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Are ALL saturated fats good for you?

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  • #16
    Originally posted by Paleobird View Post
    I highly recommend this book for the ultimate definitive guide to fats:

    Know Your Fats : The Complete Primer for Understanding the Nutrition of Fats, Oils and Cholesterol: Mary G. Enig: 9780967812601: Amazon.com: Books

    Also this post by Mark is a good general one and includes some good resource links.
    The Definitive Guide to Fats | Mark's Daily Apple
    Thanks, I've actually seen Dr. Enig's work before in defence of saturated fat, I'll make sure to get a look at that book.
    Last edited by Lukey; 04-23-2013, 01:55 PM.

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    • #17
      Originally posted by Neckhammer View Post
      Check out the right hand bar and look under posts for Plamitic acid.

      Hyperlipid: Palmitic acid: the horror never ends

      Plenty of studies showing its evil! Particularly some stuff about it causing insulin resistance. But, as usual Peter logically refutes these and offers additional studies to back his stance. Fun stuff.
      I really like Peter's writing style, He explains things thoroughly and scientifically but has a great sense of humour too! I'll definately be reading his blog from now.

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      • #18
        If it says "Crisco" on the can, it's not good for you.

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        • #19
          Originally posted by Neckhammer View Post
          Check out the right hand bar and look under posts for Plamitic acid.

          Hyperlipid: Palmitic acid: the horror never ends

          Plenty of studies showing its evil! Particularly some stuff about it causing insulin resistance. But, as usual Peter logically refutes these and offers additional studies to back his stance. Fun stuff.
          Indeed. Hyperlipid is one of my favourite sites.

          All of the studies trying to indict saturated fats do so by overdosing experimental subjects with palmitic acid and then feigning shock and surprise when they discover that *GASP* it induces insulin resistance!

          So how would one go about getting high circulating levels of free palmitic acid in one's blood stream in the absence of some boffin directly infusing them there via a catheter?

          Well, one pretty good way of doing this is to stop eating, which will cause insulin levels to drop and this will allow adipose tissues to start liberating the storage form of triglycerides via the action of hormone sensitive lipase. What is the predominant fatty acid stored in adipose triglycerides? Well, I'll be darned if it isn't our good friend palmitic acid. So, stop eating, and we can reasonably expect that we'll see elevated FAs bound to serum albumin in your bloodstream, as well as an increased quantity of glycerol.

          So, now, we have all those tissues that can oxidize fatty acids doing so, and keeping their grubby hands off the glucose that absolutely must be delivered to obligate glycolitic tissues like red blood cells, parts of the brain, and the kidney medulla, to name a few.

          Later on, with a bit of luck, you come upon some food, eat it, and get a concomitant rise in your serum insulin levels as a result. Now you find yourself in a situation where you have elevated levels of free palmitic acid and elevated insulin. This is a bit of an odd state of affairs, because the only way for you to get free fatty acids is via release from adipose tissue. Dietary fats come parceled as triglycerides in chylomicrons via the lymphatic system. From a metabolic perspective, you are sending two signals : 1) I haven't eaten for a while and I'm relying on stored energy ( elevated levels of Palmitic FFAs ), and 2) I have just eaten ( elevated insulin levels )

          At this point, you body can either gamble that you have ingested enough carbohydrates and switch on full bore system wide glucose absorption and glycolysis ( a.k.a. "insulin sensitivity" ), or it can be conservative, and maintain those tissues that are capable of performing beta oxidation of fatty acids in that state ( a.k.a. "insulin insensitive" ). If you gamble and get it wrong, the downside can be a hypoglycemic coma. If you are conservative and get it wrong, that is, you actually did ingest enough carbohydrates for all tissues to consume, this situation is self correcting, as the elevated insulin levels will curtail release of adipose FAs which will in turn cause those beta oxidizing tissues to look to some other energy substrate, read glucose.

          Palmitic acid absolutely causes insulin resistance. It is supposed to. Your survival depends on it. Oh, and the preferred energy substrates for pancreatic beta cells seems to be saturated fats. The longer, the better.

          -PK
          My blog : cogitoergoedo.com

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

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          • #20
            Originally posted by pklopp View Post
            Indeed. Hyperlipid is one of my favourite sites.

            All of the studies trying to indict saturated fats do so by overdosing experimental subjects with palmitic acid and then feigning shock and surprise when they discover that *GASP* it induces insulin resistance!...
            Thanks, that makes it clear why palmitic acid causes insulin resistance. It's quite funny how the scientists doing these experiments are shocked to find palmitic acid doing its job. Just out of curiosity, Peter goes on to say that even Low concentrations of oleate (0.1mM) completely inhibited palmitate-induced oxidative stress, SAPK activation, and apoptosis. Is oleic Acid not one of the fatty acids found in human adipose tissue? I'm just wondering why breaking down the adipose tissue would realise a high concentration of Palmitic but not oleic acid.
            Last edited by Lukey; 04-24-2013, 09:14 AM.

