Aging Matters, Issue 3, 2016

No 3, 2016

US $8.00/ EU €6.00/ GB £5.00 where sold The in-house magazine for the International Antiaging Society Private Members Club.

IMPROVING GH WITHOUT INJECTIONS

WITH GHRH & GHRPs How to keep your prostate healthy • High-dose melatonin in medicine • Deprenyl and Alzheimer’s Disease Update

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Dr Ward Dean says:

“METFORMIN is Still The Most Effective Anti-ager” World famous anti-aging physician and co-author of ‘Smart Drugs & Nutrients’ says anti-diabetic biguanide drug Metformin is still his most recommended all round substance for anti-aging.

Its broad and far reaching properties include: • Increasing longevity • Anti cancer • Weight loss • Improving insulin resistance

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WELCOME Our apologies if this issue is on the technical side; it’s because this period we asked Dr. Richard Walker to detail how we can raise growth hormone via GHRH and GHRPs and we also asked Professor Jesus Tresguerres to detail his work with high-doses of melatonin.

We think it’s important that from time to time we include these journal style articles, mainly because there are naysayers out there who try to avoid looking for facts and simply state that there isn’t evidence to support benefits, or even processes.

Those of you who have a deep interest in growth hormone and melatonin, (both of which are integral antiaging hormones), may want to keep this issue on your bookshelf as reference material.

But there’s more; we have a super account of how to keep a prostate healthy and how to help address any types of prostate issues.

CONTENTS WELCOME Phil says thanks for finding the time

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FOREFRONT This month’s news

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GH WITHOUT INJECTIONS GHRH and GHRP in detail

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LOOKING AFTER THE PROSTATE GL AND How to stay healthy 12

Plus, Dr. Ward Dean begins with his account of deprenyl, (selegiline) in part 1 of his 2 part article that details this important antiaging drug.

THE HIGH DOSE USES OF MEL ATONIN IN MEDICINE

They say that the devil is in the detail, well for sure there are plenty of details in this issue!

Professor Tresguerres reports 18

Phil M

DEPRENYL AND AL ZHEIMER’S DISEASE UPDATE Dr. Ward Dean’s part 1 of 2 24

Phil Micans, MS, PharmB

Ward Dean, M.D.

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CROSS -REFERENCE LISTS Find what you need here

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TESTIMONIALS & EXPLANATIONS Nice comments from nice people

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CONTACT DETAILS Get in touch with IAS today

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Declaration: The IAS Aging Matters™ magazine is intended for IAS private club members (and therefore is not intended for the public).

It focuses on the latest international nutritional, hormonal and drug therapies to help combat the signs of aging. These signs include the physical, mental and internal changes consisting of the diseases and disorders such as cancer, arthritis and senile dementias etc. However, the main focus is upon the prevention of such aging diseases and disorders for the ‘healthy-aging’ individual.

Copyright 2016: All copyrights are acknowledged. Whilst every effort has been made to ensure accuracy, no responsibility can be accepted for illustrations, photographs, artwork or advertising materials while in transmission or with the publisher or their agents.

Disclaimer: All educational information is offered under IAS terms and conditions. This information does not replace the advice of your physician and restrictions may apply in some countries. The opinions expressed by the writers may not be those of IAS or the magazine. All prices shown are in US Dollars and are for reference purposes only and they do not include taxes (where applicable), nor do they include shipping & handling fees. Prices, conditions and terms are subject to change without notice.

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FOREFRONT THE THINGS YOU NEED TO K NOW FROM THI S MONTH’ S NE WS

Beta Glucan Reduces Allergy Symptoms With millions of allergy sufferers worldwide dreading the start of the fast approaching allergy seasons, there maybe solace to be found in Beta Glucan for some.

boosting the immune function of intestines, it is also known be an effective ‘normalizer’ for overactive immune systems which are synonymous with allergies.

Beta Glucan is extracted from oats and barley, yeast, algae, manin, shiitake mushrooms as well as other sources, and whilst it is successful in reducing cholesterol levels and

In studies carried out at the beginning of the allergy seasons, groups taking Beta Glucan supplements saw a significant reduction in allergy nasal, eye and non-nasal

symptoms and severity.

Beta Glucan is also proven to help with stress levels, digestive health and boosting the immune system in readiness to fight off infections and diseases.

Unrelenting March of Diabetes It affects nearly 1 in 11 adults Cases have quadrupled since 1980 1.5 million people died as a result of diabetes in 2012 2.2 million additional deaths were caused by higher than optimal blood glucose 43% of these 3.7 million people died before they were 70 years old These are just some of the worrying figures linked to the unrelenting march of diabetes in the world according to the WHO. It includes both those suffering from type 1 and type 2 but the high increase has largely been linked to a surge in type 2.

There are a number of devastating consequences of failure to control blood sugar levels including: tripling the risk of a heart attack, 20 times more likely to have 4

a leg amputated, higher risk of stroke, kidney failure, blindness and complications during pregnancy.

The easy solution is for everyone to eat better, and do more exercise, keeping waist lines down. However governments also need to do more to regulate levels of fat and sugar in food, ensuring healthy options are available.

The food industry needs to be more responsible in reducing sugar and fat levels in food,

and to stop advertising unhealthy foods to younger people.

Metformin is one drug that can help with keeping blood sugar levels lower. It has also recently been the talk of the FDA with them increasing the label indications to say that it can now ‘safely be used in patients with mild impairment in kidney function and in some patients with moderate impairment in kidney function’.

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In further news in regards to Metformin, the FDA also approved in December last year a trial into anti-aging in humans using the drug. We of course have long told about the anti-aging benefits of Metformin and it seems the FDA have finally caught up to this news!

Ref: http://www.who.int/diabetes/ global-report/en/

Boosting Growth Hormone without injections

Updating the GHRPs and Sermorelin by Richard Walker, M.D.

Ed. - Eagle eyed readers may recall Dr. Walker’s other excellent articles regarding GHRPs and GHRH in issue 3, 2014 and issue 3, 2013 of the Aging Matters™ magazines, (note, they can be downloaded from the IAS website). In them he described how bolus injections of recombinant growth hormone (rhGH) do not reproduce bioidentical patterns of GH release from the pituitary, whereas application of GHRPs and sermorelin do naturally accentuate the pulsate releases of GH that occur throughout the day. His avocation is that long-term administration of injections of GH could lead to downregulation of the pituitary’s own production, which would not be desirable. In this article, Dr. Walker continues to assert that the peptides are a more effective long-term therapy to boost GH levels and that they are effective orally (unlike GH itself). His conclusion, also confirmed to me via personal communication, is that GHRPs can be used concurrently alongside sermorelin, but that just like any hormone treatment they should not be used continuously, (i.e. there should be frequent breaks) and that they should be used judiciously and sensibly etc.

Sermorelin is a truncated analog of growth hormone releasing hormone (GHRH) and the GH releasing peptides, (GHRP’s) like GHRP2 and GHRP6 are various peptidyl analogs of ghrelin.

These substances have been used for over two decades in clinical and research protocols intended to oppose maladaptive, age-associated changes in body composition.

Specifically, these substances are secretagogues that enhance pituitary GH activity so as to sustain or increase lean body mass, while decreasing total and visceral body fat.

However, despite widespread use of these molecules in age management, some practitioners still lack a thorough understanding of their developmental histories, structural peculiarities and functional relationships. For example, recently the question was raised whether GHRP2 and/or GHRP6 are structurally unrelated analogs of GHRH or simply bioactive fragments of the 44 amino acid neuropeptide. In fact, they are neither. The GHRP’s are not related structurally or functionally to GHRH. Their structures evolved from repeated chemical modifications of met-enkephalin, an opioid that acts as a growth factor in neural and non-neural cells and tissues, in

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Ghrelin is also found in the brain where it is thought to modulate the activity of GHRH-releasing neurons in conjunction with dopamine cells (2, 3, 4). In contrast, sermorelin is a bioactive analog of GHRH that is represented by the first 29 amino acids in the 44 amino acid sequence of the intrinsic GH releasing factor. Consistent with their roles in controlling pituitary activity, both categories of GH secretagogues have their own distinct, saturable receptors on somatotrophs that have separate, complementary functions in regulating GH production and secretion(5). Not only that, but when analyzing responsiveness to GHRH and/or GHRP by double-reverse hemolytic plaque assay, the presence of at least three functionally distinct somatotroph subpopulations were identified (6).

Until the discovery of GHRPs, control of pituitary GH production and secretion was thought to be regulated by the stimulatory and inhibitory influences of GHRH and somatostatin, respectively (7). In turn, the activity of cells responsible for production and release of these neuropeptides were known to be regulated by brain catecholamines. Specifically, the neurotransmitter systems responsible for stimulating GHRH and/or inhibiting somatostatin are adrenergic catecholamines and dopamine acting via α2- receptors and D1 or D2 receptors, respectively.

Excitatory amino acids acting via N-methyl-D-aspartate (NMDA) and non-NMDA receptors also similarly influence GHRH and SRIF (somatotropin release inhibiting factor) see figure 1.

Activated NMDAR Allosteric site Glutamate

Glycine

Glutamate binding site

Glycine binding site

Figure 1: The NMDA receptor: a type of glutamate receptor that participates in excitatory neurotransmission has some influence over GHRH and SRIF.

in vivo but not in vitro, where the GH response was very weak.

However, when hypothalamic fragments were incubated with pituitary cells, the in vitro response was augmented.

Furthermore, when GHRH was incubated with pituitary cells plus GHRP, GH release exceeded even that produced by GHRH alone. In fact, the effect was synergistic rather than additive (see figure 2).

This finding suggested that GHRP and GHRH release GH by different and complementary mechanisms whereby GHRP is dependent on endogenous GHRH, which in turn plays a permissive role in releasing GH from the pituitary (8).

150

100 GH (ug L-1)

addition to being a neurotransmitter and neuromodulator(1).

However, despite their origins, GHRP’s are not opioids.

Functionally, they display the properties of ghrelin, a 28 amino acid peptide found primarily in the stomach that was discovered by Kojima and colleagues in 1999 (2).

50

0 -60 -40 -20 0

20 40 60 80 100 120 140 160 180 200 220 240 Time (min.)

Intravenous bolus

Figure 2: Comparative GH responses in individual human subjects. GH responses together with areas-under-the-curve, (µgL-1 after 4-hours). Placebo, (orange, 540); 0.1 µg kg-1 GHRP (blue, 916); 1 µg kg-1 GHRP, (green, 5319); 1 µg kg-1 GHRH, (yellow, 2590); 0.1 µg kg-1 GHRP plus 1 µg kg-1 GHRH (red, 10,065). From Bowers et al., 1990 J Clin Endocrinol Metab, 70:975-982

Note in Figure 2. that when GHRP is administered in vivo at the same dose as GHRH, it releases more GH than the primary neuropeptide, demonstrating the dependence of GHRP upon GHRH for activity. But, GHRP does not passively participate in enhancing GHRH efficacy. It also stimulates hypothalamic release of the neuropeptide. Evidence for this effect derives from several facts, GHRPs have specific receptors in the brain. and their natural analog, ghrelin also exists in the brain. Cells containing ghrelin were visualized specifically within the arcuate nucleus wherein resides GHRH cell bodies (Figures 3, 9, 10).

Cell membrane

Anecdotally, this effect accounts to some extent for the ability Intracellular space of certain amino acids such as Ca channel glutamate, glycine, D-serine and aspartate to act as weak, non-specific GH secretagogues. In contrast to the α-adrenergic neurotransmitters that enhance pituitary GH activity by stimulating and inhibiting GHRH and SRIF, respectively, β-adrenergic systems have the opposite effect, thereby providing CNS control over GH homeostasis.

2+

Before synthesis of GHRPs and subsequently the discovery of ghrelin, it was believed that the regulatory system for GHRH and SRIF previously described was complete. However, ghrelin/ GHRPs were subsequently found to also have a significant physiological role in the regulatory relationship between GHRH and somatostatin. This fact was initially implied by the finding that GHRP profoundly stimulated GH release when administered 6

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Figure 3: Ghrelinproducing neurons and binding sites in the arcuate nucleus indicate a central effect for GHRPs in modulating GHRH release and thus enhancing natural functions of GHRH neurons. Source: Kern et al., Front Endocrinol 2014.

5: 1-8.

In relation to enhancement of GHRH neuronal functions, the ghrelin-producing neurons were found in association with dopamine signaling (11). The relevance of this finding derives from the fact that dopamine provides stimulatory control of GHRH neurons as previously mentioned. That these structural relationships are functional was demonstrated by the fact that GHRP’s activate a subset of neurosecretory cells in the arcuate nucleus, of which a significant portion are GHRH-synthesizing(12, 13).

This functional relationship has been supported by measurements of GHRH in the hypothalamo-pituitary portal circulation following activation (14, 15). Finally, the synergistic effect of GHRP upon GHRH results also in part, from its ability to suppress somatostatin release from the hypothalamus and somatostatin effectiveness on the pituitary (16).

The GH-releasing activity of ghrelin/GHRP in vivo is dependent upon endogenous GHRH and GH secretion, and is not maintained in the absence of GHRH. The primary feed-forward regulator of GH secretion is GHRH. Thus, ghrelin/GHRP is considered to be a facilitator or modulator of GHRH in the regulation of GH secretion (a diagrammatic representation of these relationships is provided in Figure 4). dopamine

a2-adrenergic

-

Putative GHRP’s galanin GABA(-B)

+

+ +

GHRH

+?

+

? -

serotonin (1-D)

-

(muscarinic) cholinergic

-

Somatostatin

-

-

B-2 adrenergic

+

-

L-arginine

+

+ -

+

*

GH +

-

*

IGF-I

Figure 4: Stimulatory and inhibitory roles of neuropeptides and neurotransmitters that modulate GH secretion via GHRH or SRIF, or act directly on the pituitary gland. Ghrelin/GHRP is central in facilitating GH secretion by stimulating GHRH, inhibiting SRIF and acting directly on the pituitary. Source Muller et al. Physiol Rev 1999; 79:511-607 (130)

Clinical considerations Utilization of GHRH and ghrelin analogs to increase GH secretion- as part of an age management paradigm- requires more than an understanding of the facilitating effects of sermorelin and GHRP. Under the dynamics of natural conditions these are physiological relationships acting in balance to sustain neuroendocrine homeostasis. When the injected secretagogues are administered, they act as pharmacological agents that no longer observe such balance. On the contrary, they tend to disrupt internal order depending upon the dose, frequency and timing of their administration.

By virtue of parenteral administration, the injected secretagogues are presented as boluses that are generally larger than those which the body experiences under physiological circumstances. Hence, considerations of feedback effects and

receptor desensitization must be carefully considered. Long feedback loops with easily recognizable structural impacts on the body strikingly demonstrate the potential of hormone administration to accomplish a desired clinical outcome while bringing with it an undesirable side effect. For example, anabolic steroids such as testosterone are very effective in increasing muscle mass and reducing body fat. However, they also shrink testicular size and volume due to profound negative feedback on pituitary gonadotropin secretion.

Similarly, the use of recombinant human growth hormone (hGH) essentially shuts down pituitary somatotroph function, depending upon the dose administered. In effect, the desired pharmacological effect of improving body composition during aging is accompanied by the paradoxical side effect of accelerating pituitary functional decline that is the result of aging in the first place!

As a result of such negative effects on total body neuroendocrine homeostasis, it is advisable to select an intervention that is sufficiently high on the feedback loop to avoid negatively impacting as much of it as possible.

However, no matter how much care is taken it is inevitable that some part of the system will be “shut down.” So if possible, only the shortest feedback loop should be affected in hormone replacement therapy. As shown in Figure 5, the GH neuroendocrine axis involves many levels of feedback control including long, short and ultra-short loops.

Figure 5: Long feedback involves the somatomedins (IGF-1 et al.) having negative and positive feedback on GHRH and SRIF, respectively. Short feedback involves GH having negative and positive feedback on GHRH and SRIF, respectively and ultrashort feedback involves GH and GHRH having negative feedback on somatotrophs and GHRHproducing neurons. Thus, while “external” factors can modulate the activity of GHRH neurons, GHRH can also influence its own production and secretion.

Missing from Figure 5 is Ghrelin/GHRP, because its effect is contrary to the rest. Since GHRP stimulates GHRH neurons and inhibits SRIF neurons, it can “feed forward” so as to somewhat override negative feedback factors upon GHRH neurons.

Also, while the GHRH analog sermorelin avoids some of the short negative feedback resulting from clinical use of rhGH, chronic use of the smaller peptide is hampered by a rapid desensitization of its intended response. Such desensitization of the GHRH receptor (GHRH-R) after long and short-term exposure to its agonist has been described in vivo and in vitro (17-19).

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The combined effect of ultrashort loop feedback and GHRH-R desensitization can explain a common complaint of practitioners who use serum IGF-1 levels as a primary marker of sermorelin efficacy. The oft-repeated complaint is that unlike after rhGH administration, sermorelin causes IGF-1 levels to increase initially but then after a few months to decline. In contrast, IGF-1 levels remain elevated after GHRP (Figure 6).

and IGF-1. However, after continued daily administration of sermorelin, its negative effects on brain and pituitary GHRH receptors reduces the amount of hGH and IGF-1 that results from the same dose of analog that previously produced a robust effect (Figure 7).

As seen in Figure 7, GHRP stimulates GHRH neurons and hence sustains its receptors by direct effect and also due to association of its receptors with those of dopamine to form GHSR1a:DRD2 heteromers (11). Furthermore, GHRP does not desensitize GHRH receptors on somatotrophs while at the same time, enhancing efficacy of endogenous GHRH through synergy.

These functional differences have clinical significance when considering interventions intended to restore somatotroph functions that fail during aging, primarily because of progressive deficiency in endogenous GHRH and SRIF dominance (22).

GHRP not only stimulates GHRH and inhibits SRIF, it also enhances GHRH potency in somatotrophs by activating specific receptors that act to amplify second messenger systems leading to increased production and secretion of GH (Fig 8). Recrudescence is facilitated by GHRP, because it recruits separate somatotrophs from the 3 subpopulations (6).

Figure 6: Differential effects on sermorelin and GHRH on serum IGF-1 levels.

Chronic administration of sermorelin, but not GHRP, is accompanied by an apparent loss of sermorelin efficacy. This is due to a combination of factors, including ultrashort loop feedback resulting in depletion of endogenous GHRH along with desensitization of GHRH receptors and reduction of GHRH-R messenger RNA accumulation (20). Both of these effects are caused directly by repeated daily injections of pharmacological doses of sermorelin, since negative feedback sites, SRIF neurons and GHRH-R mRNA “see” sermorelin as excessive amounts of GHRH and thus, shut down production of the endogenous stimulatory neuropeptide and its receptors.

