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ANTIAGING magazine

BEYOND CHOLESTEROL

Know Your Heart Attack Risk Factors

LEU aging expert Dr Marios Kyriazis defines the term iltimate smart drug

Rasagiline its benefits and the ilts of the clinical trials

interview iscuss BEC5 Curaderm with Dr Bill Cham H

2006

$6.50 USA £3.50 UK €5.30 Europe W

welcome

protocols that we want to inform you about - it's also the people in antiaging medicine, the books being written, and events that are taking place.

W e l c o m e to the first issue o f 2006. W e trust that

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Medicine today. A l l their thoughts and ideas are

O u r efforts continue to expand the magazine's appeal, particularly its information breadth and its diversity o f interest.

based on the published evidence. This is apparent by the fact that the references are printed at the end, so i f you wish, you can check out the technical details yourself.

O u r approach is simple, we intend to m a k e people aware o f internationally recognised antiaging developments and breakthroughs. So i f you want to find out what is going on and keep up-to-date with w o r l d w i d e events in health and medicine, particularly those focused on

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advisors The International Antiaging Magazine is proud to be regularly contributed to by, and also aided and supported by the following professional persons: Mircea Dumitru. M.D., Ph.D. was born in Romania and speaks 6languages fluently. He is the Editor of the International Journal of Gerontology and Geriatrics, based in Mexico City. He has extensive experience in Geriatrics, having completed his externship in 1958. 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. (HI received his DO in 1958 and an honorary MD degree in 1962, He completed Radiology in 1964 and for many years was also the Medical Director of Mineral Lab. As a worldrenowned expert in chelation therapy, Dr. Gordon is 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. He has been establishing cutting-edge research into the causes and progression of numerous skin diseases. His work has lead him to develop a comprehensive diagnostic system to enable genetic identification of metabolic failures, which can then result in individualized detox and antiaging therapies.

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February/March 2006

Karen Kaufman MS. CCN is a Phi Beta Kappa graduate of Skidmore College. She received a Master of Science Degree in nutrition from the University of New Haven in Connecticut. She has worked at UMass 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 and the author of numerous articles and lectures.

Marios Kyriazis. M.D.. MSc.. MIBiol. has a postgraduate qualification in Gerontology from the King's College, University of London, as well as a postgraduate qualification in Geriatric medicine granted by the Royal College of Physicians. He has written extensively on longevity, healthy aging and anti-aging matters for both scientists and the general public. He is a founder member of the British Longevity Society.

Robert Mason, Ph.D. was schooled information technology and realized the potential for research in the (then) coming information revolution. Family health concerns and a knowledge of international research taught him many "lessons." The result was the formation of an organization conducting global database research.

As a researcher, Dr. Mason believes that aging is a disease and will be

curable.

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 co-writer of the New Millennium Guide to Antiaging Medicine. He is also the Vice President of International Antiaging Systems.

John Morqenthaler has been active in the field of nutritional medicine since 1986. As a founder of Smart Publications, John has co-authored numerous health books, including Smart Drugs, Stop the FDA, Better Sex Through Chemistry, Natural Hormone Replacement for Women, and GHB: The Natural Mood Enhancer.

Walter Pierpaoli. M.D. is a pioneering research physician who introduced the concept of melatonin supplements to the world through his best selling book, The Melatonin Miracle. He graduated in Medicine and Surgery at the University of Milano, Italy in 1960. Since then has held numerous key positions and is Director of the Jean Choay Institute for Biomedical Research in Riva San Vitale Switzerland and President of the Interbion Foundation for Biomedical

Research in Zurich, Switzerland.

Recently the Walter Pierpaoli Foundation for Life Sciences has been established in Italy.

Jonathan Wright. M.D. Jonathan Wright 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 groundbreaking publications. His pioneering books; Book of Nutritional Therapy (1979) and the: Guide to Healing with Nutrition (1984), have together sold 650,000 copies. From 1994 to the present, Dr. Wright has also written the respected monthly newsletter: Nutrition & Healing.

Imre Zs.-Naqy. M.D. is Professor of Gerontologyy at the University of Debrecen, Hungary. He is a teacher in experimental gerontology and was a pupil of the science of Fritz Verzar. He has published 275 papers, chapters and books, given 340 scientific lectures. He is founder (1982) and Editor-in-Chief of the journal Archives of Gerontology and Geriatrics; recipient of the Monte Carlo Award for Excellence in Anti-Aging Medicine in 2002. He developed the membrane hypothesis of aging, which is a universal, comprehensive explanation of the biology of aging, on the basis of

Beyond Cholesterol Heart attacks are the number one killer and most prevalent in the western world where diets and lifestyles increase the risk considerably. Yet if mainstream medicine is to be believed, cholesterol is the virtual beall and end-all when it comes to monitoring the risk of having a heart attack. Yet there is much evidence that supports many other factors to be as important- if not more important than cholesterol. Nutritionalist Karen Kaufman walks us through what we all should be looking for and doing to ensure that we have the lowest risk of cardiovascular disease.

What is antiaging medicine?

Antiaging can be described in many different ways and over the years it has been used so widely that today there is confusion over its precise meaning, especially when it is accompanied by the word- medicine. Antiaging physician Marios Kyriazis with his vast experience of practice, research, lectures/ conferences etc., explains to us his interpretation of this terminology and how antiaging medicine differs from other branches of medicine such as geriatric medicine etc.

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.

also The latest drug for Parkinson's disease Rasagiline has recently been approved in parts of Europe under the brand name of Azilect. It has a novel new approach to treat the senile dementia associated with dopamine loss. Pharmacologist Phil Micans explains its actions, benefits and the outcomes of the clinical trials.

The mitochondrial theory of aging Antiaging medicine needs a focus if it truly wants to treat the underlying cause of the "disease." As such we need to look at some of the theories of why and how we age, from this knowledge a specific regime of antiaging medicine can be prescribed. In one of his last articles, biochemist James South looks at the role of the mitochondria in aging.

The ultimate smart drug Since the invention of piracetam in the 1960's the term "smart drug" has come to mean anything that acts positively on the brain to improve memory etc. Piracetam was the original "nootropic" and others have been developed from it since then. The latest and most potent form is known as pramiracetam. Researcher Robert Mason tells us about pramiracetam and why it may be the ultimate smart drug.

regulars News

Disclaimer: The information is offered under the IAS terms and conditions and is for educational purposes only and should not replace the advice of your personal physician.

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, c/o P() Box 437, Emigsville, PA 17318-0437 Declaration The Anti-Aging Magazine focuses on the latest international 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.

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Metformin could lower the risk of cancer Patients taking the most commonly prescribed oral therapy for diabetes, metformin, may get an extra benefit - a lower risk of dying from cancer.

A retrospective study reported at the European Association for the Study of Diabetes (EASD) meeting found that patients with type II diabetes using metformin had a 23% lower risk of cancer death.

Researchers at the University of Dundee, Scotland, analyzed data from two large registries, one included data from roughly 13,000 diabetic patients in Britain.

Dr. Alistair Emslie-Smith, and colleagues, reported their findings in a report in the June 4, 2005 issue of BMJ, saying that 983 patients with type II diabetes were diagnosed with cancer within a year of being diagnosed with diabetes. Those cases were matched against 1,846 patients with type II diabetes who were cancer-free. Researchers could find no factors- age, sex, duration or severity of diabetes, smoking, cholesterol levels, weight etc., to explain the difference except metformin use.

There was an inverse relationship between metformin exposure with higher doses and longer use and cancer mortality, but the researchers said there was a trend toward lower cancer mortality even among patients who took only a single dose of metformin.

The group agreed that the finding, while provocative, is mainly hypothesis. For example, the investigators pointed out that there they have not yet linked metformin to prevention of any particular type of cancer, nor are they prepared to suggest that metformin could reduce cancer

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MlK risk in non-diabetics. "It is too early to think it (metformin) will become mainstream for patients to prevent cancer, but we know it has a role in pre-diabetics," said Dr. Emslie-Smith. "If long periods of [metformin] are shown beneficial, then maybe that will justify using it earlier in patients at high risk."

Is Alzheimer's another form of diabetes?

As reported in the Journal of Alzheimer's Disease, 2005 Feb;7(l):63-80, a study from Brown University has linked declining insulin production to Alzheimer's disease, leading to the question- is Alzheimer's a form of diabetes?

"Insulin disappears early and dramatically in Alzheimer's disease;" said Suzanne M. de la Monte, a neuropathologist at Rhode Island Hospital and professor of pathology at Brown University Medical School. "Many of the unexplained features of Alzheimer's, such as cell death and tangles in the brain, appear to be linked to abnormalities in insulin signaling. This demonstrates that the disease is most likely a neuroendocrine disorder, or another type of diabetes."

The researchers found that brain insulin produced by patients with Alzheimer's disease tends to be below normal levels and that brain levels of insulin and its related cellular receptors fall

during the early stages of Alzheimer's. Insulin levels then continue to drop progressively as the disease continues.

The scientists autopsied the brain tissue of 45 patients diagnosed with different degrees of Alzheimer's. They compared the tissues to samples taken from individuals with no history of the disease. When the team analyzed insulin and its receptor function in the frontal cortex, (an area of the brain badly affected by Alzheimer's), they found that as the severity of Alzheimer's increased, the levels of insulin receptors and the brain's ability to respond to insulin decreased. "In the most advanced stage of Alzheimer's, insulin receptors were nearly 80% lower than in a normal brain," de la Monte said.

In addition, the researchers found two abnormalities related to insulin in Alzheimer's. First, levels of insulin dropped as the disease progressed. Second, insulin and its related protein; IGF-1, lose the ability to bind to cell receptors.

This creates a resistance to the insulin growth factors, causing the cells to malfunction and die. In addition, the Brown University team found that low levels of acetylcholine, a well known indicator of Alzheimer's, is also linked to the loss of insulin.

De la Monte went on to say that; "We're able to show that insulin impairment happens early in [Alzheimer's] disease. We're able to show it's linked to major neurotransmitters responsible for cognition. We're able to show it's linked to poor energy metabolism, and it's linked to abnormalities that contribute to the tangles characteristic of advanced Alzheimer's disease. This work ties several concepts together and demonstrates that Alzheimer's disease is quite possibly a type III diabetes!"

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Cardiovascular disease (CVD) in one of its various forms is the leading cause of morbidity (illness) and mortality (death) worldwide. It would be more accurate to say that atherosclerosis is the leading cause of morbidity and mortality.

"atherosclerosis is a disease that takes root early in life and grows for decades before clinical symptoms appear The focus of public health initiatives in the

Arteriosclerosis or atherosclerosis, (the build up of plaque within the large and medium arteries of the body) is better known as coronary artery disease (CAD), carotid artery disease/ cerebrovascular disease (CVD), or peripheral artery disease (PAD). It is important to remember that atherosclerosis is one disease process that may manifest in different arteries and therefore puts different organs at risk.

Cholesterol belongs to a class of chemicals known as lipids. Cholesterol is necessary for life. It is the raw material from which the body makes steroid hormones, mineral corticoids, glucocorticoids, vitamin D and bile acids. It is present in every cell membrane and maintains cellular integrity.

It is so important that if there is not

When the coronary arteries become narrowed with plaque build up, a person can develop ischemia (transient pain due to limited blood flow), a heart attack, chronic heart disease, or congestive heart failure. When the carotid arteries of the neck are plaque laden, a person may develop a stroke or vascular dementia because the arteries can no longer carry oxygen filled blood to the integral parts of the brain. When the major arteries of the legs are compromised with plaque build up, a person develops pain when walking or peripheral neuropathy. When the arteries supplying the kidneys are compromised, renal function is impaired.

Of course, at any time plaque from anywhere in the body can rupture and form a clot (thrombus). When a clot travels to the heart, it causes a myocardial infarction (heart attack). If a clot travels to the carotid arteries it can cause an acute

World Health Organization (WHO), CVD accounted for 16.7 million deaths globally in 2003 According to the

The unfortunate reality is a significant percentage of these deaths could have been prevented by reducing the risk factors that contribute to the development of atherosclerosis.

stroke. If a clot travels to the lungs it is called a pulmonary embolism and can often lead to sudden death.

United States has been a strident campaign to reduce the major risk factors: high cholesterol, smoking, high blood pressure, and diabetes. There are additional modifiable risk factors that deserve our vigilance if we want to maintain our vitality throughout the aging process.

Novel risk factors 1. Homocysteine (a chemical that damages the vessel wall and increases the tendency to form a clot).

2. Fibrinogen (a marker of increased coagulation).

3. Lipoprotein (a) (a protein that inhibits fibrinolysis).

4. C - Reactive Protein (CRP) (a marker of inflammation).

Fifty years ago, atherosclerosis, often called hardening of the arteries, was considered a disease of older people. In 1953, fundamental theories about the pathogenesis of coronary artery disease were turned upside down with the publication of a paper in the Journal of American Medical Association describing the extent of coronary artery disease in otherwise healthy soldiers killed in combat in Korea.

Similar findings were reported in 1971 when autopsies were performed on combat casualties in Vietnam. McNamara and his group reported that out of 105 soldiers examined (average age 22) 45% had some evidence of coronary atherosclerosis, and 5% had gross evidence of severe coronary atherosclerosis. It was obvious that atherosclerosis in susceptible individuals could begin very early in life.

This new hypothesis has proven to be true in the last 50 years. The notion that atherosclerosis is a disease that takes root early in life and grows for decades before clinical symptoms appear has dramatic implications for all of us and our children.

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Atherosclerosis 101

enough cholesterol supplied by the diet, the body will synthesize cholesterol from fat, glucose and protein in the liver.

Problems arise when there is an excess of cholesterol.

Besides the cholesterol absorbed each day from the gastrointestinal tract, which is called exogenous cholesterol, a large quantity, called endogenous cholesterol, is formed in the cells of the body.

Essentially all the endogenous cholesterol that circulates in the serum is formed by the liver, but all other cells of the body are able to form some cholesterol. Cholesterol travels through the bloodstream within spherical particles called lipoproteins.

Each cholesterol fraction is made up of protein and lipid. Two lipoprotein fractions are involved in transport of lipid to peripheral tissues, very low density lipoproteins (VLDL) from the liver and chylomicrons from the intestinal tract. As the lipid portion is removed from the respective lipoproteins, the density of each fraction increases. VLDL becomes intermediate density lipoprotein (IDL) and eventually low density lipoprotein (LDL).

The chylomicrons become chylomicron remnants. VLDL contains triglycerides which are now fractionated separately and

can be an i n d e p e n d e n t risk f a c t o r f o r

can be d e s t a b i l i z e d and rupture. T h a t

a t h e r o s c l e r o s i s . High d e n s i t y lipoprotein

r u p t u r e a p p e a r s to m e d i a t e d by

( H D L ) is i n v o l v e d in r e v e r s e cholesterol

i n f l a m m a t i o n . At that point part o f the

transport. T h e H D L particle is the s m a l l e s t ,

a t h e r o m a will break o f f , recruit platelets

h e a v i e s t , and least fatty particle. H D L

and f o r m a blood clot that can lodge in a

c h o l e s t e r o l p i c k s u p the c h o l e s t e r o l f r o m

critical artery.

the p e r i p h e r y and returns it t o the liver w h e r e it b e c o m e s bile a c i d s and is

A s sclerotic p l a q u e s f o r m , n o r m a l

i n n o c u o u s l y e x c r e t e d f r o m the s y s t e m .

e n d o t h e l i a l f u n c t i o n is c o m p r o m i s e d . For y e a r s the e n d o t h e l i u m w a s c o n s i d e r e d an

T h e m e d i c a l p r o f e s s i o n ' s f o c u s on h y p e r c -

inert barrier to e l e m e n t s c o n t a i n e d in t h e

h o l e s t e r o l e m i a (high c h o l e s t e r o l ) as t h e

blood. H o w e v e r , it is n o w a p p a r e n t that

root c a u s e o f heart d i s e a s e c a m e f r o m

the e n d o t h e l i u m m a i n t a i n s t h e b a l a n c e

early t h e o r i e s a b o u t h o w h a r d e n i n g of the

b e t w e e n v a s o d i l a t i o n and v a s o c o n s t r i c t i o n ,

arteries b e g a n . T h e belief w a s w h e n there

inhibition and s t i m u l a t i o n o f s m o o t h

is an e x c e s s o f c h o l e s t e r o l in the b l o o d

m u s c l e cell proliferation and m i g r a t i o n ,

s t r e a m , n o t a b l y low d e n s i t y lipoprotein

and t h r o m b o g e n e s i s a n d f i b r i n o l y s i s .

( L D L ) , s o m e of that c h o l e s t e r o l w o u l d

[ T h r o m b o g e n e s i s is the creation o f a

leave the b l o o d s t r e a m and p e n e t r a t e the

t h r o m b u s or blood clot and f i b r i n o l y s i s is

arterial w a l l , p r e c i p i t a t i n g a series of

the 'lysis' or d i s s o l v i n g of fibrin w h i c h is

cellular e v e n t s that c u l m i n a t e d in the

formed from

fibrinogen.]

formation of plaque.

n u m b e r of T l y m p h o c y t e s , s u p p o r t i n g the T h e m a j o r v a s o d i l a t i n g s u b s t a n c e released

In the early 1990's a n e w theory, first

by t h e e n d o t h e l i u m is nitric o x i d e ( N O ) .

d e s c r i b e d by Russell Ross, posits that

O t h e r s u b s t a n c e s released such as

a t h e r o s c l e r o s i s is an i n f l a m m a t o r y disease.

p r o s t a c y c l i n c o n t r i b u t e to the inhibition o f

A t h e r o s c l e r o s i s or a r t e r i o s c l e r o s i s is a

platelet a g g r e g a t i o n . B r a d y k i n i n a l s o

g e n e r i c term for several d i s e a s e s in w h i c h

s t i m u l a t e s the release o f N O and tissue

an arterial wall b e c o m e s t h i c k e n e d and

p l a s m i n o g e n a c t i v a t o r (t-PA) w h i c h p l a y s

loses elasticity. T h e e n d o t h e l i u m b e c o m e s

a role in

d a m a g e d b y a n y n u m b e r of the risk

produces vasoconstrictor substances, most

factors, i.e. h o m o c y s t e i n e , s m o k e , o x i d i z e d

n o t a b l y e n d o t h e l i n and a n g i o t e n s i n II.

L D L c h o l e s t e r o l , etc. T h e b o d y m a k e s an

[One category of blood pressure lowering

a t t e m p t to repair this d a m a g e by r e c r u i t i n g

m e d i c a t i o n w o r k s by p r e v e n t i n g

cholesterol, platelets, s m o o t h m u s c l e cells,

v a s o c o n s t r i c t i o n by t a r g e t i n g a n g i o t e n s i n

cell a d h e s i o n m o l e c u l e s , c y t o k i n e s ,

II.]

fibrinolysis.

