Monthly Archives: October 2014

VALUE OF STROKE CLOTBUSTERS QUESTIONED

Thrombolysis review controversy

Sarah Colyer  in the Australian Jnl of Medicine MJA  Monday, 13 October, 2014 reviews the raging argument:   “LEADING neurologists have condemned an Australasian College for Emergency Medicine decision to fund its own analysis of thrombolysis for acute stroke, which the college claims would be free of the conflicts of interest that plague existing guidance on the treatment.The Australasian College for Emergency Medicine (ACEM) is inviting proposals for consultants to analyse the published literature on thrombolysis in acute ischaemic stroke, which it has refused to endorse as a standard of care. (1)

Professor Yusuf Nagree, chair of the ACEM Scientific Committee, said unlike reviews published to date, its analysis would be “uniquely independent”.

“We are trying to find researchers who have no preconceived views or biases”, he told MJA InSight. An expert advisory panel would also be established to support the project, including an emergency physician, neurologist, GP, public health expert and lay person.

A Cochrane review published earlier this year found thrombolytic therapy significantly reduced death and dependency rates at 3‒6 months after stroke, and that this overall benefit was apparent despite an increase in symptomatic intracranial haemorrhage and deaths at 7‒10 days.(2)

While we await sight of the full Cochrane  paper, it is noteworthy that the abstract fails to give the absolute numbers.

Cochrane Database Syst Rev. 2014 Jul 29;7:CD000213. doi: 10.1002/14651858.CD000213.pub3.

Thrombolysis for acute ischaemic stroke.  Wardlaw JM1, Murray V, Berge E, del Zoppo GJ.:

“Most strokes are due to blockage of an artery in the brain by a blood clot. Prompt treatment with thrombolytic drugs can restore blood flow before major brain damage has occurred and improve recovery after stroke in some people. Thrombolytic drugs, however, can also cause serious bleeding in the brain, which can be fatal. One drug, recombinant tissue plasminogen activator (rt-PA), is licensed for use in selected patients within 4.5 hours of stroke in Europe and within three hours in the USA. There is an upper age limit of 80 years in some countries, and a limitation to mainly non-severe stroke in others. Forty per cent more data are available since this review was last updated in 2009.

OBJECTIVES:

To determine whether, and in what circumstances, thrombolytic therapy might be an effective and safe treatment for acute ischaemicstroke.

SEARCH METHODS:

We searched the Cochrane Stroke Group Trials Register (last searched November 2013), MEDLINE (1966 to November 2013) and EMBASE (1980 to November 2013). We also handsearched conference proceedings and journals, searched reference lists and contacted pharmaceutical companies and trialists.

SELECTION CRITERIA:

Randomised trials of any thrombolytic agent compared with control in people with definite ischaemic stroke.

DATA COLLECTION AND ANALYSIS:

Two review authors applied the inclusion criteria, extracted data and assessed trial quality. We verified the extracted data with investigators of all major trials, obtaining additional unpublished data if available.

MAIN RESULTS:

We included 27 trials, involving 10,187 participants, testing urokinase, streptokinase, rt-PA, recombinant pro-urokinase or desmoteplase. Four trials used intra-arterial administration, while the rest used the intravenous route. Most data come from trials that started treatment up to six hours after stroke. About 44% of the trials (about 70% of the participants) were testing intravenous rt-PA. In earlier studies very few of the participants (0.5%) were aged over 80 years; in this update, 16% of participants are over 80 years of age due to the inclusion of IST-3 (53% of participants in this trial were aged over 80 years). Trials published more recently utilised computerised randomisation, so there are less likely to be baseline imbalances than in previous versions of the review. More than 50% of trials fulfilled criteria for high-grade concealment; there were few losses to follow-up for the main outcomes.Thrombolytic therapy, mostly administered up to six hours after ischaemic stroke, significantly reduced the proportion of participants who were dead or dependent (modified Rankin 3 to 6) at three to six months after stroke (odds ratio (OR) 0.85, 95% confidence interval (CI) 0.78 to 0.93). Thrombolytic therapy increased the risk of symptomatic intracranial haemorrhage (OR 3.75, 95% CI 3.11 to 4.51), early death (OR 1.69, 95% CI 1.44 to 1.98; 13 trials, 7458 participants) and death by three to six months after stroke (OR 1.18, 95% CI 1.06 to 1.30). Early death after thrombolysis was mostly attributable to intracranial haemorrhage. Treatment within three hours of stroke was more effective in reducing death or dependency (OR 0.66, 95% CI 0.56 to 0.79) without any increase in death (OR 0.99, 95% CI 0.82 to 1.21; 11 trials, 2187 participants). There was heterogeneity between the trials. Contemporaneous antithrombotic drugs increased the risk of death. Trials testing rt-PA showed a significant reduction in death or dependency with treatment up to six hours (OR 0.84, 95% CI 0.77 to 0.93, P = 0.0006; 8 trials, 6729 participants) with significant heterogeneity; treatment within three hours was more beneficial (OR 0.65, 95% CI 0.54 to 0.80, P < 0.0001; 6 trials, 1779 participants) without heterogeneity. Participants aged over 80 years benefited equally to those aged under 80 years, particularly if treated within three hours of stroke.

AUTHORS’ CONCLUSIONS:

Thrombolytic therapy given up to six hours after stroke reduces the proportion of dead or dependent people. Those treated within the first three hours derive substantially more benefit than with later treatment. This overall benefit was apparent despite an increase in symptomatic intracranial haemorrhage, deaths at seven to 10 days, and deaths at final follow-up (except for trials testing rt-PA, which had no effect on death at final follow-up). Further trials are needed to identify the latest time window, whether people with mild stroke benefit from thrombolysis, to find ways of reducing symptomatic intracranial haemorrhage and deaths, and to identify the environment in which thrombolysis may best be given in routine practice.”

Post-publication commentary:   Ryan Radecki2014 Aug 04 09:38 a.m.    “The tPA Cochrane Review Takes Us For Fools”   It’s been 5 years since the last Cochrane Review synthesizing the evidence regarding tPA in acute ischemic stroke. Clearly, given such a time span, in an area of active clinical controversy, a great deal of new, important, randomized evidence has been generated!                   Or, sadly, the only new evidence available to inform practice is IST-3 – a study failing to demonstrate benefit, despite its pro-tPA flaws and biases. So, it ought not be a very exciting update, considering the 2009 version included 26 trials, and the 2014 update now includes only 27 trials. Their summary conclusion, with only additional evidence of regression to the mean, ought remain essentially the same, or even less optimistic, right?

Interv Neurol. 2014 May;2(3):97-104. doi: 10.1159/000356087.

Future directions for intra-arterial therapy for acute ischaemic stroke: is there life after three negative randomized controlled studies?

Maingard J1, Yan B2.   Royal Melbourne Hospital, Melbourne, Vic., Australia.

