Evidence debunking low sodium diet

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Rothbard said:
If conducted properly, those studies count for a lot.

If conducted by people with conflicts of interest using arbitrary stopping parameters and endpoints, etc., then not so much.



http://www.ncbi.nlm.nih.gov/pubmed/20585067
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It's true. The study you linked there is barely statistically non-significant, with a risk ratio of .91 but a 95% confidence interval of 0.83-1.01. It's too bad that PubMed doesn't have a way to see the list of studies that cited that one to see if there was any more recent followup that might have a higher statistical power to better suss out the real result.

It's also too bad that none of those many followups give you the exact opposite result in a much more comprehensive fashion. (to just pick two. the first link supports the lowering of all-cause mortality. The second supports the $/QALY I mentioned in my post above.)

I'm happy that my peers throughout the country are being taught to adequately evaluate evidence based medicine and not take the first thing they read to be gospel.
 
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I'd just give up on this guy. http://forums.studentdoctor.net/showthread.php?t=890456&page=3

guy has some kind of bitter betty bias agains't allopathic medicine. I guess the only acceptable treatments are those that do absolutely no harm. ( tincture of rose, anyone? We could probably do some serial dilutions of it, if you'd like. )

Low disease risk inclusion criteria, from the first paper included from Raryn:
"Trials were considered to have enrolled participants at low cardiovascular risk if the 10-year risk of cardiovascular-related death or nonfatal myocardial infarction among participants was less than 20%,10 as assessed by extrapolation of observed risk in the control group of each trial. In general, this corresponded to participants who were free from cardiovascular disease (i.e., no prior acute coronary syndrome or coronary revascularization, no prior ischemic stroke and no prior revascularization or loss of limb owing to peripheral arterial disease) and diabetes. Data from trials in which some, but not all, participants had known cardiovascular disease were included if the control group had a low cardiovascular risk (as defined above)."

Inclusion critera from Rothbard's paper:
"Our predefined inclusion criteria were (1)
randomized trials of statins vs placebo/control, (2) trials that collected information on all-cause mortality, and (3) trials conducted among individuals without prevalent CVD at baseline"

There basically had the same inclusion criteria. Free of CVD as a baseline. Same ****, go be bitter somewhere else.
 
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low sodium -> food taste bad -> my fat a** patients stop eating -> their glucose and BP drops. i support low sodium diets.
 
myhandsarecold said:
low sodium -> food taste bad -> my fat a** patients stop eating -> their glucose and BP drops. i support low sodium diets.
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-->you patients go back to nice-tasting, salty (fatty,sugary) foods --> they regain their weight --> we continue to have an overweight country.

Keeping the pounds off is clearly very hard nowadays, with 1/3 of Americans classified as obese. Given limited amount of willpower on the part of our patients, and the importance of addressing the problem of obesity itself, having them dedicate much of that willpower to something that in the end does not matter for their overall health is a bad prescription.
 
Inclusion critera from Rothbard's paper:
"Our predefined inclusion criteria were (1)
randomized trials of statins vs placebo/control, (2) trials that collected information on all-cause mortality, and (3) trials conducted among individuals without prevalent CVD at baseline"

What, are you going to ignore this while being a semantic nazi on the other paper? What is "prevalent"? Does that mean some risks factors were allowed?

Also, as you said in the other thread, the trials were randomized so much of this biasing factor should be ruled out, right? Or does that only occur in meta-studies proving your point?
 
Rothbard said:
It's not that the study had that much more statistical power, it's that they used different inclusion criteria.

The trial I linked to included only people with NO evidence of cardiovascular disease. The study you linked to included some people WITH cardiovascular disease: "Data from trials in which some, but not all, participants had known cardiovascular disease were included if the control group had a low cardiovascular risk (as defined above)."

Look, very few people deny that statins positively affect mortality in people with sufficient cardiovascular disease. So yes, if you include sicker people then you will see a greater effect. This is a fairly simple concept. By using such a scheme, the authors miss the point entirely. The problem with many trials is that sick people are grouped together with healthy people and the effect on this combined group is reported. The purpose of these newer analyses is to see what effect statins have on healthy people. To achieve fine resolution and prove that healthy people should get statins, you can't include people with CVD. Conclusion: the study you linked cannot be used to argue that people with no CVD should get statins because they included people with CVD! The whole idea is to exclude people with CVD!

Now, with further analysis perhaps we can posit some criteria that can be used to categorize CVD-free people into "should treat" and "shouldn't treat" groups. We're not there yet but you still want to treat all of them! This is not good medicine. First do no harm, right?