This effect takes several weeks, and thus allows the additive effect of sermorelin and endogenous GHRH to occur. This results in an initially significant increase in circulating hGH

Somatotrophs Have Dual GH Secretagogue Receptors It is also important to note that even when GHRP is administered to older persons, GH secretion is greater even than that resulting from administration of GHRH or its analog, sermorelin, so long as some level of endogenous GHRH is present (Figure 9).

As seen in Figure 9, the response to GHRP in adolescent and adult subjects was comparable even though endogenous GHRH declines with advancing age. Thus, the data suggest that the synergistic response to GHRP is not dose related to GHRH, but rather just the presence of some is sufficient to realize the full stimulatory potential of GHRP. On the other hand, the additive effect of exogenous GHRH with endogenous GHRH reflects the age-related decline in the latter neuropeptide with

Functional Differences Sermorelin

Inhibits production and secretion of endogenous GHRH by direct negative feedback on GHRH neurons. Also Binds to receptors on somatotrophs causing them to produce and secrete GH.

8

GHRP-2

Stimulates GHRH neurons and also binds to specific receptors on somatotrophs causing them to produce GH.

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Figure 7: Differential effects of sermorelin and GHRP upon endogenous GHRH in brain and pituitary. Even though daily injections of sermorelin are capable of shutting GHRH production in neurons and synthesis of GHRH receptors in brain and pituitary, these effects are fully manifest after a period of time. Thus, initially sermorelin results in an additive effect on endogenous GHRH receptors, but after several weeks or months, the absence of natural GHRH and desensitized GHRH receptors blunt the initial response. In contrast, GHRP stimulates GHRH production and sustains its receptors (20, 21).

Hypothalamus

+ GHRH

Ghrelin/GHS

GHRH-R

GHS-R

PKA

?

+

cAMP

PKC

Ca2+ Somatotroph GH release

Figure 8: Separate somatotroph receptors for GHRH/sermorelin and ghrelin/GHRP underlie their synergy. Even in the presence of relatively low concentrations of GHRH, its effect on second messengers within the somatotroph is amplified by the activation of GHRP receptors on the same cell and in subpopulations of other somatotrophs (5, 6). Source: M.J. Lengyel. Braz J Med Biol Res 2006; 39: 1003-1011

advancing age. When GHRH was administered to adolescents, their peak response was over 10 times greater than that seen in adults. These data suggest that GHRP is a better choice for opposing pituitary dysfunction during aging than is sermorelin.

Figure 9: Comparative responses to i.v. administration of GHRH or GHRP in adolescent and adult subjects. Subjects were first administered GHRP so as to avoid possible synergy with GHRH. Accordingly, GHRH was administered separately over three hours following the first dose of GHRP. Source: Walker RF, Bercu BB JAAM 1:219-225, 1998

A paradoxical effect of GHRP to increase body fat is sometimes noted when sermorelin which has been used for prolonged periods is discontinued and immediately replaced by the ghrelin analog. As has been demonstrated repeatedly by many different researchers, GHRP increases lean body mass and reduces total body fat, presumably as the result of its ability to activate the GH neuroendocrine system. However, it is important to understand that ghrelin/GHRP is also orexigenic, and thus has the ability to increase appetite and body weight.

Generally, this effect is not observed at low doses of GHRP that stimulate the GH neuroendocrine axis. However, it is important to remember that GHRP does not release GH in the absence of GHRH (8). Such circumstances may be permissive to the orexigenic effect of GHRP which otherwise would be blocked by its low-dose, GH secretagogue activity. An animal model for this paradoxical effect is seen in rats with mutated GHRH genes (23). Because they produce no endogenous GHRH, such mutated rats gain fat and body weight when given GHRP. Since as previously discussed, chronic administration of sermorelin suppresses GHRH production of neuropepetide and synthesis of its specific receptor thereby essentially eliminating the endogenous secretagogue. Thus, if GHRP is administered immediately after cessation of sermorelin therapy without

allowing sufficient time for recrudescence of the intrinsic GHRH system, then only its orexigenic effects will be manifest and fat, rather than muscle, will increase. Accordingly, a “recovery” period of at least one or two months is recommended before switching from sermorelin to GHRP for GH secretagogue, antiaging therapy.

Alternatively, GHRP may be given in conjunction with sermorelin so as to sustain the beneficial effects of secretagogue therapy on body composition. However, the practitioner should be aware that such “combination therapy” overrides and eliminates the naturally occurring temporal relationships between the brain and pituitary governing GH secretory circadian rhythms.

In contrast, GHRP alone may not cause significant perturbation of such physiological rhythms because it facilities, rather than initiates, the process of GH neuroendocrine activity. Of course, GHRP may be used in any patient who is not taking sermorelin to achieve full benefit of its influence over the GH neuroendocrine axis.

Another issue that is of relevance to clinical use of GH secretagogues is their toxicity profile. Recently this question arose following the finding that Foreo® (teriparatide), a truncated analog of naturally-occurring parathyroid hormone (PTH) causes osteosarcoma in animals, and possibly in humans as well. Like sermorelin, which contains 29 of the 44 amino acids that make up GHRH, teriparatide contains 34 of the 84 amino acids composing PTH. Because of this structural peculiarity of the two endocrine analogs, the question of whether fragments of naturally occurring peptides are potentially carcinogenic was raised. That possibility is rather doubtful, since it is more likely that the specific impact of the peptide analog upon its target tissue is more significant than the fact that it is a fragment of the naturally occurring molecule.

For example, it has been reported by the manufacturer of Forteo that “intermittent spikes of PTH, such as given by daily injection, will cause more increase in bone formation than in bone resorption.”(24). This imbalance in bone homeostasis apparently leads to development of osteosarcoma due to abnormal proliferation of osteoblasts”.

It should be noted that unlike sermorelin or GHRP that are subject to any number of feedback controls, which prevent excessive stimulation of pituitary cells, teriparatide directly stimulates bone cells and is not under feedback control.

Accordingly, the persistent and unimpeded stimulation favoring osteoblasts over osteoclasts directly disrupts bone homeostasis. This effect probably has little to do with the fact that teriparatide is a fragment of PTH and more to do with differences in its pharmacology from the native hormone (25). This possibility is totally different from the cases of sermorelin and GHRP since both are analogs of GHRH and ghrelin, respectively, and bind to the same receptors in brain and pituitary as the natural peptides. Thus, it is unlikely that hyperstimulation of any cell population with the potential to cause hyperplasia (and worse) is not likely. In fact, unlike teriparatide, there is no evidence that sermorelin, GHRP or

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even hGH causes cancer de novo (26). However, because GH is mitogenic, the secretagogues and hGH are contraindicated in extant cancer, but they can be used in periods of remission.

GHRH activity as previously described. All ingredients have been subjected to extensive testing and clinical applications with a high safety profile. In addition to such clinical trials, there is a literature of their use in humans for up to a year or more, including children, Furthermore sermorelin and GHRP have been used in animal without a single report of toxicity. In preclinical safety testing they studies and human clinical trials for decades without any have a clean record in acute (LD50 testing), repeated study (90 day reports of serious adverse events associated with their use. A dosing/histopathologic examination of all tissues at necropsy), and comparison of mild side effects with low incidence that were genotoxicity. reported for sermorelin and GHRP is presented in Table 1.

GHRP2-Pro™ can be used in conjunction with sermorelin to promote even greater synergy between the GHRH and ghrelin ADVERSE EFFECTS systems.

But if such combination therapy is considered, the Sermorelin GHRP2 physician should advise the patient to discontinue sermorelin and • Local injection site irritation • Soft stools due to GHRP-induced, increased gastric emptying any source of GHRP including GHRP2-Pro™ until adequate recovery • Redness, pain or swelling • Itching • Drowsiness, urticarial, hives, vomiting, of endogenous GHRH has occurred. Only thereafter should GHRP headache, nausea, difficulty swallowing, • Menstrual irregularity hyperactivity, chest tightness and pallor, be employed alone as an effective GH secretagogue because of its distortion in perception of taste, and absolute dependence upon endogenous GHRH for efficacy, and to flushing of the skin • No reported side effects - multiple peer • Flushing of the face, nausea, headache, avoid its inherent ghrelin-like orexigenic effects. reviewed research studies of GHRP vomiting, dysgeusia, pallor and tightness in the chest Conclusion • Anti-GRF antibodies Based upon the data presented above, it is concluded that sermorelin and GHRP are safe and effective for use GH replacement age-management protocols. However, because of their relative positions in the hierarchy of the hGH neuroendocrine axis, GHRP offers certain advantages over sermorelin for long-term therapy.

These advantages of GHRP are summarized simply by noting that because the body “sees” sermorelin as GHRH, then normal Table 1: A comparison of adverse events reported in studies with sermorelin and GHRP. All were Grade 1 Mild AE which is the lowest level AE with Grade 5 being the physiological processes are activated so as to restrict the amount of most serious. stimulation resulting from administration of pharmacological doses The delivery systems of the GHRH analog. In other words, ultra-short loop feedback, receptor desensitization and stimulation of SRIF production and Traditionally, peptides are administered by subcutaneous or secretion occur so as to maintain homeostasis at levels consistent intravenous injection. While efficient for drug administration, the with age within the axis. delivery system has the disadvantage of presenting a secretagogue as an instantaneous “pulse” rather than a slower, more persistent On the other hand, GHRP administration creates an enhanced and longer-lasting presence in the bloodstream. “feed forward” situation in which activation of GHRH neurons increases, essentially from outside the main axis, and thus, shifts Infusions of GHRP in humans enhanced pulsatile GH secretion and activity relationships within, upward. As a result, negative increased plasma IGF-I concentrations without significant adverse feedback, receptor desensitization and SRIF secretion are reduced effects (27). These findings were in contrast to secretory responses relative to the increased GHRP influence causing in turn, greater to bolus administration, suggesting that a slower more continuous recrudescence of somatotroph function with increased hGH and presence of GHRP is more advantageous than brief, daily pulsatile IGF-1 production. exposure to the secretagogue in restoring GH neuroendocrine homeostasis. Obviously, it is impractical to even consider infusion as An additional advantage of GHRP over sermorelin is that it is orally a strategy for pituitary recrudescence during aging. However, oral bioavailable. As previously noted, slower and more extended administration which provides a slower, more constant means of exposure of the hGH neuroendocrine axis to GHRP amplifies not delivery might be more clinically advantageous and effective for only its quantitative activity but also sustains its natural rhythms that reason alone. which are disrupted by bolus injections of sermorelin. Furthermore, because of its oral bioavailability, GHRP may be incorporated in To this point, we recognized that peptidyl GHRPs are composed in formulations such as GHRP2-Pro™ with complementary ingredients large part of D-amino acid isomers which, unlike the l-isomers, are to promote a more holistic approach to therapy. resistant to endopeptidase attack in the gut (28). As a result, they are orally bioavailable and suitable for use in oral dosage forms (29).

Thus, in contrast to sermorelin, more effective, beneficial and Accordingly, we created novel oral formulae for use in opposing GH physiological outcomes in sustaining hGH neuroendocrine health neuroendocrine decline and its sequelae during aging. In addition and vitality can be expected from GHRP protocols such as to providing a more prolonged presentation of secretagogue to GHRP2-Pro™. the brain and pituitary, another advantage of such formulations References is that complementary ingredients can be included in the single References available online. formulation. Some of these were added to enhance dopamine and other neurotransmitter activity as well as to promote pituitary sensitivity and to directly increase skeletal muscle development.

GHRP2-Pro™ or Release-Pro™ are formulations that can be used in lieu of sermorelin, but will still provide all the benefits of enhanced Clinical Study Report 90 Day Phase III Clinical Trial Protocol No: ECTS/11/001. Final Report – April 28 2012 Ethicare Clinical Trial Service-CRO

Gereg package insert (Serono-US), Rev 10/97, Rec 02/11/98

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Mericq V et Al - Effects of eight months treatment with graded doses of a growth hormone (GH)-releasing peptide in GH-deficient children. J Clin Endo Metab. 83(7):2355-60, 1998 CY Bowers et Al - Sustained Elevation of Pulsatile Growth Hormone (GH) Secretion and Insulin-Like Growth Factor I (IGF-I), IGF-Binding Protein-3 (IGFBP-3), and IGFBP-5 Concentrations during 30-Day Continuous Subcutaneous Infusion of GH-Releasing Peptide-2 in Older Men and Women, J Clin Endo Metab 89(5):2290–2300, 2004 Mericq V et Al - Changes in appetite and body weight in response to long-term oral administration of the ghrelin agonist GHRP-2 in growth hormone deficient children. J Pediatr Endocrinol Metab.

16(7):981-5, 2003 Laferrere b et Al - Growth Hormone Releasing Peptide -2 (GHRP-2), like ghrelin, increases food intake in healthy men. J Clin Endocrinol Metab.

90(2): 611–614, 2005.

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GROWTH HORMONES WITHOUT THE INJECTION

Save up to $20 on GHRP2, GHRP6 & Sermorelin GHRP2™ $149.99 (save $10.00 over regular price) GHRP6™ $64.99 (save $10.00 over regular price) Sermorelin™ $179.99 (save $20.00 over regular price)

Offer valid until 30th June 2016. *Restrictions may apply in some countries. All information is educational and does not replace your physician’s advice and is subject to IAS terms and conditions which may change without notice.

Alleviating the symptoms of an

By Leslie J. Farer

AGING PROSTATE

Growing bald isn’t the only unwelcome sign of advancing years; for most men, aging also goes hand in hand with bothersome lower urinary tract symptoms: night time awakenings for trips to the bathroom, the sudden and frequent urge to urinate, painful urination, even erectile dysfunction.

At the root of these issues may be the progressive enlargement of the prostate gland, which over time can grow from its original walnut-like size to reach the proportions of a lemon. Although prostate enlargement may be a sign of cancer, the most common cause is a non-malignant condition known as benign prostatic hyperplasia, which involves the growth of excess prostate tissue that eventually can obstruct the urinary tract, leading to impeded urine flow and troubling symptoms.

The good news is, through the use of phytotherapies (plantderived treatments), nutraceuticals, dietary and lifestyle recommendations, and conventional drugs when necessary, the tissue-proliferating mechanisms that drive prostate enlargement can be attenuated, resulting in urinary symptom relief and improved quality of life for men over 40.

Age-related prostate growth and “LUTS” The prostate is a small gland of the male reproductive system that sits under the bladder and surrounds the urethra, the duct that carries urine from the bladder through the penis and out for excretion. Its main function is the production of seminal fluid. Over time, in most men, the prostate undergoes structural 12

changes. By the time a man reaches his fifth decade, prostate cells can begin to multiply and pinch off the urethra, resulting in decreased urine flow. Even a small amount of growth can produce lower urinary tract symptoms (abbreviated “LUTS”), which include: • urinary frequency and urgency • weak urinary stream • nighttime urination • painful urination • incomplete emptying of bladder • sexual problems The incidence of LUTS related to prostate enlargement is agerelated, affecting approximately 50% of men age 60 to 90% of men age 85. (1) Obviously, safe and effective treatments are needed to counter this rising prevalence.

Conditions related to prostate enlargement The most common condition associated with a swollen prostate is benign prostatic hyperplasia (BPH). As the name implies, BPH involves the non-malignant (not associated with cancer) proliferation of cells in the prostate and formation of excess

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tissue, technically called “hyperplasia.” Besides annoying urinary symptoms, BPH can increase the risk of kidney damage and bladder infections; it can even lead to erectile dysfunction (ED). (2) A major factor in the development of hyperplasia, whether benign or malignant, is the influence of testosterone metabolites on the prostate, a hormone-sensitive organ.

One of these metabolites is dihydrotestosterone (DHT), converted from testosterone by the enzyme 5α-reductase. DHT is highly potent, and increased levels are associated with BPH and prostate cancer (3) (as well as hair loss, since 5α-reductase is also found in the scalp). Aging men also exhibit higher levels of another enzyme, aromatase, which converts testosterone into estrogen. (3) Like DHT, increased levels of estrogen promote cell proliferation. (3) Since BPH is an androgen- and estrogensensitive condition, an effective therapeutic strategy is to limit the activity of these enzymes (5α-reductase and aromatase), preventing the conversion of testosterone to hyperplasiapromoting DHT and estrogen. Below, we’ll see both drug and phytotherapies that target these enzymes.

Besides BPH, another non-malignant condition linked with prostate enlargement is prostatitis, which involves inflammation and/or infection of the prostate and shares many of the symptoms of BPH. Prostatitis can be chronic or acute, and is usually treated with anti-inflammatories or antibiotics. Prostate enlargement may also be a result of the malignant proliferation of tissue (i.e., prostate cancer). If you experience any urinary symptoms, see your health care provider as soon as possible to determine the cause, whether prostate enlargement (due to BPH, prostatitis, or prostate cancer), or a kidney problem or bladder infection. If prostate enlargement is detected, prostate cancer should be ruled out, but if diagnosed, must be treated with an individually-designed comprehensive medical and nutritional protocol as directed by your health care professional.

Note: This discussion focuses on the major non-malignant cause of prostate enlargement, BPH, although occasional reference will be made to prostate cancer prevention (since many of the natural and pharmacological agents outlined below have multiple mechanisms and benefits). A full discussion of prostate cancer is outside the scope of this article.

Normal Prostate

Enlarged Prostate

Treatment options for BPH/LUTS The foundation that all men should establish to avoid the risk of, or ameliorate, prostate-related symptoms are a low fat, vegetable-rich whole foods diet and a healthy lifestyle.

Meat and dairy products should be limited or eliminated, while generous servings of vegetables (including those high in carotenoids and Vitamin C) should be piled high on most plates. Additional nutritional support from supplemental zinc, selenium, vitamin C, lycopene, and essential fatty acids (EPA, DHA, and GLA) is also recommended, since all of these are beneficial in cases of BPH. Losing extra pounds, if necessary, maintaining an ideal body weight, controlling blood sugar, and exercising regularly will all lower the risk of BPH (and contribute to overall good health). These guidelines also apply to prostate cancer prevention (where cruciferous vegetables are particularly important in the diet, in addition to green tea, soy products, etc.).

On top of this foundation, the next level of support includes phytotherapies to alleviate symptoms in mild to moderate cases; in moderate to severe BPH/LUTS, drugs will likely be necessary.

Peptide bioregulators may be beneficial in all cases, regardless of severity. Most men probably want to avoid surgery, especially in a sensitive part of the body, but surgical options do exist to either remove the prostate or reduce its size in order to relieve symptoms (although some readers might squirm to read this).

