About a year ago, I also finally started taking a statin after 2 years keto and one carnivore.
I know it is against the general opinion here, but we each have to weigh all of our health factors and risks, and go with our gut.
High CAC Score
if the animal is a ruminant, the rumen of the ruminant converts the polyunsaturated fats to saturated fat. Thereâs not much difference between 100% grass fed beef and corn-fed beef. Is there some? Yes. Is it a huge amount? Not really.
As for slaughtering the animal, thatâs a different story.
For older women, itâs complex:
https://agsjournals.onlinelibrary.wiley.com/doi/full/10.1111/jgs.16302
And of course, you can find studies indicating statins should always be taken.
I would think seriously about prolonged fasting.
I mean more than 5 days every 2 weeks.
@mnl1 Thereâs a lot of discussion here (and I didnât read every word) but I would strongly encourage you to do some additional specific research on CAC (âAgatstonâ) scores and calcium plaque density.
First of all, a CAC test (CT scan) only measures calcified plaque - which is the resulting scabbing over of prior soft plaque damage. Whereas soft plaque (not captured on a CAC CT scan) is the more dangerous unscabbed plaque at risk of dislodging - which is then where blockages in the heart, brain, elsewhere are likely to result.
Put differently, your hard calcified plaque is evidence of scabbing over of prior damage. Cholesterol plays a role in that scabbing - not in causing the damage itself. Sure, Iâd rather not have bleeding ⌠but if I did Iâd rather have scabbing thereafter.
CalcDensityPlaque-Criqui-2014.pdf (323.7 KB)
CalcDensityPlaque-Criqui-2017.pdf (508.4 KB)
CalcDensityPlaque-Criqui-2021.pdf (110.7 KB)
Taking a statin will do nothing to reduce your risk of CVD. Yes, it will lower overall cholesterol (LDL and HDL included) but this is associated with increased overall mortality, not lower.
[Separately, I would encourage you to learn more about the role of Vitamin D3 and Vitamin K2 in the process of increasing calcification of bones/teeth at the expense of calcification elsewhere - although that becomes a more nuanced issue if additional calcification is needed in the arteries due to ongoing damage. Reducing inflammation - e.g., through a restricted carb WOE - goes a long way in reducing arterial/systemic inflammation.]
I may just be being a little dense here. The vitamins D3 and K2 help keep the calcium from being deposited into places it doesnât belong such as arteries and soft tissue. So, âat the expense of calcification elsewhereâ is referring to the fact that the calcium gets put where it belongs (teeth and bones) and not put where it doesnât belong (arteries and soft tissue)?
Nothing dense about the question at all! Although somewhat off the OPâs original topic and concern:
My understanding is that the availability and uptake of calcium involves a kind of homeostatic dynamic: thereâs the possibility of too much and also of too little.
Few of us in the West have a genuine calcium deficiency ⌠on the contrary, we often consume (and over-supplement) more calcium than our bodies truly need (or are even able to deposit where needed).
A combination of Vit D, K, and A work together to regulate the uptake of calcium. Too much calcium vis-a-vis levels of D, K & A will tend to overwhelm the uptake of calcium where it is âmostâ needed in an otherwise healthy body - namely, bones and teeth.
However, in the face of soft plaque arterial damage due to systemic inflammation, yes, calcium is needed for âscabâ-like repair. But generally, required amounts will be readily availability for such purposes (since itâs present in the circulatory system).
But bones need the calcium to be redeposited ever more as we age in order to stave off osteoporosis. And that doesnât happen nearly as effectively without those three vitamins mentioned above. [Studies of Japanese women and their ingestion of ânattoâ (super rich in K2) showed a strong association with higher vs lower levels of bone density health.]
If you want a food source of K2, natto is it. I mean really it. As in one ounce of natto has more K2 (of a different type though) than 3/4 pound of cheese.
Iâve been making my own natto:
Iâve seen some people who think that the Japanese ingestion of natto is a main reason they tend to have long lives.
Thatâs how I understand it ⌠natto is without competition in the food world for K2.
But after hearing that natto tastes like smelly old gym socks, I opted for the K supplementation route. So⌠how bad is it, really?
[Perhaps we should move this section of the thread to âSmelly Old Gym Socksâ category?]
I think itâs fine. But I am a former body builder, so I have drank/swallowed a lot of nasty stuff.
You can make it more palatable by adding soy sauce (I usually add), green onions, etc. The only thing I add is soy sauce.
If youâre close, you can get it from some locations:
NOTE: mine looks like beans, without a lot of the strings shown there. Youâre supposed to mix it and itâll get really stingy, but I donât do that. Also, they say a âservingâ is 3.5 ounces, but I eat a lot less per day.
Unfortunately, Iâve never seen it anywhere near me. It would be nice to try once instead of ordering a ton of it.
According to Ivor Cummings, itâs the progression in the CAC score that you need to monitor.
50% of people in a study that had a CAC score that increased by over 15% per year had heart events.
People who only progressed at 7 to 8% per year, but who also had a high score, saw about a 3% rate of heart events.
Ivor infers that the lower rate of progression suggest that the body is still repairing as it goes along.
Ivor says if they do everything right (eat real food, get vitamin D + Sun exposure, fasting) they can overcome the genetic sensitivity.
Source Video: https://youtu.be/GC488McH2eU?si=LKQBKCb30ZhZvNEY
Presumably, that repairing is the calcification of soft plaque, which doesnât show up on a CT scan upon which a CAC Agatston score is based. Nor does the Agatston score factor in density of that scabbing calcified plaque.
My opinion after reading as much as I could find on this topic is that an Agatston score is an interesting starting point - but it provides less than half the story of whatâs actually going on in terms of arterial-plaque related risk.
n=1 DisclaimerâŚ
FWIW, my own (annual) CAC scores have both risen (reflecting reparation of pre-keto soft plaque damage) and have also fallen (as density has steadily increased reflecting decreasing surface area/volume of calcified plaque) - but after 5 yrs of carb-restriction, the scores have essentially stabilized at this time.
And as a LMHR, my total cholesterol would send shivers down the spine of an ill-informed doctor given how high it stays. Fortunately our internist is well-informed - taking note of my HDL well over 100 with Trigs in the 40s.
⌠and finally, back to @mnl1âs concern: statins have never been considered as a solution to anything seen in this labwork or CAC scores, nor has our family internist suggested otherwise.
You clearly have more experience than me in this regards. Would you add/remove/change any of the actions suggested by Ivor on how to manage a high CAC score?
Were your lipid panels high before keto? Family history? I assuming you are under the age of 60? Have you also done an ApoB test? A CAC score this high warrants action. Could there have been a mistake? Please seek out qualified medical doctors.
I would have a look at the work of Dr. Ethan Weiss, M.D. and Dr. Allan Sniderman, M. D.
As one who raises cattle I can assure you that they are all grass fed or silage fed for 99% of their lifespan. It is only in the last few months they are put on a grain diet to put more fat on them.
This conversation may not be that off topic. Making sure one gets enough D3 and K2 allows the calcium to be absorbed like itâs supposed to instead of floating around in the bloodstream, settling into joints, soft tissues, etc. I imagine if calcium is needed to help scab up some arterial damage, it is not needed in large quantities. Iâm sure the body is smart enough to funnel some Ca to scab over a plaque even if itâs being absorbed into teeth and bones.