Nevada Homeopathic Integrative Medical Association conference: the brain trust - part 2.
|Article Type:||Conference notes|
(Conferences, meetings and seminars)
Medical societies (Conferences, meetings and seminars)
Integrative medicine (Conferences, meetings and seminars)
Telomeres (Conferences, meetings and seminars)
Telomeres (Health aspects)
Homeopathy (Materia medica and therapeutics)
|Publication:||Name: Townsend Letter Publisher: The Townsend Letter Group Audience: General; Professional Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2012 The Townsend Letter Group ISSN: 1940-5464|
|Issue:||Date: April, 2012 Source Issue: 345|
|Product:||Product Code: 8622000 Medical Associations NAICS Code: 81392 Professional Organizations SIC Code: 8621 Professional organizations|
|Geographic:||Geographic Scope: Nevada Geographic Code: 1U8NV Nevada|
The October 2011 Nevada Homeopathic Integrative Medical Association
(NHIMA) annual conference produced an incredible number of revelations
in health medicine. This brain trust of treasured, integrative
physicians and innovative scientists has profoundly enhanced my view of
medicine on many levels. The following reviews of that conference will
hit the high points of these great presentations. The whole conference
is available on DVD for $145. Contact firstname.lastname@example.org or
Tiffany at 775-742-4695.
Bill Andrews, PhD
Telomere Diagnostics and Therapies: The Future of Medicine
Bill Andrews, PhD (cure-aging-or-die-trying.com), was the cover story for Popular Science magazine in August 2011 ("The Man Who Would Stop Time"). He is the discoverer of human telomerase and has been a telomere researcher for 18 years. Working in biotech research for 30 years, he has 42 US patents on telomerase and is the founder, president, and CEO of Sierra Sciences in Reno, Nevada. He has lectured around the world on telomeres and telomerase and this was his first lecture in Reno. At 59, he is also an ultramarathon runner - which, by the way, increases telomere length.
Telomeres are the end plates of our chromosomes. Telomeres get shorter each time a cell divides, and when they get too short, the cell can no longer make fresh copies of itself. Telomeres are made of repeating sequences of six DNA bases - two thymine, one adenine, three guanine (TTAGGG) - that serve to cap chromosomes, preventing potentially cancerous breaks; the analogy usually is the plastic covering that prevents a shoelace from fraying at the ends.1 Every time a cell splits, the ends of its chromosomes fail to get fully copied in the two new daughter cells, and a bit of telomeric DNA get lost. Tehmerase's job is to synthesize new DNA to add to the shrinking telomeres, slowing down the decline.
Diseases Affected by Telomere Shortening
Dr. Andrews gives a list of conditions affected by telomere shortening, including: cardiovascular, cancer, COPD, degenerative disc disease, Alzheimer's, osteoarthritis, rheumatoid arthritis, osteoporosis, general immunity, skin aging, macular degeneration, liver cirrhosis, muscular dystrophy, cell and tissue transplants, AIDS, progeria, dyskeratosis congenita, idiopathic pulmonary fibrosis, cri du chat syndrome, Down syndrome, Fanconi's anemia, tuberous sclerosis, Werner's syndrome, and aging itself.
Managing Telomere Length
Thousands of natural and chemical substances have been studied by Dr. Andrews in his research of telomerase activity. His has endorsed a product called TA-65, which sells for over $200 per month and a new one called Product B from Isagenix for around $80 per month. He has been heroically pressing on in his study of compounds which increase telomerase-building activity in the last decades, working with many funding challenges. Tune in to his progress online. This knowledge is a game changer for our longevity.
