Hunter-Gatherers and Health - Part 6

The Carbohydrate Insulin Model & Others

Last time we saw that Pontzer's explanation for rising rates of obesity and metabolic disease around the world was that we eat too much. The reason we do so is because of the high amount of artificially-engineered, ultraprocessed foods that are available in modern societies, coupled with the extreme variety in flavors, colors, textures, and so on, that we encounter.

An alternative explanation that has gained popularity in recent years among a growing number of scientists, doctors, and popular authors is the Carbohydrate Insulin Model of Obesity.

In this model, obesity is not conceived as primarily an energy balance disorder, although it does acknowledge the thermodynamic basis of energy and calories. However, it conceptualizes obesity primarily as a hormonal disorder in which the body's metabolic apparatus goes awry. The cause, in this model, is abnormally high levels of the hormone insulin, which is a byproduct of modern Western-style eating patterns centering around processed, carbohydrate-rich foods such as refined grains and sugar. As Gary Taubes puts it, just as lung cancer would be a rare disease if tobacco smoking were never introduced, obesity and type 2 diabetes would be rare conditions if these eating patterns hadn't become entrenched and widespread (GB: 108).

Persistently high levels of insulin disrupt the body's evolved hormonal systems which naturally regulate appetite and fat storage leading to excessive weight gain. This is the reason why we eat too much, rather than eating too much as the cause of the hormonal disregulation.

It is well-known that insulin causes increased adiposity (i.e. fatness). This is beyond any doubt. You can inject someone with insulin and they will become fatter, independently of the amount of food consumed or the amount of exercise they get. As Dr. Jason Fung says, "I can make you fat. I can make anyone fat." All he has to do is inject someone with insulin (as the picture above demonstrates). Since we know for sure that insulin causes weight gain and increased fat storage, might it be the culprit behind rising rates of obesity?

Here is how Dr. Pontzer describes the Carbohydrate Insulin Model:

[E]ating carbohydrate-rich foods, particularly those high in easily digested sugars, raises your blood glucose levels (blood sugar). In response, the pancreas produces the hormone insulin. Insulin [moves] glucose out of the blood and into cells to store as glycogen or to make ATP.

But there's a limit on how much glycogen our body can hold, and insulin stimulates the the conversion of excess glucose into fat and inhibits the pathways that metabolize and burn fatty acids. Consequently...carbohydrate-rich diets lead, paradoxically, to less fuel circulating in the bloodstream, as the glucose is converted to fat and stored away in our adipose tissue; the body responds as though it were starving, reducing energy expenditure and increasing hunger, promoting overconsumption...the accumulation of fat is the cause of overeating, not the other way around; focusing on calories misses interplay of carbs and insulin, and therefore misses the point.

While the focus tends to be on carbohydrates, all carbohydrates are not created equal. Some can raise blood sugar a great deal; others less so. This contradicts the common myth that "a calorie is a calorie is a calorie," since clearly different foods have different physiological effects when consumed even if the calorie content is the same. Also, the amount of calories we can absorb from foods differs depending on the type of food.

Carbohydrates are simply long chains of sugar molecules, as distinguished from fat (chains of fatty acids), protein (chains of amino acids), and DNA. But...not all carbohydrates...are treated equally by the body. The differentiating feature is how much a certain carbohydrate will raise blood sugar and, in effect, insulin. Meals that are higher in carbohydrate, and especially those that are higher in simple glucose, cause the pancreas to increase its insulin output in order to store the blood sugar in the cells. (GB: 106)

In the Carbohydrate Insulin Model, it is not simply the amount of carbohydrates consumed, but the subsequent rise in insulin which matters. The amount of insulin secretion caused by various foods is determined by its glycemic index. However, this does not take into account how much of a particular food consists of carbohydrates by weight or volume, and thus can be misleading. Therefore, the glycemic load index was developed to compensate for this:

The glycemic index uses identical 5-gram portions of carbohydrates. For example, you might take foods such as carrots, watermelon, apples, bread, potatoes, a candy bar and oatmeal, measure out a portion of each to contain 50 grams of carbohydrate, then measure the effect on blood glucose. Then you compare the foods against the reference standard—glucose—which is assigned a value of 100.

However, a standard serving of food may not contain 50 grams of carbohydrate. For example, watermelon has a very high glycemic index of 72, but contains only 5 percent carbohydrate by weight. Most of watermelon's weight is water. You would need to eat 1 kilogram (2.2 pounds!) of watermelon to get 50 grams of carbohydrate—far in excess of what a person would eat at one sitting. A corn tortilla, though, has a glycemic index of 52. The tortilla is 48 percent carbohydrate by weight, so you would only have to eat 104 grams of the tortilla (close to what a person would reasonably eat during a meal) to get 50 grams of carbohydrate.

