Nov 23

#CholesterolScience with Kevin Bass

Many of you who follow my work know I actively pursue challenge. Part of that process of engagement is in initiating contact with people who may not only disagree with me — but might be very polarizing for many in the low carb community. Certainly Kevin Bass fits this description.

I had booked Kevin for an appearance with #CholesterolScience a few months ago, but between then and the show we recorded yesterday, a controversy arose that involved Dr. Ken Berry. We address this briefly at the beginning of the interview.

All in all, there were many things I liked about this interview. It was a Friday night and we were both a bit loose and not always as articulate as our A Game might allow, but that also created a much more stream-of-consciousness kind of honesty that came through at multiple times.

Reference Links

We mentioned several things throughout the broadcast that I’ll link below.

Names mentioned:

NHANES Material

LDL Level Changes during Inflammation

Kevin provided this study — The Effect of Inflammation and Infection on Lipids and Lipoproteins

While I haven’t had a chance to read the study in full, I can say that it appears this had more to do with the serum levels of lipoproteins, not specifically the production. The blood levels don’t tell us much regarding production without knowing the other side of the ledger regarding how much is subtracted via endocytosis, scavenger receptor removal, etc.

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KidPsych1`q2w]Siobhan HugginsKetoCandySam P. Recent comment authors

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Sam P.

IIRC low-level of LDL are correlated with some cancers. Not that they cause cancer, which would be preposterous since the >70mg/dL is the threshold to prevent atherosclerosis, but rather some forms of cancer directly lower LDL level through diverse pathways.

It is the main reason why mortality is higher in this category. If all of the participants in the low-LDL group were exclusively vegan/vegetarian, the mortality rate would be close to nil.


Your talk was great. I am 73 years old with Latent T1D controlled at 5.5 A1C. My docs are pushing for me to take a STATIN based on the LDL which is 100. I have been on the Keto diet since 2016 when my LDL was 64,HDL was 48, Total C was 130 and TC 92. As of 11-2019 LDL-100,HDL-58,Total C- 171 TG-66. since Keto, I don’t bolus and am on basal insulin only. I am a STATIN SKEPTIC since the FDA writes ON THE 2019 Guidelines for Statins that they are well known to cause Type 2 diabetes and Neurological problems and more. I just got back the CAC and I have a ZERO score. The reason I am writing to ask you both Is it possible that genes play more of a role in the determination of how low or high our lipids and HDL will be. Prometheus came back with a 2 to 3 fold lower risk of heart disease. The R461 is a SNP in the PCSK9 gene. It’s reported to be associated with lower LDL cholesterol levels and low risk for both early and late onset of cardiovascular events and disease. ( Not out of the Woods) While doing the CAC scan it showed a small amount of plaque in the Thoracic Aorta which I will check out with a Cardiologist. Love my results with the Keto. My docs want my LDL under 70 and don’t seem to care about the 1.2 ratio for TG/HDL Thanks for all you do. Candy Bridgman

Siobhan Huggins

Hi – I think it is possible for there to be a genetic component for both high and low LDL, but I’m not sure how common it really is. There are certainly other factors that play in – the composition of the diet, how much fat mass you’re carrying (from what we’ve seen people who are obese/overweight and on ketogenic diets tend to have lower LDL), etc, but it definitely doesn’t seem to be the *main* component in most of the people we’re seeing (that appears to be diet). But that’s not to say that genetics don’t play a role at all.
Are you relatively lean (normal weight)? Out of curiosity, what does a typical day of eating look like for you? Just curious about if this might explain something about the profile. 🙂


Thank you for your response. I am correcting my post above. On Promethease DNA, I do have the R46L or RS11591147 (G;T) on the PCSK9 gene, a SNP with greatest effect on lower LDL-C and 2-3 fold lower for cardiovascular risk reduction. The reason my doctor wants me on a Statin is because my LDL is now above 70 and she said its based on the guidelines that state “all people with diabetes must take a Statin.” I am Insulin Sensitive” according to my Endo and am a latent T1D. My Diet: 75% Fat, 25% Proteins and 5% Carbs. I use a Keto Calculator to stay on track. I am quite religious about it as I am also Gluten Intolerant. My weight is 5 pound above the normal range for my height on the weight chart. As a dog walker I average 15,000 steps/day five days a week. I do IF (16/8) eating in the 8 hour window. I mainly eat a variety of food: 2 cups coffee ( one black and one with heavy cream) eggs, salad greens, cabbage and kale with veggies, oil and vinegar or < 1 c Ranch ,nuts, cheese (more than I should.) Also about 5 ounces /day of one form of chicken, hamburger, steak, salami, salmon, sardines.

