(No emergencies or surgery- these must go to nearest polyclinic or hospital ER). .
or consultations by Telephone/email where appropriate.
for appointments for consultations, or non-xray procedures by registered practitioners : Sure Touch breast prescreening on Saturday mornings next on 7 February 2015 by Sister Zeneath Ismail – cash R650 (then R450 if followup scan desired within 3 months); -QUS ultrasound quantitative bone density cash R450 -tariff item 3612- anytime; Unlike radiologists’ and thermography reports (which describe only the imaging finding), the rates quoted include relevant breast or bone consultation and management planning by specialist nurse & physician.
IF BOOKED TOGETHER, (not necessarily the same morning) then combined breast and bone screening is R1000.
OTHER SERIOUS health problems ARE DEALT WITH BY CONSULTATION DURING THE WEEK (OR ON A DIFFERENT SATURDAY MORN) : heart- ECG, fatigue, HRT, sexual health, hypertension, depression, memory/dementia, lung & lungfunction, anaemia-haematology; kidney/bladder/pelvic, hormone-endocrine, depression, osteoporosis, sleep, diabetes, thyroid, adrenal; cramp; skin, infection including STDs & HIV/AIDs, stroke, epilepsy-neurology, dizziness, heartburn/digestive/liver, neuropathy, sexual health, menopause, HRT, genitourinary; immune problems, or arthritis relief;
Thermography no-touch infrared screening for suspicious cancer /inflammatory changes: by Radiographer Melinda-next 23 March 2015. R900 breasts; R1100 head and upper; or lower body & pelvis; R1300 whole body.
Bookings/queries contact Evelyn/ Reyhana / Val at the Natural Medicine Clinic, 1st Floor no 15, Grove Medical Bldg, opp ABSA (parking ABSA Parkade ) near Warwick/Cavendish Square Claremont Cape Town RSA, ph +27216831465 or a/h +2783 4385248 or firstname.lastname@example.org .
For the disabled – by arrangement drive up the ramp to the Clinic door on the Grove Bldg 1st floor parking deck.
Under CMS Council for Med Schemes Reg 10(6), open Medical schemes eg hospital plans have to pay from their own funds (not members’ savings) for appropriate outpatient consultation (tariff item 0191) for PMBs ie major conditions eg cancer, depression, neck/spinal problems, serious heart, lung, other disease., etc. Breast and osteoporosis concerns are generally part of menopause consultations N95.9 (if not already eg breast cancer code C50) and thus are often billable med scheme benefits. The menopause billable item only applies if you are 45yrs upwards, unless you have had total hysterectomy.
On patients’ requests, appropriate invoice can be prepared and submitted to your scheme for refund of your due benefits. Some schemes eg hospital plans falsely deny due benefits until reported to their regulator CMS. For medical plans where the billable tariff benefit rate is higher than the breast screening fee paid, the med plan rate 0191 will be charged eg R790 by the contracted specialist, and refundable by Discovery to the member. some basic schemes eg Keycare, Bonitas require preauthorization, or referral by their contracted GP .
: ABSTRACT: since last review in this column 5 years ago, what progress has there been with ovarian cancer OvCa? On Pubmed there are 81000 references, 45500 reviews on OvCa
5 Oct 2014: Ovarian Cancer Often Arises from Precursor Endometriosis Frontline Medical News, 2014 Sep 29,
29 Sept 2014 The good news is that if ovariectomy is not done at hysterectomy, then at least salpingectomy should be done- it does not cause earlier menopause. And the modern fashion for progesterone cream as baseline hormone balancing in this age of estrogen dominance, the feminization of nature, also adds major protection for heart, bone, memory, mood, and against cancer, without the risks of estrogen.
Before this month’s update, the latest, an Australian cancer review Mette ea 2013, shows that cigarette smoking increases the risk of OvCa by 30% to 60%.
The latest review 2013 Modugno ea at Univ Pittsburgh/Mayo Clinic Hormone response in ovarian cancer: time to reconsider as a clinical target? said “Ovarian cancer is the sixth most common cancer worldwide among women in developed countries and the most lethal of all gynecologic malignancies. There is a critical need for the introduction of targeted therapies to improve outcome. Epidemiological evidence suggests a critical role for steroid hormones in ovarian tumorigenesis. There is also increasing evidence from in vitro studies that estrogen, progestin, and androgen regulate proliferation and invasion of epithelial ovarian cancer cells. Limited clinical trials have shown modest response rates; however, they have consistently identified a small subset of patients that respond very well to endocrine therapy with few side effects. We propose that it is timely to perform additional well-designed trials that should include biomarkers of response.The most consistently reported reproductive and hormonally related factors found to protect against EOC are use of oral contraceptives (OCs), increasing parity, and having a tubal ligation. In contrast, increasing age and nulliparity have been consistently shown to increase EOC risk.
