Statin drugs (Lipitor, Crestor, Zocor etc) are the single most prescribed medication in the developed world. The profits associated with these drugs are truly eye-popping. Satins were first introduced to reduce cholesterol in individuals at high risk of heart disease and with high levels of total cholesterol as well as high levels of the bad variety (LDL) cholesterol. As our populations age, as obesity and diabetes become more and more prevalent, so too the concern about high cholesterol levels. Sales of statins have dominated the pharmaceutical market in recent years, consistently ranking as the number one class of drugs, peaking in 2006 with annual sales of $23 billion, primarily driven by the unprecedented success of Pfizer’s Lipitor. Eight statins have made it onto global pharmaceutical markets and until last year sales of these cholesterol-lowering drugs had accumulated a staggering $216.6 billion since they came on the scene. Let’s face it – the pharmaceutical industry knows a good thing when it sees it and pushes for ever lower levels of cholesterol as a desirable target – the number of people on these drugs is skyrocketing. I am willing to bet a good 50% of our patient group is on one or other of these brand name drugs.
Statins and Cancer
The point of this article is not to talk about statins and their role in controlling high cholesterol and thereby reducing heart disease. What I want to focus on is the role of statins in the cancer patient. Do statins help in preventing or slowing down cancer? Can statins reduce or prevent the incidence of cancer in high risk patients? If we are worried about the familial nature of CLL, should we be encouraging our children to consider daily regimen of stain drugs? What is the risk and how much of a reward is there? I think it is time to take a hard look at this controversial subject. As always, you have the right – and the duty – to mkae up your own mind.
Over the years, there have been reports that suggested using statin drugs may be beneficial in decreasing the incidence and/or decreasing the aggressiveness of colorectal cancer, melanoma, prostate cancer and breast cancer. The big four “C”s, they don’t get any bigger than that. Let us start off by looking at the latest information on these four cancers are influenced by statin use, then finish the story with the potential impact of statins on our very own favorite cancer, CLL.
Statins and Colorectal Cancer
Colorectal cancer was thought to be the most likely cancer to benefit from statin use. I know, I researched this possible chemoprevention benefit on account of my husband because his father died of colorectal cancer at an early age (55 years). There is a strong familial aspect to colorectal cancer, risk of getting this disease increases significantly in first degree blood relatives of patients with colorectal cancer. The potential benefit fo statin therapy to reduce risk of colorectal cancer seemed reasonable. It helped that my husband PC also had slightly elevated cholesterol and there was no problem getting him a prescription for Zocor. Where do we stand today in our understanding of the beneficial effects of statin use and colorectal cancer? After all, our guys are at increased risk of secondary cancers and colorectal cancer is among them. Should CLL patients go the extra distance to be on statin therapy? Here is the latest information on this subject.
Cancer Prev Res (Phila Pa). 2010May;3(5):588-96. Epub 2010 Apr 19.
Statin use and colorectal adenoma risk: results from the adenoma prevention with celecoxib trial.
Bertagnolli MM, Hsu M, Hawk ET, Eagle CJ, Zauber AG; Adenoma Prevention with Celecoxib (APC) Study Investigators.
Brigham and Women’s Hospital, Boston, MA 02115, USA.
Statins are widely prescribed for cardiovascular disease prevention and also commonly used in patients at high risk for colorectal cancer. We report the results of a planned secondary analysis of the relationship between statin use and colorectal adenoma risk in a large chemoprevention trial.The Adenoma Prevention with Celecoxib (APC) trial randomized 2,035 adenoma patients to receive placebo (679 patients), 200 mg celecoxib twice daily (bid; 685 patients), or 400 mg celecoxib bid (671 patients). The study collected complete medical history and medication use data and performed colonoscopic surveillance to 5 years after study enrollment. The effects of statin use on newly detected adenomas and cardiovascular adverse events were analyzed as time-dependent variables by multivariable Cox regression. Statins were used by 36% (n = 730) of APC trial participants. When adjusted for covariates including cardioprotective aspirin use, age, and sex, participants on the placebo arm who used statins at any time had no benefit over 5 years compared with never users (risk ratio, 1.24; 95% confidence interval, 0.99-1.56; P = 0.065). Statin use for >3 years increased adenoma risk over 5 years(risk ratio, 1.39; 95% confidence interval, 1.04-1.86; P = 0.024). For all comparisons of patients treated with celecoxib, adenoma detection rates for statin users and nonusers were equivalent. Consistent with their use in patients at high risk, cardiovascular serious adverse events were more common among statin users. For patients at high risk of colorectal cancer, statins do not protect against colorectal neoplasms and may even increase the risk of developing colorectal adenomas.
