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Part 4 Fats role in CVD

transports fats and cholesterol from intestines

Low Density Lipoprotein; transport from liver

The page and the subsequent 8 parts are being updated so as to better account for the evidence of infective agents in the cardiovascular disease process. It will be completed by October of 2015.  For the evidence in support of infection in the artery walls,  for an evaluation of the cholesterol myth

    Part 4  Fats role in CVD  http://healthfully.org/rh/id4.html   (8/23 /15)

AS        Atherosclerosis


N3         Omega 3 fatty acids   

CVD     Cardiovascular disease


N6         Omega 6 fatty acids   

HT        Hypertension


MeS      Metabolic syndrome[1][1]

IR         Insulin resistance


NALFD  Non-alcoholic fatty liver disease

KOL     Key opinion leader


T2D       Type 2 Diabetes

MI        Myocardial infarction


TC          Total Cholesterol


Background: Building on Part 1 the cause of cardiovascular disease (CVD) was not dyslipidemia, but rather reactive chemicals damaging LDL within the muscular part of the artery wall and the subsequent immune response which resulted in atherosclerosis (AS).   Part 1 went to list the vital roles of cholesterol and that lowering cholesterol levels does not prevent CVD since it doesn’t prevent atherosclerosis (AS).  Part 2 follows from part 1; it sets out the cholesterol myth (that cholesterol does not cause CVD) and thus using statins to lower cholesterol not only doesn’t prevent CVD or AS, but given the importance of cholesterol and other products of the mevalonate pathway, that disruption by statins of the synthesis of these essential bioactive chemicals is a very bad idea, especially for the elderly.   Part 3 is on the role of carbohydrates through glycation and oxidative products of metabolism that is the leading causal factor for AS and CVD, and an assortment of chronic age-related conditions.  First among the carbohydrates is fructose, which is one half of the disaccharide sucrose.  Fructose in high amounts damages the liver which leads to the development of insulin resistance (IR) and metabolic syndrome (MeS)--how.  We will be exploring the fat myths. 


Saturated Fats are safer than carbohydrates:  in 11 out of 12 studies reviewed in Wikipedia, results did not show a benefit from low fat, or increased ratio of polyunsaturated fats  A meta-analysis of 21 studies considered the  effects of saturated fat intake and found that Intake of saturated fat was not associated with an increased risk of CHD (coronary heart disease), stroke, or CVD (cardiovascular disease)" Wiki.  Low fat entails more carbs for energy with their negative consequences.  Indeed, recent prospective cohort studies have not supported any significant association between saturated fat intake and cardiovascular risk.  Instead, saturated fat has been found to be protective. The source of the saturated fat may be important. Dairy foods are exemplary providers of vitamins A and D. As well as a link between vitamin D deficiency and a significantly increased risk of cardiovascular mortality, calcium and phosphorus found commonly in dairy foods may have antihypertensive effects that may contribute to inverse associations with cardiovascular risk.  Meat is another major source of saturated fat. Consumption of processed [luncheon] meats has been associated with coronary heart disease and diabetes mellitus, which may be explained by nitrates and sodium as preservativesBMJ 10/22/13.  And it gets worse:  instead endpoint deaths and ischemic events, pharma uses the surrogate endpoint increased serum levels of LDL, Cholesterol, and triglycerides.  However in quality studies the associate is non-existent or nearly so.  There are no clear health benefits of replacing saturated fats with starchy foods (reducing the total amount of fat we eat). Heart and vascular disease includes heart attacks, angina, strokes, sudden cardiovascular death and the need for heart surgery” the prestigious Cochrane Review.  It get worse, for saturated fats  have been replaced by the unhealthy polyunsaturated fats, and the recommended low-fat diet entails entails more from carbohydrates and thus an increase in sugars, which has produced the health disaster of the Western diet that has cause the obesity, diabetes, and MeS epidemic.  Having said all this, there are important details.  For one, that a high carb diet low on sugar (the traditional diet of Orientals with the high glycemic index white rice and but 14 grams of sugar does not result in an association with CVD; and also for tribes on a high carb paleo-diet.  As pointed out at http://healthfully.org/rc/id23.html the combination of high fructose with glucose (mainly from starches) as a steady diet causes a fatty liver which results in mucking up the metabolic regulatory system.  This and other factors determine risk (see http://healthfully.org/rh/id12.html).  Thus like fats, all carbs are not equal, and lifestyle difference influence risk—click on link.          

.   http://upload.wikimedia.org/wikipedia/commons/thumb/a/a9/Isomers_of_oleic_acid.png/300px-Isomers_of_oleic_acid.png Cis-2-butene.svgcis-2-butene


Saturated fats are best, polyunsaturated fats worse:  The truth lies in the details:  one, health science has been kicked under the bus by corporate influence which produces tobacco science and uses its influence in the process and among politicians to promote financial gains.  In particular the agriculture and manufactured food lobbies have shaped government regulations around the world, starting with the US in 1977 and UK in 1983 to recommend cutting the intake of fats by 25% and reducing saturated fats as much as possible on the bogus claim that they cause dyslipidemia (high serum fatty acids and triglycerides) and coronary heart disease (CHD).  For an excellent historical thorough recount of how this happened plus a summation of the benefits of saturated fats, click on the link to Prof. Miller’s lecture (notes are in supplement below).  However saturated fats don’t go rancid:  they are not subject to oxidation on the shelf or in your body.  All the carbon bonds are taken—unlike monounsaturated fats such as the cis and trans-oleic acid shown above and polyunsaturated fats are subject to a much higher rate of oxidation and glycation[2].  This oxidation and glycation is called rancidification.  Rancid fats cannot be safely disposed of because of lack of enzyme for that purpose.  They accumulate in your body and mess up various systems.  Moreover they also in the process of their product give rise to reactive oxygen species (ROS), which cause more damage.  It is to prevent ROS and rancidification that milk fat is very low in polyunsaturated fats (under 5%) and so too for beef fat (<10%).  Evolution has set it up so that milk is low in the unhealthful polyunsaturated fats.  And it gets worse.  Polyunsaturated fats are high in omega-6 fatty acids and they block the healthful  omega-3.  Omega-3 fats (EPA and DHA—not plant ALA)[3] have important immune system functions.  This unhealthful low omega-3 has many chronic conditions relating to the immune system.  Vegetable oils are high in omega-6 and high in polyunsaturated fats.  Nut oils are low in polyunsaturated fats as too are animal sources of fats.  The highly processed vegetable oils are high in polyunsaturated fats.  Moreover to improve their flavor when used with starches, food manufactures buy the partially hydrogenated plant fats.  Like with rancid fats, they too lack enzymes for their disposal, and thus contribute to cardiovascular disease.  These are the best kind. Eat more of them and less carbs.  At the end of this paper this topic is further developed as to diet.     