Conventional drugs for BPH First, let’s look at standard pharmacological agents, of which there are several classes: • 5-α-reductase inhibitors block the conversion of testosterone to DHT, helping to reduce the size of the prostate and ease symptoms, while preventing further growth. Finasteride (Proscar®) and dutasteride (Avodart®) are two FDA-approved 5α-reductase inhibitors that have been shown to improve urinary symptoms and reduce the risk of disease progression in BPH patients, (4,5) although they may cause some degree of sexual dysfunction. Both of these DHT-suppressing drugs have also been shown to reduce the risk of prostate cancer. (6,7) • Aromatase inhibitors such as anastrozole (Arimidex®) have potential use in preventing the age-related increases in aromatase and estrogen that stimulate hyperplasia. (3) In men age 60 and older with low testosterone levels, one mg anastrozole daily increased testosterone and decreased estradiol production. (8) However, studies are few and further research is needed to confirm whether the estrogen-lowering capacity of aromatase inhibitors can significantly inhibit the prostate tissue over-proliferation that eventually leads to urinary symptoms.

• Phosphodiesterase-5 (PDE-5) inhibitors that are popular treatments for ED, such as tadalafil, (Cialis®), can also markedly improve LUTS in men with BPH. (9-11) (We saw earlier that BPH is a risk factor for ED and that the two conditions are related, so it follows that tadalafil can treat both.) Tadalafil is well tolerated with a favorable safety profile (10) and is approved worldwide for treating BPH-related urinary tract symptoms (whether or not they are accompanied by ED (11)).

Ref: Health-headlines.org

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“The incidence of LUTS related to prostate enlargement is age-related, affecting approximately 50% of men age 60 to 90% of men age 85. (1) Obviously, safe and effective treatments are needed to counter this rising prevalence.”

• Desmopressin (Minirin®), another useful agent for BPH/ LUTS, is particularly effective in reducing symptoms of nocturia (night time awakenings to urinate) that many men experience.

Desmopressin is a synthetic analog of the natural antidiuretic hormone vasopressin, which plays a key role in regulating the body’s water balance, including promoting the reabsorption of water by the kidneys and reducing urine output. Vasopressin is approved as a drug for the treatment of diabetes insipidus and associated frequent urination, but its therapeutic use in nocturia is limited due to its short serum half-life. (12) Its analog desmopressin, on the other hand, with its longer activity in the bloodstream, (12) is more suitable for overnight use in limiting urination. (Note: Both vasopressin and desmopressin are also used off-label as potent memory and cognitive enhancers.) A review of 10 controlled trials on over 2,000 adults with nocturia found that desmopressin is effective in reducing the number of nighttime voids, and delaying the time to the first void. (13) A study specifically on men with LUTS/BPH and nocturia found that three months of desmopressin treatment cut the number of nocturnal voids by about half (from an average of 3.8 to 2), decreased urine volume, prolonged the number of hours of undisturbed sleep (due to fewer awakenings to void), and improved quality of life, with good tolerability. (14) (An interesting parallel study would have been to determine if the increased hours of sleep came with heightened memory of dreams, due to desmopressin’s cognitive-enhancing effects.) Desmopressin is used once daily before bedtime, starting with a low dose and increasing gradually until an effective dose is reached. Side effects are mild, but may include hyponatraemia (low serum sodium concentration) in patients age 65 years or older; serum sodium levels should be monitored while using desmopressin in these patients.

• Other drugs used to ease urinary symptoms include α1adrenergic receptor blockers which increase urinary flow rate (though with sexual side effects) and antimuscarinics which relieve urinary urgency.

The above drugs are often used in combination. Although many of these are available through IAS, they should be used under the supervision of a physician. Note that certain of these conventional treatments for BPH (α1-adrenergic receptor blockers and 5α-reductase inhibitors) can cause sexual side effects, in addition to the ED that already accompanies many cases of BPH. Use of the natural remedies below combined with the lifestyle recommendations outlined earlier may decrease the need for, or lower the necessary dosage of, pharmacological agents, which will also result in a reduction of side effects.

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Phytotherapies treat BPH safely and effectively As a side effect-free alternative to drugs, numerous phytotherapies have been shown to successfully treat mild to moderate BPH/LUTS. Prostate Pro-2™ is a comprehensive formula containing four plant extracts that work synergistically to relieve troublesome urinary symptoms and promote overall prostate health, without unwanted side effects. Dozens of trials have been performed on the efficacy of these medicinal plants in treating BPH/LUTS, separately or in combination, and in comparison against conventional drugs.

• Urtica dioica (stinging nettle) root is a well-researched phytotherapy that acts by multiple pathways, including inhibition of aromatase in prostate tissue, (3) the same enzyme targeted by the drug anastrozole. In a placebo-controlled study on 558 patients with BPH/ LUTS, an impressive 81 percent of those who received Urtica for six months reported an improvement in symptoms (compared with 16 percent in the placebo group), and without side effects. (15) Other trials have demonstrated similar improvements, leading researchers to conclude that Urtica is a “safe therapeutic option for BPH, especially for reducing irritative symptoms and BPH-associated complications.” (16) Urtica also protects against prostate cancer by inhibiting proliferation of cancerous cells. (17) • Pygeum africanum (African plum tree) bark extract has been used for decades in Europe and more recently in the USA to treat BPH/LUTS. Its active constituents include phytosterols (such as beta-sitosterol) that inhibit pro-inflammatory prostaglandins in prostate tissue. (18) Pygeum also suppresses 5α-reductase and aromatase, and when combined with Urtica, the enzyme-neutralizing effects are synergistic. (19) In one of the numerous studies on Pygeum, 50 mg of the extract twice daily for two months reduced nocturnal frequency of urination and increased urinary flow in BPH patients, side effect-free improvements that were maintained even one month after treatment. (20) A Cochrane Database review analyzing results of 18 randomized placebo-controlled trials on Pygeum involving a total of 1562 men with BPH concluded that the phytotherapy produced a “moderately large improvement” in overall urinary symptoms (including nighttime urination, urine flow, etc.) and that adverse effects were minimal and comparable to placebo. (21) In addition to its use in BPH/LUTS, Pygeum inhibits prostate cancer both in vitro and in vivo and is recommended for men at high risk for developing prostate cancer. (22,23) • Seronoa repens or Sabal serrulata (Saw palmetto) berry extract has been treating prostate problems since the 1800’s, and today, it is probably the most widely used and well-known

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phytotherapy for BPH/LUTS. Saw palmetto contains several active compounds, including phytosterols, and has been shown to inhibit 5α-reductase (24) and reduce chronic inflammation of the prostate (25) which may contribute to BPH-related symptoms.

Multiple trials have demonstrated its efficacy and safety, either singly, or combined with drugs or other phytotherapies. In the first clinical trial to evaluate the effect of saw palmetto on both BPH and sexual dysfunction, 320 mg of the extract daily for eight weeks cut urinary symptoms in half with a corresponding improvement in sexual performance. (2) Saw palmetto has been shown to be equally effective as some standard drugs, including finasteride or tamsulosin, (26) and when taken concurrently, it also augments their actions. A year-long study compared the efficacy and safety of saw palmetto plus tamsulosin (Flomax®, an α1-adrenergic receptor blocker) with tamsulosin alone and found that the combination treatment was more effective in improving LUTS, especially what the authors refer to as “storage symptoms,” (i.e., urinary urgency, frequency, and nocturia) than tamsulosin alone. (26) (About 20 percent of patients in each treatment group experienced adverse effects, however, due to tamsulosin.) Another trial compared a combination saw palmetto and Urtica extracts with finasteride. Both treatments produced equivalent improvements, but with more adverse events in the finasteride group than the phytotherapy group. (27) These studies underscore the safety and efficacy of saw palmetto, and its suitability for long-term use was demonstrated in an observational study on BPH patients taking 320 mg of the extract once daily for 10 years without disease progression or side effects. (28) In addition to BPH/LUTS and sexual dysfunction, saw palmetto may be helpful for chronic prostatitis (29), likely due to its anti-inflammatory action. It also exhibits chemopreventive properties. (29,30) (And, as a bonus, due to its DHT-inhibiting action, saw palmetto can potentially treat male pattern baldness! (31)) • Trifolium pratense (Red clover) is an emerging phytotherapy that may hold promise in treating BPH/LUTS and preventing prostate cancer. Studies show that isoflavone components in Trifolium can inhibit the proliferation of prostate cells, reduce their potential to become cancerous, and promote apoptosis (programmed cell death). (32,33) To put it in a nutshell, these clinically proven phytotherapies act by different pathways to target the underlying mechanisms leading to prostate-related urinary symptoms (and even cancer). In a combination formula, such as Prostate Pro2™, their potencies are even further enhanced, making this an invaluable product to include in your regimen to improve and support prostate health.

The peptide bioregulator Libidon® rejuvenates the aging prostate Now let’s discuss the prostate peptide bioregulator Libidon®.

A major innovation in longevity therapies over the past few decades, led by Russian scientist Vladimir Khavinson, was the development of peptide bioregulators − short chains of amino acids (peptides) isolated from various animal tissues and organs.

When purified and administered therapeutically, these peptides act at the genetic level to regenerate age-damaged tissues and restore the function of a particular organ. For example, retinal peptides initiate the formation of retinal and pigment cells in patients with retinal degeneration, thymic peptides stimulate immunity, and pineal peptides induce the aging pineal gland to manufacture melatonin. The mechanism behind these rejuvenating effects is complex: each short-chain peptide interacts with a gene’s DNA, transferring information encoded in its amino acid sequence and stimulating a process called protein synthesis, the manufacture of proteins according to the encoded genetic information. By “switching” on genes to synthesize specific proteins, peptide bioregulators can recover the structure and function of tissues and organs undergoing age-related deterioration. IAS carries a full range of 21 of these bioregulators (for organs ranging from adrenals to thyroid), including Libidon® for the prostate.

Khavinson and his team at the St. Petersburg Institute of Bioregulation and Gerontology have performed extensive research on the broad range of peptide bioregulators, including Libidon®, which was evaluated for its effect on a variety of prostate diseases. Khavinson’s experiments specifically on BPH involved administering, both intramuscularly and orally, prostate peptide bioregulators similar to Libidon® to BPH patients, which resulted in full or partial restoration of the normal tissue structure of the gland in 21 out of 27 cases; (34) in other words, in the majority of patients, age-related changes in prostate tissue were partially and in some case completely corrected. As a result of their regenerative potential, Khavinson recommends prostate peptide bioregulators (i.e., Libidon®) for all cases of BPH, from mild to severe.

Putting it all together - your plan for prostate health Troubling symptoms resulting from an enlarged prostate are increasingly common in aging men; fortunately, as we’ve just seen, they are not inevitable, thanks to a variety of natural treatments and, if necessary, drugs.

The first step in preventing or ameliorating symptoms is to establish the foundation of dietary strategies and life style recommendations that we covered previously, with additional

“Troubling symptoms resulting from an enlarged prostate are increasingly common in aging men; fortunately, as we’ve just seen, they are not inevitable, thanks to a variety of natural treatments and, if necessary, drugs.” www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

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support from targeted nutraceuticals (zinc, selenium, etc.).

Next, phytotherapies should be added to relieve symptoms in mild to moderate cases of BPH/LUTS; Prostate Pro2™, a synergistic blend of four clinically proven botanical extracts, is an ideal choice for this purpose.

The peptide bioregulator Libidon® that acts by a unique and independent mechanism can also be included as another natural therapy for further support. If additional relief is needed in more severe cases, work with your health care professional in incorporating one or more conventional drugs to your regimen.

As mentioned, the use of phytotherapies combined with drug treatments will not only enhance the potencies of all of the active substances (pharmacological and natural), but will lower the necessary dosage of drug, and result in fewer side effects.

Obviously, symptom relief may take some experimentation on your part − the natural therapies may be sufficient alone (Prostate Pro2™, Libidon® or both), or, in the worst cases, it may require the addition of a conventional drug(s) to reach an acceptable level of improvement.

However, by following the recommended lifestyle and dietary guidelines as a foundation to which you add an individuallytailored combination of natural treatments (and drugs, if necessary), you can relieve bothersome symptoms, while improving your overall health and quality of life.

List of abbreviations BPH

benign prostatic hyperplasia

ED

erectile dysfunction

LUTS

lower urinary tract symptoms

DHT

dihydrotestosterone

PDE-5

phosphodiesterase-5

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2. Suter A, Saller R, Riedi E, Heinrich M. Improving BPH symptoms and sexual dysfunctions with a saw palmetto preparation? Results from a pilot trial. Phytother Res. 2013 Feb;27(2):218-26.

3. [No authors listed] Urtica dioica; Urtica urens (nettle). Monograph. Altern Med Rev. 2007 Sep;12(3):280-4.

4. Pirozzi L, Sountoulides P, Castellan P, et al. Current Pharmacological Treatment for Male LUTS due to BPH: Dutasteride or Finasteride? Curr Drug Targets.

2015;16(11):1165-71.

5. Oelke M, Martinelli E. Pharmacological treatment of benign prostatic hyperplasia.

Urologe A. 2016 Jan;55(1):81-96.

6. Chau CH, Price DK, Till C, et al. Finasteride concentrations and prostate cancer risk: results from the Prostate Cancer Prevention Trial. PLoS One. 2015 May 8;10(5):e0126672.

7. Andriole GL, Bostwick DG, Brawley OW, et al; REDUCE Study Group. Effect of dutasteride on the risk of prostate cancer. N Engl J Med. 2010 Apr 1;362(13):1192-202.

8. Burnett-Bowie SA, Roupenian KC, Dere ME, Lee H, Leder BZ. Effects of aromatase inhibition in hypogonadal older men: a randomized, double-blind, placebocontrolled trial. Clin Endocrinol (Oxf). 2009 Jan;70(1):116-23.

9. Brousil P, Shabbir M, Zacharakis E, Sahai A. PDE-5 Inhibitors for BPH-Associated LUTS. Curr Drug Targets. 2015;16(11):1180-6.

10. Yokoyama O, Igawa Y, Takeda M, Yamaguchi T, Murakami M, Viktrup L. Tadalafil for lower urinary tract symptoms secondary to benign prostatic hyperplasia: a review of clinical data in Asian men and an update on the mechanism of action.

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Ther Adv Urol. 2015 Oct;7(5):249-64.

11. Zhang LT, Park JK. Are phosphodiesterase type 5 inhibitors effective for the management of lower urinary symptoms suggestive of benign prostatic hyperplasia? World J Nephrol. 2015 Feb 6;4(1):138-47.

12. http://uroweb.org/wp-content/uploads/BPH-20101.pdf (Guidelines on Conservative Treatment of Non-neurogenic Male LUTS) 13. Ebell MH, Radke T, Gardner J. A systematic review of the efficacy and safety of desmopressin for nocturia in adults. J Urol. 2014 Sep;192(3):829-35.

14. Berges R, Höfner K, Gedamke M, Oelke M. Impact of desmopressin on nocturia due to nocturnal polyuria in men with lower urinary tract symptoms suggestive of benign prostatic hyperplasia (LUTS/BPH). World J Urol. 2014 Oct;32(5):1163-70.

15. Safarinejad MR. Urtica dioica for treatment of benign prostatic hyperplasia: a prospective, randomized, double-blind, placebo-controlled, crossover study. J Herb Pharmacother. 2005;5(4):1-11.

16. Schneider T, Rübben H. Stinging nettle root extract (Bazoton-uno) in long term treatment of benign prostatic syndrome (BPS). Results of a randomized, doubleblind, placebo controlled multicenter study after 12 months. Urologe A. 2004 Mar;43(3):302-6.

17. Konrad L, Müller HH, Lenz C, Laubinger H, Aumüller G, Lichius JJ. Antiproliferative effect on human prostate cancer cells by a stinging nettle root (Urtica dioica) extract. Planta Med. 2000 Feb;66(1):44-7.

18. [No authors listed] Altern Med Rev. 2002 Feb;7(1):71-4. Pygeum africanum (Prunus africanus) (African plum tree). Monograph.

19. Hartmann RW, Mark M, Soldati F. Inhibition of 5 α-reductase and aromatase by PHL-00801 (Prostatonin®), a combination of PY102 (Pygeum africanum) and UR102 (Urtica dioica) extracts. Phytomedicine. 1996 Sep;3(2):121-8.

20. Breza J, Dzurny O, Borowka A, et al. Efficacy and acceptability of tadenan (Pygeum africanum extract) in the treatment of benign prostatic hyperplasia (BPH): a multicentre trial in central Europe. Curr Med Res Opin. 1998;14(3):127-39.

21. Wilt T, Ishani A, Mac Donald R, Rutks I, Stark G. A. Pygeum africanum for benign prostatic hyperplasia. Cochrane Database Syst Rev. 2002;(1):CD001044.

22. Shenouda NS, Sakla MS, Newton LG, et al. Phytosterol Pygeum africanum regulates prostate cancer in vitro and in vivo. Endocrine. 2007 Feb;31(1):72-81.

23. Larré S, Camparo P, Comperat E, et al. Biological effect of human serum collected before and after oral intake of Pygeum africanum on various benign prostate cell cultures. Asian J Androl. 2012 May;14(3):499-504.

24. Habib FK, Ross M, Ho CK, Lyons V, Chapman K. Serenoa repens (Permixon) inhibits the 5alpha-reductase activity of human prostate cancer cell lines without interfering with PSA expression. Int J Cancer. 2005 Mar 20;114(2):190-4.

25. Latil A, Pétrissans MT, Rouquet J, Robert G, de la Taille A. Effects of hexanic extract of Serenoa repens (Permixon® 160 mg) on inflammation biomarkers in the treatment of lower urinary tract symptoms related to benign prostatic hyperplasia.

Prostate. 2015 Dec;75(16):1857-67.

26. Ryu YW, Lim SW, Kim JH, Ahn SH, Choi JD. Comparison of tamsulosin plus serenoa repens with tamsulosin in the treatment of benign prostatic hyperplasia in Korean men: 1-year randomized open label study. Urol Int. 2015;94(2):187-93.

27. Sökeland J. Combined sabal and urtica extract compared with finasteride in men with benign prostatic hyperplasia: analysis of prostate volume and therapeutic outcome. BJU Int. 2000 Sep;86(4):439-42.

28. Aliaev IuG, Vinarov AZ, Demidko IuL, Spivak LG. The results of the 10-year study of efficacy and safety of Serenoa repens extract in patients at risk of progression of benign prostatic hyperplasia. Urologiia. 2013 Jul-Aug;(4):32-6.

29. Zhan XX, Shang XJ, Huang YF. Zhonghua. Application of saw palmetto fruit extract in the treatment of prostate diseases. Nan Ke Xue. 2015 Sep;21(9):841-6.

30. Zhou T, Yang Y, Zhang H, et al. Serenoa Repens Induces Growth Arrest, Apoptosis and Inactivation of STAT3 Signaling in Human Glioma Cells. Technol Cancer Res Treat. 2015 Dec;14(6):729-36.

31. Prager N, Bickett K, French N, Marcovici G. A randomized, double-blind, placebocontrolled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment of androgenetic alopecia. J Altern Complement Med. 2002 Apr;8(2):143-52.

32. Chen MY, Yan SC, Yin CP, et al. Red clover isoflavones inhibit the proliferation and promote the apoptosis of benign prostatic hyperplasia stromal cells. Zhonghua Nan Ke Xue. 2010 Jan;16(1):34-9.

