Book Review: Secrets from the Eating Lab

Book Review: Secrets from the Eating Lab by Dr. Traci Mann

Review on Amazon

How our well-meant attempts to address the health implications of our increasing body fat are making the problem even worse.

This is a very well written and uniquely informative book in a field glutted with opinions and weak and conflicting advice. It is not a how-to book on losing weight, although it has a few solid behavioral suggestions for making modest healthy changes. This is primarily an interpretation of much of the available evidence regarding obesity and health by psychologist who runs an eating lab at the University of Minnesota and publishes a lot of scholarly peer reviewed work in the field.

Although she is a researcher, Dr. Mann takes pains to distinguish herself from obesity researchers with a public health focus who are motivated to warn people about the dangers of increasing body fat. Her interpretation of the data is often the opposite in some ways from theirs, she sees the growing incidence of body fat and she sees the growing incidence of adult onset diabetes, but she reports that the link between body fat and health problems is far weaker than is implied by the rhetoric of most obesity researchers and much weaker than the popular impression has become. In addition, our efforts to fight obesity have, she concludes, actually become counter-productive because of the manner in which we typically attempt to fight our own biology by restricting calories and exercising in ways that increase our stresses and increase our preoccupation with food, and that both of these things feed back into exacerbating the original problem.

The book starts off ripping into both the commercial diet industry and the focus of a lot of articles by doctors and obesity researchers by announcing that their "3 pillars" are all simply false:

1. That some diets work for losing weight

2. That some diets are healthy for losing weight

3. That obesity itself is deadly 

Among the central and most compelling aspects of this book is where Mann observes that our ideal body image often tends to be outside of the range that we can reasonably sustain. And this becomes confused with health concerns and fed by commercial interests. We could transform our bodies potentially through diet and exercise, but at the cost of altering or entire lives in the service of that goal and experiencing extended self-denial and obsession with food.

And the clincher for her argument is that all this self-denial and obsession would be mostly serving our aesthetic ideal rather than actually improving health. She finds that according to best available evidence upon close inspection mortality is not significantly improved by losing weight, unless you are already extremely obese and still have a long life ahead of you. The population in that category is far smaller than the one targeted by both the diet and fitness industries and most obesity researchers.

Mann finds that diets consistently fail in two ways: (1) only a tiny percentage of dieters retain their weight loss, regardless of which diet it is, and (2) even when people lose enough weight to satisfy the goals of improving their risk profile, they rarely lose enough to satisfy their aesthetic preference. This means that according to the person themselves, their diet failed even when for health purposes it succeeds. Our aesthetic goals trump our health goals for the purpose of satisfaction with the diet.

If we should want to attempt small changes that help us regulate our own eating so we can maintain a sustainably lower body weight, Mann offers several well-tested behavioral suggestions along the lines of "nudges" that help us avoid being triggered to eat excessively.

I think her principles seem sound and her use of evidence is compelling. I do have one criticism of her otherwise superb and unique exposition though. She argues for a set point model of body weight regulation that maintains our weight within a fairly narrow range but she doesn't really address the obvious question of why people are statistically getting fatter if we are so consistent at maintaining our weight in such a narrow range.

 

She puts most of her focus on obesity not being as deadly as it appears except at the extreme, and she explains why people can't simply diet away unwanted body fat, but she doesn't at all dive into the reasons for our growing bodies. That's a big topic and it isn't her area of research so I can understand leaving it to others to try to explain, but for me it left a logical hole in her argument that begs to be filled and should have been addressed with at least some general thoughts.

Book Review: The GenoType Diet

The GenoType Diet: Change Your Genetic Destiny to live the longest, fullest and healthiest life possible

By Catherine Whitney (Author), Peter J. Dr D'Adamo (Author)

[Review based on Kindle version]

From my Amazon review:

"... is it plausible in general that metabolic traits cluster along with personality traits, and that these clusters imply different health regimens? Of course it's possible. I'm strongly disposed from my own experience to think there are personality traits that lead us to construct particular rough kinds of niches, and it makes sense that these might have distinct metabolic patterns. But does the author get it right that eating Turkey vs. Chicken or Beef vs. Pork for a particular type really is a difference that makes a difference? That part needs more research."

The question this book raises in my mind is whether the author's GeneTypes significantly improve the guesses we make about the best nutrition for us as individuals, compared to just knowing our medical risk factors and knowing our rough somatotype.

This book takes off from the author's previous writings about how blood type can predict a cluster of traits that include individual response to nutrients, and modifies it into a 6 part theory of types. The 6 part model is given an evolutionary rationale and the author links metabolic differences, personality traits, and speculation about ecological niches where those traits and metabolic differences might be especially adaptive. The resulting categories are so clean and tell such a compelling sort of story that they seem to invite accusations of similarity to fortune telling. But if they're right, then this would a pretty cool system, wouldn't it? At least in theory.

• The Hunter: Tall, thin, and intense, with an overabundance of adrenaline and a fierce, nervous energy that winds down with age, the Hunter was originally the success story of the human species. Vulnerable to systemic burnout when overstressed, the Hunter’s modern challenge is to conserve energy for the long haul.

