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If people let the government decide what foods they eat and what medicines they take, their bodies will soon be in as a sorry state as the souls who live under tyranny. Thomas Jefferson Slide 2 Prevention and Cures for Neurologic Diseases New Paradigms of Freedom Slide 3 The Goal Significantly reduce or eliminate most cases of neurodegenerative disease including: Macular Degeneration Diabetic Retinopathy Central Serous Retinopathy Alzheimers Multiple Sclerosis Depression (a dying brain) Slide 4 The Challenges This is raw, unprocessed stuff. Do not expect now, or possibly ever; Expensive Big Pharma sponsored clinical trials written up in prestigious journals. More than minimal acceptance or cooperation from the medical community. Other professionals to wait for us to step up and start using this information. Someone will! Slide 5 Athletes Bodybuilders Gym Rats New Age & Alternative Healing Supplement Gurus Anti-Aging Medicine Chiropractors Naturopaths Homeopaths Dedicated, Educated Scientists and Researchers HEALTHY & HAPPY Slide 6 The Ugly Business of Disease Virtually every new disease fighting agent available to doctors is filtered through a corrupt and self-serving process. Whistleblowers are emerging telling tales of suppressed technologies, shelved patents and huge payoffs. Dont ever expect safe, cheap, effective, legal products to emerge from the current system. Slide 7 Slide 8 Marcia Angell MD Former editor-in-chief of The New England Journal of Medicine On the faculty of Harvard Medical School Time magazine named her one of the 25 most influential people in America Slide 9 Why Most Published Research Findings Are False John P. A. Ioannidis MD PLoS Med. 2005 August; 2(8): e124 There is increasing concern that in modern research, false findings may be the majority or even the vast majority of published research claims. However, this should not be surprising. It can be proven that most claimed research findings are false. (Science compromised by financial interests) Slide 10 Reyes Syndrome Repeat it till its truth Caused by aspirin right? Kills kids right! Mechanism clear as day right? The only study to compare rates of Reyes syndrome in children using aspirin vs. acetaminophen showed kids using acetaminophen had Reyes 600% more often. (Pediatrics. 1987 Nov;80(5):638-42. A catch in the Reye.)Pediatrics. Slide 11 Paediatr Drugs.Paediatr Drugs. 2007;9(3):195-204. Aspirin and Reye syndrome: a review of the evidence. Paediatr Drugs. ...there were probably no new Reye-like diseases reported during the last 10 years that could not be explained by an inherited disorder of metabolism or a misdiagnosis. The suggestion of a defined cause-effect relationship between aspirin intake and Reye syndrome in children is not supported by sufficient facts. Slide 12 Slide 13 Slide 14 If we dont understand it, lets blame it on Autoimmunity The theory that the body is too stupid to recognize its own tissue and attacks it, so we throw corticosteroids at the problem. Genetic defect/predisposition Looking for genes that correlate to diabetic retinopathy, ARMD, Alzheimers etc. while ignoring the gross deficiencies in neuroprotective hormones. Slide 15 The Big Black Hole in Medicine Hormones Theyre not patentable Theyre not profitable They arent taught properly in medical school. Theyve been demonized by Big Pharma interests. Slide 16 Slide 17 Blood Testing I dont recommend doing anything, ever without first getting hormone levels checked. You can go through an MD whose response will vary from helpful to hostile. Or you can set it up yourself using an online vendor such as privatemdlabs.com using a local outfit to do the draw and mail it off. Direct testing of CNS neurosteroids can only be done at the autopsy (too late). Slide 18 Four Principles for Understanding Neurodegenerative Disease 1. When youre losing lean mass, youre losing CNS health and function. 2. Men and women dont do well on high levels of the others sex hormones. 