Small Write-Up on Mead Acid - An Interesting but Understudied Fatty Acid

[Deleted member 3990]

"Synthesis of Mead acid
In animals, it can be produced de novo from oleic acid (18:2n-6).
The enzymes that catalyze the conversion of oleic acid (18:1n-9), linoleic acid (18:2n-6) and alpha-linolenic acid (18:2n-3) to the C20 n-9, omega-6 polyunsaturated fatty acids and omega-3 polyunsaturated fatty acids are the same but omega-6 and omega-3 families have greater affinity for them than does the omega-9; from a biochemical point of view this is competitive inhibition.
In essential fatty acid deficiency competitive inhibition is lack and enzymes will desaturate oleic acid to 18:2n-9 (Δ6 desaturase), which is further elongated and Δ5 desaturated to form Mead acid."

In contrast to n-3 and n-6 fatty acids, the role of n-9 fatty acids in breast cancer has not been studied in detail. One study showed that <15% of breast cancers could be prevented if the populations of high-income countries shifted to the traditional Mediterranean diet. The Mediterranean diet contains high amounts of olive oil rich in n-9 oleic acid (OA), and the possible effect of OA in suppressing breast cancer has received attention. However, another study was inconclusive in showing that olive oil consumption lowers the breast cancer risk. In cell culture, although OA causes growth inhibition at higher concentrations, it produces growth acceleration of human breast cancer cells at lower concentrations. Thus, the effects of OA on breast cancer appear to be complex. Mead acid (MA) is an n-9 fatty acid produced from OA when essential n-3 and n-6 fatty acids are deficient; mammals elongate and desaturate OA to make the end product MA. Epidemiologically, MA was inversely associated with breast cancer risk as well as overall cancer risk. Experimentally, MA suppressed MCF-7 and KPL-1 human breast cancer cell growth in culture. MCF-7 and KPL-1 are luminal A subtypes according to intrinsic subtype classification. MA also suppressed the growth and metastasis of KPL-1 cells transplanted in female athymic mice.

According to in vivo and in vitro studies using breast cancer cell lines, MA suppressed the promotion/progression phase of carcinogenesis; however, the role of MA in the initiation phase remains to be elucidated.

N-methyl-N-nitrosourea (MNU)-induced mammary cancers in Mead Acid (MA) Group and the Control (CTR) Group

MA dose-dependently inhibits vascular endothelial growth factor (VEGF)-stimulated angiogenesis. The VEGF pathway may act indirectly via endothelial cells and may be involved in tumor angiogenesis; or the VEGF pathway may act directly via the VEGF receptor in cancer cells and participate in the growth modification of breast cancer cells. The VEGF-VEGFR interaction on cancer cells may partially explain the actions of MA in modifying cancer cell growth.

Addition of 20:3n-9 and n-3 eicosatrienoic acid (20:3n-3) dose dependently inhibited VEGF-A-stimulated angiogenesis (more than the positive control suramin). Arachidonic, eicosapentaenoic, dihomo-γ-linolenic (20:3n-6) and oleic acids did not affect VEGF-A-stimulated angiogenesis even at 10 μmol/L. Arachidonic and dihomo-γ-linolenic acids enhanced angiogenesis without VEGF-A.
We suggest that the presence of 20:3n-9 in cartilage may be related to its vessel-free status and that 20:3n-9 may be useful for the treatment of disorders with excessive vasculature.

5,8,11‐Eicosatrienoic acid (20∶3ω9), a fatty acid increased in the platelet phospholipids of man and animals fed saturated fats, was either added to human platelets simultaneously with the aggregating agents, or incorporated into the platelet phospholipids by preincubation. 20∶3ω9 markedly increased the response of platelets to all aggregating agents tested when added simultaneously with the agent, but solely to thrombin and ionophore, after incorporation into the platelet phospholipids. The potentiating effects of 20∶3ω9 on thrombin aggregation do not appear to be related to prostaglandin formation, but rather to the production of a monohydroxy derivative through the lipoxygenase pathway.

Osteoclastic activity was not affected either by 20:3n-9 or by oleic acid. In the case with the cell line, osteoblastic activity was again significantly decreased with 20:3n-9 (10–30 μM) after 6-h incubation but not after 18 h incubation. The presence of 20:3n-9 in fetal cartilage may be important for the prevention of calcification in the cartilage. 20:3n-9 could be applied to some clinical situations where bone formation should be inhibited.

Thus, by changing its substrate specificity in an EFA-deficient state, Elovl5 is able to regulate the synthesis of Mead acid to maintain levels of long-chain PUFAs.

