The book Mastery by George Leonard has been recommended to me by many people, including chess grandmaster Maurice Ashley, swimming legend Terry Laughlin, and drumming phenom Dave Elitch.

One of my favorite sections is the epilogue, titled “The Master and the Fool,” which I’ve posted below with permission from Plume, an imprint of The Penguin Publishing Group, a division of Penguin Random House, LLC.

It explores a question: What are the keys to rapid and lifelong learning?

There are many keys, but arguably the most important is found in this five-minute read…

The Master and the Fool

“I want you to tell me how I can be a learner.”

It was not so much a query as a demand, almost a threat. He was a mountain man, with the long black hair, bold moustache and rough-hewn clothing of a nineteenth-century outlaw, one of a breed that lived illegally in the rugged hills of the Los Padres National Wilderness Area along the Big Sur coast of California—a place of buzzards and hawks, mountain lions and wild boar. Having just turned in the final proofs of a book on education (it was in the late 1960s), I had driven four hours south from San Francisco for a weekend of relaxation at Esalen Institute.

As I approached the lodge—a rustic building built at the edge of the Pacific on one of the few areas of flat land between the sea and the mountains of the Los Padres—I heard the sound of conga drums. Inside, the mountain man was sitting at one of the drums, surrounded by eight other people, each also at a drum. He was apparently giving an informal lesson to whoever cared to participate. One of the drums was unoccupied. I pulled up to the unoccupied drum and joined the others, following the instruction as well as I could. When the session ended I started to walk away, but the mountain man came after me, grasped my shoulder, and fixed me with a significant look.

“Man,” he said, “you are a learner.”

I stood there speechless. I’d never met this person, and he certainly had no idea I had just finished a book about learning. My conservative city garb had probably led him to think that I was a complete novice at the conga drum, the instrument of choice of the counterculture, and thus he must have been impressed by my seemingly rapid progress. Still, I was so pleased by his words that I didn’t inform him I’d played before. He proceeded to tell me that he was a sculptor who worked metal with an acetylene torch, and that he was badly stuck and had been for a year; he was no longer a learner. Now he wanted me, a learner in his mind, to come up to his place in the Los Padres, look at his work, and tell him how he could be a learner. He was leaving right away and I could follow him in my car if I wished.

The invitation baffled me, but I realized it was a rare opportunity to visit the forbidden haunts of one of the legendary mountain men of Big Sur, so I immediately accepted. I followed his battered sedan up a steep and tortuous dirt road, then across a mountain meadow to a driveway that was nothing more than two tire tracks through a forest of live oak, madrone, and bay trees. For what seemed a long time, the car lurched and labored steeply upward, coming at last to a clearing near the top of the coast range. In the clearing stood several wooden structures: a two-room cabin, a tool shed, a crude studio for metal sculpture, and something that might have been a chicken or rabbit coop. At one point during my visit, I spotted a slim young woman with flowing blonde hair and a long dress standing like a ghost near the edge of the clearing. He never mentioned her.

The mountain man showed me into a sturdily built cabin with a large front window looking 4,000 feet down to the Pacific, now shining like a sheet of metal in the late afternoon sun. We sat and made disjointed conversation for a while. I found myself somewhat disoriented. But for the presence of several conga drums, we might have been sitting in an early nineteenth-century pioneer’s cabin. It was all like a dream: the unlikely invitation, the rugged drive, the mysterious woman, the expansive gleam of the ocean through the trees.

When the mountain man announced that we would now go and look at his work so that I could tell him how to be a learner, I dumbly followed him out, having no idea of what I could possibly say that would be of any use to him. He walked me through his sculpture chronologically, showing me the point at which he had lost his creative spark, had stopped being a learner. When he finished, he fixed me with his eyes, and repeated his question one more time.

‘Tell me. How can I be a learner?”

My mind went absolutely blank, and I heard myself saying, “It’s simple. To be a learner, you’ve got to be willing to be a fool.”

The mountain man nodded thoughtfully and said “thanks.” There were a few more words, after which I got into my car and went back down the mountain. Several years were to pass before I considered the possibility that my answer was anything more than a part of one of those slightly bizarre, easily forgotten sixties episodes. Still, the time did come when ideas from other places—all sorts of ideas—began to coalesce around my careless words of advice, and I began to see more than a casual relationship between learning and the willingness to be foolish, between the master and the fool. By fool, to be clear, I don’t mean a stupid, unthinking person, but one with the spirit of the medieval fool, the court jester, the carefree fool in the tarot deck who bears the awesome number zero, signifying the fertile void from which all creation springs, the state of emptiness that allows new things to come into being.

The theme of emptiness as a precondition to significant learning shows up in the familiar tale of the wise man who comes to the Zen master, haughty in his great wisdom, asking how he can become even wiser. The master simply pours tea into the wise man’s cup and keeps pouring until the cup runs over and spills all over the wise man, letting him know without words that if one’s cup is already full there is no space in it for anything new. Then there is the question of why young people sometimes learn new things faster than old people; why my teenage daughters, for example, learned the new dances when I didn’t. Was it just because they were willing to let themselves be foolish and I was not?

Or you might take the case of an eighteen-month-old infant learning to talk. Imagine the father leaning over the crib in which his baby son is engaging in what the behaviorist B. F. Skinner calls the free operant; that is, he’s simply babbling various nonsense sounds. Out of this babble comes the syllable da. What happens? Father smiles broadly, jumps up and down with joy, and shouts, “Did you hear that? My son said ‘daddy.’” Of course, he didn’t say “daddy.” Still, nothing is much more rewarding to an eighteen-month-old infant than to see an adult smiling broadly and jumping up and down. So, the behaviorists confirm our common sense by telling us that the probability of the infant uttering the syllable da has now increased slightly.

The father continues to be delighted by da, but after a while his enthusiasm begins to wane. Finally, the infant happens to say, not da, but dada. Once again, father goes slightly crazy with joy, thus increasing the probability that his son will repeat the sound dada. Through such reinforcements and approximations, the toddler finally learns to say daddy quite well. To do so, remember, he not only has been allowed but has been encouraged to babble, to make “mistakes,” to engage in approximations—in short, to be a fool.

But what if this type of permission had not been granted? Let’s rerun the same scene. There’s father leaning over the crib of his eighteen-month-old son. Out of the infant’s babble comes the syllable da. This time, father looks down sternly and says, “No, son, that is wrong! The correct pronunciation is dad-dy. Now repeat after me: Dad-dy. Dad-dy. Dad-dy.”

What would happen under these circumstances? If all of the adults around an infant responded in such a manner, it’s quite possible he would never learn to talk. In any case, he would be afflicted with serious speech and psychological difficulties.

If this scenario should seem extreme, consider for a moment the learnings in life you’ve forfeited because your parents, your peers, your school, your society, have not allowed you to be playful, free, and foolish in the learning process. How many times have you failed to try something new out of fear of being thought silly? How often have you censored your spontaneity out of fear of being thought childish? Too bad. Psychologist Abraham Maslow discovered a childlike quality (he called it a “second naivete”) in people who have met an unusually high degree of their potential. Ashleigh Montagu used the term neotany (from neonate, meaning newborn) to describe geniuses such as Mozart and Einstein. What we frown at as foolish in our friends, or ourselves, we’re likely to smile at as merely eccentric in a world-renowned genius, never stopping to think that the freedom to be foolish might well be one of the keys to the genius’s success or even to something as basic as learning to talk.

When Jigoro Kano, the founder of judo, was quite old and close to death, the story goes, he called his students around him and told them he wanted to be buried in his white belt. What a touching story; how humble of the world’s highest-ranking judoist in his last days to ask for the emblem of the beginner! But Kano’s request, I eventually realized, was less humility than realism. At the moment of death, the ultimate transformation, we are all white belts. And if death makes beginners of us, so does life—again and again. In the master’s secret mirror, even at the moment of highest renown and accomplishment, there is an image of the newest student in class, eager for knowledge, willing to play the fool.

And for all who walk the path of mastery, however far that journey has progressed, Kano’s request becomes a lingering question, an ever-new challenge:

Are you willing to wear your white belt?

From Mastery by George Leonard. Published by Plume, an imprint of The Penguin Publishing Group, a division of Penguin Random House, LLC.  Copyright © 1992 by George Leonard.

George Leonard was an American writer, editor, and educator who wrote extensively about education and human potential. He served as president emeritus of the Esalen Institute, past-president of the Association for Humanistic Psychology, and co-founder of Integral Transformative Practice International.

The post The Master and the Fool appeared first on The Blog of Author Tim Ferriss.

When Dr. Rhonda Patrick returned to the podcast for a Q&A episode, I figured it would be popular. But I didn’t realize it would quickly become one of the most downloaded episodes of all-time.

As a result, many of you asked for the transcript of our conversation, so here it is. Dig in and enjoy the notes from this fascinating episode with Rhonda Patrick!

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Question (from Tim): “What new areas, experiments, discoveries or hypotheses are you most excited about these days?”

Rhonda Patrick: Thankfully, because I’ve put a certain percentage of my brain out here on the internet… much of what I’m actively interested in these days or have been interested in is actually elucidated a little bit as necessary context for some of the questions I’m going to answer here shortly.

But, Tim’s question does sort of give a nice opportunity for an overview. As a rule, the things that usually get me really revved up are ultimately optimizations that we can make to our lifestyles that might increase our functional healthspan, well-being, and lastly …cognitive and physical performance… usually through deeper understandings of biology. Healthspan, or healthy functional lifespan, is especially of interest to me. I sort of lead with that.

To me, “healthspan” is living for as long as we can while doing our best prevent deterioration from the diseases of aging.

Talking about increasing healthspan is one thing though. Often achieving it is a different thing altogether. The reason this is tricky is that the most reliable way to treat aging is to try to, instead, prevent it. A natural extension of that fact means that the earlier we start, the better shot we have of making a large cumulative effect over the course of our lives.

The specifics of how to best mitigate the damaging effects of aging, specifically, is subject to a little bit of individual variation as a consequence of each of our little genetic idiosyncrasies, the combination of which are unique to each of us. This is an area that I’m especially interested in and that I plan to invest a bit more into intellectually in the coming months, especially the interface between nutrition and genetics, known as nutrigenomics.

The good news is there are certain rule of thumb strategies that are able to have a positive effect on health and possibly even longevity. In some cases, it might mean optimizing our diet around inclusion of specific nutrients. One of the most interesting and exciting of which, to me, right now is a compound known as sulforaphane, spelled s-u-l-f-o-r-a-p-h-a-n-e. But also other related compounds that fall into the same class of compounds broadly known as isothiocyanates, all of which, including sulforaphane, being derived from cruciferous vegetables.

What’s interesting about sulforaphane is that this compound, richly found in broccoli sprouts at 50 to 100-times what’s found in mature broccoli, is that it activates a special genetic pathway in our cells known as Nrf2 and it does so more potently than any other known naturally-occurring dietary compound. This gene, a master regulator, controls over 200 other genes… affecting whether or not they’re activated and doing work. These include genes that affect our own anti-inflammatory processes, antioxidant processes, and even the ability to inactivate potentially harmful compounds we’re exposed to on a daily basis from breathing in carcinogens like benzene from air pollution.

In a sense, we’re talking about an on-switch for some of our native stress responses. Our ability to cope with physiological stress, down to the cellular level, ultimately affects how rapidly we accumulate the damage which we often refer to as aging. But, here’s the interesting thing. The reason Nrf2, a stress-response pathway, is activated by sulforaphane is because the compound itself functions as what is know as a xenohormetic, a compound that by virtue of being actually slightly stressful to cells, elicits a biological stress response that has a cumulative effect that is otherwise a net gain in resilience that creates benefit to the organism as a whole.

This is actually somewhat unintuitive if you really think about that. We sort of have this very natural notion that because excess stress is bad, we should venture to avoid stress at all costs. It turns out though, that, in fact, perhaps as a consequence of having received stressful compounds in our diets for millions of years, things that evolved in plants as insect anti-feedants that help ward off insects, we sometimes function better for having them. They can even induce neurostress responses that boost neurotrophic factors that lead to the growth of new neurons and promote the survival of existing neurons, which may function to help make compounds like sulforaphane potentially a candidate as a mild nootropic. We’ll probably come back to that in a little bit… but the bottom-line is that If we take this same concept that stress can be beneficial, known as hormesis, and apply it to other things like exercise, fasting, heat stress, cold stress, some of the various benefits that may be had from many of these strategies similarly come about as a consequence of sometimes overlapping stress-response pathways.

This idea of hormesis and trying to improve our capacity to be resilient to environmental stress and even the stress generated as a byproduct of normal metabolism and immune function, in particular, is a very useful framework for evaluating the potential of strategies that might have promise in preventing even aging. Okay, all of that said, this is a great opportunity to jump from these sort of big picture ideas back to things of a more practical application variety. Specifically, the next question evaluates a straightforward technique that has caught my interest and also happens to be broadly applicable to almost anyone.

Brandon Beckett: Dr. Rhonda Patrick: You interviewed Dr. Valter Longo, Dr. Satchin Panda, and Dr. Ruth Patterson on time-restricted feeding and fasting. Can you summarize your best practices for “time-restricted” eating and who it might not be a good fit for?

Rhonda Patrick: Okay, this is a fun question, but before we dive right into best practices on time-restricted eating, it probably helps to know what it is for the rest of you that may be listening. Time-restricted eating, as it’s called in humans, or time-restricted feeding as it’s referred to in animal research, is this idea that by constraining our eating within a certain time window during the day ranging from only 8 hours to up to 12 hours per day, usually earlier in the day to align better with our circadian rhythm, we stand to benefit from a variety of different angles.

On the more extreme end of 8 hours you’re engaging in a slightly more extreme type of time-restricted eating which is more well-known in the fitness world in particular as 16:8 intermittent fasting. Simply maintaining a slightly more conservative time window than you usually might has started to show advantages as well, potentially functioning as a lifestyle intervention that may be able to protect people from obesity, metabolic related disease and more at a population level. For example, even an 11-hour eating window has been associated in one study with a reduced risk of breast cancer and potential recurrence by as much as 36% in women. We’ll get back to what the research, both mouse and human, says about the duration of the time windows involved, but first let’s talk a little about this circadian aspect.

When healthy adults eat meals that are identical in terms of both their macronutrient and caloric content at breakfast, lunch, or dinner, the postprandial glucose increase is lowest after breakfast and highest after dinner even though the meals were 100% identical. This is just one example that suggests metabolism changes throughout the day. We also know that in humans metabolic genes are more active during the day and less active at night. The underlying reason for this is because humans are diurnal creatures which means we conduct most of our activities during the day, including feeding, exercising, and working, and then resting at night.

What makes humans diurnal creatures is the presence of an internal clock in the brain referred to as the suprachiasmatic nucleus, or SCN for short. The part of this internal clock that interacts with the external cue of light, the SCN, is also referred to as the master oscillator. But light isn’t actually the only external cue we have, we also have food influencing what are known as peripheral oscillators that occur in peripheral tissues such as the liver and influence metabolism. Whereas light is the major cue for circadian rhythm, timing of food intake regulates circadian rhythm in peripheral tissues as well. This fact sort of helps to explain why time-restricted eating as it’s defined by Dr. Panda’s work and that of others begins with the eating period with the very first bite or drink of ANYTHING non-water, because even compounds that exist in black coffee such as caffeine, can be reasonably expected to produce metabolic effects that influence these peripheral oscillators, including activity in the liver.

Everything from making neurotransmitters, to insulin, to glucose transport inside of cells, to oxidizing fatty acids, to repairing damage is on a 24-hour cycle clock that is influenced by these external cues involving metabolism.

To sort of illustrate the importance of circadian rhythm: these clocks regulate thousands and thousands of genes which is somewhere in the neighborhood of around 10 to 15% of the expressed human genome, which means that our basic metabolic physiology is meant to be tuned to behave differently depending on the time of day that is. Even the bacteria that we harbor in our guts have a circadian rhythm with the species of bacteria changing according to the time of day. Some bacteria dominate during the morning and others during the evening. Unfortunately, with the invention of artificial lighting and varying work schedules it has extended people’s eating times to occur much later in the evening and this can have very negative consequences.

Eating late at night also may “reset” peripheral clocks and result in misalignment of metabolism, which means when you wake up your metabolism is already at end of its cycle. So that’s the logic behind the circadian aspect which gets left out of some of the intermittent fasting philosophies that are popular and explains why time-restricted eating emphasizes an earlier eating window and includes non-caloric xenobiotics as a breaking of the fast, something I’ve learned is a specific point of contention for people.

Okay, but shifting away from the xenobiotics and circadian aspects to talk more about the time window itself: animals that have been limited to a 9-12-hour feeding window in which they can eat but otherwise allowing them to eat the same amount of calories that they normally would, they have shown that they can attain some pretty amazing benefits, including:

• decreased fat mass
• increased lean muscle mass
• improved glucose tolerance
• improved lipid profile
• reduced inflammation
• higher mitochondrial volume
• protection from mild-age related fatty liver
• protection from obesity
• generally favorable improvements in gene expression
• Increased production of ketone bodies, which is interesting for another reason we’ll get back to in a minute Time-restricted eating also has a growing body of research in humans.

Recent studies suggest that…

• Eating within an 11-hour window was associated with a decreased breast cancer risk and reduction in recurrence by as much as 36%.
• Earlier meal timing associates with improved effectiveness of weight-loss therapy in overweight and obese patients.
• For each 3-hour increase in nighttime fasting duration was linked to a 20% lower odds of elevated glycated hemoglobin (HbA1C), which is a more long-term marker of blood glucose levels.
• For each 10% increase in the proportion of calories consumed after 5pm there was a 3% increase in the inflammatory biomarker c-reactive protein otherwise known as CRP.
• Eating one additional meal during the day (instead of the evening) was associated with an 8% decrease in CRP.
• Eating within a 12-hour window improved sleep and increased weight loss in normal weight people.

As a rule of thumb, anything that has the potential to mitigate chronic systemic inflammation is something I personally consider worth trying to dial in since suppression of inflammation is thought to be one of the most important predictors of successful longevity that increases in importance with advancing age and also influences risk of cancer and even potentially mental health. So putting aside the potential to have better glucose control or protect myself from obesity without actually changing the composition of my diet, reducing systemic inflammation has a lot of appeal to me.

Now that we are all on the same page in terms of what some of the research shows on the benefits of time-restricted eating, I would like to go back and address Brandon’s question about what my best practices are surrounding time-restricted eating. How you choose to implement some of this information is ultimately going to be dictated by life circumstances that include practical realities surrounding work schedule and probably a million other things. The flexibility of my schedule, however, has made implementing time-restricted eating admittedly a bit easier. Unless I have a social reason that forces me to eat later in the day, I usually start my clocks as soon as I wake up. Thus, I don’t concern myself a whole lot about what counts as breaking the fast and what doesn’t and go by the strictest of definitions: if it’s not water, it breaks the fast… unless it’s just brushing my teeth. I don’t count that.

I wake up at 8 am and have my first sip of coffee at 8:15 then I make a note to myself or I set an alarm on my phone to go off 1.5 hours before the clock ends, which is usually around 6:15 pm since I aim for a 10-hour eating window and and 14-hour night time fasting window. When I’m feeling especially motivated I eat within an 8 or 9-hour time window and fast for 15-16 hours during the night, which means if I have my first sip of coffee at 8:15 am then I stop eating by either 4:15 or 5:15 pm.

I follow the same procedure on days I sleep in, even though some animal research shows that this pattern has benefits even if you cheat on the weekend. Now, the reason why I choose a 10-hour window is because it’s a sufficiently tight window of time to likely confer some of the advantages of time-restricted eating without being unduly burdensome. Personal compliance here being the issue. Stretching for the 9-hour or even 8-hour window, however, can be also interesting and may appeal to some. Some animal research has shown a certain aerobic endurance benefit for time-restricted feeding in this 9-hour range but not for shorter fasts. And, if you think about it, mice that only feed for 9-hour periods are fasting the other 15 hours.

It takes around 10-12 hours for liver glycogen stores to be depleted which is then followed by fatty acids being liberated from adipose tissue…these fatty acids then are transported to the liver where they are converted into ketone bodies like beta-hydroxybutyrate, which are then transported to a wide-variety of tissues such as the muscle and used for energy. So it sort of makes sense that eating within a 9-hour window and fasting for 15 hours overnight may lead to endurance enhancements if we’ve managed to kick off a little more ketone production the evening before a run. Anecdotally I’ve observed that personally I feel an improvement in endurance ranging from slight to pretty significant in my morning runs when I’ve tried a little bit harder to eat strictly within just 8 or 9 hours. As a closing thought, I think there’s still a lot of room for more emerging research in this area to teach us things that may be important. Questions like:

• What influence later day endurance or weight training has at mitigating the deleterious effects of other sub-optimal parameters like a later-in-the-day eating window?
• How large the effect of xenobiotics like caffeine in black coffee is compared to potentially more important factor like just keeping an otherwise tighter time window with a slightly looser definition of what is considered eating?

If you’d like to see interesting questions answered about time-restricted eating, you can actually participate in a mobile app-powered, distributed clinical trial by heading over to Dr. Satchin Panda’s lab website, which can be found at mycircadianclock.org.

Available for iPhone and Android. Basically, you commit to a baseline and then one of the patterns of time-restricted eating and then proceed to submit timestamped pictures of your food over the course of 12 weeks.

Of course, I’d also be remiss if I didn’t mention a that mutual friend and someone that has repeatedly been on the Tim Ferriss show, Kevin Rose, has developed a cool mobile app to help keep track of intermittent fasting and time-restricted eating windows. You can also check that out if you’re an iPhone user, it’s in the app store under the name “Zero”… as in the number of calories you consume while fasting.

To sort of finish off this question, as for who time-restricted feeding may not be a good fit for, well, I’m not sure! As an intervention I believe it actually is broadly applicable, however, I’m 100% certain that there there is someone somewhere for which a unique medical condition may make time-restricted eating inappropriate… especially if you expand the definition of time-restricted eating to mean long, multi-day fasts which are the subject of Dr. Valter Longo’s research in particular. Definitely check in with a physician, particularly if you’re going to do prolonged fasting or if you’re thinking of trying out time-restricted eating but may have a medical condition that for some reason might somehow make it unsafe. It is far better to be safe than to be sorry.

Jasky Singh: For all those that don’t understand the benefits of fasting. How does doing a fast differ from say eating a diet LCHF that puts you into ketosis? And what key metrics (blood tests etc) should someone look at to know it is benefiting you?

Rhonda Patrick: Very interesting question, because, as implied by the question, there are at least a few similarities between a LCHF diet and fasting, but there are also, obviously, some key differences. Probably the main similarity between the two is that metabolism shifts from using glucose as a major source of energy to primarily oxidation of fatty acids and ketone bodies as energy. When it comes to fasting there are a few things that really differentiate it from a low-carb-high fat diet.

One of the major benefits of fasting, particularly prolonged fasting, which is around 4-5 days in humans that is not found on a low-carb, high-fat diet is a dramatic increase in autophagy and apoptosis followed by a massive boost in stem cell production. Autophagy is a genetic program that is very important: it clears away damaged cells to use for energy, while apoptosis is a genetic program that causes damaged cells to self-destruct. Both of these processes prevent damaged cells from becoming cancer cells. When we clear away damaged cells this also means those cells are less likely to become senescent, which is what can happen when too much damage accumulates. A senescent cell is technically a living cell but it is not functioning in a way that is consistent with maintaining the overall health of an organ, in fact, quite the opposite. Senescent cells can accelerate the aging of nearby cells and promote tumor growth by secreting pro-inflammatory molecules and other factors.

Senescent cells are bad news and as we age they are everywhere from our livers to our hearts to our brains and they accelerate the aging process. It has been shown that mice, when given a compound that increases the clearance of senescent cells, it actually extends their average lifespan by 20 percent! Another way that fasting really shines particularly prolonged fasting is that prolonged fasting has a very robust effect on increasing stem cell numbers.

The regenerative power of tissues and organs declines with age. It is the stem cells that provide this regenerative power and because stem cell numbers decline with age so does organ function which means anything that can counter that is a win! Fasting also causes cells to clear away damaged mitochondria and recycles their defective components for energy, called mitophagy followed by a concomitant generation of new mitochondria (called mitochondrial biogenesis). This is really a great thing because mitochondria accumulate damage with age (just as cells do) and this can accelerate the aging process.

So not only does fasting clear away old, damaged mitochondria, it also generates new young healthy mitochondria to replace the damaged ones. There has been some evidence suggesting a low-carb, high fat diet may modestly increase mitochondrial biogenesis but not mitophagy. Another thing fasting does is it increases the levels of something called nicotinamide adenine dinucleotide (or NAD+ which I will just refer to as NAD). NAD levels always increase during a fasted state and decrease during the fed state (no matter what food type). NAD is a very important cofactor for many metabolic enzymes, which just means you need it for these enzymes to work properly.

Your mitochondria need NAD to produce energy from glucose or fatty acids. Any time there is chronic inflammation or DNA damage occurring, this sucks up the NAD and so the mitochondria suffer. Also, NAD levels decrease in multiple tissues with aging. There are several different compounds which are various forms of vitamin B3 that dramatically increase NAD levels and have been shown to delay aging in multiple tissues in mice. Yet another difference between fasting and a low-carb, high fat diet is that fasting activates many repair processes including repair of damaged DNA, damaged cells, damaged mitochondria, and damaged proteins.

You must be in a fasted state to repair damage which is why most repair processes occur during sleep because that is when most people are in a fasted state. Fasting improves blood sugar, insulin sensitivity, and blood lipids and improves inflammatory markers, including C-reactive protein and tumor necrosis factor-alpha (TNF-α), and improves adiponectin, leptin, and brain-derived neurotrophic factor in humans. A low-carb, high fat diet has also been shown to improve blood glucose and insulin levels and reduce inflammation but not consistently and may be highly variable depending on the individual which is likely due to the fact that the way our bodies respond to food is also complicated by genetics.

We have 8 variations in our genes that make them operate a little differently from similar versions in other members of the human population. These variations are known as genetic polymorphisms. One of the best examples I have seen yet demonstrating the immense variability in how people respond to the same foods was a publication that came out in 2015 in the Journal Cell. The study looked at the blood glucose responses of over 800 different people to various foods including fat. Without getting into all of the details of this study what is important to the topic of this discussion is that while most people had a low glucose response to dietary fat some people had a high glucose response.

There have been a few important gene polymorphisms that have been identified to play a role in a context of a high-fat diet such as FTO, PPAR-alpha, PPAR-gamma and APOE4. PPAR-alpha is one of the most important genes that I’ll mention because it plays a very important role in the process of ketogenesis. Activation of PPAR-alpha promotes uptake, utilization, and catabolism of fatty acids by activating genes involved in fatty acid transport, fatty binding and activation, and fatty acid oxidation. There is a polymorphism in this gene that has been associated with lower PPAR-alpha activity and a 2-fold higher risk of type 2 diabetes, increased levels of triglycerides, increased total cholesterol, increased LDL cholesterol, and especially important, increased small-dense LDL particles in the context of high saturated fat intake and low polyunsaturated fat intake. Obviously measuring these blood biomarkers will help illuminate whether any type of diet works for you.

