Current theories of the obesity epidemic are inadequate. None of them hold up to closer scrutiny, and none can explain all of the mysteries mentioned in Part I. But these mysteries are real, puzzling data about the obesity epidemic.
You’re probably familiar with several theories of the obesity epidemic, but there is strong evidence against all of them. In this section, we focus on the case against a couple of the most popular theories.
2.1 Calories In, Calories Out
A popular theory of obesity is that it’s simply a question of calories in versus calories out (CICO). You eat a certain number of calories every day, and you expend some number of calories based on your metabolic needs and physical activity. If you eat more calories than you expend, you store the excess as fat and gain weight, and if you expend more than you eat, you burn fat and lose weight.
This perspective assumes that the body stores every extra calorie you eat as body fat, and that it doesn’t have any tools for using more or less energy as the need arises. But this isn’t the case. Your body has the ability to regulate things like its temperature, and it has similar tools to regulate body fatness. When we look closely, it turns out that “calories in, calories out” doesn’t match the actual facts of consumption and weight gain.
“This model seems to exist mostly to make lean people feel smug,” writes Stephen Guyenet, “since it attributes their leanness entirely to wise voluntary decisions and a strong character. I think at this point, few people in the research world believe the CICO model.”
It’s not that calories don’t matter at all. People who are on a starvation diet of 400 calories per day will lose weight, and as we will see in this section, people who eat hundreds of calories more than they need will usually gain weight. The problem is that this ignores how the body accounts for the calories coming in and going out. If you don’t eat enough, your body finds ways to burn fewer calories. If you eat too much, your body doesn’t store all of the excess as fat, and compensates by making you less hungry later on. Calories are involved in the math but it’s not as simple as “weight gain = calories in – calories out”.
2.1.1 Common Sense
First, we want to present some common-sense arguments for why diet and exercise alone don’t explain modern levels of obesity.
Everyone “knows” that diet and exercise are the solution to obesity. Despite this, rates of obesity continue to increase, even with all the medical advice pointing to diet and lifestyle interventions, and a $200 billion global industry devoted to helping people implement these interventions. It’s not that no one is listening. People are exercising more today than they were 10 or even 20 years ago. Contrary to stereotypes, more than 50% of Americans meet the HHS guidelines for aerobic exercise. But obesity is still on the rise.
It’s true that people eat more calories today than they did in the 1960s and 70s, but the diﬀerence is quite small. Sources have a surprisingly hard time agreeing on just how much more we eat than our grandparents did, but all of them agree that it’s not much. Pew says calorie intake in the US increased from 2,025 calories per day in 1970 to about 2,481 calories per day in 2010. The USDA Economic Research Service estimates that calorie intake in the US increased from 2,016 calories per day in 1970 to about 2,390 calories per day in 2014. Neither of these are jaw-dropping increases.
If we go back further, the story actually becomes even more interesting. Based on estimates from nutrient availability data, Americans actually ate more calories in 1909 than they did in 1960.
Finally, there are many medical conditions that cause obesity. For example, Prader-Willi Syndrome, a genetic disorder characterized by intense hunger and resulting obesity, hypothyroidism, an endocrine disorder where people experience loss of appetite yet still gain 5-10 pounds, and lesions to the hypothalamus, which often lead to intense weight gain, sometimes accompanied by great hunger but many times not.
2.1.2 Scientific Evidence
In addition to these common-sense objections, decades of research suggests that diet and exercise are not to blame for rising rates of obesity.
Studies of controlled overfeeding — you take a group of people and get them to eat way more than they normally would — reliably find two things. First, a person at a healthy weight has to eat huge amounts of calories to gain even a couple pounds. Second, after the overfeeding stops, people go right back to the weight they were before the experiment.
The great-grandaddy of these studies is the Vermont prison experiment, published in 1971. Researchers recruited inmates from the Vermont State Prison, all at a healthy weight, and assigned some of them to eat enormous amounts of food every day for a little over three months. How big were these meals? The original paper doesn’t say, but later reports state that some of the prisoners were eating 10,000 calories per day.
