Haven't read the full paper yet but the abstract says it all: Extra lipid lowering does nothing to alter the trivial benefits seen with statin therapy.
"Conclusions The combination of fenofibrate and simvastatin did not reduce the rate of fatal cardiovascular events, nonfatal myocardial infarction, or nonfatal stroke, as compared with simvastatin alone. These results do not support the routine use of combination therapy with fenofibrate and simvastatin to reduce cardiovascular risk in the majority of high-risk patients with type 2 diabetes."
IT'S NOT THE CHOLESTEROL
EDIT from the full text, it's not the triglycerides either. Why not just eat less sugar as per Nigel's comment? Simple but scary! To me this is pretty convincing that trigs are harmless, they are a surrogate for carbohydrate/fructose...
Peter
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Fenofribrate doesn't do squat for diabetics by itself according to the FIELDS trial.
http://www.diabetesincontrol.com/index.php?option=com_content&view=article&id=5732
Why would it do any better with a statin? Lowering LDL with fenofribrate didn't halt atherosclerosis. To establish something as scientific fact, you need repeatability. With the LDL hypothesis, the repeatability just isn't there.
Fibrates are for lowering serum triglycerides (TGs). I was on fenofibrate due to TGs = 4.97mmol/L. The maximum dose didn't get my TGs into the Reference Range (RR) of <1.8mmol/L.
What did get my TGs into the RR was me stopping ramming too much carbohydrate into my mouth that wasn't being burned due to a sedentary lifestyle or stored due to full glycogen stores. I didn't need fenofibrate.
Are high TGs harmless? I thought that high TGs shifted LDL from the large type A towards the small, dense type B. Or is that just an association?
Dear Peter,
How do I know my lipase is working to shift the fat out. So, ASP puts the fat nicely into storage, but, how do i know i actually have any hormone sensitive lipase shifting it back out- I suspect not. have been living on saturated fat and fois gras and... am getting fatter. A good thing in my particular case but... where, if anywhere, is the HSL?? How does one know these things exist outside of the research papers?
Thanks,
Elizabeth ( posting form a somewhat warmer geneva at last)
@Nige
It's fasting TG that are a marker for liver damage and are associated with sdLDL. I don't think TGs per se are lipotoxic - that's more lipid hypothesis nonsense.
Hi Nigel,
You have also to be very careful with semantics here. Do fasting triglycerides shift anything to anything? They are undoubtedly a marker that your liver has more carbohydrate derived lipid than it requires, mostly from fructose. It is perfectly possible to understand how fructose in the portal vein or hyperglycaemia in the systemic circulation might modify the apoB100 to reduce the residual moiety's ability to be endocytosed. But that's glucotoxicity, not lipotoxicity. Equally you might have alterations in the lipid composition in VLDLs specifically caused by fructose detoxification to palmitic acid. Those changes give a lipid pattern which is a clear flag for fructose intake. So you have to ask whether that alteration in the fasting triglycerides is toxic per se, ie your liver is out to kill you, or if it was the fructose you chose to eat which is killing you and fasting trigs are merely the messenger telling you that there is an assassin on your plate.
We are very good at shooting the messenger. Fenfibrate shoots the messenger while the disease of fructose poisoning continues... Lots of nice CVD with "normal" fasting triglycerides...
I like this study!
Peter
BTW, nice car, but no pop up eyes! My son would not approve of fixed headlights but he would love the colour.
Elizabeth,
As Kurt has commented, everything is a balance. If you eat a single huge high fat meal a day (as JK prefers) you will store almost all of that fat. Otherwise it will just slosh around in your circulation like trigs in the blood of a diabetic on a low fat diet!
So ACS and HSL will be working all the time, but at different relative rates mostly controlled by insulin with help from other lipolytic hormones...
The balance of lipid in vs out will be controlled by total calorie intake.
BTW HSL knockout mice do lipolysis perfectly well. I doubt evolution would not have a backup system for something as essential as accessing stored energy. The fact we don't know what that system is is not too important!
Peter
Peter,
Would you care to comment on Dr. Davis' most recent post - says butter raises insulin and makes you fat:
http://heartscanblog.blogspot.com/2010/03/butter-and-insulin.html
Peter, trigs aren't even a surrogate, they're merely a telltale of the action of carbs. Just like cholesterol, VLDL, and pretty much everything else carbs act on. Calling trigs surrogate means we can still blame the trigs for the damage done because they act on behalf of carbs. Instead, trigs are acted upon, i.e. they are the ones suffering the damage being done.
AGEs is a good example. AGEs are corrupted protein. They don't act on behalf of carbs, the are acted upon by carbs. Whether they do damage on their own after that is besides the point.
wait a minute, FIELD showed a statistically significant reduction in visual loss from diabetic retinopathy from fibrates, backed up by ACCORD study.
It's important to cover all the facts and not just pick and choose what fits your hypothesis
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