Calcium Score after long term statin usage...
I am 54, I was put on 10 mg of Lipitor 20 years ago by my previous doctor. Don't remember the LDL but total cholesterol was 240±. Had one grandfather die of a stroke in his early 80's, the other died at 72 from a heart attack at 72. Latter emigrated from Belarus late 1930's and probably didn't see a "real" physician until well into his 30's (and he wasn't a model of fitness). I have always worked out a lot, but didn't really eat well until I turned 50. At 52 my doc and I decided to do a test - I went off Lipitor for 3 months and my LDL was just over 100 and total cholesterol was under 200, so I stopped it. On Lipitor I think total was around 170 or so (never paid close attention to it). 18 months later I go to a new concierge doc, LDL is around 107 and we do a calcium score. One ventricall is over 600. I'm in really good shape (VO2 Max of 52.2), low body fat, etc. Also found a huge thymoma (12 cm) that was removed last year via DaVinci robotic surgery. I know that the calcium score of that high means some serious stuff happened. Apparently the statin could raise that score (my cardiologist said we aren't going to repeat, but continue to to carotid artery test each year which shows very minor blockages). The question is as follows - is my risk really as high at the CAC score says it is? Isn't some of that calcium from the statin? Had I had a better diet over the prior 20+ years (and maybe taken my K2) would/could the calcium have gone elsewhere? Just trying to understand this phenomenon better. Seems like all the data/research doesn't really give you proper statistics for a high CAC that could have been driven (or partially driven) but statin use. Thanks for the insight.
Hypothalamic regulation of response to food scarcity or fasting
Following #194 with Rick Johnson: How Fructose Drives Metabolic Disease, I became very curious what the top level control of the metabolic responses to food scarcity or fasting (or ketosis). Found research indicating it is POMC (anorexigenic proopiomelanocortin) neurons and orexigenic agouti-related peptide (AgRP) neurons in the arcuate hypothalamus that are central to the regulation of energy expenditure/conservation, food seeking, satiety signaling and weight regulation. Insulin and leptin are hormones that control food intake via regulating POMC and AgRP expression. FOX01 and SIRT-1 are both expressed in these neurons with opposing effects. And the "master regulator" in the hypothalamus may be SRC-2, (steroid receptor coactivator-2 in the POMC neurons. Fascinating! Would love to have you address and unpack this level of control of food/energy metabolism. Thank you. Links: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8715676/ https://pubmed.ncbi.nlm.nih.gov/20103739/ https://pubmed.ncbi.nlm.nih.gov/21048357/
New car regulations F1 2022
Greetings, I am just generally curious about your view on new regulations for F1 cars for the upcoming season. Honestly, I find the new weight of the cars somewhat disappointing. I oft find myself missing the olden days with feather-light cars (sub-600 kg weight). How do you see the new rules for reducing dirty air and yet increasing grip of the cars? Thank you.