Aluminum, Alzheimer, EDTA, and P5P

[Guest guest]

So that you don't get confuse with the issue of B6,

here is the information that will open your eyes on

the dangers of aluminum, and where DMSO, MSM, EDTA,

and p5p (B6) fits in. It explains how aluminum is a

cause of so many maladies and what you can do about

it.

 

Ted

 

 

 

source: http://www.vrp.com/art/728.asp

and

http://www.vrp.com/art/765.asp

 

 

Crosslinkage Theory of Aging: Part III

The Neurotoxic Effects of Aluminum

Ward Dean, MD

 

Introduction: Sixty years ago Dr. Johan Bjorksten

introduced his theory on the role of protein

crosslinking as a process involved in many of the

debilitating effects of human aging. In Part I of The

Crosslinkage Theory of Aging we examined this theory

and explained its relevance to ongoing anti-aging

research. In Part II we examined ground-breaking

research into compounds that can potentially repair

the effects of protein cross-linking and reverse some

of the most debilitating effects of aging at the

molecular level.

 

Aluminum

Aluminum is a highly reactive metal that occurs freely

in nature, and comprises over 8% of the earth’s crust.

Although it also occurs very widely in human nutrition

(most people ingest 10-100 mg of aluminum daily), it

does not play a role in any known metabolic process.

Since the human digestive system rejects all but

traces of ingested aluminum, aluminum has historically

been regarded as a relatively non-toxic substance.

However, we are now learning that aluminum is highly

toxic, even in extremely small amounts.

 

The neurotoxic effects of aluminum have been known for

many years. (1) More recently, scientists have shown

that aluminum accumulation may contribute to

Parkinson’s disease (2,3) Down’s syndrome (4) and

Alzheimer’s disease. Crapper, et al injected 100

nanamoles of aluminum chloride into cats’ brains. (5)

Ten days after the aluminum injections, the cats’

short term memories were completely gone, causing a

condition similar to Alzheimer’s disease in humans.

 

There are a number of reasons which explain the toxic

effects of aluminum. First, aluminum is a powerful

flocculant (an agent that precipitates suspended

solids in turbid water) commonly used in municipal

water treatment processes to purify drinking water.

These properties also cause shrinkage of colloids

(suspended microscopic particles). Since the human

brain contains large amounts of colloidal gels as

essential constituents, abnormal coagulation of these

gels will cause shrinkage—and possibly sever

interneuronal connections—in a process similar to ones

known to occur in aging. If aluminum de-flocculates

our brains, however slowly, it might be a high price

to pay for absolute clarity of our drinking water.

 

 

 

 

 

Second, aluminum is a powerful crosslinking agent. The

reason for this is that the aluminum atom has a very

small diameter (Fig. 1), and a very high surface

binding energy. Therefore aluminum can penetrate

almost everywhere and displace any of the other common

metals in soluble compounds. In particular, aluminum

readily displaces calcium, which is present in every

living cell. The mechanism of how aluminum can cause

crosslinkages and age-related changes becomes clear

when we consider a critical property of aluminum in

relation to calcium. Calcium atoms have only two

binding sites. Aluminum atoms, on the other hand,

possess three binding sites (Fig. 2).

 

With only two binding sites calcium is restricted to

combining in straight lines only (Fig. 3). Thus, when

calcium combines with anything else with two binding

sites, there is no way in which branching

(crosslinking) can occur.

 

 

 

 

 

However, when even the smallest trace of aluminum

displaces anything with two binding sites, there is no

way in which branching can be avoided! This is because

aluminum has an extra valence, or hook, which can

combine with an unsatisfied binding site in another

bi-valent (two binding sites) chain. Therefore each

aluminum replacement of calcium results in a new

branching (crosslinking). Repeated branching, coupled

together with growth, makes tangling unavoidable (Fig.

4).

 

 

Thus, we can see that it takes very few aluminum atoms

to totally interrupt and change the simple and orderly

chains of calcium atoms — and to introduce all sorts

of surprising complications.

