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haidut

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Some good evidence on the role of PUFA and inflammation in obesity and diabetes. The findings that FFA are elevated in obese people is not surprising and even mainstream medicine has wisened up to that fact. The surprising (for the authors) part was that unsaturated fats were involved in the development of metabolic syndrome and diabetes. In fact, unsaturated fats were a highly sensitive biomarker capable of separating healthy from unhealthy people in the study, and predicting diabetes development a decade in advance. Quite contrary to the common story fed to us through mainstream media that PUFA protect from diabetes and obesity. The study also found that levels of SFA increased when obese patients lost weight, while the levels of PUFA declined. Perhaps unsurprisingly, the proposed mechanism of the deleterious effects of PUFA on metabolic health was related to their role as precursors to inflammation.
Another reason I find this study important it that it confirms something Peat has stated repeatedly in his articles and over email, but for which not many references were given. Namely, that when fat is released from its storage through lipolysis, PUFA is preferentially released while SFA is mostly kept stored. This explains to a great degree the negative effects of fasting, stress, and other events that elevate FFA in the blood. The opposite happens when fat is eaten through the diet - i.e. SFA is preferentially oxidized while the PUFA is stored. The study did not confirm the latter point but there are other studies providing indirect confirmation of the latter.

@Travis @Such_Saturation

Circulating Unsaturated Fatty Acids Delineate the Metabolic Status of Obese Individuals. - PubMed - NCBI
"...Using a targeted mass spectrometry metabolomics approach, we analyzed serum samples of a total of 452 subjects from four independent studies and identified a panel of UFAs whose fasting serum concentrations at routine examination delineates the metabolic status of obese individuals. In the cross-sectional study, FFA levels were found significantly elevated in overweight/obese subjects with T2D compared to their healthy counterparts. A panel of UFAs, DGLA in particular, was closely associated with metabolic markers, and was a significant marker to distinguish metabolically healthy and unhealthy individuals. We also analyzed the baseline FFAs of subjects from a longitudinal study, and found that fasting concentrations of a similar panel of UFAs were elevated up to 10 years before the onset of MS. Finally, in the two weight loss intervention studies, obese participants experienced significant beneficial effects including weight loss and improved metabolic characteristics. A panel of UFAs decreased significantly in response to the surgical or dietary interventions."

"...UFAs, as compared to SFAs, were decreased more significantly after weight loss interventions, and increased more significantly in obese subjects with MS. Additionally, UFA signatures were more closely associated with metabolic markers. To date, SFAs have been generally thought to have detrimental effects on health. However, conflicting evidence was reported regarding the effects of high SFA intake on the risk of diabetes (Micha and Mozaffarian, 2010). A large cohort study recently suggested that different individual plasma phospholipid SFAs were not homogeneous and associated with incident T2D in opposite ways (Forouhi et al., 2014). They reported that even-chain SFAs (those containing an even number of carbon atoms) including palmitic acid (C16:0) were positively associated and odd-chain (those containing an odd number of carbon atoms) and longer-chain SFAs (those with 13 to 21 carbon atoms) were inversely associated with incident diabetes. In our study, most SFAs did not show strong correlations with metabolic markers, except C16:0 that was decreased significantly in obese individuals after metabolic surgery, and increased significantly in the UO group of the cross-sectional study. "

