Don't lose your head over a diet - Toronto Sun

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The large majority of diets are ineffective because they cause an intense feeling of hunger that discourages and frustrates those looking to lose weight. A recent study has shown that this hunger is provoked by the destruction of certain neurons involved in controlling appetite.

Obesity and weight gain tied to excessive calorie intake is often the culprit behind many chronic illnesses that affect portions of the population, particularly type 2 diabetes, cardiovascular disease and several types of cancer. Even if we have a lot of hope for medicines that could cure these diseases in the future, we can't forget that a simple reduction in body weight could have a major impact on the incidence of these diseases and save many lives.

Over the years, an incalculable number of diets have been publicized to help people looking to shed pounds.

In theory, the principle is simple: because weight gain is tied to food intake, the solution is to reduce caloric intake. In reality, the situation is not nearly so cut-and-dried: the body sees this lack of calories as a signal of difficult conditions and therefore lowers the metabolism to make up for the lack of food.

These hypocaloric diets also lead to an intense sensation of hunger that can be suppressed in the short-term, but becomes intolerable over time. Consequently, the enthusiasm of people who lose a few pounds quickly vanishes when the pounds stop falling off. Not only are these people hungry, but they aren't losing the weight they were promised. That's why it's pretty normal for people to give up on these diets, and the pounds come back on.

Another danger associated with these diets is that it can, over the long-term, destroy our great relationship with food: the act of eating is no longer pleasurable, and instead is just seen as a threat to our weight. It's an activity that we can no longer take part in without feeling guilty.

A recent study showed that the hunger sensation associated with food deprivation is due to a physiological disruption of the process involved in appetite regulation (1). Researchers from New York found that a reduction in food intake caused significant damage to certain neurons located in the hypothalamus. As a response to the lack of calories, these neurons begin to digest themselves, meaning they feed off their own energy, which ultimately leads to their destruction. It's like cellular cannibalism.

Because these neurons play a key role in appetite control, their destruction causes various disruptions, most notably the production of certain peptides involved in the stimulation of appetite. Being hungry while on a diet is therefore not the result of a lack of self-control, but a physiological response from the body to an abnormal situation which is interpreted as a threat to the body's integrity.

These observations offer a scientific explanation for what people who have dieted know from experience: there is no miracle solution to lose weight, especially through diets that cause a drastic drop in calorie intake. The hunger always beats us, regardless of how committed we might be.

The only realistic way to maintain a healthy weight is to change our lifestyle habits to adopt certain simple behaviours that could have an enormous difference. Here are some suggestions:

- Eat slowly to give your body the time to control how full it feels.

- Eat low-calorie foods that take up a lot of stomach space without containing too much energy. Good examples are vegetables and greens.

- Adopt a defensive approach to the omnipresence of junk food in our environment: snacks, pop, fast-food, etc. are not daily foods, but rather, occasional treats.

- Enjoy whole grains: the quick rise of insulin caused by foods with refined flour causes the creation of fat.

- Finally, be active! Physical activity improves the general working condition of the metabolism and allows the body to better manage the calories it takes in.

(1) Kaushik et al. Autophagy in hypothalamic AgRP neurons regulates food intake and energy balance. Cell Metab. 2011 ; 14 : 173-183.

12 Sep, 2011

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