In many people it is an insulin imbalance that leads to the physiological dysfunction that characterizes carbohydrate addiction. There are a range of models and explanations for overweight conditions in general (almost a dozen have been identified and described in research animals). In humans, we have found hyperinsulinemia to be the one that best explains the recurring craving and hunger and the body’s tendency to store fat that we have identified in our work with carbohydrate addicts.
Our research suggests that overweight may be better described as a symptom of an underlying disorder rather than the disorder itself. A variety of underlying biologically based imbalances can result from altered interactions between the factors involved. Precipitating factors may include the kinds of foods eaten, the frequency and quantities in which they are consumed, and less easily understood factors, like the body’s use of the foods due to inherited metabolic tendencies and the interactions and nature of neurotransmitters, enzymes, hormones, and hormone receptors.
We believe that, at least in part, all of these factors in a significant portion of the population may contribute to what we call glucose-transport disorder. In examining the dysfunctions characteristic of glucose-transport disorder, however, it is necessary to understand the basic workings of part of the body’s endocrine system—namely, the pancreas and its hormones.
The pancreas is an elongated, narrow organ approximately the length of the human hand. Located behind the stomach, the pancreas plays an essential role in controlling the fuel that is made available to the cells of the body. It manages this fuel through the release of three hormones—insulin, glucagon, and somatostatin.
After carbohydrates are consumed, the level of the basic fuel from which the cells of the body derive energy, the blood-sugar, glucose, begins to rise. The pancreas responds to the intake of carbohydrates by releasing insulin.
The insulin reaches the cells via the bloodstream. There it binds with receptor sites on the membranes of the cells, increasing their ability to “transport” the glucose from the blood to the interior of the cells themselves. This means the so-called insulin receptor sites located on the surface of the cells are activated. In that way, muscle and fat cells are stimulated to absorb the elevated levels of glucose through these “doors” in order to fuel their activities.
The insulin also facilitates conversion of glucose to glycogen and triglycerides for storage in the liver. A second pancreatic hormone is concerned with another stage of the glucose-glycogen cycle. That hormone, glucagon, is called upon to break down the stored glycogen when energy is required. It is also released into the bloodstream, and its action is effectively to raise the blood sugar level. The role of the third pancreatic hormone, somatostatin, is not yet fully understood, but it is thought to play a role in regulating the production and release of both the insulin and glucagon.
Insulin also acts directly on central nervous system regulators, serving as an intermediary to communicate the need to eat or stop eating. Insulin keys the action of substances that function as regulators— norepinephrine, serotonin, and mesolimbic dopamine—in a complex way that is still not fully understood. In normal functioning, that means insulin alerts the brain to release the neurotransmitter serotonin after each meal. This neurotransmitter then advises the cells of the body to no longer feel hungry.
In a normal person, glucose levels in the blood change in response to a wide variety of events but always remain within set limits. The pancreas of the normal eater releases just enough insulin to support the person’s nutritional needs; the receptors allow the cells to receive the right amount of glucose; the insulin helps convert the proper amount of blood glucose to glycogen. Changes in brain chemistry are also cued, leading to the sensation of satiety. The ratio of insulin to glucose changes gradually.
It is important to understand that in normal persons and carbohydrate addicts alike, the body releases insulin in two phases. Researchers call the nature of this process biphasic.
The first phase is termed the preload phase and begins within minutes of consuming carbohydrates. In this phase, the pancreas releases a fixed amount of insulin, regardless of how much carbohydrate is being consumed at the time. The amount of insulin is determined by previous carbohydrate intake—that is, by the amount of carbohydrate eaten in the preceding meals. It doesn’t seem to matter if the insulin release is cued at a given time by the consumption of one slice of cake or four—the initial phase of insulin release will be a set amount.
Conversely, the second phase of the insulin release, which takes place about seventy-five to ninety minutes after eating, is dependent upon how much carbohydrate is actually consumed at that meal. The body will recognize whether the first phase of insulin was sufficient to handle the carbohydrates consumed. This phase adjusts insulin production and release to the need of that particular meal. If the amount of carbohydrates consumed requires more than the initial quantity of insulin released, then a second measure of insulin will be issued.
In the carbohydrate addict, several of these biological processes fail to perform as they are supposed to, starting at the stage of the glucose transport. For reasons that are not yet clearly understood, sustained high levels of insulin in the blood (hyperinsulinemia) result. Studies have found that overweight people have much higher serum (in-the-blood) levels of insulin than do normal individuals.
High levels of insulin have been observed to coincide with a decrease in the number and sensitivity of insulin receptor sites in the muscle and adipose (fat) cells. This state, in which the cells are less able to absorb insulin and glucose, is called insulin resistance. Although the cause-and-effect relationship has not yet been clearly demonstrated, there is a clear suggestion of such a causal relationship between the decrease in insulin-binding sites and the occurrence of insulin resistance. This is reinforced by findings in many overweight people of changes in insulin responsiveness and sensitivity. In genetically obese mice, hyperinsulinemia has been observed to precede the occurrence of obesity.
That means that when too much insulin is in the blood for too long, the cells, paradoxically, change in such a way that less insulin is able to enter the cells and facilitate the entry of serum glucose to the tissues. Just as a floodgate may close as water levels rise, in an ever larger spiral, the longer the levels of insulin remain high, the greater is the decrease in the number of insulin receptor sites.
Taking an alternate route, the glucose, facilitated by the insulin, appears to be converted to glycogen and triglycerides via the liver. In animals, insulin injections have produced obesity, because insulin appears to stimulate fat synthesis, which means, in the simplest possible terms, overweight occurs in the presence of excess insulin.
Malfunctions extend to the brain chemistry as well. The sensation of being satisfied is never delivered, so the person continues to eat. The disordering effect of the excess insulin is such that a craving for carbohydrate foods results; an attempt is made to satisfy that craving, yet it seems impossible to do so. Thus, the pattern of sustained hyperinsulinemia contributes both to weight gain and continued carbohydrate hunger.
To make matters worse, this pattern can also mean a higher loading of insulin for the next episode of carbohydrate consumption. Researchers have demonstrated that overweight people have a significantly greater insulin release at the preload phase than do thin normals. That means that too much insulin will be released when carbohydrate foods are next consumed, continuing and exaggerating the biochemical cycle.
There are other ramifications of the excess insulin as well. Some of these are only now being studied and observed for the first time. Among these avenues of research are the effects of insulin on the metabolism of amino acids (the building blocks of proteins) and lipids (fats) in the blood, as well as on other intracellular processes.
In summary: the carbohydrate addict falls victim to this sequence of events:
Too much insulin is produced for the amount of carbohydrate that is consumed.
This excess of insulin results in a decrease in the number of receptors (with an accompanying decrease in removal of insulin and glucose from the blood).
Serotonin levels do not rise sufficiently to cause the sensation we identify as satisfaction; the carbohydrate addict does not get the signal to stop eating and continues to eat carbohydrate-rich foods.
Production of insulin rises with each subsequent carbohydrate intake.
Greater and more frequent quantities of carbohydrates may be consumed with no increase in satisfaction.
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