I N T E R N A T I O N A L

ANTI

April/May 2006 Volume 6 Issue 2

$6.50 USA £3.50 UK

€5.30 Europe

Are You Concentrating? Improve your mind

plus

T h e Need For Antiaging Medicine Why Preventative medicine is a must

T h e Oldest Smart Drug T h e continuing benefits of Pyritinol

Inhibit Your AGE Prevent your cross - linking

BEC5 Cream Su Real people di they reversed

interview

Eat Yourself Fit We taljt t tionist Karen Kaufman about

weight loss

i

c u t t i n g - e d g e i n f o r m a t i o n t o i m p r o v e y o u r o p t i m a l h e a l t h s p a n

European Congress on Anti-Aging and Preventative Medicine

Dear colleagues

A new Europe is being formed, resulting in fresh cultural, societal and scientific-perspectives. Europe is becoming strongly integrative while assuming a new role on the world stage. Vienna at the very heart of this expending Europe offers all conference participants a sophisticated overview of State-of the-Art anti aging research, a distinguished panel of speakers and a superb social programme with a strong cultural emphasis. W e want to show you why Vienna enjoys a reputation as central Europe's prime conference address. Its role in historical anti-aging science, its significance as the founding city of ESAAM, its scientific energies and its unparalleled chic beauty combine to make an outstanding confer-ence experience. Amongst Vienna's roll-call of artists, scientists and thinkers, 2006 also sees major anniversaries of Sigmund Freud and W.A. Mozart, part of a superb social programme. Welcome to Vienna, welcome to the heart of Europe.

Hofburg Congress Centre - Vienna - Austria October 18th - 21st 2006

Congress Office Tra\ el Agency: AUSTROPAINTERCONVENTION Verkehrsburo Group Mrs. Kristin Volmer Friedrichsrrasse 7 A 1010 Vienna Austria Tel: +43 i 588 00 518 Fax: +43 I 588 00 520 I Mail: antiaging200661interconvention.at v\ \vv\ .antiaging \ i enna2006 .a t

i a m April/May 2006

welcome All too often some people react incorrectly when they hear the term "antiaging medicine." Some think they are too young for it, others too old! The reality is that antiaging is for everyone who has reached adulthood.

The concept of an "old" person being an incapable one is changing fast. Today, people in their 60's and well beyond that are literally climbing mountains, pushing themselves both physically and mentally to levels that were unheard of just a few decades ago.

But much more can be done, the future will be full of "old" people (by today's standards), however they will be lucid and agile, fully supportive and contributing to the community, enriching society with their vast range of experience and skills.

Yet some think that dying young is the only way the planet can survive! They

point out that over population will lead to disaster and that as "mainstream" medicine can't afford comprehensive health-care at today's prices and numbers of people, how could it possibly manage in such a future?

The answers to such derisory questions are featured in this magazine. When you begin to comprehend the hurdles that we face and the position we are currently in, then the choices are few. Any sane individual can understand that preventative medicine, as a life long holistic health program- is the only sensible choice.

I hope that after reading this issue of the Antiaging Magazine with the facts and figures we place before you, will allow you to understand more clearly why we believe that there is a real need for antiaging medicine.

Phil Micans Editor-in-chief

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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.

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 correct 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.

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

advisors The Internat ional Ant iag ing Magaz ine is proud to be regular ly

contr ibuted, a ided and suppor ted by the fo l lowing leading professionals:

Mircea Dumitru, 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.

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.

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 member of the British Longevity Society.

Robert Mason. Ph.D. was schooled in information technology and realized the potential for research in the (then) coming information revolution. The result was the formation of an organization conducting global medical database research.

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 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 expenmental 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-in-Chief of the journal Archives of Gerontology and Geriatrics.

Listed alphabetically by last name

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 tor Women, and GHB: The Natural

Mood Enhancer.

April/May 2006 i a m I 3

Advertisement Feature

Detox naturally - and remove unwanted heavy metals > Optimal Health can only be achieved once toxins have been removed - the simplest, effective method is oral chelation

The principle behind chelation is simply that of

binding metals - the word chelation came from the Greek word 'chele' which means claw, as in a lobster claw. The idea being that when the chelating or metal binding agent is introduced into the body, it would have a particular attraction or affinity to those toxic metals that otherwise may remain trapped in your body for years and possibility most of your life.

No one chelating agent can remove all toxic metals from our body. There are different chelating agents that may have better affinity for certain metals i.e., mercury, lead, cadmium etc. such as EDTA (4 molecules found in vinegar), malic acid (found in apples), selenium (found in walnuts) succinic acid and allicin (found in garlic).

You can now use the science of natural biochemistry to protect your health. The regular oral use of the these substances can

help clean your body

of

numerous toxic burdens.

EDTA

EDTA is one of, if not the prime chelator used today. It has a very strong affinity for removing lead. EDTA has also been shown to remove iron, cadmium, aluminium, and even mercury.

Garlic

The main active ingredient in garlic is allicin. It is widely known that garlic can chelate heavy metals, particularly lead and mercury. It also helps to protect blood cells against high levels of lead.

Selenium

Selenium is a trace element that binds to mercury and effectively deactivates it. It is also a potent antioxidant and helps the body to use vitamin E.

Succinic acid

Succinic acid or DMSA (Dimercptosuccinic acid) is noted as being one of the most potent chelators of mercury and cadmium. It is often used prior to an i.v. chelation therapy in more acute cases.

Others

V

There are a number of other substances proven to be effective chelators. One is malic acid which is

found in apples and chelates aluminium and iron.

We all do what we can to avoid toxins, but ultimately, none of us can completely avoid them. As heavy metals accumulate and deposit themselves in our membranes and bones, it is up to us to do what we can through chelation to reduce these burdens.

Detox using oral chelation should be the first phase of attack in the fight for optimal health.

Specialist oral supplements are now available, specially designed to chelate heavy metals from the body and detox naturally.

YOUR QUESTIONS ANSWERED

What are the best chelation products available?

Dr. Garry Gordon is considered by many to be the world's leading expert on oral chelation and has formulated some specialist products. Dr. Gordon's two core chelation products are called Essential Daily Defense and Heavy Detox.

What does a 3-capsule daily supply of Essential Daily Defense supply?

Niacin 20 mg Vitamin B-6 20 mg Garlic (organic Allicin) 800 mg Calcium Disodium

EDTA 400 mg MSM 100 mg Malic Acid 25 mg Betaine HCL 50 mg Carrageenan (Red Algae) 600 mg Papain 100 mg Silica 40 mg Red Yeast 100 mg dl-Methionine 50 mg Beta-Sitosterol 100 mg Crataegus 6 (Hawthorne Berry) 5

mg

What does 1-capsule of Heavy Detox supply?

Succinic Acid 65 mg D-Glucuronolactone 250 mg Selenium 100 meg

How much are Essential Daily Defense and Heavy Detox?

Essential Daily Defense is available from IAS for $24.95 for 100 capsules (plus S&H).

Heavy Detox is available from $48.95 for 45 capsules (plus S&H).

Where can I buy all these chelation products?

These and other forms of detox agents are available from IAS

International Ant iaging Systems

fi-J-Tlhjl Q Jlly OefeK*

www.antiaging-systems.com

Call: 1 800 866 4677 (toll-free in USA)

Rest of the wor ld call +44 208 123 2106

4 i a m A p r i l / M a y 2 0 0 6

This article presents facts and figures from the world's governments and regulatory bodies illustrating the changing make up of our societies. As the baby boomer generation reach their 50's and 60's, they are set to change the face of health and medicine. Conventional medicine is too costly and too immobile to cope with a "top heavy" population model. Antiaging/ preventative medicine offers a real alternative solution, as the holistic and versatile for the new century. d

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BEC5 cream success stories As we produce our articles and editorials we are aware that they should feature the clinical references, but we also know that people do like to read about people! In this contribution, you can read real people's comments on how they reversed their skin cancers with the remarkable BEC5 skin cream.

Pyritinol: The Oldest Smart Drug We shouldn't believe that because something is old that it is of no use, or for that matter has even been surpassed yet! So we thought we would remind you of one of the first smart drugs to be developed. Pyritinol is a vitamin B6 derivative that has been shown not only to improve brain energy and memory, but also to enhance the activity of the immune system.

Inhibit Your AGE One of the major theories of aging is associated with proteins cross-linking or glycosylation. This process creates "harder" and more impervious membranes and cells creating molecules known as: Advanced Glycated End products or AGEs. In this article you can learn more about AGE itself and the products and protocols that can slow and even reverse their impact.

regulars

news P12

, letters

interview

classifieds

Attention deficit disorder (or ADHD) is a virtual plague, affecting not only millions of adults, but millions of children too. This article is the first of 3 to feature the numerous proven techniques that can be used to enhance concentration and improve vigilance and awareness.

V V • • • • • • M • I B • • • • • • • • • a s s e s s - - M i

contents P 6 Are you conce

April/May 2006 i a m 5

Are you

Concentrating? The deterioration of concentration

'Concentration' is the ability to sustain focused attention on a given object. In fact, you are concentrating right now, as you read these words (lets see if you can make it right to the end!).

Concentration can be external - such as relating to other people, driving a car or eating your lunch - or internal - such as thoughts, feelings or sensations. Although animals can concentrate to some extent (a lion, for example, focusing on its chosen prey), only humans can concentrate on

"It Is lileely that w.p to a

third of adults w i l l

experience a gradual decline

I n their m e n t a l capabilities, as they get older"

things that do not yet exist (such as a building that exists only in the mind of its architect), or on such abstract notions as 'infinity', 'justice' or 'eternity'.

Paradoxically, the power of concentration also involves the ability to pay no attention to irrelevant distractions. These are things that can intrude on your concentration to divert or disrupt the sustained, focused attention. Like concentration itself, these intrusions can be divided into external and internal distractions.

External distractions relate to the physical environment: Noise, interruptions from other people, television, work responsibilities... Once identified, these distractions are often easy to deal with. Internal

distractions relate to your body, your thoughts and your emotions: Hunger, tiredness, illness, boredom, stress, daydreaming... Some of these can be easily dealt with once they are identified. Others require practice and/or additional help before they can be managed.

The reasons behind continuing poor concentration - that is, when it feels like a permanent, irreversible condition - are either related to some form of brain impairment (due to an impact or disease) or to a number of age-related changes that take place in the brain. This article will focus on the latter of these causes, the gradual deterioration of concentration and general mental dexterity with age.

The causes of age-related mental decline

As most people age they will experience symptoms of mental deterioration, such as short-term memory loss and difficulties learning new information. Aside from the various forms of age-related dementia, it is likely that up to a third of adults will experience a gradual decline in their mental capabilities as they get older. This, while not interfering with everyday life, is sufficient to impair concentration and memory.

This decline is due to many factors that accumulate over the years, contributing to damaging changes in our brains as we get older:

Diet - Clinical tests demonstrate that diets with a high fat intake produce

i n the f i r s t of three articles, on overcoming age-related

m e n t a l decline, we look, at the power of concentration,

a n d Wow to m a i n t a i n It Into

old age.

6 i a m April/May 2006

significantly higher risks of mental

deterioration. The same has been

found for a diet high in saturated fat

and cholesterol. Fish, on the other

hand, was found to produce a much

lower risk of mental decline.1

Free radicals - These are unstable

molecules that are prone to react with

other molecules in a damaging

process known as oxidation. Areas of

the body with high energy output,

such as the brain, are particularly

vulnerable to damage from free

radicals. Animal studies have

suggested that diets high in

antioxidants (including, for example,

superoxide dismutase and glutathione

peroxidase, as well as vitamins C and

E) can delay age-related memory loss.

4

Stress -Studies have shown that

stress, both everyday stress and

major traumatic stress, causing a rise

in the stress hormone epinephrine

leads to mild cognitive impairment

compared with those possessing

normal levels of epinephrine.2

Vascular disease - Cerebrovascular

disease occurs in the arteries that

pass blood to the brain. The result is

a reduced rate of blood flow which in

turn causes nerve cells in the brain to

die prematurely. This was

demonstrated in a study of 400

"Arms, o f t h e b o d y w i t h h i g h e^vergy o u t p u t , s u c h a s t h e brcdiA-, a r e p a r t i c u l a r l y v/uli/verable t o d a m a g e f r o m , f r e e r a d i c a l s "

middle-to-old aged men, which

revealed that vascular risk factors,

such as excessive alcohol intake and

higher than normal homocysteine

levels, are associated with reduced

mental processing capacity and

information processing speed. 3

April/May 2006 i a m 7

Inflammation - A number of studies have found a clear link between inflammation and cognitive impairment. One study, for instance, of 2632 elderly participants found that those suffering from metabolic syndrome (a group of symptoms including high blood pressure, high insulin levels, obesity and abnormal blood lipid levels) as well as high inflammation levels were more likely to experience cognitive impairment than those suffering from neither. Those with metabolic syndrome and low inflammation, however, were found not to be at increased risk of mild cognitive impairment. That is, it appears that the level of

"All of these health tssw.es bring about changes to the brain that are associated with a lessening of mental capacity.'

