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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
    "Right is right, even if no one is doing it; wrong is wrong, even if everyone is doing it." - St. Augustine

    B*tch-lite

    Who says back fat is a bad thing? Maybe on a hairy guy at the beach, but not on a crab.

    Comment


    • 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, 01:21 PM.
      Make America Great Again

      Comment


      • 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.

        Comment


        • 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
          Make America Great Again

          Comment


          • 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, 01:56 PM.
            Don't put your trust in anyone on this forum, including me. You are the key to your own success.

            Comment


            • 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.

              Comment


              • 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.

                Griff's cholesterol primer
                5,000 Cal Fat <> 5,000 Cal Carbs
                Winterbike: What I eat every day is what other people eat to treat themselves.
                TQP: I find for me that nutrition is much more important than what I do in the gym.
                bloodorchid is always right

                Comment


                • 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.
                  Make America Great Again

                  Comment


                  • Damn, derp.


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                    Comment


                    • 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

                      Comment


                      • Originally posted by dilberryhoundog View Post
                        PKlopp I'm on my iphone so I can't leave a big reply quoting all your rebuttals so I will leave you to ponder a few things.

                        1. The definition of anabolism is to synthesize larger molecules from smaller ones. You mentioned the synthesis of muscle cells from amino acids, this is definitely a form of anabolism. BUT THERE ARE OTHERS... The synthesis of triglycerides in adipocytes and glycogen in liver and muscle cells is also an anabolic process, what do all these processes have in common? They happen in the presence of insulin. Carbs promote insulin secretion from the pancreas which kicks off anabolic processes all over the body, proteins do this too to a lesser extent. Carbs are anabolic.

                        2. In the islet of langerhans in the pancreas there are alpha & beta cells which produce glucagon and insulin(and another I forget the name of) these cells are paracrine cells meaning they can directly "communicate" with each other. It just so happens that they "communicate" a message to be directly inversely proportional to the output of the other cell. Ie if the alpha cell output is 100% then the beta cell output MUST be 0%, if the beta cell output is 50% then the alpha cell output must also be 50%.

                        Now the body decides the ratio of the output of these 2 cells by the amount of blood sugar present in the serum. Ingested Carbs means predominantly insulin output and little glucagon. Proteins (your big steak example) results in a near 50 / 50 split between insulin and glucagon wich is perfect because half of the amino's are broken down by glucagon to become a mildly useful glucose source and the other half are transported by insulin to be anabolised into body cells. Note this insulin response can't be as significant as you make out because of the paracrine action with glucagon. Fats result in predominant glucagon release because the body still detects low blood glucose. Fatty acids can only be released from adipocytes by glucagon, although they can be transported by insulin as you mention.
                        I'm not sure I agree with you here, but the argument would be esoteric and probably better suited to a different thread, if you'd care to start it. ( BTW I think you were thinking of amylin )

                        Originally posted by dilberryhoundog View Post
                        from the above it is easy to affirm that given equal caloric amounts of a macro substrate the body will respond differently depending on the macro in question, I cannot see where the contradiction lies.
                        When you say this:

                        Originally posted by dilberryhoundog View Post
                        It is not the calories, all calories are basically equal, it is the body's different response to different macros.
                        You literally say that 1 calorie from carbs = 1 calorie from fats ( "all calories are basically equal" ), but you also literally say it isn't because "the body's different response to different macros" means that carbs do not equal fats. This is inherently contradictory, and if you cannot see that then we are at an impasse.

                        People have been speaking off and on about the specific dynamic action of food, or TEF in current terms, and I have a post about this on my blog, but the gist of it is, protein is the most metabolically expensive food to process, so the net energy yield of a meal can vary by as much as 20% depending on how much protein it contains. The takeaway from all of this is that yes, calories count, and yes, calorie sources count. It is not an either or proposition.

                        -PK
                        My blog : cogitoergoedo.com

                        Interested in Intermittent Fasting? This might help: part 1, part 2, part 3.

                        Comment


                        • 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.
                          The body is ALWAYS in a constant state of EVERYTHING.

                          You are always storing fat.
                          You are always burning fat.
                          You are always burning glucose.
                          You are always breaking down proteins.
                          You are always building proteins.

                          If any of these processes stop, you're dead. You lose body fat when you're overall consuming more stored fat than you're taking in usable calories. Just because there is always cortisol breaking down protein in your body doesn't mean that gluconeogenesis is a good thing. There is a huge difference between someone's cortisol level who is eating appropriate calories and 200 grams of carbohydrate a day compared to someone forcing themselves to consume <30g of carbohydrate a day on a diet supplemented with refined fats. The latter person is going to likely have much more cortisol in their system, and as with anything and the human body, poison is in the dose. The issue isn't whether or not you have cortisol in your system - I hope you do or you're a corpse - the issue is whether or not you have too much, and HFLC diets generally push you closer to that threshold.
                          Don't put your trust in anyone on this forum, including me. You are the key to your own success.

                          Comment


                          • Originally posted by ChocoTaco369 View Post
                            The body is ALWAYS in a constant state of EVERYTHING.

                            You are always storing fat.
                            You are always burning fat.
                            You are always burning glucose.
                            You are always breaking down proteins.
                            You are always building proteins.

                            If any of these processes stop, you're dead. You lose body fat when you're overall consuming more stored fat than you're taking in usable calories. Just because there is always cortisol breaking down protein in your body doesn't mean that gluconeogenesis is a good thing. There is a huge difference between someone's cortisol level who is eating appropriate calories and 200 grams of carbohydrate a day compared to someone forcing themselves to consume <30g of carbohydrate a day on a diet supplemented with refined fats. The latter person is going to likely have much more cortisol in their system, and as with anything and the human body, poison is in the dose. The issue isn't whether or not you have cortisol in your system - I hope you do or you're a corpse - the issue is whether or not you have too much, and HFLC diets generally push you closer to that threshold.
                            Doesn't have anything to do with my post though.
                            Make America Great Again

                            Comment


                            • Originally posted by Derpamix View Post
                              Doesn't have anything to do with my post though.
                              It was in reference to the post you quoted. You summarized what you believed I meant, I clarified.
                              Don't put your trust in anyone on this forum, including me. You are the key to your own success.

                              Comment


                              • Originally posted by ChocoTaco369 View Post
                                It was in reference to the post you quoted. You summarized what you believed I meant, I clarified.
                                Ah I see
                                Make America Great Again

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