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Book on fructose, mitochondria, and the sickest of mammals

2:6 Rancid Unsaturated fatty acids in cell membranes


2:6    Rancid unsaturated fatty acids in cell membranes   8/31/2020 5-12  COPIED FROM 4B-5-rancid-PUFA-in cell membranes     8/29/2020   split-original in older-misc. folder


Chapter 6:  Rancid UFAs membranes MTDD & CAWD:  1, Introduction   2. Science exposing 6 simple, profitable fallacies   3. The value of the omega 3 fatty acids    4. Furan fatty acids and the need for omega 3 and 6 fatty acids   5 Cell membranes    6. Why UFAs become rancid in cell walls    7. Mitochondrial membranes, the assault on UFAs   8.  Mitochondrial repair and prevention systems:  membranes     9.  Linoleic acid, is it essential?    10. Health consequences of rancid fats.    11.  Oxidized cholesterol and lipoproteins as the cause for atheromas?    12. Neurons and oxidized UFAs   13. About the rancid compounds?



Evolution made them a healthy mammal; capitalism made us the sickest of mammals


 


AD Alzheimer’s disease    AGE Advanced glycation endproducts    AHA  American Heart Association         CL cardiolipin     RAGE receptors for advanced glycation endproducts   


On naming of fats (some examples, saturated mainly):


·  Butyric (C4)  ·  Valeric (C5)  ·  Caproic (C6)  ·  Enanthic (C7)  ·  Caprylic (C8)  ·  Pelargonic (C9)  ·  Capric (C10) 


·  Undecylic (C11)  ·  Lauric (C12)  ·  Tridecylic (C13)  ·  Myristic (C14)  ·  Pentadecanoic (C15)  ·  Palmitic (C16) 


·  Margaric (C17)  ·  Stearic (C18)  ·  Nonadecylic (C19)  ·  Arachidic (C20)  ·  Arachidonic acid (c20:4)   Heneicosylic (C21)  ·  Behenic (C22)   ·  Tricosylic (C23)  ·  Eicosapentaenoic (C20:5)  the 5 indicates the number of double bonds, also 20:5(n-3) indicating it is an omega-3 fatty acid.  It is one of two omega-3 found in fish oil which was falsely claimed to be essential (#3 & 6) ·  Docosahexaenoic (C22:6) the other “essential” omega-6.  ·  Lignoceric (C24)  ·  Myristoleic (C14:1)  ·  Lauroleic (C12:1)  ·  Laurolinoleic (C12:2)  · Stearidonic acid (18:4 )  α-Linolenic acid C(18:3)  Linoleic acid (18:2)  γ-Linolenic acid (18:3)  Linolelaidic acid (C18:2)  Dihomo-γ-linolenic acid (20:3)  1Nervonic acid (C20:3)   1-Eicsenoic acid, also called gondoic acid   Nervonic acid (C24:1)    Herring acid (C224:6)  and many, many more.  The short chain, medium and long chain fatty acids are all saturated (by naming convention).  Short chain fatty acids start with Formic acid (C1:0), to Valeric acid (C5:0) of which there are 3.  Medium chain fatty acids are from Caproic acid (C6 to Lauric acid (C12:0). approximately 10–20% of the fatty acids in milk from horses, cows, sheep, and goats were medium-chain fatty acids.


SCFAs [short-chain fatty acids] are produced when dietary fiber is fermented in the colon.  SCFAs and medium-chain fatty acids are primarily absorbed through the portal vein during lipid digestion,[5] while long-chain fatty acids are packed into chylomicrons, enter lymphatic capillaries, then transfer to the blood at the subclavian vein.[1]  Medium chain fatty acids comprise from 10 to 20% of milk,[2]  


 


1,       Introduction:  Until the mid-twentieth century over 80% of dietary fats were animal derived, and were mostly SFA, about 70% or more.[3]  Milk (cattle or mother’s) is over 70% SAF.   Many of the plants from areas are high in SAFs and MUFAs.  Coconut oil has 83% SAF and 6% PUFA; palm oil is 10% PUFA with about 50% SAF and 40% monounsaturated fatty acids.[4]  Peanuts are 16% SAF, 57% MUFAs, 20% PUFAs.  Many of the commercial seeds are high in MUFAs, olive, rapeseed, (canola oil), and some cultivars of sunflowers are over 70% MUFAs   Most common nuts are high in MUFAs:  cashews are 65% MUFAs, pistachios 54% MUFAs.  In the 1930s extract with organic solvents became common, most commonly hexane was used to remove the seed oils from the mesh of crushed seeds.  The defatted seeds are then fed to cattle and pigs to fatten them up—fattening carbs.  The widely marketed seed corn is 55% PUFAs.  Lard, for example, has about 80% SFA.   Nature has its reasons: and for mammals it is high in SFAs and low in PUFAs because they become rancid in cells walls.  Thus, cow’s milk is approximately 70% SFA, 25% MUFAs, and 5% PUFA.  Human milk has a similar percentage.  Most of the fatty acids are in the storage from of triglycerides. Pasturization at high temperature (UHT) will cause oxidation reactions and cause fat deterioration and disrupt of proteins[5]  On the paleo-diet the amount of PUFA is far lower than those on the recent western diet.  


UFAs are the second major CC for CAWD.  While it probably won’t cause like fructose, IR, it will both increase the risk factors for CAWD and through MTDD promote IR.  UFAs have  double bonds between carbon on the chain permits reactive electrophilic chemicals to bond there.  This has been known for over a hundred and fifty years.  Rancidification is the process of complete or incomplete oxidation or hydrolysis of fats and oils when exposed to air, light, or moisture, or by bacterial action, resulting in unpleasant taste and odor…. Animal studies show evidence of organ damage, inflammation, carcinogenesis, and advanced atherosclerosis,’ [6]  Rancid fats are the second most significant cause of MTDD and CAWD (though possible drugs, recreational and pharmaceutical, holds second place.  For those who take more than 4 or more drugs (polypharmacy) [7] would place it in second place, and some of the drugs such as statins and the sedative, taken in sufficient does would place that person in higher risk than a diet high in PUFAs.  Unlike fructose which in sufficient excess causes MTDD, rancid UFAs, merely lower the bar, a lesser CC.  Since rancid UFAs are in mitochondrial membranes, UFAs contribute to the risk for CAWD.  Both UFA and fructose increase the release of ROS from MTD, thereby increasing the rate of damage to MTD.  The words of the surgeon captain UK Thomas Cleave (1906 to 1983) known as Peter among friends. 


I don’t hold the cholesterol view for a moment.  Mankind has been eating saturated fats for hundreds of thousand of years.  For a modern disease to be related to an old-fashioned food is the most ludicrous things I have every heard in my life.  If anybody tells me that eating fat was the cause of coronary disease, I should look at them in amazement.  But when it comes to the dreadful sweet things that are served up… that is a very difference proposition.[8]


 Cleave was a recognized expert on nutrition with books and journal articles.  He called conditions of affluence, the saccharine disease.  Cleave pointed out that the paleo peoples on a high fat diet did experience CVD.  Examples include the Maasai of Kenya and Tanzania whose diet consisted of meat, milk, and blood form cattle, a diet 66% saturated fat.  The Eskimos of Artic whose diet consisted--75% of saturated fat.  The Rendille of the Kaisut Desert of NE Kenya, a diet of camel milk, meat and Banjo which consists of a mixture of camel milk and blood—63% saturated fat.  The Tokelau of three atoll islands off of New Zealand, a diet of fish and coconut—60% saturated fat.  The lesson is that claiming nature functions contrary to evolutionary survival for the village.is tobacco science.  Over and over again, I find tobacco science violating evolution.  


Two reasons for villages, one that most of our primate evolution occurred in the paleo group including villages and they ate saturated fats.  Retain this since I will repeatedly use the evolutionary argument.  Second the village benefits by culling the elderly to make room for younger villagers.  Retain the culling of elderly, for when nature removes a substance from an elderly, such as sex hormones and melatonin it is to cull the elderly (I have yet to find a counter example).  I take those supplements and a high saturated fat diet. 

The content of human milk is for 4.2 gram per 100 of milk, with 3.8 SFA and just 0.6 g PUFAs, and cow’s milk is 69% SFA, 28% MUFA, and 4% PUFA, similar percentages for goat and sheep milk.[9]  Are these mammals making the worse of fats and the least of the best?  When someone tells me that cow’s milk and its extract budder cause coronary disease and type two diabetes, I look at them in amazement.  But when it comes to the dreadful sweet things that make up 20% of calories in the US, that is a different thing. 

