Category Archives: sexual health


Dr Neil D Burman MBChB(UCT) 1966, MRCP(UK 1974) Senior  Family General (all-ages) & Internist  practitioner in Claremont Cape Town,  has left Grove Bldg moved his rooms to
 13 Stafford St Harfield  Village, 50m down from Harfield station subway above corner of 1st Ave. .
Consultations  by appointment only 1600-1800, sometimes from 0900 weekdays and public holidays/weekends.   .  Holistic integrative chronic natural medicine practice (HRT, pain relief, infection eg HIV AIDS, TB, /cancer/obesity screening & prevention) .
(No emergencies or surgery- these must go to nearest polyclinic or hospital ER). .

or consultations by Telephone/email  where appropriate.

appts: ph Reception office hrs  021 6717797.   .
doctor personal email  or sms or whatsapp (or as last resort  try ph) 0836299160 all hrs 07.00 – 21.00. .   or    or fax 0865657215
Fellow of  Kronos Longevity Research Foundation Phoenix Arizona.

MEMBER OF  Royal Society SA; Kidney Association;Faculty of Consulting Physicians of South Africa; Kingsbury Hospital Forum;  and Local & International Societies for Study of: ; Menopause and Aging Males, Hypertension, Sexual Health, Vitamin D3-Autoimmune Disease  CGCoimbra network;  SASIM SA Society of Integrative Medicine; LDN Trust; .  Insurance, and Professional Driving Permit Assessments. mornings SASSA Disability Grant med officer Cape Town Clinics.  (formerly practicing/lecturer  in Port Elizabeth;  Hypertension, Renal & Transplant  med   GSH UCT, Leeds Hospital  England: Tygerberg Hospital Univ Stellenbosch; Libertas Hospital G/wood; and Univ W Cape.

Preferred Provider: Discovery Health & FedHealth


Accompanying his 32year old partner (with like her mother  BRCA+ breast cancer ), a   young man this week complains sorrowfully  of total erectile failure within three  days every time he resumes fluoxetine for longstanding depression.

This may suit those patients who eschew sexuality, who knowingly choose chemical castration.. But the drug doesnt fix the causes of depression, merely palliates, often no better than a placebo, sometimes worse- compared to natural multibeneficial  antidepressant supplements.

We already long  live in a sea of estrogenic endocrine disruptors decimating many species including humans,  like pesticides and PCBs, as so aptly described by Deborah Cadbury and Prof Nils Skakkebaek in classic books  eg The Feminization of Nature and The Estrogen Effect.

The commonest prescription  drugs (synthetics- antidepressants; major psychotropes;  amoxicillin,   oxidants ( betablockers eg atenolol;  nonsteroidal anti-inflammatory NSAID (which block antidepressant effects –the Paul Greengard hypothesis 2011 Rocherfeller Inst NY);  statins (cholesterol -steroid and insulin disruptors), and patent synthetic sex hormones-  are  now routine if not mandatory prescription  worldwide due to ruthless relentless marketing pressure-  disease-mongering for profit-  even in children, and worse,  in patients with cancers. The  commonest cancers- breast, prostate, uterus-  are estrogen-driven.

Such environmentally and biologically hostile designer patent drugs-for-profit   are increasingly detectable in surface wastewater globally  from human excretion, and thus drinking  water supplies .

Endocrine disruption studies of antidepressants  (eg fluoxetine Prozacs, mianserin Lantanon (its commercial analogue successor is now Remeron), Bupropion Wellbutrin Zyban;  Venlafaxine Effexor  and desimipramine)  in surface water in Canada,  USA,  Mexico, Brazil and Belgium since 2006, and longer for antipsychotics, statins  and NSAIDS, show estrogenic  ie antiandrogenic risks  for eg gender development and thus for breast/prostate cancer,   for  virility and fertility..

Doctors  mostly blithely  ignore that reproductive young females  have by evolutionary reproductive  necessity  100fold  lower androgenic:estrogenic balance (eg 3:1) than men (eg 300:1), and are also far more prone  than males both to estrogenic contraception prescription harm, and  to common  major depression and autoimmune disease like rheumatod arthritis and lupus, and thus to  the double peril of mutiple estrogenic  prescription.

Recently common NSAIDs eg ibrufen, diclofenac  and mefanemic acid have been shown to be estrogenic in fish.

But such elective  prescription of ( endocrine disruption) cancer- and infertility- promotors (antidepressants, NSAIDS, hormone contraception and HRT etc) ,  is hardly desirable or ethical  at any age, especially when patients and their parents  are not informed of the grave risks of these drugs with no proven longterm benefits (except for contraception).

new reviews  gives more insight  from a plastic surgeon into prevention, including the harms of xray mammography.

and into the gross dangerous overprescription  of diabetogenic depressing  hepato-nephro-myotoxic  statins for all.

Popular painkillers eg opioids like oxycodin, fentanyl, tramadol on the other hand are similarly also  powerful longacting hypoandrogenism–inducing drugs   promoting estrogen dominance – which further complicates the misery and depression of those in chronic pain or depression,  including from  cancer, especially in women as well as men;  who thus  require monitoring of gonadal hormone levels and, if deficient, testosterone replacement. Aloisi ea Univ Siena 2012.


Reprod Toxicol. 2012:34:80-5. In vivo and in vitro estrogenic activity of the antidepressant fluoxetine.Müller JC, Imazaki PH, Boareto AC, Lourenço EL, Golin M, Vechi MF, Lombardi NF, Minatovicz BC, Scippo ML, Martino-Andrade AJ, Dalsenter PR.  University of Paraná,  Brazil.     .Recent years have seen an increase in the use of antidepressant drugs, especially fluoxetine (FLX), in sensitive populations, such as pregnant and lactating women. Although some evidence suggests a possible endocrine action of FLX, no specific studies have been performed to investigate this hypothesis. In the present study, we investigated the possible (anti)androgenic and (anti)estrogenic actions of FLX using Hershberger, uterotrophic (0.4, 1.7, and 17mg/kg), and reporter gene (7.6-129μM) assays. In the Hershberger assay, no differences were observed in androgen-dependent organ weights. However, the uterotrophic and gene reporter assays indicated a possible estrogenic action of FLX. Uterine weight increased in the 1.7 and 17mg/kg/day groups in the 3-day uterotrophic assay in immature rats. Additionally, noncytotoxic concentrations of FLX induced estrogenic responses and increased the estrogenic response of estradiol in MCF-7 breast cancer.    Recent years have seen an increase in the use of antidepressant drugs, especially fluoxetine (FLX), in sensitive populations, such as pregnant and lactating women. Although some evidence suggests a possible endocrine action of FLX, no specific studies have been performed to investigate this hypothesis. In the present study, we investigated the possible (anti)androgenic and (anti)estrogenic actions of FLX using Hershberger, uterotrophic (0.4, 1.7, and 17mg/kg), and reporter gene (7.6-129μM) assays. In the Hershberger assay, no differences were observed in androgen-dependent organ weights. However, the uterotrophic and gene reporter assays indicated a possible estrogenic action of FLX. Uterine weight increased in the 1.7 and 17mg/kg/day groups in the 3-day uterotrophic assay in immature rats. Additionally, noncytotoxic concentrations of FLX induced estrogenic responses and increased the estrogenic response of estradiol in MCF-7 breast cancer cells transfected with luciferase.
Pharmacol Biochem Behav. 2013103: 659-65..Participation of estrogen receptors in the antidepressant-like effect of prolame on the forced swimming test. Lemini C, Cruz-López B, Martínez-Mota L  Universidad Nacional Autónoma de México, Mexico.Estrogen therapy may produce antidepressant-like actions, but the side effects, such as thromboembolic events, may restrict its use among women. The 17β-aminoestrogens (AEs) [prolame [17β-(3-hidroxy-1-propylamino)-1,3,5(10)-estratrien-3-ol)], butolame [17β-(3-hidroxy-1-butylamino)-1,3,5(10)-estratrien-3-ol)], and pentolame [17β-(5-hidroxy-1-pentylamino)-1,3,5(10)-estratrien-3-ol)] induce estrogenic and anticoagulant actions, effects that could prove advantageous in an estrogen therapy; however, their antidepressant-like effects have not been described. The objective of this study was to determine the effect of these 17β-AEs (prolame, butolame and pentolame) in the forced swimming test (FST), an animal model sensitive to antidepressant drugs, and to establish the role of estrogen receptors in such actions. Ovariectomized female rats treated with prolame (10-200 μg/rat) showed a reduction in immobility and an increase in active behaviors in the FST, while this effect was not produced by butolame and pentolame (10-200 μg/rat). The antidepressant-like effect of prolame was similar to that of 17β-estradiol (E2, 5-20 μg/rat), sharing with it a biphasic profile but at higher doses. Antidepressant-like actions of prolame and E2 were not associated with changes in locomotor activity. With respect to a control group tamoxifen (15 mg/kg) by itself produced no changes in all behavioral evaluations, but canceled the antidepressant-like effect of prolame and E2. It is concluded that estrogen receptors participate in antidepressant-like effect of both estrogens in the FST. Antidepressant-like activity of different AEs is discussed considering their differences in chemical structure and the schedule used. Our results show additional central actions of prolame besides its pro-sexual, anti-coagulant, estrogenic and anxiolytic activity.
Aquat Toxicol. 2011:104::38-47. Selective uptake and biological consequences of environmentally relevant antidepressant pharmaceutical exposures on male fathead minnows. Schultz MM, Painter MM, Bartell SE, Logue A, Furlong ET, Werner SL, Schoenfuss HL  The College of Wooster, OH   USA   Antidepressant pharmaceuticals have been reported in wastewater effluent at the nanogram to low microgram-per-liter range, and include bupropion (BUP), fluoxetine (FLX), sertraline (SER), and venlafaxine (VEN). To assess the effects of antidepressants on reproductive anatomy, physiology, and behavior, adult male fathead minnows (Pimephales promelas) were exposed for 21 days either to a single concentration of the antidepressants FLX, SER, VEN, or BUP, or to an antidepressant mixture. The data demonstrated that exposure to VEN (305 ng/L and 1104 ng/L) and SER (5.2 ng/L) resulted in mortality. Anatomical alterations were noted within the testes of fish exposed to SER and FLX, both modulators of the neurotransmitter serotonin. Additionally, FLX at 28 ng/L induced vitellogenin in male fish–a common endpoint for estrogenic endocrine disruption. Significant alterations in male secondary sex characteristics were noted with single exposures. Effects of single compound exposures neither carried over, nor became additive in the antidepressant mixtures, and reproductive behavior was not affected. Analysis of brain tissues from the exposed fish suggested increased uptake of FLX, SER and BUP and minimal uptake of VEN when compared to exposure water concentrations. Furthermore, the only metabolite detected consistently in the brain tissues was norfluoxetine. Similar trends of uptake by brain tissue were observed when fish were exposed to antidepressant mixtures. The present study demonstrates that anatomy and physiology, but not reproductive behavior, can be disrupted by exposure to environmental concentrations of some antidepressants. The observation that antidepressant uptake into fish tissues is selective may have consequences on assessing the mode-of-action and effects of these compounds in future studies.