There are also a variety of resources on the web that can help you take your raw genetic data from services like 23andMe and find out whether you have some of these polymorphisms. I similarly offer some resources for this on my website foundmyfitness.com for this purpose. In terms of biomarkers, things I would monitor, particularly if I were doing a ketogenic diet might include biomarkers for lipid and glucose metabolism, such as LDL cholesterol, small dense LDL particles, total cholesterol, triglycerides, glycated haemoglobin (HbA1c). You can also measure your fasting blood glucose levels and ketone levels at home using something like precision xtra (which I use and find to be mostly reliable).

I also like to be aware of any inflammatory biomarkers I can get my hands on, there’s some common measurements like high sensitivity CRP and also IL-6 and TNF-alpha. For those people experimenting with a strict ketogenic diet for greater than 6 months it may be wise to measure thyroid function by doing a full thyroid panel. There was a recent publication where a ketogenic diet for 9 months caused thyroid dysfunction in children with epilepsy. This may not be something to worry about in everyone but it does not hurt to be cautious.

For autophagy-related and stem cell related biomarkers, there are some used in research that you can’t really get ahold of for self-monitoring purposes. For autophagy, LC3-II and for stem cell renewal lin-CD184+CD45- cells. Okay, one quick closing point to sort of finish this section off. It’s important when we talk about fasting that we make clear distinctions between the various duration of fasts we’re talking about. If we discuss prolonged fasting, as I have done a lot of in answering this question, that means we are talking about water fasting on the order of 4 to 5 days. However, in mouse research, this level of fasting is actually achieved in 2-3 days. This has lead to some confusion, because people often attribute the so-called benefits of prolonged fasting to shorter intervals that are a bit more manageable because they might have ran across this rodent research.

The fact is that we may see some of the same benefits such as autophagy even with shorter fasts, but on an order of magnitude greater with prolonged fasts. Also, with a prolonged fast we see entire organ systems can shrink and then experience renewal during the re-feeding period. So, it should be pretty clear we’re actually talking about a whole different level of cellular clean-up that can occur, which is above and beyond what we get in shorter fasts. There’s still a lot of research going on to better tease out the differences between shorter, let’s say 2 day fasts, and fasts that meet the definition of being a “prolonged fast.”

I’m optimistic that evidence will continue to merge that even shorter duration fasts, are still beneficial. That said, as Tim likes to say, I’m not a medical doctor and don’t play one on the internet. If you’re thinking about giving prolonged fasting a shot, make sure to follow the prudent podcast listener’s rule and run it by an actual physician. There is also an emerging body of literature surrounding a fasting-mimicking diet that lasts 5 days instead of 4 and can be prescribed by a doctor via a packaged meal plan, if having that structure is helpful.

Jeff Norton: Rhonda, can you please share your thoughts on the “minimum effective dose” for sauna benefits: session time, temperature, and frequency. From this “minimum effective dose,” what types of changes/benefits can someone expect?

Rhonda Patrick: I’m going to start with the benefits since, as a point of logical progression, it’s helpful to establish what the science says about benefits before we talk about how to dose it. The good news is, I’ve actually partly done a pretty good job of talking about some potential benefits for sauna use in a guest post that’s featured on Tim’s blog entitled: Are Saunas the Next Big Performance-Enhancing “Drug?”

It’s possible Jeff’s already seen that, but, for the rest of you, make sure to check it out. Since that initial blog post, however, some pretty cool research has come out related to sauna use and it touches on areas that I spend some time thinking about: longevity and also Alzheimer’s disease.With this question I’m going to start with the benefits since, as a point of logical progression, it’s helpful to establish what the science says about benefits before we talk about how to dose it.

So humor me for a minute while we talk about that and then I’ll come back to Jeff’s question surrounding what the minimum effective dose might be with respect to temperature, sauna session time, and frequency to elicit some effects that might be loosely characterized as ergogenic or enhancing physical performance in some respects. A study published in JAMA Internal Medicine in 2015, showed that sauna use was associated with longevity. The study recruited over 2000 middle-aged men in Finland and compared frequency of sauna use with sudden cardiac death, fatal coronary heart disease, fatal cardiovascular disease, and all-cause mortality including cancer over the course of 20 years. Heart disease is the LEADING cause of death in the United States and many other countries as well, so that should be a cue to listen up.

Here’s what the study found: that fatal cardiovascular disease was 27% lower for men who used the sauna 2 to 3 times a week and 50% lower for men who used the sauna 4 to 7 times a week compared with men who just used the sauna once per week. In addition to lowering cardiovascular-related mortality, however, the study also found that sauna use lowered all-cause mortality full stop. Using the sauna 2-3 times per week was associated with 24% lower all-cause mortality and 4-7 times per week lowered all-cause mortality by 40%.

Let’s talk about all-cause mortality… what does it mean? Does it mean using the sauna 4-7 times per week made 40% of people immortal? No, what it means is that for the individuals being studied, they had 40% less mortality than those of a similar age not being subjected to these same conditions and this reduction in mortality wasn’t strictly tied to heart disease, but instead something potentially more general. Keep in mind this study also adjusted for other parameters that may affect the data including body mass, serum cholesterol, blood pressure, smoking, alcohol consumption, type 2 diabetes, physical activity, and socioeconomic status. We’ll come back to talk more about this generalized longevity effect in a minute since it’s interesting to discuss plausible mechanisms that underlie that effect.

The effects on heart disease, however, are a little more straightforward to try to explain: some of the positive benefits of sauna use on heart health may have to do with similar benefits seen with regular physical exercise. Heart rate can increase up to 100 beats per min during moderate sauna bathing sessions and up to 150 beats per min during more intense warm sauna use. 150 beats per minute corresponds to moderate-intensity physical exercise, which as we already know, also has a positive effect on cardiovascular health.

Heat stress from sauna use also increases plasma volume and blood flow to the heart, known as stroke volume. This results in reduced cardiovascular strain so your heart has to do less work for each beat that it does to pump oxygen-rich blood to your tissues and brain. Additionally, long-term sauna use has been shown to generally improve blood pressure, endothelial function, and left ventricular function. But… crossing over from the theory to the more practical: what if improving heart health really just meant having a boost of endurance? In fact, this is exactly what’s been demonstrated.

One study demonstrated that a 30-minute sauna session two times a week for three weeks POST-workout increased the time that it took for study participants to run until exhaustion by 32% compared to baseline. If you start to think of mild adaptation to heat stress as a proxy for some of the benefits of exercise, the generalized longevity effect starts to make sense. But there may be molecular mechanisms for this as well. There’s two pathways in particular I’d like to briefly highlight: heat-shock proteins produced by our cells in response to heat stress and also another pathway known as FOXO3. Sauna use robustly activates a class of stress response proteins known as heat shock proteins, and heat shock proteins have been implicated in aging, where increased expression has been shown mechanistically in lower organisms to confer increased longevity, and, similarly, polymorphisms in human populations that increase heat shock protein production have also been shown to have an association with increased longevity.

To understand why this is the case, it is helpful to know the purpose of heat shock proteins. HSPs help all other proteins maintain their proper 3-dimensional structure in the cell which is important for each protein in order for it to be able to perform its function. If various interactions that can occur disrupt the structure of that protein, denaturing it for example, then this prevents the protein from doing its function and changing the half life of it. As I briefly mentioned earlier, damaging products get created from normal immune system function and metabolism. These damaging molecules, produced at a low level every day even in the best of circumstances but made worse by poor lifestyle choices, damage proteins and disrupt their structure. Moreover, once a protein’s structure is damaged it can then misfold, preventing degradation and can lead to the accumulation of toxic protein aggregates that can themselves damage cells as well.

Protein aggregates, something heat shock proteins specifically help prevent the accumulation of, are associated with neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease and Huntington’s disease. In fact, when you take normal mice that have been engineered to accumulate amyloid-beta plaques characteristic of Alzheimer’s, they do begin to manifest a pathology in the brain that is similar to what we might call Alzheimer’s in 12 humans, but if you engineer these same mice to over-produce one of the more well-known heat shock proteins, HSP70, it reduces the severity of this condition, including reducing the associated loss of neurons and synapses. So, if you think about it, this might suggest something interesting.

We know that heat shock proteins are produced in response to heat stress, and they seem to help prevent symptoms of Alzheimer’s in mice by reducing protein aggregation and by helping keep proteins from losing their structure in the first place. What if, by naturally increasing our heat shock protein expression, we could reduce the risk of Alzheimer’s? The same group that studied over 2000 male sauna goers found a very interesting association from the same cohort that they later published in another paper: they found that men that used the sauna 2-3 times per week had a 22% lower risk of dementia and a 20% lower risk of Alzheimer’s disease compared to men that only used the sauna one time per week. Men that used the sauna 4-7 times per week had a 66% lower risk of dementia and a 65% lower risk of Alzheimer’s disease compared to men that used the sauna once a week. Once again, just as before, this is after adjustment for age, alcohol consumption, body mass index, systolic blood pressure, smoking status, type 2 diabetes, previous myocardial infarction, resting heart rate and serum ldl cholesterol.

Now, whether or not it was the heat shock proteins may be a great idea for future research. But, as a plausible mechanism, heat shock proteins seem like a very good explanation for what’s going on there. Since we’ve also mentioned, briefly, the endurance and cardiovascular benefits of sauna use, particularly in a trial involving run-until-exhaustion aerobic activity it’s also worth mentioning that VO2 max, which is the body’s maximum capacity to transport and use oxygen during exercise, has a strong association with cognitive capability in old age, which may have something to do with brain perfusion and even the ability for blood perfusion to wash away metabolic waste products, including amyloid-beta. The other molecular pathway of interest that may help to explain some of what’s going on with this association between a type of longevity and sauna use mentioned earlier is a pathway known as the FOXO3 pathway.There is some evidence that part of the natural cellular stress response when confronted with heat is an activation of this pathway. FOXO3 is one of the big aging genes for which regular ol’ fashioned genetic variation has shown is involved in longevity: humans with a polymorphism that makes more FOXO3 have up to a 2.7-fold increased chance of living to be a centenarian and in mice, having more of their homologous version of this same gene can extend their lifespan by up to 30 percent!

As a pattern of aging, our FOXO3 activation trends downward… decreasing in expression with age., FOXO3 is a master regulator is involved in: autophagy, DNA repair, metabolism, endogenous antioxidant production, stem cell function and Immune function. Since we’ve already spent so much time navigating the especially relevant waters of HSPs, I’ll leave the discussion of FOXO3 alone for now.

Okay, so we got a little bit distracted talking about mechanism and other various odds and ends surrounding sauna use, but to return to part of the core of the question asked by Jeff, we need to address minimum effective dose. For the minimal benefits of lower cardiovascular disease mortality, lower all-cause mortality, and lower Alzheimer’s disease risk, we have to address the literature that actually observed these effects. In this case, that would be 20 minutes at 174º F (or 79º C) 2-3 times per week. Remember, however, those that used the sauna for 4-7 times a week, had an even more robust effect. This is actually a pretty great guide because we’ve got a range of effects based on dosing and a pretty large trial of 2,000 participants.

If we turn our attention to smaller studies, such as the run-until-exhaustion endurance trial we mentioned earlier, the minimum effective dose for endurance appeared to be 30 minutes in a 194 fahrenheit (90C) sauna twice a week… a dose which, by the way, produced a maximum heart rate of 140 beats per minute. This last point is especially interesting if you consider the fact that maximal heart rate might be an appealing candidate for “quantified-selfers” to track their physiological response to heat stress when other variables may differ.

Take for example the fact that not all saunas get as hot, especially the infrared ones that run cooler. It does seem reasonable to think, however, that turning the nobs on other aspects of the sauna session by making changes to the duration, for example, you can probably still elicit comparable effects. What I have not discussed yet, but mentioned in the guest post on Tim’s blog, certain studies have demonstrated some effects on muscle mass and recovery in animal and human trials. For endocrine effects in the area of growth hormone, for example , multiple studies report ranges of 20-30 minutes and around 176°F (or 80°C ) in the neighborhood of 2-3 times a week. Again, pretty similar to the larger 2000 person mortality and alzheimer’s studies mentioned earlier. Finally, molecular evidence for heat-shock protein induction seems to indicate that healthy young men and women sitting in a 163 F (73 C) sauna for 30 minutes are able to increase their heat shock protein levels including hsp72 by 49% and that the elevation in heat shock protein levels persist for 48 hours after the initial heat stress, suggesting 2-3 times per week is again a good moderate frequency to hit a threshold for some sustained effects.

So it’s pretty clear we have a few options available to us. Some more mild than others. More popular here where I live in the United States are infrared saunas, which don’t get quite as hot, often limited to about 140 degrees fahrenheit or 60 celsius. For reasons of practicality and because I believe that benefits from the sauna are primarily conferred directly by heat, I tend to prefer a hotter sauna. But it seems wholly reasonable that making other adjustments, like preceding the sauna session with light cardio, for example, might help make up for other differences. It’s hard to know for absolute certain, but I’m optimistic.

All of that said, I think it’s a good moment to make a point to give the same warning Tim gives on his blog surrounding sauna use and heat stress in general: try to exercise good judgment, if you have some sort of medical condition all bets are off even if you don’t think you have a medical condition, it’s reasonably worth checking in with a doctor before becoming some kind of mega sauna enthusiast. Heat can be no joke and it’s important that you don’t hurt yourself. Cool? Finally, there’s other so-called benefits that I’ve suggested may exist on Tim’s blog that didn’t get talked about here today. Areas where the science may be promising but maybe not quite as robust or otherwise confer itself well to talking about a minimum effective dose, including:

• The possibility that that sauna use could play a role in mood and attention by increasing norepinephrine and affecting our sensitivity to and production of beta-endorphin, giving us a sort of runner’s high… the potential of which was something that initially appealed to me when experimenting with my own personal sauna use.
• The possibility that sauna use may reduce muscle atrophy and then muscle regrowth — an effect which, while very interesting, is mostly shown in animal studies that might be hard to try to then apply back to humans So definitely go check out that post. Moving forward we can now talk about the flip side of the coin with our next question from….

Thanatos Mors: I would like to know about the interaction between heat and cold exposure and if they will cancel one another out. Example: If I do a workout and then sauna for 10-20 mins to engage the heat shock proteins to maximize the hormonal response and then proceed to take a cold shower will that cancel the benefit of the sauna and heat exposure? Also will that make the cold exposure less effective?

Rhonda Patrick: For this question, I’m going to choose to focus on discussing the question of a combining heat stress and cold stress in rapid succession rather than a discussion of the combination of either with exercise, which is sort of a different if overlapping discussion which comes up in a different question I’ll get to in a moment. So, to answer this question with our slightly narrowed parameters: I have been trying to find to find empirical evidence in the scientific literature discussing various aspects of combining heat stress and cold stress and have come up pretty dry when it comes to answering a lot of the big questions surrounding the combination of both of these modalities in rapid succession.

Frankly, it’s hard to find good information whether we’re talking about winter swimming, as is done by sauna-goers in Finland… or simply a cold shower… or, far more extreme, alternating between a sauna and an ice bath as described by Rick Rubin and Tim Ferriss during their sauna podcasting experience. One thing we can do a little bit of, however, is turn to the molecular evidence. What may surprise many of you is that both heat stress from the sauna and even cold stress are both able to activate heat shock proteins. This is because heat shock proteins respond to cellular stress in general and not exclusively heat stress. Heat, as a cellular stress, does cause a more robust activation than cold though.

Still, it’s sort of good to know that both types of thermal stress seem to positively affect heat shock protein expression which we’ve sort of established may have something to do with some of the benefits we might ascribe to sauna use. But, it’s sort of important to ask yourself what you’re trying to accomplish with the cold exposure aspect.

One of the main reasons I like to expose myself to the cold are the effects it seems to have on the brain, mood and possibly attention. One of the most likely candidates for eliciting an effect is norepinephrine, which is also the catecholamine that is actually responsible for triggering the browning of fat, making our fat more metabolically active. In fact, in terms of pathways or physiological responses to cold, the release of norepinephrine into the bloodstream, as well as in the locus coeruleus region of the brain, is one of the more profound. Guess what else increases norepinephrine release? Heat as from sauna use. So this is a second way in which both hot and cold, instead of having opposing effects where one cancels out the other, at the molecular level are nudging some of the same pathways in the same direction.

But, to elicit these overlapping stress responses, you actually have to get cold enough for that to happen. Otherwise, you’re actually just taking some of the heat burden you created on your own body and removing it. How cold is cold is the real question we have to ask here. In the case of an ice bath, I suspect the stress is almost certainly additive in nature.

The extremes of going from a 200 fahrenheit sauna to near-freezing water isn’t a walk in the park. In the case of a 30 second cold shower that isn’t sufficient to even trigger momentary discomfort, it is probably not adding stress but in fact simply removing it. This isn’t strictly a bad thing, if that’s what you’re wanting to do. That said, to give you an idea for some of the threshold temperatures involved to elicit the norepinephrine response of cold stress: studies have shown that people that immersed themselves in cold water at 40°F (4.4°C) for 20 seconds increased their norepinephrine 2 to 3-fold (200 to 300%) and this release of norepinephrine didn’t seem to be reduced with habituation to cold. Long durations of cold water exposure under more moderate temperature have a more potent effect on norepinephrine release.

For example, in another study, people that spent 1 hour in 57°F (14°C) water increased norepinephrine in their bloodstreams by 530% over baseline. As anyone who has swam in the pacific ocean knows, this is still quite cold and certainly sufficiently uncomfortable but it’s probably very possible, depending on where you live and the season, to get a shower that is similarly cold or even more cold! Something I’ve personally observed that’s sort of interesting is that after a sufficiently intense sauna session, it can be very hard to stop sweating even potentially hours after you’ve cooled down — unless you’ve had a very borderline painfully cold shower. For social reasons, at least for me personally, it can almost be a requirement.

One last quick note before we move onto our next question which shares some overlap with this one. I mentioned a moment ago that information surrounding going from hot to cold, such as combining ice baths with the sauna or even just doing the sauna and winter swimming combination as done in Finland and elsewhere, is lacking. One of the areas I’d like to see more information on is actually safety. There’s clearly a cultural history in some places of going from a hot sauna right into an icy lake, but there is at least one case study reported in the literature of a heavy smoker having a heart attack, possibly as a result of a plaque rupture caused by coronary artery spasm after doing many, many rounds of contrast immersion over several hours.

I’ve personally done ice baths interspersed with sauna use Rick Rubin style and found it to be very, very enjoyable. It seemed to help me sleep better and I definitely felt like my mood was significantly affected for even the next 24 hours. More so than either alone… so I’m hopeful we’ll see some research come out that proves the case report to be an irrelevant association and somehow demonstrating ultimate safety, but in the meantime I’m hesitant and a little cautious. For the broader audience listening now I will make the same advice I made earlier, please please be careful what you subject yourself to, especially if you have a condition that might warrant such caution. If in doubt, check with a physician before you take up a new polar plunge habit.

Rob Schlicker: Dr. Rhonda Patrick, can you explain your thoughts on how regular hyperthermic conditioning and hypothermic stress relate to muscle hypertrophy and strength training?

Rhonda Patrick: First, for our listeners since Rob is clearly in the know, let me define what hyperthermic conditioning is: hyperthermic conditioning refers to deliberately acclimating yourself to heat, either independent of or in conjunction with exercise. I typically refer to hyperthermic conditioning in the context of using the sauna because this is where the most empirical evidence is. But there are other modalities of heat exposure including hot baths, steam showers, and hot yoga… and they probably create a qualitatively similar type of heat stress that approximates sauna use on some level, depending on intensity.

There are a couple of main mechanisms that hyperthermic conditioning through using the sauna may plausibly affect muscle hypertrophy. First, is through the robust activation of heat shock proteins. I mentioned earlier how heat shock proteins play a role in preventing neurodegenerative diseases such as Alzheimer’s disease by helping proteins maintain their proper 3-dimensional structure. Not only does this have a role in preventing the aggregation of proteins but it may also plays a role in muscle hypertrophy.

Here’s why: muscle hypertrophy is ultimately the delta between protein degradation and new protein synthesis. When we train for muscle hypertrophy we often put a lot of thought into how to increase muscle protein synthesis… but if we reduce protein degradation, which is an effect heat shock proteins have, we are still increasing our net protein synthesis by increasing the difference between the amount of new synthesis of muscle protein versus the amount of degradation that is happening. This type of effect has been shown in rats where it was shown that a 30-minute heat treatment at a temperature of 106°F (41°C ) given every 48 hours over a 7 day period caused a sustained increase in heat shock proteins during that time frame… big surprise… but more importantly, this actually correlated with a whopping 30% more muscle regrowth than a control group during the seven days after immobilization. Not bad, right?

Putting aside heat shock proteins for a moment, the other way that hyperthermic conditioning through using the sauna could plausibly affect hypertrophy is by robustly increasing growth hormone. For example, two 20-minute sauna sessions at 176°F (80°C) separated by a 30-minute cooling period elevated growth hormone levels two-fold over baseline. An even more robust effect was found with men using higher sauna temperatures.

For example, two 15-minute sauna sessions at 212°F (100°C) separated by a 30-minute cooling period resulted in a five-fold increase in growth hormone. The boost in growth hormone levels is transient and only lasts a couple of hours. To understand why this might be useful, it’s helpful to understand a little more about this pathway. Many of the effects of growth hormone are mediated through another hormone known as IGF-1 or insulin-like growth factor-1. IGF-1 activates another pathway in skeletal muscle known as mTOR, which is responsible for new protein synthesis. Muscle cells require amino acids for both growth and repair so if we can also plausibly activate mTOR we’re now sort of completing the circle. With heat shock protein induction we reduce protein degradation and through these endocrine effects, actually increasing protein synthesis… by increasing net protein synthesis, we effectively increase hypertrophy.

In fact, if you sort of reverse engineer the habits of bodybuilders: IGF-1 is actually one of the major pathways most robustly activated by dietary protein intake. So the next time you’re shoveling down protein powder or essential amino acids like leucine… you can be aware that part of what you are doing in the first place is robustly activating the production and release of IGF-1 and thus mTOR. Protein (and specifically essential amino acids) are the major dietary regulators of IGF-1. IGF-1 plays a very important role in muscle growth and repair.

For example, mice that have been engineered to express high levels of IGF-1 in their muscle develop a greater degree and diversity of skeletal muscle hypertrophy. Similar experiments have also shown some promise in combating age-related muscle atrophy, especially the kind found in a mouse model of duchenne muscular dystrophy. I’ve previously talked a little bit about a so-called trade-off when it comes to IGF-1… I’m not going to dive into that yet. We’ll talk about that more in some of the diet-related questions, but suffice to say that I think in the context of sufficient physical activity this so-called trade off may become a bit less important. That said, let’s take a minute to talk about TIMING of sauna use in particular and then we can talk about cold showers or ice baths.

I like to sauna after a workout. First, there’s entirely practical reasons: doing an intense sauna session prior to working out can increase exhaustion a little bit too quickly, making it very hard to finish a workout. Studies have shown that to be the case empirically too, but it’s also intuitively obvious. Adding on top of that, the social aspect of potentially drenching gym equipment with your profuse sweating makes it more sensible to sauna afterward. But, if it were not for those reasons in particular, there’s also just the issue of when we most want a boost of IGF-1. To answer that question, it’s helpful to be aware of a mechanism involved in hypertrophy. One which, in fact, becomes especially relevant when we talk about the effect of cold stress after training in a moment. That mechanism is inflammation.

When we train, as a result of the mechanical work being done we produce metabolic byproducts like reactive oxygen species and we also activate inflammatory cytokines. This is actually necessary to activate genetic pathways that contribute to creating more mitochondria (mitochondrial biogenesis as we talked about) and also plays a role in muscle hypertrophy. In fact, it is inflammation that recruits immune cells such as macrophages to skeletal muscle in order to produce IGF-1 that helps induce acute muscle repair. There has been some experimental evidence that indicates that these specific immune cells are also likely involved in satellite cell migration, which is a type of muscle stem cell that serve as precursors to actual muscle cells and for which the raw number of are actually associated very closely with the amount of actual hypertrophy that occurs as a result of strength training.

As we can see, inflammation seems to play a pretty important role in the benefits of actual training. And this inflammation, as measured by an inflammatory cytokine known as IL-6, actually peaks during training and also right after but then falls by 50% of its initial peak after the first hour. So, in a way, if you’re going to try to pick a time to increase growth hormone or IGF-1 activity, it makes sense to probably do so in close proximity to when it’s actually peaking. In my mind, I interpret this to be pretty much immediately on the tail end of my work out. But this peak of inflammation potentiating IGF-1 synthesis that then goes on to play a role in hypertrophy may become especially relevant if we talk about the mixed research surrounding cold stress, such as ice baths or cryotherapy, especially when used in conjunction with working out.

Whereas the sauna seems to be just fine and maybe even beneficial to do immediately after exercise, cold water immersion and possibly other modalities of cold exposure are a bit more nuanced in the context of strength conditioning. Specifically, studies have shown mixed results when paired with strength training. For example, one 2015 study in the Journal of Physiology showed that a 10 minute cold-water immersion immediately following heavy leg training dramatically decreased hypertrophy by almost 2/3rds at 10-weeks follow-up. The active cold treatment group also had a reduction in muscle strength and showed smaller increases in type II muscle fibers which are required for very short-duration, high-intensity bursts of power and all of this coincided with a reduction in biomarkers that are usually associated with hypertrophy, including the activation of satellite cells. That’s pretty alarming, if you think about it.

But maybe it shouldn’t be too surprising. Let’s unpack this anti-hypertrophy effect of cold a little bit. One of the reasons ice baths became popular in professional sports, for example, is because cold exposure blunts inflammation and, specifically, it’s been shown to dramatically decrease the production of what are known as E2 series prostaglandins, which are one of the factors that have specifically been shown to induce the synthesis of IGF-1 by macrophages, that growth factor mentioned earlier because it’s important for hypertrophy. In addition to this, cold exposure also causes vasoconstriction which may also acutely prevent immune cells from migrating to places like muscle tissue. Knowing how to reduce inflammation when needed is good, but only if we account for the various downstream effects that this may have.

This is not the only study (although it is the best one) that has showed that cold water immersion done immediately after strength training may blunt some hypertrophy. There are others but again all of those studies used cold exposure sometime immediately after strength training. So that leaves us with a few open questions, but the most important one is this: would we still have seen the blunted or reduced hypertrophy effects if cold-water immersion was done at literally any point other than immediately after strength training.

