Category Archives: Obesity - Page 3

Jay Wright’s Weight Loss Journey

Posted by on December 1, 2011 133 comments

Jay Wright, who comments as “Jaybird,” has had a remarkably successful weight loss story. He adopted our diet in March at a weight of 250 pounds, and reached his normal weight of 170 pounds at Halloween, seven and a half months later.

I met Jay at Wise Traditions in November and can attest that he is now a handsome, slender man.

Jay’s weight loss was remarkably consistent at about 2.5 pounds per week. He agreed to describe his weight loss journey in a guest post; my questions are in italic, Jay wrote everything else. Welcome, Jay! – Paul

I would like to thank Dr. Paul Jaminet and Dr. Shou-Ching Jaminet for writing a great diet book and website!  You have been instrumental in helping me achieve the long elusive goal of great health and weight. For me, this truly is the Perfect Health Diet!

Before PHD

Paul: Jay, what do you think caused your overweight condition in the first place?

1. Ignorance and confusion. I believe I would have eaten the PHD way and remained at a healthy weight if I was taught to eat this way from the beginning. Instead, the government promotes the anti-saturated fat, pro-seed “vegetable” oil, and whole grains food pyramid. The belief formed from trusting the experts is a lot to overcome. I remember a decade ago during the Atkins’ hype that I thought that he must be crazy to recommend such a dangerous diet that would go against the “entire” medical establishment.  Then, even after I stopped believing the Lipid Hypothesis, I was still confused by all of the rest of the diet claims out there. While I was uncertain, I thought I might as well enjoy a “normal” diet until I can figure it all out.

2. Eating Habits. Besides the high carbs, food toxins, and malnourishment of the food pyramid diet, a few other factors may have affected my eating habits. I was a normal weight child growing up and I could eat anything and everything in sight and not get even pudgy in the slightest. When all foods have the same effect – none – you don’t worry about whether the food is healthy. Also, I spent my childhood playing one sport after another which might have actually worsened my eating habits. At least here with Texas football, we were constantly encouraged to stuff ourselves and put on more weight.  When sports ended for me after college, normal amounts of food looked like a starvation diet on a plate!

3. Carelessness toward health.  Was I careless because I was told “healthy” meant a yucky salad and “unhealthy” meant a yummy steak?  A young boy always chooses the steak especially when I was constantly hungry from 3 hour practices!  This all started to change after my dad was diagnosed with heart disease and started eating a “healthy” low-fat diet. However, the real wake-up call came when my mother was diagnosed and eventually died of breast cancer! To fight the cancer, she put up a courageous fight by being the most dedicated eater of an “alkalizing” vegetarian diet ever! Yet, even though I began to care more about health, I continued to allow myself to eat anything while I learned more and took breaks from trying different diets.

4. Lack of exercise because of a bad back.  I have had a herniated disc in my lower back for about 10 years now. When I changed careers and became even more sedentary, my back problem only worsened from bad posture while sitting. I should have at least continued to walk short amounts, but at the end of the day, I didn’t even feel like tolerating even a little pain after dealing with it so much during the day. The recliner offered relief.

5. Convenience.  As a single guy, I relied on eating out for convenience over the years and pre-made frozen dinners when I ate at home mostly. Starting a diet always meant making big changes to my routine and giving up a lot of time to cook.

6. Diets were Too Low in Food Reward.  Looking back, all the diets I tried were much lower in food reward than the “regular” American diet with lots of sweets that kept calling to me! All of the previous diets required a Herculean will power just to fight the temptations. It was mental torture being on a diet!

Paul: Jay, what were your experiences on the various diets you tried – and what caused you to give them up?