          John Yudkin, the leading UK nutritionist (2:1) appeared before the Commission.  “Yudkin blamed heart disease exclusively on sugar, and he was equally adamant that neither saturated fat nor cholesterol played a role.  He explained how carbohydrates and specifically sugar in the diet could induce both diabetes and heart disease, through their effect on insulin secretion…. [He said to McGovern], I believe that high blood cholesterol in itself has nothing whatsoever to do with heart disease. [10] 

This is exactly what I will present in this book, and in this chapter why fructated and oxidized UFAs is a second major CC for CAWD.  Government politics and the Sugar Research Institutes have shortened the lives of every human on the western diet, a reasonable estimate is 8 years and enduring on an average increase in infirmity of 16 years.  A devilish example of how profits come first, tobacco ethics. 

Calling in those holding the opposite views is a common move of blue-ribbon panels; gives the claim of objectivity, but the results were decided before the process began.  The list of critic causes the gullible to believe that the panel came to the table, evaluated both sides, and fairly chose the one supported best by the evidence.  The back door evidence supports that the US government prior decision to support major corporate farms and food manufacturers, and at the same time give cigarettes a free pass on all cancers and CVD.  Excess deaths for those who smoking long-term a pack a day or more is greater for CVD than excess deaths from cancer, including those not exposed such as the pancreas, which is 2.5 times greater than the rate for nonsmokers.[11]  For these smokers every tissues has excess cancers. 

 

2.      Science exposing 6 simple, profitable fallacies:  One way to win the battle over which fat to eat the KOLs produce tobacco science:  1) PUFAs are better than SFA for cell walls, 2) needed for the essential anti-inflammatory Omega 3, 3) UFA oils are heart healthy.  4) SFAs are toxic:  5) SFAs cause fatty liver, 6) SFAs cause CVD including MI, and 7) SFAs cause diabetes.  The American Heart Association (AHA) recommends under 6% of calories from SFAs, 24% UFAs, and a total 30% of calories from fats, as too most governmental health agencies and all the well-funded organizations similar to the AHA.


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.[12]


          By the way, the AHA was established in 1924, but remained small until funding by the marketer of Crisco, Proctor & Gamble, in the 1940s[13] (more at 2:7).  Given that over 95% of dieticians and physicians have swallowed the castor oil of the AHA, I shall at the start here and confront 7 crapolla examples—5 of them briefly.  Oh, recall the words of Thomas Cleave (in Introduction) that it is ridiculous to suppose that which we ate for hundreds of thousands of years is the cause of the recent plague of CVD—that is a dispositive statement.  Cleave went on to do a population study which found sugar is the cause of the recent CVD plague.  Our government and others used the obviously flawed Ancel Keys’ 7-Countries Study (he had figures for 22 counties, cherry picking).    


          It is necessary to clean the slate as to the good calories and the bad calories, a theme in this book,[14] since bad calories are the major CC for CAWD.  1) The body needs PUFAs there for cell walls. “The length and the degree of unsaturation of fatty acid chains have a profound effect on membrane fluidity as unsaturated lipids create a kink, preventing the fatty acids from packing together as tightly, thus decreasing the melting temperature (increasing the fluidity) of the membrane.  The ability of some organisms to regulate the fluidity of their cell membranes by altering lipid composition is called homeoviscous adaptation.” [15]  This is bad science since the mechanism for rigidity of cell membranes is controlled by sterols for fluidity,[16] and glycolipids for rigidity.  It is known that the behavior of lipids under physiological (and other) conditions is not simple” [17]  Another case of a simple answer being wrong, that PUFAs play an essential role in cell wall.



Alpha-linolenic acid (ALA)


An essential omega-3 fatty acid, cis9-12-15-ocatdecatrienboic acid


          It is wrong for 3 reasons, they become rancid in the cell membranes thus the control of rigidity by sterols and glycolipids, and secondly because those on a paleo diet have a very small amount of dietary UFAs; third in their cell walls the UFAs are not straight thus affecting rigidity and barrier functions therefore, resulting in SAFs being the main fat in cell walls. The importance of UFAs is another case of tobacco science exaggeration, in this case the role of UFAs essential for cell membranes.  Most populations eat little seed oils, especially in the colder inland climates.  These populations did not have significant CAVD, heart attacks. or diabetes.  The food and drug industries have promoted UFAs as essential in cell walls. 


          The need for omega 3 lacks quality studies showing a causal method for improving health.  Moreover, the inland Eskimos were fine without significant source UFAs and the omega 3 PUFAs to lower their inflammation (a topic examined in #3 and #4 here).  The body can synthesize them as needed.  It turns out that furans found in fish oil prevents the chain reaction caused by the oxidation of PUFAs (more on furans #3)


          For the next four putative adverse health consequences, the modus operandi for SFAs causing health conditions is lacking.  The stability of SFAs is dispositive.  This is further supported by various paleo peoples that are on a high saturated fat        diet.


          This brings me to the attack on SFAs, number 3 heart healthy.  Epidemiological study show association of UFAs with CVD.  A BMJ meta-analysis found 21 of 22 studies found no association of SFAs with CVD.  The complexity and contravening variables make the conclusion of fats associated with CVD determined by the authors’ beliefs.  However, the method of rancid fats promoting CVD is known, as described in the previous chapter.  Secondly, the low-fat diet is high carbs including sugars, the second CC for CVD.    


          Fourth, there isn’t quality evidence that SFA are toxic for those who are slim.  Rather the association of fat with pathology is a result of large lipid droplets. It is not caused by SFAs in the diet, but instead by sugars causing MTDD and IR.  


          Item 5, the claim that SFAs in the diet cause NAFLD (and by implication MeS).  Evidence for harm is that DNL produces mainly palmitic acid a saturated fat.  Following from that argument, it would entail that evolution promoted one of the worse fats.  The issue of toxicity used by KOLs arises not from SFAs but over stuffed cells with glucose and the PP and DNL removing the excess, Again the formation of excessive size of lipid droplets causing stress upon cells (4:1).  Again, we have the firemen--palmitic acid--phenomena again, guilt by association.  Palmitic fatty acid is there because of DNL and the western diet causing IR which can result in large LD.  Insulin stops the metabolism of fatty acids which are turned to the storage form triglycerides which are then stored in the adipose tissue and some in the different types of cells that make up organs and other tissues as organelles called lipid droplet.  When the fat organelles reach a certain size the performance of the cell stops.[18]  We have western diet, not SFAs being pernicious.   


          Sixth causing CVD and MI, quality studies support the opposite.  A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.” [19]  Again there is opposite, and again I go back to Cleave’s statement about violation of evolution. 


          Seventh diabetes is a way of deflecting the cause, the western high fructose diet to the innocent SFAs. The association with high sugar diet is strong: a trial in a clinic of students with fed 40% of calories from sugar; this diet produced insulin resistance and elevate blood glucose in 2 weeks.  The march toward IR and t2d has been similarly demonstrated on feeding experiments on mammals.     


Metabolic syndrome represents a collection of abnormalities that includes fatty liver, and it currently affects one-third of the United States population and has become a major health concern worldwide. Fructose intake, primarily from added sugars in soft drinks, can induce fatty liver in animals and is epidemiologically associated with nonalcoholic fatty liver disease in humans. Fructose is considered lipogenic due to its ability to generate triglycerides [palmitic acid and others] as a direct consequence of the metabolism of the fructose molecule. Here, we show that fructose also stimulates triglyceride synthesis via a purine-degrading pathway that is triggered from the rapid phosphorylation of fructose by fructokinase. Generated AMP enters into the purine degradation pathway through the activation of AMP deaminase resulting in uric (4:2) acid production and the generation of mitochondrial oxidants [ROS].  Mitochondrial oxidative stress results in the inhibition of aconitase in the Krebs cycle, resulting in the accumulation of citrate and the stimulation of ATP citrate lyase and fatty-acid synthase leading to de novo lipogenesis. These studies provide new insights into the pathogenesis of hepatic fat accumulation under normal and diseased states. [20]


I am very, very tired of the crapolla built upon audience ignorance of this topic:  The KOLs and their dupes roll out lipotoxicity.  Mixing the two types of fats, then blame the saturated fats, pure tobacco science (4:1).  The lack of CVD, virtual unknown among those on a paleo diet (1:3) and supported by animal experiments is ignored by KOLs.  Like with cholesterol, the myth has been thoroughly exposed, yet it thrives upon a broth of ignorance spiced with dollars and social conditioning.  Mother nature hasn’t given us CVD. 


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.  Donald Miller is Professor of Surgery, Division of cardiothoracic Surgery, University of Washington.  He gave a lecture to audience of physicians, https://www.youtube.com/watch?v=vRe9z32NZHY.  By now you too should be saddened by our system.  There is also a BMJ meta-analysis 21 of 22 articles failed to find an increase-risk in MI with a diet high in SFAs.[21] 

Thanks food manufacturers for protecting us with a low-fat high-sugar diet.  I think of my brother-in-law Ginter with t2d.  He is 13 years my junior and died in 2005 at the age of 49, after 6-years of disability with broken ankle that wouldn’t heal.  He died in the hospital while treating his lower limb, likely of arrythmia; found dead in his room.  His photo at the age of 18 with my wife is on the wall.  He was visiting us in Escondido, CA. 

