Category Archives: menopause



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  .

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, B Jancin

   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).             

     Reproductive disorders and other reproductive factors :  Factors affecting childbearing have also been shown to be associated with EOC. In most studies, infertility has been associated with an increased risk, which may be greatest among women who fail to conceive (Vlahos et al. 2010). In general, infertility treatment does not appear to increase EOC risk, although the subset of treated women who remain nulliparous may be at an increased risk (Vlahos et al. 2010).

         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).

    Estrogens and androgens –  The evidence linking these  to EOC are mixed. The majority of women who develop ovarian cancer are postmenopausal at the time of diagnosis. In postmenopausal women, the major source of circulating estrogen is from the peripheral conversion (in skin and adipose tissue) of androstenedione by the enzyme aromatase.

    Progesterone and progestins- Epidemiological data suggest that progestins and progesterone may have a protective role against EOC. Importantly, there is some evidence that progesterone might synergize with chemotherapeutic drugs to induce apoptosis.

Now this month  comes exciting news about  a  Paradigm Shift: Prophylactic Salpingectomy for Ovarian Cancer Risk Reduction   Frontline Medical News, 2014 Sep 24, B Jancin     :   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/]).
   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.

17 July 2009     A new cancer study of  over 7 million women years is another major coffin for unopposed estrogen ET, for progestin Pg, and for oral  sex hormone therapy SHT.

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.



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.


  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


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.


20 July 2014 HIGH CARBS OR LOW CARBS?  THE BIG FAT SURPRISE  – which is best for weight loss?  a collaborative literature metanalysis study  July 2014 by Naude ea the universities of Stellenbosch, Cape Town and Liverpool (UK)  claimed to compare the effects of low CHO and isoenergetic balanced weight loss diets in overweight and obese adults,  stratified by outcomes at 3-6 months and 1-2 years.  Of nineteen trials  (n = 3209), 3 had adequate allocation concealment. In non-diabetic participants, analysis showed little or no difference in mean weight loss in the two groups at 3-6 months (MD 0.74 kg) or  for blood pressure, LDL, HDL and total cholesterol, triglycerides and fasting blood glucose. In diabetic participants, findings showed a similar pattern.  CONCLUSIONS: Trials show weight loss in the short-term irrespective of whether the diet is low CHO or balanced. There is probably little or no difference in weight loss and changes in cardiovascular risk factors up to two years of follow-up when overweight and obese adults, with or without type 2 diabetes, are randomised to low CHO diets and isoenergetic balanced weight loss diets.

‘But  Noakes points outLow-fat, high-carb, high-sugar diet a likely cause of obesity/diabetes  “I refer to the report in the Cape Times of July 10,  “Noakes’s popular low-carb diet is not healthier, better for weight loss – study “. Since the authors of that study (Naude ea) do not understand either what constitutes a low-carbohydrate diet or the unique biological effects of such diets, they were predisposed to produce a biased report that comes to exactly the wrong conclusion.

‘First, the conclusion of their study was predictable since the authors chose to review only studies in which subjects ate the same number of calories on both diets. It is not clear how the authors conceived that diets that provided exactly the same number of calories would produce different outcomes. Indeed, a core teaching of these nutritional scientists is that the degree of weight loss is determined by the reduction in calorie consumption. Thus the authors knew the outcome of their study even before they undertook it. This is not good science.

‘Second, the studies included in their meta-analysis are not of the low-carbohydrate diet described by either Dr Robert Atkins or ourselves in Real Meal Revolution. Dr Atkins realised in the 1970s that the majority of overweight/obese persons can only reduce their weights successfully, and keep that weight off in the long term, if they eat less than 60g carbohydrate/day for the rest of their lives. Higher intakes are increasingly less effective. In Real Meal Revolution we stress that those with insulin resistance/ type 2 diabetes need to keep their carbohydrate intakes even lower, ideally to about 25g/day. The  “low-carbohydrate ” diets included in the meta-analysis provided a minimum of 200g carbohydrate/day (or 4-8 times higher than the carbohydrate content that is known to be effective). As a result this is a meta-analysis of studies providing a high, not a low-carbohydrate load for those with obesity/insulin resistance/type 2 diabetes.

‘Third, the extent of weight loss in the studies included in he meta-analysis is small, the greatest values being about 10kg. For most people with significant weight problems, such small weight losses are probably relatively meaningless and should be classified a diet failure, not a success. But freeliving persons who follow individually prescribed carbohydrate diets providing about 25g carbohydrate/day report quite remarkable degrees of weight loss, not infrequently up to 40-80kg, usually achieved effortlessly if the low-carbohydrate rules are followed.

‘Fourth, the unique biological effects of the properly-defined low-carbohydrate is that (i) It reduces hunger, allowing subjects to eat fewer calories without experiencing continual hunger. The point, as stressed by Dr Atkins, is that the low-carbohydrate diet is a low-calorie, no-hunger diet. (ii) The diet lowers blood insulin concentrations. In those with obesity/insulin resistance/metabolic syndrome, it is continually elevated blood insulin concentrations that cause ill-health (as clearly established by the work of Dr Gerald Reaven of Stanford University over the past 50 years).

‘The authors  found that health benefits were no different on either diet.    A number of properly designed, peer-reviewed meta-analyses of the real low-carbohydrate diets show that weight loss and health benefits are superior compared with higher-carbohydrate diets. Unfortunately, the authors appear to be ignorant of those studies since neither they nor your reporter refers to them. This implies the presence of bias, questioning the true intent of the report.

‘The report also includes the statement of the Heart Foundation of South Africa (HFSA) to the effect that a diet high in saturated fat causes heart disease. Unfortunately, the HFSA spokesperson appears unaware of Nina Teicholz’s recentbook, The Big Fat Surprise: Why Butter, Meat, Cheese Belong in Healthy Diet, and the  June 23 Time Magazine  Ending the War on Fat, which show that this dogma is false and is not based on any credible science.     It is  time  the HFSA updated its understanding of what actually causes heart disease. They might also want to consider whether their promotion of their unproven low-fat, high-carbohydrate, high sugar diet for the past 37 years is the most likely direct cause of the obesity/diabetes epidemic that has since engulfed South Africans.

‘Indeed on a practical side, I wonder if the authors have ever considered studying the dietary intakes of the obese diabetic patients they treat at Tygerberg and Groote Schuur hospitals. Do patients with these diseases eat either high- or low-carbohydrate diets? Why is is that these twin diseases, which are crippling the health services of the Western Cape, began to increase exponentially only after the 1977 Dietary Guidelines that institutionalised the low-fat, high-carbohydrate diets? Surely these are the critical questions that should really be exercising the minds of the Western Cape’s nutritional scientists? The best conclusion that can be drawn from this study is that diets providing more than 10 percent of daily calories in the form of carbohydrate are equally ineffective in producing meaningful degrees of weight loss in those with obesity/insulin resistance/type 2 diabetes.”

15 June 2014    DIET RISKS FOR BREAST CANCER, INFECTION & ALL ELSE:   Sugar? Fats? Vitamins?

already 30 years ago Seely and Horrobin in ‘Diet and breast cancer: possible connection with sugar consumption’ hypothesized: younger and older  (possibly pre- and post-menopausal )women differ with respect to such correlations. In older women a strong correlation was found between breast cancer mortality and sugar consumption (correlation coefficient = 0.9).. In younger women the correlation with diet is weak. A possible connecting link between sugar consumption and breast cancer is insulin. This is an absolute requirement for the proliferation of normal mammary tissue and experimental mammary tumours may regress in its absence. Insulin secretion occurs in response to blood glucose level and could be excessive if the regulatory mechanism is overtaxed by large sugar intake. The same mechanism might account for the increased risk of mammary cancer in diabetics.
  A  major decades-long Nurses’ Health  Study  review from Harvard shows no relationship between fat intake and breast cancer.
By contrast, studies from  Mexican  2004,  Canada 2005, Italy 2006 , and New York  2009 confirm direct association between sugar intake and breast cancer. . Only a study from Denmark 2005  shows no relationship.
Hence the HighFat LowCarbs (William Banting 1863) diet is now established by the rigorous scientific references of the past 150 years  assembled by science writer Gary Taubes in The Diet Delusion ,  and advised to all  for prevention and management of obesity and all other common major diseases including breast and all cancers.
      As investigative journalists write recently, like Taubes and rational scientists the past 50years,  the major cause of all common chronic degenerative disease including cancer and immunoincompetence is not fat but refined carbs – the root cause of the SACCHARINE DISEASES  that Cleave, Campbell, Burkitt reported occurring in pastoral tribes converting to the western commercialized diet of sugar, refined cereals and rice .                   They note that in the Mouse Cancer Study in cancer-prone mice,