Modafinil & Adrafinil are class-leading eugeroic drugs that reinvented

stimulatory alertness for millions of people around the world.

These are remarkable products that offer stimulation without affecting sleep. They increase mental & physical alertness and concentration, reducing the desire to nap (sleep), and yet at the same time display no addictive or "coming-down" side effects.

For further details about Modafmil & Adrafinil

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inflammation was the decisive factor. 5

All of these health issues bring about changes to the brain that are associated with a lessening of mental capacity. A crucial consequence is the decrease in the number of neurotransmitters in the brain, such as serotonin and acetylcholine. In addition, the number of nerve impulses and nerve cells will also reduce, and the quantity of blood passing through the brain will diminish. This is particularly important as the oxygen and nutrients that are required for the brain to function correctly are carried into the brain by the blood.

Fortunately, many of the problems associated with memory loss and other neurological disturbances are correctable. However, too often in the past, physicians have viewed these detrimental changes to the brain as

an inevitable consequence of aging. Indeed, conventional medicine has had little to offer people who visit their physician describing a small decline in their memory or mental abilities. Recent

developments, however, have uncovered a number of possible causes behind 'age-related' mental decline and identified therapies to enable people to confront it.

How can I have increased alertness

& concentration, without the usual

'highs & lows' from stimulants that

disrupt my normal sleep pattern?

'too oftew i n the past, physicians have viewed these detrimental c h a f e s to the brain as an inevitable oo^sequeM'e of aging."

i a m April/May 2006

What can be done about it?

The best way to maintain a healthy, active brain is to maintain a healthy, active body. This means plenty of exercise, a balanced diet and a good night's sleep.

On top of this, there are a number of supplements that can compensate, at least partially, for the causes of age-related mental decline that I've mentioned. In general these supplements fall into one of three categories: brain stimulants, nerve cell enhancers and blood flow promoters. There are often secondary benefits, however, that cross the category

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boundaries. The following examples of supplements indicate some of the more popular choices from each of the categories.

Brain stimulants

Adrafinil and Modafinil are the sole members of a new class of drugs called Eugeroics, which literally translates as 'good arousal'. Adrafinil is designed to bring about increased levels of vigilance and alertness, while Modafinil is a psychostimulant used to improve memory and brighten moods. The basis of Eugeroics' uniqueness lies in their ability to stimulate only when stimulation is required, unlike most other 'brain wakening' drugs.

Adrafinil and Modafinil selectively stimulate adrenergic receptors in the brain that normally respond to norepinephrine (noradrenaline), a neurotransmitter linked to alertness,

April/May 2006 i a m 9

" i i a c r e a s e d m a o levels m-ay be associated with age-related iA.ewr0n,fll d e t e r i o r a t i o n a n d

Parkinson's disease. " learning, and memory. This highly focused activity profile may account for Adrafinil and Modafinil's relative lack of adverse side effects compared to conventional stimulants which have a much broader spectrum of activity. Unlike these other stimulants, there are no 'highs and lows'; minimal anxiety, agitation and insomnia; sleep patterns remain unaffected; and they are non-addictive.

Nerve cell enhancers

Deprenyl is a potent neuro-protector and a selective MAO-B inhibitor. MAO-A and MAO-B are the primary enzymes responsible for degrading

neurotransmitters in the central nervous system and peripheral tissues. Increased MAO levels may be associated with age-related neuronal deterioration and Parkinson's disease.

Although Parkinson's disease remains the only FDA approved indication for Deprenyl in the USA, with a number of ongoing clinical studies evaluating its efficacy in Alzheimer's disease, anecdotal reports from both physicians and patients refer to dramatic improvements in an impressive range of diseases.

Centrophenoxine rejuvenates nerve cells by reducing their levels of lipofuscin. Lipofuscin is the name given to the biochemical clutter that accumulates in the body's cells over time. The more lipofuscin a cell accumulates, the less functional it becomes. In aged animals, levels of

lipofuscin can reach up to 30% of cell volume.

Numerous animal experiments measuring memory and learning abilities have demonstated how aged animals with their lipofuscin levels reduced by Centrophenoxine have their memory and learning abilities restored to a level similar to that of a healthy young animal.

Blood flow promoters

Hydergine has been known of since the 1940s. It stimulates blood flow to the brain, increasing the delivery of oxygen and relieving symptoms of deteriorating mental activity. This was demonstrated in an experiment where two groups of cats were anaesthetized and their brains electronically monitored. The blood supply to all the cats' brains was reduced (and therefore the oxygen supply). The cats in the 'no Hydergine' group had brain damage within 5 minutes and died within 15 minutes. However, the cats in the 'Hydergine treated' group had strong brain wave patterns up to 45 minutes later.

Nicergoline has alpha-adrenolytic action which activates the brain's metabolism and improves arterial flow, lowers vascular resistance and improves the use of glucose and oxygen. Currently used in the battle to treat senile dementia, Nicergoline has been found to improve mental agility through enhancing perception and vigilance. In this way it differs from the effects of Hydergine (to which it is chemically similar). That is, Hydergine extends the period of useful mental workload, and has been designated as an IQ booster, whereas Nicergoline appears to enhance clarity, perception and vigilance.

Xanthinol Nicotinate (XN) is a form of Niacin (vitamin B3) that passes easily through cell membranes. It is the most potent form of Niacin available. XN has been shown to increase brain glucose metabolism and boost brain ATP levels as well as improve brain blood flow. As such, XN has been used to treat insufficient blood flow to the arteries and the extremities, short-term memory disorders and lack of brain energy

Make a difference to mood, memory and life enhancement...

for less than 50 cents per day

Deprenyl (selegiline) has long been approved for use in Parkinson's disease, but the work of Professor Knoll and others shows that regular low dose use of deprenyl can J i aid in the general protection®!' age related memory g j decline, supporting libido function and increasing well f t being.

Just a few milligrams a day can make a difference M to mood, memory and life enhancement.

The liquid is ideally supportive for low dose use because 1 drop = 1 mg.

Furthermore its cost effectiveness means that most individuals pay less than 50 cents per day.

We offer Deprenyl in both a 1 liquid, and a 50 x 5mg tablet format.

Further details available at: www.antiaging-systems.com/a2;

Call: (USA) 1 415 992 "5563" Outside USA +44 208 123*2106

Restrictions on its sale/ delivery may app||fp some countries.

10 i a m April/May 2006

that compromises vigilance, concentration and attention. Furthermore, XN has been clinically shown to improve the reaction speed of the elderly.

Picamilone is a chemical derived from gamma-amino-butyric acid (GABA) and nicotinic acid. It rapidly crosses the blood-brain barrier to increase the rate of intracranial and cortex blood circulation. Picamilone has been cited as a better vasodilator than either Hydergine or Vinpocetine. Studies carried out in Russia have shown that patients with mild to moderate memory impairment and emotional, hearing and speech difficulties, noticeably improved after taking a course of Picamilone.

Aging is all in the mind

Your brain is the most intricate part of your body. Which is not surprising, as it controls virtually every metabolic function required to keep you alive. Held within the compact and remarkable structure of the brain are several thousand miles of interconnected nerve cells which control not only every movement, but every thought, sensation and emotion that make us what we are.

Just a few years ago, doctors and scientists assumed that the process of age-related cognitive decline was unavoidable and unstoppable. They believed that the number of neurotransmitters would decrease, the quantity of nerve impulses and nerve cells would go down, and the amount of oxygen reaching the brain would dwindle. Now, however, opinions have changed and it is generally accepted that mental decline is no longer an inevitable consequence of aging.

The same lifestyle factors that

"it is general ly accepted that \M£\Atal decline is ko l o v u ^ e r a i t i i / u e v i t a b l e

co\A,s,ec\y.e\^ce of agu/vg."

govern physical health can also help to preserve mental health. By identifying areas of risk now, such as in your diet and lifestyle, you may be able to stave off any serious mental decline in the future. And, thanks to the rejuvenating powers of supplements, only some of which have been mentioned in this article, it may be possible to pre-empt mental decline and maintain youthful mental agility for the rest of your life.

If you're still reading this article then your concentration can't be too bad. But remember, prevention is better than cure. It's never to late, or too early, to get a better brain!

In the following articles in this series, I will discuss specific mental difficulties, such as Attention Deficit Disorder and Alzheimer's Disease, and how supplements can help to overcome them. Then, in the third and final article, I will focus on 'smart drugs' and how they can be used to turbocharge the mind!

References:

1 Solfrizzi V et al 2005; Solfrizzi V et

al 2003; Solfrizzi V et al 1999;

Panza F et al 2004; Capurso A et al

2000. 2 Karlamangla AS et al 2005.

3 Aleman A et al 2005. 4 Joseph JA

et a I 1998; Perrig WJ et al 1997. 5

Yaffe K et al 1998.

For details on how to advertise in the International Antiaging

Magazine, email your media pack request to: advertising@antiaging-

magazine.com

BRAIN F O O D TO I M P R O V E M E M O R Y

& I N C R E A S E LUCIDITY

P h o s p h a t i d l y s e r i n e

This nutrient enhances the function of Nerve Growth Factor and increases production of the brain neurotransmitter acetylcholine (most affected in Alzheimer's disease).

• Enhances brain glucose • Prevents brain dendrite

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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.

addition to my smart-nutrient regime. H.C, Washington

For more information about this unique brain enhancer go to: www.antiaging-systems.com

Call: (USA toll-free) 866 800 4677

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60 x 250mg capsules

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April/May 2006 « a m 11

in the news calendar of events Memantine effective in Alzheimer's disease over long term

Memantine is safe and effective in the long term, according to an open-label 24-week extension of a 28-week, randomised, double-blind trial in patients with moderate to serve Alzheimer's disease. Patients taking placebo in the initial trail were switched to Memantine for the 24-week extension, and the authors saw significant benefit for these patients relative to the rate of decline experienced while on placebo (using the same efficacy measures). Patients switched to active treatment did not completely catch up with the patients who continued taking Memantine throughout the whole trail. The study is published in the Archives of Neurology (2006; 63:49).

Switch to aromatase inhibitor improves survival

Replacing Tamoxifen with Anastrozole (Arimidex) improves survival of patients with early breast cancer compared with continuing on Tamoxifen for five years, according to results from the first study to show a survival benefit of changing hormonal therapy. The meta-analysis of three trials with similar design included 4,600 women with hormone-sensitive early breast cancer who were randomised to switch to Anastrozole after two to three years of Tamoxifen or to remain on Tamoxifen for five years. The results showed that women changing to an Anastrozole gained a 29 percent improvement in survival compared with those remaining on Tamoxifen. The risk of diseases recurrence was reduced by 45 percent and risk of distant recurrence fell by 39 percent. Reporting the findings at the San Antonio breast cancer symposium last week, Walter Jonat, of the University Of Kiel, Germany, said: "Results from previous study showed that survival is improved if patients start treatment with an aromatase inhibitor rather than Tamoxifen. This meta-analysis shows that survival is

also increased if patients already on Tamoxifen are switched to anastrozole." Geoff Saunders, Macmillan cancer network pharmacist for Greater Manchester commented: "These findings are encouraging us towards using aromatase inhibitors at an earlier stage in the treatment of breast cancer. The evidence indicates that's we should start women with early breast cancer with an aromatase inhibitor at diagnosis. Those already on Tamoxifen should be switched early, rather than remaining on Tamoxifen foe five years."

Could health professionals be recommending the wrong sun protection message?

It has been suggested that the so-called Sunsmart campaign, which encourages people to "always cover up" is killing more people than it is saving! This is due to the association between vitamin D deficiency and various diseases, in particular various types of cancer. According to Oliver Gillie, author of; "sunlight robbery" the Sunsmart programs should be abandoned. Dr. Gillie said that the advice aims to try to prevent skin cancer, but that the evidence now indicates that skin cancer is associated with sunburn rather than normal exposure to the sun. Instead, Dr. Gillie proposes a new policy, which he calls "Sunsafe" this recommends: • To sunbathe without burning, everyday if possible. • The middle of the day (in the UK) being a good time for sunbathing. Brian Diffey, Professor of medical physics, University of Newcastle thinks that it is irresponsible to expose ourselves randomly to ultraviolet and suggests that vitamin D deficiency could be addressed through supplements. He stated: "It may not be reasonable to expect people to modify their lifestyle to get more sun exposure. We live in a time-poor society and on average spend only 14 minutes a day outside."