I don’t think that, based on the current literature, that we can state this 100% certainty at this stage, but if we take into account this potentially inflammatory-mediated anabolic window that seems to peak especially in the first hour post exercise, then it might help explain some of the mixed results we see surrounding the use of cold stress with various forms of strength training. Specifically, one 2013 study from the Scandinavian Journal of Medicine & Science in Sports showed the almost exact opposite effect — this study showed that whole body cryotherapy for a couple minutes done 1 hour after squat jumps and leg curls was actually associated with performance enhancements which included improvements in power at the start of the squat jump, and squat jump work-up and improved pain measures up to 72 hours after the cold treatment.

This isn’t the only study showing an enhancement in performance from cold either. We see in a study published in PloS one in 2011 that Elite runners that engaged in whole body cryotherapy 1 hour, 24 hours, or 48 hours after doing some hill sprinting ultimately had a 20% increase in speed and power up to two days later. What’s interesting about the cold is that it may also be conducive to enhancing endurance-related activities in particular. Like fat, whereby cold can increase the number of mitochondria in white adipose tissue in order to transdifferentiate it into brown fat, a form of fat that is metabolically active, protective against obesity, and naturally declines as we age muscle also experiences an increase in mitochondria as a consequence of cold exposure. These mitochondria are the energy producing machinery of our muscle cells. The density or number of them on a per cell basis, affects our aerobic capacity. Mitochondria are what give us the ability to use oxygen in order to produce cellular energy, and if we have more of them, it can be said we may be more adapted to aerobic activity. Mitochondria are what give us the ability to use oxygen in order to produce cellular energy, and if we have more of them, it can be said we may be more adapted to aerobic activity.

OKAY! All of that said… to sort of get to the point and to summarize my thoughts on sauna and cold-water immersion or cryotherapy in the context of exercise, I think that:

• sauna use after exercise seems to be a good time to do it, generally
• we need more research but cryotherapy or cold-water immersion may be better to hold out on until at least an hour after training
• And, finally, the effects of and appropriateness of cold-related activities on performance may be, for a few different reasons, very dependent on the actual activity we are actively training for.

Kevin Noonan-Fick: What are your thoughts on nootropic/cognitive-enhancing supplements and do you take any yourself? Ie. choline, lion’s mane mushroom, etc.

Rhonda Patrick: I do take some things that might qualify as nootropics. I am, however, very cautious in what I choose to experiment with, at least over the long-term. My biggest concern comes down to one simple fact: when we introduce outside compounds that too directly perturb complex biological systems, we open up the possibility of triggering feedback systems that can result in unintended consequences such as receptor down-regulation. What do I mean by that? For example, let’s say we take pharmacological drugs that inhibit transporters that re-uptake and metabolize neurotransmitters. This causes these neurotransmitters to then stay around in the synapse for a longer period of time, exerting more biological effects.

This might be perceived as a good thing. BUT the trade-off is this causes the receptors that bind to these various neurotransmitters, which is how they exert their biological effect to decrease in number. This is what we call downregulation. So what happens when you do not take that same drug for a few days? Your baseline level has changed so that, in the absence of those drugs that inhibit reuptake, your neurotransmitters will not by themselves exert the same effect that they might have before your pharmacological intervention due to changes in receptor density or the number of receptors we have for the neurotransmitter to interact with.

This is one reason why I prefer to, instead, focus primarily in the realm of nutrition since it usually works a little bit more indirectly by providing compounds that are found in and needed by the body, and, in the context of this conversation, the brain.

When compounds are identified in food (such as xenohormetic compounds) we have a better chance of achieving benefit without deleterious effects because of the fact that we’ve likely evolved alongside the presence of that compound. If the compound or compounds don’t have that same history it takes a little bit more scrutiny before we can be sure that there isn’t some sort of significant side effect we just haven’t taken the time to observe yet. Maybe we won’t even know about it for years. For this reason, I tend to stay away from compounds that are inhibitors of enzymes in the brain (which I know are ubiquitously found in many nootropic stacks) even though they likely work in the short term, we don’t have good evidence what if any long-term effects may occur.

With that said there are some nootropics that I have tried. Choline is one of them. Choline can either be used to make acetylcholine (acetylcholine is a neurotransmitter that connects neurons together) or phosphatidylcholine or methyl groups. In humans, choline supplements increase choline plasma levels within 1 hour after ingestion and with brain concentrations peaking around 2 hours until at least up to 3 hours after ingestion. Cholines effects on the cholinergic peripheral system peaks between 1 and 2 hours after ingestion. Choline itself (without forming acetylcholine) acts on a subtype of nicotinic receptors (alpha 7 nicotinic receptor) that is involved in long-term memory. Acetylcholine also acts on all the nicotinic receptors. Choline does not cause desensitization of this receptor like other agonists do (like nicotine). In fact, supplementing with choline increases this receptor subtype.

Certain neurodegenerative disorders like AD are linked to decreased acetylcholine so there has been a lot of interest in investigating whether certain choline supplements and other compounds that affect the cholinergic system can improve cognition and memory in people with cognitive decline, dementia, AD. There are different forms of choline supplements but I think the choline that is complexed to phosphatidylcholine is the best because it is 12 times more bioavailable and gets into the brain faster. There is a decent body of evidence that has looked at the effects of various types of choline on brain function.

L-Alpha glycerylphosphorylcholine (more commonly known as alpha GPC) is a naturally occurring form of choline and is thought to be a form of choline that crosses the BBB quickly. I came across this compound when doing a literature review of various phospholipids and their role in Alzheimer’s disease. The study that put it on the map was an old study published in 2003 that demonstrated 1200 mg/day split up over 3 daily doses was able to enhance cognitive performance and slow cognitive decline in Alzheimer’s patients. The problem is this study was done in Mexico city 13 years ago. Since then, another study in 2011 attempted to repeat this but in addition to alpha-GPC about ten other compounds were given. It improved cognitive function but it’s impossible to pinpoint this effect specifically to alpha-GPC. Finally, there is yet another interesting study that showed that alpha-GPC along with other natural compounds reduced reaction times and prevented mental exhaustion after intense exercise, an effect that is likely due to the replenishment of choline that is actually temporarily reduced in the brain as a consequence of endurance exercise (such as long runs).

I have personally tried alpha-GPC before at a dose of around 600 mg per day… an amount that is half the dose that was given to the demented patients in Mexico city and noticed that it did seem to help improve my focus and attention. You should always leave a little room for the possibility that it may be placebo effect, but since it’s my anecdote… a smaller dose of 300mg didn’t really seem to have as much of an effect. In general, I do not take alpha-GPC everyday. I’ll take it on rare occasions when I’m doing a lot of writing or there’s some sort of event I’m speaking at. There is another popular form of choline called CDP-Choline which is an intermediate produced during the generation of phosphatidylcholine from choline. There are a couple human studies looking at the effects of CDP-choline in the cognitive function of healthy young or middle-aged adults… usually in the range of around 1000 mg per day. The only benefits were seen in young adults that had poor processing speed and verbal memory at baseline. Strangely, those individuals that performed well at baseline actually had impaired performance after supplementation which may have to due with genetic variance in the receptor density, etc. which just sort of goes to show how complicated neurobiology is and how even seemingly straightforward relationships can turn out to not be so straightforward.

I have personally tried CDP-Choline and never really noticed any enhancing effect like I seemed to with alpha GPC. The other nootropic I have tried and use semi-frequently is Yamabushitake extract which is also more commonly known as……. Lion’s mane! The main active compound in lion’s mane is hericenones (found in the fruit body of the mushroom). This compound is capable of activating nerve growth factor (NGF). NGF is essential for the growth of new neurons and survival of existing neurons. NGF acts on cholinergic neurons in the central nervous system. What got me interested in lion’s mane as a nootropic was a Japanese study which was a double blind, placebo controlled trial where elderly men with cognitive decline were given 1 gram doses of 96% Yamabushitake dry powder three times a day for 16 weeks for a total of 3 grams per day. Those individuals given the lion’s manes extract but not placebo had a significant improvement in cognitive function at weeks 8, 12 and 16 of the trial. But the cognitive effect wore off 4 weeks after discontinuing the treatment suggesting that continuous intake was necessary to maintain the effect, at least in cognitively impaired older adults.

Lately, I do use lion’s mane extract pretty regularly from Four Sigmatic. They come in packets and each packet contain 1.5 grams of lion’s mane extract from the fruit body only (which would contain hericenones). Note: I have no affiliation with them. They sent me some free packets a couple of years ago, and I liked them so I continue to buy them. When I use them, which only again — tends to happen during periods of intense writing or creative work, I actually like to use 2 packets, a dose that is around 3 grams of lion’s mane extract and the same dose used in the clinical study I mentioned a moment ago out of Japan.

No discussion of nootropics would be complete if I didn’t at least briefly mention two hobby horses of mine: Vitamin D and omega-3. The effects of both of these are pretty far reaching and extend far, far beyond the realms of just cognition, but even if one were concerned with just cognition they would both still have special relevance. First, let’s talk vitamin D. This one is near and dear to my heart since it was my in silico work that actually identified that Vitamin D affects serotonin production, which I believe has very far reaching implications not just for adults trying to stay healthy and live optimally but also for neurodevelopmental disorders as well, where impaired serotonin production may be particularly important for early brain development when the foetus relies on the mother as its source for vitamin D. A whopping nearly 70% of people in the U.S. can be classified vitamin D insufficient and that includes pregnant women.

Returning to the main topic after that brief digression, Vitamin D is something that should be periodically monitored via blood test in order to titrate to a dose that is appropriate. I personally shoot for 40 to 60 ng/ml since there have been a few all-cause mortality studies that seem to indicate that this may be a so-called sweet spot. Because vitamin D can be toxic in the high upper ranges, doing too much can also be problematic. It’s an absolute fact that what may work for one person, especially in terms of dose, may not for another because of the individual variation involved that can affect how deficient you are, including genetic polymorphisms, weight, age, the latitude you live at, ethnicity, how much time you spend outdoors, whether you wear sunscreen and more.

I’ve personally found that the tolerable upper intake level recommended by the institute of medicine of just 4000 IU, usually taken with a vitamin K2 supplement, is actually the amount that lands me right in the middle of that target range. That said, I’m probably not even in the highest risk category for vitamin D deficiency. Next, a quick mention for omega-3.

Approximately 8% of the brain’s weight is actually omega-3. The number of studies that demonstrate optimizing intake of omega-3 has some effect on cognition or behavior are extremely diverse. Today we’ve talked a little about nerve growth factor… so just by way of example… I literally just ran across an animal study that showed that supplemental omega-3 increases nerve growth factor which increases the enzyme responsible for producing acetylcholine, it increases vascular endothelial growth factor, and brain-derived neurotrophic factor and has generally been shown to improve cognition.

Getting past all of the usual suspects on our list of nootropics here, the other nootropic that I actually take frequently is SULFORAPHANE! It’s not even usually considered a nootropic by most people but I think it has potential to be considered at least a mild nootropic for a variety of reasons. One of the the best reasons to make this argument is the fact that sulforaphane crosses the blood-brain barrier, at least in mice. This is the first criteria that a substance must meet in order for there to be a compelling argument that it somehow exerts effects on the brain — but, in addition to that, it also affects the activities of the immune system which is now known to affect the brain through a series of lymphatic vessels. this new understanding of the immune system’s ability to interact with the brain also helps to explain why manipulating levels of systemic inflammation has, in clinical trials, been shown to affect feelings of depression either inducing depression in the presence of an artificial increase in activity in the immune system by injecting things like interferons into human trial participants or reducing depression caused by this artificial increase in inflammation through the co-administration of a natural anti-inflammatory, such as eicosapentaenoic acid, better known as the omega-3 fatty acid EPA.

In addition to sulforaphane crossing the blood-brain barrier in mice, the compound has been shown in a couple of randomized, double-blinded, placebo-controlled studies in humans to have one sort of effect or another on brain and behavior. For example, treatment with sulforaphane extracted from broccoli sprouts at doses ranging from about 9 mg to about 25 mg, which is an amount that might be found in around 65 grams of fresh broccoli sprouts on the high end, was able to improve autistic behavior checklist scores by 34% and significantly improved social interaction, abnormal behavior, and verbal communication in young men with autism spectrum disorder. Similarly, some measurable effects have been shown in a small trial of people with schizophrenia.

The fact that sulforaphane is exhibiting clear effects on the brain and behavior of people, such as those with autism spectrum disorder, hints that it might continue to show promise in other areas of cognition too. This is because animal studies have really shown a diversity of very interesting effects that are really just waiting to be replicated in humans.

For example: Sulforaphane has been shown to improve spatial working memory and short term memory in mice in the context of conditions that can affect memory in a deleterious way, such as Alzheimer’s Disease. It has been shown to increase neurite outgrowth, which is how damaged neurons and synapses repair themselves after damage from traumatic brain injury. The effect of sulforaphane on a rodent model of Alzheimer’s Disease in some respects is particularly interesting, because, if we go back to our conversation a little bit earlier about the potential choline may have for mitigating some of the negative effects of this disorder, sulforaphane has also been shown to significantly reduce memory impairment that has been experimentally induced by a drug that works specifically by interfering with the effects of acetylcholine in the nervous system, a drug known as scopolamine.

Sulforaphane was, in this animal trial to which I am referring, able to improve the cholinergic system by increasing acetylcholine levels, decreasing acetylcholine esterase activity, and increasing choline acetyltransferase, which is the enzyme responsible for synthesizing acetylcholine in the hippocampus and frontal cortex. This ties in nicely with some of our discussion earlier about the potential importance of the choline system in cognition. Finally, sulforaphane has been shown to have a positive effect on mood and alleviated depressive symptoms and anxiety as effectively as the antidepressant Prozac in a mouse model of depression and I understand that there is at least one trial currently in the beginning stages looking to confirm this effect in humans as well.

If you consider the variety of brain and behavioral effects demonstrated already in humans, I’m optimistically hoping that some of the groups out there working on these questions will have something good to show for it in the future. If you’re looking to supplement sulforaphane there’s a few options available. First of all, the most confusing thing that is necessary to understand when gauging the various supplements for usefulness is that sulforaphane is made from a precursor known as glucoraphanin. Many supplements on the market are actually JUST glucoraphanin. You know this because it either says glucoraphanin or it says sulforaphane glucosinolate on the bottle, which is actually somewhat confusingly just another name for glucoraphanin. Then there are a few supplements on the market that is glucoraphanin and the enzyme needed to convert it into sulforaphane, an enzyme called myrosinase. One example of this combination is a product known as Avmacol.

Finally, there is actual stabilized sulforaphane. This includes a french product that hasn’t been introduced to the U.S. known as prostaphane. These three categories of products that I’ve mentioned have very large differences in terms of bioavailability: around 10% on average for glucoraphanin by itself, 40% for the glucoraphanin and myrosinase combination, and then around 70% for stabilized sulforaphane. The dosage range that strike me as particularly interesting because they have showed up often in clinical trials range between 30 to 60 mg of sulforaphane. These doses, however, actually make most of the supplements out there somewhat costly in my opinion. The good news is that many studies seem to be showing promise even at a lower dose and if you’re doing an n=1 experiment it may be useful to be able to get a reliable product like the ones i just mentioned.

That said, this cost factor has been a big reason for why I’ve simply taken up growing broccoli sprouts at home, which is extremely inexpensive. The main challenge being keeping a clean environment with little possibility of contamination from pathogenic bacteria, which can happen. Some estimates land fresh broccoli sprouts at a concentration of about 1 gram fresh weight to around 0.45mg of sulforaphane, but it depends on the seed quality and genetic background, the age of the sprouts, how you consume the sprouts, whether you froze them and threw them immediately into a blender which is what I do and tends to increase the amount of sulforaphane derived… or if you, instead, just chewed them up fresh, the good ole fashioned way.

The drawback to using sprouts is that the dosing becomes tricky. The fact of the matter is that I’ve found that my personal digestion is probably a more reliable source of feedback than trying to work out the dosage math. That’s kind of embarrassingly imprecise to have to admit… but it just comes down to the fact that there’s a tremendous number of variables that can influence how much sulforaphane in a given dose of broccoli sprouts and on top of that what an appropriate amount of sulforaphane to even supplement is. I’ve been known to consume up to 4 ounces of broccoli sprouts a few times per week and will likely continue for the foreseeable future. That said, there are concerns that isothiocyanates like sulforaphane may reduce iodine uptake by the thyroid gland.

While right now I don’t think the evidence is especially strong that this is a cause for great concern unless a person is iodine deficient, an uncommon deficiency, it may be prudent to exercise some degree of caution. Some of the effects from these compounds present in cruciferous vegetables and broccoli sprouts in particular are persistent for several days so one does not need necessarily take an extreme approach in order to reap some effect. Again, run it by your doctor, etc. etc.

Jez Thierry: Is one able to cold press juice broccoli sprouts and still receive high amounts of sulforaphane from ingesting in this way?

Rhonda Patrick: To answer your question, yes you should be able to also cold press broccoli sprouts and make a juice. The myrosinase enzyme (which again is needed to activate sulforaphane) begins to get activated once you “cold press” the sprouts because by cold pressing you are breaking open the plant cell walls and causing the mixing of glucoraphanin in the plant with the myrosinase enzyme stored away in specialized vacuoles. This mixing then allows sulforaphane to form. Ultimately you would not get the same dietary fiber which is why I prefer to blend things rather than juice them but the sulforaphane would be concentrated and since it may be less aversive, it seems like an interesting option.

William McGrath: Besides a low carb diet (which reduces inflammation), what is the most effective non-pharmaceutical pain reliever for arthritis/sport injury sufferers?

Rhonda Patrick: Okay, William’s question here is an interesting one. The reason for that is because of the fact that many NSAIDs, as in non-steroidal anti-inflammatory drugs, which are often used for mild pain relief are actually not especially safe to take on a daily basis. This is even more true of people that tend to take them in larger than recommended doses and it is why the FDA recently strengthened their warning that non-steroidal anti-inflammatory drugs (known as NSAIDs), with exception to aspirin, significantly increase the risk of heart attack or stroke even with short-term use. What these NSAIDs, including ibuprofen, that cause this increased risk have in common is that they all inhibit COX-2, an enzyme involved in inflammation and pain.

There are a few fundamental mechanisms that increase the risk of heart attack and stroke. First, NSAIDs that inhibit COX-2 inhibit the production of a molecule called prostacyclin which is produced by cox 2 and relaxes blood vessels and sort of “unglues” platelets. Second, they inhibit the production of nitric oxide (which is also regulated by cox 2 to some degree) and needed for proper vascular function. Finally, one more mechanism by which chronic NSAIDs use may increase heart attack risk is through a disruption mitochondrial function in heart cells. Knowing these risks sort of motivated me to put avoiding the use of NSAIDs such as ibuprofen, alieve, and naproxen, just to name a few, at a generally higher priority than it may have been previously for me on a personal level.

As an alternative to the use of NSAIDs, however, I’ve found curcumin is actually very helpful. Curcumin is sort of an interesting compound. It exhibits a pretty diverse array of potentially beneficial properties but as a xenobiotic that the body actively makes an effort to get rid of, its activity can be limited unless care is taken to try to make it more bioavailable. There’s a few different formulations that attempt to do that, but the one I’ve found the most interesting is a formulation known as meriva which has been shown to exhibit certain pain-relieving properties.

Meriva, a form which is available from a few well-known brands, consists of a phospholipid complex with 20% curcumin dispersed throughout the phospholipid. This helps to get the curcumin past the stomach lining and from being cleared by enzymes in the liver too rapidly. A few clinical trials have looked into the effects of meriva on pain and inflammation. For example, runners that were given 1 g of meriva twice a day found that it reduced delayed onset muscle soreness about 2-fold and caused a 60% decrease in markers of muscle damage and inflammation, specifically IL-8 and C Reactive Protein, after running until exhaustion downhill. There have also been a couple of other clinical studies published looking at the efficacy of 1 g of meriva per day in reducing symptoms of osteoarthritis and increasing mobility.

After 3 months of treatment, people with osteoarthritis and joint pain had a 4-fold increase in mobility, CRP (decreased by 67%, and they had a around a 58% reduction in arthritis symptoms including pain. There was a similar study that included a longer follow-up (8 months) and found similar increases in mobility and reductions in inflammation and pain. What’s interesting is that meriva has also been compared directly to common pain relievers in terms of ability to give pain relief in a small clinical study, which found that people taking 2 grams of a Meriva per day experienced a pain relief equivalent to 1 gram of acetaminophen or tylenol… an amount, by the way, which has been associated with liver damage in conjunction with long-term use.

Another study also found that 2 g per day of meriva for 6 weeks was equivalent to around 800 mg per day of ibuprofen for pain relief. The study found that the analgesic effect of curcumin lasted for approximately 4 hours, and a second dose, administered 6–12 hours after the first dose, was necessary for controlling pain. On the whole, curcumin is also a surprisingly safe compound. One study out of Japan published in 2011 in the Journal of Cancer Chemotherapy and Pharmacology showed that curcumin in amounts as high as even 8 grams per day for up to 14 days at a time was safe and tolerable. These were cancer patients and this wasn’t a meriva formulation. However, seeing how well tolerated very high clinical doses are generally… for occasional pain relief I tend to be pretty liberal with popping a few grams of curcumin in the form of meriva throughout the day.

There’s a few popular brands offering meriva or sometimes simply marketed as phytosomal curcumin. Right now the one I’m taking is the product from Thorne. Again, like every other supplement brand I’ve mentioned on this podcast, no affiliation whatsoever. Since I’ve sort of put curcumin and meriva out there specifically as a nice NSAID alternative, I need to address the gorilla in the room. Quite recently a very sensational scientific review was making the rounds claiming that curcumin basically had no health benefits and that, because of a quirk of an investigative method used to look at protein-to-protein interactions that may be subject to some degree of imprecision because of how it can behave in a manner that produces background noise, all curcumin research up until this point should be more or less considered null and void. That was sort of the crux of the argument.

A handful of unsuccessful trials were also cited to support, in my opinion poorly, this argument. The problem is that the specific quirk of the research assay being discussed is rendered absolutely and completely irrelevant in the context of the massive body of clinical curcumin research done in humans that has showed the compound exceedingly versatile.

Moreover, even if we put aside the enormous amount of clinical research, it’s been demonstrated that curcumin works in a manner that, at the cellular level, exhibits broad changes in gene expression. Something that cannot be dismissed simply because one specific assay which does not even measure gene expression exhibits some degree of artifact. If you couldn’t tell, I’m not a big fan of this particular review article published and may even feel a little bit of desire to sort of heep mountains of admonishment on the authors. That said, I will concede that there is a need for more double-blinded placebo controlled studies on curcumin and specifically the meriva phytosomal complex of curcumin which does significantly bypass the bioavailability issues associated with the compound, which has also been the source of some criticism. I am, however, very very optimistic about future research surrounding curcumin in general and meriva in particular.

Finally, one more thing I should bring up in the context of joint health is hydrolyzed collagen powder. What first sparked my interest in this was a study shared with me by a colleague that established the fact that, at least in an animal model, hydrolyzed collagen supplemented in the diet did find its way into the cartilage. Sometimes in nutrition relationships don’t tend to be so straightforward as may seem intuitive on the surface, cholesterol is a great example of this.

We actually create cholesterol and consumption of dietary cholesterol is not necessarily strictly a cause of high cholesterol as we think of it. In the case of hydrolyzed collagen powder, however, the relationship does seem to be straightforward: the study to which I’m referring used radiolabelled collagen which allowed the scientists that were doing the investigation to see what happened after the hydrolyzed collagen was consumed. They saw two things happened: that the collagen ended up being broken down into amino acids, but, more importantly, that some of it was also absorbed intact and shown to accumulate in cartilage long-term, which is pretty cool.

So a little bit about collagen. Collagen is an important component of tendons, ligaments, cartilage, and skin, but also an important component of gums, muscle and the gut. About 33% of collagen is made from proline and glycine, which most dietary protein sources are not especially high in. Proline may also have a special place in wound healing as well. The first 10 days after a wound occurs proline levels at the site of the wound are 50% higher than plasma, which might suggest that proline is actively being transported to the site of the wound and probably a necessary part of the wound healing process.

As an interesting aside, proline can also be used by the mitochondria to produce energy. It is converted to glutamate and alpha-ketoglutarate and used by mitochondria to produce energy. The reason this pathway exists is because during conditions when glucose levels drop, proline is released from connective tissue to be used to make energy. I’ve heard Tim mention great lakes brand hydrolyzed collagen powder, which happens to be the same brand I’ve used for the last few years. It does not have a particularly strong taste, so it can pretty much be added into anything, including a beverage like tea or coffee or pretty much anything else.

Guy Fasciana: What brands can we trust for dietary supplement brands? How can we find trustworthy brands?

Rhonda Patrick: This is a great question and an important question because the FDA does not require dietary supplements to be tested before they are marketed. As a result, products may contain unlisted ingredients and contaminants; some products have even tested positive for prescription drugs not listed on the label. Many supplements do not contain what they are actually supposed to contain and instead may be a combination of fillers like clover leaf.

So there’s a few things you can do…. One thing you can do is make sure the product is certified by NSF International, which stands for the National Sanitary Foundation, which independently tests and certifies dietary supplements and nutritional products and ensures that they do not contain undeclared ingredients or contaminants. To earn NSF Dietary Supplement Certification, products must undergo rigorous testing and inspection. The standard requires label claim testing/verification, a contaminant review and a facility audit.

You can look for products containing the NSF label by searching their dietary supplements online product database found at info.nsf.org/Certified/Dietary I usually will just type in the manufacturer name (for example nordic naturals) or I will type in a specific product that I am looking for like Meriva. The drawback to relying on this particular certification is that their database can be pretty restrictive.

While being in the NSF database is a good sign, not being in it isn’t strictly a deal breaker. So here’s another option: Look for products that are USP-certified. The USP, which stands for The United States Pharmacopeial Convention, is a scientific nonprofit organization that sets standards for the quality, and purity of dietary supplements that are manufactured, distributed and consumed worldwide. In the United States, the FDA relies on standards the USP has developed. So you can just go to their website, which is USP.ORG and click “Verified Supplements” to see a list of brands and products within brands that the USP verifies.

In addition to the USP and the NSF, there are independent companies that also test supplements and then rank those products and provide reports to customers, sometimes for a cost. However, I’ve found these to be either misleading or sometimes coming to conclusions that gives me pause. Doing the type of validation necessary may require technical skills that might be executed poorly or sometimes just plain weird ranking criteria may be at play. For that reason, I don’t trust these independent ranking companies as much, but absent other information it may still be better than just blindly grabbing something off a supermarket shelf.

James Enright: Rhonda, what are your core supplements and core foods for health or brain and daily/weekly health routine?