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            • #21
              Originally posted by Lukey View Post
              Thanks, that makes it clear why palmitic acid causes insulin resistance. It's quite funny how the scientists doing these experiments are shocked to find palmitic acid doing its job. Just out of curiosity, Peter goes on to say that even Low concentrations of oleate (0.1mM) completely inhibited palmitate-induced oxidative stress, SAPK activation, and apoptosis. Is oleic Acid not one of the fatty acids found in human adipose tissue? I'm just wondering why breaking down the adipose tissue would realise a high concentration of Palmitic but not oleic acid.
              Actually, the human body tends to store fatty acids of 16 carbon atoms in length or greater. Shorter chains fatty acids are mostly oxidized. Palmitic acid is a 16 carbon saturated fat, or in other words, the shortest fatty acid that the body stores and the predominant one that it synthesizes.

              The point Peter is making is that your body is quite capable of synthesizing oleic acid from palmitic acid in the liver via fatty acid elongase and desaturase enzymes. This means that in a biological system ( i.e. you ) it is impossible to _exclusively_ deliver palmitic acid to a cell, there will always be some accompanying oleic acid, and it doesn't take a whole lot of it to mitigate any potentially negative effects of palmitic acid. So, he's calling out the researchers for stacking the deck against palmitic acid.

              Incidentally, researchers are quite aware of the specific metabolic effects of palmitic acid, and fatty acid metabolism in general. The name of the game, however, is to get funded and published, and the funding people often have an agenda, and if you hope to get more money from them in the future, you'd better produce results that they like. So if some "heart healthy" whole-grain peddler or vegetable oil concern is funding your lipid research ... I can pretty much predict your results aren't going to be kind to saturated fats even before looking at your paper.

              -PK
              My blog : cogitoergoedo.com

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

              Comment


              • #22
                Hey, PKlopp! Where ya been?

                Quick question: When one goes LC for a while, they often find their fasting blood glucose approaching pre-diabetic levels of 120mg/dl. This has been explained as a result of the body not being able to differentiate well between exogenous and endogenous glucose. Often, adding in carbs reduces this high FBG. What's your take on this? Should one be concerned with high FBG on LC?

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                • #23
                  Originally posted by otzi View Post
                  Hey, PKlopp! Where ya been?

                  Quick question: When one goes LC for a while, they often find their fasting blood glucose approaching pre-diabetic levels of 120mg/dl. This has been explained as a result of the body not being able to differentiate well between exogenous and endogenous glucose. Often, adding in carbs reduces this high FBG. What's your take on this? Should one be concerned with high FBG on LC?
                  Hyperlipid: Axen and Axen (4) Ketogenic insulin resistance. It's all over now...

                  Here it is pointed out that reintroducing carbs can correct the high blood sugar (insulin resistance from a ketogenic diet) within a week.

                  But Peter ALSO suggests that the resistance caused by ketosis is quite normal, not worrisome, and even NECESSARY for people to survive on a ketogenic diet. He seems to be saying not to be concerned about it if I read this right.
                  "The cling and a clang is the metal in my head when I walk. I hear a sort of, this tinging noise - cling clang. The cling clang. So many things happen while walking. The metal in my head clangs and clings as I walk - freaks my balance out. So the natural thought is just clogged up. Totally clogged up. So we need to unplug these dams, and make the the natural flow... It sort of freaks me out. We need to unplug the dams. You cannot stop the natural flow of thought with a cling and a clang..."

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                  • #24
                    I've read that, too. Here's my deal: I was pre-diabetic prior to PB, on LC Paleo, I lost weight, improved cholesterol, and all that jazz, but FBG remained high, A1C remained high. My FBG was consistently in the 115-125 range. Adding daily starch, as in 1-2 potatoes a day, since Jan 1st, has brought my daily FBG into the 85-95 range.

                    Hoping PKlopp takes a stab at whether walking around with high FBG is OK on LC.

                    Comment


                    • #25
                      Originally posted by otzi View Post
                      I've read that, too. Here's my deal: I was pre-diabetic prior to PB, on LC Paleo, I lost weight, improved cholesterol, and all that jazz, but FBG remained high, A1C remained high. My FBG was consistently in the 115-125 range. Adding daily starch, as in 1-2 potatoes a day, since Jan 1st, has brought my daily FBG into the 85-95 range.

                      Hoping PKlopp takes a stab at whether walking around with high FBG is OK on LC.
                      Well, if such a resistance is normal and even NECESSARY in a low carb state, then it would be my assumption that having a low fasting blood sugar might not be a good thing when eating very low carb.