On this olympian diet, the prisoners did gain considerable weight, on average 35.7 lbs (16.2 kg). But following the overfeeding section of the study, the prisoners all rapidly lost weight without any additional eﬀort, and after 10 weeks, all of them returned to within a couple pounds of their original weight. One prisoner actually ended up about 5 lbs (2.3 kg) lighter than before the experiment began!
Inspired by this, in 1972, George Bray decided to conduct a similar experiment on himself. He was interested in conducting overfeeding studies, and reasoned that if he was going to inflict this on others, he should be willing to undergo the procedure himself. First he tried to double each of his meals, but found that he wasn’t able to gain any weight — he simply couldn’t fit two sandwiches in his stomach at every sitting.
He switched to energy-dense foods, especially milkshakes and ice cream, and started eating an estimated 10,000 calories per day. Soon he began to put on weight, and gained about 22 lbs (10 kg) over 10 weeks. He decided this was enough and returned to his normal diet. Six weeks later, he was back at his original weight, without any particular eﬀort.
In both cases, you’ll notice that even when eating truly stupendous amounts of food, it actually takes more time to gain weight than it does to lose it. Many similar studies have been conducted and all of them find basically the same thing — check out this recent review article of 25 studies for more detail.
Overfeeding in controlled environments does make people gain weight. But they don’t gain enough weight to explain the obesity epidemic. If you eat 10,000 calories per day, you might be able to gain 20 or 30 pounds, but most Americans aren’t eating 10,000 calories per day.
We can compare these numbers to the increases in average calories per day we reviewed earlier. Sure, consumption in the US went from 2,025 calories per day in 1970 to 2,481 calories per day in 2010, a diﬀerence of 456 calories. But consider Poehlman et al. (1986), where researchers fed a group of 12 men 1,000 extra calories a day for 22 days. On average the men gained about 5 lbs (2.2 kg), but some of them actually lost weight instead.
And it’s not as though these participants are eating 1,000 extra calories of celery and carrots. In one study, the extra calories came from “sherbet, fruit juices, margarine, corn oil, and cookies”. But the content doesn’t seem to matter very much. Another study compared overfeeding with carbohydrates (mostly starch and sugar) and overfeeding with fat (mostly dairy fat like cream and butter). The two groups got their extra calories from different sources, but they were overfed by the same amount. After two weeks, both groups gained the same amount of fat, 3.3 lbs on average. A similar study overfed volunteers by 1,194 calories on either a high-carb or a high-fat diet for 21 days. Both groups gained only about 2 lbs of fat.
The fact that many of these are twin studies provides even more evidence against CICO. In groups of twins that are all overfed by the same amount, there is substantial variation between the different participants in general. Some people gain a lot of weight, others gain almost none. But each person gains (or loses!) about the same amount of weight as their twin. In some cases these correlations can be substantial, as high as r = 0.90. This strongly suggests that genetics plays a large role in determining how the body responds to overfeeding.
The story with exercise is the same as with overeating — it makes a difference, but not much. One randomized controlled trial assigned overweight men and women to different amounts of exercise. More exercise did lead to more body fat loss, but even in the group exercising the most — equivalent to 20 miles (32.0 km) of jogging every week for eight months — people only lost about 7 lbs.
You might think that hunter-gatherers have a more active lifestyle than we do, but this isn’t always true. The Kitavans examined in 1990 by Staffan Lindeberg were only slightly more active than westerners, had more food than they knew what to do with, and yet were never obese. “Many Westerners have a level of physical activity that is well within the range of the Kitava population,” he wrote. “Hence, physical activity does not seem to explain most of the differences in disease pattern between Kitava and the Western world.”