Richard Kunin, MD
Mega Vitamins and Orthomolecular Health Medicine
Dr. Kunin is our much-beloved dean of orthomolecular health medicine. His curriculum vitae is most impressive, beginning with his graduation from the University of Minnesota School of Medicine in 1955 and the start of his publishing career in 1964. He has written scores of articles and several books, including Meganutrition and Meganutrition for Women.4-5 A champion of nutritional medicine from the beginning of his career as an orthomolecular psychiatrist and health practitioner, he has lectured at Stanford Medical School and University of California San Francisco Medical School and has been the president of the Society for Orthomolecular Health Medicine since 1994 to the present. He is a library of biochemical information that surpasses most medical minds. Gratefully, he has imparted these biochemical pathways to his colleagues, students, and friends through all these years and their nutritional and functional medicine interdependence. Of tangential interest is his service as a captain in the US Army Medical Corps, 121st Evacuation Hospital (Korea), and the Valley Forge Army Hospital (Pennsylvania), 1959 to 1961.
Lest We Forget
Dr. Kunin begins with homage to two-time individual Nobel Prize winner Linus Pauling, PhD, and his neologism orthomolecular medicine: "the use of substances normally present in the human body for the maintenance of health and resistance to disease."
He notes that ascorbate (vitamin O directly protects the vascular endothelium from free radical damage. It also restores oxidized vitamin E to assist in protection of membrane lipids. L-ascorbate reduces iron in neutrophils to generate hydroxyl radicals with antibiotic action against bacteria and viruses. COMT (catechol-O-methyltransferase) is inhibited by ascorbate, thus preserving catechol intermediates, much like a reuptake inhibitor. Collagen tensile strength has a linear relationship to ascorbate concentration, important in wound healing and connective tissue strength.
B12 deficiency are often due to TC II transcobalamin transport protein, which is also caused by mercury, lead, antimony, and halogenated hydrocarbons such as PCB, PBB, DDT, and so on, that block methionine synthase enzyme. Cobalamin malabsorption at the terminal ileum is linked to acid pH, often due to pancreatitis, lactose, dysbiosis, or ileocolitis. Folic acid deficiency is most often due to gluten enteropathy, MTHFR (methylenetetrahydrofolate reductase) mutation and/or ingested oxidants, especially chloramines and fluoride. Fluoride kills MTHFR; vitamins C and B3 can normalize it.
Dr. Kunin also reviews many flawed studies on vitamin C and the common cold, noting that upon increased scrutiny almost all studies were favorable to vitamin C in reducing morbidity and especially pneumonia and other more serious side effects of influenza. He catalogs many nutrients and their beneficial effects on treating illness along with their minimal side effects. In atherosclerosis he cites the positive effect of vitamin C on blood lipids, fibrinolytic activity, and platelet adhesiveness in patients with coronary artery disease.7 Forty survivors of Ml were treated with placebo or vitamin C twice daily, either at 0.5 g or I g and followed for 6 months. After 6 months the 1000 mg dose was associated with a 45% increase in fibrinolytic activity, a 27% improvement in platelet adhesiveness, and a serum cholesterol decrease of 12%.
Megavitamin B3 in Psychotic States
In 1939 Drs. Sydenstricker and Cleckley reported 10 cases of atypical states responsive to nicotinic acid at doses up to 300 mg per day. In 1941 they reported an additional 29 cases treated with doses up to 1500 mg per day. "Usually the response to nicotinic acid was prompt, often it was spectacular." This breakthrough in the treatment of organic psychoses and schizophrenia was lost for the next decade, until the double-blind studies of Hoffer, Osmond, and Smythies and the birth of megavitamin therapy for schizophrenia. Subsequently, Hoffer and Osmond's research with double-blind assessment of schizophrenics in 1964 revealed that 75% of niacin-treated patients and 36% in the placebo group did not require readmission.
