The LDN Research Trust is proud to offer presentations introducing virtually all a practitioner would need to know about the effective use of LDN. For more extensive information on the use of LDN, be sure to register for a Full Ticket or Livestream so that you can also access our additional recorded sessions.
Advances in basic and clinical LDN research are expanding exponentially, yet remarkably, traditional medicine continues to be slow to incorporate LDN into traditional treatment protocols.
Drawing upon the lessons learned from the clinical experience of a highly successful compounding pharmacy, it is clear that being fluent in the languages of research, clinical medicine, and pharmacy is critical to translate the latest findings into directly applicable clinical indication specific dosing protocols, as well as creating the guidance on expected dosing and timeframes necessary to achieve therapeutic success for the patient.
Widespread acceptance of LDN depends upon the clinician’s understanding of its proven safety and efficacy—the science continues to grow daily—what’s needed now is the development of comprehensive, standardized educational tools to provide the practitioner the knowledge and confidence to utilize LDN on behalf of their patients.
This lecture will describe some of the clinical trial evidence supporting well-accepted chemotherapy regimens for advanced cancers in adults, as well as some of the published human research about LDN. The audience will be challenged to decide if the “standard proven” therapies are actually better than LDN, which is still considered “unproven” by mainstream medicine.
In the dawning of the immunotherapies era, nearly 80% of patients undergoing these treatments will experience adverse events. Understanding what is happening to the immune system when met with these medications and then knowing what to do to lower risk and negative outcomes with LDN will be discussed
Little is known about cancer and degenerative diseases in correlation with multiple infections with viruses and bacteria. There is more known about single infections with Coxiella burnetii or Epstein Barr Virus in Non Hodgkin Lymphoma, but nothing is known about the possibility of combined multiple infections in cancer.
Traumatic Brain Injury (TBI) is defined as an alteration of brain function or other evidence of brain pathology, which is attributed to an external mechanical force. This emerging epidemic targets the predominately male, able-bodied workforce, and will become one of the leading causes of death in the next decade. TBI affects every aspect of an individual. Leaky gut equals leaky brain. After brain injury, tight junctions connecting the mucosal epithelial cells become dysfunctional and allow large macromolecules (food antigens) to cross into the bloodstream, which activate the immune system. The mucosal lining often atrophies and dies with changes occurring within minutes after brain injury. Similarly, tight junctions of the blood-brain barrier (BBB) also break down, and neuroinflammatory chemicals enter and wreck havoc. Brain injury often contributes to over or under-activation of the immune system, which may lead to autoimmunity or immune compromise. TBI can trigger autonomic dysfunction, disorders of visceral sensing and processing, and impair gut motility. As the macrophages of the central nervous system (CNS), microglia are the first line of defense of the immune system. In response to TBI, microglia migrate to site of injury and eliminate cellular/molecular debris. Activated microglia release noxious chemicals including pro-inflammatory cytokines, reactive oxygen species (ROS) and nitrogen species, and cause persistent neuro-excitation via glutamate release, which exacerbates existing damage and precedes neurodegeneration. The role of microglia activation in TBI is more highly nuanced than previously described, in which microglia are activated in different phenotypes. These correspond to neurotoxic or neuroprotective priming states. Low Dose Naltrexone (LDN) is a powerful microglial modifier and use in TBI may help prevent neurodegeneration and immune dysfunction. The mechanism is LDN’s antagonist effect on non-opioid receptors (Toll-Like Receptor 4, TLR4), found on macrophages including microglial cells.
Medical research has recently been bringing into question the safety and effectiveness of many of our most popular pharmaceutical treatments for mental health issues. With its extremely low risk-profile, its ability to treat autoimmune and mental health issues simultaneously with only transient side effects, LDN offers an attractive, inexpensive, non-addictive, alternative.
Dosing of opioid antagonists for traumatic stress syndromes and dissociative symptoms is discussed. Case studies are used to illustrate the need for different dosing and how this relates to minimizing adverse effects and maximizing beneficial effects. A neurobiological rationale for adverse effects on emotional functioning in these cases is provided, as well as specific strategies how to address such issues. Moreover, different dosing strategies and their integration with psychotherapeutic interventions are discussed.
Persistent symptoms associated with Lyme disease is a controversial topic with conflicting data and clinical opinion regarding the etiology of this illness. Underlying this controversy is research showing the persistence of Borrelia despite repeated courses of antibiotics. This data combined with the observation that there is a clear gender disparity in the development of post-treatment lyme syndrome suggests the common denominator is a maladapted immune-mediated inflammatory response.
