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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.

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.

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).

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

Fish consumption shifts lipoprotein subfractions to a less atherogenic pattern in humans. Li Z, Lamon-Fava S, Otvos J, Lichtenstein AH, Velez-Carrasco W, McNamara JR, Ordovas JM, Schaefer EJ. J Nutr. 2004 Jul;134(7):1724-8. PMID: 15226460 The effect of fish consumption on plasma lipoprotein subfraction concentrations was studied in 22 men and women (age > 40 y). Subjects were provided an average American diet (AAD, 35% of energy as fat, 14% as saturated fat, and 35 mg cholesterol/MJ) for 6 wk before being assigned to a National Cholesterol Education Program (NCEP) Step 2 high-fish diet (n = 11, 26% of energy as fat, 4.5% as saturated fat, and 15 mg cholesterol/MJ) or a NCEP Step 2 low-fish diet (n = 11, 26% of energy as fat, 4.0% as saturated fat, and 11 mg cholesterol/MJ) for 24 wk. All food and drink were provided to study participants. Consumption of the high-fish NCEP Step 2 diet was associated with a significant reduction in medium and small VLDL, compared with the AAD diet, whereas the low-fish diet did not affect VLDL subfractions. Both diets significantly reduced LDL cholesterol concentrations, without modifying LDL subfractions. Both diets also lowered HDL cholesterol concentrations. However, the high-fish diet significantly lowered only the HDL fraction containing both apolipoprotein (apo) AI and AII (LpAI:AII) and did not change HDL subfractions assessed by NMR, whereas the low-fish diet significantly lowered the HDL fraction containing only apo AI (LpAI) and the large NMR HDL fractions, resulting in a significant reduction in HDL particle size. Neither diet affected VLDL and LDL particle size. Our data indicate that within the context of a diet restricted in fat and cholesterol, a higher fish content favorably affects VLDL and HDL subspecies

"A friend has emailed me the full text of Pawel Grieb's paper documenting a number of physiological parameters of medium to long term Optimal Diet (OD) eaters in Poland, as pointed out by Flo and Stan. There are a few points worth making. The biggest mistake, BTW, is that the authors claim (correctly) that the OD diet aims for >70% fat with (incorrectly) "no restriction on the type of fat (saturated or unsaturated) or cholesterol level". I think they meant that the OD does not ban saturated fats. This is of course true but the impression given is that the OD allows "healthy" fats, which are, of course, inedible. So the heavy emphasis on saturated fats is missed by the paper. A pity, anyone might be left thinking corn oil is a human food... The first positive aspect is that this is a multi author study, eleven authors from several medical centres/unversities. So it's not a one man band case report. I like that. The second is that it is remarkably positive about the findings throughout. Even the elevated LDL cholesterol levels are not taken as extreme and are not trumpeted from the rooftops as the portent of imminent cardiovascular doom. So refreshing!"

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.

Choose healthy fats, limit saturated fat, and avoid trans fat.\n\nThe total amount of fat you eat, whether high or low, isn't really linked with disease. What really matters is the type of fat you eat.\n

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

"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."

"Aug. 31, 2009 -- Eating a Mediterranean-style diet may help people with type 2 diabetes keep their disease under control without drugs better than following a typical low-fat diet. A new study from Italy shows that people with type 2 diabetes who ate a Mediterranean diet rich in vegetables and whole grains with at least 30% of daily calories from fat (mostly olive oil) were better able to manage their disease without diabetes medications than those who ate a low-fat diet with no more than 30% of calories from fat (with less than 10% coming from saturated fat choices). After four years, researchers found that 44% of people on the Mediterranean diet ended up requiring diabetes medications to control their blood sugars compared with 70% of those who followed the low-fat diet. It's one of the longest-term studies of its kind, and researchers, including Katherine Esposito, MD, of the Second University of Naples, say the results "reinforce the message that benefits of lifestyle interventions should not be overlooked.""

"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. "

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.

"Some people promote coconut oil as a healthy addition to a weight-loss diet, even though it has higher levels of saturated fat. WebMD Feature Reviewed By Brunilda Nazario Is it possible to add fat to your diet and lose weight? Yes, if it's the right fat, says naturopath Bruce Fife, ND, author of Eat Fat Look Thin. He recommends adding coconut oil and substituting it for polyunsaturated oils to suppress appetite, boost metabolism, and bring about weight loss. "Lots of people have reported that when they add coconut oil to their diet, it was enough to promote weight loss," says Fife. "Some people don't notice a drop in weight, which often means they're simply eating too much. Calories are important." His own experience with coconut oil produced a gradual weight loss over six months of about 20 pounds, which he'd been unable to lose previously through diet and exercise. He advises using about three tablespoons of natural coconut oil, either virgin or processed, daily. His patients use it in place of polyunsaturated fats for stir-frying and salad dressings, add it to other foods, or take it straight. The fat is also present in canned coconut milk (not the liquid inside the coconut), which can be substituted for milk in many recipes, and fresh coconut fruit, which can be eaten as a snack or grated over fruits and salads"

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.

Cardiovascular disease risk of dietary stearic acid compared with trans, other saturated, and unsaturated fatty acids: a systematic review1,3. Hunter JE, Zhang J, Kris-Etherton PM. Am J Clin Nutr. 2009 Nov 25. [Epub ahead of print] PMID: 19939984 doi:10.3945/ajcn.2009.27661 Conclusions: TFA intake should be reduced as much as possible because of its adverse effects on lipids and lipoproteins. The replacement of TFA with STA compared with other saturated fatty acids in foods that require solid fats beneficially affects LDL cholesterol, the primary target for CVD risk reduction; unsaturated fats are preferred for liquid fat applications. Research is needed to evaluate the effects of STA on emerging CVD risk markers such as fibrinogen and to understand the responses in different populations.

Giving saturated fat another chance. Saturated fat has long held a bad rep and been noted for its potential to contribute to cardiovascular disease. So you might understand why I was a bit skeptical of all the hype surrounding the supposedly miracle-working power of coconut oil, which is composed of saturated fatty acids. However, if there's one thing I have learned as a nutrition student, it is that research has the potential to change our views as we continue to expand our knowledge and make new discoveries. Coconut oil may prevent and alleviate disease. Both research and clinical studies have shown that MCFA may be useful in treating and preventing diseases such as diabetes, osteoporosis, virus-related dieases (mononucleosis, hepatitis C, herpes, etc.), gallbladder disease, Crohn's disease, and cancer. The smaller size of MCFA (compared to LCFA) allows them to be digested more easily, making them ideal for those suffering from digestive diseases. Coconut oil may assist in the absorption and retaining of calcium, thereby benefiting bones. Coconut oil has antimicrobial, antiviral, and antifungal properties. Lipid-coated bacteria and viruses contain a lipid coat which encloses their DNA among other cellular materials. When consumed by humans, coconut oil disrupts the lipid membrane, killing the pathogens without damaging the host or harming health-promoting intestinal bacteria. The antimicrobial properties stem from the monoglycerides and free fatty acids (mainly lauric acid and capric acid) that compose coconut oil.

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

Not all steaks are created equal. Thus choosing the right grade and the right cut of meat makes all the difference in how tender the steak is and how much saturated fat and cholesterol you end up ingesting. Never mind the calories. The tenderness of a steak depends on where the steak is cut from. Beef is a muscle and the more the muscle is worked, the less fat it has. Steaks that have less fat are not as tender.

Scientific evidence points to the fact that eating sugar and fat may stimulate the pleasure at the same body receptors (opioid receptors) that respond to the drug morphine. Thus, eating fat can make us, if not addictive, at least very close to it. And here is why.