The three randomised controlled trials, Interventional Management of Stroke III (IMS3), Mechanical Retrieval and Revascularization of Stroke Clots Using Embolectomy (MR RESCUE) and Synthesis Expanasion: A Randomized Controlled Trial on Intra-Arterial Versus Intravenous Thrombolysis in Acute Ischaemic Stroke (SYNTHESIS EXP) showed no significant difference in clinical outcomes comparing intra-arterial (IA) therapy with intravenous thrombolysis. This article will explore the reasons for failure to show superiority of IA therapy.:

There are many reasons for the disappointing results of the three randomised controlled trials. Opposing views on IA therapy exist. Critics argue that only a small percentage of patients will be eligible for IA therapy and that it will never be cost-effective. Additionally, current trials have failed to address superior recanalization rates of new generation devices and lack of patient selection by advanced imaging. Time-to-treatment is longer in these randomised controlled trials and stroke outcomes were worse than anticipated. The current randomised controlled trials also took long periods to complete. There is emerging evidence that general anesthetic negatively influences outcome. Next generation trials will attempt to address these issues. Key Messages: There are disparate explanations for the disappointing results from the three IA therapy randomized controlled studies. Poor recanalisation rates with first generation endovascular devices, lack of advanced neuroimaging to aid in patient selection, lack of data surrounding the use of general anaesthesia, and prolonged time-to-treatment are potential contributors to negative results. The new generation of trials has the potential of addressing these pressing issues.

update: COMPLEMENTARY, HOMEOPATHIC MEDICINE APPROVED IN SWITZERLAND, DEBATED IN AUSTRALIA, GERMANY AND SWEDEN

20 Oct 2014  an update Swedish perspective;

Forsch Komplementmed. 2013;20(5):376-81. doi: 10.1159/000355916. Epub 2013 Oct 17.  Homeopathy: meta-analyses of pooled clinical data.
Hahn RG.    Research Unit, Södertälje Hospital, Södertälje, Sweden.

In the first decade of the evidence-based era, which began in the mid-1990s, meta-analyses were used to scrutinize homeopathy for evidence of beneficial effects in medical conditions. In this review, meta-analyses including pooled data from placebo-controlled clinical trials of homeopathy and the aftermath in the form of debate articles were analyzed. In 1997 Klaus Linde and co-workers identified 89 clinical trials that showed an overall odds ratio of 2.45 in favor of homeopathy over placebo. There was a trend toward smaller benefit from studies of the highest quality, but the 10 trials with the highest Jadad score still showed homeopathy had a statistically significant effect. These results challenged academics to perform alternative analyses that, to demonstrate the lack of effect, relied on extensive exclusion of studies, often to the degree that conclusions were based on only 5-10% of the material, or on virtual data. The ultimate argument against homeopathy is the ‘funnel plot’ published by Aijing Shang’s research group in 2005. However, the funnel plot is flawed when applied to a mixture of diseases, because studies with expected strong treatments effects are, for ethical reasons, powered lower than studies with expected weak or unclear treatment effects. To conclude that homeopathy lacks clinical effect, more than 90% of the available clinical trials had to be disregarded. Alternatively, flawed statistical methods had to be applied. Future meta-analyses should focus on the use of homeopathy in specific diseases or groups of diseases instead of pooling data from all clinical trials.

German perspective:      Homeopathy. 2010;99(1):76-82. Placebo effect sizes in homeopathic compared to conventional drugs – a systematic review of randomised controlled trials.     Nuhn T1, Lüdtke R, Geraedts M.1Klinik Roderbirken, Roderbirken, Leichlingen, Germany.  It has been hypothesised that randomised, placebo-controlled clinical trials (RCTs) of classical (individualised) homeopathy often fail because placebo effects are substantially higher than in conventional medicine.  OBJECTIVES:  To compare placebo effects in clinical trials on homeopathy to placebo effects on trials of conventional medicines.         METHODS: We performed a systematic literature analysis on placebo-controlled double-blind RCTs on classical homeopathy. Each trial was matched to three placebo-controlled double-blind RCTs from conventional medicine (mainly pharmacological interventions) involving the same diagnosis. Matching criteria included severity of complaints, choice of outcome parameter, and treatment duration. Outcome was measured as the percentage change of symptom scores from baseline to end of treatment in the placebo group. 35 RCTs on classical homeopathy were identified. 10 were excluded because no relevant data could be extracted, or less than three matching conventional trials could be located.       RESULTS:  In 13 matched sets the placebo effect in the homeopathic trials was larger than the average placebo effect of the conventional trials, in 12 matched sets it was lower (P=0.39). Additionally, no subgroup analysis yielded any significant difference.     CONCLUSIONS: Placebo effects in RCTs on classical homeopathy did not appear to be larger than placebo effects in conventional medicine

and an Australian perspective from the MJA on a recent Australian ethics review: :

J Bioeth Inq. 2014 Jul 19.    A Gentle Ethical Defence of Homeopathy.
Levy D1, Gadd B, Kerridge I, Komesaroff PA.    1Centre for Values, Ethics and the Law in Medicine, School of Public Health, Faculty of Medicine, University of Sydney, 92-94 Parramatta Rd., Camperdown, NSW, 2006, Australia, David.c.levy@sydney.edu.au.

Recent discourses about the legitimacy of homeopathy have focused on its scientific plausibility, mechanism of action, and evidence base. These, frequently, conclude not only that homeopathy is scientifically baseless, but that it is “unethical.” They have also diminished patients’ perspectives, values, and preferences. We contend that these critics confuse epistemic questions with questions of ethics, misconstrue the moral status of homeopaths, and have an impoverished idea of ethics-one that fails to account either for the moral worth of care and of relationships or for the perspectives, values, and preferences of patients. Utilitarian critics, in particular, endeavour to present an objective evaluation-a type of moral calculus-quantifying the utilities and disutilities of homeopathy as a justification for the exclusion of homeopathy from research and health care. But these critiques are built upon a narrow formulation of evidence and care and a diminished episteme that excludes the values and preferences of researchers, homeopaths, and patients engaged in the practice of homeopathy. We suggest that homeopathy is ethical as it fulfils the needs and expectations of many patients; may be practiced safely and prudentially; values care and the virtues of the therapeutic relationship; and provides important benefits for patients.

Jane McCredie
Monday, 20 October, 2014
Jane McCredie

YOU don’t see the word “gentle” in the title of a scientific paper all that often.

But there it is atop a paper coauthored by two homeopaths and two prominent Australian medical ethicists, Associate Professor Ian Kerridge and Professor Paul Komesaroff: “A gentle ethical defence of homeopathy”.

Homeopathy doesn’t usually keep that kind of company. Medical leaders are generally more likely to lambast the alternative health practice than to defend it.

These authors, however, suggest those who criticise homeopathy as unethical have “an impoverished idea of ethics — one that fails to account for either the moral worth of care and of relationships or for the perspectives, values, and preferences of patients”.

“The choice to seek care from a homeopath can be just as valid and as ethically sound as any other health care choice that a patient or consumer makes, and the notion that consent or agency is untenable in respect to homeopathy is deeply paternalistic and challenges the very idea of moral autonomy”, they write.

I can’t help gently suggesting that perhaps the authors are setting up a bit of a straw man here.

I’m not sure that even the most virulent critics of homeopathy would argue an adult seeking homeopathic care was acting unethically, though they might criticise that choice on other grounds.

But what of the homeopaths? Is it unethical to provide a treatment that comprehensively fails to meet the normal standards of evidence-based medicine (EBM) (see this MJA review)?