Gemma Llaverias ea, Jefferson University, Philadelphia   2011,  which claimed that high (fat)cholesterol intake promotes breast cancer, the control mice  (not major carnivores but omnivores) were fed a balanced natural chow with 4.5% fat, 23% protein, and 50% carbohydrate, whereas the test mice were fed a totally synthetic chow meant to represent a western human  cholesterolemic  diet: 20% fat, 17% protein, and 48% carbohydrate. So in fact the high risk factor for cancer and all disease was not the higher fat intake (20%  as dairy fat) vs 4.5%- from fish meal and soy/cereals) but the 48% carbs (2/3  sucrose, 15% (malto)dextrins -which absorb as rapidly as glucose) intake and 19% casein (a major health problem)   in the test chow. They failed to include a control group on what is natural mouse diet ie free of refined carbs and milk :  RSPCA 2014:   Wild mice – opportunistic omnivores- will eat a wide variety of seeds, grains, and other plant material as well as invertebrates, small vertebrates and carrion“. Thus plenty of natural seed/grain fats and mixed protein and plant carbs,  zero sugar or refined carbs- ie the Banting diet. ..
A new 18year observational  followup  study from Sweden last year in 62000 people assessed total energy intake – carbohydrate  from median 61 to 39% , protein 11 to 19% , and  fat 27 to 42% . LCHP scores were positively related to intake of animal protein, but negatively related to plant protein. For carbohydrate and fat, associations were consistent in sucrose and whole grain and saturated and unsaturated fat, respectively. Across the range of macronutrients, there was no clear significant trend for particular cancers. This is not surprising as the intake of carbs ranged from 40 to 60% and fat from 27 to 42%. Thus no cohort was on a highfat low carbs ketogenic diet as Banting, Noakes  et al find successful. . the lowest % carbs group at best had similar fat % intake ie there was no low-carbs cohort taking below 30% carbs..There is a vast difference in calorie intake  between their “optimal’  LCHP 42:40 fat:carbs ie 1:1  , versus the  true ketogenic HifatLowcarbs diet of eg 50:<30 fat:carbs ie >1.66:1.
       Allowing up to 20% protein in total energy intake, for real weight loss- especially with insulin resistance- diet  fat needs to  be  >50% energy and carbs <30%, thus ensuring ketogenesis to shed excess fat and avoid depositing more glycogen and adiposity ; so eg for a tall fat person, thats  up to 80gms protein 320kcal mostly from flesh; carbs below 50gms 200kcal (  rainbow vegs) , and fat ~1480 kcal ie ~160gms from cream (not milk),   eggs, butter, cheese, avo, and fatty flesh; and mixed nuts cautiously due to their ~20% carbs content. .

It is no wonder the public is confused.

The truth of more than four decades worth of research is now very clear: the potential benefit of mammography screening is small and the harms are substantial at all ages, but especially so for women in their 40s.

The bottom line is that mammography screening, implemented to reduce breast cancer deaths due to earlier detection of breast cancer, has been eclipsed by therapy and increased awareness.

– See more at:

It is no wonder the public is confused.

The truth of more than four decades worth of research is now very clear: the potential benefit of mammography screening is small and the harms are substantial at all ages, but especially so for women in their 40s.

The bottom line is that mammography screening, implemented to reduce breast cancer deaths due to earlier detection of breast cancer, has been eclipsed by therapy and increased awareness.

– See more at:


VITAMIN C  each 100mg/day increment reduces allcause mortality by 27%, and breast cancer mortality by 22%:   a metaanalysis by the Karolinska- Harris ea   last month found 10 trials of vitamin C use and intake  in breast cancer, included 17,696 breast cancer cases, 2791 total deaths, and 1558 breast cancer-specific deaths. The summary RR (95% CI) for post-diagnosis vitamin C supplement use was 0.81 (95% CI 0.72-0.91) for total mortality and 0.85 (95% CI 0.74-0.99) for breast cancer-specific mortality. The summary RR for a 100mg per day increase in dietary vitamin C intake was 0.73 (95% CI 0.59-0.89) for total mortality and 0.78 (95% CI 0.64-0.94) for breast cancer-specific mortality- ie 25% lower mortality for every 100mg higher daily vit C intake..

Johnston CS1,ea., Arizona State University.            The early indications of vitamin C deficiency are unremarkable (fatigue, malaise, depression) and may manifest as a reduced desire to be physically active; moreover, hypovitaminosis C may be associated with increased cold duration and severity.. Healthy non-smoking adult men (18-35 years; BMI < 34 kg/m2; plasma vitamin C < 45 µmol/L) received either 1000 mg of vitamin C daily (n = 15) or placebo (n = 13) in a randomized, double-blind, eight-week trial. In the final two weeks of the trial, the physical activity score rose modestly for the vitamin C group vs. placebo after adjusting for baseline values: +39.6% p = 0.10). The number of participants reporting cold episodes was 7 and 11 for the vitamin C and placebo groups respectively during the eight-week trial (RR = 0.55;  p = 0.04) and cold duration was reduced 59% in the vitamin C versus placebo groups (-3.2 days; 95% CI [-7.0,0.6]; p = 0.06). These data suggest measurable health advantages associated with vitamin C supplementation in a population with adequate-to-low vitamin C status.

A 49-year-old man presented to hospital with severe orthostatic hypotension, gingival dysplasia and a purpuric rash involving his extremities. The orthostatic hypotension failed to respond to fluids and, on the basis of physical examination and dietary history, the patient was given a preliminary diagnosis of scurvy (ascorbic acid deficiency). Serum ascorbic acid levels were undetectable and the orthostasis resolved within 24 h of ascorbic acid replacement. The pathogenesis of orthostatic hypotension in the setting of scurvy appears to involve impaired catecholamine synthesis and attenuated vasomotor response to α-adrenergic stimulation. We believe that this case describes a rare presentation of scurvy and highlights a previously under-reported connection between scurvy and vasomotor instability.         

Br J Community Nurs. 2013 Suppl:S6, S8-11.Vitamin C: a wound healing perspective.   Moores JVitamin C, also known as ascorbic acid (AA), is involved in all phases of wound healing. In the inflammatory phase it is required for neutrophil apoptosis and clearance. During the proliferative phase, AA contributes towards synthesis, maturation, secretion and degradation of collagen. Deficiencies affect the maturation phase by altering collagen production and scar formation. The body strives to maintain homeostasis of AA, thereby ensuring availability for collagen synthesis. After wounding, plasma and tissue levels of AA diminish and, as a consequence, supplements may be useful for healing, although levels beyond saturation are excreted. Clinicians need to be aware of both the nutritional status of patients with either acute or chronic wounds and the possibility of any AA deficiency which may hinder healing.
Nat Commun. 2013;4:1881. Mycobacterium tuberculosis is extraordinarily sensitive to killing by a vitamin C-induced Fenton reactionVilchèze C1,ea .Einstein College New York.  Drugs that kill tuberculosis more quickly could shorten chemotherapy significantly.  we show that vitamin C, a compound known to drive the Fenton reaction, sterilizes cultures of drug-susceptible and drug-resistant Mycobacterium tuberculosis, the causative agent of tuberculosis. While M. tuberculosis is highly susceptible to killing by vitamin C, other Gram-positive and Gram-negative pathogens are not. The bactericidal activity of vitamin C against M. tuberculosis is dependent on high ferrous ion levels and reactive oxygen species production, and causes a pleiotropic effect affecting several biological processes. This study enlightens the possible benefits of adding vitamin C to an anti-tuberculosis regimen and suggests that the development of drugs that generate high oxidative burst could be of great use in tuberculosis treatment.
20 years  ago Newmark from Sloan Kettering NY wrote :  High dietary fat increases mammary epithelial cell proliferation, particularly the “hormonally driven” hyperproliferation during breast growth and development in young animals. Increased dietary calcium (and probably vitamin D) lessens the increase of proliferation induced by high fat. These data, although limited, suggest that the maximum effect of diet (high fat increase, as well as calcium and vitamin D modulation) on eventual breast cancer may be during puberty, and adolescence, when the mammary gland is actively growing and developing. (3) An inverse epidemiological correlation exists between sunlight availability as a source of vitamin D and the risk of breast cancer in the U.S. and Canada. (4) Current vitamin D and calcium dietary intake in the U.S. is far below the RDA in all female age groups, particularly for the elderly. (5) Reduction of breast cancer risk, and simultaneously osteoporosis, might be achieved by increasing dietary intake of calcium and vitamin D to RDA levels. This may be particularly applicable to females during puberty and adolescence.
                    20 years later we now still find:                 Vitamin D and Cancer: The promise not yet fulfilled(California) ; and is there a link (France)?