How do you like that for a punch line, that last sentence in the abstract!? You can read the whole article for free, just click on this link. Or, you can read an easier to read review of it published on Medlineplus. This is a very credible report of research findings in a large group of people and conducted by a highly regarded institution. And it blew a huge hole in theory of statins as chemoprevention agents to reduce risk of colorectal cancer. This is a stunning development to say the least. “For those who took statins for three years or longer, the chances of developing the adenomas were nearly 40 percent higher than those not on statins”. Not only does statin use not protect against colorectal cancer, it may even increase the risk of developing colorectal adenomas! Who knew.
OK, we struck out on colorectal cancer, big time. How about melanoma? After all, CLL patients are at much higher risk of all kinds of skin cancer. Does statin therapy give us an extra dose of protection? Here is another hot off the presses article that dashes our hopes on this front as well. Better living through chemicals does not seem to be working all that well in this instance either. You guys still need to stay out of the sun, avoid excessive UV exposure and if your self image makes it mandatory, use on of those tan-in-a-bottle thingies. And don’t forget to schedule regular full body dermatological exams.
Eur J Epidemiol. 2010;25(1):29-35. Epub 2009 Oct 21.
Can statin therapy reduce the risk of melanoma? A meta-analysis of randomized controlled trials.
Bonovas S, Nikolopoulos G, Filioussi K, Peponi E, Bagos P, Sitaras NM.
Department of Pharmacology, School of Medicine, University of Athens, 75 Mikras Asias Str., 11527 Athens, Greece. firstname.lastname@example.org
A growing body of literature suggests that statins may have a chemopreventive potential against melanoma through pleiotropic anti-inflammatory, immunomodulatory, and antiangiogenesis mechanisms. Our aim was to examine this association through a detailed meta-analysis of randomized controlled trials (RCTs). A comprehensive search for trials published up to June 2009 was performed, reviews of each study were conducted and data were abstracted. Prior to meta-analysis, the studies were evaluated for publication bias and heterogeneity. Pooled relative risk estimates (RR) and 95% confidence intervals (CIs) were calculated using the fixed- and the random-effects models. Subgroup and sensitivity analyses were also conducted. Sixteen RCTs of statins for cardiovascular outcomes, involving 62,568 individuals with a mean age of 60 years and an average follow-up of nearly 4.7 years, contributed to the analysis. We found no evidence of publication bias (P = 0.47) or heterogeneity among the studies (P = 0.25). Statin use did not significantly affect the risk of developing melanoma assuming either a fixed- (RR = 0.92, 95% CI: 0.67-1.26), or a random-effects model (RR = 0.92, 95% CI: 0.62-1.36). This neutral effect was further supported by the results of subgroup and sensitivity analyses.Our findings do not support a protective effect of statins against melanoma.
Another biggie cancer that gets a lot of press and attention. I hope you guys out there in the right age bracket are getting regularly scheduled prostate check-ups. What do we know about the use of statins and the risk of prostate cancer, either its incidence or its aggressiveness? Here is a very recent article on the subject from Johns Hopkins.
BJU Int. 2010 May;105(9):1222-5. Epub 2009 Nov 3.
Is statin use associated with prostate cancer aggressiveness?
Loeb S, Kan D, Helfand BT, Nadler RB, Catalona WJ.
Department of Urology, Johns Hopkins School of Medicine, Baltimore, MD, USA.
OBJECTIVE: To further examine the association between statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) and pathological features in a large group of patients undergoing radical prostatectomy (RP), as epidemiological studies have suggested that statins, in addition to their beneficial cardiovascular effects, might reduce the risk of aggressive prostate cancer. PATIENTS AND METHODS: From 2003 to 2009, 1351 men with data on preoperative statin use had RP by one surgeon. The clinical and pathological tumour features were compared between 504 users of statins and 847 who were not users. RESULTS: Statin users were significantly older and had a higher mean body mass index than non-users. The preoperative serum prostate-specific antigen levels, tumour volume and percentage of cancer in the RP specimen were significantly lower in patients taking statins. Overall, statin users had a proportionately lower rate of adverse tumour pathology features, including a significantly lower risk of positive (cancerous) surgical margins. CONCLUSION: Our results suggest that the use of statins might be associated with more favourable pathological features at RP. The long-term disease-specific outcomes and the underlying link between statins and prostate cancer require further investigation.