Here is my weight history:

After college sports, I struggled with my weight. I was a yo-yo dieter – I could lose weight but it always ended up even higher. I tried meal shake replacements, frozen dinners to limit calories, no meat/meat, no dairy/dairy, acid/alkaline, exercise/no exercise while dieting, no cash or credit cards in my wallet going to work so I wouldn’t stop at a fast food, punishment where I had to eat a raw tomato if I cheat (I hate raw tomatoes), and many other vegetarian leaning and mental tricks.  A pattern emerged with these diets.  I would starve with low energy for about a week or two until my will power ran out. Then, I would go eat something “bad.”  If I continued to repeat the pattern and managed to be “successful,” I stayed hungry even once I reached my goal weight.  I tried to transition to a “regular” amount of food to stop starving and just maintain but to no avail.  My weight went right back up even higher than before even without cheating on the diets.

Paleo was finally the exception to the starving rule, but only at first.  I felt great on a very low carb paleo for a couple of months.  I ate a pound of meat a day and mostly vegetables with a little fruit and nuts and a lot of coconut oil. The extra fat and meat seemed to enable me to lose weight and not be hungry. I lost nearly 40 lbs and halfway to my goal.  However, I started to not feel so well and hunger was returning, too. I had headaches and energy fluctuated throughout the day. I never liked the taste of vegetables and I began dreading the need to eat more vegetables than I had ever cared to eat in my life. Also, the sugar cravings never stopped just like on the vegetarian diets. Eventually, will power ran out eventually on paleo just like on the other diets.

Here’s what I looked like at 250 pounds. I’m the one on the left in the gray shirt; the one on the right is my brother Craig Wright:

I knew I had better find an answer when my family and friends would laugh each time I declared, “Diet starts tomorrow!”

Paul: Jay, it’s very interesting that on pre-Paleo diets you were always hungry, and when you ate to satisfy your hunger, your weight returned to as high or higher than when you began. That’s consistent with the set-point theory of obesity: your set-point hadn’t changed, and so when you reduced weight below the set-point, you got hungry; when you ate to satisfy your appetite, you were obese. The Paleo experience could also be said to be consistent with the set-point theory: it reduced the set-point so you lost 40 pounds without hunger, but weight was still above normal and hunger returned as your weight got below the new set-point.

An interesting data point, which I see as a challenge for the setpoint theory because it suggests an alternative view, is that on VLC Paleo your hunger returned at the same time you began to feel unwell. This suggests that hunger and setpoint are really an index of health, and when the body is not being properly maintained the brain manufactures hunger. When nutrients are abundant and the body has all it needs to establish good health, the setpoint is reduced to normal weight, hunger disappears, and weight loss resumes.

Perfect Health Diet

Paul: Jay, what was your experience on PHD? I’m especially interested in whether you experienced plateaus where weight loss stalled, and whether you experienced hunger as on other diets.

I recorded my weight every day from April 15 through November, and enough days in March and early April to give a clear picture. Here is what happened:

As you can see, there was no stall in weight loss until I hit my target weight of 170 pounds.

Here’s my after photo, again with my brother Craig. This time Craig is on the left in black, I’m on the right in green:

Interestingly Craig has eaten pretty much the same foods as I have throughout life, and always maintained a normal weight. On my recommendation he adopted PHD soon after I did, and he also experienced health improvements – psoriasis, which he’s had for 20 years and used to leave red scales over much of his body, is nearly gone.

Hunger

I followed the PHD weight loss protocols and felt virtually no hunger throughout the 7 months. Intermittent fasting with one meal a day worked best for my schedule; I coconut oil fasted earlier in the day and 1 day per week.  After the first month, I coconut oil fasted for an entire week since I figured I should clean out my system. Then I dropped the calories to only 1200 to get some faster results early on to help my back. I thought I would readjust the calories up or the eating schedule according to my hunger, but I did not experience any hunger and had great energy so I left the plan alone. What little hunger I did experience was very mild and just meant it was time to drink another bottle of water or swig a tablespoon of coconut oil before the evening dinner. Interestingly, I ate some birthday cakes toward the end and experienced stronger and more uncomfortable hunger the following days than the previous months. The lack of hunger was definitely a key to my weight loss success.