3. A brain thats losing function sends up depression as a warning flag. 4. The health and function of both the CNS and the immune system are based upon the same basic principles. Slide 19 The Good Guys! Neuroprotective Hormones 1. DHEA Dehydroepiandrosterone 2. Testosterone/DHT Increases insulin sensitivity (think DR!). 3. Estrogen is like taxes. You do not want this stuff too high. More than the minimum usually causes problems. 4. Allopregnanolone progesterone metabolite in the CNS 5. HGH and its more active form: IGF Slide 20 Neurosteroids are a group of steroid hormones synthesized by the brain in the presence of steroidogenic enzymes. Specific neurosteroids modulate function of several receptors, and also regulate growth of neurons, myelinization and synaptogenesis in the central nervous system. Some neurosteroids have been shown to display neuroprotective properties, which may have important implications for their potential use in the treatment of various neuropathologies such as: age-dependent dementia, stroke, epilepsy, spinal cord injury, Alzheimer's disease (AD), Parkinson's disease (PD) and Niemann-Pick disease (NP-C). Pharmacol Rep.Pharmacol Rep. 2006 May-Jun;58(3):335-40. Endogenous neuroprotective factors: neurosteroids. Slide 21 The Enemy Fight or Flight Hormone Cortisol trumps all the other hormones because the body thinks its in survival mode. Virtually all anabolic functions (healing and growth) are ceased until the crisis is over. Catabolic processes begin immediately to increase blood sugar and blood pressure. High cortisol levels are deadly to central nervous system neurons. Slide 22 Slide 23 Adrenal Fatigue/Failure/Insufficiency Slide 24 Compounding Lifestyle Issues that Raise Cortisol Levels Sleep deprivation defined as lack of proper amount of deep restful sleep, not the time youre unconscious. Distance/Endurance exercise A bad idea for older athletes. HIIT training superior. Calorie deficits, dieting Alcohol toxic, catabolic and estrogenic Caffeine Squeezes everything out of the adrenal glands, norepinephrine and cortisol. Slide 25 Chronic Elevated Cortisol Effects Raises blood sugar Promotes insulin resistance Promotes angiogenesis (think PDR and wet macular) Highly catabolic to protein based tissues (muscle) Promotes fat storage Lowers sex hormones, HGH and thyroid hormone (T3) Slows cellular metabolism Raises blood pressure constricts mid size arteries Weakens immune function promotes activation of herpes viruses and mycoplasmas Major cause of depression Kills CNS neurons (think retina and optic nerve) Slide 26 J Clin Endocrinol Metab.J Clin Endocrinol Metab. 1993 Mar;76(3):554-8. Diabetic neuropathy is associated with increased activity of the hypothalamic-pituitary-adrenal axis. J Clin Endocrinol Metab. integrated secretion of both ACTH and cortisol was increased specifically in the 25 diabetic patients with symptomatic polyneuropathy compared to 19 diabetic patients without neuropathy. ACTH and cortisol concentrations correlated with most clinical and neurophysiological parameters of neuropathy Slide 27 Cortisol Secretion in Patients With Type 2 Diabetes Relationship with chronic complications Diabetes Care January 2007 vol. 30 no. 1 83-88 CONCLUSIONS In type 2 diabetic subjects, hypothalmic-pituitary-adrenal (HPA) activity is enhanced in patients with diabetes complications and the degree of cortisol secretion is related to the presence and number of diabetes complications. cortisol level was significantly associated with diabetic retinopathy Slide 28 Routine Psychological Screening in Youth With Type 1 Diabetes and Their Parents Diabetes Care October 2007 vol. 30 no. 10 2716-2724 10-year point prevalence and lifetime prevalence rates of psychiatric disorder in diabetic youth were found to be 47% and 37%, respectively. Mood disorders such as major depressive disorder and dysthymia are the most frequently reported diagnoses in youth with type 1 diabetes. Neurohormonal changes related to stress and mental illness may directly influence metabolic control through endocrine pathways. Slide 29 Central Serous Retinopathy Endogenous Cortisol Profile in Patients with Central Serous Chorioretinopathy Br J Ophthalmol. 