The danger of our ancient sugar cravings
The changes we see and feel that we collectively label “aging” are the result of complex biological processes occurring at the cellular level. One of these processes that increases with age is glycosylation, in which excess blood glucose (sugar) cannot get into the cells, where it would be used as energy, and attaches to molecules outside the cells instead.
A basic explanation of how type 2 diabetes develops also explains how glycosylation in general proceeds. For most of human history, getting enough food was difficult. When humans were hunter-gatherers, we had to work hard all the time to obtain enough calories to stay alive. We developed an efficient metabolism to extract the maximum amount of energy from small amounts of food. Sugars, which provided concentrated energy, were in short supply, so we developed cravings for them. When we were lucky enough to find, for instance, patches of wild berries, scarfing down every one in sight was smart; it was a behavior that helped the human species survive.
In the last 150 years or so, though, much of the world has exchanged the problem of too little food for the problem of too much food. We have too much of it all the time and most of us do not have to work hard physically to obtain it. This overabundance of food in the developed world is mismatched with a metabolism designed for food scarcity. When we give in to the mismatch and interpret our ancestral cravings as physiological hunger, we are likely to overeat and tax our systems in ways that cause dysfunctional adaptations.
Metabolism breaks everything down into glucose for energy, so this mismatch applies to eating too much in general, not just to consuming too much sugar. Insulin acts as a key that unlocks cells to let the glucose in. Overeating causes a sharp increase in blood sugar, and the pancreas answers with a sharp increase in insulin. If this is a person’s usual pattern over decades, it can result in insulin resistance. The extreme outcome of this pattern is type 2 diabetes.
Diabetes, with its detrimental effects on multiple physiological systems, is often viewed as a kind of accelerated aging. Glycosylation can disrupt the normal function of cells, and when it affects protein molecules, the resulting products are called advanced glycosylation end products (AGEs). The acronym fits because they actually age us; they have a pronounced role in diseases that increase with age.
If we look at those diseases as occurring along a spectrum rather than as either/or, we can understand how the process can rob us of wellness even if we never get to the point of having a particular disease. Consider its effects in the following systems:
Arteries: Glycosylation weakens the links between cells in the arterial walls and makes them more vulnerable to tears, which the body repairs by filling them with cholesterol. While this kind of repair is a vital function, arteries that are in a continual state of tear and repair are prone to atherosclerosis.
Eyes: When glucose attaches to protein molecules in the lens of the eye, it changes the lens cells from clear to cloudy in a process we know as cataract formation. Glycosolation can also occur in retinal blood vessels. In diabetic retinopathy, a leading cause of blindness, the vessels have become so fragile that they bleed chronically.
Alzheimer’s disease: Proteins damaged by glycosylation in the brain are implicated in plaque formation that is one of the markers of Alzheimer’s disease. In diabetes, high levels of insulin produced as the pancreas tries to keep up with high levels of blood glucose stimulates plaque buildup. Along with arterial damage resulting from high blood glucose over time, diabetes increases the risk of developing Alzheimer’s disease. In fact, many doctors and researchers now call it type 3 diabetes.
A tenet of successful aging is that lifestyle choices give us a great deal of control over much of what we used to accept as inevitable. Successful agers — those of us looking for a fountain of health, not a fountain of youth — know this and also know that “normal” is not optimal. Most doctors still view a fasting blood sugar below 100 milligrams per deciliter as normal, but research shows that people who keep their fasting level below 92 do not develop diabetes, whereas many with “normal” readings above 92 do develop the disease. Many doctors also accept a gradual increase with age and tell older patients that fasting blood sugar levels of 100, even 105 mg/dl, are normal and nothing to worry about.
But now that we know such increases can signal the detrimental systemic effects of glycosylation, maybe we should tell our doctors we are interested in optimal, not normal. Better yet, let’s work with them to make “optimal” the new normal.
Angelyn Frankenberg is a wellness coach and writer living in Carbondale. She has a master’s in physical education and an undergraduate degree in music. Reach her at firstname.lastname@example.org.
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