A recent meta-analysis of 36 studies compared the effects of interval training exercise with more traditional moderate-intensity continuous training. The authors call interval training “the magic bullet for fat loss” (this is literally in the title) and trumpet that it provides 28.5% greater reductions in total absolute fat mass than moderate exercise. But what they don’t tell you is that this is a difference between a loss of about 3 lbs and about 4 lbs, for an exercise program running 12 weeks long. Needless to say, this difference isn’t very impressive. Other meta-analyses find similar results: “neither short-term HIIT/SIT nor MICT produced clinically meaningful reductions in body fat.”
Maybe diet and exercise together are worth more than the sum of their parts? Sadly this doesn’t seem to be the case either. If anything, when combined they are worth less than the sum of their parts. One meta-analysis comparing interventions based on diet, exercise, and diet plus exercise found that people lost about 23.5 lbs (10.7 kg) on diets, 6.4 lbs (2.9 kg) on an exercise regime, and 24.2 lbs (11.0 kg) on diet plus exercise. After a year, diet plus exercise was down to 18.9 lbs (8.6 kg). Other meta-analyses are more tempered, for example, finding a loss of about 3.6 lbs (1.6 kg) after two years of diet plus exercise interventions. Again this is more weight loss than zero, but it clearly rules out diet plus exercise as an explanation for the obesity epidemic. People in 1950 were a lot leaner than they are now, but it’s not because they ate less and exercised more.
[Edit: We’ve added an interlude clarifying this section on CICO in response to reader questions and objections. Read it here.]
2.2 Good Calories and Bad Calories
Ok, calories themselves may not be the villain here. But maybe it’s not that we’re eating more than we used to — maybe it’s that we’re eating diﬀerently. Maybe one particular macronutrient or source of calories is to blame.
2.2.1 Dietary Fat
Dietary fat seems like a possible culprit. After all, fat makes you fat, right? Turns out it’s not so simple.
To begin with, fat consumption has actually fallen over the past few decades, while obesity has skyrocketed. This isn’t consistent with an explanation where dietary fat leads to obesity.
Plenty of cultures eat extremely high-fat diets and remain very lean indeed. You’ll remember that the Maasai diet is about 3000 calories per day, and 66% of that is from fat. But the Maasai don’t suﬀer from obesity. In fact, Kalahari Bushmen love fat and apparently wax poetic about it.
Clinical results agree: dietary fat doesn’t have much of an impact on long-term weight. Putting people on a low-fat diet reduces their weight in the short term, but in trials lasting for longer than one year, they tend to return to normal. When they are directly compared, low-fat and high-fat diets have about the same impact on weight loss.
This is a little diﬃcult to square with animal studies that find that a high-fat diet reliably leads to obesity in monkeys, dogs, pigs, hamsters, squirrels, rats, and mice. It could just be that humans are not monkeys, dogs, pigs, hamsters, squirrels, rats, or mice, and that while dietary fat has an adverse effect on these species, it doesn’t do much to us. Some of the hamster studies, for example, induced obesity simply by giving the hamsters extra sunflower seeds, a phenomenon not observed in humans. Pigs, in particular, will become obese even on low-fat diets when given the opportunity.
We even see differences within a specific kind of animal. The same high-fat diet will make one species of hamster (Syrian hamsters) obese and leave another species of hamster (golden hamsters) merely chubby. If the findings can’t generalize between different species of hamsters, we shouldn’t expect them to generalize to humans.
It could also be that dietary fat leads to obesity in mammals held in captivity, possibly due to factors like stress. Metabolic ward studies restrict your movement, but it’s not exactly like living your whole life in a laboratory cage. And it’s worth noting that about 10–15% of macaque and rhesus monkeys in captivity become obese when they reach middle age, despite the fact that they are fed a relatively low-fat (10% of energy) diet.
In any case, it’s hard to square a fat-based explanation for the obesity epidemic with the fact that fat consumption hasn’t increased in step with the rise of obesity and the fact that low-fat diets don’t lead to much weight loss.
Ok, maybe fat doesn’t make you fat. How about carbohydrates? All this bread can’t be good for us.
