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2:7 THE FAT STORY. History and Science

2:7    The fat story, history and science   8/23/2020, 5-12-2020  edited


  1. UFAs won the fat battle 


By attacking the competition, saturated fatty acids, food manufacturers have established their PUFA as the preferred fat in cooking and at the same time have used the less expensive fats for their manufactured foods, fast foods, and in restaurants.  Like tobacco they have buried the critics, and only a few who research recognized the pathogenic consequences.  By 1970 I didn’t buy vegetable oils, my deep fryer had lard, as to my cakes and pie crusts.  Butter won the taste contest.  Taste is important.    

The history goes back to cottonseed oil, the first major seed oil.  Prior to that with—few  exceptions, PUFAs made up under 4% of calories our 8% of fats (pig fat is 9.6% PUFA, butter is 2.6%).  The sources a waste product of cotton that was ground and fed to livestock, its price was low.  In 1857 an effective way to separate the hull for the seed permitted the extraction of cheap cottonseed oil.  In 1858 it was widely used in the US as an additive to lard and olive oil.  A congressional investigation exposed the practice in 1884 and legislation the resulting legislation required the label of lard compound.  Olive oil continued to be diluted. In 1902 Wilhelm Normann patented a process for hydrogenation of vegetable oils, and he set up a facility from 1905 to 1910.  Procter and Gamble bought the patent and in June of 1911 introduced hydrogenated cottonseed oil branded as Crisco.  Hydrogenation improves flavor and extends shelf life. Starting in 1911 Crisco advertise it as heart health. Conflicting claims were made for SFAs and PUFAs.  Articles soon appeared in journals on rancid fats, but that message wasn’t disseminated to the public, restaurants, or physicians.  The fight was over the fluff, not the science, the chemicals used to extra seed oils, or the conditions of the slaughter houses.  Healthy heart falls under the umbrella of fluff, but unhealthy for the heart PUFAs weren’t.  As the market for manufactured food grew, and science progressed a number of tobacco claims were made; I shall comment on three of them.  These are examples of myth making to expose the way  food manufacturers use science.    

The AHA remained small until the 1940s when it was selected for support by Procter & Gamble, via their PR firm, from a list of applicant charities. Procter & Gamble gave $1.5 million from its radio show, Truth or Consequences, allowing the organization to go national.[8] Procter & Gamble turned cottonseeds from a waste product of cotton production into something that could be sold as a supposedly "heart-healthy" alternative to its competition - animal fats, which were mostly saturated. Procter & Gamble were the inventors of the fake trans-fat margarine called Crisco (Crystallized Cottonseed Oil), which was touted by the AHA as healthier than butter.

          With its climb to national recognition and as an authority the public turns to, there is a lack of awareness of its funding from pharma and food manufacturers.  The AHA publishs 13 medical journals.  In 1994, the Chronic le of Philanthropy released result of their survey: “The study showed that the American Heart Association was ranked as the fifth "most popular charity/non-profit in America" of over 100 charities researched with 95 percent of Americans over the age of 12 choosing Love and Like A lot description category.[1]  This is the charity which sells their heart healthy logo to company’s to put on their products such as sugar coated cereals and grape juice. 


2.  Trust in government shot in the foot, almost—I missed  I shall try to limit my frustration over the harm done by promoting the unhealthy fat as healthy and the healthy fat as artery clogging, but such is the track record of unmanaged capitalism; its tobacco ethics creating tobacco science.  It has a personal ring:  everyone I know has been over the healthful sugar limit of 36 grams daily for men and 24 grams for women (World Health Organization recommendation), which comes to about 5% of total calories—the US average is over 20% (2:1). With age and its diminished autophagy (RRA) we have the health disaster for seniors. Then add to this the rancid PUFAs in cell membranes. and as developed in 4:6 incorporated also in the MTD’s membranes, and thus a CC for MTDD. 

I was consuming about 20% of calories from sugar all sources as a child, and continued at about 15% until 2014, when I investigated the claims made about sugar by Prof. Robert Lustig.  I had been since 1992 on a low-fat diet until 2014, which the high glucose potentiates the harm done by fructose by delaying its metabolism.  I thus avoided the PUFAs, which I had done since 1970 when I learn about rancid fat,  My purchase of manufactured over the years would put at the bottom 20%, with the only major one being Raisin Bran for 15 years, then I found out that it was 17 sugar by weight,  Today I know of only one senior, a long-term friend, who is both thin and free of conditions.  As for restaurants I am in the bottom 15% since about 1980, thus avoiding their PUFAs.  Of all those I know over the age of 60 and for 3 years or more (over 100) they weren’t as fortunate with the exception of Joe, Bob and me; we all have maintained our youthful weight. 

,In June I lost to cancer a friend age 64 whose fitness and diet was like mine.  At the age of 59 he was diagnosed with stage 3 colon cancer.  In June of 2020 he died from the cancer.  We don’t know:  Staffan Lindeberg the Swedish Professor of family medicine University of Lind, who studied the Kitavans (see 1:1) (lecture on YouTube), he died of prostate cancer at the age of 66 in 2016.  He was a leading advocate of the paleo diet, and looked it.    

I missed the bullet (so far) by chance:  I was on long-term aspirin for chronic bad back.  I averaged over a half gram a day from 1992 until 2018.  I am a sports-fitness addict, (since 1975), as policy to diet whenever I gained 5 pounds, I take it off (weight watching since 1969).  Exceptions were in 1969, 1998, and  2003 when I put on 10 to 20 pounds in 3 months, I then lost those pounds in a couple of months, before the complex weight regulatory set reset.  I have been taking sufficient testosterone lotion to returned me to a youthful level since 2004, and DHEA since 2002—both are natural and thus supplements. At 77 years in 2020, I am still drug free, but my risks are well above the LSPs.  Though I have written of this before, I feel compelled to repeat a healthful example and to direct you the details on the supplements see 6:2, the diet you know, avoid fructose and PUFAs.  These 2 chapter is on the evidence that raises PUFAs to stand next to fructose.     


3.   Organizations for hire, AHA:  Storage fat can be used for energy or for cell membranes.  PUFAs will become rancid at room temperature.  I threw out 2 bottles of oil in my S.O’s. pantry with the last 2 months (6/2020) because they stunk, and the crackers she had also stunk.  The ducks at our pond wouldn’t eat them.  That happened in a tightly sealed jar with no air circulation; that is a measure of the instability of PUFAs at a temperature 20 degrees below our body’s.   Body fluids supply a large number of reactive chemicals, and being packed in a membrane doesn’t fully protect the PUFAs from those chemicals.  Moreover, prior to incorporation in cell wall, some of PUFAs have formed aldehydes with their distinct odors (more on aldehydes below).  In addition, a number of reactive substances can diffuse through the membrane and react with the electron rich PUFAs.  There is strong evidence of rancidity in cell membranes and that it is pathogenic.  The degradation of MTD membranes promotes MTDD.   Phospholipids in cell membranes also become rancid.  Read on about the rancid fats and fats in general.   “You can brown your meat at 375 degrees for one hour, or you can brown your meat at 98.6 degrees for 75 years.”[2]  So why are we told the bad is good and good is bad?  “It is as impossible for a lawyer to wish men out of litigation as for a physician to wish them in health” [3]  On point “impossible for a large corporation to wish a lower profit percentage.”

          Follow the dollar and the KOL system, and we get every major national private organization saying the opposite of science: 

The effect of saturated fat on heart disease has been extensively studied.[25] There are strong, consistent, and graded relationships between saturated fat intake, blood cholesterol levels, and the epidemic of cardiovascular disease.[8] The relationships are accepted as causal. Many health authorities such as the Academy of Nutrition and Dietetics,[28] the British Dietetic Association,[29] American Heart Association,[8] the World Heart Federation,[30] the British National Health Service,[31] among others,[32][33] advise that saturated fat is a risk factor for cardiovascular disease. The World Health Organization in May 2015 recommends switching from saturated to unsaturated fats. . . . Recommendations to reduce or limit dietary intake of saturated fats are made by the World Health Organization,[56] American Heart Association,[8] Health Canada,[57] the US Department of Health and Human Services,[58] the UK National Health Service,[59] the Australian Department of Health and Aging,[60] the Singapore Ministry of Health,[61] the Indian Ministry of Health and Family Welfare,[62] the New Zealand Ministry of Health,[63] and Hong Kong's Department of Health.[4]

This crapolla we have was through Ancel, who was in the pay of the food industry and soy farmers, and probably others.  He was the leading figure promote the low fat and low cholesterol diet for over 30 years.  He was a vitriolic critic of John Yudkin, as industry went after the leading nutritionist of the UK for fingering Sugar as Pure White and Deadly.[5]

