My Paleo f(x) presentation was on using fat-soluble vitamins to optimize sex hormones, but I also discussed the importance of body fat and carbohydrate intake for fertility and in this podcast I also discuss why using a low-carbohydrate diet to treat type 1 diabetes could negatively affect thyroid hormone and sex hormones.

Mastering Nutrition Episode 11: Paleo f(x) Grab Bag: Carbs, Sex Hormones, Type 1 Diabetes, and More

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My Paleo f(x) presentation was on using fat-soluble vitamins to optimize sex hormones, but I also discussed the importance of body fat and carbohydrate intake for fertility and in this podcast I also discuss why using a low-carbohydrate diet to treat type 1 diabetes could negatively affect thyroid hormone and sex hormones.

In this episode, I discuss some important insights from my Paleo f(x) talk and audience responses to it, including the potential dangers of treating type 1 diabetes with a low-carb diet, the importance of carbs and body fat for fertility and sex hormones, and why some people might have a great sex hormone profile on a long-term ketogenic diet despite the importance of insulin's contribution to fertility.

I also discuss Headspace meditation, contrast showers, Snapchat, U.S. Wellness Meats liverwurst, Kettle and Fire's upcoming chicken broth and chicken mushroom broth, and my interview with Ben Greenfield.

Listen on ITunes or Stitcher.
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Read on for the show notes and relevant links.

Show Notes for Episode 11

If you only want part of what's in here, you can use this to navigate:

1:30 Meditating with Headspace
2:40 Contrast showers
3:40 Snapchat
5:50 Paleo f(x)
U.S. Wellness Meats liverwurst
9:05 Kettle and Fire chicken and chicken mushroom broth
10:18 Ben Greenfield interviewed me for his podcast
12:00 The importance of body fat and carbohydrate intake for fertility
23:30 Low-carb diet for type 1 diabetes, with low thyroid and sex hormones as side effect
29:30 Great sex hormone profile on a long-term ketogenic diet
36:25 Upcoming stuff

Relevant Links for Episode 11

Here is the link to Headspace, although I would recommend downloading it from your app store if you use a smart phone.

I learned the science about cold showers and contrast showers from FoundMyFitness, specifically the February 11 and May 3 episodes. A major point of inspiration for me to “take the plunge” (lame pun completely intended) was Chase Jarvis's interview with Kevin Rose on 30 Days of Genius, where they discuss why they both use cold showers every day. I highly recommend the entire series as a source of creative inspiration.

My Snapchat username is chrismasterjohn.

This is the US Wellness liverwurst.

Here is the link to Kettle and Fire broth sold by Thrive. That's the beef broth. The K&F folks told me when the chicken and chicken mushroom come out in four weeks, Thrive will be carrying them.

Here is the link to my podcast interview with Ben Greenfield.

Here is the link to my Examine.Com editorial on carbs and insulin support for the antioxidant system and protection against glycation.

Here is a review about leptin and fertility.

Here is a review about leptin and thyroid hormone.

Some studies on insulin's effect on genes related to thyroid hormone production and activation: 1, 2, 3

Colpo vs. Perfect Health Diet debate about carbs and thyroid: Colpo, PHD, Colpo, PHD, PHD (while the limitations and implications are debated, these posts contain references clearly showing that low-carb diets as tested decrease thyroid hormone levels)

A classic and highly related post of mine: The Central Role of Thyroid Hormone in Governing LDL Receptor Activity and the Risk of Heart Disease

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  1. Hi Celeste,

    Thank you for your comment.

    I think you are missing my point here. I wan’t talking about autoimmune thyroid disorders. I was talking about thyroid hormone production.

    Less carbohydrate and less insulin will mean less production and activation of thyroid hormone, all other things being equal. This is a physiological principle that is unrelated to autoimmunity. It is also derived from mechanistic evidence as well as randomized controlled trials, and it is not an example of a mere correlation.


