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4:4 Polyunsaturated fatty acids in cell membranes

Sample Chapters  --  Book in Progress, pending final editing



SECTION 4:4    PUFAs in cell membranes 8/3/19

 1. Diet and their message   2. Nature’s choice   3. Extraction vegetable oil, and rancidification     4. Why rancid in cells?  5. Health consequences   6. Palmitic acid, omega 3 & 6, and their health consequences   7.  Oxidized cholesterol, how much?   7. Trans-fats, are they bad?  8. What are the regulations on TFA?  9. What is good?



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1.Diet and their message:      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 on unmanaged capitalism; its tobacco ethics.  It has a personal ring:   everyone I know has been and nearly all are still over the healthful 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).  Then add to this the rancid in cell membranes PUFAS. 

I was about 20% of calories from sugar all sources as a child, and continued at the 20% 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 2015, which the high glucose potentiates the harm done by fructose.  Iin 1992 I jumped into the fire of more sugars by eating more carbs.  Only one senior friend I know is thin and of good health.  All others I know (over 100) weren’t as fortunate as Bob and me.  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).  I put on 20 lbs. 1969, and forth starting in 2004, I have been taking sufficient testosterone lotion to returned me to a youthful level.  I think of harm done to friends and relatives, thus the label of bad before pharma and food manufacturers.  And don’t expect corporate media to educates us contrary to what their major advertisers expect.  I tell you this to wet your pallet for details on the supplements see 6:3. 

They and governments throughout the world have swallowed new western diet low in natural SFAs and high in PUFAs.  PUFAs being electron rich have a much higher rate of oxidation, glycation, and fructation than  MUFAs of which there are only a few common ones, and for which evolution limits their use in membranes.[1]  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 and MUFAs.  That is why dairy products are high in SFAs including mother’s milk, but food manufacturers prefer the much cheaper PUFAS.  Thus in the sales play book they claim their fats are health and the expensive saturated ones are bad for health. This chapter is about the science as to the good and bad fats.


2.  Nature’s choice:  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 with water buffalo having 8% fat while cows 4% and humans 4.2%.  The percentage difference is strong evidence that there is a health advantage for SFAs compared to PUFAs

Human milk is low in protein and as a percentage high in casein and correspondingly low in whey protein.  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?  Protein content per cup is 2.8 g. for humans, 7.9 for cows, 8.7 for goats.  The major drop in protein content of human milk is because of the much slower rate of bodily growth compared to other mammals.  However, sugars (mainly the disaccharide lactose) for human is 17 g/cup, cows 11g, and goats 11 g—sugar makes up all the carbs in milk.  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, the need for cholesterol is 1/3rd higher than the cow or goat’s milk.  The neonate fastest growing organ is the brain.  SFAs make functionally better cell membranes.      

Business certainly doesn’t care, I just examined the leading infant milk substitute, Similac, and found its main ingredient is sugar and it uses plant oils high in PUFAs.  (It was developed at Tufts University and 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, for increasing the probability of development of childhood insulin resistance.    

So what is the evidence that PUFAs are a major part of the causal path to CAWD? 


3.   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.

          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 PUFAs. The main vegetable oils 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 grains and 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.[2]    “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.  Seed oils except for corn are high in oil content:  sunflower seed (28%), soybean dry (56%), and canola dry (43%), corn (2.8%).” [3]  These oils are high in polyunsaturated oils:  sunflower 69%, soybean 58%, canola 28%, corn 55%.  Because of in vivo rancidification of PUFAs as well as in cooking, they pose a serious health risk—see rancidification section below for the consequences.   Claims of dietary safety are suspect since nearly all studies are industry funded, and the few government reports are equally of low quality.  The lack of cases for violation of regulation is strong evidence that they aren’t unenforced.

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 influence research based on heated PUFA in conditions that paralleled the use of a restaurant deep fryer.[4]   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] [5]  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 [sic] human health” (supra). This is supported by the animal studies using the oil are non-volatile extracts, that were referenced in the article.

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” [6]  “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.[7]    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 [8]   For over 50 years the warning flag has been waved in journals, but not in our media.  I knew of this when I was in graduate school. 

[1] This occurs through preferential metabolism of the common ones, thereby making them less likely to be utilized for cell membranes.  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, but in the cell wall as just stated the functionality were less.  Thus we have evolution working to make 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. Oleic is a an 18:1 cis 9 fat; elaidic is an 18:1 trans-fat.  This or course doesn’t by extension apply to the dozens of common trans fatty acids compared to their cis brethren. Amazing how evolution in a incredible complex system of mammals deals with so, so many health issues!  This is not to imply that plants aren’t complex with many parallels see ???? Plant abstract on trans

[2] Wiki, corn oil, Aug 2016

[3] 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.

[4] 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 1971 a deep fryer and used 4 pounds of lard.

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

[6] Wiki rancidification July 2016

[7] Dormandy, TL, Sept 1969, (The Lancet) Biological Rancidification (not sure if this is the right article???)

[8] Wiki lipid_peroxidation June 2016

4.  Why rancid in cells? 


Lipid peroxidation, a free radical chain reaction


I am going to dwell on the chemistry of what has gone wrong.  It is to understand why the stable SFA are so much better than the PUFA, and a bit better as a source of energy than glucose.  PUFAs in excess are pathogenic; SFA aren’t.  Because of their structure with electron dense double bonds on the carbon chain, electrophilic chemical can from covalent bonds with those electrons.  There are several major types of electrophilic molecules which bond intercellular to PUFAs, or remove the hydrogen adjacent to the double bond.  The reaction shown above requires a hydroxyl radical[1] to strip the hydrogen for the adjacent to the double-bond carbon, the hydrogen to form a lipid radical in an aerobic environment.  The major ones being ROS,[2] reactive chemicals as byproducts of non-enzymatic reactions, and bonding by various sugars, called glycation (see 2:4, 4 to 7, the nuts and bolts of the process are there covered.)  The change in structure can result in further reactions, or be a final stage, but whichever the results are negative for the cell wall.  If the PUFA is in a membrane it compromises the performance of the membrane.  The greater the number of modified PURAs in the membrane the worse the effect.[3]  Because there are many PUFAs and their small amounts in the paleo diet, the body lacks enzymes for their metabolism.  They not being metabolized entails that they accumulate and are incorporated into cell membranes. 