The endothelium also

i n f l a m m a t o r y theory. T h e r e is e v i d e n c e that fatty streaks begin to a p p e a r in c h i l d h o o d . In fact, a l m o s t e v e r y N o r t h A m e r i c a n child o v e r the a g e o f 3 y e a r s old has s o m e d e g r e e o f aortic fatty streaks.

T h e role o f o x i d i z e d L D L c h o l e s t e r o l c a n n o t be m i n i m i z e d . Studies h a v e s h o w n that o x i d i z e d L D L ( o x - L D L ) p r o m o t e s t h e p a t h o g e n e s i s and d e v e l o p m e n t o f atherosclerosis. Obviously the process of atherosclerosis occurs over decades.

Clinical s y m p t o m s m a y b e g i n to a p p e a r in high risk i n d i v i d u a l s in the third or f o u r t h

m o n o c y t e s , and m a c r o p h a g e s . O t h e r

d e c a d e . S y m p t o m s in m a n y i n d i v i d u a l s

i n f l a m m a t o r y m o l e c u l e s are called into

In addition to v a s o c o n s t r i c t i o n , e n d o t h e l i n

a p p e a r m u c h later. In general w o m e n

action. T h i s site b e c o m e s a w e i g h station

and a n g i o t e n s i n II p r o m o t e p r o l i f e r a t i o n o f

p r e s e n t with s y m p t o m s a d e c a d e later than

w h e r e m o r e o x i d i z e d L D L cholesterol can

s m o o t h m u s c l e cells and in so d o i n g

m e n . T o o o f t e n a p e r s o n ' s first s y m p t o m of

deposit. T h e d e p o s i t i o n of platelets,

c o n t r i b u t e to p l a q u e f o r m a t i o n .

a t h e r o s c l e r o s i s is death f r o m a m a s s i v e

c y t o k i n e s , cell a d h e s i o n m o l e c u l e s , etc

T h e m a c r o p h a g e s and v a s c u l a r s m o o t h

m y o c a r d i a l i n f a r c t i o n ( M l ) or heart attack.

c o n t i n u e s . C a l c i u m in the b l o o d stream

m u s c l e cells that constitute the a t h e r o m a

U n d o u b t e d l y , it w o u l d be best to p r e v e n t

also d e p o s i t s and a c o m p l e x lesion or

a l s o p r o d u c e large a m o u n t s o f e n d o t h e l i n

the early lesions in the first place. S i n c e

so this u n h e a l t h y c y c l e can self p e r p e t u a t e .

that a p p e a r s unlikely, strategies s h o u l d

plaque forms.

T h i s endothelial d y s f u n c t i o n upsets the

f o c u s on s l o w i n g or r e v e r s i n g this p r o c e s s

T h i s c o m p l e x lesion is called an a t h e r o m a

v a s c u l a r h o m e o s t a s i s and initiates a

that e v e r y o n e s e e m s v u l n e r a b l e to.

or p l a q u e and it can interfere with blood

n u m b e r of e v e n t s that p r o m o t e and

How b y n a r r o w i n g the lumen (the f r e e

exacerbate atherosclerosis. These

s p a c e in the c e n t e r o f the artery t h r o u g h

p r o c e s s e s include increased e n d o t h e l i a l

w h i c h t h e blood f l o w s ) . In addition, it will

permeability, platelet a g g r e g a t i o n ,

c o n t i n u e to collect L D L cholesterol,

l e u k o c y t e a d h e s i o n , and p r o d u c t i o n of

particularly o x i d i z e d L D L , and o t h e r lipid

inflammatory cytokines.

particles until the artery b e c o m e s completely occluded. A complex plaque

"obesity contributes dramatically to inflammation and other risk factors that promote

atherosclert

How to delay the

inevitable

If y o u are at all like me, by n o w y o u are t h i n k i n g w h a t h o p e is there for m e ? I'm a bit o l d e r than 3, and there is that c h u n k of

T h e very first e v e n t in t h e a t h e r o s c l e r o t i c p r o c e s s is a focal t h i c k e n i n g of the intima,

t i m e I c o n s i d e r as m y m i s s p e n t y o u t h !

O b v i o u s l y o n e o f the m o s t e f f e c t i v e w a y s

(the inner m o s t layer o f the artery) with an

o f e n s u r i n g health and longevity is to

increase in s m o o t h m u s c l e cells w h i c h is

a d d r e s s t h o s e risk factors that are

called a fatty streak. T h i s fatty streak i iV " a l s o c o n t a i n s m a c r o p h a g e s and a

m o d i f i a b l e f r o m this point on. C e r t a i n l y r e g u l a r e x e r c i s e is critical. T h e r e is

February/March 2006 a a i t l

7

probably nothing that will take the place of a healthy, low calorie, nutrient dense diet.

It is also important to keep your weight as close to your ideal weight as possible.

Obesity contributes dramatically to inflammation and other risk factors that promote atherosclerosis.

Everyone knows about the major risk factors - hypercholesterolemia (high cholesterol), hypertension (high blood pressure), smoking, and diabetes. It is time to address the 'novel' or emerging risk factors that may be equally as important if not more important than the risk factors we have focused on for the last 50 years.

In general, each factor detailed below is considered 'an independent risk factor' for atherosclerosis. However, when one looks at the actual biochemistry and mechanism of action of the various factors discussed, it will be evident there is a tremendous inter-relationship and inter-dependency of these factors.

Homocysteine Homocysteine (Hey) is an aminoacid produced by the body usually as a byproduct of consuming meat. It is chemically related to the aminoacid

homocysteine

cysteine. In the presence of , high levels of can be adequate levels of vitamin B6, B12, and folic acid; Hey is converted into reduced easily and inexpensively with the neutral aminoacids methionine and (vitamin B6, B12 and cysteine. In addition, any methyl donor such as s-andenosyl-l-methionine (SAMe) Folic acid) Betaine and and betaine will aid in the conversion of this benign amino acid into the innocuous There is also evidence that Hey oxidizes aminoacids.

LDL cholesterol which makes cholesterol even more dangerous. High Hey may In 1969, Kilmer McCully suggested that contribute to chronic disease in a more high levels of Hey in the blood contribute insidious way. People with elevated levels to atherosclerosis. He noticed that children of Hey may have a deficiency in the with an inborn error of methionine ability to perform methylating functions. metabolism developed homocysteinuria Methylation of D N A plays a critical role in (high levels of Hey in the urine) or protecting D N A from damage. In fact, homocysteinemia (high levels of Hey in high Hey has been implicated in such the serum). This error in metabolism can diverse conditions as Parkinson's disease, be caused a disruption of any of three Alzheimer's disease, cognitive interrelated pathways: dysfunction, osteoporosis, and peripheral neuropathy.

1) deficiency in cystathionine B- synthase As mentioned above, high levels of enzyme homocysteine can be reduced easily and inexpensively with the B vitamins 2) defective methyl cobalamin synthesis, (vitamin B6, BI2, and folic acid), betaine, and SAMe.

B vitamins

3) an abnormality in methylene tetrahydrofolate reductase (MTHFR).

SPECIALLY DESIGNED HIGH DOSE VITAMIN C • WITHOUT STOMACH UPSET Beyond C is an exciting new form of Vitamin C that safely allows you to take daily high doses without the normal side effects of stomach upset, cramping or diarrhea.

t -o

Beyond C contains additional supplements that are beneficial to health:

Children with homocysteinuria or homocysteinemia died in their 20's with premature atherosclerosis. One does not have to have this inborn error of metabolism to develop high serum levels of Hey. It is now thought that Hey can cause direct damage to the endothelium prompting the atherogenic cascade described above.

MSM - (methylsulfonomethane) which provides dramatic immune enhancing and anti-inflammatory j activities.

TIWIG/Betaine - (Trimethylglycine) which helps keep homocysteine levels (associated with heart attack, cancer and aging) at safe levels.

Ribose - benefits the heart

Bioperine - aids nutrient uptake

Beyond C provides a number of nutrients that offer free radical protection, detoxification, increased energy levels, enhanced digestion and an improved immune system.

You will find more information about the benefits of high dose vitamin C, and how to order Beyond C at the IAS website:

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a a m

February/March 2006

The pathway starts with methionine, progresses to homocysteine, and then to cysteine. This is a transsulfuration pathway.

Conversion of Hey back to methionine, catalyzed by methyl tetrahydrofolate and methlycobala in is considered a methylation pathway.

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+44 208 123 2106 (Outside USA)

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In addition, homocysteine promotes hypercoagulation of the blood leading to thrombosis. Hey also promotes inflammation. Apparently Hey can interfere with the release of nitric oxide by the endothelium thereby preventing vasodilation, the relaxation of the artery.

SAMe "

Fibrinogen Fibrinogen is a protein that plays a critical role in clot formation. Fibrinogen is the direct precursor to fibrin, a coagulation protein that binds platelets together to form a blood clot.

It is important to note that not all clot formation is bad. If we did not have the ability to clot, we could 'bleed out' with a minor cut. Clot formation is completely normal and necessary. It is when the atheroma or plaque that resides in the lining of an artery breaks or ruptures that the blood clot becomes deadly. A plaque ruptures, combines with fibrinogen which then releases fibrin. The fibrin forms scaffolding and releases peptides that draw blood platelets in the matrix. When this process occurs to stop a cut from bleeding it is a scab. When these blood clots form within the circulatory system they can become life threatening. A clot like this can cause a sudden and acute myocardial infarction (when it winds up in a coronary artery) or a devastating stroke (when the clot travels to the carotid arteries).

The coagulation cascade is extremely complex and involves at least a dozen proteins, proteases, and enzymes. A defect in any one of those proteins leads to a

d i s r u p t i o n in healthy blood activity called

T h e r e is a l w a y s the risk t h e c o a g u l a t i o n

h e m o s t a s i s . Just as t h e b o d y h a s the

p a t h w a y tips in t h e w r o n g direction

m e c h a n i s m s to f o r m blood clots, it also

l e a d i n g to too m u c h 'blood t h i n n i n g ' w h i c h

has t h e m e c h a n i s m s t o d i s s o l v e t h o s e

can lead to internal b l e e d i n g o r

clots.

h e m o r r h a g i c stroke.

A s w e h a v e seen, s o m e o f t h e blood clots

In a d d i t i o n , the a n t i - c o a g u l a n t e f f e c t s of

or t h r o m b i are p a t h o g e n i c . It is i m p o r t a n t

C o u m a d i n 速 can be n e g a t e d by f o o d s

to p r e v e n t t h e c l o t s f r o m f o r m i n g and

c o n t a i n i n g v i t a m i n K. T h e d r u g c o m p a n y

w h e n they d o f o r m , it is equally i m p o r t a n t

e n c o u r a g e s patients t a k i n g the d r u g to stay

that they be d i s s o l v e d .

a w a y f r o m d a r k , leafy, green v e g e t a b l e s .

T h e b o d y d i s s o l v e s b l o o d clots with

A s a nutritionist, I o b j e c t to this

plasmin. Plasmin c i r c u l a t e s in the blood in an inactive

m i s r e p r e s e n t a t i o n w h i c h can lead to nutrient d e f i c i e n c i e s . People on C o u m a d i n 速 can and s h o u l d c o n s u m e dark, leafy green v e g e t a b l e s on a c o n s i s t e n t

f o r m . It

basis (not erratic) basis. T h e p h y s i c i a n can

b i n d s to

and s h o u l d a d j u s t t h e d o s a g e o f t h e d r u g in

both fibrin

a c c o r d a n c e with patients' dietary habits.

and f i b r i n o g e n and

A recent study actually f o u n d that f r e q u e n t

becomes incorporated

c o n s u m p t i o n of n u t s and s e e d s r e d u c e d

into the b l o o d clot.

inflammatory markers of inflammation

Inactive tissue

and d e c r e a s e d f i b r i n o g e n levels.

plasminogen activator

T h e r e are s o m e novel p r o t e o l y t i c e n z y m e s

(tPA) is released f r o m

that s e e m to h a v e the ability to digest

vascular endothelial cells u p o n injury; it b i n d s to fibrin and f i b r i n o g e n and is consequently activated.

fibrinogen

T h e plant p r o t e o l y t i c e n z y m e s b r o m e l a i n , p a p a i n , and rutin h a v e a long history of use, particularly in G e r m a n y , as a g e n t s that e f f e c t i v e l y r e d u c e the i n f l a m m a t i o n that a c c o m p a n i e s i n f l a m m a t o r y and

and r e d u c e the risk o f clots.

osteoarthritis. T h e ability of t h e s e e n z y m e s

T h e interesting t h i n g a b o u t t h e s e plant

to 'lyse' or d i s s o l v e i n f l a m m a t o r y p r o t e i n s

d e r i v e d e n z y m e s is they d o not carry the

s y s t e m i c a l l y a c c o u n t f o r their t h e r a p e u t i c

risk of h e m o r r h a g e or h y p e r c o a g u l a t i o n .

properties.

O n e of the m o s t interesting of t h e s e e n z y m e s is called N a t t o k i n a s e ( N K ) . It is

B r o m e l a i n in particular h a s also b e e n

Inactive p r o u r o k i n a s e is also released by

an e n z y m e that is e x t r a c t e d f r o m a

the e n d o t h e l i u m o f the e x c r e t o r y d u c t s and

traditional J a p a n e s e f o o d , natto. N a t t o is a

its role ( w h e n c o n v e r t e d to u r o k i n a s e ) is to

c h e e s e like f o o d m a d e f r o m f e r m e n t e d

d i s s o l v e clots that d e p o s i t in t h o s e ducts.

s o y b e a n s and h a s b e e n part o f the

T h e s e very s a m e novel plant e n z y m e s literally d i s s o l v e the u n w a n t e d p r o t e i n s

F o l l o w i n g the r e l e a s e o f p l a s m i n o g e n and

traditional J a p a n e s e diet f o r 1,000 years.

that c o n t r i b u t e to h y p e r c o a g u l a t i o n .

p l a s m i n , t h e y a r e rapidly inactivated by

N a t t o k i n a s e closely r e s e m b l e s p l a s m i n and

their r e s p e c t i v e inactivators. T h e r e h a v e

t h e r e f o r e it acts directly on the

b e e n at least f o u r inactivators identified

fibrin clot .

the t w o m o s t i m p o r t a n t o f w h i c h are

In a d d i t i o n , it e n h a n c e s the b o d y ' s

p l a s m i n o g e n a c t i v a t o r - i n h i b i t o r s type I and

ability to p r o d u c e p r o u r o k i n a s e ,

type II (PAI-I) and (PAI-1I).

tPA, and P1A-1. In an a n i m a l

s h o w n t o inhibit platelet a g g r e g a t i o n .

m o d e l , N a t t o k i n a s e w a s s h o w n to T h e p h a r m a c e u t i c a l industry h a s not really

s u p p r e s s initial t h i c k e n i n g a f t e r

d e v e l o p e d an e f f e c t i v e t r e a t m e n t for

v a s c u l a r injury, as a result o f its

elevated

It is a delicate

ability to inhibit t h r o m b i

fibrinogen

formation.

Reduce high levels of homocysteine and at the same time re-energize yourself...

and a p r e d i s p o s i t i o n to t h r o w a clot. T o o

In s u m m a r y , it replicates the action

little

of the b o d y ' s natural fibrinolytic

1 iomocysteine has also been implicated in suc h diverse conditions as:

fibrinogen.

balance. Too much

and the risk

is high blood viscosity, h y p e r c o a g u l a t i o n fibrinogen

and there is a risk o f

h e m o r r h a g e . C o u m a d i n 速 ( w a r f a r i n ) , the current m e d i c a l therapy, is o f t e n not a

agent plasmin.

Alzheimer's disease

Osteoporosis Peripheral neuropathy

T h e r e are a n u m b e r of p u b l i s h e d

Parkinson's disease

viable c h o i c e since b l e e d i n g t i m e s m u s t be

s t u d i e s d e m o n s t r a t i n g the e f f i c a c y

Cognitive dysfunct ion

m o n i t o r e d closely.

of Nattokinase. The beauty of

,

...

.

too much fibrinogen and the risk is high blood viscosity, hypercoagulation i

and a predisposition

to throw a dot

yy

N a t t o k i n a s e is it can b e safe|y used |ong term w i t h o u t the risk o f

You will find more information about t he benefits of SAMe. and how t o order your supply of our p h a r m a r e u tiral grade SAMe brand name Samyr at the IAS website:

h e m o r r h a g e or e x c e s s bleeding.

www.antitiging-systems.com ,

February/March 2006 a a m

9

'numerous studies have now shown a strong

T h e r e a r e still m a n y p e o p l e with normal cholesterol and n o r m a l CRP w h o h a v e an a c u t e

correlation between high CRP scores US a

event such as a heart attack or

_

predictor offuture

stroke. Often these individuals

R i d k e r , M D w a s t h e first t o d e v e l o p a

T h e y don't k n o w they are walking time

' h i g h s e n s i t i v i t y ' o r ' c a r d i a c s p e c i f i c ' test

b o m b s b e c a u s e l p ( a ) is n o t a risk f a c t o r

for CRP. N u m e r o u s studies h a v e n o w

t h a t is r o u t i n e l y t e s t e d for. P e r h a p s it

shown a strong correlation between high

should be.

C R P scores as a predictor of future

Lp(a) also appears to be the

factor that differentiates patients w h o

c o r o n a r y e v e n t s . C a r d i o v a s c u l a r d i s e a s e is

experience rapid progression of

t h e n u m b e r o n e k i l l e r w o r l d w i d e . A n d yet

atherosclerosis to occlusion f r o m patients

conventional algorithms that predict future

w h o do not progress so quickly . Linus

c a r d i o v a s c u l a r events such as the o n e f r o m

Pauling had an interesting theory about

t h e F r a m i n g h a m H e a r t S t u d y fail t o

lp(a) and based upon that theory, very high

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

doses of vitamin C would neutralize the

at risk. A l t h o u g h f u r t h e r r e s e a r c h is

a t h e r o g e n i c properties o f lp(a).

Lipoprotein (a) T h e various cholesterol fractions can be confusing.

W i t h a d v a n c e s in m o l e c u l a r b i o c h e m i s t r y , s c i e n t i s t s a r e a b l e to f r a c t i o n a t e t h e v a r i o u s lipid f r a c t i o n s e v e n f u r t h e r .

