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Follow Up - Insulin Resistance

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  • Follow Up - Insulin Resistance


    Was chatting with a friend about the topic of Insulin Resistance (IR) after re-watching Dr. Brewer's March 25, 2018, video and she suggested the main cause of IR are fats, both dietary fat (primarily Saturated Fat) along with fats released by the body, referencing information from Dr. Michael Greger (eg ) and Dr. Joel Fuhrman (she copied a page from one of his books that states about the same thing). She also mentioned this video where another MD, Dr. Davis, also states it is the fat in the muscles. Also mentioned in the video is the impact of fat on blood flow, etc., and yet another MD, Joel Kahn, who has done work in this area.

    Soooo...I started doing some digging and found information backing what Davis, Greger, etc., discuss.



  • #2
    Preed: That theory has been floating around for about 15 years. It goes something like this:

    "Insulin sensitivity is also affected by the quality of dietary fat, independently of its effects on body weight. Epidemiological evidence and intervention studies clearly show that in humans saturated fat significantly worsen insulin-resistance, while monounsaturated and polyunsaturated fatty acids improve it through modifications in the composition of cell membranes which reflect at least in part dietary fat composition."

    I have not seen any epidemiological reports or other quality studies that support this theory. Do you have links that support this?

    The science is overwhelming that insulin resistance is a condition of poor carbohydrate metabolism driven by age, obesity, sedentarism and overabundance of carbohydrate intake. My insulin resistance improved on high-fat, low-carb and moderate.

    I don't believe much of anything Greger promotes in his videos. He is a evangelical vegan and well known animal rights activist. I find his agenda is unclear, but he is clearly biased.


    • #3
      Hi John,

      Here are a few of the items that I had found:

      A change of the proportions of dietary fatty acids, decreasing saturated fatty acid and increasing monounsaturated fatty acid, improves insulin sensitivity but has no effect on insulin secretion. A beneficial impact of the fat quality on insulin sensitivity is not seen in individuals with a high fat intake (> 37E%).

      Taken together, the evidence suggests that replacing saturated fats and trans fatty acids with unsaturated (polyunsaturated and/or monounsaturated) fats has beneficial effects on insulin sensitivity and is likely to reduce risk of type 2 diabetes.

      Moreover, the diet for the treatment of the metabolic syndrome should be limited in the intake of saturated fat, while high fibre/low-glycaemic-index foods should be used without specific limitations. Moderate amounts of monounsaturated fat could be permitted as they do not induce detrimental metabolic effects.

      I used to have a copy of Dr. Barry Sears' book, Enter the Zone, and he had a section dedicated to Saturated Fats as I recall that recommended against them for similar reasons as well as their being very inflammatory (quite a bit of information on that):

      However, there are some fats you want to restrict in your diet. These are saturated fats, trans fats and (AA) arachidonic acid. I consider these to be really "bad" fats. Arachidonic acids are found primarily in fatty red meats, egg yolks and organ meats.


      • #4
        One other consideration: if science has shown Saturated Fatty Acids are inflammatory (perhaps a point of agreement?) -- after all, bodyfat is stored triglycerides aka SFAs, if I recall and we know the bad affects internally -- and speakers like Dr. Davis and Dr. Greger focus on the **potential** harmful affects regarding Insulin Resistance via SFAs, but, no mention of Omega 3s or MUFAs, wouldn't that be a smarter option?

        (Dr. Brewer - Didn't you mention something about the consumption a liter of olive oil per week and its beneficial affects?)


        • #5
          One follow up: PLOS Medicine, July 19, 2016, Effects of Saturated Fat, etc. ( - Page 13 of 16:

          In vitro, even-chain SFA, including myristic acid (14:0) and palmitic acid (16:0), activates pro-inflammatory cascades, induces skeletal muscle insulin resistance, and damages pancreatic β-cells, while the MUFA oleic acid (18:1) may partly protect against some of these effects [35,4749]. However, in vivo, dietary SFA and MUFA may be readily oxidized as energy sources [50,51], while tissue levels of major SFA and MUFA may be at least equally influenced by endogenous hepatic synthesis of fatty acids rather than direct dietary intake [52]. This explains why dietary starch and sugars, which activate hepatic de novo lipogenesis, are positively associated with blood levels of major SFA and MUFA [5254]. Thus, effects of blood and tissue SFA and MUFA may not inform and should be separately considered from biologic effects of dietary SFA and MUFA.