I'm happy that my peers throughout the country are being taught to adequately evaluate evidence based medicine and not take the first thing they read to be gospel.
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You left out the rest of the paragraph:"Trials were considered to have enrolled participants at low cardiovascular risk if the 10-year risk of cardiovascular-related death or nonfatal myocardial infarction among participants was less than 20%, as assessed by extrapolation of observed risk in the control group of each trial. In general, this corresponded to participants who were free from cardiovascular disease (i.e., no prior acute coronary syndrome or coronary revascularization, no prior ischemic stroke and no prior revascularization or loss of limb owing to peripheral arterial disease) and diabetes. Data from trials in which some, but not all, participants had known cardiovascular disease were included if the control group had a low cardiovascular risk (as defined above)."

The larger sample size equaled more statistical power. You can argue about their inclusion criteria if you'd like. The reasoning is certainly debatable, and there have been plenty of responses both ways in the scientific literature regarding primary prevention in lower risk groups. There's problems with some of the studies included in your paper and there's debate on inclusion of other ones.

You most certainly have no leg to stand on when it comes to secondary prevention though, which makes your "Wait until you folks start re-thinking statins and cholesterol." that started this discussion even sillier.

Now, do I think every single person on the planet should be started on a statin? Of course not. Do I think they have robust evidence at being effective (and cost effective!) for primary prevention of morbidity and mortality? Yes. The absolute benefits of statins are smaller in primary prevention than in secondary prevention, but the effects are real. And I definitely think everyone with mid-high risk or a history of CAD should be on a statin, except in the rare circumstances they can't tolerate it.

I think I'm done posting in this thread, simply because the evidence is there for people who want to look it up and I don't have the time, especially this close to the end of a clerkship. A quick summary for those of you actually here with an open mind:

You're medical students (or people who want to be medical students), so presumably you trust in (at least some parts of) medicine. You're paying schools tens of thousands of dollars to learn medicine, and I would assume you trust the experienced clinicians teaching you. When you come across claims, in person or on the internet, that are the exact opposite of what you're being taught, there are two possibilities: Your preceptors are wrong/out of date, or the source of conflict is wrong/out of date. Is the former possible? Yes, though most academic clinicians are better than others on keeping up with the evidence. For minor things especially, they can be wrong. (Ex: I've had people tell me to never use lidocaine w/ epi on fingers/toes/nose/penis b/c of the necrosis risk. There's been papers that have examined this medical fact and found there to be no evidence behind it, just a case report or two from before the 1950s when there was no such thing as lidocaine and epi doses in locals were far from standardized)

But the simpler explanation if you see something that disagrees with a major medical fact you were taught is that there's something wrong with the claim. Do the research. Go to uptodate or look at the actual trials. You might find conflicting trials, look at the further papers that are replies to them. Keep in mind levels of evidence and things like statistical power. Or you might find the claims are made based on misinterpretations or they're made based on old data that has since been debunked. Lots of things are up for debate, but extraordinary claims (such as "the entire medical establishment is wrong and has been wrong for 50 years about xyz that has been researched to death but there's a conspiracy to tell people otherwise") require extraordinary evidence.

Edit: I just looked at that homeopathy thread one of you linked above and see Rothbard arguing against not just statins but chemotherapy and for God's sake *vaccines*! Anyone who would even think to say "allopathy is a joke" is someone that should be laughed out of this forum, not taken seriously. A "practicing homeopath" is a woo-woo idiot taking advantage of poor naive people. Either way, I'm done.
 
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Raryn said:
You left out the rest of the paragraph:"Trials were considered to have enrolled participants at low cardiovascular risk if the 10-year risk of cardiovascular-related death or nonfatal myocardial infarction among participants was less than 20%, as assessed by extrapolation of observed risk in the control group of each trial. In general, this corresponded to participants who were free from cardiovascular disease (i.e., no prior acute coronary syndrome or coronary revascularization, no prior ischemic stroke and no prior revascularization or loss of limb owing to peripheral arterial disease) and diabetes. Data from trials in which some, but not all, participants had known cardiovascular disease were included if the control group had a low cardiovascular risk (as defined above)."

The larger sample size equaled more statistical power. You can argue about their inclusion criteria if you'd like. The reasoning is certainly debatable, and there have been plenty of responses both ways in the scientific literature regarding primary prevention in lower risk groups. There's problems with some of the studies included in your paper and there's debate on inclusion of other ones.

You most certainly have no leg to stand on when it comes to secondary prevention though, which makes your "Wait until you folks start re-thinking statins and cholesterol." that started this discussion even sillier.

Now, do I think every single person on the planet should be started on a statin? Of course not. Do I think they have robust evidence at being effective (and cost effective!) for primary prevention of morbidity and mortality? Yes. The absolute benefits of statins are smaller in primary prevention than in secondary prevention, but the effects are real. And I definitely think everyone with mid-high risk or a history of CAD should be on a statin, except in the rare circumstances they can't tolerate it.

