Friday, August 12, 2011

Comment on Guyenet vs. Taubes; or Why I Don't Give a Crap What the Kitavans Eat

This post started as a comment to Stephan Guyenet's excellent post on the carbohydrate hypothesis of obesity, got too long, and so I'm putting it here. Do read Stephan's post, and keep an open mind. It's got loads of interesting and cutting-edge science, and this sort of debate and information exchange is how science progresses. If you find yourself experiencing cognitive dissonance, remember that absolute belief is antithetical to science. We always must update our beliefs as new information emerges.

Short summary of Stephan's blog post: the hypothesis that carbohydrates in general are fattening is probably over-simplified and does not reflect the most recent scientific understanding of metabolic regulation. It also leads one into a variety of paradoxes, a la the "French Paradox" of the diet-heart hypothesis.

I think part of what we're seeing here is the rather poor taxonomy of nutrition. We discuss things in terms of macronutrients, but those macronutrients come with (or without) all kinds of other metabolically relevant substances. And even within a given macronutrient group there can be significant metabolic differences, e.g. for fatty acids of different chain lengths, or between glucose and fructose (though Dr. Feinman might have something to say about the latter).

I've posted here before on my favorite example of this, and it seems like a good time to revisit (working from memory and about 4 hours of sleep, so please correct me if necessary). The Aztecs had a corn-based diet. They did experience obesity, but despite documenting a wide variety of health issues in detail never described diabetes. The Egyptians ate a wheat-based diet, also experienced obesity (along with heart disease, cancer, and the whole host of other fun "diseases of civilization"), and did document diabetes. Two high-carb diets, both resulting in some level of obesity, but from what we can tell (thousands of years later), both having radically different metabolic endpoints.

Two take-home points here. First is that we likely need to consider a broader dietary context than that imposed by our artificial macronutrient classification scheme, i.e. wheat and corn both provide primarily carbohydrates as energy, but probably do not have the same metabolic effects, particularly when considering over the timescale of a human life. Second, obesity is a symptom. A given symptom may result from multiple underlying conditions. We need to focus the discussion on more specific pathologies than just "obesity".

In the US and many other Westernized countries, one can take a look around and do a "liver check". How many people do you see with a protruding pot belly as opposed to a general body-wide distribution of fat? Most people I see have the big belly, sometimes even being very lean elsewhere (particularly in the arms and legs); there are a few "Rubinesque" figures as well, but the pot bellies seem to be running away with the obesity stakes. The big belly is indicative of fatty liver. Considering how central the liver is in metabolic regulation, it should come as no surprise that an inflamed fatty liver could lead to a whole host of metabolic disturbances: obesity, abnormal lipid profile, elevated blood sugar, elevated insulin, etc. In other words, metabolic syndrome.

I would argue that the rapidly growing health problem is not simply obesity, but metabolic syndrome (remember obesity is only one symptom, and there are thin people with metabolic syndrome too). We want to understand both how we arrive at metabolic syndrome (so our children can avoid it), and also how to treat it for those who did not avoid it. It is clear "carbohydrates" across the board are not causal in the development of metabolic syndrome. Stephan provides several counter-examples; another is the Tarahumara, who like the old-school Pima subsist largely on corn, beans, and squash, but who have one of the lowest rates of Type 2 diabetes in the world.

But the cure is not necessarily the reverse of the cause when it comes to disease. Metabolic syndrome brings a whole host of issues, not the least of which is broken carbohydrate metabolism. So while carbs in general may not lead to metabolic syndrome, once you've arrived dumping carbohydrates on your broken carbohydrate metabolism is tantamount to doing jumping jacks on two broken legs. I believe the science (along with a massive stack of anecdotal evidence) is pretty clear here, in that the most successful treatment for metabolic syndrome is carbohydrate restriction.

