Continuing my inquiry into this matter, one question that hasn’t been satisfactorily answered is why has the obesity rate shot up in the past few decades? As I’ve made plain in previous posts, variation in obesity between individuals within a group at any given time is largely heritable, as is a good portion of the variation between groups. But, the variation over time – particularly the short timeframes seen over the last few decades couldn’t be due to genetic forces, since evolution doesn’t proceed that quickly. Something(s) in the environment must have changed. But what? Pinning these factors down has been an elusive quest, but I wanted to take a look at where the evidence stands. So I did a quick look into the matter, and this is what I found.
Here’s a graph of the U.S. obesity rate. We a fairly sharp rise beginning around 1980ish.
Of all the explanations for this pattern, by far the simplest explanation is that we’re just eating more. And indeed, that is the explanation pursued by Stephan Guyenet in his post Seduced by Food. Here is the same graph with calorie intake over that time superimposed on it:
So it would seem there it is: we are apparently eating more. But if so, then why? Advocates of particular diets, particularly low-carb and “paleo” diets, like to blame particular nutrients. At first glance, sugar, particularly fructose, seems a prime candidate:
Rates of sugar consumption seems to track the obesity rate. One might naively concluded that that’s the culprit. However, what if sugar was only one ingredient in a larger pie, so to speak?
What if consumption of many things increased, of which sugar is only one? Guyenet explains:
The reward system does the same thing with foods/beverages that contain drugs, such as coffee and beer, gradually making bitter fluids palatable and then delicious. Eventually, you may go out of your way to purchase the cheese or beer at the grocery store, and maybe you’ll consume cheese or beer even if you aren’t hungry or thirsty, simply because you like it. This is an example of the reward system reinforcing and motivating behaviors related to foods it considers desirable. What does the reward system consider desirable? Calorie density, fat, starch, sugar, salt, free glutamate (umami), certain textures (easily chewed, soft or crunchy, solid fat), certain flavors, an absence of bitterness, food variety, and drugs such as alcohol and caffeine. Our brains are highly attuned to these qualities because they’re all elements of nutritious, calorie-dense foods that would have sustained our ancestors in a natural environment, but today, the exaggerated combinations of these qualities used by processed food manufacturers, chefs and sometimes even home cooks overstimulate our natural reward pathways (19). Commercial foods are professionally designed to maximize reward, because reward is precisely what keeps you coming back for more. Processed junk foods such as ice cream, fast food, sweetened soda, cookies, cake, candy, pizza and deep fried foods are all archetypal hyper-rewarding foods.
Palatability is a related concept—it’s determined in part by inborn preferences (e.g., a taste for sugar and energy dense foods), and in part by the reward system (acquired tastes). Palatability is governed by the hedonic system in the brain, which is closely integrated with the reward system. Imagine yourself sitting at the dinner table, stuffed after a large meal. Then the cake and ice cream appear, and suddenly you have enough room left for another 250 calories of food. Would you have eaten a large, unseasoned baked potato (250 calories) if someone had put one in front of you at that point? Foods that stimulate the hedonic system have a well known ability to increase food intake, and this effect can be replicated using drugs that activate these circuits directly (20). The reward system is what motivates you to get food and put it to your lips, every time you eat. When scientists shut it down in mice, they stop seeking food, even though they’ll still eat if it’s put into their mouths (21). The hedonic system influences how much you eat once you begin a meal (22). Together, reward and hedonic circuitry in the brain determine in large part how often you seek food, what foods you select, and how much you eat at a sitting.
Reward and hedonic systems, if stimulated in the right way by food or drugs, can increase food intake and body fatness. The marijuana ‘munchies’ (whose existence have been confirmed by science) are a good example of what happens when they’re chemically stimulated via the CB1 cannabinoid receptor in the brain (23). One of the most effective weight loss drugs ever developed, Rimonabant, is basically ‘reverse marijuana’, blocking the very same CB1 receptor that marijuana activates. Although it clearly reduces food intake and body fatness, it has failed to gain FDA approval because of negative psychological side effects (big surprise).
