MORE EVIDENCE THAT BUPRENORPHINE AND METHADONE OPIOID SUBSTITUTION TREATMENT (OST) IS WORSENING AMERICA’S LETHAL EPIDEMICS – ONTARIO, CANADA
Increases in injection-related infective endocarditis over pre-pandemic years are the opposite outcome predicted if the increasing provision of MAT opioids methadone and buperenorphine had been protective against high-risk use
by Clark Miller
Published March 13, 2019
Updated April 10, 2021; March 24, 2022
The numbers, as they say, are staggering.
Opioid-related and other drug overdose deaths increasing steadily, now sharply, over decades, 70,000 last year. Seemingly perversely, as population “dose” of the promised, publicly funded U.S. medical industry cure for the medical model “brain disease” of compulsive substance use – dose of substitute opioids that are addictive, diverted and abused – has expanded over the same years.
The more medical cure provided to the diseased brains, the more deaths mount.
The national trends hold in Kentucky, where overdose deaths due to synthetic opioids (like fentanyl), also to heroin, and prescribed opioids each continued to increase following and concurrently with increases in provision of the medical “fix”, the designated “treatment” for the non-medical behavioral symptom of compulsive opioid use.
Below – from Ontario, Canada additional evidence of harm, not treatment benefit, from provision of buprenorphine and methadone OST: high-risk opioid use and infective disease.
Provision by medical prescription of the substitute opioid buprenorphine (Subutex, Suboxone), funded by expanding allocation of public healthcare funds to greatly increase its availability follows the model of France’s decades-long opioid substitution treatment (OST) experiment with essentially unrestricted dispensing of “bupe” by primary care doctors.
France, for those efforts, remaining fifth highest among 20 European nations in high-risk opioid use and where levels of diversion, illicit trafficking, and abuse are . . . staggering, and where opioid-related overdose deaths have increased, not fallen, over most recent reporting periods.
As outlined and discussed in a series of posts on the opioid epidemic and its causes, the false promise of medication assisted treatment (MAT) as implemented is increasingly exposed by critical evaluation of diverse lines of evidence and research from U.S. MAT outcomes and from France’s decades-long, least restrictive, most intensive opioid substitute treatment (OST) campaign in the world, held out as the model for a U.S. medical “fix” with substitute opioids.
As established for the lethal iatrogenic opioid crisis the fix is a response to, the research “evidence” was never credibly supportive and predictive of benefit, instead predictive of a mounting body of evidence of failed outcomes and steadily worsening lethal public health epidemics associated with population “dose” of the medical cure increasing substantially and steadily in the U.S. and model country France. That research – vetted by the same expert professional class responsible for ensuring a research evidence base for the medically appropriate, safe, effective use of addictive opioids for the non-medical condition of common chronic pain – was never subjected to competent critical analysis of research design, interpretation and validity, never subjected to a critical discourse, instead successfully endorsed by popularizing writers in mass media.
That mounting evidence has included –
Retention rates (patients staying in and successfully completing MAT treatment programs) low and trending to zero in natural community treatment settings, with concurrent misuse of other opioids, other drugs – described in this post:
Evidence in the anomalous case of a Plumas County, California reversing opioid-related OD deaths pointing to Naloxone as the effective protective factor and against OST – described in this post:
Consistent evidence – as the national “dose” of substitute opioid medical “fix” and “anti-addiction drug” buprenorphine has steadily and substantially increased – of a concurrently worsening, lethal epidemic – outlined in this post:
Rampant, runaway diversion and abuse of the prescribed, addictive substitute opioids in France and the U.S., enough in France to fuel buprenorphine abuse epidemics in another country – described in this post:
The French Connection France’s Decades-Long Unrestricted Buprenorphine (Substitute Opioid) Campaign – Promoted as the “Fix” for U.S. Opioid Crisis – is Fueling Widespread Prescribed Opioid Diversion, Trade and Abuse
Lack of evidence to support the claim of efficacy for MAT/OST in reducing OD deaths or for other benefit, instead evidence for diverse harms – described in this post:
OST falsely constructed, branded as “treatment” thereby diverting public resources, attention, and policy away from existing evidence-based treatments for problem substance use including opioid use – described in this upcoming post:
Opioid Epidemic: For Worsening Crisis French and U.S. Medical Systems Dispense Ongoing Addictive, Abused Substitute Opioids With No Evidence-Based Treatments, Predictable Outcomes
and these posts at A Critical Discourse:
Effective Substance Use Treatment Requires Ending All Funding and Treatment for “Addiction” – A Fabrication that Diverts Healthcare Resources to the Criminal Treatment Scams Driving Lethal Public Health Epidemics
Evidence falsifying and dismantling claims by the medical/harm-reduction industry that diverted substitute opioids are primarily or largely used in self-treatment by individuals motivated to stop high-risk opioid use, instead affirming misuse and abuse of diverted prescription opioids – described in this upcoming post:
But that research was never critically analyzed, instead promoted by popularizing writers with interpretations flawed by the most basic of errors: attributing cause-and effect in “before and after” comparisons, when alternative factors were not accounted for and, on examination, have provided the explanation supported by evidence.
Consistently, evidence has supported the OD death-reversing drug naloxone as accounting for any reductions in OD deaths, and not buprenorphine MAT (OST)
Newly emerging and accumulating evidence explained in previous posts with links to primary research includes:
A new, large study of opioid-dependent patients in the UK, followed for 12 months after opioid substitute treatment with buprenorphine and methadone, with no findings of significant benefit in reduction of OD deaths, “drug related poisonings” = DRP.