Statin use may change pathological features of prostate cancer, but we don’t really know how it pans out in the long run. Hmmm. That did not sound like a really strong endorsement to me, so I looked further. Lucky I did, because I found the single most definitive review article yet! Abstract is below for your reading pleasure. Talk about large scale studies, this one looked at over 2 million people aged 30-84 years. There were about a quarter of a million new statin users in the lot. This very detailed study looked at a laundry list of things, not just cancer. The researchers did find decreased risk of oesophageal (throat) cancer in statin users. That is good news.
Most of us know that statin use increases risk of liver toxicity and muscle damage; sure enough the researchers found increased risk of moderate to severe liver problems as well as moderate or serious myopathy (muscle damage). I was not aware that statin use also increased risk of cataracts, that was a new one. All of these adverse effects were real, well documented and statistically valid. All of these adverse effects were more or less reversible and faded away in a few years after stopping use of statins.
But here is the punch-line: With the exception of throat cancer, none of the other potential benefits of statins that we hoped to see were noted. No benefit for gastric cancer, colon cancer, lung cancer, melanoma, renal cancer, breast cancer, or even prostate cancer. Bummer!!
BMJ. 2010 May 20;340:c2197. doi: 10.1136/bmj.c2197.
Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database.
Hippisley-Cox J, Coupland C.
Division of Primary Care, University Park, Nottingham NG2 7RD. email@example.com
OBJECTIVE: To quantify the unintended effects of statins according to type, dose, and duration of use. DESIGN: Prospective open cohort study using routinely collected data. SETTING: 368 general practices in England and Wales supplying data to the QResearch database. PARTICIPANTS: 2 004 692 patients aged 30-84 years of whom 225 922 (10.7%) were new users of statins: 159 790 (70.7%) were prescribed simvastatin, 50 328 (22.3%) atorvastatin, 8103 (3.6%) pravastatin, 4497 (1.9%) rosuvastatin, and 3204 (1.4%) fluvastatin. METHODS: Cox proportional hazards models were used to estimate effects of statin type, dose, and duration of use. The number needed to treat (NNT) or number needed to harm (NNH) was calculated and numbers of additional or fewer cases estimated for 10 000 treated patients. MAIN OUTCOME MEASURE: First recorded occurrence of cardiovascular disease, moderate or serious myopathic events, moderate or serious liver dysfunction, acute renal failure, venous thromboembolism, Parkinson’s disease, dementia, rheumatoid arthritis, cataract, osteoporotic fracture, gastric cancer, oesophageal cancer, colon cancer, lung cancer, melanoma, renal cancer, breast cancer, or prostate cancer.RESULTS: Individual statins were not significantly associated with risk of Parkinson’s disease, rheumatoid arthritis, venous thromboembolism, dementia, osteoporotic fracture, gastric cancer, colon cancer, lung cancer, melanoma, renal cancer, breast cancer, or prostate cancer. Statin use was associated withdecreased risks of oesophageal cancer butincreased risks of moderate or serious liver dysfunction, acute renal failure, moderate or serious myopathy, and cataract.Adverse effects were similar across statin types for each outcome except liver dysfunction where risks were highest for fluvastatin. A dose-response effect was apparent for acute renal failure and liver dysfunction. All increased risks persisted during treatment and were highest in the first year. After stopping treatment the risk of cataract returned to normal within a year in men and women. Risk of oesophageal cancer returned to normal within a year in women and within 1-3 years in men. Risk of acute renal failure returned to normal within 1-3 years in men and women, and liver dysfunction within 1-3 years in women and from three years in men. Based on the 20% threshold for cardiovascular risk, for women the NNT with any statin to prevent one case of cardiovascular disease over five years was 37 (95% confidence interval 27 to 64) and for oesophageal cancer was 1266 (850 to 3460) and for men the respective values were 33 (24 to 57) and 1082 (711 to 2807). In women the NNH for an additional case of acute renal failure over five years was 434 (284 to 783), of moderate or severe myopathy was 259 (186 to 375), of moderate or severe liver dysfunction was 136 (109 to 175), and of cataract was 33 (28 to 38). Overall, the NNHs and NNTs for men were similar to those for women, except for myopathy where the NNH was 91 (74 to 112). CONCLUSIONS:Claims of unintended benefits of statins, except for oesophageal cancer, remain unsubstantiated, although potential adverse effects at population level were confirmed and quantified. Further studies are needed to develop utilities to individualise the risks so that patients at highest risk of adverse events can be monitored closely.
