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Articles by Robert C. Block
Total Records ( 3 ) for Robert C. Block
  Robert C. Block , E. Ray Dorsey , Christopher A. Beck , J. Thomas Brenna and Ira Shoulson
  Huntington disease is an autosomal-dominant neurodegenerative disorder characterized by behavioral abnormalities, cognitive decline, and involuntary movements that lead to a progressive decline in functional capacity, independence, and ultimately death. The pathophysiology of Huntington disease is linked to an expanded trinucleotide repeat of cytosine-adenine-guanine (CAG) in the IT-15 gene on chromosome 4. There is no disease-modifying treatment for Huntington disease, and novel pathophysiological insights and therapeutic strategies are needed. Lipids are vital to the health of the central nervous system, and research in animals and humans has revealed that cholesterol metabolism is disrupted in Huntington disease. This lipid dysregulation has been linked to specific actions of the mutant huntingtin on sterol regulatory element binding proteins that result in lower cholesterol levels in affected areas of the brain with evidence that this depletion is pathologic. Huntington disease is also associated with a pattern of insulin resistance characterized by a catabolic state, resulting in weight loss and a lower body mass index than individuals without Huntington disease. Insulin resistance appears to act as a metabolic stressor attending disease progression. The fish-derived omega-3 fatty acids, eicosapentaenoic acid and docosahexaenoic acid, have been examined in clinical trials of Huntington disease patients. Drugs that combat the dysregulated lipid milieu in Huntington disease may help treat this perplexing and catastrophic genetic disease.
  Seth J. Baum , Penny M. Kris-Etherton , Walter C. Willett , Alice H. Lichtenstein , Lawrence L. Rudel , Kevin C. Maki , Jay Whelan , Christopher E. Ramsden and Robert C. Block
  Research dating back to the 1950s reported an association between the consumption of saturated fatty acids (SFAs) and risk of coronary heart disease. Recent epidemiological evidence, however, challenges these findings. It is well accepted that the consumption of SFAs increases low-density lipoprotein cholesterol (LDL-C), whereas carbohydrates, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) do not. High-density lipoprotein (HDL)-C increases with SFA intake. Among individuals who are insulin resistant, a low-fat, high-carbohydrate diet typically has an adverse effect on lipid profiles (in addition to decreasing HDL-C, it also increases triglyceride and LDL particle concentrations). Consequently, a moderate fat diet in which unsaturated fatty acids replace SFAs and carbohydrates are not augmented is advised to lower LDL-C; compared with a low-fat diet, a moderate-fat diet will lower triglycerides and increase HDL-C. Now, there is some new evidence that is questioning the health benefits of even MUFAs and PUFAs. In addition, in a few recent studies investigators have also failed to demonstrate expected cardiovascular benefits of marine-derived omega-3 fatty acids. To clarify the clinical pros and cons of dietary fats, the National Lipid Association held a fatty acid symposium at the 2011 National Lipid Association Scientific Sessions. During these sessions, the science regarding the effects of different fatty acid classes on coronary heart disease risk was reviewed.
  Scott J. Cameron , Robert C. Block and John Franklin Richeson
  Lipoprotein(a) [Lp(a)] is a lipoprotein subclass well-known among the lipid community to accelerate atherosclerosis and promote thrombosis through incompletely understood mechanism. We report a case of a young man with a healthy lifestyle and no major coronary or vascular risk factors who presented to the emergency department with an acute coronary syndrome and was ultimately found to have severe coronary artery disease. A diagnostic workup revealed elevated Lp(a). He was treated with consequent reduction in Lp(a) concentration. This case highlights the need to better understand atypical lipoproteins, how they relate to cardiovascular disease, the implications for screening family members, and the need to standardize patient management guidelines for the purpose of mortality risk reduction.
 
 
 
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