Presentation - The VDR nuclear receptor is key to understanding ‘diseases of the aging’

Type: Conference presentation
Presenter: Trevor Marshall, PhD
Conference: Aging 2008
Location: UCLA
Date: April 17-19, 2008
Additional content: Reflections from the Aging Conference by Amy Proal; additional video footage from the Conference


In 2006 we reported routinely inducing recovery from chronic inflammatory disease, including 'autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body' syndromes. In 2008 we additionally reported inducing recovery from chromic neurological disease, including neuropathies, cognitive and memory deficiencies, depression, Bipolar and Obsessive Compulsive Disorders. These chronic diseases are all caused by an intraphagocytic biofilm A structured community of microorganisms encapsulated within a self-developed protective matrix and living together.-like metagenomic microbiotaThe community of bacterial pathogens including those in an intracellular and biofilm state which cause chronic disease. which has apparently been part of the human experience since Neolithic times, but which, due to changes in lifestyle and medicine during the 20th century, has expanded into epidemic prominence over the last three decades. Located in the phagocyte cytoplasm, this microbiotaThe bacterial community which causes chronic diseases - one which almost certainly includes multiple species and bacterial forms. has direct access to both the transcription and translation machinery of Homo sapiens. We have demonstrated that the intraphagocytic pathogens have evolved a survival mechanism whereby VDRThe Vitamin D Receptor. A nuclear receptor located throughout the body that plays a key role in the innate immune response. transcription is inhibited. Transcription of a minimum 913 genes is thus directly affected by the pathogens, notably including MTSS1. Life Extension research can derive much from our observations on this cohort, as they transition to recovery.

Firstly, we now have objective data showing that chronic organ damage, including fibrotic tissue deposition, can be reversed, even in patients who are beyond middle-age. Further, we have shown that neurological damage can be reversed, and that neurological recovery appears complete. After recovery, patients are left re-invigorated, and report levels of cognition and memory often described as “feeling 20 years younger”. Recovery is induced by activation of the VDR Nuclear ReceptorIntracellular receptor proteins that bind to hydrophobic signal molecules (such as steroid and thyroid hormones) or intracellular metabolites and are thus activated to bind to specific DNA sequences which affects transcription. with OlmesartanMedication taken regularly by patients on the Marshall Protocol for its ability to activate the Vitamin D Receptor. Also known by the trade name Benicar. , an agonist, and long-term (3-6 years) administration of low-dose sub-inhibitory antibiotics which target protein synthesis by the bacterial 70S ribosome.

Aging-related diagnoses already shown to be reversible include: osteoporosis, periodontal disease, uveitis, arthritis, hypertension and cardiovascular disease. It should be noted that as the pathogens are killed, the infected cells often undergo apoptosis. This immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. manifests itself as an exacerbation of symptoms, and can make the patient quite ill. It is therefore important to start therapy early. A small German pilot study in Dementia had to be terminated, even though the subjects were responding to therapy as expected, because subjects were too ill to rationalize what they were experiencing. We propose that further studies of individuals recovering from chronic illness will quickly yield insight into not only the diseases of the aging, but also into the processes of aging.

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