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Contrary to widespread belief, the energy factor is secondary (which does not mean that it is
to be disregarded) to weight gain. Epidemiological studies show that there is no correlation
between calorie intake and obesity. There is even proof to the fact that the contrary is true in
many cases. Since 1960, the daily average caloric intake in Western countries has decreased
by approximately 35%.Notwithstanding, during the same period obesity has jumped by
400%.
For further information on the lack of scientific conceptualization behind the calorie theory
The functional cause for gaining weight is hyperinsulinisme /high blood sugar
levels
When we eat carbohydrates / glucidic foods (bread, pâte, potatoes, fruit, sugar…) they are
transformed into glucose. Glucose passes our intestinal wall and goes into our bloodstream.
This provokes glycemia peaks; increases in blood sugar levels which on an empty stomach
are approximately 1g par liter of blood. Glycemia triggers insulin secretion which is what
sends excess glucose into our bloodstream so that it may be stored in our liver and muscular
tissue. This reverses glycemia to its original levels.
In some people, however, insulin response is out of proportion with regards to glycemia. This
excessive insulin secretion is what is known as hyperinsulinism.
For the past 25 years, numerous scientific studies have shown that hyperinsulinismis always
tied to excess weight and à fortiori to obesity. Medical researcher B. Jeanrenaud has
described this process quite well: "In all cases of obseity, regardless of species and
mechanism, hyperinsulinism is always present, and this hyperinsulinism is directly
proportional to Body Mass Index (BMI) which measures the degree of excess weight." He
adds that, "In animals, excess weight can be provoked by injecting insulin. Excess weight is
reversed when the treatment is stopped."
Excess insulin results in weight gain and, conversely, reduced insulin results in weight loss.
Since the beginning of the 1980s, proof has been given to the fact that the 980 carbohydrates
which fall into the same category (two complex starches like for example lentil and potatoes)
can contain the same amount of calories and yet provoke totally different blood sugar levels,
possibly twice to three times as high from one to the other.
In order to reflect how our bodies really respond to carbohydrates, carbs have been ranked on
a scale according to their potential to raise blood sugar levels. Carbs with low GIs are those
that provoke low blood sugar levels whereas carbs that provoke high sugar levels are ranked
in the high GI category.
Insulin resistance
A person who occasionally consumes one or more high-GI carbs will secrete the insulin
required to lower blood sugar levels. However, when a person has the habit of consuming
high-GI carbs, his body generates insulin resistance (also known as low insulin sensibility).
Glucose, in effect, despite inusulin secretion, will tend to stay in this person's bloodstream.
This condition is known as the insulin resistance syndrome and it is particularly marked in
cases of Type II diabetes.
What happens is that insulin receptors cease to function adequately and gluco--dependent cell
tissues fail to recognize the presence of insulin. High sugar levels settle in as glucose builds
up in our bloodstream instead of going into the cells. As a result of this inertia, our organism
becomes « impatient » and orders our pancreas to secrete more insulin, that which only
contributes to aggravating hyperinsulinism. This then becomes a vicious circle where
hyperinsulinism ensues in insulinoresistance.
As remarked by numerous authors, one of the essential properties of insulin is that it acts on
fatty metabolism. This is known as lipogenesis.
The right question to ask would be what would have become these fatty acids if they had not
been stored through lipogenesis. The answer is simple, although surprising: if they had not
been activated by lipoproteine lipase (because of insulin), these fatty acids wouls simply have
been burned by our organism which, under these circumstances, tends to adjust metabolic
performances in an adequate manner.
As we can see, lipogenesis is the metabolic process which results in fat reserves, and so, in
gaining weight. Lipolysis, is exactly the opposite: it is the metabolic process which results in
freeing fats, and so, in losing weight.
Our organism finds itself in a situation that forces it to seek fat in fat cells les cellules
graisseuses (adypocites) to use as carburant, thus reducing their volume. In order for this to
work, insulin has to be low. The mechanism is as follows: low levels of insulin activate the
triglyceride-lipase enzyme, which is responsible for evicting fatty acids from adipose tissues
(adypocites) by bringing them into our bloodstream so that they can be used as carburant. Our
organism will then try to use them (burn them) by modifying its energetic performance,
according to its needs.
As a conclusion, we can say that insulin is what catalyzes weight gaining. Thus, in order to
lose weight, we have to control insulin levels by trying to keep them as low as possible. To
achieve this, we should try to keep after-meal (post-prandial) glycemia peaks at their lowest.
The only solution will naturally be to eat only low, and preferably very low, GI carbs.
Experience indicates that, by eating solely low (35 or lower) GI carbs, insulinic response
stays low enough to allow our weight-losing enzyme —triglyceride-lipase— to work and to
thus provoke a weight-losing process.
The key factor to gaining weight is, as we have just seen, consuming high GI
carbohydrates
The lipogenesis phenomenon, described above, explains why and how. Likewise,
understanding the lipolysis phenomenon makes us aware of the fact that if we want to lose
weight, we have to eat low GI carbohydrates.
We realize, however, that weight gain is not solely the result of storing the fats eaten in our
meals. Insulin also affects surplus glucose resulting from excessive consumption of high GI
carbohydrates.
For many years, nutritionists believed that glucose could not be converted into fat. This is
why they recommended diets rich in carbohydrates pretending that they did not make people
gain weight. Professor Walter WILLETT denounced this fact when he said, « by advising
people to eliminate fats from their diets and recommending that they eat carbohydrates,
nutritionists have contributed to spreading obesity.” Uniformed or recalcitrant nutritionists’
failure to advise their patients on which carbs to eat left people suffering from obesity to their
own devices and to their tendency to eat high-GI carbs. This made their bodies secrete more
insulin and generate greater amounts of surplus glucose which their bodies did not need and
which was eventually stored as fat.