Anti-Invasive Action of Niacin and Trigonelline Against Cancer Cells
Trigonelline is N-methyl nicotinamide. Niacin, nicotinamide, and trigonelline suppressed the free radial potentiated invasive capacity of cancer cells from rat hepatoma AH109A cell culture.6 This is the first demonstration of anti-invasive action of niacin and trigonelline against cancer. Nicotinamide induces p-53 independent apoptosis in pancreatic ceils and caused cell cycle G2 arrest in all four tested pancreatic tumor cell lines. Nicotinamide inhibits TNF alpha and inflammation via inhibition of NF-kappa B. It exhibits potent antiinflammatory and antitumor properties by inhibition of NF-kappa B and TNA alpha, thus inducing apoptosis.8
Nutritional Deficiency Diseases
The medical mind was slow to accept the concept of vitamin deficiency disease and it still resists the idea of vitamin dependency disease. James Lind cured scurvy (with vitamin C in limes for British sailors, hence the moniker 'limey") in 1747 but was rejected by the British Admiralty for 60 years, and another 100 years passed before Casimir Funk coined the term vitamine in 1911 and thereby raised up the concept of essentiality. Niacin emerged as a miracle in the treatment of epidemic pellagra, the scourge of the Southern states at the turn of the 20th century. Goldberger's proof that it was not an infectious disease (but due to the corn-based diet) led to the discovery of niacin in 1935, and vitamin therapy was quickly accepted and mandated by the enrichment of flour in 1939. However, the megavitamin revolution that began in the 1930s presented a conceptual challenge to the medical community: megavitamins as drugs, now in competition with pharmaceuticals for the treatment of disease. Economics and politics now blur the science! (Let's not forget beriberi and B1 deficiency from polished rice and alcohol excess, which caused epidemics of heart disease, weakness, and death around the world.)
Methylation Pathway is Environmentally Sensitive and Responds to Megadose B6, B12, Folate, and TMG (Trimethylglycine)
Cobalamin is sensitive to metals, oxidizing agents, nitric oxide, ethanol, and pesticides. Folates are sensitive to oxidizing agents, fluorides, chloramines, and phenothiazines (riboflavin blockers). Pyridoxine (B6) requires zinc. Adequate methionine, phenylalanine, and tryptophan are required for optimal health.
TMG-Betaine Nature's Survival Tool
TMG (trimethylglycine) bypasses the need for pyridoxine, folate, and B12. TMG upregulates a host of enzymes and recycles homocysteine to methionine and enhances transmethylation processes. Additional meganutrients help many processes, including lipoic acid for neuroregeneration and enhanced mitochondrial function; carnitine for cardiac survival and endurance advantage; carnosine for neuroprotection and cataract reversal; and pantetheine for high cholesterol, obesity, acne, and fatigue. Riboflavin is indicated for inflammation, headache, obesity, and photosensitivity. Pyridoxine helps tic douloureux, and selenium neutralizes methylmercury toxicity. Ascorbate enhances MTHFR single nucleotide polymorphism (SNP; genetic glitch) and glutathione. Manganese supports SOD and libido and reverses tardive dyskinesia.
Megavitamins: An Open-Ended Subject
Kunin ends his presentation with no formal conclusion other than that megavitamin therapy is ready to emerge from controversy and enter the mainstream of medical practice. The indications are applicable to almost all patients and will lead to advances in all medical specialties. "Anything that can be cured by nutrition should not be treated by any other means." (Maimonides; 12th century)
Ron Hunninghake, MD
Ascorbic Acid and Adjunctive Cancer Care: New Science Regarding an Old Vitamin
Dr. Hunninghake (chief medical officer, Riordan Clinic, Wichita, KS; www.riordanclinic.org) was raised and educated in Kansas and has a distinguished CV of hospital affiliations as well as being an associate professor of family practice, University of Kansas School of Medicine, from 1982 to 1989. His publications include eight books and hundreds of articles and conference presentations. I was honored to return to my home state and present at his Riordan Biannual Conference in 2010 on Vitamin C and Cancer. At that conference were representative physicians from around the world and especially from Japan. Japanese medical school professors lectured on the positive impact of vitamin C and the quality of life parameters they measured. Vitamin C IV is available in every prefecture (state) in Japan and many of their positive outcome patients were presented. I encourage everyone to attend this year's presentation on vitamin C and integrative approaches for cancer patients at the Riordan Center in Wichita on October 17 and 18, 2012.
