Sugar (from Wiki)
John Yudkin - High intake of sucrose and heart attacks(*)
In spite of these difficulties, such studies have already shown that sucrose, in proportions within the range found in current human dietaries, produces an increase in plasma lipids, uric acid, insulin and cortisol; abnormalities in platelet behavior; reduction in glucose tolerance; tissue resistance to insulin; damage to the liver and the kidney, and an increase in lipid in the aorta.
Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease, by Johnson et al.
It is our opinion that the potential mechanisms underlying the epidemic should be carefully reappraised. On the basis of both he experimental studies performed in our laboratories and an extensive review of the literature, we revisit an old hypothesis hat a simple dietary substance may have a significant role in driving the epidemic. Interestingly, reappraising the role of sugar nd its influence in the development of cardiorenal disease may lead to a new understanding of why certain populations, such as African Americans, Native Americans, Maori, and Australian Aborigines, are at greater risk of developing the disease. Similar to the relation between high intakes of salt or protein and the risk of developing kidney disease or to the relation between a high-fat diet and the atherosclerotic phenotype, we propose that sugars containing fructose may play a major role in the development of hypertension, obesity, and the metabolic syndrome and in the subsequent development of kidney disease. Although physical inactivity and overeating are major contributors to the obesity epidemic, we present evidence that fructose may be the "caries" to the epidemic’s root.
One unique aspect of fructose is that it is the only sugar that raises uric acid concentrations, and this can be shown in both humans (56) and rodents (57). Fructose enters hepatocytes and other cells (including tubular cells, adipocytes, and intestinal epithelial cells), where it is completely metabolized by fructokinase with the consumption of ATP; unlike in glucose metabolism, there is no negative regulatory mechanism to prevent the depletion of ATP. As a consequence, lactic acid and uric acid are generated in the process, and uric acid concentrations may rise by 1–4 mg/dL after the ingestion of a large fructose-based meal (58). Although the rise in uric acid concentrations has historically been viewed as simply a potential risk factor for inducing gout, recent studies suggest that this may be a key mechanism to explain how fructose causes cardiovascular disease. In addition, it also provides a mechanism to explain why rodents are relatively resistant to the effects of fructose (see below).
FRUCTOSE-INDUCED HYPERURICEMIA AS A MECHANISM FOR CARDIORENAL DISEASE
Nakagawa et al (51) recently showed in experimental animals that lowering uric acid concentrations could largely prevent features of the metabolic syndrome induced by fructose, including weight gain, hypertriacylglycerolemia, hyperinsulinemia and in-
sulin resistance, and hypertension. The protective effect of lowering uric acid concentrations on the development of the metabolic syndrome was shown regardless of whether the uric acid concentrations were lowered by using a xanthine oxidase inhibitor or a uricosuric agent (51). These studies were surprising, because most authorities had considered uric acid to be either biologically inert or an important antioxidant in the plasma (59). However, uric acid was found to have numerous deleterious biologic functions. For example, uric acid stimulates both vascular smooth muscle cell proliferation and the release of chemotactic and inflammatory substances (60–62), induces monocyte chemotaxis (63), inhibits endothelial cell proliferation andmigration (64, 65), and causes oxidative stress in adipocytes, which results in the impaired secretion of adiponectin (66).
In animals, the effect of elevated uric acid concentrations is even more pronounced. For example, mildly hyperuricemic rats develop hypertension because of the inhibition of nitric oxide synthase in themacula densa, the stimulation of intrarenal renin, and a reduction in endothelial nitric oxide bioavailability (67). Over time, hyperuricemic rats develop renal arteriosclerosis that then causes the animals to develop a salt-sensitive form of hypertension.
WHY ARE AFRICAN AMERICANS SUSCEPTIBLE TO CARDIOVASCULAR DISEASE?
It is well known that African Americans have higher rates of obesity, hypertension, diabetes, kidney disease, and heart disease. ... Recent studies also have documented that the sugar intake of African Americans is greater than that of whites (110, 111). Similar high sugar intakes were noted in studies of Australian Aborigines and Samoans living in New Zealand (112,113). Furthermore, it is known that African Americans have higher concentrations of uric acid (114); in the African American Study of Hypertension and Kidney Disease, the average uric acid concentration was 8.3 mg/dL (115).
If the hypothesis is correct that fructose has a role in the epidemic of cardiovascular disease, then a number of predictions should arise from future studies. First, fructose intake will be a risk factor for hypertension, insulin resistance, hypertriacylglycerolemia, obesity, type 2 diabetes, preeclampsia, chronic kidney disease, stroke, cardiovascular disease, and mortality. Second, reducing uric acid in patients with uric acid concentrations [greater than] 6.0 mg/dL will improve endothelial dysfunction, decrease systemic vascular resistance, lower blood pressure, lower triacylglycerol concentrations, improve body weight, lower the risk of the progression of renal disease, and reduce cardiovascular disease risk. Third, low-fructose diets coupled with mild purine restriction will improve weight and reduce cardiovascular disease risk. Fourth, fructokinase will be identified as a key enzyme mediating the cardiorenal disease syndrome; genetic polymorphisms will be associated with cardiovascular disease risk, and blocking the enzyme will provide a novel way to prevent cardiorenal disease. Clearly, much more work needs to be done to prove or disprove this hypothesis.
*) Found that through Mark's blog - The Definitive Guide to Saturated Fat