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From the Townsend Letter
June 2016

The 5th Annual Low-Dose Naltrexone Conference: A Review
by Emily Kane, ND
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As daily opioid overdose surpasses motor vehicle accidents as a cause of premature death in the US, interest in naloxone and naltrexone has spiked. Training primary-acare providers, pharmacists, friends and relatives of addicts, and legislators in the judicious use of the various forms of naloxone (Narcan, Vivitrol) will save many lives. Naloxone is an opioid antagonist that binds to the mu opioid receptors found on most cells, preventing activation of the opioid response, and mostly used in emergency settings to prevent opioid (e.g., heroin) overdose death. Naltrexone is a similar opioid antagonist but with a shorter half-life and slower uptake than naloxone. Unlike naloxone, naltrexone is well absorbed orally and transdermally. My purpose in reviewing the 5th Annual LDN conference in Orlando, Florida (February 29–21, 2016), is to increase awareness of the broad-spectrum efficacy of naltrexone, used in very low doses, in alleviating human suffering.
The conference organizer, energetic LDN patient and advocate Linda Elsegood, along with many volunteer members of her family and staff, runs the LDN Research Trust, based in England. A summary fact sheet for everything LDN, including the 176 disease indications, per published research, is available on its website.1 Another available resource is a video of Dr. Alex Vasquez interviewing a seasoned LDN prescriber.2
The trust has, hot off the press, an informative and fascinating book about the mechanism and uses of LDN that would be a good investment for anyone interested in the topic: The LDN Book.3 One of my favorite chapters in the book is a delightful romp through LDN history, starting with early humans' fascination with narcotics, by Scottish pharmacist and pharmacy owner Stephen Dickson.
The more recent backstory for LDN starts with the late researcher and neurologist Bernard Bihari. Bihari considered himself a primary-care physician and was living in New York City during the height of the AIDS epidemic in the 1980s. The city commissioned him to study the disease and gave him a large budget, because new victims were dropping like flies. Bihari noted that many of the advanced AIDS patients were also heroin addicts, and he became interested in measuring endorphin levels. This was an expensive undertaking, but Bihari had the funds and knew that helping addicts get off heroin could only improve their health. Bihari was able to show in an AIDS patient group that taking naltrexone regularly slowed or even halted the gradual destruction of CD4 cells. His trial group death rate was vastly lower than controls. This effect was not from LDN alone, but synergistic with the newer (at the time) antiretroviral drugs. Bihari also noted, almost incidentally, that when lower doses of naltrexone were given, there was a positive endorphin response compared with the endorphin suppression found when doses more typical for opioid addition were given. Opioid addiction is treated by blocking the effect of the opiate with 50 to 200 mg of naltrexone or naloxone daily, which inhibits any desired effect of the opioid for 24 hours. Bihari was assessing different dosing schedules and saw that giving very low doses of naltrexone actually stimulated endorphin production, rather than blocking it. At first he didn't believe these results, so he repeated them. A colleague in Milan (Dr. Maria Garoni) verified this finding. Bihari's work triggered a flurry of research assessing the importance of endorphins in the regulation of the immune system. A few years later, Dr. Ian Zagon speculated that low doses of naltrexone, producing rebound uptick in endogenous endorphins, could be used therapeutically. In 1986 Zagon demonstrated that opiate receptors were present inside multiple types of immune cells, and published nearly 300 research papers on LDN and endorphins. Quoting directly from The LDN Book, per Zagon, the basic mechanism of action for LDN is as follows:
1.  Many outward diseases are expressions of a malfunctioning immune system.
2.  The immune system is regulated by endorphins, which have a primary action on opiate receptors.
3.  Blocking opiate receptors briefly using naltrexone causes an upregulation in the production of endorphins, which can act in an immunomodulatory way to correct immune system malfunction.
4.  Cell proliferation is also mediated by a subtype of endorphins and can be suppressed by endorphins, which is applicable to some forms of cancer.
Endorphins and inflammation are not the whole picture, however. Naltrexone also binds to the group of receptors called toll-like (TLRs), first demonstrated by Christiane Nüsslein-Volhard in 1985 to recognize a wide range of antigens and initiate signaling pathways that trigger the appropriate immune response.
Now, in 2016, we also know that the broad mechanism of action of LDN is at least in part due to racemic isomers which have different and complementary functions. Mostly humans only have receptors for one isomer of a given molecule. However, in the case of naltrexone, the levorotating molecule fits into mu opiate receptors and causes a brief suppression, then rebound proliferation of endorphins, mostly beta-endorphin and met-enkephalin. The dextro isomer fits into receptors for various mediators of inflammation (cytokines, NF kappa-b) and suppresses them, via TLR antagonist mechanism.