So while yes, Virginia, the Kitavans eat a very high-carbohydrate diet and exhibit general metabolic health, for my personal dietary choices I don't really give a crap. The Kitavans have healthy carbohydrate metabolisms, but I don't (prior to going low carb I had a trophy beer gut, which in retrospect was my liver telling me "You're killing me slowly"). If you look down toward your feet and can see only your protruding liver, you might consider trading in the bagels for bacon (better yet, get yourself a blood glucose meter and check your post-bagel blood sugar - it might frighten you). It is important to remember that carbohydrate restriction is successful as a treatment for a disease, but it doesn't necessarily follow that all carbs are bad for everybody. We have several examples of cultures who thrive on diets of lean protein and whole food sources of carbohydrate, like starchy tubers and fruit. We also have examples of cultures thriving largely on protein and fat. Humans appear to have a remarkable ability to survive as omnivores eating whole foods, which in no small part explains why we are one of the most widely spread species on the planet. So if you have a healthy metabolism, you probably can choose from a wide variety of whole foods (and by "whole food" I mean something you could plausibly obtain from Nature without the aid of much more technology than fire and a sharp stick). Once your metabolism is broken, you will likely need to make some choices to avoid those things which, due to your disease state, have become effectively toxic. In other words, make your nutritional choices based on actual knowledge of metabolism and your own state of health rather than picking a buzz-phrase and applying it blindly.

And for God's sake, stop eating wheat ;-)

Saturday, January 29, 2011

On Taubes and Toilets

One of our toilets has been acting balky lately. Last night I went to flush it and nothing happened. I started pondering on the possible causes of this, and had a brief vision of a bunch of Ph.D's standing around, stroking their chins and sagely examining the toilet through glasses perched on the ends of their noses. After a few knowing glances at each other, they pronounced: "From the First Law of Thermodynamics, we know the problem with your toilet is that, at some point in the past, less water came in than left!"

Maybe I should have skipped that last martini at dinner last night.

Anyway, my imaginary colleagues were only acting as scientists often do, pronouncing "truth" without getting to the root cause of the issue. Or perhaps my subconscious has been imprinted from too many conversations like this with my children:

Me: "How did you get so dirty?"
Child: "I was playing in dirt."

Back to the toilet. My imaginary scientist friends, while technically correct, were (as scientists often are) totally unhelpful. If I were to fix my toilet, I would need to know how it works, particularly the possible failure modes. In other words, I need to get to the root cause of why it didn't flush. Once I know what's actually broken, I can fix it. Invoking the First Law of Thermodynamics might make one sound smart, but it doesn't get my toilet flushing again. And believe me, in this case it was a vital importance to identify and repair the root cause, posthaste.

The toilet is actually an example of a self-regulating system, by which I mean that when it works correctly, I don't have to pay attention to it. If you're not familiar with the workings of the common toilet, check out this entry at Basically, there's some clever gadgets in there that make sure things go smoothly. When you push the handle down, it pulls up the flapper, basically a rubber stopper with a hole in the bottom. There's air inside the stopper, which causes it to float open as long as the water level is above the stopper. Once the water is gone, the stopper closes. That's the output side. The input side is controlled by a float-activated valve. When the water level falls, so does the float, which opens the valve and lets water into the tank. As the tank fills, the float rises until it hits the switch and shuts the valve, turning off the water. This whole setup is basically tuned to ensure that you have enough water leaving the tank at the proper rate to get a good flush, while not having too much water enter the tank and thus flooding your bathroom. The toilet has an additional fail-safe to avoid the latter fate, in the form of an overflow pipe. If your float switch doesn't work, then the water goes down the overflow pipe instead of all over your floor.

My particular problem was too little water, not too much. Since I have confidence in the First Law of Thermodynamics (at least in approximately flat regions of spacetime, like my bathroom), I know that something caused the tank to not fill. The water didn't fill the tank at some point then magically vanish. One possibility was that my water main had broken. Checked the sink faucet, plenty of water there. Rather than stand around and be mystified by the inner workings of my toilet, I opened it up and took a look inside. No water alright, and it looked like the float was stuck. A quick poke and the toilet started filling. The moral of the story is that the laws of physics don't tell you how things work, but rather the constraints under which they work (e.g. the amount of water leaving the toilet in a flush is the same as the amount that entered when it filled). To solve my problem I needed to understand the mechanism by which the toilet regulated water flow and level, and how that regulation could go wrong. In other words, if you know what causes the toilet to work correctly, then you can infer what might cause it work incorrectly, and take appropriate action.