BUT The Vitamin D Council    sums up the study evidence eg in a major Brit J Cancer metaanalysis last month of 30 prospective studies in 32000 BRCA  patients, and a Chinese study a year ago,   show  that  those with highest  vitamin D levels have 50-90% lower risk of  breast cancer risk, and mortality, and the chance of breast cancer spreading.  so far all they can recommend is that  vitamin D dose should for a robust adult not exceed  10 000 iu/day, or pro rata at longer intervals eg 150 000iu a fortnight.  Compared to those with the lowest quartile of plasma 25(OH)D level, women with highest quartile 25(OH)D level showed a significant decreased breast cancer risk (Q4 vs.Q1: OR = 0.10, 95% CI = 0.06–0.15) and every 1 ng/ml increment of plasma 25(OH)D level led to a 16% lower odds of breast cancer.

         It is likely that- given the limits on vitamin C intake due to diarrhoea, and cost, and bloating-  increments in vit D3 intake well above the current mediocre antirachitic 400iu/d norm- up to the generally well-tolerated 10 000iu/day, (after a loading dose of 200 000 to 600 000iu).  with supplement of vitamin K2-  will give even better benefit against breast cancer than vitamin C.     


IT IS COMMON CAUSE THAT ONE DOESNT, CANNOT   PREVENT OR TREAT INFECTION BY POOR NUTRITION OR LOWDOSE ANTI- MICROBIALS- such policy is futile if not dangerous for breeding resistance as well as disease extension.   The studies below confirm the obvious, (as Klenner, Pauling,  Cameron ea showed the past 50 years with highdose vit C injection), that  vitamin D3 orally also works as a multiantimicrobial agent if given as early as possible in safe very high dose and bloodlevel eg 600 000iu monthly (in the first month, – in Salhuddin’s  Pakistan PTB patients (presumably also Sunni muslim) initially mean wt 45kg, thats vit D3 ~440iu/kg/d) for two doses ie a mean of 300iu/kg/day over 90days;   not the current preventative recommendation of 80iu/kg /day to a safe blood level of around 50-60ng/ml. As Holick has said, with adequate water intake  even 50 000iu vit D3 a day ie 1.5million iu/month for months causes no toxicity. Given the 40% mortality rate in the frail Saudi MERS patients, and in acute severe influenza and other serious viral infections, it can be expected that such  highdose immediate vitamin D3 therapy orally with eg 600 000iu, combined with highdose vitamin C, zinc and some multivite,  (never mind appropriate antibiotics in acute bacterial infection) will similarly virtually eliminate mortality.


But no KSA Govt website mentions this- except the Saudi Gazette a year ago which strongly urged vitamin D supplement in the KSA as even daily sun exposure does not bring most Saudi women above the vitamin D deficiency threshold. It says Since Muslim women can only reveal the hands and face, they may need to be out in the sun for longer than 30 minutes. But the review conspicuously  fails to mention that in public outdoors in KSA, women must have even the head and face covered. It also  propagates surprising  dangerous  nonsense that “severe deficiency needs monthly vitamin D injectionMom, have you taken your vitamin D injection this month?, when all it requires is an oral daily, weekly  or fortnightly  dose vitamin D3  at trivial cost.” It does stress  “One of the main reasons why vitamin D deficiency is so common in the Kingdom is because there are very few food sources of vitamin D. Foods which have fairly good amounts of vitamin D are fish liver oil, sweet potatoes, egg yolks, vegetable oils, butter, and fatty fish such as salmon, sardines, and tuna,” said Dr. Rasha Jameel, a consultant in family medicine at a local hospitalIn the United States, all milk and dairy products are fortified with vitamins A and D, but no such measures are in place in the Kingdom“.


This correlates with a new metaanalysis (in the  BMJ this month) of observational studies from Europe and USA, that all-mortality hazard ratio over a mean of 10 years  increases by 57% as vit D level falls from the highest to the lowest level. The KSA apparently chooses to ignore that, as this column reported recently from WHO data, despite  apparently being the wealthiest country per capita  of bigger populations  in the world,  KSA’s population life expectation is about 5 years lower than eg far less sunny Britain’s; ie KSA  all-cause mortality rate is avoidably materially higher. Despite KSA medical professors  having reported in studies  that most of the KSA population is deficient in vits D and C, the  KSA Govt website  chooses to ignore this on official websites;  unlike other even Middle-Eastern governments promoting vit D fortification or meaningful safe supplements costing trivial amounts.


Even a new study last year from KSA universities confirmed that ” Most commonly consumed food products by Saudi population which are supposed to be fortified by vitamin D are either not fortified or contain an amount less than  (apparently  from their table 2 ~ half of)  recommended by guidelines set for US marketplace”. Even a UAE authority recently stressed “Can fortified milk fight Vitamin D deficiency? Shockingly low levels of D3 among UAE population cannot be rectified by milk alone.” As Holick ea, including  a Turkish University 2010  trial report,  oral vitamin D3 is far more  effective , and safer than,   either vitamin D2, or vitamin D injection -never mind much cheaper. This current ostrich-head-in-the-sand denialism by the KSA government is like that of the RSA govt under Presidents Mbeki and Zuma 10-15 years ago about preventing and treating HIV-AIDS  – considering that the safe and beneficial daily intake of vitamin D3 is now universally recognized as 4000 if not 10 000iu/day (ie about 80iu/kg/day or pro rata up to perhaps fortnightly) , to a mean blood vit D  level of about 60 to 80ng/ml. .

As Prof Mike Holick pointed out a few years ago, “Even in Saudi Arabia, Qatar and South Africa, more than 50% of the population is deficient in vitamin D, all because of their avoidance of sun. Based on some of the literature, it seems that we could probably decrease health care costs across the board by 25% if everybody had optimal vitamin D status.” As Al Faraj ea reported in Riyadh in 2003,   Prof Zahid Naeem from a KSA university wrote in 2010,Vitamin D deficiency is an ignored epidemic in KSA  and globally“; confirmed by a KSA study by Ali ea in 2012: “Even in a sunny country like Saudi Arabia the prevalence of vitamin D deficiency in young female is high“..  One does not need to  speculate why the KSA and all governments globally choose to ignore this inconvenient truth,  downplay effective vigorous  vitamin C and D3 (sunshine) supplements-  such widespread vitamin D and C deficiencies, like cigarette smoking and alcohol abuse,   suit governments and Big Pharma-  the Disease Industry- in reducing populations growths and creating jobs for the highly profitable Disease Industry and it’s shareholders-   for whom Only Disease Pays. Cheap safe natural  Prevention Does not Pay since it at least halves sickness never mind disease industry jobs, taxes  and profiteering in the global $multitrillion Disease and Diet and Vaccine and Invasive Screening Industry scams.