• The Gatherer: Full-figured, even when not overweight, the Gatherer struggles with body image in a culture where thin is “in.” An unsuccessful crash dieter with a host of metabolic challenges, the Gatherer becomes a glowing example of health when properly nourished.

• The Teacher: Strong, sinewy, and stable, with great chemical synchronicity and stamina, the Teacher is built for longevity—given the right diet and lifestyle. This is the genotype of balance, blessed with a tremendous capacity for growth and fulfillment.

• The Explorer: Muscular and adventurous, the Explorer is a biological problem solver, with an impressive ability to adapt to environmental changes, and a better than average capacity for gene repair. The Explorer’s vulnerability to hormonal imbalances and chemical sensitivities can be overcome with a balanced diet and lifestyle.

• The Warrior: Long, lean, and healthy in youth, the Warrior is subject to a bodily rebellion in midlife.With the optimal diet and lifestyle, the Warrior can overcome the quick-aging metabolic genes and experience a second, “silver,” age of health.

• The Nomad: A GenoType of extremes, with a great sensitivity to environmental conditions—especially changes in altitude and barometric pressure, the Nomad is vulnerable to neuromuscular and immune problems. Yet a well-conditioned Nomad has the enviable gift of controlling caloric intake and aging gracefully.

If the model is right, it is a pretty remarkable and perhaps revolutionary approach to making better guesses at how to improve our own nutrition based on our biochemical individuality. The evidence for its plausibility seems reasonable, but there is still little evidence validating the particular categories here.

Full review on Amazon here.

The argument for a SANE diet

This is the second in a series of commentaries on the ideas promoted in Jonathan Bailor's book "The Smarter Science of Slim."

This one presents my own spin on his argument for a SANE diet as an effective long term strategy for counteracting the trend toward obesity and obesity-related chronic illness.

In addition to recommendations for brief, infrequent, high intensity exercise to counter insulin resistance and reset metabolism, Bailor promotes what he calls a SANE diet. This is an acronym for satiety, "aggression", nutrition, and efficiency. Rather than duplicate his explanation, I'll just summarize by saying this refers to the quality of food rather than the quanitity, and takes a number of different quality factors into consideration. This note is intended to present my version of the argument for a mixed collection of quality factors in an anti-obesity strategy.

1. Human biology tends to regulate its body weight in a very narrow range for long periods under a wide range of natural and ancestral environments.

I came to understand this well over a decade ago and in my opinion the evidence base for it has grown rather than being seriously questioned in any significant way. This model does have a potentially misleading aspect to it in practice. Many people seem to assume that a body weight set point means different people are predisposed to different body weights. That is only partly true. The set point model does not assume a fixed value, it assumes that we tend to regulate our weight within a narrow range for long periods of time. It is obvious that the body fat set point changes over time, otherwise creeping obesity simply wouldn't happen. The issue is not whether the set point can change, but whether (and how) we change it in the other direction. The forces on it appear to be asymmetric.

My 1998 article on body fat regulation, showing the weak understanding I had at that point of the specifics but I think accurately depicting the concept and showing its historical origins and scientific rationale.

There have also been a number of helpful popular press articles expanding on the dynamic set point concept and its relation to weight loss plateau.

Obesity expert Arya Sharma discusses the set point concept and a unique theory of how it works.

2. Increasingly throughout the contemporary world, a combination of global economic drivers and local environments has created conditions that defeat the biology of weight regulation and cause body weight to creep upwards, resulting in an "obesity epidemic."

A recent Lancet special issue on obesity gave a summary of the current perspective on factors in obesity.


3. Clinical studies suggest a role for dietary glycaemic index (GI) in bodyweight regulation and diabetes risk.

There are a number of lines of evidence leading to the conclusion that glycemic index plays a central role in weight regulation through glucose homeostasis. I singled out this article because it also describes why some of the implications of that conclusion are controversial.

4. The effect of lowering GI is a dynamic change to metabolism, not a static linear dropping of weight because the body adapts to the loss of energy in order to maintain its set point. Static models of calories in vs. calories out do not take the effects of metabolism into consideration and therefore do not accurately predict weight loss.

Even though glycemic load is an important factor in obesity, we can't just cut out starches and sugars without making any other change and expect to keep losing weight. We will tend to compensate in other ways because of the significance of metabolism in weight regulation. As a result it is now considered essential to consider metabolism in predictions of weight loss rather than just calorie balance.

5. Solely manipulating GI in isolation has a diminishing return over time in weight loss because the reduction of calorie intake tends to slow metabolism and because of changes in potentially confounding dietary factors such as fiber content, protein content, palatability, and energy density.

This is a continuation of the previous claim, based on the evidence gathered from trying to control weight solely by reducing glycemic load.

6. CONCLUSION: An individual nutrition strategy that replaces high GI foods by taking energy density, palatability, fiber, protein, energy density, ad other factors into account can more successfully use a reduction in glycemic index to control body fat by improving fat metabolism, slowing or stopping the accumulation of insulin resistance, and reversing the upward creeping of the body fat set point..

None of that is particularly surprising scientifically as far as I know. The set point model of weight control has been standard in both human and animal research for a long time, it is not at all controversial among obesity and physiology researchers. You simply have to take metabolism into account when considering how the body absorbs, utilizes, and catabolizes nutrients and energy. You can't just assume that everything we take in minus some estimate of what we are "burning" is going to be an accurate model of body weight fluctuation.