If you've read Gary Taubes most recent work, Why We Get Fat, you probably have realized by now that my toilet story is a bit of a setup. Why We Get Fat (WWGF) is generally described as "Good Calories, Bad Calories" lite, but it is a bit more than that. Taubes has focused on obesity in particular, and honed his arguments and presentation, and brought in some more recent research as well. It's an excellent and fast-paced read, and I highly recommend it.

The key hypothesis of WWGF in terms of obesity is the same as GCBC: that obesity is the result of a failure in the regulation of metabolism, specifically carbohydrate metabolism. A broad set of critics attack both GCBC and WWGF on various detailed points, while missing the big picture. For instance, there's much ado about the specifics of Taubes' hypothesis on how this failure in carbohydrate metabolism arises. Taubes posits that overconsumption of carbohydrates basically leads to insulin resistance (though notes that the situation may not be so simple), while others point to various evidence that it may be specific carbohydrates (fructose), or vegetable oil, lack of physical activity, etc. These make for nice academic discussions, but if you're one of the millions of people with a broken metabolism, none of this is very helpful. Much as was the case with me and my toilet, if you're going to fix your metabolic machine, you need to have some idea of how it works and what might be go wrong. WWGF is a great place to start educating yourself, provided you don't fall in the trap of running around screaming "I can't see the forest because I've got blood in my eyes from running into all of these damned trees!"

The publication of WWGF has also revived the strident preaching from the members of the Holy Church of the First Law of Thermodynamics. Now, I'll give you a pass if you read GCBC and perhaps came away thinking that Taubes implied that low carbohydrate diets somehow got around energy conservation. GCBC was a dense book, and Taubes (who was a degree in physics) no doubt thought that the First Law was just generally held to be true and that nobody would question his belief in it, and so didn't focus on it much. Taubes clearly learned the hard way that you can't take these things for granted. WWGF has two chapters on this topic, and makes it very clear that 1) Yes, Virginia, the First Law of Thermodynamics is alive and kicking, but 2) that the First Law adds no information as to the cause of obesity, or what you might do to fix it. If you read WWGF and still think Taubes is claiming that thermodynamics doesn't apply to biological organisms, then you either didn't really read the book, weren't paying any attention, or have the logical facilities of a monkey on crack.

The real lesson of WWGF is the same as my toilet story: just knowing the constraints on the workings of your body (e.g. conservation of energy) is not the same as knowing how the pieces actually fit together, the cause-effect relationships that make the whole machine go. You can't fix something without having some idea of how it works, whether it is a toilet or the human body. Like my toilet, your metabolism (and that of all living organisms) is self-regulating. Humans seem to be control-freaks in general, and we think that every aspect of life needs constant attention, much like driving a car (I wish people paid as much attention to driving as they do to other less consequential things, like whether or not their children poop enough times a day). But when my toilet works right, I don't have to sit in the bathroom and monitor it, waiting to shut off the water if there's an overflow, or fiddling with the float valve switch. It just does it's thing. Metabolism is the same way. Energy regulation is the key aspect of life, from bacteria to humans, and most life doesn't have the capacity to fret about how many calories it ate or how much it exercised. If your metabolism is operating correctly, by definition it is impossible to eat too much. When you have too much energy stored, the body has ways of eliciting biochemistry and behavior (which is just complicated biochemistry) to bring things back into balance: appetite is decreased, thermogenesis is increased, you have the urge to move around, etc.

If you're obese, you don't have a character or mental defect any more than my balky toilet does. You have a physical problem in metabolic regulation. Invoking the First Law of Thermodynamics and berating obese people as having a behavioral issue does not address the root cause of obesity, any more than a similar approach would have worked in fixing my toilet (I'm having visions of registered dieticians bitching out my commode for lack of self-control). WWGF is a great place to start "opening the box" and empowering yourself to start giving the "experts" the finger, stop feeling like a failure because your experience doesn't agree with their beliefs, and get down to actually solving the problem.