MAY 2006 Date: May 3-6, 2006 Name: 3rd International Conference on Antiaging and Longevity Medicine Place: Acapulco, Mexico Contact: www.med-estetica.com

JUNE 2006 Date: June 16-18, 2006 Name: 1st International Anti-Aging Symposium Place: Tokyo, Japan Contact: www.imagina.jp/aiset/english

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 Anti-Aging 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. longevity-international.com

Date: October 5-8, 2006 Name: Antiaging and Integrative Medicine Place: Geneva, Switzerland Contact: www.saaam.org

DECEMBER 2006 Date: December 7-10, 2006 Name: International Anti-Aging Congress Place: Las Vegas, Nevada, USA Contact: www.worldhealth.net

If you organize or attend an event that you think will be of interest to our readers please contact: editor@antiaging-magazine.com

i a m April/May 2006

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It's generally known that the average life expectancy is getter longer, increasing

year on year, figure illustrates the life expectancy for the USA from 1900 to 2050 and similar trends can be presented for all the developed and indeed developing countries.

Presently, the average 65-year old in the developed world can expect to live to be 79 and the average woman can expect to live to be 82. The changes taking place can be exacerbated when you realise that a child born in 1997 can expect to live 29-years longer than one born in 1900, representing a 60% increase.

Yet this could just be a "drop in the bucket" compared to what some scientists believe is already possible. Many believe that today's existing knowledge about the human biological system and the technology that is already available, will mean that many more people will be able to regularly live beyond 100, perhaps even regularly beyond 120 and who knows where. For the theory is- that the longer you live, the more chance you have to expose yourself to new technologies that can further extend lifespan.

Naturally none of this is worthwhile, unless we are also

iFigure 1

1900 1910 1920 1930 1940 1950 1960 1970 1930 1990 2000 2010 2020 2 0 M 2040 2050

enhancing or maintaining a good standard of health, thus improving the optimal health span as well as the life span.

April/May 2006 i a m 13

"extending life span based upon the costs and impracticalities of the current standard healthcare system, is unlikely to be feasible" Simply extending life span based upon the costs and impracticalities of the current standard healthcare system, is unlikely to be feasible.

The life span of the baby boomers

Not only is the average life-span becoming much longer, (thus increasing the numbers of elderly individuals in the population), but we are also about to see the impact of the baby boomers upon society. The baby boomers are those individuals born between the Second World War and the Korean War and they represent the largest single section of the population and for whom as they age, are now beginning to move into their geriatric period. As they have impacted every single area of commerce and society of their generation because of their sheer numbers, we can now expect this same impact for all their geriatric requirements.

Taking Italy as an example, we can study their current and forecasted populous. Figu is for the year 2000, here we can see a typical apple shaped graph with still seemingly reasonable numbers of the working age-group, (i.e. income generating). is

the graph for 2025 and it changes quite dramatically, it looks more like one of those old-fashioned spinning tops for children. Now there are now many more people in the over 50's age groups. And when we look at the projections for 2050 in we see that the

demographics appear to look like an inverted pyramid, with for the first time, massive numbers in their 60's, 70's and 80's. But we don't have to wait until 2050, as it is estimated that the 65 plus age group will start to experience a surge of growth from 2010.

To see how obvious it is that the elderly population is growing at a

far greater rate than any other part of society, look at igure . This graph illustrates that individuals over the age of 65

are expected to grow at a rate of 200% between 2000 and 2050. Whilst the growth rate of those between the ages of 15 and 64 will expand at 16% and those under 15 years of age at only 5%. But the single biggest increase is attributable to those over 80, with an expected increase of more than 400%! Indeed, this 80+

Source: US Census Bureau www.census.gov/ipc/www/idbpyr.html

age bracket is by far the fastest growing population group. Putting this into perspective; in the year 2000 there were 600 million people in the world aged 60 and over. There will be 1.2 billion by 2025 rising to 2 billion in 2050. And this is not singularly a developed world issue. Today, about two thirds of all older people are living in the developing world; by 2025, it will be 75%.

Aging factors

Whilst it's common knowledge that the older one is, the more likely we are to be treated for a disease or ailment, figure helps to highlight this. It shows by groups of varying ages, their percentage of the total drug consumption. This particular study looks at the years of 1990, 2000 and 2001 and whilst there are variations between the years, it is clear that the overall trend is up, and that apart from birth and childhood diseases, the older you are, the more likely you are to be prescribed medication. For example, someone who is 75 is likely to use 4-times as many drugs than someone who is 45.

The question we have to ask ourselves is, what does this mean to society if we let these facts meet our previous graph showing the over 65's increasing by 200%?

Another factor that advances with age is disability, as shown in . While the graph shows similar results for France, Germany, the Netherlands and the UK, the consensus is that the older we are, the more likely we are to suffer from some form of disability- many of which may need some type of care with its concurrent cost. Indeed, as

1 7 highlights at the age of 55 there is a 1 in 5 chance of having a disability, rising to 1 in 2 at the age of 75 and so on.

Again, let us pose the

j a m April/May 2006

question, what happens if we let these figures meet those in the aging population demographics already mentioned?

Consider that old-age dependency rates will rise in every major world region over the next 20-years, and that the burden in 2025 is expected to be at least 50% larger than it was in 1998. In just 14-years time society will consider 1 in 5 of its population as elderly.

However an aging populous could have benefits; on the up-side, an increase of just 6-years extra life expectancy in the United States, between the years of 1970 and 1990 translated into an additional gross national product of $57 trillion dollars, and those figures were based on a 1992 report.

But for those who say we can't afford to introduce preventative medicine, consider that in June 2000 the University of Chicago estimated that curing heart disease would be worth $48 trillion Dollars, and curing Cancer would be worth $47 trillion Dollars. Perhaps the question should be, can we afford not to introduce preventative medicine!

Aging's financial burden

Looking more closely at one example of an aging disease, we can begin to see more clearly the financial costs involved. Alzheimer's Disease is currently the 12th leading cause of death and it is perhaps an accurate example of an aging disease, because it very rarely affects anyone under the age of 60. At present, there is a 1 in 7 chance of being diagnosed with Alzheimer's Disease if you are over the age of 65. That figure rises to a massive, and rather alarming 1 in 2 chance if you are over the age of 85. In fact, the risk of Alzheimer's Disease doubles every 5-years after the age of 65. In the United States alone, $80 to

Source: World Health Organisation Ageing & Health: www.who.int/hpr/ageing

Source: Lehman Brothers Equity Research

France (Male)

Germany

The Netherlands

i « u >« n !* Ti

Source: Association for the advancement of assistive technology in

Europe

$100 billion Dollars is spent every-year on Alzheimer's health-care, or lost in earnings, and it has been estimated that curing Alzheimer's Disease could be worth as much as $1.5 trillion Dollars. If we take into account all the age-related diseases and disorders, is it possible to get an overall view of the financial costs involved? Essentially all

diseases fall into one of four categories, they are either:

Inherited or genetic disease. Infectious disease. Trauma. And finally,

degenerative diseases- which for argument, we can suggest are attributable

to aging- for by literally being older it dramatically increases our chances of acquiring them.

According to the statistics, only 10% of all health-care costs are spent on the first three. In other words, 90% of the total health-care budget is spent on degenerative disease.

In the United States alone, that translates into around $700 billion Dollars every year! Thus, if we really want to make a big impact on health-care in the world, we must focus on this 90%, we must focus on the degenerative diseases of aging. If we can slow or prevent the signs of aging from occurring, we could eliminate overnight the majority of disease and therefore the majority of its cost, both in financial and human terms.

But why are health costs so high? Clearly there are a number of factors here, including the need for highly trained staff, specialist equipment and premises, as well as liability insurance etc. All these factors are clearly present in the treatment of a disease, and obviously it could all be significantly reduced if far fewer people were actually sick in the first place!

Looking more closely at drug development, we see that the pharmaceutical companies are mainstays of the Fortune 500. Indeed, 10 drug companies registered more profits than the 490 remaining Fortune 500 companies combined!

We are reminded that high margins/ profits are required for R&D and the approval process. Naturally, not all drugs become approved and thus the average cost of approving a new drug- just in the United States- was estimated in 2002 to be $800 million.

"90% of the total health-care

budget is spent on degenerative

disease"

April/May 2006 i a m I 15

"the average cost of approving a new drug- just in the United States- was estimated in 2002 to be $800 million"

When going for approval, the most important question is-can the molecule be patented? After all, who is going to risk millions of Dollars to approve a molecule that anyone can sell? But as it is so difficult to patent a natural molecule, it means the accent is upon the artificial. Then once approved, a flood of press releases and marketing follows with the blessing of the authorities, after all they have approved it for use in disease X etc. This then leads to greater public

perhaps just biochemical changes. For example, rather than treating an end-point disease to

accept that hormonal change itself, or reduced inflammatory markers is good enough to prove a substance's worth, leaving the physician free to

use these tools as they see fit. Another issue is the fact that most often substances for approval are tested singularly. Whilst more often than not, a combination of substances work synergistically together, and is especially true of natural molecules and is the foundation of a holistic approach to medicine. Unfortunately, single item

awareness. This is a reality of the way things work, and as such greatly impedes the small guys and the natural molecule brigade and is one of the major obstacles to be faced. For the commercial reality is, that claims can't be made about substances that aren't approved and approval is expensive and requires strong patents.

Problems for the widespread introduction of preventative medicine

There are a number of issues that impede the introduction of preventative/ antiaging medicine, these include:

Patents: Which have already been mentioned.

Approval: Apart from the prohibitive cost of the approval process, there is also the fact that products have to be tested to correspond to a given disease or disorder. There is no current acceptance of disease prevention, or of aging itself, therefore if the category fails to exist it is clearly difficult to start an approval process! There will have to be a change to the categories to accept

1 6 i a m April/May 2006

substances are tested individually to prove their lone merit, however the results could be so much greater when combined with its methylation agents, enzymes etc.

c Studies: In preventative medicine, we really need negative studies. By this I mean, we want to keep healthy people healthy. The types of clinical trials that need to be run mean using healthy people, utilizing the substances in question and then showing that over time the people who were in the trial were less prone to disease etc. Again, all to often the trials run are the exact opposite, take a

sick person and try to

make them healthier. That is not the ultimate goal of preventative medicine and therefore it becomes another hurdle in the battle of the current approval mechanism.

d) Time: As usual it is not on our side. Once again the ultimate goal of antiaging medicine is to extend both the optimal health and the life span. Trials in humans need to be run over decades to prove their worth, although many are willing to accept that when we see positive results in a short to medium period that we can't afford to wait for the end-point, otherwise the data is of little relevance to today's generation.

Insurance: Very little tends to be reimbursable through insurance at present. Therefore as preventative/ antiaging medicine falls to cash-only patients, the numbers of people engaging in it is restricted.

f: Scope: Asking the question-what do you prevent in your healthy patient? Brings up numerous issues of the vastness of the possible scope. In its widest sense the

"we need to develop techniques to measure healthy people, to try to determine just how healthy the healthy patient is!"

adopting preventative medicine?

goals and aims are enormous, obviously because aging is affecting every part and every system of our body's. Of course, one can concentrate on specific areas, perhaps those that are most likely to be lethal, or even be of the greatest concern to the patient themselves. In its broadest sense, using all the skills and technologies that are available to us, including examination, observation, blood work, scanners and good old-fashioned questions and family background etc., the testing could potentially become enormous and is clearly limited by the issues of cost and convenience.

Measurement: Finally on the issue of measurement, we need to develop techniques to measure healthy people, to try to determine just how healthy the healthy patient is!

Furthermore, we need to move away from the idea of normal and think more along the lines of optimal. A major criticism of antiaging medicine is that it is suggested that advice and substances are given "ad-hoc", and that, as by definition, healthy patients don't feel much difference in some cases, so the advice and recommendations are taken on "faith."

So is there any way that we can show that the use of various protocols or products, such as the bio-identical hormones, are not only impacting the level of that particular hormone, but are also affecting the aging status of the patient as a whole?

Clinical application issues

Looking at the status of the actual measurement of aging and health today, what challenges do clinics face in

Firstly, we can recognise that there is a lack of

scientific measurement within the industry, with no clear path to follow.

b Secondly, any solution requires it to be quantitative, and standardization is lacking within the field.

Plus, consider that any measurement that takes place has to be seen to be changeable within a relatively short period of time. From the patient's perspective, results have to be achievable within a reasonable time frame.

Ward Dean, M.D., noted in his 1988 publication, Biological Aging Measurement: "It is assumed that with increased automation and computerization, that data will be more easily collected and analyzed, to rapidly improve the accuracy and cost effectiveness of aging measurement. I hope this book will be useful in assisting to accomplish this goal."