I think I'm done posting in this thread, simply because the evidence is there for people who want to look it up and I don't have the time, especially this close to the end of a clerkship. A quick summary for those of you actually here with an open mind:

You're medical students (or people who want to be medical students), so presumably you trust in (at least some parts of) medicine. You're paying schools tens of thousands of dollars to learn medicine, and I would assume you trust the experienced clinicians teaching you. When you come across claims, in person or on the internet, that are the exact opposite of what you're being taught, there are two possibilities: Your preceptors are wrong/out of date, or the source of conflict is wrong/out of date. Is the former possible? Yes, though most academic clinicians are better than others on keeping up with the evidence. For minor things especially, they can be wrong. (Ex: I've had people tell me to never use lidocaine w/ epi on fingers/toes/nose/penis b/c of the necrosis risk. There's been papers that have examined this medical fact and found there to be no evidence behind it, just a case report or two from before the 1950s when there was no such thing as lidocaine and epi doses in locals were far from standardized)

But the simpler explanation if you see something that disagrees with a major medical fact you were taught is that there's something wrong with the claim. Do the research. Go to uptodate or look at the actual trials. You might find conflicting trials, look at the further papers that are replies to them. Keep in mind levels of evidence and things like statistical power. Or you might find the claims are made based on misinterpretations or they're made based on old data that has since been debunked. Lots of things are up for debate, but extraordinary claims (such as "the entire medical establishment is wrong and has been wrong for 50 years about xyz that has been researched to death but there's a conspiracy to tell people otherwise") require extraordinary evidence.

Edit: I just looked at that homeopathy thread one of you linked above and see Rothbard arguing against not just statins but chemotherapy and for God's sake *vaccines*! Anyone who would even think to say "allopathy is a joke" is someone that should be laughed out of this forum, not taken seriously. A "practicing homeopath" is a woo-woo idiot taking advantage of poor naive people. Either way, I'm done.
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:clap:
 
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Rothbard said:
Why is this true? This is an appeal to authority: if my professors say it, then it must be true. Is it so hard to believe that bad ideas sometimes persist, supported (consciously or subconsciously) by financial motives? (<- here is your conspiracy theory)

What is this bullsh*t? Not once in any of my posts have I alluded to a "conspiracy". Stop putting words in my mouth. I don't believe in any conspiracies regarding medicine, apart from those that are already well accepted. Ie, that pharma will occasionally cover up negative research, something I think we're all familiar with.
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I get you're doubting statins as a primary prevention method. That's fine, many people argue about that.

Arguing about if statins should be used as a secondary preventive measure makes you very ill informed. Why don't we start doubting everything we do, if we're going to head down that road?
 
Rothbard said:
Statins do work if you don't do anything else. There are, however, other options that can be pursued that render statins nearly useless. Detoxification, avoidance of pro-inflammatory foods, supplementation with antioxidants, stress reduction, etc. Doctors are not familiar with any of these and jump straight to statins.
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I have nothing else to add here. Why did you go into medicine?
 
ya! if you give statins you will automatically give someone diabetes. listen to this guy hes 101% correct
 
we had this same discussion with rothtard in the homeopathy thread in pre-allo. when he stopped responding there I was kinda hoping he had just left.... nope... trolling another thread.
 
did you see the homeopathy thread? the guy has gone into more than 1 thread now and derailed based on statin bullcrap (and in that one, the argument was statins cause diabetes so we shouldnt use them for cholesterol control)

you can also be critical of someone's actions without being a presumptuous douche.... my issue with Roth has much more to do with the insistence on this topic and poorly supported and sometimes directly self-contradicting evidence which he uses to spread bad information. I think venting that in a little harmless sarcasm is passable
 
SpecterGT260 said:
did you see the homeopathy thread? the guy has gone into more than 1 thread now and derailed based on statin bullcrap (and in that one, the argument was statins cause diabetes so we shouldnt use them for cholesterol control)

you can also be critical of someone's actions without being a presumptuous douche.... my issue with Roth has much more to do with the insistence on this topic and poorly supported and sometimes directly self-contradicting evidence which he uses to spread bad information. I think venting that in a little harmless sarcasm is passable
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Fair enough

There was obviously some history here I didn't understand
 
jdh71 said:
Fair enough

There was obviously some history here I didn't understand
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:thumbup:

partly my bad lol. i saw a few of the other links, quotes, ect.... (basically I only had 2 examples but had already committed to a short list :cool:) and figured he was already known as a troll
 
Raryn said:
It's true. The study you linked there is barely statistically non-significant, with a risk ratio of .91 but a 95% confidence interval of 0.83-1.01. It's too bad that PubMed doesn't have a way to see the list of studies that cited that one to see if there was any more recent followup that might have a higher statistical power to better suss out the real result.

It's also too bad that none of those many followups give you the exact opposite result in a much more comprehensive fashion. (to just pick two. the first link supports the lowering of all-cause mortality. The second supports the $/QALY I mentioned in my post above.)

I'm happy that my peers throughout the country are being taught to adequately evaluate evidence based medicine and not take the first thing they read to be gospel.
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lol they are trying their darndest to salvage statin's rep. and a bigger lol @ the HYOOGE financial conflicts of interest involved with the key authors of both the papers you linked.