Food Reward

For me, PHD is a high food reward diet. It tastes great every meal! Even in the beginning of the diet, I enjoyed the PHD meal just as much mentally as thinking about eating my old food. Later, my taste buds changed and PHD became clearly the more rewarding food. However, at least part of the PHD was bland. The coconut oil provided calories with no taste and helped keep my calories low. Yet, I really believe I would not have lasted on the diet if the food was bland. Having a neutral taste reminds me of the very low carb paleo diet that didn’t allow the safe starches and even small amounts of dairy. The white rice and white potatoes enabled me to eat vegetables regularly by buffering the taste until my taste buds adjusted and I began to like them. Avoiding milk but having small amounts of other dairy also went a long way in the enjoyment of the food and menu options. The safe starches, dairy, and a little bit of fruit also seem to be responsible for satisfying my sweet tooth cravings. I’m not sure if the high food reward PHD would have controlled my calorie intake since I counted calories. Nonetheless, compared to the other past diets I dreaded to eat, I prefer the high food reward of PHD. I use to say, “Why does all of the food that’s good for you taste so bad and all of the food that’s bad for you taste so good?” I don’t say that anymore with PHD.

Plateau

My belief is that total calories do matter. I’ve always been able to lose the fat and get back to my original weight provided that I lower my calories enough to accomplish it. However, my will power usually ran out before I accomplished it many times. The constant hunger and low energy with lower calories exhausted my desire to lose the weight on previous diets. In contrast, I experienced the opposite on PHD. While the PHD food and supplements provided satiety and energy, I controlled my calories by exercising, counting calories, eating only a single meal, and having oil fast days. Even after only a month, I experienced such a surge in energy even on lower calories that I increased my exercise to 2 hours of walking. Having established such a low calorie amount in the beginning with a challenging exercise and eating plan, I simply had to maintain the routine until the goal was reached.

I believe the key was PHD enabled me to maintain low enough calories to not experience a plateau as on other diets.

Set Point

My experience might show some truth to the concept of a set point. For instance, prior to starting PHD my weight stayed consistently within a 5 lb range for about 2 years. During this period I was eating whatever I wanted. My experience on PHD could be construed as the resetting of my set point to my normal weight – 170 lb. I was never hungry on PHD as long as my weight was above 175 lb. I started feeling more hunger once I got close to my normal weight in the 170s.  Unlike previous diets, I was able to eliminate the hunger by eating a little bit more — just upping my calories slightly.

Although other diets could get me to this weight point before, I had to stay in a perpetual starving mode to remain at this level. Unlike on PHD, on other diets adding enough calories to stop hunger always led to a rebound of weight that leveled out at a higher level than before I started.

When I started PHD my intended target weight was 175 pounds. With PHD, I actually continued to lose a little more than the 175 down to 170 without planning on it. Then, my weight slightly increased with obvious cheats like some birthday cake. While eating the normal amount the following days without the cheats, the weight returned to previous levels without an effort to compensate. After the weight loss, my weight has become more stable. The last month I have had several repeating days on the weight scale with the same exact weight number to the tenth of a point. This occurred even though I ate more on a few of the previous days. My weight history shows a stair stepping up higher with each diet attempt until PHD stabilized my weight back to its original healthy level.

Closing Thought

During the middle of my weight loss, I was at a restaurant eating a salad with balsamic vinegar and olive oil dressing, 8 oz steak, and a baked potato with butter and sour cream and some water with lemon, but without a dinner roll.  I paused and proclaimed, “I can’t believe I’m eating this and still losing weight! This is the BEST DIET EVER!”

A Paleo Pregnancy Pitfall?

Posted by on September 22, 2011 29 comments

On Saturday’s Around the Web I linked to a study [1] that tied low-carb dieting early in pregnancy to obesity in the child at age 9. This made Ana concerned:

I’m somewhat worried about the pregnancy diet study. Actually I am trying to conceive, 3 months ago my husbund and I changed my diet to Paleo.

Now I see this study and even though I feel great, better than before, I’m not sure, how much credibility would you give it?

I presume that perhaps there could be too little fat, and with that too low calorie intake for a pregnant woman, perhaps that could be the case, opinions please!!!

