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Risks Associated with Low HGH in Men

Men are extremely different than woman when it comes to the risks which arise from low

(HGH) Human Growth Hormone. Men with risky low levels of HGH will suffer from

extraordinary lack of energy and motivation.

HGH in men is exceptionally crucial as the man’s two most significant hormones which build

them up physically and even emotionally are HGH and Testosterone. Women are much more

complicated hormonally speaking.

Please let us make this very clear Protein has been scientifically proven to build human beings

up. Therefore we call the building up process Anabolic…which has NOTHING to do with

steroids…HGH is NOT a steroid but it is the single most important hormone in a man’s body.

Conversely, there are substances that tear the body down and that is called the Catabolic

process and this is highly dangerous for men to be in a catabolic state, ever.

Simply put, if a man is low in HGH he is automatically catabolic.

What exactly does that mean and just how dangerous a risk is this?

It means that when a man is in a catabolic state from low HGH he is not able to replace cells

and tissues faster than his body is breaking them down. What exactly does that mean?

According to Dr. Sam Baxus, one of the world’s foremost authorities for over 40 years on low

HGH…it means that you as a man are needlessly slowly dying faster than their male friends who

do not yet have low human growth hormone blood levels.

There also exits a direct relationship between HGH and testosterone in men such that if a man

is low in HGH it is very likely to have a negative impact Testosterone production. Thus more

muscle weakness, fatigue, more fat lower lean muscle mass, and depression in men.

It means, that every aspect, every part of your body is being torn down piece by piece.

And the leading first symptom for men is lack of energy and low motivation.

Then men notice an increase in fat around the belly area and a loss of tone to their muscles.

This alone is a risk which is certainly not acceptable once a man understands that inner fat

increased around the waistline has clearly been established by cardiologists as an INCREASED

risk of having a sudden and severe Heart Attack.

Demographic studies at the University of North Carolina (chapel Hill) often referred to as the

little Harvard of the South… is known to produce the best studies of risk for illnesses of every

type according to age and the numbers of folks in each age group.

Regarding their study on HGH by age groups something enormously profound was gleaned.

Age 18, is the best age group nationwide according to HGH levels and the almost complete lack

of illness in that age group. We noticed that every 8 years after age 18 there was and is a

dramatic rise in age related disease so if one takes age 18 as nearly perfect for HGH purposes

and we times 18 by 3 we get age 54 the highest group of men by age for heart attacks each

year. Between age 45 and 55 men are at severe risk for heart attacks

Thus if we look at all age related disease due to lack of HGH by this best demographic study

ever done so far, we find an enormous mistake. Generally it has been said we lose 50% of our

HGH output every 30 years past age 20. So it has been said for years that age 50 you make only

half the HGH as you did at 20

BUT if one delves deeply into the University of North Carolina’s massive demographic research

study on age related illness and relationship to HGH levels we easily see that after age 18 we

lose 50% of our HGH output every 8 years after the age 18.

So for men the risks come on generally around age 35 to 40 with belly fat and lack of energy

and motivation.

Next there are changes in the make-up of cholesterol with an increase in the bad LDL and also

an increase in the dangerous Triglyceride levels going up for men.

A man’s stamina decreases when HGH levels are low.

Men experience less lean muscle with low HGH

Men also complain about being more sensitive to heat and cold with low HGH. Men are more

sensitive to light. Especially bright light, which is an indication of breakdown of eye tissue.

Men experience as an early warning sign of low HGH a lack of sexual desire and function.

Eventually, bones density becomes more porous and fractures from a simple trip fall can occur

The immune system starts to breakdown for men if they do not take action and get themselves

on more optimal youthful blood levels of HGH.

Men, you can forgo all these dangerous risks. AAI provides true expert advice and expert HGH

treatment protocols. Women live 10 years longer than men. Come on guys 10 years is a mini


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Glycomics, One of the 10 emerging technologies that will change the world.

MIT said the field of Glycomics, is “One of the 10 emerging technologies that will change the

world.” Notice, they did not say, one of the 10 medical technologies but one out of ALL

technologies that will change our world. It is as important as DNA and the Genome because the

8 major fundamentals of Glycobiology control both DNA and RNA. We even have the

Glyconome! Glycobiology controls our hormones and how they function…If you cannot get

enough of these 8 essentials life sustaining Glyconutrient’s, no matter how much HGH you take

it will have no effect or a neg. effect I am one of the few true experts in this exploding field. The

value to this more ramped up scientific language is so unique in this article that Google will

get in on these words I am using, KEY in on them and our standing in Google will go up

and up because no other competitor knows the scientific language of this anti-aging

breakthrough.. but Google’s algorithm’s and scrubbers places a very high value when you

write what others cannot or have not. When it is singular, as mine is and only on our

website blog Google loves that! That is why I want to write several articles on this topic so

germane to regeneration and living heathier for much longer. AND, there is big money in

this field selling sugars that heal. Please let me know what you think.


Seminal Research by Larry Sosna N.D. PhD HHP


See and hear what the true great university scientists are saying. “This is the future

today”, declares Dr. Gerald Hart of John Hopkins University…The number one rated

medical/scientific teaching hospital in the entire USA. “We won’t understand

Immunology, Neurology, Developmental Biology or Pathology until we get a handle on

Glycobiology.” ….. “If you ask, what is the Glycome for a single cell type it will be many

thousands of times more complex than the genetic Genome,” says Ajit Varki past

director of the Glycobiology Research and Training Center at Cal Tech. Professor

Raymond Dwek, head of the University of Oxford’s Glycobiology Institute, who

coined the term Glycobiology in 1988 says, “ As recent advances in genetics have

unfolded, the importance of sugars which heal has become ever more apparent.”…..

Varki said, “It’s like we just discovered the continent of North America. Now we have to

send out scouting parties to find out how big it is…..”

New Scientist Magazine, October 2002

I’m certain you have been told many times, sugar is one of the main enemies in life

causing all kinds of disease states and folks that can indeed be true. There are harmful

sugars and there are sugars so vitally important to vigorous good health that without

them we would all have suffered and died a long time ago. In fact, without these

miraculous special sugars we never would have made it out of infancy.

Glyco means sweet, there are bad sugars and ones we cannot live without, they are the

healthy Glyconutrients. If you are on one of those fad diets that does not allow the life

enhancing complex carbohydrates then you cannot make Glycoproteins which are

molecules that combine sugars with proteins as well as glycolipids, which are

combinations of healing complex sugars with fats. The term for these life giving

combinations are called glycoconjugates. These glycoconjugates have brought together

the world’s most brilliant medical scientists to comprehend a field so sophisticated the

combinations of glycoconjugates are infinite in how they arrange themselves to yield a

healthy body free from disease if you have them in high enough blood levels.

It will be useful to provide one with a high level of education concerning the immense

healing powers of a strong personal Glycobiology. Let’s shine some light on what

healthy levels of Glycoconjugates can do for the human body to improve both structure

and function.

Immune System Modulation:

Glyconutrients are necessary for healthy immune cells and a body wide capable

immune system function. They have been shown to:

Play a key role in many aspects of cell and tissue regeneration and repair, as well as

cell survival. They have strong positive effects on asthma and allergies in general.

Glyconutrients are one of the very few methods of preventing and or slowing down even

rheumatoid arthritis, lupus, and improves the symptoms of periodontal disease, canker

sores and herpes simplex 1 of the lips.

They have a favorable outcome in suppressing skin reactions and contact dermatitis as

well as inhibiting bronchitis. Many studies show they can prevent arthritis, substantially

reducing pain and increasing joint mobility in osteoarthritis, the most common form of



Glyconutrients and glycoconjugates help to inhibit growth and or tumor cell metastasis

in certain types of cancer. They do this by instructing white blood cells called Natural

Killer Cells to mobilize and seek out and destroy cancer cells. Today there is an entire

field of Glycobiology devoted to cancer research and the NIH and CDC have received

hundreds of millions in government funds to further enhance the field of Glycobiology

and cancer control.


An adequate supply of dietary glyconutritional healing sugars is vitally important during

periods of body wide stress, since glycoconjugates synthesized from eight key sugars

play key roles in many aspects of tissue healing and repair as well as cell survival

during extremely stressful periods. Corticotropin-releasing factor receptor is hormone

glycoprotein that regulates responses to emotional and other types of stress by

coordinating the endocrine, behavioral and immune responses to stress through

hormonal actions in the brain.

The Heart and Glycobiology

Glycolipid Conjugates are responsible for correct Low Density Lipid receptor site

instruction…These Low Density Lipids are the kind of cholesterol that can cause a

blocked artery and thus a heart attack…. But regulation of the dreaded LDL’s by

Glycolipid Conjugation makes the likelihood of artery blockage by LDL’s a very unlikely


Most of us have heard that cold water fish oil is protective to the arteries of the heart.