We all know of dear ones who have suffered with diabetes a progressive condition (not a disease like TB) because the drugs increase insulin resistance and celebrates who suffered, Elea Fitzgerald and Jerry Garcia come to mind.  I still listen to them.

 

3.    The value of the omega 3 fatty acids: 

                Full structural formula of furan       

                     Furan                              Furan fatty acid 

Roll out the essential healthful PUFAs, omega 3 & 6; however, they aren’t.  It is part of the pitch for PUFAs, another magic supplement.  Over and over again, I find industry generated healthful advice isn’t healthful.  Given the belief in healthful, the size of the sales of omega 3 supplements, and that innocently physician recommend omega 3, it merits a few paragraphs.  Another less in tobacco science. 

I have failed to find strong evidence for biological process producing salubrious intermediates from omega 3.  The claims of a bad ratio of omega 6 to omega 3 is strong on claims, but weak on science.  The lower of inflammation by eicosapentaenoic acid (EPA)[22] is not a vital function and a bad thing for the paleo peoples and us.  Lowering inflammation is like lowering fever, it doesn’t treat the underlying cause, and both inflammation and temperature rise are part of natures way of fight infection. 


Evidence in the population generally does not support a beneficial role for omega−3 fatty acid supplementation in preventing cardiovascular disease (including myocardial infarction and sudden cardiac death) or stroke.  However, omega−3 fatty acid supplementation greater than one gram daily for at least a year may be protective against cardiac death, sudden death, and myocardial infarction in people who have a history of cardiovascular disease.  With the possible exception of breast cancer,[4][14][15] there is insufficient evidence that supplementation with omega−3 fatty acids has an effect on different cancers. Multiple studies[14][15] have shown a relationship between α-linolenic acid and an increased risk of prostate cancer.  There is a decreased risk with higher blood levels of DPA, but an increased risk of more aggressive prostate cancer was shown with higher blood levels of combined EPA and DHA.   ALA does not confer the cardiovascular health benefits of EPA and DHAs.[23]


Most paleo peoples are very low in omega 3 since seeds for many are dietary low.[24]  It might be of benefit for those on the western diet, but as stated in quote an increase in cancer and a failure to reduce CVD.  Inflammation is part of our healing; a response to toxic and foreign substances such as bacteria and pernicious chemicals.  To block what evolution has given us to be health is likely net harmful long term.  Don’t mess with evolution.   To lower immune functions has major risks, tough it might reduce arthritic pain.  For example, taking a drug that reduces ATP and thus immune response promotes mainly among the elderly a higher death rate from the COVID 19 virus.  There is a long list of drugs, besides statins, such as most neurotropic drugs, that reduce ATP production; the leucocytes run on ATP. 


Our 1 to 16 ration of omega 3 to 6 isn’t pathogenic though the western diet is: its   high in seed oils and fructose.  Secondly, as needed, the body will make EPA & DHA from oleic acid (fatty acid) the needed two omega acids.  Lowering immune response is likely a bad idea, yet good for pharma.   Association does prove cause.. 


At first, I was a believer the ration of omega 3 to 6 PUFAs is a CC our health disaster (I wasn’t at that time searching for the cause of CAWD, which came 6 years later).  I studied for several days a seminal long article by a researcher for USDA. But with further research several years later as part of my looking into the issues of good and bad fats and business’ pattern promoting cognitive dissonance, this caused me to reverse my acceptance.  The evidence for modus operandi of the omega 3 & 6 proposed by KOLs is far from convincing.  Just because Americans average 16 times as much omega 6 as 3, while some paleo peoples average between 1:1 and 1:4 does not prove that American have a pathogenic imbalance.   We found no convincing evidence for the efficacy of omega3 PUFA supplements in the treatment of mild to moderate AD.” [25]  α-Linolenic acid is relatively more susceptible to oxidation and will become rancid more quickly than many other oils.” [26]    Slowly since 2009 I had come to realize that claims of healthful substance coming from the highest levels and promoted in the media were nearly always grossly inflated or worse. The fish oil omega-3 acceptance fits that pattern.  This skepticism was confirmed in a 2007 seminal article which found excess omega 3s are toxic:


Because fish is rich in n-3 fatty acids such as eicosatetraenoic 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.[27]


It is not the omega 3 that is salubrious, and not the real cause of protection, it is furan fatty acids.  This effect of extinguish radical only with fish oil explains why plant sources of omega 3 sources have failed to be significantly salubrious.  Nature wouldn’t select for a fat that is the quickest to become rancid. 


 


 




[1] Wiki,, Short_chain_fatty_acid, Feb 2022

[2] Wiki, Medium_chain_fatty_acids, Feb 2022.  Again, the KOLs have left out a benefit for a product on the shit list; in this case, that medium chain fatty acids promote the production of brain derived neurotropic factors (BDNF), promote growth and thus healing.  BNDF explains why MCT oils are used in a keto diet for epilepsy and dementia with significant success.  

[3] The major exception was in some countries olive oil which had been extracted since 6,000 BCE, and cotton seed oil from 1857.  It was used as an unreported diluent for lard, butter, and olive oil.  In 1857 extraction became practical by removing the husk. 

[4] At Wiki, Coconut_oil, June 2019, there is a table for percentages of 19 oils. 

[6] Wiki, Rancidification, Feb 2020

[7] There is no standard definition.  I count the regular usage of both classes of drugs including over the counter drugs.  Those most susceptible to harm, seniors, over 70% of them qualify.

[8] Gary Taubes, Good Calories, Bad Calories, 2008, P 123.  Quoting Cleave’s interview with Kenneth Scholsbern, the staff director of the McGovern’s Committee.  The Committee based on new corporate farming policy, and probably tobacco, food manufacturers, and pharma decided for profits before people , thus, the FDA came out with the food pyramid and their unhealthful SFAs and cholesterol warning which was written on the mountains by corporate media and the dupes, physicians and dieticians repeated their crapolla. 

[9]  Wiki, milk, Feb 2022

[10]  Gary Taubes, Good Calories, Bad Calories, 2008, P 123

[11]  The reason for this as explained prior is the biological stress placed by the one-two punch of the western diet and the toxic compounds which overwhelm the healing processes (autophagy) of which tobacco smoke is a major stress source. This analysis explains why the Kitavans and oriental on a traditional diet have a very low risk for both cancer and CVD.      

[12] Wiki, saturated fat, Aug 2020

[13] Wiki, American Heart Association, August 2020.  The flow of funds explain why they gave the heart healthy emblem to sugar coated cereals and grape juice, and why Ancel Keys became one of their directors. 

[14] The title of Gary Taubes 2006 book which contracted Keys’ lipid hypothesis as too a pile of journal articles.  Keys late in life lamented the harm his promotion of the lipid hypothesis.  

[15] Wiki, cell membrane, March 2020

[16] Wikipedia, sterol, Aug 202  “For example, cholesterol [a sterol] forms part of the cellular membrane in animals, where it affects the cell membrane's fluidity.” 

[17] Wiki, phospholipids, Aug 2020

[18] If that cell is a beta cell in the pancreas the production of insulin declines and the blood glucose increases until it becomes symptomatic of t2d.  Before that point, the cells to prevent overstuffing with glucose,  they withdraw the GLUT receptors for glucose, raising moderate blood glucose which is a sign of insulin resistance.  More on this in Volume 2, 

[19] Siri-Tarino, Patty, Qi Sun, et al, March 2010, Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease

[21] Malhora, Aseem, May 2013, BMJ, Saturated fat is not the major issue “Let’s bust the myth of its role in heart disease”

[22] A two carbon PUFA with 5-cis double bonds. It is synthesized from oleic acid and has several biological functions.  Like other systems excess offer no advantage and with 5 double bonds it is prone to becoming rancid and thus not used in cell membraines.