Ah, on the run right now so no time to give an in-depth comment. But to anyone whose interested in the various sides, this site might be helpful ~~> http://www.thennt.com/statins-for-heart-disease-prevention-without-prior-heart-disease/
(oh, and http://www.thennt.com/statins-for-acute-coronary-syndrome/ is a fun read as well)
 
Rothbard said:
A number of studies have shown a causative link between statins and diabetes. This isn't really debatable, the only question is how this changes the risk:benefit analysis.
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and since that isnt what i debated..... what's ur point?

(ill give you a hint like we had to do in the other thread.... there is a massive qualifier on my post concerning the diabetes stuff.....)
 
mTOR said:
lol they are trying their darndest to salvage statin's rep. and a bigger lol @ the HYOOGE financial conflicts of interest involved with the key authors of both the papers you linked.

Ah, on the run right now so no time to give an in-depth comment. But to anyone whose interested in the various sides, this site might be helpful ~~> http://www.thennt.com/statins-for-heart-disease-prevention-without-prior-heart-disease/
(oh, and http://www.thennt.com/statins-for-acute-coronary-syndrome/ is a fun read as well)
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We aren't really debating the usage of statins for primary prevention. I think it's very easy to say either way if they should be used for primary prevention.

I think we, well myself anyway, are arguing about its usage as a secondary event prophylaxis. The literature clearly says it helps after a primary event and Rothbard isn't buying it.
 
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there are half a dozen papers posted in the homeopathy thread that show a shaky correlation between statin use and diabetes to begin with. I havent seen a good study yet that really accounts for the convoluting factors that contribute to both hypercholesterolemia AND diabetes.
A morbidly obese person developed type 2 diabetes? You don't say.....

the best paper ive seen rothbard cite is a meta analysis between high and moderate dosing. but the random placebo controlled studies are not conclusive - I even posted some where glucose sensitivity was increased with statin use...
 
tiedyeddog said:
We aren't really debating the usage of statins for primary prevention. I think it's very easy to say either way if they should be used for primary prevention.

I think we, well myself anyway, are arguing about its usage as a secondary event prophylaxis. The literature clearly says it helps after a primary event and Rothbard isn't buying it.
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Did you mean it's not very easy? My understanding has been that the evidence for primary prevention is much weaker than that for secondary prevention.
 
mTOR said:
lol they are trying their darndest to salvage statin's rep. and a bigger lol @ the HYOOGE financial conflicts of interest involved with the key authors of both the papers you linked.

Ah, on the run right now so no time to give an in-depth comment. But to anyone whose interested in the various sides, this site might be helpful ~~> http://www.thennt.com/statins-for-heart-disease-prevention-without-prior-heart-disease/
(oh, and http://www.thennt.com/statins-for-acute-coronary-syndrome/ is a fun read as well)
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HOOOOOOLD the f****in phone......

your last link.... "none were helped" followed by "an unknown number were harmed"....
how do you not see the problem here? until you report a number I am assuming this unknown = 0

This is the same absurd bullcrap that was pulled in the homeopathy thread.

Statin positives: Absense of evidence = evidence of absense
Statin negatives: absense of evidence = damning

That site is not objectively reporting the findings or interpreting the paper.... Although yes.... it is a good read... only in the sens that it illuminates how warped people are willing to go to validate pre-conceived notions. god..... they even lose their fancy "laymans terms" angle from the first link.... the "in other words" is actually IN THE SAME DAMN WORDS! was this page put together by middle schoolers? nitpicky... I know.... but if you want to attack the credibility of papers posted by others make sure not to post sites which nothing but an agenda and some fancy rhetoric.

"Untold MILLIONS suffer from side effects!" = "x*(10^6) pts w secondary endpoint" and x doesnt necessarily exclude 0 here.....
 
you know the overarching topic and point of contention is whether statins should be avoided due to this small risk, right?
 
facetguy said:
Did you mean it's not very easy? My understanding has been that the evidence for primary prevention is much weaker than that for secondary prevention.
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My bad, I meant to say it's easy to spin it however you want it for primary prevention, meaning the evidence is as you say, somewhat shaky. I am not saying it's wrong for either stance, I am just saying you have evidence coming from both sides and it's hard to tell what is really going on. If you take all the research at face value, it appears statins have a large role in primary prevention. If you assume some kind of hidden agenda, then I guess you can say whatever you want.

It is pretty strong for secondary, however.
 
Would love to hear what you think about the low-fat diet for obesity.
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facetguy said:
FDA issues warning on statin side effects today:
http://www.nytimes.com/2012/02/29/health/fda-warns-of-cholesterol-drugs-side-effects.html?_r=1
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I saw this on yahoo today, too, kind of funny in light of this thread.

http://www.reuters.com/article/2012/02/28/us-fda-statins-idUSTRE81R1O220120228
"The value of statins in preventing heart disease has been clearly established," Amy Egan, deputy director for safety in FDA's Division of Metabolism and Endocrinology Products, said in a statement. "Their benefit is indisputable, but they need to be taken with care and knowledge of their side effects."
 
