Great article by Mark Sisson of Mark’s Daily Apple, a blog I follow daily, discussing potential reasons for elevated LDL in people who eat Primal (a paleo low carb variation). Potential explanations include:
- Weight Loss
- Micronutrient deficiency
- Grazing all day
- Activity levels that don’t match carb intake
- Not moving frequently at a slow pace
- Not lifting heavy things
An interesting point is his description of the role iodine and thyroid hormone plays in the expression of LDL receptors and subsequently LDL-C which pretty much is in line with everything I’ve been reading about.
Another factor that I’ll need to explore in the future is whether I was over training during my time with nutritional ketosis. I was doing Crossfit and BJJ fairly regularly which are both very glycolytic.
Well, if you’re hitting the metcons regularly without the necessary glucose infusions, your body conserves what glucose is available. We needsome glucose for brain function (ketones and other sources can handle a lot of our brain’s needs, but not all of it), so in order to preserve what little glucose is available, T3 thyroid hormone is reduced. Normally, T3 increases glucose utilization, but when the body doesn’t have enough due to mismatched exercise output and carb input, T3 must drop to conserve glucose. Unfortunately, this lowered T3 can lead to lowered LDL receptor activity, which leads to increased lipid levels.
Here’s a podcast from Relentless Roger and the Caveman Doctor where they discuss a really great study in which 12 physically active and healthy subjects ate a ketogenic diet for 38 days. Ketones were measured with urine dip sticks. Here are some interesting points:
- Surprisingly, the literature on the effects of KDs in healthy and physically active individuals is scarce, although in our experience such diets have some popularity among metabolically normal people and even athletes.
- The results of an experiment published by Matthew Sharman, Jeff Volek and colleagues indicate that despite a rise in LDL concentrations, the overall cardiovascular risk profile could change in a favourable way during a KD, e. g. by increased HDL and lowered triglyceride concentrations.
- That LDL concentrations levels stay elevated during long- term consumption of a KD is further suggested from a Polish cross-sectional study of 31 healthy individuals who ate according to the so-called “optimal diet” for at least one year. Although not strictly ketogenic, the “optimal diet” consisted of about 75 % energy from fat. Most of the LDL and total cholesterol concentrations exceeded the reference ranges, yet the “optimal” dieters showed very low risk for CVD as judged by other predictive parameters.
- The most frequently missed food items were fruits (eight subjects) followed by unlimited amounts of vegetables (four subjects). Only two subjects reported a craving for other foods like baked goods.
- Most subjects were able to continue with their usual training, albeit with minor problems including in- creased perceived exertion and subjectively increased needed time of recovery.
- Most subjects experienced a decrease in body weight over the course of the study.
Perhaps the most interesting part of the study is this table taken from the study illustrating the changes in the various biomarkers:
Many of these subjects were triathletes and weight lifters and they all consistently showed a bump in their LDL-C levels and TSH levels, pretty much what we’ve seen in my bloodwork and the bloodwork of many of the commenters here. They discuss these findings by saying:
Interestingly, subject 11 who took a thyroxin substitute experienced the least dramatic rise in LDL levels. Furthermore, positive associations between TSH and LDL as well as total cholesterol levels have been found in cross-sectional studies in euthyroid healthy subjects, and the strength of these associations seems to depend on an individual’s insulin sensitivity. We therefore hypothesize that the KD has diminished the production of T3 from T4, thereby reducing the number of LDL receptors and thus reducing LDL particle clearance which might be further impaired due to the missing stimulating effect of insulin on LDL uptake into cells.
Which pretty much agrees with my line of thinking. If you have a chance, feel free to read through all 27 pages of the study… or the 1 page abstract of you’re short on time.
Here is a great post by Peter Attia from the Eating Academy where he goes into an in depth discussion on fat metabolism. When I say in depth, I’m talking about going deep into the abyss. I had to read it a couple times… and still don’t have a strong understanding of it. My definition of understanding by the way is whether or not I’d be able to explain it to my non-science-background mother in way that she can comprehend it… and I’m definitely not there yet.
Here’s another podcast from Jimmy Moore’s Ask the Low Carb Experts where he interviews Dr. Michael Ruscio, a functional medicine physician. The entire podcast is dedicated the thyroid, aptly titled, ‘All Things Thyroid.’ They address a lot of common paleo and low carb thyroid issues. It was interesting to hear his take on thyroid hormone and high LDL-C and hear him basically say that we just don’t know enough. Still… a good listen if you have the chance.