The hypothesis that saturated fat has a detrimental effect on human health gained prominence in the 1950s as a result of the work of Ancel Keys, a US nutritional scientist.[16] At that time in the USA, the incidence of heart disease was rapidly increasing, for reasons that were not clear.[16] Keys postulated a correlation between circulating cholesterol levels and cardiovascular disease, and initiated a study of Minnesota businessmen (the first prospective study of CVD).[17]

Keys presented his diet-lipid-heart disease hypothesis at a 1955 expert meeting of the World Health Organization in Geneva.[18] In response to criticism at the conference, he set out to conduct the years-long Seven Countries Study.[19][6] Ancel Keys joined the nutrition committee of the American Heart Association (AHA) and successfully promulgated his idea such that in 1961, with the result that the AHA became the first group anywhere in the world to advise cutting back on saturated fat (and dietary cholesterol) to prevent heart disease.[20] This historic recommendation was reported on the cover of Time Magazine in that same year[7]

These subscribers to the marketplace theory have their journal articles to support their findings.  For example, SFAs cause IR, and PUFAs don’t. “Saturated and certain monounsaturated fats have been implicated in causing insulin resistance, whereas polyunsaturated and omega-3 fatty acids largely do not appear to have adverse effects on insulin action.” [8]  I have sat through a CME class and heard the lecturer say “We all know it is true that we can manage type 2 diabetes with a low-fat diet.  I have in my clinic [in Clairemont, CA] reversed diabetes with that diet.” [9]  

What have we had for the last 50 years with this change in diet:  the diabetes pandemic caused by an increase in carbohydrates and thus sugar to make up for the reduced calories from fatty acids.  With IR there is a daily 250-calorie increase.  Welcome to the world of capitalism, where profits trump science.  


 4.    Fat compositions:  AHA, FDA, and governments throughout the world have swallowed the western diet low in natural SFAs and high in seed oils and carbs.

 PUFAs being electron rich have a much higher rate of oxidation, glycation, and fructation than MUFAs which have only one double bond, their rate of reaction with electrophilic compounds and hydrogen ion is at 1/3rd the rate.  Even so the animal making MUFAs is low, SFAs are the preferred fats (see table below for percentages).  There are only a few common ones, and for which evolution limits their use in membranes.[10]  SFAs, lacking double bonds don’t become rancid.  Oxidized and glycated fats when incorporated into cell membranes perform poorly.  This is why evolution favors saturated in long lived animals.  That is why dairy products are high in SFAs including mother’s milk, but food manufacturers prefer the much cheaper seed fats.  Thus, in the sales play book, they claim their fats are health and the expensive saturated ones are bad for health.

The importance of this message merits a second presentation.  Nature selected the best fats for mammals: cow milk is 67% saturated fat, 28% monounsaturated, and 3% PUFAS (numbers rounded off and an average for cows which of course vary with breeds); human milk is 14% PUFAs, and the remaining 86% mostly SFAs. The numbers are similar for the main breeds of milk producers:  water buffalo having 8% PUFA; cows 4% PUFA, and humans 4.2% PUFAs.  The percentage difference is strong evidence that there is a health advantage for SFAs compared to PUFAs, nature doesn’t select the worst fat and minimize the best, yet we hear over and over again that PUFAs are the best, and SFAs are deadly, thus we evolved to harm the off-spring, the opposite of evolution, and this occurs for other species: 


Milk composition per 100 grams








Water g






Protein g






Fat g
























Cholesterol mg






Calcium mg












Caseins to whey proteins






Given the slow growth rate of humans, but for the brain, the amounts of calcium and protein are less but sufficient to sustain growth, but for the brain and thus higher cholesterol,  Carbohydrates are nearly all lactose, however, a significant percentage is not the simple disaccharide but chains up about 20 lactose molecules. 

Human milk is high in protein and as a percentage high in caseins to whey ratio is nearly the reverse of the others in the chart. Human milk is 29:70 Caseins to whey proteins, while bovine is 82:18 (human upper range is 33:66); goat is 78:22, reindeer 83:17, pig 76:24.  Mystery, why the difference in whey and caseins?  Another example of nature sculpturing human milk is that of vitamin C, 12 mg/cup, cows 0, and goats 3.2 mg—both cows and goats are ascorbate producers, while humans rely upon foods.  Faster growth of cows and goats requires a greater amount of calcium; their milk is 3 and 4 times that of human milk.   Since the growth of the brain is a major difference, human milk cholesterol is higher than the cow and goat’s milk.  SFAs make functionally better cell membranes thus a higher percentage than in cow or goat milk, and also humans live much longer.      

Evolution has also provided a warning system, the rancid smell, and the aversion response.  That mammals have this warning system is suggestive that the stench response to rancid fats is a way of limiting foods with rancid fats. 

Business certainly doesn’t care, I just examined the leading infant milk substitute, Similac, and found its main ingredient is sugar and plant oils high in PUFAs.  (It was developed at Tufts University and Similac is marketed by Abbotts Laboratories. That is smart business for the drug company which knows of sugar addiction and that early development of a craving for sugar will increase its sales of Similac and later its sales of drugs.  A mother who tastes Similac will assume that the baby like that flavor.  Similac’s quantities of fats and sweeteners vary according to formula.  The Similac name is on 34 products some of which are supplements or for special conditions such as diarrhea, low birth weight, protein fortifier, and a couple of products for the mother—August 2019 from their website.  Thank you, Abbott Laboratories, a $30 billon income (2018) and 99,000 employees and assets of $76.25 billion (2017) for your gift to neonates of sugar and PUFAs, thanks for increasing the probability of development of childhood insulin resistance. 

Gerber merged with Sandoz Laboratories of a major pharmaceutical company of Switzerland in 1994, which the merged the follow year with CBIA-Geigy to from Novartis, one of the largest pharmaceutical companies.  In 2007 Gerber branch was sold to Nestle for $5.5 billion.  In 2017 Gerber had 61% of the U.S. baby-food market and are also in another 60 countries.  Of the more than 60 products for babies, only 3 have moderate protein, e.g., Turkey rice has 3 grams of protein, 2.5 of fat and 12 of carbohydrates per 113-gram portion.   Of the others with 0 to 1% protein, a typical serving is of 113 grams, has 13 grams of sugar and 1% of fat.   Calcium varies between 0 to 150 mg per 113-gram portion.  Fats and cholesterol, both need by the infant’s brain in high quantity and quality are mostly zero.  Convenient but not healthy Gerber promotes sugar addiction and insulin resistance. 


5.     Extraction vegetable oil, and rancidification    


Trilinolein (linolein) a triglyceride formed from 3 linoleic acids which are attached in the middle of the molecular representation above by glycerol, the 3-carbon molecule which has lost 3 hydroxyl groups in forming trilinolein. “It’s a primary constituent of sunflower oil and multiple other vegetable fazts.”[11]

          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 and wholesomeness; and the lack of court cases for violation of regulations.  I steer clear of the highly processed seed oils. The main seeds used contain under 3% oil (the seed have more oil), and the byproduct is mainly used for animal feed.  The wholesome sound vegetable oil isn’t from vegetables, but seeds.   A description of the production of corn oil: 

Almost all corn oil is expeller-pressed, then solvent-extracted using  hexane or  2-methylpentane (isohexane). 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.[12]  


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; 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.[13]

The major seed oil undergoes similar processes. 

          Canola oil is unique among the major cooking oils in that it is 61% Oleic acid, a monosaturated oil, that is supposedly heart health—see 2:6, 3.  This is similar to olive oil which is 70% oleic acid, and it is about 1/5th the price of the popular virgin olive oil. Another 15 % is PUFAs of olive, canola is 21 PUFAs.[14]  Yield explain in part the use of these old, with palm oil having the highest yield per hectare per year 4.0, canola 1.4, soybean 0.6, sunflower 0.6.[15]  In 2012 PO [palm oil]  accounted for 32% of global fats and oils production and it has overtaken soybean oil as the most important vegetable oil in the world.” [16]

Seed oils except for corn are high in oil content:  sunflower seed (28%), soybean dry (56%), and canola dry (43%), corn (02.8%).” [17]  These oils with significant production that are high in PUFAs:  sunflower 69%,[18] soybean 58%, corn 55%, and just 21% for canola. World product Palm 2006-07 palm 41.3, soybean 41.2, rapeseed 18.2, sunflower 9.9, cottonseed 5.0 peanut 4.8, coconut[19] 3.5, olive 2.8.[20]  

The in vivo rancidification of PUFAs as well as in cooking, they pose a serious health risk—see rancidification (2:6, 5 & 6).  The evidence of PUFA oxidation has been established firmly by the 1960, with some articles going back decades before. A warning was issued in 1969 that influenced research based on heated PUFA in conditions that paralleled the use of a restaurant deep fryer.[21]   In 1973 a major study of the products of deep frying simulating commercial conditions (74 hours at 185 degrees centigrade) using 5 common commercial oils:  corn oil, hydrogenated cotton seed oil, trilinolein and triolein (two long chain fatty triglycerides with multiple double bonds), and tristearin (triglyceride of stearic—saturated—acid).  “A total of 211 compounds were identified.” [later stated they are the non-volatile compounds] [22]  Missed in the article is that the used oils are saved, picked up and many of the restaurants by the cheaper  reprocessed oils—oils that weren’t tested because they were a mixture of all types of oils.  “In addition, both volatile and non-volatile may affect human health” (supra). This is supported by the animal studies using the seed oils.