          While the damage may when extensive the repair mechanisms are limited for practical reasons.  One is the large number of PUFAs and another is the many types of membranes.   Autophagy, the orderly dismantling of damage parts is a costly process, so nature supplies us with a large battery of antioxidants as a preventative.  One important antioxidant is vitamin E. Another important antioxidant is vitamin C. Other anti-oxidants made within the body include the enzymes superoxide dismutase, catalase, and peroxidase.” [4]  I would add to the list glutathione and CoQ10.   So why is pharma telling us and physicians that antioxidants aren’t important? 

 “Autoxidation, a destructive interaction between PUFAs and molecular oxygen, accounts for many industrial and natural-decay processes. The possibility that the body fats might undergo a similar kind of degradation is still largely ignored.”[5]   

The fatty acid radical is not a very stable molecule, so it reacts readily with molecular oxygen, thereby creating a peroxyl-fatty acid radical. This radical is also an unstable species that reacts with another free fatty acid, producing a different fatty acid radical and a lipid peroxide, or a cyclic peroxide if it had reacted with itself This cycle continues, as the new fatty acid radical reacts in the same way.[1]  The end products of lipid peroxidation are reactive aldehydes, such as malondialdehyde (MDA) and 4-hydroxynonenal (HNE), the second one being known also as "second messenger of free radicals" and major bioactive marker of lipid peroxidation, due to its numerous biological activities resembling activities of reactive oxygen species[6] 

This is not a new finding, just ignored:

Autoxidation, a destructive interaction between unsaturated fats and molecular oxygen, accounts for many industrial and natural-decay processes. The possibility that the body fats might undergo a similar kind of degradation is still largely ignored—perhaps because the irregular irreversible pattern of this type of process seems at odds with the enzyme-controlled reversible pathways of traditional biochemistry. Yet work with mitochondria and other biological preparations has shown that the processes commonly grouped together as " degeneration ", " fatigue ", and " ageing " (none of which have a basis in classical enzymology) develop in close parallel with evidence of rancidification.[7]




FIGURE 3. The lipid bilayer. Substances like protein and cholesterol are found in, and as part of, the plasma mem-brane.  Hydrophobic associations keep the nonpolar molecules close together when they are surrounded by aqueous media. Since cell membranes have aqueous media on both sides of their surfaces, the polar end groups are attracted outward and the hydrophobic end groups are directed inward, toward each other and away from the water. [8]

The process by which an ROS attaches to a PUFAs in membranes is explained using the anti-Markovnikov’s rule.  This is why PUFAs are pathogenic in cell walls.

Quite simplified, the plasma membrane is bio-molecular leaflet of phospholipids, with hydro-phobic, hydrophilic, and amphipathic substances interdigitated into and interacting with the leaflet by hydrophobic and ionic forces. As shown in figure 3 the plasma membrane lipid bilayer has a hydrophobic mid-zone area. This is the nonpolar medium in whichO2 is so soluble. It is also the location of the polyunsaturated fatty acids with their allylic carbon-hydrogen bonds which are so susceptible to free-radical attack (fig. 2). Thus, the normal membrane has the highest concentration of O2 (with its diradical potential) in the hydrophobic mid-zone area, where it has the potential for doing the most damage to the membrane's polyunsaturated fatty acids, i.e., the membrane is poised for disruption. . . . In the absence of sufficient cholesterol and in the presence of iron and copper complexes, catalysis of free radical reactions would proceed unchecked, disrupting membrane integrity. And anything that disrupts the normal integrity of the plasma membrane (such as lipid peroxidation) must, as a consequence, also disrupt that membrane's functions, e.g., permeability, transport, barrier capacity, bioenergetics. The ultimate result would be cellular damage, necrosis, cerebral edema, and all the complications thereof.[9]

The article goes on to describe how compromised membranes cause ischemic events.    

Another source of PUFAs is cooking:

The oxidative deterioration of polyunsaturated fatty acids (PUFAs) in culinary oils and fats during episodes of heating associated with normal usage (80-300 degrees C, 20-40 min).  . . . the thermal oxidation of PUFAs is a free radical chain reaction, in which hydroperoxides are generally recognized as the primary major products. Hydroperoxides of PUFAs are easily decomposed into a very complex mixture of secondary products with the decrease in unsaturation. . . . The results show there is a decrease in unsaturation starting at 150 degrees C and becoming more pronounced at temperatures around 250 degrees C [deep frying temperature is 176 degrees C].[10] 


As Prof. Lustig warns about fructose applies not just to proteins (the Maillard reaction), and the browning process not just happening to food but also to your PUFAs.  “You can brown your meat at 375 degrees for one hour, or you can brown your meat at 98.6 degrees for 75 years.”[11]  Any electron rich molecule will do for an unbound electrophilic chemical. 

          This brings us full circle, back to the ways in which fructose damages the MTD.  It is not just mtDNA and proteins that are a target, so too is PUFAs, and since fructose has caused MTDD, and the increased rate of release of ROS therefrom, we have an increased bonding of the ROS above the normal LSPs’ rate.  And this is occurring in nearly every cell because of PP producing endogenous fructose from glucose.  Moreover, the repair systems can’t keep with the unnatural rate of reactions.  To this we add liver and kidney damage, and the consequences of their underperformance.  Compromised membrane are a major CC for CAWD.