Tuesday, November 16, 2010

Have We Reached the Tipping Point?

A very quick post here. Take a look at this article:

If the American Dietetic Association is flipping on low-fat diets, I'd say that signals the beginning of the end (hat tip to the Hold the Toast blog). Still waiting for Dean Ornish to jump out tell us we've been punk'd.

Also check out the Fat Head take on the Twinkie diet. Nice analysis of the food logs.

Wednesday, November 10, 2010

If you are what you eat, what does that say about "The Twinkie Diet" professor?

I've had a few questions on the "Twinkie Diet" that's been buzzing about the Internet, so here's a few thoughts...

The gist of the Twinkie business is that professor of human nutrition Mark Haub lost 27 pounds over 10 weeks by eating largely "junk food", like Twinkies. The "secret" was that he cut calories from 2600/day to 1800/day. Haub's point was to show "in weight loss, pure calorie counting is what matters most -- not the nutritional value of the food". This gets the "well DUH!" award for the month. Suppose you ate nothing at all. You'd be getting zero nutritional value. Do you think you might lose weight? Hmmmm, could be, doc.

The deeper issue here is apparent ignorance of people like professors of human nutrition about the basics of metabolic regulation. To first order, if you keep the macronutrient ratios about the same in your diet and reduce calories, you will also reduce the amount of insulin your body secretes in response to that food. As oft noted on this blog, insulin is a major metabolic hormone, governing a wide variety of processes having to do with the utilization and storage of energy, not the least of which is driving fat storage. More insulin means more fat storage. Less insulin means less fat storage. Drop insulin enough and on average more fat leaves the fat cells than is stored. The root cause of fat loss under calorie restriction is NOT simply restricting calories, but the result that calorie restriction has on your hormones, particularly insulin. For anecdotal evidence of this, you could ask a Type II diabetic who has to take insulin injections how hard it is to lose fat even by starving. More controlled experiments have been performed in animals. For instance, you can take an obese rat, keep it's insulin levels artificially high, and starve it. Said rat will literally starve to death while obese, consuming it's internal organs for energy, because the high insulin level effectively keeps fat locked up in fat cells.

So yes, of course, you can eat a calorie restricted diet of Twinkies and lose fat. But failing to understand how all of the metabolic dots are connected leads to several common backwards assertions made in the article, e.g. "Being overweight is the central problem that leads to complications like high blood pressure, diabetes and high cholesterol". Sure about that doc? Or do obesity, high blood pressure, diabetes, and high (LDL) cholesterol have a common cause, like say excess insulin? After all, there are skinny people with high blood pressure, diabetes, and high cholesterol. There are obese people who otherwise tape out as very healthy. So obesity is clearly not a cause, at least not the root cause. Insulin modulates a large number of genes, and so the precise set of symptoms a person experiences from hyperinsulinemia is going to be a function of their specific genetic makeup. A key test of a scientific hypothesis is its predictive power. The hypothesis that obesity causes Type II diabetes misses by tens of percent. But 100% of Type II diabetics are hyperinsulinemic, whether or not they are obese. Where would you put your money?

The key take-away here is that there is a large body of "health professionals" who essentially view the human body as a black box, and as such tend to come up with hand-waving and over-simplified "rules" linking various externally observable effects, like "calories in, calories out" (strictly true, but pointless because it makes no connection between cause and effect). As such, the recommendations of these people rarely rise above the level of old-wives' tales, in terms of the strength of evidence supporting them. When we "open the box", and begin to understand how the inputs and outputs are connected, and further how the body maintains control over metabolism and behavior in an attempt to maintain "health", things become much clearer. If your health expert has this knowledge, you are very lucky. Most are ignorant, and likely will remain so, as once a person deems themselves an "expert", they no longer feel the need to learn anything new (particularly if it contradicts their "expertness"). So it is going to be up to you to gain some measure of knowledge, so that you can make informed decisions for yourself.

