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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.

"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. "

"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. "

The Diet-Heart Hypothesis: Subdividing Lipoproteins Two posts ago, we made the rounds of the commonly measured blood lipids (total cholesterol, LDL, HDL, triglycerides) and how they associate with cardiac risk. It's important to keep in mind that many things associate with cardiac risk, not just blood lipids. For example, men with low serum vitamin D are at a 2.4-fold greater risk of heart attack than men with higher D levels. That alone is roughly equivalent to the predictive power of the blood lipids you get measured at the doctor's office. Coronary calcium scans (a measure of blood vessel calcification) also associate with cardiac risk better than the most commonly measured blood lipids. Lipoproteins Can be Subdivided into Several Subcategories In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source): The plasma lipoprotein profile accompanying a preponderance of small, dense LDL particles (specifically LDL-III) is associated with up to a threefold increase in the susceptibility of developing [coronary artery disease]. This has been demonstrated in case-control studies of myocardial infarction and angiographically documented coronary disease. Krauss found that small, dense LDL (sdLDL) doesn't travel alone: it typically comes along with low HDL and high triglycerides*. He called this combination of factors "lipoprotein pattern B"; its opposite is "lipoprotein pattern A": large, buoyant LDL, high HDL and low triglycerides. Incidentally, low HDL and high triglycerides are hallmarks of the metabolic syndrome, the quintessential modern metabolic disorder. Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily

"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."

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.

Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. Prior IA, Davidson F, Salmond CE, Czochanska Z. Am J Clin Nutr. 1981 Aug;34(8):1552-61. PMID: 7270479 Two populations of Polynesians living on atolls near the equator provide an opportunity to investigate the relative effects of saturated fat and dietary cholesterol in determining serum cholesterol levels. The habitual diets of the toll dwellers from both Pukapuka and Tokelau are high in saturated fat but low in dietary cholesterol and sucrose. Coconut is the chief source of energy for both groups. Tokelauans obtain a much higher percentage of energy from coconut than the Pukapukans, 63% compared with 34%, so their intake of saturated fat is higher. The serum cholesterol levels are 35 to 40 mg higher in Tokelauans than in Pukapukans. These major differences in serum cholesterol levels are considered to be due to the higher saturated fat intake of the Tokelauans. Analysis of a variety of food samples, and human fat biopsies show a high lauric (12:0) and myristic (14:0) content. Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations.

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.

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

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).

"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."

"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. "

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

Food Choices and Coronary Heart Disease: A Population Based Cohort Study of Rural Swedish Men with 12 Years of Follow-up. Sara Holmberg, Anders Thelin and Eva-Lena Stiernström. Int. J. Environ. Res. Public Health 2009, 6(10), 2626-2638; doi:10.3390/ijerph6102626 - published online 12 October 2009 Coronary heart disease is associated with diet. Nutritional recommendations are frequently provided, but few long term studies on the effect of food choices on heart disease are available. We followed coronary heart disease morbidity and mortality in a cohort of rural men (N = 1,752) participating in a prospective observational study. Dietary choices were assessed at baseline with a 15-item food questionnaire. 138 men were hospitalized or deceased owing to coronary heart disease during the 12 year follow-up. Daily intake of fruit and vegetables was associated with a lower risk of coronary heart disease when combined with a high dairy fat consumption (odds ratio 0.39, 95% CI 0.21-0.73), but not when combined with a low dairy fat consumption (odds ratio 1.70, 95% CI 0.97-2.98). Choosing wholemeal bread or eating fish at least twice a week showed no association with the outcome.

"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."

Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study. Ebbesson SO, Roman MJ, Devereux RB, Kaufman D, Fabsitz RR, Maccluer JW, Dyke B, Laston S, Wenger CR, Comuzzie AG, Romenesko T, Ebbesson LO, Nobmann ED, Howard BV. Atherosclerosis. 2008 Aug;199(2):346-53. Epub 2007 Dec 4. PMID: 18054937 doi:10.1016/j.atherosclerosis.2007.10.020 Conclusions Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs.

The serum LDL/HDL cholesterol ratio is influenced more favorably by exchanging saturated with unsaturated fat than by reducing saturated fat in the diet of women. Müller H, Lindman AS, Brantsaeter AL, Pedersen JI. J Nutr. 2003 Jan;133(1):78-83. PMID: 12514271 We conclude that, to influence the LDL/HDL cholesterol ratio, changing the proportions of dietary fatty acids may be more important than restricting the percentage of total or saturated fat energy, at least when derived mainly from lauric and myristic acids, both of which increase HDL cholesterol.