 

Natural Defenses Against Aluminum

Our bodies have five defenses against aluminum. These

are:

 

1. The Stomach and Intestines: These organs block

aluminum, allowing only about 0.015% of ingested

aluminum to be absorbed.

 

2. The Kidneys: The kidneys are highly effective in

excreting most of the aluminum that we do absorb.

 

3. The Bones: Our bones take up and store most of what

little aluminum remains in the blood stream.

 

4. The Blood-Brain Barrier: Only minute amounts of

aluminum get past this barrier, which resists the

passage of anything that does not belong in the brain.

 

 

5. The Neuronal Cell Wall: This is the final barrier

blocking aluminum.

 

Despite these barriers, nothing works perfectly, and a

small amount of aluminum is still absorbed. Using

another one of his charming stories, Bjorksten (6)

described how this might happen: If I were an aluminum

atom and wanted to get into the nucleus of a neuron,

past the body’s defenses, I would watch for a calcium

transport and board it. Calcium is needed in every

cell, so calcium has (relatively) free access. I, as

aluminum, am only half as big as the calcium, but have

50% more strength, and, as an ‘ace in the hole,’ I

have a third arm! So I would board the calcium

transport, occupy a calcium compartment, and use my

totally unsuspected resource, the third arm, either to

hold camouflage or to defend my place against all

comers. The calcium shuttle might be chosen from any

of the four groups of calcium-binding proteins. I

might slip out inconspicuously once inside the last

defense, or I might even use my third free arm to

kidnap the entire transport, converting it to a free

radical by the force in my third arm, and then

maneuver the entire unit to combine with literally

anything it happened to hit.

 

Unfortunately, our defenses against aluminum were not

designed to last much more than the 60 years or so

required for the average human to have children and

help them get a good start in life.

 

 

Aluminum Uptake Increases with Age

In 1955, during a talk on gelatin crosslinkages and

aging at the Gerontological Society in Baltimore,

Bjorksten discussed the probable relationship of

aluminum to crosslinking. One of the attendees, Prof.

H.H. Zinsser of Columbia University, was so interested

in the concept that he and Bjorksten began a fruitful

collaboration that was to last for seven years. Using

spectrographic analysis, they examined the aluminum

content of 84 persons, ranging in age from 10 to 90

years (Fig. 5). They found peak levels at age 40-50,

followed by a drop and then leveling off, indicating

that those whose aluminum accumulation peaked in

middle age did not survive the next ten years. (7)

 

Zinsser’s data were confirmed independently by

Markesbery and colleagues, who demonstrated a

progressive increase of aluminum concentrations in the

brain (Fig. 6). (8) Extrapolating from these values,

Bjorksten concluded that the finding of progressive

increases of aluminum with age were of great

theoretical importance, and indicate that humans, in

their natural state, will die between 110-120 years of

age as a result of the aluminum mechanism alone, even

if no other cause of death intervenes. (9) Bjorksten

is so convinced of the profound toxicity of aluminum

in contributing to the aging process, that he

predicted that even if cancer and atherosclerosis were

completely eliminated as causes of death, aluminum

accumulation would be the foremost cause of

age-related human disease.

 

Preventing Aluminum Accumulation and Crosslinking

Clearly, it is important to reduce our exposure to

aluminum. The most obvious steps are to drink only

filtered water, and to avoid aluminum cookware,

aluminum foil-wrapped food, beverages in aluminum

cans, aluminum-containing anti-acids,

aluminum-containing anti-perspirants, and foods made

with aluminum, like baking powder and most non-dairy

coffee creamers.

 

 

However, when preventive methods are not enough—and

Dr. Zinsser’s data cited above indicate that they

obviously are not enough—we must consider ways to

remove as much accumulated aluminum as possible.

 

Bjorksten and his staff evaluated the ability of

chelating agents to remove aluminum from the aortas of

5-6 month-old hogs, which had previously been stained

with an aluminum-containing stain (Fig. 7). (10) It

can be seen that EDTA was the most effective. Lactic

acid, similar to blood concentrations generated by

exercise were moderately effective. Of interest was

the fact that 0.5 % procaine—the active ingredient of

Gerovital (the Romanian anti-aging drug)—was also

moderately effective in reducing the aluminum. This

raises the question whether the metabolites of

GH3—DMAE and PABA—might also have some effect in this

regard.