Basics on fatty acids (fats) and triglycerides:  the dietary significant fats consist of a chain of 4 to 28 carbon molecules with an organic carboxylic acid group on the last carbon.  Fatty acids are derived from triglycerides  or phospholipids.  Each carbon can have 4 single bonds because there are just 4 valance electrons.  If the carbon has a double bond with another carbon it is ”unsaturated”, and “polyunsaturated” with 2 or more double bonds.  Having a double bond entails that there is only a single hydrogen (see stick drawing above) on each of the carbons in the double bond; and if they are on the same side it is called “cis” and if on opposite sides “trans”.  Natural trans-fats occur only in trace amounts.  A few polyunsaturated fatty acids are termed “essential” because they are used to synthesize a number of important bioactive compounds and they come only from food sources.  They are grouped into omega-3 (N-3) and omega-6 (N-6) fatty acids.[4]  Compared to carbohydrates and protein, fatty acids yield the most ATP on an energy per gram basis—9 calories of energy per gram, digestible sugars and starches 4.  Free fatty acids can be converted to triglycerides and stored in adipose tissue.  “They are consumed in the mitochondria to produce ATP through beta oxidation, whereby they generate acetyl-coA, which enters the citric acid cycle, and NADH andFADH2, which are used by the electron transport chainWiki.  Fatty-acid catabolism involves three stages. The first stage is beta-oxidation. The second stage is acetyl CoA oxidation to carbon dioxide. The third stage is electron transfer from electron carriers to the electron transfer chain.  α-Oxidation is used for branched fatty acids that cannot directly undergo β-oxidation such as phytanic acid. Fatty acids with very long chains (20 or more carbons) are first broken down to a manageable size in peroxisomes.  Nearly every type of cell can produce its own ATP from fatty acids.  Muscle cells also contain globules of fat, which are used for energy during aerobic exercise. The aerobic energy systems take longer to produce the ATP and reach peak efficiency, and requires many more biochemical steps, but produces significantly more ATP than anaerobic glycolysis, which produces 2 lactic acid molecules” Wiki.   Because of the lack of glycation type reaction, fats are a preferred ATP source.

Role of dietary fats:  “Knowledge of the nutritional importance of dietary fats has greatly expanded since the time when fats were considered only a source of calories.  We now know that dietary fats supply the essential fatty acids (linoleic and linolenic acid) that are precursors for prostaglandins and they are important components of membrane structures.  Fats also influence cell functions, serve as carriers for fat-soluble vitamins, affect immunological function, and are associated or involved with a number of diseases and disorders” Am Rev Nut, 1984 pgs.339-364.     Though we have heard much about the importance of the omega-3 fatty acid, saturated also have important bodily functions.

Reversal on saturated fats, history of dogma and its decline:  The confusion comes from using the surrogate marker cholesterol level instead of CVD, though it isn’t a causal factor.  This is compounded by the association of the artificially high dietary omega-6 fats (see below section) causes of CVD. Without a mechanism for the association of CVD with saturated fats and the failure to find evidence in a meta-analysis of 21 studies,[5] the current government position on dietary fats (recommending reduction) is in error.  A hundred years ago 1 in 100 obesity and cardiac heart disease was unknown.  The primary causes of death were enteritis [intestinal infection], TB, pneumonia, and diarrhea.   Heart disease and cancer today account for 75% of death.  There were 500 cardiologists practicing in 1950; there are 39,000 now.  In 1911 Procter and Gambled stared marketing manufactured Crisco, which they marketed it as more healthful than animal fat.  It was hydrogenated vegetable fat.  In 1913 Nikolaj Anitschkow (Russian) fed rabbits cholesterol and showed that it caused atherosclerosis. In 1948 Framingham Study a comprehensive study of a town in Massachusetts funded by the government; it showed that those with elevated cholesterol were more likely to die of heart disease.   Six years later the American Heart Association 6 years later promoted with the prudent diet.  Ancel Keyes Six Country study found the highest percentage of carbohydrates and the lowest of fats in their diet have the lowest incidence of heart disease.  This study was flawed:  Keyes had the data on 22 countries and picked out 6 to support his hypothesis.[6] Moreover, those who have the highest saturated fat in their diet have the lowest rate of coronary disease:  Maasi of Kenya 66% saturated fats; Inuit of Canada, 75%; Rendille tribe of Kenya, 63%; Tokelau of New Zealand, 63%.  Most hunter gatherers groups eat high amounts of saturated fats, up to 93% of their calories.  The Framingham Study[7] reversed its position:  “(1) over the age of 50 there is no increased overall mortality form either high or low serum cholesterol levels, and (2) in people with a falling cholesterol level (over the first 14 years of the study, before statins) for each 1% mg/dl drop in cholesterol there was an 11 percent increase in all-cause mortality (over the next 18 years).  Dr. William Castelli, the third director of the Study, states: “In Framingham, Mass., the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person’s serum cholesterol… We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least, and were the most physically active” quoted from the lecture to a professional audience by Dr. Donald Miller, professor of Surgery at the Cardiothoracic Division of the University of Washington, July 17,2011, at https://www.youtube.com/watch?v=vRe9z32NZHY.  These statements by Dr. Miller are supported in the journal literature.  Dr. Miller also listed on a slide the importance of saturated fats:

“Cell membranes:  Require (50%) saturated fatty acids to be waterproof and function properly.

Heart:  Prefers saturated long-chain 16-carbon palmitic and 18-C stearic (over carbohydrates) for energy

Bone: needs saturated fats to assimilate calcium effectively

Liver:  Protects from adverse effects of alcohol and medications like acetaminophen

Lung: Lung surfactant, which prevent asthma and other breathing disorders, is composed entirely of 16-C palmitic acid

Hormones:  Function as signaling messengers for hormone production

Immune system:  Saturated fats play an important role here.  They prime white-blood cells to destroy invading bacteria, viruses and fungi, and to fight tumors.  Medium Chain 12-C lauric acid and 14-C mystic acid (in butter) kill bacteria and candida in the gut

Signal satiety:  Promotes satiation through slowing digestion

General health:  Eating saturated fats lowers the consumption of health when compared to polyunsaturated fats which due to high content of omega-6 fat acids reduce the positive immune system effect of omega-3 fatty acids.