When we all have high levels of Glycolipids the Omega 3 fatty acids become like a

super biological Teflon…coating the linings of the arteries so the bad types of LDL

cholesterol cannot aggregate and build up on the artery linings from both sides of the

coronary arteries thus in the scientific review of many research cardiologists who have

researched Glycolipid conjugation they have published findings that are very highly

suggestive that proper amounts of Glycolipids in the blood protects against a buildup of

bad LDL aggregation, such that the arteries seem to be fully protected from a heart

attack. The problem is a mass of Americans do not have adequate blood levels of

Glycolipid Conjugates especially, Galactose which is of great importance for normal

heart and brain health.

Glyconutritional high levels of galactose, mannose, galactosamine and sialic acid binds

vitamin B12 to make B12 bioavailable to the cells. In other without the above mentioned

healing sugar combinations you can inject all the B12 in the world and it will not work.

The same combination of Glucoconjugates helps people from drug and alcohol cravings

all of which are injurious to the heart and liver.

AND the exact same above described combination, seriously reduces HUNGER

Hormone Function

Gonadotropin hormones are glycoproteins derived from the pituitary gland which

controls the release of many other hormones throughout the body including human

growth hormone (hgh).

Glycosylation of gonadotrophin hormones affects their size, circulatory life span, ease

of movement through cells, storage and secretion, clearance, immunoreactivity and

hormone bioactivity within the entire human body.

Glycosylation of IGF receptors contributes to their tissue regeneration and tissue

differences, which affects their biological activity. If an individual does not have

adequate blood levels of Glycoconjugates (the healing 8 combined sugars) all hormone

activity no matter how much one takes will be seriously insufficient to do their job in the

human body and that can be a health crisis.

Glycoconjugation which does not occur in its proper sequence will lead to a disruption

of insulin formation and correct synthesis and can be causal in some types of diabetes.

The sugars I am about to share with you are so incredible they actually have a

language all of their own. I call them the great hidden code of human life itself. They are

every bit as important as DNA. Amazingly, when these life giving sugars are combined

they can even change mistakes in DNA expression. Mistakes… that can lead to cancer

and every other nightmare type of nightmare illness. However, I am going to show you

how to take a true and certain quantum leap in your ability to regenerate, fight off

virtually all illness, protecting you’re cells, tissues and all of the organs, collectively in all

of our bodies.

You may be thinking this is absurd, sugar is bad for us, correct? Not so simple, just the

sugar D-Ribose is so vital to life that without it we cannot make Messenger RNA and

without messenger RNA you may as well not even make DNA because both are

needed for correct structure and proper functioning of each and every cell, tissue and

organ our bodies. You might even remember from high school biology in the 9th grade

that RNA stands for Ribo Nucleic Acid…and it’s very back bone comes from our good

friend, the amazing D-Ribose SUGAR.

I am very excited to share this science with you. Unfortunately this is a science within

the medical field that is so complex it was not until the 1960’s to 1980’s that we got our

arms around this field of Molecular Glyco-Synthesis. And just like the field of DNA it took

the most brilliant hand full of scientists in molecular bio-science to advance this new

field and show how massively important it is. The field is so important to every phase of

our life cycle; I still study it weekly even though it has been a 20 years endeavor. That is

how important this field is and it is an honor to share this life enhancing information with

you, our family of friends here at AAI …. Though the field to this day is not being brought

to the public with much attention or consistency.

We have given you a small taste of the importance of the 5 carbon sugar D-Ribose now

let’s really delve into the Art and Science of the other life giving sugars.

There are eight Essential Sugars called Saccharides required for Glycoprotein

Synthesis…They are as follows Xylose, Fucose, Mannose, Galactose, Glucose, N-

Acetylglucosamine, N-Acetylgalactosamine, and N-Acetylineuraminic Acid.

What does this mean? It means no expression of protein’s abilities to build up the cells

into tissues and then into organs can occur. No Protein, no big muscles no matter how

hard you work. Actually, no protein , means death That means that without these eight

amazing sugars which create Glycoprotein Synthesis we would not have a body to even

take care of. That is why you must learn how to obtain these super regenerative eight

sugars…if you want to be in a perfected state of excellent health.

Guess what else? We cannot make any HORMONES or even utilize them efficiently

without these super eight sugars but wait there is more good news. Since the early

1990’s Gluco-Scientists found 200 other super sugars from plant based sources,

funding to scientifically evaluate all 200 found so far has several years ago reached the

many hundreds of millions of dollars so are discovering the roles of all 200 sugars.

Mother Nature’s vast array of biochemistry, including these 200 sugars has a specific

purpose. The overwhelming majority of them will be to create an even more complex

language to further healing, cell regeneration and repair. So please don’t be stuck on

eating (sucrose white ultra-refined table sugar) as sucrose in that form is BAD for

human consumption.

Speaking of Hormones, about 10 years ago I learned from Dr. David Wesser M.D.

DDS, a very close friend and teacher, taught if you combine a significant dose of D-

Ribose with Galactose, the human body will regenerate all hormones that have reached

the end of their life cycle, bringing them right back to the top of their life cycle. If you

want to feel like a Greek God, put this into you’re program.

Remember the eight super sugars are a code containing an extensive language. Each

sugar is like a 1000 page book in terms of its ability to communicate instructions

throughout the entire body. Each page in any of the eight books can code and give

hundreds of millions of directions throughout the body. So, we are talking about a code

of life capable of issuing Trillions of life enhancing instructions from the molecular level

to the cells, tissues and organs and even the brain itself gets its instructions to develop

into a brain, as well as sustain you’re brain.

For Illustrative purposes, these molecular communication codes are like precisely

shaped words that protrude from the cells surface and are recognized and understood

by neighboring cells, we call this Glycoform Cellular Communication. It is these eight

amazing Glycoforms that determine your blood type. Imagine that, a sugar

molecule called a Glycoform, N-Acetylgalactosamine will make your blood type A … and

type B blood types are determined by the sugar Galactose. How IMPORTANT are these

eight sugars? You cannot make blood without them, need I say more. Yes indeed there

is so much more but to go further I would need to speak in the language of advanced


The important factor really is on a practical level which asks the question where do I get

these eight super regenerative sugars? Simply call us at AAI and you can learn how to

obtain the Super Eight!

Mechanisms of the Sialidase and Trans-sialidase Activities of Bacterial Sialyltransferases from

Glycosyltransferase Family 80 (GT80).

Mehr K, Withers SG.

Glycobiology. 2015 Nov 17. pii: cwv105. [Epub ahead of print]



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Development of Heptylmannoside-Based Glycoconjugate Antiadhesive Compounds against

Adherent-Invasive Escherichia coli Bacteria Associated with Crohn’s Disease.

Sivignon A, Yan X, Alvarez Dorta D, Bonnet R, Bouckaert J, Fleury E, Bernard J, Gouin SG,

Darfeuille-Michaud A, Barnich N.

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Identification of Arsenic Direct-Binding Proteins in Acute Promyelocytic Leukaemia Cells.

Zhang T, Lu H, Li W, Hu R, Chen Z.

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Comparative study of structural models of Leishmania donovani and human GDP-mannose


Daligaux P, Bernadat G, Tran L, Cavé C, Loiseau PM, Pomel S, Ha-Duong T.

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Synthesis of di- and tri-saccharide fragments of Salmonella typhi Vi capsular polysaccharide

and their zwitterionic analogues.

Fusari M, Fallarini S, Lombardi G, Lay L.

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Imaging. RNA catch and release.

Larochelle S.

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Merging carbohydrate chemistry with lectin histochemistry to study inhibition of lectin binding by

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André S, Kaltner H, Kayser K, Murphy PV, Gabius HJ.

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Synthesis of cholesteryl-α-D-lactoside via generation and trapping of a stable β-lactosyl iodide.

Davis RA, Fettinger JC, Gervay-Hague J.

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Enhanced Cross-Linking of Diazirine-Modified Sialylated Glycoproteins Enabled through

Profiling of Sialidase Specificities.

McCombs JE, Zou C, Parker RB, Cairo CW, Kohler JJ.

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Glycoconjugates distribution during developing mouse Spinal Cord motor organizer.

Fazel A, Vojoudi E, Ebrahimi V, Ebrahimzadeh A.

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Identification and functional analysis of two Golgi-localized UDP-galactofuranose

transporters with overlapping functions in Aspergillus niger.

Park J, Tefsen B, Heemskerk MJ, Lagendijk EL, van den Hondel CA, van Die I, Ram


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Candida albicans β-1,2-mannosyltransferase Bmt3 prompts the elongation of the cell-

wall phosphopeptidomannan.

Sfihi-Loualia G, Hurtaux T, Fabre E, Fradin C, Mée A, Pourcelot M, Maes E, Bouckaert

J, Mallet JM, Poulain D, Delplace F, Guérardel Y.

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HDL Cholesterol and Risk of Type 2 Diabetes: A Mendelian Randomization Study.

Haase CL, Tybjærg-Hansen A, Nordestgaard BG, Frikke-Schmidt R.

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Glypican4 promotes cardiac specification and differentiation by attenuating canonical

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Strate I, Tessadori F, Bakkers J.

