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Better markers of heart disease risk than total and LDL cholesterol concentrations
Recent reviews indicate that biomarkers other than total and LDL-cholesterol concentration are better predictors of atherosclerotic heart disease risk. Amongst these are inflammatory markers, other lipid components (triglycerides, LDL particle number, HDL cholesterol) and coronary artery calcium scores. LCHF and keto diets consistently result in superior improvements in the lipid components mentioned above – specifically resulting in reductions in triglycerides and elevations in HDL concentrations compared to conventional dietary interventions [27-29], indicating a protective cardiovascular effect. Contrastingly, replacing dietary saturated with carbohydrate, as seen in conventional low-fat diets, raises triglycerides and atherogenic small dense LDL cholesterol, while lowering HDL cholesterol concentrations – a profile associated with increased heart disease risk [30]. LCHF and keto diets also consistently lower inflammatory markers [31] and prevent further deteriorations in CAC scores [32]. These improvements clearly indicate that rather than LCHF and keto diets’ high saturated fat and cholesterol contents increasing heart disease risk, they’re far more likely to lower it.

If LDL-cholesterol is bad, as we have been told for many years, those with the highest values should of course have a shorter life than those with low values because, as we have been told as well, high LDL-cholesterol is the main cause of all kinds of cardiovascular diseases, and cardiovascular disease is the commonest cause of death in most countries. But as I have told in a previous newsletter, we have found that elderly people with high LDL-cholesterol live the longest.

. Our paper was published in BMJ and hitherto no one has been able to point at a study documenting the opposite. On the contrary, after the publication of our paper similar findings have been found in six studies including about 750 000 individuals in all ages from eleven countries.
. In a 10-year Slovakian follow-up study of almost 500 elderly people with high blood pressure, those with high total cholesterol and those with high LDL-cholesterol lived just as long as those with low values.
. In a British study of almost 100,000 people above the age of eighty followed for 15 years, those with the highest total cholesterol lived the longest; both among those on statin treatment and those without.
. In an Australian study of almost 1300 men about the age of seventy followed for about six years, those with the highest cholesterol and without statin treatment lived the longest, and those with the lowest levels suffered more often from cardiovascular disease.
. In a five-year American follow-up study of more than 2600 healthy people above the age of 75, those with the highest LDL-cholesterol did not suffer more often from cardiovascular disease than those with the lowest values.
. In two Korean studies of more than half a million young and middle-age people without statin treatment followed for about five years, mortality was highest among those with the lowest LDL-cholesterol.
. In a review of five studies from Latin America including almost 28 000 people of all ages followed for 5-12 years; none of the studies showed strong associations between individual lipid biomarkers and all-cause or cardiovascular mortality
. In a Chinese study including almost 70 000 elderly people followed for 3-4 years, those with high LDL-cholesterol lived just as long as those with low values.

Probably you wonder why many previous studies of young and middle-aged people have shown that high cholesterol is a risk factor for cardiovascular disease. Most likely, stress is a more common phenomenon among young and middle-aged people than among senior citizens, and stress is able to raise cholesterol by up to 50 per cent and may cause heart disease by other mechanisms than by raising cholesterol.

The Food and Drug Administration on Friday approved the first non-statin oral medication for high cholesterol in almost two decades, giving patients and doctors another weapon against heart disease, the No. 1 killer in the United States and around the world.

..best survival are from feeding the dreaded animal fats from lard, combined with CRON. The fish oil group, full of EPA and DHA, did worst of the three CRON groups with soy oil being intermediate.

I think beef dripping would have done better than lard and beef suet even better still, but then I would think that.

Peter, saturophile.

a diet containing a low proportion of PUFAs and high proportion of monounsaturated and saturated fats may maximize life span in animals maintained on CR.

Also, how can it be possible that the adverse effects of the placebo, and the statin, are always, almost exactly the same, in all trails – no matter the absolute figure. I believe that this could not possibly occur unless:
-The placebos in each trial were carefully formulated to cause adverse effects at the same rate as the statin
-The statistics on adverse effects were manipulated

"Patients who had hyperlipidemia had lower mortality than patients who had no hyperlipdemia. That's the primary finding."
Yousufuddin said that high LDL cholesterol decreased the risk of mortality by 24 percent after heart attack, and 20 percent after heart failure. The study also found this seemingly protective effect of high LDL effect was dose-dependent. In other words, the higher the LDL, the lower the risk of mortality after a cardiac event, and the lower the LDL, the higher the risk.

If you're on statins for prevention of a heart attack (primary prevention) you should know that there is near-zero transparency of the data on which this advice is based. I.e., independent researchers can't get access, thus cannot confirm. In US or Europe.

As noted above, a measurement derived from a standard lipid panel that is more strongly related to ASCVD risk than LDL-C, particularly in patients with features of the ectopic fat phenotype, is non-HDL-C (total cholesterol minus HDL-C), which comprises the cholesterol content of VLDL and atherogenic remnant lipoproteins, in addition to LDL.72 However, measurements of plasma apoB5–7 and/or LDL-P subclasses55 provide more specific measures of atherogenic lipoprotein burden that can also serve as guides for therapeutic management of ASCVD risk. In this regard, LDL-P subclass analysis has the potential to detect atherogenic lipoprotein patterns, which are below the discrimination level of standard lipid testing in MetS.60