Tuesday, May 25, 2010

Book Review: S.P.E.E.D.

This book was sent to me by Matt Schoeneberger, who co-authored it with Jeff Thiboutot. Both have master's degrees in exercise science and health promotion. S.P.E.E.D. stands for Sleep, Psychology, Exercise, Environment and Diet. The authors have attempted to create a concise, comprehensive weight loss strategy based on what they feel is the most compelling scientific evidence available. It's subtitled "The Only Weight Loss Book Worth Reading". Despite the subtitle that's impossible to live up to, it was an interesting and well-researched book. It was a very fast read at 205 large-print pages including 32 pages of appendices and index.

I really appreciate the abundant in-text references the authors provided. I have a hard time taking a health and nutrition book seriously that doesn't provide any basis to evaluate its statements. There are already way too many people flapping their lips out there, without providing any outside support for their statements, for me to tolerate that sort of thing. Even well-referenced books can be a pain if the references aren't in the text itself. Schoeneberger and Thiboutot provided appropriate, accessible references for nearly every major statement in the book.

Chapter one, "What is a Healthy Weight", discusses the evidence for an association between body weight and health. They note that both underweight and obesity are associated with poor health outcomes, whereas moderate overweight isn't. While I agree, I continue to maintain that being fairly lean and appropriately muscled (which doesn't necessarily mean muscular) is probably optimal. The reason that people with a body mass index (BMI) considered to be "ideal" aren't healthier on average than people who are moderately overweight may have to do with the fact that many people with an "ideal" BMI are skinny-fat, i.e. have low muscle mass and too much abdominal fat.

Chapter 2, "Sleep", discusses the importance of sleep in weight regulation and overall health. They reference some good studies and I think they make a compelling case that it's important. Chapter 3, "Psychology", details psychological strategies to motivate and plan for effective weight loss.

Chapter 4, "Exercise", provides an exercise plan for weight loss. The main message: do it! I think they give a fair overview of the different categories of exercise and their relative merits, including high-intensity intermittent training (HIIT). However, the exercise regimen they suggest is intense and will probably lead to overtraining in many people. They recommend resistance training major, multi-joint exercises, 1-3 sets to muscular failure 2-4 days a week. I've been at the higher end of that recommendation and it made my joints hurt, plus I was weaker than when I strength trained less frequently. I think the lower end of their recommendation, 1 set of each exercise to failure twice a week, is more than sufficient to meet the goal of maximizing improvements in body composition in most people. My current routine is one brief strength training session and one sprint session per week (in addition to my leisurely cycle commute), which works well for me on a cost-benefit level. However, I was stronger when I was strength training twice a week and never going to muscular failure (a la Pavel Tsatsouline).

Chapter 5, "Environment", is an interesting discussion of different factors that promote excessive calorie intake, such as the setting of the meal, the company or lack thereof, and food presentation. While they support their statements very well with evidence from scientific studies, I do have a lingering doubt about these types of studies: as far as I know, they're all based on short-term interventions. Science would be a lot easier if short-term always translated to long term, but unfortunately that's not the case. For example, studies lasting one or two weeks show that low glycemic index foods cause a reduction in calorie intake and greater feelings of fullness. However, this effect disappears in the long term, and numerous controlled trials show that low glycemic index diets have no effect on food intake, body weight or insulin sensitivity in the long term. I reviewed those studies here.

The body has homeostatic mechanisms (homeostatic = maintains the status quo) that regulate long-term energy balance. Whether short-term changes in calorie intake based on environmental cues would translate into sustained changes that would have a significant impact on body fat, I don't know. For example, if you eat a meal with your extended family at a restaurant that serves massive portions, you might eat twice as much as you would by yourself in your own home. But the question is, will your body factor that huge meal into your subsequent calorie intake and energy expenditure over the following days? The answer is clearly yes, but the degree of compensation is unclear. Since I'm not aware of any trials indicating that changing meal context can actually lead to long-term weight loss, I can't put much faith in this strategy (if you know otherwise, please link to the study in the comments).