"...Compared to SFAs, convincing evidence observed in our study was that UFAs are more closely associated with metabolic status in obese individuals. The fluctuations of circulating FFAs in obese phenotypes may be due to the different FA mobilization mechanisms from adipose tissue to blood, where SFAs were found much less mobilized than PUFAs (Connor et al., 1996). Our findings particularly highlight a panel of UFAs that was consistently associated with metabolic status in obese individuals across four independent studies. Two UFAs, PA and DGLA may be potential inflammation markers in predicting the risk of developing MS and monitoring the metabolic status among overweight/obese individuals. PA has been proposed as a lipid-controlling hormone (lipokine) used by adipose tissue to communicate with distant organs and regulate systemic metabolic homeostasis (Cao et al., 2008). Increased levels of plasma PA indicate an increase in stearoyl-CoA desaturase (SCD1) activity (increased DNL) in the liver as it is virtually absent in the diet and thus can be used as a marker for upregulation of this usually inhibited hepatic lipid metabolic pathway (Supplementary Figure S2B) (Gong et al., 2011). Increased DNL means increased formation of diacylglycerol (DAG), which, in turn, contributes to inflammation via release of arachidonic acid (AA) from the plasma membrane. DGLA is a key player in the synthetic pathway for pro-inflammatory series 2 prostaglandins and leukotrienes and elevated levels of this PUFA may contribute to the inflammatory phenotype in obesity/MS (Supplementary Figure S2C–D). Recently, it has been proposed that the distinction between HO and UO groups is related to the degree of chronic inflammation present (Perreault et al., 2014, Steffen et al., 2012a). This has led to several studies comparing inflammation markers such as levels of TNF-α, adiponectin, leptin, resistin, C-reactive protein, plasminogen activator inhibitor-1 and complement component c3, between HO and UO populations (Steffen et al., 2012a, Phillips and Perry, 2013). The major conclusion derived from these studies was that no significant differences were seen for inflammation markers between HO and NW subjects but inflammation markers were found to be elevated in the UO groups. A previous study on 2848 adults found that obese individuals had significantly higher levels of n − 6 PUFAs (e.g. DGLA, GLA, and AA) compared to normal and overweight subjects, and DGLA showed strong associations with inflammatory and endothelial activation markers in obesity, e.g. IL-6 and sICAM-1 (Steffen et al., 2012). It was also reported that a high proportion of DGLA in serum cholesterol ester was associated with high concentrations of C-reactive protein, which is a sensitive marker of low-grade inflammation and associated with insulin resistance and T2D (Kurotani et al., 2012)."
 

Wagner83

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Namely, that when fat is released from its storage through lipolysis, PUFA is preferentially released while SFA is mostly kept stored. This explains to a great degree the negative effects of fasting, stress, and other events that elevate FFA in the blood. The opposite happens when fat is eaten through the diet - i.e. SFA is preferentially oxidized while the PUFA is stored. The study did not confirm the latter point but there are other studies providing indirect confirmation of the latter.
Why would the body release PUFAs in times of stress?
 

MrSmart

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Why would the body release PUFAs in times of stress?
It's part of a long series in the stress response cascade.

If you mean the rationale, stress is fairly one-dimensional in the human body, and the release of cytokines and eicosanoids instigates wound-healing and macrophage activation.
 

haidut

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Why would the body release PUFAs in times of stress?

In addition to what @MrSmart mentioned, I would also add that structurally PUFA is estrogenic, and just like estrogen causes water retention, cell-division, growth, de-differentiation, etc all of which may be needed during injury and healing. In addition, PUFA stimulates cortisol release even in the absence of ACTH. So, this could help ensure adequate cortisol response in people with blunted ACTH response to stress (which is common in chronically stressed ones). But if that process becomes chronic, you see how this quickly becomes pathological.
 

Wagner83

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Ok thanks to both.

I see the point for physical stress. In case of mental/environmental stress why not release SFAs which would help the body deal with the stressor bettter? After all this is one of the goals of depleting PUFAS in tissues: not release them in times of stress.
In addition to what @MrSmart mentioned, I would also add that structurally PUFA is estrogenic, and just like estrogen causes water retention, cell-division, growth, de-differentiation, etc all of which may be needed during injury and healing. In addition, PUFA stimulates cortisol release even in the absence of ACTH. So, this could help ensure adequate cortisol response in people with blunted ACTH response to stress (which is common in chronically stressed ones). But if that process becomes chronic, you see how this quickly becomes pathological.
So basically these could be all aspects which mean crashing estrogens too low daily would be bad, even more so in the context of exercising. I never heard Ray Ray buy into the theory of low estrogens, also I doubt people would use topical estrogens to heal wounds, rather co2, dhea, vit k, t3 etc...It would make sense that some would be needed though. How would you identify and address a "blunted ACTH response to stress"?
 

MrSmart

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Ok thanks to both.

I see the point for physical stress. In case of mental/environmental stress why not release SFAs which would help the body deal with the stressor bettter? After all this is one of the goals of depleting PUFAS in tissues: not release them in times of stress.