The authors of the current paper argue the EBM approach alone is not enough, but that we need “a more sophisticated approach to evidence in medicine” in this and every other field of health care.

“This approach would recognise that what constitutes evidence can be defined and measured in different ways by different people or groups and that judgements about competing epistemes are ultimately statements about the ‘value’ of particular data or outcomes”, they write.

“When looked at in this way, it then seems completely appropriate that congruence with patients’ values, goals and preferences as well as their reported experiences and outcomes from homeopathic interventions should be included in any comprehensive evaluation of the efficacy of homeopathy.”

That’s all getting a bit postmodern for me.

I have no doubt many patients experience benefit from seeing a homeopath, and I support their right to keep doing it. I also don’t doubt the vast majority of homeopaths hold a sincere belief in the value of what they do.

But I don’t believe their medicines “work”, other than by triggering a sometimes powerful placebo effect, and I am disturbed when claims are made for them that go beyond that.

I wrote last year, for example, about homeopathic remedies being sold in pharmacies with claims they were effective against fever and other symptoms in children, claims that were withdrawn after a successful complaint to the Therapeutic Products Advertising Complaints Resolution Panel.

Randomised controlled trials (RCTs) are far from perfect but, as Winston Churchill famously said about democracy, they’re the worst system we have, except for all the others.

I’d certainly rather base my decisions about health care on RCTs than on a bunch of patient anecdotes.

Others have different values and different decision-making processes and that’s fine. I have friends who attest to the mental health benefits of past-life regression and tarot readings and I respect that.

My own ethical concerns about homeopathy arise when attempts are made to place it in contexts where it doesn’t belong, when the public purse subsidises it through private health insurance rebates, for example (something that may come to an end next year).

And I think it’s fundamentally misleading for a practice without a conventional evidence base to be promoted in a scientific context — as happens when pharmacists endorse homeopathic products or universities teach homeopathy as part of a science degree.

The ethics of that, I’d gently suggest, are troubling.

 

Jane McCredie is a Sydney-based science and medicine write

June 2009   editorial comment on `HOMEOPATHIC BASICS (June ’09)   Dr. Ron Beare ND., DHomMed, South Africa below:

On May 17, 2009, in a unique referendum ” the people of Switzerland voted by a two-thirds majority  to force Parliament to pass  a constitutional amendment that supports the use of complementary medicine (CAM), incorporating admission of doctors of anthroposophical medicine, homeopathy, neural therapy, phytotherapy and Traditional Chinese Medicine (TCM) into obligatory health insurance; integration of complementary medicine into teaching and research; and safeguarding of proven remedies.”

This vote by the  notoriously conservative rightwing Swiss  is a stunning precedent for enforcement of the peoples’ sensible rights and wishes irrespective of the machinations of  politicians and Big Business, the inconvenient truth of  oligarchy disaster capitalism especially when it manipulates organized religion as extremist  “right wings” do everywhere from Islam to Baptist America to C of E Britain to Rome to  India, China, Japan and without exception in Africa. Especially in South Africa where the AK47-brandishing State President Rev Jacob Zuma- a habitual serial adulterer  (never mind polygamist) supported by acolytes swearing to kill for him – announces that he will rule until the Christ comes….

Phytotherapy, anthroposophical and TCM deal with foodstuffs, natural plant remedies- the origin and foundation of modern drugs. But what of homeopathy?

In 2005 the University of Berne published a major meta-analysis comparing homeopathy with allopathy (Hahneman’s reference term for conventional modern medicine)  in comparable chronic conditions including respiratory-allergy, musculoskeletal, neurological and gastrointestinal. They concluded that “Biases are present in placebo-controlled trials of both homoeopathy and conventional medicine. Discounting these biases, there was weak evidence for a specific effect of homoeopathic remedies, but strong evidence for specific effects of conventional interventions.”

But “110 homoeopathy trials and 110 matched conventional-medicine trials were analysed. 21 homoeopathy trials (19%) and nine (8%) conventional-medicine trials were of higher quality. When the analysis was restricted to large trials of higher quality, the odds ratio was 0·88 (95% CI 0·65–1·19) for homoeopathy (eight trials) and 0·58 (0·39–0·85) for conventional medicine (six trials).”  This outcome statistically favours alopathic medicines and not homeopathy. .

But such analysis does not address the risk:benefit ie the adverse effects of allopathic drugs; it did note the small number of large trials of high quality.  So what this study largely raises is the power of placebo, belief ie autosuggestion and spontaneous resolution in both homeopathy and alopathy, and the fallacies of randomized controled trials and metanalyses.

It also highlights the paradox that while western medicine aims, claimsto be science-based, for daily minor consultations in the better-off  it is largely in daily practice  the art of  temporizing medicine, symptom-based palliation while the underlying stressor, be it emotional or infection, subsides spontaneously. And apart from trauma, or infection, or the small percent of adults with the most common deadly genetic diseases  eg Huntingdon’s chorea or haemophilia which can only be palliated,  for chronic common  diseases of aging there are no modern drugs which address the rckbasic degenerative pathogenesis.

Metformin the 85year old extract of the age-old medicinal galega officinalis is the only prescription “drug” which does so, in the appropriate dose and patient a true panacea since (like fish oil)  it addresses virtually every pathogenetic mechanism of obesity- lipidemia- diabetes, hypertension- heart-vascular-renal, retinopathy, dementia and hypoimmunity. Quality cannabis the Forbidden Medicine is similarly a powerful multidisease therapy, while vastly safer as a recreational dependency than heavily marketed tobacco smoking, gratuitous sex, alcohol and sugar products-the four horsemen of the apocalypse-  after human bloodlust- mass starvation, violence,  murder and warfare the greatest killers of all ..

But  homeopathy is like religion: ineffable, unprovable. As  the great Dane Søren Kierkegard the founder of modern psychology and  fierce critic of the Church wrote almost two centuries ago,  personal religion (as opposed to tribal membership) can only be by a leap of faith, a suspension of reason. The theologian Karen Armstrong, the scientist Steven Jay Gould, the London philosophers AC Greyling and John Gray, and many top novelists – George Elliott,   Hermann Wouk, Margaret Attwood and John Fowles – have written perceptive books dissecting  true religion- which is at worst a harmless fulfilling moral code – and caring calling-  for many, except when (like religion and medicine through the ages) abused for political domination and greed in the pursuit of power by the ruthless. Homeopathic physicians surely  cannot be thus accused, unlike the Disease Industry and Big Pharma ..  Homeopathy did not, like mainstream medicine in Hahneman’s time, incarcerate and even neuter  like animals the feeble and the  sad with the bad irrespective.

It is commonly said that one in three admissions to USA hospitals, and thousands of premature deaths there  each year, are iatrogenic, contributed to by modern medicines and rash surgery. Except in nondiagnosis of serious treatable illness which progresses by neglect, this cannot happen with homeopathy.