Chapter 6, "Diet", is a very brief discussion of what to eat for weight loss. They basically recommend a low-calorie, low-carb diet focused on whole, natural foods. I think low-carbohydrate diets can be useful for some overweight people trying to lose weight, if for no other reason than the fact that they make it easier to control appetite. In addition, a subset of people respond very well to carbohydrate restriction in terms of body composition, health and well-being. The authors emphasize nutrient density, but don't really explain how to achieve it. It would have been nice to see a discussion of a few topics such as organ meats, leafy greens, dairy quality (pastured vs. conventional) and vitamin D. These may not help you lose weight, but they will help keep you healthy, particularly on a calorie-restricted diet. The authors also recommend a few energy bars, powders and supplements that I don't support. They state that they have no financial connection to the manufacturers of the products they recommend.

I'm wary of their recommendation to deliberately restrict calorie intake. Although it will clearly cause fat loss if you restrict calories enough, it's been shown to be ineffective for sustainable, long-term fat loss over and over again. The only exception is the rare person with an iron will who is able to withstand misery indefinitely. I'm going to keep an open mind on this question though. There may be a place for deliberate calorie restriction in the right context. But at this point I'm going to require some pretty solid evidence that it's effective, sustainable, and doesn't have unacceptable side effects.

The book contains a nice bonus, an appendix titled "What is Quality Evidence"? It's a brief discussion of common logical pitfalls when evaluating evidence, and I think many people could benefit from reading it.

Overall, S.P.E.E.D. was a worthwhile read, definitely superior to 95% of fat loss books. With some caveats mentioned above, I think it could be a useful resource for someone interested in fat loss.

Monday, May 24, 2010

Thank You

I'd like to extend my sincere thanks to everyone who has supported me through donations this year. The money has allowed me to buy materials that I wouldn't otherwise have been able to afford, and I feel it has enriched the blog for everyone. Here are some of the books I've bought using donations. Some were quite expensive:

Food and western disease: health and nutrition from an evolutionary perspective. Staffan Lindeberg (just released!!)

Nutrition and disease. Edward Mellanby

Migration and health in a small society: the case of Tokelau. Edited by Albert F. Wessen

The saccharine disease. T. L. Cleave

Culture, ecology and dental anthropology. John R. Lukacs

Vitamin K in health and disease. John W. Suttie

Craniofacial development. Geoffrey H. Sperber

Western diseases: their emergence and prevention. Hugh C. Trowell and Denis P. Burkitt

The ultimate omega-3 diet. Evelyn Tribole

Our changing fare. John Yudkin and colleagues


Donations have also paid for many, many photocopies at the medical library. I'd also like to thank everyone who participates in the community by leaving comments, or by linking to my posts. I appreciate your encouragement, and also the learning opportunities.

phil heath Kai Greene Branch Warren after the 2009 Mr Olympia video phil heath met rx

phil heath

phil-heath

video of phil heath Kai Greene and Branch Warren after the 2009 Mr Olympia, phil heath was unlucky at the 2009 mr olympia due to some illness going into the mr olympia bodybuilding contest.

but aspect to see phil heath pushing for the 2010 mr olympia title and in much better condition then the 2009 mr olympia contest.

phil heath is wearing a met rx t-shirt in the video not sure if phil heath is still sponsored by met rx or not now.