And Karen Hansen ea at Univ Wisconsin 2014 have  just shown  that  giving vitamin D2  (not D3)  50 000iu fortnightly for a year is actually adverse – as Holick and others have  show – IT DEPRESSES – perhaps halves – THE BIOLOGICALLY ACTIVE blood 25OHVIT D3 while boosting perhaps 5 fold the far less active blood 25OHvit D2 levels , and actually worsens  rheumatoid arthritis clinically and serologically . One can speculate whether vit D2 actually blocks optimal function of VDRs vitamin D receptors. Trials published 2012 from Japan and Netherlands showed that vitamin D3 – blood 1,25(OH)2D3 (but not TNFalpha blockers) blocked  inflammation (ie TNF tumour necrosis factor alpha activation of vascular calcification).                                                 

Salahudfin ea’s new randomized controlled trial  from Pakistan Vitamin D3 injection accelerates clinical recovery from tuberculosis  shows “impressive clinical (weight gain, chest xray and sputum clearing)  improvement  over 3 months on outpatient TB therapy (Directly Observed Therapy (DOTS) with 2 months of 4 antituberculous drugs [Isoniazid, Rifampicin, Ethambutol and Pyrazinamide] followed by 6 months Isoniazid and Ethambutol)  with two doses 600 000iu vit D3 imi  (vs placebo inj)  a month apart-  ie equivalent to about 7 000iu/day over the 3 months treatment period . This dose  of vitamin D is as recommended for vitamin D supplement by the Pakistan Endocrine Society.  Trough  25OH vit D levels increased from about 20 to 90ng/ml.    After 12 weeks, the vitamin D supplemented pts (mean 28 yrs, BMI 17.2kg, 85% moderate to far advanced lung disease)  had  significantly greater mean weight gain (kg) + 3.75, (3.16 – 4.34) versus + 2.61, p 0.009; lesser residual disease by chest xxray-  30% fewer zones involved 1.35 v/s 1.82 p 0.004,   and 50% or greater reduction in cavity size 106 (89.8%) v/s 111 (94.8%), p 0.035. Vitamin D supplementation led to significant increase in MTBs-induced IFN-g secretion in patients with baseline ‘Deficient’ vitamin D serum levels (p 0.021). Patients in the vitamin D arm and serum < 30 ng/mL (‘Insufficient’ and ‘Deficient’ groups) at enrollment had significantly greater improvements in TB severity scores compared to patients with normal baseline vitamin D levels; p 0.014. This corresponds with the earliest reports of the benefits of vitamin D in TB patients published in 1848 [21] that describes disease arrest, weight gain and reduction in mortality in patients with TB treated with cod liver oil compared to standard therapy alone. More recently, Martineau et al  [7]  demonstrated that a single oral dose of 2.5 mg (100,000 IU) of vit D2 significantly reduced growth of mycobacteria . A randomized, placebo controlled study on 67 Indonesian patients, by Nursyam et al , Jakarta  [22] reported that pulmonary TB patients given 420,000 IU of vitamin D over 6 weeks  ie 10 000iu/day had significantly higher sputum conversion rates as compared to placebo (p 0.002). Martineau et al. [8] showed that 100,000 IUs of 25-hydroxyvitamin D3 supplementation significantly improved sputum conversion rates in patients with the Taq1 25-hydroxyvitamin D receptor polymorphism of the tt genotype.                                                                     .        

            As Salahuddin ea note, the good results in Pakistan in only 3 months with vigorous  INITIAL dose vit D3  contrasts with Two recently published large randomised, controlled trials of conservative vitamin D3 over months  that achieved far lower blood vitamin D levels found no difference in clinical outcomes or mortality after 400,000 IU of 25-hydroxyvitamin D3 or placebo were given by   Martineau ea  in London, UK to 146 pulmonary TB patients – where mean (trough  or midpoint)  vit D level  (after 100 000iu vitamin D(3) or placebo at baseline and 14, 28, and 42 days after starting standard tuberculosis treatment) – was surprisingly only  40ng/ml at 56days – ie after a mean of 7000iu/d by  56 days,  vs 10ng/ml  on placebo)- less than half of the bloodlevel  achieved on vit D3  in the Pakistan trial ;      


        and  by Wejse et al  2009  in  Guinea-Bissau to 365 TB patients  – who received  300,000 IUs of vit D3   ie only 100,000 IU or placebo at inclusion and again 5 and 8 months after the start of treatment,  ie below 1000iu vit D3 per day over the 12 month trial period “. The Guinea-Bisseau pts thus might have achieved a mean blood vit D level boost of only  10ng/ml.. and now Havers ea (Baltimore)   show Low 25(OH)D is common in diverse HIV-infected populations and is an independent risk factor for clinical and virologic failure; Low 25(OH)D was associated with high body mass index (BMI), winter/spring season, country-race group, and lower viral load. Baseline low 25(OH)D was associated with increased risk of human immunodeficiency virus (HIV) progression and death (adjusted hazard ratio (aHR) 2.13; 95% confidence interval [CI], 1.09–4.18) and virologic failure (aHR 2.42; 95% CI, 1.33–4.41). and Shepherd ea (Eurocoord) Low Vitamin D predicts short term mortality in HIV-positive persons Odds of death decreased by 46.0%( P = .04) for a 2-fold increase in latest 25(OH)D level.. In patients with current 25(OH)D <10 ng/mL, hsIL-6 concentration increased by 4.7%(95% CI, .2,9.4, P = .04) annually after adjustment for immunological/inflammatory markers, and no change in hsCRP rate was observed (P = .76)


1/1/2014  again, its comforting that no new evidence of hepatotoxicity of genuine black ohosh; or kava; or (USA-grade) Herbalife  products have been reported  the  past two years.

Teschke ea from Germany make the important point that herbaltoxicity is  likely due to the “kava paradox”,  that no toxicity is reported  with  ancient time-tested herbal remedies used appropriately by tradition in their fresh natural state and their countries of origin eg Pacifi islands; ,

but that adverse events occur with commerial eg alcohol-extracted and often preserved and old  preparations, and in untested combinations with other substances especially statins,  ethanol, and unknown viruses. .

The Herbalife company has just had to publish again  an update rebuttal of bad papers wrongly implicating and accusing Herbalife.  Their summary says:

World J Hepatol. 2013 Oct 27;5(10):601-2..              A correction of misinformation regarding Herbalife. Appelhans K, Najeeullah R, Frankos V. Herbalife International of America Inc, Torrance, CA     The authors of the subject article by Senadhi et al from Indiana State University  have misrepresented the safety and regulatory status of Herbalife‘s products. While we are very concerned with the unwarranted and unfavorable publicity that the inaccuracies listed could generate for Herbalife, we would welcome any inquiries that these authors may have to better clarify our commitment to the safety and quality of our products as has been demonstrated in part by our ability to establish positive relationships with regulatory authorities worldwide through continued cooperation and compliance. This letter clarifies the misinformation presented about Herbalife in the subject article

16 March 2012   it is comforting to note that there have been no new reports the past year of toxicity from these products.

In fact  some lab work seems to favour black cohosh for cancer prevention;

Anticancer Res. 2012 Jan;32(1):21-30.   Chemopreventive potential of black cohosh on breast cancer in Sprague-Dawley rats. Einbond LS, Soffritti M, Degli Esposti D, Tibaldi E, Lauriola M, Bua L, He K, Genovese G, Su T, Huggins L, Wang X, Roller M, Wu HA.  Columbia University, HHSC-1518, 701 W. 168th Street, New York, NY 10032, USA.     This study examines the chemopreventive potential and action of the herb black cohosh on Sprague-Dawley rats. CONCLUSION:Our results suggest that black cohosh may have chemopreventive potential for mammary cancer.
while Herbalife has published objective rebuttals of toxicity from Herbalife other than in isolated countries where irregular ingredients were used in local manufacture:
World J Hepatol. 2011 Oct 27;3(10):275-7. Revisiting acute liver injury associated with herbalife products.  Appelhans K, Smith C, Bejar E, Henig YS  Herbalife International of America Inc., Torrance, CA 90502, United States.   In the November 27, 2010 issue of the World Journal of Hepatology (WJH), three case reports were published which involved patients who had consumed various dietary supplements and conventional foods generally marketed as weight loss products. The reference to Herbalife products as contaminated and generally comparable to all dietary supplements or weight loss products is not scientifically supported. The authors provided an insufficient amount of information regarding patient histories, concomitant medications and other compounds, dechallenge results, and product specifications and usage. This information is necessary to fully assess the association of Herbalife products in the WJH case reports. Therefore, the article does not objectively support a causal relationship between the reported cases of liver injury and Herbalife products or ingredients.
Pharmacoepidemiol Drug Saf. 2012 Mar;21(3):333-4. doi: 10.1002/pds.3203. Misconceptions regarding the association between Herbalife products and liver-related case reports in Spain.
Appelhans K, Frankos V, Shao A.  Source  Product Compliance and Safety, Herbalife International of America, Inc, Torrance, CA, USA.

