I've heard recently heard that HDL is no longer considered to be protective. I may have misheard, so be sure to take it with a grain of salt.
LIPITOR....avoid at all costs if you can..
- Thread starter El OchoCinco
- Start date
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524519/
Nonfasting plasma triglycerides are strongly predictive of ischemic events in both sexes, even taking into account differences in plasma HDL17. As nonfasting triglyceride levels increase, so does the risk of all-cause mortality16. In addition, in patients with already low LDL cholesterol, elevations in plasma triglycerides increase CVD risk, and the greatest reduction in CVD risk occurs when both LDL and triglycerides are reduced18.
This relationship between plasma triglycerides and CVD is in part because increased plasma triglycerides are associated with the generation of a greater proportion of smaller, dense LDL, which are highly susceptible to oxidation, resistant to removal from the blood, and these LDL particles easily bind to the arterial wall18–20. In addition to promoting the formation of these atherogenic LDL particles, plasma triglycerides are themselves atherogenic since their hydrolysis by LPL results in the release of free fatty acids and other inflammatory mediators at the arterial wall2
APOCIII and diet:
Modulating apoC-III through dietary approaches may be another opportunity to beneficially change circulating apoC-III levels, though this may prove complex. In the liver, apoC-III expression is inhibited by insulin and stimulated by glucose via transcriptional regulatory elements in the promoter region75,76. ApoC-III expression is also sensitive to fibrates, which reduce levels of apoC-III in addition to lowering plasma triglycerides77,78. It is important to note that very little is known about how intestinal apoC-III is regulated, and this may be quite different than hepatic apoC-III regulation, since hepatic and intestinal lipoprotein synthesis pathways are unique and regulated at different steps79–81. There may be a valuable difference in the regulation and function of apoC-III in these tissues, and it is likely that dietary nutrients moderate this effect. This is a critical gap in understanding how this nutrient-rich food impacts a key cardio/metabolic risk factor.
Nonfasting plasma triglycerides are strongly predictive of ischemic events in both sexes, even taking into account differences in plasma HDL17. As nonfasting triglyceride levels increase, so does the risk of all-cause mortality16. In addition, in patients with already low LDL cholesterol, elevations in plasma triglycerides increase CVD risk, and the greatest reduction in CVD risk occurs when both LDL and triglycerides are reduced18.
This relationship between plasma triglycerides and CVD is in part because increased plasma triglycerides are associated with the generation of a greater proportion of smaller, dense LDL, which are highly susceptible to oxidation, resistant to removal from the blood, and these LDL particles easily bind to the arterial wall18–20. In addition to promoting the formation of these atherogenic LDL particles, plasma triglycerides are themselves atherogenic since their hydrolysis by LPL results in the release of free fatty acids and other inflammatory mediators at the arterial wall2
APOCIII and diet:
Modulating apoC-III through dietary approaches may be another opportunity to beneficially change circulating apoC-III levels, though this may prove complex. In the liver, apoC-III expression is inhibited by insulin and stimulated by glucose via transcriptional regulatory elements in the promoter region75,76. ApoC-III expression is also sensitive to fibrates, which reduce levels of apoC-III in addition to lowering plasma triglycerides77,78. It is important to note that very little is known about how intestinal apoC-III is regulated, and this may be quite different than hepatic apoC-III regulation, since hepatic and intestinal lipoprotein synthesis pathways are unique and regulated at different steps79–81. There may be a valuable difference in the regulation and function of apoC-III in these tissues, and it is likely that dietary nutrients moderate this effect. This is a critical gap in understanding how this nutrient-rich food impacts a key cardio/metabolic risk factor.
https://www.prnewswire.com/news-rel...pociii-rx-in-patients-with-fcs-273002711.html
ISIS Pharma in Phase 3 study of drug targeting APOCIII in patients with extremely high triglycerides. Probably people who don't respond to dietary changes and just have high fasting Tri's. This could be a new drug used by people over statins in general to reduce tri's and cholesterol levels.... watch out Lipitor haha.
ISIS Pharma in Phase 3 study of drug targeting APOCIII in patients with extremely high triglycerides. Probably people who don't respond to dietary changes and just have high fasting Tri's. This could be a new drug used by people over statins in general to reduce tri's and cholesterol levels.... watch out Lipitor haha.