Reduces age related chronic conditions which are a result of the monosaccharides obtained through digestion of carbohydrates which damage proteins through the process of glycation. Eating less fats entails replacing them with carbohydrates as a source of energy.  The high carbohydrate Western diet has brought about the sharp rise in obesity, metabolic syndrome, insulin resistance, and type-2 diabetes all of which are strongly statistically associated with an assortment of chronic and fatal conditions.   

Saturated fats:  Saturated fats were linked to CVD by failing to control for the transfats, high N-6 to N-3 ratio and transfats produced through hydrogenation of unsaturated oils.   Though these flaws have been pushed by business, surprising, 22 metastudies found no association of saturated fats with CVD.  If you have any doubt over the venal nature of governments, read about the disjunction between government holdings around the world, read this footnote. [8]  In general, a more reliable way to solve biological question is in the laboratory where analysis reveals the disease causing process, and this is confirmed in animal experiments.  At Scholar.Goolge.com, a search of “rats + saturated fats + cardiovascular disease” had zero studies. Wikipedia also under saturated fats doesn’t have a section show the bio-pathway for causing CVD. The proposed association with elevated LDL is without sound, consistent evidence; moreover, elevated LDL does not promote CVD, though pharma promotes that myth for to sell cholesterol lowering drugs—see cholesterol myth.  The lack of modus operandi based on laboratory experiments is a major reason to question the putative causal connection to CVD.  A high saturated fats diet lowers the consumption of sugars and is low in vegetable oils (lower trans-fats and high levels of n-6), and thus lowers risk for CVD and obesity.  The recommendations of the national health agencies around the world are another example of marketing before science and the politicalization of the guideline process.  It stands in contrast to science:  A meta-analysis of 21 studies considered the effects of saturated fat intake and found that "Intake of saturated fat was not associated with an increased risk of CHD (coronary heart disease), stroke, or CVD (cardiovascular disease)” Wiki. Moreover the main saturated fatty acid from tropical trees (coconut and palm kernel oil), lauric acid is cardiovascular protective because it increases HDL.[9]  Finally “the energy yield from a gram of fatty acids is approximately 9 kcal (37 kJ), compared to 4 k cal/g (17 kJ/g) for carbohydrate, and compared to carbohydrates fatty acids can hold more than six times the amount of energy per unit of storage space.  Put another way, if the human body relied on carbohydrates to store energy, then a person would need to carry 31 kg (67.5 lb) of hydrated glycogen to have the energy equivalent to 4.5 kg (10 lb) of fatWiki.  Fats don’t cause glycation.  For these reasons a diet low in (a) fructose, (b) those starches that are quickly absorbed (have high insulin index) and (c) omega-6 and trans-fats, and are high in saturated fats and most starches is the best source for ATP (energy).  Pharma, food industry, and government have done it again:  turned good into bad, and the bad into good, and we the consumers pay with the length and quality of our lives.

Essential fatty acids (EFAs) “are fatty acids that humans and other animals must ingest because the body requires them for good health but cannot synthesize them.  Only two fatty acids are known to be essential for humans: alpha-linolenic acid (an omega-3 fatty acid, N-3) and linoleic acid (LA, an omega-6 fatty acid, N-6).  They are modified to make.  Omega-6 fatty acids are a family of unsaturated fatty acids that have in common a final carbon-carbon double bond in the n-6 position, that is, the sixth bond, counting from the methyl end.  Functions  (The biological effects of the ω-3 and ω-6 fatty acids are mediated by their mutual interactions):

A few of the polyunsaturated fats in the human diet are EFAs. Essential fatty acids play an important role in the life and death of cardiac cells” Wiki.  “Following WWI large-scale production of vegetable oils and the shift to o grain-fed cattle (from grazing cattle) caused a marked increase in the ratio of the omega 6 to 3 oils from 2:1 to 16:1.  Man evolved in a world for which n-6 to n-3 ratio was around 2:1; the gross 20th century deviation from this ratio has dire consequences.  Proof of this causality is demonstrated both in laboratory analysis and clinical trials, but only when the ratio of N-6 to N-3 is 4:1 or less” A. P. Simopulos. “The actions of the N-3 (omega-3) and N-6 (omega-6) essential fatty acids (EFAs) are best characterized by their  interactions; they cannot be understood separately” Wiki.  They compete for the same receptors during synthesis, see above.  Some older clinical studies indicate that the ingested ratio of omega-6 to omega-3 (especially linoleic vs alpha-linolenic) fatty acids is important to maintaining cardiovascular health. However, three studies published in 2005, 2007 and 2008, including a randomized controlled trial, found that, while omega-3 polyunsaturated fatty acids are extremely beneficial in preventing heart disease in humans, the levels of omega-6 polyunsaturated fatty acids (and, therefore, the ratios) did not matter” Wiki. 


Omega-3 fatty acid:  Out of a total of 11, there are three types of omega-3 fatty acids involved in human physiology are ALA (found in plant oils), EPA, and DHA (both commonly found in marine oils)” Wiki.   “Many experimental studies have provided evidence that incorporation of alternative fatty acids into tissues may modify inflammatory and immune reactions and that omega-3 fatty acids in particular are potent  therapeutic agents for inflammatory diseases [AS, Alzheimer’s, arthritis, etc.]  Supplementing the diet with omega-3 fatty acids (3.2 g EPA and 2.2 g DHA [N-3s]) in normal subjects increased the EPA content in neutrophils and monocytes more than sevenfold without changing the quantities of AA [arachidonic acid] and DHA.  Inflammation plays an important role in both the initiation of atherosclerosis and the development of atherothrombotic events. When humans ingest fish or fish oil, the EPA and DHA from the diet partially replace the omega-6 fatty acids, especially AA, in the membranes of probably all cells, but especially in the membranes of platelets, erythrocytes, neutrophils, monocytes, and liver cells.  Inflammation plays an important role in both the initiation of atherosclerosis and the development of atherothrombotic events” 2002 Biomed.  And again pharma’s devil is in the details of this 2002 Biomed article:   the negative results of some studies arise from the failure to limit dietary N-6, which blocks the positive effects of the N-3 supplement.  The same is confirmed in Am J Clin Nutr, Sept 1999, 560—569 and supported by the reduction in diabetes, arrhythmia, hypertension, and cardiac arrest.  Another detail is related to source, with vegetable oil derived N-3, ALA; it has “only about 1/10th the active of EPA and DHAWiki.[10]  I find the evidence convincing for N-3, but there are critics:  Wikipedia, e.g., states “but the health benefits of supplementation appear to be few if any.”  This is contradicted at Wiki. Those who challenge the claims for N-3 rely on studies with the principle source of N-3 coming from vegetable oil and/or a high ratio of N-6 to N-3; who’s right?    


