Group items matching

in title, tags, annotations or url

Vitamin D and mood disorders among women: an integrative review. Murphy PK, Wagner CL. J Midwifery Womens Health. 2008 Sep-Oct;53(5):440-6. Review. PMID: 18761297 Four of six studies reviewed imparted significant results, with all four showing an association between low 25(OH)D levels and higher incidences of four mood disorders: premenstrual syndrome, seasonal affective disorder, non-specified mood disorder, and major depressive disorder. This review indicates a possible biochemical mechanism occurring between vitamin D and mood disorders affecting women, warranting further studies of these variables using rigorous methodologies.

Effect of fish oil on heart rate in humans: a meta-analysis of randomized controlled trials. Mozaffarian D, Geelen A, Brouwer IA, Geleijnse JM, Zock PL, Katan MB. Circulation. 2005 Sep 27;112(13):1945-52. Epub 2005 Sep 19. PMID: 16172267 doi: 10.1161/CIRCULATIONAHA.105.556886 Conclusions- In randomized controlled trials in humans, fish oil reduces HR, particularly in those with higher baseline HR or longer treatment duration. These findings provide firm evidence that fish oil consumption directly or indirectly affects cardiac electrophysiology in humans. Potential mechanisms such as effects on the sinus node, ventricular efficiency, or autonomic function deserve further investigation.

Fish intake is associated with a reduced progression of coronary artery atherosclerosis in postmenopausal women with coronary artery disease. Erkkilä AT, Lichtenstein AH, Mozaffarian D, Herrington DM. Am J Clin Nutr. 2004 Sep;80(3):626-32. PMID: 15321802 Conclusions: Consumption of fish is associated with a significantly reduced progression of coronary artery atherosclerosis in women with coronary artery disease.

Serum 25(OH)-vitamin D concentration and risk of esophageal squamous dysplasia. Abnet CC, Chen W, Dawsey SM, Wei WQ, Roth MJ, Liu B, Lu N, Taylor PR, Qiao YL. Cancer Epidemiol Biomarkers Prev. 2007 Sep;16(9):1889-93. PMID: 17855710 doi: 10.1158/1055-9965.EPI-07-0461 Background: Squamous dysplasia is the precursor lesion for esophageal squamous cell carcinoma, and nutritional factors play an important role in the etiology of this cancer. Previous studies using a variety of measures for vitamin D exposure have reached different conclusions about the association between vitamin D and the risk of developing esophageal cancer. Conclusions: Higher serum 25(OH)D concentrations were associated with significantly increased risk of squamous dysplasia. No obvious source of measured or unmeasured confounding explains this finding. In conclusion, we found that a higher serum 25(OH)D concentration was associated with an increased risk of esophageal squamous dysplasia, the precursor lesion for ESCC. This finding concurs with our previous prospective study which found that higher vitamin D status was associated with increased risk of incident ESCC in this same population. These unexpected findings suggest that further studies of the association of vitamin D and digestive tract cancers are needed before the effect of vitamin D in different populations can be elucidated.

Fats and Fatty Acids in Human Nutrition Annals of Nutrition and Metabolism 2009, Vol. 55, No. 1-3 Also available as ISBN 978-3-8055-9261-1

Review of fat and fatty acid requirements and criteria for developing dietary guidelines. Smit LA, Mozaffarian D, Willett W. Ann Nutr Metab. 2009;55(1-3):44-55. Epub 2009 Sep 15. PMID: 19752535 DOI: 10.1159/000228995

The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures Author: Amy Proal

How to optimize vitamin D supplementation to prevent cancer, based on cellular adaptation and hydroxylase enzymology. Vieth R. Anticancer Res. 2009 Sep;29(9):3675-84. Review. PMID: 19667164

Phytase activity in the human and rat small intestine. Iqbal TH, Lewis KO, Cooper BT. Gut. 1994 Sep;35(9):1233-6. PMID: 7959229

Meat eating made us human. The anthropological evidence strongly supports the idea that the addition of increasingly larger amounts of meat in the diet of our predecessors was essential in the evolution of the large human brain. Our large brains came at the metabolic expense of our guts, which shrank as our brains grew.

"One of the problems - if it could be called a problem - in writing this blog and moderating the comments is most readers are pretty intelligent. Occasionally I have the angry vegetarian wander in, take me to task for my errant ways, and, after a comeback or two on my part, drift away to never be heard from again. Thanks to the confirmation bias, this blog pretty much selects against the non-meat eater. So, I tend to forget how many people there are out there who are pretty much clueless about basic nutrition, and how many people there are who bobble through life spouting cliches they've heard along the way as great nutritional truths. Based on the comments I get on this blog, it seems to me that most people are pretty nutritionally sophisticated and reasonable."

Dr. Staffan Lindeberg has published a new study using the "paleolithic diet" to treat type II diabetics (free full text). Type II diabetes, formerly known as late-onset diabetes until it began appearing in children, is typically thought to develop as a result of insulin resistance (a lowered tissue response to the glucose-clearing function of insulin). This is often followed by a decrease in insulin secretion due to degeneration of the insulin-secreting pancreatic beta cells. After Dr. Lindeberg's wild success treating patients with type II diabetes or glucose intolerance, in which he normalized the glucose tolerance of all 14 of his volunteers in 12 weeks, he set out to replicate the experiment. This time, he began with 13 men and women who had been diagnosed with type II diabetes for an average of 9 years.