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” [23]  “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.” [24]   

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 hydrogens.  If not terminated fast enough, there will be damage to the cell membrane.[25]  

For over 50 years the warning flag has been waved in journals, but not in our media, USDA, FDA, or NIH.  I knew of this when I was in graduate school in 1968.  And it gets worse, article after article in journals fails to find an association of saturated fats with CVD, yet the myth has been swallowed by physicians, dieticians, and the public.  The official government message is positive, for example for canola oil:

In 2006, canola oil was given a qualified health claim by the United States Food and Drug Administration for lowering the risk of coronary heart disease, resulting from its significant content of unsaturated fats; the allowed claim for food labels states:[43]

"Limited and not conclusive scientific evidence suggests that eating about 1 ˝ tablespoons (19 grams) of canola oil daily may reduce the risk of coronary heart disease due to the unsaturated fat content in canola oil. To achieve this possible benefit, canola oil is to replace a similar amount of saturated fat and not increase the total number of calories you eat in a day.[26]

So, is Wikipedia inconsistent and wrong?   

Lipid peroxidation is 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. This process proceeds by a free radical chain reaction mechanism. It most often affects polyunsaturated fatty acids, because they contain multiple double bonds in between which lie methylene bridges (-CH2-) that possess especially reactive hydrogen atoms.. . .  If not terminated fast enough, there will be damage to the cell membrane, which consists mainly of lipids.[27]

The oil story is one more example of our corporatist state; of tobacco ethics and science by the government departments set up to promote corporate profits while faking public protection.

[1] Wiki, American Heart Association¸ August 2020

[2] Prof. Robert Lustig, Fat chanced, P 123

[3] Jeremy Bentham his little book on A fragment on government 1776.  In today’s world it is the corporate hospital and clinics that can’t “to wish them in health.”

[4] Wiki, Saturated fat, August 2019

[5] Title of Yudkin’s book in 1972, shortly after he was forced to retire in 1971.  The book is still in print with the new edition having a forward by Robert Lustig.  (I have the book).  He was Chair of Physiology at Queen Elizabeth College in London, and then at the highly rated University of London, where he established the first in UK Department of Nutrition.   His warning of sugar as causal for CAWD was made at least from 1957, and he recommended a low-carb diet in This Slimming Business (1958).

[6] This study has been repeated held up as an example of scientific fraud, because Keys had the results of 22 countries with sufficient details to be included.  He picked out the 7 countries that showed a relationship between diet and CVD; there by skipping aver 6 countries that supported the opposite theory, that carbohydrates were associated with CVD.   

[7] Wiki, Saturated fats and cardiovascular disease, August 2020

[8] Lovejoy, Jennifer, Oct 2002, The influence of dietary fat on insulin resistance

[9] Dr John McDougall, CME class on YouTube, entitled The Latest Scams from the diabetic Industry. 

[10] Surprising in the liver (and presumable in other tissues) the metabolism of elaidic acid (a trans-fat) was at a higher rate than oleic acid.  Evolution selects to build better wall by lowering the amount of trans-fats.  See Guzman, Manuel, Will Klein, et al April, 1999, Metabolism of trans fatty acids by hepatocytes.

[11] Wiki, Linolein, August 2020

[12] Wiki, Corn oil, Aug 2016

[13] Wiki, Canola oil, August 2020

[14] Wiki, Canola oil,  & Olive oil, April 2020. 

[15] Wiki, Vegetable oil, August 2020

[16] Mancini, Annamaria, Ester Imperlini, et al, Sept 2015, Biological and Nutritional Properties of Palm Oil and Palmitic Acid: Effects on Health FULL

[17] WIKI, Canola oil, Aug 2016. I consider canola oil the 2nd best of oil behind non-virgin olive oil.  It has a similar amount of monounsaturated fatty acid.  Non-virgin because virgin contains chemicals found in the olives, which I presume some of which are toxic.  I am one of the few who can taste them, and they loudly ring in my brain the rancid warning bell.

[18] Sunflower oil standard; however, two others types ar listed, linoleic with 40% PUFA, and oleic with 4% PUFA.  Labeling in the supermarket might not distinguish which of the 3 are on the shelf. 

[19] Wiki, Coconut oil, Aug 2020 lists the 2006 at 5.5, and the 2015-6 at 5.4, down form 6.66 in 2009-10.  It makes up 40% of the oil I consumer, with butter another 25%, canola about 10%, and nuts, fish dairy, chocolates the remaining. 

[20] Wiki, Vegetable oil, August 2020

[21] Dormandy, TL, Sept 1969, (The Lancet) Biological Rancidification.  I remember while in graduate school articles on restaurant deep fryers in McClean’s Magazine.  I bought in 1970 a deep fryer and used 4 pounds of lard.

[22] Chang, Robert Peterson, et al, 1973, P 718, Chemical reactions involved in the deep frying of foods.

[23] Wiki Rancidification July 2016

[24] Dormandy, TL, Sept 1969, (The Lancet) Biological Rancidification

[25] Wiki lipid_peroxidation June 2016

[26] Wiki canola oil April 2020

[27] Wiki lipid peroxidation April 2020

6.       In praise of carbs: 

In 2:6, 2, I covered briefly some of the tobacco science used to sell the UFAs as healthful and SFA as toxic.  Six examples were included, 5 briefly and that of essential omega 3 at length 3:6 at length, including the salubrious furan fatty acids found in fish and some seed oils along with the omega 3.  Fatty furan acids are one of the systems inhibiting damage by ROS to UFAs.   Here for the sake of completeness I am covering some of the other examples of tobacco science praising carbs and claim toxic effects of SFAs.  There are numerous claims as to health and illness made concerning fats, palmitic acid and the omega 3 & 6 PUFAs, and the need for glucose, glycogen.  Over and over again I read that 1) carbohydrates are the preferred source of energy, 2) brain must have carbohydrates, and thus carbs are essential for life[1]; 3) that omega 3 and 6 have vital functions (2:6, 3) and that we need omega 3 PUFAs because they are significantly heart health; 4) that the western diet ratio of omega 6 to omega 3 of 15:1 is abnormal.  The ratio should be 4:1 or less; 5) that palmitic acid and other saturated fats promotes CVD, MI, IR , NAFLD, MeS, and t2d, and Wikipedia adds osteoporosis, and cancers.[2]  There is not one word about the rancid alternative UFAs, brain derived neurotropic factor, paleo diet, or the quality studies that find it to be heart healthy.[3]  Missed also is that the body makes the saturated palmitic acid.  It is produced in the liver when there is an excess of glucose or fructose and not a need for more ATP.  It is created and the most common fat in human milk.  Assuming the negative claims are correct, this entails that evolution is promoting those negative consequence to harm humans and other mammals.

          The assault upon SFAs is all marketing ethics and tobacco science.  The evidence is in the details, and the details confirm that industries are about profits.  A focus on basic science peels off the layers of deceptions and cognitive dissonance.  Here we go again, instead of forward, I am sweeping off crapolla from the table made by the industry’s harpies.  The harpies’ deposits:      

1)     Carbohydrates are preferred to fats.[4]   There are many reasons for the opposite, that the body prefers fats.  One, is that the storage of glycogen in quantities to promote survival during extended periods of starvation would reduce survival during times of sufficient food; they are two bulky.  Fats are stored as triglycerides; they provide over 2 times more ATP per gram than does glycogen of the same weight which include 3-4 water molecule per glucose molecule. The storage of glycogen with water prevents reactions with amino acids.[5]   The average normal weight adult who is not obese and on the western diet has about 22% fat by weight.  The stored glycogen is under 600 grams.  There is a major survival advantage to storing triglycerides compared to glycogen.  To store instead of triglycerides, glycogen would be about 44% of the body’s weight, which would hinder hunting, waring, and other activities, moreover, more calories would be need for storage and to move that mass.  Only a small amount of glycogen is needed, the liver releases it prevents hypoglycemia which would affect the erythrocytes that depend upon glucose because of a lack of mitochondria. Muscles during prolonged strenuous activity metabolizing fatty acids.  A trend has started where by athletes in endurances sports go on a ketogenic diet.  Much smaller amounts are stored by the kidneys, pancreas, blood cells, and for pregnant women in the womb.