Recent studies, including the prospective Women’s Health Initiative (WHI) (Anderson et al. 2003) and the Million Women Study (Beral et al. 2007), report an increase in risk for both estrogen-only (ET) and estrogen–progestin (EPT) formulations, although the risk associated with EPT was lower than that of ET. A recent meta-analysis of 14 published studies found risk increases 22% per 5 years of ET use compared with only 10% per 5 years of EPT use, suggesting that risk differs by regimen (Pearce et al. 2009). Exogenous androgens may be associated with EOC. One case–control study found that use of Danazol, a synthetic androgen commonly used in the treatment of endometriosis, significantly increased EOC risk (Cottreau et al. 2003), although this finding has not been replicated (Olsen et al. 2008). Ever use of testosterone (tablets, patches, troches, or cream) has been associated with a threefold increase in EOC (Olsen et al. 2008).
Endometriosis, defined as the presence and growth of endometrial tissue outside the uterine cavity, has also been associated with EOC. A recent pooled analysis of 13 case–control studies showed a threefold increase in the incidence of clear cell EOC and a twofold increase in endometrioid EOC among women with a self-reported history of endometriosis (Pearce et al. 2012).
An increased risk of EOC was reported by one case–control study (Schildkraut et al. 1996) among women with polycystic ovary syndrome (PCOS), a condition associated with menstrual dysfunction, infertility, obesity, the metabolic syndrome, hyperandrogenism, and insulin resistance. However, the finding was based on a small number of cases (n=7) and the association was limited to nonusers of OCs and thin women. Further case–control and prospective studies have failed to confirm this relationship (Pierpoint et al. 1998, Olsen et al. 2008, Brinton et al. 2010).
Tubal ligation has been consistently shown to be associated with reduction in EOC risk (Cibula et al. 2011). This protection appears similar in magnitude to OC use and child bearing (about 30%) and is protective in high-risk women (i.e. BRCA1/2 carriers) as well. Hysterectomy has also been shown to reduce EOC risk, although the magnitude of the association is not as great nor as consistent as that reported for tubal ligation (Riman et al. 2004). Finally, reproductive factors associated with other hormonally linked cancers, such as age at first menarche, age at menopause, and length of reproductive years, have not been consistently associated with EOC (Riman et al. 2004).
Now this month comes exciting news about a Paradigm Shift: Prophylactic Salpingectomy for Ovarian Cancer Risk Reduction Frontline Medical News, 2014 Sep 24, Removing the fallopian tubes at the time of pelvic surgeries as a potential means of reducing ovarian cancer risk appears to be a movement that’s picking up steam in clinical practice.
A recent survey of 234 U.S. gynecologists showed prophylactic bilateral salpingectomy is catching on when performed in conjunction with hysterectomy, but far less so for tubal sterilization, Dr. Austin Findley observed at the annual Minimally Invasive Surgery Week. A total of 54% of respondents indicated they routinely perform salpingectomy at the time of hysterectomy in an effort to reduce the risk of ovarian cancer as well as to avoid the need for reoperations. However, only 7% of the gynecologic surgeons said they perform salpingectomy for tubal sterilization, even though 58% of respondents stated they believe the procedure is the most effective form of tubal sterilization (J. Minim. Invasive Gynecol. 2013;20:517-21).
“In my experience at various hospitals, I think these numbers are a pretty accurate reflection of what folks are doing,” commented Dr. Findley of Wright State University in Dayton, Ohio.
The prophylactic salpingectomy movement is an outgrowth of the tubal hypothesis of ovarian cancer.
“There is now increasing and dramatic evidence to suggest that most ovarian cancers actually originate in the distal fallopian tubes. I think this is a concept most people are unaware of or are just becoming accustomed to. The tubal hypothesis represents a major paradigm shift in the way we think about ovarian cancers. The previous belief that excessive ovulation is a cause of ovarian cancer is no longer regarded as accurate,” he explained at the meeting presented by the Society of Laparoscopic Surgeons and affiliated societies.
