An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial pipemic responses compared with a low fat diet in normal weight, normolipidemic women.
Volek JS, Sharman MJ, Gómez AL, Scheett TP, Kraemer WJ.
J Nutr. 2003 Sep;133(9):2756-61.
PMID: 12949361
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.
"Coconut oil is extracted from the kernel or meat of matured coconut harvested from the coconut palm (Cocos nucifera). Throughout the tropical world it has provided the primary source of fat in the diets of millions of people for generations. It has various applications in food, medicine, and industry. What makes coconut oil different from most other dietary oils is the basic building blocks or fatty acids making up the oil. Coconut oil is composed predominately of a special group of fat molecules known as medium chain fatty acids (MCFA). The majority of fats in the human diet are composed almost entirely of long chain fatty acids (LCFA).
The primary difference between MCFA and LCFA is the size of the molecule, or more precisely, the length of the carbon chain that makes up the backbone of the fatty acid. MCFA have a chain length of 6 to 12 carbons. LCFA contain 14 or more carbon
Historically, many populations within the tropics have used coconut medicinally as a treatment for a wide variety of ailments.[8]
A study into the effects of a "diet rich in.." medium-chain fatty acids (such as in coconut oil and butter) concluded that "MCFAs in the form of MCTs significantly increased plasma triacylglycerol and LDL-cholesterol concentrations and the ratio of LDL to HDL cholesterol and thereby resulted in a less beneficial lipid profile overall."[9]
Further, research done by nutritionist Mary Enig has found that non-hydrogenated coconut oil (i.e. extra-virgin) consumed in moderate amounts "is at worst neutral with respect to atherogenicity of fats and oils and, in fact, is likely to be a beneficial oil for prevention and treatment of some heart disease."[10] The lack of negative effects of a diet rich in coconut oil on cardiovascular health is born out in studies of Polynesian populations who consume as much as 65% of their calories in the form of coconut oil and yet, have almost no incidence of heart disease and normal blood lipid profiles.[11]
Acute Ingestion of Long-Chain (n-3) Polyunsaturated Fatty Acids Decreases Fibrinolysis in Men with Metabolic Syndrome.
Montegaard C, Tulk HM, Lauritzen L, Tholstrup T, Robinson LE.
J Nutr. 2009 Nov 4. [Epub ahead of print]
PMID: 19889809
doi:10.3945/jn.109.111427
Individuals with metabolic syndrome (MetS) often have elevated plasma plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (t-PA), contributing to an increased risk of cardiovascular disease. PAI-1 and t-PA may be affected by chronic (n-3) long-chain PUFA [(n-3)LCPUFA] supplementation; however, the acute impact of fat ingestion on these risk factors has not been established. Our objective was to investigate the acute effect of (n-3)LCPUFA on plasma PAI-1, t-PA, and platelet aggregation. We conducted a randomized crossover study in which men (n = 8, ≥45 y) with MetS consumed water or a high-saturated fat beverage (1 g fat/kg body weight) with either a high or low content of (n-3)LCPUFA. Blood samples were collected over 8 h to measure triacylglycerol (TAG), PAI-1, t-PA, and platelet aggregation. Both fat loads resulted in a significant increase in whole blood TAG concentration, plasma PAI-1 and t-PA concentrations, and PAI-1 activity, as well as a significant decrease in t-PA activity during the postprandial period. Interestingly, PAI-1 concentration and activity increased more following the high (n-3)LCPUFA compared with the low (n-3)LCPUFA beverage (P < 0.05). Furthermore, the high (n-3)LCPUFA beverage resulted in a lower t-PA activity (P < 0.05), whereas the effects of the 2 fat loads on the plasma t-PA concentration and platelet aggregation did not differ. Overall, acute intake of a high (n-3)LCPUFA beverage shifted the balance between plasma PAI-1 and t-PA, which might indicate a lower capacity for fibrinolysis
n-3 fatty acids and cardiovascular disease.
Breslow JL.
Am J Clin Nutr. 2006 Jun;83(6 Suppl):1477S-1482S. Review.
PMID: 16841857
The results of prospective cohort studies indicate that consuming fish or fish oil containing the n-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) is associated with decreased cardiovascular death, whereas consumption of the vegetable oil-derived n-3 fatty acid {alpha}-linolenic acid is not as effective. Randomized control trials (RCTs) in the context of secondary prevention also indicate that the consumption of EPA plus DHA is protective at doses 3 g/d, EPA plus DHA can improve cardiovascular disease risk factors, including decreasing plasma triacylglycerols, blood pressure, platelet aggregation, and inflammation, while improving vascular reactivity. Mainly on the basis of the results of RCTs, the American Heart Association recommends that everyone eat oily fish twice per week and that those with coronary heart disease eat 1 g/d of EPA plus DHA from oily fish or supplements. Directions for future research include 1) RCTs to confirm the initial trials showing that EPA plus DHA decreases cardiovascular death and additional studies to determine whether this effect is due to EPA, DHA, or the combination; the dosage of the effective components; and whether the mechanism of action in humans is prevention of fatal arrhythmias. 2) Clinical studies to determine whether the reduction in cardiovascular disease risk factors is due to EPA, DHA, or the combination and the dosage of the effective components. 3) Clinical studies to determine whether vegetable oil-derived {alpha}-linolenic acid added to a diet enriched in n-6 fatty acids can effectively substitute for fish oil-derived EPA plus DHA.
Ordovas JM.
Genetic interactions with diet influence the risk of cardiovascular disease.
Am J Clin Nutr. 2006 Feb;83(2):443S-446S. Review.
PMID: 16470010 [PubMed - indexed for MEDLINE]
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