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Gary Taubes and Stephan Guyenet: Three Views on Obesity

Posted by on August 11, 2011 108 comments

In a post titled “Ancestral Health Symposium Drama”, Stephan Guyenet begins to expound his scientific differences with Gary Taubes.

Since my views differ a bit from both Stephan and Gary, I thought readers might enjoy a third view.

My General Perspective on Obesity

My view is that obesity is caused in the first place by malnutrition, toxins, and infections. Each can contribute in multiple ways:

  • Malnutrition can affect appetite and energy utilization. Micronutrient deficiencies will increase appetite, regardless of energy balance. Macronutrient deficiencies may also do this. The resulting increased calorie intake may be only partially balanced by increased activity and thermogenesis; fat gain in caloric surplus tends to be more weakly opposed by brain regulatory circuits than muscle loss during caloric deficit. Malnutrition can impair energy utilization by several pathways: for instance, loss of mitochondrial antioxidants may lead to oxidative damage that impairs mitochondrial health. Choline deficiency induces metabolic syndrome and obesity (see Choline Deficiency and Plant Oil Induced Diabetes, Nov 12, 2010). Long-term, malnutrition may induce methylation defects which affect epigenetic regulation of metabolism. These can be passed on from mother to child.
  • Toxins also have multiple pathways by which they induce obesity. For example, diets that combine fructose or alcohol with polyunsaturated fats are very effective at producing metabolic syndrome and obesity in animals, and food opioids affect the endocannibinoid pathways which can be important in obesity and appetite regulation. See Why We Get Fat: Food Toxins (Jan 20, 2011) and Wheat and Obesity: More from the China Study (Sep 4, 2010) for more.
  • Infections have also been linked to obesity. I’ve blogged about how adenovirus infections of adipose cells promote obesity (Obesity: Often An Infectious Disease, Sep 22, 2010), but another very important pathway is from gut infections to obesity. Briefly, gut pathogens release fat-soluble toxins which can enter systemic circulation, and also modulate immune function. Toxins from pathogens have been shown to induce metabolic syndrome in the liver, promoting obesity. Via the immune system, gut flora can promote obesity. I’ve briefly mentioned one pathway (in Thoughts on Obesity Inspired by Stephan, Jun 2, 2011): gut immune modulation in the gut has been shown to determine whether adipose tissue macrophages are in a pro-inflammatory or anti-inflammatory state. A pro-inflammatory state promotes obesity. Research into the many ways gut flora influence obesity is in early stages, but it’s clearly important.

Due to the diversity of factors which conspire to cause obesity, it is a rather heterogeneous disease. Its unifying character is that some combination of causal factors induces “metabolic damage,” such as leptin resistance, in a variety of organs, including the brain. Metabolic damage can affect both appetite regulation and energy homeostasis.

I’ve discussed Stephan’s views and food reward theory (Thoughts on Obesity Inspired by Stephan, Jun 2, 2011). Food reward theory offers a plausible explanation for many aspects of obesity. I agree that food reward is an important factor in obesity, but consider it one among several factors, and believe that different factors may dominate in different people. Also, it seems likely to me that food reward becomes a dominant factor in obesity only after some form of metabolic damage from malnutrition, toxins, or infections begins to affect the brain’s regulatory systems. In a healthy person a highly palatable diet might have little effect on weight for quite some time. Nor am I convinced that low food reward diets are necessarily the best approach for long term weight loss or for the health of the obese, though I do believe they are great for short-term weight loss.

Distinguishing my view from Stephan’s is difficult because the obesity-inducing diets used in animal studies are generally both toxic and malnourishing and highly palatable. The “cafeteria diet” of Cheetos and such – rich in wheat, sugar, and vegetable oil – is an example.

I haven’t previously blogged about Gary’s views, but I consider very low carb dieting to be an imperfect solution for good health generally. (NB: Low-carb, which I endorse, is for me 400-600 carb calories, very low-carb, which I deprecate, is <200 calories.) Ketogenic diets may be beneficial in some cases of obesity, but I believe they should still include some starchy carbohydrates.

The Exchange

Stephan has transcribed the Q&A between Gary and himself and offers revised answers. I’ll insert my thoughts:

GT: How does your food reward hypothesis hypothesis explain a culture in which mothers are obese and their children are starving?  Are the mothers eating Snickers bars and not sharing them with their children?