[23] Wiki, Omega 3 fatty acid health effects, August 2020

[24] Ratio of 3 to 6 omega oils:  Avocado  1:13, brazil nuts 1:420, corn 1:58, olive 1:13, peanut above 1:100,, sunflower above 1:100, from Wiki table saturated fat, August 2020

[25] Burckhardt, Marion, Jax Herke, et al, April 2016, Cochrane Library, Omega‐3 fatty acids for the treatment of dementia

[26] Wiki, alpha-linolenic acid, potential role in nutrition and health, August 2020

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



4.  Furan fatty acids and the need for omega 3 and 6 fatty acids:


   Full structural formula of furan     Shape

Description automatically generated with medium confidence


                                 Furan                              Furan fatty acid      


 

The furans extinguish the chain reaction that occurs when ROS bond to PUFAs.  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.[1] 


Furan fatty acids are very effectively acting as radical scavengers. In this process dioxoenoic fatty acids are formed, which are by themselves very unstable and form thioethers with thiols such as cysteine or glutathione.[17] As potent antioxidants, they specifically trap hydroxyl radicals. [2]  


This process and the value of furan fatty acid has been repeated, all the major points, and with Spiteller are supported by other journal articles.  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].[3]


Since it is the furan fatty acids that are protective, and it is found in fish oil and plants, the claims for DHA and EPA are based on mere association.  I would put it a bit stronger in that with MTDD the need for the Furan fat acids is greater since the release for the release of ROS are much greater from the MTDD and that RRA and other factors such as RAPT increase the need for quenching LOO, thus the need of HSPs compared to the LSPs is greater for furan fatty acids.  Studies fail to show a benefit.[4]          


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 and net healthful drugs.  It is devilish when profits trumps science and those at the highest place are enablers. 

 


5.      Cell membranes:  A view of the complexity of mammalian biology.  The assault of reactive chemical is why evolution favors the production of SFAs.  It is why milk contains mostly SFAs and why in DNL it is again SAFs that are mainly produced.    


https://upload.wikimedia.org/wikipedia/commons/thumb/d/da/Cell_membrane_detailed_diagram_en.svg/500px-Cell_membrane_detailed_diagram_en.svg.png


alt text


A transport channel in a membrane, such as GLUT-1


Glucose transporter member 1, it accounts for 2% of the protein in the plasma membrane of erythrocytes.  The number varies according to tissue type and need. There are hundreds of different transporters in cell membranes, each specified by associated gene.  Fourteen GLUTS are encoded in the human genome.[5]   


 


Cell Membrane Color Sheet and Build a Cell Membrane - Activity ...


 


Scientific Videos: Cell Membrane Structure and Function 


 


 


Cell membrane also known as plasma membrane is a biological membrane that separates the interior of cells from the outside environment or the organelle from the cytosol (the intracellular fluids).  The cytosol is the liquid matrix around the organelles.  Membranes within cells separate and control the movement of substances within an organelle and substances outside the organelle.  Cell membranes are involved in a number of cellular processes, including ion conductivity, storage of molecules, transport of chemicals in and out of cells and organelles either active requiring energy or passive, rigidity of organelle, chemical signaling, cell adhesion, cell potential, o name some key functions. 

Example of major membrane phospholipids and glycolipids;

Phosphyatidylcholine (PtdCho), phosphatidylethanolamine (PtdEtn)

Phosphatidylinositol (Ptdins) phosphatidylserine (PtdSer)

 

Skeletal formula of sphingosine

Sphingosine the simplest of sphingolipids

Another family besides phospholipids is that of sphingolipids “a class of lipids containing a backbone of sphingoid bases, a set of aliphatic amino alcohols that includes sphingosine.”[6] There are over a dozen different types, each with a molecule attached to a of saturated carbon but for a double bond on the 1:2 carbs.  They have a number of functions including mechanical stability, chemical resistance on the outer leaf of the membrane, and other functions such as “cell recognition, cascades involving apoptosis, proliferation, restress responses, necrosis, inflammation, autophagy, senescence, and differentiation.” [7]  There are other classes of compounds in cell walls: glycolipids and glycerophospholipids.   

Because of this bonding there are system that restore the walls and reduces the damage caused by ROS, by glycation, by oxidized UFAs, and by the products that they form.  Like everything, it is complex:  membranes are fine tuned for their functions.  Look at the 2nd illustration above, this transport channel through the membrane, look at the careful folding of the amino acids in the protein.  The folding is controlled by genes, and it is conserved across species:  sequence of amino acids of different species often differ under 5% in their amino acid sequences.  The sequence of amino acids determines the folds.

Plasma membranes are composed of a double layer of lipids (phospholipids, cholesterol, etc.).  They serve as an internal and external barrier.  Membranes in general have a polar hydrophobic head consisting of a phospholipid.   “The phospholipid allows the liquid portion of a biological membrane to be self-assembling and to reseal (repair itself quickly when torn)...  The lipid layer contains about 10% of the externally facing lipid molecules with an attached sugar group (glycolipid). . . integral proteins are firmly inserted in the lipid bilayer . . . of which most are transmembrane and protrude on both sides. ” [8]  For entry into a cell and organelles, there is active transport, simple diffusion, and selective permeability in an aqueous solution.  Macromolecules such as LDL are transported through plasma membranes by bulk transport energized by ATP.  With exocytosis the product from within the cell is encapsulated, fuses with the membrane, and ruptures spilling the sac contents outside the cells.  With endocytosis macromolecules enter the cell contained in a membrane where its contents are digested and/or dispersed.  

There are many variations of functions and specialty molecules to promote functions.  The variations for functions could fill a book and has.  There are over 14 major types of organelles and many more specialty organelles for the 200 tissue types.  The immediate concern here is the deleterious role oxidized UFAs play and the system to mitigate the consequences of oxidation.  The illustrations above speak louder than words. 




[1] Spiteller supra, abstract.  M        

[2] Wiki, Furan fatty acids May 2020

[3] Spiteller,Gerhard, August 2007, The important role of lipid peroxidation processes in aging and age dependent disease

[4] Dr. Paul Mason confirming my search of the journals states that the studies of omega 3 fail to find significant health benefit (https://www.youtube.com/watch?v=sNz2gWqL0Ng), and backs it up by a meta-analysis.

[5] Wiki, GLUT transporters, Sept 2020

[6] Wiki, Sphingolipid, Sept 2020

[7] Wiki, Sphingolipid, Sept 2020

[8] Elaine Naruebm Human anatomy and physiology, 2 Edition, 1992, P 64



 


6. Why UFAs & PUFA become rancid in cell walls:



Hydroxyl radical are one of the main causes through a chain reaction—below-- in the modification of cell walls


http://upload.wikimedia.org/wikipedia/commons/thumb/9/9e/Lipid_peroxidation.svg/350px-Lipid_peroxidation.svg.png


Lipid peroxidation, a free radical chain reaction


 


Besides the formation of the lipid radical, the lipid peroxide (illustration below is called a lipid hydroperoxide) being unstable has several possible paths including forming a stable lipid alcohol, an aldehyde, or a lipid radical.  The consequence of these reactions is to compromise the functions of the membrane.   See illustration below


 



What is said about PUFAs also applies to their phosphorylated. The phosphate group doesn’t protect the carbon chain with its double bonds.


 


Because of UFAs 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 intramembrane to UFAs, one is the just described OH radical with its unpaired electron.  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] and there are other reactive chemicals created in the MTD.  Some of them are a product of sugar bonding to a protein--called glycation--in the Milliard reaction and the Strecker degradation (2:4, 6).  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 UFA is in a membrane it compromises the performance of the membrane.  The greater the number of modified UFAs in the membrane the greater is the dysfunction.[3] 


This is not a new finding, just ignored:


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. . .  The toxicity of lipid hydroperoxides to animals is best illustrated by the lethal phenotype of glutathione peroxidase 4 (GPX4) knockout mice. These animals do not survive past embryonic day 8, indicating that the removal of lipid hydroperoxides is essential for mammalian life. Antioxidants such as vitamin C and vitamin E may inhibit lipid peroxidation.[4]


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.[5]


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.” [6]  

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. The current evidence for the implication of LPO in pathological processes is discussed in this review. New data and literature review are provided evaluating the role of LPO in the pathophysiology of ageing and classically oxidative stress-linked diseases, such as neurodegenerative diseases, diabetes and atherosclerosis (the main cause of cardiovascular complications). Striking evidences implicating LPO in foetal vascular dysfunction occurring in pre-eclampsia, in renal and liver diseases, as well as their role as cause and consequence to cancer development are addressed.[7]


        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.” [8]  I would add to the list glutathione and CoQ10.   So why are not pharma, media, and physicians telling us that antioxidants are important?[9] 


          There are other types of reactions such as with reducing sugars.  When the reducing sugar reacts with an amino acid it is known as the Maillard reaction.[10]  The reactive compounds produce can then react with lipids.  Methylglyoxal is 50,000 more reactive than glucose.  “During the metabolism of carbohydrates, otherwise known as glycolysis methylglyoxal is formed, which is a major precursor to the formation of AGEs.  It is the dicarbonyl compound that can inhibit mitochondrial respiration and other physiological pathways.” [11] Among the reactive chemicals to bond to PUFAs are the reactive nitrogen species.  Reactive nitrogen species derived from nitric oxide are potent oxidants formed during inflammation that can oxidize membrane and lipoprotein lipids in vivo. . .  several of these species react with unsaturated fatty acids to yield nitrated oxidation products.” [12]  And there are other types of reactive chemicals such as hypochlorous acid.[13] 

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 which O2 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.[14]


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].[15]  [16]


As Prof. Lustig warns about fructose applies not just to proteins (the Maillard reaction), and the browning process, but fructose and ROS can bond non-enzymatically to UFAs.  “You can brown your meat at 375 degrees for one hour, or you can brown your meat at 98.6 degrees for 75 years.”[17]  “The most apparent feature of the oxidative breakdown of lipids is rancidity, a problem that was recognized centuries and half ago during the storage of seed oils. Rancidity persists as a widespread problem in today's society because of the common use of polyunsaturated fats and seed oils.” [18] Any electron rich molecule will do for an unbound electrophilic chemical.  Sounds like the fructation scenario again.


