Below is the confirmed line up for the conference. The Schedule may change without prior warning.
LDN clearly has a major role in disease associated with an auto immune component. Some physicians have hypothesised that patients with autoimmune diseases have less cancers, possibly due to the enhanced immune activity. If this were the case then LDN would not be expected to have a role in the management of cancer. However, it is clear that this is not always the case. My own group has shown that in addition to modulating the opiate receptors, LDN is a powerful antagonist of TLR 9 with similar activity on TLR 7 and 8. TLR 9 is overexpressed in inflammatory states such as Crohn's disease and may explain the rapid benefit seen when LDN is given to patients with Crohn's disease. A link here is that inflammation can drive cancer and that some tumours also overexpress TLR9.
In addition to direct activity against tumour cells, LDN clearly acts on the immune response attenuating overactive Th-2 responses and in some cases enhancing cell mediated immune responses. It is therefore more of an immune modulator as opposed to an immune suppressor which is the main function of steroids normally the main treatment of many auto immune diseases. We have previously published that LDN induces a completely different gene expression set compared to the normal dose used for the management of opiate addiction and as such is a unique clinical entity. The genes involved include those which affect the cell cycle and those involved in immune responses. The mechanisms of reported clinical benefit will be discussed together with its potential for enhancing the anti cancer activity of other agents.
With billions of dollars being infused into immune therapy research, two inexpensive and affordable prescriptions already exist and appear to have a synergistic as well as accumulative effect on immune function while mitigating the impact of conventional treatments such as chemotherapy, targeted therapies and immune therapies.
This presentation will describe the unlicensed medicine segment of modern healthcare and explore the supply chain challenges and key governance measures required when supporting patients with unmet needs
Lyme-Borreliosis and coinfections are the chameleon of symptoms, laboratory tests and therapies. Many patients can be infected after tick-bites with several bacteria within the ticks (͞multiple infections͟). There is more tendency by the entomologists to look at different kinds of ticks by PCR for other bacteria like Ehrlichia/Anaplasma, Rickettsia, Babesia and Bartonella. There are many evidence-based studies about Borrelia burgdorferi and for example Ehrlichia/Anaplams as the causing agents in patients with inflammatory arthritis. Modern diagnostic laboratory tests with the highest sensitivity and specificity for Lyme and coinfections are for example T-cell based like EliSpot testings.
At the Dove Clinic, we have used Synthetic Cannabidiol on over 260 cases over the last three years, prescribed under the Pharmaceutical Specials scheme. Of our cohort, approximately a third had been taking Cannabis Extract obtained over the Internet, and had no response. On switching to Synthetic Cannabidiol, they got a response.
During the session, Dr Kenyon will share his clinical experiences of using pharmaceutical grade CBD.
The conventional approach to managing Hashimoto͛s hypothyroidism is rigid and uncompromising; providing relatively limited scope for the testing and management of thyroid issues. This is not without significance for the patient. Conventional medicine is not able to differentiate between hypothyroidism and Hashimoto͛s - the treatment of both remains identical - leading to a significant shortfall in autoimmune treatment for those with Hashimoto͛s. It is therefore time to consider a new approach to the disease, and to consider if we are asking the right questions in diagnosis and management. In adopting a functional and hormonal approach to Hashimoto͛s, we afford ourselves the opportunity to ask different questions and to translate these answers into more suitable treatments for our patients.
"Hysteria has its laws, its determination, precisely like a nervous system ailment with a material lesion. Its anatomical lesion still eludes our means of investigation..."(Dr. Jean-Martin Charcot, 1890).
Medical science has established that neuroinflammatory lesions correspond, in part, to the functional lesions (physiological/biochemical) that Charcot first envisioned as underlying certain neurological and neuropsychiatric disorders. Close connections between neuroinflammation, neuroautoimmunity, and pain/autonomic/movement disorders are now well established. Neuroinflammatory lesions can be directly visualized through PET scans, or detected indirectly by abnormal pro-inflammatory cytokine profiles and/or neuroautoantibodies in bodily fluids. Effective therapies for neuroinflammatory disorders require an understanding of how neuroinflammatory lesions are established and maintained. This problem involves conceptualizing neuroinflammatory lesions as altered states of intercellular communication, within networks of neurons, glia, endothelial cells, and components of the circulatory immune system (leukocytes, antibodies, and complement proteins), which can cross into the nervous system through extravasation.
