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  1. #151
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    Choco is absolutely correct on the hormones in the US - they can only be given to beef producing animals. "Hormone free" chicken, pork, etc., is merely marketing. (It's at the USDA website.) Notice it doesn't state, "antibiotic free" or "GMO free." And I think most people on this forum know, but just in case, "cage free" only means access to outdoor space. It doesn't define how much space or much of anything. I believe it can even be a slab of concrete.

    As a note: $4.99/lb? Holy feces - it's cheaper at Whole Paycheck! Still CAFO, but some of their chicken is at the very least being treated more humanely according to some hippie self-appointed watchdog organization. LOL
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  2. #152
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    Quote Originally Posted by pklopp View Post
    This is beneath even you, Choco. That was the first study in an 80+ year history of research into lipids. The fact that you pretend that it is the only such study that ever drew a similar link is laughably disingenuous. Further, that you would choose to ignore the other four much more recent studies that I posted, is also quite telling.

    So Choco, debunk this study:

    Title : The essentiality of arachidonic acid and docosahexaenoic acid
    Journal : Prostaglandins, leukotrienes, and essential fatty acids
    Published : 2009 Aug-Sep

    It is the most recent one that I posted.

    Oh, and while hiding behind your keyboard, you can call me whatever names you want, I don't expect that people will be very impressed with that tactic.

    -PK
    Your study debunks itself, and I already explained why earlier. In case it's not clear enough:

    EFAD typically occurs when less than 1-2% of total calories are provided from EFAs. In the general population, EFAD is extremely rare.
    Because LA is abundant in the human diet, the amount of AA available almost always exceeds the level needed to maintain a triene-tetraene ratio below 0.2. It was only upon the introduction of parenteral nutrition (PN) that EFAD became more common. It was first reported in patients who received PN without dietary fat supplementation
    lol!!! so essential

    To date, there have not been any dose response studies in animals or humans investigating the ability of ALA, EPA, or DHA to reverse omega-3 FA deficiency. Perhaps this is because symptoms of omega-3 FA deficiency are difficult to diagnose and monitor.
    there is no adequate control group, typically one group are given fish oil whilst the other are likely eating a diet high in omega 6 PUFA, so yes the fish oil can produce some anti-inflammatory effects, but to really get an idea of what’s going on you’d need an additional group eating an essential fatty acid deficient diet (no omega 3 or 6), such studies are lacking although there are some indications that “essential” fatty acid deficiency produces less inflammation than fish oil supplementation as shown in this study in rats (Ling et al. 2012).

    now debunk these:

    PUFA (omega 3 and 6) inhibit pyruvate dehydrogenase, a key enzyme that links glycolysis into the Kreb’s (TCA) cycle (Da Silva et al. 1993). Inhibition of pyruvate dehydrogenase is known to contribute to the Warburg effect, the aerobic glycolysis characteristic of cancer (McFate et al. 2008).

    PUFA breakdown products (acrolein, malondialdehyde, hydroxynonenal, crotonaldehyde) inhibit mitochondrial respiration (Humphries et al. 1998, Picklo and Montine 2001).

    PUFA (including fish oil) promote cancer (Griffini et al. 1998), high DHA is associated with prostate cancer (Brasky et al. 2011).

    Linoleic acid (omega 6) is required for carcinogenesis in some animal models (Ip et al. 1985).

    PUFA suppress metabolism, this can be seen most obviously in the elevated metabolisms of lab animals fed an “essential” fatty acid deficient diet, (Burr and Beber 1934), “essential” fatty acid deficiency is associated with increased activity of cytochrome oxidase a fundamental mitochondrial respiratory enzyme (Kunkel and Williams 1951).

    Animals fed “essential” fatty acid sufficient diets gain more weight than deficient animals (Rafael et al. 1988).

    PUFA inhibit thyroid hormone activity (Clarke and Hembree 1990).

    PUFA, LA(omega 6), ALA (omega 3), AA (6), DHA(3) all cause brain swelling, oleic acid (MUFA) and palmitic acid (SFA) do not (Chan and Fishman, 1980).

