The LLVLC Show (Episode 635): Encore Week 2013 – Dr. Thomas Dayspring

Hi Jimmy,

Thanks for this interview — I have a ketogenic diet and lipid numbers just like yours. It’s nice of Dr. Dayspring to take an interest in this phenomenon, which I think is not that uncommon. By looking at studies of epileptics on ketogenic diets and other crude means, I would guess that more than 1 to 2 in 10 people will have this response to a ketogenic diet — I believe that it has not been much noticed until recently because very few people are actually ketogenic or even very low-carb. Eric Westman seems to have enough clinical experience to be familiar with it, and I suspect he probably has a higher percentage of patients compliant to a serious low-carb diet than most other bariatric physicians (and there are not many of these out there in any case).

It is interesting that Dr. Dayspring hypothesizes an increased VLDL synthesis as the cause, especially since he thinks saturated dietary fat is involved. I would have thought LDL clearance by one of at least two commonly discussed mechanisms more likely:

1. LDL receptor downregulation (activity/number): This is a favorite theory in the medical community, in response to dietary saturated fat in particular. There are tons of papers on it — it is much loved because via the lipid hypothesis and this supposed mechanism a diet rich in animal foods (e.g. meat, eggs, dairy) can be demonized. Maybe it has been discredited in recent years, but if so I am not aware. I personally do not believe it is involved in my own response to ketosis, however.

2. “Low” tissue thyroid hormone: This is known as nonthyroidal illness syndrome (NTIS) in the medical literature. It really cannot be measured directly, but clinical measurements for serum free T3 and rT3 are commonly used as markers. Here’s one relevant link for anyone interested in a little reading on the subject: http://jcem.endojournals.org/content/84/1/151.long

Of course, the normal range for our population as a whole is probably very misleading for what is healthy on a ketogenic diet. My own readings are over three times lower for the free-T3/rT3 ratio than the commonly cited minimum ratio for “tissue euthyroidism”, and so some fringe clinicians who look at these things might consider me to be “tissue hypothyroid” (for which they would probably prescribe T3 hormone supplementation). I am in perfect health as far as I know, though, and have come to the conclusion that my tissue (including liver) thyroid activity and concentrations are probably at a healthy homeostatic level in relation to my diet.

I do believe, however, that my jump up in LDL-c after going onto a VLC diet (over three years ago) probably resulted from a downregulation of hepatic thyroid hormone activity. This, in addition to low insulin (my fasting insulin is < 2mcIU/L which is the lowest reading the lab equipment could detect), is well known to result in significant downregulation of hepatic LDL receptors and this is (ala Brown and Goldstein) well known to result in increased serum LDL concentrations. After all, statins induce the liver into upregulation of LDL receptors and thereby have a powerful effect in the opposite direction.

What baffles me is why so many in the medical profession, such as Dr. Dayspring, believe that manipulating LDL serum concentrations using drugs will decrease risk of CVD. LDL-P is just a weak marker for risk (albeit somewhat stronger than LDL-c) — its correlation is much too weak to be a possible causal factor by standard epidemiological rules of measure. In addition, the drug trials' data has seemingly disproven a causal relationship in so many ways and instances that it is difficult to count (e.g. lack of dose-response relationship for hard end points). Statins work by various pleiotropic mechanisms that are pretty well known by now (e.g. Rho inhibition), and all the many other cholesterol-lowering drugs have no efficacy at all because they only reduce LDL without added beneficial pleiotropic effect. LDL is clearly a marker for something related to CVD (unIDed as yet, but maybe diet via a deleterious chronic postprandial endothelial response for example). Statins have a weak beneficial effect for a subpopulation in secondary prevention only. They are harmful in many ways, and their biological mechanism is truly terrifying IMO. I tried a couple for a few months to humor my medic, but never again. I had myopathy and a dangerous allergic reaction. And the statins were quite effective in lowering my LDL serum concentrations, but so what? Oh well…..

By the way, I had a coronary multi-slice CT done, yielding a zero calcium score (like yourself) at age 54. I am mulling over the idea of getting an Endo-PAT (digital flow-mediated dilation / reactive hyperemia / endothelial function) test done to establish a baseline for future monitoring (even though I suspect I will die of something else, other than CVD — I think my genetic susceptibilities lie elsewhere). Have you any thoughts about this test, Jimmy?