This theory is dead on the starting line, though, because as obesity has gone up, consumption of carbohydrates has gone down (see figure).
This is enough to make it clear that carbohydrate consumption isn’t driving the obesity epidemic, but we can take a slightly closer look anyways, just to be sure.
Eating lots of carbs can actually make you lose weight. High-carbohydrate diets cause weight loss, even when not restricting calories. A study from 2003 examined low-fat diets in 16 overweight people. Naturally, this low-fat diet was high in carbohydrates. When patients started the low-fat diet and were told to eat as much as they wanted, they actually ate 291 calories less per day.
But their carbohydrate intake increased, from 253 grams per day to 318 grams per day. On this diet they lost 8 lbs (3.8 kg) on average over a 12-week period. In the DIETFITS randomized controlled trial, 609 people fed a whole-food, high-carbohydrate diet lost 12 pounds (5.3 kg) over one year, not significantly different from the 13 pounds (6.0 kg) of weight lost on a whole-food low-carbohydrate diet. The high-carbohydrate diet also supplied about 1.5 times as much sugar as the low-carbohydrate diet.
The residents of Kitava, mentioned earlier, have a diet of starchy roots and tubers. Almost 70% of their calories come from carbohydrates, but they don’t suﬀer from obesity, diabetes, or heart disease.
(Lindeberg also says: “The long primate history of fruit eating, the high activity of human salivary amylase for effcient starch digestion, and some other features of human mouth physiology … suggest that humans are well prepared for a high carbohydrate intake from non-grain food sources. … in contrast to most other animals including non-human primates, humans have an exceptional capacity to produce salivary amylase in order to begin hydrolysis of starch in the mouth.”)
In general, cultures with very high intakes of carbohydrate tend to be lean. Most agricultural societies around the world have a diet that is high in carbohydrates and low in fat. Agricultural societies are different from industrialized ones in many ways, of course. But even in those agricultural cultures with abundant food, people are typically lean, with low rates of diabetes and cardiovascular disease.
This is true even if the carbohydrate is white rice. In Japan, white rice is a primary staple food (p. 338), and has been for a long time. About 62% of the Japanese diet is carbohydrates, and most of this is white rice. Despite this, Japanese rates of obesity have been, and continue to be, the lowest of any industrialized nation.
In fact, people who move from Japan to the US and begin eating less white rice become much heavier. This suggests that the diﬀerence isn’t simply genetic. These immigrants do end up eating a diet much higher in fat — but of course, from the previous section, we’ve seen that fat can’t be responsible for this change.
Nor is it likely to be some other carbohydrate staple. Wheat consumption, for example, has been falling for a century. People in the US ate almost twice as much wheat (primarily in the form of bread) in the 1880’s than they do today. If wheat were responsible, people would have been massively obese during reconstruction and entirely lean today. Obviously that is not what we observe.
If the historical data isn’t enough for you, there are entire reviews devoted to the health impacts of wheat, pretty conclusively showing that it isn’t a cause of obesity.
Everyone knows that added sugar is the real villain, right? Wrong again.
Sugar consumption has been declining for 20 years in the US, while obesity and diabetes rates have increased. The sugar data in the figure below includes all added sugars such as honey, table sugar, and high-fructose corn syrup, but doesn’t include sugars naturally occurring in fruits and vegetables.
We see something similar in what has been called The Australian Paradox, where obesity in Australia nearly tripled between 1980-2003, while sugar consumption dropped 23%.
Multiple lines of evidence confirm that sugar consumption is falling worldwide. In the US, consumption of sugary beverages dropped between 1999 and 2010. We see the same trend in longitudinal studies of a particular cohort tracked from 1991 to 2008. It’s not that consumers can’t find the sugar they crave, of course — there have been no major changes in the availability of sugary foods.
We see that public health efforts to reduce sugar consumption have worked. In fact, they’ve worked very well. But they don’t seem to have made any difference to the obesity epidemic.