Aquat Toxicol. 2010 ;100:354-64    .Waterborne fluoxetine disrupts the reproductive axis in sexually mature male goldfish, Carassius auratus.nMennigen JA, Lado WE, Zamora JM, Duarte-Guterman P, Langlois VS, Metcalfe CD, Chang JP, Moon TW, Trudeau VL  University of Ottawa, Ontario, Canada.    Fluoxetine (FLX) is a pharmaceutical acting as a selective serotonin reuptake inhibitor and is used to treat depression in humans. Fluoxetine and the major active metabolite norfluoxetine (NFLX) are released to aquatic systems via sewage-treatment effluents. They have been found to bioconcentrate in wild fish, raising concerns over potential endocrine disrupting effects. The objective of this study was to determine effects of waterborne FLX, including environmental concentrations, on the reproductive axis in sexually mature male goldfish. We initially cloned the goldfish serotonin transporter to investigate tissue and temporal expression of the serotonin transporter, the FLX target, in order to determine target tissues and sensitive exposure windows. Sexually mature male goldfish, which showed the highest levels of serotonin transporter expression in the neuroendocrine brain, were exposed to FLX at 0.54μg/L and 54μg/L in a 14-d exposure before receiving vehicle or sex pheromone stimulus consisting of either 4.3nM 17,20β-dihydroxy-4-pregnene-3-one (17,20P) or 3nM prostaglandin F₂(α) (PGF₂(α)). Reproductive endpoints assessed included gonadosomatic index, milt volume, and blood levels of the sex steroids testosterone and estradiol. Neuroendocrine function was investigated by measuring blood levels of luteinizing hormone, growth hormone, pituitary gene expression of luteinizing hormone, growth hormone and follicle-stimulating hormone and neuroendocrine brain expression of isotocin and vasotocin. To investigate changes at the gonadal level of the reproductive axis, testicular gene expression of the gonadotropin receptors, both the luteinizing hormone receptor and the follicle-stimulating hormone receptor, were measured as well as expression of the growth hormone receptor. To investigate potential impacts on spermatogenesis, testicular gene expression of the spermatogenesis marker vasa was measured and histological samples of testis were analyzed qualitatively. Estrogen indices were measured by expression and activity analysis of gonadal aromatase, as well as liver expression analysis of the estrogenic marker, esr1. After 14d, basal milt volume significantly decreased at 54μg/L FLX while pheromone-stimulated milt volume decreased at 0.54μg/L and 54μg/L FLX. Fluoxetine (54μg/L) inhibited both basal and pheromone-stimulated testosterone levels. Significant concentration-dependent reductions in follicle-stimulating hormone and isotocin expression were observed with FLX in the 17,20P- and PGF₂(α)-stimulated groups, respectively. Estradiol levels and expression of esr1 concentration-dependently increased with FLX. This study demonstrates that FLX disrupts reproductive physiology of male fish at environmentally relevant concentrations, and potential mechanisms are discussed.

Pharmacol Biochem Behav. 2008 ;88:332-40.Estrogens participate in the antidepressant-like effect of desipramine and fluoxetine in male rats.Martínez-Mota L, Cruz-Martínez JJ, Márquez-Baltazar S, Fernández-Guasti A  Instituto Nacional de Psiquiatría  Mexico City In male rats, the antidepressant-like effect of fluoxetine (FLX) and desipramine (DMI) in the forced swimming test (FST) is reduced by orchidectomy and partially restored by testosterone (T). It is unknown if this modulation of T is produced by its estrogenic metabolites. The objectives of this study were to evaluate if the aromatase inhibitor, formestane, interferes with the antidepressant-like effect of DMI and FLX in intact male rats, and to analyze if 17beta-estradiol (E2) modifies the FST and interacts with the antidepressants in orchidectomized (Orx) males. Intact males received DMI (1.25-5.0 mg/kg) and FLX (2.5-10 mg/kg) alone or in combination with formestane (17.5 mg/kg). Orx rats received E2 (5, 10, 20 and 40 microg/rat) or the combination of E2 [at sub-threshold (5 microg/rat) and optimal (10 microg/rat) doses] plus sub-effective doses of DMI (2.5 mg/kg) or FLX (10 mg/kg). Serum testosterone and estradiol levels were measured in intact-control and -formestane treated animals as well as in castrated males replaced with various doses of E2. Formestane in intact males lacked of an action in the FST, but cancelled the antidepressant-like effect of DMI and FLX. E2 at the supra-physiological doses of 10 and 20 microg/rat produced antidepressant-like effects. E2 at 5 microg/rat (that re-established the levels of this hormone to physiological levels) and at 10 microg/rat restored the antidepressant-like action of DMI and FLX in Orx rats. It was concluded that estrogens participate in the antidepressant-like effect of DMI and FLX in the FST.

Chemosphere. 2006:;65:1836-45.. Effects of the antidepressant mianserin in zebrafish: molecular markers of endocrine disruption.van der Ven K, Keil D, Moens LN, Hummelen PV, van Remortel P, Maras M, De Coen W. University of Antwerp,  Belgium.    Due to their environmental occurrence and intrinsic biological activity, human pharmaceuticals have received increasing attention from environmental and health agencies. Of particular, ecotoxicological concern are drugs that affect nervous- and endocrine-systems. Zebrafish genome-wide oligo arrays are used to collect mechanistic information on mianserin-induced changes in gene expression in zebrafish. Gene expression analysis in brain and gonad tissue clearly demonstrated the estrogenic activity of mianserin and its potency to disrupt normal endocrine (estrogenic) signaling, based on induction of molecular biomarkers of estrogenicity (e.g., vitellogenin1 and zona pellucida proteins). The possible mechanism underlying this estrogenic activity of mianserin is disturbance of the Hypothalamo-Pituitary-Gonadal (HPG) axis by direct interference of mianserin with the serotonergic and adrenergic systems in the brain of zebrafish. Taking into account the importance of the HPG-axis, and considering the concept of ‘critical window of exposure’, our results reveal the importance for more elaborate testing of endocrine disruptive effects of aquatic antidepressants at different lifestages and during longer exposure periods (e.g., life cycle studies). Although there is a low concordance between the gene expression results in this study and previous cDNA microarray hybridizations, the global mechanistic expression patterns are similar in both platforms. This argues in favor of pathway-driven analysis of gene expression results compared to gene-per-gene analysis.