SG: The food reward/palatability hypothesis of obesity is not mine, it’s a hypothesis that originated in the 1970s, perhaps earlier, and is a major subject of ongoing obesity research.  I don’t expect it to explain every instance of obesity.  Obesity involves multiple factors, an important one of which is food reward and palatability.  That being said, you have to examine a culture’s food habits in some detail, both before and after a change in obesity prevalence, to determine if reward/palatability may have played a role.  I don’t know enough about that specific culture to judge whether food reward would have played a role there.

PJ: Famines occur in impoverished societies with disrupted social institutions. People in these cultures are driven to eat the cheapest calories, which are the toxic grains such as wheat. They also tend to be malnourished, especially during famines. Malnutrition and toxic foods can create the disease of obesity, especially in a suitable infectious disease context.  Once the disease of obesity is induced, periods of caloric availability lead to weight gain which may be defended during subsequent famines. This explains maternal obesity persisting during a period of food scarcity. The slenderness of their children is a result of the disease process not having had enough time to work. It may take decades for malnutrition and food toxicity to induce obesity in the child.

So the element of long-acting causal factors and history eliminates the apparent conflict between an obese mother and a starving slender child.

Because food reward could induce obesity in the mother prior to the famine which is defended later, and food reward may act differently in growing children, food reward theory may be able to explain the situation. But Stephan prudently allows for the possibility that other causes of obesity besides food reward may be at work.

GT: The Pima indians were obese in 1902, following 20-30 years of famine.  How would your theory explain this?

SG: The Pima were first contacted in 1539 by the Spanish, who apparently found them to be lean and healthy.  At the time, they were eating a high-carbohydrate, low-fat diet based on corn, beans, starchy squash, and a modest amount of gathered animal and plant foods from the forest and rivers in the area.  In 1869, the Gila river went dry for the first time, and 1886 was the last year water flowed onto their land, due to upstream river diversion by settlers.  They suffered famine, and were rescued by government rations consisting of white flour, sugar, lard, canned meats, salt and other canned and processed goods.  They subsequently became obese.  Their diet consisted mostly of bread cooked in lard, sweetened beverages and canned goods, and they also suddenly had salt.  I don’t see why that’s incompatible with the food reward hypothesis.  It is, however, difficult to reconcile with the carbohydrate hypothesis.

PJ: The Pima Indian story seems compatible with both Stephan’s and my views, since they ate a nourishing, low-toxicity, low-food reward diet when they were lean but a malnourishing, toxic, high-food reward diet when they became obese. It seems incompatible with Gary’s ideas, since the Pima ate a high-carb diet at all times. Thus it’s a bit surprising Gary is so fond of the Pima story. It weakens, not helps, his case.

GT: There are two possible hypotheses here.  The alternative hypothesis is that sugar and refined carbohydrate consumption changes the regulation of fat tissue, leading to obesity.  The studies you cited in which people lost weight by consuming bland liquid diets would have been low in sugar as well.  “We need an observation that can refute one of the two hypotheses”.

SG: The bland liquid diet in Hashim et al. that caused massive weight loss is called “Nutrament”.  It is 50% carbohydrate, 30% fat and 20% protein.  The primary three sources of carbohydrate in this formulation are lactose (from milk), sucrose (table sugar) and corn syrup.  The bland liquid used in the study by Cabanac et al. (Renutryl), which also caused weight loss, was high in refined glucose and sucrose.  I find this rather difficult to reconcile with the idea that sugar and refined carbohydrate are inherently obesogenic.

PJ:  It’s unclear to me what Gary’s “alternative hypothesis” is. Why are refined carbohydrates different from unrefined carbohydrates? Both may raise blood glucose and insulin levels similarly. If toxic plant foods are the problem, then he should say toxins rather than carbohydrates are the problem. If it’s the macronutrient that’s the problem, why does refining matter?

Stephan scores a point against both Gary and me here, but especially against Gary, since the liquid diets are fairly high in carbs. As there was some sucrose and polyunsaturated fat, this was not a non-toxic diet, and I don’t know if adequately micronutrients were provided – probably not – but on its face the food reward theory seems to work best in explaining this experiment.

GT: “How was it bland then?”

SG: The diet was a liquid formulation that (judging by the ingredients) probably tastes like powdered milk.  The subjects were drinking that for 100% of their calories.  That fits any reasonable definition of a low reward/palatability diet, regardless of the sugar.