Rhonda Patrick: Okay, first: my perspective on food. I think it’s helpful to understand what I’m about to say because it, to a great degree, informs other opinions I may have about different approaches on diet. Food is, in a big way, a vehicle to deliver micronutrients, or compounds that are beneficial to health but not just micronutrients other compounds such as polyphenols and other xenohormetic compounds as well. Approximately 22% of all the genes that encode for enzymes require micronutrients as cofactors, which means that the machinery doing work inside your cells actually needs micronutrients to function properly. These are enzymes that are involved in metabolism, neurotransmitter production, repairing damage, basically everything that you want to be working optimally needs more than just energy. It needs micronutrients. It needs minerals, like magnesium, which we find particularly abundant in green leafy vegetables because it is at the center of the chlorophyll molecule.

Micronutrients are about 30 to 40 essential vitamins and minerals that we must get from our diet because they are essential for life. That means without them you die. Recommended daily intakes of these vitamins and minerals have been set to ensure we get adequate amounts of them but we really do not know how much of these micronutrients we need to stave off aging as best we can. If the proteins in your body start operating more poorly, let’s say they stop repairing DNA damage quite as well, or they aren’t cleaning up amyloid-beta as well or any of an almost infinite number of other potentially affected processes, you might not notice this as a disease, instead, we might just call it aging.

It’s important therefore to keep in mind that preventing aging is not the goal of RDA — it is to prevent easily observable, obvious diseases of deficiency… and figuring out what those optimal levels are for this more subtle and widespread thing we call aging is a bit more challenging. Adding some complication to this is the fact that this optimal level is probably not the same for everyone. Perhaps as a function of the agricultural practices or constraints placed by foods dictated partly by the geographic area our ancestors resided in, there is a great degree of genetic influence in how we absorb, metabolize, and use micronutrients. Understanding just some of these interactions between genetic polymorphisms and food is an area of study known as nutrigenomics. It is fascinatingly complex and there is a great opportunity for understandings in this area to improve the human condition. As an extension of this fact, I think the specifics of diet will eventually be better understood to NOT BE a one-size-fits-all.

That said, I’ve found some things that have worked for me personally and some of them are probably still relatively generalizable enough as to be useful for others. Here they are: I know most people are very focused on macronutrients. That makes sense in certain contexts so long as it isn’t to the complete and utter exclusion of all else. Instead, I just mainly follow a rule of thumb that I should eliminate refined carbohydrates in particular, and refined sugar especially and then try to eat with a special attention to nutrient density. I often enjoy wedging a smoothie in, sometimes as a partial meal substitute, that is particularly focused on cramming in some extra servings of some fruits and vegetables. I consider this a pretty important lifestyle hack that can sort of just be thrown on top of whatever else you’re doing and will help recalibrate a lot of important health parameters in a useful way.

As for actual meals, I always eat breakfast and as I mentioned earlier I practice time-restricted eating so that all of my meals are consumed earlier in the day and within a sensible time window. While some degree of diversity is ideal, for breakfast I do often rotate between a few reliable meals.

First, one of the main meals that I eat for breakfast are scrambled eggs usually topped with tomatillo salsa (which helps make the eggs less boring), sauteed kale and garlic topped with olive oil salt, and mustard powder and a grapefruit on the side. I scramble my eggs and sautee my kale in avocado oil because it is high in monounsaturated fat, low in polyunsaturated fat (I stay away from cooking oils that are high in polyunsaturated fat because it is so easily oxidized and it can be very harmful consuming oxidized fat), the avocado oil also has a very high smoke point so it can withstand some heat. The reason why I sautee the kale is very practical… it’s easier to eat. I add mustard powder to the kale as well as other cruciferous vegetables I may cook at other meals to facilitate conversion of precursors into isothiocyanates, like the sulforaphane from broccoli. One of the main reasons I eat eggs is that eggs is provide me with choline. We already talked about how choline affects acetylcholine but it also serves as a methylation source and thus affects global epigenetics, which is a way of changing the activation or deactivation of various genes.

One extremely common genetic polymorphism is in a gene that encodes for an enzyme that catalyzes the synthesis of phosphatidylcholine and thus choline. Post-menopausal women in particular with this polymorphism need to increase their dietary intake of choline. Eggs happens to be a great source of choline. I spread some tomatillo salsa on top of my eggs because I like it, foremost but it helps that it’s also high in tomatidine, which has been shown to boost muscle mass in mice by reducing the activity of a gene called ATF4, known for inhibiting muscle protein synthesis.

One reason why I like Kale a lot is because it is one of the vegetables that is highest in lutein and zeaxanthin, two carotenoids that most people associate with eye health because they accumulate in the rods and cones of the eye and protect them from singlet oxygen which is generated from blue light and can be very damaging to the eye. But recently there have been a fair amount of studies published showing that these carotenoids accumulate in large quantities in the brain. I mean what are they doing in the brain? There is no singlet oxygen from light exposure in the brain. Plasma and brain levels of lutein turn out to be associated with a higher volume of grey matter in the brain and improved crystallized intelligence in elderly, which is the ability to use the skills and knowledge that one has acquired over a lifetime.

A double-blinded, randomized controlled trial showed that lutein and zeaxanthin supplementation including 8 mg of lutein and 26mg of zeaxanthin improved neural processing speed time in young individuals. Decreased processing speed is a major hallmark of cognitive decline. Lutein and zeaxanthin have also been shown to improve memory recall while using less brain brain power in older individuals, something that’s known as neural efficiency.

An aging brain has to use more and more energy to maintain normal brain functions and so neural efficiency is said to have declined. The icing on the cake is that eating eggs with a salad increases the absorption of carotenoids like lutein and zeaxanthin, which are found in dark leafy greens particularly high in kale by up to 4-fold. Which is one reason why I do like a side of eggs with my kale. The grapefruit provides me with ferulic acid, a potent molecule that inhibits the proinflammatory cytokine TNF-alpha and E2 series prostaglandins, also inflammatory. Ferulic acid has also been shown to be anti-carcinogenic. The grapefruit is also a source of naringenin has a variety of interesting properties.

Another breakfast that I have is a nut and berry cereal with hydrolyzed collagen powder and coconut milk. My cereal also contains an array of chopped nuts including walnuts, pecans, and macadamia nuts. The nuts provide me with a host of micronutrients including magnesium, calcium, zinc, a modest amount of protein and the omega-3 fatty acid ALA which is not meant to be a substitute for the marine omega-3s. Along with the nuts, I often toss in some blueberries for pterostilbene, which is a plant compound present in blueberries that is chemically related to resveratrol except it is about four times more bioavailable than resveratrol.

Test-tube and rodent studies also suggest that pterostilbene is more potent than resveratrol when it comes to improving brain function, warding off various kinds of cancer and preventing heart disease. The blueberries are also high in anthocyanins, which evidence suggests can lower DNA damage. DNA damage has been shown to cause cancer and lead to depletion of stem cell pools so it also plays a role in the aging process as well. I also like to add some pomegranate into the cereal. One of the compounds in pomegranate is transformed by gut microbes into a molecule called urolithin A, which causes mitophagy a process important for the renewal of mitochondria, mentioned in an earlier question. Urolithin A has shown some pretty spectacular things in research on other organisms, including improving muscle function and endurance by up to 42% in mice and increasing lifespan by more than 45% in worms.

Finally, as a finishing touch to the breakfast cereal I often throw in some flaxseeds for more of the omega-3 ALA and fiber, some unsweetened coconut milk which contains some medium chain triglycerides, some raw cacao nibs which have a plethora of polyphenols including EGCG which activate many antioxidant genes and has been shown to kill cancer cells, occasionally some almond butter for some protein and to sort of make it delicious, hydrolyzed collagen powder which provides me with proline (as I mentioned is important for wound healing) and glycine (an important inhibitory neurotransmitter).

One reason I use coconut as opposed to milk is because milk contains salivary proteins which bind to anthocyanins and polyphenols and limits their bioavailability. Sometimes I’ll also throw in the cereal concoction some yogurt and possibly a packet of the probiotic VSL#3, which contains 450 billion probiotic cells per serving. Okay, let’s talk lunch. This is where the smoothie often comes in. As a base, it can often contain kale, frozen berries, avocado, hydrolyzed collagen powder and water… then a number of variations on top of those.

I have a couple of popular smoothie recipes that are floating around on the internet and a person can find by searching “Rhonda Patrick smoothie.” As a breakfast or lunch I occasionally have an avocado topped with fresh lemon juice and wild Alaskan salmon roe, possibly accompanied by a side of sauerkraut. This another variation I sometimes do. Avocados are really high in potassium and provide all of the various forms of vitamin E (in other words both tocopherols and tocotrienols), something it’s good to get a balance of via diet instead of only one form as from some supplements.

The avocado is also a great source of monounsaturated fat. Salmon roe caviar is a very good source of omega-3 fatty acids (~438 mg of EPA and 514 mg of DHA per ounce). I particularly like this source of omega-3 because the fats are in phospholipid form which has greater bioavailability to be transported into the brain via the mfsd2a transporter. This is the form that is best taken up by the brain (including the developing fetal brain). It also has a good amount of astaxanthin which protects the omega-3’s from oxidation and does the same for neurons. Studies looking at DHA and EPA levels in red blood cells have shown a correlation between higher omega-3 status and having a to 2 cm larger brain volume… getting omega-3 into and keeping it in the brain is definitely a brain aging priority for me.

The sauerkraut is a good source of fermentable fiber aka prebiotics that is fuel for the commensal gut bacteria so that they can produce compounds (such as short chain fatty acids) that feed more commensal bacteria and feed gut epithelial cells which are required to make the gut barrier. These compounds produced by the gut bacteria serve as signaling molecules to make specific types of immune cells, an important indirect role that fiber also has in the diet that helps it influence immune activities. The sauerkraut itself contains various probiotics (mostly the lactobacillus strains) which are beneficial lactic acid producing bacteria which have recently been suggested to possibly play a role in cancer prevention.

For dinner, I usually have some cooked vegetables like sauteed spinach which is very high in folate (as are all greens). Folate provides a precursor that makes a DNA nucleotide called thymine. Every time you repair a damaged cell or make a new cell in your liver, muscle, brain etc., you need to make new DNA which means you need folate. Folate was also very recently shown to increase the growth of stem cells, which is important because stem cell pools deplete with age and are a major cause of organ aging and dysfunction. Folate has recently been shown to play a role in protecting telomeres, the tiny caps on the ends of chromosomes that are a biomarker for age because they get shorter every year.

A recent study showed that mothers with highest folate levels had newborns with telomeres 10% longer and every 10 ng/ml increase in serum folate levels, newborns had a 5.8% increase in telomere length which actually suggests that maternal nutrition may actually play a role in determining the length of telomeres that we have to start with. Sometimes, instead, I’ll have some collard greens, bok choy, broccoli, brussels sprouts, parsnips (of course, since these are all cruciferous vegetables I eat these usually with mustard powder sprinkled on top since that provides an additional source of myrosinase). Cruciferous vegetables in general are among my favorites types of vegetables to eat because they contain isothiocyanates. Associative studies have shown that the top 20% of consumers of cruciferous vegetable have a 22% reduction in all-cause mortality.

Or, instead, I’ll have a big salad full of greens which provide me with a cornucopia of micronutrients including folate, magnesium, calcium, vitamin K1, lutein, zeaxanthin and sulfoquinovose, a prebiotic that feeds beneficial bacteria in the gut. For my protein I often have a big serving of baked wild Alaskan salmon.

I try to eat salmon 2-3 times per week, which is what the American Heart Association recommends. They recommend that adults consume 500 mg/d of EPA and DHA (~2-3 servings of fatty fish per wk or ~8 oz of fish/wk). However, the mean intake in Western society is ~135 mg/d and about ~2 servings of fish/mo. EPA, as mentioned in another question earlier, is a powerful anti-inflammatory fatty acid that has been shown to lower brain inflammation. As I mentioned earlier DHA is a critical component of all cell membranes that makes up 30% of the fatty acids in the brain, or about 8% of the total weight. Omega-3 fatty acids have recently been shown to positively change gene expression in several brain regions and also generally shown to stave off brain aging. But also important is just not dying. People with the highest omega-3 fatty acid intake have been associated with having a 9% reduced risk of all-cause mortality. For each 1% increment of omega-3 fatty acids in the blood there was associated a 20% decrease in risk of all-cause mortality. Another protein that I rotate for dinner is chicken legs from pasture-raised chicken which I like because in addition to the protein I also get some cartilage which is high in collagen, proline and glycine which is interesting for reasons already discussed earlier.

Sometimes I throw the chicken bones in some water with some spices and vegetables and make chicken bone soup which gives me all the same goodies I talked about with hydrolyzed collagen powder. Chicken is also very high in selenium which is a cofactor needed for all glutathione-related enzymes to work and also has a modest amount of zinc, copper, and iron.

Finally, I also sometimes have a grass-fed filet steak a few times per month which is a good source of vitamin b12, iron, and zinc. ~16% of all menstruating women are actually iron deficient. For the vegetarians out there…it has been recommended to take in about twice the RDA for iron since iron which is bound to phytate in plant sources is ~2-times less bioavailable. As I mentioned earlier I also make a broccoli sprout smoothie usually consisting of anywhere between 100 g fresh weight or sometimes a bit less of frozen since freezing them actually increases the sulforaphane content. I do this about 3 times a week usually.

I talked about some interesting effects that sulforaphane has on the brain but I actually think that it may be, in some respects, a compound versatile enough to actually possibly even slow the aging process in general. We’ll need more studies to establish that fact, but I’m optimistic because of the already numerous associative studies showing that humans that have a high intake of cruciferous vegetables have 40%-50% reduction in multiple cancers ranging from bladder to breast to prostate to lung cancer. But that’s the associative studies… What gets me really excited are the clinical studies on sulforaphane that show some pretty amazing things. For example, men with prostate cancer that were given 60 mg of stabilized sulforaphane per day resulted in slowing the doubling rate of a cancer biomarker (known as prostate-specific antigen or PSA) by 86% compared to placebo, which is pretty amazing! Another really cool thing about sulforaphane is that it activates detoxification enzymes and causes our bodies to excrete carcinogenic compounds.

For example, people that were given a daily broccoli sprout beverage containing around 262 mg of glucoraphanin (the precursor to sulforaphane) plus an additional 7 mg of sulforaphane increased the rate of excretion of benzene by 61% and acrolein by 23% beginning on the first day of consuming the drink and continuing throughout the entire 12-week period of the trial. Benzene is a nasty carcinogen that is known to cause cancer in humans and animals, particularly leukemia. Some of the major sources of benzene that people are exposed to are from automobile exhaust fumes and air pollution and cigarette smoke. Acrolein is found in most of the major sources already mentioned for benzene including air pollution, but it is also be formed when carbohydrates, proteins, and fats are heated. So we get exposed to a fair amount of acrolein from cooking food. Sulforaphane has been shown to improve markers of cardiovascular health.

For example, people with type 2 diabetes given 10 grams of broccoli sprout powder per day for 4 weeks, lowered their serum triglycerides by around 19% and lowered oxidized LDL to total LDL cholesterol ratio by around 14% and reduced their atherogenic index by 50%, which is a measure of cardiovascular disease that incorporates a wide variety of factors. Again, pretty amazing results for not changing anything else in the diet/lifestyle except adding sulforaphane to their diet. Finally, sulforaphane also lowered inflammatory biomarkers in people with type 2 diabetes who were given broccoli sprout powder containing approximately 40 mg of sulforaphane for four  weeks, reducing TNF-α, by 11% and lowering C-reactive Protein by 16%. I can tell you from my experience being involved in clinical trials with unhealthy people with metabolic syndrome, it is VERY hard to get drops in biomarkers of inflammation after just one month with no other dietary or lifestyle changes.

The fact that sulforaphane has such a profound impact on lowering inflammation is of great interest to me because it is now believed that suppression of inflammation is the single most important driver of successful longevity and that this actually increases in importance with advancing age. And I don’t just mean living long either but also a strong association with capability, meaning the ability to adequately perform activities of daily living, as well as cognition in all major age groups: elderly, centenarians (100), semi-supercentenarians (105-109), and supercentenarians (110+). In fact, inflammation has been shown to be the single most important predictor of cognitive ability, surpassed in its predictive ability only by a person’s chronological age itself. This Japanese study that I’m referring to was a bit of a surprise to be because several different biomarkers were looked at including blood glucose levels, insulin sensitivity, blood glucose levels, and even telomere length but none of those predicted successful aging in each age group up to supercentenarians. Low inflammation was the only predictor of successful aging in all age groups.

So now you know in a more comprehensive way, for those of you that have heard me mention sulforaphane a few times already, what’s behind some of that. To sort of dive into some of the supplements I happen to be taking this moment: I’m taking a multivitamin called ONE by a company called pure encapsulations. People ask the brand, so I’m sharing that. I like this multivitamin because it covers some bases for various micronutrients I just talked about and also, interestingly, has some trace elements including boron which has been shown to reduce double stranded breaks, accelerate wound healing, significantly increased mean plasma free testosterone in a small trial in men, and increased the half-life of vitamin D. Boron is definitely sort of interesting and has caught my attention recently.

The multivitamin I just mentioned also has 2,000 IU of vitamin D. So if I’m getting a lot of sunshine, I might leave it at that… or more often, I’ll add an additional 2,000 IU of vitamin D. I also usually take around 135 mg of magnesium citrate-malate from Thorne. I try to get most of my magnesium from my foods since it’s a measure of how many green leafy’s I’m getting. Even with my modest supplementation, I get a good bit… but around 45% of the US does NOT have an adequate intake of magnesium which, for adults, is roughly 400 mg/day. For a little perspective, 1 cup of cooked spinach contains around 156 mg. I’ll save a little bit magnesium for some later discussion in a few moments, but it’s important.

Another supplement that I take every other day is vitamin K2 which is found in fermented foods particularly natto but also in organ meat. This is thought to be a good one to take with vitamin D since both are involved in calcium homeostasis. I usually take 100 micrograms in the form of menaquinone otherwise known as MK4. Lastly as a part of the core supplements I take daily is… fish oil, which I take a lot of. I usually take two omega-3 phospholipid gel capsules by nordic naturals (which is omega-3 isolated from herring roe) because the DHA is in a specific form known as lysophosphatidylcholine-DHA. This form has been shown to be taken up by the brain best via the mfsd2a transporter. This is also the form you can get from krill oil as well.

In addition to this, I also take 4 gel capsules of promega 2000 fish oil by nordic naturals. One of the key things to know about fish oil is that it’s one of the supplements that you really need to watch out for quality on. It should be kept refrigerated and you ideally want a brand that is trustworthy and not arriving to you already oxidized. In fact, varying degrees of fish oil oxidation is of great concern to scientific study design when it comes to fish oil if researchers fail to ensure the fish oil used in their study is high-quality, weird mixed results surrounding supplementation can very well be expected. This is a characteristic that is sort of unique to fish oil unfortunately.

What I like about Nordic Naturals is that they are NSF certified, which is one of the certifications for quality I mentioned when responding to an earlier question. In addition to that, my understanding from having inquired is that they also isolate their fish oil under nitrogen conditions (meaning no oxygen present) so as to minimize any oxidation during the isolation process. They are by no means the only option out there, but I’ve felt pretty good about using their products and have used them for many years.

Okay, a little bit more about the fish oil habit. I’ve taken fish oil daily for about 9 years now. Some of the studies that have kept me taking fish oil have to do, in particular, with brain health. For example, supplemental fish oil DHA (2g/day) has been shown to increase the clearance of amyloid plaques in people with mild cognitive impairment after 4-17 months. But I also take it because it has been shown to slow the aging process in general. For example, supplemental fish oil of 2.5g/day has been shown to slow telomere shortening (a biomarker for aging) and lowers biomarkers of oxidation in blood cells in overweight middle-aged and older adults. In another study, supplemental fish oil of 1g/day increased muscle mass, handgrip strength, upper- and lower-body muscle strength, and leg power in older women after 6 months.

Another study showed that high dose supplemental fish oil of 3g/day increased resting metabolic rate by 14%, energy expenditure during exercise by 10%, and the rate of fat oxidation during rest by 19% and during exercise by 27%, lowered triglyceride levels by 29% and increased lean mass by 4% and functional capacity by 7% in healthy older females. There’s been studies that even show that it can affect the metabolic activity of brown fat. There are hundreds of studies like these that have convinced me to take fish oil daily but you get the point. Moving on from fish oil, I also take the probiotic VSL#3 sachets either once a week or once every two weeks.

I’ll talk a bit more about probiotics and this one in particular when following up in another question. I mix in some other supplements like the meriva formulation of curcumin, which I already talked about earlier, and I am just starting to mix in a little nicotinamide riboside into the mix. Nicotinamide riboside is a form of vitamin B3 that gets converted into NAD+ , which I already explained the importance of when I talked about fasting… but a brief recap: NAD+ status improving is generally perceived as one of the benefits of fasting that improve mitochondrial and metabolic function. Declining NAD+ status can be one of the unfortunate negatives of inflammatory processes. Nicotinamide riboside supplementation (100 mg up to 1000 mg) has been shown safe in humans and increased NAD+ levels in a dose dependent manner with 1,000 mg per day raising NAD+ levels up to 2.7 fold over baseline.

There have been several animal studies showing nicotinamide riboside improves mitochondrial function, mitochondrial biogenesis, muscle mass, and metabolism but this is important and easy to miss.. the doses that were given to animals involved in studies were so high that I’m afraid that the supplement I’m taking right now, which is by Thorne and only has 125 mg per capsule, won’t quite cut it to meet some of the robust results being seen in animal studies. I think there is potential here but more studies in humans definitely need to be done at this point. Still interested though.

The last part of my weekly health routine has to do with exercise. I like to mix up my weekly exercise routine with aerobic exercise, high-intensity training, strength training, and yoga/ballet exercises. I usually do some form of exercise everyday even if it is only 15 minutes. I usually like to do a 20 to 30 minute sauna 3 times a week but I recently moved and have not got back in the sauna routine but I hope to change that soon.

Usually I go for about 3 mile run about three times a week. I’m not really an endurance athlete, clearly, but I do enjoy it for the cognitive boost it gives me. Whenever I have a big decision to make or if something is causing me anxiety, these are times I’m especially enthusiastic about going for a run. Aerobic exercise has been shown to increase the growth of new neurons in the brain by two-fold. Aerobic exercise even starting in mid life has been shown to almost completely reverse the structural changes that occur in the brain with aging.

It has been shown that 20-40 minutes of aerobic exercise can increase serum brain-derived neurotrophic factor (in healthy men) by up to 30%, and similarly even 15 minutes of aerobic exercise can increase some BDNF albeit to a lesser extent. BDNF robustly increases the growth of new neurons in the brain and… sort of interestingly, in the muscle it plays a role in repairing damaged muscle. It combats brain atrophy which actually begins at 20 years of age and by the time a person reaches 100 (if they do) they usually will have lost an average of about 20% of their brain mass. BDNF is not only good for combating brain atrophy by growing new neurons, it also has been shown to help prevent neuropsychiatric disorders like bipolar disorder, schizophrenia, and depression. Good stuff you don’t want in short supply.

To try to get a little bit of high intensity workout I’ll do squat jumps for a few of minutes at a time. High Intensity training has been shown to improve learning and memory and when done for 8-20 minutes it increases the production of the neurotransmitters glutamate by 5% and GABA by 7%, as well as norepinephrine, a catecholamine involved in attention and focus. Interestingly, the production of norepinephrine is associated with the amount of lactate generated from the high intensity workout. A highly vigorous exercise causes demand for energy to become too high for the mitochondria to use glucose or fatty acids to generate energy so glucose is used as energy without the mitochondria via a process called glycolysis.

Lactate is then produced as a byproduct. Lactate is very similar to ketone bodies in that it is transported to other tissues including muscle, brain, heart, liver, utilizing the same transporter known as the monocarboxylate transporter which is used by ketones. Then lactate is able to shunt into the mitochondria to be used as an energetically favorable source of energy, such as in the brain, where it can then be used preferentially as a source of energy by these norepinephrine producing neurons. This idea that we can use lactate, possibly produced by our muscles to help out brain tissue or other tissues not responsible for its generation, is known as the lactate shuttle theory which is an idea that was pioneered by Dr. George Brooks that lactate produced by the muscles might be utilized or “shuttled” elsewhere.

In addition to squat jumps and running, I also lift some weights and do lunges and squats with weights either two to three times per week. It is really important to maintain muscle mass. Starting in middle age, people lose between 0.5% to 1% of muscle mass per year. One study involving over 300 twins speaks to the importance of the legs in particular: greater strength and power in the legs in particular was associated with an increased brain volume 10 years later and less brain aging in over 300 twins. Other fitness measures besides that of the legs, such as forced expiratory volume or grip strength, were not associated with brain aging when leg power was excluded. Other lifestyle and health measures such as frailty and telomere length indicated that reverse causation is not likely. To get right down to it: don’t skip leg day.

Lastly, I do some yoga and ballet exercises 3-4 days a week. I really like to do these exercises because they increase my flexibility and tone very specific muscle groups. I like it… but your mileage may vary.

Russ Thallheimer: What small change can you make in your lifestyle that leads to the biggest impact on your health and wellbeing? Essentially, what is the 80/20 of lifestyle changes?

Rhonda Patrick: Okay, so to summarize Russ’s question: what 20% of lifestyle inputs are leading to 80% of the positive effects. I think for people starting from ground zero one of the easiest lifestyle changes to make with the biggest impact on health is to cut out refined sugar. Meaning any processed cookies, cakes, candies, crackers, drinks, etc. Refined sugar intake in the US is a big problem. Around 10% of adults in the United States get 25% or more of their daily calories from added sugar and over 70% get at least 10% of their daily calories from sugar! It has been estimated that consumption of sugar-sweetened beverages in 2010 may have been responsible for approximately 133,000 deaths from diabetes, 45,000 deaths from cardiovascular disease, and 6,450 deaths from cancer worldwide. Let that sink in. We’re not talking about smoking or alcoholism.

We’re not even talking about just sugar in general, we’re talking about sugar sweetened beverages by themselves. But to give an idea of some of the magnitude of effect that sugar consumption can have in terms of sodas: associative studies have shown that adult Americans who consumed roughly one can of soda per day had a 46% higher risk of developing prediabetes compared to low- or non-consumers over the same 14-year period. In a similar vein, another study showed that replacing ONE sugar-sweetened beverage such as a soda or a sweetened juice with water or unsweetened coffee or tea reduces the type 2 diabetes risk by up to 25 percent.

Dropping refined sugar seems to also be able to take effect pretty quickly too: in another study in obese children that were put on a diet with no added sugar for just 10 days, it was shown to decrease fasting blood glucose by 5 points, reduce insulin levels a third, and also improve cholesterol and blood pressure. Cutting out the refined sugar may be the single easiest thing a person can do to dramatically improve their health. Not only is refined sugar associated with higher risk of many diseases, refined sugar literally accelerates the aging process itself.