J Hazard Mater. 2013 Jun 15;254-255:242-51. .Effects of non-steroidal anti-inflammatory drugs on hormones and genes of the hypothalamic-pituitary-gonad axis, and reproduction of zebrafish.  Ji K, Liu X, Lee S, Kang S, Kho Y, Giesy JP, Choi K. Seoul National University,  Korea.This study was conducted in two experiments, to identify non-steroidal anti-inflammatory drugs (NSAIDs) with high endocrine disruption potentials, and to understand consequences of exposure to such NSAIDs in fish. In the first experiment, the effects of five NSAIDs on hormones and gene transcriptions of the hypothalamic-pituitary-gonad (HPG) axis were evaluated after 14 d exposure of adult zebrafish. Ibuprofen and mefenamic acids were identified to increase the concentrations of 17β-estradiol and testosterone in females significantly, while decreased those of testosterone among male fish. Significant up-regulation of fshβ, lhβ, fshr and lhr were observed in females, whereas down-regulation was observed in males exposed to each NSAID. In the second experiment, ibuprofen was chosen as a model chemical. Adult zebrafish pairs were exposed to ibuprofen for 21 d, and the effects on reproduction and development of offspring were examined. The egg production was significantly decreased at ≥1 μg/L ibuprofen, and parental exposure resulted in delayed hatching even when they were transferred to clean water for hatching. The results demonstrated that ibuprofen could modulate hormone production and related gene transcription of the HPG axis in a sex-dependent way, which could cause adverse effects on reproduction and the development of offspring.

University of Algarve, Portugal  .buprofen (IBU) is one of the most sold over-the-counter non-steroidal anti-inflammatory drugs (NSAID) and widely detected in the aquatic ecosystems. Nevertheless, the information regarding IBU effects in biota is still sparse. The goal of this study was to assess IBU potential effect as oxidative stress and endocrine disruption inducer in mussel Mytilus galloprovincialis applying a battery of biomarkers. Over two weeks of exposure to IBU (250 ngL(-1)), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), phase II glutathione S-transferase (GST) activities and lipid peroxidation (LPO) levels were determined in the digestive gland and alkali-labile phosphates (ALP) were carried out in sex-differentiated mussels’ gonads. The results confirm a transitory induction of antioxidant activities responses concomitant to lipid peroxide formation outline and an increase of ALP levels over time, particularly in exposed males which may lead to mussels’ reproductive fitness impairment highlighting a higher impact of IBU as an endocrine disruptor than as a short-term reactive oxygen species (ROS)-generator.


Aquat Toxicol. 2011 ;105:264-9..Non-steroidal anti-inflammatory drug (NSAID) ibuprofen distresses antioxidant defense system in mussel Mytilus galloprovincialis gills.Gonzalez-Rey M, Bebianno M   University of Algarve,  Portugal.Active pharmaceutical ingredients (APIs) are presently considered an emergent class of environmental contaminants. Ibuprofen (IBU) is one of the most applied non-steroidal anti-inflammatory drugs (NSAIDs) in the world. Several authors report the occurrence of IBU in influents and effluents of waste water treatment plants (WWTPs), surface, river and public tap water in numerous countries. However, very little is known about the risks and chronic effects of IBU exposure in non-target organisms. This approach undertakes the assessment of several oxidative stress biomarkers responses through the analysis of antioxidant enzymes activities (superoxide dismutase – SOD, catalase – CAT, glutathione S-transferase – GST, glutathione reductase – GR) and lipid peroxidation (LPO) levels in sentinel species mussel Mytilus galloprovincialis gills exposed for 2 weeks to an environmental realistic concentration of IBU. Results clearly show the significant induction and positive correlation between SOD activity and LPO in exposed gills, concomitant to an antioxidant defense depletion of CAT, GR and GST compared to controls. The integration of all biomarkers in mussels’ gills separates non- and exposed groups supporting the breakdown of the redox defense system and IBU’s pro-oxidant action. Further studies are needed to test possible endocrine disruption effects in mussels’ reproduction fitness as IBU is involved on prostaglandins biosynthesis inhibition.

BMC Med. 2013; 11:57..  The effect of statins on testosterone in men and women, a systematic review and meta-analysis of randomized controlled trials. Schooling CM, Au Yeung SL, Freeman G, Cowling BJ. CUNY School of Public Health  York, .Statins are extensively used for cardiovascular disease prevention. Statins reduce mortality rates more than other lipid-modulating drugs, although evidence from randomized controlled trials also suggests that statins unexpectedly increase the risk of diabetes and improve immune function. Physiologically, statins would be expected to lower androgens because statins inhibit production of the substrate for the local synthesis of androgens and statins’ pleiotropic effects are somewhat similar to the physiological effects of lowering testosterone, so we hypothesized that statins lower testosterone.   METHODS:A meta-analysis of placebo-controlled randomized trials of statins to test the a priori hypothesis that statins lower testosterone. We searched the PubMed, Medline and ISI Web of Science databases until the end of 2011, using ‘(Testosterone OR androgen) AND (CS-514 OR statin OR simvastatin OR atorvastatin OR fluvastatin OR lovastatin OR rosuvastatin OR pravastatin)’ restricted to randomized controlled trials in English, supplemented by a bibliographic search. We included studies with durations of 2+ weeks reporting changes in testosterone. Two reviewers independently searched, selected and assessed study quality. Two statisticians independently abstracted and analyzed data, using random or fixed effects models, as appropriate, with inverse variance weighting.RESULTS:Of the 29 studies identified 11 were eligible. In 5 homogenous trials of 501 men, mainly middle aged with hypercholesterolemia, statins lowered testosterone by -0.66 nmol/l (95% confidence interval (CI) -0.14 to -1.18). In 6 heterogeneous trials of 368 young women with polycystic ovary syndrome, statins lowered testosterone by -0.40 nmol/l (95% CI -0.05 to -0.75). Overall statins lowered testosterone by -0.44 nmol/l (95% CI -0.75 to -0.13).    CONCLUSIONS:  Statins may partially operate by lowering testosterone. Whether this is a detrimental side effect or mode of action warrants investigation given the potential implications for drug development and prevention of non-communicable chronic diseases. See commentary article here


