ALZHEIMER’S TREATMENTS THAT ACTUALLY WORKED IN SMALL STUDIES BUT WILL NEVER BE TESTED & YOU WILL NEVER HEAR ABOUT FROM YOUR MD OR BIG PHARMA BECAUSE THEY ARE UNPATENTABLE, UNPROFITABLE, AND EASILY OBTAINABLE. Jeff T. Bowles This Book is Owned and published by Jeff T. Bowles Publishing LLC All Rights Reserved This book is dedicated to The pioneering research and theoretical works of Dr. Vladimir Dilman and Dr. Ward Dean. Introduction Chapter 1. Foundations of the Theory Chapter Two—Lupron for Alzheimer’s disease. The Story behind the Story. Chapter 3—Treatments for Alzheimer’s that Work for Men and Women Chapter Four—Pharmaceuticals for Alzheimer’s? Chapter Five—More Treatment Regimens for Alzheimer’s that Work Chapter Six--Melatonin Chapter Seven—Origins of Aging: Evolution, Cells, Plants, and Animals— Influence of Hormones Chapter Eight—Anti-Aging Effects of Caloric… and Water Restriction Chapter Nine—LH Causes Alzheimer’s--History of the Theory The evolution of aging: a new approach to an old problem of biology. NIH News: New paper suggests elevated LH behind AD Appendices Appendix A: melatonin treatment on secretion of steroid hormones Appendix B: Two twins with Alzheimer’s Appendix C: Alzheimer’s Disease—Clinical Stages Apppendix D: Smoking Prevents Alzheimer’s Appendix E: Do Aricept and Namenda really help Alzheimer's symptoms? Appendix F: Voyager Pharmaceuticals Press Release Appendix G: Voyager Pharmaceuticals’ Therapeutic Approach to Alzheimer’s Appendix H: Lupron-Drug Facts Appendix I: Pregnenolone Sex- and age-related changes in epitestosterone in relation to pregnenolone sulfate and testosterone in normal subjects. Appendix J: Scientists Pinpoint How Vitamin D May Help Clear Amyloid Plaques Found in Alzheimer's Appendix K: New Findings Contradict Dominant Theory in Alzheimer's Disease Book Overview About The Author Introduction I apologize for not writing this book 15 years ago in 1997, when I first developed a novel, compelling theory about the cause of and potential treatments for Alzheimer’s disease. Why did I sit on this information for so long? Let me explain by giving you a little of its history. I personally have seen the toll that Alzheimer’s can take on a great mind. My grandfather got the disease in his 60’s, when he was a very well-respected lawyer/real estate investor/ politician. When it first hit him, we noticed he would keep driving with the turn indicator on. After he was diagnosed, we noticed his vocabulary started a rapid decline, when he would look out the window and talk about the birds he would like to feed, and would refer to them as tails. He would drive my grandmother crazy by getting up at night and being all agitated. They finally sent him to a nursing home. I remember that when I went to visit him (when I was 14), he would just sit in a wheel chair and could not hold his head up, could not speak, and would drool a lot. He looked terrible! He died of pneumonia not too long after I saw him like that. They probably decided not to treat him. 1997 was the year when I was the first who theorized that the dramatic increases of human Luteinizing Hormone (LH) that occurs in aging people (by up to 1,000’s of percent) is the culprit that causes Alzheimer’s disease. At the time, this was quite a radical idea that had never been seen before in print or even mentioned by anyone, sane or insane! You see, Luteinizing Hormone (LH) was supposed to be a hormone that only affected, controlled, and acted upon sex-related tissues. By June, 1997, I had finished a theoretical paper describing this crazy idea, and it was accepted for publication by the British journal, Medical Hypotheses, and eventually made it into print in September, 1998. The theory was still quite speculative at the time, but little by little, supporting facts started trickling in. About a year after my paper was published, LH receptors were found all over the body (and in the brain), not just in the sex tissues. About a year after that, the Mayo clinic found that autopsied brains of Alzheimer’s victims were loaded with LH, with the heaviest concentrations being found in the most damaged parts of the brain. Just last year, a paper by a scientist at the NIH (the conservative US government-run National Institutes of Health) agreed that he (and they) now believe the premise is correct--that LH does cause Alzheimer’s! Quite a turnaround from the initial ridicule I got from various Alzheimer’s researchers to whom I’d mentioned the LH idea. I remember one researcher from Northwestern University, standing in front of his highly complicated amyloid beta poster, telling me, “I wish it were that easy,” and then smugly turning his back on me. But that is typical behavior when you are proposing unfamiliar ideas to most scientists. In my experience, I have not found much difference in my dealings with scientists and with autistic children. How are scientists like autistic children? They both usually share these characteristics: they are socially awkward they have and concentrate intensely on peculiar interests they are usually pedantic (enjoy correcting others and demonstrating their detailed knowledge of a topic) they love repetition