The Endogenous Opioid System: Role and Dysfunction Caused by Opioid Therapy

Toubia, Tarek; Khalife, Tarek

doi:10.1097/grf.0000000000000409

Cited by 41 publications

(31 citation statements)

References 25 publications

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“…(c) Guidelines discourage the use of opioids, for example for IBS (Drossman, 2019), fibromyalgia (MacFarlane et al, 2017) or migraine (American Headache Society, 2019). (d) Patients with primary pain syndromes may be less responsive to opioids due to higher endogenous opioid levels and more susceptible to worsening of hyperalgesia by opioids (Toubia & Khalife, 2019).…”

Section: (B)mentioning

confidence: 99%

European* clinical practice recommendations on opioids for chronic noncancer pain – Part 1: Role of opioids in the management of chronic noncancer pain

Haüser

Morlion

Vowles

et al. 2021

European Journal of Pain

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Section: (B)mentioning

confidence: 99%

European* clinical practice recommendations on opioids for chronic noncancer pain – Part 1: Role of opioids in the management of chronic noncancer pain

Haüser

Morlion

Vowles

et al. 2021

European Journal of Pain

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“…However, repetitive stress exposure (which is characteristic of ELS) leads to an imbalance between CRF and opioids such that opioid inhibitory tone is favored [258]. Although the relationships require further testing, there is some evidence that chronically high tonic levels of endogenous opioids may trigger downregulation or reduced affinity of µ-opioid receptors (MOR) and lower phasic release of opioid peptides, resulting in hypoactivity of this system [259,260].…”

Section: Effects Of Els On Endogenous Opioid Functionmentioning

confidence: 99%

Early Life Stress and Risks for Opioid Misuse: Review of Data Supporting Neurobiological Underpinnings

Oswald

Dunn

Seminowicz

et al. 2021

JPM

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A robust body of research has shown that traumatic experiences occurring during critical developmental periods of childhood when neuronal plasticity is high increase risks for a spectrum of physical and mental health problems in adulthood, including substance use disorders. However, until recently, relatively few studies had specifically examined the relationships between early life stress (ELS) and opioid use disorder (OUD). Associations with opioid use initiation, injection drug use, overdose, and poor treatment outcome have now been demonstrated. In rodents, ELS has also been shown to increase the euphoric and decrease antinociceptive effects of opioids, but little is known about these processes in humans or about the neurobiological mechanisms that may underlie these relationships. This review aims to establish a theoretical model that highlights the mechanisms by which ELS may alter opioid sensitivity, thereby contributing to future risks for OUD. Alterations induced by ELS in mesocorticolimbic brain circuits, and endogenous opioid and dopamine neurotransmitter systems are described. The limited but provocative evidence linking these alterations with opioid sensitivity and risks for OUD is presented. Overall, the findings suggest that better understanding of these mechanisms holds promise for reducing vulnerability, improving prevention strategies, and prescribing guidelines for high-risk individuals.

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“…In terms of function, enkephalins exhibit a wide array of effects involving multiple systems. Enkephalins play major roles in analgesia, emotional behaviors, and stress response regulation [ 277 , 278 ]. However, of particular interest are studies that focused on their role in regulating cell proliferation.…”

Section: Neuropeptides and Melanomamentioning

confidence: 99%

Neuroendocrine Factors in Melanoma Pathogenesis

Scheau

Drăghici

Ilie

et al. 2021

Cancers

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Melanoma is one of the most aggressive skin cancers with a sharp rise in incidence in the last decades, especially in young people. Recognized as a significant public health issue, melanoma is studied with increasing interest as new discoveries in molecular signaling and receptor modulation unlock innovative treatment options. Stress exposure is recognized as an important component in the immune-inflammatory interplay that can alter the progression of melanoma by regulating the release of neuroendocrine factors. Various neurotransmitters, such as catecholamines, glutamate, serotonin, or cannabinoids have also been assessed in experimental studies for their involvement in the biology of melanoma. Alpha-MSH and other neurohormones, as well as neuropeptides including substance P, CGRP, enkephalin, beta-endorphin, and even cellular and molecular agents (mast cells and nitric oxide, respectively), have all been implicated as potential factors in the development, growth, invasion, and dissemination of melanoma in a variety of in vitro and in vivo studies. In this review, we provide an overview of current evidence regarding the intricate effects of neuroendocrine factors in melanoma, including data reported in recent clinical trials, exploring the mechanisms involved, signaling pathways, and the recorded range of effects.

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The Endogenous Opioid System: Role and Dysfunction Caused by Opioid Therapy

Cited by 41 publications

References 25 publications

European* clinical practice recommendations on opioids for chronic noncancer pain – Part 1: Role of opioids in the management of chronic noncancer pain

European* clinical practice recommendations on opioids for chronic noncancer pain – Part 1: Role of opioids in the management of chronic noncancer pain

Early Life Stress and Risks for Opioid Misuse: Review of Data Supporting Neurobiological Underpinnings

Neuroendocrine Factors in Melanoma Pathogenesis

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