Omega-6 fatty acid and CVD:  Excess omega−6 fatty acids from vegetables oils interfere with the health benefits of omega−3 fats, in part because they compete for the same rate-limiting enzymes” Wiki .  The disease promotion effects of N-6 come from its “conversion to omega-6 eiscosanoids that bind to diverse receptors found in every tissue of the body…. The eicosanoids from AA [derived from omega 6 linoleic acid] are biologically active in very small quantities and, if they are formed in large amounts, they contribute to the formation of thrombus and atheromas, to allergic and inflammatory disorders, particularly in susceptible people, and to proliferation of cells [tumors].  Thus a diet rich in omega-6 fatty acids shift the physiological state to one that is pro-thrombotic and pro-aggregatory, with increases in blood viscosity, vasospasm, and vasoconstriction and decreased n bleeding time [promotes ischemic events].  The higher the ratio of omega-6/omega-3 fatty acids in platelet phospholipids … caused the higher the death rate from cardiovascular disease [65,100]. Biomed.  Other disease conditions in this article by A. P. Simopulos for which the evidence from laboratory research, clinical trials, and epidemiological studies link the unhealthful 16:1 ratio of N-6 to N-3 to  CVD asthma, breast and colon cancers, arthritis and Alzheimer’s disease.  In Paleolithic and hunter-gatherer times the ratio was 2:1.  N-6 competes with N-3 for cellular receptors.   This attack on omeg-3 follows the pattern of bad pharma ran by its marketing department which promotes profits first.   

 Essential fatty acids and arachidonic acid (AA):  Arachidonic acid (AA) is a 20-carbon N-6 conditionally essential fatty acid.[1] It sits at the head of the "arachidonic acid cascade" – more than 20 different signaling paths that control a wide array of bodily functions, but especially those functions involving inflammation and the central nervous system.  Most AA in the human body derives from dietary linoleic acid (another essential fatty acid, 18:2 N-6), which comes both from vegetable oils and animal fats ….  EPA (20:5 N-3) provides the most important competing cascade…. These two parallel cascades [second fat is GLA (18:3 N-6)] soften the inflammatory effects of AA and its products.  Animal studies show that increased dietary N-3 results in decreased AA in brain and other tissues. The reverse is also true – high dietary linoleic acid decreases the body's conversion of α-linolenic acid to EPA.  Low dietary intake of these less inflammatory essential fatty acids, especially the N-3s, is associated with a variety of inflammation-related diseases…. These changes have been accompanied by increased rates of many diseases – the so-called diseases of civilization – that involve inflammatory processes. There is now very strong evidence that several of these diseases are ameliorated by increasing dietary N-3, and good evidence for many others. There is also more preliminary evidence showing that dietary N-3 can ease symptoms in several psychiatric disordersWiki.  The totality of evidence support dietary changes with reduced N-6 and N-3 supplementation. 


So what is driving this high ratio:  Among the changes have been the effects of grain fed livestock and chicken.  For example USDA eggs have a ratio of 20 to 1, while Amplelistra farms in Greece the ratio is 3 to 1.3, 2002 in Biomed.  Other sources rich in N-6 include vegetable oils and nuts.  On these grounds it is a good course to increase intake of fish over meats[11] and limit vegetable oils and nuts.  Based on the totality of evidence, a prudent course is to lower the ratio of N-6 to N-3 both by changes in diet and taking fish oil pills high in N-3, which can be obtain quite economically from Costco.  Thus to maximize benefits limit n-6.


Health benefits of Omega-3:  The American Heart Association in a 2003 on intake of omega-3 made finds and issued recommendations.  “Research to date suggests that they {omega-3] can decrease risk for arrhythmia, thrombosis, triglyceride and lipoprotein levels, rate of growth of growth of the atherosclerotic plaque, improve endothelial function [arteries], (slightly) lower blood pressure, and inflammatory responses.  The AHA recommends that all adults eat fish (particularly fatty fish) at least two times a week.  For patients with documented CHD, the AHA recommends ≈1 g of EPA and DHA (combined) per day. … An EPA+DHA supplement may be useful in patients with hypertriglyceridemia. Two to four grams of EPA+DHA per day can lower triglyceride 20% to 40%. 


100 gm portions in gm, omega 3 & 6 fatty acids, omega-3 listed first (blank when under gm  http://nutritiondata.self.com/tools/nutrient-search   (a user friendly resource)

Safflower oil                   -       75

Walnuts                           9.0     38

Canola Oil                 7.6         19

Sunflower oil               0.9      66

Bread shortening             -       37

Potato chips               -           16

Commodity food oil    7.0    50

Margarine  hard              -       36

Peanuts raw               -           15

Corn oil                         1.1     53

French fries                      -        13

Pistachio                     -           13                

Mayonnaise               3.0       52  

Shortening vegetable   4.7     26

Lard                            1.0        10

Soy oil                          6.7      50

Pecans                           1.0       20

Salmon oil                 35         01.5

Salmon baked            4.0     1.2

Chicken fat                   1.0       19

Butter                         1.1       02.7    

Plant sources of N-3 are mostly ALA, of which about only 1/10th is converted to the essential EPA and DHA.   Another source on content of oils is at eat real food site. 

Fishes high in Omega-3 p er 85 gm serving in grams:  herring & sardines 1.3-2, mackerel 1.1-1.7, salmon 1.1-1.9, halibut 0.60-1.12, tuna 0.21-1.1, swordfish 0.97, shark 0.84, flounder 0,48


Fatty Acids in Dietary Fats -- Wiki





Vitamin E


















Coconut oil






Palm kernel oil






Corn oil






Sunflower oil






Canola/Rapeseed oil






Olive oil













Saturated fat profile of common foods; Esterified fatty acids as percentage of total fat[5]


Lauric acid

Myristic acid

Palmitic acid

Stearic acid

Coconut oil





Palm oil










Ground beef





Dark chocolate










Egg yolks










Soybean oil






[2] Glycation is a type of oxidation in which a monosaccharide--most often glucose or fructose—attaches to a unsaturated fat molecule.  Fructose is 7 times more reactive than glucose and serum level remain higher longer. 

