Sunday, February 26, 2012

My Interview With "Ask Bryan" Davis on his "Doc Fermento Discovers the World" Podcast is Now Up!

by Chris Masterjohn

Last Friday I recorded a podcast interview with "Ask Bryan" Davis, and it's now available for listening.  We talked mostly about cholesterol and fat-soluble vitamins, but also about my experience with vegetarianism, my encounter with T. Colin Campbell, the harms of micromanaging your diet, surviving in an academic environment, and the philosophy of science.  Below I've included a table of contents to help you navigate.

Unfortunately I had some internet trouble while we recorded this so there are a couple of audio glitches in the first seven minutes.  At that point I switched to my cell phone so the audio quality isn't the best, but it's not too bad and the glitches came to an end.

Here it is folks:

0:00:00 -- Bryan introduces me.

0:01:26 -- How I got into nutrition.

0:05:45 -- My encounter with T. Colin Campbell.

0:08:10 -- Remarkably, Bryan and I have never met, yet we share the same favorite sterol -- cholesterol!

0:08:45 -- The quick scoop on cholesterol, no biochem attached.

0:11:25 -- Is there an optimal cholesterol level?

0:14:30 -- Total cholesterol substantially above 220-250 mg/dL is no reason for panic but may suggest a metabolic problem.

0:14:40 -- LDL and HDL are not "bad" and "good" cholesterols, but when elevations of total cholesterol are due primarily to rises in LDL-C, a metabolic problem is more likely.

0:17:20 -- Triglycerides substantially over 120-150 mg/dL likely indicate insulin resistance, especially when they rise above this range in response to eating carbohydrate.

0:19:20 -- Why LDL-C and HDL-C never add up to total-C.

0:21:17 -- Since all non-HDL-C can usually be lumped together for purposes of indicating CVD risk or metabolic issues, it doesn't matter whether LDL is calculated or directly measured.

0:23:10 -- There's no verified, clinically useful measurement for LDL oxidation yet available.

0:24:50 -- Let's not be moleculists -- we want to understand processes.

0:27:59 -- Is small, dense LDL a cause of heart disease or just a metabolic marker?

0:31:30 -- LDL particle size conveys information about CVD risk, but it appears to redundantly convey the same piece of information conveyed by the total-to-HDL-C ratio.  Thus, we should ask what this snippet of information is that lies behind each of them.

0:34:08 -- In the general population, the most common cause of blood lipids being out of whack is probably low thyroid activity induced by a deficiency of insulin signaling.

0:39:12 -- What do I call my diet?

0:40:15 -- Weston Price's and Robert McCarrison's approaches.

0:45:20 -- Functionally, I'd lump vitamin E with vitamin C rather than A/D/K.

0:46:30 -- How we forgot about vitamin K2 (and how I forgot the name of my article about vitamin K2).

0:50:05 -- Vitamin A and osteoporosis.

0:53:50 -- One of the sloppiest ways to make inferences from science is to ignore context.

0:54:50 -- Gravity would be thoroughly unconvincing if there were only one study supporting it.

0:56:40 -- The proper ratios of vitamin A to D probably lie somewhere between 1:1 and 10:1.

0:59:59 -- Micromanaging your diet can be bad for you.

1:01:39 -- I'm a survivor of nutritional nonsense.

1:04:25 -- Scientists experience conflicting pressures, but the good ones prepare them to be open to evidence.  How to survive in an ideologically antagonistic scientific environment.

1:06:15 -- Upcoming plans.

1:08:10 -- Goodbye!

Read more about the author, Chris Masterjohn, PhD, here.


  1. Thanks, Chris. That was a very informative interview. I'd already heard the lipid info via your interviews with Chris Kresser, but I still learned plenty.