GT: What about the Mexican-Americans in Star county, Texas, who were obese despite the fact that there was only one restaurant in the whole town?

SG: Again, you have to examine a culture’s food habits in some detail, both before and after a change in obesity prevalence, to determine if reward/palatability may have played a role.  I don’t know enough about that specific culture to judge whether food reward would have played a role there.

GT: How can we differentiate between altered palatability and altered carbohydrate intake as important factors in the rising obesity prevalence of industrializing nations?

SG: Increased carbohydrate intake is a particularly poor explanation for obesity in industrializing populations, as the majority of them (for example, most of Asia and Africa) are going from a diet very high in carbohydrate, to one that is lower in carbohydrate and higher in fat.  There are also a smaller number of cultures that developed obesity as they went from high-fat to higher carbohydrate, industrialized food.  Therefore, the ideas that carbohydrate or fat are inherently fattening don’t appear consistent with the evidence as a whole.  An alternative explanation whereby both fat and carbohydrate, as well as other factors, are important for reward/palatability, an excess of which contributes to obesity, fits the evidence better.

PJ: It seems to be easiest to induce obesity with a roughly equal mix of carbs and fat; both low-carb and low-fat diets tend to be less obesogenic. This result is compatible with Stephan’s views because carb and fat together are more rewarding than either alone, and with my views because carb-fat combinations can be highly toxic – for instance, a fructose-PUFA combination is more toxic than either alone; or carbs feed gut pathogens while fats carry their toxins into the body.

It is unclear how Gary would explain the evidence from both animal studies and human populations that obesity becomes more likely as high-carb diets shift toward more fat.

Of Glass Houses

Stephan is a model of scholarly virtue, so Gary’s challenge at the end of his talk was a shock. I thought Stephan’s original reply – “Thank you for the advice” – was perfect, but Stephan revises it:

GT: “I would just recommend in the future you should pay attention to populations that might refute your hypothesis rather than just presenting populations that support.  That’s always key in science.”

SG: People who live in glass houses shouldn’t throw stones.

Presumably Stephan is challenging Gary to address some of the populations who seem to refute his hypothesis: Asian populations that have become more obese while dropping carbs from 75% to 50% of diet, or the Pima who remained lean on a high-carb diet for centuries.

In other words, to seek a theory that can explain all phenomena, as a scientist should.

In general, I find Gary’s work rhetorically artful but not very helpful to scientific progress. He often neglects to consider the full implications of his own evidence. This is especially true when he ventures into molecular and cellular biology.

For instance, he uses genetic lipodystrophies to illustrate that fat storage can be a disease of molecular biology, rather than excess food consumption. Now, the mutations in these lipodystrophies are generally not in insulin, the insulin receptor, or even centrally located on insulin pathways. So the lipodystrophies show that other molecules besides insulin can be responsible for fat storage (or negative regulation of fat storage), and may be relevant to obesity.

But when he looks into which molecules might be responsible for obesity, he offers only one candidate: insulin.

More startling is his neglect of perhaps the single most important molecule in obesity, leptin. Stephan writes:

[H]e sent me a manuscript for his book Why We Get Fat and asked for my advice prior to its publication.  I explained to him that he needed to use the word “leptin” in the book, particularly when discussing animal models of obesity that are obese because of defects in leptin signaling (ob/ob mice and Zucker rats, for example).

This is just like his use of lipodystrophies: mice get obese due to mutations in leptin, but he doesn’t discuss the role of leptin, preferring to keep the spotlight on insulin.

I don’t want to sound harsh because I think Gary is on the side of the angels. He has done very beneficial work refuting saturated-fat-phobia and encouraging low-carb diets, which improve the health of nearly all westerners who adopt them (although the reason is probably reduced toxicity from wheat and sugar, rather than reduced carbohydrate calories).

But I think he would do well to be more generous to others. I was excited when he began blogging, but disappointed by his first post:

conventional wisdom … almost incomprehensibly naïve and wrong-headed … nonsensical notion … I’ve been consistently amazed at the ability of researchers … to accept some of the rote ideas … without seemingly giving it any conscious thought whatsoever, or without wanting to ask the kinds of questions that a reasonably smart junior high school student should ask if given the opportunity…. I don’t understand this failure of intellect … nonsensical explanations … he falls short, as he’s working outside his area of expertise … we’re being fed nonsense … we will typically pass that nonsense along … If the experts had ever been open to a little skeptical thinking from others or had they been appropriately skeptical themselves … What’s been needed (and still is) was for someone (a reasonably smart 14-year-old would suffice) to ask the obvious questions and then insist on intelligent answers.