1997 November; 81(11): 962964. S Garg, T. Dada, D. Talwar, and N Biswas Increased levels of endogenous cortisol are present in patients with CSCR. Slide 30 Thyroid Hormone Basics T4 (thyroxine) has minimal activity. T4 must be converted to the biologically active form of T3 (Triiodothyronine). High cortisol levels block the conversion of T4 to active T3. People with low T3 tend to have low levels of sex hormones & neurosteroids. T3 is now being used as an anti- depressant. This makes sense! Slide 31 Excess cortisol Biologically Inactive Slide 32 Slide 33 Benign Intracranial Hypertension Aldosterone excess has been definitively linked to cases of BIH. (Am J Med Sci. 2002 Jul;324 (1):45-50. Idiopathic intracranial hypertension with primary aldosteronism: report of 2 cases. Weber KT, Singh KD, Hey JC.Am J Med Sci.Weber KTSingh KDHey JC T3 is antagonistic to Cortisol and Aldosterone. Treatment should consist of a test for active T3, and supplementation of T3 to high-normal levels. Theyll love you for the weight loss effect! Slide 34 Slide 35 Neurosteroid Dehydroepiandrosterone Interacts with Nerve Growth Factor (NGF) Receptors, Preventing Neuronal Apoptosis (PLOS Biology April 2011) ...DHEA produced by neurons and glia, affects multiple processes in the brain, including neuronal survival and neurogenesis during development and in aging. ... we provide evidence that DHEA exerts its neurotrophic effects by directly interacting with the TrkA and p75 NTR membrane receptors of nerve growth factor (NGF)... Slide 36 Clinical Implications of DHEA as a Neurosteroid Since DHEA is neuroprotective before any further enzymatic reduction, then adding downstream metabolites like testosterone, DHT and estrogen might be less effective for the treatment of neurodegenerative disease. Yet these downstream metabolites are all that are Rxed by the medical profession, and often in the form of toxic synthetics. Slide 37 Slide 38 High Estrogen Ratio in Men Causes upregulation of SHBG, further reducing free test. Has a greater inhibitory effect on the HPTA than testosterone, thus resulting in lower total testosterone production. Makes us pudgy, bloated, grumpy and hyper-emotional. High estrogen swells the prostate gland and feeds certain cancers. Slide 39 Slide 40 Test/Estrogen Ratio in Men One simple compound can fix a faulty T/E ratio: An Aromatase Inhibitor. (AI) The better examples include; 1. Formestane (transdermal) 2. Exemestane (Aromasin) available as a research chemical or by Rx (yeah right) 3. Androst-3,5-dien-7,17-dione (Erase) 4. DHT (or a DHT prohormone) Slide 41 Amazon.com Rx or Research Chemical Slide 42 Is Testosterone Neuroprotective? Testosterone improves neuron survival in brain regions vulnerable to neurodegenerative disease. This may explain the association of low testosterone levels in men with neurodegenerative diseases (Hogervorst et al 2004, Ready et al 2004). Studies demonstrate testosterone loss occurred 5 to 10 years prior to Alzheimers disease diagnosis. Slide 43 The Journal of Neuroscience, June 9, 2004 24(23):53155321 We conclude that estrogen and androgens protect human neurons against beta-amyloid toxicity by increasing the levels of Hsp70 (heat shock protein) in the neurons. Hsp70 completely protects against beta- amyloid mediated toxicity. Slide 44 But Testosterone causes cancer, right? In 1941, Dr. Charles Huggins showed that castration slowed the progression of prostate cancer. He assumed that reducing testosterone reduced the growth of the cancer. This incredible blunder can now be understood since we know about the activity of the enzyme aromatase which increases with age in virtually all adult men. Yet, most of the medical world will still quote the results of this 70 year old study. Slide 45 J Cell Biochem.J Cell Biochem. 