33. Slater M, Brown D, Husband A. In the prostatic epithelium, dietary isoflavones from red clover significantly increase estrogen receptor beta and E-cadherin expression but decrease transforming growth factor beta1. Prostate Cancer Prostatic Dis. 2002;5(1):16-21.

34. www.antiaging-systems.com/articles/364-influence-of-peptide-bioregulatorson-morphology-of-parenchymatous-organs

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THE THERAPEUTIC EFFECTS OF HIGH-DOSE MELATONIN ADMINISTRATION

By Jesus A.F. Tresguerres1, M.D, Ph.D.

This article reviews the effects of high-dose melatonin administration on several diseases. Experimental studies performed over more than 20 years have shown that oxidative stress and inflammation increase in nearly all tissues with many degenerative diseases or aging. We have measured several parameters related to oxidative stress, inflammation and apoptosis both in several models of aging and also after ischemia in the liver or brain. The effect of treatment with melatonin has been evaluated showing a significant reduction of inflammation markers (tumor necrosis factor-alpha, interleukin 1 and 10, NFkBp50 and NFkBp52), apoptosis markers (BAD, BAX and Bcl2) and parameters related to oxidative stress, (heme oxygenases 1 and 2, endothelial and inducible nitric oxide synthases) in several tissues. Inflammations, as well as, oxidative stress and apoptosis markers were increased also in degenerative diseases like diabetes, hypertension or Parkinson disease so treatment with melatonin should also have very positive effects.

When the skin is submitted to ionizing radiation like radiotherapy a marked release of free radicals inducing inflammation and oxidative stress is obtained giving rise to radiodermitis. All of the above mentioned parameters have been also shown to be increased in the skin. Melatonin treatment was able to reduce those markers and oxidative stress preventing the appearance of radiodermitis.

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The conclusion is that melatonin administration exerts beneficial effects against age- or degenerative diseases induced changes in several tissues and functions.

Introduction According to the free radical theory of aging, which is one of the most widely accepted, the physiological decline that occurs with age is, at least in part, due to accumulative oxidative damage to cells and molecules. This oxidative damage is induced by reactive oxygen (ROS) and nitrogen (RNS) species, which are highly reactive. ROS have been implicated as major initiators of tissue damage and can up regulate enzyme activity, signal transcription, and gene expression of several compounds that can exert deleterious effects on proteins, lipids and DNA which in turn are responsible of all the age related alterations in the different tissues.

Cellular enzymatic antioxidant defenses which are present in young persons are able by scavenging ROS, to decrease the oxidative damage that could give rise to irreversible damages of structure and functions of cellular macromolecules. Loss of theses defenses with age enhances oxidative damage and has been suggested to contribute importantly to the aging process and to the pathogenesis of many age-related diseases.

Melatonin, an indolic hormone secreted by the pineal gland, is a substance closely related to biological rhythms and has been

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used since decades for the induction of sleep and the treatment of jet lag. In addition to its role as a chronobiotic hormone, melatonin is an ubiquitous direct free radical scavenger and an important indirect antioxidant. Moreover, melatonin is a small, lipophilic and hydrophilic molecule, what allows it to easily cross biological barriers and membranes, and diffuse throughout cell compartments, reaching the place where the free radicals and reactive species are generated in all tissues: the mitochondria.

which reduces the risk of exhaustion of these cells and thus allowing the maintenance or restoration of normoglycemia.

Melatonin and skin – its topical effects Some studies have been performed by our group to investigate also the role of melatonin in the aging skin showing an improvement in several parameters related to oxidative and inflammatory damage in the old skin. (Fig. 1)

Besides to these direct scavenging actions, melatonin stimulates also a host of endogenous antioxidant enzymes, including Superoxide Dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GRd), and inhibits the activity of Nitric oxide synthase (NOS) thus making possible to effectively fight against free radicals but also against inflammation, apoptosis and also in several age associated diseases.

In this paper a review of the effect of high doses of melatonin administration on several diseases related to oxidative injury are reviewed.

Melatonin and Diabetes type 2 Diabetes type 2 appears in the 4th decade of life in persons with a genetic predisposition and that generally show overweight. The first indication of glucose metabolism impairment is the appearance of peripheral insulin resistance.

Pancreas reacts initially with beta cell hypertrophy leading to hyperinsulinemia and thus making it possible to maintain normoglycemia and later on, after some months or years, with beta cells getting exhausted or entering apoptosis with the corresponding reduction in plasma insulin levels and the appearance of hyperglycemia. Aging as well as insulin resistance has been shown to be associated with significant alterations in the expression of pancreatic genes involved in both insulin secretion and glucose metabolism.

Drugs used until now allow the treatment of diabetes as a chronic disease but are not able to cure it. The elements responsible for insulin resistance in peripheral tissues are related with oxidative stress and inflammation and the same occurs in the endocrine pancreas itself. Melatonin when given both to experimental animals (1-10 mg/Kg) that show already insulin resistance and hyperinsulinemia but also to humans (40-60 mg) with increased HOMA index, is able to revert the situation reducing plasma insulin levels and enhancing the islet production of insulin by reducing several inflammation and oxidative stress associated factors present both in the peripheral tissues like muscle or fat tissue such as TNF alpha, NFkB and IL1;2.

The administration of melatonin to experimental animals was able also to increase in pancreas genes of survival like Sirt 1 and FOXO as well as genes of differentiation like PCNA, Pdx and Sei1 and to reduce apoptosis markers restoring its normal function.

These effects have been observed also in humans with insulin resistance in which besides of a reduction in plasma insulin levels a potentiation of the beta cell capacity to produce insulin,

Figure 1: The effect of melatonin treatment for two months on the skin of old rats. When compared with the old control, an increase in epidermal thickness, a restructuration of dermis and a significant reduction of fat content of the hypodermis can be detected.

Radiotherapy is one of the most utilized treatments used in oncology to destroy tumoral cells. It is a local treatment in which only the area with sick cells is irradiated. Radiotherapy is used both as a principal, and as an adjuvant therapy together with other type of treatments such as surgery or chemotherapy, etc.

The biological response to radiation starts with the generation of reactive oxygen species (ROS) This free radical excess released by ionizing radiations induces structural changes and damage in the cells that are sometimes irreversible.

The skin is the first barrier of defense of our organism from the outside and also is a rapid growing tissue. Thus, during radiotherapy, the skin, although not being the primary objective is at the end target of this therapy, since ionizing radiation needs to pass through it to arrive to the tumoral area. Hence, radiotherapy can produce adverse reactions, (radiodermitis) on the skin, during or after the treatment period.

In the majority of patients the effects of radiotherapy on the skin are scarce and transitory but in 20-25% of them, patients show severe reactions that are dependent of several factors that can predispose to radiodermitis: For example, total doses of radiation, doses per session, body area involved, genetic factors etc.

The application of a moisturizing cream with a 0.5% content of melatonin has been shown to very efficiently reduce the incidence of radiodermitis in women submitted to radiotherapy as complementary therapy after the surgical removal of mammary tumors. Normally after 15-20 sessions of radiotherapy

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“The effect of treatment with melatonin has been evaluated showing a significant reduction of inflammation markers, apoptosis markers and parameters related to oxidative stress, in several tissues.” the skin of the mammary gland is burned showing an important affectation. All the more than 30 women treated topically with melatonin showed no significant modifications of the skin.

Treatment of mucositis When patients with several types of cancer are treated with chemotherapy and or radiotherapy, especially in the area of the throat or lungs very often all the mouth pharynx and gastrointestinal tract develops ulcers and inflammation on the mucosa, the so cold mucositis, which is associated with pain and great difficulties in eating. The administration of 1% melatonin in a specially developed gel that is first used for gargling and then swallowed 3 times a day completely prevents or cures the process. In our experience several patients have been treated with very good results. The method has been patented and is in the final steps of approval by the European health authorities.

Treatment of Fibromyalgia The pathogenesis of Fibromyalgia is at this time being unknown and the treatments assayed until now including corticoids, analgesics and opiates have shown no significant responses.

However, the disease affects mainly women in their 4th or 5th life decades and is extremely debilitating. The possibility of the existence of a high level of oxidative stress and inflammation in this disease as indicated by high levels of C reactive protein, TNF alfa and IL1, opened the doors to a melatonin treatment that has shown very interesting results. In our experience, women are treated with doses ranging from 10 to 40 mg every day experience a very significant improvement in less than one month. The treatment needs to be maintained all the time taking also advantage of the sleep inducing properties of the compound. Women that were treated already with opiates could abandon these drugs and were able to reassume a normal life. My experience at this moment is of more than 20 women treated with a 90% rate of success.

Effect of Melatonin on ischemia reperfusion in the liver and brain Ischemia/reperfusion injury of the liver or brain is a complex process involving numerous intracellular signalling pathways, mediators, cells, and pathophysiological disturbances The enhanced expression of these mediators’ leads to a second phase of injury characterized by the induction of secondary mediators that induce an additional damage.

The aging liver has been shown to display an increased susceptibility to Ischemia/Reperfusion (I/R), which may contribute to increased morbidity and postoperative mortality in liver transplantation which involves the maintenance of the 20

donor liver in a protective solution at low temperatures. With increasing age, the capacity of liver cells against I/R damage is reduced due to decreased production of endogenous antioxidants and to a more evident inflammatory response, which might also contribute to the increased susceptibility for tumour growth. Other of the important age-related changes is a decrease in its regenerative capacity. Nevertheless, livers from older subjects have been used successfully for transplantation, although data published on 91 seniors who underwent transplantation at the University of Wisconsin showed poor longterm patient survival after receiving livers from older donors.

In our experimental approach, the expression of proinflammatory cytokines was significantly increased in liver after ischemia and 36 h of reperfusion. Our findings were in accordance with previous studies, in which an increase in proinflammatory cytokines, such as TNF-α, IL-6, IL1β was observed.

In our research, the increased mRNA expressions of IL1β, MCP-1 and INFγ were more evident in older animals after I/R as compared with younger ones.

Treatment with melatonin significantly attenuated the increased level of serum aminotransferase, reduced the severity of hepatic cell damage, diminished steatosis and the immigration of inflammatory cells. Furthermore, melatonin was shown to decrease serum levels and tissue content of inflammatory cytokines (TNFα, IL6, IL1β, and MCP-1), to reduce neutrophil infiltration and to inhibit apoptosis of hepatocytes. Melatonin was able to ameliorate oxidative stress and to inhibit proinflammatory cytokines production and reactive oxygen species, protecting against hepatic damage.

The key mechanism of liver damage after I/R has been identified as increased apoptosis. Our results have shown also that melatonin treatment was able to diminish the expression of proapoptotic genes like Bax, AIF or Bad, together with restoring ATP content. So melatonin administered to donor livers probably could ameliorate the long term survival of patients by reducing the oxidative stress and inflammation and apoptosis induced by ischemia.

Another study from our group has initially developed a valid model for studying cerebral ischemic lesions induced by introducing a nylon catheter in the medial cerebral artery of rats.

The achieved ischemia is associated with a very high release of free radicals shows a high damaging potential that is age dependent, being more important in the older animals.

Ischemic damage after the blockade of the medial cerebral artery determines a lesion that can be detected in the hippocampus and the cerebral cortex, with increases in TNF

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alpha or IL1 as markers of inflammation and with reduction of Bcl2 and the increase of BAX that are showing the increase of apoptosis.

The effect of treatment with melatonin (10 mg/ Kg/ bodyweight/ day) was investigated. A significant reduction in the inflammatory and apoptotic parameters was seen indicating a reduction in the size and intensity of the lesion. This opens the possibility of treatment of stroke with around 100 mg of melatonin.

Melatonin on the heart In old experimental animals we have observed in the heart increased levels on mRNA expression of cytokines such as TNFα, IL-1β (Fig 6), HO-1, iNOS and NFkB together with a decrease in the expression of eNOS and IL-10.

Studies have also reported that oxidative stress can induce apoptosis in cardiac myocytes and that excessive ROS production can cause mitochondrial damage and dysfunction.

All these situations lead to endothelial cell dysfunction in many diseases, such as hypertension with reduced availability of endothelial nitric oxide.

The existence of age-dependent increases in oxidative stress, in heart mitochondria of senescence prone mice has also been observed. Iinflammatory stimuli can induce the expression of iNOS in cardiocytes whereas endothelial NO synthase that is needed for a normal endothelial function is reduced.

Melatonin treatment for one month to 10 month old senescence prone mice exhibited improvements in inflammation and oxidative stress in the heart and was able to counteract the age dependent increased production of pro-inflammatory cytokines, (TNFα, IFNγ) and NO. It has been widely documented that, melatonin exerts its protective effect as a result of its antioxidant scavenging properties, its direct detoxification of free radicals and its ability to preserve efficient oxygen metabolism in mitochondria. These facts support the concept that melatonin exerts profound protective effects against aging, at least, blocking the inflammatory and oxidative processes.

Melatonin can also be used for the prevention of damage induced by ischemia in the heart. (Fig. 2) When given previously in a similar way than in the liver or brain the substance is able to reduce the areas of necrosis after coronary obstruction.

Figure 2: The effect of melatonin treatment on experimental myocardial infarction.

Melatonin and Parkinson disease Parkinson disease appears when the dopamine producing neurons of the basal ganglia from and specially the substantia nigra degenerate, depleting the striatum from dopamine. When the number of surviving dopaminergic neurons arrives at less than 20% of the original number, the disease appears with a combination difficulty to initiate movements, the muscles becoming rigid and showing a characteristic resting tremor.

Untreated these signs gradually worsen rendering the patients at the end totally unable to move voluntarily.

Restoring the dopamine content of the brain by giving the precursor L-dopa that crosses the blood brain barrier is able to significantly ameliorate the disorder by increasing the amount of dopamine in the substantia nigra allowing the increase in the amount of dopamine available at the synapses of the striatum.

L-dopa treatment however does not cure Parkinson disease and in fact the continuous degeneration of the dopaminergic neurons leads to a reduction in the treatments effectivity.

Also although the transplant in the substantia nigra area of dopaminergic neurons obtained from different sources like the carotid body or the adrenal medulla is able to significantly ameliorate the disease, with time ,also the transplanted neurons undergo degeneration and the effect can be abolished.

Degeneration of the dopaminergic neurons is caused finally by increased oxidative stress and inflammation. Treatment with melatonin at doses between 25 mg and 100 mg are able to significantly reduce oxidative stress in the substantia nigra thus blocking neuron death. This treatment needs to be started at the initial steps of the disease since it is not able to reverse the already degenerated neurons. The combined treatment with L-dopa and melatonin reduces the doses needed of the dopamine agonist and blocks the evolution of the disease, by preventing the oxidative stress induced neurone death. The disease remains stable and does not continue its evolution.

Alzheimer disease and melatonin Alzheimer disease is responsible of nearly 70% of cases of dementia. The reason behind involves the degeneration of cortical neurons thin cortical gyri and enlarged ventricles is the hallmark of the disease as observed by NMR. The pathogenesis of the disease involves the presence of Amyloid plaques in the gray matter of neocortex and hippocampus of the brain although it is not clear how the deposition of this protein leads to the degeneration of neurons or ever if this substance is the real causative agent of the disease or is only an inert byproduct of neuronal death. Neurofibrillary tangles are bundles of abnormal filaments inside the pyramidal neurons as well as neuronal cell loss and changes in cellular morphology are also present in the disease.

The storage of new memory is affected very early but at the end also the previously stored memory become impaired. Patients eventually lose interest at there surroundings and become confined to wheelchair or bed. The disease can last 5 to 10 years until the total loss of body functions.

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The central question is why neurons die in Alzheimer disease.

Although several theories have been proposed, including the reduction of several growth factors it is becoming clear that again excitotoxicity leading to oxidative stress is at the end the most likely pathogenic pathway. Taking this into consideration, treatment with melatonin has been considered. The first study was undertaken in Argentina where two identical male twins developed Alzheimer at the same time. Since one was living in Buenos Aires, one had the opportunity of being treated with melatonin whereas the other was not treated. Five years later the non-treated patient died whereas the melatonin treated remained in a mild form of disease. From this moment on, other clinical trials have been carried out in which melatonin treatment was first able to allow a normal sleep patterns in those patients without the sun-downing effect. In addition and specially those patients with a very initial form of the disease showed a slowing down in the evolution of the disease. The doses used have been between 3 mg and 25 mg per day. No secondary effects were observed. Also no side effects were recorded by using 100 mg at bedtime for several years.

Malignant epilepsy Some patients suffer a very severe form of epilepsy that includes high intensity seizures 3 to 6 times a day. In children this is associated with high level of brain damage leading to death in several months. One case of a 3 year old girl was treated with 100 mg of melatonin at bedtime plus 10 mg in the morning for some months obtaining a nearly complete normalization of the electrical activity of the brain and a dramatic amelioration of the clinical situation. (Fig. 3) If the treatment was removed, the original situation appeared again.

Figure 3: The basal EEG registration of a 3 year old girl with malignant epilepsy.

Registration after 2 months of treatment with 100 mg melatonin shows a completely normal electrical activity under treatment.

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References 1. Department of Physiology, School of Medicine, Complutense University, Madrid, Spain.

2. Albarran, MT, S Lopez-Burillo, M I Pablos, R J Reiter, M T Agapito, 2001, Endogenous rhythms of melatonin, total antioxidant status and superoxide dismutase activity in several tissues of chick and their inhibition by light: J Pineal Res, v. 30, p. 227-233.

3. Azcoitia, I., Pérez-Martín, M., Salazar, V., Castillo, C., Ariznavarreta, C.,Garcia-Segura,LM and Tresguerres, J.A.F. “Growth hormone prevents neuronal loss in the aged rat hippocampus”. Neurobiology of Aging 26: 697-703, 2005 4. Benot,S, R Goberna, R J Reiter, S Garcia-Maurino, C Osuna, J M Guerrero, 1999, Physiological levels of melatonin contribute to the antioxidant capacity of human serum: J.Pineal Res., v. 27, p. 59-64.

5. Cagnoli, CM, C Atabay, E Kharlamova, H Manev, 1995, Melatonin protects neurons from singlet oxygeninduced apoptosis: J Pineal Res, v. 18, p. 222-226.

6. Cardinali DP1, Furio AM, Brusco LI. The use of chronobiotics in the resynchronization of the sleep/wake cycle. Therapeutical application in the early phases of Alzheimer’s disease. Recent Pat Endocr Metab Immune Drug Discov. 2011 May;5(2):80-90.

7. Castillo C, Salazar V, Ariznavarreta C, et al. Effect of melatonin administration on parameters related to oxidative damage in hepatocytes isolated from old Wistar rats. J. Pineal Res 2005; 38:240-246 8. Cheung,RT, 2003, The utility of melatonin in reducing cerebral damage resulting from ischemia and reperfusion: J.Pineal Res., v. 34, p. 153-160.