The major protein c o m p o n e n t of H D L

When

h i g h d o s e s o f v i t a m i n C a r e p r e s e n t in t h e b l o o d s t r e a m t h e r e is "an a c c e l e r a t i o n o f

individuals.

w o u n d healing and other cell- repair

T h e mainstay of treatment for high

mechanisms, the strengthening of the

cholesterol, (particularly elevated L D L

e x t r a c e l l u l a r m a t r i x ( e . g . , in b l o o d

c h o l e s t e r o l ) is a c a t e g o r y o f

v e s s e l s ) , a n d t h e p r e v e n t i o n o f lipid

pharmaceutical drugs colloquially referred

peroxidation" . T h e problem has always

to a s statin d r u g s . T h e s e i n c l u d e Z o c o r 速 ,

b e e n h o w c a n o n e t a k e in h i g h d o s e s o f

Mevacor速, Lipitor速, and Pravachol速.

vitamin C without incurring Gl distress?

M o s t o f t h e c h o l e s t e r o l in t h e b l o o d s t r e a m

L p ( a ) is p r o t h r o m b o t i c b e c a u s e it

composed of apoB and apolipoprotein ' s m a l l ' a. S i n c e a p o B is p a r t o f L D L c h o l e s t e r o l , it is less c o n f u s i n g to t h i n k o f lp(a) as L D L plus apolipoprotein (a). Lp(a) is a n e x t r e m e l y a t h e r o g e n i c f r a c t i o n that a p p e a r s t o b e g e n e t i c a n d q u i t e r e s i s t a n t to t r e a t m e n t . L p ( a ) is p r o t h r o m b o t i c .

a c t u a l l y i n t e r f e r e s w i t h t h o s e f a c t o r s in t h e clotting cascade that are responsible for l y s i n g a t h r o m b u s or f i b r i n c l o t . T h e r e f o r e N K would be beneficial for people with high levels of lp(a). T h e proteolytic e n z y m e s bromelain, papain, a n d rutin would also be protective against high

STRONGEST NATTO ON T H E MARKET Our plant-based enzyme Endozym Med contains Nattokinase which enhance's the body's ability to fight blood clots and reduce blood pressure

patients entering the emergency r o o m with an acute m y o c a r d i a l infarction ( M l ) had no identifiable risk f a c t o r s . P e o p l e w i t h l o w a n d normal levels of cholesterol w e r e developing atherosclerosis. There

It also contains:

h a d to b e s o m e t h i n g e l s e g o i n g o n .

Bromelain - to balance the immune system.

T h e t h e o r y t h a t a t h e r o s c l e r o s i s is a n

Papain - to degrade age-related proteins

inflammatory disease n o w seems

Rutin - to help promote a healthier joint mobility

o l d h a t , but t h i s t h e o r y w a s n o t

White Willow Bark - to help normalize inflammation

p u b l i s h e d in p e e r r e v i e w j o u r n a l s

'These statements have not been evaluated by the Food & Drug Administration This product is not intended to diagnose, treat, cure or prevent any disease

a a m

February/March 2006

o f cholesterol, the activity o f this e n z y m e

r e d u c t a s e g o e s i n t o o v e r d r i v e a n d t h e liver

baffled by the fact that 5 0 % of the

10

In a h e a l t h y p e r s o n w i t h n o r m a l o r l o w c h o l e s t e r o l l e v e l s , if t h e p e r s o n e a t s a lot

cholesterol, activity of H M G C o A

C Reactive Protein (CRP) In t h e late 1990's, c a r d i o l o g i s t s w e r e

www.antiageing-nutrition.com

l i m i t i n g s t e p in c h o l e s t e r o l p r o d u c t i o n is that very e n z y m e ( H M G C o A ) reductase.

t r u e . If a p e r s o n e a t s little o r n o

a r e i n v o l v e d in t h e d i s s o l v i n g o f b l o o d

Endozym Med is available from Antiageing Nutrition

( H M G C o A ) reductase. Actually, the rate

s y n t h e s i z e d in t h e liver. T h e r e v e r s e is a l s o

Its'

clots.

3-hydroxy-3-methylglutaryl coenzyme A

will s l o w d o w n a n d less c h o l e s t e r o l will b e

l e v e l s o f lp(a).

p u t a t i v e m e c h a n i s m o f a c t i o n is t h a t it interferes with blood protein factors that

is s y n t h e s i z e d in t h e liver. T h e p r o d u c t i o n o f c h o l e s t e r o l is r e g u l a t e d b y t h e e n z y m e

L D L ' s m a j o r p r o t e i n c o m p o n e n t is

[Lp(a)J is a d i s t i n c t s e r u m l i p o p r o t e i n

n e e d e d , it a p p e a r s C R P is t h e l e a d i n g c a n d i d a t e that will i d e n t i f y t h o s e at risk

c h o l e s t e r o l is a p o l i p o p r o t e i n A ( a p o A ) .

apolipoprotein B (apoB). Lipoprotein (a)

CO 1011(1 IJ C'VCHtS

h a v e high levels o f lp(a) and t h e r e f o r e are at m u c h h i g h e r risk o f ' t h r o w i n g a clot'.

until 1999. A g r o u p o f c a r d i o l o g i s t s w o r k i n g in t h e B o s t o n a r e a b e g a n t o i d e n t i f y n o v e l risk f a c t o r s f o r systemic atherosclerosis.

Paul

b e c o m e s a cholesterol producing factory.

Statin d r u g s a r e H M G C o A r e d u c t a s e inhibitors and lower L D L cholesterol by effectively shutting d o w n the activity of t h e e n z y m e that t e l l s t h e liver to p r o d u c e c h o l e s t e r o l . In a d d i t i o n to l o w e r i n g L D L c h o l e s t e r o l , s t a t i n s h a v e b e e n s h o w n to p r e v e n t t h e first i n c i d e n c e o f a c u t e h e a r t attacks and strokes, as well as prolong the survival of patients w h o have already e x p e r i e n c e d an a c u t e c o r o n a r y e v e n t o r w h o have had a vascular interventional p r o c e d u r e such as a stent, c o r o n a r y bypass, or e n d a r t e r e c t o m y . M a n y c a r d i o l o g i s t s suggest these statins also reduce inflammation and lower CRP. H o w e v e r the c l i n i c a l t r i a l s to c o n f i r m t h i s h y p o t h e s i s

are only now getting underway.

Researchers at Brigham and Women's Hospital in Boston are recruiting patients with normal or low cholesterol and high CRP to see if the statins do in fact lower CRP. Ridker himself states, "CRP has been demonstrated to actively contribute to all stages of atherogenesis, participating in endothelial dysfunction, atheroscleroticplaque formation, plaque maturation, plaque destabilization and eventual rupture". He suggests the pharmaceutical industry might try to develop a drug that lowers CRP.

elevate the risk of systemic atherosclerosis. The connection between insulin insensitivity and inflammation is supported by a recent report in the literature that Metformin reduces CReactive Protein in overweight patients with diabetes. Metformin is an oral diabetic agent that improves insulin sensitivity by making insulin receptors more sensitive to insulin. Therefore Metformin is important in the armamentarium against atherosclerosis.

notion that obesity, (particularly central obesity) and insulin insensitivity contribute to inflammation and therefore

Any lifestyle changes directed at glucose and insulin control would aid in reducing CRP. A whole foods diet rich in fruits, vegetables, whole grains, fiber, and omega 3 fatty acids is a diet that lowers inflammation. A diet that avoids saturated fats (fats from animal sources) and trans fatty acids (partially hydrogenated oils) is also important. Nut oils, olive oil, coconut oil are much better choices.

resistance and had lower levels of systemic inflammation "

A diet high in refined carbohydrates (highly processed, sugar laden foods) should be avoided. Some nutritionists speak in terms of a low carbohydrate diet or a diet rich in foods that have a low glycemic index. This is inaccurate advice

In the meantime, there are proactive steps people can take to lower systemic inflammation. Recurrent throughout the literature is the

"omega 3 fatty acids acids were less Hkelv to develop illSlllin

in my opinion and leads to confusion and diet failure amongst the public. The glycemic index is an artificial tool food scientists use to calculate how quickly a food will raise blood glucose in a laboratory setting. The glycemic load is a much more important number to be aware of. The glycemic load represents a number that reflects how much blood sugar is raised when a person eats a particular food. It considers the fiber content of a specific food which affects how that food is metabolized. Raw carrots have a high glycemic index, however they have a reasonable glycemic load. I've never seen anyone become obese by consuming too many carrots. I've seen them turn orange, but not obese. [Ed.- For more information concerning the glycemic load of most foods go the website www.glycemicindex.com] Regular daily aerobic exercise can improve insulin sensitivity, raise HDL cholesterol, help maintain weight, which in turn will lower the risk of atherosclerosis.

The effectiveness of lifestyle changes in reducing inflammation and CRP can be enhanced by carefully selected nutritional supplements. Dehydroepiandrosterone

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The Hollings Cancer Institute at the University of South Carolina has conducted a double blind study on a group of 500 cervical cancer patients that had everyone excited. Nine years of study have shown that a natural product called Ellagic acid is causing G-arrest within 48 hours (inhibiting and stopping mitosis-cancer cell division), and apoptosis (normal cell death) within 72 hours, for breast, pancreas, esophageal, skin, colon and prostate cancer cells.

strawberries, cranberries, walnuts, pecans, pomegranates and the best source, red raspberry seeds.

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February/March 2006

a a m

insulin

eicosapentaenoic acid (EPA) "normal weight indivduals can be and docosahexaenoic acid and individuals can (DHA) contained in fish oil have been subject of countless have norma! insulin/glucose metabolism " clinical and epidemiological studies since the I970's. The interest in inflammation. The COX enzyme acts upon these omega 3 fatty acids is a direct result the fatty acids in the cell membrane. The of the observation that Greenland Eskimos primary dietary fatty acid that provides the had noticeably low rates of coronary heart substrate for the metabolic pathway is an disease. Most of the early clinical trials omega-6 fatty, arachidonic acid (AA). If however, focused on the ability of the the AA is replaced by omega-3 fatty acids, omega 3 fatty acids to reduce the family of eicosanoids produced by the inflammation, particularly the COX enzymes is far less inflammatory and inflammation of rheumatoid arthritis . The has many health benefits. Foods high in omega 3 essential fatty acids proved to be AA include saturated fat, organ meats, and extremely effective at reducing the egg yolks. Foods that increase omega 3 systemic inflammation in both rheumatoid fatty acids in the body are cold water, deep arthritis (RA) and systemic lupus sea fish, nuts and seeds. As detailed above, erythematosus (SLE) . In retrospect, it is fish oil supplementation is also extremely logical that an agent that successfully effective. Foods made with partially reduces systemic inflammation would also hydrogenated vegetable oils (trans fatty be beneficial in atherosclerosis. After all, (DHEA) has shown to be an excellent acids) are as atherogenic as saturated fat. atherosclerosis is an inflammatory disease. agent at reducing systemic inflammation Trans fatty acids do not exist in nature and The cardioprotective properties of the which is "measurable via the are more pro inflammatory than AA. omega 3 fatty acids have many putative proinflammatory cytokines TNF-alpha, ILmechanisms of action. The essential fatty Ibeta, IL-6, and the anti-inflammatory This increase in omega 3 fatty acids is acids have antiarrhythmic properties, cytokine IL-10. DHEA has also proven to proving far more important as research improve endothelial function, demonstrate be an effective way to reduce central continues into obesity/overweight/ and anti-inflammatory action, and lower serum obesity. The omega 3 fatty acids insulin resistance. A group looking at triglycerides . The omega-3 fatty acids may also play into the heart overweight adolescents found that those disease equation by controlling with the highest plasma concentration of another risk factor that is expanded omega 3 fatty acids were less likely to - the metabolic syndrome .

How pure is your Omega fish below develop insulin resistance and had lower Researchers from the University of levels of systemic inflammation. oil supplement?

Virginia were able to demonstrate It is well known that EPA and DHA Omega 3 the low incidence of insulin Insulin resistance, inflammation, fatty acids such as those found in fish are resistance, metabolic syndrome, and very beneficial in reducing the risk of and atherosclerosis diabetes in Alaskan Eskimos when coronary heart disease. However many compared to American Indians can sources of fish are now contaminated with Insulin resistance contributes to systemic heavy metals and toxins. It is now becoming be explained by the Eskimos high inflammation and may be one of the most apparent that these toxins cause numerous consumption of fish, particularly long term health problems. important factors in preventing accelerated fish high in omega 3 fatty acids.. atherosclerosis. One assumes everyone Omega Pro formula is not only a high potency with insulin resistance is overweight or fish oil product suppling the omega-3 fats EPA An anti-inflammatory diet obese. This is not true. Normal weight and DHA., it is an ultra pure formula, certified individuals can be insulin resistant and to contain the lowest levels of common contaminants including lead, mercury, Diet is a contributor to chronic overweight individuals can have normal pesticides. PCB's and dioxins. Not only are inflammation. It is not necessary to insulin/glucose metabolism. Those the fish oils taken from Icelandic stocks (the go on a low fat diet to reduce individuals who are obese or overweight waters least affected by industry), but Omega inflammation. It simply becomes but remain insulin sensitive are not at Pro is packaged in an oxygen free environment very important to select the right and contains a special antioxidant blend of increased risk of developing rosemary extract, ascorbyl type of fats. The inflammatory cardiovascular disease. It is more likely to palmitate, and natural cascade begins with metabolic find insulin resistance amongst overweight tocopherols to assure pathway controlled by the cycloor obese individuals. I'm not sure if continued freshness. oxygenase enzyme (COX). The scientists know at this point which comes products of the COX enzymes are a first. Does insulin resistance cause To order Omega Pro formula caN series of eicosanoids that consist of abdominal obesity or does abdominal 866 800 4677 (USAToll-free) prostaglandins (PGs), leukotrienes obesity cause insulin resistance? Either +44 208 123 2106 (Outside USA) (LTs), and thromboxanes (TXs). way, dysregulation of insulin contributes or visit These eicosanoids are mediators of to systemic inflammation, and that www.antiaging-systems.com

resistant

Omega

a a m

February/March 2006

overweight

i n f l a m m a t i o n c a u s e s endothelial

s u p p l e m e n t s p r e v e n t e d transient

d y s f u n c t i o n , v a s c u l a r injury, and

e n d o t h e l i a l d y s f u n c t i o n . T h e r e is a fair

a t h e r o s c l e r o s i s . Insulin r e s i s t a n c e and

a m o u n t of e v i d e n c e a b o u t t h e b e n e f i t s o f

i n f l a m m a t i o n c o n t r i b u t e to a t h e r o s c l e r o s i s

resveratrol as an a n t i - o x i d a n t and an anti-

p r i m a r i l y b y i n c r e a s i n g o x i d a t i v e stress

i n f l a m m a t o r y . Resveratrol is the

t h r o u g h o u t the body.

p o l y p h e n o l i c a c t i v e i n g r e d i e n t in red w i n e

Oxidized LDL

( o x L D L ) c h o l e s t e r o l is a m o r e rapidly

and red g r a p e skins. It is p r o b a b l y the

d e p o s i t e d in the e n d o t h e l i u m and b e g i n s

single m o s t b e n e f i c i a l a n d versatile

the p r o c e s s o f v a s c u l a r d a m a g e .

p h y t o c h e m i c a l s that h a s yet to c o m e to

Therefore

the role o f a n t i - o x i d a n t s is e x t r e m e l y

light. Resveratrol h a s a n t i - i n f l a m m a t o r y ,

important. It is a l s o the p r o d u c t i o n of

c a r d i o p r o t e c t i v e , and c a n c e r

a d v a n c e d g l y c a t i o n end p r o d u c t s ( A G E s )

chemopreventive properties.

that a m p l i f i e s this p r o c e s s of v a s c u l a r

that o n e plant c o m p o u n d h a s such

injury. A n y t h i n g that limits the p r o d u c t i o n

p r o t e c t i v e qualities in so m a n y areas.

of A G E s w o u l d be an e x t r e m e l y e f f e c t i v e a d j u n c t for p r e v e n t i n g a t h e r o s c l e r o s i s .

A m i n o g u a n i d i n e is t h e first

It is not o f t e n

Conclusion

p h a r m a c e u t i c a l p r e p a r a t i o n to be a p p r o v e d

I h o p e this treatise h a s g i v e n y o u a lot to

for inhibiting A G E s . It has been s h o w n to

c h e w o n , literally! It is a p p a r e n t that a

i m p r o v e t h e e x e r c i s e ability of p e o p l e with

healthy heart and a healthy v a s c u l a r

peripheral v a s c u l a r disease.

s y s t e m can be a c h i e v e d if o n l y o n e can r e m a i n inspired and m o t i v a t e d to attend to the i m p o r t a n t risk factors. T h e r e are m a n y

It s e e m s o b v i o u s that a n t i - o x i d a n t s w o u l d

a g e n t s that can play a critical role in heart

a l s o b e b e n e f i c i a l . T h e p r o b l e m is o n e

health. K n o w l e d g e is p o w e r . We n e e d to

c a n n o t rely o n the f e w p u b l i s h e d , peer

u s e t h e s e a g e n t s in addition to m a k i n g

r e v i e w clinical or p r o s p e c t i v e trials. T h e r e

h e a l t h y lifestyle c h o i c e s . In m y

is a p u b l i s h e d study that d e s c r i b e s a

e x p e r i e n c e , m a k i n g healthy f o o d c h o i c e s is

b e n e f i c i a l e f f e c t o f s u p p l e m e n t a t i o n with

t h e e a s y part. N o w if I c o u l d only invent a

v i t a m i n C and E prior to the ingestion of a

pill that w o u l d t a k e the p l a c e of e x e r c i s e !

high fat m e a l . T a k i n g the v i t a m i n

Delivering excellence in complementary

medicine

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References Enos WF, Holmes RH, Beyer J. Coronary disease among United States soldiers killed in action in Korea: preliminary report. JAMA. 1953;152:1090-1093.

McNamara JJ, Molot MA, Stremple JF, et al. Coronary artery disease in combat casualties in Vietnam. JAMA. 1971; 216:1185-1187.

Biggerstaff KD, Wooten JS. Understanding lipoproteins as transporters of cholesterol and other lipids. Adv Physiol Edu. 2004;28:1056.

Ross R. Atherosclerosis - an inflammatory disease. N Engl J Med. 1999; 340(2): 115-126.

Liuzzo G, Giubilato G, Pinnelli M. T cells and cytokines in atherogensis.

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Kinlay S, Libby P, Ganz P. Endothelial

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Drexler H. Factors involved in the maintenance of endothelial function.

Am J Cardiol. 1998;82:3S-4S Kinlay S, Behrendt D, Wainstain M, et al. The role of endothelin-1 in the constriction of human atherosclerotic coronary arteries. Circulation.

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Ross R. Athersclerosis: an inflammatory disease. N Engl J Med. 1999;340:115-126.

Holman RL, McGill HC Jr, Strong JP, Geer JC. The natural history of atherosclerosis. The early aortic lesions as seen in New Orleans in the middle of the 20th century. Am J Pathol 1958;2:209-35 Zhao GF, Seng JJ, Ahzng H, et al.

Effects of oxidized low density lipoprotein on the growth of human artery smooth muscle cells. Chin Med J (Engl). 2005; 118(23): 1973-8.