MUFAs which average about 1/3rd the double bonds are oxidized at about 1/3rd the rate of PUFAs.  Rancidification is a second way to cause MTDD and to compromise cellular and tissue processes.  The first through the action of fructose has already been covered.  Together they are the major CCs for MTDD and CAWD.  Both fructose and UFAs are in that order the most significant causes for MTDD. 


           

7.  Mitochondrial membranes, the assault on UFAs:    

7.4B: Chemiosmosis and Oxidative Phosphorylation - Biology LibreTexts

The cardiolipin are the darker molecules in the membrane surrounding complexes 1-1V

This brings us full circle, back to the ways in which mainly fructose among the sugars and the compounds made from them that damages the MTD, now we have UFAs and their compounds made from them doing causing MTDD by basically different procedure.  The sugar when effecting the ATP production bonds to the amino acids in complex 1 through 5 and ATP synthase (above illustration, blue is proteins) affecting efficiency and thereby slowing up the metabolism through a feedback system which causes IR.  With the rancid UFAs, they affect the integrity of the membrane which allows the leakage of the protons.  This reduces the production of ATP. The leaked protons also start the chain reaction producing more rancid UFAs both inside and outside the membrane.  The reduction in the rate of ATP like with fructose causing MTDD, this too promotes IR in the liver.  

   Reactive oxygen species (ROS) are chemically reactive chemical species containing oxygen. Examples include peroxidessuperoxidehydroxyl radicalsinglet oxygen,[3] and alpha-oxygen.


The reduction of molecular oxygen (O2) produces superoxide (O
2
), which is the precursor of most other reactive oxygen species:[4]


O2 + e → O
2


Dismutation of superoxide produces hydrogen peroxide (H2O2):


2 H+ + O
2
 + O
2
 → H2O2 + O2 [4]


Hydrogen peroxide in turn may be partially reduced, thus forming hydroxide ion and hydroxyl radical (OH), or fully reduced to water:[4]


H2O2 + e → HO + OH


2 H+ + 2 e + H2O2 → 2 H2O[19]


          There are a number of ways the MTD reduces the damage done by ROS and other reactive compounds.

 

8.  Mitochondrial repair and prevention systems:  membranes:  To cope with these reactive chenical  tissues and mitochoindria store vitamin C and beta carotene, CoQ10, superoxided demutase, glutothionene, and other anti-oxidant enzymes.   One major system to nuetralize the chain reaction of UFAs is the incorportion of cardiolipin in MTD inner membrane—see illustration above, which shows the inner membrane, but is lacking the label for the 20% of cardiolipin in inner membrane.  The cardiolipin are the darker molecules in #6 above and in the illustration below. 

16:0-18:1 Cardiolipin | Avanti Polar Lipids

Cardioliptin  (CL)

The number of double bonds in the carbon chain is two, some that have 3.

 


Cardiolipin, CL, (IUPAC name 1,3-bis(sn-3’-phosphatidyl)-sn-glycerol, also known as Calcutta antigen) is an important component of the inner mitochondrial membrane, where it constitutes about 20% of the total lipid composition. It can also be found in the membranes of most bacteria. The name "cardiolipin" is derived from the fact that it was first found in animal hearts. It was first isolated from beef heart in the early 1940s.[1] In mammalian cells, but also in plant cells, cardiolipin (CL) is found almost exclusively in the inner mitochondrial membrane, where it is essential for the optimal function of numerous enzymes that are involved in mitochondrial energy metabolism…. In eukaryotes such as yeasts, plants and animals, the synthesis processes are believed to happen in mitochondria...  Complex IV has been shown to require two associated CL molecules in order to maintain its full enzymatic function. 


Other functions:


  • Cholesterol translocation from outer to the inner membrane of mitochondrial

  • Activates mitochondrial cholesterol side-chain cleavage

  • Import protein into mitochondrial matrix

  • Anticoagulant function

  • Modulates α-synuclein[19] - malfunction of this process is thought to be a cause of Parkinson's disease.

  • Causal for Parkinson’s disease when CL is subjected to excess oxidative stress, the results of which are mitochondrial dysfunction and neuronal loss in the substantia nigra.

  • CL has been found to be deficient in the heart at the earliest stages of type 2 diabetes 

  • Cancer, for at least some types, CL is impaired in the mitochondria, a confirmation mechanism for the Warburg hypothesis of the role of disable mitochondria, thereby turning off apoptosis process for destruction of precancerous and cancerous cells.

  • According to a study 95% of those with chronic fatigue syndrome have antibodies to cardiolipin[20]


 

This why variety of functions and the consequences when compromised explain why cardiolipin is widely preserved, including plants, bacteria, fungus, and vertebrates.

Showing CL’s function in the outer membrane; it can trigger apoptosis

CL also functions as a proton trap in oxidative phosphorylation mainly in complex IV & V. It is essential for MTD proper functions and is part of the system for prolonging the duration of optimal functions of the MTD. While the antioxidants play a vital role in reducing the damage from reactive chemicals, CL has many other functions. One other is the Furan fatty acids.  

Restoration of Mitochondrial Cardiolipin Attenuates Cardiac Damage in Swine  Renovascular Hypertension | Journal of the American Heart Association

 

9.  Linoleic acid, is it essential?:  It is an omega 6 fatty acids with 2 double bonds at the 9-10 and 11-12 carbons.  It is the most common fat in seed oils, 75% in safflower oil, 66% in sunflower, 59% in corn oil, 54% in cottonseed oil, 51% in soybean oil, 21% canola oi, 10% in olive and palm oil[21], and 2% in butter and coconut oil.

What is the evidence for essential? and how essential?  Is this another part of the healthful UFAs and harmful saturated claims.  “The consumption of linoleic acid is vital to proper health, as it is an essential fatty acid.[15] In rats, a diet deficient in linoleate (the salt form of the acid) has been shown to cause mild skin scaling, hair loss,[16] and poor wound healing.”  [22]  This is because oleic acid is converted to omega 3, and the shortage is only created in laboratory experiments, not in the real world.    

Replacing SFAs with linoleic acid ((18:2 cis 9, 12) increases death rate from CVD.


Objective:  To evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death Results:  The intervention group (n=221) had higher rates of death than controls (n=237) (all cause 17.6%v11.8%, hazard ratio 1.62 (95%confidence interval 1.00 to 2.64), P=0.05; cardiovascular disease 17.2%v11.0%, 1.70 (1.03 to 2.80), P=0.04; coronary heart disease 16.3%v10.1%, 1.74 (1.04 to 2.92), P=0.04). Clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease[23]


I hear the linoleic acid lubricating the cash register. 




[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 the functionality were less.  Thus, we have evolution working to make build better walls 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 the 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 that deals with so, so many potential health issues!

[4] Wiki, Lipid peroxidation, May, 2020.  The article stress ROS and ignores glycation and fructation and the products of the Millard reaction, and similar reactions. 

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

[6] Wiki Rancidification May 2016.  The LOX is not mentioned in the article but developed separately under lipid peroxidation. 

[8] Wiki, lipid peroxidation¸ Aug 2019. 

[9] Wiki, Unsaturated fat, August 2020.  “The greater the degree of unsaturation in a fatty acid (i.e., the more double bonds in the fatty acid) the more vulnerable it is to lipid peroxidation (rancidity). Antioxidants can protect unsaturated fat from lipid peroxidation.” 

[10]  Whitefield, Frank, Donald Mottram Sept 2009, Volatiles from interactions of Maillard reactions and lipids—SEMINAL 

[11] Nicholas Pololuk, PhD.2016,Scourge of the AGES, Glycation and Diabetes, Cancer, Heart Disease, Alzheimer’s and Aging

[12] O’Donnell, Valerie, Jason Eiserich, et al Dec 1998, Nitration of Unsaturated Fatty Acids by Nitric Oxide-Derived Reactive Nitrogen Species Peroxynitrite, Nitrous Acid, Nitrogen Dioxide, and Nitronium Ion

[13] Winterbourn, Christine, Dec 2002, Biological reactivity and biomarkers of the neutrophil oxidant, hypochlorous acid

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

[15] 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

[16] Kidd, Parris  Cell, 1996, Membranes, endothelial, and atherosclerosis—the importance of dietary fatty acid balance  FULL, seminal, similar in content. 