Detailed mechanistic studies unveiled that mead acid inhibited the directional migration of neutrophils by inhibiting the filamentous actin polymerization and leukotriene B4 production required for secondary recruitment of neutrophils. Our findings provide valuable insights into the preventive roles of coconut oil and mead acid against skin inflammation, thereby offering attractive therapeutic possibilities.

(Downstreams of Mead Acid)
We conclude that optimal activation of the OXE receptor is achieved with 5-oxo-ETE, 5-oxo-18:2, and 5-oxo-20:3, and that the latter compound could potentially be formed under conditions of essential fatty acid deficiency.
OXER1 is responsible for steroid production response to 5-oxo-ETE by human steroidogenic cells in vitro and therefore could be involved in steroid production in humans. (but also allergies)

(lymph node part is fairly interesting; something to investigate on)

Tumor angiogenesis is closely related to the growth of breast cancer, and VEGF and its receptors are essential for breast cancer growth. Cartilage is an avascular tissue and contains high levels of MA; MA dose-dependently inhibits VEGF-stimulated angiogenesis. However, MA did not alter angiogenesis as evaluated by microvessel density in KPL-1 tumors in athymic female mice. Although VEGF is well known for its key roles in blood vessel growth, it also promotes a range of other functions, such as cell adhesion, survival, migration and invasion. VEGF, VEGFR1 and VEGFR2 were immunohistochemically detected in KPL-1 cells. The presence of VEGFR1 and VEGFR2 as well as VEGF on KPL-1 cells may raise the possibility that VEGF may promote tumor growth not only by inducing angiogenesis but directly through the activation of VEGFR1 and VEGFR2.

The effect of the addition of hydrogenated coconut oil to the otherwise fat-free diets of rats has resulted in the depletion of essential fatty acids in a shorter time interval and at a lower animal weight than when the rats were fed a fat-free diet alone. However, the continued presence of hydrogenated coconut oil in the diet had no apparent inhibitory effect on the subsequent response of the animal to linoleate although the animals depleted with hydrogenated coco nut oil in the diet had a greater growth potential than the animals depleted on the fat-free diet.
In rats receiving diets deficient in essential fatty acids, there was an increased cholesterol concentration in the liver and a decreased cholesterol content in the plasma after one week. However, although the condition was further aggravated thereafter in the animals on the fat-free diets, cholesterol levels of the rats receiving hydrogenated coconut oil in the diets gradually returned to normal. This effect may be due to the availability of short-chain fatty acids contained in the hydrogenated fat for esterification of cholesterol.

the Mead fats are important factors in the stability of our mammalian tissues. This protective lipid system probably interacts with cellular proteins, modifying the way they bind water and carbon dioxide and ions, affecting their electrons and their chemical reactivity.

Concentrations of MA have long been known to be high in the cartilage of chicken and human infants, even without EFA deficiency. Based on these facts, we postulated that MA prevents the calcification of cartilage.
Cartilage contains no blood vessels, a condition that likely leads to local EFA deficiency and the synthesis of MA. Why is cartilage an avascular tissue? Is the avascular state supported by MA? If MA inhibits angiogenesis in cartilage, this fatty acid might support its own synthesis in avascular tissues, namely, MA→avascularity→EFA deficiency→MA synthesis. To examine this possibility, angiogenesis was measured in a coculture system consisting of human umbilical vein endothelial cells and diploid fibroblasts with exogenously added vascular endothelial growth factor-A (VEGF-A, 10 ng/mL) and fatty acids (0.1–10 μmol/L). Vessel areas were calculated using image analysis software. Treatment with MA was found to dose-dependently inhibit VEGF-A-stimulated angiogenesis after 10 days of incubation. We speculate that the presence of MA in cartilage is related to its vessel-free status, which is associated with local EFA deficiency that in turn leads to the stimulation of MA synthesis. The presence of MA in cartilage may also be important for the prevention of calcification. These mechanisms may also occur in other avascular tissues, such as the cornea and lens.

"Intermediate in potency is the Mead acid (20∶3ω−9) product, having roughly ten times less the chemoattractant potency on neutrophils. You might assume that this would be called leukotriene B₃.