Chemosphere. 2009 ;77 :1285-91.Occurrence and fate of rosuvastatin, rosuvastatin lactone, and atorvastatin in Canadian sewage and surface water samples.  Lee HB, Peart TE, Svoboda ML, Backus S. Aquatic Ecosystem Protection Research Branch, Environment Canada      Rosuvastatin (RST) and atorvastatin (ATO) are prescription drugs and members in the statin family used for the treatment of elevated cholesterol levels. A method using solid-phase extraction and liquid chromatography-tandem mass spectrometry (LC-MS/MS) for the determination of ATO, RST and its metabolite rosuvastatin lactone (RSTL) in sewage and surface water samples has been developed. In the influent and effluent samples collected from 11 sewage treatment plants located in Ontario, Canada, ATO, RST, and RSTL were detected in all samples with median concentrations of 166 ng L(-1) (influent) and 77 ng L(-1) (effluent) for ATO, 448 ng L(-1) (influent) and 324 ng L(-1) (effluent) for RST, as well as 158 ng L(-1) (influent) and 41 ng L(-1) (effluent) for RSTL. Due to the inter-conversion between RST and RSTL, the total concentration of RST and RSTL in a sewage sample should be reported. The median removal rate by wastewater treatment was 66% for ATO and 22% for RST and RSTL combined. These statins were quite persistent in sewage. After a storage period of 21 and 62 days, there was only a slight decrease in ATO concentration and no change in the total RST concentrations. These three compounds were also detected in a number of surface water samples at low ng L(-1) concentrations. This is the first reported occurrence and fate of RST and RSTL in the Canadian aquatic environment.
Ecotoxicol Environ Saf. 2011;74:1216-25. Chronic exposure to diclofenac on two freshwater cladocerans and Japanese medaka.Lee J, Ji K, Lim Kho Y, Kim P, Choi  Seoul National University,  Korea.
Consequences of long-term exposure to diclofenac up to 3 months were evaluated using freshwater crustaceans (Daphnia magna and Moina macrocopa) and a fish (Oryzias latipes). Marked decrease of reproduction was observed at 25 mg/L for D. magna, and at 50 mg/L for M. macrocopa. Three-month exposure of fish to 0.001-10 mg/L of diclofenac resulted in significant decreasing trend in hatching success and delay in hatch. The hatching of the eggs produced from the fish exposed to 10 mg/L was completely interfered, while fertility of the parent generation was not affected. Gonadosomatic index (GSI) of female fish was also affected at 10 mg/L. Predicted no effect concentration of diclofenac was estimated at 0.1 mg/L, which is a few orders of magnitude greater than those observed in ambient water. Therefore direct impact of diclofenac exposure is not expected. However its bioaccumulation potential through food web should warrant further evaluation.\
J Toxicol Environ Health A. 2009;72(10):633-41. Life-cycle exposure of fathead minnows to a mixture of six common pharmaceuticals and triclosan.Parrott JL, Bennie DT Water Science and Technology Directorate, Environment Canada,Fathead minnows were exposed for a life cycle to environmentally relevant concentrations of a mixture of six common pharmaceuticals and one personal care product (nominal concentrations: 1,000, 300, 100, 30, or 10 ng/L). Mean measured concentrations of each chemical in the highest fish exposure aquaria were: naproxen 793 ng/L, gemfibrozil 662 ng/L, diclofenac 331 ng/L, ibuprophen 217 ng/L, triclosan 115 ng/L, salicylic acid 67 ng/L, and acetaminophen (chemical analysis inconclusive, nominal 1000 ng/L). Fish exposed for a life cycle even to the highest concentrations of the six pharmaceuticals and personal care product (PPCP) mixture showed no significant changes in growth and development compared to control. Length, weights, condition factors, liver weights, and gonad weights of PPCP-exposed fish were similar to water and solvent controls (0.000005% ethanol v/v). There were no marked effects of PPCP mixture exposure on external sex characteristics of the fish or on egg production. The only parameter that appeared to be affected was percent larval deformities in F1, which showed a significant increase in the 100- and 300-ng/L (nominal) PPCP mixture. Larvae from control fish had 4.7% (water controls) and 3.4% (solvent controls) deformities, compared to 9.3% in the 100-ng/L (nominal) PPCP mixture and 9.2% deformities in the 300-ng/L (nominal) PPCP mixture. Chronic exposure to environmentally relevant concentrations of seven PPCP most often detected in Canadian municipal wastewater effluents (MWWE) did not appear to affect fathead minnow survival, growth, or egg production, although it produced quantitative increases in deformities in the F1 generation.
Hum Reprod. 1993 Aug;8(8):1168-72.Autonomic nervous modulation and effects of a prostaglandin synthase inhibitor on human cervical secretion.Jonsson B, Hammarström  Karolinska Hospital, Stockholm, Sweden.Modulation of cervical secretion at ovulation time was studied in 10 women with regular menstruations. In an in-vivo model with repeated collection of mucus samples during three 90-min periods, the amounts of mucus in a control cycle and in three experimental cycles were compared. Drugs interacting with the autonomic nervous system and a prostaglandin synthase inhibitor were administered at time of ovulation. The cholinomimetic drug carbacholine significantly increased cervical secretion, while the anticholinergic drug butylscopolamine markedly inhibited this secretion. A long-lasting decrease in secretion was seen after administration of the prostaglandin synthase inhibitor diclofenac. Beside regulation of cervical secretion by the ovarian hormones, these results suggest an autonomic nervous modulation of cervical secretion, and in addition an impact on cervical by a prostaglandin synthase inhibitor. The effects on fertility regulation in the female are discussed.
Water Res. 2010 Jan;44(2):555-66.   Oxidative transformation of micropollutants during municipal wastewater treatment: comparison of kinetic aspects of selective (chlorine, chlorine dioxide, ferrate VI, and ozone) and non-selective oxidants (hydroxyl radical).Lee Y, von Gunten U. Federal Institute of Aquatic Science and Technology, Duebendorf, Switzerland.  Chemical oxidation processes have been widely applied to water treatment and may serve as a tool to minimize the release of micropollutants (e.g. pharmaceuticals and endocrine disruptors) from municipal wastewater effluents into the aquatic environment. The potential of several oxidants for the transformation of selected micropollutants such as atenolol, carbamazepine, 17 alpha-ethinylestradiol (EE2), ibuprofen, and sulfamethoxazole was assessed and compared. The oxidants include chlorine, chlorine dioxide, ferrate(VI), and ozone as selective oxidants versus hydroxyl radicals as non-selective oxidant. Second-order rate constants (k) for the reaction of each oxidant show that the selective oxidants react only with some electron-rich organic moieties (ERMs), such as phenols, anilines, olefins, and deprotonated-amines. In contrast, hydroxyl radicals show a nearly diffusion-controlled reactivity with almost all organic moieties (k>or=10(9)M(-1) s(-1)). Due to a competition for oxidants between a target micropollutant and wastewater matrix (i.e. effluent organic matter, EfOM), a higher reaction rate with a target micropollutant does not necessarily translate into more efficient transformation. For example, transformation efficiencies of EE2, a phenolic micropollutant, in a selected wastewater effluent at pH 8 varied only within a factor of 7 among the selective oxidants, even though the corresponding k for the reaction of each selective oxidant with EE2 varied over four orders of magnitude. In addition, for the selective oxidants, the competition disappears rapidly after the ERMs present in EfOM are consumed. In contrast, for hydroxyl radicals, the competition remains practically the same during the entire oxidation. Therefore, for a given oxidant dose, the selective oxidants were more efficient than hydroxyl radicals for transforming ERMs-containing micropollutants, while hydroxyl radicals are capable of transforming micropollutants even without ERMs. Besides EfOM, ammonia, nitrite, and bromide were found to affect the micropollutant transformation efficiency during chlorine or ozone treatment.
Toxicol Appl Pharmacol. 2007 Dec 1;225:142-53. .Modulation of steroidogenic gene expression and hormone production of H295R cells by pharmaceuticals and other environmentally active compounds.Gracia T, Hilscherova K, Jones PD, Newsted JL, Higley EB, Zhang X, Hecker M, Murphy MB, Yu RM, Lam PK, Wu RS, Giesy JP.Michigan State University,       The H295R cell bioassay was used to evaluate the potential endocrine disrupting effects of 18 of the most commonly used pharmaceuticals in the United States. Exposures for 48 h with single pharmaceuticals and binary mixtures were conducted; the expression of five steroidogenic genes, 3betaHSD2, CYP11beta1, CYP11beta2, CYP17 and CYP19, was quantified by Q-RT-PCR. Production of the steroid hormones estradiol (E2), testosterone (T) and progesterone (P) was also evaluated. Antibiotics were shown to modulate gene expression and hormone production. Amoxicillin up-regulated the expression of CYP11beta2 and CYP19 by more than 2-fold and induced estradiol production up to almost 3-fold. Erythromycin significantly increased CYP11beta2 expression and the production of P and E2 by 3.5- and 2.4-fold, respectively, while production of T was significantly decreased. The beta-agonist salbutamol caused the greatest induction of CYP17, more than 13-fold, and significantly decreased E2 production. The binary mixture of cyproterone and salbutamol significantly down-regulated expression of CYP19, while a mixture of ethynylestradiol and trenbolone, increased E2 production 3.7-fold. Estradiol production was significantly affected by changes in concentrations of trenbolone, cyproterone, and ethynylestradiol. Exposures with individual pharmaceuticals showed the possible secondary effects that drugs may exert on steroid production. Results from binary mixture exposures suggested the possible type of interactions that may occur between drugs and the joint effects product of such interactions. Dose-response results indicated that although two chemicals may share a common mechanism of action the concentration effects observed may be significantly different.


update 4 March 2013:  the bad news for cheats – especially after cyclist Lance Armstrong’s confessions in January  2013, and the St Valentines Day massacre – the   Blade Runner Oscar Pistorius media frenzy  including unfounded accusations of steroid abuse ‘roid rage – is that testosterone is not recommended and prescribed for bodybuilding or performance enhancement, but solely where medically appropriate.

the good new news is that, while worldwide supplies of testosterone periodically run out,  it and estradiol are    now available once more in South Africa as appropriate 70-year old pellet implants for men and women needng HRT .  But the cost including implanting every 4-6 months remains likely much higher than fortnightly selfinjection or daily cream application.

at the beginning of 2013  authorities  were bemoaning the end of attempts to market depot hormone contraception for men.  But given increasing longevity, and falling male and female fertility, and potentially double the duration of fecundity of men compared to women, and the  real hazards of male and female sterilization and continuous female contraception with all current commercial ie patented synthetics,  for the determined couple  implants offer physiological reversible contaception without the risks of commercial patents.  For males implants of testosterone and progesterone, and for the female  triple implants of testosterone progesterone and estradio,  remain an option to be explored.

Jan 2010:  the important  report  from South African authorities on testosterone replacement for men  is wrong on one account:  such replacement with injection need not cost almost R6000pa  for the  ideal 3monthly German Schering AG ultralongacting brand.

as this column has repeatedly pointed out, physiological depot  injection has been available in South Africa for almost 70 years.  Currently it retails at perhaps R350 per gram as depotestosterone,  the equivalent dose to the 3monthly 1gm  injection (ie 160mg/fortnight)  being 160mg 1.6ml  every 2 weeks ie a cost of about R1400 per year.