 2)   that an average for paleo peoples (before farming) is 60% of calories come from fats.  There is great variation among regions, from the north to the tropics.  Evolution has adapted to the high fat diet, and also to the high saturated fat diet (PUFAs are under 15% of human milk fats, and over 80% of common food sources are even lower for the paleo diet).  Some suggest this was to fulfill the need of the brain which consumes 20 to 25% of calories.  I find this putative need with too many counter examples to be true. 

3)   because saturated fats are stable, a high fat diet reduces glycation that damages MTD, increases ROS, and damages nearly all the structures of cells.

4)   the most metabolically active organ by size, the heart, metabolizes mostly fats. 

5)   fats, the short chain ones, will yield BDNF (brain derived neurotropic factors) which promote growth and repair. 

6)  the high carb diet is likely to include more sugars, thereby promoting the conditions of affluence.  A few high carb areas before the 19th century, had year-round sweet fruits such as dates and figs.  Moreover, over the last 9,000 since the first farming vegetables and fruits have been selected for their sugar content.  Thus, population with short seasons would be subject to less of the selective breeding and thus fewer dietary sugars.  I hold that the difference between the two climates and their crops was a CC for the success of northern climates.[6] 

7)   paleo peoples and other LSPs lose weight with age as muscle mass declines.  The HSPs weight gain and comorbidities are signs that the high refined carb diet with its excessive sugar and UFAs are disadvantageous. 

For all these reasons I conclude that the claim that the body prefers carbs is false.    


7.  Glucose is essential for the brain, or is it?  I have failed to find evidence that some type of brain cell requires carbs—which one?  I have come to believe that the measurements of brain metabolism of carbs are based upon erythrocytes circulating in the brain and metabolizing glucose.  Erythrocytes don’t have MTD, therefore they like cancer cells[7] must metabolize anaerobically (fermentation) glucose to produce ATP.[8]  The scanning techniques used in the studies I found measured brain glucose use. 

          Turning the cart the other way, during fasting, sleep, starvation, and coma, the liver produces glucose once the limited store of glycogen (about 150 grams stored in the liver) is low, the liver then converts fatty acids to glucose in an amount sufficient to supply the erythrocytes.  Prior to that “For the next 8–12 hours, glucose derived from liver glycogen is the primary source of blood glucose used by the rest of the body for fuel. . .  muscle cells lack glucose-6-phosphatase, which is required to pass glucose into the blood, the glycogen they store is available solely for internal use and is not shared with other cells.” [9]  Since it is released into the blood, the erythrocytes absorb the glucose for fermentation (without oxygen) supplies the essential ATP. I don’t think the remaining glucose in the blood is taken up by other cells, with the possible exception of cancer.  The other cells through the Randel switch are metabolizing fats.  If there wasn’t this switch, we wouldn’t burn fat stores at the rate of a half-pound a day while fasting or under stress such as long period of physical excertion.  To have the liver convert fat to glycogen would slow its other functions, and under major stress would lower survival.  I am not aware of an on-point journal article.

          For these reasons I have come to believe that the brain runs fine on ketone bodies, and if any type of cell there requires glucose, it is only a type that is rare and thus not a major user of glucose.   Ketone bodies, mainly β-hydroxybutyrate and acetoacetate, are the primary alternative brain fuel to glucose.”  On a high fat-diet it would be the primary fuel and for neonates.[10]  That study went on to find that glucose metabolism was reduced with AD, but not the metabolism of acetoacetate (which was measured).  These results suggest that a ketogenic intervention to increase energy availability for the brain is warranted in an attempt to delay further cognitive decline by compensating for the brain glucose deficit in MCI [mild cognitive impairment] and AD. “ [11]  This is part of the evidence that has caused me to believe that a high SFA diet is good for the brain, made more so with coconut oil that provides BDNF (brain derived neurotropic factor).



Oh, and by the way, the liver during water fasting or ketogenic diet, through glycogenesis supplies sufficient glucose for the low energy erythrocytes, but often not for the high energy cancer cells.  Business needs to be taken out of politics and science



8. Saturated fats are toxic, or are they? 

In this review we provide a concise and comprehensive update on the functional role of palm oil and palmitic acid in the development of obesity, type 2 diabetes mellitus, cardiovascular diseases and cancer. The atherogenic potential of palmitic acid and its stereospecific position in triacylglycerols are also discussed.[12]

Again, we have guilt by association of the palmitic acid made by the liver is blamed for NAFLD and its excess LD and adipocyte tissue in the liver.  Skipped is the conversion of excess glucose and fructose to fats for storage, caused by a feedback system of not needing them in the production of ATP.  Evolution didn’t select palmitic acid as the preferred fat for milk and storage in the liver for to harm humans and mammals.  NAFLD is caused IR and dysregulation of WRS. 

But could there be some toxic chemicals created in the process for those on the western diet and/or in the food sources of the highly processed SFAs, in particular the palm oils?   That is what has been hauled out as a modus operandi for the toxicity.  One point to make is the theory is above the details.  Every process will have turned on genes, processes for synthesis which will differ from other processes, and so on.  To name them void of the forest they dwell in is to miss the foundation as to what is going on and why.  Thus, I have laid the foundation with LSPs, HSPs, fructose, rancid UFAs, MTDD, and CAWD.  Genes and processes aren’t going to overthrow the foundation, but could add a chapter, such as for carbon monoxide from smoking or statins lowering the production of ATP significantly.   

I couldn’t find any quality completing evidence that palmitic acid or the other natural, common SFAs are toxic.


9.  Trans-fats are bad, or are they?     

https://upload.wikimedia.org/wikipedia/commons/thumb/b/b8/Triglyceride_Hydrogenation%26Isomerization_V.1.png/330px-Triglyceride_Hydrogenation%26Isomerization_V.1.png  https://upload.wikimedia.org/wikipedia/commons/thumb/d/d4/Crisco_can_2007.128.jpg/180px-Crisco_can_2007.128.jpg

Above, all three fatty acids of the triglyceride are attached to glycerol (the 3-carbon black chain).  The double bonds in the top schematic on the red fatty acid are all on the same trans side, but following the hydrogenation of just 2 of the 3 double bonds, the remaining double bond has rotated on the carbon chain to become trans to the former 2 double bonds.  The green monounsaturated fatty acid has also been hydrogenated to become a MUFA.  Further processing will remove the glycerol and thus yield a mixture of 2 saturated fatty acids and one mono-saturated fatty acid.  I have come to believe after several weeks of research that trans-fats are the scape goat for the PUFAs.[13] 



      Trans fatty acid (elaidic acid)             Cis fatty acid (oleic acid)[14] 

          “The cis fatty acid chains have a bend at the double bond, and fit each other together—and saturated chains badly. . . . In the presence of hydrogenation catalysis, unsaturated compounds undergo not only hydrogenation, but also isomerization—shift of double bonds or stereochemical transformation. . . .” [15]  

Nature makes under 5% that are trans, both in plant and animal fats.  Butter is about 2% trans fats.  By far the largest amount of trans fats consumed today is created by the processed food industry because of incomplete (partially) catalytic hydrogenation to obtain a desired melting temperature.  How complete the hydrogenation process is determined by the product being manufactured.  Fully hydrogenated would yield a product significant harder than butter at both room temperature and refrigerator temperature.[16]  For example coconut oil at a temperature of 50 degrees is about twice as hard as refrigerated butter. It is 99% fat of which 83% is saturated mostly short chain.  Butter averages 81% fats, with 45% saturated, milk solids, salt and sugar, and 20% water.  The cheap unsaturated seed oils are hydrogenated under high pressure and temperature with a catalyst, typically powdered nickel, which is cheap. The need for the hydrogenation was driven by the demand that in some regions, such as France, exceeded production of butter.  For many cooking uses, lard was used a century ago. The high saturated fat content of butter and to a lesser extent lard improve the flavors of fried and baked foods by its retaining the aromatic chemicals, and the with low PUFAs there is little rancidification.  Lard is about 40% SFA and 45% MUFAs.  (A table of fat content is in section # With the development of extraction methods for corn, soya, rapeseed and others and the lower price compared to lard, the hydrogenated of seed oils in manufactured foods replaced lard.  Price, shelf life and flavor caused the preference for hydrogenated seed oils in manufactured foods.  “These partially hydrogenated fats have displaced natural solid fats and liquid oils in many areas, the most notable ones being in the fast food, snack food, fried food, and baked goods industries.” [17]  The common seed shortening hydrogenated is 25% SFA, 28 PUFA, and 41% mono fatty acid.  Up to 45% of the total fat in those foods containing man-made trans fats formed by partially hydrogenation.  Baking shortenings, unless reformulated, contain around 30% trans fats compared to their total fats. . . Margarines not reformulated to reduce trans fats may contain up to 15% trans-fat by weight.” [18]  Reformulated means the manufacturer reduced the amount of trans fats.  More, often they make the portion size small enough so that the amount of trans fats is under a half gram, and the label states zero trans-fats.  Given the government fails to enforce regulations, and the manufacture hiring a company to do nutritional test, there is great room for errors in labeling.  When is the last time you read of a case in the corporate media of a food manufacturer being prosecuted in the courts for incorrect labeling?  Do you trust the corporate honor system?