The lipoxygenase product of Mead acid had been presumed before it's been found in vivo due to the mythological nature of the beast. Since the de novo formation of Mead acid—an elongation product of oleic acid—requires the near-complete avoidance of all ω−6 fatty acids, Mead acid is generally not found in modern humans; nor is this found in lab animals fed the standard diet, and hence neither is its cycloxygenase product or the leukotriene derived from it. For this reason, the chemical structure of leukotriene B₃ was extrapolated from those of leukotrienes B₃ and B₅. This leukotriene has been synthesized, is an available research chemical, and has been used in white blood cell migration assays—among other assay types—where it gives comparable potency as our maligned leukotriene B₄ ultimately derived from linoleic acid.

In the early 1980s, the presumed Mead acid derivative leukotriene B₃ was found to be a unicorn. The structure extrapolated from the other, more common B-series leukotrienes contains one trans double bond; although this molecule is actually made my Mead acid through lipoxygenase, this is a relatively minor isomer. The actual main products of Mead acid + lipoxygenase are two enantiomers both having three cis double bonds having the IUPAC designations of 5S,12R-dihydroxy-6Z,8Z,10Z-eicosatrienoic acid and 5S,12S-dihydroxy-6Z,8Z,10Z-eicosatrienoic acid. I use the term all-cis-leukotriene B₃ to differentiate it from is unphysiological presumption, which goes by the names of: trans-leukotriene B₃, unicorn-leukotriene B₃, or simply leukotriene B₃ (it's too established). All-cis-leukotriene B₃ has approximately ten times less chemoattractant ability as leukotriene B₄, meaning that you'd expect all leukocytes to be inclined to home-in on the arachidonic acid product anywhere from 10 to 10³ times more than our natural eicosapentaenoic and Mead acid products—these being leukotriene B₅ all-cis-leukotriene B₃."-@Travis

“The enzyme that produces the Mead fatty acid is strongly inhibited by PUFA seed oils (less strongly by fish oils), and so the presence of the Mead acid in the tissues is taken as evidence that the animal is suffering damage resulting from the absence of PUFA. The Mead acid happens to have some valuable anti-inflammatory effects, and is associated with many biological advantages, but research in that direction is prevented by the lack of funding.” -R. Peat

My Thoughts:
In my opinion many people would do better to minder their PUFA excess. There are some people who seem to get barely any inflammatory response from eating them but I am unfortunately not one of them.
It is near impossible to eat a EFA free diet without starving yourself or meeting your (increased) nutritional needs.
For looksmaxxers I think the most interesting implication is the fact that Mead Acid in cartilage prevents its ossification which might be very useful for heightmaxxing (if you manage to utilize the MA). But during my research I also found so many other studies hinting that many people would trouble in an EFA-deficient state (dry skin, body cant keep up with the nutritional needs due to the increased metabolic rate and so forth). It would be a big fallacy to just go at it and avoid PUFA in an extreme manner without even knowing the state of your body and its needs. An important step would be to pinpoint what exactely changes in such a state so that we can counteract possible downsides.

I think for people who likely endured physical pains due to the Inflammation of PUFAs and their Prostaglandins (i.e. PGD2), likely people who are fat/skinny fat and prematurely aged and maybe Asthma aswell, a threshold of PUFA of about 4g might be appropiate for a start but it should not be your main criteria when you try to search your ideal diet.
It would be smart to increase cAMP activity to maybe deal with the fats (oleic acid, caffeine) and maybe other things which help proper fat metabolism (Biotin, B3 etc.).
At 2g PUFAs, after some while, you can actually see increased Mead Acid production (look at the pictures).

The old Tokelau and Kitavan people seem to had had a low PUFA diet alltogether and now, their modernised peers, are one of the greatest sufferers of Asthma and Obesity after introduction of Western Lifestyle

Spoiler: Sources and References

Sorry for not referencing the studies to their respective quotes above. But it is in chronological order here:

Mead acid - Tuscany Diet

Chemical structure, properties, synthesis, and metabolism of Mead acid, an omega-9 fatty acids. Essential fatty acid deficiency.

www.tuscany-diet.net

Dietary effects of mead acid on N-methyl-N-nitrosourea-induced mammary cancers in female Sprague-Dawley rats

The effect of mead acid (MA; 5,8,11-eicosatrienoic acid) on the suppression of the development and growth of N-methyl-N-nitrosourea (MNU)-induced mammary cancer in female Sprague-Dawley rats was examined. The MA diet (2.4% MA) or control (CTR) diet (0% ...

