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Melatonin - my life's work We talk to Walter Pierpaoli about the Melatonin miracle!
cutting-edge
information
June/July 2006 Volume 6 Issue 3 $6.50 USA ÂŁ3.50 UK â‚Ź5.30 Europe
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TransEuropeanStemCellTherapy CONSORTIUM
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ESAAM
EUROPEAN SOCIITY Of A N T I - A G I N G MEDICINE
3rd Annual Anti Ageing Conference London, England & Incorporating
The International Symposium on Regenerative Medicine
September 15-17, 2006
The Royal Society of Medicine, l Wimpole St, London
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Contact Information: Anti Ageing Conference London PO Box 50622, London, SW6 2YP, UK Tel: +44 (0)20 7581 6962 Fax: +44 (0)20 7589 1273 Email: conference@antiageingconference.com
www.londonantiageirigconference.com
welcome It's an escapable fact that most of the focuses of antiaging therapies today are directed at the alleviation of diseases and disorders. Whilst these "alternative" to mainstream medicine approaches are more natural, more holistic and in many cases (because of the multi-faceted approach) even more successful, they remain at heart- preventative, which also means long term. However, critics will state that today's practice of antiaging medicine does not take enough account of the theories of aging. As such very few products and protocols are formulated to attack the problem at its core (e.g. aging itself). The fact that there has not been a cause of aging that can be agreed upon doesn't help, but I believe it's a fair criticism we have to accept and that we should be doing more to address this issue, i.e. decide what and how aging is triggered. I've tried to lay these ideas out in one of the articles in this magazine entitled; "the theories and practice of antiaging medicine."
advisors However, let's also remember that mainstream medicine is just as guilty of not tackling the underlying problem. Take cancer for example, are the treatments based on preventing or stopping the disease itself, or just trying to destroy it when it appears? Hardly a case of tackling the core problem, despite the Billions that have been spent on it since Nixon's war on cancer in the 70's. We always have to remember that something is better than nothing, and that doing a little often and early is far preferable and much more effective than doing a lotlate. This is what makes the Antiaging Magazine unique, the fact that we report from the scientific and clinical evidence and not only from the approved (government) sources. This issue is no exception, and we trust that you continue to enjoy and learn from what we place before you.
The International Antiaging Magazine is proud to be regularly contributed, aided and supported by the following leading professionals:
Mircea Oumitru, M.D., Ph.D. is the Editor of the International Journal of Gerontology and Geriatrics, based in Mexico City. Dr. Dumitru was also the personal assistant to Professor Ana Asian, the famous Bucharest physician who developed Gerovital-H3.
Garry F. Gordon, M.D., DO, M.D. (H) is a world-renowned expert in chelation therapy behind many publications, including The Chelation Answer. He is advisor to the American Board of Chelation Therapy and examiner for all chelation physicians, being responsible for Peer Reviewed Chelation Therapy in Arizona.
Brian Halvorsen, BDS. LDS. RCS, FRSH is principal of a holistic practice and author of; "The Natural Dentisf a book relating nutrition to dental health. He is also the founder of the "British Dental Nutrition Society" and founding member of the British branch of "The International Academy of Oral Medicine and Toxicology".
John lonescu, Ph.D. is one of Europe's leading dermatologist researchers. His work into the causes and progression of numerous skin diseases has led him to develop a comprehensive diagnostic system to enable genetic identification of metabolic failures, which can then result in individualized detox and anti-aging therapies.
Karen Kaufman MS, CCN is a graduate of Skidmore College and received a Master of Science Degree in nutrition from the University of New Haven in Connecticut. She has worked at U-Mass Memorial Health Center and Medical School and currently maintains a private practice. She is also a member of the board of trustees of the Lupus Foundation of New England.
Phil Micans Editor-in-chief
Marios Kyriazis, M.D,, MSc., MIBiol. has a postgraduate qualification in Gerontology from the King's College, University of London, and a postgraduate qualification in Geriatric medicine granted by the Royal College of Physicians. He has written extensively on longevity and healthy aging and is a founding
Declaration The International Antiaging Magazine focuses on the latest nutritional, hormonal and drug therapies in use now that show promise in combating the signs of aging. These signs include the physical, mental and internal changes consisting of the diseases and disorders that include cancer, arthritis and senile dementia etc. However, the main focus is upon prevention of such aging diseases and disorders for the "healthy-aging" individual. Copyright IAS 2006.
Publisher: International Antiaging Publishing, PO Box 6 Sark, GY9 OSB Great Britain Tel:+44 208 181 6105 Fax: +44 208 181 6106 E-mail: editor@antiaging-magazine.com Advertising: advertising@antiagingmagazine.com Subscription Enquiries: subscription@antiagingmagazine.com Annual subscription (6 copies) UK ÂŁ21.00 Euros â‚Ź31.80 Rest of the world $39.00
All copyrights are acknowledged. Whilst every effort has been made to ensure accuracy, no responsibility can be accepted for inaccuracies, howsoever caused. No liability can be accepted for illustrations, photographs, artwork or advertising materials while in transmission or with the publisher or their agents. All information is corTect at time of going to print. Not for public broadcast or copy without written permission from IAS Ltd. Terms and conditions may change without notice.
member of the British Longevity Society.
Phil Micans, PharmB., MS has degrees in Pharmacology and Food and Vitamin Technology. Since 1986 he has been actively involved in antiaging medicine. Today, Phil is the Editor of the International Antiaging
Magazine,
Chairman to the International Antiaging Conference and is also the Vice President of International Antiaging Systems.
John Morgenthaler has been active in the field of nutritional medicine since 1986. As a founder of Smart Publications, John has co-authored numerous health books, including Smart Drugs, Stop the FDA, Better Sex Through Chemistry, Natural Hormone Replacement for Women, and GHB: The Natural Mood Enhancer.
Walter Pierpaoli, M.D. is a pioneering research physician who introduced the concept of melatonin supplements to the world through his best selling book, The Melatonin Miracle. He is Director of the Jean Choay Institute for Biomedical Research, Switzerland. Recently the Walter Pierpaoli Foundation
Disclaimer IAS 2006. The information offered within is done so under the terms and conditions of IAS Ltd., and may change without notice. It is for educational purposes only and does not replace the advice of your health professional/ physician. Furthermore all statements may not necessarily be those of IAS Ltd., and none have been evaluated by a regulatory body such as the FDA. The International Antiaging Magazine accepts no responsibility for the accuracy of advertising, or for any action bought by the person or people responding to an advert. International Antiaging Magazine is published by IAS Ltd and distributed in the USA by DSW. 75 Aberdeen Road. Emigsville PA 17318-0437. Application to mail at periodicals mailing rates is pending at Manchester, PA. Postmaster: send address changes to International Antiaging Magazine, c/o PO Box 437, Emigsville. PA 17318-0437
for Life Sciences has been established in Italy.
Jonathan Wright, M.D, is Medical Director of the Tahoma Clinic in Washington State. Working with natural medicines since 1973, Dr. Wright is a distinguished pioneer in nutrition and vitamin therapy. He is a recognised sex hormone expert and has authored and co-authored numerous ground-breaking publications.
Imre Zs.-Nagy, M.D. is Professor of Gerontologyy at the University of Debrecen, Hungary. He is a teacher in experimental gerontology and was a pupil of the science of Fritz Verzar. He has published 275 papers, chapters and books, given 340 scientific lectures. He is founder (1982) and Editor-inChief of the journal Archives of Gerontology and Geriatrics. Listed alphabetically by last name
June/July 2006 j a m
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e present a review of recent books all based on or around the concept of antiaging/ preventative medicine, or looking at new methods to prevent, reverse and treat disorders and disease.
All these books should be available via Amazon.com or through your local bookstore. If you have a book you would like us to review, please send us a copy. In the meantime please read through our synopsis to see if there is something of interest to you. N.B. Prices where shown are for indication Title: Natural Hormone Replacement for W o m e n over 45 Author: Jonathan Wright, M.D. Publisher: Smart Publications. Price: $10.95
NATIHAL I IOR.MONE'
I REPLACEMENT
This is the book that opened the eyes of thousands of women. Have you ever wondered why there are so many side effects and problems with HRT? Well HRT subjects women to horse estrogens that are not the same as natural human estrogen! Indeed this book is subtitled; "don't let your doctor give you horse urine!" How, why and what natural hormone replacement therapy can do is all explained here by world renowned bio-identical hormone expert Jonathan Wright. If you are a women approaching, or in menopause, we highly recommend this book. Title: Smart Drugs and Nutrients 1 Authors: Ward Dean M.D., John Morgenthaler. Publisher: Smart Publications. Price: $12.95
Smart
DRUGS
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Although it is now 16 years old! This is the book that started the Smart Drug revolution. It awoke the public to the fact that age-related mental decline had to be treated as it is the prelude to a senile dementia. The book goes on to cover numerous nootropic drugs (so-called smart drugs) and nutrients that can aid memory, learning and attention. If this is new to you this is still a great place to start, introducing not only new molecules, but also "old" molecules as the "alternative" uses they can be put to, in other words the very basis of antiaging medicine.
purposes only. Title: The Anti-aging Solution Author: Vincent Giampapa, M.D. Publisher: John Wiley & Sons Price: $14.95
Price: $14.95
Dr. Giampapa brings his considerable experience to bear in his new book. It looks at how our lifestyles and diets can change our DNA, and perhaps more importantly what we can change in the same to reverse the damage to our DNA, thereby slowing incorrect cell manufacture and slowing aging etc. As we say over here in England, it's a jolly good read. Title: The Cataract Cure Author: Marios Kyriazis, M.D. Publisher: iUniverse Price: $9.99 This book highlights the Russian breakthrough for the treatment and prevention of senile cataract using an eye-drop. It is the story of Nacetylcarnosine, and contains details of how it should be used to achieve the best results, what to look out for and case studies. A number of aging eye disorders are mentioned (i.e., glaucoma, macular degeneration, dry eye syndrome) and how they can be eased. This is the first book to attempt to bring to the fore the various international breakthroughs for the alleviation of eye aging. Title: The H Factor Authors: James Braly, M.D., Patrick Holford Publisher: Basic Health Publications
FACTOR .SOLUTION J A M L I DRALY,
M.D.
PATRICK H u i
l i s
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As explained in this book H (meaning homocysteine), is one of the best single indicators of whether or not you are likely to die of a heart attack! But there's much more, apart from homocysteine being one of the most important markers for heart health (and virtually overlooked by the mainstream medical community), high homocysteine levels (as an by-product of bad methylation) may also be responsible for accelerating oxidation, weakening the immune system (and leading to increased risk of cancer) and also damaging the brain and lowering I.Q. levels, going on to be recognised as a factor in senile dementias. This is a straight forward book, with level headed practical interventions in lifestyle and supplementation, for people who want to get things done. Title: The Hormone Solution Authors: Thierry Hertoghe, M.D. Publisher: Harmony Price: $19.00
HORMONE SOLUTION
LONGER
Dr. Hertoghe takes us through step by step what many hormones are responsible for. He also explains the kinds of therapies that can be adopted. It's almost a 'how-to' approach to discover how exactly you can improve your health by identifying hormone problems and then what to do about them. Here you can complete your own questionnaires and discover where you may be lacking in hormones. To see the full selection of antiaging m e d i a a v a i l a b l e g o to: www.antiaging-systems.com/ publications/index.htm
contents
also nutritional defence
The theories and the practice of antiaging medicine What is aging? How does it come about? Why does it exist at all and how do we define it? Plus how does antiaging medicine hope to conquer what appears to be a multifactional and universal problem? These and other grand questions are attempted to be answered here in a hope that an agreed direction will give better answers faster- all in order to overcome man's last true frontier.
Interview with Walter Pierpaoli, M.D. Sight is perhaps the one sense that no one wants to lose under any circumstance. It is a critical resource to make sense of the world around us. As we age however eyesight changes and once over the age of 55 there is a 1 in 5 chance of having a disorder such as a cataract which will affect the quality of vision. Other serious disorders include glaucoma and macular degeneration. Yet unlike yesteryear, there are now numerous nutritional strategies that can be used to help maintain and in some cases even reverse many of these issues.
The anti-stress, anti-ar enhancing hormone
Dr. Pierpaoli is well known within the antiaging fraternity as one of the most forthright and adventurous of researchers and physicians, and thank goodness because to push boundaries forward we need people like him. In this interview, he discusses his life work with melatonin and describes the many varied uses to which it can be put. You will learn how ardent a supporter he is of its general use and why because of its central role it has so many antiaging uses within the body.
Improving the mindtackling brain disorders In this second part of a three part series, the more serious issues of brain disorders are discussed as well as an oversight of the more successful treatments of recent times. In a period when governments want to restrict what they see as expensive senile dementia treatments to those who are the worst affected, which by definition means they will be least effective, it is becoming more and more necessary to know how to slow and prevent brain function into old age.
regulars news
It's hard to believe that one hormone- pregnenolone- can have so many diverse uses, yet when one understands that pregnenolone is the master hormone, the one that all others are made from, things begin to make sense. What's more, pregnenolone was in use many years ago with good success in treating inflammation and arthritic disorders, but its use was abandoned in favor of patentable drugs, so it's about time that both the public and the health professionals were reawakened to the potential uses for this multi-purpose, yet safe hormone.
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aging eye-care
Cutting edge defence to maintain
Vision Ed.- This article is based, and expands, on the book The Cataract Cure, by Marios Kyriazis M.D., published by iUniverse. hronic, age-related visual problems such as cataract, macular degeneration and glaucoma have one basic similarity. These are degenerative conditions caused by excessive oxidation (free radical damage). Remember that free radicals are toxic by-products of your everyday metabolism. With aging, the production of these free radicals increases, whereas your body defences against them (i.e. the production of natural antioxidants in an attempt to neutralise free radicals) becomes less effective. As a result, free radicals destroy proteins, enzymes and DNA causing chronic damage to your tissues.
C
"free radicals destroy proteins, enzymes and DNA causing chronic damage to your tissues" So, this is oxidation in a nutshell. Apart from oxidation, another important process implicated in aging is that of glycation. This is when sugar and similar molecules attack your proteins and DNA, causing abnormal chemical bonds between individual molecules. Free radicals then make matters worse by facilitating this destruction of your
6 I i a m June/July 2006
tissues. In the end, there is an increased amount of abnormal, twisted and deformed proteins in your body, worsening the risk of developing age-related c h r o n i c conditions. In the case of the eye, these deformed proteins may cause visual impairment through cataract, macular degeneration or glaucoma.
Cataract Cataract is a common age-related condition and affects one in four people over the age of 65. Basically, it is caused when the proteins inside the lens of the eye (called crystallins) become damaged. Glycation is the main culprit here, which causes the crystallins to bind to each other, clump together and become misshapen, forming opaque plaques in the lens of the eye.
1 CATARACT
CJJRE
The Cataract Cure, by Marios Kyriazis M.D., published by iUniverse.
As a result, light cannot pass through the lens and reach the inside of the eye properly, so vision is impaired. This progressive damage is made worse by free radical action on the already damaged crystallins. For more detailed information
Environmental pollution, increased ultraviolet (UV) radiation or other toxic d a m a g e , cause an increased production of free radicals in the retina. So, a logical way of preventing or treating ARMD is using
about cataract see my most recent book The Cataract Cure.
Age-Related Degeneration (ARMD)
Macular
Another degenerative condition is ARMD. This occurs when a particular part of the retina, called the macula, becomes damaged by free radicals that cause the arteries and cells of the retina to malfunction.
antioxidants to reduce the concentration of free radicals in the eye (1). The use of antioxidants in preventing ARMD has been studied in a variety of scientific trials, usually with positive results. For example, it was recently reported from the Department of Ophthalmology, Biochemistry, and Medicine, Emory University, Atlanta, Georgia in the US, that antioxidants prevent oxidation of vital amino acids in patients with ARMD (2). The role of oxidation as a cause of ARMD was explored further by a team of researchers from the Chemistry and Biochemistry Department, Northern Illinois University. The researchers suggested that one of the reasons why the macula is easily affected by free radicals is because, with aging, the melanin pigment of the retina loses its ability to
withstand damage (3). It makes sense to suggest, that in order to prevent this deterioration of the melanin pigment, antioxidant therapy must be helpful.
Glaucoma The third most common chronic eye condition is glaucoma. This is when the fluid inside different parts of the eye does not flow properly, causing increased pressure inside the eye with consequent loss of vision. The blockage is caused when free radicals damage the trabecular meshwork, a part of the eye that produces and then reabsorbs the fluid. Italian scientists from the Department of Health Sciences, University of Genoa, have recently reported the following: "There is growing evidence that reactive oxygen species (free radicals) play a key role in the pathogenesis of glaucoma. The occurrence of oxidative DNA damage in the
"Cataract is a common age-related condition and affects one in four people over the age of 65" trabecular meshwork has been demonstrated by measuring the increase of 8-hydroxy-2'-
June/July 2006 i a m
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aging eye-care hydrogen peroxide compromises the integrity of the trabecular meshwork.
deoxyguanosine, the most abundant DNA oxidative alteration, which is significantly increased in glaucomabearing subjects as compared to unaffected controls."
The trabecular meshwork is normally rich in natural antioxidants. • Patients who have glaucoma have significant increase in free radical activity.
