Group items tagged

Conclusions: Compared with a low-fat diet, a low-carbohydrate diet program had better participant retention and greater weight loss. During active weight loss, serum triglyceride levels decreased more and high-density lipoprotein cholesterol level increased more with the low-carbohydrate diet than with the low-fat diet. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. Ann Intern Med. 2004 May 18;140(10):769-77. PMID: 15148063

Plasma 25-hydroxyvitamin d is associated with markers of the insulin resistant phenotype in nondiabetic adults. Liu E, Meigs JB, Pittas AG, McKeown NM, Economos CD, Booth SL, Jacques PF. J Nutr. 2009 Feb;139(2):329-34. Epub 2008 Dec 23. PMID: 19106328 doi:10.3945/jn.108.093831 After adjusting for age and sex, plasma 25(OH)D was positively associated with ISI(0,120), plasma adiponectin, and HDL cholesterol and inversely associated with plasma triacylglycerol, but these associations were no longer significant after further adjustment for BMI, waist circumference, and current smoking status. 25(OH)D and 2-h post-OGTT glucose were not associated. Among adults without diabetes, vitamin D status was inversely associated with surrogate fasting measures of insulin resistance. These results suggest that vitamin D status may be an important determinant for type 2 diabetes mellitus.

ScienceDaily (Aug. 25, 2009) - Low levels of vitamin D are known to nearly double the risk of cardiovascular disease in patients with diabetes, and researchers at Washington University School of Medicine in St. Louis now think they know why. They have found that diabetics deficient in vitamin D can't process cholesterol normally, so it builds up in their blood vessels, increasing the risk of heart attack and stroke. The new research has identified a mechanism linking low vitamin D levels to heart disease risk and may lead to ways to fix the problem, simply by increasing levels of vitamin D.

Paradigms and Paradoxes Last month Dr. Armin Zittermann of Ruhr University, Germany, published the best vitamin D paper of the month. He reviewed the mounting evidence that vitamin D deficiency is a major cause of heart disease. Zittermann A, Schleithoff SS, Koerfer R. Putting cardiovascular disease and vitamin D insufficiency into perspective. Br J Nutr. 2005 Oct;94(4):483-92. Before we start, let's talk about paradigms and paradoxes. A paradigm is a set of assumptions, concepts, and practices that constitutes a way of viewing reality. The current paradigm is that heart disease is caused by a combination of genetics, hypertension, diabetes, cholesterol, smoking, obesity, inactivity, and diet. A paradox is a fact that contradicts the paradigm.

Tufts University Confirms That Vitamin A Protects Against Vitamin D Toxicity by Curbing Excess Production of Vitamin K-Dependent Proteins Tufts University confirmed my hypothesis that vitamin A protects against vitamin D's induction of renal calcification (kidney stones) by normalizing the production of vitamin K-dependent proteins in December, 2008, without citing my hypothesis or telling me they had confirmed it. I am, of course, very grateful that they thought it significant enough to investigate.

Egg fortification with n-3 polyunsaturated fatty acids (PUFA): nutritional benefits versus high n-6 PUFA western diets, and consumer acceptance. Shapira N, Weill P, Loewenbach R. Isr Med Assoc J. 2008 Apr;10(4):262-5. PMID: 18548978 Egg fortification with n-3 polyunsaturated fatty acids (PUFA): nutritional benefits versus high n-6 PUFA western diets, and consumer acceptance. Shapira N, Weill P, Loewenbach R. Isr Med Assoc J. 2008 Apr;10(4):262-5. PMID: 18548978 CONCLUSIONS: Effective concentration and transformation of supplemental n-3 PUFA/LCPUFA from feed to egg substantially enhanced egg n-3 PUFA %DRI, particularly of DHA, critical for health but often deficient. Such land-based n-3 PUFA/LCPUFA fortification may be applicable to high n-6 PUFA diets, fitting within cholesterol limitations and market criteria. It may contribute to general health and specific requirements (i.e., pregnancy and lactation), with possibilities of wide accessibility and standardization.

If last week's column convinced you that surgery may not be the best way to avoid a heart attack or sudden cardiac death, the next step is finding out what can work as well or better to protect your heart.\n\nMany measures are probably familiar: not smoking, controlling cholesterol and blood pressure, exercising regularly and staying at a healthy weight. But some newer suggestions may surprise you.

While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim. The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods. Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people. The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building

Imagine a superfood -- not a drug -- powerful enough to help you lower your cholesterol, reduce your risk of heart disease and cancer, and, for an added bonus, put you in a better mood. Did we mention that there are no side effects? You'd surely stock up on a lifetime supply. Guess what? These life-altering superfoods are available right now in your local supermarket.

Heart scan scores starting dropping not just 2%, or 8% . . . but 24%, 30%, 50% and more. We also began to see a larger proportion of people achieving these larger successes. Why? I attribute the surge in success to the addition of vitamin D. With vitamin D added to the mix of strategies in Track Your Plaque, HDL cholesterols went up much higher, LDL dropped further, blood sugars dropped, blood pressures dropped. People felt better, had more energy, gained more clarity in thought. And heart scan scores dropped more readily.

