What makes you obese

Body fat throughout childhood in healthy Danish children: agreement of BMI, waist circumference, skinfolds with dual X-ray absorptiometry.

Comparison of body fatness measurements by BMI and skinfolds vs dual energy X-ray absorptiometry and their relation to cardiovascular risk factors in adolescents. Comparison of dual-energy x-ray absorptiometric and anthropometric measures of adiposity in relation to adiposity-related biologic factors. Association between general and central adiposity in childhood, and change in these, with cardiovascular risk factors in adolescence: prospective cohort study. BMJ , , p. Estimates of excess deaths associated with body mass index and other anthropometric variables.

Relation of body mass index and skinfold thicknesses to cardiovascular disease risk factors in children: the Bogalusa Heart Study. Comparison of bioelectrical impedance and BMI in predicting obesity-related medical conditions. Silver Spring , 14 3 , pp. Skip directly to site content Skip directly to page options Skip directly to A-Z link.

Section Navigation. In many cases, obesity is more to do with environmental factors, such as poor eating habits learned during childhood. However, if conditions such as these are properly diagnosed and treated, they should pose less of a barrier to weight loss. Certain medicines, including some corticosteroids , medications for epilepsy and diabetes , and some medications used to treat mental illness — including antidepressants and medicines for schizophrenia — can contribute to weight gain.

Weight gain can sometimes be a side effect of stopping smoking. Page last reviewed: 16 May Next review due: 16 May Obesity is generally caused by eating too much and moving too little. Calories The energy value of food is measured in units called calories. Poor diet Obesity does not happen overnight.

It develops gradually over time, as a result of poor diet and lifestyle choices, such as: eating large amounts of processed or fast food — that's high in fat and sugar drinking too much alcohol — alcohol contains a lot of calories, and people who drink heavily are often overweight eating out a lot — you may be tempted to also have a starter or dessert in a restaurant, and the food can be higher in fat and sugar eating larger portions than you need — you may be encouraged to eat too much if your friends or relatives are also eating large portions drinking too many sugary drinks — including soft drinks and fruit juice comfort eating — if you have low self-esteem or feel depressed, you may eat to make yourself feel better Unhealthy eating habits tend to run in families.

Lack of physical activity Lack of physical activity is another important factor related to obesity. Read more about the physical activity guidelines for adults. Genetics Some people claim there's no point trying to lose weight because "it runs in my family" or "it's in my genes".

Medical reasons In some cases, underlying medical conditions may contribute to weight gain. Thus, if we take in more calories than we expend or excrete, the excess has to be stored, which means that we get fatter and heavier. So far, so obvious. But this law tells us nothing about why we take in more calories than we expend, nor does it tell us why the excess gets stored as fat.

Specifically, why do fat cells accumulate fat molecules to excess? This is a biological question, not a physics one. Why are those fat molecules not metabolized instead to generate energy or heat? And why do fat cells take up excessive fat in some areas of the body but not others? Saying that they do so because excess calories are consumed is not a meaningful answer.

Answering these questions leads to consideration of the role that hormones—insulin, in particular—play in stimulating fat accumulation in different cells. Insulin is secreted in response to a type of carbohydrate called glucose. When the amount of glucose rises in the blood—as happens after eating a carbohydrate-rich meal—the pancreas secretes more insulin, which works to keep the blood glucose level from getting dangerously high. Insulin tells muscle, organ and even fat cells to take up the glucose and use it for fuel.

It also tells fat cells to store fat—including fat from the meal—for later use. As long as insulin levels remain high, fat cells retain fat, and the other cells preferentially burn glucose and not fat for energy. The main dietary sources of glucose are starches, grains and sugars.

In the absence of carbohydrates, the liver will synthesize glucose from protein. The more easily digestible the carbohydrates, the greater and quicker the rise in blood glucose. Fiber and fat in foods slow the process. Thus, a diet rich in refined grains and starches will prompt greater insulin secretion than a diet that is not.

Sugars—such as sucrose and high-fructose corn syrup—may play a key role because they also contain significant amounts of a carbohydrate called fructose, which is metabolized mostly by liver cells. The result, according to the hormone hypothesis, is an ever greater proportion of the day that insulin in the blood is elevated, causing fat to accumulate in fat cells rather than being used to fuel the body. As little as 10 or 20 calories stored as excess fat each day can lead over decades to obesity.

The hormone hypothesis suggests that the only way to prevent this downward spiral from happening, and to reverse it when it does, is to avoid the sugars and carbohydrates that work to raise insulin levels. Then the body will naturally tap its store of fat to burn for fuel. The switch from carbohydrate burning to fat burning, so the logic goes, might occur even if the total number of calories consumed remains unchanged.

Cells burn the fat because hormones are effectively telling them to do so; the body's energy expenditure increases as a result. To lose excess body fat, according to this view, carbohydrates must be restricted and replaced, ideally with fat, which does not stimulate insulin secretion. This alternative hypothesis of obesity implies that the ongoing worldwide epidemics of obesity and type 2 diabetes which stems to great extent from insulin resistance are largely driven by the grains and sugars in our diets.

It also implies that the first step in solving these crises is to avoid sugars and limit consumption of starchy vegetables and grains, not worrying about how much we are eating and exercising.

Forgotten History Conventional wisdom did not always favor the energy-imbalance hypothesis that prevails today. Until World War II, the leading authorities on obesity and most medical disciplines worked in Europe and had concluded that obesity was, like any other growth disorder, caused by a hormonal and regulatory defect. Something was amiss, they believed, with the hormones and enzymes that influence the storage of fat in fat cells. Gustav von Bergmann, a German internist, developed the original hypothesis more than a century ago.

The lipophilia concept vanished after World War II with the replacement of German with English as the scientific lingua franca. Meanwhile the technologies needed to understand the regulation of fat accumulation in fat cells and thus the biological basis of obesity—specifically, techniques to accurately measure fatty acids and hormone levels in the blood—were not invented until the late s.

By the mids it was clear that insulin was the primary hormone regulating fat accumulation, but by then obesity was effectively considered an eating disorder to be treated by inducing or coercing obese subjects to eat fewer calories.

Once studies linked the amount of cholesterol in the blood to the risk of heart disease and nutritionists targeted saturated fat as the primary dietary evil, authorities began recommending low-fat, high -carbohydrate diets.