                      The high fasting blood glucose is probably indicating that your body is preferring fats for fuel and only those cells that absolutely REQUIRE glucose are utilizing it as a fuel.
                      "The cling and a clang is the metal in my head when I walk. I hear a sort of, this tinging noise - cling clang. The cling clang. So many things happen while walking. The metal in my head clangs and clings as I walk - freaks my balance out. So the natural thought is just clogged up. Totally clogged up. So we need to unplug these dams, and make the the natural flow... It sort of freaks me out. We need to unplug the dams. You cannot stop the natural flow of thought with a cling and a clang..."

                      Comment


                      • #26
                        Originally posted by otzi View Post
                        I've read that, too. Here's my deal: I was pre-diabetic prior to PB, on LC Paleo, I lost weight, improved cholesterol, and all that jazz, but FBG remained high, A1C remained high. My FBG was consistently in the 115-125 range. Adding daily starch, as in 1-2 potatoes a day, since Jan 1st, has brought my daily FBG into the 85-95 range.

                        Hoping PKlopp takes a stab at whether walking around with high FBG is OK on LC.
                        Hey Otzi,

                        I've been busy dealing with mini-me for the last three months. He's starting to get better at sleeping, which bodes well for the future....

                        I don't know how much sense it makes to speak of fasting blood glucose levels within the context of an HFLC adapted organism. FBG tests have an implicit assumption that you are periodically applying glucose loads throughout the day and concomitantly whipsawing your plasma glucose concentration around. Or in other words FBG != MBG ( where != means does not equal and MBG is your the average or mean blood glucose concentration ). If you are HFLC, and depending on how LC you go, it becomes increasingly likely that FBG == MBG.

                        I expect that the reason FBG creeps up over the course of an HFLC diet is due to muscles becoming increasingly insulin resistant ( read oxidizing fat for energy rather than glucose ). This has two effects. First, muscles no longer function as a sink for glucose. Second, muscles are dumping glycerol from triglyceride beta oxidation into the circulation which serves as a substrate for hepatic gluconeogenesis. So, we get a situation of more supply and less demand leading to increased stores of glucose. The liver is limited in it's capacity to store glucose, so at some point the output of gluconeogenesis will start to accumulate in the bloodstream, a.k.a. "elevated" blood glucose. Note that hepatic de novo lipogenesis from glucose would not change this cycle, it would merely alter the equilibrium point, with the liver extracting glucose to make triglycerides which would then be picked up by muscles, oxidized to glycerol, CO2, H2O, and the glycerol shipped back to the liver for gluconeogenesis. Rinse and repeat.

                        Note that I placed elevated in quotes above. This is because what constitutes an elevated level depends entirely upon our frame of reference. If our frame of reference is an individual eating a conventional diet, then an FB of 125 mg/dl is is elevated, and furthermore, we can anticipate that this level will increase during the course of the day. For the individual habitually eating HFLC, we need to consider a different question: "What is a healthy average blood glucose level."

                        With that in mind, for the HFLC individual, the number you would generally be most concerned about is your HbA1C. Glucose combines fairly readily with proteins, but most of the time this occurs under metabolic enzymatic control, and produces glycoproteins which play an important role in cell membranes, among other things. Glucose also combines spontaneously with proteins (glycation), and it is generally conceded that the higher the glucose concentration the greater the rate of glycation. Spontaneous glycation is synonymous with damage, as the resulting molecule has a different three dimensional structure, and structure is of paramount importance to the functioning of proteins. It is precisely the same as adding an additional bump to your key. That key will no longer fit the lock rendering it useless for its intended purpose.

                        While we cannot measure your average plasma glucose concentration without massively invasive testing, we can try to infer it from the rate of glucose damaged proteins that we can extract from you. Enter HbA1C. This is a blood test that measures what percent of the hemoglobin proteins in the sample is damaged by glycation. The lower the percentage that is damaged, the better. What affects the rate of glycation? Two things, glucose concentration and time of exposure. Double the average concentration of glucose, or double the time of exposure and you double the resulting glycation. An immortal blood cell would eventually have all of its hemoglobin glycated. The HbA1C test assumes an average red blood cell life span of 3 months and uses that in the model for retrospectively computing average glucose concentration. If you violate this lifespan assumption, the model's predictive ability falls apart.

                        Now, lifespan of cells is impacted by nutrient status, obviously. So diet is critical. If you had to speculate as to whether an HFLC diet increased or decreased the lifespan of erythrocytes ( red blood cells ), what would be your call? It turns out that eating LC increases the lifespan of erythrocytes, as much as doubling it. It is left as an exercise for the reader to determine whether that would increase or decrease the HbA1C numbers reported .

                        The takeaway from all of this is that you need to consider the frame of reference of diagnostic measures. If you do not slot nicely within that frame, then the validity and usefulness of the tests is compromised.