But if these beliefs and organized practices- homeopathy, reflexology, craniosacral medicine, faith healing, personal (not dictated) religion, nutritional supplements in moderation by experience –   are harmless, are they better or worse than most modern marketed chronic drugs, which mostly prove for common chronic conditions eventually  to be inferior to old and proven remedies, if they do not collapse or fall into neglect within years of their launch from adverse effects or disillusion. Examples are non-steroidal anti-inflammatory analgesics including coxibs (compare to the enduring paracetamol, and analgesic herbs); bisphosphonates (compare to appropriate ancient anabolic supplements including enduring appropriate HRT), or statins and glitazones (compare to ancient metformin and other natural antioxidants); or the troublesome angiotensin blockers for common hypertension (compare to gold standard old  low dose reserpine plus low dose coamilozide) .

In that context of inquiry one can read this exposition by a naturo-/homeopathic physician with well over 50 years of practice experience on the observations and teachings of Hahnemann, a profoundly observant and ethical medical practitioner, linguist and scientist for his times. . . he was certainly the first and most famous medical doctor of modern times. Although Edward Jenner was four years his senior and William Harvey two centuries earlier, they made their mark each in only one field, whereas Hahnemann applied his mind to all disease – both chronic, infectious, poisoning and the humane care of the insane. He was eerily prophetic of our modern Disease Industry- sell at any cost: he  claimed that the medicine of his time did as much harm as good: ‘My sense of duty would not easily allow me to treat the unknown pathological state of my suffering brethren with these unknown medicines. The thought of becoming in this way a murderer or malefactor towards the life of my fellow human beings was most terrible to me’ .” If only the FDA and it’s devotees would follow this principle before applying relatively untested new drugs where well-proven old have long existed.

It is not inconceivable that molecular biology may yet, paradoxically,  explain by quantum mechanics a theoretical basis for homeopathy, setting it aside from pseudoscience and quackery, since modern critical reviews still leave room for doubt. .

ndb

`HOMEOPATHIC BASICS (June  ’09)   Dr. Ron Beare ND., DHomMed, South Africa.

“It is amazing to think that Dr. Samuel Hahnemann MD  (1755-1843), a German physician and the Founder of homeopathy, http://en.wikipedia.org/wiki/Samuel_Hahnemann lived at a time when medicine recognized bloodletting and purging, mixtures made from vipers, opium, mercury; and other physically degrading poisons.

He was always mindful of the teachings of that other genius Hippocrates, Father of herbal medicine.

Hippocrates, the Father of Natural/Herbal Medicine, died about 400 years before the Christian era.

It is he whose Hippocratic Oath defines the Code of medical ethics even to-day.

Hippocrates denied the then superstitious causes of disease.

He stated in lectures and books that feelings and thought came from the brain, not the heart or liver (as it was thought for centuries before and after Hippocrates).

He was the first dr. to describe epilepsy and pneumonia.

He also said that physicians should do no harm.

Because health is our greatest blessing, we must always improve our lifestyles, by walking, diet and hygiene.

Some 2000 years after Hippocrates’ entreaties about Natures’ healing without perpetrating invasive harm;  Dr. Samuel Hahnemann (1755-1843) established a vibrant energy type of medicine, based on the totality of each patient’s individual symptoms.

“The Removal of the Totality of Symptoms means the Removal of the Cause” (Kent, “Lectures on Homeopathic Philosophy”).

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29 SEPT 2014 OVARIAN CANCER UPDATE: PROGESTERONE REPLACEMENT IS IDEAL; WHY USE ORAL HT? WHEN ESPECIALLY LONG TERM PROGESTINS GREATLY INCREASE RISK OF OVARIAN AS WELL AS BREAST CANCER.

: ABSTRACT:  since last review in  this column 5 years ago, what progress has there been with ovarian cancer OvCa? On Pubmed there are 81000 references,  45500 reviews on OvCa

5 Oct 2014:  Ovarian Cancer Often Arises from Precursor Endometriosis    Frontline Medical News, 2014 Sep 29, B Jancin

   29 Sept 2014  The good news is that if ovariectomy is not done at hysterectomy, then at least salpingectomy should be done- it does not cause earlier menopause.  And the modern fashion for progesterone cream as baseline hormone balancing in this age of estrogen dominance, the feminization of nature,  also adds major protection for heart, bone, memory, mood,  and against cancer, without the risks of estrogen.

Before this month’s update,  the latest, an Australian cancer review  Mette ea 2013, shows that cigarette smoking increases the risk of OvCa by 30% to 60%.

The latest   review 2013 Modugno ea at Univ Pittsburgh/Mayo Clinic  Hormone response in ovarian cancer: time to reconsider as a clinical target?   said “Ovarian cancer is the sixth most common cancer worldwide among women in developed countries and the most lethal of all gynecologic malignancies. There is a critical need for the introduction of targeted therapies to improve outcome. Epidemiological evidence suggests a critical role for steroid hormones in ovarian tumorigenesis. There is also increasing evidence from in vitro studies that estrogen, progestin, and androgen regulate proliferation and invasion of epithelial ovarian cancer cells. Limited clinical trials have shown modest response rates; however, they have consistently identified a small subset of patients that respond very well to endocrine therapy with few side effects. We propose that it is timely to perform additional well-designed trials that should include biomarkers of response.The most consistently reported reproductive and hormonally related factors found to protect against EOC are use of oral contraceptives (OCs), increasing parity, and having a tubal ligation. In contrast, increasing age and nulliparity have been consistently shown to increase EOC risk. 

    Recent studies, including the prospective Women’s Health Initiative (WHI) (Anderson et al. 2003) and the Million Women Study (Beral et al. 2007), report an increase in risk for both estrogen-only (ET) and estrogen–progestin (EPT) formulations, although the risk associated with EPT was lower than that of ET. A recent meta-analysis of 14 published studies found risk increases 22% per 5 years of ET use compared with only 10% per 5 years of EPT use, suggesting that risk differs by regimen (Pearce et al. 2009).               Exogenous androgens may be associated with EOC. One case–control study found that use of Danazol, a synthetic androgen commonly used in the treatment of endometriosis, significantly increased EOC risk (Cottreau et al. 2003), although this finding has not been replicated (Olsen et al. 2008). Ever use of testosterone (tablets, patches, troches, or cream) has been associated with a threefold increase in EOC (Olsen et al. 2008).             

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

         Endometriosis, defined as the presence and growth of endometrial tissue outside the uterine cavity, has also been associated with EOC. A recent pooled analysis of 13 case–control studies showed a threefold increase in the incidence of clear cell EOC and a twofold increase in endometrioid EOC among women with a self-reported history of endometriosis (Pearce et al. 2012).

    An increased risk of EOC was reported by one case–control study (Schildkraut et al. 1996) among women with polycystic ovary syndrome (PCOS), a condition associated with menstrual dysfunction, infertility, obesity, the metabolic syndrome, hyperandrogenism, and insulin resistance. However, the finding was based on a small number of cases (n=7) and the association was limited to nonusers of OCs and thin women. Further case–control and prospective studies have failed to confirm this relationship (Pierpoint et al. 1998, Olsen et al. 2008, Brinton et al. 2010).

