5 ms·

You replied to this person: >>are pretty good at treating symptoms, but when it comes to root causes of serious diseases, they're pretty bad at treating them w

by nunb 16y ago

You replied to this person: >>are pretty good at treating symptoms, but when it comes to root causes of serious diseases, they're pretty bad at treating them without inflicting collateral damage on some other body system. [Especially bad when messing with systems designed by evolution] saying: >Statins stop the production of cholesterol .. these get at the root cause of the problem and don't merely treat symptoms. No, statins do not treat the "root cause of the problem" and in fact, merely "treat" symptoms. In doing so they do great damage and kill people. Look up torcetrapib or clofibrate for examples. 0) Wikipedia http://en.wikipedia.org/wiki/Torcetrapib http://en.wikipedia.org/wiki/Torcetrapib 1) pubmed http://www.ncbi.nlm.nih.gov/pubmed/6147641 http://www.ncbi.nlm.nih.gov/pubmed/6147641? ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum 2) Pubmed Clofibrate http://www.ncbi.nlm.nih.gov/pubmed/20535009 http://www.ncbi.nlm.nih.gov/pubmed/20535009 Production of cholesterol is not the root cause of the problem. Starting from wrong axioms always produces wrong results. It's the kind of stuff that leads to blood-letting being the leading treatment of the age. If you're in medical school I would urge you to read Gary Taubes' book -- the man makes some interesting observations about how medical textbooks have changed over the years (esp. in the fields of diabetes, iirc). Also, sure antibiotics kill bacteria, but they also take a toll on the body (granted they get at the proximate cause of the problem).

carbocation 16y ago
You will do well to note that I said statins, not CETP inhibitors (torcetrapib) nor fibrates. There is an ocean of difference between them, so you can't just go around making it look like I endorsed a drug that never got FDA approval (torcetrapib), for example. After antibiotics, statins have the clearest risk-benefit profile of just about any drugs ever invented, and their effectiveness and safety have been under continuous study for decades. You assert that the production of cholesterol is not the problem. Since you claim that I am starting from the wrong axiom, what do you believe is the root cause of hypercholesterolemia? Since hypercholesterolemia is the canonical asymptomatic disease, I suspect you are misusing the term symptom. Finally, it is natural for medical textbooks to change as our knowledge changes. I haven't read the book you are referring to but if he says that drug companies are having an evil influence, I wouldn't be surprised and I'd probably agree.
- nunb 16y ago
  >You will do well to note that I said statins I did note that, and in my reply said that they (statins) don't treat the root cause. However, I used the example of torcetrapib and clofibrate merely to point out that "reduction in cholesterol" is done most efficaciously by other compounds too. (I don't know if the overall mortality was because of alternate toxicities of the compounds in question, other fibrates are still under consideration). I did not mean to imply that you endorsed either T or C, and I hope I didn't sound like I did. I may as well have accused you of promoting thalidomide... The intent was to show that treating lipoprotein numbers was unproductive... ie that the lipoprotein numbers are merely a symptom [2]. More on this below in the coronary calcification note below.. > statins have the clearest risk-benefit profile of just about any drugs ever invented I do not believe this to be true. For example, statins have well known effects in "worsening"[1] the lipoprotein profile (especially VLDL or Lp(A) -- can't find the reference at this moment) If dyslipidemia is a symptom, what accounts for Coronary arterial disease? What about coronary calcification? For example look at this: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16415377&ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=S... From the abstract: We did not observe a relationship between on-treatment LDL cholesterol levels and the progression of calcified coronary atherosclerosis. >Finally, it is natural for medical textbooks to change Of course I agree, with the proviso that the change is "as our knowledge changes". But what if the medical advice changes for political or commercial (drug company) reasons? So, if (let's assume) lipoproteins aren't the problem, what is? Here's an intriguing possiblity: http://www.ncbi.nlm.nih.gov/pubmed/17606264?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum http://www.ncbi.nlm.nih.gov/pubmed/17606264?ordinalpos=1&#38... [1] worsening = causing a lipoprotein profile that is positively correlated with cardiac death (correlation is not causation, there could be an underlying common factor etc. disclaimer goes here). [2] an attempt to answer your question about where it is that people think medicine treats only the symptoms
  - carbocation 16y ago
    Hmm, the point of torcetrapib was to increase HDL cholesterol, not reduce cholesterol. Most likely, it increased mortality via totally off target effects (see Rader's 2008 NEJM review on the topic). Looking at coronary calcification is no better than looking at lipoprotein fractions; both are intermediate endpoints. I see no reason to trust calcification if you don't trust LDL. Reduction in LDL correlates so well with reduction in mortality (statin trials) that fibrates got licensed on those grounds without showing reduced mortality. That is a problem, but not the fault of statins. It's an FDA-got-bought-out-by-pharma sort of problem. To reject the overwhelmingly data-backed LDL hypothesis, I'd need to see something much more compelling, I must say. Edit: your pubmed article addresses insulin resistance. Hypercholesterolemia is usually independent of that. In fact, high LDL is not even part of the metabolic syndrome... It seems as though you and I are not so much in disagreement as we are talking about different things entirely. I've been focusing on high cholesterol.