Dissolve Away those Pesky Bones with Corn Oil

I just read an interesting paper from Gabriel Fernandes's group at the University of Texas. It's titled "High fat diet-induced animal model of age-associated obesity and osteoporosis". I was expecting this to be the usual "we fed mice industrial lard for 60% of calories and they got sick" paper, but I was pleasantly surprised. From the introduction:
CO [corn oil] is known to promote bone loss, obesity, impaired glucose tolerance, insulin resistance and thus represents a useful model for studying the early stages in the development of obesity, hyperglycemia, Type 2 diabetes [23] and osteoporosis. We have used omega-6 fatty acids enriched diet as a fat source which is commonly observed in today's Western diets basically responsible for the pathogenesis of many diseases [24].
Just 10% of the diet as corn oil (roughly 20% of calories), with no added omega-3, on top of an otherwise poor laboratory diet, caused:
  • Obesity
  • Osteoporosis
  • The replacement of bone marrow with fat cells
  • Diabetes
  • Insulin resistance
  • Generalized inflammation
  • Elevated liver weight (possibly indicating fatty liver)
Hmm, some of these sound familiar... We can add them to the findings that omega-6 also promotes various types of cancer in rodents (1).

20% fat is less than the amount it typically takes to make a rodent this sick. This leads me to conclude that corn oil is particularly good at causing mouse versions of some of the most common facets of the "diseases of civilization". It's exceptionally high in omega-6 (linoleic acid) with virtually no omega-3.

Make sure to eat your heart-healthy corn oil! It's made in the USA, dirt cheap and it even lowers cholesterol!

Lindeberg on Obesity

I'm currently reading Dr. Staffan Lindeberg's magnum opus Food and Western Disease, recently published in English for the first time. Dr. Lindeberg is one of the world's leading experts on the health and diet of non-industrial cultures, particularly in Papua New Guinea. The book contains 2,034 references. It's also full of quotable statements. Here's what he has to say about obesity:
Middle-age spread is a normal phenomenon - assuming you live in the West. Few people are able to maintain their [youthful] waistline after age 50. The usual explanation - too little exercise and too much food - does not fully take into account the situation among traditional populations. Such people are usually not as physically active as you may think, and they usually eat large quantities of food.

Overweight has been extremely rare among hunter-gatherers and other traditional cultures [18 references]. This simple fact has been quickly apparent to all foreign visitors...

The Kitava study measured height, weight, waist circumference, subcutaneous fat thickness at the back of the upper arm (triceps skinfold) and upper arm circumference on 272 persons ages 4-86 years. Overweight and obesity were absent and average [body mass index] was low across all age groups. ...no one was larger around their waist than around their hips.

...The circumference of the upper arm [mostly indicating muscle mass] was only negligibly smaller on Kitava [compared with Sweden], which indicates that there was no malnutrition. It is obvious from our investigations that lack of food is an unknown concept, and that the surplus of fruits and vegetables regularly rots or is eaten by dogs.

The Population of Kitava occupies a unique position in the world in terms of the negligible effect that the Western lifestyle has had on the island.
The only obese Kitavans Dr. Lindeberg observed were two people who had spent several years off the island living a modern, urban lifestyle, and were back on Kitava for a visit.

I'd recommend this book to anyone who has a scholarly interest in health and nutrition, and somewhat of a background in science and medicine. It's extremely well referenced, which makes it much more valuable.

Sunday, May 23, 2010

Saturated Fat and Insulin Sensitivity

Insulin sensitivity is a measure of the tissue response to insulin. Typically, it refers to insulin's ability to cause tissues to absorb glucose from the blood. A loss of insulin sensitivity, also called insulin resistance, is a core part of the metabolic disorder that affects many people in industrial nations.

I don't know how many times I've seen the claim in journal articles and on the internet that saturated fat reduces insulin sensitivity. The idea is that saturated fat reduces the body's ability to handle glucose effectively, placing people on the road to diabetes, obesity and heart disease. Given the "selective citation disorder" that plagues the diet-health literature, perhaps this particular claim deserves a closer look.

The Evidence

I found a review article from 2008 that addressed this question (1). I like this review because it only includes high-quality trials that used reliable methods of determining insulin sensitivity*.

On to the meat of it. There were 5 studies in which non-diabetic people were fed diets rich in saturated fat, and compared with a group eating a diet rich in monounsaturated (like olive oil) or polyunsaturated (like corn oil) fat. They ranged in duration from one week to 3 months. Four of the five studies found that fat quality did not affect insulin sensitivity, including one of the 3-month studies.