    PUFA cause nervous system damage and impair learning, (Harman et al. 1976).

    Neuroprostanes breakdown products of DHA are implicared in Alzheimer’s, they are found in cerebrospinal fluid of Alzheimer’s patients at higher levels than age-matched controls (Roberts et al. 1998).

    PUFA, both omega 3 and 6 are involved in atherosclerosis, a study examining fatty acid composition of aortic plaques found a positive association between omega 3 and 6 fatty acids of plaques with adipose tissue content, no association was found for saturated fatty acids (Felton et al. 1994).

    PUFA, both omega 3 and 6 impair lung function (Wolfe et al. 2002).

    PUFA interfere with insulin sensitivity and increase diabetes risk, a study looking at safflower and fish oil found that both increased fasting blood glucose, the fish oil group had higher blood glucose (Borkman et al. 1989).

    PUFA promote liver cirrhosis, saturated fats and cholesterol are protective against liver cirrhosis (Nanji and French 1986). In another study fish oil promoted cirrhosis and saturated fat was found to reverse cirrhosis, whilst ethanol administration was ongoing!! So if you’re going out drinking make sure to eat lots of butter and coconut oil (Nanji et al. 2001).

    Omega 3 fats lower endurance in rats (Ayre and Hulbert 1997).

    Fish oil lowered mitochondrial activity and increased oxidative stress in… Atlantic Salmon, wow fish oil sucks even for fish (Kjaer et al. 2008).

    Omega 3 and 6, especially 3 impair wound healing (Cardosso et al. 2004).

    I noted a study above suggesting that essential fatty acid deficiency produces less inflammation than omega 3 supplementation, part of this effect occurs through inducing the synthesis of mead acid an omega 9 family PUFA (unsaturated in 3 places), the presence of mead acid is typically considered to be a marker of “essential” fatty acid deficiency, even when no pathology is present, its synthesis is inhibited by omega 3 and 6 PUFA, there are some animal studies showing anti-inflammatory effects from mead acid supplementation, mead acid because it is only unsaturated in 3 places is more stable than EPA or DHA (Yoshida et al. 2003).

    There’s good evidence that PUFA especially the longer chain highly unsaturated AA and DHA accumulate with aging (Tamburini et al. 2004, Nourooz-Zadeh and Pereira 1999).

    PUFA shorten lifespan, a number of animal studies show that the degree of unsaturation of tissue fatty acids corresponds inversely with maximum lifespan, i.e. eating lots of “essential” fatty acids will shorten your life (Bajra 2004). Naked mole-rats display unusual longevity for a rodent of their size they live around 28 years similarly sized mice live only 3-4 years. Mole-rats have low DHA (2-6%) in comparison to mice (27-57%), this low DHA means they are less susceptible to peroxidative damage (Mitchell et al. 2007).

    In a study in Italy a high PUFA to saturated fat ratio was found to increase all-cause mortality (Solfrizzi et al. 2005).

    So in summary PUFA inhibit metabolism, promote cancer, atherosclerosis, Alzheimer’s, diabetes, contribute to alcoholic liver disease, make you stupid, and generally kill you slowly, you might be thinking that’s not so bad, but wait it gets worse…. Much worse….

    A recent study suggests that PUFA contribute to… male pattern baldness, yes prostaglandin D2 inhibits hair growth and is found in higher levels in bald men, its derived from Arachidonic acid (Garza et al. 2012).

    pls go shill, you can't avoid unsaturated fats, the harm is when they're consumed in excess of ~5% daily calories depending on your ratio of saturated fats.
    Last edited by Derpamix; 10-09-2013 at 01:21 PM.
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  3. #153
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    Quote Originally Posted by Derpamix View Post
    Your study debunks itself, and I already explained why earlier. In case it's not clear enough:




    lol!!! so essential



    there is no adequate control group, typically one group are given fish oil whilst the other are likely eating a diet high in omega 6 PUFA, so yes the fish oil can produce some anti-inflammatory effects, but to really get an idea of what’s going on you’d need an additional group eating an essential fatty acid deficient diet (no omega 3 or 6), such studies are lacking although there are some indications that “essential” fatty acid deficiency produces less inflammation than fish oil supplementation as shown in this study in rats (Ling et al. 2012).

    now debunk these:

    PUFA (omega 3 and 6) inhibit pyruvate dehydrogenase, a key enzyme that links glycolysis into the Kreb’s (TCA) cycle (Da Silva et al. 1993). Inhibition of pyruvate dehydrogenase is known to contribute to the Warburg effect, the aerobic glycolysis characteristic of cancer (McFate et al. 2008).