 

Other benefits of DMAE/PABA were described in a

previous issue of Vitamin Research News. (11) Drs.

Imre Zs.-Nagy and Katalin Nagy demonstrated that both

dimethylaminoethanol (DMAE) and centrophenoxine (CPH)

are indeed able to diminish the extent of crosslinking

in old rats. (12) Professor Zs.-Nagy’s membrane

hypothesis of aging, and his studies with Idebenone

and DMAE were also described in a previous issue of

Vitamin Research News. (13)

 

In another series of innovative studies, (14,15)

Bjorksten’s team evaluated the ability of various

concentrations of lithium to remove tightly bound

aluminum from tanned leather baseball covers. Using a

0.05M concentration of lithium citrate, they were able

to displace 100% of the protein bound aluminum in the

baseball covers. They found that it took approximately

three months to completely demetalize the leather.

Lithium is used to treat manic depressive illness

(MDI)—but recent studies indicate that it may offer

benefit in the prevention and treatment of Alzheimer’s

disease, as well. (16) Safe blood lithium levels are

about 1.0 mEq/liter—about 1/50th of the concentration

used to displace aluminum from the baseball covers.

Nevertheless, it is intriguing to consider that

perhaps long-term treatment with low doses of lithium

may be an effective way to displace protein bound

aluminum in animals and humans. Lithium orotate as a

dietary supplement is the safest, most effective form

of lithium available.

 

In another series of experiments, using himself as a

guinea pig, Bjorksten applied a low voltage current to

his head, in an attempt to demetalize his own brain.

(17) His parents both died from Alzheimer’s disease,

and he believed that he was beginning to show some

early signs. After much trial and error, he designed

an electrical skull cap, which was moistened with a

solution of sodium chloride to enhance conduction. He

hypothesized that at the rate of 1/2 hour every day,

it should be possible to remove the aluminum present

in the neural chromatin in the brain in 1,538 days

(4.3 years). However, he realized that only a part of

the energy may have been applied to aluminum removal,

and that a longer time may be required.

 

 

Another theoretical approach to removing aluminum is

by the intravenous, oral, or topical use of

dimethylsulfoxide (DMSO). Bjorksten and colleagues

extracted a substantial part of the aluminum present

in human cadaver brains with DMSO. (18) DMSO is

approved for human use as a bladder irrigant in

patients with interstitial cystitis, and for use in

dogs and horses as a topical anti-inflammatory agent.

However, it is also widely used topically,

intravenously, and orally to treat a wide range of

clinical conditions, including arthritis, sprains,

atherosclerosis, burns, scleroderma, and many other

conditions. (19-21) MSM (methylsulfonylmethane) is the

active metabolite of DMSO, and shares most of its

properties, without the somewhat objectionable odor of

DMSO. An effective dose of MSM is generally in the

range of 3-5 gm daily.

 

Conclusion

Despite the sound theoretical and experimental basis,

and the apparent promise of the Crosslinkage Theory of

Aging, Bjorksten’s contributions have been largely

ignored by present-day gerontologists. Although

Bjorksten remained fully active until his death in

1996 (He published his last book in 1991, and

co-authored a yet-unpublished paper with his last

collaborator, Dr. Don Kleinsek, shortly before passing

away at the age of 89) (22) little has been written

about the crosslinkage theory since that time.

 

Nevertheless, Bjorksten’s work remains solid. He

suggested (and validated) the value of a number of

potential anti-crosslinking nutritional substances,

with primary emphasis on EDTA. Bjorksten, in his later

years focused primarily on the crosslinks caused by

aluminum (largely, I think, because this was something

which he discovered could be prevented). In recent

years, much has been written about the process of

enzymatic browning and glycation, resulting in

production of advanced glycation end products of aging

(AGEs) which result in crosslinked proteins, just as

Bjorksten predicted. We believe the currently popular

approach of preventing and breaking AGE-induced

crosslinks is in reality an outgrowth and development

of Bjorksten’s theory.