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Glucocorticoid-induced leucine zipper: a critical factor in macrophage endotoxin


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Tamoxifen regulation of sphingolipid metabolism–Therapeutic implications.

Morad SA, Cabot MC.

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product signaling in a ceramide-dependent manner.

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Internalization and accumulation in dendritic cells of a small pH-activatable glycomimetic

fluorescent probe as revealed by spectral detection.

Arsov Z, Švajger U, Mravljak J, Pajk S, Kotar A, Urbančič I, Štrancar J, Anderluh M.

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Highly Substituted Cyclopentane-CMP Conjugates as Potent Sialyltransferase Inhibitors.

Li W, Niu Y, Xiong DC, Cao X, Ye XS.

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Activation and function of murine primary microglia in the absence of the prion protein.

Pinheiro LP, Linden R, Mariante RM.

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Phospholipase D2 drives mortality in sepsis by inhibiting neutrophil extracellular trap formation

and down-regulating CXCR2.

Lee SK, Kim SD, Kook M, Lee HY, Ghim J, Choi Y, Zabel BA, Ryu SH, Bae YS.

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Activation of human naïve Th cells increases surface expression of GD3 and induces

neoexpression of GD2 that colocalize with TCR clusters.

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Glycobiology. 2015 Dec;25(12):1454-64. doi: 10.1093/glycob/cwv062. Epub 2015 Aug 11.






Kolesnikov AV, Kozyr AV, Schemyakin IG, Dyatlov IA.

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HUMAN MICROBIOTA. Small molecules from the human microbiota.

Donia MS, Fischbach MA.

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Temporary Conversion of Protein Amino Groups to Azides: A Synthetic Strategy for

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Oral Administration of Lipopolysaccharide of Acetic Acid Bacteria Protects Pollen Allergy in a

Murine Model.

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Intranuclear interactomic inhibition of NF-κB suppresses LPS-induced severe sepsis.

Park SD, Cheon SY, Park TY, Shin BY, Oh H, Ghosh S, Koo BN, Lee SK.

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Glycoprotein from street rabies virus BD06 induces early and robust immune responses when

expressed from a non-replicative adenovirus recombinant.

Wang S, Sun C, Zhang S, Zhang X, Liu Y, Wang Y, Zhang F, Wu X, Hu R.

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Stroke is the third leading cause of death in the United States


Stroke is the third leading cause of death in the United States and results in substantial health-

care expenditures; the mean lifetime cost resulting from an ischemic stroke is estimated at

$140,048 per patient, and this estimation is higher for people over 45 years. Nationwide in 2010,

the estimated direct and indirect costs of stroke totaled $73.7 billion [1]. Although many clinical

trials have been completed in stroke patients, none of these have demonstrated protective

efficacy except for thrombolysis [2, 3]. In the case of cardiac arrest and resuscitation only

hypothermia has been shown to have clinical utility [4]. In some sense the two therapies that

have been effective thus far clinically have broad targets, and do not only affect a single injury

mechanism. In contrast, of the failed trials, many targeted neuron-specific injury mechanisms

[5]. This may reflect too narrow a view of what is needed for brain preservation. A large body of

work has shown that astrocytes play key roles both in normal and pathological central nervous

system functioning [6]. Astrocytes are the most abundant brain cell type, and in addition to their

multiple important homeostatic roles, they organize the structural architecture of the brain, help

organize communication pathways, and modulate neuronal plasticity (for recent review see

[7, 8]). Thus, astrocytes are now thought to be important potential targets for manipulation.

Ischemic stroke is caused by an interruption of cerebral blood flow that leads to stress, cell death,

and inflammation. Neurons are more susceptible to injury than astrocytes when studied under

some in vitroconditions [9, 10]. Neurons have less endogenous antioxidants and are susceptible

to excito-toxicity [10]. Both normally and after ischemia, astrocytes support neurons by

providing antioxidant protection [11, 12], substrates for neuronal metabolism [13], and glutamate

clearance REF. Although astrocytes are sometimes more resilient than neurons, injury can result

in impaired astrocyte function even when astrocytes do not die. Impaired astrocyte function can

amplify neuronal death [14]. Therefore, many recent efforts have focused on the astrocyte-

neuron interaction and how astrocyte function can be improved after stroke to enhance neuronal

support and survival [10, 15, 16]. A growing body of data demonstrates that astrocytes play a

multifaceted and complex role in the response to ischemia, with potential to both enhance and

impair neuronal survival and regeneration [17]. Many recent studies focus on the astrocyte-

neuron interaction and several investigate ways in which astrocyte function can be improved

after stroke to enhance neuronal survival.

This review provides a brief overview of the pathophysiological events underlying ischemic

brain damage, and considers how these events affect astrocyte-mediated support of neurons. In

addition, we discuss some experimental approaches to enhance the neuronal supportive role of

astrocytes as a novel strategy against stroke. Finally, we explore how these approaches may

eventually be applied in the clinical setting to improve stroke outcome for patients.


2.1. In Vitro Studies

In vitro studies have provided substantial insight into the mechanisms governing the survival of

astrocytes following simulated ischemia. These investigations have shown that astrocytes are

generally more resistant than neurons to oxygen-glucose deprivation (OGD) performed in media

at physiologically normal pH, an in vitro model of ischemia [10, 18]. Most neurons in astrocyte-

neuronal co-cultures will die after 60–90 min of OGD, while astrocyte cultures only suffer a

similar extent of injury after 4–6 hours [9, 18, 19]. Different astrocyte populations exist and

astrocytes isolated from different brain regions such as cortex, striatum, and hippocampus differ

in their sensitivity to OGD [15, 20, 21]. Furthermore, Lukaszevicz and colleagues [22] reported

that protoplasmic astrocytes lose their integrity faster than fibrous astrocytes, which may explain

the regional differences in susceptibility to ischemia between white matter astrocytes which are

fibrous and grey matter astrocytes that are protoplasmic. Although less susceptible to OGD-

induced damaged in vitro studies have highlighted certain elements that are highly toxic to

astrocytes. For example, acidosis has been found to be very effective in killing astrocytes

[23–26], in contrast to neurons, which are protected in acidic conditions [24, 26].

2.2. Focal Cerebral Ischemia

Much of the information about the recovery of astrocytes in vivo has been provided by studies

using immunohistological markers for astrocyte specific proteins, such as glial fibrillary acidic

protein (GFAP) and glutamine synthetase GS; Fig. 1. Using these markers as tools, several

investigations suggest that astrocytes are better preserved than neurons in animal models of

stroke outside the core where all cells die [27–29]. Though neuronal markers are decreased as

soon as 1 hour after MCAO, GFAP expression is preserved over the first 3 hours of reperfusion

after 2 hour MCAO [29] and GS is increased 3 hours following a 3 hour MCAO [28]. At later

reperfusion periods, GFAP increases in the peri-infarct area that later develops into the glial scar

[29–32]. In contrast, Liu and colleagues [33] reported the deterioration of some astrocyte

markers prior to that of neuronal markers. Discrepancy in findings may be due to differences in

detection (i.e., protein vs. mRNA) and injury paradigms.

Fig. (1)

Expression of different astrocytic proteins following stroke. Increased expression of GFAP is a

hallmark of astrocytes activation, as is induction/re-expression of vimentin. Astrocytes normally

express glutamine synthetase (GS) and S100β, genes …

2.3. Forebrain Ischemia

Excitotoxic neuronal injury is a common mechanism in both acute and chronic

neurodegenerative diseases. It has long been appreciated that inhibition of astrocyte glutamate

uptake [34, 35], and more recently inhibition of astrocyte mitochondrial function [36], impairs

neuronal survival from excitotoxic injury. Brief forebrain ischemia is a model of the delayed

hippocampal neuronal loss seen in patients following cardiac arrest and resuscitation, and in part

involves excitotoxicity. Increased generation of reactive oxygen species (ROS) and

mitochondrial dysfunction in CA1 astrocytes contributes to ischemia-induced loss of GLT-1 and

ultimately to delayed death of CA1 neurons [15]. Our studies and those of other laboratories

have demonstrated that selective dysfunction of hippocampal CA1 subregion astrocytes, with

loss of glutamate transport activity and immunoreactivity for glutamate transporter 1 (GLT-1),

occurs at early reperfusion times, hours to days before the death of CA1 neurons [15, 37, 38].

The heterogeneous degeneration of astrocytic processes and mitochondria was tightly associated

with the appearance of disseminated selective neuronal necrosis and its maturation after

temporary ischemia [39]. By electronmicroscopy the same investigators [40] found that focal

infarction is exacerbated by temporary microvascular obstruction due to compression by swollen

astrocytic end-feet. However, hypoxia has multiple effects on astrocytes and their ability to

support neuronal viability [41]. For example, hypoxia induces astrocyte-dependent protection of

neurons following hypoxic preconditioning. Yet, hypoxia induces processes in astrocytes that

augment neuronal death in other situations, such as the coincidence of hypoxia with

inflammatory signaling.