"chronic eye conditions develop on a background of both oxidation and glycation"
• These patients appear to have a genetic predisposition rendering them susceptible to free radical damage.
They believe that there are several factors supporting the theory that free radicals play a fundamental role in glaucoma. Some of these reasons are: • In the presence of hydrogen peroxide (a well known free radical), the pressure of the fluid inside the eye increases. This is because
The scientists concluded: "These considerations could bear relevance for glaucoma prevention and suggest that ... the use of drugs or dietary measures attenuating the effects of free radicals could be useful tools contributing to the control of this disease. " (4)
Reverse senile cataracts and help prevent other aging eye disorders **
Glaucoma
•
Macular degeneration Dry eye syndrome
•
Computer vision syndrome
•
Eyestrain
^
Blurred vision
^
Corneal disorder
These NEW eye-drops are a major breakthrough in the prevention of senile cataract. They also help the aging eye to recover by improving its clarity, glare sensitivity, color perception and overall vision. These are the special nacetylcarnosine eye-drops researched, tested, approved and patented by IVP. For more information or to order go to:
www.antiaging-systems.com/a2z/can-c.htm or call: Toll-free (USA) 866 800 4677 (ROW) +44 208 123 2106 8
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June/July 2006
In summary, these three chronic eye conditions develop on a background of both oxidation and glycation. It is logical to assume that in order to prevent or even reverse this damage it is necessary to use a combination of chemicals which work both against oxidation (i.e. antioxidants) and against glycation.
N-acetylcarnosine The most recent development in the prevention of age-related eye diseases is the nutrient N-acetylcarnosine. This is a natural chemical closely related to carnosine, which itself is a combination of two amino acids (alanine and histidine). Carnosine has been investigated extensively and there are over 1000 scientific reports discussing its biological actions. It is active in almost all body tissues and works both as an antioxidant and as an antiglycator. N-acetylcarnosine (NAC) works the same way as carnosine, namely preventing free radical damage and reducing the risk of glycation. But
fI K
I
aging eye-care operation (5). Commercially available acetylcarnosine:
N-
The beneficial actions of NAC against cataract and other eye conditions have been recognised by a variety of c o m m e r c i a l companies who are now offering NAC in eye drop form. However, it is important to realise that NAC is very sensitive both during the manufacturing and r during the application stages, so it is necessary to use only a reputable supplier. Also, some commercial eye drops contain chemicals which may not be beneficial when applied directly in the eye. For example, although vitamins given by mouth may help prevent age related eye conditions as N H " will be discussed below, if these vitamins are given directly into the eye, NAC is they may cause damage to the eye particularly tissues. In addition, the Russian useful within the scientists who developed the original eye, because it remains NAC drops (Can-C®) claim that the biologically active for longer. combination of stabilising agents and other chemical Once inside the eye ~ ~ f a c t o r s needs to be tissues NAC — — — — — — taken into account transforms into pure «H-acetylcarnosine is a J when using NAC carnosine and . and this makes prevents free ™ry important their Can-C® drops radicals from further discovery because it the best available destroying eye shows that cataract choice at present. tissues such as the i t •. i Apart from t ... I+ . may be cured without crystallins. It also J carnosine, other reverses giycation, the need to resort to an good anti-glycators in other words, it operation " may be useful in are the agents curing already metformin and existing eye damage. N-acetylcarnosine aminoguanidine. Both work to reduce is a very important discovery because it the risk of giycation of proteins within shows that cataract may be cured the lens of the eye and thus prevent the without the need to resort to an harm caused to the proteins of the
lens. By helping to improve microcirculation of the blood in the eye these can be useful both in macular degeneration and glaucoma. By-products of giycation (called AGEs -Advance Giycation End-products) are frequently found in several parts of the eye, including the retina (6). It has now been proven that there are special receptors for these AGEs within the retina and this means that the blueprint for the slow and chronic destruction of the retina has already been put in place by nature. (7) However, antiglycators such as carnosine, metformin and aminoguanidine can fool nature by reducing AGEs before these have the chance to combine with the receptors and affect the eye. It may not be enough to only use one remedy in order to prevent or even reverse chronic eye conditions. Taking additional supplements will ensure that you are getting the extra insurance necessary to keep free radical action at low levels and reduce the risk of further harm to the eyes. The following are some relevant nutritional factors that have a role to play in improving vision. Current research supporting their actions is highlighted for each supplement. G i n k g o Biloba Extract Ginkgo is the extract of the maidenhair tree, used in order to improve memory and blood circulation problems. It is also a very good antioxidant, particularly if used correctly. Many people buy the 'raw leaf preparation of ginkgo which may not contain a standard amount of the active ingredients. It is best to use the standardised extract at a dose of 120 mg once or twice a day.
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aging eye-care
Scientists from the Department of Ophthalmology, Tang Du Hospital, Shanxi in China have studied the effects of ginkgo extracts on the
"chronic eye conditions develop on a background of both oxidation and glycation" retina. They first injected glutamate (a known brain chemical which is toxic in high amounts) into the retinas of one group of rabbits. This caused an increased production of free
radicals which, in turn, caused the retinal cells to wither and die. They then injected ginkgo biloba extracts into another group of rabbits before injecting them with glutamate. What they found was that ginkgo protected these retinas from any harm caused by free radicals. (8) This confirms that ginkgo may be able to protect the retina against age-related oxidation, and that gingko may thus be useful against all chronic eye conditions including macular degeneration. Although this particular experiment was performed on laboratory animals, newer research has
confirmed that ginkgo can also be useful in human eye problems. In a clinical t
r
i
a
l
performed by Polish researchers from the Department of Clinical Ophthalmology, Medical Academy of Poland, gingko was given to a group of 15 patients who had an increased risk of retinal damage (in this case t h r o u g h diabetes).
They found that ginkgo i m proved t h e s e
As we generally live longer than before, agerelated diseases such as cataract, glaucoma, macular degeneration, are now becoming more frequent and affect people for longer.
available anywhere, including lutein, zeaxanthin, lycopene and astaxanthin.
•
Vision Pro also provides a broad spectrum of additional antioxidants and vitamins to ensure maximum ocular protection from the free radical damage.
•
From a nutritional standpoint, lack of antioxidants in the diet has been shown to worsen the risk of macular degeneration. Patients with eye disorders are frequently found to be deficient in antioxidants such as vitamin A, glutathione, lutein and zeaxanthin. Riboflavin (a member of the vitamin B group) is essential in modulating the activities of certain antioxidants in the eye, and nutrients such as panthenine, folic acid and bilberry support eye health.
IAS offers Vision Pro 90 capsules for only $39.99 To order call:
Many experts recommend supplementing the diet with these nutrients as an extra insurance against eye disease. Our eye-protection supplement Vision Pro contains the most complete range of eye-protective carotenoids
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•
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Vision Pro contains: Vitamin A (carotenes), Vitamin E (d-alpha tocopherol), Taurine, Green Tea Extract, Gingko Biloba, Grape seed, Gamma Tocopherol, Vinpocetine, Lutein, Zeaxanthin, Lycopene, Astaxanthin
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Online:
www.antiaging-systems.com www.antiaging-systems.eu
patients' colour vision test results, concluding that: "Ginkgo seems to be good adjuvant in patients with long lasting diabetes mellitus" (which can cause retinal damage). (9) Finally, ginkgo can protect not only against macular degeneration, but also a g a i n s t
cataract, by reducing the injury caused by oxidation on the lens of the eye. It turns out that ginkgo increases the antioxidant enzymes
aging eye-care
superoxide d ism utase a n d glutathione peroxidase in the eye. T h i s makes it less likely that free radicals caused by radiation, (such as UV for example) can damage the lens (10).
Grape Extract
Seed
It is well known that both grapes and their s e e d s contain oxidants such as flavonoids H (catechin, epicatechin, procyanidins and gallic acid). These are strong natural chemicals with antioxidant power up to 20 times more than vitamin E, and 50 times more than vitamin C. Flavonoids from grape seeds help to protect the eyes from UV radiation and to improve overall vision. In addition, these compounds can help improve
blood circulation particularly in the small arteries of organs including the eye. (11)
diseases in other parts of the body, such as liver disease, can have an adverse impact upon the retina.
In a landmark experiment performed by researchers from the Research and Development Division, Kikkoman Corporation, Japan, it was confirmed that grape seed extracts prevent the progression of cataract formation. The researchers investigated the anti-cataract activity of grape seed extracts (containing 38.5% procyanidins) on laboratory rats with cataract. The rats were divided into
Nutritional supplements such as vinpocetine can prevent this kind of damage by improving blood circulation both in the liver and in the arteries of the eye. In this way, the likelihood of visual problems associated with systemic diseases can be reduced. (13)
"Apart from carnosine, other good anti' glycators are the agents metformin and aminoguanidine" two groups. The first group was fed a standard diet containing no grape seed extracts. The second was given 0.213% grape seed extract in addition t o the standard diet, for 27 days. As a result, the clarity of the lens was significantly better in the treatment group compared with the control group. The scientists concluded that: "these extracts significantly prevented and postponed development of cataract formation in the active group" (12).
Vinpocetine
More recently, Russian scientists found that vinpocetine can improve optic nerve atrophy caused by head injury. It improved the sensitivity of the retina and protected the optic nerve which transmits visual signals from the eye to the brain. Finally, it improved blood flow within the arteries of the eye, which means that more nutrients could reach vital eye tissues. (14)
Relief from eye allergies and contact lenses! Conjunctisan*
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Conjunctisan A is an eye drop containing natural eye lysates and macromolecular tissue extracts to help regenerate and repair the aged eye. Conjunctisan B is the sister product of Conjunctisan A and is the choice therapeutic agent for contact lens problems, especially as a regenerative and reparative therapy of the anterior segment of the eye after permanent stress caused by contact lenses cleaning solutions. No preservatives!
Although vinpocetine is a well known nootropic (brain booster), it has also a role to play in preventing chronic eye conditions, particularly if used in combinations with other supplements. Some years ago, scientists working at the Romanian University of Medicine and
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aging eye-care Lutein and zeaxanthin The two most well known supplements for eye protection are the carotenoids lutein and zeaxanthin. There is quite a lot of scientific evidence confirming that consumption of these two chemicals reduces the risk of age-related cataract. Lutein and zeaxanthin are the only two carotenoids present in the lens, and their role is to protect the lens against free radicals caused by UV radiation from the sun. In an experiment performed at the Ohio State University in the USA, scientists compared these two chemicals and vitamin E used against free radical action in lenses obtained from human eyes. They first applied the different chemicals (such as lutein, zeaxanthin, vitamin E, and astaxantin - see below) on
the lenses, and then they irradiated these lenses with UV radiation. They found that all these chemical s protect the lens against free radical damage. Specifically, there was an inhibition of 'cell stress signalling', meaning that the irradiated cells did not produce any toxic chemicals following the irradiation. Lutein and zeaxanthin was more powerful than vitamin E in this respect. (15)
Astaxanthin This is a carotenoid chemical similar to lutein and zeaxanthin. Common sources of natural astaxanthin are the green algae Haematococcus pluvialis, the red yeast, Phaffia rhodozyma and some shellfish. It is usually used to provide the pink colour of salmon and lobsters grown commercially. Astaxanthin, in association with lutein
REFERENCES 1. Gakhramanov FS. Effect of natural antioxidants on antioxidant activity and lipid peroxidation in eye tissue of rabbits with chemical burns. Bull Exp Biol Med. 2005;140(3):289-91. 2. Moriarty-Craige SE, Adkison J, Lynn M, Gensler G, Bressler S, Jones DP, Sternberg P Jr. Antioxidant supplements prevent oxidation of cysteine/cystine redox in patients with age-related macular degeneration. Am J Ophthalmol. 2005;140(6):1020-6. 3. Wang Z, Dillon J, Gaillard ER. Antioxidant properties of melanin in retinal pigment epithelial cells. Photochem Photobiol. 2006;82(2):474-9. 4. Izzotti A, Di Marco B. De Flora S, Sacca S. Open angle glaucoma: epidemiology, pathogenesis and prevention. Recenti Prog Med. 2006;97(1):3745. 5. Babizhayev M. Deyev A, Yermakova V, Brickman I, Bours J. Lipid peroxidation and cataracts: N-acetylcarnosine as the therapeutic tool to manage age-related cataracts in human and canine eyes. Drugs R D. 2004;5(3):125139. 6. Kaji Y, Usui T, Oshika T, et al. Advanced j a m
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and zeaxanthin, is a very effective antioxidant within the eye. (16) Scientific interest in astaxanthin has only recently begun to spread, and there are reports that it can be useful in a variety of conditions including bowel, brain and heart problems.
Others Apart from vitamins and nutrients, it is also necessary to protect your eyes in other ways. For example, avoid strong sunlight which facilitates free radical reactions within the eye. Instead wear good quality sunglasses, particularly if you live in a place where sunshine is strong. Wearing a hat is also a good idea, as it cuts down some of the harmful UV radiation reaching your eyes. Frequent eye tests will pick
glycation end products in diabetic corneas. Invest Ophthalmol Vis Sci. 2000;41(2):362-8. 7. Yamada Y, Ishibashi K, Bhutto IA, Tian J, Lutty GA, Handa JT. The expression of advanced glycation endproduct receptors in rpe cells associated with basal deposits in human maculas. Exp Eye Res. 2006;82(5):840-8. 8. Li YJ, Yang XG, Gao MR.Effects of extracts of ginkgo biloba (EGB) on levels of nitric oxide and apoptosis in the retina induced by glutamate in adult rabbits. Zhongguo Zhong Yao Za Zhi. 2003;28(10):9614. 9. Bernardczyk-Meller J, Siwiec-Proscinska J, Stankiewicz W, Fichna P, Pecold K. Influence of Eqb 761 on the function of the retina in children and adolescent with long lasting diabetes mellitus-preiiminary report. Klin Oczna. 2004;106(4-5):569-71. 10. Ertekin MV, Kocer I, Karslioglu I, Taysi S, Gepdiremen A, Sezen 0. Balci E, Bakan N. Effects of oral Ginkgo biloba supplementation on cataract formation and oxidative stress occurring in lenses of rats exposed to total cranium radiotherapy. Jpn J Ophthalmol. 2004;48(5):499-502. 11. Shi J, Yu J, Pohorly
up any early signs of eye disease and will give you the chance of starting or modifying your prevention nutritional programme. If you have diabetes, are a smoker or have a family history of chronic eye disease, then prevention therapy becomes even more important.
Promote your company, product or service to a wider audience!
For details on how to advertise in the International Antiaging Magazine, email your media pack request to: advertising@antiagingmagazine.com
JE, Kakuda Y. Polyphenolics in grape seedsbiochemistry and functionality. J Med Food. 2003;6(4):291-9. 12. Yamakoshi J, Saito M, Kataoka S, Tokutake S. Procyanidin-rich extract from grape seeds prevents cataract formation in hereditary cataractous (ICR/f) rats. J Agric Food Chem. 2002;50(17):4983-8. 13. Cusnir V, Slepova 0, Dumbrava V, Zaiteva N, Cusnir R, Midrigan I. Ocular manifestations of hepatitis B. Oftalmologia. 1997;41(2):25-7. 14. Aznabaev MT, Khalikov VA, Zagidullina ASh. Use of instenon in complex treatment of patients with optic nerve atrophy caused by craniocerebral trauma. Vestn Oftalmol. 2003;119(6):12-4. 15. Chitchumroonchokchai C, Bomser JA, Glamm JE, Failla ML Xanthophylls and alpha-tocopherol decrease UVB-induced lipid peroxidation and stress signalling in human lens epithelial cells. J Nutr. 2004;134(12):3225-32. 16. Waagbo R, Hamre K, Bjerkas E, Berge R, Wathne E, Lie 0, Torstensen B. Cataract formation in Atlantic salmon, Salmo salar L., smolt relative to dietary pro- and antioxidants and lipid level. J Fish Dis. 2003;26(4):213-29.
calendar of events
in the news to produce more, faster and cheaper. On top of that we also have to consider that our food chain is now contaminated by pesticides, plastics, endocrine disruptors and heavy metals such as mercury etc.] Letrozole reduces breast cancer recurrence rates Nutritional content of food continues to decline Recent data collected by the U.S. government shows that the nutritional content of fruits and vegetables has declined dramatically during the past 50 years. Donald Davis, a biochemist at the University of Texas, said that of 13 major nutrients in fruits and vegetables tracked by the Agriculture Department from 1950 to 1999, 6 showed declines in protein, calcium, phosphorus, iron, riboflavin and vitamin C. The declines ranged from 6 to 38%. Davis, who discussed his findings at a recent meeting of the American Association for the Advancement of Science meeting in St. Louis, suspects the trend in agriculture toward encouraging crops that grow the fastest and biggest is a reason for the decline. However, these faster-growing plants aren't able to acquire the nutrients that their slower-growing cousins can, either by synthesis or from the soil. Davis said he doesn't want his study to encourage people to stop eating vegetables on the grounds they lack nutrients. He contends his study shows that people need to eat more vegetables and fruits, not less. "Vegetables are extraordinarily rich in nutrients and beneficial phytochemicals. They are still there, and vegetables and fruits are our best sources for these." [Ed.- this confirms an earlier British study that showed that in some cases the nutritional value of food has declined by as much as 50% since the 1940's. The blame is being leveled at the state of agribusiness
Compared with Tamoxifen, Letrozole (Femara速) significantly reduces the risk of recurrence of hormonereceptor-positive breast cancer in post-menopausal women, new data have shown (new England Journal of Medicine 2005: 26: 2747). The study of 8,010 women compared four treatment groups: five years of treatment with Letrozole; five years Tamoxifen; two years of Letrozole followed by three years of Tamoxifen; and two years of Tamoxifen followed by three years Letrozole. At 25.8 months of follow-up, women given Letrozole monotherapy or initial Letrozole treatment showed increased disease free survival and reduced recurrence at distant sites. Although fractures were more frequent with Letrozole monotherapy or initial treatment, these regimens were associated with fewer thromboembolic events, a lower rate of vaginal bleeding and fewer endometrial biopsies. In order to determine whether Letrozole will continue to reduce the risk of relapse for several years after the cessation of treatment, longer followup studies will be needed, the author states. Ginkgo biloba and hearing problems Recent clinical studies have shown that a supplement intake of Ginkgo biloba extract can be as effective as the drug Pentoxifylline for the treatment of sudden deafness with acouphenes. Both caused a substantial restoration of hearing during the 10days of treatment. On the whole, hearing improved by around one third during that period.