If you are a person with any degree of scientific interest and background, then I hope you will have read "Good Calories, Bad Calories" (or a similar book) by now. If not, then shame on you for purposefully maintaining your ignorance. While no book (even a scientific textbook) has the whole story, GCBC does a fantastic job of delving into the very well-established metabolic science linking insulin and various health issues. As oft noted within, most of this stuff is not considered controversial at all. The processes by which insulin regulates fat storage have been established for decades. The gap is simply one of knowledge, where "professors of human nutrition", medical doctors, and the like either don't learn this stuff, or fail to connect the dots: what you eat affects your hormones, which affect biological processes like fat storage, which affect other hormones, which can ultimately affect what you eat. Behavior, after all, is just another manifestation of biology. So it's going to be up to you to educate yourself to some extent. If you're more of a right-brain person or otherwise find GCBC a daunting read, Gary Taubes' forthcoming book "Why We Get Fat" might be more up your alley.

But if you choose to remain ignorant, and blindly follow "expert advice", you deserve exactly what you get.

Monday, September 27, 2010

Stupid = Fat + Sick?

Just a quickie to point you to a great "tell it like it is" article at the Huffington post. Link below:

The short version: before taking "expert" advice, check their shoes . . . and their motivations. I'll repeat it again: the only person who truly has your best interests at heart is YOU. Everyone else has some other axe to grind. Once in awhile you might luck out and find an "expert" whose goals are aligned with yours, but don't hold your breath.

Saturday, September 4, 2010

Of Mice and Men, Meat and Wheat

Last week, I saw a very interesting show on the Science Channel (or one of the Discovery family), called "How Food Made Us Human". I don't see any more showings coming up, but recommend you keep an eye out, definitely worth watching. Much of the material will be review for those who follow recent ideas on metabolism and evolution, but it was well done: easy to follow, concise, with some nice hands-on demonstrations of the concepts. One I like in particular was the "chewing machine". Some scientists rigged up a gizmo the simulate chewing, and then put in "teeth" taken from casts of Australopithecus and (I think) Homo habilis fossil jaws. Australopithecus has flat teeth, hypothesized to be better for grinding tough fibrous vegetation, while Homo habilis' teeth are smaller with more ridges, better for tearing. And this is exactly what was demonstrated: the Australopithecus jaws made short work of a carrot in a single bite, but barely put a dent in a piece of raw meat. Homo habilis nearly cut the meat in half with a single bite.

In another fun experiment, several human subjects were "locked up" at a zoo, and fed something like the diet of our closest primate relatives (chimps and gorillas), consisting of raw fruits and vegetables. It was mostly vegetables, if I remember correctly, lots of clips of people gnawing on carrots, raw broccoli, and the like. Long story short, everybody hated it. They spent about half the day doing nothing but chewing, and were starving nonetheless. I believe the average weight loss quoted was something like 10 pounds in two weeks (I meant to watch the show again and take notes, but this is the first "free" time I've gotten, and it's only because I'm at the park with the kids). Subjects apparently spoke of the desire for meat quite a bit (when they weren't bitching about all of the chewing and frequent bathroom visits). It's a fun experiment you can try at home yourself!

One part of the show which rather surprised me: one of the scientists visited a remote tribe in Africa who were still living a fairly primal hunter-gatherer existence. What struck me was that these people looked like crap, nothing like the sort of pictures taken by Weston A. Price, or the fossilized H. habilis jaws shown in the chewing experiment. Their faces showed signs of nutritional stress, with small jaws and crowded teeth. One hint here may be the effort they went through to get meat. In the show, they had a porcupine cornered in its burrow (BTW, this thing was huge, the size of a really big dog). The tribesmen spent the better part of the day digging 6-foot deep holes, until they forced the porcupine into the Hobson's choice of which hole to get speared in. It was a tremendous amount of effort to get some meat, and one of the hunters basically said "porcupine sucks, but at least it's meat". They also discussed how socially important it was for hunters to bring back meat, that it brought them status in the tribe, etc. Clearly, meat is at the top of the menu for these people. Yet that they would go to such lengths to obtain it (particularly when they find porcupine distasteful) makes me wonder if hunting isn't so good in this region anymore. Perhaps game has become scarce, hence the appearance of nutritional stress? Yet they're hanging in there, if nothing else a testament to the tremendous adaptability of humanity, made possible by our big brains (and what do you suppose made those big brains possible?)