  2. Chris…first I have to say Thank You to you and all other Podcasters willing to give freely of their knowledge. I will admit…I am probably the most “lay” of all the people listening to you so forgive my attempt at a conflicting thought. First…no Type I Diabetic can “get off Insulin.” Prior to the use of insulin circa 1920 people with Type I Diabetes died from lack of insulin. Perhaps you meant “reduce” rather than “get off.” Dr. Richard K. Bernstein, himself a Type I Diabetic and now specializes in the treatment of Diabetics, has found that almost everyone of his patients has Thyroid Disease and come to his practice that way. They have “out of control” blood sugar due to eating the ADA high carbohydrate diet which they are chasing with insulin to no avail…so high carbs and plenty of insulin and still have Thyroid Disease. Dr. Bernstein has repeatedly stated that he believes the majority of people with autoimmune disease “always” get more than one autoimmune disease with Thyroid being the most common. I suspect (again…I am not trained) that low carb would not create an autoimmune condition on it’s own. Also…as you and all in the Paleo/low carb community have repeatedly said…”Correlation does not equal causation.” Having or seeing low thyroid function with low-carb or Type I Diabetes does not mean that the low carb caused it. I guess a study would have to look something like this: Two groups of participants all tested and free of Thyroid Disease, and Diabetes; one group eating a moderate to high carb diet and the other eating a low carb diet; they are followed for a number (?) of years and retested. As is often said…that study will not be done and control would be a nightmare. My Type I husband follows Dr. Bernstein’s protocol and is regularly told after his various checkups that he tests like a non-diabetic. Seeing he really does not have an option…why even criticize what he has. Why point out that life has dealt him a bad hand cause he is between a rock and a hard place… offer solutions…not criticism. At 64 he does not have the typical complications of Diabetes. I think you have some maturing to do. 🙁

  3. Chris- I have appreciated your perspective and contributions the last several years so I have really enjoyed your podcasts so far and was both pleased and surprised to hear you mention the liverwurst because I never hear about it even though I've thought it to be a spectacular and unique product. My children eat it (2 devour it, 2 don't mind it) along with me and it has been a staple at my house for years. I hope your podcast inspires many others to try it as long as they are able to keep it in stock for guys like us. 🙂

  4. Thanks for another great episode, Chris!

    You mention the importance of insulin secretion for hormone production and overall health. How often do you feel an insulin spike is necessary to reap these benefits? I personally cycle calories and carbohydrates to match my strength training days. On my off days (3 days a week), I am getting very few carbs (<50grams just from leafy greens) and a higher fat intake. My protein is kept constant. I only do some walking on these days so I do not require a lot of glucose. However, I know in recent podcasts you have said 100grams is about the minimum you would go to maintain adequate liver glycogen.

    Therefore, would you suggest keeping carbs to at least 100grams on off days even if I am getting a lot of carbs on my training days (~300) along with a caloric surplus?

    Just curious how often I need to elevate carbs (both across a week and within a given day) for the benefits of insulin secretion?

    1. Hi Zach,

      That's a great question and I don't have a clear and definitive answer for you.

      I think if you're getting all your carbs from leafy greens on some days, that is probably an overestimate of the carbs you are getting, because I doubt the carbohydrate is fully bioavailable in very fibrous leafy vegetables.

      I really don't know where the dividing line is between inadequate and adequate insulin signaling in the context you are asking.

      I think the best way to individualize it is to look for signs of stress. For example, if you are not recovering well from your exercise where you are not meeting your performance goals, more carbs might help. If you have signs of excess cortisol or HPA axis dysfunction, that could be from not enough carbs. But if your well-being and health and performance is right where you want it to be, then I wouldn't worry about the carbs in your case.