9. FitzGerald, Bishop M, Tillman G, Aronowitz J, Pieters R, Balducci S et al. Radiation therapy toxicity to the skin.

Dermatol Clin 2008;26: 161-72 10. Fisher TW, Slominski A, Zmijewski MA, Reiter RJ, Paus R. Melatonin as a major skin protectant: from free radical scaveniging to DNA damage repair. Exp Dermatol 2008; 17:713-30 11. Fischer TW, Zmijewski MA, Worstman J, Slominski A. Melatonin mantains mitocondrial membrane potential and attenuates activation of initiator (caspasa 9) and effector caspases (casp-3/casp-7) and PARP in UVR-exposed HaCaT keratinocytes. J Pineal Res 2008; 44:397-407 12. Fischer TW, ELsner P. Melatonin: a hormone, drug or cosmeceutical. In: Elsner P, Maibach H leds.

Cosmeceuticals and Active Cosmetics, Vol 1. Boca Raton: Taylor&Fancis, 2005:413-19 13. Fischer TW, Greif C, Fluhr JW, Wigger-Alberti W, Elsner P. Percutáneous penetration of topically applied melatonin in a cream and an alcoholic solution. Skin Pharmacol Physiol 2004;17:190-94 14. Hymes S, Strom E, Fife C. Radiation dermatitis: clinical presentation, pathophysiology, and treatment. J Am Acad Dermatol 2006; 54:28-46 15. Ianas,O, R Olinescu, I Badescu, 1991, Melatonin involvement in oxidative processes: Endocrinologie, v. 29, p. 147-153.

16. Kireev RA, Tresguerres ACF, Castillo C, Salazar V, Ariznavarreta C, Vara E, and Tresguerres JAF 17. “Effect of exogenous administration of melatonin and GH on prooxidant functions of the liver in aging male rats 18. J. Pineal Research 42;64-70 (2007) 19. Ling,X, L M Zhang, S D Lu, X J Li, F Y Sun, 1999, Protective effect of melatonin on injuried cerebral neurons is associated with bcl-2 protein over-expression: Zhongguo Yao Li Xue.Bao., v. 20, p. 409-414.

20. Magri,F, S Sarra, W Cinchetti, V Guazzoni, M Fioravanti, L Cravello, E Ferrari, 2004, Qualitative and quantitative changes of melatonin levels in physiological and pathological aging and in centenarians: J.Pineal Res., v. 36, p. 256-261.

21. Manev,H, T Uz, A Kharlamov, J Y Joo, 1996, Increased brain damage after stroke or excitotoxic seizures in melatonin-deficient rats: Faseb Journal, v. 10, p. 1546-1551.

22. Matsubara E, Bryant-Thomas T, Pacheco Quinto J, Henry TL, Poeggeler B, Herbert D, Cruz-Sanchez F, Chyan YJ, Smith MA, Perry G, Shoji M, Abe K, Leone A, Grundke-Ikbal I, Wilson GL, Ghiso J, Williams C, Refolo LM, Pappolla MA, Chain DG, Neria E. Melatonin increases survival and inhibits oxidative and amyloid pathology in a transgenic model of Alzheimer’s disease. Neurochem. 2003; 85:1101-1108.

23. Melchiorri,D, R J Reiter, E Sewerynek, L D Chen, G Nistico, 1995, Melatonin reduces kainate-induced lipid peroxidation in homogenates of different brain regions: FASEB J, v. 9, p. 1205-1210.

24. Mordenti Jy Chappel W The use of interespecies scaling in toxicokinetics en (Yacobi ,Kelly y Batra V)eds Toxicokinetics and new drug development 25. Pergamon press New York 1989 pp42-96 26. Reiter,RJ, 1998, Oxidative damage in the central nervous system: protection by melatonin: Prog.Neurobiol., v. 56, p. 359-384.

27. Reiter,RJ, 2003, Melatonin: clinical relevance: Best.Pract.Res.Clin.Endocrinol.Metab, v. 17, p. 273-285.

28. Reiter,RJ, D X Tan, S Burkhardt, 2002, Reactive oxygen and nitrogen species and cellular and organismal decline: amelioration with melatonin: Mech.Ageing Dev., v. 123, p. 1007-1019.

29. Sastre,J, F V Pallardo, J Vina, 2000, Mitochondrial oxidative stress plays a key role in aging and apoptosis: IUBMB.Life, v. 49, p. 427-435.

30. Shirazi A, Ghobadi G and Ghazi-Khansari M. A radiobiological Review on Melatonin: a novel radioprotector. J. Radiat. Res. 2007; 48:2063-72 31. Tan,D, L Chen, B Poeggeler, L Manchester, R Reiter, 1993, Melatonin: a potent, endogenous hydroxyl radical scavenger: Endocr.J, v. 1, p. 60-87.

32. Tan DX, Manchester LC, Terron MP, Flores LJ, Reiter RJ. One molecule, many derivatives: a never-ending interaction of melatonin with reactive oxygen and nitrogen species. J Pineal Res 2007; 42:28-42 33. Tresguerres JAF, Kireev R, Tresguerres ACF, Borras C Vara E , y Ariznavarreta C Mecanismos moleculares del envejecimiento y su prevencion mediante tratamiento hormonal en ratas.

34. Tricoire,H, A Locatelli, P Chemineau, B Malpaux, 2002, Melatonin enters the cerebrospinal fluid through the pineal recess: Endocrinology, v. 143, p. 84-90.

35. Witt-Enderby PA, Bennett J, Jarzynka MJ, Firestine S, Melan MA. Melatonin receptors and their regulation: biochemical and structural mechanisms. Life Sci. 2003; 72: 2183-2198.

36. Wakatsuki, A. Y Okatani, K Shinohara, N Ikenoue, C Kaneda, T Fukaya, 2001, Melatonin protects fetal rat brain against oxidative mitochondrial damage: J Pineal Res, v. 30, p. 22-28.

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DEPRENYL AND ALZHEIMER’S DISEASE UPDATE

By Ward Dean, M.D.

Deprenyl (aka seligiline, trade names Eldepryl®, Jumex®) was discovered in Hungary in the 1950s and was patented by Professor Jozsef Knoll of Semmelweis University in Hungary in 1962. Deprenyl was shown to extend maximum lifespan in animals, enhance cognition in normal healthy animals, reduce the symptoms and delay the progress of Parkinson’s and Alzheimer’s disease and act as an aphrodisiac and performance-enhancer in male animals and men.

In our book, Smart Drugs II, the Next Generation (1993), based on a number of positive studies, we wrote that deprenyl appeared to be a powerful weapon against Alzheimer’s disease.1 At about that same time, Professor Knoll recommended that; “Alzheimer’s disease patients need to be treated daily with 10 mg deprenyl from diagnosis until death.”2 Curiously, research on selegiline peaked ten years after the publication of our book and plummeted thereafter. What happened, I wondered, to the interest in what I still believe to be an effective antiaging, cognitive-enhancing substance?

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Cochrane Review Meta-Analyses Slams Deprenyl’s Value as Alzheimer’s Drug From 2000-2003, a series of articles critically reviewed deprenyl’s efficacy in Alzheimer’s disease—two in Cochrane Reviews,3,4 and one in International Journal of Geriatric Psychiatry.5 Cochrane Reviews is considered the “gold Standard” for “meta analyses,” in which the authors critically analyze a number of double-blind controlled studies to arrive at a consensus of “evidence-based medicine.” All three of these meta-analyses relied on the same

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Figure 1: Time-line of selegiline studies.19 Note the dramatic drop in annual studies following the publication of the disparaging meta-analyses.

statistician, reviewed essentially the same studies and arrived at progressively more negative conclusions in each review.

The first Cochrane Review conceded that of the 17 trials considered, 14 trials reported beneficial effects of deprenyl in the treatment of cognitive deficits, and 3 reported improvements in behavior and mood. Pooled data for all cognitive tests suggested significant benefits with deprenyl compared to controls. Two years later, a follow-up report by the same statistician (Birks)--but with different co-authors—again reported that overall, the studies indicated that deprenyl-users demonstrated improved cognition at 4-6 and 8-17 weeks. But the following year in 2003, the authors of the first Cochrane Review issued a blisteringly negative third meta-analysis.5 In this third review, the authors again positively reported that; “the meta-analysis revealed benefits on memory function shown by improvement from several cognitive tests,”6-18 and “The combined memory tests, and overall combined cognitive tests…showed an improvement due to deprenyl compared with placebo at 4-6 weeks and 8-17 weeks.” [Emphasis added] In addition, in “several studies [which] assessed activities of daily living using several different scales,6,9,11,12,14,15 “the combined tests showed an improvement due to deprenyl at 4-6 weeks.”5 Inexplicably, the reviewers then concluded paradoxically and without apparent justification that “Despite its initial promise, i.e. the potential neuroprotective properties, and its role in the treatment of Parkinson’s disease, deprenyl for Alzheimer’s disease has proved disappointing. There would seem to be no justification, therefore, to use it in the treatment of people with Alzheimer’s disease, nor for any further studies of its efficacy in Alzheimer’s disease.”5 With that disparaging conclusion, further research into the use of deprenyl for Alzheimer’s use ground to a screeching halt (Fig. 1). Another understandable reason for the fall-off in published studies about deprenyl is that brand-name protection for Eldepryl® (selegiline) in the U.S. had ended, and there was little likelihood for pharmaceutical-sponsorship of further trials.

Analysis of the Meta-Analyses--Review of the Reviewers I was thunder-struck by the negative conclusions reached by the Cochrane Reviewers, which seemed to fly in the face of the

positive clinical studies that we had reviewed in SDII—and, for that matter, which were included in the Cochrane Reviews.

Admittedly, Alzheimer’s disease is a chronic debilitating disease, that results in progressive death of brain cells, for which there is no known definitive cure. Deprenyl is not the “silver bullet” for Alzheimer’s disease that we all hope for—but it has been shown to delay neurodegeneration, and restore the catecholamine balance in brains altered by Alzheimer’s disease. Certainly, any treatment that slows or reverses this debilitating disease to any degree, with minimal or no adverse side effects, is a welcome addition to our therapeutic armamentarium.

I re-examined the 17 studies in the meta-analysis, as well as the studies which were specifically not included--as well as a major study that had not previously been considered (but which should have been)—to determine the credibility of the metaanalyses.

Of the papers included in the reviews, most reported positive results to varying degrees. Unless otherwise noted, the studies were all double-blind, placebo-controlled trials with Alzheimer’s patients, using 5 mg deprenyl twice daily. Here, in summary, are the outcomes of the positive studies I could find (several were obscure and unavailable): • Twenty patients diagnosed between stages 3 and 5 of primary degenerative dementia were treated for 90 days with deprenyl or placebo. Subjects in the deprenyl group demonstrated improvement in both attention and memory measures.6 • Ten patients were given either a placebo or deprenyl for two months, resulting in improved memory, attention, and language abilities among those who received the drug, while those on placebo showed worsened cognitive efficiency and reduction of parietal lobe cerebral blood flow.7 • One hundred seventy-three nursing-home residents with mild to moderate Alzheimer’s disease were treated with deprenyl or placebo for 24 weeks, resulting in improved cognitive and behavioral functions.9 • In a 14-week study of deprenyl or placebo in twenty-five outpatients, there was a significant benefit of deprenyl treatment on the Brief Psychiatric Rating Scale (BPRS), the Dementia Mood Assessment Scale (DMAS), and in cognitive function on the Alzheimer’s Disease Assessment Scale-Cognitive

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(ADAS-COG) with deprenyl compared to placebo. The authors concluded that “short-term selegiline treatment produced an improvement in behavior and cognition.”10 • In one hundred nineteen patients treated with deprenyl or placebo for 3 months, deprenyl significantly improved the activities of daily living, dementia symptoms and many cognitive functions including memory, attention and visuospatial ability, and was reported to be … “a useful and reliable tool … to improve cognitive functions and reduce behavioral alterations, without frequent or severe side effects.” 12 • Six months’ treatment of deprenyl vs placebo in 20 patients showed significant positive effects of deprenyl on memory and attention.13 • Of 341 patients treated with deprenyl (10 mg a day), alphatocopherol (vitamin E, 2000 IU/day), both deprenyl and alphatocopherol, or placebo for two years, “treatment with selegiline or Vitamin E slows the progression of Alzheimer’s disease.”14 • Sixty-seven patients were given deprenyl or placebo, and were evaluated every six months with the mini–mental state examination (MMSE). The deprenyl group deteriorated significantly less than the placebo group.18 • Nineteen patients were treated with deprenyl or placebo for six months. The deprenyl -treated patients showed significantly better performances in learning, long-term memory skills, cognitive functions and behavior. The researchers concluded that; “Deprenyl represents an effective treatment for memory disorders in Alzheimer’s disease.”20 • Deprenyl (10 mg/day) or placebo given to 12 patients resulted in clear positive trends in favor of selegiline on several dementia rating scales.21 Thus, at least 10 of the 17 studies showed apparent benefit from deprenyl in Alzheimer’s patients. Although 5 studies did not find any benefit from deprenyl, there were no adverse effects.

Deprenyl Studies excluded from the Meta-Analysis The Cochrane Review authors also considered but excluded an additional 16 studies, for various reasons. Of these studies which reported positive results: • Seventeen Alzheimer’s patients received deprenyl in doses of 10 mg or 40 mg per day. Total Brief Psychiatric Rating Scale (BPRS) scores improved significantly on the 10 mg dose, and measures of anxiety/depression, tension, and excitement decreased. Approximately half of the patients’ conditions improved clinically, with increased activity and social interaction, along with reduced tension and retardation. The behavioral changes were associated with improvement in performance on a complex cognitive task requiring sustained effort.

Unexpectedly, these improvements were not seen with 40 mg.22 Similarly, improvement occurred in episodic memory and complex learning tasks requiring information processing and

sustained conscious effort with deprenyl 10 mg/day, but not with 40 mg.23 • Eleven elderly female patients—7 with Alzheimer’s and 4 with multi-infarct dementia -- were treated with deprenyl.

Improvement was most notable in the Alzheimer’s patients-especially regarding self-care, short term memory, and mental alertness.24 • Twenty-eight patients treated for three-months with deprenyl or placebo resulted in a global improvement of cognitive performances in the deprenyl group compared to placebo.25 • Five patients with behavior problems, ranging in age from 50 to 82, were treated with deprenyl for 8 weeks. The authors reported; “Clinical significance was noted by improvement in cognition,” and “Alzheimer’s patients with behavior problems may benefit from selegiline therapy.”26 • A 4-week study of fourteen patients treated with deprenyl demonstrated significant improvements on the agitation and depression factors of the BPRS, the Cornell Scale for Depression in Dementia, and spouses’ blind rating (SBR). Recall improved on the Buschke Selective Reminding Task. Overall, the authors concluded that; “selegiline may be associated with improvement in behavioral and cognitive performance.”27 • Twenty-two patients (14 men, 8 women) mean age 62.8, in a double-blind cross-over study for 26 weeks, showed that deprenyl possesses significant beneficial activity on memory parameters, with an improvement both in information processing abilities and in learning strategies.28 Comparisons and Combination Therapy-- Deprenyl vs (or combined with) other Cognitive Enhancers • Oxiracetam, (a nootropic drug similar to piracetam) was tested against deprenyl in a trial involving 22 men and 18 women.

Deprenyl was given to one group and 800 mg oxiracetam per day was given to the other group. Deprenyl was more effective than oxiracetam in improving higher cognitive functions and reducing impairment in daily living. Deprenyl helped more with short­and long-term memory, sustained concentration, attention, verbal fluency, and visuospatial abilities.28 • In another 3-month study, deprenyl was compared to phosphatidylserine (100 mg twice daily) in forty patients (24 men and 16 women). For most measures of cognition, “the selegiline group showed improvements superior to those obtained in the phosphatidylserine group.”29 • Deprenyl was also compared to acetyl-L-carnitine (ALC) (500 mg twice daily) in forty patients (13 men, 27 women, 56 to 80 years). ALC and deprenyl both led to global improvements in the capacity to process, store and retrieve given information, as well as improvements in verbal fluency and visuospatial abilities.

However, the degree of improvement was even more effective with deprenyl than ALC.30

“Since Alzheimer’s disease is believed to be a byproduct of “normal” brain aging, our best hope to significantly decrease its prevalence is... by administering a protective substance like deprenyl.”

26

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• Deprenyl added to the regimen of 10 patients receiving either Tacrine® or physostigmine was assessed in a 4-week pilot study.

Deprenyl was associated with significant improvement in scores on the cognitive subscale of the Alzheimer’s Disease Assessment Scale (ADAS), suggesting additive effects of deprenyl to the effects of cholinesterase inhibitors.31

References

Largest, Most Positive Study Ignored by Meta-Analyzers

5. Birks J, Flicker L. Selegiline for Alzheimer’s disease. Cochrane Database Syst Rev. 2003;(1):CD000442.

• One large study that was not evaluated by the Cochrane Reviewers was conducted by scientists from the University of Catania in Italy. Two hundred outpatients over 65 were treated with deprenyl or placebo for 120 days. The physicians conducting the test and the patients themselves agreed that deprenyl treatment was beneficial. The 17-item scale of clinical assessment for geriatrics (SCAG) was used to determine efficacy. One element of the SCAG was the Short Term Memory scale, which indicated dramatic improvement in the deprenyl users (Fig. 2). When deprenyl treatment was suspended, the improved cognitive functions began to deteriorate.32 16

1. Dean W, Morgenthaler J, Fowkes SW. Smart Drugs II, the Next Generation. Smart Publications, Petaluma 1993.

2. Knoll J. (-)Selegiline-medication: A strategy to modulate the age-related decline of the sriatal dopaminergic system. J Am Geriatr Soc 40(8): 839-47, August 1992.

3. Birks J, Flicker L. Selegiline for Alzheimer’s disease. Cochrane Database Syst Rev. 2000;(2):CD000442.

4. Wilcock GK, Birks J, Whitehead A, Evans SJ. The effect of selegiline in the treatment of people with Alzheimer’s disease: a meta-analysis of published trials. Int J Geriatr Psychiatry. 2002 Feb;17(2):175-83.

6. Agnoli, A, Martucci, N, Fabbrini, G, et al., Monoamine oxidase and dementia: Treatment with an inhibitor of MAO-B activity, Dementia. 1990, 1:109-114.

7. Agnoli A, Fabbrini G, Fioravanti M, Martucci N. CBF and cognitive evaluation of Alzheimer type patients before and after IMAO-B treatment: a pilot study. Eur Neuropsychopharmacol. 1992 Mar;2(1):31-5.

8. Sunderland T, Molchan S, Lawlor B, Martinez R, Mellow A, Martinson H, Putnam K, Lalonde F. A strategy of “combination chemotherapy” in Alzheimer’s disease: rationale and preliminary results with physostigmine plus selegiline. Int Psychogeriatr. 1992;4 Suppl 2:291-309.