I find such talk ungenerous; and ironic, because in places in that very post Gary’s own reasoning is unsound.

Biology is complex, none of us have all the answers, and a lifetime is too short to acquire all the answers. Since we have no choice but to live in glass houses, we should all be humble, and refrain from casting stones.

The Ancestral Health Symposium

Posted by on August 9, 2011 25 comments

We’re back from the California and the Ancestral Health Symposium, which was a fantastic meeting – the most enjoyable symposium I’ve attended. Brent Pottenger, Aaron Blaisdell, and the host of volunteers who assisted them deserve tremendous credit for organizing it. Bravo!

It had the feel of a Paleo Woodstock: the leading names in the movement were gathered in one place for the first time, and there was a festive atmosphere, especially on the first day and at a pre-event party hosted by Aaron Blaisdell. For Shou-Ching and I, it was a delight to meet in person friends we had come to know through the Internet. We were pleased to meet some of our commenters – and had lunch with one, Mia.

Those who didn’t attend will be able to catch up on it later: presentation slides may be found here; videos of the talks and interviews will be posted here.

People and Pictures

Already there’s a great deal of information about the meeting online. Some participants were active twitterers – check out the Twitter tag #AHS11 for a blow-by-blow account of the meeting. I’m sure many attendees will be posting their own appreciations in coming days, but here are links to some of the early birds:

Richard Nikoley took a lot of pictures at Aaron’s Thursday night party and has more photos in his appreciation of the symposium. PaleoHacks has a thread for pictures from the meeting and a thread for recommendations about talks. Emily Deans has posts about talks and people.

Melissa McEwen, Stephan Guyenet, Chris Masterjohn, Jamie Scott, Andreas Eenfeldt, and Matt Metzgar have posts.

Many at the meeting remarked on how good looking the attendees were. You can find appreciations of looks from Melissa (“the conference was full of beautiful people”), Jamie (“I have never been around so many beautiful people in one room as I have been this past weekend.”), and Stephan (“I was very impressed by the appearance of the attendees”).

I was equally impressed, but that observation leads me to one more. Nearly everyone at the meeting had at one time been following bad diets and had to seek out Paleo. In Denise Minger’s talk, she asked how many people had been vegetarians at one time, and a startlingly large number raised their hands. To discover a healthy way of living, in a world full of mistaken information and unhealthy foods, is possible only for inquisitive, intelligent, discerning people. This was not only a beautiful, but a smart, crowd.

And so very friendly and cheerful. Good health, I believe, leads to good spirits. It was a pleasure to be around everyone, both during the meeting and after hours.

The Talks

A brief summary of the the most notable talks I saw:

S. Boyd Eaton kicked off the conference as the only speaker without a competitor in the parallel track; a well-deserved honor in light of his pioneering role in the Paleo movement. He spent only ten minutes on diet and moved on to expressing a quixotic hope for decreases in the global population in order to restore a more Paleo-like environment. Among the highlights was a picture from the Korean DMZ, a 400-square mile depopulated area that has apparently regained a flourishing wildlife.

Loren Cordain followed with an excellent talk, most of which will be familiar to his fans. I liked his talk a lot, in part because his slides on hunter-gatherer food intakes support our macronutrient ratios.

Staffan Lindeberg gave an excellent talk that also revisited material from his work. A few factoids: blame for the invention of vegetable oils goes to David Wesson, who figured out how to detoxify cotton seeds in 1899, thus giving us “Wesson oil”; and autopsy studies show that at age 40 most people already have atherosclerosis, a disease that is non-existent in wild animals and thus is presumably caused by industrial diets.

Robb Wolf finished the morning session and was his usual dynamic self. Shou-Ching, who hadn’t yet listened to one of his podcasts, was impressed.

If Friday morning felt like a celebrity fest, Friday afternoon was the meat of the symposium. Two Friday afternoon talks were among the best of the meeting.

Emily Deans’s talk was magnificent, pulling together a rich thread of material. Jamie Scott gave an inside look at the practical side of improving health in a corporate setting.