  5. [2]

    You also discuss how carbohydrates and insulin replenish glutathione pools, maintaining normal physiological status. I know you’ve studied diligently. Clearly carbohydrates are meant to be handled with feedback towards glutathione replenishment – normal physiology so far. First, if "glyoxalase-1 activity indirectly determines MG [methylglyoxal] toxicity and the rate of AGEs formation” (Allaman et al. 2015) and GSH recycling takes place at S-D-lactoylglutathione, something becomes apparent: big increases in MG levels and/or low Glo-2 activity can cause S-D-lactoylglutathione to accumulate. This has for effect of trapping GSH and rendering it unavailable for defence against oxidative stress.
    So although I agree without that carbs/insulin have a normal feedback to handle their downstream alpha-oxoaldehydes, the rate of flux down glycolysis & the pentose phosphate pathway matters as to balance the anti-oxidant status. Although lipids & protein contribute to it to, their advantage (in humans) is that it lessens the use of the major pathway producing the end-product MG that remains the major contributor to AGEs (despite it’s lower reactivity on a per-molecule basis).

    Lastly, you state that “insulin (influenced most strongly by acute intake of carbohydrate) as a metric of short-term energy status.”. This is true of course. I think it does something else which also negates the harm you seem to imply potentially occurs from insufficient insulin signaling on carb-restricted diets. Protein will stimulate insulin. It will feedback into replenishing glutathione pools. It will signal growth factors for sex hormones, leptin and insulin dependent cascades.

    I appreciate you engaging with me and will continue listening to your podcast in the hopes of more interesting discussions arising from it. Feel free to contact me at raphi.inter[at]

    1. Raphi,

      I agree that a high GLO-1 and low GLO-2 activity will lead to sequestering glutathione as S-D-lactoylglutathione. In general, GLO-1 is regarded as rate-limiting so in most cases this is not relevant. I published a paper arguing that GLO-2 is limiting in rat adipose tissue. Notably, however, it is not in liver and much more MG is made in liver. GLO-1 and GLO-2 ratios vary with the cell cycle, and it is probably the case that this occurs in a regulated fashion to control the level of glutathione, and perhaps to control the level of MG and perhaps perhaps to control the level of S-D-lactoylglutathione in order to control cellular differentiation and proliferation, which is an argument that Szent-Gyorgyi made in his day. However, I do not understand why you are bringing this up here and I do not see its relevance to this discussion.

      Your statement that the advantage of proteins and lipids is "that it lessens the use of the major pathway producing the endproduct MG" is dubious. There is no evidence that glycolysis is "the major pathway" and there is evidence that ketogenesis becomes quantitatively dominant when it occurs, so there is no basis for the idea that lessening carbohydrate load would lessen MG. I have gone over this clearly in episode 6. The evidence leans modestly in the opposite direction.

      You are very wrong about protein and glutathione. MOST of insulin's functions are inhibited by glucagon, and protein stimulates glucagon. The reason protein stimulates insulin is to drive certain amino acids into cells. Protein also stimulates glucagon so that this will not drive blood sugar down. But if you look beyond macronutrients, glucagon also antagonizes many other effects of insulin.

      Glucagon antagonizes GSH synthesis:

      So, no, protein will not achieve the effect of insulin on glutathione synthesis. Don't get me wrong. Protein is necessary to provide the amino acids and its stimulation of insulin will compensate for its stimulation of glucagon. But it will not provide the net energy signal that carbohydrate will.

      And protein should not be regarded as a stimulus for independent pathways that is interchangeable with carbohydrate. Most of these pathways should be regarded as a function primarily of carbohydrate.


    2. Hi Chris,

      I bring up Glo-1 because some authors (such as Allaman 2015) see it as a crunch point where sufficient flux through the glycolytic pathway may produce AGEs to pathological extents.

      I understood your argument about Ketogenesis vs Glycolysis in episode 6. Although it was informative, I do not remember you giving hard and fast numbers about their differential contribution to AGEs (aside from their reactivity on a per molecule basis). I could be wrong but their seems to be an implicit assumption their, that there is no inherent benefit of ketones to lowering glycation and/or oxidative stress. If this is your argument, stepping back we can see consider how ketones are simply less reactive than aldehydes (partially due to their being less steric hindrance in aldehydes than in ketones). In vitro, evidence shows that ketones reduce oxidative stress (Maalouf 2007, Kim do et al. 2007). In vivo, rats fed a ketogenic diet increased CGL activity leading to increased GSH biosynthesis in their hippocampi (Milder 2012). Most importantly maybe, BhB blocks the NLRP3 inflammasome–mediated inflammatory disease (Youm 2015).
      Although your comparison of the contribution of Glycolysis vs Ketogenesis to AGEs is welcome, without the full context their respective contributions to overall AGEs/oxidative stress is unclear.