Tightly-controlled metabolic ward studies also show that the sugar content of a diet doesn’t matter much. One study of 17 men compared a 25 percent sugar, high-carbohydrate diet to a 2 percent sugar, very-low-carbohydrate (ketogenic) diet of equal calories. After four weeks, they found that the high-carbohydrate diet caused slightly more body fat loss than the very-low-carbohydrate (ketogenic) diet, despite the fact that the two diets diﬀered more than tenfold in sugar content. We see similar results in mice and in rats: “Animals fed a low-fat, high-sucrose (LH) diet were actually leaner than animals fed a high-complex-carbohydrate diet.”
We can further cite the fact that many cultures, such as the Hadza of Tanzania, the Mbuti of the Congo, and the Kuna of Panama all eat diets relatively high in sugar (sometimes as high at 80%), and yet none of these cultures have noticeable rates of obesity, diabetes, cardiovascular disease, etc.
2.3 Diet in General
Over the past 40 years, there hasn’t been much of a change in where people get their calories from. Americans get about 50% of their calories from carbohydrates, 30% from fat, and 20% from protein, and they have for years. At the same time obesity continues to go up and up. Comparing these two trends, it’s hard to imagine that macronutrients have anything to do with the obesity epidemic.
You’ll recall that Mystery 8 is that all diets work about equally well. It doesn’t matter which diet you choose — you lose about the same number of pounds regardless.
All diets work. The problem is that none of them work very well. Stick to just about any diet for a couple weeks and you will probably lose about 10 pounds. This is ok, but it isn’t much comfort for someone who is 40 lbs overweight. And it isn’t commensurate with the size of the obesity epidemic.
Systematic comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates finds that across many different reduced-calorie diets, people lose about 13.2 lbs (6 kg) over six months, and that in all cases people began to gain weight back after 12 months. It’s not just weight loss, either. Satiety, hunger, satisfaction with the diet, and adherence to the protocol is similar for all diets.
There are too many diets to review in full, of course, but we see the same pattern in every diet that has been extensively studied. Let’s look at just a few.
2.3.1 Ketogenic Diet
We’ve already mentioned a few ketogenic diets, and as we’ve seen, they don’t work much better than other diets do.
There is one meta-analysis of ketogenic diet studies, comparing very-low-carbohydrate ketogenic diets to low fat diets in overweight and obese adults. Across thirteen randomized controlled trials, ketogenic diets only caused 2 pounds (0.9 kg) more weight loss than the traditional low-fat diets after 12 months.
2.3.2 Low-Glycemic Diet
Study after study finds that low-glycemic diets don’t work for weight loss.
One study from 2007 randomly assigned 203 women to either a high-glycemic or low-glycemic diet. The difference in glycemic index was considerable, with the high-glycemic diet having an index twice as high as the low-glycemic diet. The groups consumed the same amount of calories and reported similar levels of hunger.
Despite this, there was no difference between the groups. After two months the LGI group had lost 1.6 lbs (0.72 kg) and the HGI group had lost 0.7 lbs (0.31 kg), but this difference wasn’t sustained. After 18 months on the diet, the LGI group had lost 0.9 lbs (0.41) kg and the HGI group had lost 0.6 lbs (0.26 kg), and this difference was statistically indistinguishable (p = .93). Large differences in glycemic index have no meaningful long-term (or even short-term) effect on calorie consumption or body weight.
Another 18-month randomized trial compared a low-glycemic load (40% carbohydrate and 35% fat) vs low-fat (55% carbohydrate and 20% fat) diet in 73 obese young adults in the Boston, Massachussets area. In both diets, participants were largely eating whole foods; vegetables, beans, and fruit were major components of both diets. In both diets, people were allowed to eat as much as they wanted.
Both groups reported similar levels of hunger and consumed similar amounts of calories. The two diets were rated equally easy to stick to and equally tasty. Both groups lost about 4-5 lbs after 6 months. But both groups started to gain weight back soon after. In fact, the trajectory of weight loss is so identical, we simply have to show you the graph:
Note the p-value of 0.99, which indicates that the two trajectories are about as statistically indistinguishable as is mathematically possible.