This is easily and safely self-injected subcutaneously with a tiny (insulin) 25g needle, and gives physiological blood levels to most men – as with all chronic drugs, the dose and interval  simply needs to be titrated to individual metabolism and response, always under periodic medical screening. Eldrely men usually need and tolerate perhaps 20% less than younger men, who may well tolerate 200mg/fortnight.

It is blatantly wrong  to give the shortacting Sustanon monthly- this brand has been banned by authorities- and  unphysiological to give monthly the gold standard   depotestosterone cypionate / enanthate- with a life of about 3 weeks, since it is well known that the irrationally marketed higher dose for less frequent injection  eg 400mg imi monthly will give the adverse peaks and troughs that Dr Hafferjee notes. It’s like condemning  eg spirits or wine when 4% beer provides far less alcohol- but common sense tells us they are equally good (or bad!),  just the dose and interval needs to be proportionate.

Authoritative data on rational dose and interval of old depotestosterone has been freely available since at least 1991, so there is no justification whatsoever for proclaiming Nebido or other costly  forms of testosterone replacement  as the necessary gold standard- this is classic marketing hype.

We have long insisted that in this age of gender equity, men are as entitled as women to appropriate HRT- but the obtuse authorities and their stupid medical advisors refuse to recognize that both genders equally need all appropriate hormone replacement including physiological sex hormones for their vast life-extending multisystem benefits, least of which is sex.

Yet Discovery Health  has recently refused an elderly man testosterone replacement (recommended by his psychiatrist)  on the grounds that it is an aphrodisiac. Such refusal  of long-validated endocrine replacement (by their medical officers) amounts to medical negligence let alone defamation, fraud  and woeful ignorance.

Nebido and depotestosterone cypionate/enanthate are equally, superbly physiological if used rationally eg subcutaneously, to avoid the unnecessary multiple risks of intramuscular injection.  It can be questioned whether any patient who refuses to be taught his own injection warrants such costly replacement- the same natural selection applies to millions of insulin-dependent diabetics. And replacement of testosterone often relieves type 2 diabetics of the need to use costly and risky  insulin, when appropriate testosterone and metformin reduce all-cause mortality by perhaps half, whereas insulin in type 2 diabetics does not.

Just yesterday this column decried confusing causation with association in the comm0n  but far from majority universal problem of hyperandrogenism in women. There are only two major anabolic hormones that decline seriously with both aging and disease in both men and women, in whom appropriate physiological testosterone and vitamin D3  replacement (with appropriate physiological estrogen for women) is thus often required lifelong from what is potentially middle age to maintain health into vigorous- rather than frail- old age.


Health- slante, l’chaim!, hayah, sawubona! – in any country or language  is a blessing, a gift- not a right. It is insurance that has to be planned and enforced. Leaving it to fate, illness and hoping for a cure is often too late, sometimes crippling if not often  fatal. With comprehensive natural supplements, we can and should all die peacefully at an  active fit advanced  age  90years +  –   not old, incapacitated and demented. We owe this prevention to both ourselves, our  kids and our aging seniors.

So sensible lifestyle aside, promoting health  includes simple low-cost  (no-xray/no-laboratory) periodic screening:  for all,  from childhood:  of weight,  girth, eyes, teeth, bloodpressure, brainfunction- memory; and ultrasound bones – at any pharmacy/ optometrist, school or clinic;                         and  for women:  checking the breasts and pelvis for risk of  cancer.

The HealthSpanLife  South African Natural Medicine Clinic SANMC next to Cavendish Mall on the slopes of Table Mountain in beautiful Cape Town – one of the favourite world tourist  and heritage centres-  is a specialist clinic  staffed by experienced  registered professional practitioners- a medical internist specialist  (also UK registered);  a homeopath;  and a Muslim nursing sister.

It provides  one-stop holistic screening and diagnostics, and – uniquely-  evidence-based  natural remedies- nutritional support for all symptoms and chronic conditions-  also  for menopause-andropause-genitourinary- breast-sexual dysfunction- obesity-pain/headache –chiropractic  and detox ,

as well as if needed  appropriate modern specialized  testing and prescription medicines for all chronic major conditions including bio-identical hormone replacement for both genders (including implants);

and integrated referrals nearby (and in Gauteng)  as patients desire eg for autism, acupuncture, aromatherapy, physiotherapy, aquarobics,  advanced scopes, delicate restorative micro (eg hands, toes)-as well as major (eg bariatric, spinal,eye-, ear- neuro-)  surgery, infertility, xray/other scans, cancer, hyperbaric oxygen, spiritual intervention, psychiatric-hypno- therapy, and eg genetic profiling and counselling,   dialysis and transplantation, and stem cell therapy. …

Gentle Non-xray  ultrasound bone-density measurement (recommended by Cape Town , UK, and USA universities),  and tactile mechanical breast mapping (recommended by CANSA, UK, USA, Indian and Chinese studies) are available at SANMC (and in Gauteng) by appointment, and are covered by some medical aid plans;  whereas menopause consultations are covered by all open plans.

As typified by a new review last month,    World opinion is to use xray  mammography and  xray bone density imaging  only as last resort and only  in the elderly – or in staging those with breast cancer- because of the major problems and risks of xray imaging..   As world experts Profs Cornelia Baines epidemiologist in Canada, Mike Baum breast surgeon  in London and Peter Gotzsche epidemiologist  in Denmark  say,  there never has been any independent scientific evidence to support hazardous routine mass mammography crush xray screening of well women, let alone any repeated mass xray screening for decades, or the dangerous fictitious marketing hype of the American radiology-Breast Surgeons and Curves International nonsense  that xray mammo screening saves lives ..

While health tariffs must rise with inflation,  where med aid doesn’t cover, New Year 15% discount applies through January on cash-paid clinic services and in-house products. . .

For out-of-town/ overseas  visitors, accommodation and travel locally and throughout Africa and beyond can be arranged by outside experts around  clinic appointments. .

For appointments visit  the SANMC at 1st floor no.  15 Grove Medical Bldg on Pearce St  cnr Grove Ave (parking opposite at ABSA on Grove);    or  phone +2721-6831465/  -6717415; or fax  +27865657215; or email the manageress, doctors or Sister at  to discuss needs,  timing and preliminary costing. For details, references  and rationale for screening and prevention,  see


update 6 April 2015

In Claremont  Cape Town

A  Specialist Family Internist Clinic offers consultations by appointment especially for managing (and ideally preventing)  the major chronic degenerative diseases of aging  and  maintaining physical, mental (and why not sexual?) vigour to a ripe and healthy old age; as well as preventing and managing acute disease at all ages.

The clinic (a specialist physician and a nutritionalist)  offers all-system evaluation and if available, natural  (as well as essential prescription orthrodox) prevention/treatment including metabolic – weight-endocrine-diabetes; heart-lung -kidney; hypertension; neurological-pain; joint & muscle; abdominal, immune system ie infection, cancer and auto-immune  support;  genito-urinary, & sexual problems;

and appropriate screening – ECG, non-xray ( no-touch thermography- eg thermomammogram;   SureTouch tactile) mammograms, non-xray (ie  ultrasound) BMD ie  bone fracture risk measurement, body composition, and appropriate hormone profiling/replacement.

Phone during office hours for appointment: for Claremont office  ph 021-6717415  or 6831465 (or 083-6299160) – at Grove Medical Bldg 1st floor no 15 (opp ABSA Bank Parkade c/o Grove Ave Pearce Rd)  , or ;  or consultation by telephone/Skype or email .

by appointment only:        OFFICE HOURSby appt: ph office:  9am-5pm weekdays, 9am-1pm Saturdays.  AFTER  HOURS up to 9pm any day generally at office: –  email doctor  or ph 6am to 9pm  0836299160. EMERGENCIES  cannot be dealt with- acute emergencies and trauma, bleeding cases  must go to any  Emergency Unit .

Billing according to means ie specialist professional rates:  eg as a preferred provider for Discovery Health-  consultation procedure  0190; for needy patients, what the medical scheme pays  Detailed medical report and advice protocol provided at R300. Even Hospital Plans have to pay for outpatient consultation for scores of PMBs ie Prescribed Medical benefit conditions like Menopause.

 Needy patients desiring brief consultation can be seen by arrangement at GP rate.    Bone density scan  (covered by some medical schemes)  procedure 3612..  Non-xray mammograms are not yet covered by medical schemes codes: R650 for SureTouch including clinical consultation, R800 for thermomammogram.