Ovarian cancer is the No. 1 cause of mortality from gynecologic malignancy, accounting for more than 14,000 deaths per year, according to National Cancer Institute data. The lifetime risk of the malignancy is 1.3%, with the average age at diagnosis being 63 years.
Only 10%-15% of ovarian cancers occur in women at high risk for the malignancy because they carry a BRCA mutation or other predisposing gene. The vast majority of ovarian cancer deaths are caused by high-grade serous tumors that have been shown to be strongly associated with precursor lesions in the distal fallopian tubes of women at low risk for the malignancy.
There is no proven-effective screening program or risk-reduction method for these low-risk women. However, with 600,000 hysterectomies and 700,000 tubal sterilizations being performed annually in the United States, prophylactic salpingectomy has been advocated as an attractive opportunity to potentially reduce ovarian cancer risk. Other common pelvic surgeries in which it might be used for this purpose include excision of endometriosis and laparoscopy for pelvic pain. It also has recently been shown to be feasible and safe post partum at cesarean or vaginal delivery (Obstet. Gynecol. 2014 [doi: 10.1097/01.AOG.0000447427.80479.ae]).
But the key word here is “potentially.” It must be emphasized that at present the ovarian cancer prevention benefit of prophylactic salpingectomy remains hypothetical; in theory, the procedure should reduce ovarian cancer risk, but there is not yet persuasive evidence that it actually does, Dr. Findley emphasized at the meeting, presented by the Society of Laparoendoscopic Surgeons and affiliated societies.
In contrast, one well-established ancillary benefit of prophylactic salpingectomy is that it eliminates the need for future reoperation for salpingectomy. This was demonstrated in a large Danish cohort study including close to 10,000 women undergoing hysterectomy and a similar number undergoing sterilization procedures. Among the nearly two-thirds of hysterectomy patients who had both fallopian tubes retained, there was a 2.13-fold increased likelihood of subsequent salpingectomy, compared with nonhysterectomized women.
Similarly, Danish women who underwent a sterilization procedure with retention of the fallopian tubes – typically tubal ligation with clips – were 2.42 times more likely to undergo subsequent salpingectomy, most often because of the development of hydrosalpinx, infection, ectopic pregnancy, or other complications (BMJ Open 2013;3 [doi:10.1136/bmjopen-2013-002845]).
The most commonly cited potential risk of prophylactic salpingectomy – decreased ovarian function – now appears to be a nonissue. This was demonstrated in a recent retrospective Italian study (Gynecol. Oncol. 2013;129:448-51) as well as in a pilot randomized controlled trial conducted by Dr. Findley and his coworkers (Fertil. Steril. 2013;100:1704-8), which appears to have answered many skeptics’ concerns. Indeed, Dr. Findley’s coinvestigator Dr. Matthew Siedhoff said he has recently been approached by researchers interested in collaborating in a larger confirmatory randomized trial, but all parties eventually agreed it was a no-go.
“It’s a little hard to demonstrate equipoise for a larger randomized controlled trial. We’re beyond that now, given that prophylactic salpingectomy really doesn’t seem to make a difference as far as ovarian function,” according to Dr. Siedhoff, director of the division of advanced laparoscopy and pelvic pain at the University of North Carolina, Chapel Hill.
Another oft-expressed reservation about salpingectomy as a means of reducing ovarian cancer risk in women seeking sterilization is that salpingectomy’s irreversibility may lead to “tubal regret” on the part of patients who later change their mind about further pregnancies. However, Dr. Findley cited a recent editorial whose authors criticized colleagues who made that claim. The editorialists argued that the tubal regret concern indicates surgeons weren’t really listening to their patients’ true desires during the informed consent conversation.
“We should not have started thinking about salpingectomy for female sterilization only once a decrease in ovarian cancer risk became part of the equation,” they declared (Obstet. Gynecol. 2014;124:596-9).
Dr. Findley noted that Canadian gynecologists are leading the way forward regarding prophylactic salpingectomy as a potential method of ovarian cancer prevention. The Society of Gynecologic Oncology of Canada in a 2011 policy statement recommended patient/physician discussion of the risks and benefits of bilateral salpingectomy for patients undergoing hysterectomy or requesting permanent sterilization. The Society of Gynecologic Oncology followed suit with a similar clinical practice statement in late 2013.