So basically these could be all aspects which mean crashing estrogens too low daily would be bad, even more so in the context of exercising. I never heard Ray Ray buy into the theory of low estrogens, also I doubt people would use topical estrogens to heal wounds, rather co2, dhea, vit k, t3 etc...It would make sense that some would be needed though. How would you identify and address a "blunted ACTH response to stress"?

You can deplete PUFA from adipose tissue, but you can't deplete them completely from the cell membrane of other tissue. I'm not sure if the body can desaturate SFA to AA when it needs to. The idea for going Peat is avoiding excess AA reserves to prevent an amplified and chronic stress response, but you can't and shouldn't eliminate it completely.
 

haidut

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Ok thanks to both.

I see the point for physical stress. In case of mental/environmental stress why not release SFAs which would help the body deal with the stressor bettter? After all this is one of the goals of depleting PUFAS in tissues: not release them in times of stress.

So basically these could be all aspects which mean crashing estrogens too low daily would be bad, even more so in the context of exercising. I never heard Ray Ray buy into the theory of low estrogens, also I doubt people would use topical estrogens to heal wounds, rather co2, dhea, vit k, t3 etc...It would make sense that some would be needed though. How would you identify and address a "blunted ACTH response to stress"?

I don't think it can be concluded that estrogen crashing too low could be bad, as I don't know of such a case unless a person takes some kind of AI. The point is that there is always plenty of estrogen under natural circumstances and it is rather unfortunate that we eat PUFA because when it is released it potentiates the estrogen response tremendously. It is not the body's fault we eat so much PUFA, it releases what it has and if there is more PUFA than SFA then PUFA is what dominates in the bloodstream. There could be purely mechanical reasons for that too like PUFA being more hydrophilic and being more easily mobilized under the influence of adrenaline. In general, more hydrophilic substances leave the cell more easily. Along the lines of "accidental damage", Peat said that normally when the tissues are full of SFA instead of PUFA, when the SFA is released it ends up stopping the stress response as SFA have anti-glucocorticoid and anti-estrogen effects. A sort of negative feedback mechanism. But when PUFA is released due to us eating so much of it, it becomes a positive feedback cycle.
 
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Travis

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Why would the body release PUFAs in times of stress?

Don't glucocorticoids mobilize glucose, via hydrolysis of glycogen, in times of stress? I think I can see the physiological intent behind stress-induced fatty acid release, yet I don't what particular hormone is responsible? I suppose it could be another corticosteroid, and perhaps even a glucocorticoid; not everything with an eponymous function has merely that function.
 

Travis

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You can deplete PUFA from adipose tissue, but you can't deplete them completely from the cell membrane of other tissue. I'm not sure if the body can desaturate SFA to AA when it needs to. The idea for going Peat is avoiding excess AA reserves to prevent an amplified and chronic stress response, but you can't and shouldn't eliminate it completely.

On a diet without omega−6 fatty acids, no arachidonic acid (20∶4ω−6) is produced and endogenous Mead acid (20∶3ω−9) takes its place. Mead acid is a biomarker for the so-called 'fatty acid deficiency,' of the ω−6 type, and its so reliable that it essentially defines the 'condition.' The lipoxygenase product of Mead acid (20∶3ω−9) is leukotriene B₃, about fivefold less potent than AA-derived leukotriene B₄, yet Mead acid has no prostaglandin analogue: Endogenous Mead acid is is oxygenated by cyclooxygenase yet will not form the characteristic endoperoxide bridge.

Mead acid can be produced via stearate (18∶0ω−nothin'): and stearate, in turn, can be produced from acetate. Thus: Humans can make stearic acid, oleic acid, and Mead acid from carbons derived either from glucose or fructose.
 
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haidut

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On a diet without omega−6 fatty acids, no arachidonic acid (20∶4ω−6) is produced and endogenous Mead acid (20∶3ω−9) takes its place. Mead acid is a biomarker for the so-called 'fatty acid deficiency,' of the ω−6 type, and its so reliable that it essentially defines the 'condition.' The lipoxygenase product of Mead acid (20∶3ω−9) is leukotriene B₃, about fivefold less potent than AA-derived leukotriene B₄, yet Mead acid has no prostaglandin analogue: Endogenous Mead acid is is oxygenated by cyclooxygenase yet will not form the characteristic endoperoxide bridge.