    3. You said “But it [protein] will not provide the net energy signal that carbohydrate will.”
      Sure, but so what? Are you proposing that without this net signal some essential (in the technical sense of the word) function is lost?

      I’m not equating protein to carbohydrate but I am saying we do have insulin pulses from protein – which we need. And yes carbohydrate does things via insulin that protein doesn’t. But what is the significance of this? Do we see pathology by not including carbohydrate?
      You say “Protein also stimulates glucagon so that this will not drive blood sugar down.” Agreed, we see this in highly insulin resistant patients who not only benefit from lowering carbs but also from moderating their protein. You also say “But if you look beyond macronutrients, glucagon also antagonizes many other effects of insulin.” Agreed, Luft’s expriments in insulin -/- mice demonstrate this nicely. He also showed how glucagon has an underappreciated role in blood sugar control & provided a good argument from dropping the excessively insulinocentric view of diabetes (i agree!).

      I share your willingness to look beyond macronutrients. I do. But neither do I wish to do so whilst minimizing their importance.

      I look forward to hearing you reply here and/or discussing some of these points on your podcast.

      Cheers Chris!

    4. Raphi,

      I agree GLO-1 is relevant. Insulin stimulates GLO-1 expression. So, I don’t see how considering GLO-1 does anything other than add to my argument.

      I didn’t give “hard and fast numbers about” ketogenesis and glycolysis “contribution to AGEs” because no one has ever developed any. However, when considering all of the evidence combined there is the most in vivo evidence for ketogenesis, the least in vivo evidence for threonine, and intermediate evidence for glycolysis as a source of methylglyoxal. One thing I did point out is that insulin suppresses generation of methylglyoxal from all three sources including glycolysis. And the only study that made any attempt to look at this found higher methylglyoxal on the Atkins diet. As I noted, the study has severe limitations. But all of the biochemistry and the small amount of in vivo evidence points toward greater methylglyoxal under ketogenic conditions, so it strikes me as silly to argue the opposite point without admitting that the evidence leans quite favorably in the direction of ketogenesis increasing methylglyoxal, the quantitatively most important source of AGEs.

      Regarding the different levels of evidence for the different sources, I reviewed it in detail in my doctoral dissertation. I will try to find a way to make that freely available soon.

      I don’t see the relevance of the fact that ketones are less reactive than aldehydes. The point is that ketones generate methylglyxoxal, the principle aldehyde we care about.

      That is interesting about the rat hippocampi. I can imagine there are benefits to the hippocamus under those conditions. However, I have to assume the rat hippocampus is a miniscule source of whole-body glutathione and that it is also a minuscule source of methylglyoxal. On a ketogenic diet, most methylglyoxal should be produced in the liver, and in virtually any condition most glutathione should be produced in the liver.

      If you could please provide a pubmed link or a fuller citation, I would appreciate it as the study you cite sounds interesting and I was unaware of it. (It is very difficult to find anything with just an author and year).

      The “so what” about net energy signal is that if protein stimulates insulin and glucagon, and if insulin promotes glutathione synthesis while glucagon inhibits it, then protein does not provide a net regulatory stimulus of glutathione synthesis.

      In looking at our Twitter exchange ( it seems we are getting off track. I believe the goal here was to discuss your argument that intracellular insulin signaling is best corrected by decreasing circulating insulin, or that it is necessarily corrected by doing so. We seem to have dropped that discussion entirely. Did you have further comments on it? I intend to release a podcast about it next week.

      Thank you for the friendly dialogue.