5.   Health consequences:  The list of association found in a google scholar search parallel the list of AGE and thus the CAWD. Above in the Butterfields’ article on oxidized PUFAs in membranes there was the causal mechanism for ischemic events.  “Damage to the cellular membranes dysfunction that plays a major role in ageing and most age-related and oxidative stress-related diseases. . . such as neurodegenerative diseases, diabetes and atherosclerosis (the main cause of cardiovascular complications).[12]  In this seminal article Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), atherosclerosis (and thus CVD and other related conditions), pre-eclampsia (pregnancy disorder affecting about 4%), diabetes, renal diseases, chronic lymphedema (also known as lymphatic obstruction, causing swelling by compromised lymphatic system), hepatic diseases including liver IR, NAFLD, NASH (#16), exacerbating hepatitis C and cirrhosis of the liver, and a causal factor for cancers.  The various authors of each section of this in-depth article describe the process by which the lipid peroxidation causes pathology. “The Via a free radical process, the double bonds of an unsaturated fatty acid can undergo cleavage, releasing the volatile aldehydes and ketones.  Oxidation primarily occurs with PUFAs. For example, even though meat is held under refrigeration or in a frozen state, the poly-unsaturated fat will continue to oxidize and slowly become rancid…. Rancidification can produce potentially toxic compounds associated with long-term harmful health effects concerning advanced aging, neurological disorders, heart disease, and cancer.” [13]  Mother nature acts to protect vertebrates by producing a response to the odor and taste.

          Others have known of the health consequence going back decades.  Autoxidation, a destructive interaction between PUFAs and molecular oxygen, accounts for many industrial and natural-decay processes.   “The possibility that the body fats might undergo a similar kind of degradation is still largely ignoredperhaps because the irregular irreversible pattern of this type of process seems at odds with the enzyme-controlled reversible pathways of traditional biochemistry. Yet work with mitochondria and other biological preparations has shown that the processes commonly grouped together as " degeneration ", " fatigue ", and " ageing " (none of which have a basis in classical enzymology) develop in close parallel with evidence of rancidification.” [14]  And the association with disease has many journal articles.  Lipid peroxidation (LPO) product accumulation in human tissues is a major cause of tissular and cellular dysfunction that plays a major role in ageing and most age-related and oxidative stress-related diseases.” [15] This seminal articles goes on at length to develop the connections.  Another seminal article recommends (contrary to pharma) the antioxidant vitamins.  The healthy organism is able to prevent the over-production of free radicals. Low oxygen tension of the tissues is a basic condition. Its value is 26 mmHg or less. The primary line of antioxidants consists of representatives of the enzymatic defense. It is supplemented by antioxidant vitamins with scavenger property (vitamins C, A, E, K), the cofactors, compounds containing thiol, phosphor, amine, polyamine, phenols, quinolines, ubiquinone (coenzyme Q), flavonoids, polyenes, glucose, urate, bilirubin, etc.” [16] 

NEED to put in good order—separate SFs from Omega fats, state the theory of each, then what is wrong—currently all mixed up

6.  Palmitic acid, glycogen, and Omega 3 & 6 fatty acids:  there are numerous claims as to health and illness made concerning fats, palmitic acid and omega 3 & 6 have significant journal space. Over and over again I read that carbohydrates are the preferred source of energy, that palmitic fatty acid promotes CVD and IR, and that brain must have carbohydrates, and thus carbs are essential for life; all five are false.   SFA are preferred because they are stable (not subject to glycation in the cell membranes), emery dense, and aren’t stored with water--glycogen is.  Stored as a triglyceride, they provide 5-6 times more ATP per gram than does glycogen of the same weight which include 3-4 water molecule per glucose molecule.  The average non-obese person has about 22% fat by weight stored and under 800 grams of glycogen, that is because of their survival advantages.  As for palmitic promoting CVD and IR, it is again industry studies the details of which I have looked out but choose not to discuss; the claim is industry crapolla.  Nature doesn’t preferentially synthesize a bad fat, though industry implies it does.  And as for the brain needing carbohydrates, I couldn’t find any studies which controlled for the metabolism of carbs in the brain by the circulating erythrocytes.  Erythrocytes don’t have MTD, therefore they like cancer cells[17] must metabolize anaerobically (fermentation) glucose to produce ATP.[18]  Oh, and by the way, the liver during water fasting or ketogenic diet, through glycogenesis supplies sufficient glucose for the erythrocytes, but often not for the high energy cancer cells.  Business needs to be taken out of politics and science. 

The value of the omega 3 fatty acids, I have failed to find strong evidence for; just association, biological process producing salubrious intermediates, claims about a bad ratio of omega 6 to omega 3 PUFAs.  At first I was a believer, since it exposed a way in which PUFAs could be bad and explain our health disaster (I wasn’t not at that time onto the issues of CAWD, which came 6 years later).  But with further research and business’ pattern promoting cognitive dissonance, this caused me to reverse my acceptance, and to believe FOMAs are the monsters behind the curtain.   Among considerations would be that this is part of the general assault by FOMAs upon SFAs, which is echoed by the FDA:  more grains, less animal products and lower dietary fats as heart healthy.  Of recent (2019) there has been a push to replace meat proteins with plant proteins.  The evidence for modus operandi of the omega 3 & 6 proposed by KOLs is far from convincing. 

