Monthly Archives: September 2014

CONVENTIONAL SURGICAL HYSTERECTOMY OR MORCELLATION FOR FIBROIDS. DONT MINCE MATTERS?

The Wall St Journal this  week puts in perspective the dilemma the past decade of whether or not to have vaginal  powertool uterine morcellation – mincing- as the less risky procedure for vaginal hysterectomy, as opposed to the oldfashioned open surgery. “Gynecologists Resist FDA Over Popular Surgical Tool  Doctors Continue to Use Morcellators Months After Regulator Warned They Can Spread Undetected Cancer. These doctors say they believe the risks of unknown cancer have been overblown and the government shouldn’t interfere with patient treatment.  ”  Shades of overdiagnosis of breast and prostate cancer by mass screening of the well.

This lack of good evidence as to what is good best practice  hasnt stopped lawyers like Weitz and Luxenberg from chasing lucrative compensation claims. Their mission statement says it all: “Weitz & Luxenberg is New York City’s largest personal injury and mass-tort plaintiffs’ law firm. Built on the philosophy that every client’s case is our most important, we have won more verdicts than most other U.S. law firms.   Our goal is to set an unmatched standard of excellence for mass tort litigation — which is why, since our founding in 1986, our attorneys have relentlessly sought to deliver justice in cases involving asbestos and mesothelioma, defective drugs and medical devices, medical malpractice, general negligence, and environmental pollution, among others. We are unflinching in our belief that our clients deserve our absolute best work. ”

The  recent June analysis from Harvard – George, Muto ea- sums it up:    highly malignant LMS leiomyosarcomas in fibroids  are rare; many such sarcomas are difficult to be sure histologically;    with no reliable preoperative techniques to distinguish LMS from benign leiomyoma.

Vag hyst Morcellation studies show that it has  ~40%  shorter hospitalization time than  total hysterectomy  without morcellation  because of almost 2/3  lower surgical risks. as Wiki says,  hysterectomy Short term mortality (within 40 days of surgery) has been reported in the range of 1–6 cases per 1000 when performed for benign causes. Risks for surgical complications are presence of fibroids, younger age (vascular pelvis with higher bleeding risk and larger uterus), dysfunctional uterine bleeding and parity.[45]   The mortality rate is several times higher when performed in patients that are pregnant, have cancer or other complications.[46]

But considering perhaps more than a million hysterectomies a year worldwide,  the ?>300 000 uterine morcellations done the past almost 20 years (the procedure  has been around since at least 1949- Allen ), the incidence of missed LMS is rare, below 1:300- in fact very few cases of clinical LMS spread have been reported in morcellation reviews, perhaps ~ 1:1000.

so where hysterectomy is essential (it seldom is- but is  fashionable for sporty women, lucrative for  hospital staff),

its up to the woman to decide for herself with informed consent whether to risk the numerous complications of conventional hysterectomy/myomectomy- which with a big fibroid is high-

versus having morcellation, then awaiting the <1:300 likelihood of a positive pathology report that her fibroid contained  LMS, and facing recall for chemo.

some studies show that LMS can be suspected based on preop ultrasound.
Since LMS are highly vascular and big, thermography may also be helpful in selecting those rare  fibroids that show bright due to high vascularity,  that should not risk morcellation..
     so its like screening the well for breast, prostate or colon cancer-  are the mass programs screening everyone regularly worth while, or a huge unnecessary racket with risk of overdiagnosis and overtreatment?
    or like the hard choice we all- women and our  partners- face– with early breast cancer:    mastectomy only? or local excision plus radiotherapy? or bilateral mastectomy? when latest studies show that there is little to choose in longterm survival between the three, but if anything women having local excision and DXRT survive the longest; or with silent early prostate cancer- watchful waiting? or local excision , hormone therapy?
    It seems clear that vag. morcellation does better for most  (299/300) women, but those with big fibroids (the Rome 2007, and Japanese 1990  papers) need more careful screening for suspicion of LMS, and thus may be wiser to choose clean surgical hysterectomy/myomectomy.  If the mean LMS  recurrence-free survival is still only 40months vs 10 months after morcellation, these rare cases have grim prognosis irrespective.
Fibroids and LMS, like breast  and uterine cancer, are driven by estrogens- an increasing problem in our fattening age and the pernicious manmade Feminization of Nature that is destroying reproduction.
. So the first thing for those with growing breasts/lumps  or fibroids are to eliminate, balance  the excess estrogens. Dr Dee analyses this thoroughly at http://www.leiomyosarcoma.info/hormones.htm;
and  Dr Mostovoy at   http://www.thermographyclinic.com/hysterectomy.  We do see breast and uterine fibroids  turn around with such approach- but of course likely malignancies need to be typed by biopsy. .
 .Then consider carefully whether and what tests and surgery to have, and by whom.
Cancer. 2014 Jun 12. doi: 10.1002/cncr.28844. Retrospective cohort study evaluating the impact of intraperitoneal morcellation on outcomes of localized uterine leiomyosarcoma.

Uterine leiomyosarcoma (ULMS) is identified in 0.1% to 0.2% of hysterectomy specimens of presumed leiomyoma. To date, there is no preoperative technique that reliably differentiates ULMS from uterine leiomyoma. Increasing use of minimally invasive approaches for the management of leiomyomas may result in inadvertently morcellated ULMS with resultant intraperitoneal dissemination of tumor. The objective of this study was to assess the impact of intraperitoneal morcellation on the outcomes of patients with ULMS.    METHODS: In this retrospective cohort study, all patients with ULMS who attended the authors’ institutions from 2007 to 2012 were reviewed. Demographics and outcomes were compared between those who underwent morcellation or total abdominal hysterectomy (TAH) as their first surgery for uterus-limited ULMS.  RESULTS:In total, 58 patients were identified, including 39 who underwent TAH and 19 who underwent intraperitoneal morcellation. Intraperitoneal morcellation was associated with a significantly increased risk of abdominal/pelvic recurrences (P = .001) and with significantly shorter median recurrence-free survival (10.8 months vs 39.6 months; P = .002). A multivariate adjusted model demonstrated a >3 times increased risk of recurrence associated with morcellation (hazard ratio, 3.18; 95% confidence interval, 1.5-6.8; P = .003).   CONCLUSIONS:   Intraperitoneal morcellation of presumed leiomyoma worsens the outcomes of women with ULMS. Because there are no reliable preoperative techniques to distinguish ULMS from benign leiomyoma, all efforts to minimize intraperitoneal uterine morcellation should be considered.