The part where there is still room for argument is the specific causal sequence, and that has some additional implications. There's an old conundrum in psychology research: "do we cry because we are sad, or are we sad because we cry?" The answer seems intuitively obvious but it turns out that both causal models are partly right because there is a feedback look from our behavior to the way we feel.

There is a similar conundrum in obesity research. Do we get fat because we eat too much and don't move enough, or do we eat more and move less because of the effects of obesity. Again it turns out that both capture part of what is really going on. We do gain weight when we eat more and move less, at least in the short term before our metabolism starts to regulate our weight back to normal. But the thing that causes our weight to more permanently creep upward is the changes to our metabolism over time. And those hormonal and cellular changes make us less good at burning fat and better at absorbing it, changing our body fat set point over time.

Todd I. Stark
Nov 20,2011

Dietary fads, fictions, factions, and facts

This is my first post in a series of planned commentaries based on my reading of Jonathan Bailor's highly recommended book, "The Smarter Science of Slim."

This first commentary is my perspective on the history of the issues and how I perceive they have been resolved scientifically so far.

The Low Carb Revolution

Years ago, Dr. Atkins shocked popular culture and infuriated proponents of low fat diets with the claim that people could lose weight and reduce their risk of heart disease by minimizing the mainstay of the typical diet, carbohydrates, replacing them with proteins and fats.

This was a controversial claim not only because low fat diets were popular at the time but also because in emphasizing a low carbohydrate diet, Atkins was claiming that we could be healthy with minimal amounts of important dietary elements like fiber and the nutrition we get from vegetables. He was opposed by the people who promoted an ever higher proportion of vegetables in our diet and who encouraged us to minimize saturated fats, which were long widely thought to increase the risk of heart disease and obesity. At the same time, a lot of people argued that obesity can and should be sensibly addressed with the reasonable commonsense approach of eating a little less and moving a little more: get active and cut back a little on calories each day.

Two Battles Emerge

This turned into two polarized contests of opinion in popular culture.

First, there was a conflict between the folks who think quality of food is important in weight control and those who think that emphasis is misplaced, that we should just measure calories in and calories out. The implication of the food quality view: eating more of some things and less of others should affect our weight over time without making constant efforts to otherwise monitor and control our intake by counting calories. The implication of the calorie balance model: just eat a few calories less and move around a little bit more to burn a few more calories and you will lose weight consistently.

Second, among those who consider the quality of food to be important, there was the battle of the low-carb lobby vs. the vegetable lobby. Should you eliminate carbohydrates because of their effect on metabolism, or should you eliminate saturated fats because "fats make us fat" and raise blood cholesterol?

As is often the case in polarized positions it seems from our perspective today that both sides (in both contests) got some things right and both sides got some things wrong.

Calorie Balance vs. Metabolism: The Result

The standard and consensus view of obesity among researchers is that passive overeating is the best overall description of the cause. It is widely accepted, though not universally, that the amount of caloric energy we take in plays a causal role in obesity. Further the standard and consensus view is that this results from a combination of global economic factors and local environmental factors (the "obesogenic environment").

It is also a standard and consensus view among obesity researchers and physiologists that body weight is regulated by metabolic factors (via chemical messengers) that are not not related to the number of calories we take in and the number of calories estimated for the activity we perform.

What the calorie balance model captures: our biology doesn't violate the laws of conservation of mass and energy. Eating less and catabolizing body mass for energy does cause us to lose body mass. Eating more and demanding less energy utilization does cause us to gain body mass.

What the metabolism model captures: The calorie balance model clearly predicts that our body weight should consistently fluctuate according to the overall energy balance between what we take in and our activity. This is demonstrably not the case both from common experience and controlled studies. The prediction of the calorie balance model only apply for a short time and then our body changes internally to absorb food differently and to use it differently for energy. Our appetite and subjective energy levels are also changed. This is collectively expressed as the body regulating its mass in various ways around a relatively stable point.

The common experience of a "weight loss plateau" coincides with the concept of a "weight set point" around which our body maintains itself in a narrow range over time.

When we simply eat less, we lose weight for a little while and then the loss slows down and eventually stops and tends to reverse itself into return to baseline weight and sometimes even gain above that original level.

Further, the signficance of metabolism implies that quantity of energy taken in and demanded is only part of the causal model. Metabolism is affected differently by the specific foods we eat over time and the specific kinds of activities we engage in, not just or even primarily the total amount of energy involved. The metabolism model better captures the importance of food quality than does the calorie balance model.

Low Carb vs. Veggies: The Result

Given the consensus view that metabolism is an important factor in weight control and that the kinds of food we eat are an important factor in metabolism, we arrive at the second battle, over what it means to eat higher quality food more conducive to health and fighting obesity.

What the low carb lobby got right and the vegetable lobby got wrong: saturated fat isn't itself an important cause of heart disease and obesity. You can consume reasonable amounts of fat, including saturated fat from animal sources, and still have a very healthy diet.