Validation for this hyperactive immune response can be supported by numerous lab findings including elevations of C4a, CCL19, TGF-b1, IL-4, IL-6 and IL-10 with correspondingly depressed NK Cell function, TNF-alpha and IL-2 levels. Critical to long term recovery in these patients is modulating the immune system to correct the associated inflammatory response. By upregulating endorphins and enkaphalins in the body, Low Dose Naltrexone (LDN), acting as a non-selective opioid receptor antagonist, can inhibit proliferation of B and T lymphocytes and the corresponding immune responses. In this way, LDN can be a valuable therapeutic tool for addressing chronic inflammation secondary to persistent Borreliosis.
Naltrexone is an opioid receptor antagonist with FDA approval for treating opioid addiction since 1984. While typical dose for treating opioid addiction with naltrexone is between 50 mg to 150 mg, the use of low dose naltrexone (LDN) with doses ranging from 1.5 mg to 4.5 mg per day has been growing in popularity. The most common use of LDN has been treating autoimmune disorders; consequently, there have been clinical trials investigating the effectiveness of LDN for clinical conditions such as multiple sclerosis, systemic sclerosis, and Crohn’s disease. More recently, exploring the role low dose naltrexone and ultra-low dose naltrexone (microgram dosing of naltrexone) for chronic pain have been described in the literature. It has been proposed that LDN halts inflammatory cascades via glial cell inactivation. In addition, the role of microgram dosing of naltrexone has shown promise as a means to increase analgesia and decrease tolerance to opioid medications. This review evaluates the existing evidence for using LDN for treating pain and its microgram dosing in the potentiation of opioid medication while reducing side effects.
Fibromyalgia is a common condition of widespread pain reflecting central nervous system sensitization. Fibromyalgia pain is notoriously resistant to standard treatments, in part because they do not address the key contribution of the glial cells, the support and immune cells that surround neurons. Central sensitization is a complex process resulting in abnormal glial cell activation and inflammation.
Low-dose naltrexone (LDN) calms activated glial cells and lowers the volume of pain transmitted to the brain. Stanford University researchers found in two separate studies that LDN substantially reduced fibromyalgia pain. Clinical experience supports these research findings, and the presentation will briefly review 4 years of data from use of LDN in a fibromyalgia specialty practice and methods to avoid interactions with opiate-based pain medications.
LDN therapy has become more accepted in medicine. However, many practitioners of LDN therapy operate from the conventional wisdom of LDN for autoimmune disorders using 1.5 mg to 4.5 mg. However, the original article interviewing Dr. Bihari focus on LDN as an agent that can normalize immune system. Recent articles point to the mechanism by which normalizing immune system including modulation of glial cell function via Toll like receptor 4 (TLR4). Understanding the mechanism of TLR4 opens up whole new clinical implications not considered at this time. The clinical use for utilizing ultra low dose naltrexone or microgram dosing of naltrexone will be reviewed. Lastly, combination therapy with other therapeutic modalities including CBD oil and acupuncture will be discussed.
The presentation will review how LDN should be considered a first-line therapy for CFS/FM/Lyme and associated diseases and will discuss how it can be enhanced with other immune modulation therapies. Evidence will be presented on how a multisystem treatment protocol is a necessity for successful long-term treatment of these complex conditions. The cycle of dysfunction that results in multi-system dysfunction will be reviewed, as well as protocols that can be used as a starting point to treat these conditions.
Presented is a novel way of addressing relative nutritional deficiencies and inflammation in Parkinson's Disease which can reverse all symptoms related to these issues.
To discuss the actions LDN, combined with other therapies, to treat autoimmune movement disorders.
It has long been known that fasting can reduce inflammation and autoimmunity, and may extend life, however this strategy isn’t considered widely practical and has safety concerns.
Treatment helps mitigate activation protocols that create speech pathways, decreases disruptive behaviors, and improves immune function
Graves Disease, eponym of Robert James Graves, MD, (1835), is an autoimmune condition fraught with misunderstanding, misdiagnosis and mistreatment by the medical community. Graves’ Disease is characterized by hyperthyroidism secondary to circulating autoantibodies in which Thyroid-Stimulating Immunoglobulins (TSIs) bind to and activate thyrotropin receptors (TSH receptors), causing thyroid enlargement with subsequent thyroid hormone over-synthesis.