A little bit of history and some numbers:  First until the 1930s most fats were animal derived, and were mostly SFAs, about 70% or more.  Even milk (cattle or mother’s) is over 70% SFAs.  The remaining fatty acids are MUFs or PUFAs.  Compared to the major seed oils that are over 50% PUFAs (corn, soya, sunflower) nuts are the big exception, also olive oil, safflower, and canola oil (rape seed) that have above 70% MUFAs and about 10% SFAs, and less than 10% PUFAs.  Coconut oil has about 83% SFAs and 6% PUFAs; palm oil is about 10% PUFAs with about 50% SFAs and 40% MUFAs.[19]   In the 1930s extract with organic solvents, most commonly hexane, was used to remover the seed oils from mainly grains and some seeds.  The widely marketed seed oils are over 50% PUFAs.  The defatted grains our fed to cattle and pigs.  Lard, for example, has about 80% SAF.  Crisco which was introduced in June of 1911 by Procter and Gamble was the first shortening made entirely from seed oil (cottonseed).  This totally hydrogenated oil was marketed from its introduction as heart healthy in comparison to lard the standard oil ingredient in baked and fried products.  In 2004 a new Crisco was marketed “Crisco Zero Grams Trans Fat Per Serving All-Seed Shortening.”  A 2007 label has 12-gram portion, and claims zero grams of trans fats.  If you wonder why 12-gram portion, it is because at under 0.5 grams of trans fats the label, under USDA regulations, is entered as 0 grams, thus 13 grams of Crisco would have counted as above the 0.5 grams. If you wonder why I used the word claim, it is because this neoliberalism, corporations are on the honor system, and the courts aren’t interested in claims of lying labels.  I cannot believe that most of the product labels are truthful.  A major deception has been worked with the organic label, and the outsourced certification.  Companies won’t embarrass the company that hired than, especially when the risks are minimal at most.  All this reminds me of the American Heart Association selling to food manufacturers the certification sticker of heart health on their foods, such as sugar loaded cereals and Welshes Grape Juice.  We have gone back to the snake oil days, only now the government is in on the deception.   

Though most readers believe trans-fats are bad, I have failed on 3 attempts of over a week each to find the modus operandi for how they are bad supported by strong evidence—not just a theory and some biomarkers changes, and an association with CVD on an KOL article.  Association doesn’t prove cause, for those who eat foods high in trans-fats are on an average poorer than the general population (preferring for example margarine to butter) and consumer more sodas and manufactured foods.  A proposed causal method does entail that it a significant one.  Marketing frequently waves the chemical-biological foundation to promote sales. To sort out what is bad and degree has the obstacles of the dozens of PUFAs and thus dozens of trans-fats.  Putting the tail on the LDL donkey will satisfy most American, since most believe in the lipid fiction; but that isn’t causal proof; nor is population studies for the above reason of economy difference and their confounding variables.

Although trans fats are edible, consuming trans fats has been shown to increase the risk of coronary artery disease in part by raising levels of low-density lipoprotein (LDL, often termed "bad cholesterol"), lowering levels of high-density lipoprotein (HDL, often termed "good cholesterol"), increasing triglycerides in the bloodstream and promoting systemic inflammation. . . . Trans fats also occur naturally, e.g., the vaccenic acid in breast milk, and some isomers of conjugated linoleic acid (CLA). These trans fats occur naturally in meat and dairy products from ruminants. Butter, for example, contains about 3% trans fat [20]

This brings up other problems, such as why hasn’t evolution protected us from animal sources of trans fats?  Secondly, how does the minor change in shape of trans-fat cause adverse health consequences.  A likely way would be in cell membranes where incorporating rancid fat has been shown to adversely affect cell functions. It seems given the dozens of different fats mammals have evolved a system for metabolizing all of them.  Moreover, in the cells the trans-fat is as stable as it’s cis brother.  It is possible, if a study was done comparing a PUFA with 4-double bonds compared to a trans-fat with 2 double bonds, that this trans is healthier—fewer double bonds available for non-enzymatic bonding to become a rancid fat in the cell wall.  I don’t know of head to head animal studies comparing the 2 different oils. 

After looking at the evidence, I suspect that at the highest levels it was decided to blame trans fats (and saturated fats) as a way to support their claim about bad fats in the media manipulation of beliefs of doctors, dieticians, and the public, while creating an illusion of regulatory fixes (next section for details).  This claim about fake fixes has a mountain of examples, many of which are in Prof. Ben Goldacre’s Bad Pharma.  Whether trans-fats are bad or not, doesn’t make a big difference compared to the harm caused by fructose, PUFAs, and the weird chemicals taken in pill form (4:5).  drugs (next chapter). 

   I did find a journal article that trans-fats are safe: “They have no adverse effects on growth or reproduction in rats. Trans fats are hypercholesterolemia for rabbits and monkeys but no more atherogenic than their cis counterparts. . . .  Reviews of the literature by expert committees in the US and UK conclude that at current levels of intake dietary trans fats pose no health problems.” [21]  But nothing has changed business as usual with rancid PUFAs pushed under the rug, and trans-fats as a diversion, the big gorilla in the room is CAWD with its fructose causing MTDD also under the rug with the trans crumbs. 


10.  What are the regulations of trans fatty acids?  Official response has been prohibiting trans-fats in a number of countries, but not the US.  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 as trans-fat on the label.  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.[22]  Another gap in calculation is that trans-fat levels of less than 0.5 grams per serving are listed as 0 grams of trans-fat on the food label.  As a consequence, many foods labels list a small portion, often one ounce and 14 grams; thereby staying under the 0.5-gram reporting requirement.  Given the outsourcing of reporting to private corporations, we have the fox hiring the guard of the hen house.  The lack of court cases for fraudulent labeling reinforces my skepticism.

There are more major holes in the requirement:  There is no requirement to list trans-fats on institutional food packaging; thus, bulk purchasers such as schools, hospitals, [restaurants], jails,  and cafeterias are unable to evaluate the trans-fat content of commercial food items.” [23]   Because of the lower price of PUFAs and thus hydrogenation creating trans-fat, their resistance to becoming rancid (longer shelf life), their ability upon cooking to capture the flavor of the food, and thereby result in a product that noticeable tastes better, I can only expect that the honor system (without meaningful policy or penalties, or media coverage) that the major reduction in trans-fats is limited to Crisco and margarines.

  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 and Spain … no significant levels of trans-fats were found in any of the analysed products, regardless of brand of origin.” [24]  The regulations might make a difference assuming an association with CVD, 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.[25]   However, the highest rate of obesity, diabetes and sugar consumption is in the US, and this explains most of the difference and thus the reliance upon pharmaceutical drugs.  Let us not become distracted by what could by the minor causes such as TFAs, when the elephant in the kitchen is sugar, PUFAs, tobaccos, ethanol, and pharmaceutical drugs.  The weakness of lab work with head to heat trial of PUFA and TFA makes the case.[26]  Trans-fats is insignificant and another part of the web causing cognitive dissonance.  Why hasn’t PUFAs come to forward as a major CC for CAWD.  As my friend attorney Mike K. said yesterday, “money makes all the difference.”          

[1] It is since the erythrocytes lack mitochondria, and therefore like aggressive cancer cells cannot metabolize fatty acids; but can glucose by fermentation in the MTD.  The brain’s need for glucose is waved for the reader.  Also not mentioned is the body prefers to store fat rather than carbohydrates as glycogen, and also why the serum level in the fasting state (following sleeping) is but 4 grams for an adult of 150 lbs.  All these and others cause me to conclude the information is the product of scientist for hire (KOLs). 

[2] Wiki, Saturated fat August 2020

[3] Wiki, Saturated fat, August 2020.  This is not a balance article, were the conflicting evidence finds print, as it use-to-years ago. 

[4] In general, I will skip putting reference to the statements, the evidence is scattered throughout his book. 

[5] A similar process involves phosphates that inactivates glucose, fructose and other sugars., to prevent glycation and to prevent diffusion out of the cell.  Glucose form glucose-6-phosphate.  Other sugars have same, different, and form diphosphates  as to glucose which can also form glucose 1-phosphate.  

