Another instance of you putting things very well, Paul. 
Obvious truth, and it leaves me feeling somewhere between shaking my head at âthe state of things,â and barracading myself behind enormous obstacles with heavy weaponry⌠Good grief, what a worldâŚ
I like it! 
Itâs a little late for Bastille Day, but . . .
â. . . Aux arme, citoyens! Formez vos bataillons! . . .â
Yeah, after that post I did do a little looking around for information about statins and CAC score. I found several papers that confirm statins cause CAC to increase. That was a little disturbing to me and yes, the increase of CAC was considered good if it happened while taking the statin. 
Yes, there are quite a few papers that do show this. But there seems to be another effect in that the additions of statin and PCSK9 inhibitors seem to reduces overall risk/mortality in those with high CAC scores.
Happen to have any of those papersâ links handy? Iâd appreciate the chance to read up.
These are the ones I looked through:
https://www.sciencedirect.com/science/article/pii/S0167527315001990
So yeah, it seems like the field is a bit discombobulated.
From one paper:
Conclusion: Statins do not reduce or enhance CAC as measured by Agatston score in asymptomatic populations at high risk of cardiovascular diseases, but seem to slow down CAC progression.
From another:
Conclusions: Despite a greater CAC increase with high dose and long-term statin therapy, events did not occur more frequently in statin treated patients. This suggests that CAC growth under treatment with statins represents plaque repair rather than continuing plaque expansion.
This conflicting inherent assumption that raising CAC scores is a good thing - even as calcification is generally seen as a bad thing - seems at first to be counter-intuitive. But perhaps the mystery might be solved by incorporating the density of calcified plaque as other researchers have done.
Personally, Iâm still at a loss to see how taking a statin is helpful to oneâs overall good health. Even if it were to promote calcification of arteries, pitched here as a good thing, statins typically reduce all cholesterol - including HDL.
Our bodies need cholesterol. Our brains are made largely of cholesterol. Reducing it has been shown repeatedly to be associated with increased overall mortality risk.
Too much of a good thing can be a bad thing. If I recall from papers posted here on the forum the overall mortality curve for LDL is a U-shape. Not enough bad, too much bad. I guess what would be interesting would be to see a plot of overall mortality vs the HDL to triglyceride ratio.
âSince Miillerâs association of hypercholesterolemic xanthomatosis and angina pectoris, this relationship has been considered as important evidence supporting the hypothesis that elevated scrum cholesterol leads to coronary heart disease. Angina and myocardial infarction may be more frequent than in the general population, but exact information is lacking. It is possible that the precocious onset of coronary artery disease and the bad prognosis have been overemphasized because many of the early studies were of the relatives of patients who had sought medical attention. When an entire family is surveyed, as in our study, the outlook is not as gloomy. We have found that heterozygous hypercholesterolemic persons survive about as long as their unaffected relatives (see Section XI). Our finding that familial hypercholesterolemia is compatible with survival into the sixth, seventh, and eighth decades docs not imply that sudden death does not occur, particularly in young men in whom the diagnosis of hypercholesterolemia and coronary artery disease cannot be made without an autopsy. Available information suggests that sudden death due to coronary disease may have been the fate of several young men in the âHâ kindred but this is conjectural. Precocious coronary disease was not a common occurrence, however. It is the clinical impression of one of us (W.R.H.) after following this family and two other similar families for five years that angina may develop in the thirties or forties in males and continue for 10 to 15 years before the development of myocardial infarction. The frequency of positive exercise electrocardiograms in asymptomatic but hypercholesterolemic individuals (Tables 9) in this study and in the study of Guravich suggests some degree of underlying coronary insufficiency by the fourth decade in a sizeable proportion of hypercholesterolemics.â
From âFamilial hypercholesterolemia: A genetic and metabolic study,â W. H. Harlan, J. B. Graham, and E. Harvey Estes, Medicine, vol. 45, no. 2 (1968).
⌠just curious ⌠what is âscrum cholesterolâ?
Iâm getting a visual on this and itâs not pretty. 
Another thing to consider along the COVID line would be how many booster shots he has had. Would any of the white fibrinigen (see Dr John Campbellâs videos) found in vaccinated arteries show up in these scans?
I never took the vaccine or boosters. Whatever the cause of my CAC number is something I alone have to deal with. All the hypotheses and references to articles and doctors however well intentioned do absolutely nothing because none of them can address my situation.
I apologize, I missed the part where you said that you didnât want (medical) advice.
Good luck with your numbers.
Youâre being gracious. Kindaâ hard to start a thread around here with any sort of health-related question and not wind up getting a slew of free medical advice. Fortunately, it all comes with a money-back guarantee. 
