I found this paper from 2009 in JAMA Internal Medicine:
http://archinte.jamanetwork.com/article ... id=1108512
with the following conclusion:
In the largest prospective cohort study to date, CHD risk was not associated with APOE genotype after controlling for a variety of cardiovascular risk factors, particularly the ratio of low- to high-density lipoprotein cholesterol.
My take-away is that APOE4s have a harder time with keeping a good lipid profile but those who do manage a good lipid profile don't have a higher risk for heart disease. Has there been anything since 2009 that sheds more light on this topic? Am I interpreting this study correctly?
Thanks,
Is it the Lipids effect or the APOE4 effect on Heart Disease
Is it the Lipids effect or the APOE4 effect on Heart Disease
Chris
E4/E4
Alameda, CA, USA
E4/E4
Alameda, CA, USA
Re: Is it the Lipids effect or the APOE4 effect on Heart Disease
Using that single risk factor might be a bit of an oversimplification. However, here’s a more recent paper that expands on that work and demonstrates that the E4 allele leads to heart disease ONLY in conjunction with the presence of metabolic syndrome. The really great news: In patients without metabolic syndrome, the incidence of heart disease was even lower in E4 carriers.
Diversity of Apolipoprotein E genetic polymorphism significance on cardiovascular risk is determined by the presence of Metabolic Syndrome among hypertensive patients.
http://www.ncbi.nlm.nih.gov/pubmed/25413697
Also, remember that the E4 allele is pro-inflammatory. My guess is that plays a huge role for our genotype. I think Dr. Gundry checks for many markers of inflammation beyond CRP and homocysteine, like Lp-PLA2, etc. Controlling for all of those would also reduce our heart disease risk.
Diversity of Apolipoprotein E genetic polymorphism significance on cardiovascular risk is determined by the presence of Metabolic Syndrome among hypertensive patients.
http://www.ncbi.nlm.nih.gov/pubmed/25413697
Also, remember that the E4 allele is pro-inflammatory. My guess is that plays a huge role for our genotype. I think Dr. Gundry checks for many markers of inflammation beyond CRP and homocysteine, like Lp-PLA2, etc. Controlling for all of those would also reduce our heart disease risk.