(No emergencies or surgery- these must go to nearest polyclinic or hospital ER). .
or consultations by Telephone/email where appropriate.
update December 08, 2014
Aspirin, paracetamol, other NSAIDs, and codeine in periodic conservative analgesic use have not been reported to cause hypoglycemia eg a few gm a day solo or in combination in well adults- despite deliberate overdose of these being notorious for causing fatal bleeding or liver failure with hypoglycemia, or respiratory failure.
But increasingly tramadol is incriminated in dangerous hypoglycemia: Tramadol Use and the Risk of Hospitalization for Hypoglycemia in Patients With Noncancer Pain JAMA Intern Med.December Tramadol is an increasingly widely used weak opioid analgesic , associated with adverse events of hypoglycemia. Analysis in United Kingdom Clinical Practice of treatnent with tramadol or codeine for noncancer pain between 1998 and 2012 included 334 034 patients, of whom 1105 were hospitalized for hypoglycemia during follow-up (incidence, 0.7 per 1000 per year) and matched to 11 019 controls. Compared with codeine, tramadol associated with increased risk of hospitalization for hypoglycemia in the first 30 days of use (OR, 2.61 [95% CI, 1.61-4.23]). This 30-day increased risk was confirmed in the case-crossover analyses (OR, 3.80 [95% CI, 2.64-5.47]). Conclusions tramadol (in contrst to codeine), TRIPLED risk of hypoglycemia requiring hospitalization. Additional studies are needed to confirm this rare but potentially fatal adverse event.
update 4 March 2013 BAN DICLOFENAC? four years on, another call comes for the virtual banning of diclofenac, from no less than the Canadian Medical Association Journal , based on a new metanalysis of NSAID risks by University Toronto’s McGettigan and Henry .
As this column has long pointed out, diclofenac is apparently still the only NSAID that can kill suddenly without warning. There are many far safer alternatives eg naproxen, ibrufen; and no compelling clinical evidence or reason to use it let alone cox2 inhibitors except false beliefs and heavy marketing.
So as this columnist concluded in 2009, it is blatant fraud, negligence and potential indefensible homicide to continue recommending let alone using diclofenac simply for profiteering.
21June 2009 It is 4 months since this column last addressed nonsteroidal anti-inflammatory drugs NSAIDs.
A new study (from USA, UK and Canada – Ray 2009) of NSAIDs claims that in those with ischemic heart disease, the popular NSAIDS -diclofenac, ibuprofen or rofecoxib(Vioxx) – increased serious heart disease/ death by about 50-67% compared to nonusers; whereas naproxen over some 111000 patient years of use gives no significant risk or benefit.
A new study from Denmark (Fosbol 2009) this year looked at a million healthy individuals with no hospital admissions or selected therapy. Compared to no NSAID use, ibruprofen and naproxen gave no added risk of death/ myocardial infarction; diclofenac gave 67% increased risks, and the two coxibs (rofecoxib Vioxx; celecoxib Celebrex) increased risk 100%.
So we are led to believe that naproxen or ibuprofen is the NSAID mild-to-moderate analgesic of choice. Naturally the American Colleges and academia – who represent the Disease Industry, not patients- recommend yet other potentially toxic drugs- like the magical proton pump inhibitors- to counteract the adverse NSAIDS..
But is this just a myopic view beloved of big pharma, to promote their snake oils.?
Another new study from Denmark (Gislason 2009) of 110 000 patients after admission for heart failure in the 12 years 1994-2005, showed that 57% died; 9000 (8%) were rehospitalized with acute heart attack and 40 000 (38%) were rehospitalized with heart failure. Thus heart failure in a well-nourished population has a poor prognosis. In 36 000 who had used NSAIDs compared to non-users, risk of death was doubled on diclofenac; increased~67% on (rofe-or cele)coxibs; and was significantly increased 22-31% by all other NSAIDs including naproxen and ibruprofen.
It is common cause after 20 years that injected diclofenac is the only NSAID that can unpredictably cause sudden death. So it’s administration risks culpable homicide when it is totally unwarranted. No cases of sudden death from any oral NSAID including aspirin appear on Medline, apart perhaps from the risk of hyperacute asthma (Asamoto 1999).
But what of gastrointestinal bleeding risks of NSAIDS? a 2007 study in Japan (Yajima) scoped all orthopaedic patients who took NSAIDs for more than 4 wks: oral diclofenac increased risk of erosive gastric lesions sixfold. A new review from Seattle (Schlansky 2009) refers to Helicobacter synergism in all NSAID use.
