If mobilization of energy in response to stress works so wonderfully, why should it make us sick in face of chronic psychological stress? For many of the same reasons that constantly running to the bank and drawing cash from the savings accounts is a foolish way to handle your money.
At the most basic level, it is inefficient. Every time we store energy away from circulation and then return it, we lose a fair chunk of potential energy. In effect, you are penalized if you activate the stress response too often. You wind up expending so much energy that you tire more readily. Finally, with enough stress, you begin to have problems with one type of diabetes called Type II diabetes. This takes some explaining
Diabetes
There are two types of diabetes—the first is Type I or juvenile or insulin-dependent diabetes. For reasons that are still not clear, the immune system decides that cells in the pancreas which secrete insulin are, in fact, foreign invaders and attacks them. This leaves a person with very litde insulin and, therefore, little availability to promote the uptake of glucose (and indirectly fatty acids) into target cells. Big trouble—the cells are starving!
In addition, there is all that glucose and fatty acid circulating in the bloodstream—like gangsters with no place to go and they show their hand—blood vessels in kidneys gum up, arteries get atherosclerotic plaque and make it impossible for oxygen and glucose to be delivered to the tissues causing little strokes and chronic pain. They also link proteins together in the eyes to form cataracts. Bad news all around.
If you have insulin-dependent diabetes, you never want your insulin level to get too low. But you don’t want to take too much insulin as this deprives the brain of energy, damaging the nerves. The better the metabolic control (correct levels of insulin and food), the longer the life expectancy for diabetics.
In Type II or non-insulin-dependent or adult-onset diabetes, the trouble is not too little insulin, but the failure of the cells to respond to insulin. Another name for this is insulin-resistant diabetes. This disease arises with the tendency of many people to put on weight as they age. It is a disease of inactivity and fat surplus. With enough fat stored away, the fat cells essentially get full. Once you are an adolescent, the number of fat cells you have is fixed; so if you put on weight the fat cells are bloated.
Yet another heavy meal, a burst of insulin trying to promote more fat storage by the fat cells, and the fat cells refuse—’tough luck, I don’t care if you are insulin; I am completely full’. The fat cells become less responsive to insulin. You may be confused at this time—if insulin regulates glucose uptake, why does it influence the amount of fat being stored in fat cells? For immensely complex and dense reasons (wet-towel-around-the head explanations), the storage of free fatty acids and glycerol as triglycerides requires glucose uptake. This decreased insulin sensitivity of the cells is mostly due to cells losing their specialized receptors for insulin, in response to the constant insulin signal.1 This phenomenon is very much like that of teenage children who tune out the constant nagging from their parents!
Do the cells now starve? Of course not; the amount of fat stored in them was the source of the trouble in the first place. They get into trouble because of all that circulating glucose and fatty acids that are damaging the kidneys, blood vessels and the eyes.
How does stress affect this process? First, hormones of the stress response cause even more glucose and fatty acids to be mobilized in the bloodstream as we saw earlier.
Another subtler problem occurs with chronic stress. When something stressful happens, the brain directs the pancreas to stop producing insulin. It also seems that the brain does not quite trust the pancreas; so in a second step, the stress-response hormones act on fat cells to make them less sensitive to insulin. Stress promotes insulin resistance. When people get into this state because they are taking large amounts of synthetic steroids, they have succumbed to ‘steroid diabetes’.
Suppose you are in your mid-forties, overweight and just on the edge of insulin resistance. Along comes a period of chronic stress with those hormones repeatedly telling the cells that it is a great idea to be insulin resistant. Enough of this and you get diabetes!
For convenience, physicians usually use an absolute cutoff to decide when someone has insulin-resistant diabetes. Once you demonstrate a certain level of glucose during a glucose tolerance test, you get labelled as a diabetic. In reality, diabetes represents a continuum—there is no hard and fast point of insulin resistance at which the body suddenly gets into trouble. Instead, for every bit of insulin resistance there is a bit more of the risk of the type of damage discussed. People who are genetically susceptible have some sort of metabolic vulnerability, such that stress disrupts their metabolism to an atypical extent long before they become diabetic.
Diabetes more than doubles mortality and nearly triples the rate of heart diseases in men. It is one of the leading causes of blindness and in the top 10 causes of death. Unfortunately, the prevalence of Type II diabetes is increasing and awareness of the causes and remedies is very poor in the general population.