www.ncbi.nlm.nih.gov

Inhibitory effect of 5,8,11-eicosatrienoic acid on angiogenesis

Cartilage contains high levels of n-9 eicosatrienoic acid (20:3n-9) but no blood vessels. 20:3n-9 might inhibit angiogenesis.Angiogenesis was measured…

www.sciencedirect.com

Sci-Hub | The Significance of cis, cis, cis 5,8,11 Eicosatrienoic Acid in Essential Fatty Acid Deficiency. Nutrition Reviews, 38(7), 233–235 | 10.1111/j.1753-4887.1980.tb05910.x

JCI - The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally.

www.jci.org

Error - Cookies Turned Off

aocs.onlinelibrary.wiley.com

The Depressive Effects of 5,8,11-Eicosatrienoic Acid (20:3n-9) on Osteoblasts - Lipids

In cases of essential fatty acid deficiency, 5,8,11-eicosatrienoic acid (Mead acid, 20:3n-9) is synthesized from oleic acid as a 20-carbon analog of arachidonic acid. It was reported that 20:3n-9 levels were markedly higher in human fetal cartilage than in the muscle, liver and spleen. We...

link.springer.com

Phosphorylation of Elovl5 changes its substrate preference to synthesize Mead acid in response to essential fatty acid deficiency

Polyunsaturated fatty acids (PUFAs) of the n-6 and n-3 series cannot be synthesized in mammals and therefore are called essential fatty acids (EFAs). Mead acid (20:3n-9) is an unusual n-9 PUFA, endogenously synthesized from oleic acid (18:1n-9) in an EFA-deficient state. Although Elovl5, a fatty...

www.biorxiv.org

Error - Cookies Turned Off

onlinelibrary.wiley.com

Structural Requirements for Activation of the 5-Oxo-6E,8Z, 11Z,14Z-eicosatetraenoic Acid (5-Oxo-ETE) Receptor: Identification of a Mead Acid Metabolite with Potent Agonist Activity

The 5-lipoxygenase product 5-oxo-6 E ,8 Z ,11 Z ,14 Z -eicosatetraenoic acid (5-oxo-ETE) is a potent chemoattractant for neutrophils and eosinophils, and its actions are mediated by the oxoeicosanoid (OXE) receptor, a member of the G protein-coupled receptor family. To define the requirements...

jpet.aspetjournals.org

Mead acid inhibits the growth of KPL-1 human breast cancer cells in vitro and in vivo

The effects of mead acid (MA; 5,8,11-eicosatrienoic acid) on the suppression of breast cancer cell growth and metastasis were examined in vitro and in vivo by using the KPL-1 human breast cancer cell line. MA suppressed KPL-1 cell growth in culture with an IC50 value of 214.2 µM (65.7 µg/ml) for...

www.spandidos-publications.com

Effect of Fat Level of the Diet on General Nutrition: XIV. Further Studies of the Effect of Hydrogenated Coconut Oil on Essential Fatty Acid Deficiency in the Rat: Two Figures

Summary. The effect of the addition of hydrogenated coconut oil to the otherwise fat-free diets of rats has resulted in the depletion of essential fatty acids i

academic.oup.com

Sci-Hub: article not found

 

[Deleted member 10449]

one word

too high iq for me ngl

 

[Eezz]

Utility: 0

 

[Deleted member 3990]

Utility: 0

0

 

[Ocelot]

I've seen worse BotB threads, this effort passes.

 

[Deleted member 3990]

At 2g PUFAs, after some while, you can actually see increased Mead Acid production (look at the pictures).

I think eating Omega 3 is much more forgiving than for example omega 6. You can probably eat 4g of n3 and still produce mead acid/become "EFA deficient".
This might be a good consideration for people who suffer highly inflammatory reactions

 

[xefo]

b u m p

 

[zxz]

"Synthesis of Mead acid
In animals, it can be produced de novo from oleic acid (18:2n-6).
The enzymes that catalyze the conversion of oleic acid (18:1n-9), linoleic acid (18:2n-6) and alpha-linolenic acid (18:2n-3) to the C20 n-9, omega-6 polyunsaturated fatty acids and omega-3 polyunsaturated fatty acids are the same but omega-6 and omega-3 families have greater affinity for them than does the omega-9; from a biochemical point of view this is competitive inhibition.
In essential fatty acid deficiency competitive inhibition is lack and enzymes will desaturate oleic acid to 18:2n-9 (Δ6 desaturase), which is further elongated and Δ5 desaturated to form Mead acid."

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View attachment 884653
N-methyl-N-nitrosourea (MNU)-induced mammary cancers in Mead Acid (MA) Group and the Control (CTR) Group




View attachment 884730






View attachment 884790
View attachment 884791
View attachment 884795
(lymph node part is fairly interesting; something to investigate on)
View attachment 884800

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"Intermediate in potency is the Mead acid (20∶3ω−9) product, having roughly ten times less the chemoattractant potency on neutrophils. You might assume that this would be called leukotriene B₃.