Additionally, the Canadian group declared that a national ovarian cancer prevention study focused on fallopian tube removal should be a top priority.
Gynecologic oncologists in British Columbia recently reported the eye-catching results of a province-wide educational initiative targeting gynecologists and their patients. In 2010, all British Columbia gynecologists had to attend a course on the role of the fallopian tubes in the development of ovarian cancer, during which they were advised to consider performing bilateral salpingectomy for ovarian cancer risk reduction.
Surgical practice changed dramatically in British Columbia in response. In 2009 – the year prior to the physician education initiative – salpingectomy was utilized in just 0.3% of permanent sterilization procedures. In 2010, it was 11.4%. By 2011, it was 33.3%.
Similarly, only 7% of hysterectomies performed in British Columbia in 2009 were accompanied by bilateral salpingectomy. This figure climbed to 23% in 2010 and jumped further to 35% in 2011. Meanwhile the rate of hysterectomy with bilateral salpingo-oophorectomy remained steady over time at 44% (Am. J. Obstet. Gynecol. 2014;210:471.e1-11).
This project was conducted in collaboration with the B.C. Cancer Agency, which maintains comprehensive province-wide registries. Over time, it will be possible to demonstrate whether prophylactic salpingectomy is indeed associated with a reduction in the incidence of ovarian cancer. “I think this study demonstrated that there’s a lack of awareness on this issue, but also [that there’s] potential effectiveness of introducing an educational initiative like this in changing our practice patterns. As we start talking more about this issue amongst our colleagues and our patients, we’re more likely to see a practice pattern shift in the United States as well,” Dr. Findley commented.
Danish Universities prospectively document the incidence of ovarian cancer OvCa in a million postmenopausal women PMW from 1995 through 2005. Compared to non-users, use of HT increased OvCa (mean age 62yrs) by about 40% for up to 2 years after stopping Ht, ie increased the absolute incidence of clinically diagnosed OvCa from ~ 0.04 to ~0.052% ie per 100 patient yrs.
Transdermal TD ET alone increased risk by 13%; vaginal ET by 23%; Oral ET alone increased risk by 34%; oral E+ progestin Pg by 48%; TDE+Pg by 67%.
Thus the relative incidence of OvCa rose about 33% by 7 years on HT, to 48% if HT continued beyond 7years.
In 2004 Glud ea reported an increase risk of 31% for OvCa in Danish women on OHT use – total ET dose of ~5gm ie for about for 15yrs – at a time when the standard premarin dose was 0.625mg/d (equivalent to l mg E2) if not double that .
For perspective, the relative incidence of cancers in similar mostly 1st world European women from the the USA SEER data for 2006 age over 50 years are: BrCa 0.33%, uterus 0.07%, ovary o.03%(ie very similar to the baseline Danish figure of 0.04% above), colon 0.15%,and cervix 0.01%. The new (Norwegian) analysis in the latest BMJ suggests that screening mammography may result in overdiagnosis of BrCa by up to 50% (the other 50% may arguably never have been clinically significant-diagnosed- during life) , so the provocative could argue that the relative incidence of clinically significant BrCa to OvCa is more like eg BrCa 0.2 to ovary 0.03 ie just below 10:1. But OvCa is notoriously about 70% fatal within a few years, so the absolute mortality rate – at age 60-64yrs- from the same SEER source and period are as relevant: BrCa 0.063%, uterus 0.011%, ovary 0.033%, colon 0.03% & cervix 0.005%. ie new OvCa may be only 1/10th as common as newBrCa, but BrCa kills only twice as many PMW as OvCa.
And finally the 2007 survey by Rossing ea of Menopausal Hormone Therapy and Risk of Epithelial Ovarian Cancer in women in Washington State 2002-2005 showed that ET -mostly premarin (but not ET + progestin- MPA medroxyprogesterone provera) – especially in low-parity younger slim women increased OvCa compared to non-users, and that this risk was highest- up to 90%- in users of OET for more than 6 years.
By comparison – BREAST CANCER BrCa and HT: Hoover ea 1976 are the first on Pubmed to report doubling in risk of breast cancer BrCA after 15yrs on premarin in USA ie at least 5gm cumulative dose.
In Denmark by 1994 Ravn ea reported that if there was a risk of BrCa from OHT, it was small, and only after prolonged use of estrogen (15-20 years). But by 2004 -2005 Tjønneland ea , Stahlberg ea and Ewertz ea found increased risk for BrCa of 61 to 112% associated with current use of HT. Stahlberg ea already in 2003 concluded from recent studies from both the USA and Europe that the combined treatment regimens with estrogen and progestin increase the risk of BrCa beyond the risk of unopposed estrogen.