"Proanthocyanidin (PA or PAC), also known as procyanidin, oligomeric proanthocyanidin (OPC), leukocyanidin, leucoanthocyanin and condensed tannins, is a class of flavanols. Proanthocyanidins are essentially polymer chains of flavonoids such as catechins.[1] One was discovered in 1936 by Professor Jacques Masquelier and called Vitamin P, although this name did not gain official category status and has since fallen out of usage. It was Masquelier who first developed techniques for the extraction of proanthocyanidins from certain plant species. Proanthocyanidins have been sold as nutritional and therapeutic supplements in Europe since the 1980s, but their introduction to the United States market has been relatively recent. In the human body, they might act as antioxidants (free radical scavengers).[citation needed] OPCs may help protect against the effects of internal and environmental stresses such as cigarette smoking and pollution, as well as supporting normal body metabolic processes. The effects may include depressing blood fat, emolliating blood vessels, lowering blood pressure, preventing blood vessel scleroses, dropping blood viscidity and preventing thrombus formation [18]. Additionally, studies have shown that OPCs may prevent cardiovascular diseases by counteracting the negative effects of high cholesterol on the heart and blood vessels. Pycnogenol® is the name of such an OPCs commercial formulation. OPCs are available from fresh grapes, grape juice, and red wine. Although in milligrams per ounce red wine may contain more OPCs than red grape juice, red grape juice contains more OPCs per average serving size. An 8 ounce serving of grape juice averages 124 milligrams OPCs, while a 5 ounce serving of red wine averages 91 milligrams.[19][20] Many other foods and beverages also contain high amounts of OPCs, but very few come close to the levels found in red grape seeds and skins (which readily disperse into grape juice when crushed)

Coconut oil is one of the few saturated fats that doesn't come from animals, but like other saturated fats can raise cholesterol levels and, therefore, should play only a very limited role, if any, in your diet. In the past, it was widely used in movie popcorn, candy bars and commercial baked goods but was phased out of many of them because of consumer opposition to unhealthy tropical oils. Now coconut oil is being promoted as a weight loss aid; it is also touted in a book by a naturopathic doctor. The rationale goes something like this: as a source of medium-chain triglycerides (MCT), coconut oil isn't stored in the body as fat as readily as oils composed of long-chain triglycerides (LCT). Some research from McGill University in Canada suggests that this is true; MCTs also boost metabolism and satiety, and therefore may promote weight loss when they replace LCTs in the diet. Because they are so easily digested, MCTs are given in hospitals to provide nourishment for critically ill people who have trouble digesting fat. The benefits of coconut oil in the diet, if any, are likely to be minimal, and until we have more and better evidence about coconut oil's effect of metabolism and potential role in promoting weight loss, I do not recommend using it.

"The routine prescription of extended-release niacin, a B vitamin (1,500 milligrams daily), in combination with traditional cholesterol-lowering therapy offers no extra benefit in correcting arterial narrowing and diminishing plaque buildup in seniors who already have coronary artery disease, a new vascular imaging study from Johns Hopkins experts shows. In tests on 145 Baltimore-area men and women with existing atherosclerosis, all over age 65, researchers found that after 18 months of drug therapy, reductions in arterial wall thickness were measurably no different between the half who took dual niacin-statin therapy and the rest who remained on statin therapy alone. "

Last week, Harvard researchers reported how healthy 50-year-old men and 60-year-old women could benefit from taking a statin even if they didn't have high cholesterol. The people they studied had high levels of C-reactive protein, or CRP, which is a marker for inflammation. The study showed that risk for major heart problems was cut by about 50 percent among the statin users.\n\nBut like many industry-sponsored drug studies, the results focused on something called "relative risk," which compares differences between study groups. Relative risk has the effect of exaggerating a drug's benefits. What does a 50 percent reduction in heart risk mean? It means that just one out of 120 statin users was helped by the drug.

Judging by recent headlines, you might think so. Last week heart researchers reported that millions of healthy people could benefit from taking statins even if they don't have high cholesterol.\n\nAlthough many doctors hailed the study as a major breakthrough, a closer look at the research suggests that statins (like Crestor, from AstraZeneca, and Lipitor, from Pfizer) are far from magic pills. While they clearly save lives in people with a previous heart attack or other serious heart problems, for an otherwise healthy person the potential benefit remains small.

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. J Clin Invest. 2009 May;119(5):1322-34. Epub 2009 Apr 20. PMID: 19381015 doi: 10.1172/JCI37385. Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

Berberine inhibits adipogenesis in high-fat diet-induced obesity mice. Hu Y, Davies GE. Fitoterapia. 2009 Oct 25. [Epub ahead of print] PMID: 19861153 doi:10.1016/j.fitote.2009.10.010 Our previous studies illustrated that berberine inhibited adipogenesis in murine-derived 3T3-L1 preadipocytes and human white preadipocytes. In this study, the effects of berberine on the adipogenesis of high-fat diet-induced obesity (FD) or normal diet (ND) mice and possible transcriptional impact are investigated. The results demonstrated that in FD mice, berberine reduced mouse weight gain and food intake and serum glucose, triglyceride, and total cholesterol levels accompanied with a down-regulation of PPARgamma expression and an up-regulation of GATA-3 expression. Berberine had no adverse effects on ND mice. These encouraging findings suggest that berberine has excellent pharmacological potential to prevent obesity.

"(NaturalNews) A research team from the University of Washington (UW) recently published a study in Physiology & Behavior revealing that moderate consumption of fructose- and high fructose corn syrup-sweetened beverages leads to significant alterations of lipid metabolization in the liver. Conducted on rats, the study also noted marked increases in both cholesterol and triglyceride levels in rats that fed on fructose-sweetened beverages. Fructose is a monosaccharide sugar that is found in various fruits. It is a simple sugar that is often promoted as being a healthy "fruit" sugar, however the reality is that fructose is just one component of the complex sugar composition that occurs naturally in fruit. Most granulated fructose available today, called crystalline fructose, is derived from fructose-enriched corn syrup. Similarly, high fructose corn syrup is a fructose-enriched form of highly-processed corn syrup that is commonly found in soda, ketchup, candy, dressings, and many other processed foods. The biggest concern about fructose is the fact that, unlike sucrose, it passes undigested through the small intestine where it enters the portal vein and heads directly to the liver. "