The 2½-day conference featured 25 speakers, mostly physicians and pharmacists. The conference attendees were a mix of health-care providers, pharmacists, and patients – a format recognized as salutary at least a decade ago by this publication. It is beneficial for all to have a variety of stakeholders on site when expanding consciousness about health and well-being.
Learning of the breadth of LDN's therapeutic potential was a highlight of the conference, and this feature cannot be adequately elucidated here. Lecturers gave clinical evidence (some with patient numbers in the 100s) of benefit in chronic pain disorders, Crohn's, ulcerative colitis, IBS, SIBO, rheumatoid arthritis, sarcoidosis, psoriasis, polymyalgia rheumatica, FM, CFS, RLS, asthma, fertility, many autoimmune disorders, and many cancer types (endorphins boost apoptosis). This review will focus on the neurodegenerative disorders presented, since these are increasingly prevalent and conventional remedies are largely unsatisfactory. The brain disorder case studies helped by LDN presented over the weekend include autism, alcoholism, ALS, depression, dissociative disorder, MS, and PTSD.
Let's start with alcohol addiction disorder, a condition from which 1 person dies every 10 seconds in the US, wherein addiction is moralized ("why can't you just stop?") and monetized (detox and dry-out facilities are big business). Treatment is often punitive or court mandated. We learned about a revolutionary method for curing alcohol addiction via the Sinclair Method, which uses naltrexone in slightly higher doses than LDN, immediately before drinking, to neutralize the desire to continue to drink. This method has been used successfully in Finland to cure over 70,000 alcoholics. For more info visit or The Sinclair Method claims a 78% long-term success rate, which is unheard of with detox or Twelve-Step programs. Over 120 clinical trials document this success. Check it out and spread the work.
There was not a lot of discussion of ALS, a currently incurable condition, but it was mentioned several times during the conference, and these patients may benefit from LDN, though no clinical trials exist. As an older, generic, drug, no return on investment exists for Big Pharma to develop LDN. One of the overarching purposes of the LDN Research Trust is to stimulate interest in deep research without need for financial motive. As an aside, this problem in research is one of the many compelling reasons to have a single-payer health-care system – wherein it actually becomes financially interesting to prevent and cure, rather than "manage" disease. The neuropathology of ALS is characterized by pathologic inclusions within both upper and lower motor neurons and glia. The conference's opening lecturer, Dr. Pradeep Chopra (MD from Harvard Medical School and now instructor at Brown Medical School), emphasized that focusing on glial cells, as opposed to solely on neurons, was an important shift in thinking about treating pain and neurodegenerative diseases. Glial cells are so named because they were previously thought to be merely a "glue" for holding neurons in place. Now we know that glial cells play a critical house-cleaning role by modulating inflammation. When activated, they can release many pro-inflammatory chemicals including cytokines and chemokines, and increase TLRs on nearby cells. LDN blocks TLR4 signaling and upregulates the opioid growth factor-OGF receptor axis, which blocks the release of cytokines, including IL6, IL12, TNF-alpha, and NF-kappa-beta. This dual actual of LDN (analgesic and anti-inflammatory) was revisited numerous times over the weekend, and is presumably the mechanism of benefit for ALS.
Depression and anxiety are extremely common clinical presentations, and over time these emotional conditions can create physical problems as well. Several presenters praised the benefits of LDN in "mind-body" problems, with a focus on the critical importance of addressing the mental well-being of the patient when treating any disease. Hypnotist Lachlan Cox presented compelling evidence that emotions drive our pain. As an example, the mechanism of phantom limb pain is that the memory of the injury is stored in the limbic system. Ignoring physical sensations can amplify them. Find more about his work at
Dr. Ulrich Lanius, a psychologist, presented on "Traumatic Stress, Dissociative Smptoms and Consciousness." Dissociative symptoms include amnesia, depresonalization, inability to feel emotions, flashbacks, identity confusion, and somaticization. He talked about how, years ago, he came to an impasse with his usual method (EMDR) and recognized a similar "blankness" in patients with severe PTSD and those with high blood opioid levels. An Internet search brought him to naltrexone and he worked with a prescriber, using 50 mg at first. It worked; blocked patients opened up and therapy interventions became useful. Later, he found Bihari's work and switched dosing to 3 mg, which worked even better and remains Lanius's preferred dose. Pape and Woller have a paper on LDN and PTSD from 2015 available on PubMed; 11 of 15 subjects had positive and lasting effects.

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