The astrocyte response to ischemia has traditionally been viewed as detrimental to recovery, as

the astrocyte-rich glial scar has both physical and chemical inhibitory properties [42, 43]. As

components of the glial scar, astrocytes exhibit hypertrophied, interdigitated processes that form

a physical barrier. Astrocytes produce inhibitory molecules including chondroitin sulfate

proteoglycans (CSPGs) that contribute to chemical inhibition [44, 45]. In the acute setting,

astrocytic gap junctions may remain open following ischemia [46], allowing substances such as

proapoptotic factors to spread through the syncytium, thereby expanding the size of the infarct

[47]. As discussed below, astrocytes can also produce a variety of pro-inflammatory cytokines.

Many studies have shown that decreased astrogliosis often correlates with decreased infarct size.

Nonspecific inhibition of cell proliferation following ischemia using a cyclin kinase inhibitor

decreases astrocyte proliferation and results in improved functional recovery [48]. In addition,

treatment with alpha-melanocyte stimulating hormone [49], cysteinyl leukotriene receptor

antagonist [50], cliostazol [51], and caffeic acid [52] result in reduced infarct size accompanied

by a decrease in astrogliosis. Treadmill exercise [28] and acupuncture [53] are similarly

associated with improved outcome and reduced astrogliosis. Thus, results from several studies

suggest that treatments that decrease infarct size are often accompanied by attenuated astrocyte

response. Despite the frequent association of decreased astrogliosis with improved outcome, it is

difficult to determine cause and effect, since the extent of astrogliosis likely reflects the severity

of the injury, as well as influencing it.

In addition to their role in glial scar formation, astrocytes also respond to ischemia with functions

important for neuroprotection and repair. These include protecting spared tissue from further

damage [14], taking up excess glutamate as discussed above, rebuilding the blood brain barrier

[54, 55], and producing neurotrophic factors [10]. GFAP knockout mice exhibit larger lesions

than their wild-type littermates following focal ischemia [56], and mice lacking both GFAP and

vimentin have impaired astrocyte activation, decreased glutamate uptake abilities, and attenuated

PAI-1 expression after ischemia [57]. Application of astrocyte-conditioned media after transient

MCAO results in decreased infarct volume and regained blood-brain barrier function [58],

suggesting that factors released by astrocytes following ischemia are important for


Although few studies other than the use of animals lacking vimentin and GFAP have specifically

targeted astrocyte activation after ischemia, there is correlational evidence suggesting that

astrogliosis may be beneficial. Environmental enrichment, which results in reduced infarct size

and improved recovery following ischemia, also leads to increased astrocyte proliferation

[59, 60]. After focal ischemia, aged rats exhibit increased tissue damage and increased astrocyte

hypertrophy, but have decreased astrocyte proliferation compared to young rats [61]. Systemic

infusion of bone marrow stromal cells following MCAO increases gliogenesis and decreases

lesion size [62, 63]. In addition, administration of transforming growth factor α (TGFα), a known

mitogen for astrocytes [64], following MCAO leads to reduced infarct size and improved

functional recovery [65]. Furthermore, ischemic preconditioning that produces a neuroprotective

state leads to prolonged astrocyte expression of Hsp27 [66]. Finally, mice lacking connexin 43,

the gap junction connecting astrocyte networks that is needed for proper neurotransmitter and

potassium regulation, have increased infarcts following MCAO [67]. Thus, astrocytes have the

potential to be both detrimental and beneficial following ischemic insult, making them promising

targets for manipulation to improve outcome.



Inflammation plays both detrimental and beneficial roles in brain ischemia, depending upon the

timing and severity of the inflammation. Within minutes after injury, injured neurons in the core

and penumbra of the lesion and glial cells in the core produce pro-inflammatory mediators,

cytokines, and reactive oxygen species, which activate both astrocytes and microglia [68].

Activated astrocytes can produce the proinflammatory cytokines IL-6, TNFα, IL-1α and β,

interferon γ, and others [68–70]. High levels of these cytokines can be detrimental to ischemic

recovery [71–75] by directly inducing apoptosis of neuronal cells and/or increasing toxic nitric

oxide levels [76] and inhibiting neurogenesis [77]. Indeed, inactivation of astrocyte NfκB

signaling, shown to induce astrocyte production of pro-inflammatory cytokines [78], decreases

cytokine production and protects neurons after ischemic injury [79]. Hsp72 overexpression is

associated with lower NfκB activation and lower TNFα [80]. In addition to cytokines, reactive

astrocytes also produce chemokines following ischemia [81]. Chemokines upregulate adhesion

molecules in vascular endothelial cells, resulting in attraction of immune cells, which may

worsen ischemia-induced damage [82]. Overall, some aspects of the local inflammatory response

contribute to secondary injury to potentially viable tissue and lead to apoptotic and necrotic

neuronal cell death hours to days after injury [83], while other aspects are beneficial.

Although the potential benefits of inflammation after stroke have received relatively little

attention so far, indirect evidence suggests that some specific inflammatory reactions are

neuroprotective and neuroregenerative [84–91]. In addition to providing defense against the

invasion of pathogens, inflammation is also involved in clearing damaged tissue, and in

angiogenesis, tissue remodeling, and regeneration [89]. This is probably best studied in wound

healing, which is severely compromised if inflammation is inhibited [89, 91]. There is also

evidence suggesting that specific inflammatory factors can be protective in some circumstances.

IL-6, produced by astrocytes acutely after MCAO [69], is likely neuroprotective early after

ischemia [84]. Interestingly, ischemic preconditioning resulting in protection appears to be

dependent on TLR-4 signaling, and is accompanied by increased TNFα, NFκB, and COX-2

expression [90]. Indeed, in vitro work has shown that administration of TNFα in combination

with Hsp70 results in decreased expression of pro-apoptotic proteins following hypoxia [88].

Thus, it is important to consider these factors, along with timing, when trying to determine the

best strategy to reduce damage and improve recovery and regeneration.


5.1. Antioxidant Production

One hallmark of the cellular response to ischemia is a rapid, dramatic increase in damaging free

radicals, including nitric oxide (NO), superoxide, and peroxynitrite [92]. Nitric oxide synthetase

levels increase as soon as 10 minutes after induction of MCAO [93], followed by NO production

that persists for at least one week after MCAO [94]. Nitric oxide can cause cell death by

inducing the release of cytochrome-c from mitochondria, leading to apoptosis [95]. Nitric oxide

can also induce necrotic death [96]. Furthermore, the production of nitric oxide and other free

radicals can modify oxidative metabolism and impair ATP production [13, 19]. Changes in

mitochondrial properties can further limit oxidative metabolism [97]. Not surprisingly, several

studies have shown that antioxidant treatment enhances neuroprotection and recovery after

stroke [98–101].

The release of glutathione and SOD by astrocytes has been reported and is suggested to play an

important role in maintaining and enhancing neuronal survival, yet they are able to reduce

ascorbate for further neuronal antioxidant defense Fig. (2) [10, 102–106]. Interestingly, neurons

cocultured with astrocytes exhibit higher levels of glutathione compared with neurons cultured

alone [107]. Although astrocytes upregulate SOD after cerebral ischemia [108], they do not

appear to increase levels of glutathione in ischemic conditions [109]. It is unknown whether

ischemia alters astrocytic ascorbate levels, but osmotic swelling from ischemia results in

increased astrocyte release of ascorbate in vitro [110], suggesting that similar mechanisms may

occur in vivo.

Fig. (2)

Mechanisms of astrocyte support of neurons important in stroke. Antioxidant defense includes

release of glutathione and ascorbate. Regulation of extracellular levels of ions and neuro-

transmitters, especially K+ and glutamate, strongly influences neuronal …

Several treatments that attenuate ischemic injury result in increased glutathione levels [111, 112].

SOD converts superoxide into oxygen and hydrogen peroxide. Similar to glutathione, many

treatments that ameliorate stroke damage are accompanied by an increase in SOD [113, 114].

Furthermore, rodents overexpressing SOD1 have significantly smaller injuries after both focal

and global ischemia [115, 116], while mice with decreased SOD1 have larger infarcts [117].

Finally, ascorbate can also reduce oxidative stress [118]. Treatment with dehydroascorbic acid, a

blood-brain-barrier-permeable precursor to ascorbic acid, is protective after MCAO [119].

Dehydroascorbic acid is taken up by astrocytes and released as ascorbic acid [12], a process

increased by propofol [120], a treatment that can be protective after stroke [121]. In summary,

astrocytes are important producers of antioxidants in the normal CNS, and astrocyte production

of these molecules after stroke may enhance neuronal survival and protect astrocyte function.

5.2. Glutamate Regulation

Astrocytes are key players in the regulation of neuro-transmitters in the CNS. Astrocytes make

glutamine, the precursor for the neurotransmitters glutamate and GABA [122] Fig. (2). Astrocyte

production of neurotransmitter precursors is impaired after MCAO, and alterations in neuro-

transmitter levels occur throughout the brain following stroke, possibly contributing to neuronal

death [123, 124].