Dr. Dean's foresight has now been incorporated into systems such as Inner-Age and undoubtedly this type of information gathering and analysis will only become more common as the years go on. [Ed.- See www.inner-age.com]

What's the answer to world aging?

In the very near future, the world has to ask itself some basic questions. For example:

Can we expect the future working generations to pay 70% or even more tax, to support the same health-care program for a top-heavy society? It is estimated that if the policy of early retirement continues, (i.e. between the age of 55 and 60), that in just

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CoQ 10 is also one of many substances in the body that tend to decline as people age or develop certain diseases. It is one of the most important natural energy molecules cited as being of great

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get older, our body produces less CoQ 10 ' and so taking a supplement can help to maintain our vitality.

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April/May 2006 i a m

"in just 20-years time there will health, adopt the holistic

only be 2 people in employment for use of each retired person!" natural

20-years time there will only be 2 people in employment for each retired person! Thus, it appears that older people will be a necessary component of the workplace, continuing to contribute to society, if only in order to support themselves. That's another reason why we need a fit, lucid and agile older society.

Do we continue as we are? Can we allow an ever increasing elderly population to meet an already stretched health-care budget, and simply increase the numbers of people who are ending their lives in suffering? There are already discussions in the UK about whether or not certain drugs, particularly ones that are expensive and perhaps have a small benefit- should be given to the elderly. These questions have currently been raised in regard to certain senile dementia drugs and cancer drugs. They are likely represent the "thin end of the wedge" and that we are all going to hear a lot more debate and indeed decision on such matters.

3; At the end of the day, for those who state; "there are too many people already," one of the answers is a low birth rate. Are we ready for societies that dictate who, when and indeed if you can have children?

The only other answer to population control is a high death rate. Do you wish to live in a society that considers euthanasia necessary, perhaps dependant merely upon chronological age, or maybe a ratio of your health-care cost and age?

substances and allow our

elderly to live in dignity and self reliance, by remaining lucid and useful to the community at large.

Antiaging medicine

Whether or not one likes the terminology, antiaging medicine itself represents the ultimate preventative medicine. The model is based upon the very early detection, prevention and reversal of aging-related disorders.

The science of antiaging medicine is truly multi-disciplinary, for it is represented by advances in the fields of biochemistry, biology and physiology and enhanced by contributions from mind/ body medicine, molecular genetics and the new emerging medical technologies.

Antiaging medicine has its foundation in what Nobel Laurate, Linus Pauling described as orthomolecular. Furthermore, antiaging medicine accepts that aging diseases and disorders can and should be prevented, rather than simply treated. Today there are literally thousands of physicians, scientists and researchers around the world involved in the research and treatment of aging. Huge strides are being made in the understanding and control of the aging process. Our challenge is to bring together the international research, and to utilize whatever molecules and techniques that may be necessary for the long-term health of the patient- according to that science.

Or will we introduce antiaging medicine and revolutionise health-care by concentrating on the true prevention of disease? We could reduce the overall cost of

Ultimately, that means changing the way the patent system and the approval system operates. Big steps. But if we remember to educate and prove to the public that

this is the common sense they have been looking for, then usually no one stands in the way of a ground-up revolution for very long.

Conclusion

We stand at the threshold of a new paradigm, for the first time in history we understand some principles of why we age, how we can measure biological aging and how we can slow and treat its affects. Through the use of lifestyle choices, chelation, nutrition, hormones, drugs and the emerging technologies, we now have the ability to delay, reduce and even prevent the appearance of numerous disorders and diseases.

I envisage in the decade to come that thousands of antiaging clinics will be established. People will attend these clinics for regular checks and through the use of biological aging markers, an individual's rate of aging and risk from particular degenerative disease will be measured. Steps will then be taken to slow and eradicate these biological aging signs before they become diseases, and therefore difficult and expensive to treat.

In other words, the traditional recognition and diagnosis of disease will change forever. One could consider these aging but otherwise "healthy" individuals attending antiaging clinics, in much the same way as individuals visit the dentist today, for their preventative checks and measures.

However, as is usual with all great advances, mankind will probably experience the vested interests of the establishment and dogma, that together- will attempt to slow down, or perhaps even prevent the wide-scale use of antiaging medicine. After his discovery, Christopher Columbus said: "Human progress has never been achieved with unanimous consent. Those who are

enlightened first are compelled to pursue the light in spite of others." We could say the same today about antiaging medicine.

If we too can grasp the fundamental fact that we need to be pro-active about aging instead of just being tolerant of it, then mankind will be able take into its hands the possibility to radically alter the way we think about and approach "health." If we don't allow dogma, vested interests and other imposed restrictions to stand in our way, then the door is already open to us.

References:

1. US Department of Health and Human Services, January 2000. 2. United States Census Bureau. US Department of Commerce, May 1995. 3. American Academy of Antiaging Medicine, www.worldhealth.net 4. De Grey, A. 2004 Journal of Rejuvenation, Mary Ann Liebert Publications. 5. US Census Bureau: www.census.gov/ipc/www/idbp yr.html 6. World Health Organisation Ageing & Health: www.who.int/hpr/ageing 7. Lehman Brothers Equity Research. 8. Association for the advancement of assistive technology in Europe. 9. United States Census Bureau, May 1995. 10. United States Department of Commerce, 1992. 11. The Economist, 3 June, 2000. 12. National Vital Statistics Reports, Vol. 47, No. 20, June 30, 1999. 13. United States Health-Care and Finance Administration, 1996. 14. Physicians for a national health program, June 25, 2003. 15. Life Extension Magazine, May 6, 2002. Life Extension Foundation.

18 i a m April/May 2006

letters

Q: As a child I was operated on regularly by the drill-flll-blll brigade of dentists and as a result have numerous mercury containing amalgams. Having recently learnt many of the problems associated with even so-called relatively low dose mercury contamination and recognised many of my own personal issues such as memory below par for my age, lack of energy and irritability, I wish to start a program of amalgam removal. My dentist has recommended it is done as slowly as possible. My question is; is there any method of chelation/ protection I can be doing now and during the removal period?

A: We are very pleased to report that one of Britain's leading dentists; Dr. Brian Halverson is joining our advisory team shortly and will be offering advice on all forms of dental health. He, like us, is very concerned about the numerous health-related problems that current dental procedures may be causing, especially ones that lead to the accumulation of heavy metals such as mercury. This is a big problem, especially so for dental staff who are exposed to high levels of contaminants on a regular basis. Indeed, dentists are now in a profession that has one of the highest incidences of Alzheimer's disease. (Remember the expression "Mad as a Hatter" from the Alice in Wonderland book? That came about because the Hatters poisoned themselves by using mercury in the process of shaping the hats). Back to the problem at hand, EDTA (a type of vinegar molecule), allicin (from garlic) and malic acid (from apples) as well as vitamin C, are all excellent oral chelators of various heavy metals. In the case of mercury, which is a particularly difficult molecule to "shift" it can be rendered harmless by the regular use of selenium (found in walnuts) which binds itself to mercury. We believe that chelation, (the removal of heavy metals) is actually a lifelong requirement because we are all exposed to heavy metals through the contamination of air, food and water etc. by industry, (especially the burning of fossil fuels for electrical production).

World chelation expert, Garry Gordon, M.D. has formulated a number of high quality, efficacious products for this purpose. He recommends that 3 capsules daily of his Essential Daily Defense should be taken by everyone everyday. However during the amalgam removal period this could be increased to 6 capsules per day, (this contains all the ingredients mentioned above). In addition, as you have particular concerns of mercury, the ultimate selenium containing product is called Heavy Detox. It may be used 1 capsule, (each capsule contains lOOmcg selenium as well as Succinic acid and Glucuronolactone) per 50 lbs of bodyweight for a cycle of 1-month on, 1-month off.

Lastly, a unique chewing gum containing EDTA that is specially formulated for people with teeth amalgams is called EZ Defense Gum. One gum can be chewed after each meal, this helps grasp the mercury released from the amalgam by masticating into the gum. Once the orange flavor is finished the gum should be removed and disposed of and not swallowed, (that would simply take the captured mercury down into the stomach!)

Q: I would like to know, in your opinion what's the best smart drug?

A: This is a difficult question to answer precisely because there are so many possibilities, including what the patient

wants to achieve, where their weaknesses lie and what their medical/ family background is etc. Most folks want an improvement to their memory, but we have to go further and ask would that be short term memory, medium term, long term or is the problem one of a lack of concentration or easily induced boredom etc? Consider that if you are not learning new material well then you are less likely to remember it well later, (this is termed memory imprinting). The classic "smart drugs" are piracetam, oxiracetam, aniracetam and pramiracetam. The conclusion of Dr. Mason's article published in the February/ March 2006 Antiaging Magazine was that pramiracetam is the most potent, so that could be the simple answer, but remember that some experimentation is required, both with the product and its dose to find what's best for you. Cost may also be a factor of course, which is why most people usually begin with piracetam- as it is the cheapest. One thing to bear in mind is that combining different/ synergistic

Send your questions, letters & comments to: editor@antiaging-magazine.com

substances can often achieve the best results. Proven substances that often work well alongside those already mentioned are; centrophenoxine, deprenyl, hydergine, phosphatidylserine and vinpocetine.

April/May 2006 j a m 19

CREAM

One of the issues we often face with reporting new international breakthroughs in the Antiaging Magazine is that people (including physicians) don't understand that if the treatment is such a breakthrough why either ( I ) it hasn't been reported by the media in their country in a big way or (2) why their own authorities aren't looking at implementing it into general medical practice.

There are a number of reasons why that happens, much simply revolves around patents and the approval process, it takes an interested pharmaceutical company with very deep pockets to take on any approval process [Ed. Recent estimates place the cost of approving the average drug in the USA at over a Billion Dollars]. If a product is natural it is extremely difficult to patent, and therefore if a strong patent can't be applied no company is going to inject

millions of Dollars to start the process, hence it gets dropped by the wayside.

As the media is generally lazy and investigative reporting is all but dead, they tend to rely on press releases, which will be released by the pharmaceutical company when a product reaches stage-ll clinical trials. But naturally, if that doesn't happen there are no press releases, therefore there is not a massive generation of interest in product X etc.

This is one of the reasons why the Antiaging Magazine exists, to highlight international breakthroughs in all kinds of products and protocols, ensuring of course that the clinical and scientific studies are highlighted.

Over the years we've bought numerous interesting ideas and substances to the fore, perhaps two of the most remarkable has

Patients tell us their stories of success using a remarkable new cream in the battle against skin cancer

been work of Dr. Mark Babizayev with n-acetylcarnosine and the creation of Can-C eye-drops, in which there have been numerous cases of cataract reversal, and also the work of Dr. Bill Cham with BEC5 cream, a natural plant extract that has been clinically proven to reverse non-melanoma skin cancer. [Ed.- As reported in v5 i6 and v6 i I versions of the Antiaging Magazine],

We're aware that general articles and reports of clinical stories, even editorials do not really "bring to life" the personal side of breakthroughs, so listed below are just some of the testimonials and comments that patients have had to say about using BEC5 cream. We hope it gives you an insight into the remarkable difference this product has given for many people suffering with various forms of skin cancer.

As May has now been designated "skin cancer awareness month" we thought this was particularly appropriate for this issue.

20 i a m April/May 2006

"I have good news to report. After one month applying BEC5 cream twice a day, the lesion is now 50% covered with new tissue. It took me a while to be able to distinguish the new from the old eschar which needed debridement. I had the help of a doctor for this.

It still burns slightly when I apply it but I can deal with that. For the record the original dime sized lesion grew to a scary-looking large quarter size of raw flesh before it started to heal. I did use Neosporin twice for 4 hours only when it was oozing yellow. And I had difficulty keeping it moist when it reached as far as my hairline. But I found that as long as it was totally covered by the Micropore, it was okay.

Thank you so much for telling me about this. It is by far the best approach we have to healing

squamous cell carcinoma and keratoses."

Marie, Spain

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Karen, Australia.

Editor: We welcome your comments about any treatment you have undertaken. Please tell us about your experiences and they may become published in a future edition of the Antiaging Magazine.

Clinical diagnosis of a BCC on the nose of a patient before treatment with BEC-5 cream (a), during therapy (b),

and the site of treated BCC after completion of therapy (c).

l a m April/May 2006

in the news

Ignore the circadian clock at your peril

In the 10 November 2005 issue of Nature a physiologist at Yale School of Medicine commented on the complex factors controlling the circadian rhythm. From algae to human beings, all living things have built-in clocks that are synchronised to the earth's 24-hour rotation. When deprived of environmental factors, such as being kept in constant darkness, these clocks gradually drift out of synchrony with the earth's rotation. In animals, the clocks that control rest and activity depend on groups of neurons situated in the central nervous systems. An important question is how oscillations of the cellular clocks within the organism are co-ordinated.