In Norway, a recent Tromso study suggested that the dominant HT therapy used in Norway was oral estradiol E2 plus the progestin norethisterone acetate. . An earlier Tromso study in only 35000 PMW was too small- it showed that use of such OHT for >5yrs trebled the incidence of breast cancer BRCa, but did not influence that of OvCa.
Apart from smokers’ lung cancer, the commonest cancer in older women- BrCa- clinically affects perhaps 5% of PMW lifelong – but with prompt therapy after clinical presentation kills as few as 5% of sufferers- and with appropriate OHT (premarin +- provera) for up to 8years in the Women’s Health Initiative both the incidence of and mortality from BrCa, and all-cause mortality, were reduced by about one-third. Hence appropriate HT saves many from both BrCa and from premature death and disability from the commonest degenerative diseases- vascular, dementing and fracturing. 75% of women who develop BrCa die with it – not from it but from far more prevalent degenerative diseases after an otherwise normal lifespan. But the Danish evidence is that combined OHT will increase OvCa by >50%.
Ovarian Ca kills 70% of victims, and is it so rare compared to BrCa? .
Hence with the perhaps 2/3 lower incidence of OvCa, it is a relatively trivial problem for women overall- except for the 4 in 10 000 women who develop it, who have <50% 5year survival, ie 3 out of 4 of whom it will kill within a few years- compared to <25% of breast cancer victims who will be killed by the BrCa.
However, it becomes clear that these hormone-dependent cancers are both duration- and total-dose HT related; but even more important, that unopposed OET is a risk if persisted more than about 12 yrs; and even if used in far lower dose parenterally, the risk of OvCa is far higher if combined with the European fashion of androgenic synthetic progestins Pg – even parenterally; whereas the American MPA for up to 8years at least apparently if anything mitigates the OvCa risk of ET..
By contrast this column has repeatedly reviewed evidence that balancing physiological ERT with physiological testosterone replacement TRT eliminates the risk for BRCA and endometrial cancer of unopposed ERT +- PRT in PMW. Intuitively this should also apply to ovarian cancer.
Hence the message strengthens that PMW should not be exposed for any length of time at any stage to the much higher oro-hepatic HT doses (needed for symptom control) or OET+- Pg; but as in all other endocrine replacement for permanent multisystem prevention – let alone sexual function- patients with gonadal deficiency should have physiological sexhormone balance restored ie with balanced parenteral human androgen, estrogen and progesterone replacement.
It is common cause that (reproductive cycles and pregnancy aside) all the physiological prime sex hormones-DHEAdehydroepiandrosterone, P4, T, E2, E3 – are as important as all other human hormones, essential life long for optimal health; and that estrogen dominance (due to inadequate androgen and progesterone levels) is deleterious. Hence most PMW require both physiological progesterone and androgen replacement- sometimes to balance excessively high endogenous estrogens, usually to accompany necessary ERT for full balance.
The linked bad nutritional -and lifestyle – choices – Salt-Stroke – smoking- – hypertension- obesity – diabetes – heart – kidney disease – are quoted by S.A. Stats 2010 from death certifications as rising to 24% of deaths after age 50 years, leading even infections at 20% as the commonest causes of seniors’ death in South Africa. Nonnatural causes ie violence account for only 5%, and cancers only about 4%.
UPDATE 10 January 2014: PROTOS SUSPENDED -another snakeoil bites the dust- strontium ranelate. It has apparently never been registered in USA anyway.
Miriam E. Tucker
This does not affect the physiological use of natural strontium salts as one of a score of natural bone anabolic elements along with the other essential minerals, vitamins proteins and hormones in our Milieu intérieur .
update 11 Dec 2010
once again, a relevant comment from a reader (qv Doris Bevans below) prompts an update- and a title revision. The risk is not strontium, but the patent designer drug Protos/Proteos /Protelos – strontium ranelate- ie as this column has stressed from the start, it appears to be the synthetic anion ranelate that is the problem, not the metal cation strontium. This is similar to the sodium situation, where it is the anion chloride in table salt that is mostly the hypertension- fluid retention problem, not sodium.
These strontium comments by users mostly generalize- as this review has- about strontium . But of course as a useful comments website shows, there are many natural salts of strontium in use.