Exacoustos C1, Arduini D. ea   Univ Rome   analyzed the preoperative gray-scale and color Doppler sonographic findings of 8 patients with LMS, 21 patients with cellular leiomyomas, and 3 patients with smooth muscle tumors of uncertain malignant potential and compared these findings to 225 patients with benign LM. All patients underwent myomectomy or hysterectomy. Number, size, echotexture, degenerative changes, and vascularity (central or peripheral; absent, mild, moderate, or marked) were recorded and correlated to the histologic findings   RESULTS:   LMSs were significantly larger than other uterine smooth muscle tumors. They were all solitary, and 7/8 lesions had a diameter >or=8 cm. Degenerative cystic changes were observed in 4 lesions, and increased peripheral and central vascularity was demonstrated in 7 lesions. Sensitivity, specificity, and positive predictive value of increased central and peripheral vascularity in the diagnosis of LMS were 100%, 86%, and 19%, respectively. Combining other sonographic findings with marked central vascularity, positive predictive value increased to 60%, but sensitivity decreased to 75%.  
Gynecol Obstet Invest. 1990;30(4):242-5.   Sonographic findings of uterine leiomyosarcoma  Hata K1, Nagaoka S ea Univ Japan    describe various sonographic features of uterine leiomyosarcoma. Transabdominal scanning (TAS) revealed an image indistinguishable from benign leiomyoma, with evidence of degeneration. Transvaginal scanning (TVS) clearly showed the thinness of the myometrium, and the possibility of deep myometrial invasion was suspected at intraoperative open direct ultrasonography (ODU). A very high peak systolic velocity and a slightly increased diastolic component at the periphery of the tumor were evident with pulsed Doppler ultrasound. Thus, TAS, TVS, ODU and Doppler ultrasound will yield useful information for the physician attempting to evaluate the extent and vascularity of uterine leiomyosarcoma.

METFORMIN REDUCES ALL CHRONIC DISEASES, INCLUDING IMPROVING THYROID FUNCTION.

this new report Metformin and low levels of thyroid-stimulating hormone in patients with type 2 diabetes mellitus from  McGill University; Montréal, Quebec. says nothing that is seriously clinically significant, it is merely common sense.

It does not show that metformin causes any heart or thyroid dysfunction ie change in thyroid hormone levels,  merely that it reduces TSH  in those on thyroid replacement.- indicating that  thyroid dose may be able to be tapered.    

A parallel new study from Italy  Metformin-induced thyrotropin suppression is not associated with cardiac effects  confirms there is no heart risk- quite the contrary.

People tend to fatten and slow down as they age, and these people tend to  metabolic syndrome ie obesity, cholesterolemia, hypertension, vascular disease and thus diabetes- same as patients with hypothyroidism. So type 2 diabetes, hypothyroidism (sometimes preceded by hyperthyroidism) and aging go together- usually without demonstrable direct cause and effect.

This new McGill University metformin study does not claim any cause and effect.  The link may be simply  that metformin (which is simply a carbon-hydrogen -nitrogen molecule)  improves all metabolic functions- antioxidant, nitric oxidant- including iodine/TRH/ TSH / thyroid/insulin   hormone responses. .

So as with all nutritional supplements and exercise  that improve metabolism, metformin may improve treated hypothyroidism by improving peripheral thyrooxine receptors , and thus lower need for thyroid replacement.
Metformin or the parent galega a medicinal plant extract used for many centuries reduces new diabetes and all diseases and deaths by 1/3 to 2/3.

it is among other things a prohormone regulator, improving common insulin resistance.

the definition of low TSH is arbitrary. If much below 1, it is suspicious of thyroid overactivity, excess thyroid hormones-
but rarely may reflect central ie pituitary failure to produce enough TRH/TSH and thus cause central hypothyroidism.

so TSH unless way outside the ‘normal’ range of 1 to 2 is a poor guide to health and disease, which is based on clinical  state and the thyroid hormone and antibody levels.

Most aging people develop some degrees of thyroid underactivity, which generally responds to replacement of deficient selenium, iodine and sex hormones without addition of risky thyroid hormones- for which conventional blood levels are a poor guide.

so as in all patients whatever their state and treatment, thyroid function should like all other functions be considered periodically.

ndb.


  Metformin and low levels of thyroid-stimulating hormone in patients with type 2 diabetes mellitus  McGill University; Montréal, Quebec.

Background: Small cross-sectional studies have suggested that metformin, a first-line oral hypoglycemic agent, may lower thyroid-stimulating hormone (TSH) levels. Our objective was to determine whether the use of metformin monotherapy, when compared with sulfonylurea monotherapy, is associated with an increased risk of low TSH levels (< 0.4 mIU/L) in patients with type 2 diabetes mellitus.

Methods: Using the Clinical Practice Research Datalink, we identified patients who began receiving metformin or sulfonylurea monotherapy between Jan. 1, 1988, and Dec. 31, 2012. We assembled 2 subcohorts of patients with treated hypothyroidism or euthyroidism, and followed them until Mar. 31, 2013. We used Cox proportional hazards models to evaluate the association of low TSH levels with metformin monotherapy, compared with sulfonylurea monotherapy, in each subcohort.

Results: A total of 5689 patients with treated hypothyroidism and 59 937 euthyroid patients were included in the subcohorts. Among patients with treated hypothyroidism, 495 events of low TSH levels were observed during follow-up (incidence rate 119.7/1000 person-years). In the euthyroid group, 322 events of low TSH levels were observed (incidence rate 4.5/1000 person-years). Compared with sulfonylurea monotherapy, metformin monotherapy was associated with a 55% increased risk of low TSH levels in patients with treated hypothyroidism (incidence rate 79.5/1000 person-years v.125.2/1000 person-years, adjusted hazard ratio [HR] 1.55, 95% confidence interval [CI] 1.09–2.20), with the highest risk in the 90–180 days after initiation (adjusted HR 2.30, 95% CI 1.00–5.29). No association was observed in euthyroid patients (adjusted HR 0.97, 95% CI 0.69–1.36).

Interpretation: In this longitudinal population-based study, metformin use was associated with an increased incidence of low TSH levels in patients with treated hypothyroidism, but not in euthyroid patients. The clinical consequences of this need further investigation.

HORMONES 2014, 13(2):252-258
Carlo Cappelli,1 Mario Rotondi,2 Ilenia Pirola,1 Barbara Agosti,3 Ana Maria Formenti,1 Pasquale De Cata,2 Massimo Salvetti,1 Luca Chiovato,2 Maurizio Castellano1

1Department of Medical and Surgical Sciences, Endocrine and Metabolic Unit, University of Brescia; 2Unit of Internal Medicine and Endocrinology, Fondazione Salvatore Maugeri Istituto di Ricovero e Cura a Carattere Scientifico, Istituto Superiore Prevenzione e Sicurezza Lavoro Laboratory for Endocrine Disruptors, University of Pavia; 3Diabetic Unit, Spedali Civili di Brescia; Italy  http://www.ncbi.nlm.nih.gov/pubmed/24776625