Studies of the fruit fly, Drosophila, have revealed two anatomically distinct groups of neurons that independently control morning and evening peaks of activity. When fruit flies are synchronised to light-dark cycles and then released into constant darkness, morning and evening peaks still persist, but run free and gradually drift out phase with the earth's

rotation. An investigation has been carried out into whether the morning or evening oscillator predominates or whatever the two interact to establish a constant phase relationship. It seems that the morning peak controls the evening one, possibly by maintaining an hour-by-hour influence. An alternative explanation is that the evening peak is free-running, maintaining its own faster intrinsic period but being reset once a day by the morning surge. It is possible that the mechanism involves a neuropeptide that has been given the name pigment-dispensing-factor and is expressed by morning-peak cells. In the absence of this factor, the evening peak is advanced by some two hours in fruit flies. Whether oscillators in the human brain communicate in a similar fashion is unknown. Obviously, sleeping and waking and the functions they involve are highly important factors in determining a healthy or a hazardous lifestyle. To ignore them is asking for trouble, and our present ideas of a busy life expose us to lurking dangers.

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W H I C H T H Y R O I D -NATURAL OR SYNTHETIC?

Thyroid decline affects every cell in our body, resulting in a wide range of age-related problems , but the question many people ask is which is best - natural or synthetic?

Thyroid supplements come in two fonns . Whole-natural supplements and synthetic supplements. It is almost always better to use a whole-natural thyroid extract because the synthetic versions usually only comprise of one of the thyroid hormones, (such as, T3 or T4), whereas, whole-natural thyroids cover a fuller spectrum of thyroid hormones (including T 1 . T 2 , T3 and T4).

Scientific data strongly supports the idea that a small daily serving of whole thyroid extract as a dietary supplement can have a wide range of positive influences. Studies have shown that those who took 1/4 grain of thyroid combined with minerals and vitamins over a period of 10 years showed significant improvement in cardiovascular-protective function.

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April/May 2006 j a m 23

- L

Pyrit inol : The ongoing benefits of the oldest smart drug

Pyritinol is perhaps the oldest smart-drug (nootropic) which is still

in use- because it has been continuously used and researched in Europe since 1961. There was much published research in the 1980's and 1990's which are a testament to the wide range of uses, safety and efficacy of pyritinol.

Pyritinol is almost identical to pyridoxine (vitamin B6), yet it has no B6 activity (4). It has been used in a wide range of disorders, for example, in patients suffering from cerebral trauma (1) and pyritinol has also shown excellent benefit on the clinical course of victims of coma (caused by head injury), helping in many cases to return coma patients to more or less normal waking consciousness (2). What is more, pyritinol has also been used successfully to treat rheumatoid arthritis patients (3).

One of the keys to understanding pyritinol's wide mode of action was first revealed in 1989. Two Czech scientists, Drs. Pavlik and Pilar performed sophisticated experiments on 6 nootropic drugs to determine their free radical-quenching power, proving pyritinol to be far superior to the acknowledged antioxidant nootropics. They stated: "There is growing evidence that free-radical interactions are implicated in the pathogenesis of many diseases including radiation injury, atherosclerosis, arthritis, cancer and aging. The most dangerous [kind] of oxygen radicals is the hydroxyl radical that can attack proteins, lipids, nucleic acids and almost any molecule of a living cell. If the production of hydroxyl radical escapes the control mechanisms, then substantial damage to cell functions [and structure] may occur. It was found that pyritinol exerts a pronounced scavenger action against [the worst kind of free radicals] the hydroxyl radicals." (5) It is interesting to note that brain proteins were protected from hydroxyl radical damage by pyritinol in these experiments.

As will now be explained, the superior hydroxyl radical antioxidant effect of pyritinol is what provides much of its immune, arthritis and neuroprotective benefits.

Three of the most common 'free radicals' that are continuously being produced in human cells are superoxide radical (SOR), hydrogen peroxide (H202) and the hydroxyl radical (HR). SOR's are normally produced through white blood cell, germ killing activities, energy metabolism and in many disease states. In fact, "it is believed that the activity of superoxide is at least partly responsible for aging and most if not all degenerative diseases." (6a)

Fortunately the body has two different enzymes; copper-zinc SOD and manganese SOD, to neutralise SOR. SOD converts SOR into oxygen and H202. Whilst H202 is less cell-damaging than SOR, but it is still injurious if it accumulates in cells. However SOD production drops with age. (6b)

Although H202 has some uses in the body, (e.g. white blood cells secrete it to kill germs), the body needs to continuously rid itself of H202 and this is highlighted by the fact that our cells possess two completely different enzymes; catalase and glutathione peroxidase, to ensure neutralization of H202. Uncontrolled H202 can damage cell membranes and structures, as well as promote inflammation.

The brain is particularly vulnerable to damage by H202 (6c). Unfortunately, under conditions all too common in our cells, SOR and H202 will react with each other. The product of this reaction is a free radical even more damaging than superoxide, it is known as the hydroxyl radical. (6d) To make matters worse, human cells have no enzymatic defence against the hydroxyl radical (HR). It is normally quenched primarily by cholesterol, vitamin C or proanthocyanidins. (6e) (Thus,

the elevated cholesterol levels found in most modern humans may actually be a defensive tactic used by the body to quench the excesses of the hydroxyl radical induced by our toxic modern diet, environment and lifestyles). HR's are so injurious to cells that when huge uncontrollable numbers of them are generated in a person exposed to massive levels of X-ray or gamma radiation, the flesh may literally melt from the bones within hours!

24 i a m April/May 2006

I I I

As Pavlik and Pilar note: "There are clinical reports that support the opinion that pyritinol has a [hydroxyl] scavenger effect. Camus [et al] (1978) and Berry (1986) used pyritinol successfully for the treatment of some cases of rheumatoid arthritis. [Ed.-So did Lemmel et al, reporting in 1993. (3)] The protection of cartilage and synovial protein against free-radical induced degradation may be an important factor in the

treatment of rheumatoid arthritis. The same line of reasoning may be applied to some cases of stroke or brain trauma, where the generation of hydroxyl free-radicals is abundant and where pyritinol was successfully used for treatment. The potency of pyritinol to protect proteins in the brain against radical induced polymerization, in conjunction with recent reports that pyritinol enhances cholinergic transmission in the brain, substantiates its use for

the treatment of cognitive disorders." (5)

Increased brain cell energy

Another key benefit of pyritinol has been known since the 60's, that is its ability to enhance or normalize glucose transport through the blood-brain barrier and also to increase brain cell energy production from glucose (7). In a placebo-controlled, double-blind study, Hoyer and colleagues examined 87 patients suffering from various brain disorders. Careful measurements of cerebral blood flow, oxygen uptake, glucose uptake and cerebral metabolic rate were taken. Of the 45 patients receiving pyritinol, 27 suffered from disturbed glucose uptake/ cerebral energy metabolism. "Cerebral uptake of glucose, which was reduced to approximately 50% of the normal value, increased significantly with pyritinol treatment and returned to normal. The clinical disturbances generally also improved to the same extent as did the disturbed glucose metabolism." (7)

Enhanced glucose transport

Pyritinol's ability to enhance glucose transport through the blood-brain barrier when it is low is a highly significant benefit. Although the brain is usually less than 2% of total bodyweight, the brain must produce and use about 20% of the body's total energy production. Under normal, non-fasting conditions, the brain can only 'burn' glucose for fuel. Unlike virtually all other body cells, nerve cells cannot use fat as a fuel. Brain cells also cannot store any

significant amount of glucose, they are completely dependent upon a continuous delivery of glucose from the blood, through the blood-brain barrier. Thus, brain glucose uptake is a major rate-limiting factor for crucial brain energy production. Low cerebral glucose uptake necessarily translates into low brain carbohydrate energy metabolism.

So brain energy metabolism is very important to maintain optimal, healthy brain function and brain carbohydrate metabolism is impaired in a variety of dementias. (8) "The degree of reduction in brain carbohydrate metabolism is correlated with the severity of the dementia." Pyritinol is good for optimal brain carbohydrate metabolism, and hence good for the brain and the mind!

Effective immune enhancer

A surprising effect of pyritinol was first reported in 1993. Pyritinol can be an effective immune enhancer through its stimulation of neutrophil migration (9). Neutrophils are a major type of white blood cell (WBC), they typically constitute about 60% of the total number of WBC's in the blood. Wherever there is a wound, cut, sore, abrasion etc., neutrophils are attracted to leave the bloodstream and travel to the site of injury/ infection, this is called the process of chemotaxis. Once at the site of injury, neutrophils proceed to engulf germs, especially bacteria that may now be growing at the injury site. Neutrophils then secrete a powerful mix of free radicals and oxidants, such as SOR, H2 02 and hypochlorous acid. These destroy the germs before they can seriously

April/May 2006 i a m I 25

multiply and overwhelm the body. However, neutrophils sooner or later die "in the line of duty" from their own germ-killing free radical barrage.

One neutrophil averages 5 to 20 germ kills before succumbing. The free radicals that neutrophils release also typically promote inflammation at the site of injury, a process that all too easily gets out of control. Excessive inflammation promotes excessive swelling, tenderness, redness, heat and pain at the injury site. The pus that forms with cuts and wounds is in large part made up of dead neutrophils.

In a study with rabbit neutrophils, Elferink and De Koster found that pyritinol, used orally, strongly promoted neutrophil migration to injury site, but did not increase free radical levels or inflammation (9). Given the earlier discussion on pyritinol's antioxidant effects, this differential effect of pyritinol on neutrophil activity, (i.e. increasing migration, but not free radicals or inflammation) becomes comprehensible. When large numbers of neutrophils release huge amounts of SOR and H202, this generates huge quantities of inflammatory, tissue-damaging hydroxyl radicals. Yet pyritinol is a powerful quencher of HR's. Thus pyritinol is able to reduce HR-induced inflammation and tissue damage- the unpleasant side effect that usually accompanies successful germ-killing by neutrophils.

Immune defence

Neutrophils comprise the body's first line of the immune defence as they are normally first to arrive at wound/ injury sites. Yet our modern sugar-rich diet has been shown in multiple studies to significantly

impair neutrophil activity.

When human volunteers were given various forms and levels of sugar in drinks, the number of germs a neutrophil could kill before dying from its own free radical release typically dropped 50 to 80%! The effect began within one hour of sugar intake, peaked at two hours, and was still significant five hours after sugar ingestion (10). Thus a sugar-rich diet literally enhances neutrophil self-destruction, yet

pyritinol enhances neutrophil survival through reducing the hydroxyl radical excesses that normally lead to neutrophil death.

Another key property of pyritinol is its vigilance-enhancing effect. Pyritinol increases nerve activity in the locus coeruleus (LC). (11) "In humans, the number of neurons in the [LC] declines with advancing age. Degeneration appears to advance slightly faster in males than females. The [LC] is a brain area that is particularly susceptible to neuronal degeneration in Alzheimer's disease. Plus there are many studies indicating a role of this system in control of attention, learning and memory." (11)

EEG Power

"Pyritinol has also been shown to produce a vigilance response in healthy human volunteers. More recently, using topographic brain mapping of EEG, it has been shown that 600 mg. of pyritinol resulted in an increase of changes indicative of improved vigilance. Specific studies of the effects of pyritinol on memory using a battery of seven tests have shown that repeated daily doses of pyritinol 300 mg. improved memory performance over a wide range of measures in volunteers aged from 16 to 66 years." (4)

Who might benefit?

1. Pyritinol may be useful in various forms of dementia, organic brain syndrome, head injury, stroke aftermath, coma, and cerebral circulatory disorders. Vinpocetine, piracetam and phosphatidylserine may be useful synergists with pyritinol.

2. Pyritinol may be useful as an anti-brain aging nootropic

26 i a m April/May 2006

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3. Pyritinol may be useful as an aid to increased focus and concentration, memory, alertness and information processing in both young and old, normal or mildly brain dysfunctional persons.

4. Pyritinol may be useful in Attention Deficit Disorder (ADD), hyperkinetic, or mildly retarded children to increase drive, alertness, concentration and learning ability. (12, 13)

5. Pyritinol may be useful as part of a health-optimizing antioxidant program, along with vitamins C and E, selenium, zinc and lipoic acid.

