(08-01-2013, 10:48 AM)MonikaT Wrote: I'm not saying nicotine doesn't increase the risk, but a statistically-significant increase does not mean an overwhelming increase. All it takes is the right-sized sample space, and a difference of 1% or even 0.5% can be statistically significant. Just because something increases one's risk by 1%, doesn't mean much. Is it an increased risk? Yes. Is it a great risk? No. Furthermore, there may be other factors that the researchers did not account for that could also be contributing to the risk. If a person knows what s/he is doing, anything can be proven with statistics. And all of that pre-supposes that the initial hypothesis to be proven is actually valid and the study was constructed correctly. Think about it. We know smoking increases the risk for certain cancers, yet most smokers do not get cancer. That's all I'm saying.
Furthermore, the medical community gets it wrong all the time. In the 50s and 60s, doctors claimed smoking was healthy. Remember how HRT during and after menopause was supposed to protect bone density and protect against heart disease? When they actually did a scientific study they cancelled the study because they were deathly wrong on the heart protective effects of estrogen. That's just one example. COX-II inhibitors are another example.
While I agree with MonikaT in theory, and have even used a similar argument with regard to statistics, her arguments are specious, or perhaps just misleading at best. Her statements about "most smokers" not getting cancer or embolisms will be factually correct right up the point where "only" 49% of people are affected that way. She is also right that we each have to make a choice about what level of risk we are willing to accept. Is it 20%, or 15% or 10% or 5%? When it comes to weather and deciding to put off cutting my lawn, I am willing to accept the risk of being wrong even if there is a 60% chance of rain. I often count on the 40% chance of no rain. The down side isn't very significant, but when the down side is a serious debilitating embolic event (have you ever interacted with a severely compromised stroke patient on a daily basis, I have and it's not pretty) or even death, the equation becomes drastically different, at least for me.
The issue isn't about a single study, or even 5 studies, but about decades of research that universally (except for studies funded by tobacco companies, but as you said, you can tweak a study design and use statistics to prove anything, and it's not like they don't have a vested interest in proving their products "harmless" and keeping you addicted, right?) implicates nicotine in many more health risks than just embolism. Did you know it has historically been used as a pesticide in commercial greenhouses because of it's toxicity? It adversely affects pretty much every body system. In just about every measure of outcomes for medical intervention, smokers are on the low end of the curve. They heal slower and have worse results overall. That's in the data. Do they get better, sure, but at what cost?
Your examples of drugs that have gone wrong is also misleading. The cardiac protective function of estrogen, specifically estradiol, was not brought into question by the Women's Health Initiative. The WHI used Premarin exclusively as the source of estrogens in the study. Premarin is a cocktail of equine, conjugated estrogens, with the main active estrogen being estrone. All 'estrogens' are NOT created equally. Estrone is 80 times weaker than estradiol and requires metabolism by the liver to be effective in humans. In addition, oral premarin (used in the study) when processed by the liver, significantly increases the risk of embolism generally, but even more for smokers, primarily as a result of the high doses required to be effective and the extensive metabolism by the liver on the dreaded "first pass" after passing the GI system. As far as I know, the exact reason why the risk is higher for smokers is not known, but it's definitely in the data. The big pharma company that produces Premarin has done extensive advertising (yes to doctors) that equates all estrogen as being equal. In the WHI it was the form of HRT that was the problem, not getting HRT itself.
In the case of COX2 inhibitors, you will notice that other COX2 inhibitors are still on the market. Why? Because as a class of drugs, they have some significant benefits for folks that need to use them but who are also prone to GI complications. Are they perfect? No. Are they the miracle drug big pharma marketed them as when first released to the market? No. They have some well documented side effects that must be managed to mitigate the risk of cardiac events.
Vioxx was voluntarily removed from the market not because it didn't work, or because it had side effects, but because Merck did not disclose those side effects when it's OWN research indicated they existed, resulting in 100K+ cases of serious cardiac disease. Interestingly, Vioxx was faster acting and more effective than Celebrex but Vioxx was pulled from the market primarily because of public opinion and the liability risk Merck created by not disclosing all the results of it's research, and basically misleading the FDA in getting approval for the drug. The problem wasn't the study design, or the data or even interpretation of the data, but who controlled its release. Without ALL the information, physicians couldn't help protect the subset of patients at risk, so the drug was pulled from the market.
The studies with regard to nicotine are legion and by researchers and facilities without an agenda or axe to grind. It really sounds like MonikaT is either drinking the tobacco industry's Kool-aide or willfully in denial. That's fine, it's her choice, but let's not cloud the picture with specious and misleading arguments.
Basically, what we 'know' is that certain types of oral exogenous estrogen have significantly increased risk of cardiovascular events including death. Not all estrogens are equal in either their risk of cardiovascular problems or effectiveness. PM has highly estrogenic compounds that are relatively effective in humans. Do they act the same way as estradiol or conjugated estrogens? In some respects yes (feminization of males, amelioration of menopausal symptoms in females), in other respects no (protective function of PM with some estrogen sensitive cancer cell lines where estradiol seems to promote cancer cell growth). Is the risk the same for PM as conjugated estrogens or even estradiol? That's the big unanswered question.