Grassi M, Assanelli D, Mozzini, C, et al. Modeling premature occurrence of acute coronary syndrome with atherogenic and thrombogenic risk factors and gene markers in extended families. J Thromb Haemost.

2005;3(10):2238-44.

Lentz SR. Mechanisms of homocysteine-induced atherothrombosis. J Thromb Haemost.

2005;3(8): 1646-54.

Gori AM, Corsi AM, Fedi S, et al. A proinflammatory state is associated with hyperhomocyteinemia in the elderly. Am J Clin Nutr.

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Isobe C, Murata T, Sato C, et al.

Increase of total homocysteine concentration in cerebrospinal fluid in patients with Alzheimer's disease and Parkinson's disease. Life Sci. 2005;77(15): 1836-43.

Irizarry MC, Gurol ME. Raju S, et al.

Association of homocysteine with plasma amyloid beta protein in aging and neurodegenerative disease.

Neurology. 2005;65(9):1402-8.

Teunissen CE, van Boxtel MP, Jolles J, et al. Homocysteine in relation to cognitive performance in pathological and non-pathological conditions. Clin Chem Lab Med. 2005;43(10):1089-95.

Gjesdal CG, Vollset SE, Ueland PM, et al. Plasma total homocysteine level and bone mineral density: the hordaland homocysteine study. Arch

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Intern Med. 2006; 166(1 ):88-94.

Cohen JA, Jeffers BW, Stabler S, et al.

Auton Neurosci. 2001;87(2-3):268-73.

Cheuk BL, Cheung GC, Lau SS, et al.

Plasma fibrinogen level: an independent risk factor for long-term survival in Chinese patients with peripheral artery disease? World J Surg. 2005;29(10): 1263-7.

Jiang R, Jacobs DR Jr, Mayer-Davis, E, et al. Nut and Seed Consumption and Inflammatory Markers in the MultiEthnic Study of Atherosclerosis. Am J Epidemiol. 2005; [Epub ahead of print] Fujita M, Nomura K, Hong K, et al.

Purification and characterization of a strong fibrinolytic enzyme (nattakinase) in the vegetable cheese natta, a popular soybean fermented food in Japan. Biochem Biophys Res Commun. 1993; 197(3):1340-7.

Suzuki Y, Kondo K, Ichise H, et al.

Dietary supplementation with fermented soybeans suppresses intimal thickening. Nutrition. 2003; 19(3):261-4.

Akhtar NM, Naseer R, Farooqi AZ, et al. Oral enzyme combination versus diclofenac in the treatment of osteoarthritis of the knee - a doubleblind prospective randomized study.

Clin Rheumatol. 2004; 23(5):410-5.

Glaser D, Hilberg T, The influence of bromelain on platelet count and platelet activity in vitro. Platelets. 2006; 17(1 ):37-41.

Caten C, Novello M, Lapenna R, et al.

New risk factors for atherosclerosis in hypertension: focus on the prothromotic state and lipoprotein (a).

J Hypertens. 2005;23(9):1617-31.

Nauk M, Marz W, Wielaud H. Is lipoprotein (a) cholesterol a significant indicator of cardiovascular risk? Clin Chem. 2000; 46:436-7.

Terres W, Tatsis E, Pfalzer B, et al.

Rapid angiographic progression of coronary artery disease in patients with elevated lipoprotein (a).

Circulation. 1995; 91(4):948-50.

Rath M, Pauling L. Hypothesis: lipoprotein (a) is a surrogate for ascorbate. Proc Natl Acad Sci USA. 1990; 87(16):6204-7.

Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis: a comparison of Creactive protein, fibrinogen, homocysteine, lipoprotein (a), and standard cholesterol screening as predictors of peripheral arterial

disease. JAMA. 2001 ;285(19):2481-5.

Verma S, Szmitko PE, Ridker PM. Creactive protein comes of age. Nat Clin Pract Cardiovasc Med. 2005;2(1):2936.

Verma S, Szmitko PE, Ridker PM. Creactive protein comes of age. Nat Clin Pract Cardiovasc Med. 2005;2(1 ):2936.

Carter AM, Bennett CE, Bostock JA, Grant PJ. Metformin reduces Creactive protein but not complement factor C3 in overweight patients with Type 2 diabetes mellitus. Diabet Med. 2005'22(9): 1282-4 Hillebrand F, Pape HC, Hoevel P, et al.

The importance of systemic cytokines in the pathogenesis of polymicrobial sepsis and dehydroepiandrosterone treatment in a rodent model. Shock.

2003;20(4):338-46.

Villareal DT, Holloszy JO. Effect of D H E A o n abdominal fat and insulin action in elderly women and men: a randomized controlled trial. JAMA. 2004;292(18):2243-8.

Das UN. Beneficial effect(s) of n-3 fatty acids in cardiovascular diseases: but, why and how? Prostaglandins Leukot Essent Fatty Acids. 2000; 63(6):351-62.

Skoldstam L, Borjesson O, Kjallman A, et al. Effect of six months of fish oil supplementation in stable rheumatoid arthritis - a double-blind controlled study. Scand J Rheumatol.

1992;21:178-85.

Geusens P, Wouters C, Nijs J, et al.

Long-term effect of omega-3 supplementation in active rheumatoid arthritis - a 12 month, double-blind controlled study. Arthritis Rheum 1994;37:824-29.

Walton AJ, Snaith ML, Locniskar M, et al. Dietary fish oil and the severity of symptoms in patients with systemic lupus erythematosus. Ann Rheum Dis. 1991; 50:463-66.

Carroll DN, Roth MT Evidence for the cardioprotective effects of omega-3 fatty acids. Ann Pharmacother. 2002; 36(12): 1950-6.

Ebbesson SO, Risica PM, Ebbesson LO, et al. Omega-3 fatty acids improve glucose tolerance and components of the metabolic syndrome in Alaskan Eskimos: the Alaska Siberian project.

Int J Circumpolar Health. 2005; 64(4):396-408.

Adam O, Beringer C, et al. Antiinflammatory effects of a low

arachidonic acid diet and fish oil in patients with rheumatoid arthritis.

Rheumtol Int. 2003; 23(1):27-33.

Skoldstam L, Hagfors L, Johansson G. Mediterrean diet intervention in rheumatoid arthritis. Ann Rheum Dis. 2003; 62(3):193-5.

Mozaffarian D, Pischon T, Willett WC, et al. Dietary intake of trans fatty acids and systemic inflammation in women.

Am J Clin Nutr. 2004; 79(4):606-12.

Baer DJ, Judd JT, Clevidence, BA, et al. Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study. Am J Clin Nutr. 2004; 79(6):969-73.

Wu D. Modulation of immune and inflammatory responses by dietary lipids. Curr Opin Lipidol. 2004; 15(1):43-7.

Klein-Platat C, Drai J, Oujaa M, et al.

Plasma fatty acid composition is associated with the metabolic syndrome and low-grade inflammation in overweight adolescents. Am J Clin Nutr. 2005; 82(6):1151-2.

Haffner SM. Insulin resistance, inflammation, and the prediabetic state. Am J Cardiol. 2003; 18; 92(4A):18j-26J. Reaven G. All obese individuals are not created equal: insulin resistance is the major determinant of cardiovascular disease in overweight/obese individuals. Diab Vase Dis Res. 2005; 2(3): 105-12.

Plotnick GD, Corretti MC, Vogel RA. Effect of antioxidant vitamins on the transient impairment of endotheliumdependent brachial artery vasoactivity following a single high fat meal. JAMA. 1997; 278(14):1069-70.

Biondi-Zoccai GG, Abbate S, Liuzzo G, et al. Atherothrobosis, Inflammation and Diabetes. JACCI. 2003; 41 (7): 1071-7.

Bucala R, Makita Z, Koschinsky T, et al Lipid advanced glycosylation: pathway for lipid oxidation in vivo. Proc Nat l Acad Sci USA. 1993; 90:6434-8.

Gotto AM Jr. Antioxidants, Statins and Atherosclerosis. JACC. 2003; 41(7):1205-10.

Srivastava R, Ratheesh A, Gude RK, et al. Resveratrol inhibits type II phosphatidylinositol 4-kinase: a key component in pathways of phosphoinositide turn over. Biochem Pharmacol. 2005;70(7): 1048-55.

February/March 2006 3 3 1 1 1

R

asagiline is a novel, new treatment for Parkinson's disease and it is also under investigation for use in battling Alzheimer's disease.

N o w approved and available in parts o f Europe, (under the brand name o f Azilect速), it is expected to be officially "approved" in other parts o f the world, (for example the U S A ) late in 2006 and in some places it may appear under the slightly different brand name o f Agilect.

Rasagiline action is as a potent, selective and irreversible monoamine oxidase ( M A O ) type-B inhibitor. These types o f drugs are seemingly able to enhance memory and learning, as well as improve mood, motivation and help delay the age-related memory decline o f the general aging population.

Background Rasagiline was first synthesized and developed by the Israeli researcher, Professor Moussa Youdim and he has noted that selective M A O - B inhibitors, ( o f which deprenyl is the only other one currently available), do not display the so-called cheese effect. The cheese effect is a reaction when tyramine containing foods (such as cheese) are ingested at the same time. To date, the clinical trials with rasagiline have produced no hypertensive crises.

V

^Nfci

Rasagiline; the latest drug for Parkinson 9 s disease

By Phil Micans, PharmB

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February/March 2006

Professor Youdim believes that in the near future it may be acceptable to routinely mix "drugs" into our daily diet to protect the brain from neurodegenerative diseases. This thinking is more common than you may believe, and indeed other Professors, such as Jozeph Knoll and Imre Zs.Nagy, also believe that particular cocktails o f neuroprotective pills could help retard the aging process.

Parkinson's disease Parkinson's disease is a degenerative disorder o f the central nervous system related to the decline in dopamine levels. Whilst it is likely that both environmental and genetic factors play a role in the disease's onset, the symptoms include slowness, tremors, stiffness, fatigue, impaired balance and apathy.

Parkinson's often begins with diminished vitality and depression, with

Rasagiline is a novel, new treatment for Parkinson's disease and it is also under investigation for use in battling Alzheimer's disease the symptoms worsening as the disease progresses. In addition, likely due to the dopamine deficiency, many Parkinson patients become clinically depressed.

The worst signs of Parkinson's disease are seen when 70% to 80% of dopamine-producing neurons in the substantia nigra of the midbrain have been lost, (with 90% loss resulting in death). Naturally, subclinical signs and symptoms do appear much earlier, often when 30% to 40% of dopamine neurons have been "lost." In fact, some scientists have suggested that all of us could go on to develop Parkinsonian symptoms if we live long enough! This is because there is a disproportionate nigral dopamine cell loss during every decade of adult life, which has been estimated at 13% per decade for normal aging folks past the age of 40. However, the increased dopamine catabolism seen in Parkinson's is associated with greater oxidative stress and neuronal cell death than the "norm."

So it is that selective MAO-B inhibitors, such as rasagiline, are chosen to combat the problems, because they are known to help delay and slow the overall processes.

The clinical trials to date indicate that rasagiline can be used both on its own in early Parkinson's disease, or as an adjunct with L-dopa (levodopa) treatment in the later stages of the disorder, where it appears to be beneficial against fluctuations in motor function.

There is some evidence from invitro and animal studies that rasagiline can actually slow the progression of Parkinson's disease

prevent the onset of Parkinson's dementia.

Rasagiline vs. Selegiline The main therapeutic advantage of rasagiline over the other selective

itself, in addition to offering some symptomatic relief.

It is by inhibiting MAO-B that rasagiline prevents the loss of the neurotransmitters dopamine and phenethylamine. In so doing, rasagiline raises the levels of dopamine available and improves the survival prospects of the ailing dopaminergic neurons themselves.

This in turn restores some of the normal gait, locomotion and coordination in Parkinsonian patients, and importantly delays further physical decline.

The brain's dopaminergic neurons in the substantia nigra are linked to the basal ganglia. The basal ganglia regulates bodily movement and also plays a role in thinking and emotion. But to function adequately, basal ganglia cells require a proper balance between the dopamine and acetylcholine systems. Of course, this balance is imbalanced in Parkinson's disease as the dopamine neurons die off. Therefore, Parkinson's patients are sometimes given anticholinergic drugs like benztropine (Cogentin), to control their tremors. These drugs can themselves be dementing (sic), certainly they are well known to impair memory and cognition.

Fortunately, the benefits of rasagiline, either as a monotherapy or an adjunct to L-dopa treatment, extend beyond restoring motor activity. For rasagiline improves cognitive performance and it is speculated that a low-dosage regimen of rasagiline may slow, or

irreversible monoamine oxidase-B inhibitor deprenyl (seligiline) is that rasagiline does not transform into any amphetamine metabolic breakdown products. A very small part of selegiline is metabolized to methamphetamine and amphetamine, whereas rasagiline is metabolized to aminoindan.

Interestingly, some studies have suggested that rasagiline's biotransformation to aminoindan itself, may have its own neuroprotective qualities.

Selegiline and rasagiline are neuroprotective via numerous mechanisms, perhaps one of the most important are their ability to stabilize the mitochondrial membrane. It is this propargylamine moiety, rather than the MAO inhibition which may hold the key to their neuroprotective action.

But of particular worthy note is rasagiline's inhibition of the activation of the apoptotic cascade, which is triggered by dopamine neurotoxins and oxidative stress.

(Apoptosis is an active process of programmed cell-death induced by exposure to neurotoxins). Rasagiline can therefore rescue deteriorating dopaminergic neurons by inhibiting February/March 2006 a a m

17

dosage being 1 mg. per day).

Absorption is rapid, with peak plasma concentrations achieved in about 30 minutes.

the "death signal" of mitochondrial permeability transition and there is evidence that suggests that rasagiline may be more effective than selegiline in saving dopamine nerve cells from the neurological damage of aging.

Some researchers and scientists have suggested that if a direct dose comparison was to be made of rasagiline to deprenyl, that rasagiline is 5 to 10 times more potent than deprenyl.

Alzheimer's As rasagiline increases nerve growth factor in the brain, this acts to improve neuroplasticity and as a consequence the long-term potentiation of memory is enhanced.

For this reason, Rasagiline may be able to retard the symptoms and progress of Alzheimer's disease.

Alzheimer's disease is associated with plaques of beta-amyloid, yet rasagiline facilitates the conversion of amyloid precursor protein (APP) into the neuroprotective, neurotrophic and intracellular soluble APP-alpha. This action alone helps to explain why rasagiline is currently undergoing Stage II clinical trials with Alzheimer's disease patients.

Dosages In the clinical trials for Parkinson's disease, rasagiline has been taken orally, (with and without food), with dosages typically being 0.5 mg. to 2 mg. a day, (the average

8

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February/March 2006

should not be combined concurrently with other M A O inhibitors.

Tolerated

In addition, combining SSRIs with rasagiline is also best avoided, even at a low doses.

Rasagiline appears to be well tolerated within the normal therapeutic dosage range. The only adverse event

Whilst, no harmful effects from rasagiline have been detected either in pregnancy or post-natal

...rasagiline may be more effective than selegiline in saving dopamine nerve cells from the neurological damage of aging. reported with rasagiline is postural hypotension. Professor Youdim, observes that rasagiline when taken at a low MAO-B selective dosage typically has no adverse sideeffects. Indeed, the studies of the Parkinson Study Group confirmed an improvement in motor fluctuations and other Parkinson's disease symptoms The only adverse events significantly more common with rasagiline than with placebo were balance difficulties in the 0.5 mg. group with anorexia, vomiting and weight loss in the 1 mg. group.

However, a benefit was that fewer patients reported depressive symptoms.

development, this information is currently only based on animal studies. So it is as usual best avoided by pregnant or lactating women.

To date, there is also no evidence that rasagiline has any significant abuse potential.

Conclusion Rasagiline is a significant advance and it is a necessary one to assist the rapidly growing population of elderly Parkinsonian and Alzheimer's patients, all of whom are in need of more effective therapies with fewer risks and less adverse side-effects.

Contraindications At dosages above 2 mg. per day, rasagiline loses its selectivity for MAO type B and also inhibits MAO type A which can cause additional complications. But as a MAO-B selective regimen does not cause significant tyramine potentiation, (the so-called "cheese effect" which was common to users of older unselective and irreversible MAOIs who ate tyramine-rich foods such as dairy produce), a lowdosage rasagiline demands no special dietary restrictions (i.e. 2 mg. or less daily) and is therefore to be recommended. However, it should be noted that rasagiline

Rasagiline's mono use or effective combination with other standard Parkinson therapies such as L-dopa adds an additional tool to the armory of pharmaceuticals that can assist to help prevent, slow and delay these debilitating senile dementias.

It is going to take some time to know if rasagiline has any of the antiaging properties that have been attributed to the regular low dose use of deprenyl, but early indicators are promising and those serious about life extension will want to follow the progress of rasagiline closely.

in the news References 1. Chen J.J., Swope D.M. "Clinical pharmacology of Rasagiline, a novel second generation proprargylamine for the treatment of Parkinson's disease." J. Clin. Pharmacol, 2005 Aug. 45(8) pp878-94.

2. Blandini F. "Neuroprotection by Rasagiline, a new therapeutic approach to Parkinson's disease?" CNS Drug Rev. 2005 Summer II (2) pp 183-94.

3. Youdim M.B., Maruyama W., Naoi M. "Neurophrmacological neuroprotective and amyloid precursor processing properties of selective MAO-B inhibitor anti Parkinsonian drug Rasagiline." Drugs Todat 2005 June 41(6) pp369-91.

4. Parkinson's study group. "A randomized, placebocontrolled trial of Rasagiline in Levodopa treated patients with Parkinson's disease and motor fluctuations." Arc. Neurol. 2005 Feb. 61(2) pp241-8.

5. Parkinson's study group. "A controlled, randomized delayed start study of Rasagiline in early Parkinson's disease." Arch. Neurol. 2004 April 61(4) pp561-6.

6. Parkinson's study group. "A controlled trial of Rasagiline in early Parkinson's disease. The TEMPO study." Arch.

Neurol. 2002 Dec. 59(12) pp 1937-43.

7. Knoll J. "The brain and its self, a neurochemical concept of the innate and acquired drives." Springer-Verlag, 2005

Azilect which contains rasagiline, has recently been approved in Europe as a new treatment for Parkinson's disease.

In clinical trials, Azilect has been found to be effective as a monotherapy, or when taken together with Levodopa (Sinemet), for both early and late stage Parkinson's disease.

For information on how to order your supply of pharmaceutical-quality Azilect go to:

www.antiaging-systems.com

Breathe easy- more good news about vitamin D According to new findings, higher amounts of vitamin D could help make it easier to breathe, offering possible good news for smokers, asthmatics and other people with respiratory problems.