Rothbard said:
I spent a dozen posts explaining this to you in the other thread. The studies/analyses I linked to involved randomized interventions; "confounding factors" is not a valid criticism, since the two groups were presumably similar at baseline. Do you know what randomized means? I could just as well level the same criticism at any study that shows statins reduce cholesterol.

Are you an MS1 or 2? Have you taken any statistics classes?
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several other randomized studies did not show the same effects.

the OR of the meta you posted was 1.12 with a lower bound of 1.04 - statistically significant by the skin of its teeth.

Also, the statistical significance did not hold up under subgroup analysis - notably among BMI, baseline glucose, and baseline triglyceride groups. So ya.... there's that.

you cling to the fact that it was a randomized meta as if that dispels ALL selection bias. As I said previously - selection bias is inherent because people don't come in for statins because they are bored and feel like popping pills. These are people with known hypercholesterolemia - that is inherent selection bias due to risk factors for high cholesterol. In the study you posted and continue to leg hump due to its "randomized methodology": http://jama.ama-assn.org/content/305/24/2556.long

*Instance of diabetes (OR) was statistically INSIGNIFICANT among people with below median BMI, it was only significant for people with above average BMI.
*For people with average fasting baseline glucose levels, the OR for developing diabetes was statistically INSIGINIFICANT.
*all subgroups showed statistically significantly decreased odds ratio of primary endpoints (cardiovascular incidents) in the study provided by sir RothBard

random selection from within an inclusion group can mitigate selection bias, but it cannot completely resolve it. basically what these numbers are saying is "if you are already predisposed to diabetes, administration of this drug which has a small chance of messing with your sugar metabolism may increase chance of messing with your sugar metabolism"
OH GOOD GOLLY ME! Sure do hope I get good tickets to the RothParade after such a discovery!

you keep coming at me over grade and stats courses..... you were a homeopathist before med school.... what exactly have you had in the way of stats? When i make argumetns like this you seem to just stomp your feet, hold your breath, and shout "RANDOMIZATION!" (although the screaming while holding breath thing is impressive....) I'll put it this way, ive been in research long enough to see the shades of gray in the language of your posts and your sources which tell me you do not have a proper grasp of stats or interpretation of data.
 
tiedyeddog said:
My bad, I meant to say it's easy to spin it however you want it for primary prevention, meaning the evidence is as you say, somewhat shaky. I am not saying it's wrong for either stance, I am just saying you have evidence coming from both sides and it's hard to tell what is really going on. If you take all the research at face value, it appears statins have a large role in primary prevention. If you assume some kind of hidden agenda, then I guess you can say whatever you want.

It is pretty strong for secondary, however.
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This :thumbup:
keep in mind the conversation we are really having is whether we should discontinue statin use based on the chances of developing type 2 diabetes (compared to MI.... I prefer to call it "induced diet plan syndrome"....)

the underlying assumption here that rothy hasnt really dealt with is that there is something better out there. he mentioned homeopathy in the other thread, and even brought up things like chemotherapy as examples of how allopathic medicine does more harm than good. That is simply factually incorrect. Allopathic medicine has done more good than harm by any set of standards. However if we entertain the idea that Roth has a better system..... to DATE he has only supported it with some shaky evidence on statins and NO evidence on an alternative
 
Rothbard said:
This post will be my last response to you, as I simply don't have the time to rehash simple concepts over and over.



It's funny how a study is either "barely statistically significant" or "barely statistically non-significant" depending on how much you (dis)like its conclusion.
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you are doing the EXACT same thing but don't seem to be aware of it. you forget that the point I have been debating is not some weak correlation, but YOUR assertion that statins should not be prescribed "except in the most extreme cases". (a point ive had to make multiple times.....) and you simply have not shown effective evidence of this.



Yea, like you said in the other thread, marathoners aren't going to come in for statin treatment. Like I said in the other thread, these points are not relevant, since we want to know the effect of statins on people with hypercholesterolemia, not people who run marathons!

Similarly, these trials cannot be used to judge the effect of statins on rabbits - who cares, we're not trying to treat rabbits!

This study would be useless if it looked at rabbits and marathoners, since we're not going to be giving them statins!
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see, this is the problem we had in the other thread..... you mix and match your points an again... I just think keeping along with this is a little beyond you. I shall break it down for you

1. you said the randomized trials mean there cannot no-way no-how be any selection bias
2. I used the above explanation (marathon runners) to demonstrate that your generalization is false and it is inappropriate for you to use it as a magic shield to defend this paper
3. you backtrack and rationalize the selection bias and in the process endanger the lives of hypercholesterolemic rabbits everywhere :(. Now... this is OK to do - there will almost always be some selection bias in a study and rationalization of such bias is pretty normal. but 1 and 3.... you contradict yourself.