WHAT IS THE NEED FOR NSAIDS? The Wikipedia entry on NSAIDs sums it up: it has almost four times as much text on the numerous adverse effects of NSAIDs as on their uses- in fact the article does not discuss the advantages of NSAIDS as analgesics; in fact it states plainly that alone just “their gastrointestinal effects are estimated to result in 103,000 hospitalizations and 16,500 deaths per year in the United States”.
All designer drugs are dangerous in overdose. Without overdose, paracetamol has no risk – and the Wikipedia entry thereon is balanced and highly favourable even for infants. We know well that paracetamol- a fatal liver toxin in overdose- should not be marketed without a built-in simple liver (and antineuritic) protective of eg (carbo-or N-acetyl-)cysteine, alphalipoic acid and vitamin BCo. But the Disease – Big Pharma Industry is not interested in prevention- Only Disease Pays. And Regulators, lobbyists and legislators protect their source of work and income- the Drug Industry.
Fish oil (EPA+DHA) is probably the most beneficial NSAID supplement we have (- perhaps ahead of other front-runners like vitamins C, D, magnesium and CoQ10-) halving all sudden deaths, and reducing by at least a third all major chronic degenerative diseases from CVD to diabetes, arthritis, learning, depression, behaviour disorders. Industry wont pay for head-on comparative trials. But the trial evidence suggests that fish oil and oral EDTA have better risk-benefit than aspirin and other antiplatelet agents, NSAIDs and warfarin.
We know that for moderate trauma and small – medium (even knee) joint pain/ contusions, self-massage with any natural NSAID like arnica or wintergreen is all that is needed, combined if necessary orally with up to 3 to 4gm paracetamol /day +- if needed a little codeine. Prior 2002 found no significant difference in pain relief between paracetamol and naproxen in tension headache.
For more serious pain, short of strong opioids, there is in fact no overall trial evidence that weak opioids or NSAIDs are better than eg hypnotherapy, or acupuncture, or judicious paracetamol; to which latter if necessary a little codeine can be added as step-up analgesia. The latter agents have none of the deadly risk of NSAIDs. Amadio 1984 showed that of Peripherally Acting Analgesics: ” paracetamol at up to 4 g per day compares favorably in analgesic potency to aspirin and other NSAIDs, and should be considered the treatment of choice for mild-to-moderate pain”. Skovlund 1991 showed no significant difference between naproxen and paracetamol in postpartum uterine spasms.
Six RCTs – five in mostly European peoples and one in Hong Kong- found paracetamol equal to diclofenac (Voltaren) – March 1994 in arthritis; Brevik 1999 and Kubitzek 2003 in dental surgery; Hoogewijs 2000 and Woo 2006 after trauma; and Munishankar 2008 after Caesarian section. In a Cochrane analysis 2003, Towheed showed that in the one placebo-controlled RCT in osteoarthritis, paracetamol was clearly superior to placebo with a similar safety profile. And the general principle of therapy applies, that if required, combination of analgesics from different groups is better than single drug therapy. But given the many potentially fatal risks of the NSAIDs – compared to paracetamol, opioids and if indicated aspirin – there is no compelling reason to add NSAIDs for pain.
We know that it is negligent to initially sentence people with spontaneous mild-moderate head/neck/backache or tendonitis at the shoulder, elbow, knee etc to bedrest, NSAIDS, opioids or referral for xrays, scans or surgery. 95% will settle rapidly with reassurance, posture instruction and simple topicals and paracetamol analgesia. Otherwise most pain will disappear with firm reassurance with brief simple laying on of hands eg massage and traction with gentle rotational manipulation and instruction in auto-reinforcement – pressure point eg earlobe pressure, or acupuncture, or hypnosis. And most of the remainder resolve quickly with simple targeted injection with a little local anaesthetic plus depot steroid.
And we know that with judicious use, topical corticosteroid injection – never mind judicious brief systemic steroid (corticosteroid, calciferol, testosterone) has little or no risk and far greater target and multisystemic benefit than NSAIDs; and for chronic conditions, like fish oil at least address the underlying pathogenic mechanisms/causes- whereas NSAIDs and paracetamol ignore these.
Is drug-speeded resolution of inflammation essential and beneficial except for the drug vendor? A careful RCT by Bradley ea from Indiana University in 1992 observed that “joint tenderness and swelling, presumptive evidence of synovitis, may not be a priori indications for use of an antiinflammatory drug, or predict greater responsiveness to treatment with an antiinflammatory drug than to a pure analgesic, in symptomatic treatment of patients with knee osteoarthritis”.
So why are synthetic NSAIDs and especially the Coxibs still used? Why do academics and Regulators still allow, promote them for routine use, other than to profit Big Pharma, and cause perhaps a quarter million deaths a year globally?
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.
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.
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.
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.
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 http://www.biomedcentral.com/1741-7015/11/58.
