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 disease” NEJM.  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[1] [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.[2]  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…” NEJM—see 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 necro-inflammatory 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 evaluation” at 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[3].   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.  

Journal summation on trans fatty acids and oxidized polyunsaturated:   The Harvard Heart Letter put out a warning about a dietary causes of CVD, fructose, at http://www.health.harvard.edu/heart-health/abundance-of-fructose-not-good-for-the-liver-heart.  In the Nutrition and Metabolism Journal 2011 is pasted the evidence in support of the warning about polyunsaturated fats:  “Recent studies suggest multiple possible mechanisms that might mediate association of TFAs with CVD [12].  For example TFAs influence prostaglandins balance, which in turn promotes thrombogenesis [13] and inhibit the conversion of linoleic acid to arachidonic acid and to other n-6 PUFA, perturbing essential fatty acid metabolism and causing changes in the phospholipid fatty acid composition in the aorta [14].  TFAs have been associated with the activation of systemic inflammatory responses, including substantially increased levels of IL-6, and TNF-alpha, TNF receptors and monocytes chemo-attract protein-1 [15]. Furthermore, TFAs have been associated with increased levels of several markers of endothelial activation, including soluble intercellular adhesion molecule 1, soluble vascular-cell adhesion molecule 1, and E-selectin [10].  TFAs are postulated to be involved in promoting vascular dysfunction, as reflected by a reduction in brachial artery flow [16].  These observations suggest that TFAs are linked to development of CVD, probably via a vascular pro-inflammatory response [17].  Oxidative damage is a major contributor to the development of CVD.  Nevertheless, little is known about the effects on the liver induced lipids [6] and few studies are focused on the effect of foods rich in TFAs on hepatic functions and oxidative stress.  Oxidative stress results from an imbalance between oxidant production and antioxidant defenses [18].  Oxidative stress induced by free radicals has been linked to the development of several diseases such as cardiovascular, cancer, and neurodegenerative diseases [19].   When cellular antioxidant mechanisms are overwhelmed, a long-term decline in their antioxidant capacity causes oxidative stress [20, 21].  Oxidative stress is now believed to be an important factor in the development of non alcoholic fatty liver disease (NAFLD) [20, 22].  NAFLD is the most common liver disorder in the world, and in obesity, type-2 diabetes and related metabolic diseases, it incidence reaches 70-90% [23].   The disease is characterized by the accumulation of triacylglycerols inside liver cells, and the condition can progress into more serious liver disease, such as non alcoholic steatohepatitis, liver fibrosis, cirrhosis, and more rarely, liver carcinoma [23]. Previous works have shown that feeding rats a high fat diet (57% of energy from fat) induces hepatic steatosis and liver damage, which are characteristic of NAFLD and thus provides a suitable model for the early stages of the disease[24,25]. But, in these studies TFAs in the fat diet were not investigated and neglected. Therefore, it is necessary to examine the relationship between the liver functions and TFAs consumption in dietary lipids….” Both articles are posted at http://healthfully.org/dja/id5.html

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,[4] 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,[5] 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 rates” Wiki.   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. [6] 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. 

Commercial Production of Vegetable oils:  for those who are into natural, unmodified, the extraction of oils raises serious health concerns, made all the more alarming by the FDA’s reliance upon the manufacturers’ testing as proof of healthfulness. The main vegetable products used contain under 3% oil, the byproduct is mainly used for animal feed.   A description of the production of corn oil:  “Almost all corn oil is expeller-pressed, then solvent-extracted using hexane or 2-methylpentane (isohexane).^[1] The solvent is evaporated from the corn oil, recovered, and re-used. After extraction, the corn oil is then refined by degumming and/or alkali treatment, both of which remove phosphatides. Alkali treatment also neutralizes free fatty acids and removes color (bleaching). Final steps in refining include winterization (the removal of waxes), and deodorization by steam distillation of the oil at 232–260 °C (450–500 °F) under a high vacuum.^[1]”  Canola/rapeseed oil:  “Canola oil is made at a processing facility by slightly heating and then crushing the seed. Almost all commercial canola oil is then refined using hexane. Finally, the Canola oil is refined using water precipitation and acid, "bleaching" with clay, and deodorizing using steam distillation.^[22] About 43% of a seed is oil;^[23] the remainder is a rapeseed meal that is used as animal feed. About 23 kg (51 lb) of rapeseed makes 10 L (2.64 US gal) of canola oil. Seed oils except for corn are high in oil content:  sunflower seed (28%), soybean dry (56%), and canola dry (43%), corn (2.8%).  These oils are high in polyunsaturated oils:  sunflower 69%, soybean 58%, canola 28%, corn 55%.  Because of in vivo rancidification of polyunsaturated fats as well as in cooking, they pose a serious health risk—see rancidification section above for the consequences.   Claims of dietary safety are suspect since nearly all studies are industry funded, and the few government reports are undoubted influenced by industry. 

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[7] for cancer, heart attacks, strokes, vaccinations preventing contagious diseases, and antibiotic to treat infections,[8] 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, a diet high in refined carbs (especially the sugar fructose) and unhealthful trans and polyunsaturated oils, pesticides, and chemical additives.  Something is very wrong when business trumps science.