Graves’ Disease may present as hyperthyroidism alone (toxic diffuse goiter), or a patient may swing hyper or hypothyroid due to concomitant Hashimoto’s Disease (characterized by the production of Thyroid Peroxidase and/or Thyroglobulin antibodies). A patient may have Hashimoto’s alone (causing hyper/hypothyroid swings) or a single thyrotoxic nodule producing thyroid hormone.
In some patients, Graves’ disease is only one of a related group of existing autoimmune conditions, which leads to dysfunction of multiple organs (i.e. polyglandular autoimmune syndromes). Graves’ and Hashimotos (representing a spectrum of autoimmune thyroid disease) are associated with Celiac disease, vitiligo, diabetes mellitus type 1, autoimmune adrenal insufficiency (Addison’s Disease), systemic sclerosis, myasthenia gravis, Sjögren syndrome, rheumatoid arthritis, and systemic lupus erythematosus.
Females are more predisposed to Graves’ Disease with precipitating or causal factors including genetics, physical/emotional trauma, acute or a chronic infections, and environmental toxins/food antigens. Epstein-Barr Virus (EBV) is an example of a viral trigger via molecular mimicry. Three traditional treatments for Graves’ Disease include anti-thyroid medications, radioiodine therapy, and thyroidectomy. Our functional medicine approach has changed the paradigm of Graves’ Disease treatment to include a root cause approach of treatment. Low Dose Naltrexone (LDN) is a critical therapy in conjunction with removal of autoimmune triggers/environmental stressors, intense diet, nutritional, and lifestyle modifications, herbal therapies, and treatment of underlying causes (e.g. infections).
In line with the other presentations, causes of Hashimoto’s and other autoimmune diseases will be discussed. Treatments that include LDN will also be discussed. Hashimoto’s is often missed by standard doctors and endocrinologists because they feel there is nothing that can be done about it, which is, of course, clearly false. Studies show that lowering the autoantibodies against the thyroid tissue results in more beneficial effects than thyroid hormone replacement. Contrary to common dogma, Hashimoto’s is, however, not the most common form of hypothyroidism, but rather, it is just the easiest to diagnose. Other causes of hypothyroidism are much more common but just harder to diagnose and not taught in medical school or endocrinology residencies, so they are not considered by physicians and endocrinologist. Thus, they typically remain undiagnosed. LDN is also useful for these more common causes of hypothyroidism.
Hypothyroidism is well understood in conventional medicine as an elevated TSH along with associated symptoms. Unfortunately, TSH is determine by the levels of T3 in the pituitary as determined by the type 2 deiodinase. In the periphery, type 1 deiodinase is what converts T4 into T3 while type 3 deiodinase converts T4 into reverse T3. Understanding what might cause a decrease in either type 1 or type 2 or an increase in type 3 deiodinase coupled with low dose naltrexone treatment could greatly improve lab and symptom outcomes in patients with hypothyroidism or for those who experience classical hypothyroid symptoms but have a TSH within range on a lab report.
Like a symphony orchestra, the human body works best when all of its instruments are in tune and playing together.
However, without an experienced conductor the orchestra will fall out of harmony, as will the human body without holistic management of the endocrine systems.
It is perhaps too easy for practitioners to forget this by focussing mostly, or only, on the most pressing issue a patient has. For example, focussing only on improving thyroid function for a thyroid patient, but ignoring the rest of the body.
When we take a step and manage the body as a whole, conducting the orchestra rather than just the soloists, the effects have the potential to make a huge difference to every system in the body.
In our orchestra, Low Dose Naltrexone is the wonderful soloist who can raise the symphony to another level. But the soloists always requires the full support of the whole stage.
This presentation aims to demonstrate the importance of this concept of total management with specialist supporting acts.
This session will review the interactions and assessments in a community pharmacy practice that result in recommendations for LDN therapy initiation. The session will also review complementary therapies for patients seeking functional improvement of immune dysregulation
Fibromyalgia is a common condition of widespread pain reflecting central nervous system sensitization. To understand how to direct treatment of this complex illness one needs to understand the pathophysiology leading to abnormal spinal cord amplification of pain signals, so will start with a brief tour of our scientific understanding of fibromyalgia. With this data it will be clear why fibromyalgia pain has been notoriously resistant to standard treatments.