6. Pyritinol may be useful in the treatment of rheumatoid arthritis. In a large, double blind yearlong trial comparing pyritinol to a standard anti-rheumatoid drug (Auranofin), the response rate was superior for pyritinol (78% vs. 59%, at one year). "Every individual efficacy parameter showed a numerical trend for better results in the pyritinol group." (3)

Side-Effects

Most published studies on pyritinol report few if any side effects, with skin rashes and/or gastric upset occasionally noted. E.g. "In general, the tolerability of the drug was good. Practically no problems occurred during the trial. None of the reported symptoms were rated as serious nor persisted over a long period of time." (14) "No undesirable side-effects were observed." (13) "There were no significant differences in the incidence of adverse reactions in the drug and placebo group. No significant changes were observed in any [clinical laboratory] parameters." (1)

The one major exception to pyritinol's low side-effect profile occurred in the large-scale rheumatoid arthritis trial. The authors note that pyritinol side effects "were mostly nuisance events, which led to stopping therapy [in rare cases], but did not constitute a health risk for the patient and were fully and rapidly

reversible." (3) However, they also note a general trend in the pyritinol-arthritis literature of about 2% potentially serious adverse effects involving blood, kidney or liver, which makes it important for regular monitoring of liver enzymes, urine status and blood cell status when using pyritinol to treat rheumatoid arthritis. Therefore, pyritinol should be used in rheumatoid arthritis treatment only with the knowledge and supervision of a physician.

Doses

A wide range of doses have been used in pyritinol studies. These have ranged from as low as 100 mg. twice daily (12) to 200 mg. three times daily (14) or 200 mg. four times daily. (15) For anti-aging, cognition-enhancing or antioxidant purposes, 100 mg. pyritinol two or three times daily is generally safe and adequate. Higher doses (400 mg. to 800 mg. daily) should probably be used only with physician supervision, just to err on the safe side.

Pyritinol may be taken either on empty stomach or after food, as desired. Persons only prone to insomnia should probably only take pyritinol morning and early afternoon. There may be a mutual enhancement of action between pyritinol and other nootropic drugs, allowing/ requiring lower doses of some or all the drugs in order to avoid an over-excitation effect.

Conclusion

Pyritinol has a very long established and well tested history. The fact that it displays immune enhancing, antioxidant, anti-arthritis, anti-inflammation effects, as well as its memory/ cognitive enhancement benefits, with few contraindications and minor side effects, makes it a extremely beneficial indeed almost holistic aid, all in spite of its own old age!

References

1. K.Kitamura (1981) "Therapeutic Effect of Pyritinol on Dequelae of Head Injuries" J Int Med Res 9, 215-21.

2. G. Dalle Ore et al (1980) "The Influence of the Administration of Pyritinol on the Clinical Course of Traumatic Coma", J Neuroserg Sci 24, 1-8.

3. E.-M. Lemmel (1993) "Comparison of Pyritinol and Auranofin in the Treatment of Rheumatoid Arthritis" Br J Rheumatol 32, 375-82.

4.1. Hindmarch et al (1990) "Psychpharmacalogical Effects of Pyritinol in Normal Volunteers" Neuropsychobiol 24, 159-64.

5. A. Pavlik & J. Pilar (1989) "Protection of Cell Proteins Against Free-Radical Attack by Nootropic Drugs: Scavenger Effects of Pyritinol Confirmed by Electron Spin Resonance Spectroscopy" Nueropharmacol 28, 557-61.

6. R. Bradford & H. Allen, Oxidology, Chula Vista, CA: R.W. Bradford Foundation, 1997. A:p.65 B:p323 C:p. l42 D:p.66 E:p.l75.

7. S. Hoyer et al (1977) "Effect of Pyritinol-HCL on Blood Flow and Oxidative Metabolism of the Brain in Patients with Dementia" Arzneim Forsch/Drug Res 27, 671-74.

8. R. Branconnier (1983) "The Efficacy of the Cerebral Metabolic Enhancers in the Treatment of Senile Dementia" 19, 212-19.

9. J. Elferink & B. de Koster (1993) "Differential Stimulation of Neutrophil Functions by Pyrithioxine" Int J Immunopharmac 15, 641-46.

10. R. Huemer & J. Challem, "The Natural Health Guide to Beating the Supergerms", NY: PocketBooks, 1997. Pp.124-27.

11. H.-R. Olpe et al (1985) "Locus Coeruleus as a Target for Psychogeriatric Agents" Ann NY Acad Sci 444, 394-405.

12. G. Logue et al (1974) "The Effects of Pyrithioxine on the Behavior and Intellectual Functioning of Learning-Disabled Children" S.Afr Med J 48. 2245-46.

13. D. Lane O'Kelly (1975) "Pyritinol in the Treatment of Chronic Alcoholics" J Int Med Res

3, 323-27. 14. K. Fischhof et al (1992) "Therapeutic Efficacy of Pyritinol in Patients with Senile Dementia of the Alzheimer Type (SDAT) and Multi-lnfarct Dementia (MID)" Neuropsychobiol 26, 65-70.

15. A. Cooper & R. Magnus (1980) "A Placebo-Controlled Study of Pyritinol ('Encephabol') in Dementia"

Pharmatherapeutica 2, 317-22.

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interview

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Interviewed by Phil Micans

Karen Sadowsky Kaufman is a forthright nutritionist with a keen and open mind, as well as a passion for research. Her alternative perspective, bom from experience of her own personal needs as well as those of her patients, combined with a thirst for knowledge, has meant she has also worked alongside highly respected physicians and researchers. Her expertise gives Karen a unique and fascinating insight into numerous health problems. In this interview she outlines the issues of inflammation, insulin and their roles in diseases and weight control.

A A M : Karen, can you please tell us about your credentials?

Karen: Certainly. I have a Master of Science

degree f rom the University of New Haven in

Connecticut. I have worked in the nutrition

and antiaging field for the past 10 years and

have had the privilege of working with

James South and Ward Dean, both of whom I

consider to be mentors.

A A M : Why did you choose this particular area of specialization?

Karen: I actually developed a serious chronic

illness in 1991. Initially, 1 did not get a

diagnosis, but f rom the start it was clear I

had developed some sort of autoimmune,

inflammatory, connective tissue disease. That

disease was systemic lupus erythematosus

(SLE). I was extremely debilitated by

unremitting fatigue, severe pain in nearly

every joint and intermittent 'brain fog. ' I

realized 1 could not continue in my career

which required a lot of energy. I had always

been interested in health and nutrition, so I

went back to school to pursue a professional

degree. In addition, at the t ime I was

diagnosed with this au to immune disease, the

treatments that conventional medicine had to

offer were in many cases worse than the

disease itself! I was searching for novel and

non-toxic ways to recover my health. This

was how I became interested in innovative

groups such as IAS, because it was clear the

disease was attacking my central nervous

system- so I needed to avail myself of every

possible 'smart drug ' and nutrient to preserve

my brain function.

28 i a m April/May 2006

AAM: How did you go from that personal interest to the broader concerns you have today?

Karen: I began recovering my health through targeting the chronic inflammation in my body with diet, exercise, supplements and 'smart drugs.' Inflammation is at the root of so much 'evil ' and we are now learning that many chronic illnesses and diseases of aging are caused by inflammation, i.e. heart disease, cancer and the complications of diabetes.

AAM: Tell us why do you want to speak out about the issue of obesity at this particular point in time?

Karen: It's an interesting story. When 1 finished graduate school, 1 vowed to be a nutritionist that did not focus on weight loss, primarily because diets have a failure rate of 93% or more. Today 1 feel I no longer have that luxury because there is a pandemic of obesity. Diets may not work by themselves, but there are lifelong strategies people can adopt to preserve their health and quality of life while simultaneously extending their lifespan.

AAM: What prompted your change in focus?

Karen: The results of some provocative studies have recently made the headlines. They may seem quite opposite at first glance, but they are connected in some very important ways. The first involves the epidemic of obesity. The second involves some intriguing results from the first ever trials that have examined the affect of calorie restriction (CR) in humans.

AAM: Could you please give our readers some specifics?

Karen: The most astonishing headlines relate to the number of overweight individuals in the US, as well as the rapid rise in the prevalence of obesity. Today, two-thirds of adults in the US are overweight or obese. An individual who is overweight or obese is at risk for developing some diseases that may not necessarily shorten one's lifespan, but these diseases certainly affect one's quality of life. I am talking about diseases such as type-II diabetes, heart disease and cancer etc. Obesity is affecting children and adolescents as well. The increase in the number of overweight/ obese children and adolescents prompted the medical profession to rename

diabetes. Type-I diabetes was previously known as juvenile onset diabetes. Type-II diabetes was known as adult onset diabetes since it previously affected people at mid-life or later. So many overweight children were developing 'adult onset' diabetes, which is really a disease of excess glucose and insulin, so the disease had to be renamed. I am extremely concerned about this.

AAM: What troubles you the most about this situation?

Karen: Basically an overweight child is much more likely to become an overweight adult. Some statistical algorithms suggest if we stay on this same path, one in two children alive today will develop type-II diabetes by the time they reach adulthood. It is not just the diabetes that is the problem. It is the micro and macro vascular complications that go along with it, things such as blindness, specifically retinopathy, peripheral neuropathy, limb amputations and heart disease. It's well known that diabetes speeds up the aging process. It's the excess glucose and excess insulin that really causes the body to breakdown from the inside out. But the tragedy is that diabetes is a largely avoidable disease, but we must make some dramatic changes to our lifestyle.

AAM: You mentioned some recent studies were published that suggest there may be a way to truly extend life. Can you tell us more about that research?

Karen: Yes, although some say calorie restriction may not result in a longer life, but it will feel like it! AAM: Ha ha! Karen: No seriously, for the last six decades researchers have been extending the lives of laboratory rats, insects and worms by reducing their caloric intake.

" many chronic illnesses and diseases of aging are caused by inflammation"

The person that is best known for asserting this hypothesis was a University of California Los Angeles School of Medicine professor of pathology, Roy L. Walford, M.D. He wrote Maximum Lifespan, Beyond the 120 Year Diet, and The Anti-Aging Plan. Perhaps he is best known for the Biosphere experiment of the 1990s. Today, many more physicians and scientists are asserting that calorie restriction (CR) might extend life in a laboratory setting in animals, but it is premature and possibly even dangerous to assume that CR can work in the real world amongst humans. Before 1 get into the details, I must mention the obvious. It is very difficult to test this hypothesis in humans. It is impossible to do a 'double blind placebo controlled trial' when it comes to nutrition. The studies involve a small number of people. Non-believers would most certainly find hundreds of flaws in the research. But, personally I find the results very intriguing. I think the

Improve memory, vigilance and concentration with

Pyritinol Benefits include: • improved brain glucose uptake • potent antioxidant abilities • enhanced immune system • improved neutrophil activity

Pyritinol has a very long established and well tested history. The fact that

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indications and minor side effects, makes

it a extremely beneficial, almost

holistic aid, all in spite of its own

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For further information about Pyritinol go to: www.antiaging-systems.com/a2z/pyritinol.htm

April/May 2006 i a m 29

interview

"preliminary evidence that calorie restriction can

extend life in humans" studies provide preliminary evidence that calorie restriction can extend life in humans as well.

AAM: I know you are excited about this new data. With the above caveat, are you ready to share the specifics with our readers?

Karen: Absolutely. The first study was published in January, 2006 in the Journal of the American College of Cardiology and was the result of research undertaken at the University of Washington in St. Louis by Luigi Fontana, M.D, PhD. There are a number of people around the USA who have been voluntarily practicing CR. While they do restrict their calories, they work hard to eat a nutrient dense diet. Their diet avoids empty calories, particularly calories from white flour and sugar. The researchers looked at 25 individuals between the ages of 41 to 65 who had been reducing their calories to 1,400-2,000 calories per day for six years, and compared them with individuals who consumed the average American diet which is 2,000-3,000 calories per day. The study looked at heart function as a measure of 'primary aging. ' Although people in the calorie restriction group had been eating a low calorie diet for only six years, their heart function, when compared to the control group, resembled the heart function of people 15 years younger. In the case of the group practicing calorie restriction, many of the subjects had parents, grandparents or siblings who suffered heart attacks or strokes. That makes it unlikely that the CR group had a more favorable genetic make up. Some subjects had actually been taking medication for high blood pressure before starting the CR plan. Other biomarkers for aging were lower in the members of the Caloric Restriction for Optimal Nutrition Society (CRONS). These markers included markers of inflammation such as C reactive protein (CRP) and tumor necrosis factor alpha (TNFa). Previously, these researchers had found that people on the very low calorie diet had low blood levels of cholesterol and triglycerides, blood pressure scores equivalent to much younger individuals, a lower risk of developing diabetes and reduced body fat. The findings taken together suggest that the people practicing calorie

restriction have a longer life expectancy because they are more likely not going to die from a heart attack, stroke or diabetes. This suggests the quality of their life will also be better. Members of CRONS try to consume between 10% and 25% fewer calories than average Americans while maintaining proper nutrition. Accordingly, their diet resembles the Mediterranean diet. This published study was the first of many studies examining members of the CRONS. The research was supported by a number of organizations including the National Heart, Lung and Blood Institute and the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institute of Health.