The glycemic load index attempts to correct this distortion by adjusting for serving size. Watermelon turns out to have a very low glycemic load index of 5 while the corn tortilla still ranks high at 25. But whether you use the glycemic index or glycemic load, you'll find there is clear distinction between refined carbohydrates and unrefined traditional foods. Western refined foods have a very high glycemic index and glycemic load scores. Traditional whole foods have low glycemic load scores, despite containing similar amounts of carbohydrate—an essential distinguishing feature. Carbohydrates are not inherently fattening. Their toxicity lies in the way they are processed. (OC: 176-177, italics in original)

We can see from this that citing the carbohydrate consumption of hunter-gatherers in order to argue that carbohydrates are not inherently bad for us conceals as much as it reveals. The carbohydrate-rich foods consumed by hunter-gatherers are vastly different than the kinds of carbohydrate-rich processed foods we encounter in industrial societies. The devil is in the details. Our entire food system is designed to prod us to eat more refined carbohydrates, because that is what maximizes profits for the food industry (which is a recent development).

Refining significantly increases the glycemic index by purifying and concentrating the carbohydrate. Removal of fat, fiber and protein means that the carbohydrates can be digested and absorbed very quickly.

In the example of wheat, modern machine milling, which has almost completely replaced the traditional stone milling, pulverizes the wheat into the very fine white powder we know as flour. Cocaine users will know that very fine powers are absorbed into the bloodstream much faster than coarse grains—that's what allows for higher "highs," both for cocaine and for glucose. Refined wheat causes our glucose levels to spike. Insulin levels follow.

Second, refining encourages overconsumption. For example, making a glass of orange juice may require four or five oranges. It is very easy to drink a glass of juice, but eating five oranges is not so easy. By removing everything other than the carbohydrate, we tend to overconsume what is left. If we had to eat all the fiber and bulk associated with five oranges, we might think twice about it. The same applies to grains and vegetables.

The problem is one of balance. Our bodies have adapted to the balance of nutrients in natural food. By refining foods and only consuming a certain component, the balance is entirely destroyed. People have been eating unrefined carbohydrates for thousands of years without obesity and diabetes. What's changed, and recently too, is that we now predominantly eat refined grains as our carbohydrate of choice. (OC: 177-178)

Pontzer, however, is unconvinced, writing “It's an intriguing idea with a plausible mechanism for the etiology of obesity, fleshed out in many papers and books over the years by [Gary] Taubes and others, including David Ludwig. If only it were true.” (B: 211)

The main line of argument Pontzer uses to debunk the model are studies which compare the effects of low-carbohydrate diets versus other types of diets such as low-fat. What these studies invariably show is that there is no difference in weight loss between the various macronutrient ratios—the only thing that matters for weight loss is caloric intake: "Low carb-diets were tested in a large real-world sample, and they fared no better (and no worse) than the traditional low-fat approach." (B: 213). Even trials conducted by low-carb advocates like Gary Taubes, he notes, have failed to find any consistent benefits to low-carb diets over other competing protocols such as low-fat.

Pontzer also points out that even diets which allow terribly unhealthy foods—such as junk food—can lead to weight loss if calorie intake is strictly monitored. So-called monotrophic diets which only allow one particular type of food (such as potatoes) also work—regardless of what kind of food is consumed—because they eliminate variety thereby preventing us from overeating: "Regardless of diet, the people who adhered to them lost weight. All diets work if you stick to them." (B: 217) Intermittent fasting, which is trendy right now, only works because of caloric restriction, he tells us, and not because of any additional physiological benefits. The only thing that matters is the calories!

The other line of argument he uses is the fact that, as we saw last time, both sugar and carbohydrate consumption have actually declined, with no measurable effect on obesity rates. Sugar consumption (including HCFS) peaked around the year 2000, and yet obesity rates continued to climb even as people ate less sugar. (B: 213)

When we look at the dozens of studies that have measured metabolic rates on different diets, it's most likely that the ratio of carbs to fats has little or no effect on energy expenditure...There's no clear effect of sugar or other carbohydrates on body fat or metabolic disease beyond the usual dangers of overconsuming calories.

Sugar certainly isn't healthy (it holds zero vitamins, fiber, and other nutrients for a start), and sugary foods are easy to overconsume...but there's little evidence that calories from sugar (including high-fructose corn syrup) are any worse or better for your weight or metabolic health than calories from fat. (B: 215)

Pontzer does concede that low-carb diets do show some promise for people who are diabetic, especially for people with type 2 diabetes. But for the rest of us, he assures us, it's all just an illusion. We may think we're eating just as much as we did before when we go on a low-carb diet, but in reality, the truth is that we are eating less calories overall, and that's why the diet works—neither the amount of carbohydrate intake nor the insulin response matters whatsoever for weight loss:

"People on low-carb diets may feel like they're eating just as many calories as before, but...all of us are notoriously bad at estimating how many calories we eat each day. It's entirely possible to lose weight without counting calories, just like it's possible to drain your bank account without paying attention to your finances. But it isn't possible to lose weight without eating less than you burn." (B: 216)

The Rebuttal

However, this neglects several factors. I have to interject at this point that I find all these studies and claims and counter-claims utterly baffling, and I am way beyond my scope of expertise here, so take that for what it's worth. But hopefully I articulate the evidence somewhat correctly. I'll be referring to this blog—Confession of Supply-Side Liberal, which is actually written by an economist but has lots of resources about low-insulin diets and fasting. I'll also refer directly to The Obesity Code (OC) by Dr. Jason Fung, as well as Dr. David Perlmutter's book, Grain Brain (GB).