[3] The recommended average intake of omega-3 for adult men in the United States is only 1.6 grams/day, or less than 2% of total fat; the actual average consumption of omega-3 in the United States is around 1.3 grams/day, almost all of it in the form of ALA; [of which under 10% is converted to EPA and DHA the healthful forms] EPA and DHA contributed less than 0.1 grams/day” Wiki .

[4] High dietary level of N-6 blocks the conversion of N-3 and thus it healthful effects, and as a consequence N-6 is causal for CVD.

[5] A meta-analysis of 21 studies considered the effects of saturated fat intake and found that "Intake of saturated fat was not associated with an increased risk of CHD (coronary heart disease), stroke, or CVD (cardiovascular disease)” Wiki.

[6]  It was later exposed that he had received funding from the food industry.

[7] The Framingham Heart Study is a long-term, ongoing cardiovascular study on residents of the town of Framingham, Massachusetts. The study began in 1948 with 5,209 adult subjects from Framingham, and is now on its third generation of participants.  Prior to it almost nothing was known about the "epidemiology of hypertensive or arteriosclerotic cardiovascular disease.  Much of the now-common knowledge concerning heart disease, such as the effects of diet, exercise, and common medications such as aspirin, is based on this longitudinal study. It is a project of the National Heart, Lung, and Blood Institute, in collaboration with (since 1971) Boston University. Over 1000 medical papers have been published related to the Framingham Heart Study. It is generally accepted that the work is outstanding in its scope and duration, and overall is considered very useful.  showed the importance of healthy diet, not being overweight or obese, and regular exercise in maintaining good health, and that there are differences in cardiovascular risk between men and women.[9][10] It also confirmed that cigarette smoking is a highly significant factor in the development of heart disease, leading to angina pectoris, myocardial infarction (MI), and coronary death,. Framingham Risk Score is published, and predicts 10-year risk of future coronary heart disease (CHD) events. Recently the Framingham studies have become regarded as overestimating risk.  On the web at http://www.framinghamheartstudy.org/

[8]  Leading medical, heart-health, and governmental authorities, such as the World Health Organization,[16] the American Dietetic Association,[17] the Dietitians of Canada,[17] the British Dietetic Association,[18] American Heart Association,[19] the Indian Heart Association,[20] the British Heart Foundation,[21] the World Heart Federation,[22] the British National Health Service,[23] the United States Food and Drug Administration,[24] and the European Food Safety Authority[25] advise that saturated fat is a risk factor forcardiovascular disease (CVD).  A number of systematic reviews have examined the relationship between saturated fat and cardiovascular disease and have come to different conclusionsWiki. 

[9]  Lauric acid increases total serum cholesterol the most of any fatty acid. But most of the increase is attributable to an increase in high-density lipoprotein (HDL) (the "good" blood cholesterol). As a result, lauric acid has been characterized as having "a more favorable effect on total HDL cholesterol than any other fatty acid, either saturated or unsaturated”  Wiki.

[10] Consumption of omega-3 in the United States is around 1.3 grams/day, almost all of it in the form of ALA..  ALA can be partially converted into EPA and DHA by the human body, but the conversion rate is thought to be 10% or less, depending on diet and gender” Wiki  .

[11]  Another reasons to substitute fish for meats and poultry is the use of plant manufactured pesticide in the grains fed cattle.   There is strong evidence for serious health consequences from corn and eating corn and soya fed animals (thank you Monsanto).  

Polyunsaturated fats are subject to rancidification:  is the hydrolysis and/or autoxidation of fats into short-chain aldehydes and ketones which are objectionable in taste and odor.  Hydrolytic rancidity refers to the odor that develops when triglycerides are hydrolyzed and free fatty acids are released to form free tatty acids and salts of free fatty acids.  Oxidation primarily occurs with unsaturated fats. Microbial rancidity refers to a process in which microorganisms, such as bacteria or molds, use their enzymes such as lipases to break down fat.[1]  Rancidification can produce potentially toxic compounds associated with long-term harmful health effects concerning advanced aging, neurological disorders, heart disease, and cancer. A combination of water-soluble and fat-soluble antioxidants is ideal” Wiki.  A key source for oxidized fats comes from frying and deep frying.  The alarm was raised in work done at Rutgers University in 1978, where a team in a simulation of commercial frying where they tested commonly used polyunsaturated in simulated deep frying at 365 F for 74 hours.  One finding, for example was that “under such conditions [of commercial frying] both thermal and oxidative decomposition of the oil may take place.  Such unavoidable chemical reactions cause formation of both volatile and nonvolatile decomposition products…. Various symptoms of toxicity, including irritation of the digestive tract, organ enlargement, growth depression, and even death have been observed when highly abused (oxidized and heated) fats were fed to laboratory animals”… and the article goes on.  Lipid peroxidation refers to the oxidative degradation of lipids. It is the process in which free radicals "steal" electrons from the lipids in cell membranes, resulting in cell damage.  It most often affects polyunsaturated fatty acids, because they contain multiple double bonds in between which lie methylene bridges (-CH2-) that possess especially reactive hydrogensIf not terminated fast enough, there will be damage to the cell membrane, which consists mainly