What the low carb lobby got wrong and the vegetable lobby got right: The low carb lobby deals with the problems of insulin response in a gross and overly restrictive way by choosing proteins and fats over carbohydrates in general rather than balancing them and eliminating high glycemic carbohydrates. This makes levels of fiber too low and eliminates important sources of nutrients and often crowds out vegetable nutrition sources using animal ones. This is probably healthier than the typical high glycemic diet, but not nearly optimal. Minimizing carbohydrates is a bad strategy because we get many nutrients from carbohydrates, especially vegetables.

What both the low carb lobby and the vegetable lobby both got right from the start: Sugars and starches as a mainstay of our diet are killing many people. Insulin resistance is a precursor to type 2 diabetes and is associated with and exacerbated by a high glycemic diet as well as by obesity. Starches are high glycemic.

The low carb lobby recognizes the role of high glycemic foods in obesity and chronic illness but they generallize it too far to all carbohydrates as an overly restrictive and overly simplified strategy.

The vegetable lobby is too concerned with the role of animal fat in nutrition and focuses on that rather than the more important distinction of higher glycemic vs. lower glycemic carbohydrates and a more balanced diet.

Saturated fat doesn't itself cause heart disease or obesity. Combined with a high glycemic diet, saturated fat exacerbates the problems caused by constant massive triggering of the insulin response because of a combination of factors:

(1) fats plus sugars tend to increase appetite dramatically,

(2) fats have a high energy density compared to their nutrition,

(3) saturated fats in particular have no protective effect for heart disease compared to omega-3 from polyunsaturated fats.

People tend to lower their risk of heart disease when they switch from saturated to unsaturated fats. This is one of the strongest arguments for eliminating saturated fat from our diet. However it turns out that this benefit is probably not because saturated fats cause heart disease. It is more likely because unsaturated fats have a protective effect compared to saturated fats.

Lowering glycemic load allows us to use nutrients more effectively, to metabolize all fats more effectively, and tends to reduce the risk of heart disease and obesity far more than reducing saturated fats.

So what works?

What dietary strategy best lowers our risk of chronic illnesses and obesity? Do they all fail equally? Do different people respond differently to different regimens?

It turns out that individuality is a real factor, both biochemical and psychological, and learning to make the principles work in your own life and for your own biology is critical. Still, there are also some general principles that we can rely on as a very good start.

The low carb strategy often works for as long as people can manage to maintain it and is healthier than the typical diet but it is not optimal for health and most people find it hard to sustain and eventually have health problems or fail to sustain it. It is not balanced nutritionally, it is too severe in limiting valuable and healthy vegetable sources of nutrition.

A vegetarian strategy often works at least for a while and is also healthier than the typical diet but it is also difficult for most people to maintain and as a general strategy it is too severe in limiting valuable and healthy animal sources of protein and what for many people are satisfying sources of texture and flavor in animal fats.

Taking what they both get right and eliminating what each gets wrong, we end up with:

1. Avoid high glycemic carbohydrates as far as possible or only under very specific conditions.

As a mainstay of our diet are a primary cause of both obesity and chronic illnesses via their effect on our response to insulin and our ability to absorb and metabolize nutrients. In other words, these commonly accepted processed products of agriculture cause a "clogging" of our metabolism over time that defeats our evolved ability to regulate our own metabolism. High glycemic carbohydrates are not essential for health and we tend to become dependent on them in various ways so minimizing them is an important first step to better health. There are specific strategies you can use to minimize their negative effects if you want to use them for athletic reasons or because you can't bear to eliminate them from your life entirely, but you have to be wary of how often you do this and the timing of it.

2. Balance the remaining nutrients between proteins, low-glycemic carbohydrates, and fats.

Compared to high glycemic foods, these categories all contain many healthy and valuable sources of nutrition.

Why a balance? In addition to just having a variety of nutrients of different kinds as well as a variety of tastes and textures to make eating more satisfying, there are also some specific nutritional reasons.

A diet of too much fat and too little protein and carbohydrate fails because fat contains relatively little nutrition compared to its energy density and tends to crowd out our intake of fiber important to digestive health as well as various nutrients. A diet of too much fat also fails because we have to eat a lot of it to make us feel satisfied in lieu of protein, fiber and water because of its low nutritional density.

A diet of too much protein fails because it avoids fiber and avoids important sources of vitamins and minerals and because it requires us to limit our protein sources very severely. It is also unhealthy to take in extreme amounts of protein. You can live on a high protein diet for a while if it isn't too high, but it isn't optimal. Temporary protein-sparing fasts are effective and popular among some athletes.

A diet of too much low-glycemic carbohydrates (taken to an extreme this would basically be a vegetarian diet that not only minimizes starches and sugars, but also seeds, nuts, and soy) is not really something anyone seriously recommends or practices as far as I know, but if they did it would fail because it would not have adequate protein sources to sustain health and would be relatively unsatisfying. Even strict vegans eat vegetable protein and fat sources, they just avoid animal sources. A diet with a huge amount of low-glycemic carbohydrates is perfectly healthy and sustainable so long as it also includes a reasonable amount of plant fat and protein sources.

The lesson here is just to mostly eat natural foods while avoiding high glycemic carbohydrates rather than striving for extremes of individual components. Avoid high glycemic foods and otherwise eat to satisfy your hunger. The specifics of satisfying our hunger are important however, balance is important in order to get a good combination of fiber, protein, water, nutrition, taste, texture, and other factors to satisfy us.