JULY 2006 Date: July 14-16, 2006 Name: International Anti-Aging Congress Place: Chicago, Illinois, USA Contact: www.worldhealth.net SEPTEMBER 2006 Date: September 15-17, 2006 Name: London Antiageing Conference Place: London, England Contact: www.antiageingconference.com Date: September 7-10, 2006 Name: The Australasian Conference on Anti-Aging Medicine Place: Bali, Indonesia Contact: www.asiaantiaging.net/2006/ main/default.asp OCTOBER 2006 Date: October 18-21, 2006 Name: European Congress on AntiAging Medicine Place: Vienna, Austria Contact: www.antiaging-vienna2006.at Date: October 13-15, 2006 Name: International Conference on Healthy Ageing and Longevity Place: Melbourne, Australia Contact: www.longevityinternational.com Date: October 5-8, 2006 Name: Antiaging and Integrative Medicine Place: Geneva, Switzerland Contact: www.saaam.org NOVEMBER 2006 Date: November 10-12, 2006 Name: Clinical Applications for Age Management Medicine Place: Las Vegas, Nevada, USA Contact: www.agingoptions.org DECEMBER 2006 Date: December 7-10, 2006 Name: International Anti-Aging Congress Place: Las Vegas, Nevada, USA Contact: www.worldhealth.net MARCH 2007 Date: March 1-2, 2007 Name: Conference on Antiaging Place: Bangkok, Thailand Contact: www.bumrungrad.com/antiaging/2007 Date: March 22-24, 2007 Name: Antiaging World Congress Place: Monte Carlo, Monaco Contact: www.world2007.org
If you organize or attend an event that you think will be of interest to our readers please contact: editor@antiaging-magazine.com
June/July 2006 i a m
13
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dvancing years are said to impart us with wisdom, a certain philosophy of life; yet aging is often accompanied by functional decline, which often can include diminishing cognitive abilities. How many of us have asked ourselves, "Where the heck did I put my keys?" or "What's his name - it's on the tip of my tongue?" In addition to waning memory, other more serious conditions such as depression, Alzheimer's disease and arthritis may present themselves in later years.
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Research has shown that a naturally occurring hormone, pregnenolone, may hold the key to growing older with reduced consequences of "aging." Pregnenolone is synthesized directly from cholesterol in the mitochondria, (the cellular energy-producing "factories"). Pregnenolone may exert its biological action molecularly unaltered, or through either of two metabolic pathways, may convert to dehydroepiandrosterone (DHEA) or progesterone, before cascading down to estrogen, testosterone, Cortisol, and other hormones (see Figure 1). Since pregnenolone is a hormonal precursor, it is sometimes called the "Mother Hormone." At about the age of 35 the body's production of pregnenolone, DHEA, and other hormones begins to decline, often accompanied by age-related diseases and symptoms. In fact, blood
Figure 1: Steroid Hormone
measurements of pregnenolone and DHEA concentrations are useful tools as biomarkers of aging. Low pregnenolone levels can also be caused by stress, hypothyroidism, toxic exposure and depression. Physicians often prescribe supplemental bio-identical hormones to treat deficiencies and rejuvenate the
efficacy, it was abandoned in favor of synthetic cortisone derivatives promoted by the drug industry. (Naturally occurring compounds, like pregnenolone, are not patentable and of little interest to pharmaceutical marketers). However, interest in pregnenolone was revived in the 1990's and since that time
body to a more youthful status, but they often, leave the "Mother Hormone" out of their patients' regimens - quite an oversight for such a physiologically important therapeutic agent.
hundreds of research studies have demonstrated its physiological and cognitive benefits.
The Most Potent Memory Enhancer Yet Reported
Pregnenolone was studied as an anti-inflammatory therapy for rheumatoid arthritis during the 1940's and 1950's. Despite its proven safety and
Pregnenolone is known as a "neurosteroid," a term coined by the prominent French researcher, Dr. Etienne-Emile Baulieu - it is synthesized at
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least partially in the brain and modulates the activities of the central nervous system. Besides pregnenolone, other neurosteroids include DHEA, and the sulfate derivatives, pregnenolone sulfate (Preg-S) and DHEA sulfate (DHEA-S), among others. Interestingly, researchers have determined that pregnenolone is the most highly concentrated steroid hormone in the human brain. (1) [Note: Steroids are a class of fat-soluble compounds distinguished by a typical fused four -ring structure with differing side chains that elicit a range of biological functions. Hormones are a subset of the steroid family. The terms "steroids," "hormones," and "steroid hormones" are used interchangeably in the literature in reference to pregnenolone and its metabolites]. While the neurological benefits of DHEA have been extensively documented, recent animal studies show pregnenolone is a more potent memory-booster. In the early 1990's, Drs. Flood, Morley and Roberts conducted their pioneering research on the memoryenhancing properties of various steroids. One study, published in the Proceedings of the National Academy of Sciences, involved memory retention experiments performed on mice placed in a T-shaped maze consisting of a start box at one end and two goal boxes at the other. The animals were trained to enter a designated "correct" goal box through the use of an "active avoidance" paradigm if the mouse entered the wrong box, an electrical foot shock was applied until the correct path was taken. Solutions of Preg-S, DHEA-S and corticosterone were administered into various regions of the brain two minutes after training. One week later, T-maze training was resumed until each
Androgens
June/July 2006
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mouse successfully ran the maze in five out of six consecutive trials; retention of learned information was measured by the number of runs required for the mouse to meet this requirement. Of all steroids tested, Preg-S was the most effective in boosting performance - and at a remarkably low concentration - leading the researchers to establish it as "the most potent memory enhancer yet reported." (2)
low concentrations of Preg-S in the brains of aged rats and that memory deficits were markedly improved by intrahippocampal injection of the steroid. (The hippocampus is an area of the brain involved in the formation of memories.) The scientists concluded,
Among scores of other published research on the cognitive effects of pregnenolone, memory retention studies of rodents in an alternate contraption - the Y-maze - are noteworthy. (The Y-maze consists of three arms, one of which, the "novel arm," is selectively closed off at specific time intervals.) In one study, administration of Preg-S significantly increased recognition of the novel arm in young adult male mice. (3) Similarly, other researchers found that poor performance in the maze was correlated with
"Preg-S may reinforce some neurotransmitter systems that decline with age." (4)
gfi pregnenolone has been shown to stimulate growth of new nerve tissue
But just which neurotransmitter systems are associated with memory and cognitive function and how does pregnenolone impact these processes and stem their decline? Pregnenolone binds to and regulates several types of neurotransmitter receptor sites:
The Most Potent Memory Enhancer Yet Reported Pregnenolone, a memory-enhancing hormone, synchronizes brain cells to maintain youthful mental function. Pregnenolone is a sterone manufactured from cholesterol among the tiny mitochondria energy cells. In clinical studies, Pregnenolone was discovered to be a potent memory enhancing sterone, possibly 100 times more effective for memory than DHEA. As levels of Pregnenolone decline with age, supplements can be used t o improve energy levels, aid arthritis and enhance memory. O t h e r clinical studies show that Pregnenolone is good at reducing stress levels, possibly by reducing the age-increasing effects of Cortisol and inducing a better state of relaxation.
For further information about the effects of Pregnenolone, prices & how to purchase, go to: www.antiaging-systems.com/a2z/pregnenolone.htm
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it is a negative modulator (i.e., attenuator) of the inhibitory, calming gamma-aminobutyric acid type A (GABAA) receptor complex and positive modulator (i.e., enhancer) of the excitatory N-methyl-daspartate (NMDA) receptor complex. These mechanisms
synergistically raise the excitability of the system, (2,5,6) thus imparting a stimulatory effect on the brain. Pregnenolone also acts as sigma-1 receptor agonist, resulting in the increased release of acetylcholine, (7) a neurotransmitter involved in memory and learning. Acetylcholine typically declines in normal aging and is severely altered in neurodegenerative diseases such as Alzheimer's. Preg-S infused into the brains of rats was shown to augment acetylcholine release by more than 50% while improving recognition of a familiar environment. (8) In addition, stimulation of acetylcholine release induces an increase in paradoxical, or REM, sleep, which has been shown to influence memory processes. (9,10) Besides its function as a regulator of neurotransmitter function, pregnenolone has been shown to stimulate growth of new nerve tissue (known as neurogenesis). (7,9) Previously, scientists believed that brain damage was irreversible and that neural repair was impossible; but recently researchers discovered that the brain is, in fact, capable of generating new neurons - good news for those with neurodegenerative diseases and declining cognitive function. In a fascinating study, researchers demonstrated that infusion of Preg-S into the brains of both young (3 months) and old (20 months) rats stimulated
neurogenesis. (11)
Effects om M o o d , S t r e s s andl D e p r e s s i o n Pregnenolone modulates the response to stress, anxiety and depression (12,13,14) and may be a safe and non-toxic alternative to the panoply of side-effect laden antidepressants, anxiolytics, and other psychiatric drugs. Several studies demonstrate pregnenolone's moodenhancing effects, which may be achieved by its inhibitory effect on GABAA receptors and stimulatory action on NMDA and sigma-1 receptors. Mice medicated with DHEA-S and Preg-S exhibited a significant reduction in fear response when placed in a stressful environment in which they had previously been subjected to footshock or forced swimming. (15) In humans, pregnenolone's stress-buffering capacity was tested on army pilots undergoing rigorous activities. Daily administration of 50 mg of pregnenolone for two weeks mediated stress and improved performance with no adverse effects. (16) Low levels of pregnenolone may be associated with the incidence of psychiatric disorders. Researchers analyzed levels of pregnenolone in the cerebrospinal fluid of 27 patients with affective disorder and 10 healthy controls. Pregnenolone concentrations in the disturbed subjects were indeed lower than in the controls, especially during episodes of active depression. (17) Other researchers found reduced plasma levels of PregS in 12 male patients with generalized social phobia and anxiety disorder, compared to a group of 12 healthy men.
(18) Further investigation into pregnenolone's use as an antidepressive, anti-anxiety and stress-buffering agent in humans is clearly warranted.
the pain and inflammation associated with rheumatoid arthritis. As noted earlier, research on pregnenolone's therapeutic benefits was discontinued with the advent of synthetic corticosteroids and resumed in the past several years. A recent study demonstrated moderate to substantial improvement in joint pain and mobility in six out of 11 patients on pregnenolone therapy; interestingly, one person with previously unresolvable gout experienced a dramatic response within a few days of receiving intramuscular pregnenolone injections. (16) The daily oral dosage required for arthritis relief 500 mg - is significantly higher than the dose used for cognitive enhancement.
Cholesterol Reduction
Arthritis Relief A Medline search revealed at least two dozen journal articles from the 1950's documenting the efficacy of pregnenolone, or pregnenolone in combination with other steroids, in reducing
The damaging effects of elevated cholesterol, from heart disease to atherosclerosis, have been well documented and extensively publicized, leading to the wide array of cholesterol-lowering drugs on the market. But recent research indicates that restoration of hormonal balance to youthful levels naturally brings cholesterol
REFERENCES 1. Lanthier A, Patwardhan W . Sex steroids and 5-en-3 beta-hydroxysteroids in specific regions of the human brain and cranial nerves. J Steroid Biochem. 1986 Sep;25(3):445-9. 2. Flood JF, Morley JE, Roberts E. Pregnenolone sulfate enhances post-training memory processes when injected in very low doses into limbic system structures: the amygdala is by far the most sensitive. Proc Natl Acad Sci USA. 1995 Nov 7;92(23):1080610. 3. Ladurelle N, Eychenne B, Denton D, et al. Prolonged intracerebroventricular infusion of neurosteroids affects cognitive performances in the mouse. Brain Res. 2000 Mar 10;858(2):371-9. 4. Akwa Y, Baulieu EE. Neurosteroids: behavioral aspects and physiological implications. J Soc Biol. 1999;193(3):293-8. 5. Akwa Y, Ladurelle N, Covey DF, Baulieu EE. The synthetic enantiomer of pregnenolone sulfate is very active on memory in rats and mice, even more so than its physiological neurosteroid counterpart: distinct mechanisms? Proc Natl Acad Sci USA. 2001 Nov 20;98(24): 140337. 6. Baulieu EE, Robel P, Schumacher M. Neurosteroids: beginning of the story. Int Rev Neurobiol. 2001;46:1-32. 7. Basta-Kaim A, Leskiewicz M, Budziszewska B, Lason W. The role of neurosteroids in the central nervous system function. Przegl Lek. 2005;62(11):1287-92. 8. Darnaudery M, Pallares M, Piazza PV, Le Moal M, Mayo W. The neurosteroid pregnenolone sulfate infused into the medial septum nucleus increases hippocampal acetylcholine and spatial memory in rats. Brain Res. 2002 Oct 4;951(2):23742. 9. Mayo W, George O, Darbra S, et al. Individual differences in cognitive aging: implication of pregnenolone sulfate. Prog Neurobiol. 2003 Sep;71(1):43-8. 10. George O, Vallee M, Le Moal M, Mayo W. Neurosteroids and cholinergic systems: implications for sleep and cognitive
within the normal range. Twenty patients with hypercholesterolemia received treatment with pregnenolone, DHEA, tri-estrogen, progesterone and testosterone. Mean serum total cholesterol was impressively lowered from 264 to 188 mg/dL after treatment, with 60% of the subjects demonstrating a drop below 200 mg/dL. The researchers concluded that their findings "support the hypothesis that hypercholesterolemia is a compensatory mechanism for [age-related] down-regulation of steroid hormones and that broadband steroid hormone restoration is associated with a substantial drop in serum total cholesterol in many patients." (19) These results underscore the importance of including pregnenolone in a comprehensive hormone replacement regimen.
Conclusion) Pregnenolone is an intriguing subject of medical research. Extensive animal studies in the area of memory enhancement have been performed; future efforts should focus on clinical studies to further our understanding of this unique compound's role in human disease prevention and treatment. This safe, non-toxic substance is has widereaching therapeutic potential
- from treating neurodegenerative and psychiatric diseases and reversing age-related cognitive impairment, to alleviating the pain and inflammation of arthritis and rejuvenating the
body's hormonal balance and without the dangerous side-effects and toxicity of most drugs.