of lipids. In addition, end-products of lipid peroxidation may be mutagenic and carcinogenic.  For instance, the end-product malondialdehyde  reacts with deoxyadenosine and deoxyguanosine in DNA, forming DNA adducts to them, primarily M1GWiki.  The detailed 2010 article Pathological Aspects of Lipid Peroxidation list aging,  Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), atherosclerosis (and thus CVD and other related conditions), pre-eclampsia (pregnancy disorder affecting about 4%), diabetes, renal diseases, chronic lymphedema (also known as lymphatic obstruction, causing swelling by compromised lymphatic system), hepatic diseases including liver IR, NAFLD, NASH (#16), exacerbating hepatitis C and cirrhosis of the liver, and a causal factor for cancers.  The various authors of each section of this in-depth article describe the process by which the lipid peroxidation causes pathology.  The role of oxidation of fats and cholesterol within the artery walls as being atherogenic is clearly made in that article.  The effects of rancidification in the body are beyond dispute.  Also contributing are dietary sources of rancid oils.  The possibility that the body fats might undergo a similar kind of degradation is still largely ignoredperhaps because the irregular irreversible pattern of this type of process seems at odds with the enzyme-controlled reversible pathways of traditional biochemistry. Yet work with mitochondria and other biological preparations has shown that the processes commonly grouped together as " degeneration ", " fatigue ", and " ageing " (none of which have a basis in classical enzymology) develop in close parallel with evidence of Rancidification” at 1969.  The source can either be dietary rancid fats or in vivo oxidation—in vivo causing the greatest issues.  Now let us follow the chain of events concerning IR and CVD.  Rancid fats contribute to liver dysfunction NAFLD and IR by accumulating in the liver in a form that the liver can’t dispose of.  Similarly they contribute to atherosclerosis and CVD by being in a form with the muscle cells in the tunica media (muscular layer) of the artery walls which prevent uptake for transport and metabolized.  The macrophages in the tunica media similarly can’t dispose of the rancid fats.  Thus like transfats (see section below) rancid fats contribute to CVD and atherosclerosis.  Accumulating evidence suggests that oxidized fats and lipid oxidation products in the diet can contribute to the pathogenesis of atherosclerosis” at 2002, and 1998. Non-enzymatic oxidation causes the failure of the body to dispose of them; they accumulate like those of the unnatural, man-made trans-fats.  Thus polyunsaturated fats are unhealthful because of rancidification and because of their high N-6 content.  Like other vegetable with low yield through expeller-press undergoes a complex process involving organic solvents, distillation to remove the non-oil fraction, treatment with alkali to neutralize free fatty acids, bleaching to remove modify color, and distillation at a temperature of 480 F and under a high vacuum.   Corn oil has 55% polyunsaturated fat, Cottonseed 52%, canola 28%,[2] soybean 58%.  Moreover as stated above rancidification in the body and the high amount of omega-6 makes this and all oils high in unsaturated fats a major health concern.  Corn oils ratio of n-6 to n-3 is 49:1.[3]  (See section on n-6 and n-3 above).  So what does our corporate friendly government do?


Commercial forces behind vegetable oil:  For example, corn oil is derived from the waste part, the germ, of corn in the production of corn meal used in animal feed and various grocery foods.  Being a waste byproduct of a commercially valuable product makes it is “generally less expensive than most other types of vegetable oils.  One bushel of corn contains 1.55 pounds of corn oil (2.8% by weight) [and a lot of animal feed].  Corn oil is also a feedstock used for biodiesel. Other industrial uses for corn oil include soapsalvepaintrustproofing for metal surfaces, inkstextiles, nitroglycerin, and insecticides. It is sometimes used as a carrier for drug molecules in pharmaceutical preparations” Wiki.   Being cheap it is favored by the food manufacturers.  To promote manufactured food sales they have influenced government to subsidized crops, to recommend a low fat diet (thus high carbs), and to vilify saturated fats as artery clogging to promote their cheap polyunsaturated fats as heart healthy.  Over 95% of Federal-farm crop subsidies go to the production of grains.  The cheap subsidized grains have made it possible for the food manufacturers to sell their products abroad.  As developed in the article on diet, the global obesity & diabetes pandemics are founded upon sugar added manufactured foods combined with a diet high in grains (a one-two-punch)--see.  And it get worse since baked products which use a high ratio of polyunsaturated fats are clearly inferior in flavor, the food manufacturers hydrogenate them (a cheap process) to convert them to superior baking properties of saturated fats.  In this process about half of the polyunsaturated are converted to the equally unhealthy transfats—section below.  The transposition is lower energy, and thus favored, in catalytic hydrogenation.  Thus what is sold as heart healthy; isn’t; and what is artery clogging turns out to be healthy, viz., the best source for energy (ATP).   This is an example of what I call tobacco ethics and tobacco science:  corporations pursing the corporate imperative of maximizing profits. 


Trans-fats:  The daily intake of about 5 g of trans fat is associated with a 25 percent increase in the risk of ischemic heart diseaseNEJM.  However, this study was based on the use of questionnaire given 667 elderly 3 times over 10 years—hardly proof, at.  “Trans-fats are found only in trace amounts in meat and dairy products.  Their major source is in food production: liquid cis-unsaturated fats such as vegetable oils are hydrogenated to produce saturated fats, which have more desirable physical properties[4] [and more flavorful baked and fried foods].  Trans-fats are a contaminant introduced by a side reaction on the catalyst in partial hydrogenation of vegetable oils.  However, partial hydrogenation reconfigures most of the double bonds that do not become chemically saturated, twisting them so that the hydrogen atoms end up on different sides of the chain. This type of configuration is called trans, from the Latin, meaning "across".[39] The trans configuration is the lower energy form, and is favored when catalytically equilibrated as a side reaction in hydrogenation” Wiki.  Another study found a 30% increase—2015 BMJ.  In 1975, 5.6 billion Ib. of hydrogenated vegetable oil were produced in the United States, which is an average of 28 Ib/year/person (113)” ARN, 1984. Based on population studies and clinical trials, trans-fats are blamed for high levels of cholesterol, lower the good HDL, and as a major cause of CVD.   But as pointed out in the section on the Mediterranean diet, complex population studies are like data mining, where you dig determines what you find, and sometimes proposed mechanism and population data is only poorly related to CVD.  However, animal study using Wistar rats found that transfats in a high fat diet causes fatty liver disease at 2011.   However, the study which found oxidation didn’t control for the effects of polyunsaturated fats which are subject to rancidification (see poly section below).  Another study found the same in transfats and high-fructose corn syrup—at 2008.  By promoting metabolic dysfunction, we have the mechanism, like that of T2D for transfats, and presumable polyunsaturated fats as to their method of causing CVD.