3. Take advantage of the "Paleo" principle but don't be limited entirely by it

I think the principle behind "Paleo" diets is basically correct, that our metabolism seems to be tuned by evolution to process natural animal and plant sources of nutriton that we could hunt or gather, and has not adapted yet to our dietary preponderance of processed agricultural products. This is another way of saying that high glycemic carbohydrates (the main category of highly processed and cultivated foods in our diet: the wheat, corn, potato, and rice products) are a very bad thing to emphasize all of the time.

In general the principles behind paleo eating agree with those proposed here, however they also focus on a rationale that can be misleading, which is why I consider it a fad even though it gets things mostly right. Trying to guess what our ancestors might have eaten and in what amounts is not nearly as useful a way to figure out what is healthy as just applying general principles and nutritional research results. By all means it makes sense to look to Paleo recipes and products as candidates for making it easier to maintain good nutrition. Also it is convenient and useful to imagine whether something could be hunted or gathered to know whether it is a nutritional source likely to be compatible with our metabolism.

Just don't limit yourself to the principle that we can only eat what our ancestors ate or elaborate arguments about the Pleistocene lifestyle. You have more options which you can intelligently apply to use modern foods and still be healthy.

4. Don't expect restricting calories to help you in the long run if you are eating poorly.

If you stop eating competely, you eventually die because your body eats its own tissue to try to meet its energy requirements. So when we talk about calorie restriction we aren't talking about not eating. We are talking about changing the timing of when we eat and eating less in a given period relative to what we would normally eat. We might eat less in a given period than we otherwise would, or we might eat nothing for a specific period of time. There are many strategies for calorie restriction. Some of them have a place in athletic performance and some of them can also have a place in a health regimen, but we have to be careful about how we go about it and how much we rely on it.

Sometimes the most reasonable approach is not the best. Portion control and light or moderate exercise seem perfectly reasonable and have been long recommended as a treatment or prevention for obesity. But for the vast majority of people they don't work for this purpose. Our metabolism and appetite conspire to maintain a stable weight against our efforts to make small reasonable changes in how much we eat and how much we move. We have to more directly influence our appetite and metabolism to deal with obesity. Simply eating less of the same things we are eating does not neccessarily help because it does not address the metabolic causes of our problems.

Fasting, as opposed to portion control, is a more potentially valuable and effective health strategy. This is because it can help you learn how to better control cravings, and can help you get your body fat lower than you could reasonably get with frequent eating and for longer periods. Some evidence suggests that fasting itself might trigger healthy changes in the body, although these are hard to distinguish from just the benefits of controlling body fat and eating more healthy overall. Fasting is much more difficult to do effectively, much less sustainable, and much less effective and healthy when combined with a high glycemic diet.

Your best bet is probably to eliminate high glycemic carbohydrates and get the hang of eating well first, then try fasting as an additional strategy if you want to, to make it even more effective and sustainable.

5. Don't just load up on "low fat" foods. But do emphasize lean protein sources over fatty ones.

By the best evidence available now, it seems that reducing fat by itself plays virtually no role in controlling obesity or chronic illness. Nutritionally, fat should be considered "neutral" or "filler" compared to good nutritional sources like non-starchy vegetables and good protein sources like seafood, lean meats, and egg whites. The problem with a "low fat" strategy is that if you go out of your way to avoid fats, you will also tend to replace the missing energy with starches and sugars.

If you could eliminate fats without replacing them with high glycemic foods, this strategy would probably work a lot better. Lean protein sources are an important part of modern nutrition, not because fat is bad, but because protein is so valuable. Fatty protein sources are really fats, not proteins, so they should be considered filler in your diet, rather than assuming they are good sources of protein. You have to eat an unreasonable amount of fatty protein sources to get enough protein to be valuable for satiety and nutrition.

6. If you find yourself eating something high-glycemic, at least mitigate its effects with fiber and protein and avoid fat under those conditions.

The effect of food on our insulin levels is the primarily culprit in obesity and many chronic diseases. However this glycemic effect is not just a result of what individual foods we eat, it is result of their combined effect on the amount of glucose circulating in our blood. There is no way to simply counter-act the glycemic effect short of avoiding high glycemic foods entirely but you can reduce it by lowering the combined glycemic effect by increasing the amount of fiber and protein you eat along with high glycemic foods. If you are going to indulge in high glycemic food, you can reduce the damage it causes by avoid simultaneous eating of fats (which boost appetite strikingly when combined with starches and sugars) and eat lean protein and good fiber sources with the high glycemic foods instead.

Note: This article was inspired by Jonathan Bailor's highly recommended book, "The Smarter Science of Slim."

Todd I. Stark
Nov 20,2011

Book Review: The Smarter Science of Slim by Jonathan Bailor

My review of Jonathan Bailor's book, "The Smarter Science of Slim."

Highly recommended, he does a great job integrating a lot of research faithfully into an accessible picture and offers practical advice consistent with it.

I also mention some things I would have written a little differently, like expanding the discussion of exercise a little beyond just eccentric high resistance and popular but less well studied strategies based on nutrient timing, and perhaps incorporating some discussion of self-experimentation in that light.

