The Carbohydrate Hypothesis: Part 2:
In Part 2, we will discuss Sugar, Insulin, and Cholesterol.
Sugar and Insulin:
With the modernization of western diets came more and more processed foods and with those came added sugar. The increase in sugar consumption was the one noteworthy difference that might explain the increased incidence of diabetes, coronary heart disease, hypertension, and high cholesterol. The higher the sugar intake in different nations, the higher both the incidence of and mortality from cancer of the colon, rectum, breast, ovary, uterus, prostate, kidney, nervous system, and testicles. One researcher fed high sugar diets to college students and reported that it raised their cholesterol and particularly their triglycerides; their insulin levels rose, and their blood cells became stickier, which he believed could explain the blood clot that seemed to precipitate heart attacks. The higher the insulin levels the greater risk of heart disease. Both diabetes and metabolic syndrome are associated with an elevated incidence of virtually every chronic disease, not just heart disease. Elevated blood sugar, hyperinsulinemia, and insulin resistance may also cause these complications and the associated chronic disease. Let’s dive into the Insulin-Atherogenesis Hypothesis. This hypothesis states that the excessive secretion of insulin accelerates atherosclerosis and perhaps other vascular complications, any dietary factor, refined carbs in particular, that increases insulin secretion will increase risk of heart disease. In particular raising blood sugar will increase the production of what are known technically as reactive oxygen species and advanced glycation end products, both potentially toxic. Reactive oxygen species are generated primarily by the burning of glucose (blood sugar) for fuel in the cells, in a process that attaches electrons to oxygen atoms, transforming the oxygen from a relatively inert molecule into one that is avid to react chemically with other molecules. This is not an ideal situation biologically. One form of these are free radicals and all of them known together are called oxidants because they oxidize other molecules (the same chemical that causes iron to rust). The object of oxidation slowly deteriorates, called oxidative stress. Antioxidants neutralize reactive oxygen species. Advanced glycation end products, AGEs, can take years to form but begin with the attachment of a sugar (glucose) to a protein without the benefit of an enzyme to orchestrate the reaction. The role of enzymes in living organisms is to control chemical reactions to ensure that they conform to their programming. Without these enzymes the sugar sticks to the protein haphazardly and sets the stage for unintended and unregulated chemical reactions. If blood sugar levels are low enough the sugar and protein will disengage and no damage will be done. If blood sugar is elevated then the process continues. AGEs and the glycation process causes the oxidation of LDL particles and so causes the LDL and its accompanying cholesterol to become trapped in the artery wall. This means that anything that raises blood sugar, by the logic of the carb hypothesis, will lead to more atherosclerosis and heart disease, more vascular disorders, and an accelerated pace of physical degeneration, even in those of us who never become diabetic. If you have heard sugar and diabetes then you have also heard of the glycemic index. The lower the glycemic index, the less insulin pumps out and the more your blood sugar stays stabilized. The glycemic index of sucrose is lower than flour and starches and fructose is the reason why. The carbs in starches are broken down upon digestion first to maltose and then to glucose which moves directly from the small intestine into the bloodstream. Table sugar (i.e. sucrose) is both glucose and fructose, the bond is broken up by digestion. The glucose moves into the bloodstream and raises blood sugar and the fructose has little immediate effect on blood sugar. If sugar is the evil in the diet it would be the fructose that endows it with that singular distinction because fructose barely registers in the glycemic index it appears to be the ideal sweetener for diabetics. High Fructose Corn Syrup (HFCC-55) is effectively identical to sucrose upon digestion, the industry treated it and the public perceived it as a healthy additive whereas sucrose carried controversy. Because fructose is the primary sugar in fruit, HFCC is often referred to as fruit sugar and appears healthier by virtue of association. By defining carb food as good or bad on the basis of their glycemic index, health officials effectively misdiagnosed the impact of fructose on human health. The key is the influence of glucose or