I suspected that this is another example of tobacco science; I came slowly to this conclusion.  Lonely in since 2009 had I come to realize that a movement for a healthful substance coming from the highest levels and promoted in the media:  if it’s good; it’s not good for profit maximization. The fish oil omega-3 acceptance fits that pattern.  This was confirmed in a 2007 seminal article:

Because fish is rich in n-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), it was deduced that n-3 fatty acids are responsible for these protective properties. This view became very popular, assuming a reduction of isoprostanes by an effective competition of EPA and DHA [omega 3 fatty acids] with arachidonic acid oxidation products. Nevertheless, these deductions ignore the fact that, like all PUFAs, n-3 fatty acids suffer oxidation to toxic peroxyl radicals and that isoprostanes and related products are only generated in extremely small amounts. As shown above, fish contain, besides n-3 fatty acids, considerable amounts of F-acids [furan fatty acids].  F-acids readily undergo oxidation by LOO_ radicals to form dioxoenes. The oxidation intermediates are long-living radicals (see Fig. 8) stabilized by resonance structures, and therefore have the ability to react with a second radical, thus interrupting a chain reaction (many other compounds regarded as radical scavengers do not have this property). In addition, F-acids are absorbed with other fats in the intestine and are incorporated in membrane phospholipids instead of PUFAs exactly at the sites where they are needed in emergency cases. As a consequence, we suspect that F-acids [furan fatty acid], and not n-3 PUFAs, are responsible for protective effects of a fish diet.[19]

One more example of praising the accompanying (omega 3) and not the good real cause of protection furan fatty acid.  of the media, dupes, and scientists for hire producing crapolla, misdirected wasted research, n-3 PUFAs aren’t healthful.

          The importance of this seminal article by Spiteller calls for more space (and it has some valuable insights concerning lipid peroxidation--see #4 the reactions under heading:  Plants and algae are exposed to LOO_ [lipid] radicals generating radiation.  In order to remove LOO_ radicals, plants and algae transform PUFAs to furan fatty acids, which are incorporated after consumption of vegetables into mammalian tissues where they act as excellent scavengers of LOO_ and LO_ radicals. . . .  In order to remove LOO_ radicals, plants and algae transform PUFAs to furan fatty acids, which are incorporated after consumption of vegetables into mammalian tissues where they act as excellent scavengers of LOO_ and LO_ radicals.[20]This process and the value of furan fatty acid has been repeated, all the major points, and with Spiteller as an author in 8 of the 34 articles in the Wiki article.[21]  That the article and the role of furan fatty acids have met the standard for publication on a subject which opposes the main-stream theory--supported by pharma---on the exaggerated benefits of omega 3 is evidence of the solid foundation of the role of furan, and the greatly diminished role of omega 3.  The closing statement in the article supra explains the positive claims and its diminished role as we age: “In order to remove LOO_ radicals, plants and algae transform PUFAs to furan fatty acids, which are incorporated after consumption of vegetables into mammalian tissues where they [F-fats] act as excellent scavengers of LOO_ and LO_ radicals. These attack proteins and enzymes and other molecules necessary for life and could be a cause of death. As a consequence, we cannot escape death, but we can increase our life span by reducing the consumption of PUFAs [and thus LOO and LO radical].” 

I would put it a bit stronger in that with MTDD the need for the F-fats is greater since the release for the release of ROS are much greater from the MTD and that RRA and other factors such as RAPT increase the needs compared to the LSPs. 

I had spent several days studying the USDA research article on omega 3 and omega 6 in 2015, which made the pathogenic claims of the high ratio of omega 6 to omega 3—given at around 15 to 1.  The normal range is 1:1 to 1:4 for paleo diets.  I started taking fish oil from Costco; it was inexpensive.  In 2017 I became suspicious of the claims for benefits but continued with the fish oil.  Given that I limit my PUFAs to the extent of making my salad dressings using canola oil and coconut oil, and not eating manufactured foods, I figured that I was at sufficient low damage to membranes that the repair systems of autophagy makes the benefit of the fish oil insignificant--assuming some benefit.  Considering that there are no studies on how efficiently omega 3s are protecting the PUFAs in the cell wall or the rate of the repairing the oxidized omega 3s, therefore it is better to dodge the PUFAs than to take the omega-3 fix. Now I feel compelled to gripe about the amount of time wasted on industry influence crapolla, and my time wasted in this area on.  Overall I spend more time on bad science, bad medicine, than on the sound science.  It is devilish when profits trumps science and those at the highest place are enablers. 

Again you are to read about bad pharma framing the topic.  Wiki again supplies the example for KOL science:

Incidence of insulin resistance is lowered with diets higher in MUFs (especially oleic acid), while the opposite is true for diets high in PUFAs (especially large amounts of arachidonic acid) as well as SFAs (such as arachidic acid). These ratios can be indexed in the phospholipids of human skeletal muscle and in other tissues as well. This relationship between dietary fats and insulin resistance is presumed secondary to the relationship between insulin resistance and inflammation, which is partially modulated by dietary fat ratios (Omega-3/6/9) with both omega 3 and 9 thought to be anti-inflammatory, and omega 6 pro-inflammatory (as well as by numerous other dietary components, particularly polyphenols and exercise, with both of these anti-inflammatory). Although both pro- and anti-inflammatory types of fat are biologically necessary, fat dietary ratios in most US diets are skewed towards Omega 6, with subsequent disinhibition of inflammation and potentiation of insulin resistance.[5] But this is contrary to the suggestion of more recent studies, in which polyunSFAs are shown as protective against insulin resistance.[22]

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. Prof. Donald Miller, surgery, cardiothoracic division, University of Washington.  Clear well organized college lecture with graphics and lots of information, given to audience of physicians, https://www.youtube.com/watch?v=vRe9z32NZHY.