Anyway, "How Food Made Us Human" has spawned a couple of trains of thought, which I want to share with you here. The first has to do with a mouse experiment demonstrated on the show; the second with the correlations between diet changes and physiological changes over the course of evolution.

The mouse experiment was very interesting, intended to show the effect of cooking on caloric bioavailability. Take some mice, feed them raw sweet potatoes, and measure the change in body mass as well as activity (based on distance run on the exercise wheel). Now cook the sweet potato and do the same thing. If you're still stuck in the calories-in calories-out (CICO) paradigm, the results should spawn massive cognitive dissonance. The mice who ate the cooked food showed the following differences when compared to those eating the raw food:
  • They exercised significantly more, AND
  • They were heavier.
That's worth thinking about for a moment, particularly if you think that obesity is caused by conscious choices favoring gluttony and sloth. When the mice ate cooked sweet potato, they exercised MORE than those eating the raw version. Does cooking food spur psychological changes that cause you to become less lazy? But despite exercising more, the mice still got heavier. Put that in your pipe and smoke it, CICOs.

Of course this all makes perfect sense when considered from the standpoint of evolution and metabolic regulation. Cooking makes calories more available. Though they didn't explicitly say so in the show, one presumes that the quantity of potato was held constant between the two groups (since not doing so would void the entire point of the experiment). So the only difference (presumably) was raw vs. cooked. Mice didn't evolve eating cooked food. The higher caloric availability likely "fooled" their digestive systems into taking up calories too rapidly, faster than required to support normal metabolic operations. Rate of digestion is regulated by hormonal and nervous feedback mechanisms: when the brain and other internal sensory systems think there's enough energy around, gastrointestinal motility decreases, slowing the rate at which food leaves the stomach to be digested and absorbed in the small intestine; and of course when an energy deficit is detected, food moves more rapidly out of the stomach. When the stomach is empty AND your body senses an energy deficit, you get hungry, and are driven to find more food.

That's how it supposed to work. Like all feedback control systems, if you push outside the "designed" range of stability, it starts failing. I expect this to be particularly the case with biological systems. Biological responses tend to follow "S-curve" shapes. There's nothing deep about this. It simply reflects the fact that biological responses are limited by available resources. At some point you run out of the capacity to make more hormones, neurotransmitters, receptors, etc. Insulin response is a great example. As a function of blood glucose, the secretion of insulin follows a shape much like that seen on the Wikipedia page. At some point you either saturate the ability to detect glucose, or saturate the ability of the pancreas to crank out insulin, or both. The point is that it is possible to exceed your body's ability to effectively control blood sugar levels via the action of insulin, simply by changing the effective "sugar density" of the food you consume.

Back to our mice: when faced with an excess of calories, how can the mouse's body respond? It can either store energy, or burn it off (or both). We know some of it got stored, as the mice got heavier. The show gave one example of "burning it off", in the spontaneous increase in activity. I don't know if they measured it, but I'd wager that the mice also gave off more heat, which I think is a more effective way dumping energy. Muscles are remarkably efficient, and it is surprising how much mechanical work you can get out of a kilocalorie, when compared to the equivalent thermal energy (1 kilocalorie will raise 1 kilogram of water only 1 degree C in temperature, but raise a 1 kg mass over 400 meters against gravity). So the outcome of the mouse experiment is wildly inconsistent with the CICO paradigm, but precisely what one might predict from evolution and metabolic regulation. It would be very interesting to see what would happen if the mice were allowed to continue eating cooked sweet potatoes for a longer time period. I wonder if they would develop mouse metabolic syndrome?