The ability of reward and palatability to influence food intake and body weight is mediated by connections between reward/hedonic and energy homeostasis systems. For example, if you haven’t eaten in a while, your brain detects declining energy stores and acts to increase food intake. It does this by increasing your motivation to obtain food, and your enjoyment of food once you obtain it— known as ‘hunger’, this sensation is caused in large part by energy homeostasis systems activating reward and hedonic systems. But the connection goes both ways. Reward and hedonic systems also influence energy homeostasis systems, such that excessively rewarding/palatable food can increase food intake and the level of body fat that’s ‘defended’ by the brain (24, 25, 26, 27). According to findings from my own research group (lab of Michael W. Schwartz) and others, the hypothalamus can also develop inflammation and chronic cellular damage that likely contributes to the defense of a higher fat mass as well, contributing to fat gain and making fat loss more difficult (28, 29), but the reason for this is not yet clear.
Addiction is what happens when the reward system is over-stimulated by drugs, sex, food or other high-reward stimuli. In susceptible people (about 3 percent of the US population), highly palatable/rewarding foods are quite literally addictive, leading to binge eating behavior. For the rest of us, these foods may not literally be addictive, but they do often drive us to eat them more than we think we should, despite negative consequences to our weight and health.
“Addiction.” Guyenet is being too restrictive in his use of the word, since we are all addicts (otherwise behavioral genetics wouldn’t work); the declaration of something as an addiction is a rather arbitrary matter that is more related to social acceptability/desirability than to any biological/neurological fact (for example, no one criticizes the fact that people in high latitude civilizations seem to like to work and often need to work, ala Greg Cochran and Henry Harpending; well a few people do, and I know some of them… 😉 ).
In short, apparently, we’re eating more of a lot of stuff – not just sugar – and perhaps this is what is making us fat. And this is because of the market economy, which has made food suppliers superbly skilled at feeding our cravings and ensuring that we continue to crave their products.
Guyenet’s blog provides plenty of visual examples:
For this reason, I believe obesity is here to stay. People buy junk food and stuff themselves with it because they like it. And junk food makers continue to make it because it’s what we buy – what we want to buy. And it’s made so tgar we can’t get enough of it. In many ways, this is perhaps one of the great markers of modernity: gone are the days when food was limited, bland, and uncertain. Now every edible delight one can desire can be had. The downside is that some of us become fat.
How does heredity play into this? Well, heredity influences both our susceptibility to indulging (and overindulging) in food (through our taste and through the psychological reward we get from eating certain foods) and through our the level of body fat our bodies and brains “defend”:
Over the ensuing century and a half, researchers gradually uncovered a network of circuits in the hypothalamus dedicated to maintaining the stability (homeostasis) of body fat stores, by regulating food intake, energy expenditure, and the deposition of energy in fat tissue. This research culminated in the discovery of an extraordinary hormone called leptin in 1994. Produced by fat tissue in proportion to its mass, leptin enters the circulation and acts in the hypothalamus to regulate body fat stores. If you consistently restrict food intake, fat mass declines and so does leptin, and this signals the hypothalamus to stimulate hunger and make the body use calories more efficiently, in an attempt to regain lost body fat (4). Conversely, if you consistently overeat, the increase in fat mass and leptin suppresses appetite and increases calorie use until body fat stores have declined back to baseline (5, 6). Leptin and a few other hormones are part of a negative feedback loop that acts unconsciously to keep fat mass in a specific range, sort of like a thermostat does for temperature (7, 8). This is called the ‘energy homeostasis system’.
So if we have this built-in system to regulate body fatness, how does anyone become obese? Some researchers believe the energy homeostasis system defends against fat loss more effectively than fat gain. However, most obese people regulate their body fat just fine, but their brains ‘defend’ it at a higher level than a lean person. Going back to the thermostat analogy, in obese people it’s like the ‘temperature’ has been gradually turned up. That’s why it’s so hard to maintain weight loss—when body fat stores decline, the brain thinks it’s starving even if fat mass remains high—and it acts to regain the lost fat.
That last point is primarily why diets don’t work for most people. After “unnaturally” restricting food intake, whether it be the composition or the quantity or both (at least, in a way that has become unnatural in today’s world), appetite doesn’t diminish and indeed often ramps up in an effort to restore the lost body fat.