This whole “Statin therapy is good for cancer” is not looking very good to me at this point. Latest reports have shot down chemoprevention when it comes to colorectal cancer and melanoma. Prostate cancer protection sounds a bit iffy, with conflicting results. All in all, when it comes to delaying onset of cancer or decreased aggressiveness of cancer by means of using statins, we are looking at at marginal or even negative results on the reward side of the equation; unfortunately, on the cost side of the equation well documented adverse risk profiles (liver toxicity, muscle damage and cataracts) continue to be confirmed. I was particularly shaken by the report that statin use may actually increase the risk of colorectal cancer!! Not what I thought, not what I believed to be the case, not what I wanted to hear. Live and learn. If PC was alive today I would get him off of statin use quicker than you can say “billion dollars”.
Does Statin Therapy Help CLL Prognosis?
Now we come to the main course. All the previous reports were mere appetizers as it were, leading up to this most important item. Below is an abstract published in the ASH2009 (American Society of Hematology) conference. Reading this abstract got me started thinking about statins and trying to get my arms around this bewildering mix of claims and counter claims.
2344Influence of Statin Therapy On the Clinical Course of Chronic Lymphocytic Leukemia
Daphne R Friedman, MD1, Jeremy D Harrison, MD1*, Lindsay A Magura, MD1*, Holly A Warren, MD1*, Louis F Diehl, MD1* and J. Brice Weinberg, MD2
Medicine, Duke University Medical Center, Durham, NC
Background: Chronic lymphocytic leukemia (CLL) is a common leukemia with variability in clinical outcomes. Treatment is required for symptomatic and/or progressive disease, but many patients are followed expectantly without therapy. Various prognostic markers, including elevated levels of lipoprotein lipase (LPL) mRNA or protein, can identify patients with high risk to require therapy or with reduced survival. We recently reported that within our cohort of CLL patients at Duke University and the Durham V.A. Medical Centers, women with an apolipoprotein E4 (APOE4) genotype have longer overall survival than do those with a non-APOE4 genotype. Given these findings, we hypothesized that statin treatment would alter the course of CLL. Here we report on the clinical outcome of CLL patients treated with statins at the time of diagnosis.
Methods: 335 patients with CLL were prospectively enrolledin an IRB-approved study at the Duke University and Durham V.A. Medical Centers from 1999 to the present. CLL diagnosis was confirmed by immunophenotyping for CD19+CD5+ clonal B-cells. Prognostic markers such as lymphocyte doubling time, IgVH mutation status, CD38 and ZAP70 expression, CLL cell LPL mRNA, and interphase cytogenetics were determined as previously described. We abstracted clinical data including treatment need, time to treatment, overall survival, anduse of statins and serum lipid levels within a six-month interval of diagnosis and of first treatment.
Results: At diagnosis, 189 patients were not taking a statin, 65 were, and 81 did not have these data available. Of the 254 patients in whom statin use at diagnosis was known, 181 (71%) were male and 73 (29%) were female. Therapy for CLL was not required in 132 (52%) patients , while 122 (48%) patients received at least one treatment. Initial treatments included single agent chlorambucil with or without prednisone (n = 59, 49%), purine analogue-based regimens (n = 45, 37%), and rituximab-containing regimens (n=47, 39%). Indications for therapy were recorded in 117 of the 122 patients (96%), and included increasing lymphocyte count (n = 49, 42%), anemia (n = 14, 12%), thrombocytopenia (n = 8, 7%), splenomegaly (n = 8, 7%), and lymphadenopathy (n = 49, 42%). The entire cohort has been followed for 0.05 to 25 years from diagnosis (median, 4.5 years), with a shorter follow up time in the patients who were on a statin at the time of diagnosis (2.4 vs. 5.6 years, p < 0.001). There was no statistically significant difference between patients taking statins or not taking statins at diagnosis in terms of sex, lymphocyte doubling time, IgVH mutation, CD38 or ZAP70 expression, or cytogenetic aberrations. However,patients receiving a statin at the time of diagnosis were less likely to require therapy (p = 0.044). This effect was seen primarily in women (p = 0.009) and in patients with CD38 negative CLL (p = 0.002). Notably, even though patients taking a statin at the time of diagnosis were less likely to ever require therapy, statin use was not associated with a significant improvement in overall or treatment-free survival. While elevated lipoprotein lipase (LPL) expression correlated with worse clinical outcomes, there was no significant correlation between statin use and CLL cell LPL mRNA levels. Likewise, there was no significant correlation between statin use and apolipoprotein E genotype. In addition, statin use at time of first treatment was not significantly associated with progression or time to progression. We did not find any significant correlation between total cholesterol, LDL, HDL, or triglyceride levels at diagnosis and treatment need. However this analysis was compromised by low numbers of patients with relevant clinical data (n = 26).