and sameness (thus, they’re not particularly creative) and, they get really upset when the furniture is rearranged! Another researcher, after reading my paper at my suggestion, said that even though he wasn’t exactly sure about all the ideas presented in it, his initial opinion was that if it was a painting instead of a science article, it seemed more like something his granddaughter might have created, as opposed to a Jackson Pollock. Several times I got letters back from well-known, evolution professors that started with something like, “Unfortunately you do not understand how evolution works.” It used to make me angry, and I would go into a tirade showing them how wrong they were--but now it just makes me laugh. The mainstream science community cannot be convinced of anything new, no matter how much proof you push into their faces. That is why I no longer write papers for scientists--only for those who might be able to fairly evaluate the facts and theories I present. Today’s mainstream professional scientists will be the last to accept any changes to their beliefs. It really is a sad situation, because it leads to a snail’s pace of scientific and medical advancement on which countless suffering humans are waiting. In this book, I will discuss how the entire medical, evolutionary, biology, and science communities are all trapped in a self-policed and self-reinforced logical box which prevents them from coming up with proper, simple, approaches for treating the diseases of aging which today would be considered “outside the box.” I will also explain how to get out of the box without violating the rules of logic. Chapter 1. Foundations of the Theory When I submitted my first paper (a unified theory of aging) to the journal, Experimental Gerontology, the Editor-in-Chief was Leonard Hayflick, a paragon in gerontology. Dr. Hayflick sent me a 3-page hand-written rejection letter, explaining to me that I did not know the first thing about aging. Leonard Hayflick is famous for discovering that human cells can undergo a finite number of replications before becoming senescent and unable to divide anymore. This is now called the Hayflick limit. Before Leonard came along, everyone thought cells could divide forever. But it turned out that the scientists keeping cell cultures alive were feeding them with chicken serum which contained live cells, which kept the culture “alive.” Leonard corrected this erroneous belief, and became famous. He is now immortalized in history as the discoverer of the finite number of replications of a eukaryotic cell, this number forever being known as the “Hayflick Limit.” Congratulations, Leonard. You solved the chicken serum problem! (Actually, he’s an OK guy, and means well). What is LH? Luteinizing hormone (LH) is a huge hormone. One molecule of it weighs 28,000 grams per mole, while testosterone weighs just 288 grams per mole. (What is a mole? It is the number of molecules (atoms in this case) in 12 grams of Carbon (randomly chosen by early scientists as a standard unit). So LH is 100 times bigger/heavier than a molecule of testosterone--or estrogen, for that matter--and about 1,400 times bigger than an atom of Carbon! It consists of 2 halves--the alpha unit and the beta unit, about equal in size. The only thing unique about the LH hormone is the beta unit. The LH alpha unit is identical to the alpha unit in the other large hormone molecules, FSH (follicle stimulating hormone), TSH (thyroid stimulating hormone) and hCG (human chorionic gonadotropin) (One might guess that the larger the hormone molecule, the older it is, from an evolutionary point of view, because as the hormone molecule gets bigger, the receptor has to get bigger--and that should take time). Anyway, this is too much information! Let’s get back to what matters--the simple stuff. The conventional view is that in women, a monthly surge in LH drives the dissolution of the egg-containing follicle by triggering the production of prostaglandins and proteolytic enzymes that weaken the follicle’s wall. A follicle is basically a pimple with an egg inside that starts to get bigger and eventually pops. (LH also stimulates the remnants of the burst follicle to become a little hormone-producing gland called “the corpus luteum” which secretes various hormones after the follicle has ruptured [including lots of progesterone--this will be important later]). After the follicle bursts, the ovum (egg) is released into the Fallopian tube where it can become fertilized. The important function of LH for our purposes is that it initially drives the destruction of tissue in this process. In men, LH stimulates the testes to secrete testosterone, and is central to promoting fertility and sperm production in males. (I’m guessing that it eats away the tissue housing the developing sperm, and allows it to be released--but I don’t know for sure, as I haven’t researched it. But I’m guessing this function of LH [if it exists] probably won’t be discovered for a while). LH increases are also involved in triggering and driving puberty in both juvenile males and females. How did I come up with such a crazy idea that a sex-related hormone that was