We find this in study after study. Meta-analysis also finds that low-glycemic diets don’t do any better than other diets when it comes to weight loss. When the reviewers pick out the studies that show the best performance for low-glycemic diets, they still find a diﬀerence of only 4 lbs (1.8 kg). If that’s a success, we have to wonder what failure would look like.
2.3.3 Future Dietary Explanations
Eating fewer calories will lead most people to lose a couple pounds, and it doesn’t really matter what calories they restrict. Cutting back on fat works about as well as cutting back on carbs. In both cases, a couple pounds isn’t enough to explain the obesity epidemic.
Over the past 50 years, medical science has looked at diet from practically every angle. But none of these diet-based explanations have gone anywhere. People are still getting fatter. They got fatter over the last decade. And they got fatter over the decade before that. And the one before that. Every country in the world is growing more obese. And the trend has never once been reversed.
You could certainly cook up another diet-based explanation. But there’s no reason to expect that this explanation would do any better than any of the others.
It’s time to start looking for explanations outside the world of calories, macronutrients, and exercise. At this point, we should assume that the obesity epidemic isn’t caused by our diet.
Could it be a lifestyle difference? Possibly, but signs point against it. Smoking is more prevalent in Japan than among Japanese-Americans, yet Japanese-Americans have much higher rates of hypertension. Similarly, many hunter-gatherers are heavy smokers, including the Kitavans (76% of men and 80% of women) and the Bushmen of South Africa, but these societies have no sign of heart disease.
There is one theory of obesity which is almost entirely satisfying, based around the body’s ability to regulate its adiposity.
A house has a thermostat. The owner of the house sets the temperature to 72 degrees F. The thermostat detects the temperature of the house and takes action to drive the temperature to the set point of 72°F. If the house is too cold, the thermostat will turn on the furnace. If the house is too warm, the thermostat will turn on the air conditioning.
The human body has a lipostat (from the Greek lipos, meaning fat). Evolution and environmental factors set body fatness to some range — perhaps a BMI of around 23. The lipostat detects how much fat is stored and takes action to drive body fatness to the set point of a BMI of 23. If your body is too thin, the lipostat will drive you to eat more, exercise less, sleep more, and store more of what you eat as fat. If your body is too fat, the lipostat will turn on the air conditioning. Just kidding, the lipostat will drive you to eat less, move and fidget more, and store less of the food you eat as fat.
According to this theory, people become obese because something has gone wrong with the lipostat. If the owner of a house sets the thermostat to 120°F, the house will quickly become too hot, and it will stay that way until the set point is changed or the furnace explodes. Something similar is happening in obesity. The set point has been moved from a healthy and natural level of adiposity (BMI of about 23) to an unusually high level (BMI 30+), and all the regulatory systems of the body are working in concert to push adiposity to that level and keep it there.
The lipostat model is supported by more than a hundred years of evidence. By the 1970s, Dr. Michel Cabanac and collaborators were publishing papers in the journal Nature on what they called the “ponderostat” (pondero = weight). This was later revised to the adipostat (adipo = fat), and eventually, as we call it here, the lipostat.
Modern neuroscience and medical review articles (those are three separate links) overwhelmingly support this homeostatic explanation. In animals and humans, brain damage to the implicated areas leads to overeating and eventual obesity. These systems are well-understood enough that by targeting certain neurons you can cure or cause obesity in mice. While we don’t approve of destroying neurons in human brains with hyperspecific chemical techniques, the few weight-loss drugs approved by the FDA largely act on the brain (hopefully without destroying any neurons).
The lipostat explains why diet and exercise work a little, why they don’t work well enough to reverse obesity, and why even people who lose weight on diets generally end up gaining that weight right back.