My book review on Amazon.

http://www.amazon.com/review/R3PZVSW9HQ89D8/ref=cm_cr_pr_perm?ie=UTF8&ASIN=0983520801&nodeID=&tag=&linkCode=

Review of "Big Brain" by Lynch and Granger - an education in brain evolution and development

Big Brains: The Origins and Future of Human Intelligence
by Gary Lynch and Richard Granger
Palgrave Macmillan, 2009

There is a lot of very clearly and cleverly presented original material on brains and their evolution and development in this book. It is one of those books that constantly makes you think and has enough depth to read several times fruitfully. I highly recommend it.

See my full review on Amazon here.

Updated Book Review: David Shenk's "The Genius in All of Us"

Review of "The Genius in All of Us," by David Shenk, Doubleday, 2010.

An effective deconstruction of hereditary talent, and clues for a new model of exceptional ability

Link to the review on Amazon: http://www.amazon.com/review/R3DGLT1WYK6QRG/ref=cm_cr_rdp_perm

It is easy to like or dislike this book from a casual reading based on how you feel about the premise: that everyone has the potential for genius, and that heredity is not destiny in any sense. This sounds at first like a liberal political statement, but Shenk's treatment is far more nuanced than that characterization would imply.

In brief, Shenk's book is a very good deconstruction of hereditary talent, a competent but one-sided (or upon reflection I'll say very selectively focused) review of supporting research in several fields, and an interesting but abbreviated practical introduction to the interactionist (gene X environment) paradigm of development.

Just to be clear, this book is not about the psychometric definition of genius in terms of how far down the bell curve one is on Raven's Progressive Matrices or standardized tests of any sort. Nor is it about clever calculating tricks or precocious abilities, although it does do a very nice job putting those into a larger perspective. This book is more centrally about the expansive and inclusive sense of genius meaning people that accomplish something truly special and significant, and the potential that any given person may be able to get to that point. Somehow. And that's where the nuance is needed and appropriate.

Ok, I didn't like this book all that much when I first read it, and I at first gave it a mediocre 3 star rating on Amazon. I felt it did a great job deconstructing the concept of hereditary talent, but I strongly criticized it for leaving a gap where we need a better theory of where talent comes from and what it is, since obviously we don't all become true geniuses. Even among the folks who appear to have the seeds of genius in them from early on, most don't become genius adults in the broader sense.

In my original review I said this was a one-sided review of the evidence for the interactionist model. I do think it's a very selective review, but one-sided implies that he deliberately ignores contradictory evidence. He doesn't do that. He just doesn't talk about the evidence that led to the model Shenk says is obsolete, that genes are akin to blueprints. That is, the evidence that different variations of allele sometimes have strikingly specific effects in a seemingly "normal" range of environments. The case for the model of heredity that Shenk is deconstructing is not entirely ignored, but it is glossed over in order to make his case for the interactionist model. I think that is why hereditarians like Galton, Spearman, and Charles Murray get so apparently shorted in this book, Shenk focuses entirely on what they get wrong and glosses over the things they may get right.

I suspect that we do inherit "predispositions" in some form under a very wide range of conditions, even if the underlying mechanism is more complex than we previously assumed. Even if changes in environments do alter the expression of genes, something like inheritance of traits clearly does happen in a wide range of "normal" environments, and we can't just ignore that completely because of additional complexity and things that change at the extremes. That's why I say this is a very selective review. But no, it isn't really one-sided, the selectiveness is appropriate for a deconstruction, although it does mark this as a deconstruction rather than a scholarly review.

The more important problem is that the model of talent that arises from this book is not particularly easy to understand. The author is strongly against thinking of genes as predispositions, and rather offers the perspective that genes are akin to "settings." So it would be easy to conclude that the author is saying that we have the ability to make anyone a genius just by tweaking a few settings. He isn't. Or, if you read it as I did upon my first reading, you might hear the author saying that "anyone can be a genius, but talent is complicated process, we don't know what is happening at each step, and so we don't know how to help people get there, but we know it's possible." That's perhaps a little closer to the truth, but it didn't seem very helpful to me.

The reason I updated this review and why I'm now expressing more appreciation for David Shenk's accomplishment here is that while the "settings" model of genes doesn't quite convey the message, I did find upon close reading and careful reflection that the author captured a lot with his examples and case studies of individuals. The thing that is missing is some way of tying together how people manage to select and shape environments for themselves to accomplish great things, in spite of all the cultural, social, and physical constraints that tend to make environmental factors very hard to change for most of us. Shenk assiduously avoids attributing "predispositions" to genes, but then speculates that epigenetic factors may predispose us to things like musical ability. If non-genes can do this, why not genes? He just seems a little *too* intent on crushing hereditary talent in some places.

Geniuses don't just see things differently (although that is sometimes also going on), they don't just have unique abilities (although sometimes they do) geniuses are most distinct in that they manage to carve their own niche, exploiting their own uniqueness in a process where they are driven to mastery and are amazingly persistent, even where the goal seems way out of reach. This runs contrary to our popular wisdom that it makes sense to work toward small easily attained goals in most things. What we think of as really deep talent actually requires really deep faith in the long term process and the motivation to keep going. Shenk captures the significance of motivation, but I had to look very closely to see the patterns for it. It requires willingness to do things that others may find bizarre and to learn freely from what is available. The author illustrates this but seems to have a hard time really tying it all together, at least he did on my first reading. I've come to think of it in terms of niche construction, which to me really captures what exceptional people do that brings out and shapes their unique gene x environment combination in a targeted way. My reversal in the rating reflects my feeling that capturing this idea is more important than giving it a catchy name, which is really what the author is missing.