Dr. Hunninghake dedicated his presentation to his mentor, Dr. Hugh Riordan, MD, who passed in 2005 and endowed my alma mater, the University of Kansas School of Medicine's, 45th professorship at KU Medical School in Orthomolecular Medicine. I encourage all to enjoy the innovative architecture and patient facilities online or in person at the Riordan Clinic. Dr. Riordan supervised 78,200 infusions of vitamin C from 1975 to 2005.
We are again indebted to the discovers of the vitamins that he reviews and the groundbreaking work by Cameron and Pauling that noted a fourfold increase In life expectancy in cancer patients giving 10 grams of IV C daily for 10 days followed by 10 grams orally in terminal cancer patients in 1976. (9) Pauling postulated that higher doses would be more beneficial. He reminds us of the Mortel et al. study at the Mayo Clinic which did not replicate the Pauling study and found no statistical benefit in 200 end-stage cancer patients taking vitamin C orally only. The Mayo clinic studies were taken as definitive by the oncologic community.
In an article in the Annals of Internal Medicine 2004, Padayatty, Riordan, et al. demonstrated that intravenous administration of vitamin C can achieve 70-fold higher blood levels of vitamin C than the highest tolerated oral dose. (10)
Pro-Oxidant Properties of Vitamin C: Direct Cytotoxicity
High-dose intravenous vitamin C generates hydroxyl radicals, which can damage tumor cells. Healthy cells neutralize peroxide with catalase. Tumor cells are low in catalase and are more sensitive to the damaging effects of hydroxyl radicals and become susceptible to high-dose vitamin C at plasma levels of 350 to 400 mg/dl. (11-13) An NIH article in 2007 notes that "Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo." (14) High-dose vitamin C also drives cytokine activity in a healthier direction and is beneficial in addressing cancer-associated inflammation, particularly progression to systemic inflammatory response syndrome (SIRS) and multi-organ failure (MOF).
Tune in next month for the final installment of the Brain Trust.
(1.) Willeit P et al. Telomere length and risk of incident cancer and cancer mortality. JAMA, 2010 Jul 7;304il):69-75.
(2.) Spectracell Laboratories Houston, TX. 800-227-LABS; www.spectraceil.com.
(3.) Richards JB et al. Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women. Am J Clin.Nutr. 2007 Nov;86(5): 1420-1425
(4.) Kunin RA. Mrganutrition. New York: McGraw-Hill; 1980.
(5.) Kunin RA Meganvtrition for Women. New York: McGraw-Hill; 1983.
(6.) Hirakawa N, Okauchi R, et at. Anti-invasive activity of niacin and trigonelline against cancer cells. Biosci Biotechnol Biochem. 2005;69:653.
(7.) Bordia AK. The effect of vitamin C on blood lipids, fibrinolytic activity and platelel adhesiveness in patients with coronary artery disease. Atherosclerosis. 1980;35:181-187.
(8.) Pero RW, Axclsson B, et al. Newly discovered anti-inflammatory properties of the henzamides and nicotinamides. Mol Cell Biochem. 1999;193:119-125.
(9.) Proc Natl Acad Set. 1976
(10.) Padayatly SJ, Riordan HD, Levine M, et al. Vitamin C pharmacokinetics: implications for oral and intravenous use. Ann Int Med. 2004;140:533-537.
(11.) Benade L, Howard T, Burk D. Synergistic killing of Ehrlich ascites carcinoma cells by ascorbate and 3-amino-1,.2, 4-triazole. Oncology. 1969;23:33-43.
(12.) Koch CJ, Biaglow JE. Toxicily, radiation sensitivity modification, and metabolic effects of dehydroascorbate and ascorbate in mammalian cells. J Ceil Physiol. 1978;94:299-306.
(13.) Riordan NH, Riordan HD, (ackson )A, &t al. Intravenous ascorbate as a tumor cytotoxic chemotherapeutic agent. Med Hypotheses: 1995;44:20?-213.
(14.) Chen Q, Espey MG, Sun AY, et al. Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo. Proc Natl Acad Sci. May 14, 2007; 104(21):8749-8754.
by Michael Gerber, MD, HMD email@example.com
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