Dosage and Use Typical doses range from 25mg to 100 mg and must be followed up with blood testing within a few weeks to determine hormone levels; physician supervision is highly recommended and mandatory for those already on a hormonal replacement protocol. Higher doses, such as those prescribed for treatment of arthritis must be administered under a physician's care. Caution: Pregnenolone should be avoided by people with epilepsy, a predisposition to seizures, or hormonalrelated cancers such as prostate and breast cancer.
processes and potential role of age-related changes. Psychopharmacology. 2006 Jan 17; 1-12. 11. Mayo W, Lemaire V, Malaterre J, et al. Pregnenolone sulfate enhances neurogenesis and PSA-NCAM in young and aged hippocampus. Neurobiol Aging. 2005 Jan;26(1):103-14. 12. Maurice T, Phan VL, Urani A, Kamei H, Noda Y, Nabeshima T. Neuroactive neurosteroids as endogenous effectors for the sigma 1 receptor: pharmacological evidence and therapeutic opportunities. Jpn J Pharmacol. 1999 Oct;81(2):125-55. 13. Maurice T, Urani A, Phan VL, Romieu P. The interaction between neuroactive steroids and the sigma 1 receptor function: behavioral consequences and therapeutic opportunities. Brain Res Rev. 2001 Nov;37(1-3):116-32. 14. Rupprecht R, Holsboer F. Neuroactive steroids: mechanisms of action and neuropsychopharmacological perspectives. Trends Neurosci. 1999 Sep;22(9):410-6. 15. Noda Y, Kamei H, Kamei Y, Nagai T, Nishida M, Nabeshima T. Neurosteroids ameliorate conditioned fear stress: an association with sigma receptors. Neuropsychopharmacology. 2000 Sep;23(3):276-84. 16. Roberts E. Pregneolone-from Selye to Alzheimer and a model of the pregnenolone sulfate binding site on the GABAA receptor. Biochem Pharmacol. 1995 Jan 6;49(1):1-16. 17. George MS, Guidotti A, Rubinow D, Pan B, Mikalauskas K, Post RM. CSF neuroactive steroids in affective disorders: pregnenolone, progesterone, and DBI. Biol Psychiatry. 1994 May 15;35(10):775-80. 18. Heydari B, Le Melledo JM. Low pregnenolone sulphate plasma concentrations in patients with generalized social phobia. Psychol Med. 2002 Jul;32(5):929-33. 19. Dzugan SA, Arnold Smith R. Hypercholesterolemia treatment: a new hypothesis or just an accident? Med Hypotheses. 2002 Dec;59(6):751-6. June/July 2006
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in the news
"If sunlight is used as a source of vitamin D, exposure should be scrupulously monitored so that no burning of the skin occurs"
Vitamin D could reduce cancer risk Supplementation with 1,000 IU of vitamin D3 daily could reduce the incidence of colon, breast, prostate and ovarian cancer, at low cost and with few adverse effects. This according to researchers at the Moores Cancer Center, University of California, San Diego. They conducted a systematic review of 63 observational studies of vitamin D status in relation to cancer risk. The review included 30 studies of colon cancer, 13 of breast, 26 of prostate and 7 of ovarian cancer. The researchers found that most studies showed a protective relationship between adequate vitamin D levels and risk of cancer. The review also highlighted that African-Americans, who have higher rates of mortality for colon, breast, prostate and ovarian cancer, have approximately half the plasma level of vitamin D as white people because increased skin pigmentation reduces their ability to synthesize vitamin D. The researchers say that a dose of 1,000 III of vitamin D3 (25ug) daily should maintain serum levels of vitamin D at or above 30ng/ml in most people. Throughout the US, exposure to sunlight for 15 minutes per day between 11am and 2pm, in the summer, under clear skies, should maintain a similar level. However, the researchers warn that if sunlight is used as a source of vitamin D, exposure should be scrupulously monitored so that no burning of the skin occurs. "Oral vitamin D3 supplementation, rather than solar exposure, should be used by fair skinned or sun-sensitive persons, or by individuals taking medicines causing photosensitivity." They add that according to the National Academy of Sciences, no known health risks are associated with doses of vitamin D up to 2,000 IU
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daily. They went on to say that: "Strong evidence indicates that intake or synthesis of vitamin D is associated with reduced incidence and death rates of colon, breast, prostate and ovarian cancers." However, despite these reassuring studies, the public health and medical communities have failed to adopt its use for cancer prevention. (American Journal of Public Health 2006;96:9) Vitamin D limits require an update Reinhold Vieth, Professor in the department of nutritional sciences and the department of medicine at the University of Toronto said that: "The British public should be outraged at the restrictions placed on vitamin D." In the UK, vitamin D tablets that deliver a maximum daily dose of more than 10 ug (400 IU) either require a prescription or must be sold under a pharmacist's supervision (sic). Professor Vieth believes that the general public should be allowed free access to higher supplementary doses of the vitamin. Official UK policy (e.g. advice from the Food Standards Agency) is that most people should obtain all the vitamin D they need by eating a varied and balanced diet and through exposure to the sun. Pregnant of breast-feeding women and older people should consider supplementation with 10 ug daily. In contrast, according to the National Academy of Sciences (US), older people require 15 ug daily. These North American recommendations are matched on the Continent, Professor Vieth said, and he went on to ask why the British do not need vitamin D when Americans do? It can be difficult to get direct evidence of links between vitamin D and diseases, such as multiple sclerosis, diabetes and prostate cancer. Many studies are epidemiological and others, such as retrospective studies, involve asking people about aspects of lifetime exposure to the sun. "Assessing outdoor exposure is not easy and recall can be a problem, especially in elderly people," said Richard Strange, professor of clinical biochemistry, Keele University Medical School, Staffordshire, who
has researched the hypothesis- but they are supportive. And it is now recognised that other organs, in addition to the kidneys, are able to produce calcitriol. Although the links between vitamin D deficiency and various diseases have been questioned, the "proven part of vitamin D story" is that the supplement can prevent osteoporotic fracture, Professor Vieth said. However, he called a daily dose of 10 ug "a drop in the bucket" in terms of osteoporosis prevention. Professor Vieth cited research suggesting that just three pills of vitamin D a year, each containing 1000 IU, could decrease fracture risk (PJ, 8 March, 2003, p324). One of the co-authors of that study was Sir Richard Doll and Professor Vieth likened the vitamin D story to smoking - it took many years to convince people that smoking was harmful, despite the availability of evidence, and it may take as long as convince people that vitamin D supplements could be beneficial, he said. "Smoking is easy to deal with compared to vitamin D - it is easier to tell people not to do something," he added. Professor Vieth questioned the use of public health messages. "What is the quality of the evidence? There is no debate. If you are worried about osteoporosis, take at least 800 IU (20 ug) of vitamin D," he said. However, even this recommendation may be conservative. According to Michael Hollick, Professor of medicine, physiology and biophysics, Boston University Medical Centre, it is now estimated that 1,000 IU of vitamin D a day is needed to satisfy the body's requirement and maintain circulating concentrations of calcidio of at least 30ng/ml. There is a great need to increase our awareness of vitamin D nutritional status and its health implications, Professor Hollick said. A further problem, according to Professor Vieth, is that we are stuck with old documents, which he described as "millstones around our necks". And he called for a mandate to the Expert Group on Vitamin and Minerals to re-assess the evidence for vitamin D.
medicine
have been lucky enough to be involved in antiaging medicine for nearly 20-years. My pharmacological and food and vitamin technology experience has covered various aspects of international database research, working along with many professional people, and in helping to establish W h i l e there are a myriad of potions, lotions criteria for aging biomarkers based on and pills all claiming to slow the effects of published evidence. aging, Phil Micans investigates some of the But this isn't a job application! I am theories of aging itself! trying to impart that having attended numerous conferences and meetings, read much of the literature and communicated with leaders in the antiaging field and I believe that if we want to truly bring about an end to degenerative aging, or at least control it in a masterful way, then we must pay close attention to the theories of aging. By so doing we can truly target and test the effectiveness of different antiaging protocols. However, the theories of aging and their measurement is something that is rarely mentioned at antiaging meetings or in submissions (sic). Should we not expect that any protocol or product to give reference to the type(s) of theories of aging that it may be addressing? In this brief article I hope to outline some of the "best" proposed theories. Our first problem is to define aging itself. Once defined we can present a clear reasoning behind what we mean by antiaging medicine, i.e., what we intend to achieve as a positive outcome. A definition of aging was reported in ancient Greek philosophy. According to Aristotle the human body is composed of 4 elements: humid, dry, warm and cold.The humid and warm prevail while we are young, while the dry and cold take predominance as we get older.
I
The theories and the practice
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"There is some evidence (at least in animals) that females have less mitochondrial damage than males, which may help to explain why as a species they live longer than males "
Modern biology has produced a more sophisticated
definition of aging. Strehler ( I ) suggested that the aging process has 4 main characteristics: 1. 2.
3. 4.
It is destructive. It is progressive.
It is intrinsically determined. It is universal.
This definition of aging has never been contested, and therefore this definition is a serious consideration for any proposed aging theory.
The theories of aging Mutations: Some of the earliest theories of aging were called the somatic mutations (2-5), later versions became known as genetic mutations, or even error catastrophe theories (6-9). Much was originally made about exposure to "cosmic radiation."
Use: The wear and tear explanations of aging began with Erasmus Darwin (10). This approach does not blame external factors for aging, but the increasing incapacity of the organisms for effective self-repair.
Glycosylation: The glycosylation, or cross-linking theory of aging attributes the formation of intra and intermolecular cross-links that alter the structure of the macromolecules, so much so that their functions become compromised. [Ed.- See the article in A A M Vol. 6 Issue 2, April/ May 2006],This explanation was suggested by Bjorksten in 1942 ( I I ) and King in 1946 (12) and confirmed by experiments by Verzar in the
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I950's (13-15). In fact, Fritz Verzar somewhat jokingly said:"The main question of basic aging research was to find out, why an old chicken requires a much longer time of cooking, than a young one!" (16)
F r e e Radicals: Perhaps the best known theory of aging is the free radical. It was Denham Harman in 1956 (17, 18) who proposed that free radicals might be involved in the age-dependent deterioration of the molecular structure.There is however a paradox arising from the fact that young individuals consume more oxygen per unit mass/ time than the old ones. Consequently, there must be an even higher rate of free radical generation at younger ages.Yet young organisms are able to grow and proliferate, i.e., they remain apparently untouched by the free radicals, while the older organisms become progressively deteriorated by the very same free radicals, even at a much lower rates of formation. (19)
Accumulation: The accumulation theories of aging assume that aging is caused by the increasing prevalence of certain substances such as lipofuscin, (age pigment), aged collagen, damaged neurofibrils, damaged enzymes, etc. Indeed, lipofuscin has been considered as one of the most significant biomarker of aging (20). Chemically speaking, lipofuscin is a strongly altered, extensively cross-linked, mainly insoluble, lipoprotein mass. Its presence in cells appears to increase with age and it is found in abundance in the brain's of Alzheimer Disease patients.
Neuroendocrine First exposed by Vladimir Dilman in 1987 this focuses
on the loss of sensitivity of the receptors with aging,
along with the loss of control over the endocrine
It is clear that many theories of aging are inter-related, perhaps a case of which comes first the chicken or the egg?
system via the pituitary/ hypothalamus axis. The resulting hormonal disarray then cascading into the varying degenerative aspects of aging. (21) Mitochondrial Whilst aligned with the free radical theory and originally also proposed by Denham Harman in 1972 (22), it was expanded upon by Jamie Miquel in 1980 (23). During mitochondrial production of the universal energy molecule adenosine triphosphate, (through the facilitation of the Krebs and electron transport chain cycles), the mitochondria produce some of the most damaging free radicals, specifically the superoxide radical, hydrogen peroxide and the hydroxyl radical (24). However, the very uniqueness of mitochondrial DNA, (mtDNA) is also a weakness as it has no histone protection or enzyme repair systems to offer itself significant free radical protection (25). Linnane et al, examined skeletal muscle samples from a 5 year old and a 90 year old human.They found that whilst nearly all the mtDNA of the 5-year old were full-length, less than 5% were still full length in the 90-year old. (26) Mitochondrial oxidative damage and decreased function has been cited as a key factor in Parkinson's disease (27). The mitochondrial theory hinges on this formula: Less mitochondrial oxidant generation = less mtDNA damage and less mtDNA damage = more normal mitochondrial bioenergetics throughout life (28). There is some evidence (at least in animals) that females have less mitochondrial damage than males, which may help to explain why as a species they live longer than males. (29)
the late seventies (30, 31) and published by Imre Zs.Nagy in 1994 (20). Zs.-Nagy notes that the accumulation of dry mass is an implicit requirement during development and maturation of every living being. This accumulating dry mass and loss of intracellular water content of cells inhibits enzyme activity as well as heat and chemical transference and cell efficiency, with a consequent spiral of decreasing cell to cell communication and inability to repair etc. Others: There are numerous other theories of aging including the theory of autoimmunization, the decomposed program, the organic explanations (32), and of course the varying genetic theories of aging such as shortening telomeres. Doubtless in the years to come more will be promoted. Indeed I understand that Walter Pierpaoli intends to publish what he has named; "the rotation theory of aging" based on the cyclicity of life and the universe with its consequences of pineal alteration. Conclusions It is clear that many theories of aging are inter-related, perhaps a case of which comes first the chicken or the egg? However, the frustration present today in antiaging medicine is that the majority of therapies are based on the replacement of "missing" substances in older age, (i.e., hormones, minerals, vitamins, etc.). Many of these replacement therapies are well documented to improve lost functions, enhance immunity etc., and may likely lead onto preventative roles, but until we have a really solid and generally accepted aging theory, no real chance of a precise antiaging intervention may be designed and adopted.
Membrane: The membrane hypothesis of aging was developed in
If it were, such an approach would certainly silence the critics of antiaging medicine, i.e. those who claim that
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"accumulating diy mass and loss of intracellular water content of cells inhibits enzyme activity as well as heat and chemical transference and cell efficiency " the time accepted model of measure-treat-measure and "treatment" of the fundamental root of the "disease" is not clearly or regular practiced. Although to be fair, a very similar claim could be leveled at mainstream medicine, after all the culture of cut, burn or poison in cancer hardly "treats" the fundamental root of that disease either! However it is in my mind, that we must keep nearer and dearer to our hearts the theories of aging, constantly looking out for that aging genesis, so that it may be controlled at its base/ beginning. Naturally we must continue to use the best tools that are available to us today, whether that be bio-identical hormone replacement, nootropics, methylation, chelation, stem cell therapy or micro RNA's (add to this list as you see fit). But let us not lose sight that we need to adopt the means to measure aging itself through biological aging measurement, in order to justify and examine individual treatment methods. Ultimately we have to trigger the regenerative responses- to truly reverse and halt aging, rather than to be merely patching and slowing. Keeping a close eye on the theories of aging and evaluating how antiaging medicine may be affecting their fundamental core(s) is a real scientific step on the road to an ageless (ergo disease free) society.
References and high energy radiations on living systems. Q . Rev. Biol., 34, I 17142. 2. S. Russ and G.M. Scott, (1939) Biological effects of gamma irradiation. Br. J. Radiol., 12,440-441. 3. P.S. Henshaw, et al (1947) The biological effects of pile radiations. Radiology, 9, 349-364. 4. L. Szilard (1959) A theory of aging. Nature 184, 956-958. 5. L. Szilard (1959) O n the nature of the aging process. Proc. Natl.Acad. Sci. U S A 45, 30-40. 6. Zh. Medvedev, (1961) Aging of the organism 7. L.E.
Orgel,(l963)The maintenance of the accuracy of protein synthesis and its relevance to ageing. Proc. Natl. Acad. Sci. USA, 49, 517-521. 8. L.E. Orgel, (1970) The maintenance of the accuracy of protein synthesis and its relevance to aging. Proc. Natl. Acad. Sci. U.S.A. 67, 1476-1488. 9. L.E. Orgel, (1973) Ageing of clones of mammalian
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Gesetze des organischen Lebens. Ge-bruder Hahn, Part I. p. 144, Part 2. p. 382-384, Hannover, Germany
(in German).
I I. J.
Bjorksten, (1942) Chemistry of duplication, Chem. Industries, 50, 69-72. 12.A.L. King, (1946) Pressure volume relation for cylindrical tubes with elasto-metric walls: the human aorta. Appl. Physiol. 17, 501-505.
13. F.Verzar, (1965) Experimentelle Gerontologie. F. Enke
Verlag, p. 180, Stuttgart, Germany (in German). 14. F.Verzar, (1955) Veranderungen Sehnenfasern
der
thermoelastischen
Kontraktion
im Alter. Helv. Physiol. Acta,
von
13, C64-C67. (in
German). 15. F.Verzar, (1956) Altern des Collagens. Helv. Physiol. Acta, 14, 207-202. (in German). membrane
theory
16. Zs.-Nagy, I. (2003) "The
of aging." International Antiaging
International Antiaging Systems, Spring v4 il6. (1956): Aging: a theory chemistry. J. Gerontol.,
Bulletin,
17. D. Harman,
based on free radical and radiation I I , 298-300.
18. Harman, D. (1961)
Prolongation of the normal life span and inhibition of spontaneous cancer by antioxidants. J. Gerontol. 16, 146-154.
19. Zs.-Nagy, I.
(1986) Common mechanisms of cellular aging in brain and liver in the light of the membrane hypothesis of aging. In: K. Kitani (ed.) Liver and Aging - 1986, Liver and Brain, pp. 373-387, Elsevier, Amster-dam.The Netherlands.
20.
Zs.-Nagy, I. (1994)
The
Membrane Hypothesis of Aging, p. 207, C R C Press, Inc., Boca Raton, Fl. 21. Dilman V., Dean W „ (1992) Neuroendocrine theory of aging and degenerative diseases, Center of Biogerontology, Florida. 22.
Harman, D. (1972) "The biological clock: the
mitochondria?" J . A m Geriatr Soc 20: 145-47. 23. Miquel, J. et al (1980) "Mitochondrial role in cell aging" Exp Gerontal 15:579-91. 24. Shigenaga, M. et al (1994) "Oxidative damage and mitochondrial decay in aging" Proc Natl Acad Sci U S A 91: 10771-78. 25. Richter, C. (1995) "Oxidative damage to mitochondrial D N A
I. B.L Strehler, (1959) Origin and comparison of the effects of time
at molecular level. Usp. Sovr. Biol. 51, 299-3 16 (in Russian).
cells, Nature, 243, 441 -445. 10. E. Darwin, (1795) Zoonomie oder
and its
relationship to ageing" Int J Biochem Cell Biol 27: 647-53.
26.
Linnane, A. et al (1998) "The university of bioenergetic disease" Ann
N Y Acad Sci 854: 202-13.
antioxidant
diet supplementation
27. Miquel, J. (2002) "Can protect
against
age-related
mitochondrial damage?" Ann N Y Acad Sci 959:508-16. 28.South, J. (2003) "The
mitochondrial
theory
of aging."