[6] The observation that the northern climates dominate was popularized by Arnold Toynbee (1852-1853) and Jared Diamond, Guns, germs and steel (1997).    

[7] MTD signal apoptosis when a cell is significantly abnormal. Cancer cells disable their MTD and have the cancerous cell obtain sufficient ATP through aenerobic (in the cytosol) metabolism of glucose, and thereby avoid apoptosis.  This is known as the Warburg effect, named after Noble laureate Otto Warburg who observed this process in the 1920, and published his findings in 1924.  He tried to have medical establishment to acknowledge this finding up until his death in 1970. The logical conclusion would be that cancer could be starved with water fasting and ketogenic diet.  Currently there is research on this approach in conjunction with chemotherapy, and in particular the blocking of glutamate  which can as alpha-ketoacid , an intermediate of the Krebs cycle.

[8] There isn’t a pathway for catabolism of fats in the cytosol; there is one for glucose. 

[9] Wiki, Glycogen, August 2020.

[10] Ketone bodies (KBs) are an important source of energy for the brain. During the neonatal period, they are also precursors for the synthesis of lipids (especially cholesterol) and amino acids. The rate of cerebral KB metabolism depends primarily on the concentration in blood; high concentrations occur during fasting and on a high-fat diet.  Morris, A.A.M. April 2005, Cerebral ketone body metabolism

[11] Croteau, E, CA Castellano, et al, August 2016, A cross-sectional comparison of brain glucose and ketone metabolism in cognitively healthy older adults, mild cognitive impairment and early Alzheimer's disease

[12] Mancini, Annamaria, Ester Imperlini, et al, Sept 2015, Biological and Nutritional Properties of Palm Oil and Palmitic Acid: Effects on Health FULL

[13] This brings me to a favorite topic, we have been made to believe that global warming is the blubonic plague that will devastate mankind, while it is global banking and their neoliberalism.  Moreover, we are in an interglacial period, and the global warming might prevent the impending next ice age.  Global warm is the distraction while our pockets are picked by the financial sector. 

[14] Oleic acid makes up 55 to 89% of olive oil. 

[15] Morrison, Robert, Robert Boyd, Organic chemistry, third edition, (1969), P 1058-9.

[16] Butter is 81% fats; the remainder is milk solids and water.  Butter is 45% is saturated fats,  This combination of fats and water give it the hardness properties that contribute to its popularity.  

[17] Wiki, Trans_fat, May, 2020

[18] Wiki, Trans_fat, May 2020

[19] At Wiki coconut oil (June 2019, there is a table for percentages of 19 oils. 

[20] Wiki Trans-fat, May 2020.  

[21] Kritchevsky, D, Oct 1997, Trans fatty acid and cardiovascular risk

[22] Wiki trans fats, Jan 2016

[23] Wiki trans fats, Jan 2016

[24] At Backery Aug 2016, http://www.bakeryandsnacks.com/Processing-Packaging/Considerable-lowering-of-trans-fat-levels-in-Spanish-bakery-products  Again the same skepticism that applies to US regulations applies to EU regulations.  A read of Prof. Ben Goldacre Bad Pharma causes me to expect tobacco ethics is the norm. 

[26] There are just two studies using a Google Scholar search of the literature.  One population wing of the Nurses’ Health Study found a clear association after controlling for confounding variables of trans-fats with CHD (coronary heart disease).  But as stated elsewhere that population has a higher rate of fast food consumption and unhealthy lifestyle.  The other was trial using rats of 4 cohorts (6 in each):  trans-fat + HFCS, lard + HFCS, trans-fat, and control (without forced sedentary lifestyle).  The combo of HFCS and trans-fat had had the greatest weight gain, and liver weight gain, but there was no indication as the CHD (odd given that CHD is the reason for banning trans fats).  Liver damage is not a proven surrogate for CHD.  Tetri, Laura, Metin Basaranaglu, et al, Nov 2008, Severe NAFLD with hepatic necroinflammatory changes in mice fed trans fats and a high-fructose corn syrup equivalent The lack of an animal study is telling.  Rabbits being a vegetarian are not suitable for fat experiments.      

11.  Saturated fats are good for you: notes taken from Dr. Miller’s lecturer.  Donald Miller, professor of Surgery at the Cardiothoracic Division of the University of Washington, July 17, 2011, at http://www.youtube.com/watch?v=vRe9z32NZHY.  These statements by Dr. Miller are supported in the journal literature which he references.  Dr. Miller also listed on a slide the importance benefits from saturated fats:  The slides in Dr. Donald Miller’s Lecture:

Cell membranes:  Require 50% or more 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 unhealthy polyunsaturated fats which due to high content of omega-6 fat acids reduce the positive immune system effect of omega-3 fatty acids. [incorrect though widely supported by journal articles.  It is the furan fatty acids that quench the ROS from MTD that in a chain reaction oxidize the UFAs in cell membranes and else where]


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.[1]  


Getting ahead of the upcoming sections, an article by Mark Mattson (he is also on YouTube), sums up the finding all of which I totally support by journal articles:

Key Points

  • Brain evolution, including higher cortical functions of humans (imagination, creativity and language), was driven by the necessity of sustaining high levels of performance in a food-deprived (fasted) state

  • Intermittent metabolic switching (IMS) [Randel switch] occurs when eating and exercise patterns result in periodic depletion of liver glycogen stores and the associated production of ketones from fatty acids. IMS occurs rarely or not at all in individuals who eat three or more meals per day [with carbs] and who are fairly sedentary

  • The ketone β-hydroxybutyrate (BHB) is transported into the brain and into neuronal mitochondria, where it is used to generate acetyl CoA and ATP. BHB also acts as a signalling molecule in neurons that can induce the expression of brain-derived neurotrophic factor and thereby promote synaptic plasticity and cellular stress resistance

  • During fasting and extended exercise, adaptive cellular stress-response signalling pathways are activated and autophagy is stimulated, whereas overall protein synthesis is reduced. Upon refeeding, rest and sleep, protein synthesis is upregulated and mitochondrial biogenesis occurs, enabling neurogenesis and synaptogenesis

  • IMS can enhance cognition and motor performance and protects neurons against dysfunction and degeneration in animal models of stroke, epilepsy, traumatic brain and spinal cord injury, Alzheimer disease and Parkinson disease

  • Intermittent fasting can improve indicators of metabolic and cardiovascular health in humans by mechanisms involving reductions in oxidative damage and inflammation. However, it remains to be determined whether and how intermittent fasting impacts the brains of healthy humans and those affected with a neurological disorder. [2]

Mattson’s key points above is consistent with the program worked out by Jason Fung in treating obesity and t2d, and supported by the research in Fung’s books.  I came to the same conclusions in the research of the relevant literature starting in 2014. 


12.  Evidence that coconut and MCT oils stimulate neurotrophins:  Of course, what is best for us isn’t what is best for pharma and food manufacturers that frame the topic.  So, a KOL wrote the Wikipedia article, and unfortunately, 90% who read the article have faith in expert opinion. 

Due to its high levels of saturated fat, the World Health Organization, the United States Department of Health and Human Services, United States Food and Drug Administration, American Heart Association, American Dietetic Association, British National Health Service, British Nutrition Foundation, and Dietitians of Canada advise that coconut oil consumption should be limited or avoided.  It has various applications. Because of its high saturated fat content, it is slow to oxidize and, thus, resistant to rancidification, lasting up to six months at 24 °C (75 °F) without spoiling.  Many health organizations advise against the consumption of coconut oil due to its high levels of saturated fat, including the United States Food and Drug Administration,[ World Health Organization, he United States Department of Health and Human Services, American Dietetic Association,[ American Heart Association, British National Health Service, British Nutrition Foundation,[and Dietitians of Canada.

Marketing of coconut oil has created the inaccurate belief that it is a "healthy food". Instead, studies have found that coconut oil consumption has health effects similar to those of other unhealthy fats, including butter, beef fat and palm oil.  Coconut oil contains a high amount of lauric acid, a saturated fat that raises total blood cholesterol levels by increasing both the amount of high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol. [3]

This is expert opinion; what Wikipedia relies upon.  the case for the advantage of saturated fats not becoming rancid like PUFAs has been made above (3:4, 4 & 5). The case for of 3-hydroxybutrate which induces the active of BDNFs (brain derived neurotrophic factors) follows here.

          The article below on d-β-Hydroxybutyrate goes on to show the healthful functions not just in the brain but also in previous research on the heart, and its mechanism is through protecting the mitochondria—yes, prevents MTDD.

