hat causes obesity? You might think it's simple: when calorie intake exceeds energy
usage, the excess energy builds up as fat. But this isn't really an explanation. Energy
intake is so important that the body fiercely tries to maintain a fixed weight by
controlling our metabolic rate and our level of hunger, which one of our most basic
instinctual drives. Physiologically, it should be impossible for a human to
become obese.
Yet it happens. There are many theories about why, but they all come down to four factors: genetics, diet, lifestyle, and disease. These factors interact with each other. Lifestyle and disease affect your diet, genetics affects disease and lifestyle, and so on. Disentangling these factors is not easy.
We can rule out some theories straight away. Although some researchers still consider stress to be a contributing factor to obesity[1], it's unlikely to be a major factor: some East Asian countries have high stress levels but low obesity. By forcing people to burn more energy, stress ought to make people thinner.
Regional differences in food quality are not a factor, either; grocery stores in low and high obesity areas of the USA all carry similar if not identical types of food. Pollution and smoking can probably also be ruled out, because they've been declining in the USA since the 1960s.
Regional differences in obesity in the United States (2013). Map created by National Community Mapping Institute, Meharry Medical College. Original data source: Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion.
Despite this, it's clear, as the map above shows, that obesity is not evenly distributed. Maybe, you might think, there are regional differences in diet, with people in the dark-brown regions eating more fat or more fried food. However, this doesn't explain the checkerboard pattern in some states, the yellow swath in the eastern slope of the Appalachians, or the sharp division in eastern and western North Carolina.
The distribution actually resembles the pattern of an endemic disease. The areas with most obesity are regions with low income and high temperature + humidity, or heat index: Tampa, New Orleans, Memphis, and Birmingham all have high average humidity + heat, while Los Angeles, Buffalo, Phoenix, and Denver have very low. In general, the dry areas of the West have less obesity than other regions.
The correlation isn't perfect—northern Alaska and Maine are glaring exceptions. Other factors, such as genetics, clearly also play a role.
The Grauniad theory
George Monbiot at a newspaper called the Guraniad, or something like that, claims it's those nasty capitalist food companies forcing people to eat too much:
They hire biddable scientists and thinktanks to confuse us about the causes of obesity. Above all, just as the tobacco companies did with smoking, they promote the idea that weight is a question of ‘personal responsibility.’ After spending billions on overriding our willpower, they blame us for failing to exercise it. . . . The thrill of disapproval chimes disastrously with industry propaganda. We delight in blaming the victims.
I'm not sure what he's talking about there. I never heard any food industry spokesman blaming an obese person for being fat. Besides, taking responsibility for one's life is clearly a good thing. What Monbiot really wants is more government regulation. But what if government interference is what caused the obesity crisis in the first place? Companies are selling what people say they want, and people want what they're told—by the government—will make them thinner. But the fact is, the government doesn't really know, and neither do scientists.
The idea that humans are mindless sheep who need the guidance of a wise and powerful government to save them from predatory corporations has little currency in science.
So let us assume that food manufacturers can be ruled out. What's left?
Other theories
Most individuals who succeed in losing weight eventually regain most of the lost weight. This tells us that the body has a setpoint which it vigorously defends. Most of the new theories try to explain why this happens. The idea is that even if some populations have a higher food intake and lower metabolic rates, there must be a biological reason for it. Here are some of the more influential recent theories:
Gut microbiota, aka intestinal bacteria. The overuse of antibiotics, especially in our food, may be changing the composition of our intestinal bacteria. For instance, people from Latin America living in the USA have an increased prevalence of diabetes and obesity[3]. According to this theory, geographical differences in obesity correspond to regional differences in gut microbiota.
Genetic and epigenetic factors. Scientists have found connections between obesity and PPARg, or peroxisome proliferator-activated receptor gamma[4], Wnt/beta-catenin signaling[5], and single-nucleotide polymorphisms, or SNPs. Over 80 SNPs are associated with type 2 diabetes. For example, TCF7L2 is associated with less weight loss during dieting. A low frequency missense mutation in LGR4, a Wnt-FZD-LRP5/6 coreceptor, may increase obesity risk.
These genetic mutations could tip the balance from brown adipose tissues, which burn fat to produce heat, to white adipocytes, which serve mainly as fat reservoirs. However, genetic mutations for obesity are found in only a small percentage of the population.
Carbohydrates. A current fad is the idea that carbohydrates, not dietary fat, cause obesity. In a recent meta-analysis[2] it was concluded that this too is a myth that's not supported by evidence.
Inflammation. Intestinal bacteria produce lipopolysaccharides and other substances that can lead to low-grade inflammation. This is called endotoxemia, and it can damage the gut barrier function. Perhaps this can affect hunger signaling in the brain. Surprisingly, there's a lot of evidence that metabolic syndrome (abdominal obesity, high LDL, etc.) may be caused by inflammation.