International
Antiaging Bulletin, International Antiaging Systems, Summer v4 i 17. 29. Sastre, J. et al (2002) "Mitochondrial damage in aging and apoptosis." Ann N Y Acad Sci 959:448-51. 30. Zs.-Nagy, 1.(1978) A membrane hypothesis of aging* J. theory. Biol. 75, 189-195. 31. Zs.-Nagy, I. (1979) The role of membrane structure and function in cellular aging: a review. Mech.Ageing Dev. 9,237-246.32. J.L.
Esposito,
(1983)
Conceptual
gerontology. Biol. Med., 26, 522-546.
problems
in
theoretical
letters Q:. I recently used bromocriptine. My reason for taking bromocriptine was because of its action as a free radical scavenger, but I found that it had an additional beneficial effect. I have had tinnitus for many years. I found to my surprise and delight that bromocriptine stopped the ringing. I did a literature search for bromocriptine and tinnitus coming up with an interesting article that suggests dopaminergic pathways are related to tinnitus. (Medical Hypotheses, 2005,65, 349). Have you found this to be the case? A : Thank you for letting us know what is a most interesting development. Bromocriptine is one of those drugs with a very wide range of uses, the literature reports that it has mild vasodilatation effects which may have been responsible for the relief of tinnitus, (You've probably tried other specific vasodilators in the past for that purpose). Bromocriptine is also a prolactin inhibitor and growth hormone agonist as well as a dopamine agonist and as usual doubtless has several other actions not yet discovered. Q: I just want to say that Milnacipran is truly a wonder drug. For the past 6 months I've been accumulating over 1000 hours of research on different drugs for attention deficit disorder (ADD), to deal with stress, COD, work and school anxiety, social anxiety, chronic fatigue, insomnia, fibromyalgia (TMJ), panic disorder, and alcoholism. I honestly think all the OCD (obsessive compulsive disorders) and morbid conditions came from ADD and low serotonin. Milnacipran has solved or is solving all these disorders. I believe that if it is approved by the FDA it will revolutionize pharmacology. It has certainly been extremely effective with my ADD. As it increases Norepinephrine (NE) in the brain's cortex, it also increases dopamine (DA) in a pharmacological manner called piggyback. The frontal cortex doesn't have dopamine reuptake channels, so blocked by NE blockers, creating a higher concentration of DA in the cortex. I also take very low dose of deprenyl ( l m g . per day) to keep the DA elevated and also for a little bit more energy and sex drive. All my research led me to Milnacipran, a drug not even
indicated for ADD. but has an ideal pharmacological profile for ADD. I'm advocating it heavily for ADD. I've spent 20 years researching drugs, have degrees in zoology (human physiology) chemistry and minors in philosophy and mathematics, so I know how to read journals, and I know the potential pharmacodynamics behind milnacipran, especially for ADD. A: Once again thank you for your welcome report, we believe this kind of information is most useful to others and we also agree that Milnacipran is a novel new drug with many benefits. Q: I am interested in using laetrile, but someone told me that it contains cyanide. Does laetrile contain cyanide? A: The anti-cancer drug laetrile is a controversial subject. Its ardent proponents consider it to be a natural cancer cure, one that is in the normal "vitamin architecture" of mammalian food (sources include apricot kernels, bitter almonds plus certain grasses and berries), as the primary natural exogenous cancer control for humans and animals, which is why they have called laetrile; "vitamin B17." On the other hand laetrile's opponents consider it quite simply, as a toxic drug because it contains cyanide. But before anyone jumps, consider that the cyanide portion of laetrile is tightly bound, in the same way that chlorine is tightly bound in salt (and no one thinks of chlorine when using salt- right!) Two specific properties of cancer cells, (an excess of glucuronidase and a deficiency of rhodanese), are believed to release the cyanide from the laetrile in the presence of cancer cells- killing them, but as this is not the case with normal cells laetrile is harmless to them. The main story that is highlighted by critics of
laetrile is the "laetrile toxicity study in dogs," that took place in 1978. Ten dogs were force fed a special mixture of 1-4 grams laetrile combined with a finely ground raw almond paste/water mixture, which had been pre-incubated at body temperature in blood bags for 15-60 minutes. Almonds are one of the highest beta-glucuronidase (i.e. laetrile cyanidereleasing) containing foods known. Incubating laetrile with an almond/ water paste at body temperature for 15-60 minutes thus served to pre-release the cyanide normally "locked up" in the laetrile. So the dogs were force-fed large quantities of free hydrogen cyanide! Not surprisingly, four of the dogs were neurologically impaired, while 6 died. What this experiment proved is that large amounts of hydrogen cyanide, force-fed, are toxic. This experiment did not prove anything about the normal action of laetrile when taken intravenously or on an empty stomach, which is the standard protocol for laetrile use. The dog experiment was like trying to prove that all cars are inherently deadly, on the grounds that everyone who drives a car at 100 mph into a brick wall, without a seatbelt will be killed! However, this experiment does form the basis of advice, for if you are using an oral form of laetrile (i.e. tablets), they should not be ingested at the same time with foods that contain the cyanide-releasing beta-glucosidase such as raw almonds, raw apricot kernels, raw vegetables such as bean sprouts etc. If using laetrile tablets the simplest answer is to take them only on an empty stomach. However the use of laetrile injections or a topical transdermal cream overcomes this problem as they bypass the stomach. There are perhaps two simple ways of looking at laetrile use, if you are concerned about cancer and want to start a "preventative" program use a cream version. If on the other hand you have cancer and want the laetrile to treat it, use the injectable version. If this entire subject intrigues you there is a super book on the subject called: "World without cancer" written by Edward Griffin and published by American Media.
Send your questions, letters & comments to: editor@antiaging-magazine.com
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WORLD MEDICAL EXPERTS PUT PREVENTATIVE HEALTHCARE AT TOP OF AGENDA AT ANTI-AGEING CONFERENCE LONDON 2006 T h e U K think-tank, the Office of Health Economics recently reported that the life expectancy gap between men and women is shrinking. Women can now expect to live just four-and-a-half years longer than men — the smallest difference for almost thirty years. So a female born in 2002 has an expected life expectancy of 80.7 years, while a boy born the same year has a life expectancy of 76.2 years. T h e report concludes that the reason for this slowing in life expectancy is that women are adopting the same lifestyles as men - smoking, binge-drinking and suffering workplace stress. W h a t is far more worrying is that very few of us - men or women - die a " n a t u r a l " death from old age. Most of the illnesses from which we suffer and die are far from natural - obesity, heart and cardiovascular disease, cancer, Alzheimer's, stroke, cirrhosis and diabetes. Nevertheless improved medical intervention and nutrition, has resulted in a huge spurt in longevity in the 20th century. An extra 20 years has been added to the average lifespan, bringing the average global life expectancy to 66 years. Life expectancy in Ancient Rome was 22 and in the Middle Ages 35. Today there are some people who live to more than 115 years. Although medical science is a long way from the discovery of a longevity pill, there is a growing community of doctors worldwide who believe that we can change our biological biomarkers to those of a younger person, so that we can live healthier, longer and more productive lives. These doctors take rejuvenation beyond the superficial limits of cosmetic surgery through a combined regime of exercise, diet, supplements and hormone replacement. Anti-Ageing Conference London (AACL) 2006 would like to invite to you to discover how medicine and science are
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pushing back the boundaries of the diseases of ageing. This year we have the largest ever gathering of experts at our 3rd conference to be held at the Royal Society of Medicine from September 15-17. We are particularly pleased to be able to incorporate the International Symposium on Regenerative Medicine This event offers a unique opportunity to learn from scientists and physicians about the latest medical advances from what some may consider controversial, to the proven and new treatments for the diseases of ageing. This event is of importance to all medical professionals who wish to be cogniscent on the latest medical and scientific developments in anti-ageing and rejuvenatory medicine from around globe. I t is of particular importance to scientists, nutritionists, gerontologists, chiropractors, pharmacists, pharmaceutical chemists and research specialists, nursing practitioners, naturopathic doctors, dentists, bariatricians and weight management specialists. In most societies around the globe people are living longer so the importance of healthy ageing has never been greater. It is possible for older people to live full and healthy lives well into the latter part of their years but in most cases this does not happen because they and the medical professional are not always aware of the new opportunities that are available to them through antiageing medicine. T h a t is what this conference is all about and why this knowledge is so vital. T h e speaker programme for Anti-Ageing London 2006 is as follows: Friday, 15 September Regenerative and Preventative Medicine Introduction: Heather Rird-Tchenguiz MBA P r o f Larry Benowitz - ( T B A ) Prof Geoffrey Raisman: Spinal cord injury
Prof David N a o r P h D : I n v o l v e m e n t of CD 44 in s t e m cell d i f f e r e n t i a t i o n P r o f S t e p h e n Minger - (TBA) Prof S t e f a n K r a u s s P h D : N e u r a l Cell D a m a g e D r D a s a Ciscova P h D : T h e efficacy of s t e m cell t h e r a p y in a n i m a l models of a u t o i m m u n e diseases P r o f T o m a s E k s t r o m : K a r o l i n s k a I n s t i t u t e t Sweden: Epigentics principles D r Tony Pellet: Umbilical Cord stem cells Dr Miomir Knecevic - (TBA) D r Ralf Toenjes P h D : P a u l - E h r l i c h - I n s t i t u t : S t e m Cell s i g n a t u r e s as a tool for q u a l i t y control of I n n o v a t i v e medicinal p r o d u c t s A n d r e a s J u n g e MBA: Knowledge M a n a g e m e n t D r O c t a v i Q u i n t a n a Trias: E U politics Dr Marco T r a u b : S y m p o s i u m Overview Saturday, 16 September Professor Dr I m r e Z s - N a z y : T h e T h e o r i e s of Ageing Dr Ben P f e i f e r M D Pli.D: P r o s t a t e Cancer - U n i q u e Protocols f e a t u r i n g P h o t o n u t r i e n t s a n d t h e Immounomodulator Dr M a r k Babizayev: H u m a n C a t a r a c t s — t h e role of Lipid P e r o x i d a t i o n a n d the efficacy of N - a c e t y l c a r n o s i n e as a treatment Phil Micans P h a r m B : Biological Age M e a s u r e m e n t Practicalities a n d Issues Dr J e n n i f e r K r u p M D A B A A M : H R T in W o m e n : Questions, answers a n d more q u e s t i o n s Dr B r i a n H a l v o s e n : D e n t i s t r y — Advances w i t h an e m p h a s i s on chelation a n d p r e v e n t a t i v e h e a l t h care Dr R o b e r t G o l d m a n M D P h D F A A S P D O FAOASM: Prof Alfred Wolf: Chronic s t r e s s , b u r n - o u t a n d CFS, A new insight a n d preventive o p t i o n s P a t r i c k H o l f o r d BSc D i p I O N F B a n t - N u t r i t i o n and Ageing Sunday, 17 September Dr D e e p a k C h o p r a Dr J u l i a n K e n y o n : P h o t o d v n a m i c a n d S o n o d v n a m i c Therapy Professor J o h n Ionescu P h D : N e w Strategies to slow skin photoageing
Skin Cancer Breakthrough After two decades of research and clinical trials, biochemist. Dr. Bill E. Cham, has discovered that BEC5 cream when applied topically can eradicate non-melanoma skin cancers, specifically: Basal cell carcinomas (BCC) and Squamous cell carcinomas (SCC). BEC5 cream has also been shown to be efficacious with benign tumours and other skin irregularities, including keratoses, keratoacanthomas, sun spots and age spots.
The figure above shows a large BCC on the temple This BCC had been surgically removed and skin grafts applied on two previous occasions, only to return {above left). Just four weeks treatment with BEC 5 cream resulted in full regression and no recurrence after 5-years (above right).
Numerous clinical trials have confirmed BEC5's ability to regress non-melanoma skin cancers. Recent trials in 10 UK hospitals found that a twice daily topical application of BEC5 cream to the affected areas gave a complete remission to 78% of the patients within 8-weeks.
S a r a h Noble: Advances in Spa Medicine Dr Eric B r a v e r m a n , MD: Subclinical H y p e r p a r a t h y r o i d i s m : A precursor of Osteoporosis a n d Dementia? Dr Michael K l e n t z e M D P h D A B A A M : Male H o r m o n e Replacement D r P a u l Clayton: Alzheimer's Disease: P l i a r m a c o n u t r i t i o n a l strategies t o m a i n t a i n t h e ageing b r a i n Dr Ron K l a t z T h e Conference Overview T h e p r o g r a m m e m a y be s u b j e c t to c h a n g e As well as t h e o p p o r t u n i t y to h e a r f r o m these world e x p e r t s a n d put q u e s t i o n s t o our s p e a k e r panel, t h i s event provides a u n i q u e n e t w o r k i n g o p p o r t u n i t y for h e a l t h c a r e professionals. All delegates receive a h i g h - q u a l i t y b o u n d conference m a n u a l including speaker p r e s e n t a t i o n s a n d b i o g r a p h i c a l m a t e r i a l s . T h e fee also includes a b u f f e t l u n c h , on all t h r e e d a y s , r e f r e s h m e n t s a n d a n i n v i t a t i o n to t h e conference cocktail r e c e p t i o n . I n a d d i t i o n t h e latest a n t i - a g e i n g p r o d u c t s f r o m a r o u n d t h e world will be on show in t h e e x h i b i t i o n hall. Full details of t h e speaker p r o g r a m m e a n d speaker b i o g r a p h i e s can be viewed at www.antiageingconference.com T h e r e are various categories of r e g i s t r a t i o n for t h i s event: Full r e g i s t r a t i o n £350; D a y 1 O n l y £200; D a y 2 only £200; D a y 3 £200. Book on-line on t h e r e g i s t r a t i o n page at www.antiageingeonference.com. M e m b e r s h i p of c e r t a i n medical societies m a y q u a l i f y for a discount. F u r t h e r i n f o r m a t i o n m a y also be requested f r o m conference@antiageingeonference.com. Telephone: +44 ( 0 ) 207 581 6962 T h e events sponsors a n d s u p p o r t e r s include H B H e a l t h , t h e British Society of Anti-Ageing Medicine; t h e E u r o p e a n Society of A n t i - A g i n g Medicine; t h e World A c a d e m y of A n t i - A g i n g Medicine a n d T h e T r a n s E u r o p e a n S t e m Cell T h e r a p y C o n s o r t i u m .
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J?
www.antiaging-systems.eu June/July 2006 i a m
interview
Melatonin, Immunity & Cycicity what does it mean for us
W
alter Pierpaoli, M.D., is one of the great avant-garde professional researchers and physicians today who are searching for the central cure for aging disorders. He describes himself thus:
I am not a wizard or a sorcerer but simply a man curious of nature and biology who has spent almost 40 well documented years in the merry companionship of mice, waiting for them to teach me how and why we age and die. My main feature is endurance and a deeply rooted ability to escape from the fashion of science. I have definitely interpreted the biological expression of the genetic programme of aging in the "pineal network," and am now trying to stop and also reverse aging. My solitary path has not yet been followed, but the crowd generates aggressivity and confusion because many motivations in health care are not addressed to disease prevention but, on the contrary, to there maintenance. The "ultimate defiance" has started and the answer can only be through strict scientific documentation. Mice live two to three years, humans sometimes 100 and over. Some may care to wait to see, but in the meantime I protect my pineal gland from aging by using melatonin.
An interview with Walter Pierpaoli, M.D.
iaill
June/July 2006
In this interview with Dr. Pierpaoli, we discuss in detail his views on aging and what his research on melatonin, immunity and cyclicity means for all of us.
interview AAM: Dr. Pierpaoli, perhaps the most obvious first question I should ask you is what is your interpreation of melatonin? Dr. Pierpaoli: Well Phil, melatonin is ubiquitous, because it is present everywhere in nature. It is highly concentrated in the pineal gland of man, mammalian species and vertebrates. Here it is produced during the night, resulting in a typical "night peak" of melatonin which can be measured in blood. In humans, blood melatonin levels reach their highest night values before sexual maturation, i.e. at puberty and then they constantly decline. The decline of the melatonin night peak signals the progression of aging. We have found and described in many scientific publications and in a bestselling popular book, [Ed.- The Melatonin Miracle, Simon & Schuster, New York, translated into 17 languages] that nocturnal administration of melatonin to aging rodents results into a significant prolongation of their life. Melatonin in fact, when taken chronically in the late evening, protects the pineal gland from aging by simply putting the pineal gland "to sleep!" This means that other molecules are produced in the pineal gland which dramatically postpone and even reverse aging. These other molecules are presently under experimental and clinical testing, but people should be aware that the transplantation of a pineal gland from a young into an old animal delays aging in a very pronounced manner. Melatonin does not itself affect functions such as immunity directly. Melatonin protects from us from aging thanks to its protecting action on pineal function. This interpretation, which is based on experimental work and clinical observations, explains the many beneficial effects of melatonin on all organs and functions. AAM: So what does aging mean to you? Dr. Pierpaoli: We have demonstrated that typical metabolic aging is an evolutionary "programme" in the pineal gland that follows a very precise time schedule, which depends on the evolutionary development of mammals. In all mammals, including man, aging follows the strict neuroendocrine programme of growth, puberty and fertility. Aging does not depend on diseases, but diseases can profoundly affect and accelerate aging. Under ideal conditions of life and genetics with no diseases, the programme of aging will take its course until the emergence of
a "death clock" in the pineal gland, which is totally separated from aging. Therefore growth, puberty, fertility, aging and death are all expression of the genetically determined neuroendocrine programme of the mammalian brain, endowed in the hypothalamic-pituitary-pineal area of the brain. Evidence is dramatically emerging that aging is amenable to control and reversal, similar to other neuroendocrine mechanisms such as growth and reproduction. There is nothing mysterious in aging, for we can delay and even reverse aging now! A AM: So why is the pineal gland so important? Dr. Pierpaoli: The pineal gland or in its Latin and anatomical name the "epiphysis cerebri," is a tiny bean-size brain organ or "gland" which is connected to the brain and to the neuroendocrine/ hormonal and nervous systems, through a complex network of bidirectional links and, in particular, to the anterior hypothalamic nuclei (suprachiasmatic nuclei), the pituitary gland (hypophysis), the eyes (the retina) and via the supracervical nervous ganglia, to the thyroid, the thymus and all other glands such as the adrenals and the gonads.