   Tubal ligation has been consistently shown to be associated with reduction in EOC risk (Cibula et al. 2011). This protection appears similar in magnitude to OC use and child bearing (about 30%) and is protective in high-risk women (i.e. BRCA1/2 carriers) as well. Hysterectomy has also been shown to reduce EOC risk, although the magnitude of the association is not as great nor as consistent as that reported for tubal ligation (Riman et al. 2004). Finally, reproductive factors associated with other hormonally linked cancers, such as age at first menarche, age at menopause, and length of reproductive years, have not been consistently associated with EOC (Riman et al. 2004).

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

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

Now this month  comes exciting news about  a  Paradigm Shift: Prophylactic Salpingectomy for Ovarian Cancer Risk Reduction   Frontline Medical News, 2014 Sep 24, B Jancin     :   Removing the fallopian tubes at the time of pelvic surgeries as a potential means of reducing ovarian cancer risk appears to be a movement that’s picking up steam in clinical practice.
       A recent survey of 234 U.S. gynecologists showed prophylactic bilateral salpingectomy is catching on when performed in conjunction with hysterectomy, but far less so for tubal sterilization, Dr. Austin Findley observed at the annual Minimally Invasive Surgery Week.                                                                       A total of 54% of respondents indicated they routinely perform salpingectomy at the time of hysterectomy in an effort to reduce the risk of ovarian cancer as well as to avoid the need for reoperations. However, only 7% of the gynecologic surgeons said they perform salpingectomy for tubal sterilization, even though 58% of respondents stated they believe the procedure is the most effective form of tubal sterilization (J. Minim. Invasive Gynecol. 2013;20:517-21).
  “In my experience at various hospitals, I think these numbers are a pretty accurate reflection of what folks are doing,” commented Dr. Findley of Wright State University in Dayton, Ohio.
     The prophylactic salpingectomy movement is an outgrowth of the tubal hypothesis of ovarian cancer.
    “There is now increasing and dramatic evidence to suggest that most ovarian cancers actually originate in the distal fallopian tubes. I think this is a concept most people are unaware of or are just becoming accustomed to. The tubal hypothesis represents a major paradigm shift in the way we think about ovarian cancers. The previous belief that excessive ovulation is a cause of ovarian cancer is no longer regarded as accurate,” he explained at the meeting presented by the Society of Laparoscopic Surgeons and affiliated societies.
      Ovarian cancer is the No. 1 cause of mortality from gynecologic malignancy, accounting for more than 14,000 deaths per year, according to National Cancer Institute data. The lifetime risk of the malignancy is 1.3%, with the average age at diagnosis being 63 years.
       Only 10%-15% of ovarian cancers occur in women at high risk for the malignancy because they carry a BRCA mutation or other predisposing gene. The vast majority of ovarian cancer deaths are caused by high-grade serous tumors that have been shown to be strongly associated with precursor lesions in the distal fallopian tubes of women at low risk for the malignancy.
            There is no proven-effective screening program or risk-reduction method for these low-risk women. However, with 600,000 hysterectomies and 700,000 tubal sterilizations being performed annually in the United States, prophylactic salpingectomy has been advocated as an attractive opportunity to potentially reduce ovarian cancer risk. Other common pelvic surgeries in which it might be used for this purpose include excision of endometriosis and laparoscopy for pelvic pain. It also has recently been shown to be feasible and safe post partum at cesarean or vaginal delivery (Obstet. Gynecol. 2014 [doi: 10.1097/01.AOG.0000447427.80479.ae]).
   But the key word here is “potentially.” It must be emphasized that at present the ovarian cancer prevention benefit of prophylactic salpingectomy remains hypothetical; in theory, the procedure should reduce ovarian cancer risk, but there is not yet persuasive evidence that it actually does, Dr. Findley emphasized at the meeting, presented by the Society of Laparoendoscopic Surgeons and affiliated societies.
            In contrast, one well-established ancillary benefit of prophylactic salpingectomy is that it eliminates the need for future reoperation for salpingectomy. This was demonstrated in a large Danish cohort study including close to 10,000 women undergoing hysterectomy and a similar number undergoing sterilization procedures. Among the nearly two-thirds of hysterectomy patients who had both fallopian tubes retained, there was a 2.13-fold increased likelihood of subsequent salpingectomy, compared with nonhysterectomized women.
        Similarly, Danish women who underwent a sterilization procedure with retention of the fallopian tubes – typically tubal ligation with clips – were 2.42 times more likely to undergo subsequent salpingectomy, most often because of the development of hydrosalpinx, infection, ectopic pregnancy, or other complications (BMJ Open 2013;3 [doi:10.1136/bmjopen-2013-002845]).
     The most commonly cited potential risk of prophylactic salpingectomy – decreased ovarian function – now appears to be a nonissue. This was demonstrated in a recent retrospective Italian study (Gynecol. Oncol. 2013;129:448-51) as well as in a pilot randomized controlled trial conducted by Dr. Findley and his coworkers (Fertil. Steril. 2013;100:1704-8), which appears to have answered many skeptics’ concerns. Indeed, Dr. Findley’s coinvestigator Dr. Matthew Siedhoff said he has recently been approached by researchers interested in collaborating in a larger confirmatory randomized trial, but all parties eventually agreed it was a no-go.
    “It’s a little hard to demonstrate equipoise for a larger randomized controlled trial. We’re beyond that now, given that prophylactic salpingectomy really doesn’t seem to make a difference as far as ovarian function,” according to Dr. Siedhoff, director of the division of advanced laparoscopy and pelvic pain at the University of North Carolina, Chapel Hill.
         Another oft-expressed reservation about salpingectomy as a means of reducing ovarian cancer risk in women seeking sterilization is that salpingectomy’s irreversibility may lead to “tubal regret” on the part of patients who later change their mind about further pregnancies. However, Dr. Findley cited a recent editorial whose authors criticized colleagues who made that claim. The editorialists argued that the tubal regret concern indicates surgeons weren’t really listening to their patients’ true desires during the informed consent conversation.
     “We should not have started thinking about salpingectomy for female sterilization only once a decrease in ovarian cancer risk became part of the equation,” they declared (Obstet. Gynecol. 2014;124:596-9).
           Dr. Findley noted that Canadian gynecologists are leading the way forward regarding prophylactic salpingectomy as a potential method of ovarian cancer prevention. The Society of Gynecologic Oncology of Canada in a 2011 policy statement recommended patient/physician discussion of the risks and benefits of bilateral salpingectomy for patients undergoing hysterectomy or requesting permanent sterilization. The Society of Gynecologic Oncology followed suit with a similar clinical practice statement in late 2013.
        Additionally, the Canadian group declared that a national ovarian cancer prevention study focused on fallopian tube removal should be a top priority.
    Gynecologic oncologists in British Columbia recently reported the eye-catching results of a province-wide educational initiative targeting gynecologists and their patients. In 2010, all British Columbia gynecologists had to attend a course on the role of the fallopian tubes in the development of ovarian cancer, during which they were advised to consider performing bilateral salpingectomy for ovarian cancer risk reduction.
              Surgical practice changed dramatically in British Columbia in response. In 2009 – the year prior to the physician education initiative – salpingectomy was utilized in just 0.3% of permanent sterilization procedures. In 2010, it was 11.4%. By 2011, it was 33.3%.
           Similarly, only 7% of hysterectomies performed in British Columbia in 2009 were accompanied by bilateral salpingectomy. This figure climbed to 23% in 2010 and jumped further to 35% in 2011. Meanwhile the rate of hysterectomy with bilateral salpingo-oophorectomy remained steady over time at 44% (Am. J. Obstet. Gynecol. 2014;210:471.e1-11).
     This project was conducted in collaboration with the B.C. Cancer Agency, which maintains comprehensive province-wide registries. Over time, it will be possible to demonstrate whether prophylactic salpingectomy is indeed associated with a reduction in the incidence of ovarian cancer. “I think this study demonstrated that there’s a lack of awareness on this issue, but also [that there’s] potential effectiveness of introducing an educational initiative like this in changing our practice patterns. As we start talking more about this issue amongst our colleagues and our patients, we’re more likely to see a practice pattern shift in the United States as well,” Dr. Findley commented.