  2. As always, a very informative interview. Thanks!

  3. Question (apologize for the length).
    Small LDL particle sizes (typeB) appear to be correlated with high TG levels. It seems to me to be a consequence of lipoproteins being used to transfer both TGs but also cholesterol. When TG levels are high initial VLDL particles should have a higher TG/cholesterol mole ratio (though I cant find any data on this). After VLDL particles have passed on most of the TG to cells the resulting LDL particles will be smaller because the total cholesterol per VLDL particle is low. Of course we have the CETP mediated between HDL/LDL that complicates matters.
    What do you think?

    1. Hi Aleck,

      Cholesterol is denser than triglycerides, so the higher the ratio of cholesterol to TG, the smaller and denser the LDL particle. One theory of why carbohydrate restriction increases LDL particle size and why eating eggs does the same thing is because as carbohydrate intake increases, VLDL begins with more TG, whereas with egg-feeding, VLDL begins with more cholesterol. The theory is that if VLDL is higher in TG and lower in cholesterol, it will be metabolized more extensively by lipases rather than by the LDL receptor, which will leave small, dense, cholesterol-rich LDL particles in the blood.

      As you point out, CETP also makes LDL small and dense. By transferring TG from LDL to HDL and by transferring cholesterol from HDL to LDL, it makes LDL particles rich in cholesterol and poor in TG, which makes them small and dense. This also decreases HDL-C and increases LDL-C.

      Various lipases take TG from LDL. This makes LDL small and dense, because it increases the cholesterol-to-TG ratio in the LDL particle.

      Oxidation makes LDL small and dense because it oxidizes phospholipids first, and the phospholipids are removed. Since they are less dense than cholesterol, the removal of phospholipids makes LDL particle smaller and denser.

      If you have primary increases in any of the relevant enzymes (CETP, lipases, etc), you will get small, dense, LDL. If you increase the TG-to-cholesterol ratio of VLDL, you affect its affinity as a substrate for these various processes and you get smal, dense, LDL. If you simply let LDL spend more time in the blood, it gets subjected to all of these processes for a longer period of time, so the metabolism is more extensive and you get small, dense LDL.

      The question is, are ALL of these processes responsible for the correlation with heart disease risk, or only SOME of them or even ONE of them?

      And that is the difference between regarding small, dense LDL as a cause of heart disease or just a marker.


  4. Thank you for your detailed reply Chris. Always informative!

  5. Chris, thanks for the blog post!

    I love how the science geekery is much more digestible in text (at least for me).
    I have to see numbers/facts, I prefer to hear ideas.

    You are an incredible resource.
    Thanks so much for the interview.

    Best to you!

  6. You mentioned A & D work for (and sort of against) each other, and how some places like Sweden, where VitaminD exposure is low, you get Vitamin A toxicity. But what about the reverse? Let's say you have lots of Vit. D, either from diet or just being outdoors, and very little Vitamin A, either because of a poor diet, or inefficient conversion of beta-carotene to VitaminA. Is there toxicity evidence in the other direction?

    Finally, regarding A/D ratios (10:1 - 1:1) does the actual quantity matter if the ratios are good? I've been a member of the Calorie Restriction Society (CRS) for over 3 years, and have a BMI of 22, so supplements and IUs are a part of life for me. I'm wondering if taking 2 fermented cod liver oil Capsules (the one recommended in the Weston Price article) ,

    have enough Vitamin A (<<10000 IU), D2 (<<2000 IU), EFAs, and K (in the case of the capsules containing butter oil), or would separate D3, A, Omega3, and K2 capsules be better if concerned about dosage amounts. And not sure how crucial, but with the latter approach you can also be more selective (Vitamin D3 instead of D2) and only Omega3s (instead of 3/6/9), etc.

  7. Hi Chris,

    Love your method of explaining things in a fundamental and practical way.

    I have a question about cholesterol level variations. I'm listening to Chris Kresser's presentation on cholesterol for Paleo Summit and he suggests having your cholesterol tested several times to get a more accurate figure through observing potential variations. It may be a moot argument (or incorrect altogether), but even if cholesterol levels can be expected to vary up to 35 points, isn't that variation built into the results that we draw correlations from? Obviously if subjects are being tested multiple times in a study then my point is moot, but I don't know if that's happening since it sounds like the variation is not common knowledge. I know there is a justification that over many measurements the randomness of variation is expected to level out significantly, I guess I'm just not sure that the reasoning works as well in this context.