2007 Nov 1;102(4):899-911. Estrogen and prostate cancer: an eclipsed truth in an androgen-dominated scenario. J Cell Biochem. The association between plasma androgens and prostate cancer remains contradictory and mostly not compatible with the androgen hypothesis In summary, although multiple consistent evidence suggests that estrogens are critical players in human prostate cancer, their role has been only recently reconsidered, being eclipsed for years by an androgen-dominated interest. (drug companies selling 5a-reductase inhibitor drugs) Slide 46 Oestrogen and benign prostatic hyperplasia: effects on stromal cell proliferation and local formation from androgen Clement K M Ho, Jyoti Nanda1, Karen E Chapman and Fouad K Habib1 Clement K M HoJyoti Nanda1Karen E ChapmanFouad K Habib1 Clement K M HoJyoti Nanda1Karen E ChapmanFouad K Habib1 Oestradiol (E2)increased the proliferation of stromal cells in culture these findings support the hypothesis that oestrogens play a role in the pathogenesis of BPH, a disease characterised predominantly by stromal overgrowth. Slide 47 Dovepress Journal - Therapeutics and Clinical Risk Management The benefits and risks of testosterone replacement therapy: a review Authors: Nazem Bassil, Saad Alkaade, John E Morley Published Date June 2009 Volume 2009:5 Pages 427 - 448 DOI: http://dx.doi.org/10.2147/TCRM.S3025http://dx.doi.org/10.2147/TCRM.S3025 Perhaps the most controversial area is the issue of risk, especially possible stimulation of prostate cancer by testosterone, even though no evidence to support this risk exists. Slide 48 DHT The Real Kicker Evidence is mounting that the CNS effects attributed to testosterone are more likely due to its conversion to DHT The effects of DHT on the central nervous system include increased neurological efficiency, strength, increased resistance to psychological and physical stressnot to mention optimal sexual function and libido. Slide 49 DHT - Dihydrotestosterone Causes prostate enlargement and maybe cancer right? Absolutely wrong Clinicaltrials.gov - Effect of Dihydrotestosterone (DHT) on Prostate Tissue [Short Title: DHT-3] DHT may shrink the prostate, suggesting it may be beneficial for some men. The placebo group had more hyperplasia! DHT antagonizes estrogen in men. Slide 50 Dihydrotestosterone for use in androgenotherapy United States Patent 5648350 The present invention is directed to the administration of dihydrotestosterone (DHT) for preventing prostate cancer in male patients more than 50 years old A short-term study with an aromatase inhibitor in men suffering from BPH has shown a mean reduction of 26% of the prostate volume, which reinforces the hypothesis of the responsibility, also for men, of certain estrogens. Slide 51 Post-Finasteride Syndrome 5 -reductase inhibitors have been shown to have persistent side effects that can continue after quitting the treatment, including diminished libido, erectile dysfunction, male breast cancer, depression, brain fog and memory loss. Both DHT and allopregnanolone require the 5 -reductase enzyme for synthesis. Propeciahelp.com chock full of stories of ruined lives, depression and suicides...why? Slide 52 Healthy human salivary glands contain a DHEA- sulphate processing intracrine machinery, which is deranged in primary Sjgren's syndrome. J Cell Mol Med. 2009 Jul;13(7):1261-70. Epub 2009 Feb 27. J Cell Mol Med. J Cell Mol Med. Sjogrens patients have low DHEA and high estrogens. Some Sjogrens patients respond well to DHEA supplementation. Some do not because of defective enzymes related to the production of DHT. Nobodys giving DHT to females of any age. Slide 53 Testosterone, Androgens and Anabolics There are two major types of effects of testosterone on adults. One is the androgenic effects which include facial hair, hematopoiesis, libido, strength and neurologic motivation. The other effect is known as anabolic which includes healing of damaged tissue, bone growth and increases in muscle mass. Testosterone has an anabolic/androgenic ratio defined as 1/1. Slide 54 Anabolic Steroids Most anabolic steroids reduce levels of the neurosteroids by suppressing natural DHEA, testosterone