Abstract

OBJECTIVE: Metformin treatment may induce a decrease/suppression in serum TSH levels, mimicking sub-clinical hyperthyroidism (SHT). The aim of the present study was to retrospectively evaluate changes in several electrocardiographic indices in euthyroid subjects with diabetes who, after starting metformin treatment, developed a low serum TSH as compared to patients with SHT resulting from an underlying thyroid disease or TSH suppressive treatment with L-thyroxine.
DESIGN: Heart rate, P wave duration, P wave dispersion, QTmax, QTmin and QT-dispersion were assessed in 23 patients with diabetes treated with metformin before and after 6 months of TSH-suppression and in 31 control patients with SHT.
RESULTS: No significant changes in electrocardiographic parameters were observed from baseline to the TSH-suppression measurement. A significant difference in P wave duration (102.9±7.4 vs. 92.1±5.8 ms, p<0.001), P wave dispersion (13.1±3.4 vs. 7.1±3.5 ms, p<0.001), QTmax (399±18 vs. 388±16 ms, p=0.024), QTmin (341±14 vs. 350±17 ms, p=0.038) and QT dispersion (49.9±9.6 vs. 30.9±9.2 ms, p<0.001) were observed between the control group with SHT and the group of diabetic patients with low serum levels of TSH.
CONCLUSIONS: Our results show that the TSH-suppressive effect observed in patients taking metformin is not associated with peripheral markers of thyroid hormone excess, at least at the cardiac level.

THE STATIN- FOR- ALL -SENIORS HOAX: FOR WHOM TOLLS THE BELL? FOR WHOM ARE STATINS EXCEPT RARE HIGH-RISK PATIENTS’ SEVERE HYPERCHOLESTEROLEMIA, AND PROFITEERING? FURTHER DISCREDITED FOR PRIMARY PREVENTION:

neil.burman@gmail.com

19 Sept 2014 update:     ABSTRACT:  readers  of this column recently commend its statin commentary, last updated in June, about the controversy of statins  in primary prevention of cardiovascular disease CVD. This update now  reviews crucial major recent evidence that the marketing hype  of “statin deficiency” in the average aging population is a  dangerous fabrication (eg Vytorin) of the $billion Disease and Drug corporate industry  – especially when statins inhibit omega3  and CoQ10 which like other human micronutrient protectors- magnesium, iodine, arginine, carnitine, ribose, vitamins , B, D3, C & K2,   and human  sex hormones – are increasingly deficient  or imbalanced in an aging western population and urban convenience food  diet.

     The prizewinning immunologist   Dr Duncan Adams from Univ Otago   in the elite QJM 2011 pithily demolishes The Great Cholesterol ie Statin Myth, commends the statin trials metanalysis of  Ray ea from Cambridge 2010 that showed no benefits of statins in mild to moderate cholesterolemia. .     More evidence says  dont use  natural supplements along  with statins to reduce statin risks and enhance statin benefits, but better to avoid the risks  from statins, smoking and excessive alcohol eg ROS reactive oxygen species , in an aging slothful  fattening population:  with improved exercise, more water, a Banting-type low-carbs high-fat and -greens – fermented (ie high in vit K2)  diet, a multivite-multimineral plus vigorous well-tolerated supplements of CoQ10,vits D3 and C, fish oil,  magnesium, sulphur, coconut oil, and appropriate metformin and human sex hormone replacement.
     Rather than  Big Pharma’s promotion of  Statinopause, statin deficiency ,  we need to address the multiple age-and diet-related deficiencies (and some excesses)  that lead to the preventible degenerative diseases of aging- and which are worsened by the Food Factory chain  promotion that has dictated the (Gary Taubes’  Diet Delusion  and Nina Teicholtz’ The Big Fat Surprise) expose  of processed grain-fed nutrient-depleted (but fructose-loaded) foods, high carbs low animal fat/cholesterol diet for forty years. This has   compounded the deficiency of -fat-soluble micronutrients   like vitamins D3, CoQ10, A,  E & K2,  lecithin and marine omga3 – EPA and DHA; and naturally compounded pollution  by environmental-  radioactivity, electromagnetic and radiofields-,   and air, foodchain and drug pollution the past 50 years years by plastics, CO2 and volatile emissions, mercury, aluminium, fluoride, lead, bromide;   micromineral depleted salt, fatally potent endocrine disruptors, antibiotics, xenohormones, pesticides  and numerous other synthetic drugs launched on the public until they are recognized to kill humans.        
                                                                                    

  Margaret McCartney  general practitioner, Glasgow writes : We lack the tools to help patients decide about statins BMJ 2014; 349 doi:     The National Institute for Health and Care Excellence (NICE) recently approved atorvastatin for people in England and Wales who have a 10% risk of a cardiovascular event within 10 years; it had previously been a 20% risk.1 GPs are advised to treat such people—which includes everyone older than 85—and to continually review everyone else in case they pass the 10% threshold.

          This decision on funding statins is based primarily on cost effectiveness to the NHS.2 The press release from NICE mentioned the potential benefit to the population (namely, it “could help prevent up to 28 000 heart attacks and 16 000 strokes each year”3) but not the absolute benefit to the individual.

But life is more complicated than that: people make choices for multiple reasons. Many patients stop taking statins after starting them4; others, faced with the choice of taking a drug with a small chance of benefit, would rather not do so; and some people will want to take them no matter how low their risk may already be.

We lack the tools to accurately predict individual risk at such low thresholds—leading to overtreatment and, to a lesser extent, non-identification of risk.5 The general practice cake is finite; cutting a bigger slice for healthy people at lower risk means a smaller slice for people who have symptoms and are unwell. The chance of a longer life is offered to people who are willing to take tablets consistently, but we know that these compliant patients are already more likely to live longer, even when taking a placebo.6 7 This policy, which benefits people who are already the healthiest, has the potential to widen health inequalities.

       Who is keeping an overview of where NICE is taking us? The conflicts of interest among the members on its drafting panels are buried in minutes rather than in the guidance itself, and we still lack public access to most of the trial data that NICE uses.8 But we are told to press ahead regardless when, most bewildering of all, we don’t have a decent shared decision aid—designed and tested for the five million more people advised to take statins—about the benefits and harms of statinisation and the management of cardiovascular risk.

      “Should I take statins?” is a question asked of GPs every day. We urgently need better tools to allow guidance to guide, rather than dictate new targets. Our lack of resources to deal with such a common question simply isn’t acceptable.

Background:
2013 Italian  Statin HMGA   study Pasin ea shows that statins- cholesterol-busters- do not help patients with sepsis.
A 2010   review Yue ea of all published studies in  3,022 postmenopausal women (mean age, >62.7 y), showed  that statin use doesnt prevent fractures or increases bone density.

why should synthetic designer metabolic poisons – statins-  be expected to help peripheral  conditions like fracture risk and menopause?  when statins promote diabetes – insulin resistance, and  block healthy  metabolism throughout the body, in brains, muscles, kidneys, skin- but especially  lowering liver manufacture of cholesterol that is one of our top lifegivers  for our needed reproductive and adrenal steroids- including our two prime anabolic steroids( vitamin D3 and androgen). And statins increase the risk of highly malignant Merkel Cell skin carcinoma by 25%, as well as dermatitis eg Ma .  ..