Is there laboratory evidence that trans-fats cause CVD?   Back to the cholesterol myth:  trans-fats increases the risk of coronary heart disease by raising levels of the lipoprotein LDL (so-called "bad cholesterol") and lowering levels of the lipoprotein HDL ("good cholesterol") “ Wiki.  “It is now well known that the hydrogenation process and particularly the formation of trans-fatty acids has led to increases in serum cholesterol concentrations whereas LA [linoleic acid] in its regular state in oil is associated with a reduced serum cholesterol concentration” Biomed.  This has been confirmed with high trans-fat in clinical experiment on volunteers.  But it has been shown (see part 2) that pharma pushes the high LDL, high TC, and high-fat diet as causes of CVD for to promote drug sales; they are not causal factors, rather it promotes sales of statins.  The cause of CVD from a 2006 review article on trans-fats besides changes in LDL and HDL:  “Because of their effects on the metabolism of gamma-linoleic and arachidonic acid, ingestion of trans-fatty acids can affect the metabolism of prostaglandin and other eicosanoids and may alter platelet aggregation and vascular function [negative effect upon inflammation (causal of AS) and clotting functions (causal of MI)].  In addition incorporation of trans-isomers into membrane phosopholipids may influence the physical properties of the membrane as well as the activities of the membrane-associated enzymes …. Effect collagen induce platelet aggregation.…  inhibit activities of Na+ , K+-ATPase and adenylate cyclase and reduce density of B-adrenergic receptors in rat heart membranes [raise blood pressure]…. Recent evidence indicates that trans-fats promote inflammation…. Increased tumor necrosis factor (TNF) system, levels of interleukin-6 and C-reactive protein…. Several studies suggest that trans-fats cause endothelial dysfunction [affects wall of arteries and other tissues]… soluble vascular-cell adhesion factor…reflected by reduction in brachial artery flow-mediated vasodilation by 29 percent [raises blood pressure], as compared with intake of saturated-fats.  Other effects include consumption of trans-fats reduced the activity of serum paroxonase, an enzyme that is closely associated with HDL cholesterol, and impaired the postprandial activity of tissue plasminogen activator.  Trans-fats appear to affect lipid metabolism through several pathways….”  The same finding with much greater detail is in the 1984 thorough review by the Department of Agriculture.  Several epidemiological studies found a significant association of trans-fats with CDV and MI, including those studies which controlled for contravening variables.[5]  As previously stated LDL and high TC are again bystanders, and trans-fats affects some of the same processes as omega 6.  Given the clear association in dozens of population studies and clinical trials of trans-fats to CVD, governments have responded to this health hazard created by the food industry.  With the body of experimentation upon rats a mechanism for the deleterious effects of trans-fats has been established, the principle one being it effect upon blocking the conversion of the essential omega-3 fatty acid, at.  The smoking gun lines with the fact that trans-fats exert a pro-inflammatory effect, and the inflammatory processes in artery walls in response to damaged LDL causes atherogenesis.  “Because the presence of inflammation is an independent risk factor for atherosclerosis… the production of interleukin-6 and TNF-a by cultured mononuclear cells was grater after one month…” NEJMsee also, a 2006 summary article.   Laboratory experiments on rats are revealing.  Strong association with NAFLD, obesity, and MeS are associated in rats with a diet high in trans-fat.  By 16 weeks, trans fat-fed mice became obese and developed severe hepatic steatosis with associated necroinflammatory changes… severe hepatic steatosis… glucose intolerance developed within 2 and 4 weeks… plasma insulin resistance…  Because dietary transfats promoted liver steatosis and injury, their role in the epidemic of NASH needs further evaluationat 2008, and like findings 2011. This is an extremely important health finding, the causal change to obesity risk and MeS and T2D starts with accumulation of fat within the liver, which mucks up the liver’s metabolic regulatory function.  Now in addition to fructose with a high starch diet, we can add unhealthful trans and polyunsaturated fats.  The omega-6, transfats are pro-inflammatory because of the inhibition of on EFA metabolism, 1984.  This effect on n-6 is associated with heart disease in rats on trans-fats--1997 .  It thus based on lab and population studies to assiduously avoid artificially produced trans-fats[6].   The zero trans fats on food label is deceptive for 2 reasons, at 0.5 grams the entry is 0, and since no one is checking food content, there is an incentive to manufacture numbers on product labels.  


What are the regulations:  Official response has been prohibiting trans-fats in a number of countries, but not the U.S.  According to the FDA, the average American consumes 5.8 grams of trans-fat per day (2.6% of energy intake).  This is government figure is low because trans fatty acids that are part of mono- and diglycerides [bound with glycerol] are not required to be listed on the ingredients label as making contributions to calorie count or trans fatty acid content.  Trans-fats in the form of monoglycerides and diglycerides are not considered fats by the FDA, though upon absorption from digestive track they yield trans-fats.  Another gap in calculation is that trans-fat levels of less than 0.5 grams per serving are listed as 0 grams trans-fat on the food label.  There is no requirement to list trans-fats on institutional food packaging; thus bulk purchasers such as schools, hospitals, [restaurants]  and cafeterias are unable to evaluate the trans-fat content of commercial food items [nor is there an incentive to spend more for trans-free foods]” Wiki.  The major source of trans-fats in the U.S. is in fried foods from restaurants, and this source is not included in US dietary figures for trans-fats.   A number of countries have simplified the process of controlling trans-fatty acids by banning them, starting with Denmark in 2003 and now also Iceland, Sweden, Switzerland .  “Spain … no significant levels of trans-fats were found in any of the anaylsed products, regardless of brand of origin” at Bakery.  The regulations might make a difference, because death rate per 100,000 2011 from coronary heart disease is 80.5 US, 55.9 for Denmark, for Spain 43, Switzerland 52 ,Japan 31, Israel 46, Italy 51, Greece 60, U.K. 69, and France 29, source LeDuc Media.  However, the highest rate of obesity and diabetes is in the US, and the US allows GMOs.  Let us not become distracted by what could by the minor causes such as fats when the elephant in the kitchen  are refined carbs and sugars.  The weakness of  lab work on fats make the case,[7] we need to look at the Western high carb diet.          


The Western diet:  Avoid the western diet and avoid fructose, trans-fats, and high ratio of n-6 to n-3 and fats subject to rancidification (main source vegetable oil), but not starches, saturated fats, and polyunsaturated fats low in n-6.  Note, since the process of AS is initiated by NAFLD mucking upon metabolic regulations which starts with the combination of high fructose and high insulin caused by carbs, avoid the Western diet.  Thus instead of high fat diet and high levels of cholesterol being the chief villains in the life ending CVD, it is the Western diet with large amount of fructose, sucrose, refined carbs,[8] tobacco smoke, and polyunsaturated and transfats that has caused most of the spike in CVD and varied health problems facing the elderly, especially those involving oxidative damage and immune responses   (arthritis, Alzheimer’s & Parkinson’s diseases, macular degeneration, CVD, and insulin resistant diabetes).  Place sugars as first, refined carbs second, and vegetable oils third on the dietary avoid list—the carbs connection see part 4.   


