Group items tagged

Conclusion: The associations suggest that replacing SFAs with PUFAs rather than MUFAs or carbohydrates prevents CHD over a wide range of intakes. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Jakobsen MU, O'Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Am J Clin Nutr. 2009 May;89(5):1425-32. Epub 2009 Feb 11. PMID: 19211817 doi:10.3945/ajcn.2008.27124

A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer's disease. Van der Auwera I, Wera S, Van Leuven F, Henderson ST. Nutr Metab (Lond). 2005 Oct 17;2:28. PMID: 16229744 doi:10.1186/1743-7075-2-28 CONCLUSION: Previous studies have suggested that diets rich in cholesterol and saturated fats increased the deposition of Abeta and the risk of developing AD. Here we demonstrate that a diet rich in saturated fats and low in carbohydrates can actually reduce levels of Abeta. Therefore, dietary strategies aimed at reducing Abeta levels should take into account interactions of dietary components and the metabolic outcomes, in particular, levels of carbohydrates, total calories, and presence of ketone bodies should be considered.

Fernandez ML, West KL. Mechanisms by which dietary fatty acids modulate plasma lipids. J Nutr. 2005 Sep;135(9):2075-8. Review. PMID: 16140878 [PubMed - indexed for MEDLINE]

It was observed that in post-menopausal women with documented heart disease from the Estrogen Replacement and Atherosclerosis (ERA) trial, a multicenter clinical trial evaluating the effects of hormone replacement therapy on atherosclerotic progression, in the group consuming the highest-saturated dietary fat diet (12.0% Sat Fat), an enlargement in coronary diameter of 0.01 mm and a 0.1% regression in coronary artery stenosis

Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Jakobsen MU, O'Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Am J Clin Nutr. 2009 Feb 11. [Epub ahead of print] PMID: 19211817 doi:10.3945/ajcn.2008.27124

A reappraisal of the impact of dairy foods and milk fat on cardiovascular disease risk. German JB, Gibson RA, Krauss RM, Nestel P, Lamarche B, van Staveren WA, Steijns JM, de Groot LC, Lock AL, Destaillats F. Eur J Nutr. 2009 Mar 4. [Epub ahead of print] PMID: 19259609 DOI: 10.1007/s00394-009-0002-5

"Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell."

"The diet-heart hypothesis is the idea that saturated fat, and in some versions cholesterol, raises blood cholesterol and contributes to the risk of having a heart attack. To test this hypothesis, scientists have been studying the relationship between saturated fat consumption and heart attack risk for more than half a century. To judge by the grave pronouncements of our most visible experts, you would think these studies had found an association between the two. It turns out, they haven't. The fact is, the vast majority of high-quality observational studies have found no connection whatsoever between saturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years."

According to Dr. Willcox, Principal Investor for the Okinawa Centenarian Study that started in 1975, "Among the entire population, which takes a sparing approach to food, there is 90 percent less coronary artery disease than in the wider world, a third less incidence of cancer, and breast cancer is virtually unheard of." HERE. In long-living Okinawan and Japanese, their dietary intake as surveyed in the 1970s was higher in both protein and dietary saturated fatty acids (see below abstract) compared to their shorter-lived peers at that time. When Okinawans move away (like to Brazil) heart disease risk factors appear (see last abstract). Diet is 80-90% of our health I believe because our bodies are designed to express what is dictated by our environment and food macro- micronutrients (foraging/hunting v. lounging; fecundity v. fasting). (These are the PPAR alpha gamma and delta receptors; their role is to 'sense nutrients' and to 'sense energy demand' in order to ultimately balance our energy needs). To me, the observations from blue zones and centenarian data always seem to reinforce that the physically active, low carb mod-high fat Paleo/TYP approach is the most optimal at this time, as it was for centenarians studied in the 1970s.