We have known for  ~forty  years that while anticholesterol drugs  are  valuable for  rare people with severe hypercholesterolemia HCH risk of  vascular disease, statins’  longterm adverse effects are numerous, and there has never been evidence to justify their routine mass  use  for mild to moderate HCH- ie CVS risk below ~15 to 20% in 10 years-   despite the Cholesterol-statin industry investing multimillions in their promotional trials and in their lobbyists.

The Sheffield Cholesterol  and Multiple Risk Table by Jackson ea 25 years ago in the Lancet  was impressive  as a guide to  life extension by taking a statin permanently. When used for secondary prevention of coronary heart disease CHD , treatment with an inhibitor of hydroxymethylglutaryl-coenzyme-A reductase HMGA results in worthwhile benefit that clearly exceeds any risk in patients whose risk of coronary death is 1.5% or more per year ie >15% per 10 years. This evidence can be extrapolated logically to primary prevention of coronary disease provided that treatment is targeted at those with similar or higher risk. The table highlights the predominant effect of age on coronary risk; a person who is free of vascular disease and younger than 52 years is unlikely to have the specified degree of risk. Even in older people (60-70 years) several risk factors are generally required to attain this degree of risk. Some people are candidates for lipid- lowering drug treatment with serum cholesterol as low as 5.5 mmol/L, whereas others with cholesterol as high as 9.0 mmol/L are not. Although cholesterol lowering is a powerful method for preventing coronary events in people at high risk, cholesterol measurement by itself is not a good way to identify those with high risk. At that stage I had already been advised for 20 years , and declined on the evidence,  to take an anticholesterol drug , since in my early 50s despite my cholesterol of 6-7, my normal weight, HDLC, Hcy, Lpa,  bloodpressure, blood glucose, lifestyle and diet  put me at low risk
.Now the updated Sheffield 2011 Table  is  by  Jackson et al  in the prestigious QJM. At my age and low risk factors (no FH of CHD despite familial risks  (diabetes, atrial fib and mild lipidemia), my  Sheffield score of about 10 barely  puts me into the statin benefit range of 5 months gained. My coronaries and carotids are clear of plaque at last imaging, on all the natural supplements mentioned in this review, but not statin or any other designer hypolipidemic drug. If my patients have already been started elsewhere on a statin, I suggest they try just 5mg/day to minimize risks. . .
ADVERSE EFFECTS:  by design, they are antimetabolic;  oxidant ie increase ROS reactive oxidant species;  reduce CoQ10 by 39%.  Although these adverse effects are dose dependent and may be rare, they are cumulatively serious against muscle, liver, kidneys, memory, mood,  pancreas,  skin, sexual function; they cause diabetes, neuropathy and perhaps worsen cancer.  Thus they are like cancer chemotherapy, only for severely ill patients ie those with severe familial hypercholesterolemia..
     As  Beyond Health summarizes last year,      “Cholesterol does not cause heart disease. The French  Paradox- they have the highest average cholesterol in Europe, around 250mg(6mmol/L), but the lowest incidence of heart disease and half the heart attacks we have here in the U.S. In Crete, the home of the healthy Mediterranean diet, a 10-year study failed to find a single heart attack despite average cholesterol levels well over 200 (5 mmol). There are as many heart attacks in people with cholesterol levels over 300 (7.5mmol) as those whose levels are under 200 . Half of all heart attacks occur in people with normal cholesterol levels.   Cognitive problems affect about 15 percent of statin users, including episodes of temporary amnesia called transient global amnesia (TGA). Statins have an adverse effect on tau, a protein made by brain cells that helps maintain their structure. Abnormal tau proteins are linked with neurodegenerative diseases like Alzheimer’s, Parkinson’s and ALS.  Statins  cause progressive cognitive decline, ranging from mild to severe, and anxiety, depression, inability to deal with stress, and violent behavior. Statin-takers are more likely to develop peripheral neuropathy, and to experience tremors and vertigo.  Other health issues linked with statins include cancer, suppressed immunity, cataracts and optic nerve problems, liver damage, impotence and loss of libido, hypersensitivity reactions that can lead to the autoimmune disease lupus, birth defects if taken by pregnant women, skin rashes and dryness, hair loss, gastrointestinal problems, insomnia, and pancreatitis. “
LESSONS FROM FAMILIAL HYPERCHOLESTEROLEMIA:
Wiki says In FH, Initial studies showed increased activity of HMGA but more showed that this did not explain the very abnormal cholesterol levels in FH patients. The binding of LDL to its receptor, and effects of impaired binding on metabolism  proved to be the underlying mechanism for FH.  Heterozygous FH is a common genetic disorder inherited   in 1:500 people in many “European”   populations – the Afrikaner, French Canadians, Lebanese Christians, and Finns have high rates of specific mutations that make FH particularly common in these groups. Homozygous FH is much rarer, occurring in 1 in a million births. Heterozygous FH is normally treated with lipid lowering agentsstatins, bile acid sequestrants.. . Homozygous FH often does not respond to medical therapy and may requires radical  other treatments.
 
       But search of Pubmed and Google  for STATIN mortality reduction IN FAMILIAL HYPERCHOLESTEROLEMIA gives few reports showing  that statins meaningfully reduce mortality  and add  QALYs quality life years.
                        A current comprehensive  Medscape review August 2014 Familial Hypercholesterolemia Medication  does not specify any  % reduction in mortality on statins or any other drugs, despite lowering LDLc levels 50-60%.
and  Familial Hypercholesterolemia.  Youngblom E, Knowles JW. Editors.  GeneReviews® Univ. Washington 2014 Jan  says Familial hypercholesterolemia (FH) is characterized by severely elevated LDL cholesterol (LDL-C) levels that cause atherosclerotic plaque deposition in arteries and a markedly increased risk of coronary artery disease at an early age. In FH, the more common CVD is coronary heart disease (CHD), which may manifest as angina and myocardial infarction; stroke occurs more rarely. Heterozygous FH is relatively common (prevalence 1:200-500). Persons with untreated FH are at an approximately 20-fold increased risk for CHD. Untreated men are at a 50% risk for a fatal or non-fatal coronary event by age 50 years; untreated women are at a 30% risk by age 60 years. In contrast, homozygous FH (HoFH)  is much rarer (prevalence 1:160,000 to 1:1,000,000). Most individuals with HoFH experience severe CHD by their mid-20s. The rate of either death or coronary bypass surgery by the teenage years is high.
Indeed,  Fred Raal, Dave Marais ea from their clinics’  long term results at   Wits and UCT showed Reduction in Mortality in Subjects With Homozygous Familial Hypercholesterolemia Associated With Advances in Lipid-Lowering TherapyCirculation 2011 but the ~60% reduction in mortality in the statin era in this rare group (187 such subjects, mostly Afrikaners, very few smokers) was even so statistically barely significant. When the patients lost to follow-up in the statin-naive group were included in the analysis and censored on the date that statin therapy became available, the hazard ratio for the end point of death remained barely significant at 0.38 (95% CI 0.15–0.94; P 0.04), and the hazard ratio for the end point of MACE was not significant 0.54 (95% CI 0.25–1.18; P=0.12)
However, a  new JAMA study   from the Netherlands paints a gloomy picture- following almost 277  kids from age ~14 years for  Ten-Year Follow-up After Initiation of Statin Therapy in Children With Familial Hypercholesterolemia, after 10 years twice as many of those on statins were smoking  compared to their “normal” sibs, but worse, the FH sibs on statins, despite 20% lower cholesterol,  had the same increase in carotid artery thickening as their sibs without FH.
 