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

Danish  Universities prospectively document  the incidence of ovarian cancer OvCa in a million postmenopausal women PMW  from 1995 through 2005.  Compared to non-users, use of HT increased OvCa (mean age 62yrs) by about 40%   for up to 2 years after stopping Ht, ie increased the absolute incidence  of clinically diagnosed OvCa from ~ 0.04 to ~0.052% ie per 100 patient yrs.

Transdermal TD ET alone  increased risk by 13%; vaginal ET by 23%;                                            Oral ET alone increased  risk by  34%; oral E+ progestin Pg by  48%;          TDE+Pg by 67%.

Thus the relative incidence of OvCa rose about 33% by 7 years on HT, to 48% if HT continued beyond 7years.

In 2004 Glud ea reported an increase risk of 31% for OvCa in Danish women on OHT use – total ET dose of ~5gm ie for about  for 15yrs – at a time when the standard premarin  dose was 0.625mg/d (equivalent to l mg E2)  if not double that .

For perspective,  the relative incidence of cancers in similar mostly 1st world European women from the  the USA SEER data for 2006 age over 50  years  are: BrCa 0.33%,  uterus 0.07%, ovary o.03%(ie very similar to the baseline Danish figure of 0.04% above), colon 0.15%,and cervix 0.01%. The new (Norwegian)  analysis in the latest BMJ suggests that screening mammography may result in overdiagnosis of BrCa by up to 50% (the other 50% may arguably never have been clinically significant-diagnosed- during life) , so the provocative could argue that the relative incidence of clinically significant BrCa to OvCa is more like eg BrCa 0.2 to ovary 0.03 ie just below 10:1. But OvCa is notoriously about 70% fatal within a few years, so  the absolute  mortality rate – at age 60-64yrs-  from  the same SEER  source and period are as relevant: BrCa 0.063%, uterus 0.011%, ovary 0.033%, colon 0.03% & cervix 0.005%. ie new OvCa may be only 1/10th as common as newBrCa, but BrCa  kills only twice  as many PMW as OvCa.

And finally the 2007  survey by  Rossing ea of  Menopausal Hormone Therapy and Risk of Epithelial Ovarian Cancer in women in Washington State 2002-2005 showed that  ET -mostly premarin (but not ET + progestin- MPA medroxyprogesterone provera) – especially in  low-parity  younger slim women increased OvCa compared to non-users, and that this risk  was highest- up to 90%-  in  users of OET  for more than 6 years.

By comparison – BREAST CANCER BrCa and HT: Hoover ea  1976  are the first on Pubmed to report doubling in  risk of breast cancer  BrCA after 15yrs on premarin in USA ie at least 5gm cumulative dose.

In Denmark by 1994 Ravn ea reported that if there was a risk of BrCa from OHT, it was small, and only after prolonged use of estrogen (15-20 years).  But by 2004 -2005 Tjønneland ea , Stahlberg ea  and Ewertz ea  found increased risk for BrCa  of 61 to 112%  associated with current use of HT.  Stahlberg ea already in 2003 concluded from recent studies from both the USA and Europe that the combined treatment regimens with estrogen and progestin increase the risk of BrCa  beyond the risk of unopposed estrogen.

In Norway, a recent Tromso study suggested that the dominant HT therapy used in Norway was oral estradiol E2 plus the progestin norethisterone acetate. . An earlier Tromso study in only 35000 PMW was too small- it showed that use of such OHT for >5yrs trebled the incidence of breast cancer BRCa, but did not influence that of OvCa.

Apart from smokers’ lung cancer, the commonest cancer in older women- BrCa- clinically affects perhaps 5% of PMW  lifelong – but  with prompt therapy after clinical presentation kills as few as 5% of sufferers- and with appropriate OHT (premarin +- provera)  for up to 8years in the Women’s Health Initiative both the incidence of and mortality from BrCa, and all-cause mortality,  were reduced by about one-third. Hence appropriate HT saves many from both BrCa and from premature death and disability from the commonest degenerative diseases- vascular, dementing and fracturing. 75% of women who develop BrCa  die with it –  not from it but from far more prevalent degenerative diseases after an  otherwise normal lifespan. But the Danish evidence is that combined OHT will increase OvCa by >50%.

Ovarian Ca kills 70% of victims, and is it so rare compared to BrCa? .

Hence with the perhaps 2/3  lower incidence of OvCa, it is a relatively trivial problem for women overall- except for the 4  in  10 000 women  who develop it, who have <50% 5year survival, ie 3 out of 4  of whom it will kill within a few years- compared to <25% of breast cancer victims who will be killed by the BrCa.

However, it becomes clear that these hormone-dependent cancers are both  duration-  and total-dose HT related; but even more important, that unopposed OET is a risk if persisted more than about 12 yrs; and even if used in far lower dose parenterally, the risk of OvCa is far higher if combined with the European fashion of androgenic synthetic progestins Pg – even parenterally; whereas the American MPA for up to 8years at least apparently if anything mitigates the OvCa risk of ET..

By contrast this column has repeatedly reviewed evidence that balancing physiological ERT with physiological testosterone replacement TRT eliminates the risk  for BRCA and endometrial cancer of unopposed ERT +- PRT in PMW.  Intuitively this should also apply to ovarian cancer.

Hence the message strengthens that PMW should not be exposed for  any length of time at any stage to the much higher oro-hepatic HT doses (needed for symptom control) or OET+- Pg; but as in all other endocrine replacement for permanent  multisystem prevention – let alone sexual function-  patients with gonadal deficiency should have physiological sexhormone balance restored  ie with balanced parenteral  human androgen, estrogen and progesterone replacement.