We don't know exactly how to take advantage of the dynamic nature of heredity and development, although the study of achievement and expertise reviewed by Shenk gives us many tantalizing clues to go on. And if knowing that the potential is there inspires the faith to keep going, then more and more of us will eventually learn to become better and better at using our minds, constructing our own niches from our own individuality, and the promise of "The Genius in All of Us" will eventually begin to be realized. There is a lot in this book that will repay careful reading and re-reading, as I discovered by doing exactly that.

Related Reading:

See also this classic manifesto of genetic interactionism: The Triple Helix: Gene, Organism, and Environment(Lewontin R (1998/2000) Triple Helix: Gene, Organism, Environment. Cambridge, MA, Harvard)

This superb earlier popular introduction to the emerging model Shenk offers: The Agile Gene: How Nature Turns on Nurture(Ridley, The Agile Gene)

This similar treatment of trait development in interactionist terms, but focused on personality: The Temperamental Thread: How Genes, Culture, Time and Luck make Us Who We Are(kagan, temperamental thread)

This alternative and original interactionist account of how personality develops: No Two Alike: Human Nature and Human Individuality (Judith rich harris no two alike)

This interesting challenge to some widely help assumptions about influence: Stranger in the Nest: Do Parents Really Shape Their Child's Personality, Intelligence, or Character?(Stranger in the Nest, D. Cohen)

This little known treasure by an old friend that offers its own unique challenges about human uniqueness and what it means: rebellion: physics to personal will (Brody, Rebellion)

This on the classic view from the perspective of behavior genetics: Genetics and Experience: The Interplay between Nature and Nurture (Individual Differences and Development)(Plomin, Genetics and Experience)

This on the fascinating broader biological implications of interactionism from a gene perspective, how the genes of organisms construct niches even beyond the organism itself: The Extended Organism: The Physiology of Animal-Built Structures(Turner, The Extended Organism)

And finally this wonderful broad account of biology and the role of heredity that appreciates the complexities of gene function in a demanding but uniquely engaging way: The Logic of Life(The logic of life, francois jacob)

Book Review: "The Imprinted Brain" - A fascinating genetic theory of mental illness

Book Review: "The Imprinted Brain: How Genes Set the Balance of the Mind between Autism and Psychosis" by Christopher Badcock

Review by Todd I. Stark

A bold new theory of mental illness that could revolutionize our understanding, if it is right.

[See my reviews on Amazon.]

This is a deeply fascinating theory. I gave it lots of stars because of the importance of its ideas, even though it is not a great book in literary or stylistic terms.

The relatively uncommon collaboration of a sociologist (Badcock) and a biologist (Crespi) produced a compellingly simple and symmetric theory of the biology of the human mind which remains remarkably explanatory and coherent around just a few central ideas:

1. The "selfish gene." William Hamilton's insight that genes can sometimes serve their own reproductive ends as much as or more than those of the organism they build.

2. The "imprinted gene." Some genes may be inherited by either parent but only be expressed when inherited from one parent vs. the other.

3. The clinical observation that autism and psychosis are expressed in opposite versions of the same kinds of symptoms.

4. The theory that autistic symptoms represent an extreme of thinking in mechanical terms, and psychosis an extreme of thinking in mentalistic terms, with the two kinds of illness forming a single spectrum of disorders from autistic at one end to schizophrenic at the other.

This is not one of those relatively dull or unlikely theories about how schizophrenics might really be geniuses, or how mental illness might somehow be adaptive. The speculations of the imprinted brain theory go well beyond that sort of thing, making it distinctively broad and potentially testable. Although the book has a few philosophical turns in it, the technical journal articles by Badcock and Crespi make it clear this is a scientific theory that will live or die on empirical data, not primarily a philosophical idea.

The theory itself is half about how paternal imprinted genes serve their own reproductive ends by increasing growth and testosterone and by laterallizing the brain and helping to produce thinking that is optimized for dealing with inanimate things in particular ways. The other half of the theory is about how maternal genes serve their own reproductive ends by cutting back on growth, reducing testosterone, and fostering the development of a kind of thinking optimized for interpreting human intentions.

The theory explains the symptoms of autism as an "extreme male brain" which deals well with things but poorly with people. The symptoms of paranoid schizophrenia are seen as "cancers of the mind" resulting from an "extreme female brain," the extremely fertile creation of human intentions and minds around us from little basis. The idea that the autistic end of the spectrum may be an exaggeration of what we think of as stereotypical male cognitive processes has been suggested by many others since the autism was first identified, but the possibility of the other end of the spectrum being a symmetric case of mentalistic overdrive is a little more original. It also seems to be less well supported by the genetic data so far. But the possibility that a beautifully symmetric theory like this might possibly be validated is the kind of thing theorists get very excited over.