Researchers at the University of Auckland in New Zealand found people with higher levels of the vitamin in their systems showed better lung function than those with lower amounts.

While the vitamin, which people get mostly from sunlight, is linked to lung health, the exact relationship is unclear, they said. Their findings appear in the December 2005 issue of the American College of Chest Physicians' journal. Vitamin D can also be found in certain foods like fortified beverages and fatty fish like salmon and mackerel as well as dietary supplements.

"Although there is a definite relationship between lung function and vitamin D, it is unclear if increases in vitamin D through supplements or dietary intake will actually improve lung function in

patients with chronic respiratory diseases," said Dr. Peter Black, who led the study. Black, an associate Professor in the University's Department of Medicine, and his team analyzed information from the U.S. National Health and Nutrition Examination Survey, which collected data on 14,091 people from 1988 to 1994. Their new analysis found those who had higher levels of vitamin D were able to inhale and exhale more air.

That link was seen in blacks and non-Hispanic whites and was stronger in people older than 60 and smokers. NonHispanic blacks and Mexican-Americans showed lower levels of the vitamin compared to whites.

The study, also found levels of the nutrient were higher among men and lessened as people aged or gained weight.

Dr. Rosalind Wright, a Professor at Harvard Medical School's Department of Society, Human Development, and Health, said; "the vitamin could be an easy way to boost lung function. Vitamin D would be a relatively simple, low-cost intervention that would likely have high compliance to prevent or slow loss of lung function in susceptible subgroups."

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T

he mitochondrial theory of aging ( M T A ) w a s first proposed in 1972 by Denham Harman w h o is regarded as the "father" of the free radical theory of aging (1).

T h e MTA was further refined and developed in 1980 by Jaime Miquel (2) and there is such a strong connection between the MTA and the free radical theory that they are often discussed together. (3) Yet the MTA concerns itself far more than with "just" free radicals themselves. To understand the MTA, it is first necessary to have an overview of the mitochondrion and their pivotal role in the life of biological organisms.

Mitochondria basics Mitochondria are organelles (little organs) found in all cells in the animal and human body, (see figure 1) with the exception of red blood cells. Typically, there can be from 20 to 2 5 0 0 per cell (4). These n u m b e r s can be understood when one realises that the mitochondria are the energy generators of the cell, typically producing 9 0 % or m o r e of all the ATP bioenergy m a d e in the body (4).

T h e production of ATP within the mitochondria occurs from the interaction of two metabolic cycles- the tricarboxylic acid ( T C A ) cycle, (also called the "Krebs" or "citric acid" cycle) and the electron transport chain (ETC).

(4) T h e mitochondrion is essential for life, it generates the energy from the food w e eat to p o w e r all our cellular activity, muscular activity, heart and brain functions, breathing, walking, talking etc. Without ATP there is no life, and without well-functioning mitochondria, there is (almost) no ATP.

To truly understand how and why aging takes place and therefore be able to target regimes that can slow and reverse its affects, it is necessary to review the various theories of aging. From this we can attempt to identify which of the problems are most relevant to our own personal aging and therefore act accordingly. In this article, James South MA looks at the mitochondrial role in aging.

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Interestingly, one of the unique features of mitochondria is that they contain their own D N A (7), specifically mitochondrial DNA ( m t D N A ) , gleaned entirely from our mother's.

A theory of aging The very feature that makes mitochondria unique a m o n g the various cell organelles, (i.e. having their own

"mitochondria are the energy generators of the cell, typically producing 90% or more of all the ATP bioenergy made in the body "

The evidence It is generally accepted that oxidative mitochondrial decay is a major contributor to aging. (10) Dr. Sastre points out that: "The role o f

D N A ) gives rise to a major

( H 2 0 2 ) and hydroxyl radical (8). It

problem. Mitochondrial D N A has

is generally estimated that 1% or

no protection or significant enzymes

2 % o f all oxygen consumed by

repair systems to ofier significant

mitochondria, (by the way they

free radical protection (6), as such,

consume 85% o f all body oxygen)

they are far more likely to be

is converted into damaging S O R

subject to free radical damage. (6)

free radicals (8).

One study investigated 10 normal

In turn S O R can be converted

humans aged 42 to 97 years,

into H 2 0 2 (9), which causes

checking three brain regions. There

scissions (breaks) and cross linking

was a 10-fold increase in m t D N A

o f D N A (9). Thus, in the very act o f

damage as compared to normal

doing its j o b o f making ATP, the

D N A found in the entire group o f

ETC inadvertently damages

samples, with a 15-fold increase in

m t D N A , on which the viability o f

persons over 70 (6).

current and future mitochondria

As mitochondrial D N A damage

depends. As Dr. Linnane notes: "As

accumulates over the lifetime of an

tissues age, m t D N A mutations

individual, the functionality o f the

accumulate in individual cells;

energy processes that produce ATP

eventually some cells will reach the

decreases dramatically and

point at which the ability to make

gradually produces a cellular energy

the m t D N A is seriously impaired. I f

crisis. Another study found that in a

m t D N A mutations occur in a

90 year old man, only 5 % o f the

significant number o f cells in a

total mitochondrial D N A from

tissue, the function o f that tissue

muscle tissue was still in the form

will be comprised and consequently

o f full-length, normal D N A (5).

will contribute to such age-

To make matters worse, the

associated pathologies as skeletal

mitochondrial ETC is the main

muscular and neurological

source o f cellular free radicals/

degeneration, heart failure, strokes,

oxidants, especially superoxide

... other diseases [and death!]." (5)

radical ( S O R ) , hydrogen peroxide

old mitochondria in cell aging has been emphasized by the finding that cells injected with mitochondria isolated from old rats degenerate to a much greater extent than those injected with mitochondria from young rats." ( I I ) One area o f evidence for the MTA comes from the structural differences between young and old mitochondria. Studies in both humans (9) and rats (7, 11) show a similar picture. In young organisms, there are a large number o f small mitochondria that provide needed ATP. In aged rats and humans, there are a smaller number o f large mitochondria. The total volume o f the cell that consists o f mitochondria, (which can be up to 20% o f the total cell volume), remains roughly the same in young and old rats/ humans. These larger mitochondria are not as efficient as the youthful, normal, small mitochondria (7, 11). As Dr. Sastre and colleagues noted; "... mitochondrial size increases and mitochondrial membrane potential decreases with age. This may reduce the energy supply in old cells since the mitochondrial membrane potential is the driving

Rough endoplasmic reticulum

force for ATP synthesis." (12)

Nuclear p o r e Nucleolus

- Nucleus

Dr. Linnane and colleagues compared skeletal muscle tissue

Ribosome

samples from a 5-year old and 90Golgi apparatus

year old human. They analyzed the

Centriole

samples for m t D N A content, as well

Lysosome

as C O X activity in muscle cells.

They found that less than 5 % o f the total m t D N A from the 90-year old was still in the form o f full-length m t D N A , while the bulk o f m t D N A

Smooth endoplasmic reticulum Mitochondrion

Cytoplasm

molecules were made up seriously mutated m t D N A . Meanwhile the 5year olds m t D N A were almost

Cell membrane

Figure 1: indicates the presence of mitochondria within a cell.

entirely normal m t D N A . There were only rare COX-deficient muscle fibers in the 5-year old, but COXdeficient muscle fibers were very

February/March 2006 a a m

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canaries (24 years) have similar body size and oxygen consumption to mice (3.5 years), yet also have much lower mitochondrial oxidant generation (13). Less mitochondrial oxidant generation = less m t D N A d a m a g e , and less m t D N A d a m a g e = more normal mitochondrial bioenergetics = a longer/ healthier life.

Glutathione plays a key role in protecting mitochondria and c o m m o n in the 90-year old. They m t D N A f r o m oxidative d a m a g e . conclude that: "This provides Glutathione protects against compelling support for the hypothesis of m t D N A mutationm t D N A - d a m a g e in the inner driven bioenergy degradation is a mitochondrial m e m b r a n e . (14) key feature of the aging process."

Glutathione breaks d o w n H 2 0 2 , a (5) free radical normally produced within mitochondria and which A comparison of three bird d a m a g e s m t D N A . (9) Mitochondria species to rats and mice also lack the ability to synthesize provides support for the MTA. Pigeons have a body size and basal glutathione, or to rid themselves of metabolism similar to rats. Yet oxidized glutathione. (10) pigeons have a nine-fold higher Glutathione levels and peroxide median life span (35 years) than production m a y also explain the rats (4 years). It w a s discovered that differential in life spans that occurs pigeons have significantly less between males and females in m a n y mitochondrial free radical/ oxidant species, including h u m a n s . Brain generation than rats. (13) It w a s also and liver mitochondria f r o m males found that parakeets (21 years), and have higher H 2 0 2 production than females, yet glutathione levels in James South: 1947 • 2006 mitochondria of males It is with much sadness that we announce the death of are generally lower James South in January 2006 after a battle with a rapid than females (12). form of brain cancer. Those who knew James understood T h u s females should that he was a private man who was passionate and suffer less m t D N A dedicated about many subjects and deeply damage, with knowledgeable about each of them. Indeed his breadth and depth of detail as a biochemist devoted to nutrition consequently slower could quickly identify him as a "walking encyclopedia." aging. [Ed.- This may His style and his passion will be missed by his friends help explain why and family and he is a great loss to the antiaging/ f e m a l e s live longer!] optimal health field at large. He leaves behind his wifeThis evidence for Anne. the MTA is just a brief "snapshot" of the vast array of evidence that REVERSE MITOCHONDRIAL AGING has accumulated to support the MTA. In Acetyl-L-Carnitine is a naturally occuring amino acid that preparing this article I has been proven to treat age-related mental decline with studied far more effects including: scientific papers on Enhanced cognitive function the MTA than I can Increased motor ability refer to here and Lessening of depression Improved short-term memory having looked Enhanced attention to detail carefully into the Improved mitochondrial condition MTA, I am personally Order Now at www.antiaging-systems.com convinced that the

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February/March 2006

mitochondria theory of aging represents one of the most important causes of aging and agerelated diseases.

Fortunately, there are various practical measures that w e can take to minimize or reduce m t D N A / mitochondrial d a m a g e and aging.

Caloric restriction is the best-proven anti-aging regimen because it significantly reduces m t D N A / mitochondrial oxidant damage. (13) [Ed.- For further details on regimes to induce/ improve calorie restriction, please see the S u m m e r 2 0 0 4 Antiaging Magazine, pages 49]. However, there are a n u m b e r of nutrients and antiaging drugs that will combat m t D N A / mitochondrial oxidative d a m a g e and thus aging itself, and we shall outline some of them here.

T h e B vitamins Most of the ATP m a d e by mitochondria is produced by the E T C . (16) T h e E T C requires three products- N A D H , succinate and F A D H 2 - to initiate itself. (16) N A D H is the reduced c o e n z y m e f o r m of vitamin B3, while F A D H 2 is the reduced c o e n z y m e form of vitamin B2. It is in the c o e n z y m e f o r m that B vitamins serve to activate enzymes, as well as begin the activity of ETC complexes. Dr. A m e s and colleagues point out that: "High levels of vitamins have been used successfully to treat m a n y h u m a n genetic diseases.... the therapeutic vitamin regimens work by increasing intracellular c o e n z y m e concentrations, stimulating a defective e n z y m e . " (10) Dr. A m e s believes that during aging, oxidation of proteins d e f o r m s them and; "...thus decreases the affinity of m a n y e n z y m e s for their substrates or c o e n z y m e s . " (10) So, through the law of mass action, supplying higher-than-RDA levels of B vitamins increases c o - e n z y m e binding to the (oxidant d a m a g e d ) e n z y m e s , thereby decreasing age damaged e n z y m e activity.

A typical daily regime may want to include: • 10 mg. to 100 mg. vitamin B1 and B2.

• 2 5 mg. to 100 mg. vitamin B6.

• 50 meg. to 250 meg. vitamin B3.

• 50 mg. to 200 mg. vitamin B5 (pantothenic acid).

• 150 meg. to 1 mg. biotin.

• 100 meg. to 1000 m e g vitamin B12.

This may help stimulate the TCA activity, with a consequent increase in ATP production.

Acetyl-L-Carnitine & lipoic acid Acetyl-L-Carnitine is a natural constituent of the inner mitochondrial membrane, especially in heart, brain and muscle (8, 10).

Feeding Acetyl-L-Carnitine to rats reduces lipofuscin accumulation in the prefrontal cortex and hippocampus neurons. (8) Lipofuscin is in large part the waste product of mitochondrial membrane debris. (9) Feeding Acetyl-LCarnitine to rats completely reverses the age-related decrease in the critical membrane phospholipid cardiolipin, this is essential for the proper structural positioning and

functioning of key membrane components, necessary to send ATP from the mitochondria to the cell where it is needed and for more besides. (8) When Acetyl-L-Carnitine is combined with lipoic acid, there was a profound regeneration of aging rats. (17) Together they partially reversed the age-related decline in the average mitochondrial membrane potential, (which drives ATP production).

A daily dosage of 250 mg. to 500 mg. Acetyl-L-Carnitine three times daily plus 15 mg. to 50 mg. lipoic daily seems to be a prudent way to help reverse mitochondrial aging.

they could alter the morphology of aging mitochondria in rats. They found that with aging there was no significant changes in the cellular volume of mitochondria, but that there were fewer mitochondria and they were of large size when compared to the large numbers of small mitochondria in young adult rats.

When they fed hydergine to old rats they were able to significantly reverse this trend. [Ed.- As reported in detail and shown on page 16 of the Fall 2005 Antiaging Magazine], Using hydergine they reduced by a massive 4 5 % the number of extremely large, inefficient, mitochondria in old rats, to levels

"The rejuvenation of aging brain mitochondria may be one more indication for using the smart drug hydergine " Hydergine

close to those of young adult rats.

(7) It is widely documented that hydergine increases stores of ATP, stabilizes nerve cells, improves brain glucose utilization and in turn, increases ATP production. (7) Based on the facts about hydergine, Dr. Bertoni-Freddari used it to see if

They were also able to increase the numerical density of mitochondria in neurons of old rats to a level close to that of young rats.

In addition, hydergine reduced the mean size of aged rat mitochondria to a number similar to that of young adult rats. (7) They conclude that hydergine treatment is able to induce smaller, more numerous brain synaptic mitochondria in old rats, presumably leading to increased mitochondrial energy production as well.

For humans, a daily dose of 4.5 mg. to 9 mg. of hydergine has been shown to be safe. The rejuvenation of aging brain mitochondria may be one more indication for using the smart-drug hydergine on a regular basis.

ATP

Figure 2: W i t h h e a l t h y energy/ m e t h y l a t i o n p r o c e s s e s 1 m o l e c u l e of glucose can b e c o n v e r t e d into 36 m o l e c u l e s of A T P .

In his 1981 article on bio-energy supplements, Dr. McCarty notes that nucleotides such as adenosine triphosphate (ATP) are quickly

February/March 2006 a a m

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converted when given by injection or sublingually, but that ATP is digested (destroyed) when swallowed. (18) Since cells can absorb blood-carried adenosine and convert it to A M P and ADP, (the precursors of ATP), sublingual ATP supplements promise a "short cut" w a y to quickly raise cellular ATP levels. Indeed, this activates the mitochondrial energy metabolism which activates the E T C into "higher gear" ATP production. (19) This is why Dr. Lund w a s able to increase (in-vitro) liver cell ATP by 3-fold within 60 minutes by adding 0.5 rnM of adenosine. (20) Since G e r m a n studies have found even 2 mg. to 3 mg. of sublingual adenosine effective (18), a sublingual dose of 5 mg. to 10 mg. of ATP daily should be useful to stimulate mitochondrial energy production.

Figure 2 shows the m a x i m u m achievable molecules of ATP (36) that can be produced through efficient, healthy mitochondrial production from 1 glucose molecule.

NADH N A D H is the reduced (high energy) c o e n z y m e form of vitamin B3. (21) It is also the product that initiates ATP production by the E T C . (16) In a small scale double blind study with chronic fatigue s y n d r o m e patients, Dr. Forsythe found a significant improvement in energy levels a m o n g patients receiving 10 mg. of N A D H daily for four weeks, ( 3 1 % improved, versus placebo of 8% improved).

Furthermore, 18 of 25 (or 7 2 % ) of the study patients in a longer open label follow-up study reported significant improvement in their energy levels. (22) N A D H has also shown impressive improvement in doubleblind studies with Parkinson's patients at a G e r m a n clinic. (23) Mitochondrial oxidative d a m a g e and decreased function is a key factor in Parkinson's disease. (24) A

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February/March 2006

sublingual form of N A D H may be C o Q I O mice were still alive, versus optimal, since s o m e swallowed only 2 5 % of the controls. Average N A D H might be broken d o w n by life span for controls w a s about 31 digestion, while sublingual N A D H months, versus 37 m o n t h s for the will penetrate right into the bloodstream. "the CoQIO content in hearts from 5 mg. to 10 mg. humans 77 to 81 years old is only 43% of N A D H daily is of that present in 19 to 21 year old ' a typical therapeutic dose.

CoQIO C o Q I O is a key player in the mitochondrial ETC. (25) It has been reported, that the normal level of C o Q I O in the mitochondrial m e m b r a n e is below that required for m a x i m u m activity. This finding indicates strongly that C o Q I O might be a rate-limiting c o m p o n e n t in the E T C . (26) C o Q 10 is also a p o w e r f u l antioxidant that protects the E T C from the oxidants they produce (27). The fact that the biosynthesis of C o Q I O in aging tissues is inadequate is obvious f r o m the fact that, the C o Q I O content in hearts f r o m h u m a n s 77 to 81 years old is only 4 3 % of that present in 19 to 21 year old hearts. (26) Figure 3 highlights the similarity b e t w e e n C o Q 10 and its synthetic analogue idebenone.

In a m o u s e life-span C o Q I O study, at the 39th month 5 0 % of the Coenzyme Q10

C o Q I O mice. Even more noticeable was the far greater activity level in the C o Q I O mice, an obvious sign of the reversal of the typical age drop of mitochondrial energy production.

(26) Dosages obviously vary greatly upon need, but 60 mg. to 120 mg. of C o Q I O daily is a useful basic dose.

Idebenone Idebenone is a special synthetic analogue of C o Q I O (see figure 3) sharing most of its features, but it also has many additional features that appear not to be present with C o Q I O (such as enhancing serotonin levels or nerve growth factor). In itself, it is recognised as the most potent anti-oxidant available, with studies indicating it to be more than 30-times as effective as a free radical quencher than vitamin E. [Ed.- for further details about idebenone, please see the Fall 2004 issue of the Antiaging Magazine, pages 14-15].

Idebenone m a y be a useful adjunct to C o Q I O for mitochondrial energy enhancement at 30 mg. to 90 mg. daily.