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.
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.
Already just since April 2010, Pubmed (the on-line catalogue of peer-reviewed medical journal papers) reveals four reviews – from USA, Mexico, Ireland and Cambridge UK- on the huge socioeconomic impact of neglect of long-available safe cheap measurement and prevention of osteoporosis in aging populations. Especially that osteoporosis is underdiagnosed, and hence the need for improved use of diagnosis screening and preventatives.
And another study from France reviews the deadly potential cutaneous (let alone gastrointestinal and other) risks of bisphosphonate and strontium drugs prescribed for osteoporosis . Their risk of serious adverse effects may be <1:10 000 – but no study has ever been done comparing such $billion raincheck designer drugs with simple balanced lowcost safe combination of the score of natural supplements (some 7 vitamins, about 8 minerals and 5 human biologicals- costing as little as about US$10 a month) that are proven to prevent and heal osteoporosis let alone have major benefit on most major chronic diseases. .
The analogy is so simple- one does not treat :
anything but major pain with opioids or risky non-steroidal drugs (or a sore throat with antibiotics) when simple safe modest-dose non-addictive analgesics and local therapy suffice; or
overweight, or type 2 diabetes , or common mild to moderate hypercholesterolemia with any designer drug but metformin until control (with diet, lifestyle, supplements including metformin and appropriate other hormone adjustments) is no longer good enough; or
mild to moderate hypertension requiring drug therapy with anything but perfectly safe lowdose reserpine plus lowdose amilozide – which suffice in almost 90% of mild to moderate cases- when more modern designer drugs (eg betablockers, angiotensin-converting – enzyme inhibitors and even the older methyldopa and calcium channel blockers) and newer drugs both have infrequent but serious adverse effects, and are less effective (they do not have the long duration and safety record of reserpine plus amilozide that makes it so effective even with erratic use) .
The socioeconomic model that measures the impact of a therapy only on one disease eg osteoporosis obviously also by intent supports the global profiteering and job-creation interests of Big Pharma and their well-rewarded allies – Government, Regulators, Universities, Research, Corporations and private practice. For these big-money industries, the use of a safe shotgun of unpatented and nonprescription supplements that more than halves the incidence, premature disability and mortality of both fractures AND all the common major aging degenerative diseases is anathema, since it reduces the Aging Diseases Industry from a $trillion goldmine in the aging who still vote, travel and earn, to a $billion expense when it matters far less- in the very old.
Hence Big Pharma is fighting a global war to abolish free choice of foodstuffs and supplements, conspire with governments to dictate what sources of foodstuffs must be eaten, and put all micronutrient supplement under doctors’ prescription! and above all else, suppress comparisons of designer prescription drugs with the gold standard old drugs and highly effective safe combinations of supplements.
This column has regularly published the growing irrefutable proof that high technology appliances and drugs are simply not needed to measure, prevent and treat common fragility fracture risk or any of the associated linked common chronic degenerative aging diseases.
And Guglielmi ea from Italian and Singapore Universities recently published another landmark review confirming the voluminous evidence, recent reviews from UK, that quantitative ultrasound QUS scan has replaced Dual Xray DXA bone mass density BMD scan as the goldstandard fracture risk measurement test in common practice . Portable lowcost and therefore far more widely available QUS avoids the irradiation risk of costly centralized DXA, and the increasing overreading of bone density and hence risk score with aging due to accumulating calcification over the lower spine and hips.
It is of course intuitively and logically obvious that QUS devices that fix the target bone at a standardized site between the QUS heads as with eg the heelbone in eg the Norland CUBA footbox will eliminate most performer technique variation with a manually moved contact as in eg the Sunlight Beammed system.
Southampton University UK has also just published a study showing good correlation between peripheral QUS measurement and direct bone density measurement of excised fractured femoral heads from elderly hip replacement patients. . .
And a Madrid team has just published a survey showing good correlation in children between 5 and 12 years between QUS measurements and calcium-vitamin D intake.
CONCLUSION: Safe and lowcost QUS can and thus should be used for bone risk measurement at all ages and locations – including schools and even the bedside; in contrast to DXA which must not be used in those who are pregnant or not at least post reproductive if not post-middle-aged.
Even in the chronically frail or mentally dependent, periodic QUS screening is as crucial as eg bloodpressure screening since eg hypertensive , elderly, dementing or stroke patients share so many risk factors, and are thus are even more prone to osteoporosis- and incidental osteoporotic fracture easily converts the walking wounded from needing supervised care to being totally wheelchair- or- bed- dependent.
This blog is irregularly updated with the latest detailed pharmacological information on the ingredients of anti-aging preparations, the powder blend compositions, and mail-order/wholesale prices.
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