    5. Hi Chris,

      I am taking us a bit off track 🙂

      I'll just provide full links from now on (duh, haha). The point about rat hippocampi I referenced I got from "Acute oxidative stress and systemic Nrf2 activation by the ketogenic diet" (Milder et al. 2010 Another relevant one is "The ketogenic diet increases mitochondrial glutathione levels [in rats]" (Jarrett, Milder et al. 2008

      I need to read up more on glutathione synthesis (you clearly have a better overall view of it) so that I can make it fit into my understanding of oxidative stress. Rather than immediately carrying on the discussion I should first finish listening to your last podcasts on HbA1c & glycation (part 2) as well as your upcoming one on insulin signaling.

      Looking forward to it!


    6. Hi Raphi,

      Thank you for providing the references.

      I will have to look at the study in further detail for my definitive interpretation. The abstract of the first study indicates that a ketogenic diet causes oxidative stress. Stimulation of Nrf2 is accomplished by a variety of things that are both good and bad. For example, cigarette smoking does it, and so do the polyphenols in fruits and vegetables. Everything that activates Nrf2 does it by causing oxidative stress. Nrf2 upregulates antioxidant defense in response to oxidative stress.

      This indicates that a ketogenic diet is a stress that, if provided in the right dose in the right circumstance with the right adaptive capacity, can provide a benefit through hormesis.

      However, in perusing the figures I see that this study shows that throughout its length hepatic glutathione was obliterated and lipid peroxidation was increased. I therefore find it doubtful that the ketogenic diet is overall beneficial, and I am surprised that you mentioned it as such.

      The second study appears to have only looked at hippocampi. I would have wanted to know what happened in tissues that would be expected to account for most of the glutathione, such as the liver.

      It also isn't clear to me whether the rats were fasted before the measurements. Fasting causes a dramatic decrease in glutathione. So, I wouldn't be surprised if fasting levels of glutathione could be similar or higher on a ketogenic diet, yet total exposure to glutathione be lower as a result of poor glutathione status in the fed state of the ketogenic diet compared to the fed state of the non-ketogenic diet.

      In any case, it seems like the first study gives a better impression of what happens in the whole body, and is consistent with what I would expect.


  6. [1]

    Hi Chris,

    This is @raphaels7, you invited me to leave a comment on your blog about Extracellular insulin damage vs Intracellular insulin signaling damage (that you brought up on an episode of the Ben Greenfield's podcast).

    Some of the points you brought up there were also discussed in your Examine Editorial “Sugar is the ultimate antioxidant and insulin will make you younger: Appreciating a few poorly recognized but critical contributions of carbohydrate” which I have read.

    In the editorial, you say “Insulin would protect against 3-deoxyglucosone accumulation by clearing glucose from the blood and stimulating its downstream intracellular metabolism”.
    I take this to mean that this action is intrinsically protective. However, 1 prediction that comes from this is that administering insulin to diabetics (suffering nephropathies, neuropathies etc.) or stimulating its release via more carbohydrate would reduce the damage to the small vasculature in their kidneys, eyes and feet. But it does not. In fact, it get worse. Moving glucose from the blood into different does not mitigate the damage & may in fact worsen it. We have an inkling as to why this is by looking at the electron transport chain (ETC).

    Superoxide production at Complex 1 exiting the mitochondria as H2O2 puts the brakes on PTP 1B. This allows insulin receptor autophosphorylatin, enabling insulin signaling to occur. Thus, “mitochondrial superoxide/H2O2 controls insulin function and subsequent blood glucose levels” (Petro Dobromylskyj). It is ground-zero for insulin signaling. Pancreatic release is secondary to lower-level mitochondrial signaling (how can it not be?). You contend increasing carbohydrate content will improve poor intracellular insulin signaling, the locus of damage in diabetics. But if cycles of hyperinsulinemia cause insulin resistance (like cycles of antibiotics cause anti-biotic resistance), how is it that more insulin will increase the low levels of intracellular signaling? Would it not be more straight forward to generate reverse electron flow to Complex 1 by feeding FADH2 at Complex 3? You get *physiological insulin resistance* (rather than pathological insulin resistance) because another substrate provides adequate NAD+/NADH redox status all the while limiting the need for the substrate entering the mitochondria as pyruvate. Hence, less total insulin production is required, breaking the hyperinsulinemic cycle that lowered the intracellular insulin signaling in the first place.