Healthy adults that drink 12 fluid ounces (or roughly a can) of soda per day had much shorter telomeres in their white blood cells than people the same age but do not drink soda everyday, a reduction in telomere length roughly equivalent to 4.6 years of biological aging. Telomere length is a well-established biomarker for aging since our telomeres get shorter every year… and for that reason, it should be at least a little alarming when you see an amount that is equivalent to 4.6 years of aging getting trimmed off. Inflammation, one of the factors that are very important to aging, may also be at play here. One trial found that giving healthy, normal weight young men 20 ounces of a sugar-sweetened beverage that was more or less similar to drinking a similar amount of soda daily for 3 weeks was enough to trigger an increase in the biomarker of inflammation C-Reactive Protein between 60% to 100% higher levels than they started with.

What about hormones? In one study, men experienced a 25% decrease in testosterone for up to 2 hrs after 75g of sugar intake. There is nothing good about consuming refined sugar except for that short-lived dopamine hit you experience, which by the way, it’s also been shown that refined sugar increases dopamine and activates the brain’s reward pathway in a way that is in some respects similar to other drugs like tobacco, cocaine, and morphine. It also affects the opioid system. The effects in terms of magnitude are smaller than these substance abuse drugs. But the pattern ultimately follows a similar trajectory: you continually activate the brain’s reward system, you begin to lose self control, start to crave it, and eventually build up a tolerance to it so you need more and more.

These same mechanisms are at play when we talk about sugar addiction too. In my opinion, the best thing you can do is to cut it out!! You will be so much healthier by just cutting out this one thing. Once you stop eating refined sugars foods begin to actually taste sweeter that’s a real effect that’s been shown in clinical studies. Moving on, the second thing easiest thing you can do that will have a big impact on health is to begin doing time-restricted eating within a 9-12 hour time frame in accordance with circadian rhythm where, unless you are a night shift worker, you try to eat your meals earlier in the day as possible like discussed earlier.

If you’re looking to start out, I think 10-hour is a very good middle of the road approach. A fact I mentioned earlier does a great job at establishing magnitude of impact: women that previously had breast cancer and ate all their food within an 11-hour time period and changed nothing else in terms of their dietary composition reduced their breast cancer recurrence by 36%. Mice that were fed a high sugar, high fat diet but could only eat within a 12-hour window and still ate the same number of calories as mice that were allowed to eat within a 15-hour window ended up being 28% leaner, had 70% less body fat, did not get fatty liver compared to the mice splitting their meals over a longer period of time which did end up with fatty liver. The timed-restricted mice also had better blood glucose levels, cholesterol profile, and were more active, and could do complex motor tasks better.

This even included two cheat days per week in which the time restriction wasn’t in place to sort of simulate a human weekend off. It’s really important to drive home the fact that the impact of time-restricted eating was made without other improvements in food quality… the versatility factor is of huge benefit here and what makes it appealing is it is broadly applicable for people. So that’s two. So far to answer this question, the big lifestyle inputs I’ve suggested are: remove all refined sugar as much as humanly possible, especially sodas… and implement time-restricted eating regardless of diet, preferably earlier in the day.

The third huge lifestyle input that I think can make a big, big difference is simply doing whatever it takes to potentially triple the amount of vegetables you take in on a daily basis. For me, the way I’ve gone about this has been to make a habit out of creating a micronutrient smoothie, as I’ve termed it. Basically, I grab various combinations of vegetables and sometimes a few fruits to balance it out, drop them all into a powerful blender or food processor and drink drink it down.

Going about it this way means that all of the hugely beneficial fiber still gets ingested. This is important because commercial juicers remove the fiber, which is problematic since fiber is highly beneficial for the microbiome, important for health and the regulation of blood glucose levels, and often in short supply in the diet of the typical Westerner. We’ll talk about the implications of that in a question that comes up later. One important tip is that using an especially powerful blender makes sure that the smoothie has a consistent texture, enhancing palatability, which may be a drawback for some folk that may otherwise have prefered juicing. You learn over time adding in certain things like avocado also can greatly change the texture, usually improving it. Having done this micronutrient smoothie “hack” 4-5 times per week for the past 6 years, often without great regard of where it may fit in with the rest of my diet, even adding it on top, I noticed something pretty interesting early on: I noticed that the amount of vegetables I was buying almost quadrupled. Vegetables are a rich source of many important micronutrients and other compounds like lutein and zeaxanthin that have important functions that I mentioned earlier when talking about the foods I eat.

The smoothie that I make at the very least usually has kale, berries, and an avocado but I usually also add chard and possibly some other veggies like carrots and a tomato. In the U.S. micronutrient deficiencies are especially common, but this is probably true elsewhere abroad as well. RDA’s have been set to make sure people meet their daily intakes but even still people don’t meet them.

Some micronutrients that are abundantly found in greens just happen to be the ones that people in the US are the most deficient in somewhere around 45% of people are deficient in magnesium, 35% in vitamin K, 24% in vitamin C, 34% in vitamin A, 38% in calcium, 8% in folate. Magnesium, because of it’s location at the center of the chlorophyll molecule, is especially telling when it comes to the root cause of the problem… a lack of consumption of green leafies.

Earlier I mentioned that around 22% of all enzymes require a micronutrient to function. These micronutrients are necessary for metabolic pathways that are essential for short-term survival and metabolic processes that are important for long-term health. Sometimes these different processes both require the same micronutrient to function. So what happens in a person that happens to be deficient in that particular micronutrient? My former postdoctoral mentor, Dr. Bruce Ames, proposed that those metabolic processes that are required for short term survival will get their share of the micronutrient first because nature wants you to survive long enough to reproduce and pass on your genes, whereas processes that are more concerned with the long-term maintenance, processes involved in mitigating aging in the long-term ultimately get neglected.

Bruce calls this evolved strategic rationing of micronutrients the triage theory. It’s a helpful way to think about how the body deals with micronutrient inadequacies and deficiencies and he’s published a couple of studies providing the theoretical backing to support the idea. While nature has devised this elegant way of allocating vitamins and minerals to ensure survival during periods of food scarcity, which has occurred throughout evolution, the tradeoff is it results in insidious types of damage that accumulate with age, accelerates the aging process and leads cancer and neurodegeneration.

In the case of magnesium over 300 different enzymes in the body require magnesium, including all the enzymes that use and produce ATP, the energetic currency of the cell. ATP must be bound to a magnesium ion in order to be biologically active. These functions of magnesium are required for short term survival. If you can’t make ATP you simply can’t live. But the enzymes that are involved in the generation of ATP are not the only enzymes in the body that require magnesium.

Magnesium is also required for enzymes that repair damage to DNA which has been shown to lead to cancer and damage mitochondria, which can accelerate the aging process. But optimal DNA repair function is not critical for short-term survival so those enzymes, it would logically follow, would not not get their first pick of magnesium. Putting aside the micronutrients for a moment, of course, along with the kale you get some isothiocyanates like sulforaphane which we talked about quite a bit earlier. Finally, for lifestyle input #4, the other really, really easy lifestyle change that I think has a potentially big impact, for many, many people, is probably taking a vitamin D supplement.

Vitamin D is actually converted into a steroid hormone in the body and regulates around 5% of the human genome. Let that sink in and recall back to the fact that approximately 70% of the US population does not have adequate levels of vitamin D, which is an amount of 30 ng/ml or greater. Or 75 nmol/L if your test uses that unit. That means 70% of people in the U.S. are experiencing some dysregulation of their genes due to poor vitamin D status.

As I mentioned earlier this is largely due to people spending more time indoors, wearing sunscreen which blocks the ability of your skin to make vitamin D, darker skin pigmented people living in more northern latitudes age etc. Earlier when discussing vitamin D in the context of serotonin production as a nootropic, I mentioned that I like my vitamin D levels to be between 40-60 ng/ml.

Here’s part of the basis of that: a meta-analysis including around 30 studies from 1960 to 2013 showed that people with vitamin D levels between 40-60 ng/ml had the lowest all-cause mortality and another study found that people with those same vitamin d levels had the longest telomeres compared to age-matched controls with lower vitamin D levels. And sort of just generally establishing again the importance of vitamin D: yet another study involving a couple thousand twins found that those with the lowest vitamin D levels had shorter telomeres that corresponded to 5 years of accelerated aging.

Vitamin D activates the expression of DNA repair genes and anti-inflammatory genes and thus lowers DNA damage and inflammation, both of which accelerate the attrition of telomeres. So I think having adequate vitamin D levels definitely has an effect on long-term health. But it also affects short-term health as well. A meta-analysis of 25 randomized clinical trials conducted in 14 countries showed that vitamin D supplementation cut infection risk by 50% in people that were deficient and by 10% in people with normal vitamin D levels. It also affects muscle mass and exercise performance. For example, 2,000 IU of vitamin D3 per day for 2 weeks increased exercise performance (cycling) by 30% while lowering physical exertion. Postmenopausal women receiving a vitamin D supplement had a significant increase 25% in muscle strength, while those receiving the placebo actually lost an average of 7% of muscle mass.

There are so many studies showing that vitamin D improves health including brain health, you do not want to be deficient in this and yet so many people are. The solution is to take a vitamin D supplement. Generally speaking, as a rule of thumb, 1,000 IU of vitamin D usually raises serum levels of vitamin D by 5 ng/ml. This is sort of useful as a course correction when you’ve got a vitamin D test coming back outside of the range you want to see it. It really is important, however, to measure your blood levels of vitamin D after supplementing as well. Okay, so with that last one I think that sort of wraps up my high level thoughts on lifestyle strategy choices that might drive big changes in a pareto’s principle sort of fashion.

To recap:

• #1 – Eliminate refined sugar from the diet to the greatest extent possible.
• #2 – Practice time-restricted eating and eat generally in accordance with your circadian rhythm.
• #3 – Do everything in your power to maximize vegetable intake, possibly using the micronutrient smoothie method as a way to jumpstart the habit.
• #4 – Enlist your physician in helping you monitor your vitamin D blood status and then attempting to titrate your dose to an above 30 ng/ml range, possibly trying to land between 40 and 60 ng/ml.
• #5: try to get some form of meaningfully vigorous cardiovascular exercise, at least 30 minutes, a few times per week.
• And #6: get bright blue light during the day, as early as possible, and avoid that same blue light as much as you can in the evenings.

Sean Ballard: Rhonda, have you considered taking meat completely out of your diet? Also, which meats do you consume, where do you get them, and how frequently do you consume meats

Rhonda Patrick: The truth of the matter is that there have been many, many correlative studies that have found that higher meat consumption is associated with a significantly higher risk of cancer and cancer mortality. This fact alone should be enough to at least make a person give thought to their position on the subject especially when it’s a relationship that keeps showing up.

That said, one of the largest studies to-date, which was published in JAMA Internal Medicine in 2016, and looked at meat consumption and all-cause mortality and cancer-related mortality found something interesting that is important to the narrative: specifically, it found that a high intake of meat from animal sources was only associated with a higher mortality rate and cancer mortality rate in people that had at least one other factor associated with an unhealthy lifestyle such as being obese, or having a history of smoking or being physically inactive or being a heavy consumer of alcohol.

Meat consumers that were healthy by not having any of these aforementioned unhealthy lifestyle factors did NOT have a higher mortality rate or cancer mortality rate. Critical to the meat consumption and cancer link is the fact that protein increases IGF-1, something that research suggests may be an important link in this meat-cancer relationship.

Earlier we talked a little about the importance of IGF-1 in its beneficial context for muscle hypertrophy, but this cancer link is a trade-off that’s worth paying attention. Amino acids and particularly essential amino acids (such as leucine) which are more abundant in meat are the most potent dietary activators of the IGF-1 pathway. IGF-1 does a lot of stuff. It’s a growth factor that plays a very important role during early growth development and also is important in promoting and maintaining muscle mass, as we discussed, and also neuronal function.

There are many positive benefits to IGF-1 but there is also a tradeoff, as there so often is in biology. IGF-1 is a very potent growth factor that allows cells that have been damaged to survive when they otherwise would die. It is important to understand that IGF-1 does not cause damage to the cell, rather, it allows damaged cells to live and reproduce so that it can make more copies of the damaged cells. IGF-1 is known as a tumor promoter because it promotes the growth of cancer cells.

Other factors that cause DNA damage such as reactive oxygen species (byproducts of metabolism) and inflammatory cytokines (byproducts of immune activation) can initiate cancer by causing DNA damage, which is the initial insult that can lead to a damaged cell. Our body has protective mechanisms that sense a damage cell and kill it but the presence of an abundance of IGF-1 overrides this mechanism and can allow that damaged cell to survive. This is why IGF-1 can be fuel for cancer growth. Not initiation, but growth. That distinction may be important.

As a pathway, IGF-1 is actually of great interest in both cancer and longevity research. We know from animal evidence that growth hormone and IGF-1 deficient mice are resistant to cancer. Interestingly, this evidence isn’t limited to animal research: some humans also have polymorphisms in the gene that encodes for the IGF-1 receptor, which leads to a decrease in IGF-1 activity in these individuals. Similar to animal research, we see a decreased incidence in cancer and also longer lifespans in these people.

Human evidence also exists for the exact opposite, where people that have genetic polymorphisms that cause them to have increased IGF-1 also have an increased cancer risk. If we get away from genetic polymorphisms and just look at people with higher circulating IGF-1 in their serum, something that can be quantified, this has also been associated with an increased risk of several common cancers, including breast, colon, and prostate.

So, high IGF-1, higher cancer risk. Low IGF-1, reduced cancer risk and even longevity. With this new understanding of the relationship of meat consumption to IGF-1 production and IGF-1’s relationship with cancer and longevity, where it even inhibits the longevity gene FOXO3, it would be very tempting and very easy to take an absolutist position and never touch meat again, putting aside all of the other reasons why someone might make such a choice.

But as I mentioned there are good aspects to IGF-1. IGF-1 has been shown to increase lean muscle and and reduce adipose tissue simultaneously, it acts as a neurotrophic factor increasing the growth of new brain cells, it prevents brain cells from dying. It’s pretty clear that I actually want some IGF-1 activity. I think this is a really important take-home with respect to IGF-1 because IGF-1 has a good and a bad side but I think exercise is a way to tip the balance towards the good. Exercise, whether we’re talking about aerobic or resistance training has been shown to to lower serum IGF-1 because exercise causes our muscles to take up IGF-1. Additionally, IGF-1 has been shown, in rat studies, to cross the blood-brain barrier in response to exercise and increases neurogenesis.

This also means the exercise lowers circulating concentrations of IGF-1 which means it has less of a chance to promote the growth of damaged cells or inhibit Foxo3 in other tissues. If we circle back to the original study I mentioned where meat consumption was only associated with a higher all-cause mortality if one other unhealthy lifestyle factor was present this makes perfect sense if most of the bad effects are mediated through IGF-1.

Since I do not have any of those unhealthy lifestyle factors and I understand what I perceive to be the mechanism behind the relationship between cancer and meat consumption, I have decided to keep some meat in my diet. Since I already got into a meal breakdown where I talk about the meals I eat in a typical week in another question, I’lI skip to the last part of the question which is where do I get my meat from: I usually get them from the local grocery store or the farmers market. I buy wild fish (mostly Alaskan salmon), grass-fed beef, and pasture-raised chicken with no antibiotics or hormones.

Andrea Kurland: I would like to hear your thoughts on some of the fad diets that have been circulating. Paleo/ketogenic/vegetarian. Advocates of each of these often claim that their diet is the best for inflammation…yet they are all different.

Rhonda Patrick: I think there are benefits to the perspectives that are brought by each of these various philosophies, though there might be contexts that may make one or another make more sense. I personally choose a more middle of the road route and eat what might be loosely termed a Paleo-ish type of diet. The good news is that some of these diets have aims that sort of overlap with one another.

For example, both paleo and ketogenic-style diets emphasize cutting out refined carbohydrates and refined sugar which in and of itself has a dramatic effect on lowering inflammation, lowering cancer risk, cardiovascular disease risk, dementia risk, and delays aging all of which we talked about in more detail a minute ago when discussing how cutting out refined sugar is one of the big changes a person can make to have a rapid impact on personal health. The paleo diet, in contrast to some of the popular culture’s flavors of keto, emphasizes eating a lot of vegetables and fruits, which also comes with the package in vegetarian diets as well.

As I mentioned earlier fruits and particularly vegetables are a great source of micronutrients and other important compounds such as folate, magnesium, vitamin K1, calcium, vitamin A, vitamin E, vitamin C, potassium, lutein, zeaxanthin, pterostilbene, anthocyanins and other polyphenols and flavanols.

I already mentioned how incredibly important these micronutrients are, how 22% of all enzymes require some micronutrient to work properly and how important they are for metabolism, mitochondrial function, neurotransmitter production, antioxidant and anti-inflammatory pathways, immune function, brain function, repair enzymes…basically everything important for preventing disease and healthy aging.

One of the problems with certain variations of the ketogenic diet is that, without a great deal of care to avoid this pitfall, it can lead to inadequacies or deficiencies in some of these micronutrients and you may not get as many of the other beneficial compounds present in plants as well. A great example of this might be the flavanols in blueberries, just by way of example. Fruits and vegetables, which, again, it seems like the paleo diet and vegetarian diet focus a bit more on, are also a great source of various types of fiber including fermentable fiber and non-fermentable fiber. Fiber is not a single nutrient, which is why fiber supplements are no magic bullet either. It’s not just about quantity, but also diversity of complex carbohydrates.

There are hundreds of different polysaccharides — complex carbohydrates, in plants. Gut microbes reflect this same diversity, specializing in using different types of complex carbohydrates and even the metabolic byproducts of other microbes. These microbes then produce short-chain fatty acids that impact our health in a variety of ways. This is why eating only one type of fiber, as from supplementation, is ultimately a failed strategy.

The best way to increase your microbial biodiversity is to actually eat a variety of polysaccharides from a diverse diet of plants and vegetables as well as fruits. For example, lignins and cellulose (which are found in plant cell walls) are non-fermentable fiber that help move food and other byproducts through the intestines. Examples of fermentable fiber that are eaten by a wide-variety of commensal bacteria in the gut include pectins (which are found in fruits and berries,), gums (which are found in seeds), inulin (which is found in plants and onions, garlic, and artichokes), resistant starch (which is found in legumes like beans also in bananas).

Green leafy vegetables also contain a prebiotic known as sulfoquinovose which also feeds beneficial gut bacteria in the gut. In addition to diversity, however, we also need volume of dietary fiber. Figuring out what this golden amount is to keep our microbes metabolically satisfied and not literally starving is a tricky issue. The institute of medicine recommends men 50 years of age and younger get at least 38 grams of fiber per day and women 50 years of age and younger get 35 grams of fiber per day. Those numbers drop slightly for adults older than 50. But traditional societies, for example those that still exist in places like in Tanzania that are living a hunter gatherer lifestyle, can get around 200 grams of fiber compared to the norm for U.S., which is shockingly only about 15 grams per day on average. Either by comparing to traditional societies or just taking the institute of medicine’s recommendation most miss this mark.

It is therefore, important that whatever diet you do choose you ultimately ensure your microbiome has adequate substrate which survives digestion to make it toward the end of the digestive tract where the majority of these microorganisms live and interact with our immune systems and our brains. The big problem with a low fiber diet which in the context of this discussion may possibly be a version of the ketogenic diet — again, unless special care is taken, is that it may not provide this substrate. Fats, proteins, and sugar are all absorbed in the small intestine earlier on but all the 100’s of trillions of bacteria that are in our gut and regulate our immune system, brain function, and more are at the end or “distal” part of our large intestine, called the colon.

When we eat fiber-deficient foods, our gut microbes starve but to keep from starving they eat and cannibalize the gut barrier (which is made of carbohydrates and mucin). In terms of magnitude, low fiber has the largest negative effect on breaking down the gut barrier. Additionally, one study showed that a low-fiber diet caused up to 75% depletion in half of gut bacterial species. That’s a magnitude of effect that sounds almost on par with actually taking a round of antibiotics, if you think about it.

Okay, so I’ve voiced some real concerns about possible implementations of certain variations of ketogenic diets. But there are other benefits of a ketogenic diet. In my opinion one of the main benefits from the ketogenic diet is a steady stream of ketone body production particularly beta-hydroxybutyrate (BHB). BHB is a fascinating mostly anti-inflammatory compound and plays an anti-oxidative role as well. Altogether, most studies in animals link the production of beta-hydroxybutyrate to lower oxidative stress, lower inflammation, improvements in mitochondrial respiration and ATP production, and improved brain function. It also may change gene expression in a positive way by regulating class 2 histone deacetylases.

As I mentioned earlier in another question, the ketogenic diet has also been shown to lower blood glucose levels and improve insulin sensitivity and lead to weight loss in some individuals. But this is not true for everyone as some people do experience negative metabolic effects likely due to genetic variation which is why it may be helpful, if you experiment with this diet, to keep an eye on some of the blood biomarkers mentioned earlier to make sure that, if you do experiment with it, you’re not one of the folk that it may not be ideal in the long-term for. It’s also possible to ramp up ketone body production for short bursts by kicking off evening fasts a bit earlier, playing it strict and following some of the time-restricted eating or intermittent fasting protocols out there.

Going back to the paleo and vegetarian diets, while they both focus on eating whole vegetables and fruits…they obviously differ in that vegetarian diets lack meat and have an even heavier emphasis on plants, obviously. One potential drawback from the vegetarian diet is that people on this type of diet must put in a little more effort to get some of the micronutrients that are found in meat such as the marine omega-3 fatty acids (EPA and DHA), iron, zinc, vitamin B12, selenium. For example, iron (which in addition to being important for red blood cells to carry oxygen to all tissues, is also required to produce neurotransmitters and myelin).

Non-meat sources of iron such as kidney beans or lentils contain iron that is bound to something in the legumes called phytate. There are large bioavailability differences between iron that is in heme (which is how it is found in meat) compared to iron that is in in phytate from a plant source. The bioavailability of iron in phytate is about 1.8 times lower than the iron bioavailability from heme. The poor bioavailability of iron that is bound to phytate has to do with the fact that humans cannot digest phytate so most of that iron does dot get absorbed. For this reason, the RDA for iron for vegetarians should be 1.8 higher.

The RDA for adult males is 8 mg and pre-menopausal women is 18mg. A lot of iron is lost during menstruation which is why menstruating women are at high risk for deficiency. In fact, approximately 16% of all menstruating women are iron deficient. Too much iron, however, can cause serious oxidative damage and other problems, which is why it’s a good idea to get iron levels measured instead of blindly supplementing.

This is just one example of what I mean by vegetarians having to work a little harder and think about complexities like this to make sure they get all of their micronutrients. There are other examples. A great one I mentioned earlier are the omega-3 fatty acids. It may be tempting for vegetarians to dose up on conventional plant sources, like flaxseed. Some people have a gene polymorphism in the gene that encodes for the enzyme that converts the plant omega-3, ALA, into EPA and DHA, the ones I referred to as marine omega-3 fatty acids a moment ago, and this can cause them to not convert as well others.

This can be circumvented by supplementing with microalgae oil and possibly eating higher concentrations of ALA, however. Or you may just be lucky and be a highly efficient converter of ALA in which case, it may not be a problem. Similarly, essential amino acids are much more abundant in meat and may be something that vegetarians may need to work a little harder to make sure they are getting enough of particularly in older age.

One study looking at people over 65 found that there was an increased mortality with low protein intake, likely due to frailty. As I mentioned earlier, Starting in middle age we lose about 0.5-1% of muscle mass a year and essential amino acids are important for maintaining muscle mass along with putting those muscles to work, of course. But, if you recall earlier, there may be a flip side to that. Folks on paleo or keto diets do include meat. This means that they may need to take special care to be active and not sedentary to put that IGF-1 to use. Remember that eating meat increases IGF-1 and for people that have even one component of an unhealthy lifestyle such as obesity (without trying to lose weight…paleo and keto diets have been shown to result in weight loss), being sedentary, smoking, or excessive drinking… this may increase all-cause mortality and cancer-mortality.

So that is my sort of high level general summary of these three diets. Like I said, I personally choose to try and get the best of all worlds. I eat paleoish, including fish and other meats, but with a big emphasis on plants that might be more common among vegetarian eaters. I am very vigilant about avoiding refined or processed foods and especially sugar.

I practice  time-restricted eating and intermittent fasting to get the occasional dose of the ketone body beta-hydroxybutyrate. I do not smoke or drink excessively, and I make sure to exercise! This protocol works really well for me. But there may be life contexts, being honest-to-god sedentary for example, or possibly even genetic backgrounds in which we need to emphasize one philosophy more over another. Similarly, a person might have important clinical reasons for pursuing a ketogenic diet, in which case, avoiding pit-falls like poor micronutrient intake can become especially important.

Either way, I think there’s a rich future in figuring out where individual variation and genetic polymorphisms come into play in the pursuit of a healthy lifestyle… and conversely, what approaches are more broadly applicable, like time-restricted eating.

Luke Hoskovec: Do probiotics need to be taken forever or do the different strains of bacteria gain a foothold at some point? If I take probiotics for six months and stop, will the introduced colonies survive?

Rhonda Patrick: Your question actually highlights one of the important drawbacks of taking supplemental probiotics. In order for probiotics that are introduced to actually remain in the colon (which is where the majority of our gut microbiome resides) there has to be space for these tiny microbes to stay.

The predominant way bacteria take up residence long-term in the large intestine is by sticking to the mucin, which is the mucus-like material that makes up the gut barrier and lines the interior of the gut. The problem is that unless a person has just taken a course of antibiotics that mucin is already effectively colonized with bacteria that already reside there, which can be a limiting factor that reduces the foothold that new species are able to gain. What this effectively means is that often the probiotics that make it to the colon, if they were alive when you took them, end up being flow through instead of sticking around. BUT! What’s interesting, however, is that probiotics can, while passing through, facilitate population shifts that may be otherwise less than straightforward while they pass through. Sort of like you introduce population A and B but resident populations X is diminished and resident population Y is increased… or, alternatively, the probiotics may also interact more directly with our immune system while they pass through.

Basically, there’s still a ton of research to be done on probiotics… it’s clear that, in some cases, they can be highly, highly effective for a variety of purposes, but sometimes the exact mechanism is a bit elusive and may not be strictly intuitive. This issue of already being colonized and existing biota taking up space does, however, come with certain obvious conclusions. The first of which is that you are perhaps most advantaged in taking probiotics shortly after you’ve wiped out your existing populations with antibiotics. It’s important to note, however, that the cumulative effect of repeated use of antibiotics is pretty much unambiguously negative from the perspective of gut microbial communities, with each additional course causing even greater changes that shifts the community further away from its natural starting state… so it would not be prudent to seek out antibiotics strictly to try to liberate a little space in the gut. Interestingly, another good time to take them may be while taking antibiotics too.