Mead acid can be produced via stearate (18∶0ω−nothin'): and stearate, in turn, can be produced from acetate. Thus: Humans can make stearic acid, oleic acid, and Mead acid from carbons derived either from glucose or fructose.

Do you think arachidic acid can displace arachidonic acid as a substrate for the COX/LOX enzymes, or antagonize its effects in other, non-enzymatic pathways? In addition to being a driver of inflammation arachidonic acid can also activate various fatty acid receptors and possibly even steroid receptors. So, it would be nice if there was a "competitive antagonist" of sorts for arachidonic acid.
 

Travis

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Do you think arachidic acid can displace arachidonic acid as a substrate for the COX/LOX enzymes, or antagonize its effects in other, non-enzymatic pathways? In addition to being a driver of inflammation arachidonic acid can also activate various fatty acid receptors and possibly even steroid receptors. So, it would be nice if there was a "competitive antagonist" of sorts for arachidonic acid.

If arachidonic acid can be said to have an antagonist, I think it would have to be eicosapentaenoic acid (20∶5ω−3). Under the action of cycloxygenase, this membrane lipid forms 3-series prostaglandins—those with reduced activity—and is the only other proto-prostaglandin besides dihomo-γ-linolenic acid (20∶3ω−6). I am under the impression that Mead acid is a cyclooxygenase substrate yet will not form a prostaglandin, so it can perhaps be views as a competitive inhibitor in that way. Although Mead acid is a good sign, α-linolenic acid (18∶3ω−3) can antagonize arachidonic acid yet another way: Alpha-linolenic acid (18∶3ω−3) competes with γ-linolenic acid (18∶3ω−6) and linoleic acid (18∶2ω−6) for elongation & desaturation enzymes, thereby restricting the very synthesis of arachidonic acid (20∶4ω−6). And then to add insult to injury, α-linolenic acid (18∶3ω−3) becomes eicosapentaenoic acid (20∶5ω−3) and antagonizes it directly. Much of the perceived benefit of fish oil is on account of arachidonic acid inhibition, yet because long-chained ω−3 fatty acids are also lipofuscin hazards it would be best to restrict those too. Avoiding ω−6 fatty acids negates the need for their antagonism in the first place, and also lowers ω−3 requirement.
 
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haidut

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If arachidonic acid can be said to have an antagonist, I think it would have to be eicosapentaenoic acid (20∶5ω−3). Under the action of cycloxygenase, this membrane lipid forms 3-series prostaglandins—those with reduced activity—and is the only other proto-prostaglandin besides dihomo-γ-linolenic acid (20∶3ω−6). I am under the impression that Mead acid is a cyclooxygenase substrate yet will not form a prostaglandin, so it can perhaps be views as a competitive inhibitor in that way. Although Mead acid is a good sign, α-linolenic acid (18∶3ω−3) can antagonize arachidonic acid yet another way: Alpha-linolenic acid (18∶3ω−3) competes with γ-linolenic acid (18∶3ω−6) and linoleic acid (18∶2ω−6) for elongation & desaturation enzymes, thereby restricting the very synthesis of arachidonic acid (20∶4ω−6). And then to add insult to injury, α-linolenic acid (18∶3ω−3) becomes eicosapentaenoic acid (20∶5ω−3) and antagonizes it directly. Much of the perceived benefit of fish oil is on account of arachidonic acid inhibition, yet because long-chained ω−3 fatty acids are also lipofuscin hazards it would be best to restrict those too. Avoiding ω−6 fatty acids negates the need for their antagonism in the first place, and also lowers ω−3 requirement.

Thanks. I guess if one wanted to go the displacement route, displacing linoleic acid by consuming stearic acid would be the better approach as it kills 2 birds with one stone.
 

Obi-wan

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"Mead acid can be produced via stearate (18∶0ω−nothin'): and stearate, in turn, can be produced from acetate." ACV/BS is acetate...
 

haidut

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"Mead acid can be produced via stearate (18∶0ω−nothin'): and stearate, in turn, can be produced from acetate." ACV/BS is acetate...

I thought ACV is not acetate but malate?? Grape vinegar is acetate. Maybe I am wrong...
 