The past year has seen not just catastrophic oilleaks, earthquakes  and thus marine and radiation disaster  accross the world, but also in Big-Business -driven campaigns to promote invasive radiation  screening mammography. Is the Disease-industry-driven screening   xray mammography tsunami fearmongering    to inflate the $trillion cancer industry ?

A tsunami is an overwhelming and non-tidal deluge. What does the screening mammogram xray deluge  for ever-younger  women bode for their later years?

Any intelligent consumer, not just a  specialist for 40 years, should  look very critically at all technology marketing  and products, and ignore most as unjustified.

Winifred Cutler from the Athena Institute writes this month: it is claimed that screening xray mammography and early treatment of silent breast (pre)cancer has greatly reduced  breast cancer mortality. But she points out that such mortality has also fallen in unscreened women, and given the incidence of overdiagnosis, “the adjusted mortality reduction that can be attributed to widespread  xray mammographic screening may be even more modest than reported by Kalager and colleagues: instead of the 7.2 reduction per 100,000 person-years that they report, a number somewhere between 5.99 and 5.54 should be compared to the 4.8 reduction per 100,000 person-years found in non-screened women. Hence, between 80% (4.8/5.99) and 88% (4.8/5.54) of the reduction in mortality may be attributable to issues other than mammogram screening”.

Another paper this month   reviews “Antidepressants and breast and ovarian cancer risk  and researchers’ financial associations with industry” – concluding that “Researchers with industry affiliations were significantly less likely than researchers without those ties to conclude that ADs increase the risk of breast or ovarian cancer. (0/15 [0%] vs 20/46 [43.5%] (Fisher’s Exact test P = 0.0012).”  ie in studies independent of AD manufacturers,  there is strikingly significant increase in breast cancer risk in those on antidepressants. With all the focus on the overblown risk of womens’ cancers, and the oft-reported discomforts and recalls from  screening xray mammography, no wonder that depression and breast cancer risk may be increased not just by stress (including the dreaded annual mammogram)  but more so by estrogenic ADs .

In view of the controversies about both necessity for well-breast screening, and patient complaints and cost-benefit doubts about xray mammography,  we consider  two of the options that radiologists dont  generally offer – thermography recommended by a recent patient with her thermography report, and tactile pressure-transducer  mapping recommended and used by CANSA the Cancer Association of South Africa, and the breast clinic at Newcastle-on-Tyne University.  

Both equipment technologies  are approved  in eg USA/ UK/ Europe/ Australia, and have been screened and not disapproved by regulatory authorities since the latter have no experience of such, and they are approved overseas, and there are no usage hazards, and as yet no standards locally, and no claims are made about their efficacy for diagnosis, prevention or treatment.

Thermography is used in clinics around South Africa; while pressure transducer tactile breast mapping is recommended and offered by CANSA for the poor in the main centres. In Gauteng one  radiologist does ultrasound followup in the ~10% of breasts where cancer cannot be confidently excluded.

There are obviously at least three major separate issues:

1.REAL RISKS OF COMMON CANCER?  Is the risk – incidence and mortality- of presymptomatic cancer in well patients without genetic risk of developing breast or prostate cancer high? and does early detection of presymptomatic breast or prostate cancer in patients not at high risk do more good than harm? Careful analysis of all available unbiased data suggests not- in fact such early diagnosis possibly  does more harm than good. 

2. RISKS OF REPEATED INVASIVE XRAY SCREENING: are  the risks of breast cancer increased by repeated xray screening?

3. IS ANY MAMMOGRAPHY METHOD TRULY SUPERIOR OR MORE RISKY?  Are the alternative screening mammography options- MRI, tactile mapping, thermomammography,  ultrasound- significantly different from each other and from invasive xray compression  mammography in risks and in sensitivity/ specificity? The evidence suggests that thermomammo, MRI and tactile mapping are safer and more sensitive and specific than xray mammography, and more sensitive than ultrasound as primary screening.

BACKGROUND:     Screening in medical practice thirty years ago used to refer to xay fluoroscopy – viewing through a fluoroscope screen- as is done of passengers at airports; but now refers to any preventative ie screening tests for silent undetected early disease. The most validated screening for cost-benefit – apart from taking a complete history- remains objective ie electronic bloodpressure monitoring.

However, is there still  justification for ever exposing younger healthy tissue- especially the thyroid, breasts and gonads- to repeated preventative invasive  xray “screening” under any circumstamces including for mammography and bone densometry? Especially not children, and especially not well younger (pre or peri)menopausal women  with already fluctuating endogenous estrogen dominance, who now with safe lifestyles have an average life expectancy ahead of them of perhaps 40 years. And when so many older middle-aged women simultaneously have been exposed needlessly to long-known carcinogenic smoking, alcohol and other oral estrogenics- soya, psychotropes, estrogens and progestins- recent use of oral contraceptives increases the risk of breast cancer. 

 The ongoing argument for and against screening is hotly debated by specialists opposed by the vested interest of the Screening Industry.  

XRAY MAMMOGRAPHY:    A Sherbrooke University Quebec paper published in 2011  seems unique- Irradiation (30Gy) of normal mouse tissue increases by some 30fold  the invasiveness of subsequent subcutaneously injected induced mouse breast cancer cells after 6 weeks  . There is nothing like it before on Pubmed nor apparently on Google – that recent normal-thigh irradiation vanquishes cancer resistance. This may explain why  breast cancer incidence, and mortality,  may be the same, if not higher  than in non-screened women after 10 years of   regular xray screening mammography of healthy breasts (the Norwegian and Danish studies of last year- see below) . The mouse irradiation study tries to simulate with one-off irradiation  the situation in women who have breast cancer removed and then a course of fractionated radiotherapy – which may eradicate most existing cancer but promotes fibrosis, but may promote  growth of metastatic   cancer cells into surrounding previously cancer-free subcutaneous tissue. This correlates with the shrunken hard breast we see in women who have had breast cancer excision and then breast radiotherapy.

Whether this applies to repeated (bi)ennial  screening xray mammography of “well” breasts over many years  with perhaps a few milliGy of diagnostic xray each time remains to be clarified.   Ruth Kleinerman’s followup of children does suggest possible risk,  that modest irradiation for diagnostic or therapeutic purposes with 0.1 to 0.7Gy increases breast cancer risk up to 2.5fold a decade to fifty years later.   This especially when the breast sceening industry claims that breast cancer lifetime risk is already above 10% eg 1 in 10, and increases with aging.

And correlates with work 30 years ago –Brian Henderson ea San Fransisco -that even ‘modest’ dose of another indisputable secondary carcinogen – oral ie megadose xeno-estrogen-progestin eg PremPro – started soon after menopause- progressively increases breast cancer risk when continued ie > 1500mg premarin for much more than a decade . .

Are women   reaping the harvest of liberal combined (post)menopausal oral (in North America, mostly (xeno)-estrogen therapy) – ERT – since the 1990s – ie to women born after WW2 – with liberal screening mammography?  – “a social obligation” according to xray-screened British women recently canvassed by Frances Griffiths ea .

Have either of these universal prescriptions for women ever been justified by independent longterm (ie well over 10 year) cost-benefit trials? since the 1980s Canadian Breast Screening Trial (1990 Brian Miller ea  )  cast doubt on the benefit over 5 years of  Xray screening mammography . . 

 A practicing USA radiologist like Dr Jeff Dach argues realistically against all such screening based on the evidence.  . He says, ‘just switch off the screening imaging machines, stop calling ductal carcinoma in situ of the breast a cancer.’  This may enrage radiologists offering screening xray mammography, and breast surgeons specializing in early breast cancer surgery.

IS RISK INCREASED BY XRAY SCREENING?  OVERDIAGNOSIS BY XRAY MAMMOGRAPHY SCREENING?          Despite numerous modelling studies trying to theorize – model  the safety of xray mammography, eg from Netherlands and Canada , a Spanish study has just confirmed that breast cancer is overdiagnosed by screening mammography by almost 50% in younger women so screened.  This bears out the observed greater Danish decline in overall mortality after about a decade  (2%) in those not screened than in those screened (1%) by Jorgensen Zahl and Gotzche;     and the lack of decline in incidence of breast cancer over the decades from screening mammography in the English-speaking continents, Sweden and Norway,  documented by Jorgensen and Gotzche. These studies contrast with other studies quoted by the mammography industry. Each group disputes the statistics of the other. .

The recent review in NEJM by Kalager ea of screening xray mammography in Norway similarly showed that such repeated breast screening irradiation if anything saves 1 in 40 000 lives from breast cancer, and barely reduces the longterm risk of breast cancer- contrary to what the dominant Xray Screening Industry would have us believe the past 20 years. .