We certainly don’t want Ana to be stressed out, and it’s hard to turn down three exclamation marks, so I thought I’d interrupt the cancer discussion to address her concerns.

The Study

The study [1] claimed two things:

  1. Women who ate less than a thousand carb calories per day during the early part of pregnancy were more likely to give birth to babies with an overly silenced gene for the Vitamin A receptor RXR-alpha.
  2. Babies born with an overly silenced gene for RXR-alpha were more likely to be overweight at age 9.

Let’s look at the second point, which is more solid, first.

RXR-alpha silencing is associated with obesity

Here is the data:

It looks like it’s normal to have about 50% RXR-alpha methylation in this promoter region and if you have 80% methylation, you’re likely to become a pudgy 9-year old.

How solid is the correlation? They replicated it in a second cohort. Their first study produced two epigenetic marks that were strongly associated with childhood obesity, RXR-alpha and eNOS. A replication study confirmed the RXR-alpha but not the eNOS association.

How plausible is it that RXR-alpha silencing would contribute to obesity? Very plausible, because RXR-alpha is the hub of a network of genes regulating most aspects of metabolism and cell activity.

Vitamin A binds to two types of nuclear receptor, RAR and RXR. When it binds to RXR, a vitamin A – RXR complex is imported into the nucleus. This then looks around for a partner. Partners of RXR-alpha include:

  • Vitamin A – RAR complexes.
  • Vitamin D – VDR (vitamin D receptor) complexes.
  • T3 thyroid hormone – TR (thyroid hormone receptor) complexes.
  • LXR (liver X receptor).
  • CLOCK, the circadian rhythm regulation gene.
  • PPAR-gamma (peroxisome proliferator-activated receptor), a regulator of lipids whose deficiency leads to high cholesterol and hyperglycemia.
  • MyoD, a factor that triggers muscle creation.
  • Many others; a list can be found at Wikipedia.

The vitamin A – RXR-alpha complex “dimerizes” with these other nuclear receptors, forming a new complex that acts as a transcription factor to turn on gene expression. Most of those other partners cannot act to turn on DNA transcription unless they dimerize with RXR.

This means that the absence of RXR-alpha would be functionally equivalent to being low in vitamin A, vitamin D, T3 thyroid hormone, CLOCK, and all those other partners. It is like being born a sun-starved hypothyroid with messed up circadian rhythms who can’t form muscle and is hyperglycemic and dyslipidemic.

All of those things are associated with obesity.

RXR-alpha silencing might be a universal component of the metabolic damage in obesity:

[A]n association between increased RXRA methylation and adiposity is consistent with the observation of strongly diminished RXRA expression in visceral white adipose tissue from obese mice (35).

Personally, I think it’s very likely that silencing of RXR-alpha promotes obesity. This is the most solid part of the paper. They have data, and the mechanism makes sense.

Conclusion: some babies are getting off to a bum start in life due to epigenetic silencing of an important gene.

Does maternal diet affect RXR-alpha silencing?

This is the really weak part of the paper. Here was their data:

When I say this was their data, this was all of it. No scatter plots, no information about how other characteristics of the diet correlate with RXRA methylation, no information about health or lifestyle characteristics of the various carbohydrate intake cohorts so that we can evaluate the possibility of confounding factors.

It is unlikely that low carbohydrate intake was causing the problem. Aside from the fact that dietary carbohydrate intake is only weakly correlated to any factors seen by the baby in the womb (eg blood glucose, insulin, etc), 261 g/day is a substantial amount of carbohydrate – well above physiological needs. So the low-carb quartile included women in glucose deficiency, glucose moderation, and glucose excess; the other quartiles only women in glucose excess. If a glucose deficiency caused RXRA hypermethylation and glucose excess caused RXRA, there would have been a much larger scatter in RXRA methylation levels among the low-carb quartile compared to the 3 higher-carb quartiles. But we can see from the graph that the standard deviations are the same in every quartile.

So there is likely to be some other factor besides carbohydrate intake that was responsible for the RXRA hypermethylation. What are the possibilities?