    PUFA breakdown products (acrolein, malondialdehyde, hydroxynonenal, crotonaldehyde) inhibit mitochondrial respiration (Humphries et al. 1998, Picklo and Montine 2001).

    PUFA (including fish oil) promote cancer (Griffini et al. 1998), high DHA is associated with prostate cancer (Brasky et al. 2011).

    Linoleic acid (omega 6) is required for carcinogenesis in some animal models (Ip et al. 1985).

    PUFA suppress metabolism, this can be seen most obviously in the elevated metabolisms of lab animals fed an “essential” fatty acid deficient diet, (Burr and Beber 1934), “essential” fatty acid deficiency is associated with increased activity of cytochrome oxidase a fundamental mitochondrial respiratory enzyme (Kunkel and Williams 1951).

    Animals fed “essential” fatty acid sufficient diets gain more weight than deficient animals (Rafael et al. 1988).

    PUFA inhibit thyroid hormone activity (Clarke and Hembree 1990).

    PUFA, LA(omega 6), ALA (omega 3), AA (6), DHA(3) all cause brain swelling, oleic acid (MUFA) and palmitic acid (SFA) do not (Chan and Fishman, 1980).

    PUFA cause nervous system damage and impair learning, (Harman et al. 1976).

    Neuroprostanes breakdown products of DHA are implicared in Alzheimer’s, they are found in cerebrospinal fluid of Alzheimer’s patients at higher levels than age-matched controls (Roberts et al. 1998).

    PUFA, both omega 3 and 6 are involved in atherosclerosis, a study examining fatty acid composition of aortic plaques found a positive association between omega 3 and 6 fatty acids of plaques with adipose tissue content, no association was found for saturated fatty acids (Felton et al. 1994).

    PUFA, both omega 3 and 6 impair lung function (Wolfe et al. 2002).

    PUFA interfere with insulin sensitivity and increase diabetes risk, a study looking at safflower and fish oil found that both increased fasting blood glucose, the fish oil group had higher blood glucose (Borkman et al. 1989).

    PUFA promote liver cirrhosis, saturated fats and cholesterol are protective against liver cirrhosis (Nanji and French 1986). In another study fish oil promoted cirrhosis and saturated fat was found to reverse cirrhosis, whilst ethanol administration was ongoing!! So if you’re going out drinking make sure to eat lots of butter and coconut oil (Nanji et al. 2001).

    Omega 3 fats lower endurance in rats (Ayre and Hulbert 1997).

    Fish oil lowered mitochondrial activity and increased oxidative stress in… Atlantic Salmon, wow fish oil sucks even for fish (Kjaer et al. 2008).

    Omega 3 and 6, especially 3 impair wound healing (Cardosso et al. 2004).

    I noted a study above suggesting that essential fatty acid deficiency produces less inflammation than omega 3 supplementation, part of this effect occurs through inducing the synthesis of mead acid an omega 9 family PUFA (unsaturated in 3 places), the presence of mead acid is typically considered to be a marker of “essential” fatty acid deficiency, even when no pathology is present, its synthesis is inhibited by omega 3 and 6 PUFA, there are some animal studies showing anti-inflammatory effects from mead acid supplementation, mead acid because it is only unsaturated in 3 places is more stable than EPA or DHA (Yoshida et al. 2003).

    There’s good evidence that PUFA especially the longer chain highly unsaturated AA and DHA accumulate with aging (Tamburini et al. 2004, Nourooz-Zadeh and Pereira 1999).