II o

Conclusion o

o Idebenone

Figure 3: similarity between CoQIO and its synthetic analogue idebenone.

Mitochondrial decay with aging is a basic fact of life. It is a m a j o r contributor to aging and ultimately death. Thus, the earlier in life one starts an anti-mitochondrial decay program, such as the types outlined in this article, the greater the chance to postpone until a ripe old age the mitochondrial grim reaper.

References 1. H a r m a n , D. ( 1 9 7 2 ) "The biological clock: the mitochondria?" J A m Geriatr Soc 20: 145-47.

2. Miquel, J. et al (1980) "Mitochondrial role in cell aging" E x p Gerontal 15: 579-91.

3. B e c k m a n , K. & A m e s , B. (1998) "The free radical theory of aging matures" Physiol Rev 78: 548-81.

4. Pike, R. & B r o w n , M. Nutrition: An Integrated A p p r o a c h N Y C : M a c m i l l a n . 1984. Pp. 4 5 0 - 8 4 .

5. Linnane, A. et al ( 1 9 9 8 ) "The university of bioenergetic disease" Ann N Y A c a d Sci 854: 202-13.

6. Richter, C. ( 1 9 9 5 ) "Oxidative d a m a g e to mitochondrial D N A and its relationship to ageing" Int J Biochem Cell Biol 27: 647-53.

7. Bertoni-Freddari, C. et al (1994) " M o r p h o l o g i c a l alterations of synaptic mitochondria during aging" Ann N Y A c a d Sci 717: 137-49.

8. Shigenaga, M. et al ( 1 9 9 4 ) "Oxidative d a m a g e and mitochondrial decay in aging" Proc Natl A c a d Sci U S A 91: 10771-78.

9. Miquel, J. ( 1 9 9 2 ) "An update on the mitochondrial D N A mutation hypothesis o f cell aging" Mutat Res 275: 209-16.

EES

10. Liu, J. et al ( 2 0 0 2 ) "Delaying brain mitochondrial decay

and aging with mitochondrial antioxidants and metabolites" A n n N Y A c a d Sci 959: 133-66.

11. Sastre, J. et al ( 1 9 9 8 ) "A g i n k g o biloba extract ( E g b 7 6 1 ) prevents mitochondrial aging by protecting against oxidative stress" Free Rad Biol M e d 24: 298-304.

12. Sastre, J. et al ( 2 0 0 2 ) "Mitochondrial d a m a g e in aging and apoptosis" A n n N Y A c a d Sci 959: 4 4 8 - 5 1 .

13. Barja, G. (2002) " E n d o g e n o u s oxidative stress: relationship to aging, longevity and caloric restriction" A g e i n g Res Rev 1: 397-411.

14. H r u s z k e w y c z , A. ( 1 9 9 2 ) "Lipid peroxidation and m t D N A degeneration. A hypothesis " Mutat Res 275: 24348.

15. Yen, T.C. et al ( 1 9 8 9 ) "Liver mitochondrial respiratory f u n c t i o n s decline with age" B i o c h e m Biophys Res C o m m 165: 994-1003.

16. C h a m p e , P. & Harvey, R. Lippincott's Illustrated Reviews: Biochemistry. Philadelphia: J.B. Lippincott. 1994.

Pp. 66-73, 105-09.

17. Hagen, T. et al ( 2 0 0 2 ) "Feeding acetyl-L-carnitine and lipoic acid to old rats significantly i m p r o v e s metabolic function while decreasing oxidative stress" Proc Natl A c a d Sci U S A 99: 1870-75.

18. McCarty, M. ( 1 9 8 1 ) "Toward a 'bio-energy supplement' - a prototype for functional orthomolecular supplementation" M e d Hypoth 7: 515-38.

19. M a t h e w s , C. & van Holde, K. Biochemistry. R e d w o o d City C A : B e n j a m i n / C u m m i n g s Pub Co. 1990. Pp. 83-5.

20. Lund, P. et al (1975) "Effect of adenosine on the adenine nucleotide content and metabolism of hepatocytes" B i o c h e m J. 152: 593-99.

21. Pike & B r o w n , op. cit., p.99.

22. Forsyth, L. et al (1999) "Therapeutic e f f e c t s o f oral N A D H on the s y m p t o m s of patients with chronic fatigue s y n d r o m e " A n n Allergy A s t h m a I m m u n o l 82: 185-91.

23. Birkmayer, G. N A D H - T h e Energizing C o e n z y m e . N e w C a n a a n : Keats. 1998.

24. Miquel, J. ( 2 0 0 2 ) "Can antioxidant diet supplementation protect against age-related mitochondrial d a m a g e ? " Ann N Y A c a d Sci 959: 508-16.

The most potent a n t i o x i d a n t available Idebebnone's potential Idebenone is a cerebral benefits fall into 4 stimulant that increases categories: brain energy levels and has a rejuvenating effect on the whole body. It is a 1 Anti-aging synthetic variant of one 2 Energy enhancement of life's most essential 2 Cognitive biochemicals, Coenzyme enhancement Q10 (Co Q10).

4 Organ protector

Idebenone is simply one of the best supplements I've come across. I'm an otherwise healthy person but I can feel the difference it makes .

D.C., New York.

To order Idebenone call: or visit 866 800 4677 (USAToll-free) www.antiaging-systems.com +44 208 123 2106 (Outside USA)

25. Wallace, D. et al ( 1 9 9 8 ) "Mitochondrial biology, degenerative diseases and aging" BioFactors 7: 187-90.

26. Bliznakov,E. ( 1 9 9 9 ) "Aging, mitochondria and c o e n z y m e Q 1 0 : the neglected relationship" Biochimie 81: 1131-32.

27. Lenaz, G. et al ( 2 0 0 0 ) "Mitochondrial bioenergetics in aging" Biochim Biophys Acta 1459: 397-404.

28. Latini, S. et al ( 1 9 9 3 ) "Effect of idebenone on a d e n o s i n e o u t f l o w and adenine nucleotide level in h i p p o c a m p a l slices under ischemia-like conditions" Eur J Pharmacol 249: 6570.

29. Borgstrom, L. et al ( 1 9 8 6 ) " P h a r m a c o k i n e t i c s o f Nacetylcysteine in man" Eur J Clin Pharmacol 31: 217-22.

30. B o n a h o m i , L. & G a z z a n i g a , A. ( 1 9 8 0 ) "Toxicological, p h a r m a c o k i n e t i c and metabolic studies on acetylcysteine" Eur J Respir Dis 61 (Suppl 111): 4 5 - 51.

31. Miquel, J. et al (1995) "N-acetylcysteine protects against age-related decline o f oxidative phosphorylation in liver mitochondria" Eur J Pharmacol 292: 333-35.

February/March 2006 a a t t l

letters Q: I have a question about Wobenzym tablets. What is the established protocol? i.e. when surgeons prescribe Wobenzym to help the healing process as the literature says, do they tell you to start taking it before surgery or wait until after the surgery?

A: Wobenzym is Europe's best selling systemic enzyme formula and has been popular with atheletes for years to help speed the healing of injuries.

Mainly used as tablets, it is now also available in cream form for application directly to painful joints etc. Its results can be easily tested, next time you have a bruise use Wobenzym and you will see how much more quicker it disappears.

Regarding surgery, as you may imagine this does depend on the circumstance. However the majority appear to wait until after the surgery is complete before using. For such use, the standard dose for Wobenzym is 5 tablets twice a day, (normally upon rising and going to bed), however some physicians, including Dr. Garry Gordon have recommended as many as 10-tablets three times a day post-operation.

Q. Can I use the BEC5 cream even though I have had surgery to remove my BCC skin cancer?

A. As we reported in the Fall 2005 issues of the Antiaging Magazine, the development of the all natural BEC5 cream is showing remarkable results in the clinical trials for the reversal of BCC and SCC skin cancers, often avoiding the need for chemotherapy, radiation and surgery! However it is a fact that many people who have had previous treatment for such cancers are more likely to see a reoccurrence within the next 5-years. Surgery in particular does highlight one particular problem, that is the removal of cancer cells is very dependant upon the eye and hand skill of the surgeon. If after surgery a few cancer cells remain below the level of the skin surface (which can happen), then it is very hard for the BEC5 cream to find them. The cream needs to follow a trail of cancer cells, entering into the skin, for it to be effective. This is why Dr. Bill Cham always recommends the use of the

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one takes several thousand times the recommended dose. This is an alarmist and naive statement that has no bearing on scientific truth. High amounts of carnosine in the blood are not the equivalent of the medical condition called carnosinemia. There are over 1000 scientific trials showing the benefits of carnosine, and none supports the above statement. In fact, the latest research supports the use of carnosine AGAINST chronic brain disease. [Ed.- this is an abbreviated form of Dr. Kyriazis statement which is on file].

BEC5 cream before surgery.

Q. A certain doctor in the United States has been publishing that carnosinemia is a condition caused by carnosine overload.

This being perpetrated either by a genetical defect due to a lack of production of the detoxifying enzyme carnosinase, or that it can occur from the inhibition of the enzyme by too much of its substrate- carnosine. He states that an overload of l-carnosine will cause the inhibition of the degradation/ detoxifying enzyme, carnosinase. As a result he suggests that there will be an accumulation of high concentrations of carnosine in the blood and tissues, with this carnosine accumulation being the same as induced carnosinemia and that over time would potentially cause deleterious effects. How do you answer this statement that supplemental, orally taken l-carnosine may induce this condition?

A. We put this doctor's entire statement to carnosine expert, Marios Kyriazis, M.D., he answered us: "This is an exaggerated version of the truth. Carnosinemia is a very rare genetic condition due to lack of carnosinase, which allows extremely high amounts of carnosine in the blood. It is simply impossible to induce carnosinemia by taking too much carnosine by mouth, unless

Q. I just finished reading Dr. Wright's great little book on HRT. Wow! More succinct than all those other books out there. At the end of the book, which admittedly was 1997 when published, he put the estrogen rations at 80/10/10. Have you found other ratios more accurate? As it's almost nine years later and tons more research later I'd appreciate your time, help and consideration. Thank you.

A. Indeed Dr. Jonathan Wright's book, Natural hormone replacement for women over 45, which was also subtitled- don't let your doctor give you horse urine (published by Smart Publications), still remains a best seller today. You may remember that in that book Dr. Wright refers to the fact that his research found that the most normal/ average ratio of estrogens in women was 90/7/3, (that's 90% estriol, 7% estradiol and 3% estrone). I believe he only referred to 80/10/10 at the end because at that time in 1997 that was all that was available. Since then a bio-identical transdermal estrogen cream with the exact ratios of 90/7/3 has become available, it's called; "Esnatri." Remember that estrogens are best taken along with progesterone as highlighted by the work of the late John Lee, M.D. A recommended read in that regard is his book; What your doctor may not tell you about the menopause, published by Warner books.

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

remember that on my 71st birthday, I woke up to the phone ringing. It was sister from Dallas, and as she wished me a happy birthday, I realized the reason for the early morning call. After the conversation, I sat and reflected. What had happened to the time?

Many of my closest friends were gone. Too many more are waiting to die. At night we are bombarded with television commercials telling us that we need scooters so that we don't have to walk too far after a certain age.

I

Paul Bernstein, aka Mr. Physical Fitness USA™ is now 72 years young and reaching for 100+. He shares his views on optimal healthy aging and how he has achieved his remarkable psyche and fitness, even though he is approaching his 8th decade.

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This cheery news is followed with another company explaining how they can bury you inexpensively! As if this were not enough to totally depress you, your children get ads from homes that will take their parents off their hands and take care of them so that they don't have to. "Out of sight; out of mind."

Then your spouse receives offers in the mail for long-term home health care implying that if you live long enough, you are going to be a liability to her and those around you that may care.

"Aging is inevitable; growing old is optional" growing old is optional."

I make a positive goal daily and the picture you see of me is a current photo. It is how I look now and I know that I can continue to look like this for years to come; in fact I can grow younger as I grow older.

I work out 5 days a week at one of several fitness centers near my home in Houston. Almost every time I go to one of these clubs, I am asked the same question, "What is my secret?" There is no secret formula, it is called knowledge gleaned from 50 years in the fitness industry. Allow me to pass on an abbreviated version of the knowledge that I have gained through my experience and contacts.

When I was born in 1933, one was considered lucky to live to age 65. Hardly anyone lived to see his or her grandchildren grow up. Thank God, I have had the opportunity to see my great-grandchild be born, what's more I intend to take her through her first workout.

longer? My suggestions follow this introduction.

Remember what they always say; "The buck stops here." It is your responsibility to take charge of your health and learn how to extend your life and improve the quality of your life now and later.

I break down my suggestions into three parts; one-third mental attitude; one-third, exercise and one-third life-style: 1 My mental attitude: "The glass is always half full." Think young; enjoy your family; get in touch with that teenager inside of you. When I get up, the first thing I do is open the door and look up. If it's sunny, it's a great day! If there are clouds, I admire the beautiful patterns they make. If it is raining, I enjoy the fresh, clean smell. Use your mind for constructive things, such as, mentoring a young person, helping your community,

My answer to all of this is to say, "BALONEY!" Actually, what I really said could not be printed here! When I look in the mirror, I see a 21-year old, and I feel that way, too. This 72-year old intends to be young until 100 and then some. If you want to change a few of your life-threatening habits, you can come along and learn that whilst "Aging is inevitable;

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" M y mental attitude: The glass is always half full"

business. Right now I am developing three new projects. Get rid of anger.

Clean the garbage out of your mind. Leave more room for good thoughts and great ideas. Give yourself a goal each day, no matter how small.

2. Getting in Shape or shape up: These two expressions refer to two different things though they are often used interchangeably. Getting in shape refers to internal changes, like strengthening the heart and lungs, improving circulation, getting more flexible, and increasing stamina. These things are usually accomplished best by aerobic exercises.

Choose an activity that you truly enjoy: bike riding, swimming, jogging, skating, or walking. Your gym will have aerobic classes for those times when outdoor activities are impossible. Shaping up refers to the external or physical appearance.

Most people have one or more body parts that they

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do not like about themselves. Making physical changes is done by means of exercising with weights. Notice I said, "with weights." This does not mean HEAVY weights. Use a weight that you can move comfortably. Free weights or exercise equipment with weights can be used.

Choose the one that feels more natural for you. You may start an exercise program at any age, whether or not you have ever exercised, or it has been a long time since your last workout. Studies have been done in hospitals and retirement homes with seniors over 70, 80, and 90. In a matter of just a few months, these elderly people, who are usually couch potatoes, gained an average of 20% in muscle mass and lost around 10% of their body fat. We are lucky today. There are fitness centers on every corner in most major cities. There are more fitness centers than there are 7-11 s! No matter what your age, you will meet some nice people there. Most of these fitness centers have good trainers who will be happy to show you how to use the machines to your best advantage. If you don't live near a fitness center, or the cost is prohibitive, there are websites where you can get good exercise information, dozens of books on exercising, and many

excellent tapes and CD's with simple instructions.

3. Lifestyle/ medical: Most people in the fitness industry usually feel that there is no need for a doctor. They prefer to find a vitamin or an herb on their own; or as they often say, a "natural" remedy.

Don't self-medicate without advice. To live a VERY long and healthy life (and enjoy life to its optimum), the most important factor will be finding the right wife/ husband. Your other lifepartner is going to be your physician, your companion, your cheerleader, etc. This may confuse you coming from Mr. Physical Fitness, USA, but let me continue.

Doctors don't have a partnership with God. You must look around and ask questions. Be informed.

To me there are two kinds of doctors, (a) The traditional doctor that we are most accustomed to is the old-fashioned doctor who makes you feel better by treating your

symptoms when you get sick. I call them the "Sick Doctors." (b) But today there is another type of a doctor in a new field of medicine called, "AntiAging Medicine." This doctor should become your closest and most trusted friend. They are doctors dedicated to "wellness." Have a fullspectrum blood test at least twice a year, replacing those hormones that decline with age, to help keep the body working smoothly at optimum efficiency, like maintaining the fluids in your automobile. Work out your wellness plan with your doctor. Doctors list their specialties. Two of my favorite antiaging medicines are growth hormone and piracetam, they've made a big difference for me. If you

do not find antiaging doctors in your telephone book, visit A4M or IAS and ask about antiaging physicians in your area.

The right advice can literally add years to your life.

Always be good to yourself. Treat yourself to a spa treatment, good skin care, the right diet, activities you enjoy, and a healthy environment. The dividends will be a longer life that is more fun, and your family will love you better for it.

Paul Bernstein, Mr. Physical Fitness, U S A ™ has been a pioneer in the Health & Fitness Industry for more than 45 years. He has owned many health clubs, written articles, lectured at Senior

Seminars, publishes a Health & Fitness Digest, appears on television talk shows, and occasionally plays a "heavy" in movies.

Skin Cancer Breakthrough BEC5 cream the answer for skin c a n c e r Doctors & dermatologists of highly respected hospitals now advise that skin cancers may not require surgery, chemo or laser therapies!* Dermatologists at the Royal London Hospital recently concluded their stage III clinical studies by saying: "BEC5 is a topical preparation which is safe and effective, an ideal therapy for outpatient...it is a cost effective treatment for both primary and secondary skin cancer."

A natural cream with a 78% success rate within 8-weeks BEC5 Curaderm is a glycoalkaloid extract of the Australasian plant, the "Devil's apple" (Solanum sodomaeum). It has been shown to shown to selectively destroy cancer cells. Over 50,000 patients have already had success with BEC5 Curaderm.

"Dr. Rino Ceno & Sangesta Punjabi, St Barts Hospital, London (letter on file). **BEC5 cream applied twice daily, success measured as zero presence of basal cell carcinomas.

Note restrictions may apply in some countries.

This product and its statements have not been evaluated by the FDA.This product is not intended to treat, cure or prevent any disease.

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echnically speaking a "smartdrug" should be called a "nootropic." This was a term originally coined by Dr. Giurgea in the 1970's and taken from Greek to mean; "acting on or towards the mind." (1,9) In the medical sense a nootropic is restricted to a particular specialist class of drugs (2), but today the public are more likely to use the term "smart drug" to refer to any substance that has a positive effect on memory and cognition.

Ever since the publication in the 1990's of Dean, Morgenthaler and Fowkes best selling books; Smart Drugs and Nutrients (3) and Smart Drugs II (4) the term "smart drugs" has become much more familiar.

The first true smart-drug was piracetam and it was first developed nearly 40 years ago, heralding a "revolution" in pharmacology. This then continued with the development of piracetam's "cousins;" oxiracetam, aniracetam and pramiracetam.

Nootropics are revolutionary for two reasons, firstly they combine efficacy with extremely low toxicity and few side effects, (something rarely seen with "regular" drugs), plus they also offer promise to postpone or help reverse brain aging, and they may even be able to make "normal" brains work better!

