A brand new paper offers GREAT news for E4 carriers. New research suggests that the E4 allele leads to heart disease ONLY in conjunction with the presence of metabolic syndrome.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
Abstract
BACKGROUND:
Hypertension has a significant relevance as a cardiovascular risk factor. A consistent increase on world's Metabolic Syndrome (MetS) incidence has been associated with an epidemic cardiovascular risk in different populations. Dislipidemia plays a major role determining the epidemic CV burden attributed to MetS. Apolipoprotein E (ApoE) is involved on cholesterol and triglycerides metabolism regulation. Once ApoE polymorphism may influence lipid metabolism, it is possible that it brings on individual susceptibility consequences for the development of MetS and cardiovascular risk. The objective of the study is to measure the discriminatory power of ApoE polymorphism in determining cardiovascular risk stratification based on the presence MetS in a cohort of hypertensive patients.
METHODS:
It was enrolled 383 patients, divided in two groups, classified by MetS presence (IDF criteria): Group 1: 266 patients with MetS (MetS +) and Group 2: 117 patients without Mets (MetS -). Patient's data were collected by clinical evaluation, physical exam, file reviews and laboratory testing. Polymorphic ApoE analysis was performed by PCR amplification. Groups were compared on clinical and laboratory characteristics as well as allele and genotype distribution towards ApoE polymorphism. Mets CVD prevalence was analysed according to E4 allele prevalence.
RESULTS:
The results evidenced 184 men (48%), 63,7% whites, 45,1% diabetics and 11,7% of patients were smokers. Mean age was 64,0 +/- 12,0 years. When genotypic distribution was analyzed, E3/3 genotype and E3 allele frequencies were more prevalent. Among patients with MetS, we observed an independent association between CVD prevalence and E4 allele frequency (OR 2.42 (1.17- 5.0, p < 0,05)). On the opposite direction, in those without MetS, there was lesser CVD burden in E4 allele carriers (OR 0,14 (0,02-0,75)). These associations remained significant even after confounding factor corrections.
CONCLUSIONS:
The results presented demonstrate that the association between ApoE gene and CVD may be modulated by the presence of MetS, with an increased CV burden observed among E4 allele carriers with the syndrome. On the opposite way, E4 allele carriers without visceral obesity had lesser prevalence of CVD.
Yes, it made sense to me. My reasoning:
It's black and white about how toxic hyperinsulinaemia and hyperglycaemia are, it has never ever been a subject of controversy. Its always been a clear linear relationship. Whereas lipids are still so controversial - yes there is a relationship between LDL and CVD risk BUT there are still so many unknowns.
On an aside: when I said that IMO glucose control trumps lipids, I never meant that lipids were irrelevant. Just that I feel we (and everyone) need to first optimise our glucose control then look at what is left to tweak lipid wise. And that a good lipid profile should never justify poor glycaemic control.
Wow. Love the thought that for e4s lower blood sugar "protects" from CVD and we already talked about how important lower BS is to protect the brain! My father, who had at least one E4, died almost 30 yrs ago of CVD and he had metabolic syndrome.
Another point is the use of statins to bring down cholesterol. So sugar can be made into cholesterol, and lipids go up, so the doctor prescribes a statin which has been shown in some people to increase BS levels. So the drug to decrease heart disease risk may actually increase heart disease risk in those that it drives up BS and have an E4 gene.
For those of you that have missed and enjoyed "THE COBBLER", your wait is over as he/she is back.
Vitamin D3 supplementation improves insulin sensitivity in subjects with impaired fasting glucose
as well as
Large study to examine if Vitamin D prevents diabetes
You may want to do some of your own cobbling research with vitamin k reading as well.
So this appears to resolve the cad and metabolic syndrome issues presented in class today. You have to just love "THE COBBLER". Your job if you choose to accept it before this tape self destructs in 60 seconds is to determine if "THE COBBLER" is onto something after being into something or is just discussing something about something. We believe that something may be wrong in Denmark and only "THE COBBLER" knows the truth. "SSSSSSSSSSSSSSSSSHHHHHHHHHHH"
On an aside: when I said that IMO glucose control trumps lipids, I never meant that lipids were irrelevant. Just that I feel we (and everyone) need to first optimise our glucose control then look at what is left to tweak lipid wise. And that a good lipid profile should never justify poor glycaemic control.
Of course. I did not mean to imply otherwise. Commonly high Tg's are thought to represent too much carb intake/poor glucose control. In my unusual case, eating high vegan carbs gives a stellar lipid panel, but less stellar glucose. I've taken the position to optimize glucose and then tweak lipids. E4's are known for poor lipid clearance. I certainly see this. Eating animal (and perhaps some other fat - haven't worked that out yet) fat shows a spike and a long slow decline (clearance). I'm thinking of doing detailed Tg testing. Eating a set amount of some kind of fat (or carbs) and testing Tg's before then periodically (maybe at 2, 6, 9, 12 hours... until <50 mg/dL). I've just been testing at ~12 hours, but the "decline" or "clearance" curve may be interesting. Even longer fasting shows elevation, so looking to see where the minimums are would allow me to optimize low Tg's. From my results, TC, LDL, HDL all correlate with Tg's & even some of the LDL-P & small LDL-P measurements. So if I minimize Tg, I optimize everything else.
WA,
I optimize 25 OHD for ~70 nmol/L (28 ng/ml). ~200 mcg of K2-MK7 is considered therapeutic. I've seen data showing a dose response relationship for K2-MK7 & arterial calcification. Hence I consume 270 mcg 2x/day. Also, supplementing with D3 to this level w/o K2 can lead to negative results IMO.
On an aside: when I said that IMO glucose control trumps lipids, I never meant that lipids were irrelevant. Just that I feel we (and everyone) need to first optimise our glucose control then look at what is left to tweak lipid wise. And that a good lipid profile should never justify poor glycaemic control.
Of course. I did not mean to imply otherwise.
oh! wasn't specifically talking about anyone or you, just clarifying in case what I said was ambiguous. Sorry in case it sounded accusatory, wasn't meant to be at all.
And your reactions to food are very....um what's the best word here.....interesting!! I have no idea what to suggest for you actually. I'm stumped. But what I do know is that you have a very healthy lifestyle in so many respects so I'm confident that you will remain healthy
Stavia, I appreciated the clarification and fully concur with your position. Of course lipids matter, esp. advanced lipids; but addressing MetS matters MORE.
Because of THAT, I think you're focusing in the right place, George. I suspect that the longer you follow Dr. Gundry's plan, all will fall in line. Fingers crossed.