    1. Hi Dylan,

      Yes he is correct, and his data derives from our second podcast together. If you follow my recent blog links you should find that quickly, or click on "podcasts" in the tab.

      Yes, the variation is built-in to these correlations. This means that there is somewhat more random error than would otherwise be the case, which decreases the strength of the correlation. Since the correlation nevertheless exists, all we can say is that its strength is probably somewhat underestimated.

      This reason is also the reason I have used the population means for groups like the Masai and tropical islanders rather than the ranges there, because most of the inter-individual variation shown in those studies is really an artifact due to intra-individual variation, so the population means are probably a reasonable estimate of what most of the individuals have for their own mean.


  8. Even though TG/HDL and HDL/TotalC as measures of heart disease risk are in some sense the same, some references suggest that TG/HDL is a sharper or more sensitive indicator. Do you have any view on this?

    1. Hi Anonymous,

      TG are not an independent predictor of CVD risk, whereas HDL-C and non-HDL-C are. Please see the second-to-last graph in this post, as well as reference 16:

      If you have references that indicate otherwise, please let me know.

      Thanks for writing,

  9. Hi Chris, this was really interesting as usual, I particularly liked the warning against micromanaging your diet, and the stress obsessing over every last detail can cause. On that note, I wonder if you can advise me - you seem to be the only voice of scientific reason when it comes to an objective analysis of gluten and whether it is the universal killer so many other bloggers and professionals make it out to be! Basically, do you feel that to err on the side of caution it would be better never to ingest the smallest molecule of gluten just in case you have an (as yet unobvious) autoimmune reaction to it or that it might cause a leaky gut thus making an autoimmune reaction inevitable?
    I have done a gluten free trial of a couple of months and tried a small amount of sourdough bread to no, I think, noticeable ill effect. If anything I felt better with the small amount of bread, though why this would be I don't know, we are talking a tiny (half an ounce) probably piece with a slab of butter! In brief I have no terrible health problems although a history of eating disorders, which makes me nervous of obsessing over what gluten might/might not do to me, and also osteopenia, probably as a result of the anorexia and also my mother has osteoporosis. I eat an almost grain-free WAPF diet with CLO/butter oil, fermented veg, raw dairy etc but wonder if those odd aches and pains that I had attributed to a busy life with small children are in fact, a terrible gluten-induced autoimmune disaster waiting to happen! Sorry for the long question but I really find it difficult to decide whether to go gluten free or not and if the stress of this will be more detrimental than a small slice of sourdough. Thanks in advance, all the best

    1. Hi Karen,

      Thanks for your appreciation! I've never seen any convincing evidence that gluten causes leaky gut either in healthy people or in putatively gluten sensitive people, so I think you should go with the results of your trial and your experience.

      Hope that helps,

  10. It does, thanks, Chris, keep up the good work!

  11. Great information. Looking forward to your next post Chris.

  12. is there a healthy range for both Large LDL particles and small LDL particles? How much of this is genetic vs. diet related?

  13. It is worth checking what the TG fraction is in the blood
    B-48 CE or fat food, an endogenous
    B-100 CE exogenous fat, liver
    the rest of the LDL, HDL are less important



  16. Hi Chris,
    Paul Jaminet has been saying lately on his blog that he is skepical of the benefits of fermented cod liver oil. More precisely, he is saying that Vitamin A combined with DHA and oxidative stress can lead to 'highly tooxic endproducts'. Do you give any credence to this at all? Can you reassure those of us who take the fermented cod liver oil? Thanks very much, Adam

  17. Whats up with these findings? Should we make sure to be eating resistant starch from tubers!

  18. Very good podcast interview I can see that you worked hard in order to create this post. The writers who share resume writing service reviews work hard as well because they want to share their feedback and experience.