A diet rich in coconut oil reduces diurnal postprandial variations in circulating tissue plasminogen activator antigen and fasting lipoprotein (a) compared with a diet rich in unsaturated fat in women. Müller H, Lindman AS, Blomfeldt A, Seljeflot I, Pedersen JI. J Nutr. 2003 Nov;133(11):3422-7. PMID: 14608053 In conclusion, our results indicate that a coconut oil-based diet (HSAFA-diet) lowers postprandial t-PA antigen concentration, and this may favorably affect the fibrinolytic system and the Lp(a) concentration compared with the HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy seem to have a beneficial influence on Lp(a) levels. The connection between Lp(a) and atherosclerosis is not entirely understood. Different studies have provided strong evidence that Lp(a) level is an independent risk factor for developing coronary artery disease in men (47,48), but the question of causality continues to be debated. Recent data suggest that Lp(a) might be atherogenic (49), in particular when combined with other risk factors. High levels of Lp(a) combined with other risk factors such as the ratio of plasma total/HDL cholesterol have been shown to increase the risk for coronary heart diseases (50). It has also been reported that when substantial LDL cholesterol reductions were obtained in men with coronary heart disease, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening (51). In conclusion, the present results show that the HSAFA-diet lowered postprandial t-PA antigen and thus potentially improved fibrinolysis compared with the HUFA-diet. Diets with either high or low levels of saturated fatty acids from coconut oil beneficially decrease Lp(a) compared with a HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy may be of importance if the goal is to decrease Lp(a).

"I've always read that you should avoid coconut oil because of its high level of saturated fat. But I recently heard it is actually healthful and can help you lose weight. Is that true? Most nutritionists don't believe consuming coconut oil will help with weight loss -- the evidence is far from conclusive on that point. But most will also concede that the oil may not be the demon many think it is. To be honest, when it comes to nutrition research, the "truth" often seems elusive. Studies pronounce one verdict and then new findings point in another direction. That's simply the nature of the scientific process and the complexity surrounding nutrition and health. As long as we persist in hunting for more precise answers, we'll continue to encounter surprises. "

"Jennifer Aniston uses it and the England rugby squad swear by its metabolism-boosting qualities. Coconut oil is being touted as the health food of 2008 - but is this just more 'superfood' hype? By Lucy Atkins"

"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]

No one can dispute that mother's milk is the ideal nutrition, as far as the biochemical composition is concerned. It contains 3 to 11 grams of fat per 1 gram of protein (0.4% unsaturated fat). The conclusion is obvious - if Nature included such a minute quantity of that constituent in such a wonderful food, then we should respect it. Meanwhile, people are being persuaded that plant-derived fats containing polyunsaturated fatty acids which do not exist in mother's milk, are healthy. Nothing is more misleading. The best are the fats which contain the highest percentage of energy contributing constituents, or in other words, such in which COOH group is attached to the longest fatty acid chain. Short fatty acid chains contain around 30-40% of energy-contributing constituents, the longest ones over 90%. Long-chain fatty acids fully saturated with hydrogen, yields approx. 10 cal/g when metabolised, the same as petrol. Fat's value as a "fuel" for our body increases with the increase in the amount of hydrogen per gram of carbon in its molecule, with the increase in the energy-contributing constituents. Chemically, the best are long-chain fully saturated fatty acids, that is to say, solid fats of animal origin. Only fats with the length of the chain above 10 carbon atoms are suitable to be utilised by our cells and tissues without conversion. These fats are directed straight to the blood stream via the lymphatic system, and they do not have to be converted and made suitable by the liver, as is the case with inferior fats (with shorter chains), or all other constituents of consumed and digested foods

How could changes in diet explain changes in coronary heart disease mortality in Spain? The Spanish paradox. Serra-Majem L, Ribas L, Tresserras R, Ngo J, Salleras L. Am J Clin Nutr. 1995 Jun;61(6 Suppl):1351S-1359S. PMID: 7754987 We review and compare trends in coronary heart disease (CHD) and stroke mortality in Spain from 1966 to 1990 and changes in food consumption at national and regional levels. Since 1976, a decrease in cardiovascular disease (CVD) mortality in males and females has been observed, and standardized CHD mortality rates have fallen. Stroke mortality decreased during the same period. Trends in food consumption show increases in intakes of meat, dairy products, fish, and fruit, but decreases in consumption of olive oil, sugar, and all foods rich in carbohydrates. Although fat and saturated fat intakes increased, these changes were not accompanied by an increase in CHD mortality rates. This paradoxical situation can be explained by expanded access to clinical care, increased consumption of fruit and fish, improved control of hypertension, and a reduction in cigarette smoking. Diet appears to have an important role in this paradox, but it may not be as critical as other factors. Nevertheless, we suggest dietary guidelines for prevention of CHD in Spain.