After my third child , I became a Triathlete and had trouble losing weight Even with diabetes, all doctors told me to increase my carbs for energy and now I know that made losing the weight difficult. I lost the weight when I dropped my carbs under 100g a day taking away the oatmeal of 27 grams a day just alone for my daily breakfast. I was an adult when I was found to have autoantibodies and my diabetes diagnosis was changed to T1D putting me on insulin. I had to bolus with each meal to cover the carbs and now with virtually no carbs I keep my A1c almost normal between 5.5% and 6% and am only on basal insulin.

As said, I don't believe a Statin is good for me and I do much reading and listen to Podcasts and talks from Ivor, Dave and Low Carb Down Under. I went to the Adapt lecture when Dr. Westman was in my town. With all the knowledge, I took the CAC Scan (November 2019) and got a Total 0 score. I have a Cardiology appt in March. I plan to push my opinion on why I don't believe I need to start with a Statin at my age. I am happy to finally speak up about my beliefs on my health.

Siobhan, thank you for your thoughts. By the way, after the beginning of the year, I plan to make a donation to Dave's "amazing" work as I think he is onto something BIG. Thanks for any thoughts on my Keto diet and R46L variant and how much that gene could play in keeping my heart healthy. Happy Holidays.

Siobhan Huggins

Thanks for getting back to us with additional info! Sounds like you are on your way to figuring out what you are comfortable with long term – and thanks so much for the support as well. 🙂


Thanks for your response. I am letting you know that I am “old school.” I followed what I was told even if I knew it wasn’t right for me. Eat carbs for all my sports, and for G-d sakes don’t ever eat Butter!!! But thanks to my CGM, my Twitter friends, my LCHF Keto diet I see why nothing worked before. And now I feel I am the best I can be. It’s a great discovery to find what works and stick with it. No one really knows the future, but what we do know is a feeling that something is right with what we are doing. I will always support Dave Feldman’s research. Thank You.
Best, Candy Bridgman (KetoCandy)
PS haha. It’s not surprising I left the butter and bacon off my last post while giving details of what I eat. …. but letting you know, I eat lots of it.!!!! Thanks Siobhan.


Fascinating discussion. I was struck by the lack discussion around risks/potential rewards for statin use. From Kevin’s perspective, there seemed to be a persistent belief that interrupting or discouraging statin use was exceptionally harmful (or potentially so), despite what I’ve seen reported that statin use requires an NNT of 100 or so. In other words, most persons using statins are not conferred any benefit. Further, while he touched on the idea that statins might provide anti-inflammatory benefits, I didn’t hear him discuss the possibility that, if this were so, why not engage in other activities that might boost nitric oxide production? Exercise, keto, beat juice, L-citruline, etc. Malcolm Kendrick has a blog post on the use of viagra and the like, which appears to confer more protective benefit than statins (without disrupting a vital biological system, as statins clearly do).

The cancer discussion interested me too. I recall reading research from Japan showing increased risk of cancer in long-term users of statins. I couldn’t help but wonder if these risks are muted in these shorter trials. My own father in law developed skin cancer (and dementia!) after long-term statin use. Fellow with two PhDs (and a three time Jeopardy winner) can now barely hold a coherent thought. But he’s in his seventies, so maybe this is just how it goes, right?

I have a friend who has been on statins for the past year, and last week he’d seen his doctor to find out he was now pre-diabetic. With the caveat that I’m not a physician, I suggested doing the above. However, when push comes to shove, and he’s sitting across from his doctor, who recommends continuing treatment (despite blood glucose levels rising), he can’t make that change. And so it goes.