Again - we're trying to treat neither rabbits nor skinny healthy people. Of course the effect will be more pronounced on people who are fatter and have more risk factors. That's ok, since these are the people we're trying to treat with statins!

The effect will be less on skinny/healthy people, but they will also benefit less from statins (skinny/healthy people don't have a lot of heart attacks for us to prevent)! (That's assuming we even give them statins, which we probably will not!)
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and here it is. you have made my point for me. :love:

Bold: you admit to a convoluting factor i.e. BMI or other such DM2 risk factors
Underlined: you admit statin use has a positive impact on high risk individuals (by admitting that there is a correlative relationship between risk and efficacy)


those at higher risk of cardiovascular event - those who stand to benefit more from statin use. these are the people who now have an increased chance of being diagnosed with DM2.


you said it yourself.... im just paraphrasing what you've said here, and because I (dis)like whatever conclusion so much, im even willing to ignore the previous self-contradiction in favor of this new position! (im just a gentleman like that ;))


(may want to do some stretching people.... about to commit arithmetic)

lets look at those numbers quick, since we are on the subject..... absolute value was 2 additional cases in 1000 pts. The OR was 1.12. That means that with x original cases, (x+2)/1000 = 1.2x/1000 or x=20 cases expected anyways.

Given the points YOU made (bold and underlined), the people who were already at increased risk for DM2 are the ones likely to get it and these are the people who are in greatest need of the statins - not a solid argument for discontinuation in primary prevention.





Of course, a valid criticism of any randomized trial. Why this suddenly becomes a focal point of studies you don't like, I'm not sure.


Watch me do the same thing with CVD: basically what these numbers are saying is "if you are already predisposed to CVD, administration of this drug which has a small chance of messing with your cholesterol metabolism may increase chance of messing with your cholesterol metabolism"

Uh, no kidding. The point is to quantify these effects. That's the point of EBM. The pro-diabetic effect is quite significant relative to the beneficial effect of statins. The NNT's are of similar magnitude.
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the NNTs differ by a factor of 3, but hey maybe we should only accept treatments that have an offset impact of orders of magnitute... :thumbup:

BOLD: you forget that messing with cholesterol is the POINT here.... also, you are still stuck in the notion that a negative side effect negates any benefit automatically.

if I had a drug that was guaranteed to give every pt I prescribed it to a headache for the day, but it cured or prevented cancer in 30% of people - every one of my patients would get it. you dont seem to understand the relative nature of this. an additional 2/1000 DM2 patients in an already increased risk population is more than acceptable to me if it means that those 2 plus 4 of their buddies dont die of a heart attack (actual numbers from your paper). top prescription for DM2 is diet and exercise.... oh heavens whatever will these poor people do who now DIDNT DIE OF A HEART ATTACK? side point..... diet and exercise will also reduce their need for statins in many cases....



What does it matter? Although some (most) on this forum will question my judgement and intelligence, it's obvious to anyone reading these threads that I understand the basic statistical concepts. It's obvious to me that you don't, regardless of how much "research" experience you have. I encourage you to revisit this thread after finishing up MS2, you will better understand some of the points I'm making.
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ya ok that will sure happen, and given the vast support youve gotten in both threads it is blaringly obvious that everyone believes you understand the basic concepts :confused:

how about instead of going around this merry-go-round again for the umpteenth time, you answer the question you have avoided time and time again - if statins bad? what good?

hit me with it.... what secret mystical treatment is so much better than the allopathic approach of pushing pills and never prescribing something as natural as diet and exercise do you have? and pullleaassseee show me the blinded randomized trials that support your claim :laugh:

or you can go back and edit all of your posts back to "nm" again until the next time you get butthurt enough to re engage in this....
 
You guys are ridiculous. I knew I shouldn't have mentioned the low-fat diet here.

Why should anyone have to listen to your baseless diatribes backed by only randomized, double-blind, placebo-controlled crossover studies
when we can get our medical knowledge from world-renowned physicians like Dr. Oz?

But don't me, guys. Just enjoying my low-fat Cinnabons here. Losing weight has never tasted so good!


[YOUTUBE]cLoeNBHEoqI[/YOUTUBE]
 
If you just break it down to its most fundamental level--evolution--it just makes no sense that fat is the culprit in our diet. For hundreds of thousands of years we weren't eating pasta and bread, we were by and large eating meat. Think about all the problems we have today-almost EVERYONE has to have braces--why is that? It can't be normal, nature would NEVER select for crooked teeth. So what's going on? Why is Type 1 diabetes so prevalent? These questions are answerable. Anyway, I'll leave this alone for now, because a single paragraph is not going to convince anyone. This summer, though...