Nordestgaard, Tybjærg-Hansen ea for the European Atherosclerosis Society Eur Heart J. 2013 say . Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population:  to prevent coronary heart disease: consensus. .  Of the theoretical estimated prevalence of 1/500 for heterozygous FH, <1% are diagnosed in most countries. Recently, direct screening in a Northern European general population diagnosed approximately 1/200 with heterozygous FH. All reported studies document failure to achieve recommended LDL cholesterol targets in a large proportion of individuals with FH, and up to 13-fold increased risk of CHD. Based on prevalences between 1/500 and 1/200, between 14 and 34 million individuals worldwide have FH. We recommend that children, adults, and families should be screened for FH if a person or family member presents with FH, a plasma cholesterol level in an adult ≥8 mmol/L(≥310 mg/dL) or a child ≥6 mmol/L(≥230 mg/dL), premature CHD, tendon xanthomas, or sudden premature cardiac death. In FH, LDLC targets are <3.5 mmol/L(<135 mg/dL) for children, <2.5 mmol/L(<100 mg/dL) for adults, and <1.8 mmol/L(<70 mg/dL) for adults with known CHD or diabetes. In addition to lifestyle and dietary counseling, treatment priorities are (i) in children, statins, ezetimibe, and bile acid binding resins, and (ii) in adults, maximal potent statin dose, ezetimibe, and bile acid binding resins. Lipoprotein apheresis can be offered in homozygotes and in treatment-resistant heterozygotes with CHD.                                                                                                                                                            
THE FAILURE OF EZETIMIBE, VYTORIN:
But ezetimibe as an addon to statin eg in  Vytorin has been thoroughly discredited.  As Forbes.com said last year,   Pharma & Healthcare 2013   The Fate Of New Cholesterol Drugs Depends On IMPROVE-IT   “.But  Improve-It was not completed as planned in 2013. The new American  guidelines delivered a strong statement questioning the increasingly controversial theory that LDL lowering by itself is beneficial. “We found that non-statin therapies really didn’t provide an acceptable risk reduction benefit compared to their potential for adverse effects in the routine prevention of heart attack and stroke,”  IMPROVE-IT is the large, seemingly endless outcomes trial studying Vytorin, which has been a blockbuster drug for Merck. But the drug’s reputation, and its sales, have diminished in recent years because of a raging controversy over the lack of any evidence for clinical benefit. Vytorin lowers LDL cholesterol but no one knows if it improves outcomes. The IMPROVE-IT trial is supposed to resolve this controversy next year, but it will do so only as the patent on the drug nears expiration.     There’s a really good analogy to help understand the way IMPROVE-IT could impact the fate of the PCSK9 inhibitors. Just recently supporters of Amarin’s fish oil pill Vascepa thought the drug would coast to approval for a broad new indication. Their optimism was based largely on an agreement with the FDA that did not require a large outcome study before approval. But over the past few years several large outcome trials– not entirely dissimilar to IMPROVE-IT– failed to demonstrate clinical benefit for drugs that, like Vascepa, lowered triglycerides. The FDA tore up its earlier agreement with Amarin. In all likelihood Vascepa will not gain the new indication it seeks until an ongoing outcome study is successfully completed. The other Merck CVS drug trial of Tredaptive, a combination of simvastatin and niacin B3 vitamin, failed to show the new drug was better than a statin alone.

However, the Improve-It trial already failed when it showed no significant target benefits of more intensive LDLC lowering by it’s planned   2.5  years finish ie  2010 ; so numbers  (10 000 to 18000)  and time were increased to 18000 subjects, to finish now.. The latest is that results will be released  17 November…

what do other  STATIN  trials show? A Canticle for Statins?

COMPARISON OF THE 2011 CAMBRIDGE METANALYSIS AND  2013 COCHRANE STATIN METANALYSES:

 Ray et al from Cambridge Univ UK in Arch Intern Med. 2010:  a   meta-analysis of 11 randomized controlled trials (Jupiter, Allhat, Ascot, Mega, AfCaps, WOSCOPS, ASPEN, CARDS, Prevend-it, PROSPER, HYRIM) involving 65,229 participants  ie ~244,000 person-years , mean age 62yrs,  systolic BP 141, LDLC 3.45, mean duration 3.7yrs (Jupiter only 2.2yrs), 19% diabetics,   found no  benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up.
and 3  years later Taylor ea (London Univ Cochrane Database Syst Rev. 2013)  concluded  in   their abstract: Statins for the primary prevention of cardiovascular disease THAT  Evidence available to date showed that primary prevention with statins is likely to be cost-effective and may improve patient quality of life. In Eighteen randomised control trials   in  56,934 participants , mean age 57yrs, cholesterol baseline 6.17mol/l, LDLC 4.1;  duration 1 to 5.3years ie mean about 3.15 years ( they did not report mean bloodpressure). . Fourteen trials recruited patients with specific conditions (raised lipids, diabetes, hypertension, microalbuminuria). All-cause mortality was reduced 14%  by statins (OR 0.86, 95% CI 0.79 to 0.94).  as was combined fatal and non-fatal CVD RR 0.75 (95% CI 0.70 to 0.81) There was no evidence of any serious harm caused by statin prescription .                         

BUT
t
heir full published paper tables   showed that statin use – in a mean time of only 3 years-   ” increased Diabetes 18% from 2.4% on placebo to 2.9% on statin; with  more fatal strokes,  liver, renal, arthritis adversity. and all-cause mortality from 5-1 to 4.4%; NUMBER NEEDED TO TREAT NNT 96. THE ABSTRACT DOES NOT GIVE THESE GLUM NUMBERS, that statins benefit  only 1 in a hundred.  BUT the dull paper states  Only the JUPITER trial showed strong  evidence of a reduction in total mortality.
As this column has previously pointed out, the Jupiter Trial was clearly flawed when we first reviewed it, and further debunked by diverse major groups by 2011/2 .
so while  the Cochrane study patients were 5 years younger but had baseline LDLC 19% higher,  than in the Cambridge analysis,   ie by age and LDLC, the Cochrane analysis could still not show meaningful reduction in mortality other than in the disputed Jupiter study.. But the Cochrane trials had only 1/8th of the diabetics in the Cambridge analysis.
 