The second line of thought follows the main line of reasoning from the show, which is thus: by incorporating more nutrient dense foods into their diets, our hominid ancestors set in path a major evolutionary shift, where gut size was exchanged for brain size. The argument is elegant: if you eat food with greater bioavailable caloric density, you can spend less energy on digestion. That opens up an evolutionary pathway to increase brain size and energy expenditure at the expense of the gut, because you can extract the same energy from food with a smaller and less-demanding digestive system. And indeed, the fossil record seems to indicate that the major jumps in hominid brain sizes came at two critical nutritional junctures. The first was around the time we started eating meat. The second was when we started cooking food, and cooking is hypothesized to have led to modern humans.

It's interesting to consider the evolutionary advantage brought about by our big brains. What advantage did they bring our hominid ancestors? The scientist visiting the African hunter-gatherers went on a bit about how hunting is a fairly complex behavior, particularly as practiced by humans. But there's a lot more to it than that. The brain remembers - it stores information. And an "advanced" brain not only remembers information, but can extrapolate it to the future, making choices now that create advantages later. For instance, it's good to know that when the rains come, wildebeest are going to show up and a certain place, and that there's an effective method for cutting one out of the herd, how to make the tools you need to kill and butcher it, which parts are good to eat, etc. In the context of hunting and gathering, there's a positive feedback loop between the increase in nutrient density and encephalization, each reinforcing the other.

Of course, there's been another major shift in nutrient density since the advent of cooking: agriculture. The advent of agriculture is an interesting case. At first blush it doesn't seem so hot. The main thrust of human agriculture has been domestication of annual grasses for their seeds, i.e. grains. Across the world, in geographically separate locations, populations growing different crops (wheat, corn, rice) uniformly appear to show significant increases in the chronic "diseases of civilization". But evolution doesn't care if your teeth fall out or you drop dead from cancer at age 40. All evolution cares about is reproductive fitness, and agricultural humans had an undeniable reproductive advantage over hunter-gatherers; otherwise we wouldn't be having this conversation.

We had a hint from the mouse experiment above that an increase in dietary effective energy density could lead to "metabolic overload", exceeding the body's ability to balance and regulate the intake and expenditure of energy. And indeed, the evidence continues to mount that a good chunk of our modern epidemic of chronic diseases may be attributable to such metabolic malfunction. It makes me wonder what happened to our Australopithecus ancestors when they started eating meat: did they suffer metabolic disease as well? It's an academic question, of course, as chronic disease or no, meat-eating proved to increase reproductive success. We might ask a similar question about what occurred as cooking gained popularity. These are hard questions to answer from the fossil record. Agriculture happened much more recently, and further is amenable to archaeology (agriculturists tend to gather in large numbers in one spot, as opposed to wandering all over the place looking for food).

But here's a thought: we noted above that big brains are useful for remembering lots of stuff. This is important when living as a hunter-gatherer, because the dynamics of nature are complex. Maximizing reproductive potential in this context means being able to remember and extrapolate the myriad (and often subtle) cause-and-effect relationships of the natural world, along with whatever technological innovations are required to take advantage of this knowledge. This information does not get passed on genetically, but rather through communication, i.e. parents teaching children. Knowledge is power, in a very tangible sense, when talking about hunter-gatherer survival. Greater knowledge implies greater ability to obtain nutrient-dense food, hence greater reproductive fitness; it also means that it takes longer to get that knowledge into the brains of your offspring. It is often argued that diseases of civilization have little effect on evolution, because they generally kill you after the reproductive years. But that assumes the only information being passed along is genetic. If memories are also required for the reproductive success of your offspring, it pays to live long enough to pass along that information. And if you follow this line of reasoning, it's clear there's a volume of information at which the parent will not be able to effectively communicate the body of knowledge while still performing hunting and gathering activities required for survival. Enter Grandma and Grandpa. If the information volume for reproductive effectiveness is sufficiently large, it pays to live long enough to pass along that information to your offspring, their offspring, and so forth. Correspondingly, adoption of new dietary practices must either preserve this longevity, OR require less information to be effective.