Leptin. Leptin is a hormone made by adipocytes that tells the hypothalamus to inhibit hunger. A deficiency in leptin causes hyperphagia and obesity in both humans and animals, but there is no evidence that human obesity is due to a deficiency in leptin.
There are many other theories, such as imbalances between saturated and unsaturated fat, sedentary lifestyle, pollutants such as organochlorine pesticides and polychlorinated biphenyls, which accumulate in adipose tissue[1], and even lack of caffeine[6]. The short answer is that nobody really knows.
Some popular theories, such as that obesity is an evolutionary trade-off to protect against starvation or even epidemics of diseases like tuberculosis, are still around, but in general they're regarded as speculative. Most biologists seem to have the view that, as one author put it, obesity is the disease and overeating is the symptom.
The Endocrine Society released a statement in 2017 [7] basically saying that the cause of obesity is a mystery. They wrote
Although there are many interventions that can cause obesity in an experimental setting, the key question is whether they do cause obesity in a naturalistic environment. . . . Growing evidence indicates that obesity pathogenesis involves processes far more complex than passive accumulation of excess calories. We need to elucidate the mechanisms underlying this upward setting or ‘resetting’ of the defended level of body-fat mass, whether inherited or acquired.
Food quality
Just looking at the food in our grocery stores is enough to make one feel anorexic. Beef has every trace of fat carefully shaved off. Pork chops have only the tiniest sliver of fat. Fat-free milk and fat-and-salt-free potato chips sit in plump, nitrogen-filled, ultraviolet-absorbing metallized bags on our shelves. The result: all of it tastes like airplane food. And good luck finding any soda in the USA that contains any actual sugar.
Back in the 1970s, before the obesity epidemic started, that wasn't the case. Beef and pork were sold much as our ancestors saw it: with big chunks of fat around the outside. I had occasion to find a sample of fat-containing beef last month. It was every bit as tasty as the beef we used to get in the 70s, yet I found myself eating much less of it.
Could our attempts to fight fat actually be causing the obesity crisis? In the past, dietary fat was blamed for obesity. But fat has now been almost completely eliminated from our grocery stores and obesity continues to increase. It was one of the biggest experiments ever conducted on humans, and the results are now in: it does not work.
It's well established that lack of energy-producing nutrients leads to feelings of low energy. The body adapts by cutting energy expenditure. If you deprive the body of nutrients, it continues to signal that it needs more until it gets enough.
There's a clue there: we need to eat fat, which is why we're programmed to think it tastes good. Once we get what the body requires, it signals that we've had enough. Without those signals, which good quality food would provide, we just keep eating and eating.
Just keep in mind the four food groups: salt, nitrites, sugar and caffeine.
1. Tomiyama AJ (2018). Stress and Obesity. Annu Rev Psychol. 2018 Jun 21. doi: 10.1146/annurev-psych-010418-102936 Abstract
2. Sartorius K, Sartorius B, Madiba TE, Stefan C. (2018). Does high-carbohydrate intake lead to increased risk of obesity? A systematic review and meta-analysis. BMJ Open. 2018 Feb 8;8(2):e018449. doi: 10.1136/bmjopen-2017-018449. Abstract
3. Elena RM, Gabriela GD, Arnulfod GC, Enrique CA. (2018). Studying the Gut Microbiome of Latin America and Hispanic/Latino populations. Insight into Obesity and Diabetes. Systematic Review. Curr Diabetes Rev. 2018 Jul 30. doi: 10.2174/1573399814666180730124817. Abstract
4. Huang Q, Ma C, Chen L, Luo D, Chen R, Liang F. (2018). Mechanistic Insights Into the Interaction Between Transcription Factors and Epigenetic Modifications and the Contribution to the Development of Obesity. Front Endocrinol (Lausanne). 2018 Jul 6;9:370. doi: 10.3389/fendo.2018.00370. Abstract
5. Chen N, Wang J. (2018). Wnt/β-Catenin Signaling and Obesity. Front Physiol. 2018 Jul 17;9:792. doi: 10.3389/fphys.2018.00792. Abstract
6. Wu L, Meng J, Shen Q, Zhang Y, Pan S, Chen Z, Zhu LQ, Lu Y, Huang Y, Zhang G. Caffeine inhibits hypothalamic A1R to excite oxytocin neuron and ameliorate dietary obesity in mice. Nat Commun. 2017 Jun 27;8:15904. doi: 10.1038/ncomms15904. Abstract
7. Schwartz MW, Seeley RJ, Zeltser LM, Drewnowski A, Ravussin E, Redman LM, Leibel RL (2017). Obesity Pathogenesis: An Endocrine Society Scientific Statement Endocr Rev. 2017 Aug 1; 38(4): 267–296. Abstract
aug 16 2018, 5:42 am; last edited aug 18, 2018, 4:20 am