Conclusions: Statin use at the time of diagnosis of CLL is associated with an improved clinical course, specifically a reduced likelihood of progressing to require therapy. This benefit is seen particularly in women and in those with low risk (CD38 negative) CLL. The mechanism of action of statins in altering the clinical course of CLL is unknown. Statinscould be directly cytotoxic for CLL cells, could influence lipid-LPL-CLL biology, alter B-cell receptor signaling, or modify autocrine/paracrine survival signals. The benefit of statin use in women with CLL might reflect an interplay between estrogen, lipids, and CLL cells. Our findings have the potential to improve our understanding of CLL biology and possibly lead to novel CLL treatments.
This study conducted at Duke University Hospital looked at a cohort of CLL patients, of which 189 were not taking statins and 65 were taking them. More men were taking statins than women (71% versus 29%). There were no big differences between the group taking statins compared to the group not taking statins, in terms of the usual patient profiles and prognostic indicators.
Here is what the researchers noted. Patients taking statins were less likely to need therapy right away, compared to those that were not taking statins. Sounds good! It is encouraging if taking statins delays the dark day when the CLL has progressed to the point that therapy is needed, right?
Not quite. Use of statins did not cause any significant improvement in how patients responded to treatment, or even how long they lived. Say what?! Statin use had no effect on response to therapy or overall survival. I chalk that up as a real disappointment. As for why patients taking statins took longer before they needed therapy for their CLL, I have a theory to explain that. It is just my take on this point, you have to decide whether it makes sense to you or not. Since it is my two cents and not expert opinion, it goes under the heading of “Editorial”.
Many CLL patients are diagnosed with CLL as a result of a routine blood test that shows the white count is unexpectedly high. Very often, the patient is stunned with the diagnosis, he / she had no clue there was anything wrong. There you are, going about your business in a nice peaceful fashion, you go for the usual annual check up, your GP does the usual blood test, and the next thing you know he is sending you to his friend the oncologist down the road.
Diagnosis of CLL has gone up dramatically since the advent of cheap and automated CBC tests and as more of us become conscientious about getting annual medical checkups. If you are like most people, the temptation is to skip this annual hassle, go for a couple of years between getting a CBC blood test. Many CLL patients probably had CLL for a couple of years or more, they had no symptoms and never knew they had the disease until the WBC got high enough or they noticed a couple of swollen lymph nodes. PC was formally diagnosed with CLL in the summer of 2001. But with 20/20 hindsight and going back to look at prior year blood tests, it was easy to see he had the tell tale signs as far back as the fall of 1999, it was just that no one commented about it and we knew no better.
But what about people who get put on statin therapy for cholesterol control? Because of the well documented risk of liver toxicity and muscle damage in a small percentage of patients prescribed statin therapy, the standard guidance is to make sure patients on statins must get regular blood checks. My doctor will not renew my statin prescription unless I have blood tests at least once every quarter. Good safety procedure and I heartily approve. But what is the effect of this frequent blood testing? I think it dramatically increases the chances that patients with CLL lurking undetected in the background are likely to be diagnosed as a result of blood tests done to monitor for statin safety. This is a huge difference in the two groups of patients studied in the Duke University Hospital study. Earlier diagnosis means it takes longer before the CLL percolates sufficiently to need therapy. Patients who are diagnosed with CLL at a later point have already had a couple of years on the clock, it makes sense that they would need therapy sooner. So, if my theory is right, the fact that statin using CLL patients did not need therapy quite as soon as their counterparts who were not using statins – the difference could be entirely due to the statin users being diagnosed with CLL as soon as it showed its ugly hear, while CLL stayed hidden and under the radar in the case of the non-statin users. All a question of how frequently the patients had blood tests.