The fifth study, which is the one that's nearly always cited in the diet-health literature, requires some discussion. This was the KANWU study (2). Over the course of three months, investigators fed 163 volunteers a diet rich in either saturated fat or monounsaturated fat.
The SAFA diet included butter and a table margarine containing a relatively high proportion of SAFAs. The MUFA diet included a spread and a margarine containing high proportions of oleic acid derived from high-oleic sunflower oil and negligible amounts of trans fatty acids and n-3 fatty acids and olive oil.
Yummy. After three months of these diets, there was no significant difference in insulin sensitivity between the saturated fat group and the monounsaturated fat group. Yes, you read that right. Even the study that's selectively cited as evidence that saturated fat causes insulin resistance found no significant difference between the diets. You might not get this by reading the misleading abstract. I'll be generous and acknowledge that the (small) difference was almost statistically significant (p = 0.053).

What the authors decided to focus on instead is the fact that insulin sensitivity declined slightly but significantly on the saturated fat diet compared with the pre-diet baseline. That's why this study is cited as evidence that saturated fat impairs insulin sensitivity. But anyone who has a basic science background will see where this reasoning is flawed (warning: nerd attack. skip the rest of the paragraph if you're not interested). You need a control group for comparison, to take into account normal fluctuations caused by such things as the season, eating mostly cafeteria food, and having a doctor hooking you up to machines. That control group was the group eating monounsaturated fat. The comparison between diet groups was the 'primary outcome', in statistics lingo. That's the comparison that matters, and it wasn't significant. To interpret the study otherwise is to ignore the basic conventions of statistics, which the authors were happy to do. There's a name for it: 'moving the goalpost'. The reviewers shouldn't have let this kind of shenanigans slide.

So we have five studies through 2008, none of which support the idea that saturated fat reduces insulin sensitivity in non-diabetics. Since the review paper was published, I know of one subsequent study that asked the same question (3). Susan J. van Dijk and colleagues fed volunteers with abdominal overweight (beer gut) a diet rich in either saturated fat or monounsaturated fat. I e-mailed the senior author and she said the saturated fat diet was "mostly butter". The specific fats used in the diets weren't mentioned anywhere in the paper, which is a major omission**. In any case, after 8 weeks, insulin sensitivity was virtually identical between the two groups. This study appeared well controlled and used the gold standard method for assessing insulin sensitivity, called the euglycemic-hyperinsulinemic clamp technique***.

The evidence from controlled trials is rather consistent that saturated fat has no appreciable effect on insulin sensitivity.

Why Are We so Focused on Saturated Fat?

Answer: because it's the nutrient everyone loves to hate. As an exercise in completeness, I'm going to mention three dietary factors that actually reduce insulin sensitivity, and get a lot less air time than saturated fat.

#1: Caffeine. That's right, controlled trials show that your favorite murky beverage reduces insulin sensitivity (4, 5). Is it actually relevant to real life? I doubt it. The doses used were large and the studies short-term.

#2: Magnesium deficiency. A low-magnesium diet reduced insulin sensitivity by 25% over the course of three weeks (6). I think this is probably relevant to long-term insulin sensitivity and overall health, although it would be good to have longer-term data. Magnesium deficiency is widespread in industrial nations, due to our over-reliance on refined foods such as sugar, white flour and oils.

#3: Sugar. Fructose reduces insulin sensitivity in humans, along with many other harmful effects (7).

As long as we continue to focus our energy on indicting saturated fat, it will continue distracting us from the real causes of disease.


* For the nerds: euglycemic-hyperinsulinemic clamp (the gold standard), insulin suppression test, or intravenous glucose tolerance test with Minimal Model. They didn't include studies that reported HOMA as their only measure, because it's not very accurate.