So where does agriculture fit in? Is the adoption of agriculture, which brings with it ever-increasing energy density in food, driving us toward the next phase of "big brain" evolution? Good question - but consider this: how much do you need to know to be an effective agriculturist? I would argue rather little, compared to hunting and gathering. A hunter-gatherer may have thousands of foods in their diet, and they have to know where and when to find them, how to prepare them, etc. Agriculturists have relatively narrow diets, and there's a relatively simple and fixed pattern to the whole business: plow the land, plant the seeds, keep out the weeds, harvest. Lather, rinse, repeat. So I think you can argue that agriculture has a much smaller information burden than hunting/gathering. The tremendous technological increases since the advent of agriculture are a testament to how relatively little brain-power is needed for obtaining food anymore, as we apparently had plenty of spare brain capacity to monkey around with things not directly related to getting fed.

Now it is well known that brain volume decreased dramatically with the advent of agriculture. So did adult lifespan. Yet the agriculturists clearly laid the smack-down on the hunter gatherers, evolutionarily speaking. So neither long-term health nor brain size is a reproductive advantage once you start growing your own food (or at least the foods that our ancestors chose to cultivate). There's no point in fueling a big brain if you've got nothing to put in it. And there's no point in keeping old people around if they are not able to contribute directly to the reproductive fitness of their offspring. If you can't work the fields, don't make babies, and we don't need your accumulated wisdom, then you're pretty much just eating food better used for making more genetic copies. So for an agriculturist, dropping dead at 35 may actually have been an advantage.

It makes me wonder what direction agriculture (and more recently, industrial food processing) is driving our "humanness". Does the ever-growing energy density and general availability of food imply we'll evolve even smaller guts and bigger brains? I'll put my money on "No". After all, look around you: it's not like the smartest people are the most successful reproductively. You can damn near be vegetative, contribute nothing to society at all, yet we will ensure you've got all the Big Macs and Twinkies you can stuff in your face to fuel the generation of lots of babies to do the same thing. In our current environment, evolution favors being chronically ill and stupid. It doesn't really matter how much we wring our hands about ethics, culture, and society: reproductive success always wins. So if humanity wishes to achieve its stated long-term goals of giving people long and healthy lives while living sustainably on Earth, we'd better figure out how to align those goals with Nature's overriding law of reproductive fitness.

Friday, July 23, 2010

Cognitive Dissonance: Not Just for the Layperson

I must admit, I had not carefully read Dr. Campbell's "last word" from the "discussion" of his reply to Denise Minger. His refusal to engage in discussion told me everything I needed to know. But in spelunking around for something else on that page, I came across this quote:

I had hoped to have had a civil discourse, but this is difficult when the questions come from uncivil people. I also don’t have time to answer superficial questions of others like ‘what is the detailed mechanism of protein induction of high cholesterol levels’ – that easily could become an entire but relatively useless dissertation when the “mechanism” most decidedly is a symphony of mechanisms, as I explained in our book. At this point, the far more important observation is the dramatic increase in serum cholesterol.

Hmmm, I wonder what Campbell's definition of "uncivil" is? Seems to have some conceptual overlap with the second sentence, i.e. those who ask "superficial" questions are being "uncivil". The question in question came from me, and I'm glad to see it had one of the desired effect. My preferred outcome would have been that Dr. Campbell actually answered the question. Then I would have learned something. It is unfortunate that he instead evaded the question as above, because then all we learn is that a) he doesn't have an answer, but b) thinks he does, and is thrown into painful cognitive dissonance when confronted by the truth of his ignorance. The nonsense about there being a "symphony of mechanisms" is, I believe, a subtle trick played on Dr. Campbell by his own mind. There are indeed many possible causes, and may be several interacting processes. But he confuses "I don't know which of the many possibilities contributes to the effect" with "here is what we know, a complex process". Classic mental band-aid for cognitive dissonance.

Anyway, I think my goal has been accomplished. I wanted to know if Dr. Campbell had any relevant information. If not, I wanted him to publicly torpedo his own credibility. Mission accomplished. Next time he wants to show up and bash a low-carb or paleo book an Amazon, you have ample material to demonstrate his irrationality.