Stephen T. Sinatra

The Saturated Fat, Cholesterol, and Statin Controversy A Commentary

In the 1930s, there were advertisements run in JAMA with testimonials from MDs saying that smoking cigarettes did not harm your lungs. It took many years of increasing lung cancer incidence to convince people that this was not a true statement. The current situation with serum cholesterol and coronary heart disease is very similar in concept, though this time doctors are widely convinced that the former causes the latter, despite a glaring lack of scientific evidence. There have been no studies that prove dietary cholesterol levels directly cause atherosclerosis. There are many correlation studies that may suggest an association but none that show cause and effect. In fact, if analyzed carefully, there are more studies that disprove the “cause and effect” hypothesis than even come close to proving it. One basic tenant of biostatistics and epidemiologic research is that you can never prove a hypothesis you can only fail to disprove it. Experimental design has three essential components: 1) Estimate of error, 2) Control of error and 3) Proper interpretation of results [1]. Correlation studies indicate a possible relationship between two factors, i.e, blood cholesterol and CVD, but they do not prove cause and effect. Correlations are often observed in epidemiological studies, but carefully designed studies with sufficient control of confounding factors and avoidance of other potential bias needs to be conducted to demonstrate cause and effect. In these cases, small differences in the design of the study can cause different outcomes. Most of the studies in animal models are not a good model to compare the same systems as in humans. They may give hints,

Recent Science and Clinical Application of Nutrition to Coronary Heart Disease

ABSTRACT One of the greatest threats to mortality in industrialized societies continues to be coronary heart disease (CHD). Moreover, the ability to decrease the incidence of CHD has reached a limit utilizing traditional diagnostic evaluations and prevention and treatment strategies for the top five cardiovascular risk factors (hypertension, diabetes mellitus, dyslipidemia, obesity, and smoking). It is well known that about 80% of CHD can be prevented with optimal nutrition, coupled with exercise, weight management, mild alcohol intake, and smoking cessation. Among all of these factors, optimal nutrition provides the basic foundation for prevention and treatment of CHD. Numerous prospective nutrition clinical trials have shown dramatic reductions in the incidence of CHD. As nutritional science and nutrigenomics research continues, our ability to adjust the best nutrition with an individualized approach is emerging. This article reviews the role of nutrition in the prevention and treatment of CHD and myocardial infarction (MI).

d-Ribose Supplementation in the Equine: Lack of Effect on Glycated Plasma Proteins Suggesting Safety in Humans

Background: d-Ribose is a popular dietary supplement for humans and the equine because of its crucial role in cellular bioenergetics. However, as a reducing sugar, it has been suggested that ingestion of d-ribose might promote the formation of glycated proteins in vivo with potential adverse consequences. Objective: The aim of this study was to examine if d-Ribose would promote the formation of glycated proteins in vivo following exercise in training thoroughbred racehorses. Methods: Two groups of horses received the supplement (30 and 50 g d-Ribose daily) for 17 weeks, during which period the horses were subjected to low-intensity exercises followed by high-intensity exercises. Blood samples were analyzed for glycated plasma proteins at baseline and following the 2 exercise regimens. Results: This study shows that long-term ingestion of d-Ribose at 30-50 g a day does not promote the formation of glycated plasma proteins in thoroughbred racehorses. Ribose supplementation also protected the horses from cramping while enhancing muscle recovery at the same time. No adverse effects were reported. Conclusion: Ribose supplementation is safe and does not cause glycation in vivo. This investigation also establishes safety of d-Ribose in thoroughbred racehorses, suggesting similar implications in humans as well.