But as Welch’s accompanying editorial on Kalager’s Norway study points out,  (and sent by the South African Menopause Society January 2011 email Menopause Matters newsletter) “The risk of a 50 year old woman dying from breast cancer in the next 10 years of her life is 0.4% (or 40 per 10 000) – this calculation includes (xray) screening. Put in the obverse frame of reference 9 960 per 10 000 will not die from such cause. Screening contributes 10% to this survival so without screening 9 956 women will not die. The number of lives saved by screening is thus 4 per 10 000 women per 10 years of screening. Using “numbers needed to treat” 2 500 women would need to be screened for 10 years to save one life. This is the benefit of screening. The harms are what happen to the 2499 women who are screened that do not die. Depending on screening techniques roughly 1 000 of the 2 499 (ie 40%) can anticipate a false-positive  and some sort of recall for further screening  This number rises with the frequency of mammography and is here calculated on screening every 2 years. Over-diagnosis and over-treatment is more sinister and would occur in 10 of the 2 499 survivors. This is needless (iatrogenic) treatment of a condition that was never going to bother them. False-positive diagnoses and over-treatments are the harms of screening.”

Is there any  objective evidence for the marketing slogan of the American Radiological and Breast Surgeons’ Associations- and the Curves International website-  that Screening Xray Mammography Saves Lives – in order to promote the $8billion a year xray screening mammography industry and the $trillion a year cancer industry?

And it needs to be stressed that the above concerns about screening mammography are directed at XRAY mammography, since due to heavy marketing and promotion,  Xray mammography is the only mammography method in use in all papers and studies of widespread primary screening of well breasts in women not at high risk from eg family history, previous cancer or already having breast lump or bleeding or pain.

It may be asked again: what male doctor would have biennial let alone annual crush xray imaging of his testes from age 40years to reduce his theoretical risk of silently developing testicular cancer, even if the hypothetical risk were 1 in 10?

THERMOGRAPHY:    A practicing academic gynecologist speaks for thermomammography from good  experience for years. Whether his esperience and opinion is  more or less valid that that of breast surgeons  who claim they can run and report xray mammography machines without a radiologist  is as usual a matter of hotly divided opinion.

 Far more important is that recent trials from Cornell , Cambridge UK and Shanghai   universities speak for the comparable effectiveness of thermography .

COMPUTERIZED TACTILE PRESSURE TRANSDUCER BREAST MAPPING  has evolved over the past decade, with applications in prostate and colorectal cancer mapping heavily funded by US Govt agencies. It ( computerized palpation tactile pressure mapping of breasts eg SureTouch) has been validated by academics such as Prof Cary Kaufman  and in controlled studies, at least eight the past decade  eg at the Necastle on Tyne Breast Clinic by Prof Clive Griffith and team (paper under peer review by the British Journal of Surgery). A recent abstract from Griffith(2009) describes study of 137 patients at a UK NHS breast clinic, 66 of whom had palpable breast masses. Seventy-seven of these were chosen at random to have a SureTouch examination in addition to CBE. Use of SureTouch reduced the percentage of missed lesions by senior and junior surgical trainees. The reproducible reports allowed efficient review by examiners with various levels of experience. Authors state that SureTouch imaging improved patients’ safety in breast clinic and likely had a role in the training and assessment of surgical trainees.

All the above options are now accepted in many western countries including South Africa, for both screening and diagnostic breast imaging, since the evidence  supports each of the options.

DEFINITION OF WHAT CONSTITUTES OPTIONS FOR MAMMOGRAPHY:   It is common sense that equipment methods involving the prefix/suffix gram eg ECG/ EKG/EEG/ spirogram/ renogram/ gramradio  often dont involve xrays. Equally, there are many established useful reliable alternative types, options for imaging the heart/lung/ breast. Neither the pre/suffix ‘gram’ nor the prefix ‘mammo’ are exclusive to the xray breast image, there are many established comparable modern breast imaging techniques from physiologicalthermomammography which reflects temperature ie bloodflow,  – to anatomical eg xray, ultrasound; magnetic resonance; and the past decade to computerized palpation tactile  pressure mapping (eg SoftTouch). This is despite van Steen and Van Tiggelen’s semantic  illogic  in regarding only xray breast imaging as mammography in their 2007 Belgian History of Mammography.   Already in 1999, the Dutch used mammography interchangeably for both xray and ultrasound screening.  But the earliest apparent Pubmed reference to ultrasound mammography is in 1982. .

RISK OF BREAST (AND PROSTATE) CANCER: it is common cause that in a first world population- where most die of “natural” degenerative aging diseases rather than classic malnutrition, plagues, exposure and violence –  these cancers cause about 4% of all deaths. But most sufferers do not die from these cancers. Hence their clinical occurrence over a lifetime may be around 10% risk ; although silent – never suspected- cancers may be found in far more people at autopsy. .

With routine repetitive xray mammography screening, the annual risk of breast cancer detection is generally reported  to be about 6 per thousand.

But Winifred Cutlers’ influential Athena Institute group from USA and Switzerland recent study Breast cancer in postmenopausal women: what is the real risk? concluded that regular xray screening of well not-at-high risk breasts, in the 18 published major studies without obvious vested interest bias involving over a million women screened, the annual incidence is more like 1 in a thousand. Her group questtions the bias, data massage of SEER statistics to inflate ie fearmonger. They thus question the cost-benefit of repeated xray screening of all older women from midlife to find 1 silent cancer in every thousand women- many of which cancers may be overdiagnosis since without intervention many will never present clinically diuring lifetime..

But it is also common cause that, apart from those with strong genetic risk (at least 2 close relatives who get one of the five hormonal cancers young ie prostate, colon, breast, ovary and womb),  the risk of cancer lifelong may be 10% or less since without screening, many never present during lifetime and are found incidentally at autopsy. There are many putative avoidable – preventable- causes: obesity, diabetes and bad food choices; and drugs- alcohol; sugar; smoking; aspartame; high cortisol (stress, lack of exercise), and oral estrogenic drugs like unfermented soya, the birth control and hormone therapy pills,. The risk of cancer subsides once these risk factors are minimized – this applies even to the familial cancers- eg after more than 5 years off oral birth control or sex hormone therapy. All diabetics- and all who stay overweight, or have raised cholesterol (mostly caused by insulin resistance) – should take the best preventative all-purpose prescription drug there is, the natural plant extract-  metformin- in appropriate tolerated dose- as well as abundant all-system-protectant antioxidant insulin sensitizer nitric oxide promoting eg vitamins, minerals, biologicals including fish oil; and appropriate human HRT. .

So the only women who justify early and ongoing screening for breast cancer may in fact be those who are at high risk from the above factors; and those who want to use appropriate HRT. For such women, even if if they have no breast symptoms or lumps, thermomammogram and/or tactile breast imaging (SureTouch) screening may arguably  be started young since they are at least harmless, to indicate whether there is need for further screening with ultrasound, xray, MRI etc. . .

Obviously the (Xray and thermo- and Tactile mapping and ultrasound and MRI) mammography machine suppliers and users are not going to fund a head-to-head comparative trial of the five methods . But if we collaborate as Griffith’s Newcastle-on-Tyne group did in an observational study ie recruiting enough women to have two or more of the mammography methods each time they elect to have screening, with screening staff blinded to what is suspected and shown on other and previous mammograms, and have central co-ordination – registration and independent collation- of results, we will soon have answers, as was invaluably shown without error in eg the major longterm Nurses Study.

With already available statistics, it will not take statisticians long to calculate how many women – maybe as little as 100 in each set- will need to have at least a preset minimum of at least two different mammography options, ideally say a year apart for baseline comparison and standardization.. This will be as simple as the Groote Schuur Hospital evaluation of the quantitative ultrasound bone risk system versus xray bone densometry in over a thousand women reported in 2009-  it showed equivalence.


update Feb 2011: WORLD CANCER DAY DOES NOT MEAN WORLD INVASIVE CANCER SCREENING:   the 2010  World Cancer Day email from the South African Medical Association  claims that “People should get tested by means of screening, it is a simple test that will identify if an individual have an unrecognised disease” ?

Where is cancer screening simple ie no invasive and technological cost? And without false negatives? Even faecal occult blood screening is both distasteful and thus anything but simple to many patients, requires some skill in interpretation, and the test kit has a cost. This SAMA message sounds like the Curves- Breast cancer Industry’s mantra slogan that Xray Mammography Saves Lives?   

 The huge problem is to get people to report and investigate SYMPTOMS, bleeding, bowel changes, lumps promptly.  

 For SCREENING of the well ie those who dont already warrant diagnostic tests due to symptoms or family history-  the definitive diagnostic imaging screens- of cervix,  prostate, colon and breast  –  are anything but simple,   non-invasive , low-cost tests  .   Except in the small minority who have a compelling family history of any of the five interlinked genetic  (breast, womb, ovary; colon; and prostate) cancers, prostate  & breast screening  of the well for early diagnosis of asymptomatic cancer have not proven to make significant difference in long term health let alone survival except create more worry & discomfort when positive?  