Astrocytes are primarily responsible for glutamate uptake in the normal brain using the astrocyte

specific glutamate transporters GLAST and GLT-1 (Fig. 2) [125–127], as excess glutamate leads

to cell death via excitotoxicity [128]. Glutamate transporter levels in astrocytes decrease acutely

following global ischemia [38, 129] and neonatal hypoxia-ischemia [130], most likely

exacerbating neuronal death as a result of glutamate-induced excitoxicity. Despite the therapeutic

potential of increasing astrocyte glutamate transport after stroke, few groups have explored this

possibility. Carnosine, shown to be protective after focal ischemia, may partially be effective

because it prevents loss of GLT-1 on astrocytes, resulting in attenuated excitotoxicity [131]. In a

more direct assessment of how post-ischemic astrocyte glutamate transporters contribute to

neuronal survival, our laboratory has shown that upregulation of GLT-1 on astrocytes using

ceftriaxone protects CA1 neurons after global ischemia [129], similar to its effects in focal

cerebral ischemia [132].

5.3. Potassium Uptake and Energy Metabolism

Astrocytes also regulate neuronal activation by extracellular potassium uptake [133] Fig. (2).

Neurons release potassium after activation, and increased extracellular potassium leads to

neuronal hyperexcitability [133], a phenomenon that occurs in ischemic conditions [134]. In

addition to regulating neuronal activation, proper maintenance of ion gradients, such as

potassium, is important in regulating cell volume in both normal and ischemic conditions

[135, 136]. Astrocytes increase potassium transporter activity in response to transient in

vitro ischemia [137]. Due to its effects on both neuronal activity and cell volume, increasing

astrocytic potassium uptake may be a possible therapeutic target for stroke.

Astrocytes are also integral to normal maintenance of neuronal metabolism. When astrocytes

take up extracellular glutamate as a result of neuronal activity, the Na+/ K+-ATPase, along with

AMPA signaling, triggers astrocyte uptake of glucose from the blood, as astrocytic endfeet

contact capillaries [138, 139]. This glucose is then made into lactate, a substrate for neuronal

energy, to further “fuel” active neurons [140] Fig. (2). As mentioned above, astrocytes produce

glutathione. In addition to its antioxidant properties, glutathione is needed for the conversion of

methylglyoxal, a toxic by-product of metabolism, into D-Lactate by glyoxalase 1 [141].

Although the role of astrocyte metabolism is relatively well-established in normal tissue, the

post-ischemic role of astrocyte metabolism maintenance is less clear [142]. After ischemia,

astrocytes upregulate glucose transporters in order to provide energy to stressed/dying neuronal

cells [143,144]. Ethyl pyruvate, a derivative of the energy substrate pyruvate, is neuroprotective

after stroke only when astrocytes are viable, suggesting that astrocytes are necessary for

improvement in post-ischemic energy metabolism [122].



Although few studies have specifically targeted astrocytes for repair after stroke, there is some

evidence that this can be a successful strategy. Recent results indicate that induction of BDNF in

astrocytes by galectin-1 reduces neuronal apoptosis in ischemic boundary zone and improves

functional recovery [145]. In addition, protection by pyruvate against glutamate neurotoxicity is

mediated by astrocytes through a glutathione-dependent mechanism [146]. Our recent study

demonstrated that enhancing astrocyte resistance to ischemic stress by overexpressing protective

proteins or antioxidant enzyme results in improved survival of CA1 neurons following forebrain

ischemia Fig. (3) [16]. Two well-studied protective proteins, heat shock protein 72 (Hsp72) and

mitochondrial SOD, were genetically targeted for expression in astrocytes using the astrocyte-

specific human GFAP promoter. In both cases protection was accompanied by preservation of

the astrocytic glutamate transporter GLT-1, and reduced evidence of oxidative stress in the CA1

region [16]. Similarly, selective overexpression of excitatory amino acid transporter 2 (EAAT2)

in astrocytes enhances neuroprotection from moderate hypoxia-ischemia [147].

Fig. (3)

Targeted over-expression of Hsp72 in astrocytes reduces the vulnerability of CA1 neurons to

forebrain ischemia. Selective overexpression of Hsp72 in astrocytes by expressing it from the

astrocyte specific GFAP promoter was achieved by unilateral stereotaxic …


Many factors have been identified that likely contribute to the failure in translation seen so far

with stroke therapies. Currently, the only approved stroke therapy is thrombolysis induced by

intravenous administration of recombinant tissue plasminogen activator [148]; however, because

of a short therapeutic time window, only a small fraction of patients benefit from this treatment.

Hypothermia is the only accepted acute treatment to reduce brain injury following cardiac arrest

and resuscitation [4]. Thus far many clinical trials have focused on treatments that would likely

be beneficial to neurons, with fewer studies focused on mechanisms that might benefit all cell

types or specifically targeting other cell types, such as astrocytes. Often the consequence of these

treatments on the astrocyte response is not considered. Several examples of past and ongoing

clinical trials are discussed below, with specific attention to how these treatments may alter

astrocyte response or viability.

Several clinical trials have targeted manipulation of the inflammatory response to ischemia, as

stroke patients with systemic inflammation exhibit poorer outcomes [149]. Although anti-

inflammatory therapy decreases infarct size and improves neurological sequelae in experimental

animal models of stroke [150], human trials with anti-neutrophil therapy have not shown a clear

benefit [151, 152]. In addition, recent clinical trials in which anti-CD11/18 antibodies were

administered to human subjects were unsuccessful [153]. Likewise, a double-blinded, placebo-

controlled clinical trial in which anti–ICAM-1 antibody was administered within 6 hours of

stroke symptoms showed disappointing results [151]. In understanding these results it is

important to recall that while experimental stroke is relatively homogeneous concerning size,

territory, and etiology, with more consistent inflammatory response, human stroke is extremely

heterogeneous [154], with different vascular territories and extents of injury. In addition, these

mediators are known to affect many organ systems beyond the central nervous system. Systemic

administration of anti-inflammatory agents may have exacerbated the relative state of

immunocompromise seen in stroke patients, thereby confounding the outcome. Furthermore,

inflammation and astrocyte response are likely closely connected. Although there is little

evidence for a direct relationship between neutrophils and astrocytes, it has been shown that

mice with a blunted inflammatory response exhibit increased loss of GFAP-positive astrocytes

after cortical stab injury [155]. Because astrocytic glial scar formation is important in protection

of spared tissue from further damage [156], it is possible that treatments that drastically attenuate

inflammation lead to a stunted astrocyte response that is deleterious to recovery.

Another drug that has advanced to clinical study is DP-b99, currently in phase III studies for

acute stroke. DP-b99 is a membrane active chelator derivative of the known calcium chelator,

BAPTA spell out [157]. A lipophilic chelator of calcium, zinc and copper ions, DP-b99

sequesters metal ions only within and in to cell membranes. This clinical trial is especially

attractive because sequestration of calcium, zinc, and copper are potentially beneficial not only

to neurons, but also to astrocytes. It has been shown in Alzheimer’s disease that beta amyloid

increases astrocyte calcium influx, which causes decreased glutathione levels [158]. Zinc

chloride is toxic to astrocytes as well as neurons in vitro [159]. Similarly, astrocytes exposed to

neocuprine exhibit increased copper influx and undergo apoptotic cell death [160]. Approaches

that benefit multiple cell types, including astrocytes, are more likely to be successful.

Other current ongoing clinical trials focus on neuroprotective agents for the purpose of aiding

neurological recovery after stroke. Minocycline (Phase I), edavarone (Phase IV), propanolol (a

β-blocker; phase II and III), and more recently arundic acid have been previously shown to be

protective and enhance neuronal survival in stroke [161–165], though by targeting different

mechanisms. Some additional completed and ongoing trials are summarized in Table 1.

Preclinical research needs to consider these clinical results, and assess effects on astrocytes as

well as neurons.

Table 1

Overview of Some Completed and Ongoing Clinical Trials for Stroke

Although anti-inflammatory strategies to diminish ischemic brain injury have failed thus far,

continued elucidation of the complex interactions involved in modulating the inflammatory

response may still enable novel therapeutic approaches that translate successfully into clinical



Traditionally, stroke research has focused on neurons and often ignored effects on glial cells. It is

increasingly evident that glia are vital to both normal CNS functioning and also play important

roles in neuropathological conditions. Although astrocytes form an inhibitory glial scar following

ischemia, they also perform functions necessary for neuronal survival and well-being, such as

maintaining low extracellular glutamate levels and providing antioxidant protection. Because

they have a great many functions, astrocytes are attractive candidates as therapeutic targets. By

striving to shift astrocytes towards a pro-reparative, neuronal-supportive phenotype following

stroke, future clinical therapies may well be more successful in protecting neurons from ischemic

damage and promoting repair.


This work was supported by NIH grants CM49831, N5053898, and NS014543 to RGG.