The focus of this strontium review column the past three years has naturally been on the potentially hazardous designer patent drug Proteos, Protos, Protelos strontium ranelate StRan – for which there is absolutely no need considering the numerous perfectly safe and multisystemically far better alternatives.
Perusal of Google makes it obvious that StRan is not a natural salt- in fact there is no mention of ranelic acid or strontium ranelate (Sr2SN2O8) until some 20 years ago when someone first created it- to enable patenting of a strontium salt for osteoporosis. Imagine how long industrial chemists must have schemed to find a new molecule to carry the useful strontium cation? But the story has apparently yet to be revealed on the internet. One can only speculate why the story of it’s invention has not been put on the internet.
But the common earth metal strontium was already ‘discovered’ over 200 years ago – in Scotland- and has numerous industrial uses as diverse natural salts. Ward Dean MD points out that strontium salts have been used medicinally for well over a century- against osteoporosis but especially painful cancer in bone, against dental caries and arthritis; with the optimal dose apparently around 600mg strontium a day. Usefully, this is about the same optimal dose as calcium, since as Dean says “a comprehensive regimen of synergistic bone-enhancing substances should provide the optimum regimen for preventing and treating osteoporosis. We know that obviously the optimal regime includes appropriate sex hormones.
So far there are at least twelve agreed biologically valuable metal(oid)s ie cations for humans: sodium, potassium, calcium, magnesium, iron, zinc, copper, boron, manganese, chromium, molybdenum, chromium, vanadium, cobalt; and arguably lithium, gold, silver, silica and nickel.
However, no-one has yet shown that strontium is an essential (trace) element like the recognized lighter metals.. .
But just as lithium salts were recognized to have major multiple medicinal benefits within 50 years of discovery ( by the mid 19th century), natural strontium salts have been recognized and promoted as useful for osteoporosis prevention and management since at least Shorr and Carter 1950 .
And of course the designer StRan has still not been registered for use in the USA. The detailed data sheet for strontium ranelate warns chillingly of its deadly risks of venous thromboembolism and dermatitis; that it contains phenylalanine; and that it confounds calcium level measurement.
So the glowing testimonials by consumers to the benefits of strontium salts in USA can only be from the use of natural strontium salts there, unless Protos/Proteos was brought into that country by patients.
And indeed, there do not appear to be any adverse effects to natural strontium salts used in sensible dose the past century.
Rousselet ea showd already in 1975 tight feedback regulation between calcium, strontium and vitamin D: “Oral administration of strontium to calcium wellfed rats blocks intestinal absorption of calcium. When high doses of vitamin D are given over long period, the inhibition of calcium intestinal absorption disappears. Under these conditions the absorption of strontium is increased. It is suggested that there is only one absorption mechanism for these two cations. An overdose of vitamin D increases the renal elimination of strontium but under these conditions the plasma concentration of the strontium is unchanged. Vitamin D brings about the same action on bone fixation of the strontium as it does on bone fixation of calcium. Bone fixation is increased with low dosages, decreased with high dosages.”
So like lithium and silica, there is no apparent reason not to use moderate doses of natural strontium salts orally in supplements.
Phosphates are indeed , like zinc and copper , calcium and magnesium, biologically essential in the right balance. It looks like strontium may be the same. . But that doesnt make the synthetics bisphosphonates or strontium ranelate safe- indeed they may cause deadly complications. So why risk them when the only winner is the manufacturer?
And this time the FDA has been wise to deny registration of StRan. As a designer drug it is not in the category of lithium and metformin, enormously beneficial drugs in recommended doses which the FDA denied without reason to Americans for at least 20years, (except could it have been to protect their own drug company profits?) costing vast numbers of lifeyears and lives.
Hence in future correspondents praising strontium need to state what form of strontium they are taking.
update 14 November 2010
Crystal comments today: “My mother has taken strontium Sr for the past 2 years and her bone density from her last bone scan has improved greatly. I am a believer!
Assuming you are talking about the topic of this column- strontium ranelate- is that great? I am also a believer in faith and prayer; but faith doesnt prove anything objectively, in fact it still leaves billions starving and in abject poverty, and all of us in major jeopardy from mankind’s madness, greed and ruthlessness .
If doctors rely on faith, prayer and Big Pharma, regulators- not critical evidence, common sense and experience – heaven help Mom, all patients.