Dr. BG and Dr Tim Gerstner gave an outstanding talk, one of the best of the meeting. Dr BG’s story was fascinating and fast-paced. She and her sister are writing a book, “Jillian’s story,” about Dr BG’s autistic niece who has seen great improvements from chelation therapy. Heavy metal toxicity is an important subject and it looks like Dr BG and her collaborators are going to make an important contribution. We went to dinner Friday night with Dr BG, her sister, Dr Gerstmar, and J. Stanton of gnolls.org, and had a wonderful time.

In attending these two great talks, I missed two of the star attractions of the meeting – Stephan Guyenet, whose talk I would dearly love to have seen, and Gary Taubes. The buzz of the main ballroom when we got back was that Gary had, in the question session, cut to the front of the question line in order to challenge Stephan in some fashion. I expect this video will be the most downloaded one of the conference. UPDATE: Video of Gary’s questioning is here and a detailed account here.

Curious to hear about Stephan’s talk, we had returned to the main ballroom during the break, and stayed to watch Michael Eades. He gave a very nice talk focusing on the pre-history of the Paleo diet – going back to some early clinicians, one of whom was a friend of Vilhjalmur Stefansson, who had tried low-carb Paleo diets on their patients with success.

Again, I was torn between two great speakers as I very much wish I could have heard the talk of anthropologist Craig Stanford, who was opposite Eades. I had a pleasant chat with Dr. Stanford at Aaron’s pre-meeting party and it turns out our professional paths seem to be criss-crossing: I am working on a book on evolutionary biology, applying my economics ideas to the problem, and he is considering writing a book on diet. Small world!

Friday’s last talk was by Chris Masterjohn, who gave a superb exposition on LDL receptors, how LDL-R status can influence LDL time in the blood and oxidation status and, therefore, health. I had read most of the material on Chris’s blog, but still took copious notes. Chris is a most impressive and well-organized speaker.

On Saturday I started with Seth Roberts and Tucker Max. Seth’s talk was excellent – the gist can be found in recent blog posts, such as the one on butter reducing his coronary calcium score.

Tucker Max’s talk was fascinating in light of Todd Hargrove’s recent guest post here (How to Do Joint Mobility Drills, July 26, 2011). Tucker’s idea was that violence, both against animals (hunting) and people (warfare, homicide), must have been a critical factor shaping Paleolithic culture, and that this had important implications: Paleolithic peoples must have spent a lot of time play fighting as practice and as a fitness technique; and they must have developed philosophies, like those associated with all modern martial arts, to develop calmness and serenity in the face of violence – since the natural human reaction, panic, is unhelpful. It sounds as though mobility and serenity practices such as Tai Chi or yoga, which Todd endorsed, and components of religions such as Zen Buddhism may be modern descendants of Paleolithic martial arts. I liked this talk because it reminds us that “ancestral health” encompasses more than diet.

Mat Lalonde’s talk was outstanding. The subject of food toxins is extremely important for health, under-researched by scientists, and lacking in good overviews. (Step Two of our book is among the best, but only scratches the surface.) Mat reviewed research on a number of major food toxins, and discussed the ability of these toxins to survive cooking, enter the body, and contribute to disease. The talk had only one disappointment: Mat dis-associated himself from what he called “your movement.”

Mark Sisson and Denise Minger gave two of the most pleasant, fun talks at the meeting, as befits their super-positive personalities. Luckily on Saturday the two sessions were in neighboring rooms and it was possible to see some of each.

Nora Gedgaudas gave an excellent talk on the use of diet as a clinical approach to mental health disorders. It had plenty of citations that I’m eager to track down. We are fans of ketogenic dieting for neurological diseases, and Nora obviously is too – indeed she promotes a diet that verges on zero-carb. I think this will work well as a fast-acting therapy until she meets a patient with toxoplasmosis or some similar protozoal brain infection, but that the benefits of ketosis have to be balanced against long-term risks of glucose deficiency.

Melissa McEwen gave a fantastic talk about the evolution of the gut. It was fact-filled, science-rich, and entertaining. Interesting part: there is significant human variability in, for instance, colon size and structure. This is important because the digestive tract is really the only part of the body that evolves in response to changing diets. There has been some talk about different populations needing different diets; Melissa’s work suggests that instead of “metabolic typing” we may some day do “gut typing” to determine an optimal personal diet.