One problem with a lot of these studies is that “low-carb” diets are typically evaluated against diets which also lower insulin levels. These diets also eliminate "bad" foods, therefore it's not surprising that there is no clear difference between them. Focusing on macronutrient ratios ignores the critical role of insulin levels. It is the insulin level—and not the amount of carbohydrates per se—that is important in the model. A low-insulin diet is not the same thing as a low-carb diet.

For example, in the DIETFITS study (cited by Pontzer), both protocols effectively reduced insulin levels. Both diets replaced low-quality foods with higher-quality ones. Both diets reduced the amount of sugar consumed:

A low-insulin-index diet is not the same thing as a "lowcarb diet" either as the phrase "lowcarb diet" is used in common speech or as "low-carbohydrate-diet" is used in nutrition research. All of these involve avoiding sugar, refined grains and processed foods, which is a big deal. But beyond that, they are different.

It is unfortunate that the results of the DIETFITS study were reported as showing that a lowcarb diet and a lowfat diet were equally good, when in the nontechnical sense of what most people mean when they say "lowcarb diet" both diets were "lowcarb" because they both involved avoiding sugar, refined grains and processed foods...Note here that the researchers who did the DIETFITS study did not question the idea that sugar is bad, despite the dispute about just how bad sugar is...

Why a Low-Insulin-Index Diet Isn't Exactly a 'Lowcarb' Diet (CoaSSL)

Another issue is that, according to advocates of the Carbohydrate Insulin Model, the beneficial effects of low carbohydrate diets take a certain amount of time to manifest. Therefore, too short a study will not properly measure its benefits. Dr. David Ludwig—one of the main proponents of low-carb diets—argues that it takes at least three weeks minimum for the brain to switch to powering itself from fat instead of carbs. Therefore the length of time of the study, as well as the eating habits of subjects beforehand, are relevant and need to be taken into account.

David Ludwig: It Takes Time to Adapt to a Lowcarb, Highfat Diet (CoaSSL)

When it comes to dietary studies, the gold standard are those which take place in a metabolic ward where what the patients eat can be strictly monitored. Most studies, however, rely on subjects accurately keeping track of what they eat and sticking religiously to their diet plan which, as we’ve seen, is notoriously difficult to do in real life.

The problem is that confining people to a metabolic ward is prohibitively expensive (you’re effectively a prisoner). Therefore, these studies are rare and usually short-term. Most studies in which people follow certain prescribed diets—both in terms of caloric intake and macronutrient ratio—are less reliable since people tend to cheat or underreport calories. Therefore these studies tend to be longer-lasting, but are much less reliable because of compliance issues. There are also numerous confounding factors in larger and longer-term studies (what other behavioral habits are affecting subjects' health outcomes besides their diet?). These are things to keep in mind when reading about any dietary study in the media.

Ludwig notes that in one meta-analysis allegedly used to "debunk" the benefits of low-carb diets, the studies lasted an average of less than six days. In longer-length studies, he contends, low-carb diets have in fact shown an increase in energy output. Even though the increase is only a few hundred calories on average, he argues that this can make a big difference over time.

Also, Ludwig notes that people's insulin response varies a great deal from person to person. Some people are "high insulin secreters," while others are "low insulin secreters." Therefore, the effectiveness of a low-glycemic diet for weight loss will vary from person to person, and this needs to be taken into account as well.

Of these recent studies by Ludwig, Pontzer notes:

A recent study by David Ludwig and colleagues examined metabolic rates in men and women before and after weight loss. They reported that the subjects had somewhat elevated daily energy expenditures when eating a low-carb diet during the period after they lost weight. A reanalysis of their data by Kevin Hall challenges this conclusion, and it's likely that the effect, if it's there, is quite small.

Regardless of whether the low-carb diet led to somewhat elevated energy expenditures after weight loss, the results don't do much to resuscitate the carbohydrate-insulin model. For one thing, weight loss was achieved through straightforward calorie reduction, not through carbohydrate restriction. And second, there's no indication that the greater daily energy expenditures initially reported for the low-carb group made weight maintenance any easier. (B: 214-215)

Another common criticism is that the CIM engages in "magical thinking" regarding calories. CIM advocates are portrayed as denying that calorie intake has any bearing on weight loss whatsoever, as long as we restrict carbohydrates. Pontzer himself takes up this line of attack:

While [Gary] Taubes doesn't reject the laws of physics, he has argued extensively that calories aren't important in tackling obesity. In his view, the calories we eat have no meaningful effect on body fat and weight gain unless those calories are carbohydrates...In its purest form, the argument that calories don't make you fat makes as much sense as the argument that money doesn't make you rich. It's magical thinking...Energy balance is the only thing that alters our weight. That's the inescapable reality of physics. (B: 186-187; emphasis in original)