and DHT production. They dont feel good. Low DHT plus high estrogenic effects are known as roid rage. The CNS doesnt like synthetics. Anabolic steroids have a higher anabolic ratio that is known as the myotrophic ratio or the Q ratio. Slide 55 SARMs (Ostarine, Andarine) Selective Androgen Receptor Modulator A new class of drug that is not a steroid hormone, but acts as an androgen receptor agonist. Advantages include oral dosing, low toxicity, minimal suppression, and high anabolic ratio. Recent studies have been very successful in helping cancer patients and the elderly gain lean mass. Neuroprotective effects are unknown. Slide 56 HRT for Women Good or Bad? The synthetic versions of both estrogen and progesterone are strongly linked to higher cancer rates and autoimmunity. Natural hormones cannot be patented by drug companies, their synthetic analogs can. Thus, most HRT involves the use of synthetic estrogen (Premarin PREgnant MAre urINe) and/or a synthetic progesterone (Provera/Norplant). Slide 57 Slide 58 Nandralone (Deca) Levonorgestrel (Norplant, Mirena) Slide 59 Levonorgestrel Progesterone Allopregnanolone (a healthy neurosteroid) 5-dihydrolevonorgestrel (toxic, androgenic metabolite) 5-reductase Slide 60 Levonorgestrel A Bad Idea? Its in vitro relative binding affinities at human steroid hormone receptors are: 323% that of progesterone at the progesterone receptor, 58% that of testosterone at the androgen receptor. Loading up a female with large doses of an androgenic substance is not a good idea. Blocking the progesterone receptors with something 3X as strong is not a good idea. Slide 61 J Neurobiol.J Neurobiol. 2006 Aug;66(9):916-28. Reduced metabolites mediate neuroprotective effects of progesterone in the adult rat hippocampus. The synthetic progestin medroxyprogesterone acetate (Provera) is not neuroprotective. J Neurobiol. In conclusion, our findings indicate that progesterone is neuroprotective against kainic acid excitotoxicity in vivo while the synthetic progestin MPA is not and suggest that progesterone metabolism to its reduced derivatives DHP and THP (allopregnanolone) is necessary for the neuroprotective effect of the hormone. Slide 62 Allopregnanolone Formed in a 2 step conversion from progesterone. Uses the 5 -reductase enzyme. Research with animal models shows allopregnanolone effective against neuroinflammation, myelin and axonal injury and reduced neurobehavioral deficits. Severely reduced or absent in MS, schizophrenia and bipolar. (Tx options???) Slide 63 Brain (2011) 134 (9): 2703-2721. These multi-platform studies point to impaired neurosteroidogenesis in both multiple sclerosis and experimental autoimmune encephalomyelitis. The findings also indicate that allopregnanolone and perhaps other neurosteroid-like compounds might represent potential biomarkers or therapies for multiple sclerosis. Slide 64 StAR - Steroidogenic acute regulatory protein Regulates cholesterol transfer within the mitochondria, which is the rate-limiting step in the production of steroid hormones. In persons with high or normal cholesterol and low levels of steroid hormones, suspect low StAR levels. Alcohol suppresses StAR activity. DAA d-aspartic acid. Upregulates StAR, makes more steroid hormones! Slide 65 Amazon.com Slide 66 P450scc Slide 67 Human Growth Hormone 0 10 20 30 40 50 60 70 80 90 Slide 68 Slide 69 Make Your Own HGH & IGF Take niacin at bedtime on an empty stomach. Start with a low dose (50mg) to avoid a severe flushing reaction and build tolerance until youre up to 1000mg. 4 hours later, eat something high in simple carbs to spike your insulin. HGH + Insulin = IGF Slide 70 Niacin better than Statins! Slide 71 Benfotiamine Fat soluble Vitamin B-1 Great for peripheral neuropathies Easily crosses the blood-brain barrier Powerful inhibitor of the formation of advanced glycation endproducts (AGE) Discussed in peer reviewed literature as a cure for diabetic retinopathy Will soon play a role in the treatment of AMD since AGEs are found in drusen. Slide 72 Amazon.com