by nunb 16y ago

carbocation 16y ago

You will do well to note that I said statins, not CETP inhibitors (torcetrapib) nor fibrates. There is an ocean of difference between them, so you can't just go around making it look like I endorsed a drug that never got FDA approval (torcetrapib), for example. After antibiotics, statins have the clearest risk-benefit profile of just about any drugs ever invented, and their effectiveness and safety have been under continuous study for decades. You assert that the production of cholesterol is not the problem. Since you claim that I am starting from the wrong axiom, what do you believe is the root cause of hypercholesterolemia? Since hypercholesterolemia is the canonical asymptomatic disease, I suspect you are misusing the term symptom. Finally, it is natural for medical textbooks to change as our knowledge changes. I haven't read the book you are referring to but if he says that drug companies are having an evil influence, I wouldn't be surprised and I'd probably agree.

nunb 16y ago
>You will do well to note that I said statins I did note that, and in my reply said that they (statins) don't treat the root cause. However, I used the example of torcetrapib and clofibrate merely to point out that "reduction in cholesterol" is done most efficaciously by other compounds too. (I don't know if the overall mortality was because of alternate toxicities of the compounds in question, other fibrates are still under consideration). I did not mean to imply that you endorsed either T or C, and I hope I didn't sound like I did. I may as well have accused you of promoting thalidomide... The intent was to show that treating lipoprotein numbers was unproductive... ie that the lipoprotein numbers are merely a symptom [2]. More on this below in the coronary calcification note below.. > statins have the clearest risk-benefit profile of just about any drugs ever invented I do not believe this to be true. For example, statins have well known effects in "worsening"[1] the lipoprotein profile (especially VLDL or Lp(A) -- can't find the reference at this moment) If dyslipidemia is a symptom, what accounts for Coronary arterial disease? What about coronary calcification? For example look at this: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=16415377&ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=S... From the abstract: We did not observe a relationship between on-treatment LDL cholesterol levels and the progression of calcified coronary atherosclerosis. >Finally, it is natural for medical textbooks to change Of course I agree, with the proviso that the change is "as our knowledge changes". But what if the medical advice changes for political or commercial (drug company) reasons? So, if (let's assume) lipoproteins aren't the problem, what is? Here's an intriguing possiblity: http://www.ncbi.nlm.nih.gov/pubmed/17606264?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum http://www.ncbi.nlm.nih.gov/pubmed/17606264?ordinalpos=1&#38... [1] worsening = causing a lipoprotein profile that is positively correlated with cardiac death (correlation is not causation, there could be an underlying common factor etc. disclaimer goes here). [2] an attempt to answer your question about where it is that people think medicine treats only the symptoms
- carbocation 16y ago
  Hmm, the point of torcetrapib was to increase HDL cholesterol, not reduce cholesterol. Most likely, it increased mortality via totally off target effects (see Rader's 2008 NEJM review on the topic). Looking at coronary calcification is no better than looking at lipoprotein fractions; both are intermediate endpoints. I see no reason to trust calcification if you don't trust LDL. Reduction in LDL correlates so well with reduction in mortality (statin trials) that fibrates got licensed on those grounds without showing reduced mortality. That is a problem, but not the fault of statins. It's an FDA-got-bought-out-by-pharma sort of problem. To reject the overwhelmingly data-backed LDL hypothesis, I'd need to see something much more compelling, I must say. Edit: your pubmed article addresses insulin resistance. Hypercholesterolemia is usually independent of that. In fact, high LDL is not even part of the metabolic syndrome... It seems as though you and I are not so much in disagreement as we are talking about different things entirely. I've been focusing on high cholesterol.