A new, anomalous case of significantly reduced incidence of OD deaths against the continuously worsening national trend – in Dayton, Ohio – where evidence can directly link the reduction to a naloxone campaign, not to OST/MAT.
Additional outcome measures from France inconsistent with benefit from decades of unrestricted medical provision of substitute opioids as “treatment” – France remaining 5th worst of 20 European nations in “high risk opioid use”.
In the U.S., opioid substitution treatment (OST) primarily with buprenorphine has been successfully branded,
marketed and funded with public healthcare resources on claims that research has established effectiveness in reducing opioid-related OD deaths. But that research was never critically analyzed, instead promoted by popularizing writers with interpretations flawed by the most basic of errors: attributing cause-and effect in “before and after” comparisons, when alternative factors were not accounted for and, on examination, have provided the explanation supported by evidence.
Prevention of a lethal opioid-related OD resulting from use of naloxone is directly observable and attributable as such in cases in which naloxone was administered to an opioid user who was evaluated as medically at risk of death.
In contrast, to attribute prevention of OD deaths to use of buprenorphine in MAT programs requires additional and different evidence. It would require 1) a “natural experiment” in which buprenorphine MAT was implemented for a population without the concurrent associated increased availability and successful recorded use of Naloxone, 2) and/or that observed longitudinal decreases in incidence of lethal opioid-related ODs could not be accounted for by naloxone reversals, and 3) that the recorded decreases corresponded to treatment-related psychosocial gains required to explain decreases in high-risk opioid use (e.g. disengagement from drug use culture; decreased use for social and euphoric benefits; gains in treatment and community engagement; evidence of decreased use of bupe to manage withdrawal symptoms when cheaper, more euphoric illicit opioids are unavailable) and/or drug use behavior changes (significant decreases in population illicit “street” opioid use, like heroin and fentanyl) attributable to bupe programs.
More simply: a decrease in opioid-related overdose deaths over time raises the a critically important question for addressing the worsening opioid crisis: what protective, preventative, and/or life-saving factors can be identified as effective? Attributing decrease in lethal ODs to naloxone use is simple and direct – collecting evidence of cases of opioid users at risk of OD death having naloxone successfully administered. Attributing decrease to prescribed Suboxone/buprenorphine requires hypothesis testing, because there is conjecture, not direct observable effect. Attributing a causal relationship to two phenomena simply because they are concurrent is a naïve and primitive error of interpretation, in this case potentially lethal if the error leads to bad public health policy.
Testing the hypothesis that prescribed buprenorphine has prevented and prevents lethal opioid-related ODs requires evaluating evidence that psychosocial benefits of buprenorphine use cause behavioral and other changes that reduce prevalence of high-risk opioid use.
This post discussed in detail, with links to primary research, multiple lines of evidence pointing away from benefit attributable to OST, instead to use of naloxone and/or other supports in reducing opioid-related deaths.
New evidence from Canada
provides additional, clear evidence pointing away from OST providing benefit by reducing high-risk opioid use. In Ontario, Canada, as in other provinces, over past decades and years provision of methadone and buprenorphine has steadily and significantly increased.
Among the health ministries that did respond, overall methadone and suboxone patient counts and costs have increased, perhaps unsurprisingly, just as rates of overdose deaths have continued to rise. And methadone was usually prescribed at much higher rates than suboxone. Recent guidelines published in the Canadian Medical Association Journal deemed suboxone the “preferred first-line treatment” for opioid addiction.
The Ontario health ministry provided the number of patients receiving methadone going back to 2013 — the first year for which data on this is available. The number of methadone patients rose from 39,796 in 2013 to 44,554 in 2017. And the Ontario Drug Benefit program increased its spending on methadone by more than $12 million over four years, paying $46,320,288 for methadone in 2012/2013 and $58,446,216 in 2017/2018. Those amounts do not include patients who received treatment provided in other settings such as in hospitals, so the spending figures are likely an underestimation.
The number of pharmacies in Ontario offering methadone went from 631 in 2008/2009 to 1,234 in 2017/2018.
While Ontario has one of the highest number of patients in Canada, Alberta saw a 50 percent spike in the number of people receiving methadone and suboxone over the last four years: 4,200 patients in 2014/2015 to 8,200 in 2017/2018. British Columbia’s health ministry said the province’s PharmaCare program covered methadone or suboxone for 10,365 patients in 2008/2009 and 22,012 patients in 2016/2017.
Over the same time period of significant increase in provision of methadone and buprenorphine MAT, what should be a valid indicator and measure of changes in prevalence of high-risk opioid use – incidence of injection-related endocarditis – has increased steadily and significantly as well. That’s the opposite of predicted if OST by provision of methadone and bupe were providing benefit by reducing high-risk opioid use.
Significant, extended increases in medical provision of buprenorphine and methadone OST should necessarily have resulted in the opposite outcome – decreases over the same time period of high-risk opioid use . . . unless . . . as is generally and predictably the case, the provision of a medical model “treatment”, unsupported and indicated against by research evidence for an entirely non-medical condition – compulsive problem opioid use – has predictably resulted in a worsening of an iatrogenic lethal opioid crisis rather than providing benefit.