                        I cannot say whether your FBG and HbA1C signify or are indicative of pathology. I can say that we should not jump to conclusions as there are fairly obvious reasons as to why you would observe those numbers given your dietary approach.

                        With respect to the reintroduction of starches in your diet and their effects on the test results, all that accomplished was to shift your dietary context to more closely match the assumptions of the diagnostic framework. Whether that has any impact on your health, well being, and longevity is highly debatable.

                        -PK
                        Last edited by pklopp; 04-26-2013, 08:17 AM.
                        My blog : cogitoergoedo.com

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

                        Comment


                        • #27
                          You said it yourself.

                          The body synthesizes palmitic acid and prefers it as a storage fat.
                          The primary fat in breast milk is palmitic acid.

                          It sounds to me like the body really likes the stuff. The stuff that I believe are incredibly unhealthy - omega 6 and omega 3. Our body synthesizes very little of them - and for a damn good reason. Toxic stuff.
                          Don't put your trust in anyone on this forum, including me. You are the key to your own success.

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                          • #28
                            Originally posted by ChocoTaco369 View Post
                            You said it yourself.

                            The body synthesizes palmitic acid and prefers it as a storage fat.
                            The primary fat in breast milk is palmitic acid.

                            It sounds to me like the body really likes the stuff. The stuff that I believe are incredibly unhealthy - omega 6 and omega 3. Our body synthesizes very little of them - and for a damn good reason. Toxic stuff.
                            You are right that it would be incredibly odd for the body to have evolved to use a poisonous substance as its preferred storage medium. With respect to the PUFAs being toxic ... you should consider that studies that show toxicity do so in pretty much the same way that palmitate toxicity is "proven" ... by administering fats in ways that never occur in nature.

                            PUFAs are very prevalent in nature, which is why the body in general would not need to synthesize them. PUFAs are also highly reactive due to the prevalence of double bonds, especially with Omega 3 FAs. Because of this, it is imperative that your PUFAs be as fresh as possible ( i.e. from living food, not some bottle ). Further, PUFAs incorporated into the cell membrane increase the fluidity of the membrane, thereby increasing the metabolic rate of the cell as it is capable of more quickly responding to changes in the environment. This is a GOOD thing.

                            As with all things, it is possible to overdo it, however, and that's when toxicity sets in. Water is toxic in the right dose as well.

                            -PK
                            My blog : cogitoergoedo.com

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

                            Comment


                            • #29
                              Originally posted by pklopp View Post
                              You are right that it would be incredibly odd for the body to have evolved to use a poisonous substance as its preferred storage medium. With respect to the PUFAs being toxic ... you should consider that studies that show toxicity do so in pretty much the same way that palmitate toxicity is "proven" ... by administering fats in ways that never occur in nature.

                              PUFAs are very prevalent in nature, which is why the body in general would not need to synthesize them. PUFAs are also highly reactive due to the prevalence of double bonds, especially with Omega 3 FAs. Because of this, it is imperative that your PUFAs be as fresh as possible ( i.e. from living food, not some bottle ). Further, PUFAs incorporated into the cell membrane increase the fluidity of the membrane, thereby increasing the metabolic rate of the cell as it is capable of more quickly responding to changes in the environment. This is a GOOD thing.

                              As with all things, it is possible to overdo it, however, and that's when toxicity sets in. Water is toxic in the right dose as well.

                              -PK
                              I believe PUFA's exist in nature because everything on Earth is supposed to age. We are born, we live and we die. I believe PUFA's are crucial to accelerate the aging process because we are supposed to age. While eating fresh fish and raw nuts is much healthier than eating fish oil and canola oil, I believe that a diet rich in salmon and walnuts will age you faster than a diet rich in pastured beef, potatoes, watermelon and coconut. PUFA's are in everything because we are all supposed to get old and die.

                              That being said, I'd never advocate the ingestion of fully hydrogenated oils. Even though they may technically be "safer" because they're PUFA-free, I don't agree with eating laboratory generated foods. Ray Peat, even with all his anti-PUFA talk, recommends coconut oil over MCT oil because he specifically states to always choose real food over laboratory food. This is why I avoid fully hydrogenated oils. Partially hydrogenated is a no-brainer.
                              Don't put your trust in anyone on this forum, including me. You are the key to your own success.

                              Comment


                              • #30
                                Originally posted by ChocoTaco369 View Post
                                I believe PUFA's exist in nature because everything on Earth is supposed to age. We are born, we live and we die. I believe PUFA's are crucial to accelerate the aging process because we are supposed to age. While eating fresh fish and raw nuts is much healthier than eating fish oil and canola oil, I believe that a diet rich in salmon and walnuts will age you faster than a diet rich in pastured beef, potatoes, watermelon and coconut. PUFA's are in everything because we are all supposed to get old and die......
                                Dude.... what an utterly strange philosophy

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