Improvement in bone density doesnt translate into longterm benefit, healthy longevity. What real benefit is strontium ranelate having for Mom, on fracture rate, muscle ie strength, and all other aging systems?
The biggest risk for osteoporotic fracture is not low DXA bone density (a very profitable designer hi-tech technology that irradiates patients totally unnecessarily) but failing muscle, co-ordination, balance- for which strontium apparently does nothing. Overall, the top disablers and killers of old age are not fractures but vascular disease, cancer, dementia, strokes. At no age do fractures appear in the top 10 causes of death in the USA.
And there is still no evidence of StRan’s longterm SAFETY- in fact the potential risk of the DRESS syndrome makes strontium ranelate contraindicated when the proven safe more-than-twenty natural proven bone multinutrients that greatly improve all systems are so effective and available.
Why take a snakeoil designer drug like Proteos when natural works both better and safer?
Look at how bisphosphonates improve bone density- but at terrible multihazard risk of later disaster – teeth and jaw loss, fractures from harder but more brittle bones, skin & gullet complications.
Why risk strontium ranelate’s “memory loss and diarrhoea during longer-term treatment” (Deeks ea 2010), or venous thromboembolism (Osborne 2010) . And in a massive study, Guerra-Garcia ea 2010 have just shown that over the 5 years 2004-2008 in 12 000 patients, the prescription of StRan has risen 10fold and bisphosphonates 50%- but without reduction in the incidence of hip fracture.
Yet the current Wiiki entry on strontuim ranelate still omits the horrendous risk of the DRESS syndrome; and still tells the lie that the drug reduces hip fractures by a third. Presumably the StRan manufacturer Servier uses Wiki as its carefully sanitized advertorial.
Focusing just on medium-term fracture benefit (up to 5-10years) and ignoring all-system benefits and risks, is absurd negligence- the criminal deception practiced by Big Pharma and blissfully ignored by the FDA and the leading journals and “expert reviewers” who depend on big pharma’s handouts .
Appropriate natural supplements reduce premature ALL-CAUSE disease and deaths by almost half.
If you are taking StRan, you and your doctor have conned yourselves, as intended by Big Pharma, ( the Disease Industry and the Governments- politicians- who are well paid to support their Disaster Capitalism ) . Only Disease Pays. And worst of all, they have conned you into taking potentially lethal costly poison that does overall no good. Has anyone checked her height, her spinal xray, her memory, bloodpressure, carotid calcification, kidney function to show that these markers havent deteriorated despite StRan?
update: 22 Dec 2009: on this radiant southern summer solstice day, there is no good news on strontium ranelate because no new trials have been published in the past 19 months.
In their Cochrane Review of 2006, Reginster ea could find just 4 trials of strontium ranelate for 3 to 4 years ; these showed 37% fewer spinal fractures but only 14% fewer non-spinal fractures -results no-where near as good as with safe lowcost multisystem protection with appropriate non-oral human estrogen and testosterone, and vigorous dose of a blend of calmag boron zinc manganese, proline, the vitamins B6-9-12, C, D and K .
And as with SERMS eg tamoxifen, and bisphosphonates, why use StRan for osteoporosis when there is better safer natural multisystem prevention and treatment? Severe complications may be rare (<1 in 10,000 cases) but as reported by Reginster ea, except for the profit of manufacturers, why risk life-threatening reactions? – Stevens Johnson syndrome (SJS) and TEN toxic epidermal necrolysis with bisphosphonate, but with StRan TEN syndrome, and DRESS – angioedema, drug rash with eosinophilia and systemic symptoms (DRESS), let alone renal failure and alopecia..
Again, Prescrire sums it up: “Strontium: confusion and hallucinations. Do not use strontium”. We now acknowledge this should read strontium ranelate.
Only the crazy or the malicious would recommend aspirin or designer anti-inflammatory drugs (with their major risks) for mild to moderate pain when paracetamol or, better, a simple safe mix of natural anti-inflammatory-analgesics would suffice eg MSM-curcumin-pantothenate-catsclaw-bromelain-boswelia.
Osteoporosis occurs mostly in the elderly ie those at far higher risks- osteoporosis is a late sign of multisystem deficiency risks, with patients far more likely to die from the concomitant other degenerative diseases – frailty, vascular, malignant, dementing- than from fractures . So it is criminal to delay effective prevention till osteoporosis is present, then prescribe risky drugs like SERMS, bisphosphonates or StRan when far more multisystem effective and safe therapy has long been available and proven.