By the way, a similar study looking at the effect of statin use in early stage CLL patients conducted at the Mayo Clinic (Rochester, MN) shows no beneficial effect. Not even on time to first treatment, thereby contradicting even the small benefit that the Duke researchers saw.
Leuk Lymphoma. 2010 Jul;51(7):1233-40.
Statin and non-steroidal anti-inflammatory drug use in relation to clinical outcome among patients with Rai stage 0 chronic lymphocytic leukemia.
Shanafelt TD, Rabe KG, Kay NE, Zent CS, Call TG, Slager SL, Bowen DA, Schwager SM, Nowakowski GS. Division of Hematology, Mayo Clinic, Rochester, MN, USA. firstname.lastname@example.org
Statins and non-steroidal anti-inflammatory drugs (NSAIDs) are among the most commonly prescribed medications. In vitro studies suggest that statins and NSAIDs may have potential as anticancer therapies in low-grade non-Hodgkin lymphomas including chronic lymphocytic leukemia (CLL), and a recent observational study found statin use was associated with improved event free survival in patients with follicular lymphoma. Other studies have suggested that statins reduce the efficacy of rituximab by inhibiting binding to CD20. We therefore conducted an observational cohort study of 686 patients with newly diagnosed Rai stage 0 CLL to evaluate whether statin or NSAID use was related to their clinical outcome or influenced the efficacy of rituximab therapy. At diagnosis, 136 (20%) patients took statins and 230 (34%) scheduled daily aspirin, ibuprofen, or naproxen. No difference in time to treatment was observed based on statin or NSAID use. Among patients receiving a rituximab-containing first-line therapy, no difference in time to salvage treatment was observed based on statin use. Although previous studies suggested statins may improve event free survival among patients with follicular lymphoma, we find no impact of statins on time to initial therapy in this large study of patients with Rai stage 0 CLL. The in vitro observation that statins reduce rituximab efficacy does not appear to have clinical significance in CLL care.
What does all this mean?
- “Better living through chemicals” has been de-bunked so many times it is not even funny anymore. A healthy and varied diet rich in fresh fruit, vegetables, whole grains and easy on the fats and junk food; plenty of exercise to keep your muscles well toned and your body in the healthy weight range; fresh air, plenty of rest, an optimistic attitude to life and commonsense things like not smoking or indulging in too much alcohol or UV radiation – these are the things to do to stay as healthy as possible. Good health does not come in a pill bottle or as a result of fad diets. I wish I had a dollar for every patient who wrote to me about “juicing”. Eat the darned vegetables the way your mom told you to eat them!
- It means you continue to take statins if you are at high risk of heart disease and your cardiologist wants you to take statins. I have significant history of cardiac disease in my family (both my parents have heart issues, my only brother died at the tender age of 32 due to heart disease). I have high cholesterol as well. For these reasons I have been on statin therapy for several years now.
- If you do not need to be on statin therapy for cholesterol or cardiac issues, think twice (or even a couple more times) before you push your doctor to put you on statin therapy in the fond hope it will help prevent or decrease the aggressiveness of your CLL – or any cancer for that matter. It is not looking very good, this whole theory of cancer prevention by taking statins.
- Say it aint so Joe, have we been had yet again, has the industry hype about statins sold us a bill of expensive goods? There were folks talking about putting statins in the drinking water – only half jokingly – because these drugs were thought to be good for so many things. Once again, we see the emperor is not wearing too many clothes – heck he may be stark nekked!!
- Be a smart consumer. Stay smart, stay informed, hang on to your wallet. Way too many smart folks out there who would like to take some of the hard earned cash from your pocket and straight into their bottom-line profits.
I love a good conspiracy yarn as well as the next guy, a good way to spend a lazy afternoon. But I request that you folks stay on topic, and stay well grounded in reality in your comments. Careful weighing of risks and rewards is very important, but I really do not want to see people scared off of taking necessary therapy when they clearly need it and may benefit from it. That goes for chemotherapy and statins too. Staying away from drugs that we do not need does not mean we do the “back to nature” stuff with a vengeance, revert to juicing and cottage cheese as the sole means of nutrition or cancer control.