 

The next installment of the Crosslinkage Theory will

address the glycation of proteins in detail, and

suggest specific anti-aging approaches based on

preventing and eliminating these AGE-induced

crosslinks.

 

 

 

 

Email this article to a friend

 

Crosslinkage Theory of Aging: Part IV

AGEs and Crosslinkages - New Respect for Crosslinkage

Theory

Ward Dean, MD

 

Introduction and review: The Cross-linkage Theory of

Aging was first proposed by Dr. Johan Bjorksten in

1941. Bjorksten believed that aging was caused by

inter- and intramolecular crosslinks in proteins,

nucleic acids, and other vital macromolecules that

caused them to gradually stiffen and lose their

function.

 

Bjorksten initially searched for enzymes capable of

dissolving damaging crosslinks. But as he grew older

he realized that he didn’t have enough years of life

left ahead of him to allow for the identification and

isolation of these enzymes. Consequently, he shifted

his line of research to a more imwww.ely solvable

approach—using chelating agents to remove toxic heavy

metals (especially, aluminum)—that were known to be

one cause of crosslinking. He hoped that by

eliminating the crosslink-promoting tri-valent (three

points of attachment) aluminum atoms (which he

believed displaced di-valent [two points of

attachment] calcium atoms, he would reduce one of the

major sources of crosslinking, and thereby buy enough

time to solve the rest of the crosslinkage problem.

This has been explained in greater detail in the first

three parts of this series (see Crosslinkage Theory of

Aging on the VRP online library at www.vrp.com).

 

Bjorksten ended his active research career in 1991

with one last publication that summarized his progress

up to that point. Ironically, at about the time

Bjorksten was retiring from his quest to unravel the

crosslinkage problem, other scientists were picking up

the baton—although they approached the problem from a

slightly different direction.

 

Advanced Glycation End Products of Aging (AGEs)

A characteristic of all long-lived proteins in the

body is that as they age, they turn brown and become

fluorescent (under UV light), become more

cross-linked, less soluble, less elastic, and less

digestible by enzymes. In 1965, Dr. H.B. Bensusan

first proposed that it was a process known as the

Maillard reaction that caused these changes. The

Maillard reaction is named for the noted French

scientist, Louis Camille Maillard (1912), who

described the non-enzymatic chemical reactions between

proteins and carbohydrates that cause cooked foods to

turn brown. This time-honored bit of kitchen chemistry

has been used by cooks for centuries to enhance flavor

and transform plain foods into delicacies by adding

flavor and color to recipes.

 

 

In 1985, Monnier, Kohn and Cerami provided further

details of the role of the Maillard reaction as a

major source of the age-dependent increase in

browning, fluorescence and crosslinking of collagen

and other tissues. (1) They further developed the idea

that it is the Maillard reaction that results in

premature aging and degenerative diseases such as

diabetes and heart disease. In this regard, many

scientists think the human body may be viewed as a low

temperature oven with a relatively long—approximately

75 year —cooking cycle. (2)

 

The Maillard reaction involves a chemical reaction

(condensation) between a sugar (usually glucose) with

a protein. This complex is known as a Schiff base. In

the human body, this is a reversible reaction which

reaches equilibrium (i.e., stabilizes) within several

hours.

 

With continued exposure to the sugar, the Schiff base

undergoes a rearrangement known as non-enzymatic

glycosylation that results in a more stable, less

reversible substance, known as an Amadori product.

Again, in the human body, this process reaches

equilibrium over several weeks. (Fig. 1)

 

 

The Amadori product further degrades irreversibly into

a number of highly reactive carbonyl (C=O) compounds.

These reactive substances, called Advanced Glycation

End products have been designated by the acronym AGE.