But this isn't my understanding at all. My understanding is that, by preferring lower glycemic foods, our hormonal signals can more accurately match appetite to energy expenditure. Consequently, our inner sense of how much to eat to maintain a healthy weight will be restored without having to painstakingly count calories, which is how people managed to maintain a healthy weight for pretty much all of human history until very recently. Consuming a diet heavy in refined carbohydrates, on the other hand, upsets our natural hormonal signals and causes us to get hungry sooner, making us want to eat more (the so-called "Chinese restaurant effect"). As I argued in the previous post, it's hard to believe everyone, everywhere, intentionally maintained a permanent negative energy balance throughout their entire lives without even trying:

People often say the way to lose weight is to "Eat less, move more." By itself that is not so stupid, but what is off track is to think that you "Eat less, move more" by trying to "Eat less, move more." Instead, just keep your insulin levels down, and your body will automatically make you want to eat less and move more without you trying at all—other than whatever effort it took to keep your insulin levels down. (Here I am taking a bit of poetic license in counting a rise in basal metabolism as "moving more.")

Some aspects of a low-insulin strategy for weight loss will look very similar to what you might try to do anyway under the naive take on calories in/calories out that surrounds us in our culture: for example, eat lots of greens, avoid anything with added sugar; avoid eating late at night. But many other aspects of a low-insulin strategy are quite different than the conventional wisdom.

What I think is the correct advice—and hope will become conventional wisdom in a better future—is to avoid all foods and beverages that cause the body to produce a lot of insulin and to lean towards foods and beverages that cause the body to produce relatively little insulin...

Forget Calorie Counting; It's the Insulin Index, Stupid (CoaSSL)

Finally, what most of these studies miss is the crucial role of insulin resistance. This is neglected even by the conventional Carbohydrate Insulin Model.

Insulin resistance is somewhat analogous to drug resistance. If someone does cocaine or heroin on a regular basis, after a while they notice that the drugs no longer have the same effect. They've developed a tolerance for it. They need to increase the amount of cocaine or heroin they do in order to get the same high. Eventually, they become accustomed to that as well, meaning they need to increase the amount of the drug still further (which can result in death if taken to extremes).

Insulin resistance is a similar phenomenon. The key is not just the amount of insulin secreted, but how often our cells are exposed to it. If our cells have become resistant to insulin’s (necessary) effects, the pancreas has to secrete higher amounts of it. This causes higher levels of insulin to circulate in our bloodstream than is natural or healthy. Higher amounts of insulin, in turn, promote still more insulin resistance. As insulin resistance develops, it forces the body to secrete yet more insulin in a self-reinforcing cycle which, if left unchecked, will eventually lead to obesity and type 2 diabetes for those who are susceptible. This is why obesity and type 2 diabetes are so closely intertwined.

Insulin...is one of the most important biological substances for cellular metabolism. Its job is to ferry glucose from the bloodstream into muscle, fat, and liver cells. Once there, it can be used as fuel.

Normal, healthy cells have a high sensitivity to insulin. But when cells are exposed to high levels of insulin as a result of persistent intake of glucose (much of which is caused by an overconsumption of hyper-processed foods filled with refined sugars that spike insulin levels beyond a healthy limit), our cells adapt by reducing the number of receptors on their surfaces to respond to insulin. In other words, our cells desensitize themselves to insulin, causing insulin resistance, which allows the cells to ignore the insulin and fail to retrieve glucose from the blood.

The pancreas responds by pumping out more insulin. So higher levels of insulin become needed for sugar to go into the cells. This creates a cyclical problem that eventually culminates in type 2 diabetes...Unfortunately, insulin doesn't just escort glucose into our cells. It's also an anabolic hormone, meaning it stimulates growth, promotes fat formation and retention, and encourages inflammation. When insulin levels are high, other hormones can be affected adversely, either increased or decreased due to insulin's domineering presence. This, in turn, plunges the body further into unhealthy patterns of chaos that cripple its ability to recover its normal metabolism. (GB: 28-29)

Another source of insulin resistance is overconsumption of fructose. Foods which combine fructose and glucose—like table sugar, honey and high fructose corn syrup (it's right there in the name)—are metabolized differently by the body than foods which contain glucose alone. The excess fructose eventually leads to fatty liver disease, which also contributes to insulin resistance and other metabolic disorders:

Glucose and fructose differ in many significant ways. Whereas almost every cell in the body can use glucose for energy, no cell has the ability to use fructose. Where glucose requires insulin for maximal absorption, fructose does not. Once inside the body, only the liver can metabolize fructose. Where glucose can be dispersed throughout the body for use as energy, fructose is targeted like a guided missile to the liver.

