There are various reasons why people are overweight. These include genetics (suggested by studies of twins), overeating, stopping smoking, alcohol consumption, lack of exercise, a change in life style, more energy intake than energy expenditure (taking into account resting metabolic expenditure), environmental factors, sodium retention, hidden food allergies, major depression/anxiety/other psychological, medical illness, medications, during and after pregnancy, cultural (perceptions on obesity), and socioeconomic factors.
In the US, 20 to 30% of children are either overweight or at risk of becoming so. Kids who weigh too much are at a greater risk of becoming heavy adults, are more likely to suffer from low-esteem and have a greater chance of developing health problems such as diabetes.
Set Point Theory
Obesity is not strictly the product of sloth and gluttony. Everybody has a weight that their body can defend and most people know what that weight is. You lose a little weight, but tend to bounce back to your original weight again and again. That weight is called the “set point”. Although weight is influenced by what and how much one eats, and by such things as exercise, ordinarily it will revert to its most comfortable level.
One thing that is not well recognized is the fact that weight loss itself is not a particularly difficult problem. If a human being is put on an 800 or 1000 calorie diet, they lose weight. There do not appear to be a large number of people who have undesirable responses to a 1000 calorie diet that prevents them from losing weight: the few claims that have been investigated have not held up to scrutiny. In other words, there are no people who are totally resistant to weight loss. However, the vast majority of humans are very resistant to the maintenance of a body weight below whatever their set point is.
A person’s set point is the approximate weight and fat percentage that their body settles into during adulthood. Body fat is actually regulated by the brain’s weight regulating mechanism in the hypothalamus. This mechanism chooses the amount of body fat it considers ideal for the body’s needs and then works tirelessly to maintain that level.
The regulating mechanism controls body weight in two critically important ways. First, it has a profound effect of the amount of food you eat. It is responsible for dramatically increasing or decreasing appetite to maintain the set point weight. As you lose weight, it signals hunger; as you gain weight, it reduces appetite. Second, the regulating mechanism can trigger the body’s systems to waste excess energy if you overeat or conserve energy if you don’t eat enough. Energy conservation may lead to muscle loss and a slow down of the endocrine system due to the body’s attempts to protect its fat stores for use in the future. In addition, less muscle mass means the body requires still fewer calories.
An individual’s set point is genetically determined. There are those who are able to eat anything and everything they desire and still maintain a low body fat percentage, but others who continually struggle with their genetic set point and constantly diet and exercise to lose weight. Often this weight loss is a loss of both muscle and fat tissue. Once they stop dieting, those who have battled fat loss incorrectly or are simply unable to maintain the proper lifestyle will inevitably return to their original body composition or gain additional body fat. The subsequent weight gain consists primarily of fat tissue.
If you go to a doctor and tell them you need to lose weight, the doctor is not likely to tell you that are at your set point, so there is not need to treat you. That thought usually has nothing to do with how people are treated. The diet industry also is not based primarily on medical complications, but cosmetics and profit.
One way to rationalize the treatment of obesity is to treat only individuals who have medical causes and complications. Treat the individual who has hypothyroidism, hyperlipidemia, gall bladder disease, or type II diabetes, to the point where the cause and risks are reduced. Don’t treat the obesity per se. Treat the cause or the body fat content until you relieve the metabolic consequences. It turns out that just a 10% body fat reduction can produce increases in insulin sensitivity and blood pressure reduction.
Leptin
Molecular biologists first identified leptin in 1994. Since then, the fat hormone has been the subject of intense speculation among scientists. Leptin has prompted research into eating disorders, obesity and diabetes. The obesity hormone leptin appears to reduce cravings for sweet foods by targeting taste receptors on the tongue. Therefore, it is possible that a lack of leptin, or the body’s failure to respond to the hormone due to defects in leptin receptors (leptin resistance), may contribute to the so called sweet tooth that affects so many.
Leptin, a hormone produced by fat cells, is involved in weight regulation. It is thought that the hormone signals the brain when fat cells are full, but exactly how the hormone controls weight is not entirely clear. Animals and humans without leptin, or with defective leptin receptors, become obese. As one becomes fatter, the body makes more leptin and the likelihood of leptin resistance increases . Men whose bodies produce more insulin also tend to have increased leptin levels.
Exercise decreases the amount of leptin in the blood of both overweight and normal weight individuals. Recent research shows that only 3 hours of exercise per week lowers leptin levels by about 10%. Exercise can lower the levels of leptin no matter how fat a person is. Lowering leptin levels reduces the risk of leptin resistance seen in obesity; raising leptin levels does not appear to be an effective weight loss mechanism in humans. However, trials have shown that large supplemental doses of leptin can result in some weight loss in obese individuals.
In short, leptin levels should be kept within the normal range: low levels can result in food cravings and higher levels tend to suppress appetite but are also associated with tissues becoming less sensitive to the hormone and contributing to craving and more weight gain. Exercise can lower leptin levels, but caution must be taken in some individuals that levels do not go too low. Researchers have long been busy searching for the key to safely control a person’s weight. It remains to be seen if they will ever be successful. Products like Leptoprin and Anorex do not contain leptin, though their high price would suggest otherwise.
Research on leptin levels indicate that once weight is lost, the key to maintaining the loss, in spite of increased calorie consumption, is exercise!
Ghrelin
The recently discovered “hunger hormone” called ghrelin is gaining a solid reputation for regulating how much food we eat and how much weight we gain. Pronounced (GRELL – in), it is produced mainly by the stomach, although it is also made in other organs, such as the intestines and the kidneys. Ghrelin has been dubbed the hunger hormone because in previous experiments people given the hormone became so ravenous, they ate markedly more than their usual food intake. So, increased ghrelin equals increased hunger.
Another study found that in slim people, ghrelin levels peaked right before a meal but rapidly declined soon afterwards. In contrast, levels of the hunger hormone were lower than average in obese individuals, but they remained steady before and after a meal, suggesting obese people might still feel hungry after eating.
Although scientists only identified ghrelin in 1999, more than 200 papers on the substance have already been published. Ghrelin acts to stimulate food intake but blood levels are reduced in obese patients suggesting that this mediator represents a key regulator of food intake. Metabolism 2002;87: pp.3997-4000, 4005-4008]
Nearly two-thirds of American women are either clinically “overweight” or “obese.” As women are more at risk for being overweight or obese than men, and women are at risk for gaining weight as they age, postmenopausal women are a particularly vulnerable population.