It is common cause that (reproductive cycles and pregnancy aside) all the physiological  prime sex hormones-DHEAdehydroepiandrosterone, P4, T, E2, E3 – are as important as all other human hormones, essential life long  for optimal health; and that estrogen dominance (due to inadequate  androgen and progesterone levels) is deleterious. Hence most PMW require both physiological progesterone and androgen replacement- sometimes to balance excessively high endogenous estrogens, usually to accompany necessary ERT for full balance.

ndb

All Artificial Sweeteners Raise Your Risk of Diabetes by Altering Your Gut Microbiome

why we must avoid all artificial sweeteners – if you must sweeten, use only the natural ie herbal intense sweeteners  stevia;  xylitol or  lo han go. available from Natural Medicine Clinic, 15 Grove Bldg, Grove Ave, Claremont Cape Town ph +27216831465)

By Dr. Mercola Oct 1st 2014: Artificial Sweeteners Raise Your Risk of Diabetes by Altering Your Gut Microbiome

Both artificial sweeteners and certain gut microbes have previously been linked to obesity, and according to the latest research, artificial sweeteners may raise your risk of diabetes by disrupting your intestinal microflora. According to the authors of the widely publicized study:1
“[W]e demonstrate that consumption of commonly used non-caloric artificial sweeteners formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota.
The researchers found that artificial sweeteners alter certain metabolic pathways associated with metabolic disease, and that it can induce gut dysbiosis and glucose intolerance in otherwise healthy people.
Glucose intolerance is a condition in which your body loses its ability to cope with high amounts of sugar, and it’s a well-known precursor to type 2 diabetes. It also plays a role in obesity, because the excess sugar in your blood ends up being stored in your fat cells.
The fact that artificial sweeteners may exacerbate metabolic disorders like diabetes is a severe blow to diabetics who dutifully follow recommendations to switch to diet foods and beverages in order to control their diabetes.
The fact that artificial sweeteners are NOT a dieter’s nor a diabetic’s best friend has been known by researchers for some time. The problem is that it hasn’t received the necessary traction in the media—until now.2, 3
“Collectively, our results link non-caloric artificial sweeteners (NAS) consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage,” the researchers note.
Artificial Sweeteners Can Cause Glucose Intolerance by Altering Your Microbiome
The researchers initially started out testing the artificial sweeteners saccharin, aspartame, and sucralose in mice, and were “surprised” when the mice developed glucose intolerance.
As noted by New York University microbiologist Martin Blaser,4 no one had previously considered that artificial sweeteners might exacerbate metabolic disease by way of the microbiome.
Of the three non-caloric sweeteners tested, saccharin had the most pronounced effect on glucose levels. This led to a human trial, in which data from 400 people enrolled in a nutritional study were assessed.
Those who consumed high amounts of artificial sweeteners were found to have higher levels of HbA1C—a measure of blood sugar—compared to non-users or occasional users of artificial sweeteners.
Seven volunteers who did not use artificial sweeteners were then recruited, and asked to consume the equivalent of 10-12 single-dose packets of artificial sweeteners daily for one week.
Four of the seven people developed “significant disturbances in their blood glucose,” according to the researchers. Some became pre-diabetic within just a few days!
The reason for this dramatic shift was traced back to alterations in gut bacteria. Some bacteria were killed off, while others started proliferating. As noted in the featured NPR article:5
“It could be that for some people who responded negatively to the artificial sweetener, the bacteria that got crowded out were helping to keep glucose in check.”
This mirrors previous research,6 which has found that bacterial populations in the gut of diabetics differ from non-diabetics.
Another 2008 study demonstrated that sucralose can alter the microbiome in rats by reducing colonies of beneficial gut bacteria, and research published in Clinical and Experimental Rheumatology7 in 2012 revealed a potential link between aspartame and irritable bowel syndrome (IBS). Imbalanced gut flora has also been linked to obesity.
Compelling Results Suggest We Should Reconsider Widespread Use of Artificial Sweeteners
In sharp contrast to many other studies, this one was actually able to clearly show causality, meaning there’s a direct cause and effect relationship between consuming artificial sweeteners and developing elevated blood sugar levels. As reported by The Scientist:8
“Four weeks of treatment with gut bacteria-depleting antibiotics reversed the glucose intolerance in mice that continued to receive saccharin. This led the team to examine whether the microbiomes of the mice were somehow altering glucose metabolism.
Transplantation of feces from non-antibiotic-treated mice that consumed saccharin- or glucose-containing water into germ-free mice within six days induced the same blood-sugar elevations in animals that were never themselves exposed to the sweeteners.
‘This is the elegant and home run experiment that shows causality in mice,’ said [pathologist Cathryn] Nagler.
Using shotgun metagenomic sequencing on the fecal samples, the researchers showed that mice given saccharin or those that received a fecal transplant from saccharin-fed mice had a different microbiome composition compared to mice given sugar or no sweeteners.”
Cathryn Nagler, who wrote an accompanying commentary9 in the journal Nature, said the findings were “very compelling,” noting that “the study suggests… we should step back and reassess our extensive use of artificial sweeteners.”
Aspartame Raises Insulin Levels as Much as Sugar
Other studies have also linked artificial sweeteners to metabolic alterations that promote type 2 diabetes—contrary to conventional thinking and health recommendations.
For example, one 2012 study10 found that chronic lifetime exposure to aspartame, commencing in utero, produced changes in blood glucose parameters in mice. Not only was aspartame found to decrease insulin sensitivity compared to controls, it also wrought havoc on brain function…
Another study published in 2007 in the journal Diabetes Care11 found similar results. Here, the researchers investigated the effect of different macronutrient compositions on plasma glucose and insulin levels during an acute bout of exercise in men with type 2 diabetes.
They hypothesized that using fructose or aspartame would have a lower impact on insulin release and glucose response than a sucrose-sweetened meal. Those of you who have been reading my articles featuring experts on sugar and fructose like Dr. Richard Johnson and Dr. Robert Lustig will immediately recognize this as a fatally flawed hypothesis. And indeed, that is what they discovered. According to the authors:
“Contrary to all expectation, the aspartame breakfast induced a similar rise in glucose and insulin levels at baseline than the sucrose meal, even if the aspartame meal had the same taste, and was 22 percent lower in calories and 10 percent lower in carbohydrates, with an inferior glycemic index… Considering the lack of evidence on the aspartame utilization in patients with type 2 diabetes, we consider that these clinical observations, in an exercise setting, raise important concerns regarding the safety of aspartame as suggested by international guidelines.”
Obesity Continues to Rise
According to a recent JAMA study,12, 13 the obesity rate among American adults has continuously climbed over the last decade. Between 1999 and 2012, the average age-adjusted waist circumference increased from 95.5 centimeters (37 19⁄32 inches) to 98.5 centimeters (38 25⁄32 inches). Abdominal fat also rose from 46.4 percent in 1999-2000 to 54.2 percent in 2011-2012. The United Kingdom is facing a similar health crisis. According to September 17 article in Mail Online:14
“Obesity is a ‘slow-motion car crash’ which is threatening to bankrupt the NHS, according to its chief executive. Simon Stevens said the problem is now more deadly than smoking and causing millions to suffer life-long illness and disability. He also revealed that – absurdly – the NHS is spending far more on drastic weight loss surgery than trying to prevent the problem in the first place. A quarter of adults and a fifth of children are now considered obese and the rates have almost doubled in 20 years…
Next month, Mr. Stevens will publish a set of plans to tackle the problem which will see the NHS and private firms urged to do more to help staff lose weight. Doctors and nurses will be encouraged to be healthy role models for patients and hospitals told to ban junk food from canteens. NHS trusts and private companies will also be urged to help staff lose weight by holding slimming classes, running clubs or just providing bike racks at work. Mr. Stevens, who took up post last April, said: ‘Obesity is the new smoking, and it represents a slow-motion car crash in terms of avoidable illness and rising health care costs…” [Emphasis mine]
Artificial Sweeteners Can Severely Hinder Weight Management Efforts
Those who switch to artificial sweeteners are typically carrying extra pounds and/or are diabetic, or prone to these conditions. Unfortunately, this may be the absolute worst diet change you could implement if you’re overweight or diabetic. Research has repeatedly shown that artificially sweetened no- or low-calorie drinks and other “diet” foods tend to stimulate your appetite, increase cravings for carbs, stimulate fat storage and weight gain, and promote insulin resistance and diabetes.
There are a number of different reasons for this. First of all, artificial sweeteners basically trick your body into thinking that it’s going to receive sugar (calories), but when the sugar doesn’t arrive, your body signals that it needs more, which results in carb cravings. This connection between sweet taste and increased hunger can be found in the medical literature going back at least two decades (see list of selected studies below). But artificial sweeteners also produce a variety of metabolic dysfunctions that promote weight gain—and now we can add gut dysbiosis and altered microbiome to that list!
In 2011, the UT Health Science Center in San Antonio publicized the results of two important studies, saying:15
“In the constant battle to lose inches or at least stay the same, we reach for the diet soda. Two studies presented [June 25, 2011] at the American Diabetes Association’s Scientific Sessions suggest this might be self-defeating behavior. Epidemiologists from the School of Medicine at The University of Texas Health Science Center San Antonio reported data showing that diet soft drink consumption is associated with increased waist circumference in humans, and a second study that found aspartame raised fasting glucose (blood sugar) in diabetes-prone mice…
‘Data from this and other prospective studies suggest that the promotion of diet sodas and artificial sweeteners as healthy alternatives may be ill-advised,’ said Helen P. Hazuda, Ph.D., professor and chief of the Division of Clinical Epidemiology in the School of Medicine. ‘They may be free of calories but not of consequences.’” [Emphasis mine]
Sampling of Studies Refuting ‘Diet’ Claims
Here’s a sampling of some of the studies published through the years, clearly refuting the beverage industry’s claims that diet soda helps with weight management. The 2010 review in the Yale Journal of Biology and Medicine16 is of particular relevance here, as it offers a great historical summary of artificial sweeteners in general, and the epidemiological and experimental evidence showing that artificial sweeteners tends to promote weight gain. It also illustrates that as usage of artificial sweeteners has risen, so has obesity rates—despite all these “diet friendly” products.