At the liver, fructose is rapidly metabolized into glucose, lactose and glycogen. The body handles excess glucose consumption through several well-defined metabolic pathways, such as glycogen storage and de novo lipogenesis (creation of new fat). No such system is present for fructose. The more you eat, the more you metabolize. The bottom line is that excess fructose is changed into fat in the liver. High levels of fructose will cause fatty liver. Fatty liver is absolutely crucial to the development of insulin resistance in the liver. (OC: 163-164, italics in original)

Insulin resistance is the major player in metabolic diseases like obesity and diabetes according to Dr. Jason Fung. As he describes it, obesity is a progressive disorder that manifests itself over long periods of time. Therefore, if we neglect the time dependent nature of the disease, he says, we will not understand it.

He compares it to rust (iron oxide). You can immerse a piece of iron in water for a long time and not see any change. You might conclude that water exposure does not cause rust. But oxygenation of iron is a progressive process. Left outside exposed to the elements for a year or more, that same metal object will be covered with rust. It is this time-dependent nature of obesity, Fung says, that is missing in the standard Carbohydrate Insulin Model.

The longer you are obese, the harder it is to eradicate....Most current theories of obesity cannot explain this effect, so they instead ignore it. But obesity is time dependent. Like rust, it takes time to develop. You can study moisture conditions and metal composition. But if you ignore the time dependent nature of rust, you will not understand it.

So we know that insulin causes insulin resistance. But insulin resistance also causes high insulin—a classic vicious or self-reinforcing cycle. The higher the insulin levels, the greater the insulin resistance. The greater the resistance, the higher the levels. The cycle keeps going around and around, one element reinforcing the other, until insulin is driven up to extremes. The longer the cycle continues, the worse it becomes—that's why obesity is so time dependent...At the very beginning of obesity, a person will manifest little insulin resistance, but it develops over time. The longer you are obese, the more insulin resistance you have. Gradually, that insulin resistance will cause even your fasting insulin levels to rise.

The high insulin levels are the primary result. Persistent high insulin levels lead gradually and eventually to insulin resistance. Insulin resistance in turn leads to higher insulin levels. But the crucial starting point of the vicious cycle is high insulin levels. Everything else follows and develops with time—and the fat get fatter...Obesity at age seventeen has consequences that reach decades into the future. Any comprehensive theory of obesity must be able to explain why its duration matters so much. (OC: 107-108; 114-116)

It's not just high insulin levels alone which lead to insulin resistance—it's also the frequency and duration of exposure to high insulin levels that causes it to develop. Fung contends that the increased frequency of meals in our society has contributed just as much to rising obesity rates as the increased glycemic load of the foods we eat:

...in the development of obesity, the increase in meals is almost twice as important as the change in diet. We obsess about what we should eat. We eat foods that practically didn't exist ten years ago. Quinoa. Chia seeds. Acai berries. All in the hopes of making us slim. But we spare not a single thought as to when we should be eating. (OC: 121; italics in original)

The increase in eating opportunities has led to persistence of high levels of insulin. Snacks, which tend to be high in refined carbohydrates, also tend to cause higher levels of insulin. Under these conditions we should expect the development of insulin resistance. We never consider the implications of the drastic changes we have made in meal timing. Think about it this way: In 1960, we ate three meals a day. There wasn't much obesity. In 2014, we eat six meals a day. There is an obesity epidemic. (OC: 123)

No wonder the studies Pontzer cites don't show a difference between diets. They completely misrepresent the actual causal mechanism by which high-carbohydrate diets make us fat in the first place: insulin resistance. Insulin resistance does not develop over a short period of time, therefore it cannot be reversed in a short period of time either. Certainly not over six days, or even three weeks. High insulin levels will cause us to retain too much fat in the long term, no matter what diet we eat. Sure, we can lose weight temporarily through caloric restriction alone, as Pontzer points out. We can accomplish this on virtually any diet. But can we maintain it?

It's not that carbohydrates are inherently bad for us. That’s why hunter-gatherers can eat plenty of carbohydrates and yet have no metabolic disease. It is the highly processed refined carbohydrates of modern Western-style diets (including ultraprocessed foods)—coupled with high fructose/glucose consumption—that leads to insulin resistance. Insulin resistance leads to higher insulin levels which leads to more insulin resistance. The body's Set Point is dialed ever higher, making it harder to lose weight in the long term; consequently, this is why most diets fail. We need to reverse the insulin resistance. Dr. Fung also highlights the crucial role fiber plays in the consumption of carbohydrates in traditional societies:

It is no coincidence that virtually all plant foods, in their natural, unrefined state, contain fiber. Mother Nature has pre-packaged the "antidote" with the "poison." Thus, traditional societies may follow diets high in carbohydrates without evidence of obesity or type 2 diabetes. The one critical difference is that the carbohydrates consumed by traditional societies are unrefined and unprocessed, resulting in very high fiber intake.

Western diets are characterized by one defining feature—and its not the amount of fat, salt, carbohydrate or protein. It's the high amount of processing of foods. Consider traditional Asian markets, full of fresh meats and vegetables. Many people in Asian cultures buy fresh food daily, so processing it to extend shelf life is neither necessary nor welcome. By contrast, North American supermarkets have aisles overflowing with boxed, processed foods...