The lipoxygenase product of Mead acid had been presumed before it's been found in vivo due to the mythological nature of the beast. Since the de novo formation of Mead acid—an elongation product of oleic acid—requires the near-complete avoidance of all ω−6 fatty acids, Mead acid is generally not found in modern humans; nor is this found in lab animals fed the standard diet, and hence neither is its cycloxygenase product or the leukotriene derived from it. For this reason, the chemical structure of leukotriene B₃ was extrapolated from those of leukotrienes B₃ and B₅. This leukotriene has been synthesized, is an available research chemical, and has been used in white blood cell migration assays—among other assay types—where it gives comparable potency as our maligned leukotriene B₄ ultimately derived from linoleic acid.

In the early 1980s, the presumed Mead acid derivative leukotriene B₃ was found to be a unicorn. The structure extrapolated from the other, more common B-series leukotrienes contains one trans double bond; although this molecule is actually made my Mead acid through lipoxygenase, this is a relatively minor isomer. The actual main products of Mead acid + lipoxygenase are two enantiomers both having three cis double bonds having the IUPAC designations of 5S,12R-dihydroxy-6Z,8Z,10Z-eicosatrienoic acid and 5S,12S-dihydroxy-6Z,8Z,10Z-eicosatrienoic acid. I use the term all-cis-leukotriene B₃ to differentiate it from is unphysiological presumption, which goes by the names of: trans-leukotriene B₃, unicorn-leukotriene B₃, or simply leukotriene B₃ (it's too established). All-cis-leukotriene B₃ has approximately ten times less chemoattractant ability as leukotriene B₄, meaning that you'd expect all leukocytes to be inclined to home-in on the arachidonic acid product anywhere from 10 to 10³ times more than our natural eicosapentaenoic and Mead acid products—these being leukotriene B₅ all-cis-leukotriene B₃."-@Travis

“The enzyme that produces the Mead fatty acid is strongly inhibited by PUFA seed oils (less strongly by fish oils), and so the presence of the Mead acid in the tissues is taken as evidence that the animal is suffering damage resulting from the absence of PUFA. The Mead acid happens to have some valuable anti-inflammatory effects, and is associated with many biological advantages, but research in that direction is prevented by the lack of funding.” -R. Peat

My Thoughts:
In my opinion many people would do better to minder their PUFA excess. There are some people who seem to get barely any inflammatory response from eating them but I am unfortunately not one of them.
It is near impossible to eat a EFA free diet without starving yourself or meeting your (increased) nutritional needs.
For looksmaxxers I think the most interesting implication is the fact that Mead Acid in cartilage prevents its ossification which might be very useful for heightmaxxing (if you manage to utilize the MA). But during my research I also found so many other studies hinting that many people would trouble in an EFA-deficient state (dry skin, body cant keep up with the nutritional needs due to the increased metabolic rate and so forth). It would be a big fallacy to just go at it and avoid PUFA in an extreme manner without even knowing the state of your body and its needs. An important step would be to pinpoint what exactely changes in such a state so that we can counteract possible downsides.

I think for people who likely endured physical pains due to the Inflammation of PUFAs and their Prostaglandins (i.e. PGD2), likely people who are fat/skinny fat and prematurely aged and maybe Asthma aswell, a threshold of PUFA of about 4g might be appropiate for a start but it should not be your main criteria when you try to search your ideal diet.
It would be smart to increase cAMP activity to maybe deal with the fats (oleic acid, caffeine) and maybe other things which help proper fat metabolism (Biotin, B3 etc.).
At 2g PUFAs, after some while, you can actually see increased Mead Acid production (look at the pictures).