"Nothing in biology makes sense except in the light of evolution."

The incidence of childhood type 1 diabetes increased worldwide in the closing decades of the 20th century, but the origins of this increase are poorly documented. A search through the early literature revealed a number of useful but neglected sources, particularly in Scandinavia. While these do not meet the exacting standards of more recent surveys, tentative conclusions can be drawn concerning long-term changes in the demography of the disease. Childhood type 1 diabetes was rare but well recognized before the introduction of insulin. Low incidence and prevalence rates were recorded in several countries over the period 1920–1950, and one carefully performed study showed no change in childhood incidence over the period 1925–1955. An almost simultaneous upturn was documented in several countries around the mid-century. The overall pattern since then is one of linear increase, with evidence of a plateau in some high-incidence populations and of a catch-up phenomenon in some low-incidence areas. Steep rises in the age-group under 5 years have been recorded recently.
Click to expand...

Sugar, anyone?

http://diabetes.diabetesjournals.org/content/51/12/3353.full

The fact that SGLT inhibitors exist speaks to the size of the blinders we wear. There is a much, much more obvious solution.
 
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CaptainSSO said:
If you just break it down to its most fundamental level--evolution--it just makes no sense that fat is the culprit in our diet. For hundreds of thousands of years we weren't eating pasta and bread, we were by and large eating meat. Think about all the problems we have today-almost EVERYONE has to have braces--why is that? It can't be normal, nature would NEVER select for crooked teeth. So what's going on? Why is Type 1 diabetes so prevalent? These questions are answerable. Anyway, I'll leave this alone for now, because a single paragraph is not going to convince anyone. This summer, though...
Click to expand...

In fairness, wild buffalo, gazelles, etc, are pretty lean animals. Must hunted meats are, with the notable exception of marine and cold-weather animals.

Too much fat can be a problem, but it's also all about context. If you eat a high fat diet in the way our ancestors might have, you're probably good. Track that quart of Ben and Jerry's across the arctic tundra for a day and a half before finally cornering it and driving it into your buddy's net, and you'll both be very well served by feasting on its delicious remains. Pick it up at the grocery store on your drive home from work, and you and your roommate may be less well advised to just sit down and eat the whole thing.
 
CaptainSSO said:
If you just break it down to its most fundamental level--evolution--it just makes no sense that fat is the culprit in our diet. For hundreds of thousands of years we weren't eating pasta and bread, we were by and large eating meat. Think about all the problems we have today-almost EVERYONE has to have braces--why is that? It can't be normal, nature would NEVER select for crooked teeth. So what's going on? Why is Type 1 diabetes so prevalent? These questions are answerable. Anyway, I'll leave this alone for now, because a single paragraph is not going to convince anyone. This summer, though...

"Nothing in biology makes sense except in the light of evolution."



Sugar, anyone?

http://diabetes.diabetesjournals.org/content/51/12/3353.full

The fact that SGLT inhibitors exist speaks to the size of the blinders we wear. There is a much, much more obvious solution.
Click to expand...

you forget that selection has not been an issue for people for several thousand years. as a social animal we tend to protect even the weak or dis formed among us. only specific cultures in our history are known to not have this behavior and they are oddities because of it. I also don't know that teeth alignment needs to be that highly conserved. Neanderthal women usually had Sarah Jessica Parker tee... er... uh.... horse teeth :shifty:. The teeth would stick outward because they would hold hides in their mouthes in order to tan them for use (scraping the fat off the skin). In a time of no discernible medicine, agriculture, or pasta... these Sex in the City look-alikes did just fine

in addition (and I think this is the more important part) we were never supposed to live this long in the first place. our life expectancies have doubled since then. For most of human existence you were lucky to hit 40. A good deal of our diseases are a result of modern medicine WORKING. The human body was simply not made to last this long but we said "F YOU MOTHERNATURE!" and decided to push it up towards 80. non-familial cancers are a good example of this. You just don't see cancers in wild animals. Typically they don't live long enough. Dogs are getting cancers now - likely a result of also living longer than normal. (this isnt including genetic cancers or anything really weird like the Tasmanian Devil's lack of alloimmunity causing STD cancer)

the point is just that as we push the limits of what the human body can really do things are BOUND to start falling apart at some point. This principle holds true of classic cars - which is why anything from the 60's in cherry condition is so interesting. same with a 90 year old who can climb a mountain.


and the "simple solution" you are referring to (i believe) is simply healthy living... if only it were that simple lol. but I agree, I wish we would stop clogging our arteries and hospitals with diseases of vice and excess.
 
SpecterGT260 said:
in addition (and I think this is the more important part) we were never supposed to live this long in the first place. our life expectancies have doubled since then. For most of human existence you were lucky to hit 40. A good deal of our diseases are a result of modern medicine WORKING. The human body was simply not made to last this long but we said "F YOU MOTHERNATURE!" and decided to push it up towards 80. non-familial cancers are a good example of this. You just don't see cancers in wild animals. Typically they don't live long enough. Dogs are getting cancers now - likely a result of also living longer than normal. (this isnt including genetic cancers or anything really weird like the Tasmanian Devil's lack of alloimmunity causing STD cancer)
Click to expand...