The heroin analogue 1-methyl-4-phenylpyridinium, MPP+, both in vitro and in vivo, produces death of dopaminergic substantia nigral cells by inhibiting the mitochondrial NADH dehydrogenase multienzyme complex, producing a syndrome indistinguishable from Parkinson's disease.  [A bad batch of fentanyl caused this in about 30 street drug users in San Francisco area about 2003].   Similarly, a fragment of amyloid protein, Aβ1–42, is lethal to hippocampal cells, producing recent memory deficits characteristic of Alzheimer's disease. Here we show that addition of 4 mM d-β-hydroxybutyrate protected cultured mesencephalic neurons from MPP+ toxicity and hippocampal neurons from Aβ1–42 toxicity. Our previous work in heart showed that ketone bodies, normal metabolites, can correct defects in mitochondrial energy generation. The ability of ketone bodies to protect neurons in culture suggests that defects in mitochondrial energy generation contribute to the pathophysiology of both brain diseases. These findings further suggest that ketone bodies may play a therapeutic role in these most common forms of human neurodegeneration. . . . Brain in normal adults entirely depends on the metabolism of glucose for its energy needs, being unable to use exogenous fatty or amino acids. The single exception is the ability of brain to derive a major portion of its energy needs from the metabolism of ketone bodies, referred to as ketones. . . . Elevation of blood ketones, the brain's only alternative to glucose as an energy source, has been used for 50 years as a treatment for refractory epilepsy.[4]

This is not an isolated finding there is one of many journal articles on beta hydroxybutyrate and its benefit in stimulating neurotrophins.  Even the Wikipedia beta-hydroxybutyrate article acknowledges this function: 

β-hydroxybutyric acid has been found to increase brain-derived neurotrophic factor (BDNF) levels and TrkB signaling in the hippocampus.[10] Moreover, a rodent study found that prolonged exercise increases plasma β-hydroxybutyrate concentrations, which induces promoters of the BDNF gene in the hippocampus.[10] These findings may have clinical relevance in the treatment of depression, anxiety, and cognitive impairment[5]

The article fails to mention how short-chain fatty acids, the main source coconut oil, or the MTC oil,  are made from oils.  Instead is a chart, leucine metabolism in humans, with over 20 steps leading to many products of which one among them is beta-hydroxybutyrate.  Leucine metabolism certainly is not the main contributor.  This is more stonewalling by key opinion leaders.  So, is Beta-hydroxybutyrate derived from coconut oil through short-chain fatty acids and what of MCT oil? 

          The MCT oil makes no mention of beta hydroxybutyrate which is a BNDF.  The same is t rue of coconut oil which contains the list of warnings by government organization (see above).  Again, I find an example of regulatory capture on a global scale.  The MCT article has a warning :  They have potentially beneficial attributes in protein metabolism, but may be contraindicated in some situations due to a reported tendency to induce ketogenesis and metabolic acidosis.[6]    The article on BDNF (brain derived neurotropic factors There is no light at the end of the global pandemic caused by MTDD, and the assault upon health by pharma. To turn to Wikipedia which has much more health requires a background that few have, and certainly doctors don’t.  It is like sprinkling crushed red peppers into the filling of an eclair, it burns the brain.      

I could again scream about the divergence between science and marketing.  Wiki again is full of crap in beta-hydroxybutyrate, but one more time is not need it—is it?  It is produced not just in the liver as KOLs and Wikipedia claim but can be made in the cytosol in just about every cell in the body. But it is not Wiki, which has taken a pragmatic road, but that of industries using scientists for hire to set the standard not just in Wikipedia, but in textbooks, CME class and medical schools, and through regulatory capture in government publications.  Ketone bodies are good medicine[7] contra to pharma’s choir.  


13.  Other ways to stimulate neurotrophins:  Four acknowledge ways are through exercise, extreme calorie restriction, ketogenic diet, and neurosteroids though Wikipedia  list DHEA, testosterone and estradiol were missed.  Given the strong evidence for their inclusion, I can only draw the negative conclusion as the most likely reason.[8]  Levels of β-hydroxybutyric acid increase in the liver, heart, muscle, brain, and other tissues with exercise, calorie restriction, fasting, and ketogenic diets. . . .  Moreover, a rodent study found that prolonged exercise increases plasma β-hydroxybutyrate concentrations, which induces promoters of the BDNF gene in the hippocampus. [9] The mechanism for exercise increases neurotransmitter release through BDNF has been described.[10]  The below article names fasting and calorie restriction and ketogenic diet for increasing BDNF. 

The ketone body β-hydroxybutyrate (βOHB) is a convenient carrier of energy from adipocytes to peripheral tissues during fasting or exercise. However, βOHB is more than just a metabolite, having important cellular signaling roles as well. βOHB is an endogenous inhibitor of histone deacetylases (HDACs) and a ligand for at least two cell surface receptors. In addition, the downstream products of βOHB metabolism including acetyl-CoA, succinyl-CoA, and NAD+ (nicotinamide adenine dinucleotide) themselves have signaling activities. These regulatory functions of βOHB serve to link the outside environment to cellular function and gene expression, and have important implications for the pathogenesis and treatment of metabolic diseases including type 2 diabetes.  A major contributor to the processes of learning and memory formation involves brain derived neurotrophic factor (BDNF) signaling pathways. It has been known for over two decades [2016 article] that physical activity or neuronal activity markedly enhances Bdnf gene expression in the brain) and that this increase in BDNF protein leads to activation of signaling pathways that result in exercise-dependent enhanced learning and memory formation . . .   Though these results are widely recognized.  β-hydroxybutyrate is specifically upon HDAC2 and HDAC3, which act upon selective Bdnf promoters.[11]

Given the other evidence from a variety of sources, this satisfies me that short and medium chain SFA are more than an alternate source of energy, they are the preferred energy source, especially for one who has been on the western diet for decades.  SFA are preferred to carbohydrates.  No mechanism is known for any of the carbohydrates for which there is a mammalian biopathway that improves bodily functions.  Medium chain SFAs supply BDNFs via conversion to beta hydroxybutyrate and some sources have furan fatty acids; these are two which that have special bodily functions, and there are probably others.  One further thought is that many of the unprocessed source of carbs have toxic compound that aren’t in sufficient amounts to bring in a short time have adverse health consequence, except for insect that eat just that plant.  The work of Prof. Bruce Ames list many of them.  

 The principle sex steroids have receptors in every cell, they are produced in the brain by glia cells (and probably others) and their low levels is associated with mental illness.[12]  I have been taking sublingually DHEA since 2002, and testosterone topically from a compounding pharmacy since 2004.  I and other can testify to their positive effects upon cognitive functions and mood.  I have been told multiple times that estradiol with progesterone from a compounding pharmacy has similar effects.[13]  I am getting ahead of the topic which is developed in 6:2. 

14.  What is good?












Butter (20% water)








Palm Kernel
























Sunflower standard




 Sunflower (> 70% oleic)




Sunflower (< 60% oleic)
























Varies according to sample, method of extraction, and strain of crop

Again, I recommend the lecture by Dr. Miller as a guide which is strong on the history and with references.  What I wrote of it on my extensive video page:  For a 1-hour summation of the evidence on good and bad fats, I recommend Dr. Millers lecture:  Enjoy Eating SFAs:  They’re Good for You 53 min, 262,000 views 2016. Prof. Donald Miller, surgery, cardiothoracic division, University of Washington.  Clear well organized college lecture with graphics and lots of information, given to an audience of physicians, https://www.youtube.com/watch?v=vRe9z32NZHY.

The best oil is coconut oil because of the short chain fatty acids, about 30% which are broken down into beta hydroxyl butyrate which stimulates the product of BDNFs (brain derived neurotropic factors).  There is strong evidence that it slows the progress of AD and PD, see for the evidence d-β-Hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease[15] and it promotes neuronal health.     

Based upon flavor and value of this oil, I have developed a butter substitute which contains 20% water to which is dissolved powder sugar, powder salt, and 2 drops of yellow die dissolved in a tbs of water.  I heat 2 cups coconut oil and ˝ cup of canola oil to 150 degrees. I first blend the salt, sugar, water, and 2 drops of yellow dye.  For mayonnaise, I use 2-eggs, salt, and sugar, no water and 5 tbs. of vinegar with 2 cups of coconut oil (oil heated to 150 degrees).  I start with blending the eggs, salt and sugar, then gradually add the heated oil.  I scape the sides if needed with a spatula to improve mixing.  The butter substitute is good, and the blender mayonnaise superior.    