The old Tokelau and Kitavan people seem to had had a low PUFA diet alltogether and now, their modernised peers, are one of the greatest sufferers of Asthma and Obesity after introduction of Western Lifestyle
View attachment 885014View attachment 885016View attachment 885018

Spoiler: Sources and References

Sorry for not referencing the studies to their respective quotes above. But it is in chronological order here:

Mead acid - Tuscany Diet

Chemical structure, properties, synthesis, and metabolism of Mead acid, an omega-9 fatty acids. Essential fatty acid deficiency.

www.tuscany-diet.net

Dietary effects of mead acid on N-methyl-N-nitrosourea-induced mammary cancers in female Sprague-Dawley rats

The effect of mead acid (MA; 5,8,11-eicosatrienoic acid) on the suppression of the development and growth of N-methyl-N-nitrosourea (MNU)-induced mammary cancer in female Sprague-Dawley rats was examined. The MA diet (2.4% MA) or control (CTR) diet (0% ...

www.ncbi.nlm.nih.gov

Inhibitory effect of 5,8,11-eicosatrienoic acid on angiogenesis

Cartilage contains high levels of n-9 eicosatrienoic acid (20:3n-9) but no blood vessels. 20:3n-9 might inhibit angiogenesis.Angiogenesis was measured…

www.sciencedirect.com

Sci-Hub | The Significance of cis, cis, cis 5,8,11 Eicosatrienoic Acid in Essential Fatty Acid Deficiency. Nutrition Reviews, 38(7), 233–235 | 10.1111/j.1753-4887.1980.tb05910.x

JCI - The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally.

www.jci.org

Error - Cookies Turned Off

aocs.onlinelibrary.wiley.com

The Depressive Effects of 5,8,11-Eicosatrienoic Acid (20:3n-9) on Osteoblasts - Lipids

In cases of essential fatty acid deficiency, 5,8,11-eicosatrienoic acid (Mead acid, 20:3n-9) is synthesized from oleic acid as a 20-carbon analog of arachidonic acid. It was reported that 20:3n-9 levels were markedly higher in human fetal cartilage than in the muscle, liver and spleen. We...

link.springer.com

Phosphorylation of Elovl5 changes its substrate preference to synthesize Mead acid in response to essential fatty acid deficiency

Polyunsaturated fatty acids (PUFAs) of the n-6 and n-3 series cannot be synthesized in mammals and therefore are called essential fatty acids (EFAs). Mead acid (20:3n-9) is an unusual n-9 PUFA, endogenously synthesized from oleic acid (18:1n-9) in an EFA-deficient state. Although Elovl5, a fatty...

www.biorxiv.org

Error - Cookies Turned Off

onlinelibrary.wiley.com

Structural Requirements for Activation of the 5-Oxo-6E,8Z, 11Z,14Z-eicosatetraenoic Acid (5-Oxo-ETE) Receptor: Identification of a Mead Acid Metabolite with Potent Agonist Activity

The 5-lipoxygenase product 5-oxo-6 E ,8 Z ,11 Z ,14 Z -eicosatetraenoic acid (5-oxo-ETE) is a potent chemoattractant for neutrophils and eosinophils, and its actions are mediated by the oxoeicosanoid (OXE) receptor, a member of the G protein-coupled receptor family. To define the requirements...

jpet.aspetjournals.org

Mead acid inhibits the growth of KPL-1 human breast cancer cells in vitro and in vivo

The effects of mead acid (MA; 5,8,11-eicosatrienoic acid) on the suppression of breast cancer cell growth and metastasis were examined in vitro and in vivo by using the KPL-1 human breast cancer cell line. MA suppressed KPL-1 cell growth in culture with an IC50 value of 214.2 µM (65.7 µg/ml) for...

www.spandidos-publications.com

Effect of Fat Level of the Diet on General Nutrition: XIV. Further Studies of the Effect of Hydrogenated Coconut Oil on Essential Fatty Acid Deficiency in the Rat: Two Figures

Summary. The effect of the addition of hydrogenated coconut oil to the otherwise fat-free diets of rats has resulted in the depletion of essential fatty acids i

academic.oup.com

Sci-Hub: article not found

TL;DR please. Give example of foods to avoid or what the thing is you need to avoid. What you should do etc.
Thanks

 

[Deleted member 3990]

TL;DR please. Give example of foods to avoid or what the thing is you need to avoid. What you should do etc.
Thanks

Read "My Thoughts" if you want a tldr

 

[zxz]

View attachment 917895
Read "My Thoughts" if you want a tldr

Ok, so:
PUFA = bad
Mead Acid = good
EFA = good
???

Ok but what I don't understand is this:

and this:

Isn't vasculature a good thing btw? From what I understand is it goes down when MA increases.
What is endothelial proliferation?

 

[Deleted member 3990]

Ok, so:
PUFA = bad
Mead Acid = good
EFA = good
???

Ok but what I don't understand is this:
View attachment 921367

and this:
View attachment 921369

Isn't vasculature a good thing btw? From what I understand is it goes down when MA increases.
What is endothelial proliferation?