John Durant gave an entertaining and informative talk on the history and future of zoos. We had just visited San Diego Zoo and the San Diego Zoo Safari Park (formerly Wild Animal Park) earlier that week, and the Bronx, Washington DC, and Cleveland zoos fairly recently, so I enjoyed John’s take.

Andreas Eenfeldt and Richard Nikoley were another duo that were hard to choose between. Richard is entertaining at all times, and Andreas had an interesting story about the low-carb diet revolution in Sweden. I tried to catch both talks as best as I could.

After fitness talks from Doug McGuff, Frank Forencich, and Erwan LeCorre we chatted with friends new and old before leaving for the airport for our redeye flight back home. Shou-Ching pulled out her camera for a few photos. Here’s one:

All in all, a fabulous meeting. I think the Ancestral Health Society is going to have a big impact, and can’t wait for AHS 2012. Thanks, Aaron, Brent, and everyone else responsible for this enjoyable event!

Going to California

Posted by on July 29, 2011 5 comments

We’ll be on vacation for the next week-plus. We’re flying to San Diego early tomorrow morning to visit my brother and his family; then we’ll be vacationing in southern California and attending the Ancestral Health Symposium the following weekend.

I don’t expect to reply to comments or emails until we return.

Our best wishes to all!

Mobility and Health: Some Thoughts

Posted by on July 27, 2011 35 comments

I’d like to thank Todd Hargrove for his guest post (How to Do Joint Mobility Drills, July 26, 2011). It was thought-provoking, and I thought I’d share my reflections on it.

What Is the Goal of Exercise?

When it comes to fitness, the blogosphere tends to emphasize strength and athleticism. This is great, but there are other dimensions to health and fitness that are maybe a bit under-discussed.

As a 48-year-old recovering chronic disease patient, I am not looking to become a competitive athlete, enjoyable though that might be. Rather, I want to maximize health and longevity, and be able to freely and pleasurably move through all the challenges and opportunities life may present. I’ll be happy if I can:

  1. Be strong enough to freely manipulate my body plus a heavy load.
  2. Be fit enough to run 3-4 miles with pleasure, play an hour of tennis without getting sore, and sprint faster than common criminals.
  3. Be mobile enough to move freely and gracefully through the full natural range of motion of all joints without crackling, stiffness, or soreness.
  4. Develop good posture, circulation, and neurological function, so that my body naturally arranges itself in healthy positions.

The first three goals are not too different from Jamie Scott’s prescription for surviving a natural disaster. He asks: Could you lift yourself over a wall or up to a balcony to escape a tsunami? Sprint-jog 3-4 miles over shattered ground and obstacles to escape the liquefaction zone of an earthquake? Walk 3-4 hours over hills daily when roads are impassable? Get into a low squat to fit in a small shelter, or squeeze through a small opening?

But I have a special interest in neurological health. I had chronic ear infections as an infant, culminating in surgery, and ever since have had poor balance. My central nervous system infection made it much worse. Three years ago I had to sit down to put pants on or take them off; walked into doors; and fumbled and dropped things, as the complete loss of our former collection of wine glasses can attest. With diet and antibiotics I’ve recovered; my balance is now similar to what it was in my 20s – which is to say, poor.  I can now stand on one foot for about 20 seconds before I have to put down the other foot to balance myself; that would have been 1 or 2 seconds three years ago, but Shou-Ching can do it indefinitely. When we go hiking in the mountains, Shou-Ching clambers up or down steep rocky slopes like a mountain goat; I have to move with care.

Falls are a major cause of health impairment, broken bones, and mortality in the elderly. It would be great if I can improve nervous system function and balance before I get old and falls become dangerous.

I’m very pleased to start this blog’s discussion of fitness with Todd’s post, because mobility and neurological function are critically important to fitness at all ages – and may be crucial to good health as we age.

The Concept of Body Maps

Let me paraphrase one of the key points of Todd’s post this way:

The brain maintains “maps” of the body … These maps may become inaccurate, out of synch with the physical body … As a result the brain may believe a movement is impossible or dangerous and block its performance, even if the body is fully capable of performing the movement … With training the brain can learn the true movement capabilities of the body and revise its maps to more accurately reflect reality, thus increasing the body’s ability to move freely.