9. Filip V, Kolibás E. Selegiline in the treatment of Alzheimer’s disease: a long-term randomized placebocontrolled trial. Czech and Slovak Senile Dementia of Alzheimer Type Study Group. J Psychiatry Neurosci.

1999 May;24(3):234-43.

10. Lawlor BA, Aisen PS, Green C, Fine E, Schmeïdler J. Selegiline in the treatment of behavioral disturbance in Alzheimer’s disease. Int J Geriatr Psychiatry. 1997 Mar;12(3):319-22.

11. Loeb C, Albano C. Selegiline - A new approach to DAT treatment. Proceedings of the European Conference on Parkinson’s Disease and Extrapyramidal Disorders; 1990 Jul 10-14, Rome. 1990. http://www. psych.org/clin_res/pg_dementia_8.html.

12. Mangoni A, Grassi MP, Frattola L, Piolti R, Bassi S, Motta A,·Marcone A and Smime 1. S. Effects of a MAO-B inhibitor in the treatment of Alzheimer ‘s disease. Eur Neurol (Switzerland) 31(2): 100-7, 1991.

13. Piccinin GL, Finali G and Piccirilli M. Neuropsychological effects of L-selegiline in Alzheimer’s type dementia. C/in Neuropharmacol 13(2): 147-63, April 1990.

Deprenyl Placebo

12

14. Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, Woodbury P, Growdon J, Cotman CW, Pfeiffer E, Schneider LS, Thal LJ. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer’s disease. The Alzheimer’s Disease Cooperative Study. N Engl J Med. 1997 Apr 24;336(17):121622.

10

15. Tariot PN, Goldstein B, Podgorski CA, Cox C, Frambes N. Short-term administration of selegiline for mildto-moderate dementia of the Alzheimer’s type. Am J Geriatr Psychiatry. 1998 Spring;6(2):145-54.

14

8

16. Freedman M, Rewilak D, Xerri T, Cohen S, Gordon AS, Shandling M, Logan AG. Selegiline in Alzheimer’s disease: cognitive and behavioral effects. Neurology. 1998 Mar;50(3):660-8.

6

17. Burke WJ, Roccaforte WH, Wengel SP, Bayer BL, Ranno AE, Willcockson NK. Selegiline in the treatment of mild dementia of the Alzheimer type: results of a 15-month trial. J Am Geriatr Soc. 1993 Nov;41(11):1219-25.

4

18. Riekkinen, PJ, Koivisto, K, Helkala, EL, et al. (1994), Long-term, double-blind trial of selegiline in Alzheimer’s disease, Neurobiology of Aging, 15 (Suppl 1): S67.

2

19. Figure adapted from data obtained at: http://www.ncbi.nlm.nih.gov/pubmed/?term=selegiline

0 -2

20. Finali G, Piccirilli M, Oliani C and Piccinin GL. L-selegiline therapy improves verbal memory in amnesic Alzheimer patients. Clin Neuropharmacol (USA) 14(6): 523-36, 1991.

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21. Heinonen EH, Savijärvi M, Kotila M, Hajba A, Scheinin M. Effects of monoamine oxidase inhibition by selegiline on concentrations of noradrenaline and monoamine metabolites in CSF of patients with Alzheimer’s disease. J Neural Transm Park Dis Dement Sect. 1993;5(3):193-202.

Figure 2: Improvement in SCAG short term memory scale with deprenyl (solid line) compared to placebo (broken line).32

22. Tariot PN, Cohen, RM, Sunderland, T, et al. L-Selegiline in Alzheimer’s disease: Preliminary evidence for behavioral change with monoamine oxidase B inhibition. Archives of General Psychiatry 44: 427-33, May 1987.

Conclusion

23. Tariot PN, Sunderland T, Weingartner H, Murphy DL, Welkowitz JA, Thompson K, Cohen RM. Cognitive effects of Selegiline in Alzheimer’s disease. Psychopharmacology (Berl). 1987;91(4):489-95.

Unfortunately, Alzheimer’s Disease is presently an incurable neurodegenerative disease. Although a number of treatments are used to minimize or improve the symptoms, there is no proven treatment to reverse its downward course. By the time the diagnosis is made, the patients are usually past complete recovery, since the neuropathological changes in the affected neurons are on an irreversible downward path.

Since Alzheimer’s disease is believed to be a byproduct of “normal” brain aging, our best hope to significantly decrease its prevalence is to slow the natural aging of the threatened neurons by administering a protective substance like deprenyl.

Although deprenyl does not alter the landmark pathological changes of Alzheimer’s once they have become manifest (such as neurofibrillary tangles, amyloid beta or abnormal tau proteins), it has demonstrated over and over via multiple mechanisms that it can slow the progression of Alzheimer’s disease, and in many cases enhance cognitive and behavioral indices of the disease. Therefore, the optimum time to use selegiline is before the disease presents.

24. Martini E, Pataky I, Szilágyi K, Venter V. Brief information on an early phase-II study with selegiline in demented patients. Pharmacopsychiatry. 1987 Nov;20(6):256-7.

25. Martignoni E, Bono G, Blandini F, Sinforiani E, Merlo P, Nappi G. Monoamines and related metabolite levels in the cerebrospinal fluid of patients with dementia of Alzheimer type. Influence of treatment with Selegiline. J Neural Transm Park Dis Dement Sect. 1991;3(1):15-25.

26. Goad DL, Davis CM, Liem P, Fuselier CC, McCormack JR and Olsen KM. The use of selegiline in Alzheimer’s patients with behavior problems. J Clin Psychiatry 52(8): 342-5, August 1991.

27. Schneider LS, Pollock VE, Zemansky MF, Gleason RP, Palmer R and Sloane RB. A pilot study of low-dose L-selegiline in Alzheimer’s disease. J Geriatr Psychiatry Neurol. 1991 (USA) 4(3): 143-8.

28. Falsaperla A, Monici Preti PA and Oliani C. Selegiline versus oxiracetam in patients with Alzheimer-type dementia. Clin Ther 12(5): 376-84, Sep-Oct 1990.

29. Monteverde A, Gnemmi P, Rossi F, Monteverde A and Finali GC. Selegiline in the treatment of mild to moderate Alzheimer-type dementia. Clin Ther 12(4): 315-22, Jul-Aug 1990.

30. Campi, N, Todeschini, GP, Scarzella, L (1990), ‘Selegiline versus L-acetylcarnitine in the treatment of Alzheimer-type dementia’, Clinical Therapeutics, 12:306-314.

31. Schneider LS, Olin JT, Pawluczyk S. A double-blind crossover pilot study of selegiline (selegiline) combined with cholinesterase inhibitor in Alzheimer’s disease. Am J Psychiatry. 1993 Feb;150(2):321-3.

32. Raffaele R, Rampello L, Veccio I, Giammona G, Malaguarnera M, Nicoletti G, Ruggieri M, and Nicoletti F. The use of selegiline in the treatment of cognitive deficits in elderly patients. Arch Gerontol Geriatr. Suppl.

8 (2002) 319-326.

“...the optimum time to use selegiline is before the disease presents.“

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DEPRENYL Protecting You From Mental Decline Deprenyl has been shown to dramatically boost dopamine levels protecting the brain from the effects of dopamine decline and maintaining youthful cognitive functions.

DepPro™ 20ml 300mg bottle liquid $79.99 (save $5.00 over regular price of $84.99) DepTabs™ 50x 5mg tablets $29.99 (when purchased at 2 or more packs - save $5.00 over regular price of $34.99) Offer valid until 30th June 2016. *Restrictions may apply in some countries. All information is educational and does not replace your physician’s advice and is subject to IAS terms and conditions which may change without notice.

SPOTLIGHT: BIOCLIP ® CUFF MONITOR ING YOU R VA SCU L AR CONDITION The BioClip® Cuff is a simple way of assessing both your blood pressure condition and your arterial flexibility; plus, you can use the BioClip® Cuff in the comfort of your own home because you simply attach the device to your arm just like an ordinary blood pressure cuff.

What does the BioClip® Cuff measure?

The BioClip® Cuff provides a series of metabolic indicators that you can use to improve your lifestyle and so help to prevent the causes of cardiovascular disease. We all know the risks of being overweight, of having high cholesterol or suffering from high blood pressure. We also know how to reduce those risks – by exercising more, not smoking, reducing our alcohol intake and eating a balanced diet.

These include: • Diastolic blood pressure • Systolic blood pressure • The heart rate • Vascular condition – which linked to arterial flexibility.

Few of us know about the hidden dangers of arterial inflexibility, or how to measure it. This is where the BioClip® Cuff is unique being as it is the first at-home device able of delivering this information to you within minutes.

What is arterial flexibility?

The BioClip® Cuff works by evaluating your arterial flexibility, which experts say is one of the most important

Above: The BioClip® Cuff readout, showing both blood pressure, heart rate and vascular flexibility results.

risk factors when it comes to assessing the likelihood of a heart attack or stroke. Arteries are important because they’re responsible for blood flow around your body via your cardiovascular system. To work properly, it’s crucial that your arteries are kept healthy.

The poorer your vascular condition, the greater your chances of serious health issues Our arteries usually stiffen with advancing age. This brings with it a greater risk of a potentially fatal heart attack, heart failure or stroke, as is shown in figure 1.

You may not recognise the heart failure symptoms as your arteries begin to stiffen Unfortunately arterial stiffness can occur without warning.

Often there are no symptoms of cardiovascular disease and

people don’t suspect they are in danger until they suffer an attack. Figure 2 highlights that arterial stiffness is strongly correlated with mortality The BioClip® Cuff provides a cardiovascular condition scale, shown by LED bars - that are either within the green zone (good), yellow zone (fair) or red zone (poor).

It is important to note that like blood pressure, vascular condition should be monitored over time and not just taken as one reading. The BioClip® Cuff makes this simple by averaging your tests over time and therefore provides a more accurate result.

BioClip® Cuff provides reassurance and a vital early warning system that helps you to be aware of changes and therefore keep your vascular condition in check.

Left: Arterial stiffness is a biomarker of aging, as shown here arterial stiffness tends to increase with age.

Source: Millasseau et al., Clinical Science, 2002.

The BioClip® Cuff is easy to use The BioClip® Cuff doesn’t puncture your skin and is used on its own, without any additional attachments. The procedure is straightforward and you don’t need to link to a computer, as the results are shown on the BioClip® Cuff screen. Note: If you want to see it in action there is a video available at the IAS website.

Armed with this information it’s easy to keep a check on your cardiovascular health and the risks associated with arterial stiffness, such as heart attacks and strokes. Armed with this information it is possible to make changes to your lifestyle and supplement program to improve results and keep you biologically younger!

Above all, the BioClip® Cuff provides reassurance and a vital early warning system that helps you to be aware of changes and therefore keep your vascular condition in check.

Left: Three groups (each approximately 80 persons) were monitored over 140 months for their survivability. Those in the flexible artery groups (marked as PWV <9.4 m/s and 9.4-12.0 m/s) survive best losing approx. 25%. But those in the hard artery group (marked as PWV >12.0 m/s) 90% of them die in the same period. Source: ESRD, Blacher et al. Journal of Circulation, 1999 www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

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SPOTLIGHT: BIOIDENTICAL HORMONES NATU R AL ESTROG EN S AND PROG ESTERONE FOR WOMEN IAS carries a wide range of bioidentical hormones - a term that means ‘natural to and in the body’. In this featured section we are focusing on the use of natural estrogens and progesterone for women, which of course are normally utilised to aid the menopause.

When hormone replacement therapy (HRT) was developed in the 1920s, estrogens had to be derived from horse urine because a laboratory solution was too difficult/ expensive to synthesize. But today everything has changed, yet this ancient practice continues- these facts have been pointed out by Dr. Wright in his best-selling book ‘Stay Young & Sexy’ Horse estrogens are, as you might expect, not identical to human; after all humans don’t have manes nor do they have hooves! Yet the industry is stuck in this old loop, despite the fact that natural (bioidentical) estrogens can be easily produced now. Some people believe that the known side-effects from ‘traditional HRT’ are due to the fact that the hormones given are not correct.

Above: Stay Young & Sexy

By Dr. Wright

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Esnatri™, a unique tri-estrogen Esnatri™ is our bioidentical triple estrogen cream, which many women use, confident they have chosen the best bioidentical estrogen cream available.

It comes directly from the work of Dr. Wright who has shown that the majority of women produce estrogens in the ratios of 90% estriol, 7% estrone and 3% estrone.

Above: As Dr. Wright himself has said many times; “we only have to copy nature, the right molecules at the right times and doses.”

Most tri-estrogen preparations attempt to replicate the human hormones estriol, estradiol and estrone, apply them in the ratio of 80:10:10, while some even entirely over-look estriol, claiming

it is a weak estrogen. But, women naturally produce high levels of estriol and it is considered to have anticarcinogenic effects.

Esnatri™ use The Esnatri™ cream can be applied by daily rotation to your neck, upper chest, breasts and behind the knees, or inner thighs. A typical starting dose is 2 mg, start from day one (of what would have been the start of your menstrual cycle) and continue until day 25.

Then you should stop for five days, before repeating the application at the start of the next menstrual cycle. During these last few days, the estrogen receptors are being allowed to ‘rest’ as they have been accustomed.

Progesterone Progesterone is the counterbalance to estrogens. Indeed, whilst women can significantly decline in estrogen levels during menopausethey rarely reach zero production levels, whereas progesterone

can sometimes not be measured at all in elderly women.

It is also the low of progesterone that most significantly impacts bone strength, leading onto osteoporosis, so there are numerous reasons to ensure that progesterone is also taken alongside an estrogen therapy.

IAS provides a 5% strength natural progesterone cream.

Typical doses are 25 mg to 30 mg of progesterone applied on day 10 and continuing to 25. The start date varies according to the usual timing of your ovulation. Note: As with the Esnatri™ cream, stop for the last five days of your cycle so that the estrogen receptors have their accustomed ‘rest’ period.

Remember, your hormone replacement therapy should be overseen by a physician and should not be undertaken if you have undergone cancer treatment.

“Esnatri™ is our bioidentical triple estrogen cream, which many women use, confident they have chosen the best...”

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SPOTLIGHT: BIOIDENTICAL HORMONES OX Y TOCIN FOR PA SS ION AND S E X IAS carries a wide range of bioidentical hormones - a term that means ‘natural to and in the body’. In this featured section we are focusing on oxytocin.

What is oxytocin?

Oxytocin is a hormone produced by the hypothalamus, but excreted via the pituitary gland. Its orthodox medicine role is to help women give birth, since the large dose that’s injected helps relaxes the uterus and alleviates the passage of the child into the world for the mother.

Above: Dr. Thierry Hertoghe

However, as we will discover and has been highlighted by Dr. Thierry Hertoghe’s book; ‘passion, sex and longevity, the oxytocin adventure’ -it has many other roles to play too.

The love hormone Oxytocin has been dubbed ‘the love hormone’, why would this be? Principally because oxytocin can induce feelings of bonding and care and not just

between individuals, but even with animals too!

Oxytocin measurements have been taken between lovers, friends, relatives, parents and their children etc. From those results, it has been noted that oxytocin levels are higher when they are in their presence. Mothers naturally bond with their children, but even men, (especially those who experience the live birth), express their emotions as wanting to care and protect their offspring, these effects may be attributable to the release of oxytocin hence triggering the bond. On the other side of the coin, psychopaths are notoriously low in their oxytocin levels, which may be a cause of their uncaring feelings towards other humans.

The pain and orgasm connection Fibromyalgia can be a very debilitating disorder with a lot of pain, sometimes constant for those who suffer with it. In women it was noted that when they were experiencing an orgasm they felt no pain

at all. Later, it transpired that women undergo a burst of oxytocin during orgasm. Trials were undertaken to see if oxytocin supplementation could alleviate the pain of fibromyalgia, there was some success, but the side-effect noted was that those women now enjoyed multiple orgasms! This was a fact picked up on by the popular press and is probably singularly the action most responsible for bringing oxytocin into the public gaze.

Synergy Dr. Hertoghe has explained that some folks will not feel the effects of oxytocin. This is principally because of two reasons, (if we consider that the dose is correct for that individual). Firstly, that some people are ‘low’ in their own principal sexhormone, so if a man is low testosterone, or if a woman is low estrogen, it is possible that oxytocin will not elicit its full potential in those persons.

The other issue could be low vasopressin; vasopressin is a counterpart

to oxytocin, produced and released via the same glands. In cases of vasopressin deficiency, the patient may enhance the oxytocin experience by adding one or two sprays (10 IU each) of vasopressin via the Vaso-Pro™ nasal spray.

Dosing As might be expected doses are very dependent upon its use. However for social or sexual enhancement, one can consider 5 IU to 10 IU a ‘typical’ dose. In fact, Dr. Hertoghe has somewhat reduced the doses that he recommends in his book, (transmitted via personal conversation to me).

Currently IAS is providing Oxy-Sub™ in 20 IU trouches (a soft sublingual tablet), these can therefore be cut into half or quarter for a dose of 5 or 10 IU and should be placed under the tongue and allowed to melt.

The other option is Oxy-Pro™ which is applied intranasally delivering 10 IU per spray.

“...oxytocin can induce feelings of bonding and care and not just between individuals, but even with animals too!”

Dr. Thierry Hertoghe’s book, “Passion, sex and longevity - the oxytocin adventure”, details its roles and uses in a ‘how to’ guide form.

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SPOTLIGHT: CAN-C

™

A B R E AK THROUG H FOR C ATAR AC T Can-C™ eye-drops are the original™ brand- developed by Innovative Vision Products (IVP). This group were the first to research, publish and prove how eye-drops can reduce and even eradicate cataract. Accordingly there are active US and EU patents (and others pending) on this unique and special product.

Unique formula:

Clinical trial:

Can-C™ eye-drops are the formula from the original published human trials.

They contain a purified and racemized form of n-acetylcarnosine (made in Japan); this natural di-peptide has potent anti-glycating and antioxidant properties that prevents lipid peroxidation.

Note that the formula is important- it’s not all about the n-acetylcarnosine; the specific carrier agents and their purity are also important. If you look at the Can-C™ formula you will see differences to the copycats, (remember it is only Can-C™ that is patented in recognition of the original work). If you want the best possible results in the fastest possible time, then choose Can-C™ to deliver them according to the clinical trials.

Patients placed two-drops of Can-C™ into their eyes twice daily for a 6-month period, the outcome was:

• 90% saw an improvement in their visual acuity.

• 88.9% of patients showed improvement in the clarity of their lens.

There have been numerous reports of cataract shrinkage and even disappearance with documented evidence that Can-C™ eye-drops remain effective (and safe) more than 24-months later. The most commonly expressed initial reports are that glare is significantly improved, (for example night driving is much safer) and color perception is enhanced.

