Do you know omega-3 fatty acids promote something called reverse cholesterol transport?
https://pubmed.ncbi.nlm.nih.gov/28984832/
I couldn’t take statins because of the side effects. I went on a fish only, no plant oil diet, and my LDL is now 200 and my HDL for the first time my life rose above 35 to 52. To me, the key was getting the omega-3 level way higher than the omega six level and totally eliminating short chain poly unsaturated fatty acids.
Note that I went on this diet, because I actually know my genetics. I don’t recommend anyone do the same thing without knowing what I know.
Diet works and it’s sad people can’t commit to it. And I’m afraid for a lot of people it won’t be the vegetarian diet that is normally prescribed.
Remember as well cholesterol is not the only contributors her heart disease. Oxidative stress plays a large role in damaging, or oxidizing, the LDL to cause the plaques.
https://www.frontiersin.org/articles/10.3389/fphar.2020.6137....
Oxidative stress can be caused by external forces, but also by the lack in proper nutrients, like zinc and B6 and riboflavin, deficiency in those supplements are all linked to greater incidence of heart disease.
I am in my mid-50s and I’ve had no issues so far.
What do you use as a substitute for vegetable oils in your cooking?
You don’t need oil to cook. Your diet will look a lot different, but you certainly don’t need oil to cook.
It’s instructive to remember that two hundred years ago, palm oil/vegetable oil/canola oil/avocado oil/almond oil/etc didn’t exist, nonstick pans didn’t exist, and somehow people could still cook amazing food.
To say it is "just a fitness fad" is dismissing a ton of good research:
Here's to hoping that with the death of the dollar, the "settled science" practitioners lose their bullhorns.
HDL is an antioxidant and this why HDL rules over all:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4607861/#:~:tex....
It sounds like 200 is still trouble. Was it even higher before?
Return short, chain fatty acids into long chain fatty acids by four enzymes FADS1, FADS2, EVOL1, and EVOL2.
https://www.mdpi.com/nutrients/nutrients-06-01993/article_de...
I have polymorphisms in FADS1 and FADS2 that slow down the rate of this pathway. By the way, I have Inuit (SAMI) Heritage.
I will not give medical advice over the internet, but if I were you, I would not want to be messing around with anything short of the standards of care given those odds. Statin therapy is a core part of that standard.
Statin adverse effects do exist, but they are found to be quite rare (1-2% prevalence) when assessed for through well designed placebo-controlled trials. Additionally, there are newer statins with fewer adverse effects you could consider. Assuming you truly have FH and truly are statin intolerant (or remain at elevated LDLs despite maximally tolerated statin therapy), PCSK9 inhibitors can be considered. In the US, you would likely qualify for one if these through a good insurance plan, assuming the above criteria are met.
I’m not screwing around, I know my genetics, and I know how reverse cholesterol transport works. I also know keeping oxidative stress at a minimum is probably more important than the level of cholesterol. I actually moved to a location with extremely low air pollution for that very factor. You can’t look at LDL only to understand the risk of heart disease.
I had very good doctors and if they thought I was at risk, they would be telling me what to do because that’s what they always do. But now they say there’s no need for statins and they’re not concerned about my heart disease risk anymore.
Followingdao@proton.me
There’s no clear/satisfactory answer as to why South Asian patients have so much more heart disease, but the evidence does suggest we should be adopting more aggressive targets of risk parameters for them (A1c, LDL, BP, weight, etc.), and the clinical guidelines likely will reflect this in the future.