Slide 73 Nature Medicine 9, 294 - 299 (2003) Published online: 18 February 2003; doi:10.1038/nm834 Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy The ability of benfotiamine to inhibit three major pathways simultaneously might be clinically useful in preventing the development and progression of diabetic complications. Slide 74 Pharmacological Research Volume 61, Issue 6Pharmacological Research Volume 61, Issue 6, June 2010, Pages 482488 The multifaceted therapeutic potential of benfotiamine The anti-AGE property of benfotiamine certainly makes it effective for the treatment of diabetic neuropathy, nephropathy and retinopathy. Slide 75 Slide 76 Medium Chain Triglycerides (Ketone bodies) An alternative energy source for insulin resistant CNS neurons! Coconut oil is a cheap and readily available source for MCTs. Have already been successful as a standalone treatment for Alzheimers. Slide 77 BMC Neurosci. 2008; 9(Suppl 2): S16. Published online 2008 December 3 Hypometabolism as a therapeutic target in Alzheimer's disease This decline in cerebral glucose metabolism occurs before pathology and symptoms manifest, continues as symptoms progress, and is more severe than that of normal aging. Ketone bodies are an efficient alternative fuel for cells that are unable to metabolize glucose or are 'starved' of glucose. AC-1202 (Axona, a patented MCT) is designed to elevate serum ketone levels safely. Slide 78 VEGF and BMI* *Body Fat Percentage would have been a better control Slide 79 VEGF Origin and Function Tissue hypoxia triggers release of VEGF. In blood vessels, VEGF stimulates new vessel growth. But in CNS Neurons, VEGF directly protects cells from hypoxic, excitatory and oxidative damage. It also promotes healing and growth of CNS cells including neural stem cells. Oops, were injecting it into the CNS! Slide 80 Anti-VEGF, Pro-VEGF VEGF shows up at hypoxic tissue like firemen show up at a fire. Anti-VEGF therapy is not the best way to treat cancer or macular disease. I doubt pro-VEGF therapy will emerge as a sensible neurodegenerative disease Tx. Treat the underlying cause, hypoxia, before trying to outsmart the subsequent damage control systems. Slide 81 Opportunistic Infections Many researchers are becoming aware of infectious agents underlying human diseases that used to be classified as autoimmune. It is a simple concept that high cortisol levels suppress the immune function. Also, the lack of protective neurosteroids in the CNS leaves it wide open to attack. Slide 82 Pop Quiz What infectious agent Is widely spread throughout the population, Can live for decades undetected in the CNS, Cannot be eradicated with current medical therapy, Activates in the presence of high cortisol levels, Can cause rapid, severe tissue damage? Slide 83 Answer: Three of the eight herpes viruses. Herpes Simplex 1 (HSV-1) Herpes Simplex 2 (HSV-2) Varicella Zoster Virus (VZV) Slide 84 Heresy Food for Thought... What viruses multiply in, then destroy T-cells? Three other herpes viruses; HHV-6A HHV-6B HHV-7 Slide 85 Journal of NeuroVirology: 513528, 2002 Glucocorticoids and central nervous system inflammation under certain circumstances glucocorticoids enhance inflammation. glucocorticoids have been found to increase neuron loss. Section: Glucocorticoids and neurotropic viruses Slide 86 Herpes: the Ultimate Neurotropic Virus A neurotropic virus is a virus which is capable of infecting nerve cells, or which does so preferentially. Such viruses thereby largely evade the usual immune response, which acts only within the blood. Slide 87 More than a lip lesion Activated herpes viruses probably account for a large proportion of cases of; Rheumatoid Arthritis Thyroiditis Pancreatitis (Diabetes?) MS All of which have been labelled autoimmune. Slide 88 An Association of Herpes Simplex Virus Type 1 Infection With Type 2 Diabetes Diabetes Care February 2005 vol. 28 no. 2 435-436 A significant association of HSV-1 infection with type 2 diabetes was found in the present study. Chronic inflammation is involved closely