Kurt G. Harris MD

PāNu means paleonutrition. The "paleo" here signifies "old" and not necessarily paleolithic. The PāNu approach to nutrition is grounded on clinical medicine and basic sciences disciplined by knowledge of evolutionary biology and paleoanthropology. The best evidence from multiple disciplines supports eating a pastoral (animal-based) diet rather than a grain-based agricultural one, while avoiding what I call the neolithic agents of disease - wheat, excess fructose and excess linoleic acid.

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A quick post on FH and statins

I've had a longer post in the works for a while now about FH and the lipid hypothesis and statins, but I keep getting sidetracked.

I keep getting emails asking about it and one person on Robb Wolf's site posted the following:

  • Dr. Harris,

    In regards to your statement “the Lipid Hypothesis is BS”: is that still applicable to myself (and other FH’s) being the lucky possessor of Familial Hypercholesterolemia? After my last exam, a CT calcium score of 206, at age 48, I’m about to give into Statin therapy. After adopting Paleo 5 months ago, my LDL went to 348 with the Lp(a) at 10. The particle sizes are leaning toward the Pattern A side of the scale, and all of my inflammatory markers are low.

    Can FH patients ignore their Lipid numbers?

    My reply follows and is a short version of my views on FH and statins.

    I responded:

    I can’t give you specific medical advice. I have a post on FH coming up .The thing to understand is that there may be increased risk of coronary disease with hetFH*, but that does not mean the elevated LDL is causing the disease.
    In FH, LDL is elevated because there are fewer LDL receptors. The paucity of receptors may increase intracellular cholesterol production or may make it hard to repair vascular damage, in either case the serum LDL has little to do with it. In fact, studies in both FH and non-FH populations show no relationship between LDL reduction and risk reduction. It is independent of the LDL level. it may be that statins, via their anti-inflammatory effects and completely independent of LDL levels, may reduce risk of MI, but the same thing is true for those without FH in secondary prevention.

  • Studies of families with FH show that before the mid 20th century, mortality in those identified by screening was about the same as the normal population. And families with FH identified through early heart attacks are not the same risk as those identified through screening of aysmptomatic persons, who are more likely at lower risk.

    So what do you think they were eating back then, maybe less sugar and vegetable oil? That would be my guess. I personally can’t think of a plausible mechanism where raising your serum LDL number with sat fat in the diet (FH or not) would do anything but decrease the rate of plaque formation. If you’ve been to my site you know what I think are the important elements of an anti-inflammatory diet. It’s all about the parts that are missing, not the macro ratios.

    A score of 206 is certainly high for age 48. The decision of whether to add statins to an anti-atherogenic diet is yours alone, and must be made with the knowledge that it may help, but there may be tradeoffs due to side effects.

    You might not know it listen to cardiologists, but there have been no randomized trials of statin therapy in FH to tell us for sure whether it helps or not. There are uncontrolled and restrospective analyses that suggests lower than “expected” mortality with treatment, but you know how unreliable that kind of study is.

    So it might be reasonable to take a small dose of statin if you have FH for the pleiotropic effects, but not specifically to decrease the LDL, and the LDL change will not predict how much your risk is decreased.

    If you take a powerful statin like crestor, your LDL could become lower than mine (190 particle number 1100 pattern A, etc.) but your risk may still be higher than mine as you still have fewer receptors or altered intracellular cholesterol metabolism etc. In the same manner, folks who have already had an MI become “only” 4 times more likely to die instead of 5 times with statins, even if their LDL gets into the Davis zone of 60… More proof the serum LDL number is not "causing" anything. In the case of FH, elevated LDL is an effect of the actual abnormality, which is the receptor mutation.

    So to summarize, a person with strong family history of CAD and hetFH is probably in the same boat as the secondary prevention population, but with a mortality benefit actually less established than those who've had a heart attack.  May be at higher risk for MI (especially on the SAD), and may have reduced MI risk with statins, but may be trading MI risk for a higher risk of cancer, muscle dysfunction, liver toxicity, memory problems. etc.

    Of course, with the availability of CAC (calcium scoring) you have a little help in your decision. If you are age 50 and have a trivial or zero calcium score, you are probably like the rest of us risk wise, but if your score is sky-high, you might be more like the secondary prevention population.

    But everyone would benefit from a less atherogenic diet, I would think.


    Japanese Study

    Oxford Study

    *hetFH = heterozygous FH - the most common type, about one in 500 people