Most dietary Polyunsaturated Fatty Acids are called "Essential Fatty Acids" because your body can not produce them by its own.
Indeed, good vasculature is indeed good but if angiogenesis happens, that oftenly hints that something is wrong. Your body is likely building new vessels to nourish tissues likely because the other vessels can not do it properly anymore.
Angiogenesis is especially a start backwards if it happens in Cartilage where there should be no Vessels at all.
So, VEGF is likely upregulated because the already established vasculature is not enough. May be good under certain circumstances.

Your body produces more Mead Acid if there is a chronic lack of Arachidonic Acid (among other things). Mead Acid is mostly concentrated in cartilage and generally high in Newborns. The mechanism is not explained but drop of MA in a certain region is associated with increased VEGF expression and circulating 3 series Prostaglandins

 

[Deleted member 3990]

What is endothelial proliferation?

Compare it to blue and red light
blue light increases cell division and red light promotes proliferation and respiration

MA increases endothelial proliferation and likely works into opposite direction of VEGF, which is literally creating and growing the vascular endothelium (vasculature etc.)

 

[zxz]

Most dietary Polyunsaturated Fatty Acids are called "Essential Fatty Acids" because your body can not produce them by its own.
Indeed, good vasculature is indeed good but if angiogenesis happens, that oftenly hints that something is wrong. Your body is likely building new vessels to nourish tissues likely because the other vessels can not do it properly anymore.
Angiogenesis is especially a start backwards if it happens in Cartilage where there should be no Vessels at all.
So, VEGF is likely upregulated because the already established vasculature is not enough. May be good under certain circumstances.

Your body produces more Mead Acid if there is a chronic lack of Arachidonic Acid (among other things). Mead Acid is mostly concentrated in cartilage and generally high in Newborns. The mechanism is not explained but drop of MA in a certain region is associated with increased VEGF expression and circulating 3 series Prostaglandins

Compare it to blue and red light
blue light increases cell division and red light promotes proliferation and respiration

MA increases endothelial proliferation and likely works into opposite direction of VEGF, which is literally creating and growing the vascular endothelium (vasculature etc.)

Thanks, the question now is: what would a diet look like according to the things you stated? A diet which will promote a lot of mead acid and VEGF? Give food examples and give foods/things you should avoid.

 

[Deleted member 6892]

PUFA is in nearly in all of the modern food though
Eggs, Chicken, Beef
what would an ideal nutritionally satisfactory diet with low PUFA look like

 

[Deleted member 3990]

PUFA is in nearly in all of the modern food though
Eggs, Chicken, Beef
what would an ideal nutritionally satisfactory diet with low PUFA look like

The organizing power of energy flow is hypothesized to be the origin of biological complexity and its decline the basis of diseases & aging.
PUFAs may be integrated in the lipid layers of the cell and can aid in water balance (carbon bonds?) and you could argue that some Prostaglandins from Arachidonic Acid may be useful but the fact that endothelial Nitric Oxide is in great synergy with those Prostaglandins gives me the feeling that those are just used as substitutal stress response. So, managing the body because it is lacking primary ressources.
I still need to research but I think that CO2 is one of those "primary" ressources, specifically because it seems like that low levels of CO2 is associated with higher levels of lactic acid and NOx (maybe the latter is used as substitute vasodilator?).
The reason that mouth breathing is bad is that it reduces the amount of CO2 that you breathe. There is more anatomical "dead space" in the nasal passages to trap the air you just breathed out, which in turn has a much higher concentration of CO2 than the outside air. Nearly all animal anatomies are elegantly designed to create this "dead space" for trapping as much CO2 as the animal's metabolism needs.
If you look at the Carboniferous Era (An Era with high CO2 ppm in the air), then you might come to the conclusion that even environmental CO2 can make you grow which is in line with the findings about CO2 preventing calcification and causing bone growth.

I digress ...
PUFA are a hurdle and your body is probably decreasing your metabolic rate to prevent the oxidative damage from lipid peroxidation. Which might be a possible explanation why (FFA-) Antioxidants like Vitamin E can increase metabolism or why EFA deficient states are always correlated with higher metabolic rate and oxygen consumption ...
Maybe I answered your question or maybe not?