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

[18] Reiter, Russel, Du-Xian Tan, et al Oct 2014, Melatonin reduces lipid peroxidation and membrane viscosity

[19] Wiki, reactive oxygen species, August 2020

[20] Wiki, cardiolipin August 2020

[21]  Also 10% in lard, whoever, lard often has cotton seed oil as unreported addition.  Congress 150 years ago legislated against this practice, but given the lack of court cases I believe it is another fake fix.  Why is linoleic 5 times that of butter and not in meats?

[22]  Wiki,  linoleic acid, Nov 2020. 

[23] [23] Ramsden, Daisy Zamora, et al, Feb, 2013, Use of dietary linoleic acid for secondary prevention of coronary heart disease and death. Increased death rate by 62%.  One reason is that PUFA produces 770 units of toxic aldehyde products, olive oil 355 units butter 205, and lard 180 units.



9.  Neurons:  Because of the reactive chemical leaked in the MTD their membranes are a target, and because of the high level of lipids in axons of neuron, they too are above the norm vulnerable to reactive chemicals:


The outer limiting membrane of cells and membranes of subcellular organelles, e.g., mitochondria, liposomes, peroxisomes, etc., are generally rich in PUFA and their protection from oxidation is essential for the optimal function and survival of the cell. In addition to lipids, cell membranes also contain proteins in varying amounts depending on the unique physiology of the membrane. Thus, the inner mitochondrial membrane, because of its high density of respiratory complex proteins, contains only 20% lipids; this is also the case with chloroplast thylakoid membranes. In contrast, the myelin sheath surrounding axons are up to 80% lipid. Due to the differences in the percentage of lipids in membranes, they are subjected to different degrees of peroxidation.[1]


A function of melatonin is protective:  “Melatonin, the main secretory product of the pineal gland, efficiently scavenges both the hydroxyl and peroxyl radicals counteracting lipid peroxidation in biological membranes. . . . These lipoperoxides can induce oxidative stress linked to membrane lysis, damage to neuronal membranes may be related to alteration of visual function.[2] That lipid oxidation is toxic entails that there are systems to rectify this issue  One of these systems is melatonin:  “Melatonin is a highly evolutionarily conserved molecule that both directly and indirectly markedly reduces the breakdown of lipids in both animals and plants, especially in vivo. . . .  Currently, what is known is that both endogenously-generated and exogenously-administered melatonin has an important role in restricting lipid rancidity and preserving optimal membrane fluidity.” [3] 


          This brings us back to other CCs for MTDD and the downstream contributions of diminished heal processes as a result of RATP and RRAP which will be covered Section 3, 4, and 6.  It is not just melatonin but general poor maintenance schedule and others system stressing the neurons.   What occurs to neuron, the types of assaults, they occur to every cell in the body, with the greatest stress placed upon those that are the most metabolically active and least replaced.  Many of the neurons are never replaced.   Most of those essential tissues types, depending on their functions and their system affording protection, are at increased risks.  The following 3 sections add details and consequences.   

   


10.   What about rancid fats?

          Like so much what is of relevant for health isn’t a concern for researchers:  I entered into “google.scholar.com “Rancid fat metabolism, and out of the first 50 articles listed, just one; it was as though I entered Greek in the search engine. What happens to for example the dicarbonyl bonding to lipids?  However, there are extensive article under dicarbonyl, lipids because over 50 years ago they were being investigated mainly as products deep frying with vegetable oils.  But I haven’t found articles on how the body handles the many different dicarbonyls once formed and bonded to proteins and lipids.  I was familiar with that issue in 1969 of them forming from heating UFAs.    

There are two area in which FFAs can be prepared for metabolism in the Krebs cycle, the outer area of the MTD and also in the ER.  The process starts for both areas with the TG converted to FFA in the cytosol or in the ER.  Next acyl-CoA attaches to the FFA. 

When transported into the mitochondria outer area, a series of reactions occur which lop off 2 carbons from the chain, and to which are attached to an acyl-CoA and carnitine.  The carnitine is essential for transport into the inner membrane area (crystae) of the MTD.  In the process of passing through the inner membrane the carnitine is removed.  In the crystae the 2-carbon chain attached to the acyl-CoA enters the Krebs cycle. 

The same series of reactions can occur in the ER resulting in 2 carbon chain attached to an acyl-CoA for transport into the MTD.  There inside the MTD carnitine attaches for transport of the acyl-CoA into the inner membrane area.  In that transport process the carnitine is removed.  The acyl-CoA with 2 carbons is metabolism in the Krebs cycle.   

The UFA can be modified by reactive chemicals.  This may occur in 4 ways:  hydrolytic, oxidative, microbial, and by an assortment of reactive chemicals that haven’t been quenched.[4]  

 

                                      Skeletal formula

  Dicarbonyl                                                Methylglyoxal

Dicarbonyl is a molecule containing two carbonyl group (C=O). “The 1,2‐dicarbonyl compounds glyoxal, methyl glyoxal and diacetyl which are known to be mutagens without metabolic activation in the Salmonella typhimurium TA100 system, were detected in autoxidised edible oils (sesame, safflower and sardine oil).” [5] “Advanced glycation end products (AGEs) are proteins or lipids that become glycated after exposure to sugars. AGEs are prevalent in the diabetic vasculature and contribute to the development of atherosclerosis.” [6] 

“During the metabolism of carbohydrates, otherwise known as glycolysis, methylgloyoxal (MG) is formed.  MG is a major precursor to the formation of AGEs. . . . MG is more reactive than glucose, fructose, and even the highly reacative ribose in creating AGEs.[7]  Given what has gone before it isn’t just proteins, but also UFA that are targets.  

Proteins that function of mitigate the damage of UFAs outside the membrane I haven’t found.  This  is one of the reasons given that there are several proteins which function as receptors for advanced glycation endproducts, called “RAGE”.  RAGE exists in the body in two forms: a membrane-bound form known as mRAGE, and a soluble form, known as sRAGE. mRAGE has three domains, and sRAGE has only the extracellular domain. sRAGE is either the product of alternative splicing or the product of proteolytic cleavage of mRAGE.” [8]  “Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3‐deoxyglucosone and are regarded as major precursors of AGEs. . . . These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA.[9] 

This is a continuation of the topic in 2:4, 4, 5, and 6 as caused by fructose and focused upon bonding to proteins, here it is on UFAs. The net result is that fats are a significant CC for MTDD and thus CAWD.


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.” [10]  The association with disease of rancid fats 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.” [11]  This seminal article 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. [12] 


But where science is manipulated the invisible hand of commerce, the literature focuses on rancid fats from commercial cooking.  There is cellular mechanism to limit the utilization of PUFAs and rancid PUFAs in cell membranes.  Of course, those on the western diet with their MTDD have the protective systems operating at submaximal levels.  The HSPs experience health consequences not found in the LSPs.  


The case for UFA modification being a major CC has been made.  Now on to a lighter topic the Fat Stories, how money talks loudly. 




[1] Reiter, Russel, Du-Xian Tan, et al Oct 2014, Melatonin reduces lipid peroxidation and membrane viscosity

[2] Catala, Angel, August 2010, A synopsis of the process  of lipid peroxidation since the discover of the essential fatty acids

[3] Reiter, Russel, Du-Xian Tan, et al Oct 2014, Melatonin reduces lipid peroxidation and membrane viscosity

[4] This cause for MTD and cellular damage is missed by wiki in rancidification, Sept 2020.  Missing is a statement that saturated fats are far more stable than UFAs. Nor is there a reference to glycation or sugar. 

[5] Hirayama, Teruhisa, Naohide Yamada et al Dec. 1984, The existence of the 1,2‐dicarbonyl compounds glyoxal, methyl glyoxal and diacetyl in autoxidised edible oils

[6] Lin He-An, Chi-Hao Wu, et al Jan 2016, Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression

[7] Pokoluk, Nicholas, Scourge of the AGES 2016, Chapter 4 (no page numbers in this book).   

[8] Wiki, RAGE (receptor), August 2020.  The article go one to list eleven ligands found to bind RAGE. 

[9] Lin He-An, Chi-Hao Wu, et al Jan 2016, Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression

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

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

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



9.  Linoleic acid, is it essential?:  It is an omega 6 fatty acids with 2 double bonds at the 9-10 and 11-12 carbons.  It is the most common fat in seed oils, 75% in safflower oil, 66% in sunflower, 59% in corn oil, 54% in cottonseed oil, 51% in soybean oil, 21% canola oi, 10% in olive and palm oil[1], and 2% in butter and coconut oil.