** There's this idea that pervades the diet-health literature that all saturated fats are roughly equivalent, all monounsaturated fats are equivalent, etc., therefore it doesn't matter what the source was. This is beyond absurd and reflects our cultural obsession with saturated fat. It really irks me that the reviewers didn't demand this information.

*** They did find that markers of inflammation in fat tissue were higher after the saturated fat diet.

The Body Fat Setpoint, Part IV: Changing the Setpoint

Prevention is Easier than Cure

Experiments in animals have confirmed what common sense suggests: it's easier to prevent health problems than to reverse them. Still, many health conditions can be improved, and in some cases reversed, through lifestyle interventions. It's important to have realistic expectations and to be kind to oneself. Cultivating a drill sergeant mentality will not improve quality of life, and isn't likely to be sustainable.

Fat Loss: a New Approach

If there's one thing that's consistent in the medical literature, it's that telling people to eat fewer calories does not help them lose weight in the long term. Gary Taubes has written about this at length in his book Good Calories, Bad Calories, and in his upcoming book on body fat. Many people who use this strategy see transient fat loss, followed by fat regain and a feeling of defeat. There's a simple reason for it: the body doesn't want to lose weight. It's extremely difficult to fight the fat mass setpoint, and the body will use every tool it has to maintain its preferred level of fat: hunger, reduced body temperature, higher muscle efficiency (i.e., less energy is expended for the same movement), lethargy, lowered immune function, et cetera.

Therefore, what we need for sustainable fat loss is not starvation; we need a treatment that lowers the fat mass setpoint. There are several criteria that this treatment will have to meet to qualify:
  1. It must cause fat loss
  2. It must not involve deliberate calorie restriction
  3. It must maintain fat loss over a long period of time
  4. It must not be harmful to overall health
I also prefer strategies that make sense from the perspective of human evolution.

Strategies
: Diet Pattern

The most obvious treatment that fits all of my criteria is low-carbohydrate dieting. Overweight people eating low-carbohydrate diets generally lose fat and spontaneously reduce their calorie intake. In fact, in several diet studies, investigators compared an all-you-can-eat low-carbohydrate diet with a calorie-restricted low-fat diet. The low-carbohydrate dieters generally reduced their calorie intake and body fat to a similar or greater degree than the low-fat dieters, despite the fact that they ate all the calories they wanted (1). This suggest that their fat mass setpoint had changed. At this point, I think moderate carbohydrate restriction may be preferable to strict carbohydrate restriction for some people, due to the increasing number of reports I've read of people doing poorly in the long run on extremely low-carbohydrate diets (2).

Another strategy that appears effective is the "paleolithic" diet. In Dr. Staffan Lindeberg's 2007 diet study, overweight volunteers with heart disease lost fat and reduced their calorie intake to a remarkable degree while eating a diet consistent with our hunter-gatherer heritage (3). This result is consistent with another diet trial of the paleolithic diet in diabetics (4). In post hoc analysis, Dr. Lindeberg's group showed that the reduction in weight was apparently independent of changes in carbohydrate intake*. This suggests that the paleolithic diet has health benefits that are independent of carbohydrate intake.

Strategies: Gastrointestinal Health

Since the gastrointestinal (GI) tract is so intimately involved in body fat metabolism and overall health (see the former post), the next strategy is to improve GI health. There are a number of ways to do this, but they all center around four things:
  1. Don't eat food that encourages the growth of harmful bacteria
  2. Eat food that encourages the growth of good bacteria
  3. Don't eat food that impairs gut barrier function
  4. Eat food that promotes gut barrier health
The first one is pretty easy: avoid refined sugar, refined carbohydrate in general, and lactose if you're lactose intolerant. For the second and fourth points, make sure to eat fermentable fiber. In one trial, oligofructose supplements led to sustained fat loss, without any other changes in diet (5). This is consistent with experiments in rodents showing improvements in gut bacteria profile, gut barrier health, glucose tolerance and body fat mass with oligofructose supplementation (6, 7, 8).