In reality, almost any diet will generally cause its adherent to lose weight – if you can stick to it.The primary reason for diet failure is inability to stick to the diet (this includes low-carb and “paleo” diets). Guyenet discusses this:
Diet trials have shown that a ‘simple’ diet, low in palatability and reward value, reduces hunger and causes fat loss in obese humans and animals, apparently by lowering the ‘defended’ level of fat mass (30, 31, 32, 33). This may be a reason why virtually any diet in which food choices are restricted (e.g., Paleo, vegan, fruitarian), including diametrically opposed approaches like low-fat and low-carbohydrate diets, can reduce food intake and body fatness in clinical trials. As stated by Nora Volkow, director of the National Institute on Drug Abuse, “The common denominator of such diets is that neither allows consumption of the very caloric and seductive foods that combine high fat with high carbohydrates” (34). Hyper-rewarding/palatable foods—candy, chocolate, ice cream, chips, cookies, cakes, fast food, sweetened beverages and pizza—are uniquely fattening and should be the first foods to go in any fat loss attempt. Some people will benefit from further simplifying the diet.
The bottom line is that any diet requires discipline – indeed, an almost inhuman amount of disciple (especially for certain people). Diets are most successful amongst individuals willing to make considerable lifestyle changes, being mindful of what they’re eating at all times, and for the rest of their lives. That is, individuals with certain personality traits, particularly high on conscientiousness and low on neuroticism (and generally, higher in IQ) These individuals are highly unusual. Most people are quite incapable of living this way for the long term.
Long-term behavior modification, which would be required for successful weight loss for overweight individuals, is a central point of Daniel Callahan’s idea that obese people should be “shamed” into losing weight. Callahan’s thesis is that society is too permissive of overweight people and that is why they unable to lose weight. Numerous commenters have explained why he is likely wrong. One of his largest pieces of evidence is a study in which a treatment group received dietary guidance over two years and achieved (slightly) better weight loss than a control group that received no such counseling. Callahan believes that this is evidence overweight people can achieve permanent weight loss if they are given proper incentives.
The flaw in this idea should be obvious: there is no way to perform population-wide “counseling” necessary to achieve this effect; Callahan’s hopes are unrealistic.
It’s also worth noting that Callahan’s prime example, the decline of smoking, declines just as obesity was on the incline:
Shaming smoking didn’t get people to give up on their disgusting habits; it just caused them to trade one vice for another.
Of course, as we saw in my earlier posts, obesity is hardly everybody’s problem – even in the developed world. In the West, it’s primarily an Anglo/Celtic/Germanic problem (also a Latin American problem). Southern and Eastern Europeans seem much less affected, particularly the French. As well, it’s barely a problem in East Asia. In my previous post, I suggested genetic factors were at least partly to blame for this, and with what I’ve discussed in this post, I’m free to speculate on which genetic factors may be at play. The most obvious is metabolism: likely, these groups “defend” much lower levels of body fat. The others are behavioral, both on an individual and on a cultural level. On an individual level, taste, impulsivity, and palatability (as defined above) likely vary between groups. Perhaps the French, for example, are much less susceptible to the excesses of highly “palatable” food than say the Scots are.
On a cultural level, perhaps the collective attitudes and tastes prevents the food-industrial complex that feeds Anglos highly palatable foods from becoming established in these countries. This may explain the difference we see between France and Quebec, for example.
In any case, the existence of the food-industrial complex – one which supplies Westerners with highly palatable foods – means that it’s foolish to expect any meaningful reduction in obesity rates. The system would need to be dismantled – such that highly palatable foods were rendered scarce commodities – for reductions in obesity rates to take place. In a market economy, this prospect an exceedingly unlikely one.
Obesity may simply be a fact of life we need to accept in the modern world.
So if obesity is here to stay, what does this mean? This brings us to the key issue associated with obesity: health. Obesity is blamed for the poor health of many individuals in Anglo countries. As we saw in my previous post, the association between obesity and heart disease, while present, is weaker than we might believe. Furthermore, it’s unclear that lowering the obesity rate – even if that were possible – would improve cardiovascular outcomes.
For some food for thought, take a look at this:
Deaths from cardiovascular disease actually peaked during the Baby Boom years and have been declining ever since, in fact decline as obesity rates have risen. In short CVD is becoming less of a problem, not more. Surely, much of that is due to advances in medicine:
While there is some inquiry into the matter, it is clear that the link between obesity and health is even more tenuous than we’ve been led to believe, especially when you compare the CVD incidence map to the map of obesity:
There may not be much we can realistically do about obesity, and its causes may ultimately be pretty simple (genetics, too much tasty food), but yet nonetheless apparently intractable. But, that may be OK. The impact on health is not as severe as we might imagine. And despite the alarm of the term “obesity epidemic“, it may turn out that concern about its effects are primarily aesthetic ones. Some people may see that as itself a cause for alarm, but (if you will excuse the pun) perhaps we have bigger things to worry about.