"Aging does not depend on diseases, but diseases can profoundly affect and accelerate aging" prioritary. Therefore the pineal gland and its "products" are fundamental for reproduction biology. In the course of evolution, the "pineal network" of each species has acquired the capacity to progressively develop and to maintain a "life, aging and death clock." The parallel genetical and developmental, evolutionary course of all species has resulted into a precise "age-clock" for each species. In other words, environmental and reproductive needs have lead to precise "clocks" for each species. Thus the "pineal network" controls the neuroendocrine programme of aging in the brain and scans the time when we grow, when we procreate and when we age. These precisely programmed events are quite distinct. Our experiments with rodents and clinical evidence show that the pineal gland and its "wonder molecules" which have been the target of mockery from "pinealogists" can truly delay and reverse aging. This is achieved by acting on those same mechanisms which make us grow and reproduce!
Thus it is thus clear that, via its direct connections with the brain centers, such as The pineal gland is the key for the suprachiasmatic nuclei, it is regulating body temperature and photoperiodic daynight and seasonal variability of hormonal synthesis and secretion. The "pineal master gland" acts as a true "director of the hormonal orchestra" in the course of growth, puberty, fertility and aging. It must be emphasized, however, that the role of the pineal gland in the maintenance of body functions is strictly Longevity related to the different Sexual function Immunity evolution of Menopause mammalian and other Andropause species, in relation to Lipid/Fat levels the survival and Hormone balance reproduction need of Macular degeneration each species. The need www.antiaging-systems.com for reproduction is Toll-free USA 866 800 4677
June/July 2006
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understanding aging because it controls
For women, menopause is the expression of
which is the most powerful natural
from birth to death the circadian and
the progressive and sometimes abrupt
antioxidant agent found to date, will
seasonal variability of hormones- which
cessation of monthly menstruations.
influence the course of aging and affect
regulate all functions of the body. Death is
Perimenopause, those being the years
longevity owing to their capacity to
a precise signal from the pineal gland
before, during and after menopause, is
neutralize "toxic" hydroxyradicals. We
which is timely programmed and does not
generally accompanied, in most women, by
think that the relevance of oxidative
depend on aging. This means that we can
a very large variety of symptoms,
damage on the expression and course of
die at the age of 120 without any disease!
disturbances, and also changes related to
aging is minimal. Nature provided many
We can stop aging and we will be able to
decline of hormonal-regulated monthly
millions of years ago through evolution the
interpret also the mechanism of the "death
ovulation. The problem is clearly
process to neutralize oxidative damage!
clock."
neuroendocrine and in fact "hormone
This commercial slogan does not serve the
replacement therapy" (HRT) can produce
purpose of fighting aging. We do not share
A A M : A lot is made by antiaging
positive reversal of menopause-related
the view that the documented anti-aging
physicians of hormones, particularly to
alterations, but HRT also produces side-
and life-prolonging effects of melatonin
treat the male andropause and female
effects!
depends entirely on its anti-oxidant activity. Melatonin is produced at night, when
menopause, what's your view of that? We are convinced, on the basis of a clinical
stress-produced oxyradicals are minimal.
Dr. Pierpaoli: Andropause is the
trial which has been reported in a scientific
Nocturnal administration of melatonin at a
expression of the progressive decline of
journal [Ed.-Experimental Gerontology,
relatively low dosage will simply prevent
reproductive functions in the male.
February 2001], that melatonin alone or in
the pineal gland from synthesizing
Although the relevance of sexual
combination with HRT can dramatically
melatonin, in particular in the course of
senescence in males is largely neglected
improve the course of menopause, to the
aging, thus allowing the pineal gland to
owing to the prejudices and ignorance
extent that it may be able to prolong
maintain the capacity to produce other,
surrounding the biological relevance of
fertility and even reconstitute cyclic
more basic molecules.
testosterone, many pathologies and
ovulation and menstruations. It is not true
symptoms clearly show, in the great
that ovaries are worn out! In fact there is a
A A M : Many people are aware that much
majority of men, an insufficient brain
progressive absorption and sclerosis (ovary
of your research has focused on immunity,
regulation of sex hormones
atresia) which is brain-programmed and
how does melatonin play a role in
(gonadotropins, LH, FSH) with consequent
does not depend on lack of ova! Melatonin
autoimmunity and the immune system?
involution of peripheral male sex organs,
can produce a progressive reconstitution of
(e.g. testes) during aging. One of the most
juvenile secretion of pituitary
Dr. Pierpaoli: Melatonin, in particular
frequent pathologies is prostate
gonadotropins and thus reverse the course
when combined with zinc, is a very potent
hypertrophy and consequent urinary
of menopause. The dramatic reconstituting
and reliable immunopotentiating agent. In
problems. Also a sudden or progressive
effects of melatonin on the synthesis and
our view, melatonin does not act directly
loss of sexual drive, inertia, apathy,
secretion of sex hormones had been
but via its synchronizing effects on the
depression, muscular weakness is observed.
demonstrated and published by us,
entire neuroendocrine system, which totally
In our experience, those symptoms and
however, as a definite confirmation, clear-
controls the immune system. Melatonin
deficiencies do not depend on a
cut evidence has emerged from the
will also profoundly affect the thymus and
quantitative deficiency of sex hormones,
placebo-controlled clinical study in
cell-mediated, transplantation immunity
but rather on a constant and progressive
perimenopausal women, which has been
and thus the resistance to viruses. The
levelling of hormone cyclicity. In fact, all
published in Experimental Gerontology,
effects of melatonin in enhancing immunity
hormones display a day-night rhythmicity
February 2001.
are truly dramatic and it seems that they are
which is under pineal-hypothalamic-
exerted via utilization of zinc, which, for
pituitary regulation. Aging of the brain
A A M : Perhaps the most well known and
example, is needed for synthesis and
results into an increasing stiffness, by
discussed treatments of aging center on the
activation of the thymic hormone thymulin.
which I mean a reduced and ineffective
role of free radicals and antioxidants, in
To summarize, melatonin will protect the
feed-back of the mechanisms which
your work what have you made of that?
pineal gland from aging and balance the
regulate hormone secretion. In fact the so-
28
gland for its optimal juvenile activity. In
called central feed-back mechanisms do not
Dr. Pierpaoli: We do not share the view
respond anymore to stimuli, this results in
that aging can be delayed with "anti-
immunodepression, melatonin will protect
alteration and de-synchronization of
oxidants" and "free radical scavengers" and
and restore immunity. In adult and elderly
case of stress, which produces profound
hormone secretion. Melatonin, by
similar fashionable and simplistic
people, melatonin will greatly potentiate
protecting the central master gland, namely
interventions! We think that oxidative
the protecting effects of vaccinations.
the pineal gland, from aging, maintains and
damage and oxyradical formation, which is
even reconstitutes normal physiological
a by-product of cell respiration, only
hormone cyclicity in the brain! In other
minimally and perhaps not at all
used in autoimmune diseases simply
words, our work has shown that it is not
contributes to aging. No experimental in-
because it will restore a normal immune
the lack of sex hormones which underlines
vivo or clinical evidence exists that an
reaction and the capacity of the immune
andropause, but rather the pattern of their
addition to the daily diet of even very large
system to recognize "self' antigens. We
circadian, day-night secretion.
amount of "anti-oxidants" such as Vitamin
have observed complete recovery! The
E, glutathione and even melatonin itself-
etiology of all autoimmune diseases
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June/July 2006
As for autoimmunity, melatonin must be
interview a f f e c t i n g t h e skin, t h e g l a n d s , t h e b l o o d
e n d o g e n o u s h o r m o n a l r h y t h m i c i t y by
a n d a n y o t h e r t i s s u e is b a s e d on c o n g e n i t a l
p r o t e c t i n g o u r m a s t e r g l a n d - the pineal
or a c q u i r e d inability to r e c o g n i z e o u r o w n
g l a n d , w i t h e v e n i n g intake o f m e l a t o n i n ,
b o d y tissues a n d t h u s to m o u n t a n
e s p e c i a l l y if it is also c o m b i n e d w i t h s o m e
a u t o i m m u n e reaction. A g i n g itself is
zinc.
largely a h i d d e n , latent a n d insidious a u t o i m m u n e p r o c e s s l e a d i n g to vasculitis
A A M : A lot o f talk is m a d e b y s o m e
(sclerosis o f vessels), a u t o a n t i b o d i e s a n d
p e o p l e a b o u t m e l a t o n i n ' s r o l e in cancer,
cancer. O u r w o r k o f 4 0 y e a r s h a s led to
w o u l d y o u c a r e to e l a b o r a t e on that
t h e d e m o n s t r a t i o n that i m m u n i t y is totally
subject?
u n d e r h o r m o n a l control. M e l a t o n i n will not increase t h e s y n t h e s i s o f a g g r e s s i v e
Dr. P i e r p a o l i : M e l a t o n i n is n o c u r e f o r
a u t o a n t i b o d i e s , on the c o n t r a r y it will
cancer. Its e f f e c t s on c a n c e r are o n l y
p r o g r e s s i v e l y lead to h e a l i n g o f the basic
visible if a s s o c i a t e d to a n u m b e r o f
h o r m o n a l d e r a n g e m e n t s u n d e r l y i n g and
i m m u n i t y - e n h a n c i n g agents. M e l a t o n i n can
initiating the a u t o i m m u n e p r o c e s s .
help i m p r o v i n g pineal f u n c t i o n in c a n c e r
A A M : So h o w d o t h e natural b i o r h y t m s o f
c a n c e r - s u r v e i l l a n c e , the natural
life e f f e c t o u r h o r m o n e s a n d o u r a g i n g ?
i m m u n o l o g i c a l a n t i - c a n c e r activity.
D r . P i e r p a o l i : R h y t h m i c i t y , periodicity,
h o w e v e r , will protect f r o m onset o f c a n c e r
cyclicity, daily a n d s e a s o n a l variations o f
o f all kind, i n c l u d i n g m a m m a r y cancer.
light a n d t e m p e r a t u r e h a v e indelibly
C a n c e r is p r e c e d e d by h o r m o n a l c h a n g e s
patients, t h u s a l l o w i n g a r e c o n s t i t u t i o n o f
Melatonin administration and prophylaxis,
inprinted t h e e v o l u t i o n o f life on o u r
w h i c h d e v i a t e t h e i m m u n e s y s t e m f r o m its
planet. N o t h i n g e s c a p e s the l a w s o f
c a n c e r - s u r v e i l l a n c e tasks. M e l a t o n i n can
p l a n e t a r y a n d c o s m i c variability a n d life
restore a d e r a n g e d i m m u n i t y a n d will t h u s
itself in all its living f o r m s h a s t a k e n its
h e l p to correct t h e n e u r o e n d o c r i n e
p r e s e n t s h a p e u n d e r t h e control o f t h e s u n ,
alterations w h i c h p r o d u c e cancer. S o by
t h e m o o n , t h e tides a n d t h e rotation o f
p r o t e c t i n g t h e pineal g l a n d w i t h m e l a t o n i n
earth a r o u n d itself a n d a r o u n d t h e sun. In
will h e l p p r o t e c t f r o m cancer. H o w e v e r ,
fact, e v e r y tiny p r o c e s s or e v e n t in o u r
o n c e c a n c e r is a l r e a d y d e v e l o p e d ,
b o d y o b e y s the natural l a w s o f
m e l a t o n i n will not s i g n i f i c a n t l y a f f e c t its
b i o r h y t h m i c i t y ! E m e r g e n c e o f a n e w life in
c o u r s e , but it will i m p r o v e the g e n e r a l
t h e m o t h e r ' s w o m b also d e p e n d s on
c o n d i t i o n s o f the patient a n d p r o l o n g life.
o v u l a t i o n , w h i c h is a m o n t h l y e v e n t .
T h e p i n e a l g l a n d is t h e k e y f o r interpreting
Fertility in w o m e n is c l o s e l y linked to
t h e c a u s e s o f a g i n g a n d cancer, night
lunar cyclicity a n d cyclical n e u r o e n d o c r i n e
m e l a t o n i n will k e e p t h e p i n e a l g l a n d y o u n g
r e g u l a t i o n . L i f e itself is t h e m a i n t e n a n c e o f
and functioning!
cyclicity o f h o r m o n e s a n d cells, w h i l e a g i n g a n d death is e x a c t l y the o p p o s i t e :
A A M : A n o t h e r k e y f a c t o r that m a n y
p r o g r e s s i v e loss o f a d a p t i v e cyclicity. All
p e o p l e w o r r y about t o d a y are their
h o r m o n e s in fact, i n c l u d i n g the c h e m i c a l
c h o l e s t e r o l levels. H a v e y o u f o u n d
m e s s e n g e r m e l a t o n i n , f o l l o w a strictly
m e l a t o n i n to play a n y role f o r a d j u s t i n g
individually s h a p e d d a y - n i g h t variability.
lipids f a v o r a b l y ?
W h e n w e a g e a n d w e a r e r e a d y to die
"Our work of 40 years has led to the demonstration that immunity is totally under hormonal control"
b e c a u s e the g e n e t i c p r o g r a m m e e x p i r e s ,
Dr. P i e r p a o l i : Naturally, lipids/ fats are
f r o m "cyclically f l u c t u a t i n g " w e b e c o m e
vital to the body, but an e x c e s s o f t h e m ,
"flat". T h i s is t h e r e a s o n w h y t h e night
e s p e c i a l l y in a s e n e s c e n t a n d sick b o d y will
m e l a t o n i n signal in the pineal gland tells us
r a p i d l y g e n e r a t e c a r d i o v a s c u l a r d i s e a s e s . It
h o w old, y o u n g or d e r a n g e d w e are. A n
is h o r m o n e s w h i c h u n d e r l i n e lipid
absent (flat) night peak o f m e l a t o n i n in t h e
metabolism and H D L and L D L cholesterol,
pineal g l a n d d o e s not n e c e s s a r i l y m e a n that
total c h o l e s t e r o l , t r i g l y c e r i d e s a n d f r e e
w e are g o i n g to die i m m e d i a t e l y , but that
fatty acids a r e part o f a b a l a n c e d s y s t e m
w e can expect degenerative and
w h i c h p r o g r e s s i v e l y d e r a n g e s with a g i n g .
a u t o i m m u n e d i s e a s e s or cancer. In fact,
A s s u c h , m e l a t o n i n can p o w e r f u l l y
m e l a t o n i n p r o t e c t s the pineal g l a n d f r o m
c o n t r i b u t e to the a d j u s t m e n t o f lipid
a g i n g and t h u s the b o d y f r o m b e c o m i n g
m e t a b o l i s m via its b a l a n c i n g e f f e c t s on the
" h o r m o n a l l y flat" a n d f r o m d e v e l o p i n g the
entire n e u r o e n d o c r i n e , h o r m o n a l s y s t e m .