    1. Hi Raphi,

      Please provide a reference that supports the statement that insulin makes diabetic complications worse.

      What I said is that insulin would help prevent 3-deoxyglucosone from forming. I believe that is correct, and I must reiterate that the blood is most likely the compartment where 3-deoxyglucosone is a quantitatively major contributor to AGEs.

      Intracellularly, type 2 diabetes and obesity-associated insulin resistance involves energy overload. I did make the point that insulin increases the synthesis of glutathione, but to be clear I am not advocating that as a treatment for diabetes. Energy overload must be resolved as it is the driving pathological feature that has implications well beyond glucose and insulin.

      I disagree that "cycles of hyperinsulinemia cause insulin resistance."

      I do not understand what you mean about reverse electron flow or why you would expect it to resolve the issue. FADH2 can contribute to oxidative stress if CoQ10 is limiting.

      I don't follow the last several sentences.


    2. Hi Chris,

      Thanks for the thoughtful reply.

      Here are just 3 references for insulin administration not helping or worsening (Type 2) diabetic complications and mortality outcomes:
      Conclusion: “In a large representative cohort of adults with type 2 diabetes, more aggressive glucose-control strategies have mixed short-term effects on microvascular complications and do not reduce the myocardial infarction rate over 4 years of follow-up. These findings are consistent with the results of recent clinical trials, but confirmation over longer periods of observation is needed”
      [As an anecdotal aside, my granmother was treated with insulin (amongst other meds for her diabetes) and was on a constant blood sugar roller coaster as her microvasculature complications only got worse. This is the norm. Many MDs I have spoken to confirmed that this is the case.]

      Conclusions: “As compared with standard therapy, the use of intensive therapy for 3.7 years to target a glycated hemoglobin level below 6% reduced 5-year nonfatal myocardial infarctions but increased 5-year mortality. Such a strategy cannot be recommended for high-risk patients with advanced type 2 diabetes”

We’ve been using insulin intensively for more than a century now and the rates have only gone up
      Conclusions: “In high-risk people with type 2 diabetes monitored for 9 years, a mean of 3.7 years of intensive glycemic control had a neutral effect on death and nonfatal cardiovascular events but increased cardiovascular-related death”

      As for 3-deoxyglucosone, first, I agree that (acutely) insulin will clear it from the blood, reducing 3-DG’s AGE effects there. Where doe insulin clear it to? Or does it just impede its production? I ask because “3-DG inactivates intracellular enzymes such as glutathione peroxidase […] thus, intracellular accumulation of 3-DG may enhance oxidative stress by inactivating the antioxidant enzymes” (Niwa et al. 2001).
      Second, “In diabetes, hyperglycemia enhances the synthesis of 3-DG via the Maillard reaction and the polyol pathway” (Niwa et al. 2001) which as you propose, is (temporarily) mitigated by insulin. However, in diabetics, we would be relying on an every-growing insulin bolus to handle this which leads to insulinotoxicity. Like you say, it’s not all about glucotoxicity. Dr.Fung has discussed the isssues insulinotoxicity associated with insulin administration in diabetics by looking at data from multiple trials ( Also, feeding more carbohydrates to diabetics (people intolerant to excessively high levels of carbohydrates) to raise their insulin is not a viable strategy as you pointed out. Furthermore, adminstration of peripheral insulin is problematic as the portal vein does not see enough and there remains proportionally too much in peripheral circulation. This leads me to your point about not agreeing that “cycles of hyperinsulinemia does not cause insulin resistance”.

    3. When sufficiently high & persistent levels of a drug lead to down-regulation of its target receptor, is that not what cycles of hyperinsulinemia do? What exempts insulin from this mechanism?
      Diabetes is a problem of energy overload. One of the main levers to pull to address that is insulin signaling, right? Biasing macronutrients to lower the insulin load is 1 tool. Another, is the frequency of energy intake (intermittent or prolonged fasting). Another yet, is improved sleep. And on the list goes. All of those I just mentioned affect energy overload and their effects are partially mediated through insulin signalling.