(3) AGE is a clever pun which reflects the proposed

relationship of these reactive substances to aging and

age-related diseases. AGEs can further react with

other fats, proteins and nucleic acids to form largely

indissoluble crosslinks. The age-related accumulation

of these AGE products has been demonstrated in many

tissues of the body (Fig. 2). (4)

 

Furthermore, during long-term hyperglycemia (elevated

blood sugar), as in diabetics, glycation and AGE

formation may increase up to four times as much! This

explains why diabetics suffer the premature onset of a

wide range of age-related complications including

cataracts, retinopathy, neuropathy, nephropathy,

atherosclerosis and osteoporosis. (5,6)

 

Crosslinkage Theory Gets New Life

Bjorksten was a talented petroleum chemist. Had he

been a food chemist instead, he may have appreciated

this link between the Maillard Reaction and

crosslinking much earlier, and made even greater

progress in developing preventive and therapeutic

approaches to crosslinkage-induced aging. Through

their insightful work in understanding this process,

scientists like Brownlee, Cerami and Monnier provided

renewed impetus and a rebirth for the crosslinkage

theory. (3) Unfortunately, they did this with little

attribution to Bjorksten, who had doggedly pursued

this approach to aging for over 50 years.

 

 

 

 

 

Crosslinkage Biomarkers

An important aspect of any comprehensive theory of

aging is the inclusion of techniques (dictated by the

theory) that can be used to accurately measure the

progress of aging. Parameters that can be correlated

with age and that can be used to evaluate the rate of

aging are known as biomarkers. (7) Scientists have

identified a number of unique biomarkers that reflect

aging in terms of the Crosslinkage/ Glycosylation

theory. (Table 1)

 

 

 

 

 

Approaches to Preventing and Removing AGE-Induced

Crosslinks

 

Khalifah and his colleagues proposed a schematic of

the formation of AGEs, which illustrates a number of

specific therapeutic targets (Fig. 3). ( 8) Here are

some of the most promising substances to use to

inhibit/dissolve AGE-induced crosslinks.

 

 

 

 

 

Goat’s rue (Guanidine)

Goat’s rue (Galega officinalis), or French Lilac, has

historically been used for the treatment of diabetes

since medieval times. The glucose and insulin-lowering

effects of Goat’s rue extract are due to the natural

substance, guanidine. Guanidine (Fig.4.) is the herbal

prototype for the insulin-sensitizing,

glucose-lowering anti-diabetic drug, Metformin

(Glucophage), and for the related substance,

aminoguanidine. The use of raw Goat’s rue is limited

in diabetes by its toxicity. The toxicity of Goat’s

rue is due to a substance known as galegine (Fig. 5),

which can cause reductions in blood pressure and nasal

discharge. Vitamin Research’s Goat’s rue extract is a

special preparation that is standardized to contain

50% guanidine, with negligible amounts of galegine.

VRP’s purified, high-guanidine form of Goat’s rue

presumably shares most of the beneficial effects of

aminoguanidine and Metformin, with none of the adverse

effects of raw Goat’s rue herb.

 

 

 

 

 

Metformin (Glucophage)

Metformin is an anti-diabetic biguanide that was

derived from the herb, Goat’s rue (Galega

officinalis). Biguanide drugs were recognized by Prof.

Vladimir Dilman as early as the mid-1970s as the most

effective anti-aging drugs in existence. Metformin is

known as an insulin receptor sensitizer, capable

primarily of lowering blood sugar and insulin. Dilman

also demonstrated that biguanides restored cortisol

receptor sensitivity. Metformin has many other

beneficial properties, including optimizing lipid

profile, reducing body fat, maintaining levels of

growth hormone, stimulating immunity, and extending

the maximum lifespan of experimental animals. I

reviewed the anti-aging/ life-extending effects of

Metformin in the November, 1998 issue of Vitamin

Research News.

 

Despite its wide range of reported beneficial effects,

Metformin has not, to my knowledge, been tested for

its ability to retard AGEs and AGE-induced crosslinks.

However, I assume that AGE-inhibiting effects would be

found for Metformin, if anyone bothered to look.