"Should you eat low carbohydrate and high saturated fat, or high carbohydrate and low fat, that is the question? This question is causing a tremendous back and forth in the medical and nutrition industry. It is unbelievable that the medical profession has not at least thoroughly tested the question. How is it that a magnificent experiment had been going on for 2.5 million years, the hunter gatherer Paleolithic life. This continued up to and until about about 10,000 years ago, with the advent of agriculture. After that time is when the diseases of the metabolic syndrome started to appear. This information is a matter of history. If a layman like me can recognize the validity of an experiment that continued for 2,5 million years, and produced healthy individuals, relative to the diseases of the metabolic syndrome, such as: obesity, diabetes type 2, cardiovascular disease and stroke, and some cancers to name just a few, then how is it, that the consensus opinion of the medical profession and nutritionists think that the hunter gatherer lifestyle of our ancient ancestors is unhealthful or dangerous? The consensus opinion says that low fat (trim all visible fat from the animal protein) and high carbohydrate food is the "healthy eating" choice for us. I personally know that instead of being healthy,it is unhealthy, because by following my doctors advice over the last 50 years many of the above mentioned diseases started to appear on my charts. "

The effect of select nutrients on serum high-density lipoprotein cholesterol and apolipoprotein A-I levels. Mooradian AD, Haas MJ, Wong NC. Endocr Rev. 2006 Feb;27(1):2-16. Epub 2005 Oct 21. Review. PMID: 16243964 One of the factors contributing to the increased risk of developing premature atherosclerosis is low plasma concentrations of high-density lipoprotein (HDL) cholesterol (HDLc). Multiple potential mechanisms account for the cardioprotective effects of HDL and its main protein apolipoprotein A-I (apo A-I). The low plasma concentrations of HDL could be the result of increased fractional clearance and reduced expression of apo A-I. To this end, nutrients play an important role in modulating the fractional clearance rate, as well as the rate of apo A-I gene expression. Because medical nutrition therapy constitutes the cornerstone of management of dyslipidemias, it is essential to understand the mechanisms underlying the changes in HDL level in response to alterations in dietary intake. In this review, we will discuss the effect of select nutrients on serum HDLc and apo A-I levels. Specifically, we will review the literature on the effect of carbohydrates, fatty acids, and ketones, as well as some of the nutrient-related metabolites, such as glucosamine and the prostanoids, on apo A-I gene expression. Because there are multiple mechanisms involved in the regulation of serum HDLc levels, changes in gene transcription do not necessarily correlate with clinical observations on serum levels of HDLc.

"Butyric acid (from Greek βούτυρος = butter), also known under the systematic name butanoic acid, is a carboxylic acid with the structural formula CH3CH2CH2-COOH. Salts and esters of butyric acid are known as butyrates or butanoates. Butyric acid is found in rancid butter, parmesan cheese, vomit, and body odor and has an unpleasant smell and acrid taste, with a sweetish aftertaste (similar to ether). It can be detected by mammals with good scent detection abilities (such as dogs) at 10 ppb, whereas humans can detect it in concentrations above 10 ppm. Butanoate is produced as end-product of a fermentation process solely performed by obligate anaerobic bacteria. Fermented Kombucha "tea" includes butyric acid as a result of the fermentation. This fermentation pathway was discovered by Louis Pasteur in 1861. The role of butyrate changes depending on its role in cancer or normal cells. This is known as the "butyrate paradox". Butyrate inhibits colonic tumor cells but promotes healthy colonic epithelial cells.[1], but the signaling mechanism is not well understood.[2]. A review suggested that the chemopreventive benefits of butanoate depend in part on amount, time of exposure with respect to the tumorigenic process, and the type of fat in the diet.[5] Low carbohydrate diets like the Atkins diet are known to reduce the amount of butanoate produced in the colon

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Am J Clin Nutr. 2010 Jan 13. [Epub ahead of print] PMID: 20071648 doi:10.3945/ajcn.2009.27725 Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.

Dietary mono- and polyunsaturated fatty acids similarly affect LDL size in healthy men and women. Kratz M, Gülbahçe E, von Eckardstein A, Cullen P, Cignarella A, Assmann G, Wahrburg U. J Nutr. 2002 Apr;132(4):715-8. PMID: 11925466 In conclusion, our data indicate that dietary unsaturated fat similarly reduces LDL size relative to saturated fat. However, the small magnitude of this reduction also suggests that the composition of dietary fat is not a major factor affecting LDL size.