In a house where the thermostat has been set to 120°F, there are a lot of things we can do to lower the temperature. We can open all the doors and windows. We can open the icebox. We can order mountains of dry ice oﬀof the internet. All of these things will lower the temperature of the house a little, but even with these measures, the house will still be hotter than the healthy temperature of 72ºF. The furnace will work double-time to push the temperature back up to 120ºF, if it’s not redlining already. And as soon as you relax any of your heat-dissipation measures, the temperature will go right back up to where it was before.
(We can also go down into the basement and hit the furnace with crowbars until it doesn’t work very well anymore. This is a pretty extreme solution and also, incidentally, why gastric bypass surgery works so great.)
When people intentionally overeat, as in the overfeeding studies we reviewed, they temporarily gain a little weight, but when they stop overeating, they quickly return to their original weight. When people intentionally undereat, as they do on a diet, they temporarily lose a little weight, but when they stop undereating they quickly return to their original weight. In fact, they usually return to near their original weight even if they keep undereating. The lipostat has a target weight and, when not actively opposed, it will push your body weight to that weight and do its best to keep it there.
There are many signals that the brain uses to measure how much fat the body is carrying. One of the most important is the hormone leptin, which is naturally produced by fat cells. Part of the action of the lipostat is making sure that leptin levels are kept within a desired range, which helps keep us at a desired weight.
Very rarely, people are born with a genetic mutation that makes it so their fat cells no longer produce leptin. The lipostat notices that it isn’t detecting any leptin, and assumes that the body has no fat stores at all, with predictable results. Usually these children are of normal birth weight, but from the first weeks of their lives, they are insatiably hungry. By age two, they weigh more than 50 pounds, and may be as high as 60% fat by weight. They have a truly incredible drive to eat:
. . . leptin-deficient children are nearly always hungry, and they almost always want to eat, even shortly after meals. Their appetite is so exaggerated that it’s almost impossible to put them on a diet: if their food is restricted, they find some way to eat, including retrieving stale morsels from the trash can and gnawing on fish sticks directly from the freezer. This is the desperation of starvation [. . . ] they become distressed if they’re out of sight of food, even briefly. If they don’t get food, they become combative, crying and demanding something to eat.
The lipostat account is extremely convincing. The only weakness in the theory is that it’s not clear what could cause the lipostat to be set to the wrong point. In leptin-deficient children, their body simply can’t detect that they are obese. But most people produce leptin just fine. What is it that throws this system so totally out of balance?
While the lipostat perspective does in a sense explain why people become obese (their lipostat is out of alignment), it’s not really a theory of the obesity epidemic, since it doesn’t explain why our lipostats began getting more and more out of balance around 1980.
Even advocates of the theory are perfectly willing to admit this. In The Hungry Brain, Stephen Guyenet writes:
Many researchers have tried to narrow down the mechanisms by which [diet] causes changes in the hypothalamus and obesity, and they have come up with a number of hypotheses with varying amounts of evidence to support them. Some researchers believe the low fiber content of the diet precipitates inflammation and obesity by its adverse effects on bacterial populations in the gut (the gut microbiota). Others propose that saturated fat is behind the effect, and unsaturated fats like olive oil are less fattening. Still others believe the harmful effects of overeating itself, including the inflammation caused by excess fat and sugar in the bloodstream and in cells, may affect the hypothalamus and gradually increase the set point. In the end, these mechanisms could all be working together to promote obesity. We don’t know all the details yet…
Guyenet favors a “food reward” explanation, where eating “highly rewarding food” causes a mild form of brain damage that turns up the set point of the lipostat. He’s even gone so far as to propose (as an April Fools joke) a collection of boring recipes called The Bland Food Cookbook.
You’ll notice that in all these theories, the factors that damage the lipostat are related to diet. But as we’ve just argued above, the persistent failure to find a solution in our diets strongly suggests that we should start looking elsewhere for the explanation.
2.6 What, Then?
We should start seriously considering other paradigms. If diet and exercise are out as explanations for the epidemic, what could possibly explain it? And what could possibly explain all of the other bizarre trends that we have observed?