The idea that brain “maps” of the physical body, rather than the actual body, are what sets the limits to motion reminded me of a TED video I had seen by Dr. Vilayanur Ramachandran. He is a neuroscientist who investigated the problem of “phantom pain” in the lost limbs of amputation victims, and showed that the pain could be cured by “mirror box” therapies that fooled the brain into manipulating the lost arm and thereby re-drawing the brain’s body maps. Here is his fascinating TED talk:

Todd explains how improper brain maps can lead to chronic pain, and how repairing the brain maps can end the pain. This is an important idea for those suffering from chronic pain.

Use It Or Lose It

Todd observes that

While movement will clarify maps, lack of movement will tend to blur them. In a famous experiment, researchers found that sewing a monkey’s fingers together for a few weeks caused its brain to map the fingers as one unit, not as two separate parts capable of individual movements.

So if I want my brain to remember what my body is capable of, I need to regularly take my body through a diversity of movements.

This is an important reminder for someone who spends 12 hours per day at a desk. Get away from the desk, even if only for a few minutes a day, and move!

The Strategy of Slow, Mindful Movement

When I was young I wanted to do everything fast. (Shou-Ching complains that when I’m behind the wheel of a car, I think I’m still young.) But now I’m starting to appreciate the benefits of slow motion.

Todd’s list of ways to “maximize the benefit of mobility exercise” emphasizes slow, mindful movements. A few thoughts on each:

“Avoid pain and threat.” Since the purpose of the brain’s body maps is to prevent dangerous movements from happening, to re-draw the maps we have to teach the brain that “dangerous” movements are actually safe. For this to be persuasive, they must actually be safe. But this corollary may be less obvious:

Make sure the movement does not … create other signs of threat such as holding the breath, grimacing, collapsing your posture, or using unnecessary tension.

I’m a fan of the mobility videos of Kelly Starrett at mobilitywod.com, and he frequently advises one never to make a “pain face” or grimace, but rather to maintain a cheerful “Zen face.” A grimace during a challenging stretch or movement may be enjoyable, but it might detract from the value of the exercise. Interesting!

“Be mindful and attentive.” This one comes easily to me: I am introspective and enjoy listening to my body and paying attention to muscles, breath, and blood flow during exercise. It’s good to know that’s beneficial.

“Use novel movements.” I like routine, but routine mobility drills are unproductive. Movements need to explore new capabilities.

“Easy does it.” Move slowly and gently. This calls to mind the classic Chinese exercise forms, like Qi Gong and Tai Chi; they are characterized by slow, flowing, graceful movements.

“Be curious, exploratory, and playful.” I like the evolutionary inference Todd makes here:

All animals engage in the most play during the times of their lives when the educational demands are the highest. This means that play is the best solution to difficult education problems that evolution has found.

I think we sometimes fall into the trap of thinking that adulthood implies seriousness and sobriety. No! Rather, good health implies lifelong playfulness.

In Boswell’s Life of Johnson, in the Dedication, Boswell writes:

It is related of the great Dr. Clarke, that when in one of his leisure hours he was unbending himself with a few friends in the most playful and frolicksome manner, he observed Beau Nash approaching; upon which he suddenly stopped. “My boys,” said he, “let us be grave – here comes a fool.”

Let us not be fools, and play!

Can Rhythmic Movement Be an Ultradian Therapy?

I’ve done several posts on the subject of circadian (day-night) rhythms, and how enhancing these rhythms with diet, light, sleep, and exercise may be therapeutic for many diseases. See, for instance, Intermittent Fasting as a Therapy for Hypothyroidism (Dec 1, 2010) and Seth Roberts and Circadian Therapy (Mar 22, 2011).

But humans have other natural biorhythms that cycle more frequently. These “ultradian rhythms” can be quite short. For instance, some hormones are released in pulses – I believe insulin and thyroid hormone may operate this way – and I believe a common interval between pulses is 6 seconds.

Many classic movement forms, like yoga or qi gong, emphasize that movement should be synchronized with breathing, and that breathing should be slow and rhythmic – often with about ten breaths per minute, or six seconds per breath.

The coincidence between these numbers intrigues me. If enhancing circadian rhythms is therapeutic for disease, might enhancing ultradian rhythms by mindful “synching” of the breath to their period be therapeutic for hormonal dysfunction?