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I'm with everything stated about the benefits of diet and exercise, as I've frequently heard stated if exercise were a drug everyone would be clamoring for it based on the benefits.
That said, dropping from 3% to 1.9% is in fact a 36% reduction (36.6% by my math actually). That's a pretty significant result, especially given that the 36.6% represents hundreds of thousands of people if it holds out over time and the drug is broadly prescribed, which appears to be the case. If I or someone I love is one of those hundreds of thousands, it's pretty damn significant to me! Again, not to dispute all the great points about better options than the drug, but as drugs go this is a pretty significant result and given that it acts on a massive population (as opposed to say, an orphan drug for a disease that only impacts a handful of people), that percentage is even more significant. Simply saying I don't think arguing the angle of "it only reduced incidence from 3% to 1.9%" is a winning argument from either a statistics or human interest perspective. Stick with the "better options with fewer side effects" argument!
Ok then how about simple math.
30000 out of a million who took a pill, compared to 19000 out of million who took nothing (a placebo pill).
Still think that is a great result? Especially weighing the cost of the drug and the fact many, probably a good size majority, will not make any substantial change in diet and exercise?
30000 out of a million who took a pill, compared to 19000 out of million who took nothing (a placebo pill).
Still think that is a great result? Especially weighing the cost of the drug and the fact many, probably a good size majority, will not make any substantial change in diet and exercise?
That's 11,000 real live breathing loved humans. Just saying there's no world where that isn't significant. Listen, I don't put in 20-25 miles running a week because I don't get the importance of exercise and diet. But when you get so hung up on your religion that you start claiming things that objectively just don't make sense, like this being an irrelevant result, you become less effective at spreading your and my message, not more.
First the data is coronary event, NOT only deaths. Second, there is no way to know if the placebo group could have improved their rate of coronary even by simply improving lifestyle. The study never addressed that. Also what if the placebo group was given strict dietary restrictions and the incidence rate dropped to 1% verus 1.9% on statins? Pharma will never fund that study.
So a pill that costs a lot of money is addressing an issue that affects 3% of the population????? And the improvement is to 1.9%.
Have you ever studied what a statin does to your body and what are the side effects? Have you seen a study where a group simply changed lifestyle and improved the 3% rate? Of course not because that does not serve the drug companie's profit aim. Separate studies have proven the efficacy of diet on lowering triglycerides and LDL and improving coronary risks. People who were not taking statins.
It is not "hung up on religion" it is basic facts. I did the detailed medical research and the fact the FDA passed the drug based on a 3% to 1.9% improvement in test groups without validating lifestyle changes.
You know why? Drug companies cannot patent/profit from diet recommendations. PERIOD.
So a pill that costs a lot of money is addressing an issue that affects 3% of the population????? And the improvement is to 1.9%.
Have you ever studied what a statin does to your body and what are the side effects? Have you seen a study where a group simply changed lifestyle and improved the 3% rate? Of course not because that does not serve the drug companie's profit aim. Separate studies have proven the efficacy of diet on lowering triglycerides and LDL and improving coronary risks. People who were not taking statins.
It is not "hung up on religion" it is basic facts. I did the detailed medical research and the fact the FDA passed the drug based on a 3% to 1.9% improvement in test groups without validating lifestyle changes.
You know why? Drug companies cannot patent/profit from diet recommendations. PERIOD.
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I don't think anyone disputes the fact that diet and exercise can solve this better than a stating. There is actually a good deal of research to support the benefits of diet and exercise, just couldn't pull one up off the top of my head on this particular topic.
Seriously preaching to the choir on the better alternatives out there, we're in violent agreement. That doesn't mean that going from 3% to 1.9% in a large population isn't significant, you're conflating the two because you want to think that statins are pure evil with no purpose. There are people who can't exercise, there are even people I love who won't exercise even though it without question would allow them to reduce or end their dependence on medication. I still love them, their early death or poor health is still a bad thing for me even if entirely preventable and their fault. Something that helps tens of thousands of people like this is still a good thing full stop, you come across as pretty callous with any other message. Which again makes people less receptive to our shared message.
BTW, if you want to shift to discussing coronay events vice deaths that might be worthwhile, just note that's a very different thing than the original line of thought. Without knowing a lot about how a "coronay event" is defined, I'd say that avoiding tens of thousands of those is a good thing even if not all or even most would result in death, but hey, maybe some people find coronay events pleasant?