The attack upon palmitic acid is more tobacco science.  It starts with the most common fat being then most common in NAFLD, in triglycerides, in atheromas, therefore by association it is casual, like the fireman.  A diet high in palmitic acid increases LDL (maybe), but what of lowering triglycerides which is actually associated with the cause for CVD (high fructose diet), while raised LDL is only through tobacco science causative of CVD.  The most common of fat made by nature isn’t the worst; nature wants us healthy.  To start with it assumes that the most common made fat in mother’s milk and the most common fat in our body is because mother nature prefers the worse of fats.  The mechanism by which it is the worst of fats is a sales pitch by KOLs and their dupes.  Since the SFAs are the best of the 4 types of fats, the claim of palmitic being different needs strong experimental evidence, not just some putative biological marker.  Third by evolution, our systems are set to function on a low fructose, low PUFAs diet.  The greater the deviation from the LSPs, the greater the need to turn up autophagy, as described in 6:1.  Finally, the inflammation process is part of the natural heal system, like fever, there are benefits, and to take a compound that lowers inflammation should delay healing.  This is a theory about the value of inflammation, again based on evolution (but a topic I haven’t researched).  I suspect that inflammation is blamed for the typical reasons of promoting drug sales and for their side effects.


7.  Oxidized cholesterol and lipoproteins as the cause for atheromas:  Over and over again when there is a claim that promotes drug sales, it is based on tobacco science.  Normally, I simply go about my studies, but this topic is part of the puzzle of what is causing CVD, atherosclerosis, and hypertension, your number 1 killer, yet unknown for LSPs.  The standard theory is the oxidize cholesterol and lipoproteins are the major cause.  Then why aren’t the LSPs having their cholesterol and lipoproteins oxidized??  Or could it be that the oxidized theory is wrong?? 

Prior, I had simply ignored the oxidized claim—I smelled the pharma skunk.  However, while researching drugs that damage the MTD in August 2019, I came across a “seminal” article that listed conditions that would have me believe that CAWD is caused by oxidized cholesterol, LDL, and PUFAs.  I shall call this claim oxidized for simplicity. Since the literature is dotted with oxidized cholesterol and LDL, a brief response should with the prima facie evidence and the also competing MTDD evidence has for me placed that claim in the slime category under corporate rocks.   

          One flag is the source of funding for the article was by the British Heart Foundation.  Foundations such as the AHA, various medical associations such as AMA, they do the biding of their major contributor.[23]  The summation seminal article Pathological aspects of lipid peroxidation (2010) has 24 contributor each writing a technical section in their area of research.  This was a major coordinated effort, much more than your typical seminal paper.   What was the role of pharma--if any--and how much did it cost British Heart Foundation? 

          Their list of claims by section headings each caused by oxidized:



Aging and oxidative stress

Historical studies on ageing and oxidative stress

Lipid peroxidation in ageing

Neurodegenerative diseases; lipid peroxidation and central nervous system

Lipid peroxidation and Alzheimer's disease

Amyotrophic lateral sclerosis  

Parkinson’s disease


Role of oxidized phospholipids in atherosclerosis

Role of aldehydes in atherosclerosis

Role of oxysterols in atherosclerosis

Long-term impact of LPO on PE infants and adolescents


Renal diseases

Lymphoedema [edema in the lymph system]

Hepatic diseases

Lipid peroxidation and cancer[24]

This list left me with the question:  Should I add to oxidized as major CC to not just CVD but CAWD???   Is the British Heart Foundation funding science? 

          First, like with glucose (as explained in 2:3 and 2:4), it is the less reactive compound, And unlike glucose, cholesterol’s dietary and synthesized supplies are far less than the PUFAs and the long list of compounds that bond with fructose and its metabolites (2:4).  Non-enzymatic bonding of cholesterol isn’t so easy, as pharma claims.  The structure shows that unlike PUFAs there aren’t electron rich double bonds (aromatic rings are stable).  A study on point used heat to oxidized cholesterol.  Cholesterol requires a heat of over 120 degrees centigrade,[25] while PUFAs become rancid at body temperature and on the shelf when exposed to air.  Secondly there is an extensive body of literature showing that oxidized PUFAs negatively affect the cell membranes that they are incorporated it, I don’t know of similar quality article for cholesterol, going beyond association and their putative effects, nor a clear indication as to the standard used for measuring oxidized. Are toxins counted in “oxidized” figures?   The oxidized claim is based on mere association. 

Even more telling is that we have the murder weapon, MTDD; thus at most oxidized cholesterol and LDL are CCs.  This still leaves me with the question, is its oxidation sufficiently pathogenic to be included with PUFAs, MSU, RATP, RRA, and RCR, for CAVD like cigarette carbon monoxide, and now also for the conditions in the above list?  Given the weak modus operandi of oxidized, it seems that there is more tobacco science. 

This seminal article is claiming much more than atherosclerosis: hepatic and renal, t2d, etc.  God, we really need to lower our cholesterol!  Pass me the Lipitor and Crestor.  Or should I?  This claim is missing the quantity of oxidized LDL and cholesterol in vivo. 

Oxysterols are oxygenated derivatives of cholesterol that are intermediates or even end products in cholesterol excretion pathways. Because of their ability to pass cell membranes and the blood-brain barrier at a faster rate than cholesterol itself, they are also important as transport forms of cholesterol. In addition, oxysterols have been ascribed a number of important roles in connection with cholesterol turnover, atherosclerosis, apoptosis, necrosis, inflammation, immunosuppression, and the development of gallstones. According to current concepts, oxysterols are physiological mediators in connection with a number of cholesterol-induced metabolic effects. However, most of the evidence for this is still indirect, and there is a discrepancy between the documented potent effects of oxysterols under in vitro conditions and the studies demonstrating that they are of physiological importance in vivo.[26]

This article indicates that the fireman has a function.  In vitro studies lack the oxysterol receptors, and fails to duplicate their cellular functions.  Oxysterols have a long history, and evolution has receptors for their functions.[27]  So far there has been identified 11 oxysterol receptors.  Could the oxidized cholesterol have a function by design, like the immune system’s use of hydrogen peroxide to destroy bacteria? 