15.  A review of palmitic acid and fructose:

Since the 1990s, these researchers have established certain findings unambiguously.  First, feed animals enough pure fructose or enough sugar (glucose and fructose) and their liver converts some of the fructose into fat—the saturated fat palmitic acid, to be precise, which is the one that supposedly gives us heart disease when we eat it, by raising LDL cholesterol [see cholesterol myth].  The biochemical pathways involved are clear and not particularly controversial.  Feed animals enough fructose for long enough and this fat accumulates in the liver, cause the kind of fatty liver seen in obese children and adults.  The fat accumulation accompanies insulin resistance, first in the liver and then other cells as well, resulting in metabolic syndrome, at least in laboratory animals.  . . . The effects may take several months to appear if the animals are fed something closer to what humans in America actually consumer—around 20 percent of calories in their diet.  Stop feeding them the sugar and the fatty liver goes away and with it insulin resistance.  In a 2011 study in which twenty-nine rhesus monkeys were given the opportunity to drink a fructose-sweetened beverage along with their unusual monkey chow, every last one of them developed insulin resistance and many features of the metabolic syndrome within a year, and four had progressed to type 2 diabetes.[16]

De novo lipogenesis produces palmitic acid.  The association with CVD is through the fructose which is converted to palmitic acid; thus, it is the fructose that is causing CVD.  This is one way that palmitic acid and in general saturated fats get blame form CVD and ischemic events.  The fire caused by the high starch plus fructose in the liver is ignored while the blamed is placed upon their conversion product palmitic acid. 


16.  Communicating with the public: a number of researchers being denied access to corporate media have gone public through YouTube.  Three on the benefits of SFAs:

§***** Diseases of Civilization:  are seed oil excesses the unifying mechanism:, 45 min, 143,000 views, Dr. Chris Knobbe, historical information of what has happened with the increase in seed oils—college level.  Then progresses to rat studies, and concludes that the rancid fats are 80% of the cause of Conditions of Civilization, sugar 15%, and refined grains 5%   Considers PUFA as the cause for MTDD, explains how; and with less metabolism an increased storage of fat though insulin resistance. He misses fructose thus its role in DNL,  insulin resistance, and hyperuricemia.   https://www.youtube.com/watch?v=7kGnfXXIKZM Excellent

***** Omega-6 Apocalypse:  from heart disease to cancer and macular degeneration—AHS19 39 min, 87,000 views, Chris Knobbe Oct 2019,  covers history above lecture; college level on how bad PUFAs are, especially linoleic acid ,a good second dose on damage to MTD big on the damage to inner membrane of MTD and leaking protons, the toxic chemicals made,  https://www.youtube.com/watch?v=pHnPinYI2Yc Excellent

The Alzheimer's Antidote: Can we prevent Type 3 Diabetes? | Amy Berger, 25 min, 180,000 views, What I’ve learned, interview with Amy Berger, starts with Gary Taubes & says what I do: the need for beta amyloid removal, the role of insulin resistance and IDE, insulin degrading enzyme which with hyperinsulinemia does not do its other function of degrading beta amyloid and tau protein. The  lowering of pyruvate dehydrogenase reduces the rate of metabolism of glucose thus lower metabolism.  Misses mitochondrial dysfunction, she uses ketogenic diet for treatment, says that the brain needs some glucose (error because it is the blood, in  the brain); was her PhD thesis & the book, https://www.youtube.com/watch?v=f-A2rIA2OTE&t=10s very good 


17. The one two punch, fructose and UFAs, the road to MTDD and CAWD

Nature converts excess fructose and glucose into palmitic acid, a stable fat, yet the KOLs tell us that it is associated with CVD and NAFLD, also cancer and dementia.  Their claim is because palmitic acid is downstream from fructose (#6 for this topic).  

Consider this dispositive experiment:  In a 2011 study in which twenty-nine rhesus monkeys were given the opportunity to drink a fructose-sweetened beverage along with their unusual monkey chow, every last one of them developed “insulin resistance and many features of the metabolic syndrome” within a year, and four had progressed to type 2 diabetes” [17]  Thus we have fructose not palmitic acid as the cause for weight gain (obesity);  the rhesus put on 12% of weight over the year, developed insulin resistance, and four of the 29 progressed to t2d.  They were on a regular primate chow mix with the modification that 25% of calories came from fructose.  I hold based on this Section 2, that fructose is the most significant of the 2-punches, while oxidized and fructated UFAs is the second blow that leads to MTDD.  In Section 3 are what I consider the major downstream consequences of MTDD that are leading to CAWD.  Without MTDD there wouldn’t be CAWD and all of the dysfunctional topics is Section 3.  We are not humming birds or Bonobos (57% of calories from fruit),[18] or a squirrel, two are sugar and fruit eaters, and the later in some areas consume mostly nuts with their high fat UFA content.

I feel that the sum total of evidence as to degree of pathological consequences and its role in causing MTDD places UFA through its oxidation and fructation second behind fructose as a cause for MTDD and together they cause the conditions of affluence currently called conditions associated with the western diet--above that of IR as causal for CAWD and MeS because oxidation of UFA directly contributes to MTDD, and MTDD to IR. The role of IR as promoting MTDD is not major, now would IR occur without fructose.  MTDD can occur without UFA, and UFA might not be sufficient in itself to cause MTDD; thus, fructose is the major cause of MTDD and CAWD.   

[1] Posted at http://healthfully.org/rh/id4.html 8/23/2015  

[2] Mattson, Mark, Keelin Moehl, et al, Jan 2018, Intermittent metabolic switching, neuroplasticity, and brain health  FULL

[3]  Wiki coconut oil (October 20190

[4] Kashiwaya, Yoshihiro, Takao Takeshima, et al, May 2009, d-β-Hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease

[5] Wiki, beta- hydroxybutyrate Oct 2910

[6] Wiki, Medium_chain_triglycerides May 2020.  “However, there is other evidence demonstrating no risk of ketoacidosis or ketonemia with MCTS at levels associated with normal consumption.”  This implies a risk taking the concentrated commercial MDT oil.  Another hatchet job by an industry that profits from illness.  

[7] Cahill, George Jr., Richard Veech, 2013, Ketoacids? Good medicine?  George Cahill was a giant in the field of metabolic research, a Harvard (died in 2012 at the age of 85).  He unconvered the five Randle (metabolic) switching during starvation.  

[8]    There is emerging evidence that testosterone-derived “androgenic neurosteroids”, 3α-androstanediol and 17β-estradiol, mediate the testosterone effects on neural excitability and seizure susceptibility. Testosterone undergoes metabolism to neurosteroids via two distinct pathways. Aromatization of the A-ring converts testosterone into 17β-estradiol. Reduction of testosterone by 5α-reductase generates 5α-dihydrotestosterone, which is then converted to 3α-androstanediol, a powerful GABAA receptor-modulating neurosteroid with anticonvulsant properties.  Reddy Deodipala, March-April 2008, Mass spectrometric assay and physiological–pharmacological activity of androgenic neurosteroids

[9] Wiki Supra. 

[10] Sleiman, Eama, Jeffrey Henry, et al Jun 2016, Exercise promotes the expression of brain derived neurotrophic factor (BDNF) through the action of the ketone body β-hydroxybutyrate.  Electrophysiological measurements indicate that hydroxybutyrate

causes an increase in neurotransmitter release, which is dependent upon the TrkB receptor. These results reveal an endogenous mechanism to explain how physical exercise leads to the induction of BDNF. . . . The ketone body D-b-hydroxybutyrate (DBHB) is a major energy metabolite that is increased in the liver after prolonged exercise. DBHB levels are frequently increased after caloric restriction, fasting and ketogenic diets and DBHB is believed to serve as a signaling molecule in response to metabolic changes (Newman and Verdin, 2014).

[11] Newman, John, Eric  Verdin, Noc 2014, β-hydroxybutyrate: Much more than a metabolite

[12] Shirayama, Yukihiko, Kenji Hasimoto, et al Nov 2002, Correlation of plasma neurosteroid levels to the severity of negative symptoms in male patients with schizophrenia

[13] Guidelines and computer program call for the addition of E3, estriol.  Its inclusion is to block the positive effects of estradiol.  I have come across numerous cases of E3 inclusion and comments such as tender breast, lack of cognitive improvement, and nausea.  

[14] Table from Wiki, coconut oil, August 2020

[15] Kashiwaya, Yoshihiro, Takao Takeshima, et al, May 2009, d-β-Hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease

[16] Gary Taubes The case against sugar, P 204-05. 

[17] Bremer, Andrew, Peter Havel, et al August 2020, Fructose‐Fed Rhesus Monkeys: A Nonhuman Primate Model of Insulin Resistance, Metabolic Syndrome, and Type 2 Diabetes FULL, and Gary Taube, The case against sugar, P 205

[18] Wiki, Bonobo, August 2020

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On how daily excessive fructose damages the mitochondria and thus is the main cause for the conditions associated with the Western diet--much, much, more than insulin resistance, type-2 diabetes, and weight gain