2 Feb 2011

Since June 2010 there have been no new cases of toxicity from Black Cohosh, herbalife or kava reported on Pubmed.


The new literature analysis Suspected black cohosh hepatotoxicity: no evidence by meta-analysis of randomized controlled clinical trials for isopropanolic black cohosh extract  by Naser et al from Yale , and Germany(the main producer of black cohosh BC products)- begs the question.

As this colunm has previously reviewd about BC,  women have died from or needed liver transplants after taking it.. Hence most Authorities have Black Box warning requirements Recurrences of liver reaction have been reported on rechallenge. These scattered cases can be argued away on metanalysis, but they cannot be ignored. One death or acute liver failure is unacceptable when BC is never an essential drug without other safe options.

Another study also published now (Wang ea from the FDA Centre for Drug Evaluation ) contradicts the German metanalysis with more basic toxicological data: “Computational analysis of positively predicted constituents showed … specifically, protocatechuic acid from black cohosh… predicted positive for liver toxicity endpoints also confirmed with literature findings”

Black cohosh is not physiological hormone replacement, BC is recommended by its proponents solely for menopause symptoms (it has no other benefits) for up to 6 months.

So why risk, use black cohosh at all?

Appropriate balanced hormone replacement – preferably human hormones, not xenohormones ie hormones not found in the healthy women, and not by swallowing it- is indicated permanently in all women .

As previouslly pointed out in this column, the International Menopause Society has summed it up in putting approriate HRT as the main agent(s) for menopause symptoms as well as  for its permanent multisuystem benefits;  and the human hormone gamma-aminobutyric acid GABA as the only alternative that is both safe and cleearly proven better than placebo for improving both hot flashes and sleep, anxiety. Used appropriately and with sensible monitoring and dose titration, all such hormone balance has no longterm risks.

MDICOLEGAL LIABILITY: under the new Conumae Protection Act CPA in South Africa, the pendulum has gone ridiculously too far. irrespective of the onus on manufacturers and promoters of any product, the onus is on the end-prescriber, end-dispenser to warn consumers of potential risks,  and any consumer claim for consequent damages is legally against only the final and retail supplier.

So no supplier of black cohosh is protected against consequent liability unless he gets a signed waiver from the purchaser after the recorded warning about its potential toxicity.

16 June 2010

there are no new adverse toxicity reports on Hebalife, black cohosh or kava  so far in 2010 .

Both Herbalife,  and black cohosh products, remain marketed and in demand  in South SAfrica.

There are  no new serious adverse reports or concerns published  on Pubmed or Google about Herbalife products in 2009.

On Pubmed there were 2 new cases of liver and coagulation problems associated with black cohosh in mid2009, from a Germanic and an Italian institute; and 14 hepatitis cases associated with kava ingestion confirmed  from around the world .

4 Jan 2009

This review  is not about benefit of black cohosh (independent trials show none for menopause symptoms) or Herbalife (trials support that Herbalife is indeed a weight loss aid), or kava (it is a confirmed anxiolytic analgesic euphoriant); but about toxicity potential however rare – considering that none of these  products can make any claim to being a necessity.

Contamination aside, there are no new  relevant reports  on Herbalife the past two months on Pubmed,

but indeed  4 new reports on black cohosh; and one on kava.

Lessons for black cohosh and Herbalife may be learnt from kava. Kava-kava was hastily banned  eg  in Europe and South Africa early this decade owing to reputed association with hepatotoxic deaths. But on careful study these toxicity claims appear to be uncertain.

The claimed benefits of kava are analgesic, euphoriant and relaxant, without addiction potential. The four trials of Kava (between 1991 and 2003, in Italy and Germany) confirmed that kava has anxiolytic benefits in the menopause syndrome.) . The hepatotoxicity (not reported from the source – Polynesia – unless taken by alcoholics) was reported largely from western countries, where commercially sold  kava extract was apparently differently extracted, and from the aerial leftovers of the kava; whereas in Polynesia it is extracted only from the root. A recent website from the NIH shows it is not banned there, but expresses much caution.

A careful analysis of kava hepatotoxicity by Teschke ea in Germany last month again finds little evidence of toxicity if kava is taken from a reputable manufacturer  at prescribed dose and for short duration  – as applies equally to alcohol, and most drugs.


An objective  NICUS  Nutritional Institute of University of Stellenbosch Report critical of  Herbalife is quoted verbatim in the Summer 2008  Newsletter of the Association of Dieticians of SA. NICUS- a world authority in Nutrition – confirms it stands by this report. It could thus be taken as a directive (to condemn Herbalife)- to dieticians for whose professional advice some patients wrongly substitute diet supplements;  where these modalities- careful  professional diet advice and counselling, and supplements-  are actually complementary..

But there does not appear to be any  more  evidence to condemn Herbalife than there was a year ago. As far as Pubmed and Google reveals,  the reports  [to date end of 2008 on Pubmed) of adverse effects  were from 4 discrete European regions [ Iceland; Switzerland; Spain & Israel) , apparently wth locally formulated Herbalife, not the USA main factory product, leading to assumption of a local production fault. There appear to have been 2 cases of liver failure in some 33 affected patients, in one of whom liver transplant became necessary but the patient died.. .

One cannot condemn all  babyfood because some is deliberately adulterated with melamine by ruthless Chinese sham factories. Commercial babyfood is arguably a necessity for many.

We await an updated rebuttal from Herbalife in the new year- but there does not seem to be anything for them to add to their rebuttal of last year..There has been no published evidence to justify update on Herbalife during 2008.

The accusation (by one patient, and a  convicted fraudster, Minkow) of a claimed lead-contaminated  Herbalife batch  in California   has, strangely, generated no updates for months now- but on the wiki herbalife update , it says “In August 2008, Minkow retracted all accusations against Herbalife and removed any mention of the company from his Web site.[30]” – there is no report of whether Herbalife bought his silence or not , which is a pity- see also. ;   but see also heavy flak against Minkow , suggesting that his whole campaign was a successful bear scam  to profit from Herbalife shares.

The  current  Wiki Herbalife  review also quotes a new trial validating benefit for weightloss. Caveat Emptor.

It may be asked why a Nutritional authority like NICUS:  warns  against Herbalife but not against the potentially fatal black cohosh. New independent analyses are both for and against them:


Black Cohosh:

Analyses of case reports from Univ Florida (Palacio 2009) and Italy (Borrelli 2008)  recommend caution about black cohosh for humans in view of adverse case reports; while a German analysis (Teschke 2008) exonerates black cohosh in every single case till then.

A trial from USA (Davis 2008) found that “black cohosh significantly increased the incidence of lung metastases in tumor-bearing mice compared with mice fed the isoflavone-free control diet”.

Clearly the valid divergence of opinion comes down to complex statistics of probability.

Black cohosh has been associated with severe liver failure and  transplantation in a number of women on a number of continents, for which reason the local Health Products Association, like all responsible authorities , finally agreed and issued recommendations that Black Cohosh label must be black-boxed- there is no justification for it’s sale as a useful product, unlike the role than can be argued for food substitute powders.

So why should anyone use black cohosh for menopause symptoms (when it’s benefit seems to be largely placebo, with grave doubt about safety) , when there are proven safe symptom relievers eg GABA (no adverse reports); or lowdose balanced appropriate parenteral human sex hormones (no adverse reports, and have numerous longterm multisystem benefits- which neither black cohosh nor GABA can claim..).

This review  is not about benefit, but safety. Regulators remain silent about drastically curtailing sale of the most lethal substances in widespread unregulated (and unnecessary)  use- paracetamol, other nonsteroidal anti-inflammatories, statins for uncomplicated  mild-to-moderate lipidemia, alcohol, tobacco and sugar, and pollution of everything by industrial adulteration with synthetic (often estrogenic) endocrine disruptors and virtually all fast foods with cornstarch and/or sugar.