A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Lindeberg S, Jönsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjöström K, Ahrén B. Diabetologia. 2007 Sep;50(9):1795-807. Epub 2007 Jun 22. PMID: 17583796 DOI: 10.1007/s00125-007-0716-y Conclusions/interpretation A Palaeolithic diet may improve glucose tolerance independently of decreased waist circumference.

The joint effects of apolipoprotein B, apolipoprotein A1, LDL cholesterol, and HDL cholesterol on risk: 3510 cases of acute myocardial infarction and 9805 controls. Parish S, Peto R, Palmer A, Clarke R, Lewington S, Offer A, Whitlock G, Clark S, Youngman L, Sleight P, Collins R; International Studies of Infarct Survival Collaborators. Eur Heart J. 2009 Sep;30(17):2137-46. Epub 2009 Jun 11. PMID: 19520708 doi:10.1093/eurheartj/ehp221 Conclusion: Apolipoprotein ratios are more informative about risk than lipid fractions are. This suggests that, among lipoprotein particles of a particular type (LDL or HDL), some smaller and larger subtypes differ in their effects on risk. Direct measurements of even more specific subtypes of lipoprotein particles may be even more informative about risk.

"I recently received an email from the Vitamin D Council regarding recent evidence that having adequate serum Vitamin D levels could be very important to avoiding illness from the H1N1 (swine) flu that is making the rounds. That will seem intuitive to those of you who read my earlier post about D, but it's good to see some real evidence. Some of you may have seen this information already on other blogs, including Richard's, but I have some new information and some comments to add."

"Peter at Hyperlipid and Stephan at Whole Health have dispelled yet again myths regarding the indictment of the 16:0 long-chained saturated fatty acid Palmitic Acid as the prime instigator of insulin resistance (IR). Researchers are always wrong -- it's... HIGH CARBS PLUS Palmitic acid. Their brilliant posts discuss below: --Sportzaid (FRUCTOSE) + Palmitate = IR RETARDNESS --High Carb Lab Chow + Palmitate = IR in the brain Yes. Such inferences applied to low carbers (LCers) is pure ridiculousness. Non-applicable. Low/no carb + Palmitic Acid = GOOD THING. All the low-carb/high saturated fat (palmitic acid) and ketosis trials by Hays JH, Volek JS, and Krauss RM have shown reductions in blood insulin, blood glucoses (BG) and peripheral tissue insulin resistance (IR). Directly contrary to the high carb animal or human studies. Palmitic acid has a special evolutionary, adaptive role in mammalian metabolism. Stephan showed that it likely 'fills in' when blood glucose starts to decline. "

"Anti-inflammatory Diet Components of an Anti-inflammatory Diet (focus on meats, fish, eggs and leafy vegetables)"

"We've been having an interesting discussion in the comments about a recently published paper by Dr. Stephen C. Benoit and colleagues (free full text). They showed that a butter-rich diet causes weight gain and insulin resistance in rats, compared to a low-fat diet or a diet based on olive oil. They published a thorough description of the diets' compositions, which is very much appreciated! They went on to show that infusing palmitic acid (a 16-carbon saturated fat) directly into the brain of rats also caused insulin resistance relative to oleic acid (an 18-carbon monounsaturated fat, like in olive oil). Here's a representation of palmitic acid. The COOH end is the acid end, and the squiggly line is the fatty end. Thus it's called a "fatty acid", various forms of which are the fat currency of the body."

"I like palmitic acid. It causes insulin resistance. Thank goodness. Ted sent me this link. It's depressing. I'm going to discuss a thought drug. I'm going to call it Palmitofake, and it can be developed by Pfizer, no, Fort Dodge. I particularly dislike FD for anaesthesia related reasons. So what does Palmitofake do? BTW, if you didn't need any other hint you can tell this drug is going to bomb as there is neither an x, y or z in its name. Trust FD to screw up (in my mind). Palmitofake is a fluoride substituted analogue of palmitic acid which irreversibly binds to the acyl-CoA interaction site of JNK1 and so inhibits the pathway by which palmitic acid keeps GLUT4 transporters off of the cell surface membrane, whole body-wide. The logic to this is that the lipotoxin, palmitic acid (nature's second biggest mistake, the biggest was obviously cholesterol) can no longer keep glucose out of cells and metabolism can run, unimpaired by fat, for ever on glucose. Woo hoo bring on the glucose."

Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy in patients with newly diagnosed type 2 diabetes: a randomized trial. Esposito K, Maiorino MI, Ciotola M, Di Palo C, Scognamiglio P, Gicchino M, Petrizzo M, Saccomanno F, Beneduce F, Ceriello A, Giugliano D. Ann Intern Med. 2009 Sep 1;151(5):306-14. Erratum in: Ann Intern Med. 2009 Oct 20;151(8):591. PMID: 19721018 Conclusion: Compared with a low-fat diet, a low-carbohydrate, Mediterranean-style diet led to more favorable changes in glycemic control and coronary risk factors and delayed the need for antihyperglycemic drug therapy in overweight patients with newly diagnosed type 2 diabetes.