It’s just a thought. Many people with glucose regulation issues have disrupted ultradian rhythms for insulin secretion. The ultradian clocks in their pancreatic beta cells aren’t working properly. Wouldn’t it be interesting if mindful breathing, as in yoga, could improve insulin secretion and glucose regulation?

This is not such a far out idea. Consider these quotations from recently published papers:

Mind-body modalities based on Eastern philosophy, such as yoga, tai chi, qigong, and meditation … have many reported benefits for improving symptoms and physiological measures associated with the metabolic syndrome…. Findings from the studies reviewed support the potential clinical effectiveness of mind-body practices in improving indices of the metabolic syndrome. [1]

Participation of subjects with T2DM in yoga practice for 40 days resulted in reduced BMI, improved well-being, and reduced anxiety. [2]

Yoga-nidra practiced for 30 minutes daily up to 90 days, parameters were recorded every. 30th day. Results of this study showed that most of the symptoms were subsided (P < 0.004, significant), and fall of mean blood glucose level was significant after 3-month of Yoga-nidra. This fall was 21.3 mg/dl, P < 0.0007, (from 159 +/- 12.27 to 137.7 +/- 23.15,) in fasting and 17.95 mg/dl, P = 0.02, (from 255.45 +/- 16.85 to 237.5 +/- 30.54) in post prandial glucose level. Results of this study suggest that subjects on Yoga-nidra with drug regimen had better control in their fluctuating blood glucose and symptoms associated with diabetes, compared to those were on oral hypoglycaemics alone. [3]

[F]asting plasma insulin was significantly lower in the yoga group. The yoga group was also more insulin sensitive (yoga 7.82 [2.29] v. control 4.86 [11.97] (mg/[kg.min])/(microU/ml), p < 0.001). [4]

There are fifty-six papers in Pubmed on “yoga diabetes”, and only four of them date before 2002. Most were published after 2008. This is an emerging area of research, but it would be interesting if slow, mindful movement proves to be an effective therapy for metabolic disorders. Maybe exercise doesn’t need to be vigorous to heal disorders like diabetes and obesity!

The Best Exercises for Mobility

I asked Todd what traditional movement forms he would most recommend. He replied:

In my blog I made some lists of exercises styles, traditional and modern, which are in line with what I recommend: the Feldenkrais Method, Z-Health, Alexander Technique, and tai chi are at the top of the list.

My favorite is the Feldenkrais method, but I think for purposes of your blog, some tai chi videos would be perfect, because they really provide a picture of what I’m talking about. You can’t do tai chi without observing all of the guidelines I provide at the end. And it looks cool.

You might include a point that the magic of tai chi is not so much in the specific forms they use, but in the WAY they move – smooth and slow. And the mind state while moving – mindful, relaxed, attention to small details and subtleties. You could apply this tai chi style to anything and get benefit – sitting, standing, walking, lifting weights or doing joint mobility drills.

All of these movement disciplines are extremely interesting, and I hope to get help exploring them in future blog posts. I know that a number of Z-Health Master Trainers have read our book, and hopefully one of them will teach us about Z-Health.

In closing, here are some videos of Qi Gong and Tai Chi movements. With videos available on DVD or on YouTube, there’s no need to join a class to learn mobility drills. You can play a video in your TV and practice slow, mindful, relaxed movements at home.

Perhaps the most valuable movements, in my view, are those used as “warm-up” exercises in Tai Chi or beginning movements in Qi Gong. Here is a well-made introductory video:

Here is a beautiful exhibition of Tai Chi:

Thanks, Todd. I very much appreciate the opportunity to learn about fitness from an expert!

References

[1] Anderson JG, Taylor AG. The metabolic syndrome and mind-body therapies: a systematic review. J Nutr Metab. 2011;2011:276419. http://pmid.us/21773016.

[2] Kosuri M, Sridhar GR. Yoga practice in diabetes improves physical and psychological outcomes. Metab Syndr Relat Disord. 2009 Dec;7(6):515-7. http://pmid.us/19900155.

[3] Amita S et al. Effect of yoga-nidra on blood glucose level in diabetic patients. Indian J Physiol Pharmacol. 2009 Jan-Mar;53(1):97-101. http://pmid.us/19810584.

[4] Chaya MS et al. Insulin sensitivity and cardiac autonomic function in young male practitioners of yoga. Natl Med J India. 2008 Sep-Oct;21(5):217-21. http://pmid.us/19320319.