    PUFA shorten lifespan, a number of animal studies show that the degree of unsaturation of tissue fatty acids corresponds inversely with maximum lifespan, i.e. eating lots of “essential” fatty acids will shorten your life (Bajra 2004). Naked mole-rats display unusual longevity for a rodent of their size they live around 28 years similarly sized mice live only 3-4 years. Mole-rats have low DHA (2-6%) in comparison to mice (27-57%), this low DHA means they are less susceptible to peroxidative damage (Mitchell et al. 2007).

    In a study in Italy a high PUFA to saturated fat ratio was found to increase all-cause mortality (Solfrizzi et al. 2005).

    So in summary PUFA inhibit metabolism, promote cancer, atherosclerosis, Alzheimer’s, diabetes, contribute to alcoholic liver disease, make you stupid, and generally kill you slowly, you might be thinking that’s not so bad, but wait it gets worse…. Much worse….

    A recent study suggests that PUFA contribute to… male pattern baldness, yes prostaglandin D2 inhibits hair growth and is found in higher levels in bald men, its derived from Arachidonic acid (Garza et al. 2012).

    pls go shill, you can't avoid unsaturated fats, the harm is when they're consumed in excess of ~5% daily calories depending on your ratio of saturated fats.
    Ill check back in a few days after you read all of that.

  4. #154
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    Quote Originally Posted by moluv View Post
    Ill check back in a few days after you read all of that.
    Here is more:

    Extremely limited synthesis of long ... [Appl Physiol Nutr Metab. 2007] - PubMed - NCBI

    these studies all suffer from the same glaring flaws which is a failure to consider all other dietary variables that affect conversion. the use of limited amounts of ALA with a huge amounts of LA would further suppress conversion through competition for enzymatic d6d activity and by LA impairing d6d production

    Extremely limited synthesis of long ... [Appl Physiol Nutr Metab. 2007] - PubMed - NCBI
    An Error Occurred Setting Your User Cookie

    the requirements are so insignificant that it renders the word "essential" literally meaningless. unless, they're considering the fact we don't synthesize it as grounds for labeling it essential. on the flip side, that's probably exactly why they aren't essential. see: mead acid Age-related changes in the retinal capilla... [Invest Ophthalmol. 1972] - PubMed - NCBI
    nihil

  5. #155
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    Quote Originally Posted by pklopp View Post
    This is beneath even you, Choco. That was the first study in an 80+ year history of research into lipids. The fact that you pretend that it is the only such study that ever drew a similar link is laughably disingenuous. Further, that you would choose to ignore the other four much more recent studies that I posted, is also quite telling.

    So Choco, debunk this study:

    Title : The essentiality of arachidonic acid and docosahexaenoic acid
    Journal : Prostaglandins, leukotrienes, and essential fatty acids
    Published : 2009 Aug-Sep

    It is the most recent one that I posted.

    Oh, and while hiding behind your keyboard, you can call me whatever names you want, I don't expect that people will be very impressed with that tactic.

    -PK
    What is beneath "even me"? You came at me, bro. Don't point out my lack of knowledge if you know even less yourself.

    The study you linked was long-debunked. Is it my fault or yours you posted the very study I was speaking of earlier? I'm a big fan of irony.

    Derp's reply is, frankly, better than what I can write because he knows more about this stuff than I do, so I'll defer to his response.

    What names did I call you? If you don't like being disproved, why did you call me out first? Did you think I wouldn't reply?



    I fail to see how ANYONE can prove ANYTHING being essential because it is impossible to limit only one variable. Are EFA's actually essential? Has there EVER been a diagnosis where someone has DIED due to a lack of omega 3 or omega 6? I'm willing to bet the answer is a resounding "NO!" Which in that case would indicate it has never been proven, yet people believe it anyway. It is marketing.
    Last edited by ChocoTaco369; 10-09-2013 at 01:56 PM.
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  6. #156
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    Quote Originally Posted by Derpamix View Post
    Here is more:

    Extremely limited synthesis of long ... [Appl Physiol Nutr Metab. 2007] - PubMed - NCBI

    these studies all suffer from the same glaring flaws which is a failure to consider all other dietary variables that affect conversion. the use of limited amounts of ALA with a huge amounts of LA would further suppress conversion through competition for enzymatic d6d activity and by LA impairing d6d production

    Extremely limited synthesis of long ... [Appl Physiol Nutr Metab. 2007] - PubMed - NCBI
    An Error Occurred Setting Your User Cookie

    the requirements are so insignificant that it renders the word "essential" literally meaningless. unless, they're considering the fact we don't synthesize it as grounds for labeling it essential. on the flip side, that's probably exactly why they aren't essential. see: mead acid Age-related changes in the retinal capilla... [Invest Ophthalmol. 1972] - PubMed - NCBI
    Kickin some knowledge today Derp.