     The 2013 Cochrane statin review’s   evidence for using statins for primary prevention in higher-risk persons without CVD  admits it’s antimortality benefit   is based solely on the weight of the seriously flawed Jupiter trial. But while the Taylor Cochrane analysis used only 8 of the trials (skipping PROSPER, ASCOT and ALLHAT)  analysed in the Ray Cambridge analysis, the Cochrane analysis added another 10 trials. Despite covering 7 more trials than the Cambridge 2010 analysis, the Cochrane analysis included 25% fewer patients than the Cambridge analysis,

     So  what the innocuous abstract of the London  UK  Cochrane review   failed to say is that, in their full paper (available on application)  weighted by the biased Jupiter trial,   to lower mortality by 14% in about 3.5years, to avoid one death,   96 well people need to take fairly vigorous dose statin for 1 to 5.4 years – or 1 patient for a few hundred years–   with serious risks of diabetes (up 18%), liver, kidney, myopathies, peripheral neuropathy, intracerebral hemorrhage (ICH), and other diseases of the central nervous system (eg  cognitive impairment, depression, sleep disorders, nightmare, and headache- . mood (suicide risk increased 2.5 fold – Davison & Kaplan 2014 Canada );

and (unlike the anticancer benefits of metformin and vitamin D3) no benefits in reducing cancers rates. Such bad risk: benefit ratio confirms what  has always been known, that there is no place for mass long-term consumption of statin whether in a mythical Polypill (Wald and Law 2003–   with adverse Bblocker, ACEI and aspirin,) or even more farfetched added to our diet staples- water, bread etc..

It is common cause that diabetes increases major  risks 4 fold; so advocating  96 well people to take a statin to lower  mortality  by 1 case in 3.5 years ie 330 patient-years while >3% develop diabetes, stroke, depression, myositis, hepatorenal  and other major complications,  is  negligence,  when patients do so much better on metformin plus other natural proven life-extending  supplements like fish oil, coconut oil, vitamins esp vit D3 & K2,  minerals etc. 

As Pubpeer said on 27  July 2014, its a crisis of  trust in what top journals (in this case the Cochrane Review) publish. For TRUST read distrust…

This is in contrast to metformin prevention in similar overweight well people,  which lowers all risks by at least a third, with no adverse effects  provided dose is started low and titrated to tolerance ie ~250 to 2500mg a day. THE BMJ STATIN FUROR JUNE 2014:
Just last month, the long-awaited independent review of the BMJ June 2014 STATIN publication (of articles denouncing the value of statins for mass primary prevention ) confirmed  that the BMJ editors under  Dr Fiona Godlee were correct in  standing by the June papers  that there is no mortality benefit from statin treatment in people at less than a 20% 10-year risk of cardiovascular disease, as Canada implements.,
The panel, chaired by Dr Heath with  six internationally renowned experts, concluded the journal had handled the two articles appropriately and that its processes were timely and reasonable. 

Now  three new 2014  studies put more wolves  among the Big Pharma profiteering disease-mongering sheep:
one from India describing many promising new competitors to displace statins;  one from Oxford University warning yet again of the adverse effects of anticholesterols, this time by CETP inhibitors; and one from New York University mocking the wannabe Statinopause, statin deficiency:

      George,  Elangovan  ea in India  J Cardiovasc Pharmacol Ther. 2014 Jul  Look  into the Crystal Ball -Upcoming Drugs for Dyslipidemia: say: . Although statins are effective anti-dyslipidemic drugs, their use is fraught with issues such as failure of adequate lipid control in 30% of cases and intolerance in select patients. The limited potential of alternatives such as fibrates, bile acid sequestrants and niacin has spurred search for novel drug molecules with better efficacy and safety, eg  promising cholesteryl ester transfer protein CETP inhibitors such as evacetrapib and anacetrapib; (MTP) inhibitors eg lomitapide; Apo CIII inhibitors eg  mipomersen;  PCSK9 inhibitors eg evolocumab, alirocumab; farnesoid X receptor modulation; and Lp-PLA2 inhibition. While it may not be an easy proposition to dismantle statins from their current position as a cholesterol reducing agent and as a drug to reduce coronary and cerebro-vascular atherosclerosis, our improved understanding of the disease and appropriate harnessing of resources using sound and robust technology could make rapid in-roads in our pursuit of the ideal anti-dyslipidemic drug.

BUT
Miller NE. University of Oxford, UK   in F1000Res.2014 Jun   warns  Time to think again about .  CETP inhibitors and cardiovascular disease:   Inhibition of cholesteryl ester transfer protein (CETP) lowers plasma LDLC concentration and raises HDLC, suggesting it might prevent CVD. From the outset, however, the concept has been controversial owing to uncertainty about its effects on HDL function and reverse cholesterol transport (RCT). Although there has long been good evidence in rabbits  that CETP inhibition reduces atherosclerosis , the first information on CETP as a CVD risk factor in a prospectively followed cohort was not published until after the first Phase 3 trial of a CETP inhibitor had begun. The worrying finding that in humans CVD incidence was related inversely to plasma CETP has since been reproduced in each of five further prospective cohort studies. Similar results were obtained in subjects on or off statin therapy, for first and second CVD events, and for mortality as well as CVD morbidity. Additionally, two recent studies have found alleles of the CETP gene to be associated with an increased risk of myocardial infarction. Meanwhile, CETP gene transfer in mice was found to increase RCT from peripheral macrophages in vivo, and human plasma with high CETP activity was shown to have a greater capacity to remove cholesterol from cultured cells than plasma with low activity. This mounting evidence  in humans and mice for a protective function of CETP has been given remarkably little attention, and indeed was not mentioned in several recent reviews.  It appears to show that CETP inhibition does not test the HDL hypothesis as originally hoped, and raises a pressing ethical issue regarding two Phase 3 trials of inhibitors, involving more than forty thousand subjects, which are currently in progress. As the weight of evidence now clearly supports an adverse effect of CETP inhibition on CVD, an urgent review is needed to determine if these trials should be discontinued.
and
Han, Weinberger, SutinNew York University. J Gen Intern Med. 2014 Aug. warn:  Statinopause.        Statins are the cornerstone of lipid-lowering therapy for CVD prevention. The  American College of Cardiology (ACC) and American Heart Association (AHA) 2013 guidelines represent a fundamental shift in how statins will be prescribed; recommending  statins for nearly all older patients up to age 75 years, including healthy adults with low normal lipid levels and no atherosclerotic cardiovascular disease (ASCVD) risk factors other than age. Under the 2013 guidelines, age becomes a main determinant for initiating statin therapy for primary prevention among older adults. Specifically, according to the new guidelines, white males aged 63-75, white females aged 71-75, African American males aged 66-75, and African American females aged 70-75 with optimal risk factors would be recommended for statin treatment for primary prevention. Based on the new guidelines, one could term these older adults as having “statin deficiency,” a condition warranting statin treatment. We call this putative condition of age-related statin deficiency “statinopause.” After careful examination of the trial evidence, we find very little support for the new recommendations for primary prevention. The lack of evidence underscores the need for clinical trials to determine the risks and benefits of statin therapy for primary prevention among older adults.                                                                                                                                                           
HALF OF PATIENTS DISCONTINUE STATINS WITHIN A YEAR IN REAL LIFE:     Already in 2009    Goldenberg N1, Glueck C: wrote  in real life practice, about half of patients who are prescribed statins discontinue the medication by the end of the year. from the  Cholesterol and Metabolism Center,  Jewish Hospital, Cincinnati, Ohio, USAin  Vasc Health Risk Manag. .    Efficacy, effectiveness and real life goal attainment of statins in managing  CVS  risk. Statins became available in 1987 for the treatment of hypercholesterolemia .   Multiple, well-designed, placebo-controlled, double-blind studies revealed that each 1% reduction in serum cholesterol level was associated with about 1% reduction in risk of CVS events. Low-density lipoprotein (LDLC) cholesterol reduction to less than 78 mg/dL may be associated with reduction of atheroma burden. Patients with high levels of high specificity C-reactive protein and having LDLC less than 3.4 mmol/L (130 mg/dL) in primary prevention settings benefited from aggressive LDLC reduction with rosuvastatin over a 2-year period.  Medication adherence is lower in younger patients, women, and absence of known CHD. Personal features of the prescribing physician and dispensing pharmacies also affect patients’ compliance. More studies are needed to evaluate if “compliance packets” would benefit patients in a real life situation.
STATINS DEPLETE  Co10, OMEGA3 AND OTHER ESSENTIALS:.
     Coenzyme q10 therapy 2014  .Garrido-Maraver J1,  Sánchez-Alcázar ea . at Seville Universities say coenzyme Q10 (CoQ10) have  key role in mitochondrial bioenergetics; antioxidant; obligatory cofactor for uncoupling proteins and a modulator of the mitochondrial transition pore; expression of genes ; human cell signaling, metabolism and transport. CoQ10 deficiencies are due to autosomal recessive mutations, mitochondrial diseases, aging-related oxidative stress and carcinogenesis processes, and statin treatment. Many neurodegenerative disorders, diabetes, cancer, and muscular and cardiovascular diseases have been associated with low CoQ10 levels as well as different ataxias and encephalomyopathies. CoQ10 causes no serious adverse effects in humans.  Oral a CoQ10 is a frequent  antioxidant used in many diseases that may provide a significant symptomatic benefit.