A A M : That sounds like extremely detailed and interesting research. You mentioned a different area of investigation. Can you tell us more about that?

Karen: Yes. The results of another investigation, called the Comprehensive Assessment of the Long Term Effects of Reducing Intake of Energy (CALERIE) study, were published in the April 5, 2006 issue of the Journal of the American Medical Association. This study recruited 48 middle aged overweight, non-obese men and women and randomly assigned them to one of four diets: control (weight maintenance diet); CR (calorie intake reduced by 25% of normal); CR with exercise (calorie intake by 12.5%, energy expenditure increased by 12.5%); very low calorie diet (890 calories per day until 15% weight loss, then weight maintenance diet). The study was conducted at Pennington Biomedical Research Center, Louisiana State University, Baton Rouge. After six months, the control group lost about 1 % of their body weight. The three intervention groups all lost significantly more weight (as expected). The CR group and the CR plus energy expenditure group lost about 10% of their body weight. The very low calorie diet group lost 14% of their body weight. However, weight loss was not the primary focus of the study and positive results were observed for markers of aging. The lead author, Leonie Heilbronn, M.D. stated: Our results indicate that prolonged calorie restriction caused a reversal in two of three previously reported biomarkers of longevity, (fasting insulin levels and core body temperature). . .and a reduction in DNA fragmentation, reflecting less DNA damage. As one of the most widely held theories of aging is that free radicals AKA reactive oxygen species- assault DNA, which therefore affects normal cell function and

3 0 i a m April/May 2006

interview

"Preventing those spikes in glucose and insulin is

also the best way to prevent diabetes,

metabolic syndrome, overweight/ obesity, heart disease, stroke

and cancer"

potentially leads to cancer, this makes sense. Another related theory of aging suggests the excess blood glucose causes the 'sugaring or browning' of all cells and all cellular function is compromised. This is one of the main reasons diabetes and metabolic syndrome causes so much morbidity and mortality. There have been extensive studies in animals, including mice. In 2004 researchers established that CR even when started in late middle age in mice, significantly extended life. So it may never be too late in life to begin CR and reap the health benefits. In 2005, a study in mice suggested one mechanism of the anti-aging affect of CR is the increase nitric oxide (NO). N O is so important in relaxing the walls of blood vessels and preventing that hardening of the arteries. So here we are beginning to understand that CR works on several important mechanisms to improve both quality of life and longevity.

AAM: That's all very interesting Karen, but what does that mean for the general population, and those of us who are interested in optimal health and longevity? Do we all have to be thinking about near starvation?

Karen: Don' t get me wrong, this is not a call for everyone to go on a very low calorie diet. Scientists would say the evidence is only preliminary and the studies were very small. Be aware that a very low calorie diet can lead to malnutrition. Those interested in this lifestyle change should make sure they do a lot of reading and get the advice of a qualified nutritional professional. Let me read you part of an editorial that appeared in the New York Times on Sunday, April 9, 2006, Frank Bruni writes: If living to 99 means forever cutting the porterhouse into eighths, swearing off the baked potato and putting the martini shaker into storage, then 85 sounds a whole lot better, and I 'd ratchet that down to 79 to hold onto the Haagen-Dazs, along with a few shreds of spontaneity. It's all a matter of priorities.

AAM: So I guess the obvious question is: is there any way of having the cake and eating it too?

Karen: My answer is a resounding yes. But it takes some strategizing. CR prevents spikes in both glucose and insulin. Preventing those spikes in glucose and insulin is also the best way to prevent diabetes, metabolic syndrome, overweight/ obesity, heart disease, stroke and cancer. The good news is that there are things known

as calorie restriction mimetics; Metformin is the best known and it also has the longest history of success. Currently Metformin is prescribed (Ed.- off label) to help prevent diabetes in susceptible individuals. I see no reason why it shouldn't be taken almost like a vitamin at this point. Acarbose is also a drug being used to prevent type-II diabetes in the prediabetic population. Acarbose is a substance that blocks the absorption of refined carbohydrates thereby preventing the spike in glucose, which would then be followed by a spike in insulin. In 2002, David Sinclair, M.D., professor of pathology at Harvard Medical School, claimed that he and a team of researchers discovered a way to genetically mimic the life-extending effects of CR, without the severe food deprivation. His studies were done in yeast and focused on the Sir2 protein. Later, he and his team asserted that the compound; resveratrol- a key antioxidant found in red wine and other substances, can slow the aging process without CR. Of course, it is important not to overeat and maintain an active lifestyle. But there are other natural products that have shown the ability to regulate blood glucose and insulin. The best of these 'weight loss' products contain the important minerals chromium and vanadium. In addition, green and black tea extracts can help boost metabolism. Cinnamon extract, gymnema sylvetra extract, and bitter melon extract may have a certain synergy that can assist in weight loss.

AAM: Karen, you've discussed a lot of important and fascinating information here. Is there anything you'd like to conclude with?

Karen: Phil, I 'd like to thank you for letting me present what I consider to be some critical health and longevity issues. The data at this point is suggesting that CR may indeed extend life while maintaining health and vibrancy. But that means one has to start thinking about eating to live, rather than living to eat. Eating after all, is one of life's greatest pleasures. You know I am a huge believer in the health enhancing power of the right foods along with an active lifestyle. I am also a realist. My guess is many people are interested in reaping all the benefits of CR, but few will be interested in the arduous lifestyle changes required. I commend organizations such as IAS for making available some important pharmaceuticals and nutrients that may well mimic CR.

AAM: Thank you Karen, as always it's a pleasure to talk with you.

April/May 2006 i a m 31

It is now well established that the

process of glycosylation is

one of the most important

causes of aging, perhaps equally as

important as the process of oxidation (free

radical damage). During everyday

metabolism, sugar molecules (such as

glucose and fructose), and reactive

aldehydes and/or ketones may attach to

free amino groups on proteins, a process

called non-enzymatic glycosylation

(glycation). This reaction is also sometimes

called the Maillard reaction. It results in a

glycated protein, i.e. a protein carrying

sugar (or similar) molecules on it. This

glycated protein (also called an Amadori

product) may then react with any other

proteins resulting in irreversible bonding

between the two. This bonding process is

named 'cross-linking'.

Affected molecules can be anything from

collagen and elastin, to enzymes and

immunoproteins. Facilitators during cross-

linking are the carbonyl groups which act

like glue, fixing the two proteins

together. Carbonyls are chemical

groups which are formed

as a result of a sugar

(or an

aldehyde

or a ketone or a

free radical) reacting

with aminoacids on a protein. In

addition, carbonyls

can be formed in other situations

involving lipids or DNA so they are not

necessarily restricted to proteins. So,

carbonyls may cause not only protein-to-

protein

cross-linking,

but also protein-to-

DNA, or protein-to-lipid

cross-linking, which is equally

damaging to the organism. Recently, a

condition called 'carbonyl stress' has been

described. It involves increased levels of

reactive carbonyl compounds which make

cross-linking much more likely (1).

Cross-linking results in formation of large

insoluble aggregates of damaged proteins

in the tissues. These aggregates have been

named AGEs (Advanced Glycosylation

End products) (or 'post-Amadori

products ' , or 'glycotoxins ') and

may then go on to

interact with free

radicals

and

cause further

tissue injury,

through chronic oxidation.

Although a steady rate of AGE

formation happens as a result of normal

aging (starting after the age of 20),

formation of AGEs is accelerated during

hyperglycemic states such as diabetes.

Copper, iron and other metals may hasten

AGE formation.

Once formed, AGEs inhibit cellular

transport processes, stimulate cells to

produce more free radicals (such as

superoxide and nitric oxide), and activate

inflammatory

cytokines such as Tumor

Necrosis Factor alpha

(TNF-a) and

interleukin 6. In

addition, some AGEs

are immunogenic (causing

age-related auto-immunity) or

mutagenic (increasing the risk of cancer),

whereas others increase the activity of

adhesion molecules, reduce protein

degradation rate and reduce cell

proliferation, all of which ensure that the

risk of degenerative disease is increased.

Also, AGEs stimulate apoptosis, resulting

in excessive loss of cells and contributing

further to the risk of degeneration. Some

AGEs up-regulate genes which are

involved in chronic inflammation

reactions.

At the clinical level, cross-linking

contributes significantly to diabetic

complications, lower immunity and

increased risk of cancer, atherosclerosis

and hypertension, Alzheimer 's disease

32 i a i t l April/May 2006

anti-

cross-

linking effects.

(through

the formation

of amyloid, which is a

type of AGE), cataract,

kidney damage, skin aging, and

other age-related diseases (2).

The process of cross-linking through

glycation was hitherto thought to be

irreversible, and this was one typical

example of the immutability of aging.

There are hundreds of compounds aimed at

preventing cross-linking, but during the

past few years, new products have also

been developed directed specifically at

breaking the abnormal bonds between

already cross-linked proteins, practically

reversing protein aging (3). Both classes of

drugs, the cross-link inhibitors and the

cross-link breakers, have been found to

offer remarkable benefits at the clinical

level.

Cross- l ink Inhib i tors

There are several commercially available

inhibitors of cross-linking. Examples of

these include carnosine, aminoguanidine,

metformin, acarbose, and pyridoxamine.

Some of these (like acarbose and

metformin) are already in use as anti-

diabetic drugs but new research coming to

light is now emphasizing their additional

Other not yet widely available

inhibitors are Tenilsetam, OPB9195,

phenazinediamine (2,3-

diaminophenazone), and many others still

in development (4).

Many cross-link inhibitors are nucleophilic

traps, (scavengers) for reactive carbonyl

intermediates. They are also copper

chelators, and so they minimize the risk of

both cross-linking and consequent AGE-

related damage. In addition, they block

soluble receptors (sRAGEs) or specific

receptors (RAGEs) which recognize AGEs.

Some soluble receptors circulate freely,

whereas specific ones can be found on

macrophages, fibroblasts and endothelial

cells. When an AGE molecule interacts

with a RAGE it forms an adduct which is

then prone to create more damage through

oxidation and increased metal toxicity.

C a r n o s i n e

The dipeptide carnosine (beta alanyl- L-

histidine) is a naturally-occurring agent

found in muscle and nervous tissue (5).

Carnosine has been hailed as one of the

most promising cross-link inhibitors. It has

multiple actions and as such it has been

called a pluripotent agent. One way

carnosine works is by scavenging for free

carbonyl groups. Carnosine is one of

the few cross-link inhibitors

that is not only active

against protein-

to-protein

cross-

linking but

also against

protein-to-DNA cross-

linking (6).

Another important carnosine activity is

'carnosinylation' , which is a process

whereby carnosine attaches to the protein

bearing a carbonyl group, thus blocking the

carbonyl from attaching to another protein.

It is just like placing a piece of paper

(carnosine) between two proteins bearing

glue (carbonyls). In other words, carnosine

reacts with carbonylated proteins to form

carnosine-carbonyl-protein adducts. These

adducts are then removed by proteolysis

and degradation. Conveniently, carnosine

also stimulates and enhances the process of

proteolysis (7).

Carnosine has a direct antioxidant action,

and it also has a sparing effect on other

antioxidants such as glutathione. It is a

strong chelator of copper thereby reducing

the copper-mediated damage during AGE

activity. Finally, it has a possible, yet

unconfirmed, bond-breaking capability by

dissolving certain bonds (S-S bonds) on

cross-linked proteins.

At the clinical level, carnosine reduced

urinary products of free radical and

glycosylation metabolism in humans (8).

One of the most important developments

regarding carnosinc is its ability to

prevent and cure age-related

cataract, and possibly

glaucoma and

other

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It is now well established that the

process of glycosylation is one of the

most important causes of aging, perhaps

equally as important as the process of

oxidation (free radical damage).

Cross-linking is the process that causes

food to turn yellow and become tough

with age. Similarly with humans, cross-

linking may be responsible for many of

the problems of old age, including senile

cataracts, thickening of the arteries,

some cancers and damage to the

immune system.

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3 4 i a m April/May 2006

age-related eye conditions (9). In this

respect the form of carnosine used is N-

acetyl-carnosine. This curative action of

carnosine is perhaps related to its ability to

stimulate proteolysis and thus dissolve

protein aggregates in the lens.

People taking 50 mg. to 300 mg. of

carnosine a day have not reported any side

effects whereas those taking higher doses

(1000 mg. to 1500 mg. a day) have

reported occasional histamine-related

allergic reactions.