fructose not on blood sugar but on the liver. Fructose passes directly to the liver where it is metabolized almost exclusively, and the liver responds by converting it into triglycerides and then shipping it out on lipoproteins for storage. The more fructose in the diet the higher the subsequent triglyceride levels in the blood. Glucose, however, is the least reactive of all sugars, the one least likely to attach itself without an enzyme to a nearby protein which is the first step in the formation of AGEs. Investigators studying AGEs have proposed that Alzheimer’s starts with glycation, the haphazard binding of reactive blood sugars to these brain proteins. Because these sugars stick randomly to the fine filaments of the proteins, this in turn causes the proteins to stick to themselves and to other proteins. This impairs their function and occasionally leaves them impervious to the usual disposal mechanisms causing them to accumulate in the spaces between neurons. Sugar intake in international comparisons is positively correlated with both the incidence of and mortality from colon, rectal, breast, ovarian, prostate, kidney, nervous system, and testicular cancer. Let’s go a little deeper into how insulin affects our bodies. Insulin-like growth factor (IGF) is sufficiently similar in structure to insulin that it can mimic its effects. Add the necessary food and IGF levels increase and so will the rate of growth. IGF and its receptors appear to play a critical role in cancer. Anything that increases insulin levels will therefore increase the availability of IGF to the cells and so increase the strength of the IGF proliferation signals (insulin has been shown to affect estrogen this way too). The extra insulin receptors will cause cancerous cells to receive more than their share of insulin from the environment which will convey to the cell more blood sugar for fueling growth and proliferation; the extra IGF receptors will assure that these cells are supplied with particularly forceful commands to proliferate. Another critical role of IGF in the development of cancer may be its ability to inhibit or override the cell suicide program that serves as the ultimate fail safe mechanism to prevent damaged cells from proliferating. IGF accelerates the process by which a cell becomes cancerous and then they work to keep the cells alive and multiplying. Diet changes the nurturing of those cells.
Cholesterol:
Cholesterol is only one of several fatlike substances that circulate through the blood and are known collectively as lipids or blood lipids. These include free fatty acids and triglycerides, the molecular forms in which fat is found circulating in the bloodstream. Both cholesterol and triglycerides are shuttled through the circulation in particles called lipoproteins. The amount of cholesterol and triglycerides varies in each type of lipoprotein. When physicians measure total cholesterol levels, they have no way of knowing how the cholesterol itself is apportioned in individual lipoproteins. It is possible that in heart disease the problem may be caused not by cholesterol but by a defect in one of these lipoproteins or an abnormal concentration of the lipoproteins themselves. Low density lipoproteins: LDL “bad”, HDL “good”, very low density lipoproteins: VLDL play a critical role in heart disease this is where more of the triglycerides are found. Carbohydrates elevate VLDL. If a physician put a patient with high cholesterol on a low fat high carb diet that may lower LDL but it would raise VLDL. Triglycerides shoot up on low fat and fall on high fat diets. High triglycerides were considerably more common in heart disease victims than high cholesterol. There are four categories of lipoproteins: (1) LDL carries most of the cholesterol, (2) VLDL carries most of the triglycerides, (3) HDL, and (4) chylomicrons which carry dietary fat from the intestine to the fat tissue. By far the most common of the 5 lipoproteins disorders was type 4 characterized by elevated VLDL, synonymous with carb induced hyperlipemia. The higher the HDL, the lower the triglycerides and the risk of heart disease. Lipid profiles provided the rationale for physicians to keep measuring total cholesterol even though it was confirmed that this was an unreliable predictor or risk. Saturated fats raise both HDL and LDL, carbs lower LDL and HDL, monounsaturated fats like oleic acid found in olive oil lower LDL and raise HDL: this principle is also found in red meat, eggs, and bacon. There are two patterns to LDL: pattern A is large, fluffy LDL low risk, pattern B is small, dense LDL high risk. The lower the fat in the diet and the higher the carb the smaller and denser the LDL and more likely for pattern B and the greater risk for heart disease.