Others articles show oxidation of LDL isn’t a demon, it has an immune function. 

Sixty years ago researchers discovered that the lipoproteins participate in our immune system by binding and inactivating bacteria, viruses, and their toxic products.  The lipoprotein immune system may be particularly important work immediately and with great efficiency.  There are many ways to demonstrate it. . . . In the laboratory it has been shown that human LDL is able to inactivate more than 90% of the most toxic bacterial products.[28]

Has binding toxic chemical has been by pharma and other included under the heading of oxidized LDL, at least in some, if not most articles?  This function of LDL ties in well with extensive finding of bacteria found in the atheroma.  It explains in part why endothelial cells actively transport through their receptors LDL into the artery walls: to mop up toxins from bacteria and to promote cell building follow apoptosis brought on by bacteria in the artery walls.    

          Nature works to keep us healthy, thus the natural cholesterol with its many uses was not selected to be an Achilles’ Heel.  The very complexity and many functions supports the proposition of survival importance.  Each cell is capable of synthesize cholesterol in a complex 57 step process.  Complexity supports its value, as too that about 75% of total cholesterol is made in the liver for transport as needed, and cholesterol is highly conserved.   A 150 lb. human synthesizes 1 gram a day mostly in the liver at night;[29] thus 0.25 grams come from dietary sources.  Total blood cholesterol is under 0.15 grams.  A 4-ounce portion of beef has about 0.70 mgs, and only 40 mgs in pork loin.  The animals we eat don’t get CVD though they have cholesterol.  Thus there is a need to explain like with LSPs what is the difference re oxidation, or is oxidation being hung out to promote drug sales. 

          I suspect that the oxidized theory is an attempt to deflect the fact that the level of serum cholesterol is at best weakly associated with atherosclerosis (See Uffe Ravhskov, Atherosclerosis caused by high cholesterol? reprinted at http://healthfully.org/rl/id5.html).  Since there is no convenient lab test for oxidized sterols,[30] the testing for serum cholesterol is a profitable surrogate. 

There is strong evidence that the bacteria within the artery wall are responsible for both the formation of plaque and modified LDL.  For those who wish to get started on this topic, I recommend looking at the articles pasted at http://healthfully.org/rl/id8.html and related article at the /rl2, ‘rl5, /rl9, /rl1 and /rl10.  The topics of pathogens, atherosclerosis, lipid hypothesis, and drugs to lower cholesterol is fit for books, and there are over a dozen quality ones in print.  It is too off course for me to continue here. Ravnskov and Calpo’s[31] are the best I have read, see appendix.    

          Again we have an example of industry Harpies snatching medical science from the table and depositing crapolla.  The “seminal” article above is one of the most brazen deposits upon the table of science.   The sum total of the prima facie evidence entails that I move on to another supposedly major cause for CVD, trans-fats. 

[1] “The hydroxyl radical has a very short in vivo half-life of approximately 10−9 seconds and a high reactivity.[7] This makes it a very dangerous compound to the organism”  Wiki hydroxyl_radical Aug 2019

[2] “Initiation is the step in which a fatty acid radical is produced. The most notable initiators in living cells are reactive oxygen species (ROS), such as OH· and HOO·, which combines with a hydrogen atom to make water and a fatty acid radical.” Wiki lipid_peroxidation, Aug 2019.

[3] 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, but in the cell wall as just stated the functionality were less.  Thus we have evolution working to make 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. Oleic is a 18:1 cis 9 fat; elaidic is an 18:1 trans-fat.  This doesn’t by extension apply to the dozens of common trans fatty acids compared to their cis brethren. Amazing how evolution in an incredible complex system deals with so, so many health issues!

[4] Wiki, lipid_peroxidationž Aug 2019. 

[5] Dormandy, TL, Sept 1969, (The Lancet) Biological Rancidification The first line of a very influential article on PUFAs.

[6] Wiki lipid peroxidation 6/2016   

[7] Dormandy, TL Sept 1969, Lancet, BIOLOGICAL RANCIDIFICATION 

[8] Butterfields, Jack, Patrick McGraw, 1979 in AHA, Storke P 444, Free Radical Pathology

[9] Butterfields, Jack, Patrick McGraw, 1979 in AHA, Stroke P 443-5, Free Radical Pathology

[10] Moreno, Moya, Olivares Mendoza, et al, Sept 1999, Analytical evaluation of polyunsaturated fatty acids degradation during thermal oxidation of edible oils by Fourier transform infrared spectroscopy

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

[12] Negre-Salvayre, Anne, Nahalie Auge, et al  Sept 2010 Pathological aspects of lipid peroxidation

[13] Wiki rancidification May 2016

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

[15] Pamplona, R, J Serrano, Oct. 2010, Lipid peroxidation in human diabetes: From the beginning to the end

[16] Raihi, Y, G Cohen et al, Dec 2010, Signaling and cytotoxic functions of 4-hydroxyalkenals

[17] 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.

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

[19] Spiteller,Gerhard, August 2007, The important role of lipid peroxidation processes in aging and age dependent disease.  Fish are a good source of protein (so too meats),.

[20] Spiteller supra, abstract. 

[21] Wiki, Furan_fatty_acids Aug 2019

[22] Wiki, Unsaturated_fat, Nov 2016.  Wiki given its standard of consensus of science on a topic, is stuck in most cases with ghost writers; the KOLs signoff on the articles.

[23] In the UK—and in other countries—the way industry gets around the band of direct-to-consumer advertising is through “informationals” given by the health associations in that country.  While they don’t favor a particular drug, they promote classes of drugs, and more significantly they implant the belief of health through drugs, and like with cigarettes and media messages, the informationals have created a population of pill poppers.  Marketing and propaganda change behavior.  They are similar to the US AHA, and their food pyramid is low fat high carbs (https://diet.com/g/british-heart-foundation-diet).  