Why the Mediterranean diet works: “The recently published PREDIMED randomised controlled trial was stopped early after it showed that in high risk people the Mediterranean diet achieved a 30% improvement over a “low fat” diet in terms of cardiovascular events”  BMJ.   There is major variation between regions of the Mediterranean.  Wikipedia concludes:  The all-embracing term 'Mediterranean diet' should not be used in scientific literature.”  Among errors:  “olive oil consumption is negligible… Mediterranean countries tend to consume relatively high amounts of fat, they have far lower rates of cardiovascular disease than in countries like the United States, where similar levels of fat consumption are found…The most popular dietary candidate, olive oil, has been undermined by a body of experimental evidence that diets enriched in monounsaturated fats such as olive oil are not athero-protective when compared to diets enriched in either polyunsaturated or even saturated fats.  A healthy active lifestyle (notable a physically active lifestyle or larbour) is also beneficial… red wine … contains flavonoids with powerful antioxidant properties… The proposed mechanism is solar UVB-induced synthesis [sun] of Vitamin D in the oils of the skin, which has been observed to reduce the incidence of coronary heart disease, and which rapidly diminishes with increasing latitude….  A recent randomized Spanish trial of diet pattern published in The New England Journal of Medicine in 2013 followed almost 7,500 individuals over around 5 years found that individuals on a Mediterranean diet supplemented with mixed nuts and olive oil had a 30 percent reduction in risk of having a major cardiovascular event and a 49 percent decrease in stroke risk.  A 10-year study found that adherence to a Mediterranean diet and healthful lifestyle was associated with more than a 50% lowering of early death ratesWiki.   Undoubted influenced by pharma’s thought leaders, the Wikipedia article basically a survey, a kitchen sink without clear guidance & no mention of sucrose, fructose, refined carbs, or glycation.  However the research in this series on CVD place as beneficial low use of sucrose first, refined carbs second, followed by saturated fats and monounsaturated fats, then physical active life style and the lower use of pharma’s patented drugs as why those on a Mediterranean diet live longer.  Moreover the first study of this diet started in the 50’s based upon Italians who ate a peasant diet. [9] Other factors include lower rate of obesity, popularity of red wine (its anti-oxidants), effective regulation of trans-fats (unlike the US), and higher intake of diary product with its vitamin D and sunlight (this combination of calcium, vitamin D, and sun light is cardio-protective).  Wikipedia’s article on the Mediterranean diet repeats the tobacco science of the food and pharmaceutical industries.    Human evolved a biological system for the hunter-gatherer life, not the modern diet. 


1871 census UK and longevity:  More evidence of the consequences of the western diet:  the 1871 census in the UK (the first of its kind) found the average male life expectancy as being 44, but if childhood mortality is subtracted, “males who lived to adulthood averaged 75 years.   The present male life expectancy in the UK is 77 years for males [the United States averages 74 for males]” Wiki.  In spite of the improved medical procedures[10] for cancer, heart attacks, strokes, vaccinations preventing contagious diseases, and antibiotic to treat infections,[11] and also a safer work environment, these benefits have been undone as to life extension by CVD, cancer, osteoporosis, Alzheimer’s disease, for which western diet and lifestyle are the major causes. 



Fats, what’s good; what’ s bad:  Omega-3 fatty acids (N-3) EPA and DHA are converted in the body to essential products that modify inflammatory and immune reactions and thus N-3 lowers the risk of autoimmune diseases including Alzheimer’s, arthritis, and CVD.    Omega-6 fatty acids (N-6) have an inflammatory effect and also block the conversion of N-3 and thereby increase autoimmune diseases including AS and CVD.  The ideal ratio of N-6 to N-3 is 4:1 or less; the western-diet ratio is 16:1.  Main source for N-6 are vegetable oils and nuts.  Canola oil[12] is the only major vegetable oil with a good ratio of N-6 to N-3 (2.5:1), although the main omega-3 is the form of alpha-linolenic acid of which only about 10% is converted to the healthful EPA and DHA.  Because Canola oil is from GMO canola, I must withhold recommending it;[13] most other vegetable oils are from GMO crops.  Main source for EPA and DHA is fish oil supplement and fish. For vegetable oils to avoid N-6, the best are coconut, palm, and olive oils and they are free of GMO.  However, I must withhold recommending olive oil; its N-6 to N-3 ratio is 14:1.  Another issue for vegetable oils is that of rancidification which makes them comparable to that of transfats.  Our body’s lack enzymes for their metabolism, and thus insufficient amounts they accumulate in our cells and causals for an assortment of conditions including CVD.  Moreover most vegetable oils come from GMO seeds which are not only Roundup read but also have a GMO pesticide that causes leaky gut.  Because leaky gut kills insects, there is a major human risk.[14]  The switch to grain fed poultry and cattle from free range has lowered the amount of N-3 in those meat sources.   In manufactured foods and restaurants trans-fats are a concern.  They are a result of partial hydrogenation of vegetable oils.  While banned in many developed countries, U.S. regulations require only listing trans-fat content on label.  However, there are several exclusions in the regulations, and those labels are based on the corporate honor system without government oversight.  Secondly, restaurant and institutions are excluded from regulations, thus their baked and fried foods are another major source. Trans and saturated fats enhance the flavor of baked goods and fried foods.  Trans-fats promote CVD and other autoimmune diseases.  The palm nut[15] are high in saturated fats including the beneficial lauric acid and thus are recommended along with animal sources of saturated fats, and also monounsaturated fats.  After them comes olive oil with its low level of polyunsaturated fats.  Thus as a policy, limit vegetable oils, commercial backed goods, and restaurant baked deserts and fried foods.  Animal fats because of the GMO plant pesticide and Roundup issues, I thus withhold recommending lard.[16]  Substitute saturated fats such as butter and vegetable oil from palm tree nuts, eat more seafood, and take omega-3 supplement. “If insulin is elevated there is a net inward flux of FFA [free fatty acids], and only when insulin is low can FFA leave adipose tissue. Insulin secretion is stimulated by high blood sugar, which results from consuming carbohydrates” Wiki.  Thus a low carbohydrate diet with saturated fats replacing them and sea foods is recommended for weight control and lowering CVD risk.  A more complete accounting of what constitutes are good diet is found at Diet recommendations and its science which is a short non-technical summation followed by diet recommendations and at Healthful lifestyle which has also a list of several healthful drugs that pharma of course opposes.