Clinical studies have shown this can reduce the potential of later c. difficile infections, among other things. Gut researcher Dr. Justin Sonnenburg out of stanford has characterized probiotics as potential placeholders that prevent pathogens from gaining a foothold during recovery, which may be an interesting way to look at it. However, with that said it is possible that with repeated use (as is the case with 6 months) that some can get a foothold in the mucin and stick there.

To have a better chance of that happening or having any sort of therapeutic effect whatsoever, however, it’s helpful to first have a product that you’re confident is alive when it arrives to you and also has a sufficient quantity of bacterial cells that it can actually make an impact. There’s one particular product that stands out for this reason and also because of the sheer volume of clinical evidence that you can find just by searching its name in google scholar or Pubmed. The product to which I’m referring is known as VSL#3, particularly the unflavored sachets, which has 450 billion probiotics per serving packet. They also get shipped in an actual cooler with ice packs to ensure they’re viable when you get it.

By way of comparison, you might be lucky to find a probiotic with 100 billion but most contain more like 10 billion or sometimes even less and the viability of those bacterial cells by the time it makes it off the shelf or out of a warehouse and into your refrigerator may or may not be effectively zero.

There are dozens of publications showing the effectiveness of VSL#3 both in humans and animals looking at its effect on a wide variety of conditions ranging from the more obvious, like antibiotic-induced diarrhea, but also its effect on insulin signalling, atherosclerosis, food allergy, colitis, liver dysfunction, lipid profile, blood pressure and more. But to speak to Luke’s question about whether species in probiotics are able to gain a foothold, I have, anecdotally, measured both mine and my husbands microbiome species using a consumer service both before and after taking VSL#3 for several months and did find that the VSL#3 caused new species of commensal bacteria to crop up that were not quantifiable when at my baseline and were not even species of bacteria that were present in the VSL#3.

I think it is possible that some of the probiotic strains that WERE in the VSL#3 produced what are known as short-chain fatty acids, small molecules like lactate, which then ultimately provide fuel for other neighboring strains of bacteria that I may have had in very small quantities already present in my gut which then became detectable once they sufficiently increase in quantity. So this sort of feeds into that earlier discussion about how probiotics can have positive effects but then once you go in to actually look at the changes from the probiotics, they may be somewhat unexpected. Additionally, however, in my experience some of the strains actually present in the super probiotic VSL#3 did begin to show up as well.

All of that said, as a person with former gut problems that seem to have been resolved, I no longer take VSL#3 everyday because, frankly, it is a bit cost prohibitive and probably not even necessary for me at this point. Instead, I take a maintenance dose every week or so and generally keep what I consider an airtight diet that promotes a healthy microbiome through the consumption of an abundance of various types of healthy fermentable fiber. If you’re listening this and look up VSL#3 online, again — no affiliation here — be aware that it can be bought direct from the manufacturer and shipped to your home without a prescription, but they do advertise it as a medical food with the expectation that you’re taking it under the care of a physician. While I don’t know of any particular risk from taking probiotics, it’s always good to follow the prudent podcast listener’s rule and consult a physician before trying to treat what may be a medical condition.

Mary Maxey: Are artificial sweeteners bad for gut health or overall health? Should they be avoided?

Rhonda Patrick: I try to avoid them because they may have adverse effects on gut health and, through that, overall health too. Once in a great while it’s probably fine but everyday use, as in the case of a daily diet soda, is not a good idea in my opinion. There was a study published in 2015 that showed that artificial sweeteners alter the gut microbiome both in mice and in a small group of human trial participants. In the mice, they tested saccharin, sucralose and aspartame and found that they increase a population of bacteria that are better at extracting energy (specifically glucose) from food and then store that energy as fat.

This ultimately altered gene expression which then allowed for increased fat storage and decreased fat burning. Similarly, humans that were given a high-dose saccharin showed a rapid alteration of the gut microbiome and also had decreased glucose tolerance sort of showing proof that the same mechanism in mice does seem to cross over when we’re talking about people too. This sort of hints at a potential bitter irony whereby people having switched to drinking diet sodas, for example, may actually be affecting their microbiome in such a way as to actually make themselves more obese, even if the empty sugar calories they’re taking in have been reduced. In general, if we think more about overall health, putting aside whether the effects mediated by the microbiome or not, artificial sweeteners in particular have been linked to metabolic syndrome, coronary heart disease and other cardiovascular events.

I’m somewhat optimistic that the effects of the natural non-nutritive sweetener stevia are somewhat more benign, especially in light of a 2016 study showing lipid improvements and even therapeutic potential in a rodent model of obesity. This sort of hints at the fact that it may be a totally different can of worms. But, even so, I do still think it may be worth exercising some degree of caution. In general, when talking about artificial sweeteners or even the non-nutritive sweetener stevia, proper randomized controlled trials are lacking. I’m sure the debate will continue until these sort of gold standard trials emerge that can move the conversation forward by firming up the details more. For now, I personally avoid artificial sweeteners altogether and only use stevia in moderation.

Emily St Clare: Is metformin really damaging to the mitochondria or is it more of a hormetic stressor?

Rhonda Patrick: Briefly for those of you that do not know what metformin is — Metformin is a drug, specifically a biguanide derivative, that is primarily used for the treatment of type 2 diabetes. It helps control blood glucose levels and restore insulin sensitivity. It decreases the amount of blood sugar that the liver produces (mostly through reducing gluconeogenesis in the liver via AMP Kinase activation). It also reduces the amount of glucose that the intestines or stomach absorb.

In addition to affecting blood glucose, metformin affects other pathways involved in metabolism, inflammation, and growth. That said, the reason why Emily may be asking this question, if I were to venture a guess, is because over the last few decades there have been hints that metformin, in addition to regulating blood sugar in people with type 2 diabetes, might also prevent diseases associated with aging.

In the late 1990’s a study in the UK found that type 2 diabetics taking metformin lowered all diabetes-related complications by 32% and also lowered the risk of cardiovascular disease. Other studies have found that taking metformin is associated with a reduced cancer risk and it preserved cognitive function. But the study that got the most attention and certainly piqued my own attention was a British study involving around 78,000 individuals that found adult type 2 diabetics who took metformin, on average, lived longer than healthy age-matched controls.

That was kind of mind blowing for me. Oddly enough among many of the compounds that have been shown to affect lifespan in animals, including metformin, rapamycin, resveratrol, etc., metformin has generally not been THAT impressive. but, metformin has a long reassuring track record since people with type II diabetes have been taking it since the 1960s. Still, I don’t take it but I’m interested for its future and will be keeping an eye on emerging research.

To more directly answer the original question, metformin does inhibit complex I of the mitochondrial respiratory chain (which is a very important complex in the mitochondria that is responsible for energy production) and, thus, inhibits oxygen consumption in the mitochondria. Believe it or not, several researchers actually think that this may be the important mechanism by which metformin affects aging. This is because, by inhibiting the mitochondria, this turns down mitochondrial metabolism which may mean the mitochondria accumulate less damage since they aren’t working as hard.

The consequence of complex I inhibition by metformin is a decline in ATP production and an increase in ADP and AMP and this activates AMP kinase. So far as I am aware, the complex I inhibition in mitochondria does not appear to cause mitochondrial toxicity. Future studies will help better illuminate if and how metformin can reliably extend human healthspan and whether or not this doesn’t come with some sort of drawback that just hasn’t been teased out yet.

Sarah Fox: For superior health, do you recommend to stay away from any alcohol? Or, are an occasional couple glasses of red wine on the weekends ok?

Rhonda Patrick: Sarah, you and, indeed, probably Tim, will be relieved to know that I think a couple of glasses of red wine on weekends are probably OK.

The post Transcript: Dr Rhonda Patrick on Exploring Smart Drugs, Fasting, and Fat Loss (#237) appeared first on The Blog of Author Tim Ferriss.

I’m often asked about my morning routine, which I detailed at length in a previous podcast.

For me, a reliable nighttime routine is just as important.

The short video below explains the exact protocol I use to wind down in the last 60 minutes of my day. Some of these tactics have been honed over many years, while others have been borrowed from guests on The Tim Ferriss Show. (Note: I’ve collected all of my favorite habits and routines from podcast guests — including some you haven’t met — in Tools of Titans.)

In my experience, these evening steps practically guarantee less stress and a better night’s sleep.

Do you have any favorite nighttime rituals? Please share in the comments below! Enjoy…

The post My Evening Routine for Optimal Relaxation and Sleep appeared first on The Blog of Author Tim Ferriss.

I’ve written about my morning journaling routine once before.

But my journaling–think of it as freezing thinking on paper–isn’t limited to mornings. I use it as a tool to clarify my thinking and goals, much as Kevin Kelly (one of my favorite humans) does. The paper is like a photography darkroom for my mind.

Below is a scan of a real page. Both entries are from October 2015.

The first entry (top half) is simply a list of “fun” things I felt compelled to schedule after the unexpected death of a close friend. Since I’ve ticked all of the bullets off. You’ll notice that I blurred out a few sensitive bits, and I won’t spend time on this entry in this post.

The second entry (bottom half) was written in Samovar Tea Lounge in San Francisco after a two-hour walk. The gestation period during walking and subsequent entry lead me to re-incorporate “deloading” phases in my life. “Deloading” is a term often used in strength and athletic training, but it’s a concept that can be applied to many areas. Let’s look at the sports definition, here from T Nation:

A back-off week, or deload, is a planned reduction in exercise volume or intensity. In collegiate strength-training circles, it’s referred to as the unloading week, and is often inserted between phases or periods. Quoting from Essentials of Strength Training and Conditioning: “The purpose of this unloading week is to prepare the body for the increased demand of the next phase or period,” and to mitigate the risk of overtraining.

So, how does this relate to creativity, productivity, or quality of life?

First, I’ll give a personal outcome — In the last 12 months, I’ve used “deloading” outside of sports to decrease my anxiety at least 50% while simultaneously doubling my income.

Deloading for business, in my case, consists of strategically taking my foot off the gas. I alternate intense periods of batching similar tasks (recording podcasts, clearing the inbox, writing blog posts, handling accounting, etc.) with extended periods of — for lack of poetic description — unplugging and fucking around.  Oddly enough, I find both the batching and unplugging to free up bandwidth and be restorative.

The unplug can still be intense (here’s a personal example in Bali), but you shouldn’t be working on “work.”

Let’s dig into the journal entry, as it provides much of the reasoning.

I’ve provided the scan (click to enlarge) and transcribed the entry below it, including many additional thoughts. The journal itself (Morning Pages Workbook) I explain here:

Now, the transcription with revisions and additional thoughts:

– TUES – SAMOVAR @ 5:40PM –

The great “deloading” phase.

This is what I’m experiencing this afternoon, and it makes a Tuesday feel like a lazy Sunday morning. This is when the muse is most likely to visit.

I need to get back to the slack.

To the pregnant void of infinite possibilities, only possible with a lack of obligation, or at least, no compulsive reactivity. Perhaps this is only possible with the negative space to–as Kurt Vonnegut put it–fart around? To do things for the hell of it? For no damn good reason at all?

I feel that the big ideas come from these periods. It’s the silence between the notes that makes the music.

If you want to create or be anything lateral, bigger, better, or truly different, you need room to ask “what if?” without a conference call in 15 minutes.  The aha moments rarely come from the incremental inbox-clearing mentality of, “Oh, fuck… I forgot to… Please remind me to… Shouldn’t I?…I must remember to…”

That is the land of the lost, and we all become lost.

My Tuesday experience reinforced, for me, the importance of creating large uninterrupted blocks of time (a la maker’s schedule versus manager’s schedule), in which your mind can wander, ponder, and find the signal amidst the noise. If you’re lucky, it might even create a signal, or connect two signals (core ideas) that have never shaken hands before.

For me, I’ve scheduled “deloading” phases in a few ways: roughly 8am-9am daily for journaling, tea routines, etc.; 9am-1pm every Wednesday for creative output (i.e. writing, interviewing for the podcast); and “screen-free Saturdays,” when I use no laptops and only use my phone for maps and coordinating with friends via text (no apps).  Of course, I also use mini-retirements a few time a year.

“Deloading” blocks must be scheduled and defended as strongly as–actually, more strongly than–your business commitments. The former can be a force multiplier for the latter, but not vice-versa.

So, how can one throttle back the reactive living that has them following everyone’s agenda except their own?

Create slack, as no one will give it to you. This is the only way to swim forward instead of treading water.

###

Did you enjoy this? Please let me know in the comments.  I’d also love to hear of how you “deload,” if you do.

If you’d like more on my morning routines, here are five habits that help me tremendously.

As always, thanks for reading.

The post Why You Need a "Deloading" Phase in Life appeared first on The Blog of Author Tim Ferriss.

This short (<5 minutes) video will teach you how to triple your reading speed in less than 20 minutes. It works nearly immediately, and there is zero loss in comprehension.

No voodoo, no pseudoscience — just two tricks for optimizing eye movement.

Some of you learn better with text, and some of you learn better with video. As one commenter who watched the above video put it:

“Tim, thanks so much for this video. I read your blog post about this like four times without being able to get it. With a video, it’s much easier.”

Have fun, and I’d love to hear your results in the comments.

If you enjoy this, you might also like my posts on rapid language learning, or my interview with champion memory competitor, Ed Cooke. You can stream the latter below:

The post Learn How to Triple Your Reading Speed in 5 Minutes (Seriously) [VIDEO] appeared first on The Blog of Author Tim Ferriss.

“It’s [about] getting closer to the source and not being distracted by any nonsense…” — Rick Rubin

Rick Rubin has been called “the most important [music] producer of the last 20 years” by MTV.

Rick is also revered as something of a Zen master, and he is as deep as he is soft-spoken. He rarely grants interviews, and one condition of doing this one was the setting: his hyper-heated barrel sauna at home.

In this episode, we delve into how Rick helps artists (e.g. Jay Z, Shakira, Johnny Cash, etc.) produce their best work. Not only that, we also discuss Rick’s step-by-step experience losing 135+ pounds. He describes underwater weightlifting stories, training with Laird Hamilton, testing different diets, and much more.

Rick’s resume includes everyone from Johnny Cash to Jay Z. His metal artists include groups like Black Sabbath, Slayer, System of a Down, Metallica, Rage Against the Machine, and Linkin Park. He’s worked with pop artists like Shakira, Adele, Sheryl Crow, Lana Del Rey, and Lady Gaga. He’s also been credited with helping to popularize hip hop with artists like LL Cool J, The Beastie Boys, Eminem, Jay Z, and Kanye West.  And that’s just a small sample.

This conversation teaches a cohesive lesson in breaking down complex skills with deep and subtle problem solving.

The sauna caused the microphones to burn our hands and us to nearly pass out. DON’T TRY THIS AT HOME, folks! I think it adds a hilarious element to the whole thing, but it’s not without risks.

[Last but not least, if you haven’t seen my new TV show, which is #1 on iTunes as I write this, please check out The Tim Ferriss Experiment! There are 13 episodes, including ones with surfer Laird Hamilton and “top 10 drummer of all-time” Stewart Copeland.]

Enjoy!

You can find the transcript of this episode here. Transcripts of all episodes can be found here.

• Listen to it on iTunes.
• Stream by clicking here.
• Download it as an MP3 by right-clicking here and choosing “save as”.

Interested in learning more about world-class musicians? — Check out my interview with Amanda Palmer who left her record label and raised more than $2 million via crowd funding. (stream episode below or right-click here to download):

Also, don’t miss Justin Boreta of The Glitch Mob, one of the biggest electronic groups on the planet. In my conversation with Justin, we play their never-before-heard draft versions of their songs and then explore what it takes for Justin to move that draft through 300+ versions to a final version which will knock your socks off (stream below or right-click here to download):

This episode is sponsored by Onnit. I have used Onnit products for years. If you look in my kitchen or in my garage you will find Alpha BRAIN, chewable melatonin (for resetting my clock while traveling), kettlebells, maces, battle ropes, and steel clubs. It sounds like a torture chamber, and it basically is. A torture chamber for self-improvement! Ah, the lovely pain. To see a list of my favorite pills, potions, and heavy tools, click here.

This podcast is also brought to you by 99Designs, the world’s largest marketplace of graphic designers. Did you know I used 99Designs to rapid prototype the cover for The 4-Hour Body? Here are some of the impressive results.  Click this link and get a free $99 upgrade.  Give it a test run…

QUESTION(S) OF THE DAY: Rick Rubin cites “heart work” as critical for creatives. What is the balance of heart work and head work in your creation process? 50/50? 70/30? How did you realize what works best for you? Please let me know in the comments.

Scroll below for links and show notes…

Selected Links from the Episode

• Slow Burn by Stu Mittleman
• Get the app that helped Rubin count calories, MyFitnessPal
• Explore world-class music lists like those Rolling Stone and/or Mojo
• Tao Te Ching translation by Stephen Mitchell
• Wherever You Go, There You Are by Jon Kabat-Zinn
• Learn more about the documentary 20,000 Days on Earth
• Learn more about the Wim Hof Breathing Technique

Show Notes

• The story of how Rick Rubin lost 135-145 pounds [7:50]
• Sleep Tools: A process for rebuilding your circadian rhythm for the first time [10:50]
• What does Rick Rubin “do”? [22:45]
• Transitioning into a career of record producing [23:35]
• On letting music be discovered vs. manufactured [24:30]
• What gets in the way of artists producing their best work [26:05]
• Recommendations for contemporary music [30:55]
• How Rick Rubin learned that music was something he could do as a career [34:00]
• Hip-hop to heavy metal and how to approach music with appreciation [38:05]
• Working with artists in different genres: LL Cool J to Slayer [40:15]
• Meditation and managing disruption [42:40]
• Who comes to mind when Rubin thinks of the word “successful” [46:50]
• Lessons learned from time spent with Don Wildman [49:45]
• Most gifted books and favorite documentaries [51:35]
• Managing the experience of overwhelm [54:30]
• About Rick Rubin’s cameo for 99 Problems and Jay Z’s creative process [56:50]
• On being introduced to the sauna/ice-bath combination [1:00:10]
• Underwater weight training and lessons from Laird Hamilton [1:02:15]
• Other exercises: Hyperbaric oxygen and the Wim Hof method  [1:08:35]
• How Rubin uses small tasks to help others [1:10:05]
• Advice for his 20-year old and 30-year old self [1:13:10]

People Mentioned

• Stu Mittleman
• Mo Ostin
• Dr. Heber at UCLA
• Black Sabbath
• Reign in Blood
• Slayer
• LL Cool J
• Don Wildman
• Laird Hamilton
• Jay Z
• Chris Chelios

The post Rick Rubin on Cultivating World-Class Artists (Jay Z, Johnny Cash, etc.), Losing 100+ Pounds, and Breaking Down The Complex (#76) appeared first on The Blog of Author Tim Ferriss.

One tiny favor! If you’re enjoying the podcast, could you please take 30 seconds now to leave a brief review on iTunes? Just click “View in iTunes” under my pic here. Once I pass 2,000 reviews, I’ll reciprocate by writing a massive, behind-the-scenes post on everything I’ve learned about podcasting. I promise tricks of the trade galore, just as in-depth as the “Hacking Kickstarter” post. Speaking of which…

Ed Cooke is a dear friend and a Grandmaster of Memory.  In 2010, he was interviewed by a journalist named Joshua Foer. Under Ed’s Yoda-like training, Joshua became the very next American Memory Champion in 2011.  It took less than a year for Ed to transform a novice from unknown to world-class.

But how?!?

Aha… This interview explores Ed Cooke’s brilliant techniques (many of which I use), strategies, and practical philosophies.  To boot, he’s also a wicked funny bastard!  If you enjoyed the epic interviews with Kevin Kelly, Josh Waitzkin, or Maria Popova, you’ll love Ed.  He’s one of a kind.

You can find the transcript of Episodes 52 and 53 here. Episode 53 begins on page 24. Transcripts of all episodes can be found here.

• Listen to it on iTunes.
• Stream it by clicking for Part 1 here and Part 2 here.
• Download both as MP3s by right-clicking and choosing “save as”: Part 1 here and Part 2 here.

This podcast is brought to you by 99Designs, the world’s largest marketplace of graphic designers. Did you know I used 99Designs to rapid prototype the cover for The 4-Hour Body? Here are some of the impressive results.

QUESTION(S) OF THE DAY: What’s one mental feat you’d love to accomplish in 2015? Any tips or tricks you can share? Please share in the comments by clicking here.

Scroll below for links and show notes…

Enjoy!

And also… please subscribe to The Tim Ferriss Show on iTunes!  A kitten gets super powers every time you do this.

Non-iTunes RSS feed

Selected Links from the Episode

• Ed Cooke on Twitter (@tedcooke). Say hello!
• Learn more about Memrise
• Learn more about the World Memory Championships
• Moonwalking with Einstein by Joshua Foer
• Theory of Colours by Johann Wolfgang von Goethe
• Read Tim’s thoughts on delayed philanthropy (and the reasons against it) – The Karmic Capitalist
• Spectacle by David Rockwell & Bruce Mau
• Station to Station by Doug Aitken
• In Praise of Idleness by Bertrand Russell
• Armando Iannucci and The Armando Iannucci Show
• Withnail and I
• Learn more about Sensory Substitution and Paul Bach-y-Rita
• Touching the Rock by John Hull
• The Blind Man Who Taught Himself to See by Michael Finkel
• The Joyous Cosmology by Alan Watts
• Is Trilled Smell Possible?

Show Notes

Part 1

• How Tim and Ed were introduced, and what it takes to be a “grandmaster of memory” [5:02]
• The dynamic that produces rapid developments in speed and capability [8:15]
• The outcome of the unusual 4-Hour Chef memory competition [13:02]
• The story of winning the US memory championships and subsequently training Joshua Foer [21:02]
• Exploring the extraordinary skill of imagination [24:22]
• Memory techniques which can be utilized in everyday life [32:02]
• Recommendations for designing house parties based on memory techniques [39:02]
• Clarifying and finding objectivity…and the value thereof [41:47]
• Rapid-fire questions [47:45]

Part 2

• Balancing intuition and analytical decision making [1:27]
• How to set up incentives to flog yourself into self-discipline and systems thinking [5:55]
• On merit and virtue [8:05]
• Contrasting homelessness with the strange selfishness of Silicon Valley [10:00]
• The conundrum of the Bill Gates model of philanthropy [18:25]
• What is financial security, and how does Ed Cooke define it? [24:20]
• Ed Cooke’s take on Burning Man [30:55]
• Quick fire theory about why Burning Man is the most brilliant institution in the world [32:20]
• How to extract the Burning Man experience for a group of 20? [41:40]
• Escaping existential doldrums [45:55]
• Balancing present-state mindfulness with building things [52:25]
• More rapid-fire questions [55:40]
• A specific defining moment from Ed Cooke’s childhood and the theory of exteroception [1:07:25]

People Mentioned

• Johann Wolfgang von Goethe
• Monty Python
• Armando Iannucci
• Alan Partridge
• Withnail and I
• Kevin O’Regan
• Paul Bach-y-Rita
• Seymour Papert
• Daniel Kish
• Alan Watts

The post Ed Cooke, Grandmaster of Memory, on Mental Performance, Imagination, and Productive Mischief (#52 & #53) appeared first on The Blog of Author Tim Ferriss.

Can you rewire your brain in two weeks?  The answer appears to be — at least partially — yes.

The following is a guest post by Shane Snow, frequent contributor to Wired and Fast Company and author of the new book SMARTCUTS: How Hackers, Innovators, and Icons Accelerate Success.  Last year, he wrote about his two-week Soylent experiment, which went viral and racked up 500+ comments.  He knows how to stir up controversy.

In this post, Shane tests the “brain-sensing headband” called Muse.

It’s received a lot of PR love, but does it stand up to the hype?  Can it make you a calmer, more effective person in two weeks?  This post tackles these questions and much more.

As many of your know, I’m a long-time experimenter with “smart drugs,” which I think are both more valuable and more dangerous that most people realize.  This includes homemade brain stim (tDCS) devices (I wouldn’t recommend without supervision) and other cutting-edge tools.  If you’d like to read more on these topics, please let me know in the comments.

In the meantime, I hope you enjoy Shane’s experimentation!…

Enter Shane Snow

The electrodes needed to be adjusted to fit my sweaty head, which was apparently the largest size the product could accommodate.

I was sitting on a porch in palpable D.C. humidity, on a midsummer’s morning at Bolling Air Force Base, trying to get a quartet of EEG sensors to connect my brain to my Samsung Galaxy. The purple box on my screen kept blinking in and out of sync.

Inside the house, my friend’s two-year-old was jumping violently on the sofa—the same sofa that the shedding 15-pound cat named Endai and I had shared for the past week. The house was in shambles; movers were busily trucking everything away to my friend’s soon-to-be new home in New Mexico. Hence the porch.

I had been sleeping on said couch due to the abrupt ending of an 8-year relationship, which had left me stunned and homeless for the preceding three weeks.  As luck would have it, the anti-anxiety pills my shrink had prescribed for me to take “as needed” were back in New York in my friend Simon’s living room. Crap. My calendar had just alerted me that I’d missed the Skype call start time for my company board meeting, right before the movers unplugged the Internet. Meanwhile, a platoon of military helicopters had decided to play what appeared to be a game of “who can hover the longest over the neighborhood”. Chuk, chuk, chuk, chuk, chuk. CHUCK. CHUCK.

My stress levels were high.

Seemed like as good a time as any to try out my new gadget: a brainwave-sensing headband called the Muse, and its companion app, Calm.

I placed the band’s centimeter-wide contact strip of electrodes against my forehead and rested the plastic against the top of my ears, fiddling with the fit until my phone finally registered a solid connection for each of the sensors, two on my temples, two behind my ears. I donned my white Audio-Technica DJ headphones and fired up the app, which in a soothing voice instructed me to sit up straight, and breeeeeeeathe.

Calm is a simple meditation exercise: Count your breaths. Don’t try to force them. Your body knows how to breathe. Simply pay attention, the female voice in my headphones told me. After Muse calibrated to my brain’s “active” state—by making me brainstorm items in a series of topics—I was given five minutes of nature sounds to breathe to. When calm and focused, I enjoyed the sound of lapping waves and birds tweeting; when my mind wandered, sturdy winds picked up and the birds flew away.

At the end of five minutes, the app confirmed: I am not very calm.

Thus began my two week experiment in brain therapy. I’d been planning on acquiring a Muse after having caught wind of its development nearly two years before, but who knew it would finally be released during the most anxious time of my adult life? Two weeks was plenty of time, Muse inventor Ariel Garten told me, for the Muse focus training exercises “to reduce perception of pain, improve memory, improve affect, reduce anxiety, and also improve emotional intelligence.”

Seemed a little good to be true, but I was willing to test it.