Obi-wan

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Many acetate salts are ionic, indicated by their tendency to dissolve well in water. A commonly encountered acetate in the home is sodium acetate, a white solid that can be prepared by combining vinegar and sodium bicarbonate ("bicarbonate of soda"): -Wikipedia

CH3COOH + NaHCO3 → CH3COO−Na+ + H2O + CO2

The acetate anion, [CH3COO]−,(or [C2H3O2]−) is one of the carboxylate family. It is the conjugate base of acetic acid. Above a pH of 5.5, acetic acid converts to acetate:[2]

CH3COOH ⇌ CH3COO− + H+
 
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haidut

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Many acetate salts are ionic, indicated by their tendency to dissolve well in water. A commonly encountered acetate in the home is sodium acetate, a white solid that can be prepared by combining vinegar and sodium bicarbonate ("bicarbonate of soda"): -Wikipedia

CH3COOH + NaHCO3 → CH3COO−Na+ + H2O + CO2

Right, but you said ACV, which I am assuming stands for "apple cider vinegar". That one contains malic acid, so if you combine with baking soda (BS) you will get sodium malate, not sodium acetate.
 

Obi-wan

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Malic acid was first isolated from apple juice by Carl Wilhelm Scheele in 1785.[3] Antoine Lavoisier in 1787 proposed the name acide malique, which is derived from the Latin word for apple, mālum—as is its genus name Malus.[4][5] In German it is named Äpfelsäure (or Apfelsäure) after plural or singular of the fruit apple, but the salt(s) Malat(e). Malic acid is the main acid in many fruits, including apricots, blackberries, blueberries, cherries, grapes, mirabelles, peaches, pears, plums, and quince[6] and is present in lower concentrations in other fruits, such as citrus[7

The salts and esters of malic acid are known as malates.

Apple cider vinegar contains malic acid, which is produced during the process of converting carbohydrates.

The acetate anion, [CH3COO]−,(or [C2H3O2]−) is one of the carboxylate family. It is the conjugate base of acetic acid. Above a pH of 5.5, acetic acid converts to acetate:[2]
 
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Obi-wan

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The most common salt of the bicarbonate ion is sodium bicarbonate, NaHCO3, which is commonly known as baking soda. When heated or exposed to an acid such as acetic acid (vinegar), sodium bicarbonate releases carbon dioxide


All vinegar is acetic acid...any vinegar plus baking soda will create acetate...ACV/BS creates potassium acetate...
 
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Obi-wan

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Acetate is a common anion in biology. It is mainly utilized by organisms in the form of acetyl coenzyme A.

Acetyl-CoA (acetyl coenzyme A) is a molecule that participates in many biochemical reactions in protein, carbohydrate and lipid metabolism.[1] Its main function is to deliver the acetyl group to the citric acid cycle (Krebs cycle) to be oxidized for energy production

Acetyl-CoA then enters the citric acid cycle, where the acetyl group is oxidized to carbon dioxide and water, and the energy released captured in the form of 11 ATP and one GTP per acetyl group.

The introduction of an acetyl group into a molecule is called acetylation. In biological organisms, acetyl groups are commonly transferred from acetyl-CoA to coenzyme A (CoA). Acetyl-CoA is an intermediate both in the biological synthesis and in the breakdown of many organic molecules. Acetyl-CoA is also created during the second stage of cellular respiration, the Krebs Cycle, by the action of pyruvate dehydrogenase on pyruvic acid.

Pyruvic acid supplies energy to cells through the citric acid cycle (also known as the Krebs cycle) when oxygen is present (aerobic respiration), and alternatively ferments to produce lactate when oxygen is lacking (lactic acid fermentation).[4]

If insufficient oxygen is available, the acid is broken down anaerobically, creating lactate in animals. Pyruvate from glycolysis is converted by fermentation to lactate using the enzyme lactate dehydrogenase and the coenzyme NADH in lactate fermentation.

Pyruvate is a key intersection in the network of metabolic pathways. Pyruvate can be converted into carbohydrates via gluconeogenesis, to fatty acids or energy through acetyl-CoA, to the amino acid alanine, and to ethanol. Therefore, it unites several key metabolic processes.

I think acetate helps Pyruvate turn into energy instead of lactate...
 
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