LDN (Naltrexone) | Misitio

LDN (Naltrexone)

LDN (Naltrexone)

Treatment for Multiple Sclerosis and Fibromyalgia

 

This pure opioid receptor antagonist has been Food and Drug Administration (FDA)-approved for medication-assisted treatment of alcoholism or opioid use disorders. Following Dr. Bihari’s initial off-label use (prepared in compounding pharmacies) of naltrexone in doses ranging from 1.5 mg to 4.5 mg as therapy for acquired immune deficiency syndrome (AIDS) in the 1980s, low-dose naltrexone (LDN) has been introduced into clinical practice for other purposes like Multiple Sclerosis and Fibromyalgia

 

Naltrexone and naloxone are classical opioid antagonists. In substantially lower than standard doses, they exert different pharmacodynamics. Low-dose naltrexone (LDN), considered in a daily dose of 1 to 5 mg, has been shown to reduce glial inflammatory response by modulating Toll-like receptor 4 signaling in addition to systemically upregulating endogenous opioid signaling by transient opioid-receptor blockade. Clinical reports of LDN have demonstrated possible benefits in diseases such as fibromyalgia, Crohn’s disease, multiple sclerosis, complex-regional pain syndrome, Hailey-Hailey disease, and cancer.

Naltrexone is classically prescribed in daily doses of at least 50 mg to be taken orally. This pure opioid receptor antagonist has been Food and Drug Administration (FDA)-approved for medication-assisted treatment of alcoholism or opioid use disorders.

The clinical phase of LDN pharmacological research preceded the bench-scientific one, thus theorizing on its exact mechanism of action has predominated until recently. Naltrexone expands the standard approach regarding a linear dose–effect curve. What is known as a ‘hormetic principle’, by which certain pharmacological or toxicological substances exert qualitatively different pharmacodynamical effects in relation to the applied quantity, seems to address properties of LDN in a more adequate manner. It implies that naltrexone, having multiple dose-dependent pharmacological targets with different respective effects, might be considered such a substance.

The ‘classical’ effect of naltrexone exerting opioid antagonism still abides by the traditional dose–effect curve, yet at low-dose range this mechanism of action of the drug may seem less important. On the contrary, instead of eliciting a permanent opioid receptor blockade by standard dosing, the transient opioid receptor blockade ensuing from low-dose use upregulates opioid signaling. This opens the perspective of LDN as modulating tool of the neuroimmune axis [25], which further intertwines with the neuroendocrine axis to form a crossroads between CNS and rest of the body.

The higher reactivity of immune cells and decreased growth of cancerous cells are both mediated by transient increase in opioid growth factor signaling. Permanent blockade of opioid growth factor receptor leads to enhanced cellular growth, which is unwanted in case of tumors, but has been experimentally used for wound or corneal abrasion healing.

Low-dose naltrexone has been shown to ameliorate and modify the course of various diseases. Low-dose naltrexone could be useful for states involving chronic inflammation or immune dysregulation, such as Fibromyalgia, multiple sclerosis, Crohn’s disease, cancer, Hailey-Hailey disease, complex-regional pain syndrome.

 

More Information and preparations, contact Dr. Aceves

Calle Guadalupe Victoria N° 24, Ajijic, Jal.

Tel: +52 (376) 766 12 44 

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