Source: Yale Journal of Biology and Medicine June 8 2010: v83(2)
Preventive Medicine 1986 Mar;15(2):195-20217
This study examined nearly 78,700 women aged 50-69 for one year. Artificial sweetener usage increased with relative weight, and users were significantly more likely to gain weight, compared to those who did not use artificial sweeteners—regardless of their initial weight. According to the researchers, the results “were not explicable by differences in food consumption patterns. The data do not support the hypothesis that long-term artificial sweetener use either helps weight loss or prevents weight gain.”
Physiology and Behavior, 198818
In this study, they determined that intense (no- or low-calorie) sweeteners can produce significant changes in appetite. Of the three sweeteners tested, aspartame produced the most pronounced effects.
Physiology and Behavior, 199019
Here, they found that aspartame had a time-dependent effect on appetite, “producing a transient decrease followed by a sustained increase in hunger ratings.”
Journal of the American Dietetic Association, 199120
In a study of artificial sweeteners performed on college students, there was no evidence that artificial sweetener use was associated with a decrease in their overall sugar intake either.
International Journal of Obesity and Metabolic Disorders, 200421
This Purdue University study found that rats fed artificially sweetened liquids ate more high-calorie food than rats fed high-caloric sweetened liquids. The researchers believe the experience of drinking artificially sweetened liquids disrupted the animals’ natural ability to compensate for the calories in the food.
San Antonio Heart Study, 200522
Data gathered from the 25-year long San Antonio Heart Study also showed that drinking diet soft drinks increased the likelihood of serious weight gain – far more so than regular soda23 On average, for each diet soft drink the participants drank per day, they were 65 percent more likely to become overweight during the next seven to eight years, and 41 percent more likely to become obese.
Journal of Biology and Medicine, 201024
This study delves into the neurobiology of sugar cravings and summarizes the epidemiological and experimental evidence concerning the effect of artificial sweeteners on weight.

According to the authors: “[F]indings suggest that the calorie contained in natural sweeteners may trigger a response to keep the overall energy consumption constant. …Increasing evidence suggests that artificial sweeteners do not activate the food reward pathways in the same fashion as natural sweeteners… [A]rtificial sweeteners, precisely because they are sweet, encourage sugar craving and sugar dependence.”
Yale Journal of Biology and Medicine, 201025
This review offers a summary of epidemiological and experimental evidence concerning the effects of artificial sweeteners on weight, and explains those effects in light of the neurobiology of food reward. It also shows the correlation between increased usage of artificial sweeteners in food and drinks, and the corresponding rise in obesity.
Appetite, 201226
Here, researchers showed that saccharin and aspartame both cause greater weight gain than sugar, even when the total caloric intake remains similar.
Trends in Endocrinology & Metabolism, 201327
This report highlights the fact that diet soda drinkers suffer the same exact health problems as those who opt for regular soda, such as excessive weight gain, type 2 diabetes, cardiovascular disease, and stroke.28, 29 The researchers speculate that frequent consumption of artificial sweeteners may induce metabolic derangements.
Nature, 201430
This study was able to clearly show causality, revealing there’s a direct cause and effect relationship between consuming artificial sweeteners and developing elevated blood sugar levels.

People who consumed high amounts of artificial sweeteners were found to have higher levels of HbA1C—a long-term measure of blood sugar—compared to non-users or occasional users of artificial sweeteners.

Seven volunteers who did not use artificial sweeteners were then recruited, and asked to consume the equivalent of 10-12 single-dose packets of artificial sweeteners daily for one week.

Four of the seven people developed “significant disturbances in their blood glucose,” according to the researchers. Some became pre-diabetic within just a few days.

The reason for this dramatic shift was traced back to alterations in gut bacteria. Some bacteria were killed off, while others started proliferating.
Are There ANY Safe and Healthy Alternatives to Sugar?
One of the best strategies to kick the sugar habit is to implement intermittent fasting, and to make sure you’re eating enough healthy fats. Once your body has the proper fuel, your sweet cravings will radically diminish. If you need a sweetener you could use stevia or Luo Han, both of which are safe natural sweeteners. For a comprehensive review of the best and worst sweeteners, please see my previous article, “The 4 Best, and 3 Worst Sweeteners to Have in Your Kitchen.” Just remember, if you struggle with high blood pressure, high cholesterol, diabetes, or extra weight, then you have insulin sensitivity issues and would benefit from avoiding ALL sweeteners.
If you’re having trouble weaning yourself off soda, try Turbo Tapping. Turbo Tapping is a clever use of the Emotional Freedom Technique (EFT), specifically designed to resolve many aspects of an addiction in a concentrated period of time. Last but not least, if you experience side effects from aspartame or any other artificial sweetener, please report it to your National or Regional Health Dept without delay. It’s easy to make a report — just go to your National  Consumer Complaint Coordinator page, find the phone number for your state, and make a call reporting your reaction.