The hysterical approval of diethylstilbestrol  DES by the FDA by 1950, and for a massive  1950 maternity trial  against all evidence (even though it’s toxicity was recognized by 1953,  it’s sale anywhaere was finally banned only 20 years later) continues to torment the original myriads of  guineapig women, their children and now grandchildren. These scandals are dictated by individual opportunist, corporate and governmental greed, and indifference to medical evidence and prevention.

The analogy for black cohosh, kava  and Herbalife  is perhaps:

#the ~20year delays before the FDA would licence the lifesaving lithium salt, and metformin, in USA;

#the ~5year hysteria over HRT after the Women’s Health Initiative – when the over-estimated risks of inapproriate use of  OHT in elderly women were stupidly and harmfully (for thousands of women) extrapolated to young women and other  HRT preparations;


#the melamine- baby milk formula catastrophe – the problem for the latter was exclusively some contaminated  babyfood batches made in China especially for the lucrative export market. .

The jury can thus be considered as still out on both black cohosh, kava  and Herbalife,  until manufacturers of commercial  products (not traditional preparations of  eg kava and black cohosh taken by residents who grow these)  can produce evidence, confirm  that the risk was limited  to specific batches of the commercial product  and adherence to accepted recommendations, and not due to other possible risk factors.


4 Sept 2007 Review
The following reports below of HerbaLife-associated liver failure appear on Medline – from Spain, then Israel and Switzerland.
:The July 2007 reports of the two dozen Herbalife-associated hepatitis cases from Israel & Switzerland reveal that liver problems occurred after about 5 months on the products; and that relapse occurred in about 20% on rechallenge with Herbalife ie in this percentage the association is proven.

Herbalife results for weight control have been reported as good. The only problem is historical according to the current Wikipedia entry: “Some of the original Herbalife weight loss products contained the active ingredient Ma Huang or Sida cordifolia, two herbs containing ephedrine alkaloids.

Adverse reactions involving the company’s Thermojetics original green tablets were recorded by the U.S. Food and Drug Administration and Herbalife subsequently stopped using ephedrine in its products in the face of rising insurance premiums.[3][4] The U.S. FDA banned supplements containing ephedra in 2004.[5]“

It is possible that the case reports below are unrelated to Herbalife itself , or that in those countries ephedra-containing Herbalife was still in use at the time, or that potentially hazardous herbs etc were added locally.

From, there is an authoritative rebuttal from Iceland dated February 2007.

A score of drugs and herbs can cause liver damage, topical ones – albeit rarely- include mushrooms; black cohosh and kava – see a recent list.

Drugs like ticrynafen, methyldopa and cerivastatin were discarded among other reasons because of liver problems, which are among many reasons why necessary sex hormone contraception and replacement should rather not use designer patent ie synthetic drugs, and especially not by mouth (hepatic first pass effect).

So it is always difficult to blame a single product, as the ongoing debate about black cohosh shows – which many “first world” regulators have “black boxed” ie added a compulsory warning to black cohosh warnings.

As with black cohosh, with a rare adverse event report, users of such products must weigh up for themselves.

As they say, since Herbalife tends to be custom-made in each country, with numerous ingredients (some undisclosed), it is so far impossible to incriminate whether the cause was local product corruption, or some appreoved component, of which the known possible culprits are ephedra and camelia.

Other known hepatotoxic herbs like black cohosh, kava and mushrooms were not mentioned. A few of the patients had viral hepatitis. Only 7 cases had also taken other known potential liver sensitizers – some synthetic sex hormones (4), aspirin (3), statin (1) and hydrochlorothiazide(1), of which 2 cases had positive recurrence of hepatitis on rechallenge with Herbalife.

UCT Medicines Information Centre is unaware of any such problems locally, and can recollect only perhaps 2 queries about Herbalife in some 23 years. Clarification is awaited from Herbalife headquarters.

From Swiss data the estimated incidence was below 2 cases per million Herbalife users, but both studies were based only on hospital records.

Considering the severe global problem of hepatitis from other causes (due to alcohol; obesity/diabetes (steatohepatitis, sulphonylureas, glitazones); numerous infections; carbon tetrachloride; synthetic sex hormones (oral contraception and postmenopausal hormone therapy) , mushrooms, antibiotics and antivirals, , autoimmune disease, antiepileptics, nifedipine, amitryptiline, allopurinol, nonsteroidal anti-inflammatories including aspirin and paracetamol , black cohosh, kava, antifungals and paracetamol), and that the rare adverse association of herbalife with liver damage may well have been limited only to Herbalife products made in those three “European” countries at that time, there is clearly no cause for alarm about Herbalife – just awareness.

The urgent problem of endemic liver disease is rather the avoidance of infections and potentially hazardous antimicrobials; mushrooms; carbon tetrachloride, alcohol excess; sale pf paracetamol without inclusion of protective vitamins and N-acetyl cysteine; and avoidance of potential hepatotoxins which are rarely if ever justified considering their risks, and safe effective alternatives available for eg statins, sulphonylureeas, glitazones, black cohosh, kava, non-steroidal anti-inflammatories; oral sex hormones; and sulphonylureas.

The centuries-proven plant galega officinalis (extract) metformin after 85years of modern use remains the only drug proven in longterm use to both reduce liver damage, lipidemia, thrombosis, adiposity and insulin resistance, and thus almost halve the incidence of new diabetes, hypertension/vascular disease, cancer and thus all-cause premature medical mortality.

Thus appropriate general use of metformin with long-proven vitamins, minerals, biologicals, safe herbs, fish oil and systemic human sex hormones – combined with prudent lifestyle and largely natural fresh foodstuffs- – does away with most of the well-known potential hepatitis drug risks listed above.

In defence of free market enterprise and choices, those who choose convenience safe proven food substitutes or other complementary products as part of an acceptable balanced regime advocated by suppliers like Herbalife do well, they should just be sure of the ingredients and supplier; and they should report and discuss what they use with some knowledgable up-to-date healthcare provider.

Response from Herbalife

Herbalife’s South Africa CEO responds reassuringly:

Good day,
Herewith a statement from Herbalife in response to the issues raised by yourself earlier in the week:

While we are aware of reports of abnormal liver function blood tests such as those reported by Dr. Oneta, our extensive consultation with internationally recognised liver experts has led repeatedly to the conclusion that these associations in time cannot be linked to any Herbalife product.

These small numbers of reports are anecdotal and millions of satisfied customers all over the world have been using our products for more than 27 years. All Herbalife products are formulated and manufactured in accordance with strict standards overseen by the Herbalife Scientific Advisory Board, which is chaired by David Heber, M.D., Ph.D., F.A.C.P., F.A.C.N. Quality control is overseen by our Scientific Affairs Group, chaired by Y. Steve Henig PhD and made up of an international panel of experts in nutrition and botanical dietary supplements.

Herbalife products, which are now sold in 65 countries, are formulated, registered and labelled in accordance with the regulatory requirements in every market where sold. All Herbalife products are safe to consume as directed.

Many consumers who choose to use Herbalife weight-management products for weight loss are overweight, some significantly so. Pre-existing medical conditions such as obesity and diabetes can be associated with non-alcoholic fatty liver disease, a disorder that may return certain types of abnormal blood test results. These test results, therefore, may have nothing to do with any herbal supplement, but rather are the result of a pre-existing medical condition. In addition, it is possible for an individual to have an allergic reaction to our products, the same way one might to any food product; for example, strawberries or shellfish. Herbalife supports the recommendation that consumers visiting their doctors for medical treatment inform them of any supplements they may be taking.

As a socially responsible company, we operate an adverse event reporting procedure that deals with the small number of queries we have from doctors and consumers and we operate an open dialogue policy with the medical community. All adverse event reports are investigated thoroughly in consultation with the consumer and the physician (if they are available) to fully understand the facts. None have resulted in the compulsory withdrawal of any product, ever. In the United States, Herbalife actively lobbied Congress to pass legislation mandating the submission of all dietary supplement and over-the-counter drug serious adverse events to the Food & Drug Administration. That new law takes effect December 22, 2007.”