One possibility alluded to in the paper is that the women had low carbohydrate intake because they were starving. The paper notes that “famine during pregnancy is associated with obesity in the adult offspring (5).” However, I am unaware of recent famines in Southampton UK.

Another possibility is an excess of some other macronutrient. Those mothers who ate fewer carbs were eating more fat and possibly more protein. Given the ubiquity of vegetable oils in modern fats, the increased fat was probably largely omega-6. This raises two possibilities:

  • High maternal omega-6 intake causes RXRA methylation.
  • High maternal protein intake causes RXRA methylation.

Both possibilities have support from studies in rodents: maternal high protein intake and maternal omega-6 fat intake are both associated with obesity in offspring. For more on the risks of high protein, see The Danger of Protein During Pregnancy, Jul 12, 2010.

Another possibility is that the low-carb high-fat diet produced a vitamin A excess. As we discuss in the book, this is a common problem, especially among people taking a multivitamin; probably due to widespread vitamin D and vitamin K2 deficiencies, large numbers of people exhibit evidence of impaired health with vitamin A intake above 10,000 IU/day. As a fat-soluble vitamin, vitamin A intake is more or less proportional to fat intake.

If a balance between vitamin D and vitamin A is needed because the vitamin D-VDR complexes and vitamin A-RXR complexes have to be in proper proportion, then the body may respond to an excess of vitamin A and a deficit of vitamin D by upregulating VDR expression and downregulating RXR expression. Such downregulation may be achieved by RXR-alpha methylation.

Another possibility is some confounding factor that happens to be correlated with carbohydrate intake. In the US Nurses Health Study, nurses with the lowest carbohydrate intake were “rebels” who rejected not only the health advice to eat vegetable-rich and whole-grain rich diets, but also every other standard bit of health advice. The low-carb nurses smoked more, exercised less, and drank more alcohol and more coffee.

So it could be maternal smoking, lack of exercise, or drinking too much alcohol or caffeine that causes RXRA hypermethylation and childhood obesity.

Another possibility, raised in the comments by Amber, is that mothers of the obese children were obese themselves, ate low-carb diets for weight control reasons, and passed on their obesity to their children. It is indeed the case that obese mothers tend to have children who are obesity-prone, and it is suspected that epigenetics may be responsible for this “inherited” obesity. If low-carb diets have indeed become popular among the obese mothers of Southampton UK, then this is a possibility that must be considered.

Low-Carb Paleo Pitfalls?

Should Ana modify her diet because of this study?

I think it’s important to avoid a glucose deficiency. But I don’t think it’s necessary to eat 1,000 calories per day of carbs to achieve that.

I think it’s important to eat a moderate amount of protein, neither too much nor too little; and to limit the amount of omega-6 fats eaten.

I think it’s a good idea to avoid alcohol or excessive consumption of bioactive beverages like coffee during pregnancy. Also to avoid smoking, and to get some exercise and sun exposure.

If you’re doing all these things, I don’t think you need to be concerned. Ana says, “I feel great, better than before”; that’s good evidence that she’s well prepared for a healthy pregnancy.

Conclusion

The paper presents solid evidence that hypermethylation of RXR-alpha in the womb predisposes children to become obese at age 9.

The paper gives us essentially no evidence at all as to what causes hypermethylation of RXR-alpha in the womb, except that it correlates with low carbohydrate consumption in the women of Southampton UK.

I hate it when journals do this. If you’re going to link carb intake to RXRA methylation, give some real data and analysis. Probably the authors are saving their dietary analysis for a future paper. The carb graph was included as a “teaser” to make the work seem more interesting.

There are many known health dangers which are known risk factors for obesity and which correlate with low carbohydrate consumption in the general population. So until more evidence emerges, I think there’s little here for low-carb Paleo dieters to be concerned about.

References

[1] Godfrey KM et al. Epigenetic gene promoter methylation at birth is associated with child’s later adiposity. Diabetes. 2011 May;60(5):1528-34. http://pmid.us/21471513.

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.

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.