 

This situation is analogous to other similar nutrients

that have been tested for specific effects, while

overlooking effects attributed to their structural

cousins. For example, Acetyl-L-Carnitine is used

primarily for its cognitive-enhancing, mitochondrial

membrane normalizing effects, while L-Carnitine is

usually used for its cardiovascular and

lipid-normalizing benefits. Dr. Brian Liebovitz,

author of L-Carnitine—Vitamin Bt, believes, however,

that L-Carnitine is equal to or better as a cognitive

enhancer than ALC—its just that no one has ever

evaluated the cognitive enhancing effects of

L-Carnitine. I think the same could probably be said

for Idebenone and its close relative, Coenzyme Q10.

They both probably have very similar actions.

 

Likewise, I think Metformin and guanidine (as in VRP’s

Goat’s rue extract) probably share the AGE and

crosslinkage-inhibiting effects of their relative,

amino-guanidine. Metformin requires a prescription in

the United States.

 

Aminoguanidine (Pimegedine™)

Aminoguanidine is a substance that has been known for

over 100 years. It is structurally very similar to

guanidine, the active ingredient in the herb, Goat’s

rue. Aminoguanidine has aroused a great deal of

interest in the last twenty years, due to its

demonstrated ability to block the formation of AGEs

and AGE-induced crosslinkages in both animal and human

clinical studies.

 

Aminoguanidine inhibits AGE formation, preventing

AGE-induced crosslinks in collagen and other tissues.

Fortunately, aminoguanidine does not interfere with

the formation of normal collagen crosslinks, which are

required for structural integrity. Another mechanism

by which aminoguanidine is believed to act is by

enhancing the action of nitric oxide (the same

mechanism by which Viagra functions). (9,10)

 

 

Aminoguanidine also reduces the formation of

lipofuscin (age pigment) and prevents or reduces

cataracts, atherosclerosis, diabetic retinopathy,

nephropathy and neuropathy (Fig. 6). (2,11-13)

 

In a study with rats, scientists occluded the arteries

that supply blood to the brain, inducing an

experimental stroke. The scientists administered

aminoguanidine in various concentrations and at

various time intervals following inducement of the

stroke. They found that the size of the brain damage

from the loss of blood flow could be greatly reduced

with aminoguanidine, even when administered as much as

two hours after the onset of the reduction in blood

flow. (14) This indicates that aminoguanidine may also

be effective in the prevention and treatment of

strokes.

 

In one study of diabetic patients, after four weeks of

therapy with amino-guanidine, LDL cholesterol

decreased almost 30%, and total cholesterol and

triglycerides both decreased almost 20%.

Hemoglobin-AGE levels, a circulating marker of the

degree of glycosylation, also decreased dramatically

(13.8 U/mg Hb at the beginning of therapy, to 10.0

U/mg Hb after only four weeks). (15)

 

Although aminoguanidine’s effects on blood sugar and

insulin have not been examined, to my knowledge, I

believe that if such studies are conducted, the

effects will be positive. For example, Metformin and

Goat’s rue (guanidine) are best known and best tested

for their beneficial effects on blood sugar and

insulin, due to their insulin-receptor sensitizing

properties. Aminoguanidine, on the other hand, is best

known and best tested for its AGE-inhibiting effects.

However, I think that if these substances were to be

comprehensively evaluated together, we would find that

they share most properties, to a greater or lesser

degree, due to their closely related structures.

Anecdotal reports from patients and physicians appear

to confirm this.

 

Aminoguanidine is very safe, as indicated by

short-term human studies which used the astronomical

dose of 1200 mg daily. (16) (This is in comparison

with a usual human dose of 100-300 mg daily). The dose

required to cause death in half the animals (mice) to

which it was administered (Lethal Dose 50 [LD50]) was

1800 mg/kg.9 That would be equivalent to a human dose

of almost 300 gm!

 

Pyridoxal-5-Phosphate (P5P)

 

P5P, the active form of vitamin B6, has been found to

significantly reduce the nonenzymatic glycosylation

(formation of AGEs) of bovine serum albumin (BSA) with

radioactive-labeled sugar. Of the substances tested,

P5P was exceeded only by aminoguanidine in its ability

to inhibit AGE formation (Fig. 7). Combining P5P with

guanidine, metformin, or aminoguanidine may enhance

their AGE-inhibiting actions even more. (17)

 

 

 

Vitamin B1 (Thiamin)

Alteon is a pharmaceutical company which is focused on

developing drugs to prevent the formation of

AGE-induced crosslinks, as well as to dissolve

crosslinks after they are formed. Several of their

products are currently undergoing FDA-sanctioned

trials. One of the products, ALT-711, improved

arterial elasticity, indicating an ability to undo

crosslinkages. (18) This is the first drug that is

specifically designed as a crosslinkage breaker.