Fiber and fat, key ingredients, are removed in the refining process: fiber to change the texture and make food taste "better," and natural fats, to extend shelf life, since fats tend to go rancid with time. And so we ingest the "poison" without the "antidote"—the protective effects of fiber is removed from much of our food. (OC: 183)

Fiber intake has fallen considerably over the centuries. In Paleolithic diets, it was estimated to be 77 to 120 grams per day. Traditional diets are estimated to have 50 grams per day of dietary fiber. By contrast, modern American diets contain as little as 15 grams per day...the removal of dietary fiber is a key component of food processing. And improving the texture, taste and consumption of foods directly increases food companies' profits. (OC: 181)

A lot of folks notice that as they get older, they tend to put on weight more easily, even while eating much the same foods as they always did. They think that this is because their metabolism slows down as they age. But Dr. Pontzer's own research shows that this is untrue! This study came out after Burn was published but was reported in the media.

According to his data, metabolism remains stable our entire lives, from age 20 to age 60, even during major hormonal shifts. This would seem to validate the progressive nature of insulin resistance and its role in obesity. Yet in interviews Pontzer still insists that the sole cause of obesity is eating too much: "Pontzer argues that if the calories we burn stay largely the same throughout life, then the real source of obesity has to be the amount we’re eating, and particularly the heavy consumption of highly processed foods."

But that doesn't make sense, does it? Do we really eat more processed foods as we get older? In my experience, we usually tend to eat less of them. Most of us are painfully aware that we can't eat the kind of junk we could in our twenties. As people get older they increasingly have to "watch what they eat." Yet despite this, they still find themselves gaining weight year after year. The insulin resistance hypothesis seems to offer an explanation other than merely overconsumption. People today start packing on the pounds well before age sixty. Why is that?

And there are other problems with the notion that ultraprocessed foods are the primary culprit behind obesity. One of them is the strong link between obesity and poverty, as Dr. Fung explains:

The basic premise of this argument is that food is more delicious in 2010 than in 1970 because food scientists engineer it to be so. We cannot help but overeat calories and therefore become obese. The implication is that hyper-palatable "fake" foods are more delicious and more rewarding than real foods, but that seems very difficult to believe. Is a "fake" highly processed food such as a TV dinner more delicious than fresh salmon sashimi dipped in soy sauce with wasabi? Or is Kraft Dinner, with its fake cheese sauce, really more enticing than a grilled rib-eye steak from a grass-fed cow?

But the association of obesity with poverty presents a problem. The food-reward hypothesis would predict that obesity should be more prevalent among the rich, since they can afford to buy more of the highly rewarding foods. But the exact opposite is true. Lower-income groups suffer more obesity.

To be blunt, the rich can afford to buy more food that is both rewarding and expensive, whereas the poor can afford only rewarding food that is cheaper. Steak and lobster are highly rewarding—and expensive—foods. Restaurant meals, which are expensive compared to home cooking, are also highly rewarding. Increased prosperity results in increased access to different types of highly rewarding food, which should result in more obesity. But it does not...

Neither food reward nor physical exertion can explain the association between obesity and poverty. So what drives obesity in the poor? It is the same thing that drives obesity everywhere else, refined carbohydrates...If refined carbohydrates are significantly cheaper than other sources of food, then those living in poverty will eat refined carbohydrates. Indeed, processed carbohydrates are an order of magnitude less expensive... (OC: 138-140)

Pontzer inadvertently provides some additional evidence for this theory. He tells about the National Weight Control Registry, an online group of over ten thousand remarkable people who've lost at least thirty pounds and kept it off for at least a year. The average member, he tells us, has lost over sixty pounds and kept it off for more than four years. Yet despite their smaller body size, their metabolisms are still apparently set to their old weight rather than their new one:

Tellingly, the Registry members...racked up more physical activity each day than the normal-weight adults who had never been obese. In other words, the Registry members worked harder than never-obese adults did to maintain the same body weight. A follow-up study that measured daily energy expenditures helps to explain why.

Despite their smaller body size and lower BMRs, Registry members had the same daily energy expenditures as obese adults. Their bodies—or more specifically, their weight management systems in their brains—were stuck at their old, pre-weight loss daily energy expenditures, targeting the same number of calories they burned before their weight loss, when they were a lot bigger. To stay in energy balance and keep the weight off, Registry members had to find a way to burn all those calories. Exercise provided the answer. (B: 257)

Pontzer lists this as a benefit of regular exercise for weight loss, but he has no explanation as to why this phenomenon occurs in the first place! If the body is a dynamic homeostatic system, why would their bodies still be trying to maintain the higher weight, even when their current body composition was so much different? Fung would have an explanation, however: the body's settling point has been increased due to the ongoing effects of insulin resistance. The brain is still trying to defend the higher set point, hence the need to exercise more often to burn off the extra calories that the body is trying to conserve. This strongly points to a malfunction in the lipostat, and not just too much variety or too many ultraprocessed foods lying around.