Electroencephalography (EEG—the recording of electrical activity emitted from the brain) has come a long way in the last 100 years, since doctors drilled holes in monkeys heads to attach sensors, and eventually glued contacts with cathode ray tubes to intact human skulls to map brain activity. They discovered that the brain emits oscillating signals of variable frequency, and the frequency of the oscillations indicates what’s happening—at a high level—in one’s mind. These “waves” are generally delineated into categories based on frequency ranges:

• Delta waves: indicate deep sleep. (1-3 Hz)
• Theta waves: indicate deep relaxation or meditation. (4-8 Hz)
• Alpha waves: indicate a relaxed brain state, what Garten calls “an open state of mind.” (9-13 Hz)
• Beta waves: indicate alert consciousness and fire up when you’re actively thinking. (14-30 Hz)
• Gamma waves: indicate high alertness and are often associated with learning. (30-100 Hz)

The original purpose of EEG was the study of epilepsy. Over the decades, however, as computers improved, neuroscientists’ increasing capability to process the enormous amount of data the brain throws off allowed them to experiment with EEG for other uses, such as attention therapy.

In his 2007 book, The Brain That Changes Itself, neuroscientist Norman Doidge made mainstream the then recent (and surprising) finding that “the brain can change its own structure and function through thought and activity.” Our intelligence and tendencies are not locked in once we’re no longer children, as popular belief once held. Once our brain was wired, it could still be rewired. Doidge called it, “the most important alteration in our view of the brain since we first sketched out its basic anatomy and the workings of its basic component, the neuron.”

This adaptability factor of the brain is called “neuroplasticity.” You may have seen dubious advertisements for “brain-enhancing games” and other gimmicks that drop the term neuroplasticity in impressive-sounding (but often meaningless) marketing speak. Despite this misuse, the plasticity of our neurons is, in fact, fact. Our brains use it to wire themselves naturally, but in the past several years scientists have developed a simple procedure to “hack” them.

Neurofeedback training, or NFT as the scientists call it, is a conditioning method wherein a patient is hooked up to an EEG and shown how active her brain is, thus allowing her to concentrate on exercises that exploit neuroplasticity to build mental muscles that allow her to consciously affect her resting brain activity. Clinical studies have shown that NFT helps the majority of patients to improve their cognitive control and have also helped ADHD sufferers significantly improve their ability to focus.  NFT has even been shown to have a positive effect on depression.

The two prerequisites to being able to pull off NFT are EEG sensors and a computer processor that can turn an EEG scan into real-time feedback. The electricity coming off the brain is orders of magnitude weaker than a standard AA battery, which means sensors must be powerful, delicate, and well-attached to pick anything up. Doctors have found that the skull reduces the signal significantly and thus would prefer if we didn’t have skulls (for examination purposes, that is), but have mostly settled on using wet sensors—electrodes affixed to the scalp or forehead using conductive gel.

The breakthrough that enabled a more practical, portable EEG device like the Muse claims to be, was the advent of dry sensors, or metal contacts that can use the skin’s own moisture or sweat to attain the necessary conductivity.

“Brain waves are very, very, very quiet.  They’ve had to make their way all the way through your thick, thick skull,” Garten says. But sensor technology is improving at a rate that indicates we’re two to three years away from non-contact sensors, she predicts.

And in 2014, processing power is no longer a problem. “Ten years ago we were using fiber optic cable to make sure that you got this extraordinary data into what was like an egg carton and an ancient Commodore computer so that they could do all the processing,” Garten says. “Now, we can just use a phone and Bluetooth.”

When I’d first laid hands on the Muse a year and a half before, it was a chunky slab of plastic and metal. Garten and I met up at a design gallery in Manhattan for a demo of the prototype headband she’d been working on for the better part of the last decade. A Canadian fashion designer turned neuroscientist, she spoke earnestly about the potential applications for measuring one’s brainstate to ameliorate stress and perhaps one day cure ADHD and anxiety.

Garten’s prototype Muse measured the activity of these waves and output them to an iPad like a seismograph. After I donned the plastic headband, I watched in real time as slowing my breathing or concentrating on something or simply talking affected the different wave forms.

“The long term vision is this tool is going to be a regular part of our daily lives,” Garten told me. “You know, like pedometers that help people manage and understand their physical exercise. Brain health is going to be something that is on everybody’s mind. Up until now, there has been no way to, basically, like put a stethoscope up to your brain and say, ‘How is it doing?’”

Ten years ago, a NFT system with Muse-like capabilities (often found in a chiropractor’s office) would cost 5 figures and a closet-worth of space. Now the processing power lives on a standard smartphone, and Muse sensors cost $299.

Eventually, Garten predicted, doctors would actively use it to treat the mentally ill. Programmers would build brainwave-control apps for gaming and smart homes and surfing the Internet on top of Muse’s technology.

But for now it just gives you tweety birds.

My porch session resulted in precisely zero of them:

This session, for which I got a score of “31% calm,” would be the first of many mental workouts in my DYI NFT experiment. Would regular usage of the Muse headband actually change my brain and help fix my anxious life? Or would it turn out to be another wearable that’s more hype than help?

THE EXPERIMENT

The hypothesis (aka sales pitch) was that by using Muse, I’d improve my ability to focus and maintain my cool during my stressful day-to-day.

So for fifteen days, I performed a five-minute Muse Calm session each morning within an hour of waking up and shaking off sleep. I’d sit in a similar setting (straight-back chair in a room alone), in similar clothing (comfortable, shorts and t-shirt, no shoes), with no distractions (accomplished via Bose noise-canceling earbuds) every time.

Additionally, I performed a series of sessions in various random non-comfortable settings, to test whether different mental exercises produced different results, or whether I could remain calm while being assaulted by various outside forces—which is the real goal of NFT, rather than simply getting better at a “game” in quiet isolation.

Though the app would tell me if my brain was getting better at calming itself during the exercise, the less easy-to-quantify result would be to see whether my level of general anxiety would decrease as I got better at the Calm app. (I.e. am I forming these alleged neural pathways?) Garten and Calm each told me that once I completed enough sessions (5,000 points’ worth), the app would unlock insights about how my brain was doing, which could shed some light on my meta-state. But I also tracked my overall emotional and mental state by keeping regular journal entries throughout the two weeks.

For a control—and as a basic BS test—I performed a session while reading a book instead of doing the breathing exercise. I read three pages of Murakami’s new one, Colorless Tsukuru Tazaki, and my brain was all sorts of active. Mr. Murakami, your work is stimulating. Science hath proven it:

THE RESULTS

Most of my morning sessions took place between 8 and 11 a.m. I keep a somewhat irregular sleep schedule (a source of anxiety, or symptom?), but aim for 7 hours a night. The important part for this experiment was to make sure that I did my Muse session within an hour of waking, but after I had stopped being groggy. In other words: before my morning exercise, after my morning pee.

I kept the morning schedule up with a few exceptions: on August 18, the Muse Calm app caused the headband to think my brainwaves had completely flatlined. I contacted the Muse team, and they confirmed that this was indeed a bug that they were working on fixing that day. On August 20, 22, 24, and 26 I skipped my morning session due to extenuating circumstances. (The 24th, for example, was my birthday, and I stayed out until 8 a.m.. My first session that day was at 4 p.m. and resulted in a hangover-level 31%.) But throughout my 15-day experiment, I never went a day without doing one or more sessions, and I never went two days without doing a standardized morning session.

In all, I completed 24 sessions. Here’s how my morning sessions went over the course of the two weeks:

You’ll notice that I did pretty poorly for the first several sessions, then experienced a jump in improvement on August 17. What this chart doesn’t show is that though it was that August 17 was actually the seventh session I’d done in total. So I was getting better, but I’m not entirely sure why such a dramatic jump. You’ll also notice a slight dip on the 25th and 27th. On these days, I was having a couple of particularly anxious mornings (due to personal issues); however, on these days I still maintained double the calm as my first few sessions—which were less emotionally fraught than these days.

My final morning session of the experiment, on August 28, was a serene 89%—my best yet, and just one spike of brain activity away from monk-like zen:

More importantly, I attracted a fucking flock of tweety birds:

Here’s how I performed on my random sessions in less-controlled environments:

Clearly, it was harder for me to focus and remain calm when I was tired or emotionally compromised.

Trains made it easier to focus (likely due to the lack of noise and abundance of leg room). Airplanes tend to give me claustrophobia, but it’s also likely that the vibrations of the plane itself caused my muscles to move (generating louder electrical signals than your brain emits) and made my results so poor during the flight. There certainly was a lot of shaking going on during my flight.

Interestingly, listening to calming music (I tend to put Blackmill’s “Miracle” album on repeat when I want to relax or single-task) outperformed no sound (simply trying to calm myself without an aid). On August 27, my regular session with the app’s wind and waves, resulted in 12% less calm than my music experiment immediately after.

As far as the meta, “how am I doing” portion of the experiment went, I eagerly awaited when I could unlock the “Insights About You” page of the app, after racking up enough “calm points”. Disappointingly, though Garten and Muse Calm both promised me these “additional features and special insights into my brain”, once I unlocked the screen, I got simply a blank, broken page:

When asked, the Muse publicist confirmed that the feature “actually hasn’t been developed yet” and relayed the (in my opinion) unlikely explanation that “there was a miscommunication between the product and dev teams.”

My journal entries indicated a general decrease in agitation and worry by the end of the experiment. My ability to focus on tasks (primarily writing) seemed to improve. I have a tendency to get distracted when I’m writing, and in the same way that the waves-and-wind exercise in the app teaches you to power through distractions and focus on your breath, I felt that I already was improving my ability to notice a distraction but keep it in the background instead of indulging it.

Furthermore, as I walked down busy streets or lay in bed—times when I normally would ruminate—I found myself subconsciously slowing breaths and counting them as a means of shoving out bad thoughts and calming down.

“Many smart people who use their brains a lot are ‘high beta,’” explained my therapist (whose name I’ll omit to maintain a shred of personal privacy) when I asked her about this. An award-winning Manhattan psychologist and author, she has used NFT herself.  A few years ago, she used a professional-grade version of Muse to teach her own active brain to be silent. “I couldn’t go to sleep without the TV on,” she said. “The minute it was quiet, my brain would explode with activity.”

With measurement and some mental situps, she calmed her own rumination—as apparently thousands of people have done at clinics that use EEG therapy. That “neuroplasticity” thing that people throw around, it turns out, is real. And it works as fast as one can form a bad habit.

“The brain can be retrained,” she said. “People think it can’t, but it can.”

POTENTIAL ISSUES

One of the main limitations of the Muse Calm app—or at least questions that I had from the beginning—was the validity of the wind-and-waves feedback sound system itself, as well as the “count your breaths” mediation exercise. My assistant, Erin, who’s a yoga instructor and meditation expert by night, was skeptical that the Muse Calm exercise was the most effective method the app could have chosen. Why would you have the distracting sounds get worse when you were most compromised? she said. Doesn’t that create a self-defeating cycle?

Garten responded: “We did a bunch of experimentation on positive reinforcement and negative reinforcement and we ultimately built an application with a mix of both. The negative reinforcements of the wind can definitely be distracting, but what you learn over time is also this lesson in not being judgmental when things don’t work.”

A 2010 study by scientists from the University of Pennsylvania and Georgetown found positive links between “mindfulness training”—the popular meditation practice of calmly noticing, but not changing what’s happening to you—has a positive effect on working memory. The Muse Calm’s “notice and count your breaths” exercise is a form of mindfulness training, and appears to hold up under scientific scrutiny, but the wind-and-waves feedback loop (NFT) throws a bit of a wrench into true “mindfulness”, since the act of being mindful ends up affecting your environment, whereas the point of mindfulness meditation is to notice but not affect.

Could a “pure” mindfulness exercise without the instant and self-reinforcing feedback outperform Calm’s NFT/mindfulness hybrid? Beats me, but it’s a question I’d want to test in future experiments.

Other limitations or potential variables that could affect the science behind my two-week experiment include the following:

• Factors such as the exact time I awoke and what kind of bed I slept in changed slightly from day to day, as I was traveling and couch-hopping. While the course of my experiment showed an upward trend in calm, I wasn’t able to duplicate the time and setting of each of my morning sessions precisely, which could affect the results to some degree.
• Since I was dealing with the fresh personal trauma, perhaps I was naturally recovering psychologically during the two weeks of my experiment (i.e. regression to the mean). My therapist insists that the relationship wound was too fresh and two weeks is not enough time to work through anything, but it still could be a factor.
• This experiment was only two weeks, which I was told would be a sufficient minimum for results. More time could certainly help verify the trends I observed in my short experiment. (And I plan to keep using Muse over the next few months to track just that.)
• And of course, my observations about how I was feeling were, by nature, subjective. (However, if my psychological improvement is all in my head, that’s okay by me—it was in my head to begin with! And actually, I’ve interviewed one scientist who’s studying how placebos actually form neural pathways that can physically cure psychological issues. Very interesting stuff happening in this field.)

EPILOGUE

The electrodes had no problem beaming the signal from my sweaty head to my Android this time.

I was sitting on a set of red bleachers in disgusting New York humidity in the middle of Times Square, Manhattan. The familiar female voice in my headphones instructed me to close my eyes, as she had two dozen times before.

Around me, a trillion stressed-out tourists were busily taking selfies and worrying about pick pockets. A troupe of Chinese activists had just accosted me with pamphlets and signs concerning some “Jesuit Father discrimination” something-or-other, meanwhile a quartet of feather-headressed ladies performed a synchronized dance on the steps below me. A bumblefoot pigeon had taken up residence on my step and didn’t seem to want to leave me alone. My entire body was sweating.

I’d just walked through my old neighborhood, a surprisingly painful reminiscence. Unexpectedly, one of my ex’s favorite songs had begun playing on shuffle as I made my way through the crowd, further dampening my mood. In the back of my head were the several overdue stories for editors of various publications in line with my book launch, and the approximately 200 priority emails stacked up in my inbox. I was lugging my entire life in an overstuffed backpack and had just spilled protein drink all over my shorts—which I just now realized were my only available leggings, because I’d left the remaining two pairs of jeans I owned back in my friend Simon’s freezer (here’s why). I was pensive and hot and frustrated and dripping.

Once again, I donned my brainwave headband, which once again told me to breeaaathe.

About halfway through my five-minute session—the twenty-fifth I’d undertaken since meeting Muse—some nearby tourists began singing “Happy Birthday” so loudly that I could hear them through my noise-canceling headphones. A fire engine blared its siren in place for a full minute, stuck one block away in Times Square traffic. My butt burned on the red steps, in the August heat. My posture was killing me.

At the end of five minutes, Muse confirmed: I was pretty damn calm.

The two spikes in active brain activity in this chart were the fire truck and the birthday party, each of which I recovered from almost instantly. Aside from that, my brain state was either neutral or calm the entire time:

Plus I attracted 15 tweety birds:

Despite the chaos in my life, there was no doubt that this little device had made me a calmer person in just two weeks. I could play through the mental and physical pain with twice the composure as just fifteen days before.

Muse has a way to go before the guy with the electric headband on in Times Square doesn’t just look like an idiot. And the Calm app could definitely use work. (Different meditation exercises, please?) However, the science behind what the Muse team is doing is real, the technology promising, and a bevy of independent programmers are already building fascinating applications on top of Muse.

With the development of cheap and portable EEG monitors like Muse, are we a few lines of code away from controlling light switches and video games with our brains? It’ll take a while.

But I, at least, am a step closer to mind over matter.

Breeeeathe….

###

Question of the day:  What do you think are the next frontiers of self-experimentation and self-tracking?  What would you like me to test for you?  Please let me know in the comments by clicking here.

The post Can You Rewire Your Brain In Two Weeks? One Man's Attempt… appeared first on The Blog of Author Tim Ferriss.

The following is a guest post by Shane Snow, a frequent contributor to Wired and Fast Company.  Last year, he wrote about his two-week Soylent experiment, which went viral and racked up 500+ comments.

This post is adapted from his new book, SMARTCUTS, and it will teach you a few things:

• How to use strategic “laziness” to dramatically accelerate progress
• How “DHH” became a world-class car racer in record time, and how he revolutionized programming (they’re related)
• A basic intro to computer programming abstraction

Note: the technical aspects of programming have been simplified for a lay audience.  If you’d like to point out clarifications or subtleties, please share your thoughts in the comments!   I’d love to read them, as I’m thinking of experimenting with programming soon.

Enter Shane Snow

The team was in third place by the time David Heinemeier Hansson leapt into the cockpit of the black-and-pink Le Mans Prototype 2 and accelerated to 120 miles per hour. A dozen drivers jostled for position at his tail. The lead car was pulling away from the pack—a full lap ahead.

This was the 6 Hours of Silverstone, a six-hour timed race held each year in Northamptonshire, UK, part of the World Endurance Championship. Heinemeier Hansson’s team, Oak Racing, hoped to place well enough here to keep them competitive in the standings for the upcoming 24 Hours of Le Mans, the Tour de France of automobile racing.

Heinemeier Hansson was the least experienced driver among his teammates, but the Oak team had placed a third of this important race in his hands.

Determined to close the gap left by his teammate, Heinemeier Hansson put pedal to floor, hugging the curves of the 3.7-mile track that would be his singular focus for the next two hours. But as three g’s of acceleration slammed into his body, he began to slide around the open cockpit. Left, then right, then left. Something was wrong with his seat.

In endurance racing, a first place car can win a six- or 12-hour race by five seconds or less. Winning comes down to two factors: the equipment and the driver. However, rules are established to ensure that every car is relatively matched, which means outcomes are determined almost entirely by the drivers’ ability to focus and optimize thousands of tiny decisions.

Shifting attention from the road to, say, a maladjusted driver’s seat for even a second could give another car the opportunity to pass. But at 120 miles per hour, a wrong move might mean worse than losing the trophy.  As Heinemeier Hansson put it, “Either you think about the task at hand or you die.”

Turn by turn, he fought centrifugal force, attempting to keep from flying out while creeping up on the ADR-Delta car in front of him.

And then it started to rain…

***

When Heinemeier Hansson walked onto the racing scene in his early 30s, he was a virtual unknown, both older and less experienced than almost anyone in the leagues. A native of Denmark, he’s tall, with a defined jaw and dark spikey hair. At the time he raced 6 Hours of Silverstone, it had been about five years since he first drove any car at all.

That makes him one of the fastest risers in championship racing.

Despite that, Heinemeier Hansson is far better known among computer programmers—where he goes by the moniker DHH— than car enthusiasts. Though most of his fellow racers don’t know it, he’s indirectly responsible for the development of Twitter. And Hulu and Airbnb. And a host of other transformative technologies for which he receives no royalties. His work has contributed to revolutions, and lowered the barrier for thousands of tech companies to launch products.

All because David Heinemeier Hansson hates to do work he doesn’t have to do.

DHH lives and works by a philosophy that helps him do dramatically more with his time and effort. It’s a principle that’s fueled his underdog climbs in both racing and programming, and just might deliver a win for him as the cars slide around the rainslicked Silverstone course.

But to understand his smartcut, we must first learn a little bit about how computers work.

Think of the way a stretch of grass becomes a road. At first, the stretch is bumpy and difficult to drive over. A crew comes along and flattens the surface, making it easier to navigate. Then, someone pours gravel. Then tar. Then a layer of asphalt. A steamroller smooths it; someone paints lines. The final surface is something an automobile can traverse quickly. Gravel stabilizes, tar solidifies, asphalt reinforces, and now we don’t need to build our cars to drive over bumpy grass. And we can get from Philadelphia to Chicago in a single day.

That’s what computer programming is like. Like a highway, computers are layers on layers of code that make them increasingly easy to use. Computer scientists call this abstraction.

A microchip—the brain of a computer, if you will—is made of millions of little transistors, each of whose job is to turn on or off, either letting electricity flow or not. Like tiny light switches, a bunch of transistors in a computer might combine to say, “add these two numbers,” or “make this part of the screen glow.”

In the early days, scientists built giant boards of transistors, and manually switched them on and off as they experimented with making computers do interesting things. It was hard work (and one of the reasons early computers were enormous).

Eventually, scientists got sick of flipping switches and poured a layer of virtual gravel that let them control the transistors by typing in 1s and 0s. 1 meant “on” and 0 meant “off.” This abstracted the scientists from the physical switches. They called the 1s and 0s machine language.

Still, the work was agonizing. It took lots of 1s and 0s to do just about anything. And strings of numbers are really hard to stare at for hours. So, scientists created another abstraction layer, one that could translate more scrutable instructions into a lot of 1s and 0s.

This was called assembly language and it made it possible that a machine language instruction that looks like this:

10110000 01100001

could be written more like this:

MOV AL, 61h

which looks a little less robotic. Scientists could write this code more easily.

Though if you’re like me, it still doesn’t look fun. Soon, scientists engineered more layers, including a popular language called C, on top of assembly language, so they could type in instructions like this:

printf(“Hello World”);

C translates that into assembly language, which translates into 1s and 0s, which translates into little transistors popping open and closed, which eventually turn on little dots on a computer screen to display the words, “Hello World.”

With abstraction, scientists built layers of road which made computer travel faster. It made the act of using computers faster. And new generations of computer programmers didn’t need to be actual scientists. They could use high-level language to make computers do interesting things.

When you fire up a computer, open up a web browser, and buy a copy of my book online for a friend (please do!), you’re working within a program, a layer that translates your actions into code that another layer, called an operating system (like Windows or Linux or MacOS), can interpret. That operating system is a probably built on something like C, which translates to Assembly, which translates to machine language (1s and 0s), which flips on and off a gaggle of transistors.

(Phew.)

So, why am I telling you this? 
In the same way that driving on pavement makes a road trip faster, and layers of code let you work on a computer faster, hackers like DHH find and build layers of abstraction in business and life that allows them to multiply their effort.

I call these layers platforms.

***

At college in the early aughts, DHH was bored. Not that he couldn’t handle school intellectually. He just didn’t find very much of it useful.

He practiced the art of selective slacking. “Some of my proudest grades were my lowest grades,” he tells me.

We all know people in school and work with a masterful ability to maintain the status quo (John Bender on The Breakfast Club or the bald, coffee-swilling coworker from Dilbert), but there’s a difference between treading water and methodically searching for the least wasteful way to learn something or level up, which is what DHH did.

“My whole thing was, if I can put in 5 percent of the effort of somebody getting an A, and I can get a C minus, that’s amazing,” he explains. “It’s certainly good enough, right? [Then] I can take the other 95 percent of the time and invest it in something I really care about.”

DHH used this concept to breeze through the classes that bored him, so he could double his effort on things that mattered to him, like learning to build websites. With the time saved, he wrote code on the side.

One day, a small American web-design agency called 37signals asked DHH to build a project management tool to help organize its work. Hoping to save some time on this new project, he decided to try a relatively new programming language called Ruby, developed by a guy in Japan who liked simplicity. DHH started coding in earnest.

Despite several layers of abstraction, Ruby (and all other code languages) forces programmers to make countless unimportant decisions. What do you name your databases? How do you want to configure your server? Those little things added up. And many programs required repetitive coding of the same basic components every time.

That didn’t jibe with DHH’s selective slacking habit. “I hate repeating myself.” He almost spits on me when he says it.

But conventional coders considered such repetition a rite of passage, a barrier to entry for newbies who hadn’t paid their dues in programming.  “A lot of programmers took pride in the Protestant work ethic, like it has to be hard otherwise it’s not right,” DHH says.

He thought that was stupid. “I could do a lot of other interesting things with my life,” he decided. “So if programming has to be it, it has to be awesome.”

So DHH built a layer on top of Ruby to automate all the repetitive tasks and arbitrary decisions he didn’t want taking up his time. (It didn’t really matter what he named his databases.) His new layer on top of programming’s pavement became a set of railroad tracks that made creating a Ruby application faster. He called it Ruby on Rails.

Rails helped DHH build his project—which 37signals named Basecamp—faster than he could have otherwise. But he wasn’t prepared for what happened next.

When he shared Ruby on Rails on the Internet, programmers fell in love with it. Rails was easier than regular programming, but just as powerful, so amateurs downloaded it by the thousands. Veteran coders murmured about “real programming,” but many made the switch because Rails allowed them to build their projects faster.

The mentality behind Rails caught on. People started building add-ons, so that others wouldn’t have to reinvent the process of coding common things like website sign-up forms or search tools. They called these gems and shared them around. Each contribution saved the next programmer work.

Suddenly, people were using Ruby on Rails to solve all sorts of problems they hadn’t previously tackled with programming. A toilet company in Minnesota revamped its accounting system with it. A couple in New Jersey built a social network for yarn enthusiasts. Rails was so nice that more people became programmers.

In 2006 a couple of guys at a podcasting startup had an idea for a side project. With Rails, they were able to build it in a few days—as an experiment—while running their business. They launched it to see what would happen. By spring 2007 the app had gotten popular enough that the team sold off the old company to pursue the side project full time. It was called Twitter.

A traditional software company might have built Twitter on a lower layer like C and taken months or years to polish it before even knowing if people would use it. Twitter—and many other successful companies—used the Rails platform to launch and validate a business idea in days. Rails translated what Twitter’s programmers wanted to tell all those computer transistors to do—with relatively little effort. And that allowed them to build a company fast. In the world of high tech—like in racing—a tiny time advantage can mean the difference between winning and getting passed.

Isaac Newton attributed his success as a scientist to “standing on the shoulders of giants”—building off of the work of great thinkers before him.

Platforms are tools and environments that let us do just that. It’s clear how using platforms applies in computer programming, but what if we wanted to apply platform thinking to something outside of tech startups?

Say, driving race cars?

***

David Heinemeier Hansson was in a deep hole. Halfway through his stint, the sprinkling rain had become a downpour. Curve after curve, he fishtailed at high speed, still in third place, pack of hungry competitors at his rear bumper.

LMP cars run on slick tires—with no tread—for speed. The maximum surface area of the tire is gripping the road at any moment. But there’s a reason street vehicles have grooves in them. Water on the road will send a slick tire drifting, as the smooth rubber can’t channel it away. Grooved tires push water between the tread, giving some rubber grip and preventing hydroplaning. The slicker the tires—and the faster the speed—the more likely a little water will cause a car to drift.

That’s exactly what was happening to the LMP racers. As the rain worsened, DHH found himself sliding around the inside of a car that was sliding all over the race track. Nearby, one driver lost grip, slamming into the wall.

Cars darted for the pits at the side of the track, so their teams could tear off the slick tires and attach rain tires. Rain tires are safer, but slower. And they take a precious 13-plus seconds to install. By the time the car has driven into the pits, stopped, replaced the tires, and started moving again, more than a minute can be lost.

DHH screamed into his radio to his engineer, Should I pit in for new tires?

Like I said, DHH wasn’t the most experienced racer. He had gotten into this race because he was skilled at hacking the ladder. A few years into 37signals’s success, and with Rails taking a life of its own, Hansson had started racing GT4—essentially souped-up street cars—in his spare time.