Unlike the commonest medical degenerative disease of adults-  vascular disease, hypertension- even breast cancer, the most feared amongst  non-smoking women, is not that common- as the South African Cancer Association says, only “1 in 29 ie 34% of women will present with breast cancer during her lifetime” – not 1 in eight as diseasemongers would have women believe. And “cervical cancer will be diagnosed in 1:35”. And prostate cancer in “1:23 men during lifetime” and  “one in 97 South African men is at risk at getting colorectal cancer while the rate for women is one in 162 “. And of course these risks are far lower in those who do not have bad family history and lifetyle. So the benefit of invasive screening is debatable, the risk of cancer is low in those who live safely, who know they do not have a bad family history or develop symptoms.

 Whether colon imaging (as opposed to faecal occult blood FOB screening) for preclinical diagnosis is any better at truly reducing morbidity and mortality  from colon cancer in low-risk well people is truly better than breast/ prostate screening remains to be validated in the same way  that 10 year retroanalysis has shown up the zero longterm benefit- if not more harm-  of xray screening mammography    

The US Preventative task Force study claims  15% reduction in colon cancer mortality from FOB screening – but all such data from the USA and its trading partners is so  notoriously tweaked to favour diseasemongering , can one believe any of them? Mainstream North American specialists who promote  screening scopes on all  well people naturally believe it is lfe-saving  –  but does it benefit the not-at-risk adult overall except the Screening Industry?  

For universal colon screening, where are objective colon screening studies like the recent Scandanavian breast studies that look at at least 10 year outcomes in the well low-risk population undergoing screening versus the population screened only because of symptoms?   The Wiki review of cancer screening pointedly highlights clear cancer screening benefit only for those at increased risk – which is by definition no longer primary screening for all, only for a small minority.  This seems to be a balanced rational view. Repeated cervix cancer screening is hardly cost-beneficial for the lifelong monogymous couple or ( careful olygamous) woman.


Posted on November 24, 2010     A still practicing radio-oncologist retired professor  writes:


“I think (xray) mammography needs to come from a request from a physician following clinical history, i.e risk factors, family at risk, or if for some reason genetic screening found BRCa1 or BRCa 2 genes, or a clinical exam suggests a lump;

Patient insistence may be OK, given informed consent about the controversy about different methods, benefits and risks.

Screening xray mammography implies Xraying all females of a population “at risk”.

 Early detection is based on physician and patient related factors, I would think.


By contrast, the evidence validating breast screening thermography  – recommended by eg a practicing gynecologist –  has been increasing for fifty years;  and for those who want screening when well, has been reported as a physiological screen with comparable high sensitivity and specificity  (as compared  to anatomical imaging- static xray or ultrasound or MRI or SureTouch tactile devices ) to pick up premalignant hyperperfusion risk about 8 years earlier (than xray mammography)..

In fact, as Dr Kaunitz points out  recently,  from the Norwegian study,  “decline in mortality attributed to screening alone may be as few as 2 deaths prevented/ 100,000 women screened[3]         ie xray mammography screening may save as few as 1 per 50 000 women screened. “

This is indeed a far cry from mammographysaveslives,  when 50 000 women with apparently well breasts   are  denied full knowledge of the actual risks and nett benefits, and driven by fearmongering   to have their breasts crushed and irradiated for decades  –  to  save possibly one  life.



update 2 Oct 2010: a practitioner asks what to do for a  white female 58years:
1998 ductal cell. lumpectomy, radiation, 15 nodes removed.  Tamoxifen  5 yrs.
2009  lobular cell. double mastectomy, nodes removed.  Aromasin  for next 5 yrs.
Osteopenia -2.3  found inside  1 yr .    on
Boniva ibandronate  4 yrs, stopped recently. 
 Doesn’t want to take IV drug for osteoporosis. 24 hr urine calcium  normal.  High vitamin d levels.
takes a lot of calcium,  vit d, vit c, vit b complex sups. Takes Prilosec omeprazole for reflux and hiatal hernia. chronic insomnia.
The questioner does not reveal her bodymass index or resting morning cortisol level or insulin resistance- all of which may well be raised; nor give her crucial vitamin D and C  intake or vitamin D  blood level. It is a question of evidence, not opinion – dogma- or laboratory average population ranges , as to what are optimal intakes and blood levels.

This column  has regularly reviewed the conflicting views and evidence  on osteoporosis;  BNP and breast cancer; and the safe multisystemic efficacy of using the score of natural supplements- including appropriate combined hormone replacement therapy – that safely oppose both osteoporosis – bone and muscle frailty-  and the associated chronic major involutionary diseases of aging especially vascular disease, dementia  and cancer. .

 The antireflux proton pump inhibitors PPI drugs notoriously aggravate osteoporosis; and for average reflux are not necessary with use of slippery elm, apple cider vinegar, simple calmag  and sensible diet and lifestyle.  It has been known for years that PPIs  more than double risk of osteoporosis, so why take them?. 

On the other hand, the pluripotential hormones of darkness and light –  vitamin D3 and  Melatonin – combined with the other mulibeneficial natural supplements that synergistically relieve/ reduce insomnia,  reflux pain,  cancer, depression, memory loss  and all other significant major chronic degenerative diseases of aging.

As this column regularly updates, Metformin too is a natural supplement (plant) co-hormone- a veritable panacea-  that reduces all major chronic disease and mortality by about a third- including cancer; and  dementia perhaps via reducing serum amyloid levels.let alone tissue oxidation, glycation, vasculopathy. BPN has none of these extraosseous benefits, only deadly risks.  

 Similarly, appropriate transdermal human estrogen but not oral xenoestrogen- CEE-  reduces serum amyloid in postmenopausal women,  while low testosterone raises serum amyloid in men.

So middleaged patients are at terrible risk of anxiety depression hypercortisolemia, frailty fractures, vascular disease , cancer and dementia after cancer, especially with sex hormone suppression or blockade. They do not need the myriad risky designer drugs touted for prevention of more cancer etc, all they need urgently and permanently is the scores of appropriate natural balanced supplements as this column regularly reviews- most of which supplements can simply be mixed in a tub of customized powder blend to be drunk twice daily. .

:Feb 13, 2009    In response to  Death-knell-for-bisphosphonates-for-osteoporosis-breast-cancer-time-for-class-action-against-bisphosphonate-damage last week,  a world-renown emeritus professor of radio-oncology comments:

“the action of the bisphosponates BPN is to inhibit osteoclastic action and thus reduces bone resorption; the patients tell the story- they get immediate and sustained relief from bone pain; if they  are on opiates the need is much reduced. Of course palliative RT is valuable, but often if pain recurs after RT the BPN give welcome relief, at least in my experience.

The  IV BPNs are also very useful in the oft-times encountered hypercalcemia often threatening myeloma- and other cancer patients. I am not however, too conversant with D3 in this setting!” But the first reference links are the latest in the clinical field of BPN and cancer.

Other than  in terminal cancer cases- when it doesn’t matter what convenient pain relief is used-  the problem with bone pain in cancer always is, what is the cause? either bone resorption from the catabolic effect of cancer (via eg high parathyroid hormone PTH);  OR cancer eating away at bone itself, OR something else common OP  unrelated to the cancer.?

But FOR CANCER-RELATED bone pain lesions – whether directly from cancer there, or from remote metabolic effect –  where are the trials comparing BPN with other antiresorptive antineoplastic ANTIINFLAMMATORY ANALGESIC ANABOLICS ie testosterone (or occasionally estrogen/ other antiandrogen)  and vitamin D3?

Obviously bone metastases are attacked with appropriate chemo-/ xray XRT, cortisone, testosterone AND if deficient, vitamin D3.

To put it the other way round: where is the evidence that BPN – at cumulative cost and risk-  adds benefit to the multiple attack? where the evidence that- unlike testosterone and vitamin D3- BPN has any benefit except on bone pain? Hypotheses based on in vitro and animal and human cell culture studies have  not translated into even good observational comparative evidence favouring BPN as good benefit:cost ratio for osteoporosis or cancer.

The oncologist answers in the traditional mode, by experience that BPN works. But evidence-based medicine EBM asks where is the comparative evidence for BPN to challenge the evidence that we have better multi-attack without BPN – when these supplements are not equally commercially promoted and tested in controlled trials for the usual commercial  reason ?

The dream of drug manufacturers is eternal, that their raincheque designer drug- statin or BPN or antihypertensive- will prove to be a safe multisystem panacea as is metformin and many  other supplements like vitamin D3 or testosterone. But after more than 30 years of BPN and statins, no trial in humans has yet shown this for BPN or  statin or any other original designer drug.