 

Interestingly, ALT-711 is a derivative of thiamin. In

their book, Life Extension, Durk Pearson and Sandy

Shaw reported that thiamin was an effective crosslink

inhibitor. They were, at that time, consuming two

grams of thiamin each day in their personal anti-aging

regimens. Thiamin, the parent compound of ALT-711, may

ultimately also prove to be an effective crosslinkage

breaker as well as inhibitor.

 

Carnosine

The anti-aging effects of carnosine were detailed in a

previous article in the November 2000 issue of Vitamin

Research News. Recently, Dr. Alan Hipkiss of the

Division of Biomolecular Sciences, King’s College

London, reviewed the anti-aging effects of carnosine

and aminoguanidine. Dr. Hipkiss believes that one of

the major mechanisms of the anti-aging effects of

carnosine is its powerful effects as a crosslink

inhibitor and breaker, and that the use of these

substances might help to control age-related molecular

dysfunction.

 

Conclusion

The venerable crosslinkage theory of aging has clearly

gained new respectability in light of the advances in

understanding of non-enzymatic glycation and the

formation of AGEs and AGE-induced crosslinks. Research

in this area is leading to the development of new

classes of crosslinkage inhibitors and breakers as

anti-aging drugs and nutrients.

 

It is also interesting to note the close relationship

between the crosslinkage, neuroendocrine, and free

radical theories. Free radicals have been proposed as

a cause of crosslinkages, as well as a factor in the

loss of sensitivity of receptors of various hormones

and neurotransmitters. Also, the loss of insulin

receptor sensitivity and impaired glucose metabolism

proposed by the neuroendocrine theory, which results

in high levels of blood sugar, is clearly a

cause/accelerator of crosslinkages.

 

Understanding these processes clearly points at a

number of ways to attempt to delay, and in some cases,

perhaps even reverse aging. One of the most effective

approaches, I believe, is to maintain low levels of

glucose and insulin, and minimize the formation of

crosslinkage-inducing advanced glycation end products

(AGEs). In addition to a low glycemic diet and

exercise, I think using either Metformin,

aminoguanidine, or Goat’s rue extract, combined with

P5P, carnosine, and possibly, additional thiamin, will

be found to be a potent anti-aging combination. In the

future, crosslinkage breakers like ALT-711 may also

become clinically available.

 

Related Products: (Click on links below to view

product(s))

 

1985-AGEBlock® , Anti Glycation Formula 90 capsules

1131-B6, Vitamin, Pyridoxal-5-Phosphate 50 mg, 60

capsules

1820-Oral ChelatoRx 360 capsules

 

 

 

The information in this article is not intended to

provide personal medical advice, which should be

obtained from a medical professional, and has not been

approved by the U.S. FDA.

 

Copyright by Vitamin Research Products, Inc. The

Vitamin Research News is intended solely for

individual, non-commercial use. All other uses are

prohibited without written permission from VRP. The

Vitamin Research News is protected by U.S. and

international copyright laws and may not be

reproduced, distributed, transmitted, displayed,

published or broadcast in any form, or by any means

whether now known or hereinafter devised, without

prior written permission from VRP.

 

Requests for permission to reproduce all or part of

the material or information contained in the Vitamin

Research News should be directed by U.S. Post to

Robert Watson at Vitamin Research Products 4610

Arrowhead Drive Carson City, NV 89706 or by fax to

Robert Watson at 775.884.1336 or via e-mail to Robert

Watson, at VRP

 

 

home | products | company | health concerns | library

| site map | catalog | newsletter | contact us

 

Vitamin Research Products . 800-877-2447 Carson City,

NV 89701