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function. Neuroscientist.2009;15:579–588. [PMC free article] [PubMed]

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Anti-Aging Answer for Women’s Health

AAI is the Anti-Aging Answer for Women’s Health

Women’s hormonal web is complicated; finding the right anti-aging serum can also be challenging. The

hormones governing women’s physical and mental function throughout their lives work together to

maintain a balance. The key hormonal players in women, Estrogen, Progesterone, Testosterone/DH EA,

Human Growth Hormone, Thyroid, & Cortisol, begin to play out of tune as their levels decrease with age.

So when hormones decline or become imbalanced, as in Peri Menopause & Menopause, we start to

notice changes in our bones, muscle strength, the elasticity of our skin, and in our energy, mood,

memory, & libido. The majority of women think that Peri Menopause and Menopause cause inconvenient

symptoms: mood swings, fatigue, hot flashes, & low libido among others. What they don’t know is that

these hormonal imbalances raise our risk for serious diseases such as heart disease, Alzheimer’s,

osteoporosis, obesity, depression, stroke, and cancers; especially breast cancer . Therefore, it is crucial

that we prevent and treat the cause of these symptoms as soon as they start to appear in our late 30’s.

Not only our well being and quality of life depends on it, but our health and risk of disease is optimized by

becoming hormonally balanced.

The “Women’s Health Initiative” (WHI 2002) was a major multi-national study that included thousands of

women on synthetic estrogens (Premarin, Birth Control Pills, Nuvaring) and/or on synthetic progesterones

(Provera, Progestins, Birth Control Pellets/Injections). This study had to be stopped abruptly:

unprecedented for any medical study around the world. The reason was that women in the study were

getting a much higher incidence of heart disease, stroke, blood clots, and breast cancer than women in

the general population. At this point, 08/GYN’s around the country took women off their synthetic

hormonal therapy (synthetic estrogens and progesterones) to prevent these problems, even though they

knew women would have to live with bothersome symptoms and their risk for serious illness would be

greatly increased. Bio-Identical or Non-Synthetic hormonal therapy is the only option for women to treat

Peri & Menopausal symptoms, decrease significantly the risk of age-related diseases, and increase well-

being & quality of life. Most doctors are not familiar with the Bio-Identical hormonal therapy, but experts in

Anti-aging Medicine specialize in this field.

Bio-Identical hormones are the answer!

Women’s reproductive life is composed of 3 stages:

1. Pre Menopause – the PMS Years

2. Peri Menopause- the Rollercoaster Years

3. Menopause/Post Menopause-the End of Periods

Pre Menopause-The PMs Years

During their 20’s and 30’s, women experience fairly regular cycles with balanced estrogen and

progesterone production. But increasingly, younger females who are prone to excess stress, crash diets,

and contraceptive use are not ovulating regularly. Anovulatory cycles can lead to symptoms of

hormonal imbalance, severe PMS, and more serious health issues, such as polycystic ovaries,

endometriosis, and infertility.

Peri Menopause – The Rollercoaster Years

Most women don’t know that there is a period of time called Peri Menopause {of 10-15 years) when the

body gets ready to start Menopause, therefore, they do not associate mood and emotional symptoms with

their hormones or menopause. But they should! Beginning in the late 30’s until menopause (average age

of 51), women begin to experience a whole new world of symptoms, as estrogen and progesterone levels

fluctuate dozens of times a day from wavering ovarian function. These symptoms range from classical

menopause symptoms like hot flashes, night sweats, and mood swings to not so typical ones like high

anxiety, foggy thinking, bone loss, weight gain, depression, fatigue, and low libido. These fluctuations in

hormone levels take women on a rollercoaster ride! At this point, the search for symptom relief begins

with Bio-Identical hormones.

Menopause/Post Menopause- The Ends of Periods

The official start of Menopause is 12 months in a row without a period, occurring around age 51. But it is

not uncommon to see symptoms much sooner. Acute/prolonged stress, for example, can negatively

impact ovarian function and can precipitate premature Menopause in vulnerable women as early as their

mid to late 30’s. Menopause can also be surgically induced through hysterectomy, radiation, or

chemotherapy. We think that hormones control only our sexual and reproductive systems, but hormones

actually regulate the entire body. With fewer hormones to go around, their important role in protecting the

health of the brain, bones, muscles, skin, breasts, and heart are diminished.

Supplementation with Bio-Identical hormones is a matter of life or death at this stage.

Common hormone imbalances in Peri Menopause & Menopause:

The right balance of anti-aging serum and hormones is vital to a woman’s health & well being. During Peri

Menopause & Menopause, hormone levels drop and hormone deficiencies take place. Logically, one

would think that hormonal deficiencies should be resolved with hormonal supplementation. Unfortunately,

there are so many hormones at work in a woman’s body that deficiencies in one hormone may trigger

excesses of ether hormones and this is how imbalances take place. (Remember, low levels of hormone

are as harmful to your health as high levels). The following are the most common hormone imbalances in

women and their symptoms:

1. “Estrogen Dominance”–mood swings, migraines, fat gain, low thyroid, breast cancer risk

2. “Low Estrogen & Progesterone”-hot flashes, night sweats, palpitations, foggy thinking

3. “High Testosterone & DHEA”-acne, hair loss, irritability, belly fat, polycystic ovaries

4. “Low Testosterone & DHEA”-decreases bone/muscle mass, energy, libido (sexual desire)

5. “High or Low Cortisol” (Stressed Adrenals): insomnia, anxiety, chronic fatigue, allergies, food

cravings, low immunity

Do you have symptoms of hormonal imbalance?

Mood Swings

Cold Body Temperature

Scalp Hair Loss

Memory Lapses


Sleep Disturbances

Can’t Lose Weight

Thinning Skin

Bone Loss

Uterine Fibroids

Hot Flashes

Sugar or Salty Cravings

Aches & Pains

Decreased Libido

Tender Breasts

Weight Gain (waist &/or hips)

Heart Palpitations

Fibrocystic Breasts



Polycystic Ovaries

Night Sweats

Increased Body /Facial Hair

Vaginal Dryness

Heavy Menses/Bleeding Changes

Foggy Thinking

Water Retention


Foggy Thinking

Troublesome or persistent symptoms during Peri Menopause & Menopause are a sign

of related imbalances that may be complicating the situation and raising disease risks of

osteoporosis, heart disease, breast cancer, obesity, and Alzheimer’s.   Symptoms from

one woman to another are as highly individual as a thumbprint! If you answered yes to 3

or more symptoms in this questionnaire, you may be hormonally imbalanced:

How can I balance my hormones naturally?

Hormone balance and the knowledge that hormones work together with a healthy mind

and body are the keys to optimal health and Peri & Menopausal relief.

1. First, determine your symptoms

2. Then, test ALL of your hormones to detect specific imbalances

3. Find a board certified doctor in Anti-Aging Medicine (specializing in Bio-Identical

hormonal therapy)

4. NEVER use Estrogen alone (even after Hysterectomy)!

5. ALWAYS use Bio-Identical hormones (the exact chemical structure as the hormones

produced by the body and derived from a natural source)

6. STOP all synthetic hormones-Premarin, Provera, Progestins, and birth control pills,

pellets, injections, & intrauterine devices (They ALL contain synthetic hormones)

7. Supplement with Nutriceuticals (pharmaceutical-grade nutritional supplements that

are prescription strength, free of harmful contaminants, and actually absorbed by the

body)-only way to have the available building blocks to regenerate the body’s tissues

and to work properly

8. Detoxify is key for Bio-Identical hormone treatment to work at its best

9. Limit “Xenoestrogens” (substances that mimic estrogen in the body & precipitate

hormonal imbalances)–for example, pesticides, nail polish, fumes,

10. Use “hormone-free” foods and products

11. Maintain ideal weight (fat cells send signals in the body that cause hormonal It is

medically proven that overweight/obesity is a major risk factor for the major killers in

the US: heart disease, stroke, and cancer. Also, breast cancer patients have a

significant increase in fat mass compared to women without cancer)

12. Boost hormones naturally with exercise-not a substitute for hormonal supplementation

with Bio-Identical hormones; exercise makes hormonal therapy more work at its best,

while becoming more stable

13. Minimize stress and use stress-handling techniques like yoga, meditation, prayer,

14. Stop smoking ASAP

15. Eat more fiber

16. Get deep, restful, uninterrupted 7-8 hours of sleep-this is the only way that body

tissues regenerate after being used during the day

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Whey Protein Facts and Application, Dr. Lawrence Sosna

by: Dr. Lawrence Sosna

The word Protein means “first substance”. Our first protein food was found in our mother’s milk. Milk

is the only food designed specifically to optimally sustain the life of a mammal. In fact, the root word

for nutrition means to suckle.  As a species, we would not have survived if not for the nutrition and

protection mother’s milk offers.

Whey is one of the two protein groups found in milk. It is a liquid complex consisting of a wide range

of proteins. The other protein group is casein, which curds are made from and then processed into


Whey is an original complete protein food and is considered number one for building and

regenerating our bodies and maintaining a strong immune system.  Our entire metabolic process

relies on the intake of complete protein.  We cycle proteins into amino acids constantly.