typical " d i s e a s e s o f a g i n g " such as c a r d i o v a s c u l a r a n d c o r o n a r y diseases, a u t o a g g r e s s i v e d i s e a s e s a n d cancer. W e can s a f e l y p r e v e n t this p r o g r e s s i v e loss o f
If y o u c h e c k y o u r lipids and then t a k e m e l a t o n i n f o r o n e to t w o m o n t h s , then c h e c k t h e m a g a i n , y o u will realize that the
June/July 2006 i a i f l
29
interview level is going back to normal. This can be even if lifestyle and diet have not changed ! Of course, improvement of life habits, in particular less stress, more sleep and better food will accelerate the lipid-lowering activity of melatonin. AAM: Are there any farther advantages to melatonin for coronary and cardiovascular diseases? Dr. Pierpaoli: The variety of diseases caused by the degeneration of vessels, which is drastically accelerated by many factors such as genetics, alimentary habits, diabetes, smoke, alcohol, stress, metal or drug poisoning and so on, comprehend a huge variety of symptoms and diseases. The most common of them are coronary, heart diseases and infarction, thrombosis, arterial and venous occlusions, embolism, brain haemorrhage or ictus and heart arithmias. It has been demonstrated that in the commonest of them, namely coronary heart disease and ictus, the patients show an extremely low level of night melatonin [Ed.- Lancet, volume 345, page 1408, 1995]. This low level is an ominous signal for a derangement of pineal function and consequently for the hormonal regulation of the body. It is certainly not melatonin itself which is missing, but melatonin is produced by the pineal gland at night and its absence shows a profound alteration of pineal control of hormones. Although its effects may require a few months, the addition of melatonin to your evening or nocturnal habits may prolong decades to your life, for besides reconstituting a "child's sleep," while you sleep, melatonin protects the pineal gland and then this "master gland" will be able to synthesize and secrete other more fundamental molecules which regulate all function of cells. In addition, melatonin is also produced by platelets/ thrombocytes, this has powerful anti-aggregating properties and will keep your vessels and capillaries free, elastic and "smooth." AAM: Another of the things that concerns many people as we get older is depression, clearly no one enjoys the experience, particularly when there doesn't seem to a good reason for it. Can melatonin help alleviate these symptoms? Dr. Pierpaoli: Seasonal affective disorders or SAD, with gloomy morning moods and depression are caused by a variety of family, social, neuro-psychological and
30
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June/July 2006
"by protecting the pineal gland with melatonin will help protect from cancer" hormonal alterations and derangements. Depression can be combined with nervousness, anxiety, fear and also be located in the subconscious without being aware of it. As such, many persons adapt to cohabit permanently with depression. Depression is the most dangerous and devastating of all diseases, in so far it deprives us of any joy and motivation of life. Depression blocks and alters mental biochemistry and creates a vicious circle of negative events in the body and in the brain. For centuries induced fear and depression have been utilized by authoritarian and tyrannical religious movements and regimes to enslave people and make them docile and subdued. One very common condition of more or less deep depression is consequent to menopause and andropause and is obviously dependent on the decline of sexual hormones. Melatonin, by reconstituting a juvenile hormonal cyclicity can, better than any drug acting on brain biochemistry, mitigate or cure depression. It restores physiological sleep and cyclicity of sexual hormones, in particular testosterone and estrogens. Short-term effects are visible but the best results in the restoration of a positive and also euphoric morning mood are achieved by a long-term treatment with melatonin, combined of course with additional interventions such as diet, exercise and sexual activity. AAM: I suppose the best known feature of melatonin has been its reported effect on improving sleep patterns and jet-lag, how do you feel about that? Dr. Pierpaoli: Well as I think everyone can see, melatonin is a remarkable molecule with many uses. But in regard to sleep, it is its effects on the regular, circadian, e.g. day and night change and cyclic, daily temporary event of life that are most
important. Insomnia is a disturbance of sleep duration and quality, leading to severe and often irreparable damage of psychic and somatic functions. I would like people to know that melatonin is not a sleeping pill and has no drug effect on the sleep quality or length. However, thanks to its central action on the re-synchronization of hormonal cyclicity, melatonin reconstitutes a juvenile and physiological sleep pattern. The reconstituting effect of sleep does not depend on its duration, but on its quality. A normal healthy sleep is characterized by an initial "rapid eyes movement" (REM) phase. If sleep is disturbed such as during "pathological aging," REM sleep disappears. All hormones follow a typical 24-hour cyclicity and variation which is being deranged by many factors such as stress, anxiety, diseases, jet-lag and so on. The melatonin-induced sleep produces a juvenile pattern of sleep with REM which perfectly restores psychic, mental and body forces. In order to cure insomnia, one must recreate a periodicity and quality of sleep which only melatonin can provide. The progressive restoration of hormonal cyclicity produced by protecting the pineal gland with melatonin, acts as a positive cascade which automatically reconstitutes a healthy and profound sleep, with no regard to its duration. With specific regard to jet-lag, the discomfort, sleep, weakness and psychosomatic and neurovegetative problems provoked by crossing within a short time one or more Oceans and Continents, and resulting in a slow and difficult adaptation to a new local daytime and environment, including the temperature and time of day, can be partially or even totally prevented or overcome by taking melatonin before leaving for a destination or at arrival. The same can be done on the way back home. In order to adapt to the destination time before leaving, one must take for two or three days before departure about 3 mg. of melatonin by calculating the late-evening time at destination of 10 to 12 pm. Then continue to take melatonin after arrival at the detination, when the brain has already adapted to local time before departure. The same must be applied when returning home. One must take melatonin for two-three days before departure by calculating the late-evening time at home. In case a prophylactic adaptation cannot be done, in order to at least mitigate the effects of jet-lag one must take melatonin at
interview the destination place only when going to bed between 10pm and 12 pin and not before! The discomfort of jet-lag becomes very significant when the time difference between home and destination time is more than 6 hours. [Ed.- It has been calculated that the body clock requires 1day to adapat to each hour of time difference]. AAM: One of the great pleasures I had last year was to be invited to one of your Stromboli conferences. For those whose European geography isn't good, Stromboli is a unique volcanic island located in the Tyrrhenian Sea off the coast of Sicily. I belive that many people won't have heard of the conference before, probably because you only invite scientists, physicians and researchers to lecture and network amongst themselves. It is a super event, and in particular I remember one fascinating piece of information imparted by Dr. Changxian Yi from China on the effects of melatonin and vision, do you recall it? Dr. Pierpaoli: Indeed I do Phil. Firstly let me say that melatonin is produced by the retina. The large clinical trial in China on the protecting and reconstituing effects of evening administration of melatonin were focused on the currently incurable diseases of the eyes that lead to blindness, namely macula degeneration and atrophy, and also in aging-related or diabetes-depending retinopathies. This was done because hundred of millions of persons are affected by fatal macula degeneration. We have documented a single case of retina degeneration close to blindness that was cured with melatonin, the patient having total clinical recovery of the retina and permanent maintenance of residual sight capacity. The almost blind subject even get his driving licence back! The case is described in my "Melatonin Miracle" book and now Dr. Yi has many before and after pictures of reversal of macula degeneration just from the evening administration of oral melatonin! A AM: The wide range of improvements that you have clinically shown melatonin to be able to perform are truly incredible. Are there any other areas you would like to mention that we haven't already covered? Dr. Pierpaoli: Indeed there are some more. For example, to our great amazement and surprise, we have documented several cases of subchronic and chronic hepatitis-C
"melatonin reconstitutes a juvenile and physiological sleep pattern" cases which have undergone rapid regression of fatty infiltration and reconstitution of liver tissue, after late evening administration of melatonin, this has been shown by repeated liver biopsy and liver enzymes measurement. The effects are visible within weeks or months after initiation of melatonin intake and depend on the degree of severity of hepatitis as well as individual health conditions and lifestyle such as diet, stress and so on. However, the reconstitution of liver tissue integrity and function was constant and has led to complete healing. We hypothesize a potent local antiinflammatory effect and a rapid enhancement of anti-viral immunity with melatonin, which has been shown in our experimental work with virus infected mice. We have also documented the reversal of osteoporosis in women after continued intake of melatonin. This has been documented with regular bone densitometry measurements. This is not astonishing if we consider that melatonin profoundly affects the levels of gonadotropins and reverses the perimenopausal syndrome in women. The positive cascade of events initiated by melatonin are also seen in the reactivation of bone metabolism and bone formation. This is one of the most easily documentable effects of melatonin in arresting and reversing menopause. Plus there is no doubt that, according to our clinical observations over many years that melatonin can rapidly or slowly ameliorate Parkinson's disease. There is no rule for it in so far the effects of melatonin greatly vary depending upon age, sex, stage of the disease, therapy and so on. However, melatonin is a fundamental therapeutical agent for improving
Parkinson's disease. We have observed patients for years and documented a constant improvement even from advanced Parkinson to its complete healing. The therapy must be continued for many years since sometimes the improvements are suddenly rapid after a long period of administration. A dosage of 3 mg. in the evening appears to be sufficient. In case of strong rigidity, recovery is slower but constant. Lasltly, let me mention sex power! The idea that melatonin affects sexual vigor is true. However, it would be misleading to think that melatonin is a kind of aphrodisiac drug, a kind of magic "sexdrive-arousing pill!" Melatonin, taken according to a circadian night rhythm certainly protects the pineal gland and thus maintains physiological and juvenile sexuality. Melatonin is not itself a sex hormone but it helps to maintain sexual functions. In spite of the fact that melatonin controls reproductive functions in many species, such as sheep, it does not do so in humans. On the contrary, if taken at a very high dosage in young fertile women, melatonin inhibits secretion of gonadotropins from the pituitary gland and consequently ovulation. If taken at a moderate dosage of a maximum of 3 mg., melatonin protects the reproductive tract both in males and females from sexual decay and aging. By maintaining the normal functions of the sex glands in both men and women, melatonin prolongs a gratifying, juvenile and active sexual life. AAM: So Dr. Pierpaoli, if I was to ask you for a one line statement about how to use melatonin what would you say? Dr. Pierpaoli: In conclusion, I recommend a regular nightly intake of melatonin of 3 mg., with additional zinc for all persons more than 40 years old. Melatonin can also be taken by younger persons for periods of weeks or months, especially when under conditions of severe stress, insomnia, jetlag and a number of pathologies, including autoimmune diseases of all kind. AAM: Dr. Pierpaoli, thank you very much for your remarkable insight into the amazingly broad properties of melatonin. Dr. Pierpaoli: Let me say that I enjoy reading the Antiaging Magazine and wish you good luck with it.
June/July 2006
iaill
31
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fna of three articles on overcoming age-related mental decline, we look at three common ailments: AD(H)D, Alzheimer's Disease and strokes.
Improving your mind: Tackling brain disorders It is important to recognise the clear distinction between the 'normal' mental impairment we associate with aging and that brought about by disease. Neurological diseases, such as dementia, have a devastating impact and on millions of people around the world. Not just on the sufferer, but also their families, whose lives can be dominated by their relative's disease. As these disorders commonly manifest themselves in the elderly, they are a matter of great concern for all of us as we approach old age. Here I will look at three widespread, but very different, forms of mental ailment AD(H)D, Alzheimer's Disease and strokes - and consider their possible causes, preventions and treatments. Attention Deficit Disorder - An overlooked condition in the elderly
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Attention Deficit (Hyperactivity) Disorder, AD(H)D, is a serious disorder of concentration that affects an estimated 4% to 8% of school-age children. The adult version of ADD/ADHD usually occurs in people who had ADD as children, with an estimated 67% of children with the disorder continuing to have symptoms as adults.
"Over-activity of the prefrontal cortex is the common denominator in all forms ofAD(H)D" Psychiatrist Daniel Amen reports that adults who come to his clinic suffering from ADD are typically concerned with poor performance caused by such concentration-related symptoms as difficulty sustaining
attention to reading or paperwork; tendency to being easily bored by tedious material; poor planning and organization; chronic procrastination; restlessness and non-phobic difficulty staying in confined spaces; difficulty listening carefully to directions; frequent lateness for work or appointments; and tendency to misplace things. They also frequently complain of difficulty thinking clearly, poor self-discipline, mood problems, anxiety, restlessness, drug abuse, temper problems, marital problems, insomnia, over impulsiveness and money problems. All of these problems in turn relate to their difficulty with sustaining attention and resisting distractions.l ADD and ADHD are caused by subtle dysfunctions of the frontal lobes and the pathways connecting them to other parts of the brain. Of all the structures in the brain, only the prefrontal cortex is embedded in such a richly networked pattern of neural pathways. Over-activity (and sometimes under-activity) of the
prefrontal cortex is the common denominator in all forms of AD(H)D. Adult sufferers of AD(H)D may benefit from counselling and behavioural skills (such as list-making, day planners and filing systems) as well as similar medication to that prescribed for children. Otherwise, antidepressants may be recommended. In some sufferers, the problem is related to food intolerance. This can be explored by the controlled elimination of certain elements of the diet (dairy products, wheat, corn, eggs, chocolate, artificial colours etc.). The more healthy the overall brain function is (especially frontal lobe function), the more effective and effortless concentration becomes. Thus, both AD(H)D sufferers and nonsufferers can improve their concentration abilities through optimising their brain function. Two popular supplements that provide a response to some of the changes in the brains of AD(H)D sufferers are Centrophenoxine and 5HTP.
Centrophenoxine is a powerful derivative of the aminoacid DMAE. Whilst it is known to enhance levels of acetylcholine (the neurotransmitter most affected in Alzheimer's disease), perhaps its most useful role it to remove the cells toxic accumulation of lipofuscin, (again, very often found in Alzheimer brains). This detoxification action cleanses the brain's cells of harmful 'debris' accumulation. The results tend to manifest themselves in improved memory, particularly speed of recall of detail. 5HTP (5-hydroxy-tryptophan) can help to alleviate many of the symptoms of AD(H)D by boosting levels of serotonin. Low serotonin levels are associated with irritability, aggression, impatience and anxiety, and significantly decreased levels in serotonin have been found in suicidal patients. Some patients that fail to respond to standard antidepressant drugs have found relief in 5HTP. Unlike other antidepressants, such as L-Tryptophan which has other roles throughout the body, 5HTP affects the brain only. Alzheimer's Disease - The most common cause of dementia Beginning with mild memory problems and leading to severe brain damage, Alzheimer's Disease (AD) affects the parts of the brain that control thought, memory and language.
Centrophenoxine increases the brain's use of glucose and improves brain energy levels. It removes lipofuscin build up in the brain, heart, lung and skin cells, and is vital for the efficient communication of a cell to transfer potassium and sodium across its membranes. It also removes the visible signs of excessive lipofuscin build up - age or liver spots.
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Although some cases occur in younger people, AD is almost entirely and age-related problem, with the number of AD sufferers doubling every 5 years beyond the age of 65. Approximately 10% of over-65s have AD, and nearly 50% of over-85s may have the disease. But it must be remembered that AD is a disease and not a normal part of aging. There are clear changes to the brains of people with AD. The hallmarks of the disease are abnormal clumps called neuritic plaques and tangled bundles of fibres called neurofibrillary tangles. In addition, there is a reduction both in the
number of nerve cells and the amount of the chemicals that carry messages back and forth between the nerve cells. By thwarting the passage of these messages in the brain, AD can disrupt normal thinking and memory processes. Failing memory is usually the first recognisable symptom. Sufferers may have trouble remembering recent events and names, and ask the same question repeatedly. As the disease progresses they may become disoriented and get lost in once familiar places. Even simple tasks, like brushing their teeth or combing their hair, may seem perplexing. Eventually, the brain damage caused by AD leads sufferers to becoming completely confused and requiring total care. Apart from Familial AD, a rare form occurring between the ages of 30 and 60 which can be inherited, scientists do not yet fully understand what causes AD. Current areas of investigation range from the sufferer's education to their diet, as well as the accumulation of heavy metals over time, in particular mercury. No treatment can stop AD. However, ensuring that the sufferer has a healthy diet, exercise, social
' I
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Improve concentration by increasing serotonin levels 5HTP is the direct precursor to serotonin, alleviating the harmful effects of worry and stress.