A change to the body's Set Point makes more sense than the prevailing "calories in, calories out" energy-balance model. Once you learn about the body's remarkable ability to modify both energy expenditure and appetite as we have over the course of this series, CICO seems inadequate to explain how almost everyone managed to effortlessly maintain a healthy weight before the present unless they had a genetic propensity to store fat (which could not explode over a single generation). Changing dietary habits and a malfunctioning lipostat make more sense to me than the idea that modern foods are simply too delicious, or a collective loss of "willpower."

Dr. Fung recommends reversing insulin resistance by eating foods which don't raise insulin levels too much and adding in more fiber (vinegar also appears to be protective) to help modulate insulin spikes. Protein also causes higher insulin levels, so he calls for moderate consumption of meat (unlike some other low-carb diets). The insulin response also tends to be higher later in the day, so eat earlier if you can.

He also recommends eating less often, which will help reset your cells' sensitivity to insulin. At minimum that means no snacking, but even better is time restricted feeding, also known as intermittent fasting.

Fung points out that most dietary strategies are additive—focusing on what kinds of foods to eat or what supplements to take. But taking things away—eating less—is hardly ever discussed because there's no product to sell (and in fact it reduces profits if people eat less). Fasting has been a part of traditional practices in many cultures all around the world going back thousands of years. In fact, before calorie counting became the norm, skipping meals and avoiding farinaceous foods used to be the standard advice for people trying to lose weight¹.

Dietary guidelines for reducing insulin levels include reducing added sugar and refined grains, keeping protein consumption moderate, and adding healthy fat and fiber. Intermittent fasting is an effective way to treat insulin resistance without incurring the negative effects of calorie reduction diets. Stress management and sleep improvement can reduce cortisol levels and control insulin. (OC: 5-6)

Once again, these recommendations are pretty much in line with both the Paleo and Weston Price approaches to diet, which revolve around the types of food eaten and how they are prepared rather than calories consumed. Some people go even further—for example, Gary Taubes has recently started recommending a Ketogenic diet for tackling metabolic syndrome.

Some of the best eating advice I’ve found comes from Dr. Bill Schindler, an experimental anthropologist who studies the ways people have made food since prehistory. He points out that we have not evolved to eat virtually any of the foods we eat today. This means that basically everything we eat is a product of our minds and our tools. The problem is that the way we get our food and the way we prepare it has changed more in the last 50 years than in the last 50,000+. Because of this, he tells us, for the first time ever malnutrition and obesity can occur in the same individual. He has a new book out called Eat Like a Human, which calls for a review of its own (meaning we'll probably be revisiting this series in the future). You can watch a presentation by him here (YouTube)

Do We Have the Guts?

Another intriguing possibility is that our fat storage mechanisms have gone awry due to a disturbance in our microbiome.

The role of the gut microbiome in metabolism is still unknown and highly speculative. For this reason, it is not considered to be related to rising obesity rates by mainstream researchers, who are conservative by nature. The human microbiome contains roughly 100 times more genes that humans themselves. Many microbial species don't even have a name yet.

It appears that people in industrial societies exhibit a significant loss of biodiversity in their gut microbiome compared to hunter-gatherer populations like the Hadza. The diversity of gut microbiota in non-Western agricultural populations is midway between those of hunter-gatherers and people living in industrial societies. Furthermore, the microbiota of people living in the past was apparently more diverse than that of their descendants living in the same societies today. Remarkably, this can be discerned by analyzing fossilized excreta (i.e. poop) from archaeological sites (known as coprolites).

This is thought to be caused by two factors: 1) A lack of dietary fiber—our gut seems to require large amounts of fiber for our microbiome to flourish; and 2.) The widespread use of antibiotics. Other environmental factors may be contributing as well (pesticides and seed oils are often mentioned).

Traditional people eat diets rich in unprocessed plant material, which are much more chemically complex compared to processed foods. The smorgasbord of chemicals acts as fuel for a higher variety of microbes. Traditional people use less antimicrobial medicines and compounds in daily life, which might also contribute to their increased gut microbe diversity.

One study of the Hadza found that their gut microbiota varied with the seasons: "In particular, a subset of microbial species' populations diminished in the wet season, when honey accounted for a significant portion of caloric intake, and rebounded in the dry season, when consumption of fiber-rich tubers peaked." This suggests that gut diversity can be restored. However, a study by the same researchers with rodents showed that if microbial diversity was lost for several generations due to a restriction of fiber, microbial species that had initially bounced back became permanently lost².

Another study had children and adults living in a village in the rainforest for two weeks and eating the local diet to see what the effects would be on their microbiome. They found that the diversity of the children's microbiome increased, but not that of the adults; that is, the children's microbiome was more "plastic." They speculate that feeding children a high-fiber, low-fat, low processed-food diet before age three might allow for a healthier microbiome to develop, and that this would persist throughout adulthood.