[24] Negre-Salavre, Anne,  Nathalie Auge, et al (22 contributors), Sept 2012, Pathological aspects of lipid peroxidation

[25] Osada, Kyoichi, Takehiro Kodama, et al P 1198-12021993, Oxidation of cholesterol by heating

[26] Bjorkhem, Ingemar, Ulf Dicfalusy Febn 2003, cited 347 times (Sept 2019), Oxysterols:  Friends, Foes, or Just Fellow Passengers?

[27] The oxysterol-binding protein (OSBP)-related proteins (ORPs) are a family of lipid transfer proteins (LTPs). Concretely, they constitute a family of sterol and phosphoinositide binding and transfer proteins in eukaryotes[2] that are conserved from yeast to humans. They are lipid-binding proteins implicated in many cellular processes related with oxysterol, including signaling, vesicular trafficking, lipid metabolism, and non-vesicular sterol transport. Wiki oxysterol-binding protein, August 2019.

[28] Uffe Ravnskov, MD, PhD, Ignore the awkward!  How the cholesterol myths are kept alive, 2010, P 137-8.  Uffe is the founder of and spokes person for THINCS at thinks.org, the International Network of Cholesterol Skeptics

[29] Given the synthesis at night, why are people given statins or taking high dose of niacin during the day? 

[30] That which is within cells, requires more than simple blood tests. 

[31] Anthony Colpo, The Great Cholesterol Con:  Why everything you’ve been told about cholesterol, diet and heart disease is wrong! (2012).  He goes beyond Uffe Ravnskov to prove that angiograms, bypass operations are based on a wrong belief of atheroma.  They are treat old stable plaque, while the young plaque (20% occlusion) that  leaks to cause ischemic events.  

8.  Trans-fats, are they that bad?     


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

Reaction scheme: By far the largest amount of trans fat consumed today is created by the processed food industry as a side effect of partially catalytic hydrogenation of unsaturated plant fats (generally vegetable oils) with cis carbon-carbon double bonds. 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.  The regulations governing reporting, test for labeling, and enforcing violations of labeling has been replaced by an honor system, #9.  

A little bit of history and some numbers:  First until the 1970s most fats were animal derived, and were mostly SFA, about 70% or more.  Even milk (cattle or mother’s) is over 70% SFA.  The remaining fatty acids are MUFs or PUFA.  Nuts are the big exception, for example, olive oil and canola oil (rape seed) have about 75% MUFAs and about 15 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.[1]   In the 1930s extract with organic solvents, most commonly hexane, was used to remover the vegetable oils from mainly grains and some seeds.  The widely marketed vegetable oils are over 50% PUFA.  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 vegetable 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-Vegetable 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 0.5 grams. And 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. 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.  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 to find the modus operandi for how they are bad supported by strong evidence—not just a theory and some biomarker change, and an association with CAWD.  One barrier is that of research, their difference in structure to the PUFA derived from


of TFAs are nearly identical to the fat that they are derived from, only they have a reduction in the number of sites that are electron rich, a good thing (but contrary to crapolla that PUFAs are heart healthy).  It is possible if a study was done comparing a PUFA with4 double bonds to its trans version with 2 double bonds, that this TFA is healthier.  I don’t know of head to head animal studies comparing the 2 oil.  Second the studies claim an unhealthy change in lipid profile, the pile gets higher.  Others changes putatively found just don’t seem to be the kind of significant difference as causative of CVD.  End-point epidemiological studies I find less than convincing, in that they don’t control for contravening variables. Those who eat the highest quartile of trans-fats also eat the highest quartile of manufactured food and thus sugars and PUFAs, which increase the risk for CVD, and its modus operandi is strongly supported by experimental evidence.  After looking at the evidence, I suspect that at the highest levels it was decided to blame trans 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.  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 drugs (next chapter). 

   I did find a journal article that TFAs 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.” [2]  But nothing has changed business as usual with rancid PUFAs, and trans-fats as a diversion. 


9.  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 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.[3]   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; 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 concerning the accuracy of the labeling requirements.  There are 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” supra wiki.   Because of the lower price of PUFAs and thus 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 there isn’t as a norm deceptive labeling. 

  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 anaylsed products, regardless of brand of origin.” [4]  The regulations might make a difference assuming an association with CHD, 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.[5]   However, the highest rate of obesity, diabetes and sugar consumption is in the US of those listed.  Let us not become distracted by what could by the minor causes such as TFAs, when the elephant in the kitchen is sugar, PUFAs and drugs.  The weakness of  lab work with head to heat trial of PUFA and TFA makes the case[6] that trans-fats is insignificant and another part of the web causing cognitive dissonance.          


10.  What is good?




















Palm Kernel




































Varies according to sample 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. Prof. Donald Miller, surgery, cardiothoracic division, University of Washington.  Clear well organized college lecture with graphics and lots of information, given to 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 d-β-Hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease[7] and other benefits.  


11.  Evidence that coconut oil stimulates 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,  [and it is resistant to rancid].  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.  [And again the message] 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,[42] World Health Organization, he United States Department of Health and Human Services,[44] American Dietetic Association,[45] American Heart Association,[4 British National Health Service,[48] British Nutrition Foundation,[49][50] 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.[52] 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. [8]

Someone is way off. The case for the advantage of saturated fats not becoming rancid like PUFAs has been made above (3:4, 4 & 5). What of 3-hydroxybutrate which induces the active of BDNFs (brain derived neurotrophic factors)?