Improving eye-sight: More evidence is mounting that Can-C™ is efficacious for many conditions

including: • Cataracts (particularly the senile version) • Glaucoma • Presbyopia • Corneal disorders • Eye strain • Ocular inflammation • Blurred vision • Vitreous opacities and lesions • Diabetes mellitus complications • Contact lens users • Dry eye syndrome Of special interest may be to persons who wear contact lenses. This is because Can-C™ inhibits the accumulation of lactic acid and therefore contacts can be worn for longer periods without pain.

We have also received reports that Can-C™ not only aids dry-eye syndrome with its lubricants, but that Can-C™ helps to unclog proteins from the lacrimal ducts, thus releasing more

Before: Right: A woman’s eye shows the cataract before treatment.

Far Right: 5-months later after use of Can-C eye-drops (two drops twice daily), there is no longer a visible cataract and eyesight has improved.

Dr. Kyriazis book, ‘The Cataract Cure’, details the usefulness and evidence of Can-C™ eye-drops.

It is now available as a FREE e-book at:

www.antiaging-systems.com/can-c-ebook

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www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

natural tears onto the eye.

In a similar way, it is also believed that the unclogging of proteins in the eye’s drain, (the Schlemm valve), helps to reduce intraocular pressure and thus aids glaucoma.

Can-C™ Plus capsules In addition to the eye-drops, Can-C™ Plus capsules are also available. They are strongly recommended to be used in combination with the eye-drops- if you have ripe (long existing) cataracts.

Above: Can-C Plus capsules

After:

SPOTLIGHT: PEOS

®

S U PPLYING AND BAL ANCING OMEGA S NATU R ALLY Most people are familiar with the benefits of omega oils for their health and in particular to reduce inflammation. Indeed cod-liver oil supplements are the world’s most popular supplement, but recently Professor Brian Peskin’s research which is all contained in his new book – the PEO solution - is causing quite a stir and may make many folks to rethink and change their stance.

Professor Brian Peskin and the cover of his latest book - the PEO solution

We are referring to his discovery that the body naturally uses plant oils to make its own omega 3 and 6, thereby satisfying a precise balance according to need- providing the ‘raw materials’ are available. Professor Peskin has termed the phrase PEO as the acronym for ‘parent essential oils.’

Professor Peskin states openly that he has found this information hidden in the scientific literature and never once found it referred to in the medical literature. Why does it matter? Because as he says, it means that physicians are unaware of these facts and therefore they continue to advocate super-physiological doses of omegas from fish oil, which may be actually doing more harm than good!

It’s a lot to swallow, (no pun

intended) and we can’t do his research justice on a single page, which is why we recommend his book, or take a look at the Aging Matters™ magazine No1, 2015 in which Professor Peskin’s article is the lead story. Let’s summarise the advantages of the PEOs: • The plant oils live in our environment, (typically around 50-60°F); hence they do not go rancid at room temperature.

Cold water fish live in a cold environment (typically around 30-40°F), therefore PEOs represent a much more stable product.

• The PEOs are obviously a nonanimal source and therefore can be considered more suitable for those wanting to avoid animal based products.

• The PEOs represent a sustainable source, since there is already too much ‘pressure’ on the seas to provide both fish and even krill stocks.

• The PEOs enable the body to produce its own internal essential fatty acids (EFAs) and correct its own balance. This has not been shown to be the case with fish oil supplements.

Why not fish oil?

Figure: How is fish oil made? It often does not start as the healthiest possible source!

Professor Peskin maintains that the super-high doses in fish oils are extreme when compared to those manufactured within the body.

Furthermore, even the omega 3 to

omega 6 balance OXYGEN MAGNETS! they provide could be EFAs work like tiny “magnets” drawing Oxygen EFAs oxygen into all cells, tissues wrong and that the and vital organs.

O O body may actually Reduce oxygen by only 1/3 and a cell O turns cancerous, forever! require more omega HEART LUNGS 6 than is currently being advocated today. Did you know that when a bear eats a fish he throws away the body? Could it be that the bear Figure: Essential fatty acids provided via wants the omega 6 provided PEOs work like magnets, drawing oxygen into cells and tissues. Reduce oxygen by the fish brain and not the content in cells by one third and they can omega 3 that is within its body? become cancerous.

(The fish uses omega 3 as an anti-freeze due to its cold water contains organically produced, environment). cold-pressed seed oils, these include high linoleic safflower PEO-Pro™ oil, sunflower oil, evening IAS has always been ‘on the primrose oil and flax oil, all in cutting-edge.’ It may remain the proportions derived from controversial, however we have Professor Peskin’s research. taken the decision to remove Maintenance doses are 1 or fish and krill based oils from 2 capsules daily; for those with our range and replace them greater need, 1 capsule per 40 with PEOs that are contained in lbs (18 Kg) bodyweight per day PEO-Pro™. may be more suitable.

The PEO-Pro™ supplement 2

2

2

Oxygen Magnets

Appetite

• Less Cravings • Less Hunger • Better Appetite Fulfilment

Heart Health

• Flexible Arteries • Clean Arteries • Fast Blood Flow • Lower Blood Pressure • Improves Lipids

Beauty

• Healthier Skin • Less Dandruff • Less Cellulite • Healthier Hair • Eczema Improved

• Less Sweet Cravings • Lower Blood Sugar • Less Neuropathy/ Retinopathy

PEOs

Anti-inflammation

SUPPORT

• Less Arthritis • Less Joint Pain/Swelling • Faster Healing

Hormones/ Endocrine

Brain Health

Endurance

Diabetes

• Better Sexual Function • Smoother Pregnancies • Less PMS • Fewer Headaches

• Better Clarity • Better Focus • Improved Memory • Helps Improve ADD & ADHD

• More Energy • Less Fatigue • Greater Intensity • Faster Recuperation

Figure: This diagram highlights the benefits of EFAs (essential fatty acids) that PEOs can deliver.

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SPOTLIGHT: PEPTIDE BIOREGULATORS THE DI SCOVERY OF G ENE SWITCHES IN FOOD Today Professor Vladimir Khavinson is the President of the European Academy of Gerontology and Geriatrics, but in the 1980’s he was a Colonel in the Soviet Union military medical corps. At the time, he and his team were approached by Kremlin officials, they wanted them to find a way to protect their troops from a myriad of problems; issues such as radiation for submariners in nuclear submarines to troops that may be blinded from known, (but thankfully unused) new weapons such as battlefield lasers.

A former Soviet military secret!

obtained from food, to act as a ‘short-cut’ to initiate protein synthesis. These peptides, What their research uncovered unlike proteins, can enter the - that was used for two blood through the stomach. decades on many thousands Through a comprehensive of men and women - was a list of patents and even remarkable link between copyrighted PowerPoint short chain peptides and DNA. slides, the Russian research This former military secret is group have shown that each now available to the public of the concentrated peptide as peptide bioregulators. bioregulators so far examined, Their published research has interact with particular strands identified that each organ / of DNA - effectively and very gland / tissue uses a highly specifically activating repair specific short chain peptide, and regenerative processes.

This is a remarkable story since what we are describing here are peptides that act as individualised gene switches. To date, they have been tested for many years on thousands Above: A short-chain peptide bioregulator

of individuals, without report of any serious side effects or contraindications. We believe that they could be set to ‘out do’ stem cells.

Why? Because this peptide therapy is relatively cheap, highly specific, can be taken orally and doesn’t require any suppression of the immune system to operate fully (as stem cells do).

Original material from the trials The peptide bioregulators available via IAS are the bovine originals; sourced from carefully chosen Danish calves and processed through pharmaceutical processes and filters. They are not the synthetic versions which have not been studied/ proven.

Peptide bioregulators act as they sound- to regulate; for example, Thyreogen®

the thyroid peptide would increase thyroid activity if it were too low, but decrease it if it were too high!

Dosing Doses are very dependent upon the need and unlike hormones these peptides do not have to be taken every day, hence making them a cost effective regime. A typical/ average use could be considered as follows: • Start with an intensive course: 2 capsules once a day for 30-days.

• Thereafter use 2 capsules once a day for 10-days, repeat every 2, 3, 4 or even as little as 6-months.

The story of the peptide bioregulators is a remarkable one and we recommend that you to read the articles and interviews and see the video on the IAS website.

interacting with DNA

PEPTIDES CURRENTLY AVAIL ABLE: Bone Marrow bioregulator: Parathyroid bioregulator: Brain peptide bioregulator: Heart peptide bioregulator: Bladder peptide bioregulator: Pineal peptide bioregulator: Adrenal peptide bioregulator: Muscle peptide bioregulator: Prostate gland peptide bioregulator: Kidney peptide bioregulator: Cartilage peptide bioregulator:

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Pancreas peptide bioregulator: Stomach mucus peptide bioregulator: Liver peptide bioregulator: Lung peptide bioregulator: Testes peptide bioregulator: Thyroid peptide bioregulator: Blood vessel peptide bioregulator: Retina peptide bioregulator: Thymus peptide bioregulator: Ovary peptide bioregulator:

www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

Suprefort® Stamakort® Svetinorm® Taxorest® Testoluten® Thyreogen® Ventfort® Visoluten® Vladonix® Zhenoluten®

SPOTLIGHT: CENTROPHENOXINE IMPROVES RECALL SPEED

C E NTRO PH E N OX I N E , (PRO N O U N C E D, C E NT- ROW- FE N - OX- I N) I S A C L A S S I C ‘ S M A RT D RU G .’

The term ‘smart drugs’ has become synonymous with substances that aid memory and cognition, although the correct medical terminology is ‘nootropics’ (which when translated from the Greek is- ‘towards the mind’). As shown in the insert, centrophenoxine is an ester of PCPA (a plant compound) and DMAE which is a natural choline-based substance found in the diet.

OCH2

Cl

A

PCPA

COO

CH2

CH2

N

CH3 CH3

DMAE

The molecular structure of centrophenoxine, showing its combination of PCPA and DMAE.

Background Centrophenoxine has been studied extensively over many decades, principally in Europe and one of its leading proponents is the Gerontology expert, Professor Imre Zs.-Nagy, whom utilises it for his own antiaging purposes, keeping his mind sharp.

later on), although the same could be said for all senile dementia medications, since trying to revert the damage of a mid-late stage dementia is very difficult. The target therefore is

be very troublesome for the cell because it inhibits proper functioning from taking place, reducing the transference of chemicals through the cell wall, thus damaging both messaging and detoxification abilities. Indeed this inhibition and the inherent loss of lipidity that accompanies it, forms a significant part of Professor Zs.-Nagy’s ‘membrane hypothesis of aging.’ What we do know, is that when significant amounts of lipofuscin are present

Professor Imre Zs.-Nagy says; “Centrophenoxine has shown many facets to improve conditions related to my membrane hypothesis of aging. For example, its ability to improve brain performance, survival time in animal experiments and to remove the cell-aging pigment called lipofuscin. It has been my antiaging supplement for more than 30-years.”

One of the actions of centrophenoxine is to improve acetylcholine levels in the brain and it is this neurotransmitter that declines in Alzheimer’s diseaseleading to its devastating effects.

Yet, centrophenoxine doesn’t make significant improvements for Alzheimer patients in this way, (note, there is another important action mentioned

Showing the typical size and placement of lipofuscin in tissues. at the earliest stage of dementia, or even before then, at the antiaging stage, wherein smartdrugs like centrophenoxine can improve/ enhance and protect the performance of an aging, but otherwise recognised as a healthy, individual.

Lipofuscin Lipofuscin is a waste material that accumulates in aging cells, especially those in the brain, heart, lungs and skin; indeed, in skin cells, lipofuscin can form part of the pigmented spots that are often referred to as ‘age’ or ‘liver’ spots.

Lipofuscin accumulation can

in the brain, they are then referred to as ‘plagues’ and then become recognised trait of Alzheimer’s.

Perhaps it is therefore centrophenoxine’s primary mode of action to help remove lipofuscin deposits. It does it so well, that it is currently believed to be the best tool commercially available to do so and so well, that in patients with visible ‘age’ or ‘liver’ spots in the skin; it is possible over several weeks of centrophenoxine supplementation to see them fade or even disappear. Such patients can also benefit from the knowledge, that at the same, lipofuscin deposits are being reduced in their heart, lungs and brain etc.

Centro-Pro™, the leading brand of centrophenoxine used by its expert, Professor Imre Zs.-Nagy and his patients.

General cognitive benefits Classifying the precise benefits of the various smart-drugs can be tricky. Most individuals often simply refer to their ailing cognitive facilities as “memory loss.” However, a quick breakdown of that statement requires further evaluation in order to determine the precise nature of the problem.

So which of the following is your main issue?

• Short term memory • Medium term memory • Long term memory • Do you get bored easily?

• Do you lack focus/ attention?

• Does your mind quickly become tired?

• Is the problem remembering new experiences later? (So called memory-imprinting) • Does it take too long time to recall memories?

Centrophenoxine is best suited to the last problem. If your speech appears to be full of “ums” and “ers” - whilst your brain tries to catch up with your mouth, then it is likely that centrophenoxine will be an aid for you. In our experience, centrophenoxine should not only be considered for those concerned with the development of Alzheimer’s, but when utilized correctly it can help many people, especially those aged over 40, to hasten their recall speed, bringing clarity and order to both speech and thought.

Doses It is of course impossible to list all details of centrophenoxine use onto one page, but interested parties should ask for further details and read the articles with references that are available on the IAS website. A typical dose for the ‘average’ person is 250 mg once or twice daily; higher doses are necessary according to the varying degrees of Alzheimer’s.

Note: Centrophenoxine is synergistic with other smart-drugs, in particular choline based forms such as piracetam (Nootropil®); these additional benefits can be experienced by using them concurrently, although naturally both doses need to be adjusted downward to suit.

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SPOTLIGHT: SMART DRUGS AND NUTRIENTS DEPR ENYL FOR FOCU S AND CONCENTR ATION Deprenyl is also known as selegiline, it was created in the 1960s by Professor Joseph Knoll from Hungary, principally as an aid to Parkinson’s patients - because deprenyl has a significant benefit to improve dopamine levels in the brain. Dopamine is the neurotransmitter most affected in Parkinson’s disease, in fact, deprenyl still remains a front line treatment for that disease.

Significant longevity studies

Morgenthaler, (as published in the book, Smart Drugs and Nutrients I), produced figure 2.

It highlights that the loss of dopamine in humans with age, can be mapped against both the development of Parkinson’s and even death.

Mode of action For a long time deprenyl has been expressed as a MAO-b inhibitor, that it to say that is prevents the enzyme monoamine-oxidase type-b from destroying dopamine, ergo leading to its greater availability in the brain. The inhibition of the more common MAO-a can be problematic, leading to something called ‘the cheese effect,’ therefore this is not a side effect of deprenyl, although it should be noted that dopamine can inhibit type-a, but usually only at very high doses of 20mg.

In more recent times, Professor Knoll has noted that there is another significant action of deprenyl and this is the raising, (albeit briefly) of PEA levels. PEA is a catecholamine activity enhancer that raises

Professor Joseph Knoll; now aged in his 90s but still active in pharmacological research.

Professor Knoll’s experiments with rats produced some of the most incredible longevity benefits that have ever been seen. When they were fed deprenyl in their food, they lived so much longer than those that were not, so much so, that even after the last non-treated rat died, the first of the deprenyl treated rats was yet to die! These results are shown in figure one: Note; interestingly and importantly, these results were verified independently in another study not conducted by Professor Knoll. Based on this research, Dean, Fowkes and

norepinephrine levels; this is a significant attention agent that is behind the primary mechanism of the famous Eugeroic drug- modafinil (Provigil®).

To learn a great deal more about dopamine and deprenyl, we would recommend Professor Knoll’s books; ‘the brain and its self’, or ‘how selegiline/ deprenyl slows brain aging.’

Typical patient responses In patients who have mild cognitive impairment, or age related minor cognitive dysfunction, the most common report is of a significant improvement in their focus and concentration.

Persons with higher dopamine levels often appear more ‘driven’ and ‘dedicated.’ Avoid overuse since it can lead to what may appear to be an oppressive behavior, as others around you are not so focused and ‘on the ball’ as you!

This is why we recommend occasional breaks from deprenyl use, some advocate one week off in the month and others use it during the

75

Dopamine Level (%)

% of animals alive

100

Deprenyl Treated Rats

50

Control Rats

25 0 140

150

160

170

180

190

200

210

220

Age of rats in weeks

Figure 1: Professor Knoll’s experiment showed that when deprenyl is given to animals it significantly extends their lifespan and their latter life activity.

36

100 90 80 70 60 50 40 30 20 10 0

Average Parkinson’s Patients Rapid Parkinson’s Patients

weekdays but not at the weekends.

Dosing Doses are as normal, based upon need and age. Whilst Parkinson’s patient will require large doses, a person wanting to improve their cognitive performance may want to typically consider 1mg to 3mg per day, with occasional breaks. Note: These doses do not take into account synergy with other dopamine enhancing agents and persons using anti-depressants should consult with their physician beforehand.

Deprenyl tablets are typically provided in 5mg form (Jumex®); some persons like to take ½ to 1 of these tablets 3-times a week; however the use of the deprenyl liquid (Dep-Pro™) is particularly attractive for those using deprenyl to generally support, protect and improve neurological function, since 1 drop = 1mg.

Therefore the liquid can be dosed very precisely by simply placing those drops into a cold drink. Avoid use in the late evening to prevent any sleep disruption.

Slow Aging People Normal People

PARKINSON’S SYMPTOMS DEATH 0 10 20 30 40 50 60 70 80 90 100 110 120 130 140

Figure 2: For humans, the normal loss of dopamine past the age of 40 is 13% per decade. As the lines suggest, if we all live long enough we all become senile!

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SPOTLIGHT: SMART DRUGS AND NUTRIENTS PIR ACE TAM, THE ORIG INAL NOOTROPIC Smart drugs and nutrients, or to give them their correct medical terminologynootropics, are agents that can not only improve conditions of senile dementias, but in recent times have become popular for older individuals to improve their mental and cognitive processes. It was Ward Dean, M.D. who highlighted these facts through his very popular ‘Smart Drug’ series of books in the 1980s, since then the term ‘smart drugs’ has become mainstream.

Piracetam, the original nootropic The smart-drug we focus on here was in fact the first, developed as it was

by Dr. Giurgea for UCB laboratories in Belgium in the 1960s. Originally it was designed to assist with travel and altitude sickness, but shortly afterward individuals realised that piracetam had positive cognitive enhancement effects.

What can piracetam do for me?

Piracetam is a cognition agent that has been used successfully to treat a

wide range of conditions, for example it has been shown to increase a person’s attention levels and improve memory and intelligence. Piracetam can help to slow down ‘senile involution’, dementia and Alzheimer’s disease. In tests and trials, piracetam induces significant improvement to memory consolidation and recall in those suffering from ‘age-associated memory impairment’.

