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Mastering Nutrition Episode 6: Why “Glycation” Is a Bad Reason to Restrict Carbs

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In this episode, I respond to a listener's question about whether glycation is a good argument against a high-carbohydrate diet. I agree that we should avoid refined carbs and empty calories, but in this episode I describe why “glycation” is really a misnomer and why carbohydrate is actually likely to protect against glycation.


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Read on for the show notes.

Show Notes for Episode 6

Glycation can be driven by the metabolism of protein, carbohydrate, and fat. Insulin protects against glycation from all three sources, and insulin signaling is strongest after eating carbohydrate.

In fact, glycation may actually serve important physiological roles under conditions of low insulin signaling, so it is important not to view it as an intrinsically “bad” process.

Although there are many unknowns, the evidence, even if relatively weak, suggests that restricting carbohydrate is more likely to increase glycation rather than decrease it. I don't think that is a good argument in favor of a high-carbohydrate diet, but it certainly means that glycation is not a good argument against consuming carbohydrate.

For my related writings (which contain the relevant references), see “Start Here for Glycation and AGEs.”

For the one study I discuss that looked at the effects of the Atkins Diet on methylglyoxal concentrations (a study with very severe limitations), see “Ketosis leads to increased methylglyoxal production on the Atkins diet.”

What do you think of the amount of biochemistry in this episode? My plan is for episodes to range from 10-30 minutes with some oriented towards biochemistry and data and others oriented towards practical tips or other insights.

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19 Comments

  1. Hi Chris,

    Well I have read all this with morbid interest, believing AGE’s were the scourge of all my problems, and now you have cast doubt in my mind. So thanks for the alternative view (I kind of hope AGE’s are NOT my main problem as it would be alot simpler lol).

    Can I just ask instead, what do you think of excess phosphate added to food? I found a study which linked diphosphates. triphosphates, calcium phosphate etc. are easily absorbed in the GI tract and can contribute to heart problems, skin thinning, diabetes, kidney problems etc. What do you think of this as a problem vs glycation?

    http://oregonstate.edu/instruction/bb317/Phosphates%20and%20aging.pdf
    https://www.sciencedaily.com/releases/2015/07/150721102751.htm

    Generally I eat a lot of fruit and vegetables and I am slim weight/no actual diseases/conditions. But last year I was eating lots of things with added phosphate (meat slices, coconut milk, cheese , cakes and biscuits etc.), in addition to high phosphorus foods like oats, sardines, dairy, etc. and I had a near heart attack (massive chest pain, weak heart etc. which doctors couldn’t actually say what caused it), plus awful thin skin in places and pains in my back near kidneys. Also shoulder pains and back problems. When I cut down on the added phosphates everything improved. Causation or coincidence? I thought it was glycation at the time (from too many sugary snacks), but now I am totally thinking ADDED phosphates (vs naturally occurring).

    Anyway, thx for your continued insights and just all round ‘masterful’ attitude 🙂

  2. Hi. We have wondered whether ketosis actually do lead to elevated methylglyoxal or not. Two recent papers might question whether it is true. The first demonstrate lower dicarbonyl during a strict diet : http://rdcu.be/u6JX . Unfortunately, the authors do not measure ketones and secondly another paper that actually shows that ketones scavenge methylglyoxal: http://www.cell.com/cell-chemical-biology/fulltext/S2451-9456%2817%2930270-2#.WZb7Wj6e2zg.safelinking. The 1000-dollar question is whether you now can trust any measurement of methylglyoxal in a matrice containing ketones and secondly what the true levels are. It has also been shown that ketones decompose to methylglyoxal on oxidation, and this could also lead to false elevated levels of MG formed during the analysis..

    1. The first paper doesn’t address that question at all, as it tested caloric restriction. The second paper is interesting but from perusing it I don’t see any test of a dietary effect, so we remain with the rather poorly designed study of the Atkins diet showing the physiologically plausible elevation of MG on that diet.

  3. Dr. Masterjohn,

    I'm a big fan of your work, theories and most of all your openess to discuss science from a sort of new point of view.
    After about a year looking for some answers to my high A1C and theorethically high average blood sugar despite a low carb diet, I finally found the answer in this podcast. I was put on a very low carb diet with the aim of reducing my A1C from 5.6 to end up at 6.1 after 6 months . I was told my average blood sugar must be in the 120 mg/dL which; was at all not possible as I was measuring my blood sugar like a freak all day long and never got any value above 110 nor stayed longer than that for more than an hour plus my FBS average was 87-90. My blood lipids were all in the healthy range, still was told I was borderline Type 2 and hypothyroid. In summary, I got worse in a very low carb diet so I did re-introduce carbs again and feel much better. I'm not and was never overweight so, not a problem at all.
    I will continue reading your posts as I'm still intrigued on why or what nutrient deficiencies are behind cases like mine as I've seen many people improving on a very low carb diet. It works but, it is not for every one.
    Thanks for sharing your work with us.
    Mónica

    1. Monica, thank you for sharing your story. I've heard others like it, and it's not surprising because it has been known for over a half century that carbs increase glucose tolerance and that was the traditional rationale of standardizing carb intake for a couple weeks before a glucose tolerance test. I'm glad you're feeling better.

      Chris

  4. AWESOME episode! Would love to hear how all this relates to a1c and diabetes. I've also heard a few people talk about how a1c is not as reliable to measure average glucose as we thought and is used in clinical practice. Can we get a glycation part 2?!

    1. Hi Tracy,

      Good idea! In short, it is useful but confounded by fructosamine 3-kinase activity (deglycates hemoglobin) and by red blood cell turnover (higher rate lowers Hba1c). Also, there is no evidence that Hba1c plays a causal role in diabetes.

      Chris

  5. The amount of biochemistry is great!

    What I enjoy most, is seeing how very smart people, can deeply analyze and research the same topic and data, yet arrive at very different conclusions! The insulin-obesity model is my favorite.. for example, Peter Attia (former President of NuSI), and Dom D'Agostino both very well credentialed, tout a low-carb ketogenic diet, and have plenty of biochemistry to show..

    https://eatingacademy.com/nutrition/ketosis-advantaged-or-misunderstood-state-part-ii

    On the other end, you have researchers like Stephen Guyenet who aren't so convinced:

    https://wholehealthsource.blogspot.com/2016/01/testing-insulin-model-response-to-dr.html

    Sugar, is also a good one.. Robert Lustic (Bitter Truth fame) say fructose (and by extension HFCS) is metabolized differently than glucose, to promote weight gain. Alan Aragon makes compelling counterpoints:

    https://www.alanaragonblog.com/2010/02/19/a-retrospective-of-the-fructose-alarmism-debate/

    While the smoke settles, any plans for podcast on Intermittent fasting?

  6. Chris, I enjoy the detailed level of biochemistry. Even when I don't follow all of it, it gives me a sense of the context and the bigger picture. It squelches the tendency to over simplify

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