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! 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. 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 .
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.
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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.
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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 5. Nrf. 2 and it does so more potently than any other known naturally- occurring dietary compound. This gene, a master regulator, controls over 2. 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 Nrf. 2, 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.
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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 1. 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 1.
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 1. 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 1. 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 2. 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 1. 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- 1. 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. 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.