Fortunately there are some newer alternative pain relief treatments that specifically target the central nervous system sensitization. One of the best studied is low-dose naltrexone (LDN) which calms activated glial cells and lowers the volume of pain transmitted to the brain.
Several case studies of fibromyalgia patients using LDN in a specialty practice will be reviewed, each highlighting one important aspect of prescribing LDN for this specific population. One challenge to prescribing LDN to patients with fibromyalgia is that many utilize opiate-based medications to manage their symptoms. There are ways to overcome this, including using ultra low-dose naltrexone along with separating dosage times adequately to lessen any interactions.
Where to focus your marketing muscle that will skyrocket your inquiries...even though it seems counter-intuitive
There is much more to compounding pharmacy than mixing ingredients. This presentation will give a glimpse into the world of compounding pharmacy, the regulations and guidelines that we strive to meet, how to choose a compounding pharmacy, and how to writefor a low dose naltrexone compounded prescription. Specifically, different bases and equipment used in the compounding of low dose naltrexone will be discussed and how to choose the right dosage form for your unique patient.
30 minute expansion on the Live Presentation
30 minute extension to Treating Depression in Patients with Autoimmune Conditions LIve Presentation
30 minute extension to Treating Psychiatric Disorders with LDN Live Presentation.
30 minitue extension on Infections in Cancer and Autoimmune Disorders Live Presentation
LDN is a potent immune modulator and analgesic, that has synergy with other aspects of an integrative approach to healing pain and inflammatory conditions
To show the audience how the use of LDN has been used to manage neuropathic pedal disorders.
Outline the problem of PMS, current treatments and new treatment with LDN
Naltrexone is used for many areas of the body. But what about the eyes? This presentation will shed light on the use of Naltrexone for ocular issues from a pharmacist’s perspective, as well as considerations for ocular naltrexone formulations.
This session will discuss compounding techniques and quality control procedures used in the process of compounding low dose naltrexone. The topics discussed will apply to compounding of capsules, oral solutions, and topical LDN preparations.
Hashimoto's thyroiditis (autoimmune thyroiditis) is the most common cause of hypothyroidism in the United States. It is characterized clinically by a gradual decline in thyroid function due to the immune-mediated destruction of the gland tissue. Hashimoto’s thyroiditis is an inflammatory process, and since low dose naltrexone (LDN) appears to act as an immunomodulator it is can be an excellent adjunct therapy in clinical practice. Additionally, LDN use in patients with Hashimoto’s not only helps reduce a myriad of thyroid-associated symptoms, but can also lead to a reduced thyroid replacement dosing. Many people with Hashimoto’s often exhibit numerous sensitivities and aggravations to different therapies.
Description: The old paradigm that immune balance is obtained by regulating T helper1 (Th1)and T helper 2 (Th2) cells has been challenged along with the idea that elevated Th1 is always associated with autoimmune disease. With the differentiation of T helper 17 (Th17) cells from Th1 cells came the realization that the immune system is much more complex than the Th1/Th2 paradigm. Decreasing autoimmunity and chronic infections involves balancing Th17 and Treg cells in addition to Th1 and Th2 cells. Understanding the imbalanced immune cycle that is common in many of our chronic disease patients leads to new treatment modalities including transfer factors, natural anti-inflammatories, and LDN.
Sjogren's Syndrome is a chronic autoimmune inflammatory disorder characterized by inflammation in the tear ducts and salivary glands causing both dryness of the eyes and mouth. In addition, chronic fatigue as well as muscle and joint pain are common features. In addition to its pain relieving properties, LDN is also has anti inflammatory benefits based on its inhibition of toll like receptors. As a result, it may be an excellent treatment for this condition which is limited by the lack of FDA approved therapies. In this session, I will present a case report of a patient with Sjogren's Syndrome who had not responded to standard treatment but had a dramatic and rapid improvement with LDN.
SIBO, small intestine bacterial overgrowth, is estimated to account for up to 60% of all IBS patients. That’s millions of patients. The core etiology of developing SIBO is due to auto-immune damage to the nerves that stimulate the muscles of the small gut to move contents forward. As a result, the colon backwashes bacteria/archae into the small gut and they proliferate, causing significant symptoms and damage to the small gut lining. Low Dose Naltrexone can be an invaluable tool in working with SIBO patients. It can help reduce the auto-immunity and acts as a gentle prokinetic, helping to move contents forward to prevent SIBO recurrence. Learn about SIBO, auto-immunity, prokinetics at this interesting lecture by a SIBO expert."