What is the evidence for essential? and how essential?  Is this another part of the healthful UFAs and harmful saturated claims.  “The consumption of linoleic acid is vital to proper health, as it is an essential fatty acid.[15] In rats, a diet deficient in linoleate (the salt form of the acid) has been shown to cause mild skin scaling, hair loss,[16] and poor wound healing.”  [2]  This is because oleic acid is converted to omega 3, and the shortage is only created in laboratory experiments, not in the real world.    

Replacing SFAs with linoleic acid ((18:2 cis 9, 12) increases death rate from CVD.


Objective:  To evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death Results:  The intervention group (n=221) had higher rates of death than controls (n=237) (all cause 17.6%v11.8%, hazard ratio 1.62 (95%confidence interval 1.00 to 2.64), P=0.05; cardiovascular disease 17.2%v11.0%, 1.70 (1.03 to 2.80), P=0.04; coronary heart disease 16.3%v10.1%, 1.74 (1.04 to 2.92), P=0.04). Clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease[3]


I hear the linoleic acid lubricating the cash register. 

 

  10.  Health consequences of rancid fats:  The experimental literature on rats as to health consequences is thin.[4]  Rats fed rancid oil 15 to 20%, they all died within 3 weeks  Found was diarrhea, “the occurrence of large livers, kidneys, and adrenals, and small spleens and thymuses.” [5]  The long list of products formed by aerated heating to create rancid fats includes reactive aldehydes and the polymerization of fats.

 

11  Oxidized cholesterol and lipoproteins as the cause for atheromas?  The autopsy Chemical structure of cholesterol

evidence for bacteria in the intima media causing atheroma goes back over 100 years[6]  Most telling is that fats and cholesterol amount to between 7 and 22% of the contents of an atheroma.  The 1974 summation article on atherosclerosis confirmed the content of fat and cholesterol as being minor.  These are prima facia reasons, along with the failure of statins and other cholesterol lowering drugs to reduce ischemic events (subtract FRUB).  The B5 and S5 explain ischemic events through the diminished functioning of the immune system and autophagy and the down-stream other major CCs in Section 4.  Why aren’t the LSPs having their cholesterol and lipoproteins oxidized?  Or could it be that the oxidized theory is wrong?  The quality Framingham Study of over 50 years found that , those with the highest 20% of cholesterol live the longest. 

Oxysterol are enzyme directed derivatives of cholesterol which “play important roles in various biological processes such as cholesterol homeostasis, lipid metabolism, apoptosis, autophagy and prenylation of proteins.” [7]

  

Chemical structure of cholesterol

Cholesterol


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.[8]


This article indicates that the fireman has a function.  Oxysterols have a long history, and evolution has developed receptors for their functions.[9]  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? 

Other 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.[10]


This function of LDL ties in well with the finding of bacteria in atheroma, which first made the literature over 100 years ago based on autopsy studies of ruptured plaque (autopsy study).  This function of LDL explains in part why endothelial cells actively transport through their receptor’s 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, and it isn’t for the LSPs.  Nature didn’t make human milk the highest in cholesterol to harm the next generation, but because of its essential functions in the nervous system.  The very complexity and many functions support the proposition of survival importance.  Each cell is capable of synthesize cholesterol in a complex 57 step process.  Complexity supports (consumption of ATP) its value.  About 75% of total cholesterol is made in the liver for transport as needed.  Cholesterol is highly conserved because of the energy consumption in converting acetyl CoA to cholesterol.  A 150 lb. human synthesizes 1 gram a day mostly in the liver at night;[11] and about 0.25 grams come from dietary sources.[12]  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, why LSP don’t have oxidation of cholesterol and its deposits in artery walls.  Marketing has no conscience or concern for its victims. 


          I suspect that the oxidized theory is an attempt to deflect the fact that the level of serum cholesterol is NOT associated with atherosclerosis but for by FRUB (See Uffe Ravnskov, Atherosclerosis caused by high cholesterol? at http://healthfully.org/rl/id5.html).  Since there is no convenient lab test for oxidized sterols,[13] 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,s and Calpo’s[14] are the best I have read on the lipid myth, see appendix.   

          Again, we have an example of industry Harpies snatching medical science from the table and depositing crapolla.  I have saved the scape-goat, trans-fats for the next chapter (2:7).  A scape-goat for UFAs, and the US regulation is Swiss cheese.  The sum total of the prima facie evidence entails that I move on to neuron. 

 

12.  Neurons: 

 

Most neurons are very long lived and some are very long.[15].  Because of the reactive chemical leaked in the MTD, cell membranes are a target, and because of the high level of lipids in axons of neuron, they are above the norm vulnerable to reactive chemicals:


The outer limiting membrane of cells and membranes of subcellular organelles, e.g., mitochondria, liposomes, peroxisomes, etc., are generally rich in PUFA and their protection from oxidation is essential for the optimal function and survival of the cell. In addition to lipids, cell membranes also contain proteins in varying amounts depending on the unique physiology of the membrane. Thus, the inner mitochondrial membrane, because of its high density of respiratory complex proteins, contains only 20% lipids; this is also the case with chloroplast thylakoid membranes. In contrast, the myelin sheath surrounding axons are up to 80% lipid. Due to the differences in the percentage of lipids in membranes, they are subjected to different degrees of peroxidation.[16]


A function of melatonin is protective:  Melatonin, the main secretory product of the pineal gland, efficiently scavenges both the hydroxyl and peroxyl radicals counteracting lipid peroxidation in biological membranes... These lipoperoxides [UFAs oxides] can induce oxidative stress linked to membrane lysis, damage to neuronal membranes may be related to alteration of visual function.[17] That lipid oxidation is toxic entails that there are systems to rectify this issue.  One of these systems is melatonin:  


Melatonin is a highly evolutionarily conserved molecule that both directly and indirectly markedly reduces the breakdown of lipids in both animals and plants, especially in vivo. . . .  Currently, what is known is that both endogenously-generated and exogenously administered melatonin has an important role in restricting lipid rancidity and preserving optimal membrane fluidity.” [18]    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. As with any radical reaction, the reaction consists of three major steps: initiation, propagation, and termination. The chemical products of this oxidation are known as lipid peroxides or lipid oxidation products (LOPs).[19]


With age its level declines.  One more way nature culls the elderly from the village.  I take the melatonin, 12 mgs daily, slow release, because half life is 20 to 50 minutes.   


          This brings us back to other CCs for MTDD and the downstream contributions of diminished heal processes as a result of RATP and RRAP which will be covered Section 3, chapters 4, and 6.  It is not just less melatonin but general poor maintenance schedule and others system stressing the neurons.  What occurs to neuron, the types of assaults, they occur to every cell in the body, with the greatest stress placed upon those that are the most metabolically active and least replaced.  Most of the neurons are never replaced.   Fructation and rancidification are the major CCs for CAWD.      

 


13.   About the rancid compounds:

           

There are two area in which FFAs can be prepared for metabolism in the Krebs cycle, the cytosol and mostly in its ER regions.  Next acyl-CoA attaches to the FFA.  However, with rancid fats they don’t enter either reaction, they aren’t metabolized.  For example, cottonseed oil made rancid by heating to 225 degrees centigrade produces “nonurea adduct-forming monomers and dimers were formed which were toxic to rats.  Analyses showed that the toxic fractions contained moderate amounts of carbonyl and hydroxyl and that they contained unsaturation difficult to remove by hydrogenation. Cyclic structures appeared to be present in the dimer fraction. The production of nonurea adducting monomers and dimers is associated with polymerization and other reactions of linoleic acid.”[20]  Diminished weight of spleen, and increased of the kidneys, liver, and thymus have been observed.[21] 

When fats are transported into the mitochondria outer area, a series of reactions occur which lop off 2 carbons from the chain, and to which are attached to an acyl-CoA and carnitine.  The carnitine is essential for transport into the inner membrane area (cristae) of the MTD.  In the process of passing through the inner membrane the carnitine is removed.  In the cristae of the MTD, the 2-carbon chain attached to the acyl-CoA enters the Krebs cycle. 

The same series of reactions can occur in the ER resulting in 2 carbon chain attached to an acyl-CoA for transport into the MTD.  There inside the MTD carnitine attaches for transport into the inner membrane area.  In that transport process the carnitine is removed.  The acyl-CoA with 2 carbons is metabolism in the Krebs cycle.  