22 May 2008
The promotion of essential micronutrients like sex hormones, vitamins and minerals for multisystem health including bones is vital.
But what evidence for longterm cost:benefit is there for strontium ranelate StRan for anything let alone bones?
A warning was published in 2005 (Prescrire Int. ) Strontium: new drug. Postmenopausal osteoporosis: too many unknowns. [No authors listed]). . No new trials have appeared since. .
There is in fact only one solitary major trial published of sodium ranelate SrR in osteoporosis, the SOTI-TROPOS trial by Reginster, Meneur ea for the strontium ranelate SrR manufacturers (Servier) at 72 centers in 11 European countries and Australia, in some 5000 postmenopausal women recruited from 1996 through 1998 ie till about 2003, with either previous postmenopausal fracture or frank osteoporosis: All on 1 to 1.5gm calcium and vitamin D 400-800iu/day, they were randomized to placebo or StRan 2gm/day. After a mean of 3 years, compared to placebo, vertebral fractures in 1442 women at a mean of 69yrs were reduced by 49% from baseline , but in the entire cohort nonvertebral fractures were reduced by only 16% from baseline at mean age of 77yrs.. All fractures were reduced from 12.9% to 11.2% ie 4.3%pa to 3.7%pa; hip fractures from 3.4% to 2.9%, vertebral fractures from 14% to 7.7%.
Are these differences significant for patient care, when the longterm effects of StRan therapy are unknown, and the longterm adverse effects of biphosphonates are becoming horrifically clear?
But these trials of StRan used only weak baseline prevention of lowdose calcium and vitamin D . Numerous other preventative bone-and muscle-strengthening supplements were apparently specifically excluded or omitted – magnesium, estrogen. vigorous-dose vitamin D eg 2000iu/d, vitamin K, androgen, boron, zinc.
And like the concurrent Womens’ Health Initiative, the SOTI-TROPOS trial was stopped woefully too soon instead of letting it run for at least 10 years to see the longterm benefit (if any). Worst of all, it did not test whether StRan adds any benefit on a sensible baseline of all the proven supplements that we have used for decades.
As Winzenberg ea ask in a recent 2007 Australian review, Strontium ranelate Does it affect the management of postmenopausal osteoporosis? Strontium ranelate did not cause gastritis, back pain or death, but more or less doubled numerous adverse effects :
*50% more (ie six out of 100 women taking strontium ranelate) experienced diarrhoea compared to four out of 100 taking placebo,
• The risk of vascular system disorders including venous thromboembolism (two trials, n=6669, 2.2 vs. 1.5%, OR: 1.5, 95% CI: 1.1–2.1) , pulmonary embolism (two trials, n=6669, 0.8 vs. 0.4%, OR: 1.7, 95% CI: 1.0–3.1) * as well as nervous system disorders such
as headache (3.9 vs. 2.9%), seizures (0.3 vs. 0.1%), memory loss (2.4 vs. 1.9%) and disturbance in consciousness (2.5 vs. 2.0%) is
slightly increased with taking 2 g of SrR daily over 3–4 years
• There were no RCTs identified which compared StRan to other treatments of postmenopausal osteoporosis.”
It is common cause that the chief risk factor for fracture is not bone density but frailty, falls; and that the only microsupplements that strengthen muscle are apparently androgen, zinc, calcium and magnesium and the vitamins D3 and B6, 9 and 12. There is no absolute contraindication to appropriate long term human androgen plus estrogen replacement .
Now Fuchs ea show that “Strontium ranelate does not stimulate bone formation in ovariectomized rats” – sex hormones are necessary for strontium to benefit bones.
With the oldfashioned calmag, zinc, boron, fluoride ,vitamins A-E, and parenteral androgen plus estrogen, we have seen bone density rise by 1%pa and hip density by 1/2% pa over 15years from age 52 in a frail woman with severe rheumatoid arthritis, despite management with corticosteroid and other remittive drugs, and repeated surgeries to replace destroyed joints. She has never sustained an osteoporotic fracture.
So what is the indication to add the costly long-term (ie >10year) unproven strontium to proven effective supplements?
Strontium ranelate may work in the medium term (3 to 5 years) but there is still apparently no more justification for using strontium ranelate routinely for preventing/ treating ageing osteoporosis than there is for biphosphonates or calcitonin.