The author put a lot into this relatively small book and made it very readable. The style however is a bit lacking and sometimes can be dull and sometimes abrasive in contrast to the fascination of the content itself. I got the feeling at various points that the author couldn't help throwing in his own editorial comments about pet peeves that might be addressed by aspects of the theory, and I think this sometimes hurt the tone of the book. With such a powerful theory it is very tempting to wield it excessively just to see what it can do.

Overall, though, this book provides a reasonable balance between technical presentation and narrative exposition. It isn't a journal article, although it is based on material that has filled a number of journal articles, and it is not a breezy introduction with award winning science writing. It is a general readership account of a technical theory that has both deep scientific and broader cultural implications ... if it turns out to be right.

The book gives a solid introduction to the patterns of symptoms in various mental illnesses and the historical interpretations that help align each of them with their theory. They introduce just enough genetics so that you can understand why they feel "imprinted genes" help explain the complex idiosyncratic inheritance pattern seen in autism and schizophrenia. They discuss the spectrum of symptoms from several different angles so that you can see just how broadly explanatory this theory could potentially be. The authors briefly discuss some cultural implications of their theory for religion, feminism, science, and so on, a deep area that they only touch on very superficially.

The end of the book raises the interesting possibility that certain exceptional kinds of geniuses may be savants at both ends of the spectrum, extreme male and female brains at the same time, capable of both the overdeveloped mechanical cognition of autistic savants and the overdeveloped intentional sensitivity that the authors hypotheize may represent "psychotic savants."

The book is scattered with supporting quotes from erudite psychotics and high functioning autistics describing in their own words how they think and experience the world.

Reading this book I got a feeling that the theory *could* very well be right and that it seemed to make sense of a lot of otherwise very diverse and sometimes puzzling findings in genetics and psychiatry. I think it's entirely accurate to say that this theory has the potential to revolutionize our understanding of mental illness, especially its genetics, and provide a coherent framework where previously we had only scattered loosely related diagnostic categories and quibbles over them.

If I were to deliberately seek out a fault here, other than the sometimes annoying cultural jabs at religion and feminism, it is that the imprinted brain theory seems to explain too much while taking too much for granted. Explaining all of the dimensions of mental illness through an all-encompassing dimension of cognitive abilities seems to explain too much about thinking and not enough about motivation. Mechanistic thinking is not just thinking about things, it is a fascination, an absorption in things, and likewise for mentalistic thinking about people. The book never really talks about how the different cognitive subsystems relate to the motivation to use them, which seems to be just as important, especially in the case of savants, who provide a significant area of data for the theory. This is a topic that I've seen addressed in Crespi's journal articles, but was not really touched on in the book very much.

As far as validation of the overall theory, I think it will depend a lot on whether both both ends of the spectrum of disorders are found to be the genetic result of a common disease pathway resulting from many different variations of rare alleles or a particular conjunction of common ones. If either end depends on rare alleles, its evolutionary significance is much less likely. The beautiful symmetry of this theory depends very much on both ends of the disorder spectrum having evolutionary significance.

See also Badcock's Edge article:
"http://www.edge.org/3rd_culture/badcock08/badcock08_index.html"

and the following books on some of the less well known speculative evolutionary genetic ideas underlying this theory:

Genes in Conflict: The Biology of Selfish Genetic Elements

Genomic Imprinting and Kinship (The Rutgers Series in Human Evolution, edited by Robert Trivers, Lee Cronk, Helen Fisher, and Lionel Tiger)

There is some good theoretical backgound to the evolution of reasoning and what we can learn about it from autism in:

Human Reasoning and Cognitive Science (Bradford Books)

The Story Behind the Landmarks in the History of Life

The Story Behind the Landmarks in the History of Life

A review of Sean Carroll's book "Remarkable Creatures: Epic Adventures in the Search for the Origin of Species" 2009, Houghton Mifflin.

This is one of those “stories behind the science” books that gives you a sense of the sort of explorations that lay behind the famous discoveries that shaped modern biology. The primary focus is on the paleontologists who made various critical fossil finds and whose scientific obsessions led the efforts to uncover the history of life. Other books have covered the stories behind the genetics and the development of evolutionary theory itself better, but this one is particularly strong on the stories of key fossil hunters and their unique fascination with deep history and what it tells us.

The thing that makes this book worthwhile is that it is not just a travelogue of fossil discoveries, it makes a good and often successful effort to tie the work of each of the paleontologists into its implications for the history of life as well as making each find an interesting discovery for the reader.

It’s a very different experience learning the principles of biology in a classroom and reading the story of biology from the eyes of the naturalists discovering it firsthand.

On the other hand, the author doesn’t always tie specific finds back to their specific implications for biology. There is story and there is explanation, and the two are hard to balance. Story sometimes gets the better of explanation in this book. Although he is often careful to give simple explanations of concepts when introducing them, in a book of this type the author can’t help implicitly assuming a fair amount of knowledge that some lay readers might not have. I’m not sure I’d recommend this book as a primer on evolutionary biology, but then it wasn’t intended to be anything of the sort and that’s part of its charm.

What better way to celebrate Darwin’s bicentennial this year than to learn about how his ideas helped inspire generations of scientist-detectives to learn about the fascinating history of living things on our planet. The story is intriguing throughout, but by the time Carroll gets to the story of discoveries close to our own species, it has become a story you just can’t put down and which is really just beginning to be told.