This is the data that is changing the world:
- 10 out of 15 meeting the criteria for a catecholamine surge (catecholamine level or above a 15% increase over the maximum normal range)
- 13 out of 15 with at least one catecholamine level elevated.
- For the mental health diagnosis known as opioid use disorder to be accurate, these blood levels would need to be normal
Normal Catecholamine Values
Norepinephrine = 0-874
Epinephrine = 0-62
Dopamine = 0-48
Estimated Cardiovascular Deaths Due to Opioid Withdrawal
Ignore Science at your own peril. Diagnosis “Opioid Addiction” as a mental health disorder and you get an epidemic of citizens dying of a heart attack during opioid withdrawal. Dying by the millions. It’s not a mental health disorder. It’s damage to the DNA by a defective product, the opioids.
THE SMITH HYPOTHESIS
100% of the deaths associated with the Opioid Crisis were premature and mostly preventable deaths.
Methylation of certain CpG islands within the promoter region of the OPRM1 gene, as seen in response to the exposure to the opioids, results in gene silencing. This gene silencing is not producing a drop in the population of the mu-opioid receptor. Rather, this gene silencing results in the formation of an abnormal mu-opioid receptor. This production of an abnormal mu-opioid receptor is due to a process we are calling partial gene silencing – the receptor was produced but it was an abnormal receptor. This abnormal mu-opioid receptor is no longer able to maintain balance and homeostasis within the Autonomic Nervous System when Opioid Abstinence is attempted. This dysfunction within the Autonomic Nervous System results in a true Neuroendocrine Emergency known as Autonomic Dysfunction. This Autonomic Dysfunction is reflected in the abnormal activity in both branches of the Autonomic Nervous System, the Sympathetic Nervous System and the Parasympathetic Nervous System. Autonomic dysfunction, and the Catecholamine Surge that results, is a condition of extreme duress and cannot long be endured by the human body. The full agonist opioids offer a partial and temporary relief. But this partial and temporary relief comes with the associated risk of the full agonist opioids. The partial agonist, Buprenorphine, is able to maintain a more complete and longer lasting relief from the autonomic dysfunction but, due to the Ceiling Effect of Buprenorphine, at a higher level of safety. Untreated, there is concern that autonomic dysfunction could be a risk factor for the development of Opioid Induced Adrenal Insufficiency. In addition, a Catecholamine Surge is known to be associated with Cardiomyocyte Necroptosis. Therefore, cardiac related death rates would be expected to be increased dramatically in any vulnerable populations which also experienced a simultaneous increase in opioid overdose deaths. These cardiac deaths would mistakenly be attributed to a non opioid related etiology.
THE TWO PREDICTIONS OF THE SMITH HYPOTHESIS
A catecholamine surge will be found intermittently in so called “opioid withdrawal.”
A detectable increase in coronary artery disease deaths in any population simultaneously experiencing an increase in opioid overdose deaths.
Catecholamine Surges Cause Cardiomyocyte Necroptosis via a RIPK1-RIPK3 Dependent Pathway in Mice
Coronary Heart Disease Deaths 1999-2011
Number and Characteristics of LA County Deaths among PEH, 12 Months Pre- and Post-pandemic Onset
OPIOID CRAVING SCALE – DATA & DISCUSSION
Opioid Craving Scale – Before Buprenorphine
Opioid Craving Scale – After Buprenorphine
AUTONOMIC DYSFUNCTION SCALE –
DATA & DISCUSSION
Autonomic Dysfunction Scale (Before Buprenorphine)
Autonomic Dysfunction Scale (After Buprenorphine)