J Hepatol. 2007 Oct;47(4):521-526. Herbal does not mean innocuous: Ten cases of severe hepatotoxicity associated with dietary supplements from Herbalife((R)) products. Schoepfer AM, ea.University Hospital Bern, Switzerland.
METHODS: To determine the prevalence and outcome of hepatotoxicity due to Herbalife((R)) products. A questionnaire was sent to all public Swiss hospitals. Reported cases were subjected to causality assessment using the CIOMS criteria. RESULTS: Twelve cases of toxic hepatitis implicating Herbalife((R)) preparations (1998-2004) were retrieved, 10 sufficiently documented to permit causality analysis. Median age of patients was 51 years (range 30-69) and latency to onset was 5 months (0.5-144). Liver biopsy (7/10) showed hepatic necrosis, marked lymphocytic/eosinophilic infiltration and cholestasis in five patients. One patient with fulminant liver failure was successfully transplanted; the explant showed giant cell hepatitis.     Causality assessment of adverse drug reaction was classified as certain in two, probable in seven and possible in one case(s), respectively. CONCLUSIONS: We present a case series of toxic hepatitis implicating Herbalife((R)) products. Liver toxicity may be severe. A more detailed declaration of components and pro-active role of regulatory agencies would be desirable.

J Hepatol. 2007 Oct;47(4):514-520. Association between consumption of Herbalife((R)) nutritional supplements and acute hepatotoxicity. Elinav E, ea -Hebrew University Medical Center, Israel.
: In 2004, identification of four index cases of acute hepatitis associated with Herbalife((R)) intake led to a ministry of health investigation in all Israeli hospitals. Twelve patients with acute idiopathic liver injury in association with consumption of Herbalife((R)) products were investigated.
RESULTS: Eleven of the patients were females, aged 49.5+/-13.4 y. One patient had stage I primary biliary cirrhosis and another had hepatitis B. Acute liver injury was diagnosed after 11.9+/-11.1 months of initiation of Herbalife((R)) consumption. Liver biopsies demonstrated active hepatitis, portal inflammation rich with eosinophils, ductular reaction and parenchymal inflammation with peri-central accentuation.
. CONCLUSIONS: An association between intake of Herbalife((R)) products and acute hepatitis was identified in Israel. We call for prospective evaluation of Herbalife((R)) products for possible hepatotoxicity.

Med Clin (Barc). 2007 Feb 17;128(6):238-9.
[Hepatotoxicity associated with the consumption of herbal slimming products] Duque JM,ea. [Article in Spanish] Letter



we were informed 36 hours ago by the Council for Medical Schemes that their Appeal Tribunal on 29 July  2013  refused the appeal by GEMS against the CMS Judgment of June 2012 ,  ie that Schemes have to pay members their due benefits for services by practitioners irrespective of PCNS registration.

Now, while the handful of schemes ( that have continued to defraud members of their benefits by illegally vilifying practitioners who refuse to pay BHF extortion money) consider their endless options to continue appealing, its up to the Media to publicise the lies of these Schemes and BHF,and force them to listen to their Regulator CMS and pay members due benefits, and stop defaming dissenting practitioners, CMS and BHF.

Its up to Practitioners and patients to join our protest, lodge complaints with CMS against schemes who continue this fraud and malpractice, who want to increasingly control and dictate  the age-old doctor-patient relationship.

Schemes and the BHF will no doubt – to continue the status quo- fight back with their endless funds (the >R70 billion  a year medical schemes premium income ) , continue to appeal the judgment endlessly and vilify the tiny group of dissenting practitioners who fight for pateints’ rights, as schemes have done for decades now.  Only increasing proaction  by patients for their and their choice of  concered doctors  will prevail.

2010   Dear PostMenopausal Woman/ older member,

Please note the reminder this month  to  medical aid patients from the commonest  Hospital Plan:   the Discovery Coastal Core benefits list (like the Council for Medical Schemes CMS) makes it clear that you are covered for PMBs Prescribed Minimum Benefits Chronic Illness Benefits. “You have cover for a list of (almost 300) chronic conditions. You have full cover for approved medicine on Discovery Health’s medicine list or up to a set monthly amount for medicine not on our list.”

This flatly contradicts the lies that patients are told when they contact their hospital plan schemes about such benefits- eg Discovery tells their members they have NO out of hospital benefits. Their  ‘consultant’ – even when  the member visits their head office in person- simply and deliberately with fraudulent intent omits to tell the member to read the rules, that all they have to do is get their doctor to complete the necessary prescribed application form to be registered for chronic illness benefit, be it for eg menopause or unipolar depression.

In the end, it is the members’ fault – caveat emptor.  Open medical schemes  and their umbrella  BHF are simply clever money-making businesses run for maximum profit, for the welfare of the owners/directors, not the patient-members.  This is the unblushing naked published mission of the Board of Health Funder BHF , a ruthless co-op representing less than half the medical scheme members in South Africa, “ to ensure that it is able to lobby government and other organisations effectively and to influence policy where necessary on behalf of the entire industry.”  The BHF is in such chaos as a private company claiming to lead a giant >R60billion a year industry that it’s  financial report for 2008 has not yet been published on it’s website.

But  despite numerous complaints of fraud against the BHF on which the  Regulator -the Council for Medical Schemes CMS -has repeatedly had to take action, – CMS has just re-awarded  the BHF an R8.5million-a-year contract to run a Practice  Code Numbering System PCNS . This cost is more than double that of the next bid of R3.5 million for a far better service.  And the CMS without explanation simply declares “closed” numerous substantiated  complaints ( by patients and their doctors)  of blatant fraud against members by the BHF and it’s constituent medical schemes. Can this criminally wrong award  action be due to anything but fraudulent collusion between the BHF and recently resigned chief executives of COMS and BHF?  Otherwise why would there mysteriously be no obvious news announcements about this award on either the CMS or BHF websites,  nor rebuttal of the accusations in the Medical Chronicle of early this month.

And why has the Statutory Regulator- the CMS- continued to allow despite regular complaints the lies on the BHF website eg “The practice number, allocated to all registered healthcare providers is  a legal requirement for the process of reimbursement of a claim to  a  service provider.” This is NOT a legal requirement.

In fact elsewhere the BHF now publishes the truth: “In accordance with the Medical Schemes Act 131 of 1998, a medical scheme reimburses a member for services rendered by a provider of service duly registered or licensed with the relevant government.. statutory council.” Thus the medical scheme is contractually bound to reimburse the member for services by eg a doctor registered with the Heath Professionals Council of SA.
The Council for Medical schemes recently confirms to me in a letter  (printed below) what their rules have stated for years, that  obligatory benefits- which are paid for by the med scheme not from your benefits-  include not just the 27 most common chronic major  disease conditions but also eg :

*Menopause Disorder –   2 visits a year and appropriate HRT;
* and Chronic  Depression including 15 psychotherapy visits a year and approved antidepressant- by a psychiatrist.

Thus if suffering from these two common conditions from mid life,  you should have had  completed a CIB form for menopause for 2 visits a year;
and you and a psychiatrist a CIB form for Depression.

Did you/we  do so? For depression Have you seen a doctor  the past 6 mo?

Check your Med aid website to see if you are registered for  both conditions, with appropriate drugs.
If not, then you and your doctor do so.  Neither your doctor nor your open medical scheme have any choice in the matter, obviously provided the diagnoses are genuine.

Your  Med Scheme is apparently under no obligation to inform your doctor  (completing the application form) of the outcome of your application  EXCEPT in rejecting the doctor’s claim  for services.