A study of paleofeces from Arizona found that the native diet was "remarkably high in fiber, low in fat, and consisting largely of foods with extremely low glycemic indices." This type of diet would theoretically allow the development of "thrifty genes" that cannot cope with modern diets, leading to the high rates of diabetes seen among native populations in the Southwest. And a study of paleofeces from miners of the prehistoric Halstatt culture in Europe found that, "ancient miners up to the Baroque period...had gut microbiome structures more like those of modern non-Westernized individuals, whose diets are also mainly composed of unprocessed food, fresh fruits and vegetables. The findings suggest a more recent shift in the Western gut microbiome as eating habits and lifestyles changed." Among the foods eaten were fermented foods like beer and blue cheese.

If our gut microbiota has indeed changed due to modern diets and lifestyles, it might explain the rise in the Set Point, especially if the change was quite recent. And if hunter-gatherers' microbiota is more diverse, it might explain why they are protected against metabolic diseases that plague the rest of the world. However, more research in this area is needed, and much more exciting work will surely be done in the future.

Environmental Contamination

Finally, another provocative hypothesis argues that one or more substances in our environment have caused us to gain weight by causing our lipostat to malfunction and adjusting our weight Set Point higher. We might label this the Environmental Contaminant Model of obesity.

This explains a few data points about obesity that don't make sense otherwise, for instance: 1.) Obesity rates are rising even in lab animals fed controlled diets, and even in some wild animals; 2.) Obesity rates seem to be correlated with altitude (the higher up, the lower the obesity rate); 3.) Obesity is correlated with certain professions independent of income or the amount of physical labor required by those professions; 4.) Obesity rates started rising precipitously only after 1980, with no sudden, obvious shifts in diet.

This thesis was put forward in a paper and an accompanying Web site by someone calling himself or themselves Slime Mold Time Mold (?). I'll let you read it for yourself. If nothing else, it's a good rundown of why many of the prevailing theories of obesity are inadequate:

A Chemical Hunger

In the end, they make the argument that the offending substances are 1.) Lithium, and 2.) PFAS, otherwise known as "forever chemicals." Lithium, for example, is already known to cause weight gain. Both of these compounds are present in our natural environment, in our food supply, and in our water supply in industrialized countries.

These contaminants are the only cause of the obesity epidemic, and the worldwide increase in obesity rates since 1980 is entirely attributable to their effects. For any two people in a group, the difference between their weights is largely genetic, because everyone is exposed to similar levels of contamination. But the difference between the average weight in 1980 and the average weight today is the result of environmental contaminants.

People were skinny before the modern era because these contaminants didn’t exist back then. People’s diets were “worse” in the past—full of lard and bread—because diet doesn’t cause obesity. The ~1% of people who were obese in the past were people with one of the various medical conditions known to cause obesity, such as Prader-Willi Syndrome, hypothyroidism, or hypothalamic lesions.

Different groups of hunter-gatherers remain lean while eating very different diets because the human body can thrive on many kinds of food. Some of the diets are extremely high-fat. Some of them are extremely high-starch. Some of them are extremely high-sugar. Some eat an extremely varied diet, while others get almost half of their calories from a single food source. But they don’t become obese, because they’re eating fat right off the gemsbok or yams straight out of the ground, and living in grass huts. When hunter-gatherers adopt an industrialized lifestyle, however, they become obese just like anyone else.

A Chemical Hunger – Part III: Environmental Contaminants

It's an intriguing hypothesis, but I'm not sure I buy it. Some of the arguments used to dismiss competing hypotheses are the same ones Pontzer uses which, as we've seen, have problems with them. Also, I just don't think they have enough evidence. The correlation with altitude in the United States seems dubious to me. Europe also has mountainous and flat terrain. Do we see a correlation there as well? If not, why not? This might be a case of spurious correlations. Also, if their hypothesis is correct, based on the data I have on PFAS contamination Colorado should be one of the most obese states, along with New Jersey, North Carolina, Massachusetts, and Michigan. But that's not what we see. Some of the most contaminated places in the Third World also don’t have particularly high rates of obesity compared to other places.

PFAS Contamination in the United States (Environmental Working Group)

And, even if true, there's not much we can do. Move to Colorado (or Vietnam)? Drink bottled water? Eat less contaminated foods? (like the Hadza, the authors are very fond of tubers). If our environments are so thoroughly suffused with these substances so as to cause a worldwide obesity epidemic, then it doesn't seem like there's much we can do about it besides trying to clean up our environment (which we should be doing anyway). But the effects would take years to manifest.

In our last installment, we'll pivot back to exercise. What can hunter-gatherers teach us about exercise and movement as well as other aspects of life like sitting and sleeping? That's what we’ll look at next time.

1. The fact that historical fasting practices go back thousands of years in many cultures also disproves the idea that everyone in the past had a difficult time getting enough food to eat. Clearly you don't need to recommend fasting to starving people!

2. One of the anthropologists, Jeff Leach, gave himself a fecal transplant from the Hadza. You can listen to an interview with him on Tangentially Speaking here.