The benefits of 5HTP are the assistance of sleep and alleviation of age related mental depression. 5HTP is a v a i l a b l e in 60 x 5 0 m g capsules from only $16.99 Call: +44 208 123 2106 or order online: www.antiaging-systems.eu June/July 2006
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activities, regular medical care and a safe environment will assist in their well-being. The use of memory aids, such as calendars, lists and written instructions, can be helpful for people in the earlier stages of AD. In addition, there are several drugs that may help some people in the early and middle stages of the disease, including Memantine and Galantamine. Memantine is a novel new drug that blocks the accumulation of excitotoxins in the brain. It is believed that too many excitoxins can lead to brain dysfunction. What's worth noting is that there are a number of food substances that rapidly increase the presence of excitotoxins, including the artificial sweetener aspartame, the flavor enhancer MSG (monosodium glutamate), as well as hydrolysed products (found in soups and broths etc). Memantine has been proven to even be efficacious in the late stages of Alzheimer's disease, which has lead to a strong focus on the role of long-term nutrition and excitotoxins in the development of Alzheimer's disease. Galantamine inhibits the reduction of
Omega How pure is your Omega fish oil supplement? It is well known that EPA and DHA Omega 3 fatty acids such as those found in fish are very beneficial in reducing the risk of coronary heart disease. However many sources of fish are now contaminated with heavy metals and toxins. It is now becoming apparent that these toxins cause numerous long term health problems. Omega Pro formula is not only a high potency fish oil product suppling the omega-3 fats EPA and DHA., it is an ultra pure formula, certified to contain the lowest levels of common contaminants including lead, mercury, pesticides PCB's and dioxins Not only are the fish oils taken from Icelandic stocks (the waters least affected by industry), but Omega Pro is packaged in an oxygen free environment and contains a special antioxidant blend of rosemary extract, ascorbyl palmitate, and natural tocopherols to assure continued freshness. To order Omega Pro formula callj 866 800 4677 (USAToll-free) +44 208 123 2106 (Outside USA) or visit
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acetylcholine in the brain, and is reported to delay, or even reverse, mental decline in some patients with mild to moderate Alzheimer's disease. In the largest long-term study of its kind, 240 AD patients were treated with 24mg of Galantamine daily for 48 months. It was found that Galantamine treatment reduced cognitive deterioration by more than half.2
"low viscosity blood is the leading factor in the avoidance of a heart attack or stroke" Research is being done into reports that Ginkgo Biloba can delay or prevent dementia in older people. Research is also in progress into the hormone Estrogen. Although studies have shown that Estrogen does not prevent AD, some research suggests that it may help prevent the disease. Strokes - Sudden assaults on the brain A stroke occurs when the blood supply to the brain is abruptly stopped or diminished, the cells affected will be injured and may die, altering the function of that area of the brain. Although some cell injury is reversible, the death of brain cells is permanent, usually leaving lasting disability. The number of brain disorders due to strokes is huge, with over 6 million cases internationally each year. In the USA, strokes are the third-leading cause of death behind heart disease and cancer. There are three common reasons for a sudden reduction in blood supply to the brain: • Thrombosis - This causes approximately 60% of all strokes. It occurs when an artery in the brain or neck narrows due to the build-up of cholesterol and fatty deposits, eventually blocking completely. • Embolism - This causes approximately 20% of all strokes. It
occurs when an artery in the brain or neck becomes blocked by a clot or 'embolus'. This may be a blood clot formed elsewhere in the body (commonly in the heart) that travels to the brain, or small pieces of fatty deposits breaking off the inside wall of the arteries. Hemorrhage - This causes approximately 20% of all strokes. Here, an artery in the brain or on its surface, ruptures. A common reason for such a rupture would be an aneurysm (a thinner than normal area on an artery wall). Transient ischemic attacks (TIAs) are often referred to as a 'mini-strokes'. The symptoms of a TIA are shortlived, sometimes lasting an hour, occasionally for 24 hours. Prompt medical attention is still essential for a TIA as about 1 in 4 people who have a TIA go on to have a bigger stroke within five years. This followup stroke could be prevented if the TIA is detected and appropriately treated. The symptoms that follow a stroke depend on the area of the brain that has been affected and the amount of brain tissue damage. The most common symptoms of a stroke are: • Weakness or numbness in the face, arms or legs, especially on one side of the body • Confusion, or difficulty speaking or understanding speech • Vision problems • Dizziness, loss of balance and coordination • Severe headache Other key symptoms that are less common, are nausea, vomiting and momentary loss of consciousness. Should any of these symptoms be identified (in yourself or someone else), the immediate action should be to call an ambulance. Every second counts when the brain is deprived of oxygen. To encourage blood flow to the brain, the affected person should lie down horizontally. Treatment of stroke depends on the areas affected and the damage
done. 'Clot busting' drugs (as used for treating heart attacks) can be helpful in the early stages of strokes caused by blood clots. To pre-empt thrombotic strokes, anti-platelet drugs, such as aspirin, are used to prevent the clots from forming in the first place. One of the most important recent developments in the immediate treatment of strokes, is tPA (tissue plasminogen activator). This is a very powerful 'clot-buster' that is infused through the veins. If given within the first three hours after the onset of symptoms, tPA can significantly improve the patient's long term recovery prospects. There are also a number of supplements that can ward off the threat of strokes as well as providing other benefits for the brain.
individuals with high levels of C-reactive protein have up to 6 times the likelihood of a heart attack or strokes as individuals with lower levels.
seemingly
Vinpocetine is a vasodilator (improves brain blood flow) that can protect against brain arteriosclerosis, which if left unchecked, can lead to strokes. A study involving thirty stroke patients treated with Vinpocetine demonstrated a greater improvement in the condition of the Vinpocetine users compared with patients not taking the drug.3 Tackle mental disorders and rescue your brain!
Omega 3 fish oils have been shown to benefit blood thinning, and so has the Japanese plant nattokinase, (often abbreviated to natto), helping to improve smooth blood flow and attributed to being one of the factors why the Japanese are the longest lived race on the planet. A recent book, The Blood Thinner Cure, by Kenneth Kensey, M.D., a leading American cardiologist, attributes low viscosity blood (in other words thin and smooth flowing) as the leading factor in the avoidance of a heart attack or stroke. In other words as a single factor, keeping blood flowing through veins has higher importance than how hard those arteries are, or how much cholesterol or triglycerides or homocysteine they are carrying.
the potentially debilitating effects of these disorders. This combination of a healthy lifestyle plus the use of medical supplements when necessary means that we need not be helpless victims of these
Enzyme preparations, such as Wobenzym lower C-reactive protein levels (a marker of chronic infection in the body) on average by 30%. The latest research, published in the New England Journal of Medicine, has documented that
Unlike the gradual slowdown in the functioning of the brain discussed in the previous article in this series, mental disorders are seemingly indiscriminate, striking randomly without reason. However, as we've seen, numerous preventative treatments exist as well as a wide range of therapies that help overcome
indiscriminate attacks on the brain. Not only can we act to prevent the attack, we can take steps to rescue the brain after the attack has taken place. References: 1 D. G. Amen, (2001) Healing ADD 2 Schwalen S, Hammond G. (2003) 3 Feigin VL, Doronin BM, Popova TF et al. (2001)
Vinpocetine Vinpocetine is a vasodilator (improves brain blood flow) that, uniquely for this type of drug, affects only the areas that need to treating. This action has lead to Vinpocetine being used to improve hearing (particularly tinnitus), eyesight and even alleviate problems related to the menopause.
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Background Coenzyme QIO (CoQIO) is an essential component of the mitochondrial membrane. It is a critical electron transfer molecule that transports electrons from Complexes I and II to Complex III. This electron transfer is essential for the production of adenosine triphosphate (ATP). CoQIO is present as an antioxidant in mitochondria and cellular membranes where it inhibits lipid peroxidation. Mitochondria are concentrated in skeletal and heart muscle.
Heart A large body of evidence confirms that CoQIO is an effective adjunct in congestive heart failure , pediatric and adult cardiomyopathy, hypertension, and angina. The administration of CoQIO to people awaiting heart transplants improves their clinical symptoms and quality of life . Pretreatment with CoQIO improves the outcome of people undergoing cardiac surgery.
Statins A report by nutritionist Karen Kaufman
There is a synergy between CoQIO and some pharmaceutical drugs. Statin drugs
COENZYME QIO
deplete the body of CoQIO and this
Also
Since so many people are taking statins
known
as
U b i q u i n o n e
depletion may account for the most common adverse side effect of these drugs - muscle pain and dysfunction .
and CoQIO together, studies now show CoQIO improves statin toxicity. In addition, recent studies have shown
Our focus section takes a direct look at some of the
the co-administration of CoQIO with a statin improves endothelial function and
most important supplements available today. It is
heart disease through a mechanism
designed to be a straight-to-detail section for those
the statin drug.
who want to get to the core of its uses immediately.
Dementias
This issue focuses on CoQIO.
independent of the depletion of CoQIO by
Coenzyme QIO exerts its effect primarily as an antioxidant in the mitochondria and
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June/July 2006
cell membranes. There is ample evidence that mitochondrial dysfunction and
Often a patient with cancer cannot
oxidative damage play a key role in the
tolerate therapeutic doses of a
pathogenesis of neurodegenerative
chemotherapy drug because the result of
diseases such as Alzheimer's disease and
administering that dose of a
Parkinson's disease.
chemotherapeutic agent results in
Animal and in vitro studies have
that administering CoQIO with
CoQIO in neurodegenerative diseases
chemotherapy improves the quality of life
that are currently untreatable, i.e.
of the cancer patient as well as
Huntington's disease, ALS.
protecting the heart of patients who
use of CoQIO to slow the
"mitochondrial dysfunction and oxidative damage piay a key role in the pathogenesis of
neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease."
damage to the heart. Studies now show
suggested a possible beneficial role for
Researchers have been looking into the
1
prostate cancer cell line .
receive the chemotherapeutic drug
1
anthracyclines.
neurodegenerative decline that occurs in Parkinson's disease. The putative
Diabetes
mechanism of CoQIO's ability to slow this decline has been described , and the
Diabetes affects virtually every biological
actual ability of CoQIO to slow this decline
system and high levels of oxidants are
in people has been established in a
associated with both macro and micro
clinical trial .
complications of the disease. Research
It is therefore not surprising that CoQIO
has shown that CoQIO may improve the
would be a logical treatment for
endothelial dysfunction that occurs in
peripheral neuropathies.
diabetes in part by increasing the amount and the availability of nitric oxide. A
Gums
controlled trial showed that supplementation.
Not all the mechanisms of action of
CoQIO improved blood pressure and
CoQIO have been fully described, however
long term glycemic control in subjects with
a couple of studies provide strong
type 2 diabetes. Lastly, this nutrient with
indications that CoQIO plays a role in
such a wide array of activity has been
reducing inflammation. When a nutrient
shown to be an effective way to prevent
is a potent antioxidant in the mitochondria
migraine headaches.
and cell membranes, that nutrient will inevitably be useful in any disease where
Bioavailability
cells are rapidly dividing. One of the first studied beneficial effects of CoQIO is in periodontal disease .
CoQIO is absorbed from the small intestine into the lymphatics, and from there it enters the blood. One can
Cancer
increase the absorption by taking it with food, particular foods with a high lipid
Another condition in which cells divide
content.
rapidly is cancer and there are reports of favorable effects of coenzyme Q10 in
Dosages
breast cancer, both regression of tumours and regression of metastases. In a mouse model of breast cancer, researchers found co-administration of
30 mgs to 60 mgs per day for antiaging. 90 mgs to 120 mgs per day for heart health.
tamoxifen and coenzyme Q10 improved
300 mgs per day for breast cancer.
the efficacy of the tamoxifen treatment.
1200 mgs per day for Parkinson's
An in vitro study demonstrated supplementation with coenzyme Q10 significantly lowered cell growth of the
disease.
Conclusion: CoQIO's primary actions Improves congestive heart failure. Treatment for cardiomyopathy. Alleviates angina pectoris. Improves hypertension. Protects against statin toxicity. Protects heart from damage due to chemotherapy. Putative role in neurodegenerative diseases particularly Parkinson's disease. Reduces endothelial inflammation. Improves insulin resistance in type II diabetes. Alleviates skeletal muscle fatigue. Improves periodontal disease. May prevent breast cancer recurrence and metastases. Prevents migraines.
June/July 2006
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transplantation: a randomized, placebocontrolled study. Clin Cardiol. 2004; 27(5):295-9 1. Lakomkin VL, Konovalova GG, Kalenikova 9. Rosentfeldt F, Marasco S, Lyon W, et al. El, et al. Changes in antioxidant status of Coenzyme Q I O therapy before cardiac myocardium during oxidative stress under surgery improves mitochondrial function and the influence of coenzyme Q I O . in vitro contractility of myocardial tissue. J Biochemistry (MOsc). 2005; 70(l):79-84 Thorac Cardiovasc Surg. 2005;129(l):25-32 2. Weant KA, Smith KM. The role of 10. Rundek T, Naini A, Sacco R, et al. C o e n z y m e Q I O in heart failure. Ann Atorvastatin decreases the coenzyme Q I O Pharmacother. 2005; [Epub ahead of print] level in the blood of patients at risk for 3. Bhagavan HN, Chopra RK. Potential role cardiovascular disease and stroke. Arch of ubiquinone (coenzyme Q I O ) in pediatric Neurol. 2004; 61(6):889-92 cardiomyopathy. Clin Nutr. 2005l24(3):331-8 11. Baker SK. Molecular clues into the 4. Fosslien E. Review: Mitochondrial pathogenesis of statin-mediated muscle medicine - cardiomyopathy caused by toxicity. Muscle Nerve. 2005;31(5):572-80 defective oxidative phosporylation. Ann Clin 12. Silver MA, Langsjoen PH, Szabo S, et al. Lab Sci. 2003;33(4):371-95 Effect of atorvastatin on left ventricular 5.Rosenfeldt F, Hilton D, Pepe S, Krum H. diastolic function and ability of coenzyme Systematic review of effect of coenzyme Q I O to reverse that dysfunction. Am J Q I O in physical exercise, hypertension and Cardiol. 2004; 94(10):1306-10 heart failure. Biofactors. 2003:18(1-4)9113. Strey CH, Young JM, Molyneux SL, et al. 100 Endothelium-ameliorating effects of statin 6. Tran MT, Mitchell TM, Kennedy DT, Giles therapy and coenzyme Q I O reductions in JT. Role of coenzyme Q I O in chronic heart chronic heart failure. Atherosclerosis. 2005; failure, angina, and hypertension, 179(1)201-6 pharmacotherapy. 2001; 21(7):797-806 14. Chapidze G, Kapanadze S, Dolidze N, et 7. Kamikawa T, Kobayashi A, Yamashita T, al. Prevention of coronary atherosclerosis by Hayashi H, Vamazaki N. Effects of coenzyme the use of combination therapy with Q I O on exercise tolerance in chronic stable antioxidant coenzyme Q I O and statins. angina pectoris. Am J Cardiol. Georgian Med News. 2005;( 1)20-5 1985;56(4):247-51 15. Kuettner A, Pieper A, Koch J, et al. 8. Berman M, Erman A, Ben-Gal T, et al. Influence of coenzyme Q I O and cerivastatin Coenzyme Q I O in patients with end-stage on the flow-mediated vasodilation of the heart failure awaiting cardiac brachial artery: results of the ENDOTACT study 16. Beal MF. Mitochondrial dysfunction and oxidative damage in Alzheimer's and Parkinson's diseases and CoQ 10 is an essential part of the mitochondrial coenzyme Q I O as a system that converts the food we eat into ATP potential treatment. the body's energy currency. CoQ 10 is found in J Bioenerg every cell in the body. CoQ 10 is a powerful natural Biomembr. 2004; antioxidant, which means that it protects us from 36(4):381-6 harmful free radicals. 17. Zeron MM, Fernandes HB, C o Q 10 is also one of Krebs C, et al. many substances in the Potentiation of body that tend to decline as NMDA receptorpeople age or develop certain mediated diseases. It is one of the most excitotoxicity linked important natural energy molecules with intrinsic cited as being of great importance in heart apoptotic pathway health. It helps the body support normal in YAC transgenic ^cholesterol levels and keeps your heart mouse model of jergized. Huntington's disease. Mol Cell As we get older, our body'e produce less Neurosci. CoQ 10 and so taking a supplement can help to maintain our vitality. 2004;25(3):469-79 18. Shults CW. This optimal health supplement comes in Coenzyme Q I O in 120 x 30mg capsulesfromjust 529.99 neurodegenerative diseases. Curr Med To order call Chem. 2003; 10(19): 1917-21 19. Shults CW, www.antiaging-systems.eu
References
Co-enzyme ENERGY FOR
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Oakes D, Kieburtz K, et al. Effects of coenzyme Q I O in early Parkinson's disease: evidence of slowing of the functional decline. Arch Neurol. 2002;59( 10): 1541-50 20. Saifi GM, Szigeti K, Snipes GJ, et al. Molecular mechanisms, diagnosis, and rational approaches to management of and therapy for Charcot-Marie-Tooth disease and related peripheral neuropathies. J Investig Med. 2003; 51(5)261-83 21. Wang XL, Rainwater DL, Mahaney MC, et al. Cosupplementation with vitamin E and coenzyme Q I O reduces circulating markers of inflammation in baboons. Am J Clin Nutr. 2004; 80(3):649-55 22. Koller WC, Cersosimo MG. Neuroprotection in Parkinson's disease: an elusive goal. Curr Neurol Neurosci Rep. 2004; 4(4):277-83 23. Iwamoto Y, Nakamura R, Folkers K, Morrison RF. Study of periodontal disease and coenzyme Q. Res Commun Chem Pathol Pharmacol. 1975; 11(2):265-71 24. Lockwood K, Moesgaard S, Folkers K. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q I O . Biochem Biophys Res Commun. 1994; 199(3):1504-8 25. Lockwood K, Moesgaard S, Yamamoto T, et al. Progress on therapy of breast cancer with vitamin Q I O and the regression of metastases. Biochem Biophys Res Commun. 1995;212(l):172-7 26. Perumal SS, Shanthi P, Sachdanandam P. Combined efficacy of tamoxifen and coenzyme Q I O on the status of lipid peroxidation and antioxidants in DMBA induced breast cancer. Mol Cell Biochem. 2005: 273(l-2):151-60 27. Quiles JL, Farquharson AJ, RamirezTortosa MC, et al. Coenzyme Q I O differentially modulates phospholipid hydroperoxide glutathione peroxidase gene expression and free radicals production in malignant and non-malignant prostate cells. Biofactors. 2003; 18(l-4):265-70 28. Roffe L, Schmidt K, Ernst E. Efficacy of coenzyme Q I O for improve tolerability of cancer treatments:a systematic review. J Clin Oncol. 2004; 22(22):4418-24 29. van Dalen EC, Caron HN, Dickinson HO, et al. Cardioprotective interventions for cancer patients receiving anthracyclines. Cochrane Database Syst Rev. 2005;(1):CD003917 30. Chew GT, Watts GF. Coenzyme Q I O and diabetic endotheliopathy: oxidative stress and the 'recoupling hypothesis'. QJM. 2004; 97(8):537-48 31. Hodgson JM, Watts GF, Playford DA, et al. Coenzyme Q I O improves blood pressure and glycaemic control: a controlled trial in subjects with type 2 diabetes. Eur J Clin Nutri. 2002; 56(ll):1137-42 32. Sandor PS, Di Clemente L, Coppola G, et al. Efficacy of coenzyme Q I O in migraine prophylaxis: a randomized controlled trial. Neurology. 2005; 64(4):713-5
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