 

[Deleted member 6892]

The organizing power of energy flow is hypothesized to be the origin of biological complexity and its decline the basis of diseases & aging.
PUFAs may be integrated in the lipid layers of the cell and can aid in water balance (carbon bonds?) and you could argue that some Prostaglandins from Arachidonic Acid may be useful but the fact that endothelial Nitric Oxide is in great synergy with those Prostaglandins gives me the feeling that those are just used as substitutal stress response. So, managing the body because it is lacking primary ressources.
I still need to research but I think that CO2 is one of those "primary" ressources, specifically because it seems like that low levels of CO2 is associated with higher levels of lactic acid and NOx (maybe the latter is used as substitute vasodilator?).
The reason that mouth breathing is bad is that it reduces the amount of CO2 that you breathe. There is more anatomical "dead space" in the nasal passages to trap the air you just breathed out, which in turn has a much higher concentration of CO2 than the outside air. Nearly all animal anatomies are elegantly designed to create this "dead space" for trapping as much CO2 as the animal's metabolism needs.
If you look at the Carboniferous Era (An Era with high CO2 ppm in the air), then you might come to the conclusion that even environmental CO2 can make you grow which is in line with the findings about CO2 preventing calcification and causing bone growth.

I digress ...
PUFA are a hurdle and your body is probably decreasing your metabolic rate to prevent the oxidative damage from lipid peroxidation. Which might be a possible explanation why (FFA-) Antioxidants like Vitamin E can increase metabolism or why EFA deficient states are always correlated with higher metabolic rate and oxygen consumption ...
Maybe I answered your question or maybe not?

Didn't really consider the CO2's role in mouthbreathing that is interesting.
Thyroid hormomes and other metabolism increasing substanes can be utilized to counteract the anti-metabolic effects of PUFA, am I wrong? It would be better of course to gradually decrease the overall PUFA amount you consume but that will prove a challenge with the amount of it inside every food. Indeed I guess it is a partial explanation for me being skinny fat. I'll try to correct my O6:O3 ratio and reduce the amount of PUFA I consume. Considering we consume a lot more of it than out ancestors it definitely played a role in worsening of our health.

 

[ReverseNorwoodPill]

I’m not convinced we are supposed to eat any fat outside of the fats naturally occurring in things like nuts etc
I seem to be doing better on raw pufa than cooked/processed sfa

as soon as I cook stuff I get inflammatory responses and lose energy in comparison to eating raw food

 

[Deleted member 3990]

Didn't really consider the CO2's role in mouthbreathing that is interesting.
Thyroid hormomes and other metabolism increasing substanes can be utilized to counteract the anti-metabolic effects of PUFA, am I wrong?

Well, they can release them and other free fatty acids.
There is a drug called Dinitrophenol which, I think, is uncoupling alot of ATP into heat and drives metabolic rate upwards significantly and literally burns off your bodyfat. But as I said, those released fats cause/are lipid peroxidation and will cause oxidative damage big time. I think many of the side effects of Dinitrophenol, like cataracts in eyes, are the damage of excessive lipid peroxidation.

 

[Deleted member 3990]

I’m not convinced we are supposed to eat any fat outside of the fats naturally occurring in things like nuts etc
I seem to be doing better on raw pufa than cooked/processed sfa

as soon as I cook stuff I get inflammatory responses and lose energy in comparison to eating raw food

Indeed.
Gravity is preventing me from flying like superman but without gravity I would float around in space.

I think it is a good step to get fresh PUFAs if you dont want to avoid them. The air can make it rancid and that rancid fat isnt even used by the body. Literal toxin you eat

 

[ReverseNorwoodPill]

Indeed.
Gravity is preventing me from flying like superman but without gravity I would float around in space.

I think it is a good step to get fresh PUFAs if you dont want to avoid them. The air can make it rancid and that rancid fat isnt even used by the body. Literal toxin you eat

Bro I’m on the chemhead diet and although my temps are dropping a bit due to low cal, everything else is improving. It’s interesting af
I think peating might not work bc digestion takes too much energy. I don’t really think we need all those micros tbh. Most holocaust and gulag survivors still had hair after years of extreme malnutrition. They must have had zero inflammation though

 

[Deleted member 3990]

Bro I’m on the chemhead diet and although my temps are dropping a bit due to low cal, everything else is improving. It’s interesting af
I think peating might not work bc digestion takes too much energy. I don’t really think we need all those micros tbh. Most holocaust and gulag survivors still had hair after years of extreme malnutrition. They must have had zero inflammation though

Good for you I guess

 

[Dainslief]

Bro I’m on the chemhead diet and although my temps are dropping a bit due to low cal, everything else is improving. It’s interesting af
I think peating might not work bc digestion takes too much energy. I don’t really think we need all those micros tbh. Most holocaust and gulag survivors still had hair after years of extreme malnutrition. They must have had zero inflammation though

What foods does chemhead diet consist of?