        Statin treatment and new-onset diabetes: a review of proposed mechanisms. Brault ,  Daskalopoulou ea .2014  at McGill and Harvard say   New-onset diabetes has been observed  involving statin therapy. To explain this association, three major mechanisms have been proposed . First, certain statins affect insulin secretion through direct, indirect or combined effects on calcium channels in pancreatic β-cells. Second, reduced translocation of glucose transporter 4 in response to treatment results in hyperglycemia and hyperinsulinemia. Third, statin therapy decreases other important downstream products, such as coenzyme Q10, farnesyl pyrophosphate, geranylgeranyl pyrophosphate, and dolichol; their depletion leads to reduced intracellular signaling.

     Michel de Lorgeril ea .Universite Joseph Fourier, Grenoble France  BMC Med.2013 ask: do statins inhibit omega-3?. Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions. .Early randomized controlled trials (RCTs) demonstrated the health benefits of omega-3 fatty acids (n-3), whereas recent RCTs were negative. We now address the issue, focusing on the temporal changes having occurred: most patients in recent RCTs are no longer n-3 deficient and the vast majority are now treated with statins. Recent RCTs testing n-3 against arrhythmias suggest that n-3 reduce the risk only in patients not taking a statin. Other recent RCTs in secondary prevention were negative although, in a post-hoc analysis separating statin users and non-users, non-significant protection of n-3 was observed among statin non-users whereas statin users had no effect. Recent RCTs testing statins – after the implementation of the New Clinical Trial Regulation in 2007 – are negative (or flawed) suggesting that the lack of effect of n-3 cannot be attributed to a parallel protection by statins. Finally, statins favor the metabolism of omega-6 fatty acids (n-6), which in turn inhibits n-3; and contrary to n-3, they increase insulin resistance and the risk of diabetes. Thus, n-3 and statins are counteractive at several levels and statins  inhibit n-3.

ie statins undo the proven benefits of omega3 and CoQ10. .

VITAMIN D AND CHD:

 Charles Glueck ea at the same Cincinnati Jewish Hospital. in  Med Hypotheses. 2011 describe HOW Vit D repletion reverses statin intolerance in 91% of statin-intolerant patients. Symptomatic myositis-myalgia in hypercholesterolemic statin-treated patients with concurrent vitamin D deficiency leading to statin intolerance may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle.   Myositis-myalgia is the most common cause of statin intolerance, leading to cessation of statin use, with consequent failure to lower LDL cholesterol to target levels for primary and secondary prevention of cardiovascular disease (CVD). Despite published and new empirical evidence, the medical establishment has refused to accept it, requiring placebo-controlled, double-blind studies, none having been reported to date.

Glueck’s promotion of vitamin D as antidote or alternative to statin is borne out by at least 5 papers on Pubmed since 2003 (Kajinami), Yavuz 2009 ea ) –  some of which show that vit D level may rise significantly on statin.
       Now a  major review from Universities of Newcastle UK and Harvard by Kunadian, Manson ea   Am Heart J. 2014 of  Vitamin D deficiency and coronary artery disease: concludes: Coronary artery disease being the leading cause of death in developed countries, older patients are at particularly high risk of poor outcomes following acute coronary syndrome,  and impaired nutrition, including low vitamin D levels, may play a role.  Longitudinal studies have demonstrated increased cardiovascular mortality and morbidity associated with vitamin D deficiency. Low vitamin D levels have been linked to inflammation, higher coronary artery calcium scores, impaired endothelial function and increased vascular stiffness. Most available trials have tested only low doses of supplementation in relatively low-risk populations.


Specific Critiques of the Jupiter study and Contrasting results from other studies: :
 Wiki quotes Dr. Michel de Lorgeril, et al  In 2010,  published “a critical reappraisal” of the JUPITER Trial in the Archives of Internal Medicine,  what they saw as flaws in the trial, pointing out that the cardiovascular mortality rate and the case-fatality rate for myocardial infarction were much lower than they expected; they also questioned whether the study had been biased and perhaps manipulated because it was sponsored by a pharmaceutical company with a strong commercial interest in the outcome. They concluded that, “The results of the trial do not support the use of statin treatment for primary prevention of cardiovascular diseases and raise troubling questions concerning the role of commercial sponsors.  In addition, some prior and some subsequent studies have contrasted with the JUPITER trial results.       Five  other major university papers in prestige journals  also criticized the Jupiter study in 2011/12: Samson ea Florida State, Serebruany Johns Hoplins; Ridker Harvard, and  Morrissey ea Cedars-Mt Sinai;  while Lopez and Wright from Spain and Canada published an exhaustive debunking of the Jupiter claims of significantly reduced mortality.
            as we have long questioned about mass use of statins, Jay Cohen MD 2014 Aug 4th asks in  the MedicationSense E-Newsletter again: what is The Truth About Crestor: Is Crestor Dangerous And, if so, Why?  Crestor is the newest statin and the strongest statin yet. Statins are highly touted drugs for reducing cholesterol. Studies clearly show that statins improve cholesterol numbers (by lowering LDL and raising HDL) and may reduce C-reactive protein. Statins impede atherosclerosis, reduce heart attacks and strokes, and cardiac death. Thus, the statins Lipitor and Zocor are not only the #1 and #2 top-selling drugs in America, but also household names.  Other statins include Pravachol, Mevacor, and Lescol–and now ultra-potent Crestor. Until 2001, there was another statin: Baycol. It was then the newest statin and a potent statin–until it was withdrawn because of dozens of deaths. Is Crestor another Lipitor or another Baycol? Although Crestor has been on the market only a year, it has already been linked to numerous cases of severe muscle breakdown, kidney toxicity, and deaths. Public Citizen recently petitioned the FDA to ban Crestor...
 