  7. #157
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    Quote Originally Posted by pklopp View Post
    This is beneath even you, Choco. That was the first study in an 80+ year history of research into lipids. The fact that you pretend that it is the only such study that ever drew a similar link is laughably disingenuous. Further, that you would choose to ignore the other four much more recent studies that I posted, is also quite telling.

    So Choco, debunk this study:

    Title : The essentiality of arachidonic acid and docosahexaenoic acid
    Journal : Prostaglandins, leukotrienes, and essential fatty acids
    Published : 2009 Aug-Sep

    It is the most recent one that I posted.

    Oh, and while hiding behind your keyboard, you can call me whatever names you want, I don't expect that people will be very impressed with that tactic.

    -PK
    Leaving the ad-hominems of Choco's reply out of it, I also thought that the 1929 paper was largely considered discredited since it ascribed behaviour to the fat that has since been understood to be related to B-vitamins.

    I still think that eating fish is good for us though.
    Disclaimer: I eat 'meat and vegetables' ala Primal, although I don't agree with the carb curve. I like Perfect Health Diet and WAPF Lactofermentation a lot.

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  8. #158
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    Unlike what you seem to believe, the body is in a constant state of gluconeogenesis. As in every second of every day of your life. Several tissues like red blood cells and the kidney medula are obligate glycolytic tissues. Lacking mitochondria, they are incapable of oxidative respiration and so can only derive energy from glycolysis. The interesting thing about this is that the end product of glycolysis in the absence of mitochondria ( or sufficient oxygen in those cells possessing mitochondria ) is lactic acid. So, of course, all of us are keeling over from extreme lactic acidosis as the lactic acid builds up in our systems catastrophically altering the pH of our bodies, right? Well, no, because lactic acid is a very nice 3 carbon chain that when combined with another such molecule in hepatocytes is used as a gluconeogenesis substrate to regenerate glucose. So, if you possess red blood cells or kidneys, guess what, you are in a constant state of gluconeogenesis.
    Just saw this: gluconeogenesis and glycolysis are coordinated so that in a cell one is mostly inactive while the other is active. Both glycolysis and gluconeogenesis are exergonic in cellular conditions, so there is no thermodynamic barrier for their simultaneous activity -- the activity of each are controlled via rate limiting steps so that both are not highly active at the same time. Gluconeogenesis is controlled mostly by concentrations of lactate. The main purpose of gluconeogenesis is to generate glucose from non-carb substrates ie; lactate, glycerol, and glucogenic amino acids. To say that we are in a constant state of gluconeogenesis is an exaggeration and a strawman.

    Choco is referring to overburdening the liver with excessive lactate, I believe. Lactate is a metabolic dead end. See: Cori cycle.
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    Quote Originally Posted by Derpamix View Post
    Just saw this: gluconeogenesis and glycolysis are coordinated so that in a cell one is mostly inactive while the other is active. Both glycolysis and gluconeogenesis are exergonic in cellular conditions, so there is no thermodynamic barrier for their simultaneous activity -- the activity of each are controlled via rate limiting steps so that both are not highly active at the same time. Gluconeogenesis is controlled mostly by concentrations of lactate. The main purpose of gluconeogenesis is to generate glucose from non-carb substrates ie; lactate, glycerol, and glucogenic amino acids. To say that we are in a constant state of gluconeogenesis is an exaggeration and a strawman.

    Choco is referring to overburdening the liver with excessive lactate, I believe. Lactate is a metabolic dead end. See: Cori cycle.
    Interesting

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