The UFA can be modified by reactive chemicals (ROS).  This may occur in 4 ways:  hydrolytic, oxidative, microbial, and by an assortment of reactive chemicals that haven’t been quenched.[22] 

 

                                      Skeletal formula

  Dicarbonyl                                                Methylglyoxal

Dicarbonyl is a molecule containing two carbonyl group (C=O). “The 1,2dicarbonyl compounds glyoxal, methyl glyoxal and diacetyl which are known to be mutagens without metabolic activation in the Salmonella typhimurium TA100 system, were detected in auto-oxidised edible oils (sesame, safflower and sardine oil).” [23] “Advanced glycation end products (AGEs) are proteins or lipids that become glycated after exposure to sugars. AGEs are prevalent in the diabetic vasculature and contribute to the development of atherosclerosis.” [24] 

“During the metabolism of carbohydrates, otherwise known as glycolysis, methylyglyoxal (MG) is formed.  MG is a major precursor to the formation of AGEs.... MG is more reactive than glucose, fructose, and even the highly reactive ribose in creating AGEs.” [25]  Given what has gone before it isn’t just proteins, but also UFA that are targets.   

There are several proteins which function as receptors for advanced glycation endproducts, called “RAGE”.  RAGE exists in the body in two forms: a membrane-bound form known as mRAGE, and a soluble form, known as sRAGE.  mRAGE has three domains, and sRAGE has only the extracellular domain. sRAGE is either the product of alternative splicing or the product of proteolytic cleavage of mRAGE.” [26]  “Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3deoxyglucosone and are regarded as major precursors of AGEs.... These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA.[27]   The net result is that UFAs are a significant CC for MTDD and thus CAWD.


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.” [28]  The association with disease of rancid fats 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.” [29] 


This seminal article 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. [30] 


         The HSPs experience health consequences not found in the LSPs to which UFAs are a significant CC.  The case for UFA modification being a major CC for CAWD has been made.  The concern demonstrated through the number of journal article from the 50s through to the 70s; but we live in a much worse world when measured by our health (1:1).  Now on to a lighter topic the Fat Stories, how money talks loudly. 




[1]  Also 10% in lard, whoever, lard often has cotton seed oil as unreported addition.  Congress 150 years ago legislated against this practice, but given the lack of court cases I believe it is another fake fix.  Why is linoleic 5 times that of butter and not in meats?

[2]  Wiki,  linoleic acid, Nov 2020. 

[3] [3] Ramsden, Daisy Zamora, et al, Feb, 2013, Use of dietary linoleic acid for secondary prevention of coronary heart disease and death. Increased death rate by 62%.  One reason is that PUFA produces 770 units of toxic aldehyde products, olive oil 355 units butter 205, and lard 180 units.

[4]  Human studies except for paleo peoples would be population studies.  The list of contravening variables is long along with the uncertainty of self-reporting over decades.  

[5]  Kunitz, Hans, Charles Slanetz, et al, April 1955, Antagonism of Fresh Fat to the Toxicity of Heated and Aerated Cottonseed Oil: Two Figures  “The inclusion in a rat diet of 15 to 20% of refined cottonseed oil, aerated and heated to 95°C. for 200 to 300 hours, led to rapid loss of weight and death within three weeks.”

[7] Wiki, oxyxterol, Oct 2020   “An oxysterol is a derivative of cholesterol obtained by oxidation involving enzymes and / or pro-oxidants. Such compounds play important roles in various biological processes such as cholesterol homeostasis, lipid metabolism (sphingolipids, fatty acids), apoptosis, autophagy, and prenylation of proteins.”

[8] Bjorkhem, Ingemar, U Dicfalusy, Feb 2003 (cited 347 times Sept 2019), Oxysterols:  Friends, Foes, or Just Fellow Passengers?

[9] 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.

[10] 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 thincs.org, the International Network of Cholesterol Skeptics

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

[12] So why the hell are they given drugs during the day when its production is at night?  Do you hear the cash register?  

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

[14] 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, angioplasty. & bypass operations are based on a wrong belief of atheroma.  They are treating old stable plaque, while the young plaque (20% occlusion) leaks to cause ischemic events.   Human brain has 10-20 billion neuons in the cerebral cortex, and 55 to 70 billion neurons in the cerebellum, and several times as many of the dozens of types of support cells (not signalling). 

[15] An axon that runs from the toe to the posterior column of the spinal cord averages over 1.5 meters in adults and is not replaced.  Stems cells can turn astocvtes (a type of glial cell) into pluripotent cell as needed for growth and repair.  What can be replaced is limited.  A neuron cannot be functionally replaced by one of another type (Llinas law, neuron usage doesn’t drive differentiation).  Peripheral axons can regrow if they are severed and dendrites form and whither govern by need. 

[16] Reiter, Russel, Du-Xian Tan, et al Oct 2014, Melatonin reduces lipid peroxidation and membrane viscosity

[17] Catala, Angel, August 2010, A synopsis of the process  of lipid peroxidation since the discover of the essential fatty acids.  Melatonin is an inexpensive supplement with 86% bioavailability.  The Wikipedia article misses this function, among others and contains the usual KOL’s warnings and claims of ineffectiveness.  If only they used the principle of consistence in their evaluation of drugs and applied medical science to CME classes and textbooks, we would live longer and better (4:5)

[18] Reiter, Russel, Du-Xian Tan, et al Oct 2014, Melatonin reduces lipid peroxidation and membrane viscosity

[19] Wiki [Lipid peroxidation], Oct 2020.  Again, I point out that the term lipid is among the worst of terms, in that it also means cholesterol.  Need I go into how pharma promotes confusion and errors on an industrial scale?

[20] Firestone, David, William Horwitz, et al, May 1961,  Heated fats. I. Studies of the effects of heating on the chemical nature of cottonseed oil

[22] This cause for MTD and cellular damage is missed by wiki in rancidification, Sept 2020.  Missing also is a statement that saturated fats are far more stable than UFAs. Nor is there a reference to glycation to UFAs or sugar. 

[23] Hirayama, Teruhisa, Naohide Yamada et al Dec. 1984, The existence of the 1,2‐dicarbonyl compounds glyoxal, methyl glyoxal and diacetyl in auto-oxidised edible oils

[24] Lin He-An, Chi-Hao Wu, et al Jan 2016, Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression

[25] Pokoluk, Nicholas, Scourge of the AGES 2016, Chapter 4 (no page numbers in this book).   

[26] Wiki, RAGE (receptor), August 2020.  The article go one to list eleven ligands found to bind RAGE. 

[27] Lin He-An, Chi-Hao Wu, et al Jan 2016, Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression

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

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

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


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. 

 Most plants use toxic chemicals a defense to promote survival.  They don't have a dinner sign, Eat Here! The exception are some fruits which use animals and insects to spread the seed. 

An example of toxic chemicals is the family of lectins. Cooking and fermentation are two ways humans get around toxicity. Another is eating moderate amount of one type of plant, A steady diet of Rhubarb would prove deadly, as it does to rabbits and insects.  

A common toxin is the family of lectins, found in beans and other plants:



Lectins are carbohydrate-binding proteins that are highly specific for sugar groups of other molecules and so cause agglutination of particular cells or precipitation of glycoconjugates and polysaccharides. Lectins have a role in recognition on the cellular and molecular level and play numerous roles in biological recognition phenomena involving cells, carbohydrates, and proteins.[1][2] Lectins also mediate attachment and binding of bacteria, viruses, and fungi to their intended targets.


Lectins are ubiquitous in nature and are found in many foods. Some foods, such as beans and grains, need to be cooked or fermented to reduce lectin content. Some lectins are beneficial, such as CLEC11A, which promotes bone growth, while others may be powerful toxins such as ricin.[3]


Toxicity


Lectins are one of many toxic constituents of many raw plants, which are inactivated by proper processing and preparation (e.g., cooking with heat, fermentation).[24] For example, raw kidney beans naturally contain toxic levels of lectin (e.g. phytohaemagglutinin). Adverse effects may include nutritional deficiencies, and immune (allergic) reactions.[25]


Hemagglutination


Lectins are considered a major family of protein antinutrients, which are specific sugar-binding proteins exhibiting reversible carbohydrate-binding activities.[26] Lectins are similar to antibodies in their ability to agglutinate red blood cells.[27]


Many legume seeds have been proven to contain high lectin activity, termed hemagglutination.[28] Soybean is the most important grain legume crop in this category. Its seeds contain high activity of soybean lectins (soybean agglutinin or SBA).


https://en.wikipedia.org/wiki/Lectin#Animals

Soybeans make a number of toxic chemicals including estrogen/testosterone mimic.  If a compound occupies the receptors for estradiol, it like has some affinity of testosterone receptors, often with the result of blocking some of their vital functions.  

I avoid soy products.    I own and read The Whole Soy Story:  the dark side of America's favorite health food, by Kaayla T. Daniel, 2007


Enter supporting content here

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 the cause than insulin resistance, type-2 diabetes, and weight gain, all of which are caused by mitochondrial dysfunction, which starts first in the liver.