Even Hippocrates, the Greek physician of the 5th century B.C., the “father of medicine”, knew the

benefits of whey protein. He stated that the body has an inner adaptive or healing power, and that to

strengthen this healing power, he prescribed serum (liquid whey) to his patients. It was true non-

denatured, native whey. It provided full biological activity and numerous health benefits. All

commercial whey proteins available now are derived from extensively processed milk and

incomparable to the vitality in that 2500 year-old prescription.

It is appropriate to review some important definitions of terms used:

Native Protein: The naturally occurring conformation of a protein. Unaltered by heat, chemicals,

enzyme action or processing. (Native is the same structure and proportion as in the original


Denatured: To cause the tertiary structure of (a protein) to unfold, as with heat, alkali, or acid, so

that some of its original properties, especially its biological activity, are diminished or eliminated. (It

means damaged.)

Undenatured: To undamage. (A term that is used without discretion in the industry and is

misleading. It is not possible for a protein to be undenatured.)

Non-denatured: The same structure and proportion as in the original substance with full biological

activity. (Never damaged.)

Presently, the various commercial methods of processing whey do not improve or even maintain the

fragile immune modulating and regenerative components or the biological activity that was originally

in the milk. Most are overly processed and damaged during the manufacturing process.

There are three commercial production methods, which comprise the majority of available whey

proteins. They are isolates (the most popular), ion-exchange and hydrolyzed forms. They are all

ultra-filtered, cross-flow filtered or micro-filtered via elaborate patented methods developed by large

dairies. The milk used in these three methods undergoes major processing that involves high heat

(often multiple times) and drastic acidification of the whey to produce curds for manufacturing

cheese. These steps denature (damage) the proteins. What is then required is extensive filtration to

remove the many denatured proteins in order to produce the highest percentage of protein.

Unfortunately the fragile vital protein components (immunoglobulins, lactoferring, serum albumin,

etc), which determine the biological activity of the protein, are not retained. The terms undenatured

and cold-processed are prevalent with these commercial products, but once a protein is denatured it

is not possible to undenature it.

The key point in regard to the quality and effectiveness of whey is that the full range of biological

activity and proportion of the protein components be preserved in their original native form as nature

provided. Only whey that is minimally processed and maintained can achieve that goal. Additionally,

the health of the milking cows and quality of the milk is the foundation of this type of product.

Non-denatured whey protein has the highest biological value of any protein. It is a complete

protein, unlike soy, and provides all the essential amino acids in the correct balance. The five major

active proteins of whey are lactoferrin, immunoglobulins, bovine serum albumin, alpha-lactalbumin

and beta-lactoglobulin. There are many whey products available; therefore it is highly advisable to

have in writing from the manufacturer, the treatment of the cows and the processing the milk


Covalent Bonded Cysteine (the non-denatured form), is the critical amino acid required for the all-

important intracellular production of the antioxidant glutathione (GSH). Glutathione is our body’s

master antioxidant and is responsible for numerous defense and repair functions and is an effective

anti-aging substance. Glutathione is best utilized when we produce it internally. Cysteine is very

scarce in our modern diet and therefore glutathione production is limited and deficiency is prevalent.

If cysteine undergoes extreme heating or processing, as most commercial whey products do, it is

denatured and converted to cystine. Covalent-bonded cysteine, active peptides, anabolic growth

factors and enzymes are also present in non-denatured whey protein.

The public is now becoming more aware of the value of quality protein and is choosing whey protein

for many good reasons. Whey protein benefits are numerous, and can yield a wide range of

immune-enhancing properties. It also has the ability to act as an antioxidant, antihypertensive, anti-

tumor, antiviral and antibacterial. A number of clinical trials have successfully been performed using

whey as an antimicrobial agent and in the treatment of cancer, HIV, hepatitis B & C, cardiovascular

disease and osteoporosis. It has a major role in red blood cell production, support in chemotherapy

treatment, safe binding and detoxification of heavy metals, wound healing, growth of new muscle,

weight regulation and the support of numerous immune functions. It is used by populations that have

Chronic Fatigue Syndrome (CFS), Fibromyalgia, Hepatitis, Cancer, HIV/AIDS, Respiratory disease,

cognitive disorder from nutritional compromise and for any sports performance improvement.

Dr. Lawrence Sosna

Dr. Lawrence Sosna Graduated first in his class from the Fairfield College of Myopractics and

Naturopathic Medicine. He is a N.D. and has a PhD in Myology with an emphasis in Orthomolecular

Biochemistry. He strictly practices Integrative Medicine – his research field being cellular

regeneration, Anti-Aging and bio-identical comprehensive hormone replacement therapy. Dr. Sosna

lectures on these topics at symposiums all over the world.

Copyright © January 2005

Whey Protein Facts and Applications


Bonang G, Monintja HE, Sujudi, van der Waaij D. Influence of breastmilk on the development of

resistance to intestinal colonization in infants born at the Atma Jaya Hospital, Jakarta. Scand J Infect

Dis 2000;32:189-196.

Bounous G. Whey Protein concentrate and glutathione modulation in cancer treatment, Anticancer

Res. 2000;20:4785-92

Bounous G, Kongshavn PA. Influence of dietary proteins on the immune system of mice. J

Nutr 1982;112:1747-1755.

Bounous G, Gervais F, Amer V, et al. The influence of dietary whey protein on tissue glutathione and

the diseases of aging. Clin Invest Med 1989;12:343-349.

Bowen J, Noakes M, Clifton P. Whey Protein and body fat loss. Asia Pac J Clinical Nut. 2003; 12:S9

Crinnion WJ. Environmental medicine, part 2 – health effects of and protection from ubiquitous

airborne solvent exposure. Altern Med Rev 2000;5:133-143.

Guimont C, Marchall E, Girardet JM, Linden G. Biologically active factors in bovine milk and dairy

byproducts: influence on cell culture. Crit Rev Food Sci Nutr 1997;37:393-410.

Ha E, Zemel MB. Functional properties of whey, whey components, and essential amino acids:

mechanisms underlying health benefits for active people (review). J Nutr Biochem 2003;14:251-258.

Hakkak R, Korourian S, Ronis MJ, et al. Dietary whey protein protects against azoxymethane-

induced colon tumors in male rats. Cancer Epidemiol Biomarkers Prev 2001;10:555-558.

Jones EM, Smart A, Bloomberg G, et al. Lactoferricin, a new antimicrobial peptide. J Appl

Bacteriol 1994;77:208-214.

Kawase M, Hashimoto H, Hosoda M, et al. Effect of administration of fermented milk containing

whey protein concentrate to rats and healthy men on serum lipids and blood pressure. J Dairy

Sci 2000;83:255-263.

Kennedy RS, Konok GP, Bounous G, et al. The use of a whey protein concentrate in the treatment

of patients with metastatic carcinoma: a phase I-II clinical trial study. Anticancer Res 1995;15:2643-


Kimball SR, Jefferson LS. Control of protein synthesis by amino acid availability. Curr Opin Clin Nutr

Metab Care2002;5:63-67.

Lands LC, Grey VL, Smountas AA. Effect of supplementation with a cysteine donor on muscular

performance. J Appl Physiol 1999;87:1381-1385.

Laursen I, Briand P, Lykkesfeldt AE. Serum albumin as a modulator on growth of the human breast

cancer cell line MCF-7. Anticancer Res 1990;10:343-351.

Levay PF, Viljoen M. Lactoferrin: a general review. Haematologica 1995;80:252-267.

Markus CR, Olivier B, de Haan EH. Whey protein rich in alpha-lactalbumin increases the ratio of

plasma tryptophan to the sum of the other large neutral amino acids and improves cognitive

performance in stress-vulnerable subjects. Am J Clin Nutr 2002;75:1051-1056.

Marshall David Jr., O.D., Ph.D. WHEY PROTEIN REPORT – Review of Various Whey Protein.

Current Concepts on Whey Protein Usage.

Micke P, Beeh KM, Buhl R. Effects of longterm supplementation with whey proteins on plasma

glutathione levels of HIV-infected patients. Eur J Nutr 2002;41:12-18.

Sawatzki G, Rich IN. Lactoferrin stimulates colony stimulating factor production in vitro and in

vivo. Blood Cells1989;15:371-385.

Smithers GW, McIntosh GH, Regester GO, et al. Anti-cancer effects of dietary whey

proteins. Proceedings of the Second International Whey Conference 1998;9804:306-309.

Shah NP. Effects of milk-derived bioactives: an overview. Br J Nutr 2000;84:S3-S10. Sundberg J,

Ersson B, Lonnerdal B, Oskarsson A. Protein binding of mercury in milk and plasma from mice and

man – a comparison between methylmercury and inorganic mercury. Toxicology 1999;137:169-184.

Takada Y, Aoe S, Kumegawa M. Whey protein stimulated the proliferation and differentiation of

osteoblastic MC3T3-E1 cells. Biochem Biophys Res Commun 1996;223:445-449.

Tsuda H, Sekine K, Ushida Y, et al. Milk and dairy products in cancer prevention: focus on bovine

lactoferrin. Mutat Res2000;462:227-233.