Initially, he finished in the middle of the pack with the other novices. But after studying videos of master drivers, he started placing higher. High enough that after six races, he was allowed to enter into GT3 races (the next level up), despite zero first-place wins. In GT3, he raced another six times, placing first once, third another time. He immediately parlayed up to GTE (the “E” is for “endurance”). While other racers duked it out the traditional way, spending a year in each league, and only advancing after becoming league champion, DHH “would spend exactly the shortest amount of time in any given series that I could before it was good enough to move up to the next thing.”

There’s no rule that says you have to win the championship to advance from GT4 to GT3. Nor is there a rule saying you have to spend a year in a given league before moving up. That’s just the way people did it. Instead, DHH compressed what normally takes five to seven years of hard work into 18 months of smart work. “Once you stop thinking you have to follow the path that’s laid out,” he says, “you can really turn up the speed.”

On the rainy Silverstone course, however, parlays couldn’t help him anymore, and slacking was not an option. DHH had to drive as fast as safely possible, and every microsecond counted. In such tight competition, the only edge a racer had was raw driving skill.

Or, as it turned out, a better platform.

SHOULD I PIT IN? The man who hates repeating himself repeated over the radio. I’m going to end up in the wall!

His engineer told him to tough it out. The rain is about to clear up.

G-force pounding his body, DHH cautiously hugged the curves for another lap, and sure enough, the downpour began to subside. By two laps the course was dry. Heinemeier Hansson’s slick tires gripped the track with more friction than his competitors’ newly fitted rain tires and he sped ahead. The other drivers now had to pit back in for slick tires, for a total of nearly two minutes’ delay that DHH entirely avoided.

At the end of his leg of the relay, DHH jumped from the car, having demolished the competition.

The slick tires provided DHH a platform advantage, more leverage to drive faster with the same pedal-to-floor effort. And though driving slick in the rain had been risky, his skill learned by imitating master racers kept him alive.

Reflecting on his rapid ascent in racing, DHH says, “You can accelerate your training if you know how to train properly, but you still don’t need to be that special. I don’t think I’m that special of a programmer or a businessperson or a race car driver. I just know how to train.”

DHH had proven he had the skill to race. Videos of master drivers had helped him to learn quickly. His tire advantage had pushed him ahead of equally skilled drivers, and propelled him to the next level. And the advanced racing leagues themselves became a platform that forced him to master the basics—and faster—than he would have at a lower level.

When DHH returned to visit his home race track in Chicago, the same set of drivers still dominated the lower leagues.

He came back and effortlessly beat them.

***

Effort for the sake of effort is as foolish a tradition as paying dues. How much better is hard work when it’s amplified by a lever? Platforms teach us skills and allow us to focus on being great, rather than reinventing wheels or repeating ourselves.

“You can build on top of a lot of things that exist in this world,” David Heinemeier Hansson told me. “Somebody goes in and does that hard, ground level science-based work…”

“And then on top of that,” he smiles, “you build the art.”

###

Question of the day (QOD):  What other selectively “lazy” innovators can you think of?  People who’ve looked at problems in novel ways, or solved them in non-obvious ways? People who’ve opted for simplicity when most “experts” are choosing complexity?

Please share in the comments.

The post The Art of Strategic Laziness appeared first on The Blog of Author Tim Ferriss.

Preface from Tim

Back in 2012, Gabriel Wyner wrote an article for Lifehacker detailing how he learned French in 5 months and Russian in 10, using mostly spare time on the subway.  That article went viral.

But don’t run off! That was nothing but version 1.0.  This post gives you version 2.0 and more.

He’s spent the last two years refining his methods and putting them on steroids. Kevin Kelly, founding editor of Wired, was the one who told me, “You have to check this guy out. His new book is amazing.” Keep in mind that I’d previously told Kevin that I thought most books on language learning were garbage.  I took his endorsement seriously, and I wasn’t disappointed.

This post gives you Gabe’s new blueprint for rapid language learning:

• A revised and updated version of his original post
• New techniques from the last two years of experimentation
• How he learned 6 languages in just a handful of years
• Tips and tricks you won’t find anywhere else

The “and never forget it” in the headline was Gabe’s idea. Read the article and let me know what you think. Is it possible? I, for one, hope it is.

And speaking as someone who’s studied 10+ languages as an adult, I can tell you: you’re much better at learning languages than you think.

Enjoy!

Enter Gabriel — An overview of what this is and why it works

Two Foreign Words

Let’s compare two experiences. Here’s the first one: you come into a language class, and your (Hungarian) teacher writes the following on the board:

Kitchen cabinet – konyhaszekrény

She tells you that this is going to be on your vocab quiz next week, along with forty other words you don’t care much about.

Experience two: You and your most adventurous friend are sitting in a bar, somewhere in Scandinavia. The bartender is a grey-bearded Viking, who places three empty shot glasses in front of you in a line. From behind the counter, he pulls out a bottle labeled Moktor and pours a viscous, green liquid into the three glasses. He then grabs a jar and unscrews the lid. It’s full of something that looks and smells disturbingly like slimy, decaying baby fish, which he spoons into each shot glass. He then pulls out a silver cigarette lighter and lights the three shots on fire.

“This – Moktor,” he says, picking up one of the glasses. The locals in the bar turn towards you and your friend. “Moktor! Moktor! Moktor!” they all begin to shout, laughing, as the bartender blows out the flame on his shot glass and downs the drink. Your friend – your jackass friend – picks up his glass, screams “Moktor!” and does the same. The crowd goes wild, and you, after giving your friend a nasty look, pick up your glass and follow suit.

As a result of this experience, you are going to remember the word “Moktor” forever, and if you still remember the Hungarian word for kitchen cabinet, you’re likely going to forget it within a few minutes.

Let’s talk about why this happens. Your brain stores memories in the form of connections. Moktor has a (bitter, fishy) taste, which connects with its (rotting) smell. That taste and smell are connected to a set of images: the green bottle, the jar of rotting fish, the grey-bearded barkeep. All of that, in turn, is connected to a set of emotions: excitement, disgust, fear. And those emotions and images and tastes and smells are connected to the writing on that green bottle and the sound of that chanting crowd: Moktor.

Konyhaszekrény, in comparison, just doesn’t stand a chance. In English, “kitchen cabinet” may evoke all sorts of multi-sensory memories – over the course of your life, you’ve probably seen hundreds of cabinets, eaten wonderful foods in their presence, and assembled your own cabinets from IKEA – but konyhaszekrény has none of these things. You’re not thinking about IKEA’s weird metal bolts or bags of Doritos when you see konyhaszekrény; you’re just associating the sound of the Hungarian word (which you’re not even sure how to pronounce) with the sound of the English words ‘kitchen cabinet.’ With so few connections, you don’t have much to hold on to, and your memory for the Hungarian word will fade rapidly. (For a more in-depth discussion about memory and language learning, check out this video excerpt)

In order to learn a language and retain it, you’ll need to build Moktor-like connections into your words. The good news is that if you know what you’re doing, you can do this methodically and rapidly, and you don’t even need to travel to Scandinavia.

The Components of a Memorable Word

If we strip a word down to its bare essentials, a memorable word is composed of the following:

• A spelling (M-o-k-t-o-r)
• A sound (MAWK-tore, or ˈmɑk.toʊɹ, if you want to get fancy)
• A meaning (A viscous green drink, served on fire with dead, baby fish in it.)
• A personal connection (Ick.)

If you can assemble these four ingredients, you can build a long-lasting memory for a word. So that’s exactly what we’re going to do. In addition, we’re going to use a Spaced Repetition System. This is a flashcard system that automatically quizzes you on each of your flashcards just before you forget what’s on them. They’re a ridiculously efficient way to push data into your long-term memory, and we’ll take advantage of that, too.

My language learning method relies on four stages: Begin by learning your language’s sound and spelling system, then learn 625 simple words using pictures. Next, use those words to learn the grammatical system of your language, and finally play, by watching TV, speaking with native speakers, reading books and writing.

Keep in mind that different languages will take different amounts of time. The Foreign Service Institute makes language difficulty estimates [Ed. note: scroll down to the heading “FSI’s Experience with Language Learning”] ​for English speakers, and I’ve found their estimates are spot on – in my experience, Russian and Hungarian seem to take twice as much time as French, and I expect that Japanese will take me twice as long as Hungarian. For the purposes of this article, I’ll assume that you’re learning a Level 1 language like French, and you have a spare 30-60 minutes a day to dedicate to your language studies. If you’re studying something trickier or have different amounts of spare time, adjust accordingly.

Here are the four stages of language learning that we’ll go through:

Stage 1: Spelling and Sound: Learn how to hear, produce and spell the sounds of your target language

1-3 weeks

One of the many reasons that Moktor is easier to memorize than konyhaszekrény is that Moktor looks and sounds relatively familiar. Sure, you haven’t seen that particular set of letters in a row, but you can immediately guess how to pronounce it (MAWK-tore). Konyhaszekrény, on the other hand, is completely foreign. What’s “sz” sound like? What’s the difference between “é” and “e”? The word is a disaster when it comes to spelling and sound, and it gets even worse if you were looking at Russian’s кухонный шкаф, or Mandarin’s 橱柜.

Before you can even begin assembling memories for words, you’re going to need to create a spelling and sound foundation upon which you can build those memories. So spend your first 1-3 weeks focusing exclusively on spelling and sound, so that the foreign spellings and sounds of your target language are no longer foreign to you.

To break down that process a bit, you’re learning three things:

•  How to hear the new sounds in your target language,
•  How to pronounce the sounds, and
•  How to spell those sounds.

We’ll tackle those in order.

How to hear new sounds

Many people don’t think about hearing when they approach a new language, but it’s an absolutely essential first step. When I began Hungarian, I discovered that the letter combinations “ty” and “gy” sounded basically identical to my ears.

Tyuk:

Gyuk:

If I had rushed ahead and started learning words and grammar immediately, I’d have been at a severe disadvantage whenever I learned words with those letter combinations, because I’d be missing the sound connection when trying to build memories for those words. How could I remember a word like tyúk (hen) if I can’t even hear the sounds in it, let alone repeat them aloud?

There are a few different ways to learn to hear new sounds, but the best that I’ve seen comes from a line of research on Japanese adults, learning to hear the difference between Rock and Lock.

I’ve made a little video summarizing these studies, but here’s the short version: to rewire your ears to hear new sounds, you need to find pairs of similar sounds, listen to one of them at random (“tyuk!”), guess which one you thought you heard (“Was it ‘gyuk’?”), and get immediate feedback as to whether you were right (“Nope! It was tyuk!”). When you go through this cycle, your ears adapt, and the foreign sounds of a new language will rapidly become familiar and recognizable.

For Hungarian, I built myself a simple app that performs these tests. In the end, it took me ten days at 20 minutes a day to learn how to hear all of the new sounds of Hungarian (of which there are quite a few!). It is a ridiculously efficient way to learn pronunciation; after experiencing it myself, I made it my personal goal to develop pronunciation trainers for 12 of the most common languages, a goal that – thanks to Kickstarter – is coming to fruition. These trainers will walk you through ear training tests and teach you the spelling system of your target language in ~2 weeks. As I finish them, I’ll be putting them on my website, here. But if I’m not covering your language yet, or if you prefer to do things on your own, I have an article on my site explaining how to make them yourself for free.

How to pronounce new sounds

With your ears out of the way, you can start mastering pronunciation. But wait! Is it even possible to develop a good accent from the start? I’ve long heard the claim that developing a good accent is only possible if you’ve been speaking a language before the age of 7, or 12, or some other age that has long since past.

This is simply not true. Singers and actors develop good accents all the time, and the only thing special about them is that they’re paid to sound good. So yes, you can do this, and it’s not that hard.

Once your ears begin to cooperate, mastering pronunciation becomes a lot easier. No one told you, for instance, how to pronounce a K in English, yet the back of your tongue automatically jumps up into the back of your mouth to produce a perfect K every time. Most of the time, your ears will do this for you in a foreign language, too, as long as you’ve taken the time to train them. That being said, there may be occasions when you can hear a foreign sound just fine, but it just won’t cooperate with your mouth. If that happens, you may benefit from a bit of information about where to put your tongue and how to move your lips. I’ve made a Youtube series that walks you through the basics of pronunciation in any language. Check it out here. It’ll teach your mouth and tongue how to produce tricky new sounds.

This gives you a few super powers: your well-trained ears will give your listening comprehension a huge boost from the start, and  your mouth will be producing accurate sounds. By doing this in the beginning, you’re going to save yourself a great deal of time, since you won’t have to unlearn bad pronunciation habits later on. You’ll find that native speakers will actually speak with you in their language, rather than switching to English at the earliest opportunity.

How to spell new sounds

Spelling is the easiest part of this process. Nearly every grammar book comes with a list of example words for every spelling. Take that list and make flashcards to learn the spelling system of your language, using pictures and native speaker recordings to make those example words easier to remember.

Those flashcards look like this:

Spelling Flashcard 1

(Trains individual letters and letter combinations)

Spelling Flashcard 2

(Connects a recording of an example word to the spelling system of your language)

And I have a guide to building them on my website.

Author’s note: For Japanese and the Chinese dialects, you’re going to be learning the phonetic alphabets first – Kana (Japanese) or Pinyin (Chinese). Later, when you get to Stage 2, you’ll be learning characters. You can find an article on modifying this system for those languages over here.

Stage 2: Learn 625 Basic Words: Learn a set of extremely common, simple words using pictures, not translations

1-2 months

To begin any language, I suggest starting with the most common, concrete words, as they’re going to be the most optimal use of your time. This is the 80/20 Rule in action; why learn niece in the beginning when you’re going to need mother eighty times more often?

On my website, I have a list of 625 basic words.  [Ed. note: This link now goes to an internet archive site. Please be patient with load times.] These are words that are common in every language and can be learned using pictures, rather than translations: words like dog, ball, to eat, red, to jump. Your goal is two-fold: first, when you learn these words, you’re reinforcing the sound and spelling foundation you built in the first stage, and second, you’re learning to think in your target language.

Often, when someone hears this advice, they think it’s a good idea and try it out. They pick up a word like devushka (girl) in Russian, and decide to learn it using a picture, instead of an English translation. They go to Google Images (or better, Google Images Basic Mode, which provides captions for each word and more manageably sized images), and search for “girl.” Here’s what they’ll see:

Google Images search for “girl” (Using Basic Mode)

It’s exactly what you’d expect. They look like girls, and you could pick out a couple of these images, slap them on a flashcard, and teach yourself devushka within a few seconds. Unfortunately, you’d be missing out on the most interesting – and most memorable – bits of the story. You already know what a girl is. What happens if you search for “девушка” (devushka) instead? 

Google Images search for “девушка” (Using Translated Basic Mode)

Russian devushki tend to be 18-22 year old sex objects. Devushka is not a word you’d use to describe your Russian friend’s 3-year-old daughter (That word is ‘devuchka’). And while knowing the difference between girl and devushka may keep you out of trouble with your Russian friends, it’s also a thousand times more interesting than simply memorizing “devushka = girl.” By searching for images in your target language, and by looking for the differences between a new word and its translation, you’ll find that the new word suddenly becomes memorable.

Devushka is not some random exception; it’s the rule. Nearly every new word you encounter will be subtly (and sometimes, not-so-subtly) different from its English counterpart. So your first step when learning a new word is to search for it on Google Images, look through 20-40 pictures, and try to spot the differences between what you see and what you expect to see. This experience is the learning process for your word. It’s the (often exciting) moment when you discover what your word actually means. Once you’ve had that experience, grab 1-2 images and put them on a flashcard to remind you of what you saw.

Note: This is why you can’t just download some flashcards and successfully learn a foreign language. If you do this, you miss out on the actual learning experience. The flashcards aren’t particularly effective, because they’re not reminding you of anything you previously experienced.

Armed with an image or two from Google Images, you’ve now managed to connect a spelling (k-o-n-y-h-a-s-z-e-k-r-é-n-y) and a sound (“konyhaszekrény!”) to a meaning (really old-fashioned looking kitchen cabinets).

At this point, the only thing separating konyhaszekrény from Moktor is a personal connection, and fortunately, you have plenty of personal connections to choose from. When’s the last time you encountered a particularly old-fashioned kitchen cabinet? Search your memories, and you’ll find that for nearly every word you learn, there is at least some experience you’ve had with that concept. In my case, my grandmother’s old house definitely was full of konyhaszekrények. Find your own personal connection with each new word, come up with a short reminder of it – in my case, I’d choose my grandmother’s name, Judith – and stick that on the back of your flashcards as well. When you include personal connections, you’ll remember your words 50% better.

Once you’ve built these connections, start making your flashcards (guide here)

Tip 1 – Regarding Word Order

When learning words, never learn them in the standard order you see in grammar books, where similar words are grouped together: days of the week, members of the family, types of fruit, etc. When you do this, your words will interfere with each other (is ’jeudi’ the word for ‘Tuesday’ or ‘Thursday’?), and on average, you’ll need 40% more time to memorize them, and they’ll last 40% less time in your memory compared to a randomized group of words. You can find more information about the effects of word order over here.

Tip 2 – Mnemonics for Grammatical Gender

If any of you have studied a language with grammatical gender, you know how much of a pain it can be trying to remember whether chairs are supposed to be masculine, feminine or neuter. Some of the friendlier languages may give you clues – perhaps masculine nouns usually end in ‘o’ – but those clues aren’t always trustworthy. So what can you do?

There’s a simple way to make abstract information like grammatical gender stick. Use mnemonic imagery, and for this particular case, use vivid, visualizable verbs. Make your masculine nouns burst into flame, your feminine nouns melt into a puddle, and neuter nouns shatter into a thousand razor-sharp shards. You’ll find that mnemonic imagery like this makes gender extremely easy to memorize, right from the start.

Stage 3: Learn the grammar and abstract words of your language

2-3 months

Now it’s time to crack open your grammar book. And when you do, you’ll notice some interesting things:

First, you’ll find that you’ve built a rock-solid foundation in the spelling and pronunciation system of your language. You won’t even need to think about spelling anymore, which will allow you to focus exclusively on the grammar. Second, you’ll find that you already know most of the words in your textbook’s example sentences. You learned the most frequent words in Stage 2, after all. All you need to do now is discover how your language puts those words together.

Grammar’s Role

So let’s talk about what grammar does, and how you should learn it. Grammar is a story telling device. It takes a few actors and actions – you, your dog, eating, your homework – and turns them into a story: Your dog ate your homework. This is a tremendously complex operation; not only can grammar tell you who’s doing what and when they’re doing it, but it can simultaneously tell you what the speaker thinks about the story. By switching from “My dog ate my homework” to “My homework was eaten by my dog,” for instance, we move from a story about a bad dog to a story about a sad, sad homework assignment.

In every single language, grammar is conveyed using some combination of three basic operations: grammar adds words (You like it -> Do you like it?), it changes existing words (I eat it -> I ate it), or it changes the order of those words (This is nice -> Is this nice?). That’s it. It’s all we can do. And that lets us break sentences down into grammatical chunks that are very easy to memorize.

How do you learn all the complicated bits of “My homework was eaten by my dog”? Simple: Use the explanations and translations in your grammar book to understand what a sentence means, and then use flashcards to memorize that sentence’s component parts, like this:

New Words (Front Side) – [Guide to construction]

New Word Forms (Front Side) – [Guide to construction]

Word Order (Front and Back Sides) – [Guide to construction]

You can memorize any grammatical form using this approach, and this has a few advantages over the standard sort of grammatical drills you’ll find in your textbook. For one, you’re learning each grammatical form in the context of a story, which allows you to connect images to abstract words. This makes them a lot easier to remember. What’s a “by” look like? For this story, it looks like a guilty dog.

Second, you’re learning grammar with the help of a Spaced Repetition System, which will provide you with the exact amount of repetition you need to definitively memorize any grammatical form. This lets you skip over the hundreds of grammar drills in your textbook. Instead, you can take just one or two examples of every new grammatical form and move on to the next section of your book. This lets you move very, very fast, and devour a textbook worth of information within a couple of months. It’s also a lot of fun; without getting bogged down with boring grammatical drills, you’re constantly learning new ways to express yourself.

Other Sources of Example Sentences

Occasionally, your textbook won’t give you the example sentences you need. Instead, it’ll throw a bunch of verb conjugations at you – I am, you are, he is – and tell you to simply memorize the forms. When this happens, you can turn to two wonderful, free resources to produce example sentences: Google Images and Lang-8.

On its surface, Google Images is a humble image search engine. But hiding beneath that surface is a language-learning goldmine: billions of illustrated example sentences, which are both searchable and machine translatable. If you mess with it just right (Instructions here), you get this (I’m searching for French’s ’peuvent’ ([they] can)):

And if you mouse over the text, you get this:

Google Images Basic Mode, jammed into Google Translate

(Mouse over to reveal original text)

Yup, that’s an effectively unlimited source of illustrated, translated example sentences for any word or word form in your target language. It’s the largest illustrated book ever written, and it’s both searchable and free. Gold.

Alternatively, you can write your own example sentences. Naturally, you’ll make mistakes, but with Lang-8.com, you can get those mistakes corrected for free by native speakers, in exchange for correcting someone else’s English. You can then take those corrected sentences, break them down into flash cards, and use them to memorize even the most complex of grammatical forms. I really like writing my own flashcard content. It makes my flashcards a lot more personal, it gives me practice using the words I already know to express myself, and the corrections show me exactly where I need additional flashcards to help push my grammar in the right direction.

Using these tools, you can easily memorize any word or grammatical concept you’d like to learn. I’d recommend using these tools to accomplish two things:

• Memorize the first half of your grammar book, since it’s the half that typically contains all the meaty, useful bits. (The second half often contains specialized stuff like reported speech, which you might not need.)
• Learn the top 1,000 words of your language. By this point, you’ve already learned many of these words from the original 625, and with your newfound ability to learn abstract words, you can learn the rest of them.

This part of the process is a lot of fun. You can feel your language growing in your head, and since you’re never using translations on your flashcards, you’ll frequently find yourself thinking in your target language. It’s a particularly weird and wonderful experience.

And by the end of this stage, you’re ready to start playing.

Stage 4: The Language Game

3 Months (or as long as you want to keep playing)

This stage is extremely flexible, and in many ways, obnoxiously simple. Want more vocabulary? Learn more words. Want to be more comfortable reading? Read some books. But there are some efficiency tweaks you can do here that will help you transition more easily from an intermediate level to full fledged fluency.

Vocabulary Customization: 

Learning the top 1000 words in your target language is a slam-dunk in terms of efficiency, but what about the next thousand words? And the thousand after that? When do frequency lists stop paying dividends? Generally, I’d suggest stopping somewhere between word #1000 and word #2000. At that point, you’ll get better gains by customizing. What do you want your language to do? If you want to order food at a restaurant, learn food vocabulary. If you plan to go to a foreign university, learn academic vocabulary. Get a Thematic Vocabulary Book, a book that lists vocabulary by theme (food, travel, music, business, automotive, etc.), and check off the words that seem relevant to your interests. Then learn those words using the methods from Stage 3.

Reading: 

Books boost your vocabulary whether or not you stop every 10 seconds to look up a word. So instead of torturously plodding through some famous piece of literature with a dictionary, do this:

• Find a book in a genre that you actually like (The Harry Potter translations are reliably great!)
• Find and read a chapter-by-chapter summary of it in your target language (you’ll often find them on Wikipedia). This is where you can look up and make flashcards for some key words, if you’d like.
• Find an audiobook for your book.
• Listen to that audiobook while reading along, and don’t stop, even when you don’t understand everything. The audiobook will help push you through, you’ll have read an entire book, and you’ll find that it was downright pleasurable by the end.

Listening:

Podcasts and radio broadcasts are usually too hard for an intermediate learner. Movies, too, can be frustrating, because you may not understand what’s going on until the very end (if ever!).

Long-form TV series are the way to go. They provide 18+ hours of audio content with a consistent plot line, vocabulary and voice actors, which means that by the time you start feeling comfortable (2-4 hours in), you still have 14+ hours of content. To make those first few hours a bit easier, read episode summaries ahead of time in your target language. You can usually find them on Wikipedia, and they’ll help you follow along while your ears are getting used to spoken content.

Speaking: 

Fluency in speech is not the ability to know every word and grammatical formation in a language; it’s the ability to use whatever words and grammar you know to say whatever’s on your mind. When you go to a pharmacy and ask for “That thing you swallow to make your head not have so much pain,” or “The medicine that makes my nose stop dripping water” – THAT is fluency. As soon as you can deftly dance around the words you don’t know, you are effectively fluent in your target language.

This turns out to be a learned skill, and you practice it in only one situation: When you try to say something, you don’t know the words to say it, and you force yourself to say it in your target language anyways. If you want to build fluency as efficiently as possible, put yourself in situations that are challenging, situations in which you don’t know the words you need. And every time that happens, stay in your target language no matter what. If you adhere to that rule whenever you practice speaking, you’ll reach fluency at a steady, brisk pace.

Naturally, you’re going to need practice partners. Depending upon your city, you may find friends, colleagues, private tutors (Craigslist.org) or large language practice groups (Meetup.com) for speech practice.

No matter where you are, you can find practice partners on the Internet. iTalki.com is a website designed to put you in touch with a conversation partner or tutor for free (if you’re willing to chat in English for half of the time), or for $4-12/hr (if you don’t want to bother with English). It’s a tremendous and affordable resource.

The more often you speak, the more rapidly you’ll learn. Speech practice pulls together all of the data you’ve crammed into your head and forms it into a cohesive, polished language.

Learning a foreign language is a fluid process; you’re building a lot of different skills that meld into each other. The more vocabulary you learn, the easier it will be to speak about a wide variety of topics. The more you practice speaking, the easier it will be to watch foreign TV and movies. So rather than be strict and methodical about this (“My reading comprehension skills are lacking; I must read 15 books to maximize efficiency!”), just do what you find most enjoyable. If you like writing about your day on Lang-8 and making flashcards out of the corrections, then keep doing that. If you like to chat with your tutor on iTalki, do that.

There’s a very simple way to figure out if you’re spending your time well: if you’re enjoying yourself in your target language, then you’re doing it right. In the end, language learning should be fun. It needs to be fun; you retain information better when you’re enjoying yourself, and the journey to fluency takes too much time to force yourself through using willpower alone. So enjoy yourself, and play around with new ways to think about the world. See you on the other side.

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Links:

• My book, Fluent Forever: How to learn any language fast and never forget it, is an in-depth journey into the language learning process, full of tips, guidelines and research into the most efficient methods for learning and retaining foreign languages.
• My CreativeLive Workshop is 18 hours of language learning insanity in video form. I go through everything I know about the language learning process, with detailed, step-by-step walkthroughs of every computerized and analog tool I recommend.

Related & Recommended Posts:

12 Rules for Learning Foreign Languages in Record Time

How to learn any language in 3 months

Why language classes don’t work: How to Cut Classes and Double Your Learning Rate

How to Learn (But Not Master) Any Language in 1 Hour

The post How to Learn Any Language in Record Time and Never Forget It appeared first on The Blog of Author Tim Ferriss.