What is clear from even a brief check of the international drug database PubMed, is that nootropics have been exhaustively researched. Since the first scientific studies began in the late 1960's over 1000 scientific papers have now been published. (4)

The action of the nootropics has been studied extensively in both animals and humans and one thing stands out, the toxicity of piracetam and its "cousins" is almost non-existent.

For example, in acute toxicity studies, intravenous doses of piracetam given to rats (8 g.l Kg. body weight) and oral doses given to mice, rats and dogs (10 g.l Kg. or more) have produced no toxicity. (6) This would be equivalent to 700 grams for a 70 Kg. (154 lb) human and therefore can be claimed to be "safer than salt." It is apparent that nootropics are among the toxicologically safest drugs ever developed.

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After examining the manufacturers leaflets for aniracetam, oxiracetam, piracetam and pramiracetam (20-24), the listed side effects are limited to excitability, headache, nausea, agitation, insomnia and anxiety, with most of those being mainly attributable to over dosage.

Nootropics enhance brain metabolism by stimulating oxidative catabolism, increasing energy levels (by improving ATP-turnover and cAMP levels), and enhancing phospholipid metabolism and protein biosynthesis. In addition they also appear to have an impact on the hippocampal release of acetylcholine and dopamine, but they do not significantly impact the release (or inhibition) of neurotransmitters, which may be a clue to their very rare occurrence of side effects (7).

Gouliaev and Senning stated; "..we think that [nootropics] exert their effect on some [molecule] present in the membrane of all excitable cells, i.e. the ion carriers or ion channels, and that they somehow accomplish an increase in the excitatory response. It would therefore seem that the [nootropics] act as potentiators of an already present activity (also causing the increase in glucose utilization observed), rather than possessing any activity of their own, [this is] in keeping with their very low toxicity and lack of serious side effects. The result of their action is therefore an increase in general neuronal sensitivity towards stimulation." (8) The most unique method of action of nootropics is the increase of communication across the corpus callosum (figure 2). This is the bundle of nerves that separate the two hemispheres of the brain. Nootropics appear to be able to enhance the communication across this network, improving intra-hemisphere contact.

(26,27,28) Some have inferred that this represents the ability to have new ideas (the right brain being artistic and creative) and putting them into action, (the left brain being logical and analytical). In other words, effectively connecting the Yin and Yang parts of the cerebellum.

These methods indicate that nootropics enhance potentiation and sensitize the activity of receptors, something very much in line with the model of improvement for the

"neuroendocrine theory of aging." (25)

In the 3+ decades that nootropics have been available in Europe, they have been used to treat an amazingly broad range of human ailments and conditions. These include: Being used successfully to treat alcoholism. (9,10,11) Improving or slowing deterioration in senile dementias such as Alzheimer's disease. (12,13) Enhancing alertness, co-operation, socialization and IQ in elderly patients. (14) Improving reading and accuracy in dyslexia, as well as the speed of reading, writing and spelling. (15,16) Reducing the severity and occurrence of the symptoms of headache, especially those associated with concussion. (18) Successfully treating motion sickness and vertigo. (19) Boosting mental performance in "aging, non-deteriorated individuals" suffering only from "forgetfulness."

(17) In regard to that last statement, nootropics have been found to boost learning, concentration and intelligence even in young people!

In a unique experiment, Dimond and Brouwers reported the results of a series of 7 double blind trials, involving 16 second and third year college students, all of them in excellent health and good physical and mental condition. After a period of 14-days, the authors reported on those receiving the nootropic by stating; "the fact is that piracetam improves verbal learning and in this it would appear to be a substance which is., capable of extending the intellectual functions of man., our subjects were not senile, suffering from generalized brain disorder, confusional states, or any other pathology of the brain... It is therefore possible to extend the power which [individuals gifted with high intelligence and good memory] possess to still higher levels despite the fact that the range of their achievement is already high." (24) This is a remarkable statement and is a clear indication of the potential of nootropics in antiaging/ preventative medicine.

Individual differences of action between piracetam, oxiracetam, aniracetam and pramiracetam and often subtle.

The Japanese, who have contributed much research on aniracetam favor it as an agent to rapidly promote clarity of thought.

One interesting benefit reported only for pramiracetam, is its ability to increase goal directed and purposive behavior (30).

Some studies on dementia comparing piracetam and oxiracetam (the two that are most chemically identical), have suggested that oxiracetam may be more effective in restoring the cognitive deficits of dementia (decreased memory, concentration and alertness). While piracetam may be

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more effective at normalizing the emotional problems of dementia such as agitation, tension-anxiety, hostility, insomnia and uncooperativeness.

Piracetam and oxiracetam are highly water soluble, while aniracetam and pramiracetam are more fat-soluble.

This fact may allow for less frequent dosing (once or twice daily) with aniracetam and pramiracetam, compared to 2 to 3 doses a day with piracetam and oxiracetam.

Quantitatively, piracetam is the least potent racetam, with clinical doses typically being 2400 mg. to 4800 mg. per day. Oxiracetam is usually given 800 mg. to 2400 mg. per day.

Aniracetam doses are typically 750 mg. to 1500 mg. per day, while pramiracetam has shown benefit even at 150 mg. to 300 mg. per day, although 600 mg. to 1200 mg. per day is more typical.

In fact, one study (31) showed significant intelligence and memory enhancement in Alzheimer's patients with just 150 mg. of pramiracetam daily, whilst the equivilant piracetam dose would have been 2400 mg. to 4800 mg. This indicates that when compared mg. to mg. pramiracetam could be up to 15-times more potent than piracetam.

Nootropics are a proven way to help improve concentration, memory, learning and attention. They have a long record in Europe of assisting with numerous disorders for the young and old alike.

Although there wasn't time to elaborate in this short article, there is also strong evidence that nootropics often work well, (i.e. they can be synergistic) when taken with some other substances such as acetyl-lcarnitine, centrophenoxine and hydergine etc.

There are a number of subtle differences between piracetam and its later derivatives. Often to get the best for an individual patient, some informed experimentation is required.

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But whilst oxiracetam and piracetam may be the most similar and aniracetam and pramiracetam the most "different," it is clear when compared mg. to mg. that pramiracetam can be considered, at least by its potency alone, to be the "ultimate smart drug."

1. Giurgea, C. (1973) "The nootropic approach to the pharmacology of the integrative activity of the brain" Cond.

Reflex 8, 108-115.

2. South J, (1998) "Reviewing the smart drugs" International Antiaging Bulletin, Spring v3 i4, International Antiaging Systems.

3. Dean W, Morgenthaler J, (1990) "Smart Drugs and Nutrients." Health Freedom Publications.

4. Dean W, Morgenthaler J, Fowkes 5.W. (1993) "Smart Drugs II." Health Freedom Publications.

5. PubMed drug database www.pubmed.gov National Library of Medicine and National Institute of Health.

6. M. Tacconi, R. Wurtman (1986) "Piracetam, physiological disposition and mechanisms of action" in Advances in Neurology V43; Myoclonus, S. Fahn, ed. 675-685, Raven Press.

7. G. Pepeu, G. Spignoli (1990) "Neurochemical actions of nootropic drugs" in Advances in Neurology V51; Alzheimer's disease, R. Wurtman ed.

247-52, Raven Press.

8. A. Gouliaev, A. Senning (1994) "Piracetam and other structurally related nootropics" Brian Res. Rev. 19, 180-222.

9. C. Giurgea, M. Salama (1977) "Nootropic drugs" Prog. NeuroPharmac.1, 235-47.

10. Paula- Barbosa, M. et al (1991) "The effects of Piracetam on lipofuscin of the rat cerebellar and hippocampa; neurons after long-term alcohol treatment and withdrawal" Alcoholism: Clin Exp Res 15, 834-38.

11. Skondia, V. & Kabes, J. (1985) "Piracetam in alcoholic psychoses: a double-blind, crossover, placebo controlled study" J Int Med Res 13, 185-87 12. Stegink, A. (1972) "The clinical use of Piracetam, a new nootropic drug" Arzneim-Forsch/Drug Res 22, 975-77.

13. Croisile, B. et al (1993) "Long-term and high dose treatment of Alzheimer's disease" Neurol 43, 301-05.

14. Chouinard, G. et al (1983) "Piracetam in elderly psychiatric patients with mild diffuse cerebral

impairment" Psychopharmacol 81, 100-06.

15. DeBerdt, W. (1994) "Interaction between psychological and pharmacological treatment in cognitive impairment" Life Sci 55, 2057-66 16. Wilsher, C. et al (1987) "Piracetam and dyslexia: effects on reading tests" J Clin Psychopharmacol 7, 230-37 17. Mindus, P. et al (1976) "Piracetaminduced improvement of mental performance" Acta Psychiat Scand 54, 150-60.

18. Hakkrainen, H. & Hakamies, L. ( 1 9 7 8 ) " Piracetam in the treatment of post-concussional syndrome" Eur Neurol 17, 50-55.

19. Gouliaev, A. & Senning, A, (1994) "Piracetam and other structurally related nootropics" Brain Res Rev 19, 180-222.

20. Aniracetam manufacturer's leaflet (Ampamet), Menarini.

21. Oxiracetam manufacturer's leaflet (Neuromet), GlaxoSmithKline.

22. Piracetam manufacturer's leaflet (Nootropil), UCB. 23. Pramiracetam manufacturer's leaflet (NeuPramir), Lusofarmaco.

24. S.J. Dimond, E. Brouwers (1976) "Increase in the power of human memory in normal man through the use of drugs" Psychopharmacol 49, 307-09.

25. Dilman, V., Dean, W „ (1992) "The neuroendocrine theory of aging and degenerative disease." Center for Biogerontology, Pensacola, Florida.

26. Buresova, O. & Bures, J. (1976) "Piracetam induced facilitation of interhemispheric transfer of visual information in rats" Psychopharmacologia 46, 93-102.

27. Dimond, S. et al (1979) "Some effects of Piracetam on chronic schizophrenia" Psychopharmacol 64, 341-48.

28. Okuyama, S. & A i h a r a , H. (1988) "Actions of nootropic drugs on transcallosal response of rats" Neuropharmacol 27, 67-72.

29. South, J. "Nootropic drugs and nutrients, pathway to brain rejuvenation." 1st Monte Carlo Antiaging Conference www.antiagingconference.com 30. R.J. Branconnier et al (1983) "The therapeutic efficacy of Pramiracetam in Alzheimer's disease- preliminary observations" Psychopharmacol Bull 19, 726-30.

31. Poschel, BPH, Marriott JG, Gluckman Ml, (1983) "Pharmacology underlying the cognition activating properties of pramiracetam."

Psycopharmacology Bulletin, Vol. 19, No. 4, pp 708-16.

W

hile everybody is talking about Antiaging Medicine nowadays, very few people agree on what the term actually means.

Some practitioners use the term very generally to include 'quack' treatments and therapies that have no scientific basis whatsoever, while others rely so much on strict scientific and academic terms that do not allow room for a common sense and practical discussion.

Between these two extreme positions, true Antiaging Medical practitioners are now getting organised to stimulate a debate aimed at clarifying what their speciality is truly about.

Setting the Scene Before discussing the exact meaning of Antiaging Medicine it is necessary to mention a brief overview of Gerontology- the science of aging. Gerontology is an academic and scientific discipline which studies every aspect of aging, not just medical matters. It is divided into three main categories. These are distinct entities but certain elements of one category may overlap with another: Social Gerontology. This is about social issues associated with J | | c l u d i n g families, ships, pensions, financial issues, retirement, employment, education, the politics of old age, and so on.

Biological Gerontology. It is the study of the biology and biochemistry of aging. It includes molecular and cellular research such as stem cells & cloning, immunology, animal research and other academic issues or basic and laboratory sciences.

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Marios Kyriazis, M.D.

Clinical Gerontology. This concerns human aging medical issues.

Clinical gerontology is further divided into two sub-categories: - Geriatric medicine, a well

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Antiaging Medicine is a branch of complementary . . practitioners are currently medical science and clinical involved in this specialty. medicine...with the ultimate goal

of extending the healthy An Antiaging medical doctor may use both conventional and lifespan of humans. alternative treatments, in an

established branch of medicine which aims to treat existing diseases affecting older people (those over the age of 65).

-Antiaging Medicine, the new medical specialty aimed both at young and old individuals who want to delay age-related problems for as long as possible, and maintain health into old age.

The Specialty

So, you can see that Antiaging Medicine is only a small part of a much bigger umbrella which covers age-related issues. A specific definition of Antiaging Medicine is the following: Antiaging Medicine is a branch of medical science and clinical medicine, aimed at treating some of the underlying processes of aging and at alleviating or postponing any age-related ailments, with the ultimate goal of extending the healthy lifespan of humans.

Antiaging medical practitioners aim not only at delaying and reducing the severity of age-related diseases (such as arthritis, dementia, cataract), but also at postponing and reducing the severity of ailments which are due to the natural process of aging (e.g. skin aging, loss of muscle tissue, loss of bone mass) and so maintain some of the characteristics of youth.

Strictly speaking, those who practice Antiaging Medicine should be fully qualified and registered medical practitioners, although other health practitioners, such as nutritionists, osteopaths and a a m February/March 2006

integrated approach for achieving the best possible result for the patient. Antiaging Medicine is a holistic discipline, seeing the patient as a whole and not just as an isolated disease. Perhaps one of the most important characteristics of Antiaging Medicine is that it is not so much concerned with treating existing diseases, rather with preventing or delaying future age-related health problems. This begs the following question: What is the difference between conventional preventative medicine and Antiaging Medicine?

Well, preventative medicine and general health promotion is directed at people of any age and uses general concepts of prevention, aiming to reduce the likelihood of any disease. It does not offer any treatments. Antiaging Medicine on the other hand, is more focused and specific, concerning itself only with agerelated issues. For example, preventing infectious diseases or diseases in pregnancy is not within the realms of Antiaging Medicine.

or health problems of aging. Some parts of aging can be really useful.

For example, wisdom and understanding of the world increases with age, spiritual matters are better appreciated, and there are even some physical areas which improve with age, for example: Âť Allergies generally become less troublesome.

- Travel sickness becomes less likely.

- Sensitivity to pain decreases.

By the same token, youth is not necessarily a good thing, but only certain aspects of it are desirable (health and appearance for example). Other aspects of youth, such as inexperience and insecurity, are definitely seen as undesirable in the eyes of many older people. Youth should not be confused with 'a young chronological age'. What most people are trying to achieve is not to have a young chronological age but a young biological age, i.e. be healthy and biologically efficient.

Aging

In addition, preventative medicine relies only on prevention, whereas Antiaging Medicine is both about prevention and cure. Some of these cures are already used by mainstream health practitioners (such as Alendronate and hormone replacement therapy for agerelated osteoporosis). Other treatments are used to cure specific age-related diseases (such as n-acetylcarnosine drops for cataract, Strontium Ranelate for osteoporosis, and Alagebrium for cardiovascular disease).

To give a better idea about Antiaging medicine, it is necessary to also explain what 'aging' actually means. There are different ways of trying to define aging, and experts in the field have been struggling for years to come to an agreement. Generally, aging can be described as: 'the progressive failing ability of the body's intrinsic and genetic powers to defend, maintain and repair itself in order to keep on working efficiently'. This highlights the fact that, as we grow older, we are subjected to an increasing number of both external and internal damaging events, which are not being properly controlled, leading to illness and disability.

Antiaging Medicine is not necessarily against all aging as such, but only against the medical

Another definition of aging is 'the process of accumulated damage to the building blocks of life (proteins,

DNA, carbohydrates etc), leading to malfunction of cells, tissues and organs, ultimately leading to death'. This is a more academic explanation of aging at the molecular level, but essentially implies that, if we somehow repair this damage to the building blocks of life, then we could retard or reverse aging at the clinical level.

Traditional scientists believe aging to be a natural phenomenon which is intrinsic (in our genes), deleterious (it is detrimental and has no benefits), universal (it affects every living thing), and progressive (it goes only in one direction and it ca not be turned back).

Cutting-edge thinking however, shows that this view is becoming difficult to support. Although aging is indeed written into our genes, it is not completely irreversible. The clock has been turned back in a number of pioneering experiments during the past few years, and on at least one occasion involving ground-breaking cloning techniques, it has been reset right back to zero. Also, aging is not necessarily detrimental, and there are several aspects of it that are advantageous, as already mentioned.

Aging is certainly not due to a simple lack of a hormone or nutrient. Taking a few supplements or replacing a single nutrient is not going to reverse aging. It is a much more complicated process, and there are several different mechanisms involved in it.

As mentioned above, Antiaging medicine aims to maintain some of the characteristics of youth. But what does 'youth' actually mean?

Youth, in the context of Antiaging medicine, does not mean 'somebody who is not old', but somebody who has some, or all, of the characteristics of idealized youth, for example, good general health, strong muscles and bones, an efficient immune system, sharp memory, a healthy brain, and

hormones working at their peak capacity.

Antiaging practitioners believe that it does not matter how old you actually are, in other words it is not a matter of chronological age, but a matter of improving biological, social, j spiritual and mental age.

'Aged' or 'old' is somebody who has succumbed to the problems related to age. You may be of an advanced chronological age but still retain some of the characteristics of youth. For example, there are 90 year-olds who look healthy, are without any significant illnesses, feel energetic and enjoy life to the full. They are content and fulfilled, and enjoy the best of both worlds: health (youth) plus wisdom (age).

Other terminology

Many people, including some respectable scientists, are in a muddle about the different terms used in the Antiaging field. They use words like 'longevity', 'immortality' and 'rejuvenation' without making a distinction. These words may sound similar but there is, in fact, a great difference between them.

Any linguist will tell you that 'longevity' simply means 'living longer'. An Antiaging physician will tell you that 'longevity' does not mean merely prolonging life for the sake of it, but also extending the years you can live in good health, your 'health-span'. Those who are opposed to longevity, thinking that the aim of longevity is merely to add years to life (with all the illnesses that come with that), are simply mistaken. 'Longevity', in the

eyes of an Antiaging practitioner, is not one, but two things: living longer and being healthier.

You will notice that 'living longer' is not specific and does not refer to any numbers. How much longer?

Longer than what? The answer is vague: By as much as possible.

Longer than others. 'Long life' to most people means an age of, perhaps, 90-95 years, whereas a minority may mean an age of over 100.

Other terms used in the Antiaging field are: 'Rejuvenation' means exactly 'to become young again.'

'Eternal life' means to live forever.

'Forever' means different things for different people. Some take it to mean 200-300 years of age, whereas others consider it to mean thousands of years. Some people even take it literally, i.e. really forever (billions of years).

'Immortality' means never to die, which is, in a sense, similar to the above.

Notice that none of the above terms say anything about being healthy or unhealthy. These terms should be used to their exact meaning. Treatment with a certain February/March 2006

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product will not make you 'immortal', but may grant you a certain degree of 'longevity'.