The central nervous system utilizes a variety of primary signaling pathways to activate neuroimmune responses. Inhibition/attenuation of upstream Toll-like receptors (TLRs), purine receptors (P2Rs), and phosphatidylinositol-linked pro-inflammatory pathways are among current strategies for the treatment of neuroinflammatory lesions. Positive outcomes for neuroinflammatory movement disorders (e.g. fixed and paroxysmal dystonias) have been obtained when LDN (low-dose naltrexone) is used in combination with other anti-neuroinflammatory agents, to reset hyperexcitable cellular states, which drive neuropathic pain and movement disorders. A collapsed transmembrane chloride gradient in post-synaptic neurons is a pervasive mechanism for the loss of inhibitory GABAergic and glycinergic synaptic tone within inflamed spinal and supraspinal sites of the CNS, including thalamic relay neurons located in the sensory and motor nuclei of the forebrain's thalami. This talk will examine how LDN can be potentially combined with other therapies to help restore normal synaptic tone within the inflamed nervous system, and treat neuroinflammation-linked movement disorders.
Mounting evidence suggests that gut health is at the root of all health, and especially autoimmunity and inflammation. A “leaky gut” appears to be a necessary condition for autoimmunity to arise, as it allows potential antigens to enter the bloodstream and trigger an immune response. We will cover some of the many steps patients can take to help “heal and seal” the gut lining. A second aspect of gut health is the microbiome, or the trillions of microbes that live in the digestive tract. These microbes exert an enormous influence on different aspects of health and immunity. Luckily, many different diet and lifestyle habits can alter gut microbes for the better, meaning that patients can largely take control of gut health to reduce or even halt autoimmunity. This presentation will share numerous practical dietary strategies for improving gut health.
Naltrexone is utilized most commonly to normalize immune function. Today many autoimmune and immune dysregulation conditions are successfully treated with LDN. The mechanism of LDN is being investigated; an interesting role of LDN as effecting Toll-Like Receptors (TLR) in addition to opioid receptors. The TRL play a key role in the innate immune system. In addition, the role of TRL in chronic inflammation is being recognized. Thus, LDN is being investigated as a novel anti-inflammatory agent. Younger et al. has published results of clinical trials on using LDN to treat fibromyalgia. Other applications include complex regional pain syndrome. In addition, author will present case histories of patients with intractable neuropathy successfully treated with LDN.
Naltrexone is utilized most commonly to normalize immune function. Today many autoimmune and immune dysregulation conditions are successfully treated with LDN. Because of LDN being a potent opioid antagonist, the use of LDN for patients on opioid pain medication is not recommended for fear of trigger opioid withdrawal reaction. However, the review of literature reveals the role of microgram dose of naltrexone commonly referred as Ultralow Dose Naltrexone (ULDN) having the role of increasing the therapeutic effect of opioid medication and decreasing side effects. This led to exploration of investigative medication Oxytrex. While Oxytrex failed to win FDA regulations, the use of ULDN remains possibility with clinical trials backing the safety profile. Given the challenge we face today in opioid epidemic ULDN is a promising therapeutic intervention.
While LDN has been a wonderful resource for thousands of people with many illnesses of immune dysfunction, treating root causes is essential for long-term healing. Join Dr Nahas to find out what yours might be, with a focus on scars. These disturbances in the autonomic nervous system can persist for decades after any infection, insult or injury, even those from childhood. Learn how they occur, how they disturb immune function and how they can be treated.
This presentation will review the use of re-purposed drugs that have anti-cancer activity via immune and metabolic mechanisms, and are also non-toxic unlike conventional chemotherapy. Therapies will be reviewed, with an emphasis on oral low dose naltrexone, dichloroacetate and dimethylsulfoxide.
This case study discusses a 26 year-old female patient that established care with the desire to wean off methotrexate for the treatment of rheumatoid arthritis. This was accomplished with an autoimmune-specific anti-inflammatory diet, management of comorbidities and psychosocial stressors, targeted anti-inflammatory supplements, correction of nutritional deficiencies, and low dose naltrexone. Subsequently, following clinical improvement and weaning of methotrexate, the patient had an uneventful pregnancy and delivery of a full-term, healthy female infant, without complications. She maintained treatment with 4.5mg low dose naltrexone throughout her pregnancy and post-partum period including breastfeeding her daughter. She flared with rheumatoid arthritis symptoms at approximately 8 weeks post-partum, which was quickly mitigated by targeted anti-inflammatory supplementation and immune system support.