Watanabe A, Okada K, Shimizu Y, et al. Nutritional therapy of chronic hepatitis by whey protein

(non-heated). J Med2000;31:283-302.

Walzem RL, Dillard CJ, German JB. Whey components: millennia of evolution create functionalities

for mammalian nutrition: what we know and what we may be overlooking. Crit Rev Food Sci

Nutr 2002;42:353-375.

Yamamura J, Aoe S, Toba Y, et al. Milk basic protein (MBP) increases radial bone mineral density in

healthy adult women. Biosci Biotechnol Biochem 2002;66:702-704.

Back to Top

Whey Protein Quality As Compared to Other Available


The quality of dietary proteins is a vital factor in determining what proteins are the most valuable in

terms of how the body assimilates and utilizes the protein as a resource.

To test these ratios in a protein source we begin with an amino acid analysis, a nitrogen analysis,

and then we proceed to the biologic testing. Measuring changes in the protein of the body is a well

accepted evaluative analysis used to determine protein quality, measured as Biologic Value (BV).

This involves the measurement of nitrogen intake from the protein and the output of nitrogen in the

feces and urine. BV is therefore a measurement of the nitrogen absorbed and utilized by the body.

  • Biologic Value (BV) of Dietary Proteins(1)
  • Protein Biologic Value
  • Whey protein 104
  • Egg 100
  • Cow’s Milk 91
  • Beef 80
  • Fish 79
  • Casein 77
  • Soy 74
  • Potato 71
  • Rice 59
  • Wheat 54
  • Beans 49

As this table shows, the animal proteins are high in BV, and are therefore complete proteins(2).

While vegetable proteins are much more incomplete and retain a lower BV rating, due as well to

their lower digestibility(1). With a mixture of these vegetable proteins the effect of a complete protein

can be produced when eaten in sufficient quantity, but this requires a great deal more total protein to

satisfy these requirements.

Whey Protein Concentrates

The benefits (as shown above) of using a whey protein concentrate (WPC) is great according to the

BV of this protein source. It fulfills the body’s amino acid intake beyond any other source of protein

listed above, as well as being a very versatile dietary food. Our Proserum® native whey protein®

concentrate contains all of the essential amino acids for the body as well as providing cysteine and

glutamine. These amino acids are precursors and are necessary for the production of glutathione, a

vital free radical neutralizer in the body.

WPC is defined as a whey protein concentrate containing approximately 80% protein. Proserum® is

a WPC.

1. Renner E. Milk Protein. In: Milk and Dairy Products in Human Nutrition. Munich:

Volkswirtschaftlicher Verlag, 1983

2. Mahan LK, Escott-Stump S. Proteins. In: Krauses Food Nutrition and Diet Therapy, 9th edition,

Philidelphia: WB Saunders; 1996

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Human Growth Hormone (HGH)

Human Growth Hormone (HGH)

Larry Sosna N.D. PhD HHP

It seems like everyone has heard about HGH Human Growth Hormone. But what is it? And is it

safe to take? HGH is 191 Amino Acids in an Exact Molecular Structure. It is NOT a Steroid! Given Correctly at the right dosage it is very Safe and Effective…

If I may be so bold as to talk to you just like we were friends and neighbors, I would be very


You see over 35 years ago, I was just about to die from a serious yet common virus

which normally just shows up on the lip as a sore. Well, that is just what happened AND for

some reason it jumped right on up through my nose, through my sinus and attacked my brain

and spinal cord. All I heard from the doctors was get ready young man, because it seems like

you’re time is up. But guess what? I sure got lucky and did not die like they all said I would. It

was really bad though. I spent 3 years in bed and another 2 years in a wheel chair until I got a

little bit better and one of my friends, also a doctor told me I should take HGH Human Growth

Hormone…and that I might get better. Well, that was the first good news anyone gave me in 5

whole years.

See, think about it like this. Growth Hormone is like a five star general. It’s very smart and just

like a five star general it can and does give orders and commands to everything in our whole

body. Amazing right! So let say you lived in the condo just down the hall on the same floor as

me and you would come and visit me so I would not get so lonely. Because that’s the kind of

friend you are, a real good and decent one.

You noticed each week I was getting a lot better suddenly, and when you came to visit you

wanted to know how in the world did I go from being flat on my back, to moving around and

even walking a bit. Naturally being a friend you had, and maybe still have lots of questions

about how in the world does Growth Hormone make a guy as bad off as me so much better

week after week.

Well, the research doctors explained it very simply by saying that HGH human growth hormone

or just plain GH growth hormone, being the 5 star general, gives orders to the cells in the body

to repair themselves. Growth Hormone can tell any cell at all…say a skin cell, or a nerve cell, or

a heart cell to repair and regenerate itself during deep restful sleep at night. In my situation I

needed lots of repair and regeneration to the nerve cells of my brain and spinal nerves.

It seemed as if I was the only person to survive this type of horrible viral damage to my brain

and spinal nerves they said maybe a few have lived but in a life long coma. So, please listen to

the next part of my journey… because it’s Super Amazing…They tell me that I am going to Italy

to be treated by a woman who won the Nobel Prize in 1985 exactly the time I needed her

because she discovered something very close to growth Hormone which I needed called Nerve

Growth Factor… which when we are in our mother’s womb…Grows all of the billions of Nerves

that become our BRAIN and spinal nerves. I was the first person on this planet to get shots of

nerve growth factor which Dr. Rita Levi Montalcini won the Nobel Prize for and guess what

happened next???

I made a discovery which made me a little famous within Nerve Scientists and Regenerative

Medicine Experts… few that existed back then. What you ask? I discovered that unless a person

with nerve damage or any other long term illness GETS very youthful blood levels of Growth

Hormone to activate the Nerve Growth Factor! Remember Growth Hormone is the Five Star

General, so I could feel the injections of Nerve Growth Factor not making me better… so I did

some basic arithmetic and decided I needed both Nerve growth Factor and Blood levels of

GROWTH HORMONE which would be normal for the average healthy 14 year old young adult.

In 12 months of doing the treatment this way, I went back to Italy 100% healed. No more wheel

chair. The new program had regenerated all of me and repaired all damaged nerves to my

brain and spine. I got better and in the process of needing to do maintenance each week and

each month throughout the years….I became an acknowledged expert in the field of Growth

Hormone Programs, Regeneration Therapies and all the Tissue Growth Factors of the body

starting with Nerve Growth Factor.

As you age, growth hormone declines dramatically. There are new studies that predict that for

every 18 years after age 18…Growth Hormone Declines by 50%. Thus, according to the University

of North Carolina at Chapel Hill….known for being the best at medical studies based on age and

by large groups of people by their age… called demographic medical research studies… We can

see that if you add 18 years to age 18 in just 3 times a person would go from age 18 to age 54

and we see in just 1 more cycle a person is then age 72  and if we go just 1 more cycle a

person becomes age 90… If we follow this very simple method, we see a virtually perfect

predictive model for all age related disease and illness. In this model, aging is an illness in and of

itself. WHY? Because there is simply not enough growth hormone available at or above age 50

to mobilize or put more simply, to turn on the specific nerve growth factor and all the other

tissue growth factors such as muscle growth factor, or skin growth factor, or liver and kidney

growth factor, BONE GROWTH FACTOR…which decline in tandem with growth hormone to be

able to do youthful levels of cell repair and regeneration and thus all the age related issues

including wrinkled skin seen on the face and age related illnesses debilitate folks in time. It is

horrible to see unnecessary Bone Lose and see little old men and women hunched way

over…unable to straighten back up.

So what can we do? We can give much more youthful blood levels of Growth Hormone by

injection, in fact by a very tiny needle so small most folks hardly if ever even feel it. I certainly

do not feel it and I have been giving myself Growth Hormone shots for 25 years.

What else can we do that very few other places can do? We can give our beloved family of

clients all of the specific Tissue Growth Factors including Nerve Growth Factor. We can get

our clients back to youthful levels of both HUMAN GROWTH HORMONE and ALL TISSUE

GROWTH FACTORS so as to be always consistent in producing cell repair and regeneration for

our client’s entire body and not just a few aspects of the body.

I am now age 63 as of Jan. 27 and I have the physiology of a 30 year old and often feel

younger than that.

Advantages to this protocol:

Better Eyesight vision… especially at Night

Increased Cardiac output (stronger more youthful heart muscle)

Enhanced Sex Drive

Loss of FAT around the waist

Increase in lean body muscle

Better metabolism

Much Faster Wound Healing

Hair and Nails Grow Longer Faster (Women Love it)

Improves Daily Energy

Increases Confidence

Emotional ability to Deal with Stress

Much Improved Sleep

Better Orgasms

According to Dr. Daniel Rudman, in New England Journal of Medicine….Age Reversal

And so much MORE

Please come to AAI and see me and the outstanding loving and caring staff….Because you will

become part of our family of beloved clients by phone or in person we live a great part of our

lives to reverse you’re age and allow you to feel incredibly youthful again.

Kindly, Larry Sosna N.D. PhD HHP

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