How to further lower ApoB?
First time poster, long time follower. Quick context, I am a fit 38 yo (been going to the gym since 14 with zero gaps in time etc) with horrific family history of heart disease. Didn't really think much of it until last year when I had a MI at 37. Doing the usual annual physical my basic lipid panels were never out of control and was never on any meds. Now I'm eating even cleaner than before. Dropped 20 lbs (was never overweight but bulky build) watching my health stats via Garmin, Zone 2 training, trying to improve my VO2 Max post MI etc. On atorvastatin 80mg and Lisinopril 40mg for blood pressure which is now 110-75 on avg. I can provide as much detail as possible while also being broad to benefit as wide an audience as possible. My question is; In my instance genetics seems to be playing an overweight role in this medical issue for me. My ApoB is still at 50. My LDL is also in the 50s but my LP(a) is 350. Listening and reading your material leads me to believe I need to get it to 30nl/dl. What else can I do to get it lower? Thanks in advance you have helped me bring my health to a new level!
GLP-1 Novo Nordisk SELECT Trial
What are your thoughts on the recent Novo Nordisk SELECT Trial announcement demonstrating a 20% reduction in MACE over a 5-year period? The trial enrolled "adults aged 45 years or older with overweight or obesity and established cardiovascular disease (CVD) with no prior history of diabetes." The study has not yet been peer reviewed and the full results are not yet available. The announcement also does not make mention of any adverse events. It is known from other studies that a large proportion of observed weight loss is lean mass. How should we think about balancing the potential benefit in the reduction of MACE with the potential risks of sarcopenia and osteopenia/osteoporosis, and the associated mortality.
Vazguard Bergamot Phytosome and effects on HMG CoA Reductase synthesis instead of statins
Have you been reading at all about this supplement and some of the publications which describe its effect on transcription of HMG CoA Reductase which may help eliminate the restricted pathway of acetoacetate production? I have been thinking that some of the glucose dysregulation related to statins may be related to the metabolic influence as a forced metabolic fuel over glucose for non-hepatic tissues. My brief personal experience is that statins on my CGM caused immediate glucose havoc and I'm pretty healthy. As soon as I added bergamot (Thorne's Vazguard product), within a day my glucose on the CGM seems to be improving.