      I apologize if my description of the ETC was unclear. I will try to simplify. I was taking your line of intracellular insulin signalin and relating it back to how electrons flow through the ETC. I was making the case that how they flow determines the redox state of the cell which is ground-zero for 1) cellular energy overload 2) intracellular insulin signaling 3) oxidative stress. 1, 2 and 3 were all of concern to you in diabetic complications. Ultimately, my point is that introducing agents (whether dietary or otherwise) that prompt more insulin to be produced too often will exacerbate insulin resistance and diabetes. But you seem to disagree with this fundamental interpretation.
      Lastly, my point about Pathological vs Physiological insulin resistance was to highlight that the former is when dietary or kind of agents prompt too much insulin too often whilst the latter occurs when the cell has access to substrates that do not drive hyperinsulinemic cycles but simply prioritize glucose for certain body parts over others (brain over muscle for example).

    4. Raphi,

      Thank you for the references on insulin’s effect on morbidity and mortality. I will check them out.

      I want to emphasize and reiterate that my point in the Examine.Com editorial was not that T2D should be treated with insulin. It was that the study I cited shows proof of principle that glycation and antioxidant defense is suffering from inadequate intracellular insulin signaling. I regard the cause of this as cellular energy overload, and administration of insulin cannot fix that.

      3-DG is significant but minor compared to methylglyoxal (MG), particularly intracellularly in cells other than blood cells, where MG is overwhelmingly the major cause of AGEs in diabetic tissue. Insulin is not as important in preventing 3-DG accumulation as it is for MG accumulation and its main effect is to move glucose into cells and stimulate its consumption for energy.

      About insulin, I regard the origin of insulin resistance cellular energy overload, not systemic circulating insulin. I will explain this in a podcast soon. Yes, of course if you keep the cause there and add more insulin, the cell will not respond to the additional insulin, but that is not, in my view, the cause of the resistance.


  7. Hi Chris,

    Great podcast again. The day before I was just thinking on insulin relationship to thyroid and sex hormones, so this came in the right moment. I'm one of those cases where low insulin because of low carb eating ruins thyroid and hormonal output. I start getting cold right after 5-7 days in a row on low carb and also, I had discovered that my body needs at least 24% body fat to function properly. I do naturally eat low carb as I am gluten sensitive and eat no processed foods at all but, have to keep an eye on my carbs intake -usually to eat more-.
    This podcast gave me a lot of information about how important insulin is for many metabolic processes rather than just keeping blood glucose under control.
    Thanks again for sharing so much knowledge with all of us.

    *excuse my english, is not my first language*

  8. Hi Chris,

    Great podcast! Would love to here your thoughts on higher dose resveratrol (500mg/day) and mitochondrial biogenesis.



    1. Hi Unknown,

      I'm weighing some options to monetize the podcast, mainly Patreon and sponsors. At the moment, I cannot afford to have transcripts made, but if I find a way to finance that I will do it.


  9. Please be careful about recommending Thrive Market. They are possibly the worst company I've ever dealt with…they make canceling your membership nearly impossible. I had to file a complaint with the BBB in order to get them to do it.

    1. I agree Janet. I thought I had it cancelled, then it showed up on my credit card a year later. Good thing I look at my credit card statements!

  10. Chris,

    As a Type 1 Diabetic on a ketogenic/low-carb diet, I too have found my thyroid hormone dropping and TSH shooting up. All other hormones are normal. The benefit is that blood sugars are almost to a normal level. In the long run, I do think that having normal blood sugars outweighs having low Thyroid hormones, although I understand that this approach is not optimal and not what I would choose if I had the choice. Is there anything you could recommend for Type 1 Diabetics, not just in terms of Thyroid and Sex Hormones, but in general for Diabetics? For instance, in one of your recent papers you discussed the use of mega doses of gamma-tocopherol to reduce MGO formation in diabetics.

    1. Unknown,

      Thanks for your comments. Supporting the antioxidant system is broader than just vitamin E, so I don't think megadosing is the right way, but broad-based nutritional support of the antioxidant system is likely to help.


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