Future treatment with genetic manipulation may give you 'rejuvenation' but not 'eternal life'.

Antiaging Medical Treatments The following treatments or therapies are currently used by Antiaging practitioners and form part of true Antiaging Medicine.

Drugs and supplements Hormonal therapies. These include treatment with bio-identical hormones such as DHEA, growth hormone, androgens, testosterone, and estrogens. Other hormones used are thyroxin, insulin and melatonin. On certain cases, hormones may be used to treat endocrine (hormonal) problems before these are picked up by conventional laboratory tests.

Examples are diabetes, hypothyroidism, menopause and andropause.

Antioxidant therapies, such as vitamins A, C and E, resveratrol, glutathione, co-enzyme Q10, polyphenols and many others.

Although many people buy some vitamins from their health food shop, this does not guarantee any Antiaging effect, because one should take into account the strength of the preparation, its quality and purity, the reliability of the supplier, the combination these supplements are taken, and many other factors.

Antiglycators, which are active against glycation, the damaging process whereby sugar molecules attach to proteins or DNA. Commonly used antiglycators are carnosine (including Nacetylcarnosine for cataract) and aminoguanidne. Less common but effective agents are tenisletam, pyridoxamine, and cross linkbreakers such as Alagebrium (ALT 711).

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February/March 2006

Antiaging medicine is a new and pioneering branch as 'brain-boosters' such as ginkgo biloba, phosphatidylserine, choline, although of medicine memantine, bacopa,

- Nootropics, commonly known

centrophenoxine, piracetam and hydergine, to mention just a few.

The general activity of nootropics is to improve circulation of the blood to the brain, protect the neural tissues against damage (including against free radical damage) and stimulate neurotransmitters.

- Other general anti-agers are deprenyl, methylators (i.e., SAMe and TMG) and Calorie Restriction mimetics, such as metformin. Less commonly-used treatments such as heavy metal chelation, human stem cells, fetal cell therapy, and other immune therapies are also available in a clinical setting.

Nanotechnology has a future potential for Antiaging medicine.

Lifestyle and appearance Lifestyle therapies including hormesis (beneficial stress), brain and sense exercises, physical exercise, calorie restriction, and general health education. Advice on these is available from books or from Antiaging clinics.

Cosmetics used against aging of the skin: Botox, Isolagen, collagen, hyaluronic acid fillers, face lifts and other surgical operations used against face skin aging.

Others Treatment for specific age-related diseases such as Alzheimer's disease, Parkinson's, osteoporosis etc is also part of Antiaging medicine although some aspects of this overlap with Geriatric medicine. Complementary treatments such as with plants and nutrients which protect against specific age-related illnesses are included.

It is worth remembering that certain treatments or approaches,

aimed at helping us live longer, are not entirely part of Antiaging Medicine. For example:

- Cryobiology and cryonics. This is not against the aging process, but against death. • Sports medicine and endurance.

Although helpful in improving the health of an older person, general sports medicine and activities such as body building or body sculpturing are not age-related therapies - Treatment for unusual or incurable diseases such as Multiple Sclerosis, ALS, fibromyalgia, chronic fatigue syndrome. These are not related to the aging process.

- Beauty treatments (aimed only at improving beauty and not aging of the skin), such as artificial nails or eyebrows, treatment of excessive facial hair etc.

- Certain cosmetic procedures such as breast enlargement, liposuction, penis enlargement etc., which do not deal with any age-related changes.

Conclusion Antiaging medicine is a new and pioneering branch of medicine. By outlining exactly what one means when using the different terms related to aging, it becomes clear that this specialty has not any mythical or unscientific connotations, but it is scientificallybased and worthy of further recognition.

No doubt, soon more treatments will become available and added onto the existing mainstream treatments offered by Antiaging practitioners, to help achieve the aim of 'living longer and healthier'.

interview

The discovery of a natural cream that eats cancer!

Dr. Bill Cham is the Biochemist who discovered and developed BEC5 Curaderm. The following interview with Dr. Cham outlines the history of medical research that BEC5 Curaderm has followed between 1979 to the present day. It highlights the personal dedication that Dr. Cham has demonstrated in achieving his ambition of developing a remarkable cream for skin cancer.

A A M : Dr. C h a m , please let o u r r e a d e r s know a b o u t the qualifications you hold.

Dr. C h a m : Certainly, m y credentials include University degrees in Chemistry from the Netherlands, as well as Biochemistry, w h i c h I obtained in Australia. I also hold a Doctorate o f Science P h . D in the field o f M e d i c i n e .

A A M : W h e r e did you complete most o f your studies?

Dr. C h a m : I was l i v i n g in Australia, w o r k i n g at the University o f Queensland Department o f Medicine. A s Queensland has a m o n g the highest rates o f skin cancer, I was pleased to be h e l p i n g people with their conditions.

However, all the research was self-funded and privately undertaken.

A A M : W h e n d i d y o u first f i n d o u t a b o u t t h e active i n g r e d i e n t in B F . C 5 C u r a d e r m ?

Dr. C h a m : It was out o f the blue in 1979, when a friend o f m i n e named M e r v Gilliver, w h o was c o m p l e t i n g his veterinarian P h . D , asked m e w hether I had heard o f the 'Devils apple Plant?' M e r v had recently discovered that the j u i c e o f the Devils A p p l e fruit had stopped the growth o f an eye cancer t u m o r in cows. That piqued m y interested and I began to research it further. At the time it was u n k n o w n what the possible active ingredient was in the fruit o f the Devil's A p p l e plant.

R e a l i z i n g that Vincristine and Vinblastine are active anticancer agents in the Periwinkle plant I embarked at looking for similar ingredients in the Devil's A p p l e . Vincristine and Vinblastine are glycoalkaloids. I discovered that there were also glycoalkaloids in the Devil's A p p l e . Bui these glycoalkaloids were very different in structure than those

Interviewed by Phil Micans

found in the periwinkle plant. O n c e the glycoalkaloids were fully characterized 1

February/March 2006 a a m

37

realized that the interest in the source material

kidneys or haematopoietic system during

went back a hundred years in the literature.

treatment. N o r m a l skin treated with B E C 5

you c o n c e r n e d a b o u t c o u n t e r f e i t p r o d u c t s ?

C u r a d e r m , was also tested and was also free

Dr. C h a m : Naturally one worries about one's

A A M : W h a t is t h e active i n g r e d i e n t in

from adverse histological clinical effects.

work being used to support products that are

B E C S C u r a d e r m a n d w h a t m a k e s it

B E C 5 Curaderm is a non-toxic product as it

not proven or tested, and that has happened.

special?

has the same active ingredients f o u n d in egg

O n e particular c o m p a n y has m a d e several

plant which is eaten every day. Therefore y o u

attempts to release cream products in the U S A

Dr. C h a m : The active ingredient in B E C 5

d o not need to worry about any side effects or

for S u n Spots and cites m y research on

Curaderm is called Solasodine Glycosides.

adverse reactions. Actually, the products

Solasodine Glycosides as evidence o f the

These active ingredients are extracted from the

natural attributes m a k e the product so simple

products efficacy. However, whilst clinical

plant S o l a n u m S o d o m a e u m , the so-called

to use w h i c h greatly contributes to the

results have been published, the specific

D e v i l ' s apple- w h i c h is f o u n d in the

products popularity.

technologies to extract and purify the active

is that the pure extract, the active substance

A A M : W h a t t y p e o f skin c a n c e r s d o y o u

d o m a i n . So these companies are using 'guess

itself, has been shown to be effective in the

r e c o m m e n d B E C 5 C u r a d e r m to t r e a t ?

w o r k ' without trials and trying to deceive the

ingredient is not available on the public

Australasia region. W h a t makes it interesting

public that they contain the same

treatment o f the m a l i g n a n t h u m a n skin tumours, basal cell carcinomas, s q u a m o u s cell

Dr. C h a m : 1 r e c o m m e n d B E C 5 Curaderm to be

pharmacologically active ingredient. This is

carcinomas as well as the benign tumours,

used to treat areas o f the skin that m a y have

clearly not the case and in some cases resulted

such as keratoses and keratoacanthomas.

become discoloured, thickened or scaly as a

in fake products being withdrawn from the

result o f exposure to sun ( U V ) light. These

marketplace. The only glycoalkaloid product

areas o f the skin are k n o w n as keratoses (sun

that is supported b y credible evidence is B E C 5

application of the B E C S C u r a d e r m cream

spots). This cream is also very effective to

C u r a d e r m . Others c o u l d potentially worsen the

been?

treat true malignant skin cancers such as the

condition, w h i c h is dangerous.

A A M : S o j u s t h o w effective has t h e

non-melanoma basal cell carcinoma ( B C C ) and s q u a m o u s cell carcinoma ( S C C ) .

A A M : S o m e d o c t o r s m a y l i k e to classify

treatment give us c o m p e l l i n g evidence o f the

A A M : Y o u say ' n o n m e l a n o m a ' s k i n

t r e a t m e n t . W h a t a r e y o u r c o m m e n t s on

efficacy o f B E C 5 Curaderm. Treated skin

c a n c e r s , w h a t a b o u t m e l a n o m a s themselves.

this?

cancer lesions have not recurred for at least 5

W h y w o u l d they be a n y d i f f e r e n t ?

Dr. C h a m : The histological analyses o f

B E C 5 C u r a d e r m as an a l t e r n a t i v e

biopsies taken before, during and after

years after cessation o f therapy. Indeed, recent

D r C h a m : There is a big misunderstanding

trials completed at respected U K hospitals

Dr. C h a m : It is often misunderstood by the

highlighted that twice daily applications o f

public that there is a very clear distinction

i f the product is natural it is an alternative

B E C S Curaderm produced complete remission

between a m e l a n o m a and a m a l i g n a n t skin

treatment. The natural active ingredients o f

o f skin cancers in 7 8 % o f the patients within

cancer. M e l a n o m a s are characteristically moles

Curaderm B E C 5 have been fully investigated

only 8-weeks.

that are changing in shape and size. A r o u n d

as i f they were synthetic c o m p o u n d s to

5 % o f all skin cancer cases are M e l a n o m a s and

establish efficacy, safety etc. O v e r 7000 o f the

A A M : That's r e m a r k a b l e , w h a t was the

their danger is that the cancer can spread

c o m m o n l y prescribed drugs in the western

s i t u a t i o n in the r e m a i n i n g 2 2 % o f p a t i e n t s ?

through the body to any other organ. B E C 5

world are derived from plants, but they are not

Curaderm is a localized cream treatment that

classified as alternative!

Dr. C h a m : A l l o f them also had reduction in

has the capacity to trace and destroy cancer

the size o f their tumors. 1 believe had the trials

cells in a specific skin area. The active has n o

A A M : C o u l d y o u please d e s c r i b e to us the

continued longer for those patients, that they

w a y o f entering the bloodstream to locate

t y p i c a l process a p a t i e n t goes t h r o u g h a n d

too w o u l d have achieved complete remissions.

cancer cells in other organs or skin areas. A t

w h a t they m i g h t expect to see?

Such results have been the case in former

the m o m e n t , the B E C Technology is being

Clinical Trials completed in Australia in the

researched by an Australian listed company,

Dr. C h a m : The most important thing to k n o w

1980's and 1990's which have been published

'Solbec Pharmaceuticals L t d ' and results for

about using B E C 5 Curaderm is the end result

in international journals such as Cancer Letters

the treatment o f internal cancers are

is smooth, fresh skin that has a normal

and Drugs o f Today. The near 100% success

encouraging. At this stage, however, absolutely

appearance. Stopping treatment before this

rate has been consistent across all clinical

n o treatment claims can be m a d e for B E C ' s

point is not advised as cancer cells may still be

trials, open studies and a m o n g consumers in

effectiveness on m e l a n o m a s or internal

present w h i c h will subsequently multiply.

general. S o m e larger skin tumours m a y take

cancers. Thus, until all clinical trial work is

Sunspots and Keratoses involves a p p l y i n g the

up to 15 weeks treatment for complete

concluded and relevant drug approvals are

cream 2 or 3 times a day and within a few

remission.

A A M : W h a t a b o u t side effects, h a v e t o x i c o l o g y studies been c o m p l e t e d on B E C S Curaderm?

Dr. C h a m : Yes, all forms o f toxicology have been investigated. B i o c h e m i c a l , hematological

finalized, B E C should never be assumed to be

days the skin will appear normal again.

a m e l a n o m a t u m o r treatment. M e l a n o m a s

case o f B C C s and S C C s , the treatment process

require the care full attention o f a Doctor w h o

is longer as the lesion is bigger a ÂŤ d malignant.

that there are no adverse effects on the liver,

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February/March 2006

In the

can perform clinical tests accessing where the

In this case it is very important for people to

cancers are located in your body. F o l l o w i n g

understand the process because, during

this, treatment options m a y be a combination

treatment the lesion usually appears worse

o f surgery and chemotherapy or other cancer

than pre-treatment. BEC-5 penetrates the skin

controlling drugs.

tissue and moves its way around the healthy cells to find the cancer infected cells. O n c e

and urine analytical studies have demonstrated

38

about alternative treatment. M o s t people think

A A M : T h i s is r e m a r k a b l e , c a n I a s k , are

these cells are located the two B E C 5 actives

interview are activated to perform their duties. The first active contains a receptor that has the key to the cancer cell door. Once inside, the second active finds the stomach of the cell and explodes the stomach, killing the cancer's life.

This killing of the cancerous cells causes a slight inflammation as the cancer cells are killed. This can be evidenced on the skin surface through the lesion appearing bigger and possibly watery material will seep from the lesion. There is no need to worry. This seemingly worsening of the lesion is just a sign that the cancer cells have been destroyed creating a disturbance to the skin tissue structure. The dead cancer cells are replaced with healthy normal cells. Despite the increase in lesion size it is most vital that you continue to apply the BEC5 cream. The continued application allows more BEC5 to locate cancer cells in the surrounding tissue. BEC5 literally traces and seeks out all the cancer cells. It is imperative that an occlusive dressing such as micro-tape is used after each BEC5 application. The treated lesion is not allowed to dry out and form a scab. The objective of BEC5 treatment is to return your skin to be absolutely back to normal. Once the skin area has a completely new layer of skin with no more sores, inflammation or break in the skin surface, then the treatment is over. We are glad that it is easy for everyone to know when the treatment is over because everyone's principal objective when treating skin cancer is to have skin return absolutely back to normal. Cancer free and scar free are of course also results you can expect from using BEC5.

AAM: So how much of the BEC5 cream does it take to treat a typical skin cancer?

Dr. Cham: On average a 20ml bottle can manage one to two large noil melanoma SCC or BCC skin cancers, two to three medium sized ones or perhaps twelve sun spots and its shelf life is 5 years.

AAM: That really must be the most economical treatment for cancer- ever!

Presumably the patient isn't undergoing any other treatments as well?

Dr. Cham: Indeed hopefully they are not! in fact, some dermatologists have remarked that BEC5 Curaderm is an ideal replacement for chemo, radiotherapy and laser treatment and an excellent therapy for outpatient treatment.

AAM: I am sure some of our readers are interested or are already using BEC5 Curaderm. What is the best advice you can give people when using this remarkable

natural cream?

Dr. Cham: There is no question that BEC5 Curaderm is the treatment of choice for non melanoma skin cancer. The disadvantages of other treatments are wel I known by doctors everywhere. Post treatment consequences include; scars from invasive surgery, recurrence of the skin cancer within a few years and drastic side-effects from the currently available "standard" drugs. I have been shocked by some of the surgical results that I have seen on patients and consequently I have worked tirelessly for 27 years so that people worldwide can be given the choice of BEC5 Curaderm. So, obviously my best advice is: use BEC5 Curaderm, it works.

Secondly, my advice is have patience. Whilst surgery can be over in a day, some patients, such as Iris Napier have been treated for up to 13 weeks. This is a long time, but remember, the BEC5 treatment is about, killing the cancer cells, building back the healthy cell tissues beneath the skin and finally regenerating the top outer skin layer.

Compared to surgery, that is simply cutting out all the tissue, both good and bad out, permanently! So, of course, BEC5 Curaderm will take longer. Incidentally, Iris was warned by her Doctor that the planned surgery would risk her nose existence! As Iris was likely to have to live with a plastic nose, she is glad that she found BEC5 Curaderm. The average treatment time is under 2 weeks, but note, if you want to speed up the treatment BEC5 Curaderm can be applied up to 10 times a day with 20 to 30 minutes in-between every application, this reduces the number of treatment days dramatically. Thus, more applications a day means faster results.

AAM: As Antiaging medicine is all about not becoming sick in the first place, is there any role for BEC5 Curaderm in preventative medicine?

Dr. Cham: Good question, to which I believe the answer is yes. After all, if you have concerns that a sun spot could be malignant, or may become so, simply apply the BEC5 Curaderm cream sparingly twice a day until it has cleared up. My vision is that as the popularity of BEC5 Curaderm increases people will learn to use the cream immediately on site of any such spot and in doing so cancer lesions will not grow. Because there is zero toxicity it is simple to apply the cream all over the face, arms and other potential skin cancer/sun spot risk areas. I actually suggest this prevention tactic to anyone who has had skin cancer in the past.

"I'm happy that the research has come to something so conclusive and extraordinary" AAM: So you have been working on BEC5 Curaderm since 1979, how active are you on the product now in 2006.

Dr. Cham: 1 recognize my work on BEC5 Curaderm as a significant life achievement and have been honored with the many hundreds of peer medical reviews that have validated the Glycoalkaloid science that I pioneered. There is no question in my mind that these 26 years have paved the way for a long commercial future for the product.

However, I have reached a point in my life, now retired in the beautiful South Pacific country of Vanuatu, where the commercial world is beyond me. I will be a life long endorser of the medical research and efficacy that distinguishes BEC5 Curaderm, however you will not see me in the board room or at marketing presentations any more like I was busy doing ten years ago when I first released the product, so really, I am not involved with the product anymore. However, I am writing a book called; "The Skin Cancer Cure" which partly explores the roller coaster ride I have experienced in getting the product this far without the support of large company budgets.

Following the release of the book next year I plan to write some more journal articles possibly on the preventative side of BEC5 Curaderm, which I feel is very important to explain.

AAM: I believe this is a great example of antiaging medicine at its best and I am glad that we've been able to expose your terrific work in the Antiaging Magazine. I see that it has been a long road for you personally, how do you feel now?

Dr. Cham: There have been many obstacles to overcome and there will be more I'm sure.

But we feel that we are now over the crest of the hill and I'm happy that the research has come to something so conclusive and extraordinary, and that we are of course, helping people's lives and saving them from a lot of discomfort and disfigurement.

AAM: Many congratulations Dr. Cham.

Dr Cham: Thank you for your interest in our work.

February/March 2006

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