When you say "most of human history", you appear to mean "most of human history since the advent of agriculture", which was actually pretty recent on an evolutionary timescale. Either that, or you're talking out of your ass. The modal age of adult deaths for hunter gatherers is upwards of 65 years. <Source>.
 
phltz said:
When you say "most of human history", you appear to mean "most of human history since the advent of agriculture", which was actually pretty recent on an evolutionary timescale. Either that, or you're talking out of your ass. The modal age of adult deaths for hunter gatherers is upwards of 65 years. <Source>.
Click to expand...

This.

Thank you for posting that, I didn't have a good source for that. Also, about the buffalo, it's because they're herbivores--their digestive systems have a much higher metabolic price than ours. Part of what allowed the bain of Homo sapiens to develop the way it did was that the shift in diet from vegetation to meat allowed more resources to be shunted away from the gut and to the brain.

The Expensive Tissue Hypothesis: http://www.jstor.org/pss/2744104

I have the full article but I'll have to dig it up, check that out for now.

Specter, that's what I was taught my whole life as well. That hunter gatherers died too long for things like diet to be an issue. But it turns out that wasn't entirely true. This is a difficult process, because it literally runs counter to the low-fat doctrine we've been taught for the past 50 years. It took me about 3 solid weeks of reading as many different sources as I could find for my resistance to the idea to finally break down.
 
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phltz said:
When you say "most of human history", you appear to mean "most of human history since the advent of agriculture", which was actually pretty recent on an evolutionary timescale. Either that, or you're talking out of your ass. The modal age of adult deaths for hunter gatherers is upwards of 65 years. <Source>.
Click to expand...


2nd paragraph under results
There is some variability among groups. Among traditional huntergatherers,
the average life expectancy at birth (e0) varies from 21 to 37 years,
the proportion surviving to age 45 varies between 26 percent and 43 percent,
and life expectancy at age 45 varies from 14 to 24 years (Figure 1; Table 2 and
Figure 3). Ache show higher infant and child survivorship than the other
groups, and Agta mortality is high at all ages. These patterns are verified in
the parameter estimates of the Siler model (Table 2). Initial immature mortality
(a1) for the Ache is about half that of other foragers, while for the Agta
it is two to three times greater.1
Forager-horticulturalists also vary significantly in infant mortality,
with a threefold difference between Neel and Weiss's Yanomamo sample
and the Tsimane. Survival to age 45 varies between 19 and 54 percent, and
those aged 45 live an average of 12&#8211;24 additional years. The Tsimane show
earlier accelerations in adult mortality than the Yanomamo and the forager
populations. The raw and simulated Gainj population shows earlier mortality
accelerations, although the raw data do not permit a strong inference about
ages greater than 55.
Acculturated foragers vary most in their likelihood of reaching age 45
(ranging from 26 percent among the peasant Agta population to about 67
percent among sedentary !Kung, Aborigines, and Ache), but show a range
of 13&#8211;27 additional years of life upon reaching age 45, similar to the range
for less acculturated foragers and forager-horticulturalists. Adult mortality
is also highly variable. For example, life expectancy at age 15 is 48 years for
Aborigines, 52 and 51 for settled Ache and !Kung, yet 31 and 36 for peasant
and transitional Agta. Hiwi show similarly low life expectancy. The acculturated
category shows a range of mortality experiences associated with
acculturation.
PDR
Click to expand...

the point I was getting at is that modern medicines has extended the lives of people as a whole.

and unless I am reading your link incorrectly I am not sure how I am "talking out of my ass". huntergatherers avg life expectancy at birth was 21-37 years... and I said "you;'d be lucky to hit 40".... its a hell of a long read so I maybe I missed something but your response is a straw man tactic for one, and doesn't exactly agree with your statement preceding it.


I am not an anthropologist.... the stuff bores me to tears. and I did see the model death charts. If you're willing to explain the difference between life expectancy and model adult death. although I still do not see this as a counterpoint to the fact that medicine and advancement as a whole are extending life expectancy
 
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^Part of it is due to modern medicine, you're right, in that we have antimicrobials and trauma surgeons, incubators for babies, etc. I have a couple articles dealing with the subject, not with mortality per se, but rather with the lack of diseases of civilization found in hunter gatherer remains. I'll have to find them though. But a large factor in mortality was due to death from trauma/infections, and that by itself brings down the life expectancy. However, of those who DIDN'T succumb to infections/trauma/infant mortality their life expectancy was quite long. I'll need to find my sources though because I realize that is pretty counterintuitive. But the main point here is that they typically didn't suffer from the diseases of civilization that are so common today.
 
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