       Conclusion: these references reviewed confirm that  is no justification for the myth of routine use of statins for primary prevention in the average population, especially in view of their risks, especially  increase in diabetes, and the availability of safe and far more globally healthgiving natural antiaging antioxidant energizing  insulin-sensitizing supplements that do a far better job of reversing both CVD and all other major diseases. .

update  16 June 2014 as this column has argued since 2008 (and this author for 40 years in refusing to take them for lack of proof)-  given their numerous serious and nuisance harms-  there never has been good enough evidence to justify synthetic designer cholesterol-busters for primary prevention with mild-to-moderate cholesterolemia ie without the presence of cardiovascular disease;

in contrast to   harmless multipurpose (antiatheroma antidiabetic antithrombotic antihypertensive anticancer all-disease prevention) micronutrient supplements like fish oil, coconut oil, DMSO, metformin,  vitamins esp C D & K2, minerals esp magnesium, chromium, zinc, iodine; , human nonoral HRT, CoQ10, arginine, carnitine, carnosine ; numerous mixed medicinal herbs; etc.

In the Statin-use debate creates furor at BMJ    CMAJ  on June 16, 2014,   Carolyn Brown argues  “Statins are beneficial for people with proven coronary artery disease, but a recent BMJ article questioned their use as a prophylactic measure.            “Are statins going to have a big impact on coronary artery disease or are they going to be one of the big mistakes that the medical profession has made?” That’s the question asked by Dr. James Wright, a Canadian who co-authored an analysis of the evidence on statins that appeared in the British Medical Journal (BMJ) in October 2013. 

      ” It seems like a straightforward question, but that article has led to a furor in the United Kingdom, with a well-known researcher calling for its retraction and the BMJ editor-in-chief Fiona Godlee defending the journal’s publishing process on radio and television. At issue is the clinical uncertainty about the preventive use of statins. “We’re fairly certain that benefits outweigh the harms in people with proven coronary artery disease (CAD). That’s based on a highly statistically significant but modest reduction in total mortality,” says Wright, who is managing director and chair of the Therapeutics Initiative (TI) at the University of British Columbia. But he says most prescriptions for statins are aimed at preventing CAD.

               “The evidence for this is not as rigorous and serious adverse effects have been documented. The UK’s National Institute for Health and Care Excellence (NICE) recently proposed extending preventive use of statins from patients who have a 20% chance of developing CAD in the next 10 years (its current guideline) to those with a 10% risk. This has led to a debate over the accuracy of risk calculators, unnecessary prescribing in seniors (since age is a major risk factor) and adverse effects. Canada’s guidelines recommend statin therapy in patients with risk below 20% only if their levels of cholesterol or other indicators exceed certain thresholds. Wright believes the statin issue has become heated because “so many people are taking them. They have been in the news so much and there [is] so much money being spent on them.” “Publication of our article has reignited the debate,” says Dr. Kamran Abbasi, international editor of the BMJ, who spoke on behalf of Godlee. “There are people who disagree vehemently on this issue. They can’t reach any sort of consensus on it at the moment.” The BMJ article re-analyzed data from the Cholesterol Treatment Trialists (CTT) Collaboration meta-analysis and cited adverse effects rates from various studies.

             ” Sir Rory Collins, a researcher at Oxford University and head of the CTT group, corresponded directly and met with Godlee in December 2013 about the article, calling for a retraction. He has also stated his view in media interviews. As a result of Collins’ complaint, the article was corrected, as the authors agreed that they had erred in reporting rates of side effects from the observational study. Wright says, “The issue around side effects is just that there is some harm.” The analysis had cited a rate of statin-related adverse effects of 18%; in fact, the original study found 17.4% of patients had a “statin-related event” but only approximately 9% discontinued statin therapy as a result. The correction affirmed that the CTT study failed to show that statins reduced the overall mortality risk in patients with a less than 20% risk of CAD over 10 years. Godlee also published an editorial explaining the journal’s decisions on how to handle the controversy and appointed an independent panel to rule on whether a retraction is warranted. Collins says he has submitted detailed material to this panel and maintains that there remain “extensive problems” with the analysis paper, beyond what the correction addressed. Charlotte Haug, vice-chair of the Committee on Publication Ethics (COPE).

update 2010   A new review, this time from a top team in France, further demolishes the deceptive  Jupiter trial promoting rosuvastatin Crestor, confirming that it was fatally flawed:

Cholesterol lowering, cardiovascular diseases, and the rosuvastatin-JUPITER Crestor controversy: a critical reappraisal.

Michael de Lorgeril ea conclude: ” The results of the trial do not support the use of statin treatment for primary prevention of cardiovascular diseases and raise troubling questions concerning the role of commercial sponsors.”

This concurs with the fraud of modern medicine increasingly pursued by combined Drug Industry and Government Regulator conspiracy, including www.lef.org/…/Media-Attempts-to-Misrepresent-Scientific-Findings.htm

and

Justice Dept declares war on doctors.

and why use a drug that can cause cancer , and tendinopathy, and  thrombocytopenia? Pubmed  shows at least 7 causally linked case reports since 1992 and 2008 , including one  now for rosuvastatin.

and Univ California San Diego alone reports 300 cases of statin-related myopathy.

contrast this with the trial report last week from a hypertension unit in Israel where a simple combination of vits C & E, coQ10 and selenium for 6 months – with no risks- lowered arterial stiffening, hypertension, lipidemia and glucose.

so why use statins except in severe familial lipidemia?

Feb 4th 2010 

 Early last year this column pointed out that the JUPITER trial was another nail in the coffin of primary use of statins.

Now a University California    Davis team concur further   in “Another look at the results of the JUPITER trial…  that many of the participants did not receive care consistent with current standards. Thus, the benefit of statin therapy would have been more difficult to demonstrate if standard therapeutic recommendations had been followed. In conclusion, these considerations cast doubt on the contention that statin therapy should be initiated in apparently healthy individuals on the basisof elevated high-sensitivity C-reactive protein levels.