and early on in the pathogenesis of type 2 diabetes. In summary, the association of HSV-1 infection with type 2 diabetes further supported the notion that inflammation and virus infection might be the risk of development of type 2 diabetes. (or are both due to elevated cortisol?) Slide 89 MS Natural killer cells are lower in MS patients (suspect high cortisol). MS patients virtually lack Allopregnanolone! The evidence continues to mount that herpes viruses HHV-6A, EBV and VZV play an important role in triggering multiple sclerosis, perhaps in different subsets. Slide 90 Guanosine Analogue Antivirals Acyclovir Valacyclovir 70% acyclovir, 30% Valine Famciclovir prodrug to Penciclovir They get incorporated into replicating DNA, but then nothing else can connect to it. Also known as a chain terminator. They cross the blood-brain barrier at low efficiency. Slide 91 Alternative Herpes Therapy Cortisol control + Neurosteroids Monolaurin Has powerful microbicidal activity against all herpes viruses, flu viruses, mycoplasmas and even MRSA. Lysine Has been definitively shown in peer reviewed literature to suppress the formation of herpes viruses when sufficient amounts are present. (Dermatologica 1978;156:257-267) Slide 92 Amazon.com Slide 93 Mycoplasmas A primitive bacteria with no cell wall resulting in antibiotic resistance. M. fermentans is the most pathogenic. There is a subspecies called M. fermentans incognitus that very well could be an escaped biological weapons project (Project Day Lily). Very common in Chronic Fatigue Syndrome, Gulf War Syndrome and Rheumatoid Arthritis. Slide 94 Mycoplasmas: The smallest known living cells.1 micron dia = the size of a herpes virus Slide 95 Presence of Mycoplasma fermentans in the bloodstream of Mexican patients with rheumatoid arthritis BMC Musculoskeletal Disorders 2009, 10:97 Increasing evidence incriminates bacteria, especially Mycoplasma fermentans, as possible arthritogenic agents in humans. Our findings show that only M. fermentans produce bacteremia in a high percentage of patients with RA. Slide 96 Slide 97 Slide 98 Basic Neuroprotection Protocol Supplement T3 to upper 1/2 to 1/3 of normal range. Control cortisol down to lower 1/2 of range. Get progesterone (allopregnanolone) levels up to the upper end of normal range. Get androgen (DHEA, T, DHT) levels up and in proper ratio to estrogens. Begin niacin protocol to raise levels of HGH and IGF Slide 99 Neuroprotection Ancillaries D-aspartic acid to augment conversion of cholesterol to steroid hormones Benfotiamine 600-1200 mg daily Medium chain triglycerides (MCT) or coconut oil as alternative energy source Creatine 1-4 g Ubiquinol (reduced CoQ10) 100-200 mg Monolaurin 6-9 g if infection is suspected. Lysine 3-6g if herpes is suspected. Slide 100 Where to get T3 Good luck getting anybody to prescribe this properly. There are discussion groups all over the internet that contain excellent information on dosing, side effects, pyramiding protocols, cruising protocols andwhere to get it. People order this stuff as a research chemical all the time. Slide 101 Slide 102 Cortisol control Amazon.com Slide 103 Progesterone and Estrogen Amazon.com Slide 104 Where to get legal Androgens You can have testosterone Rxed by a licensed physician, CNP, or sometimes a chiropractor. You can use OTC compounds containing DHEA and derivatives designed for different downstream effects. Slide 105 Steroids for the Brain High oral availability of DHEA and Pregnenolone Amazon.com Slide 106 Slide 107 DHEA and Pregnenolone Slide 108 DHT by Rx Compounded DHT Slide 109 DHT Prohormones Contains epiandrosterone Converts directly to DHT Cant convert to estrogens Amazon.com Slide 110 I believe we have a profound moral obligation to do anything in our power to assist patients in the prevention and treatment of neurodegenerative disease. Nobody can stop us from sharing information. At least a web page devoted to discussion of this material, complete with relevant links should be made available to both patients and professionals.