Metformin

Metformin (brand names Glucophage,

Metforal) is a standard anti-diabetic drug

(dimethyl-biguanide) used worldwide both

against insulin-dependent and against non-

insulin-dependent diabetes. Although it is

used primarily to increase peripheral

sensitivity to insulin and lower blood

glucose, metformin has several other

important actions which are not yet

appreciated by many physicians.

Metformin lowers cholesterol, reduces

body fat, stimulates antioxidant defenses

(10) and it is also an effective inhibitor of

glycation. It reduces the formation of

AGEs, particularly those affecting

collagen. In that respect, it prevents

diastolic stiffness in the myocardium of

diabetic dogs (11). It has direct anti-

glycation effects and improves cross-

linking induced damage to nerves in

diabetic rats. Its main mechanism of action

is its carbonyl trapping ability, as will be

explained below.

In a clinical trial examining 57 people with

type 2 diabetes, treatment with

metformin was shown to rcduce

the concentration of

methylglyoxal in a

dose dependent < |

(12). Methylglyoxal, and the related

compound, glyoxal, are both reactive

carbonyl agents (alpha-dicarbonyls) which

are blocked by the quanidine molecule,

(remember that metformin is a guanidine-

containing drug). Specifically, the

guanidine moiety of metformin combines

with methylglyoxal dicarbonyls to form

guanidine-dicarbonyl adducts which are

then eliminated from the tissues (13). With

reduced amounts of carbonyl groups in the

tissues, the likelihood of cross-linking is

reduced. This mechanism of action is

similar to that of aminoguanidine (below),

which, as the name suggests, it is also a

guanidine-containing molecule.

More recent experiments show metformin

to have widespread activities as a cross-

link inhibitor. It reduces cross-linking of

fibrin proteins which take part in the

clotting of blood. Exaggerated cross-

linking of fibrin results in abnormal blood

clotting and therefore an increased risk of

thrombosis with consequent myocardial

infarction or stroke. Metformin reduces

fibrin cross-linking and therefore,

ultimately, reduces the risk of thrombosis

(14).

In summary, with regards to glycation,

metformin has a dual effect- it lowers

blood glucose, and as new research is

revealing, it is an effective inhibitor of

cross-linking through carbonyl

trapping.

Metformin should be

used under

medical ^ M p M M

M l

supervision with monitoring of the liver

and kidney function. The dose is 500 mg.

twice to three times a day. Dr Ward Dean

recommends that everybody who is over

the age of 40 should be taking metformin,

and research into the anti-glycation

benefits of metformin supports this

recommendation, as a preventative anti-

AG E drug.

Aminoguanidine

An agent structurally similar to metformin

is aminoguanidine, (sometimes called

Pimagidine) which has been studied

relatively extensively and the reports have

been encouraging. As with the case of

metformin, aminoguanidine is also a

guanidine-containing agent, and it

therefore acts as a carbonyl trapping agent

(15).

Aminoguanidine too works by forming

guanidine-dicarbonyl adducts, thereby

reducing the numbers of free carbonyl

groups. In particular, it is active against

certain aldehydes which contribute to

cross-linking, (e.g. alpha-oxoaldehyde, and

malondialdehyde). Aminoguanidine is

active mainly during the early stages of

glycosylation.

It is an effective inhibitor of cross-linking

initiated by glucose molecules, but not as

effective in situations involving

ribose-related cross-linking. In

any case, Aminoguanidine

prevents collagen

cross-linking

tendons

and skin

which shows its

potential for prevention of

muscle and joint age-related

stiffness, and skin aging wrinkles. (16) It

limits the development of diabetic

complications in animals and it has shown

promising actions in improving diabetic

nephropathy in double blind human trials

(17). In addition, it is a weak copper

chelator. Copper chelation is important in

AGE induced damage, as high amounts of

free copper are more likely to increase

AGE-induced injury.

nausea

or headache.

There are two main

varieties of

aminoguanidine, the hydrochloride

and the bicarbonate variety. Although the

bicarbonate variety is more commonly

available, the hydrochloride version is

Aminoguanidine prevents

cardiac enlargement in animal

studies by reducing the risk of

glycation-induced damage to

cardiac collagen. Also, it

prevents cross-linking between

lipoproteins, (proteins carrying

fat molecules) and therefore

reduces the risk of blockage of

the arteries, particularly the

small arteries that feed the

nerves (18).

S o 1 Control A 5 1

Vitamin C O 1 0

% 5 1

Vitamin C O 1 0

% 5 1 DHA - 0 . 1 1

n r 1 Pyridoxa! * 5 1

Pyridoxa!

U 0 . 1 H • 1 2 0.5 1 Pyridoxamine

£ 5 1 1= S l- Aminoguanidine Aminoguanidine

0 20 40 60 80 100

% labeling

In vitro compar ing the fo rmat ion of AGEs on bovine s e r u m a lbumin when exposed to glucose. Note the dramat ic reduct ion when aminoguanid ine or pyr idoxamine are added, (khatami, et al. Life Sciences, 1988)

It is such a strong carbonyl scavenger that

it can sometimes result in excessive

removal of carbonyl groups (which, in

small quantities, are necessary for the

normal functioning of the metabolism).

This can, on rare occasions, give rise to

toxicity particularly if aminoguanidine is

used in excessive doses (over 600 mg.

daily without medical supervision). In

theory, the concomitant use of

pyridoxamine (see below) can reduce the

likelihood of this potential problem.

The dose is 150 mg. once or twice a

day, but diabetics may use

double this dose. Side

effects are rare and

mild and

include

believed to be the most active

(bioavailable) as it is more soluble.

Aminoguanidine may be used together

with carnosine which is active both in early

and late stages of glycosylation, or together

with metformin, particularly in diabetics.

Acarbose

Another drug used in diabetes, Acarbose

(Glucobay) is an alpha-glucosidase

inhibitor. Alpha-glocosidases are enzymes

which facilitate the breakdown of complex

carbohydrates, (such as starch) into smaller

sugar molecules which are then absorbed

through the intestinal wall. Acarbose

blocks this, therefore inhibiting the

absorption of certain sugar molecules such

as maltose and sucrose, while allowing the

absorption of glucose and lactose, which

April/May 2006 i a i l l 35

are needed for energy. In this way the

overall absorption of carbohydrates is

reduced and this lessens the risk of

glycation-induced damage and AGE

formation.

Acarbose's main activities include a

reduction of blood lipids (reduced uptake

of triglycerides), an aid to weight loss, as

well as being an important anti-glycation

activity (19). As with the case of

metformin, acarbose has hitherto been used

primarily to reduce blood glucose and

therefore improve the symptoms of

diabetes. However, new research is

unraveling its anti-glycation properties

which are in addition to its glucose-

lowering actions. For this reason, acarbose

is not only indicated for treatment of

diabetes, but also for treatment of diabetic

complications and other AGE-related

damage.

Several studies have shown that Acarbose

reduces the formation of glycated proteins

(including the glycated hemoglobin A l e

which is a marker for diabetes). Animal

models show an ability of acarbose to slow

down the rate of protein glycation and

delay renal, brain and eye complications of

diabetes (20).

Other studies confirm its effectiveness in

protecting against nephropathy, neuropathy

I retinopathy in diabetes, by its ability

i lower AGE formation (21). With

^regard to the kidney-

^protecting effects of

_ acarbose, it was

shown that

III*. possible

mechanism

could be its ability

to protect the glomerular

membranes, (where filtering

urine takes place in the kidney)

against the effects of cross-linking (22).

Acarbose is safe but it may have side

effects such as abdominal pain and cramps,

bloatedness and diarrhea. These are due to

excessive amounts of unabsorbed

carbohydrates in the bowel. The usual dose

is 50 mg. to 100 mg. daily but the

maximum should be kept to 300 mg a day

to prevent these side effects. For greater

benefits, it may be worth using acarbose

together with other cross-link inhibitors

such as carnosine. (Ed.- Acarbose is best

taken by chewing the tablets, usually just

before or during meals).

Pyridoxamine

There are three different vitamers of

Vitamin B6: pyridoxal, pyridoxine (the

form traditionally used in supplementation)

and pyridoxamine. All of these are

naturally occurring. Pyridoxamine is found

in animal sources, whereas pyridoxine is

also found in plant sources. All three

variants have a certain degree of anti-cross-

linking actions, but pyridoxamine is the

strongest and most significant of the B

vitamins. Trials are in progress to evaluate

the product's safety and efficacy in

preventing diabetic complications.

Pyridoxamine prevents the formation of

AGEs by 25 to 50% and ameliorates

diabetes-related kidney dysfunction, (it

improves albuminuria, plasma creatinine

hyperlipidemia). It works by

^trapping reactive carbonyl

^groups (27) and exhibits

free radical

scavenging

properties

(28). It is most

effective in the later

stages of glycosylation and

therefore, for full protection, it

may be used together with

aminoguanidine which is active in the early

stages of glycosylation. In fact, comparison

studies with aminoguanidine suggest that,

although both are effective against AGEs,

pyridoxamine may be a more versatile

agent to use against glycosylation, in order

to avoid the low risk of potential toxicity

problems with aminoguanidine mentioned

above (29).

Pyridoxamine does not affect the levels of

blood glucose. It inhibits both

methylglyoxal and glycoaldehydes which

are most active following lipid

peroxidation. It forms methylglyoxal-

pyridoxamine dimers which are inactive

and eliminated easily (30).

There have been reports of neurotoxicity

from using very high doses of pyridoxine,

but the use of pyridoxamine is thought to

be free from these side effects. The reason

is that pyridoxamine needs to be

phosphorylated (i.e. it needs the addition of

phosphate on the main molecule) before it

can become active.

Cross-link Breakers

The most important cross-link breaker is

the drug Alagebrium (ALT-711), an orally

active compound. This is a thiazolium

product (dimethyl-3-phenacyl-thiazolium

j a m April/May 2006

I

chloride)

manufactured

I t by the Alteon

Corporation in the US. A

related compound is PTB

(dimethyl-Phenacyl-Thiazolium

Bromide), which has actions similar to the

chloride variety. Alagebrium is not an

enzyme as such, but it has enzymatic

properties. It has been shown to actually

break the covalent bonds between cross-

linked proteins and free the proteins which

are then able to function again normally.

Alagebrium breaks the bonds although, in

theory, the bonds may then re-form,

(because the carbonyl group is still active

on the freed protein), Alagebrium has

benefits which persist after the drug is

stopped (Alteon Corporation, personal

communication). In other words, if the

proteins are cross-linked again, Alagebrium

will divide them once more, and if they are

then rebound, it will keep on separating

them. For this reason, it may be necessary

to use a combination of the cross-link

inhibitor carnosine together with

Alagebrium for full protection against

cross-linking. In that situation, when the

bond is broken, carnosine will immediately

bind to the carbonyl group (i.e. it will

'carnosinylate' the protein) and therefore

cross-linking of that particular protein will

not take place for the second time. The

Alagebrium molecule will then be free to

seek out other cross-linked proteins to

work on.

Alagebrium can reverse aortic stiffening in

jji; rodents,

w^r canines and

primates. A 40%

i reduction on age-related

left ventricular stiffness (in

^ ^ dogs) was reported after just one

month of treatment (37). Other

experiments support its effectiveness

against hypertension, cardiovascular

stiffness and heart failure (38).

It has also been studied in a number of

human clinical trials. It was found to be

effective in reversing some of the

complications of diabetes, improving

myocardial and arterial stiffness, heart

failure, and reducing blood pressure (39).

However, far from being unique,

Alagebrium is in a group of 375 other

cross-link breakers developed by Alteon

alone!

Summary

The best cross-link inhibitors currently

available are aminoguanidine,

pyridoxamine, carnosine, metformin and

acarbose, whereas others are now

becoming available. No cross-link breakers

are commercially obtainable as yet, but

these will be marketed within a few years.

Soon after, combinations of inhibitors and

breakers are bound to follow.

References

1. Suzuki D, Miyata T, Kurokawa K.

Carbonyl Stress. Contrib Nephrol

2001,134:36-45

2. Dukic-Stefanovic S, Schinzel R, Rieder

R AGEs in brain aging: AGE-inhibitors as

neuroprotective and anti-dementia drugs?

Biogerontology 2001, 2(1): 19-34

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body's sugar-protein bond might turn back

the clock, Sci Am 2000, 283(1): 16

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4. Bonnefont-Rousselot D, Antioxidant and

anti-AGE therapeutics, J Soc Biol

2001,195(4):391 -398

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Physiological properties and therapeutic

potential. Age Aging 2000, 29:207-210

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reacts with protein carbonyl groups:

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7. Hipkiss A, Brownson C et al. Reaction

of carnosine with aged proteins. Annals

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Efficacy of N-acetylcarnosine in the

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38 i a m April/May 2006

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