Current correspondence with CMS: (names are omitted as these statements emanate as offIcial policy statements sent me  from  the Benefit Management Unit: Clinical Analyst  and via her from the acting CEO and Legal Head):

Neil Burman to Complaints at CMS 18 Jan 2010

Dear CMS,
please clarify the status of ICD 10 item 95.1 Menopause disorder as a PMB 528M , or Unipolar Depression certified by a psychiatrist,  under your extended PMB list –
are open med schemes eg Discovery Coastal Core entitled to refuse registration of such conditions as obligatory PMBs if they are not on the core 27 list?
Last Friday  your Clinical Analyst was most helpful  over the phone ; she firmly insisted that your website is incorrect in stating:
Is my medical scheme obliged by law to provide cover for certain medical conditions? Yes, these are known as Prescribed Minimum Benefits (PMBs). They were introduced into the Medical Schemes Act to ensure that members of medical schemes would not run out of benefits for certain conditions and find themselves forced to go to state hospitals for treatment. These PMBs cover a wide range of close to 300 conditions.”
She says your list and directive is not obligatory on schemes. Surely she is contradicting your directive from your current website quoted in italics above? Perhaps I misunderstood her?
Neil Burman
the next day the Benefit Management Unit: Clinical Analyst    at CMS replied  with a changed view:

Dear Dr Burman

“The acting CEO  requested that I provide you with detailed information with regards to our telephone conversation on Friday 15 January 2010.

It seems that there has been a misunderstanding with regards to the coding of PMB conditions and the registration of PMB conditions at medical schemes.

I would like to clarify the following matters:

1.  PMB registration as discussed in Circular 37 of 2009   2.  PMB ICD-10 coded list on the CMS website      3. Requirements of a PCNS number

1. PMB registration as discussed in Circular 37 of 2009

“On 15 December 2009 we published circular 37. The circular details the findings of:

  • Evaluations of compliance with certain administration standards by medical schemes and third party administrators
  • Analysis of numerous complaints received by the CMS.

“One of the findings was that medical schemes and third party administrators require members to register their PMB conditions with the scheme. This involves the completion of a registration form and also the submission of certain clinical criteria to the scheme. Benefits were only provided once the registration was completed. This requirement is not permitted as the PMBs are a legal entitlement as detailed in the Regulations to the Medical Schemes Act 131 of 1998.

2. PMB ICD-10 coded list on the CMS website

The CMS published a document i.e. Prescribed Minimum Benefits ICD 10 Five Character Coding – Excel Version 1.04 on our website on 4/8/2008.

During our conversation I mentioned that the list is not a legislative document and the intention was that it should be used as a basic guideline to link PMB conditions to specific ICD-10 codes.

Since this is not a legislative document but a basic guideline only, schemes should not use it as the final determining factor when deciding whether a condition qualifies as a PMB condition or not.  The regulation is still the only legislative document.

PMBs consist of Diagnostic Treatment Pairs (DTP), Chronic Disease List (CDL) and Emergency Conditions.

Although PMBs are legal entitlements, certain criteria do exist in the regulation. Certain conditions e.g. Unipolar depression is included in the PMB DTP regulation but the treatment specified does not include medical management. The only treatment currently specified in the PMB regulation is Hospital-based management up to 3 weeks/year (including inpatient electro-convulsive therapy and inpatient psychotherapy) or outpatient psychotherapy of up to 15 contacts

The situation for the treatment of Bipolar Disorder did however change as the Minister of Health published the Bipolar Mood Disorder algorithm during December 2009. Medicine management as detailed on this algorithm is therefore now part of the entitlement of the condition.

Please remember that not all chronic illnesses are mentioned in the Chronic Disease List (CDL) but that a multitude of chronic illnesses are included in the Diagnostic Treatment Pairs (DTP).

Chronic conditions covered under the DTP list include for example Menopausal Management. The treatment specified for Menopausal management however details Medical and surgical management, including hormone replacement therapy.

This is the difference between Menopause and Unipolar Depression. Both are included in the PMB regulation under the DTP list but the treatment specified for each differs.

3. Requirements of a PCNS number

CMS  obtained a legal opinion on the PCNS from Senior Counsel. Their opinion is that any provider wishing to receive direct reimbursement must obtain a PCN. Should they not do so then they are not disqualified from practising medicine or from treating scheme members, but are simply NOT entitled to demand direct payment. The PCN grants them an entitlement. Schemes may also not refuse to reimburse a member who has been treated by a provider not having a PCN, but may refuse to reimburse the provider directly on the basis of him or her not disposing of a PCN.

BHF unfortunately holds a view that medical schemes are not entitled to recognise a provider not having a PCN and may not pay any claim emanating from such provider. The legal opinion does not support this view.

We have published Circular 35 of 2007 that dealt with the specific problem (attached to this mail).

Please supply your members with a copy of the circular and request them to discuss their entitlements with the medical schemes in order to receive reimbursement for the services obtained from you.”

Kind regards

Benefit Management Unit: Clinical Analyst





Answer: none provided it is safely and economically measured and safely and economically corrected at all ages from small children to dotage. It is so cheap and easy to halve  the fracture risk and rate in all, and thus save vast suffering, costs and especially deaths.

A spinal surgeon laments as we all do  the poor correlation between dual xray bone density analysis DXA and fracture risk.
The simple answer is that bone density is not the top risk factor for fractures,

The chief risk for fractures in the aging is falls and fragility ie global health balance  including agility-co-ordination, balance, and strength- muscle mass.

As this column has previously detailed, DXA is valuable for looking at risk areas in the hip or a vertebra;
but just as screening X-ray mammography overdiagnoses clinically relevant breast cancer,   trunkal DXA measurement  increasingly overreads bone density  as we age because of false densification- vascular calcification overlying hips and spine, and progressive collapse wedging of vertebrae.

That’s why,  as  this column has previously referenced,  QUS -quantified ultrasound – done mostly at the heelbone, has become the international gold standard for monitoring global fracture risk, since that bone measured in its long axis  is generally free of overlying vascular calcification and collapse wedging. It is recommended by  international bodies, many leading universities from Cape Town to Cambridge to Scotland, Japan and USA. .

There is generally  good  correlation between true DXA measurement at hip and spine, and heel QUS measurement.
And QUS lacks the cumulative radiation risks of DXA.
That’s why QUS bone density  is increasingly recommended from childhood, for monitoring and thus simple prevention of frailty   – thus avoiding  the mushrooming  fracture and frailty risk in later life Osteoporos Int. 2012 Aug  Quantitative ultrasound and fracture risk prediction in non-osteoporotic men and women as defined by WHO criteria.Chan ea  Garvan Institute of Medical Research,Sydney,  Australia. Osteoporos Int. 2012 Jan:143-53.Quantitative ultrasound of  heel and fracture risk. Moayyeri ea .University Cambridge  UK. Metanalysis: 21 studies with 55,164 women and 13,742 men were included  with a total follow-up of 279,124 person-years. All QUS parameters were associated with risk of different fracture:  1 SD decrease in BMD associated with almost doubling of  hip fracture risk.  (RR by BUA  1.69, SOS was 1.96). There was marked heterogeneity among studies on hip and any clinical fractures but no evidence of publication bias amongst them. Different validated devices predicted fracture risks with similar performance; with  similar performance in men and women. This study confirms that heel QUS, using validated devices, predicts risk of different fracture outcomes in elderly men and women.

Oct 30, 2010.


The just-published Champ study of osteoporosis in men over 70yrs in Australia shows the high risk for older men as well: 25% had vertebral fractures, but only 77% of the men with fractures had even osteopenia let alone osteoporosis on DXA screening. and this does not factor in the overreading by DXA at the spine and hip owing to the high prevalence of both calcinosis and vertebral collapse. And abysmally few of the men were taking realistic preventatives.

The study bears out:

that frailty,  usually from aging  – is the chief risk factor for non-violent fractures;

and  the low sensitivity of especially  DXA screening, never mind the folly of waiting for fractures or dementia or worse before doing safe lowcost (QUS bone risk) screening as one incentive to starting multipreventative supplements.

As the GIOS Project in Spain yet again confirms, simple  diagnosis and safe  treatment of those at risk of non-violent fractures is scandalously neglected.

And it does not require costly risky high technology – xray screening  bisphosphonates or strontium ranelate..

Like doctors, men are far more resistant than even women to heeding warning to start screening and supplements early enough.

The  CHAMP  study again highlights the importance of asymptomatic middleaged men never mind women having periodic no-xray ultrasound quantitative bone strength scans  routinely as the gold standard so as to prompt them to take the appropriate blend of the fewscore supplements effective against both frailty fractures as well as the associated lipid- diabetes- vascular -respiratory- dementia- cancer diseases.