Oligofructose is similar to inulin, a fiber that occurs naturally in a wide variety of plants. Good sources are jerusalem artichokes, jicama, artichokes, onions, leeks, burdock and chicory root. Certain non-industrial cultures had a high intake of inulin. There are some caveats to inulin, however: inulin and oligofructose can cause gas, and can also exacerbate gastroesophageal reflux disorder (9). So don't eat a big plate of jerusalem artichokes before that important date.

The colon is packed with symbiotic bacteria, and is the site of most intestinal fermentation. The small intestine contains fewer bacteria, but gut barrier function there is critical as well. The small intestine is where the GI doctor will take a biopsy to look for celiac disease. Celiac disease is a degeneration of the small intestinal lining due to an autoimmune reaction caused by gluten (in wheat, barley and rye). This brings us to one of the most important elements of maintaining gut barrier health: avoiding food sensitivities. Gluten and casein (in dairy protein) are the two most common offenders. Gluten sensitivity is widespread and typically undiagnosed (10).

Eating raw fermented foods such as sauerkraut, kimchi, yogurt and half-sour pickles also helps maintain the integrity of the upper GI tract. I doubt these have any effect on the colon, given the huge number of bacteria already present. Other important factors in gut barrier health are keeping the ratio of omega-6 to omega-3 fats in balance, eating nutrient-dense food, and avoiding the questionable chemical additives in processed food. If triglycerides are important for leptin sensitivity, then avoiding sugar and ensuring a regular source of omega-3 should aid weight loss as well.

Strategies: Micronutrients

As I discussed in the last post, micronutrient deficiency probably plays a role in obesity, both in ways that we understand and ways that we (or I) don't. Eating a diet that has a high nutrient density and ensuring a good vitamin D status will help any sustainable fat loss strategy. The easiest way to do this is to eliminate industrially processed foods such as white flour, sugar and seed oils. These constitute more than 50% of calories for the average Westerner.

After that, you can further increase your diet's nutrient density by learning to properly prepare grains and legumes to maximize their nutritional value and digestibility (11, 12; or by avoiding grains and legumes altogether if you wish), selecting organic and/or pasture-raised foods if possible, and eating seafood including seaweed. One of the problems with extremely low-carbohydrate diets is that they may be low in water-soluble micronutrients, although this isn't necessarily the case.

Strategies: Miscellaneous

In general, exercise isn't necessarily helpful for fat loss. However, there is one type of exercise that clearly is: high-intensity intermittent training (HIIT). It's basically a fancy name for sprints. They can be done on a track, on a stationary bicycle, using weight training circuits, or any other way that allows sufficient intensity. The key is to achieve maximal exertion for several brief periods, separated by rest. This type of exercise is not about burning calories through exertion: it's about increasing hormone sensitivity using an intense, brief stressor (hormesis). Even a ridiculously short period of time spent training HIIT each week can result in significant fat loss, despite no change in diet or calorie intake (13).

Anecdotally, many people have had success using intermittent fasting (IF) for fat loss. There's some evidence in the scientific literature that IF and related approaches may be helpful (14). There are different approaches to IF, but a common and effective method is to do two complete 24-hour fasts per week. It's important to note that IF isn't about restricting calories, it's about resetting the fat mass setpoint. After a fast, allow yourself to eat quality food until you're no longer hungry.

Insufficient sleep has been strongly and repeatedly linked to obesity. Whether it's a cause or consequence of obesity I can't say for sure, but in any case it's important for health to sleep until you feel rested. If your sleep quality is poor due to psychological stress, meditating before bedtime may help. I find that meditation has a remarkable effect on my sleep quality. Due to the poor development of oral and nasal structures in industrial nations, many people do not breathe effectively and may suffer from conditions such as sleep apnea that reduce sleep quality. Overweight also contributes to these problems.

I'm sure there are other useful strategies, but that's all I have for now. If you have something to add, please put it in the comments.


* Since reducing carbohydrate intake wasn't part of the intervention, this result is observational.