          The article 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 fentynol 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.[9]

This is not an isolated finding there is one of many journal articles on beta hydroxybutyrate and its benefit in stimulating neurotrophins.  Even the Wiki 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[10] thought no mention is made of short-chain fatty acids, though a synthesis from Leucine in humans is in a chart of over 20 possible steps which produced beta-hysdorxybutyrate.   A complex alternate source is indicative of its survival importance.  So is Beta-hydroxybutyrate derived from coconut oil through short-chain fatty acids? 

          I could again scream about the divergence between science and marketing.  Wiki again is full of crap in beta-hydroxybutyrate, but one more times is not need it—is it?  It is produced not just in the liver as KOLs and Wiki claim but can be made in the cytosol in just about every cell in the body.            


12.  Other ways to stimulate neurotrophins:  Four acknowledge ways are through exercise, extreme calorie restriction, ketogenic diet, and neurosteroids (the last not in Wikipedia):  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. [11] The mechanism for exercise increases neurotransmitter release that explains the induction of BDNF.[12]  The below article names fasting and calorie restriction and ketogenic diet. 

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.[13]


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 7 decades.  The short and medium chain source of SFA are preferred; and in response I consume over 5 pounds of coconut oil a month.  I use it in salad dressing and I make an imitation butter (the receipts are in the appendix).  Yes, I am on a low-carb diet, with digestible carbs making up under 20% of my energy supplying calories. 




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

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

[3] Wiki trans fats, Jan 2016

[4] 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 cause me to expect the same tobacco ethics. 

[6] 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.      

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

[8]  Wiki coconut oil (October 20190

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

[10] Wiki, beta- hydroxybutyrate Oct 2910

[11] Wiki Supra. 

[12] 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 bhydroxybutyrate

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).

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

EDIT  -NEED to add above

Coconut oil composition:  Oils had 90–98.2 % triacylglycerols, 1–8 % diacylglycerols and 0.4–2 % monoacylglycerols.  The 12 C lauric acid is the most common

Rossell, JB, B King, et al Feb 1985, Composition of oils “Palm kernel and coconut oils both contain about 47% lauric acid.”



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

^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^  Fat metabolism   ADD section

Fatty acid metabolism consists of catabolic processes that generate energy, and anabolic processes that create biologically important molecules (triglycerides, phospholipids, second messengers, local hormones and ketone bodies).[  In adipose tissue, intracellular triglycerides (the storage form of fatty acids) are broken down into 3 fatty acids and glycerol by lipase (of which there are 11 classes of, with variations in each class).  Note:  biologically the two forms of fat, triglyceride and free fatty acid are equivalent.  One role of fatty acids in animal metabolism is energy production, captured in the form of adenosine triphosphate (ATP). When compared to other macronutrient classes (carbohydrates and protein), fatty acids yield the most ATP on an energy per gram basis, when they are completely oxidized to CO2 and water by beta oxidation and the citric acid cycle. USED   Triglycerides are by far the main storage form for energy mainly because glucose must be stored in a very bulky form of glycogen which has for each glucose molecule 3 to 4 water molecules.  Put another way, fatty acids can hold more than six times the amount of energy per unit of storage mass.  Secondly, glucose is more reactive than fatty acids, thus causing damage in the cell in a process called glycation.  Moreover, glucose in excess increases osmotic pressure inside and outside the cells, which has adverse health consequences, which explains why PP is turned on to lower cytosol glucose. This is a bad thing, because the end product is fructose.  Finally, glucose in a meal high in sugar and starches very significantly delay (about 100%) the time for fructose uptake in the blood and cytosol for conversion to pyruvate, thereby increasing very significantly the amount of fructation.  Nature for these reasons has selected triglycerides rather than glycogen for energy storage.  Theupward limits of glycogen in the muscle is around 400 grams and liver 120 grams—the 2 principle storage sites.  With athletic training the amount can double.  A typical glycogen molecule consists of 300 glucose units, and 3-4 times as many water molecules. 


In the cytosol of the cell (for example a muscle cell), the glycerol will be converted to glyceraldehyde 3-phosphate, which is an intermediate in the glycolysis, to get further oxidized and produce energy. However, the main steps of fatty acids catabolism occur in the mitochondria.[15] Long chain fatty acids (more than 14 carbon) need to be converted to fatty acyl-CoA in order to pass across the mitochondria membrane.[6] Fatty acid catabolism begins in the cytoplasm of cells as Acyl-CoA synthetase uses the energy from cleavage of an ATP to catalyze the addition of Coenzyme A to the fatty acid.[6] The resulting Acyl-CoA cross the mitochondria membrane and enter the process of beta oxidation. The main products of the beta oxidation pathway are Acetyl-CoA (which is used in the Citric acid cycle to produce energy), NADH and FADH.[15] [Citric acid cycle occurs in the mitochondria.].  The acetyl-CoA produced by beta oxidation enters the citric acid cycle in the mitochondrion by combining with oxaloacetate to form citrate. This results in the complete combustion of the acetyl-CoA to CO2 and water. The energy released in this process is captured in the form of 1 GTP and 11 ATP molecules per acetyl-CoA molecule oxidized.  Each beta oxidative cut of the acyl-CoA molecule yields 5 ATP molecules.  Acetoacetate, beta-hydroxybutyrate, and their spontaneous breakdown product, acetone, are frequently, but confusingly, known as ketone bodies (as they are not "bodies" at all, but water-soluble chemical substances). The ketone bodies are released by the liver into the blood. All cells with mitochondria can take ketone bodies up from the blood and reconvert them into acetyl-CoA, which can then be used as fuel in their citric acid cycles.   The overall net reaction, using palmitoyl CoA (16:0) as a model substrate is:

7 FAD + 7 NAD+ + 7 CoASH + 7 H2O + H(CH2CH2)7CH2CO-SCoA → 8 CH3CO-SCoA + 7 FADH2 + 7 NADH + 7 H+



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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