          • Robin
            Robin commented
            Editing a comment
            My insulin resistance and cholesterol improved after 15 years of prior vegan eating....when I went low carb, high good fats...and eggs, salmon, other fish. No cow, pig, chicken, turkey or other animals though.

        • #6
          Robin: What is a "high good fat?" Thanks


          • #7
            OAG: Extra virgin olive oil, avocados, avocado oil, cold water fatty fish (sardines, salmon, halibut, herring, etc.), eggs, nuts such as raw or dry roasted macadamias, almonds, walnuts, pistachios, lean meats for good protein. Consider using MCT oil too. All of these really will help make up for carb calories that need to be drastically reduced. These fats also increase ketones and insulin sensitivity and help to decrease hunger.


            • #8
              My experience is similar to what Robin describes. Years of plant-based eating. Since it was also low-fat, I got most of my calories from grain-based carbs. My IR improved dramatically when I replaced the carbs with oils. I eat lots of olive oil. And avocado oil.


              • #9
                Yep. I always fhought nothing feeds cancer cells quite like glucose. Then this article appeared on my computer screen from MIT that claims the amino acid glutamine may be the main culprit. I have to think about this.

                ”How cancer cells fuel their growth”



                • #10

                  It would seem like the article is using an apples and oranges comparison because cells, even cancer cells, are going to by necessity use most of the existing genetic machinery to generate new cells. That those cancer cells use glucose or glutamine as fuel and don't go through the standard Kreb Cycle/ETC doesn't to me mean that they have a fundamentally different uptake of standard nutrients for the building blocks of the cancer cells. Maybe I missed something there. It might give an indication of how difficult it can be to stop cancer by limiting certain nutrients though.


                  • #11
                    I recently listened to a podcast whose guest was a researcher, Navdeep Chandel, who explained some of the more recent findings about cancer tumor growth and glucose/glutamine intake that surprised me (and probably will others). It ties in with the MIT article above in a way that I could not understand before. Navdeep Chandel was one of the authors of the below referenced 2016 paper. Otto Warburg's notable finding many decades ago was that cancer cells in vitro were using glycolosis quite a bit (producing lactate) even when oxygen was sufficient for mitochondria to produce ATP efficiently. There have been a lot of explanations about why that occurs including defective mitochondria DNA, a theory that mitochondria ROS would promote apoptosis for a cancer cell and hypoxia at least at some stages of tumor growth. Once genetic tools became available to definitely knock out the mitochondria ATP production by inhibiting ETC Complex I, Navdeep Chandel found out that in fact cancer tumors could not grow well. Despite what has been thought all of these years by many, functioning mitochondria are essential for cancer tumor growth. Going back to that MIT article, it (and the below article) indicate that the cancer cells use that extra pyruvate from the increased glucose intake and glutamine as building blocks for new cells with a focus on accelerated growth (e.g. new DNA requires ribose, etc.) being the driver rather than energy efficiency. Some slow growing cancers (e.g. standard prostate cancer) might only use their mitochondria function until a later stage. There is some work on trying to decrease ETC Complex I in cancer cells without killing nearby healthy cells. Interesting in that this is likely metformin's "anti-cancer" effect as it in fact lowers ETC Complex I activity to a small degree in some tissues. Also interesting in how this plays into using nutrients as part of a cancer treatment. If anybody wants to hear the entire Navdeep Chandel podcast, it is on Peter Attia's podcast page.



                    • #12
                      Anti-angiogenic foods help to cut off the nutrient supplies that fuel tumor growth. It works well as an adjunct therapy for people receiving standard medical cancer treatments as well