Piracetam has also been used to improve patient’s recovery from strokes, particularly improving post stroke speech impairment (aphasia). Another use has been in cases of acute and chronic cerebral ischaemia, (decreased blood flow to the brain). Using piracetam has restored speech and the use of limbs in these patients; it has also increased neuronal activity in the brain when measured with EEG.

For regular individuals, piracetam has been shown to enhance idea creation and the ability to ‘see things through,’ in other words to have ideas and bring them to fruition. The level of clarity piracetam creates is often described/ perceived as; “the fog has lifted.”

How does piracetam work?

Piracetam’s key and unique method of action is upon the Corpus Callosum, the region of the brain that links the two hemispheres.

It is this that most experts believe is the key that gives piracetam users the ability to channel greater brain potential by connecting the logical side of the brain with the creative side more effectively, Yin and Yang if you will.

“Piracetam can help to slow down ‘senile involution’, dementia and Alzheimer’s disease.”

What are the doses of piracetam?

A common dose is 800mg tablets three times a day, then lowering to 800 mg twice a day after the first month. Note: The effects of piracetam can be enhanced if taken concurrently with centrophenoxine or Hydergine®.

Side effects are minimal and seldom experienced, but should you experience nausea or headache then it is usually caused by an overdose, so in which case reduce the dose and build up more slowly, (if it is necessary).

Note: There are many articles and videos on the IAS website about smart drugs and nutrients.

Right: The Corpus Callosum

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37

SPOTLIGHT: STEM CELL WORX

®

ENHANCING AND IMPROVING STEM - CELL AC TIVIT Y Stem Cell Worx® is an intraoral spray that contains a very high-grade bovine colostrum, (with over 30% of the antibody IgG and over 54% protein) along with a 98% pure trans-resveratrol and 95% fucoidan (a seaweed extract). should not be confused with embryonic stem cells that come from an embryo.

The Stem Cell Worx® supplement is designed specifically to enhance one’s own adult stem cells naturally.

Stem Cell Worx® is an intraoral spray providing an absorption rate of up to 95% of its nutrients. This is important because in order for adult stem cells to be stimulated, it is the blood that is the principal carrier of nutrients and oxygen to our cells. In order to enhance cell activation you need three key factors, which are: • Growth factors • Immune factors and • Cytokines Stem Cell Worx® has all three of these factors in abundance and it is scientifically proven they are most effective when administered by intraoral spray delivery.

Time takes its toll on adult stem cells. At 65 years of age, the release rate of adult stem cells entering the bloodstream has dropped

1/10,000

Mesenchymal Stem Cells

Mesenchymal stem cells shown as a proportion of total cells in bone marrow.

Lots of MSCs in our younger years. MSCs repair muscle, bone cartilage and tendons.

MSCs rapidly decline with age.

Longer repair and recovery times. More prone to aging and disease.

1/100,000 1/250,000

Newborn

Teenager

Age 30

1/400,000

1/2,000,000

Age 50

Figure 1: The decline in stem cells with advancing age.

38

Age 80

90

% of Bone Marrow Cells Proliferated

This natural health supplement is designed to activate the body’s own adult stem-cells in order to provide a robust immunity. With 50 to 70 trillion cells in the body, cellular health is clearly crucial to overall well-being and good health. Hence, adult stem cells working at optimal levels provide the platform for many cumulative health benefits.

Unfortunately, as we age, our own adult stem cells decline rapidly, along with their release rates from the bone marrow, and our immune system weakens. Whilst stem cell clinics are at the forefront of antiaging medicine today, the process of full adult stem cell therapy is very expensive and has many regulatory restrictions.

Adult stem cells are the master cells of the body that have the ability to maintain, selfrenew and repair cells, tissue and muscle throughout an entire life-time. These cells are referred to as autologous, haematopoietic (blood), mesenchymal or stromal stem cells. Adult stem cells

80 70 60 50 40 30 20 10 0

25

12.5

6.25

3.12

Stem Cell Worx Concentration (mg/ml)

Figure 2: This study used blood samples from healthy humans. The adult stem cell proliferation percentages were determined by flow cytometry, measured in mgs of the Stem Cell Worx formulation. As this graph demonstrates the Stem Cell Worx formulation produces steady percentages of bone marrow stem cell proliferation being dose dependant, but still active at a relatively low dosage of mgs.

by 80% compared to youth.

It is important to keep them activated. The good news is it is now possible to reverse this statistic.

Stem Cell Worx® benefits Stem Cell Worx® contains the greatest number of natural growth and immune factors compared to any other health supplement currently on the market. This enables natural stem cell activation to be as much as 75% per 36mg of the formulation. This provides: • Support to naturally increase adult stem cells, providing the platform for many cumulative health benefits including: • Increased energy and endurance.

• Boosting the immune system.

• Improved alertness and mental clarity.

• Faster recovery after your

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exercise regime and faster repair and recovery after surgery, injury or illness.

• Helping to build muscle, burn fat and maintain natural weight loss in conjunction with a healthy diet and exercise regime.

IAS choose Stem Cell Worx® over other purported stem-cell activators on the basis of evidence. Figure 2 demonstrates the benefits of supplementing daily with Stem Cell Worx.

Dosing Six sprays into the mouth provide 36mgs of formulation.

This can be performed once or twice daily as required. Spray under the tongue, hold for 10 seconds, then swallow the remainder. It’s best taken on an empty stomach, at least 30-minutes before or after eating any food.

SPOTLIGHT: THYROID SUPPORT FOR THE HYPOTHYROID EPIDEMIC Dr. Broda Barnes in the 1970s estimated that 40% of the adult population was deficient in thyroid hormones; he published this statement in his excellent book‘hypothyroidism, the unsuspected epidemic.’ Since then, pupils of Dr. Barnes, such as Dr. Richard Wilkinson, have suggested that this figure could be even greater now!

This is important because the thyroid gland is of pivotal importance to our overall health, but like the majority of hormones as we age the production of thyroid hormones decline. This lack of thyroid function is the root cause of a wide variety of agerelated health disorders.

Ergo, supplementation with a synthetic or a natural thyroid can have a significant positive effect on a wide range of agerelated problems.

The importance of the thyroid gland The hormones produced by the thyroid control the body’s metabolism- the rate at which it burns calories for energy. It also controls the body’s utilization of fat, so a decline in the secretion of hormones from the thyroid gland, (known as hypothyroidism) can result in wide range of symptoms such as poor concentration, confusion, memory problems, cold hands and feet and weight gain.

Another serious condition which can be caused by and result from an underactive thyroid are painful musculoskeletal issues that affect tendons, muscles and ligaments.

How can I be sure if I need a thyroid supplement?

Above: The position of the thyroid gland

Apart from recognising the types of effects listed above, your doctor can of course get your blood

levels of thyroid checked, but another, simpler method is to take your body temperature when you wake in the morning.

It should be in the range of 97.8 to 98.2 degrees Fahrenheit, if it is regularly lower you could be hypothyroid and if higher then hyper-thyroid.

Choosing between synthetic and natural thyroid supplements IAS stocks a comprehensive range of both synthetic and natural thyroids, although we advocate the use of a natural supplement over a synthetic, this is because products such as Armour® are of a porcine origin, so they naturally contain the full spectrum of T1, T2, T3 and T4 thyroid hormones, (note the bottles only list the amounts of T3 and T4 because very few physicians are familiar with T1 and T2).

Conversion between synthetic and natural thyroid products The table provided is a helpful guide to what the suggested conversion rates are for those wishing to make the switch between synthetic thyroids and natural versions. As always we recommend consulting with a physician before making changes to your program.

Thyroid doses Natural desiccated thyroids are measured in grains; with one grain being equivalent to approximately 60 mg.

IAS carries doses from ¼ grain to 2 grains, with brands including Armour®, ERFA® and Nature®. IAS also provides synthetic T3 in 20 mcg and T4 in 100 mcg tablets.

Thyroid supplements provide potent antiaging protection Many aging individuals can benefit from taking a thyroid supplement because this remarkable hormone has such a profound affect across so many different conditions.

Many antiaging physicians consider thyroid support an essential part of any serious attempt to improve a person’s health-span and longevity.

Dose of Desiccated thyroid (grains)

Equivalents (mg)

Dose of T3 (lithyronine) (μg)

Dose of T4 (levothyroxine) (μg)

0.5

32

12.5

0.05

1

65

25

0.1

2

130

50

0.2 0.3

3

200

75

4

260

100

0.4

5

325

125

0.5

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39

SPOTLIGHT: YOUTH GEMS

®

THE PEP TIDE B IOR EG U L ATOR S FOR S KIN Four peptide bioregulators have now been combined into topical skin preparations so that their unique gene-switching performance can be bought to the field of aesthetic medicine.

What does each peptide provide for?

The beauty product line Youth Gems® contains the following four peptides and a ginseng extract called Neovitin®. They represent the very latest developed program of complex skin care designed for the face, neck, hands and the body.

The line includes four unique active ingredients of shortchain peptides that have a directed tissue-specific action to improve all basic skin structures: • Thymus peptide: This stimulates tissue regeneration and the synthesis of tissue-specific proteins. Thus, cells proliferative and metabolic activity is enhancedaccelerating the renewal of various cell tissues. It also has an anti-inflammatory action, improving the healing time of wounds, as well as antioxidant, immune stimulating and anti-stress actions.

• Pineal peptide: This regulates metabolic processes and increases protein synthesis in skin cells. It also possesses potent antioxidant activity, normalizes the lipid peroxidation processes in skin cells that in turn

40

promotes the elimination of negative influences on the skin from external factors.

• Cartilaginous peptide. This stimulates regeneration of fibroblasts and keratinocytes and interferes with the destructive changes in collagen skin structure; it also strengthens collagen structure of elastic skin fibers and increases elasticity.

• Blood vessel peptide: This regulates metabolic processes in the vascular wall, normalizes vascular tone and restores disturbed skin microcirculation. It strengthens and regulates the permeability of the vascular walls of skin vessels and improves skin turgor.

What else is included in Youth Gems® in addition to the four peptides?

In addition to the four peptides, the Youth Gems® also contain an incredible array of beneficial natural agents- which just by themselves would make other antiaging creams jealous! The range includes: Neovitin® (a complex isolated from ginseng), olive oil, raisin-seed oil, Argon oil, Soya oil, Jojoba oil, Bisabolol (extract from chamomile), Peony extract,

sodium hyaluronate (a derivative of hyaluronic acid), green tea extract, cocoa oil, carrageenan (from seaweed), winter bloom, almond extract and vitamin E.

What results have been seen?

Clinical trials and examinations have been conducted at the St. Petersburg Biogerontology Institute and they have concluded that these short chain peptides, when applied to skin cells, have many beneficial activities, shown below are some of those results. These include improved metabolism in vascular wall cells, the growth of new skin cells, enhanced antioxidant activity; increased blood flow circulation and greater moisturization.

The skin’s appearance becomes smoother, with fewer wrinkles and with more elasticity, all of which helps to lift the face contours producing a more radiant, youthful appearance. These beneficial effects were noted in 100% of women who took part in the voluntary clinica trial.

Right: A 68 year old female before (top) and after (below) application of Youth Gems®

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What’s available?

• Body milk: The body milk is a very light cream that can be applied to most areas of the body.

• Day cream: The day cream is the core product designed to be applied to the face and hands.

• Serum: The serum is designed to be used sparingly against the most noticeable skin aging effects on the face and neck.

• Tonic: This cleanser can be used to help any area become more firm and taught and may be splashed on as required.

All of the Youth Gems® should be applied onto clean, dry skin- avoiding the eyes; makeup can be applied after absorption - if required.

CONDITION CROSS-REFERENCE LIST This cross-reference list highlights individual products that have been used for these disorders.

Note: It does not mean that all these products are synergistic together.

Addison’s disease Aldosterone, peptide bioregulator (Glandokort®) ADHD (ADD, attention deficit disorder, see mental stimulants) Adrenal fatigue Aldosterone, Digestif®, hydrocortisone, peptide bioregulator (Glandokort®) AGE (advanced glycated end-product inhibitors) ACF228™, aminoguanidine, Can-C™ Plus, carnosine, metformin, pyridoxamine

Rotational Melatonin Telomeres Peptide biomarker (Endoluten®), TA65® Anti-biotics Ciproxin, doxycycline, penicillin, roxithromycin, tetracycline Anti-depressants Lithium, milnacipran (Ixel®), moclobemide (Manerix®), reboxetine (Edronax®), Stablon®, Valdoxan®, venlafaxine (Efexor®) Anti-oxidants (see free radical scavengers)

Age Related Macular Degeneration (see eyesight)

Anxiety (see stress)

Age Related Mental Decline (see cognitive)

ARMD (see eyesight)

Aids (see HIV)

Arterial (See heart, arterial & blood)

Alcoholism (also see compulsive disorders) 5HTP, L-tryptophan, memantine

Arthritis (rheumatoid & osteo) Andro-Pro™, Gerovital-H3®, Novisyn®, PEO pregnenolone, SAMe, thymus,

Allergies Pregnenolone, thymus

Asthma (see Allergies)

ALS (amyotrophic lateral sclerosis, Lou Gehrig’s disease) Naltrexone, TRH

Autism (also see chelation agents) Oxytocin, piracetam

Alzheimer’s disease (see senile dementia)

Back problems (see spine)

Anabolic (see growth hormone & testosterone)

Bell’s palsy Vitamin B12

Anginas (see heart, arterial & blood)

Blood disorders (see heart, arterial & blood)

Animal use Can-C™ eye-drops, deprenyl, L-tryptophan, peptide bioregulators

Blood pressure Magnesium, Neo40®, oxytocin, potassium, propranolol, vinpocetine

Antiaging (as impacting on a particular theory of aging) Calorie Restriction Carnosine, metformin, resveratrol

Bone problems (also see joints & arthritis) AndroPro™, Bone-Pro2™, Esnatri™, peptide bioregulator (Bonomarlot®), progesterone, SAMe, thyroid

Free radical ACF228™

Breathing (see lungs)

Glycation Aminoguanidine

Membrane Centrophenoxine

Cancer (also see anti-oxidants & radiation) 1st Line™, anastrozole, BEC5® Curaderm, bromocriptine, curcumin, DIM-Pro2™, laetrile, melatonin, metformin, naltrexone, oxaloacetate, progesterone, resveratrol, thymus, TRH

Mitochondrial Hydergine®, PQQ

Cardiovascular (see heart & arterial disorders)

Neuroendocrine Metformin, TRH

Cataplexy (sudden fatigue) Adrafinil, picamilone

Hayflick Carnosine, TA65®

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41

Cataract (see eyesight)

Diabetes insipidus (see urination)

Central Nervous System (CNS)

Dieting (see weight loss)

Peptide bioregulator (Cerluten®)

Digestive issues Digestif®, peptide bioregulator (Stamakort®), Symprove®

Chelation agents Carnosine, centrophenoxine, EDTA, zeolite Cholesterol (see blood disorders) Crohn’s disease Naltrexone Chronic fatigue syndrome (see mental stimulants & physical energy improvement) Cognitive (also see memory & senile dementias) Alertness Adrafinil, Xan-Pro™ Creativity Aniracetam, piracetam, pramiracetam Focus/ concentration Deprenyl, desmopressin, vasopressin Energy ATP-Boost™, centrophenoxine, Mito-Pro2™, picamilone General support Gerovital-H3®, vinpocetine

Down’s syndrome Melatonin, piracetam Energy improvement (see physical energy & mental stimulants) Enzymes Boluoke® Epilepsy GABOB, phenytoin Erectile dysfunction (also see sex-libido & premature ejaculation) Andro-Pro™, cabergoline, Cialis®, deprenyl, Neo40®, oxytocin, Viagra®, Vielight® Eyesight ARMD MZS™ Cataracts Can-C™, Can-C™ Plus Contact lenses Can-C™

Intelligence Hydergine®

Dry eyes Can-C™

Work load Hydergine®, thyroid

General support Aminoguanidine, peptide bioregulator (Visoluten®), vinpocetine

Compulsive disorder treatment (also see alcoholism) 5HTP, GABOB, L-tryptophan, picamilone Cortisol alteration (also see stress) Aldosterone, DHEA, GABOB, Gerovital-H3®, hydrocortisone, peptide bioregulator (Glandokort®), phenytoin Cross linking (see AGE) Deep vein thrombosis (see frequent fliers) Dental (see teeth & gums) Depression (also see well-being & anti-depressants) 5HTP, aniracetam, ATP-Boost™, curcumin, deprenyl, Gerovital-H3®, lithium, L-tryptophan, milnacipran, picamilone, piracetam, pramiracetam, pregnenolone, SAMe, thymus, thyroid DHT alternation (dihydrotestosterone) Dutasteride, finasteride, peptide bioregulator (Libidon®), progesterone Diabetes Acarbose, aminoguanidine, ATP-Boost™, benfotiamine, L-carnosine, metformin, Mito-Pro2™, PEO, peptide bioregulator (Suprefort®), pyridoxamine, thyroid, TRH 42

DNA support (also see telomeres) Carnosine, CoQ10, PEO, peptide bioregulators, PQQ, resveratrol, TA65®

Glaucoma Can-C™ Retinal MZS™, nicergoline, picamilone Retinal pigmentosa Picamilone, peptide bioregulator (Visoluten®) Excitotoxins (reduction) Carnosine, deprenyl, idebenone, lithium, memantine Fertility Melatonin, metformin, peptide bioregulator (Zhenoluten®), TRH Fibromyalgia (also see physical energy & mental stimulants & pain relief) 1st Line™, milnacipran, naltrexone, oxytocin Free radical scavengers ACF228™, ATP-Boost™, BHT, glutathione, idebenone, melatonin, Mito-Pro2™ Gastrointestinal (see digestive) Glaucoma (see eyesight) Glucose control (see diabetes) Glycation prevention (see AGE)

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Gout Colchicine

HGH (see growth hormone)

Growth hormone (improvement) Bromocriptine, deprenyl, GABOB, GHRP2, GHRP6, Hydergine®, Neo40®, sermorelin, thymus, thyroid

Homocysteine (see heart, arterial and blood)

Hashimoto’s Iodine, peptide bioregulator (Thyreogen®), thyroid Hair improvement Dercos®, dutasteride, finasteride, Gerovital-H3®, PEO

HRT (hormone replacement therapy for women) DHEA, Esnatri™, melatonin, progesterone Human growth hormone (see growth hormone) Hypertension (see blood pressure)

Headaches (see migraines)

Hypothyroidism Iodine, peptide bioregulator (Thyreogen®), thyroid

Heath diagnostics (see at home test kits)

IBS (irritable bowel syndrome) Symprove®

Hearing disorders Aldosterone, Anacervix®, nicergoline, picamilone, vinpocetine

Immune system improvement (also see infections) 1st Line™, ATP-Boost™, carnosine, melatonin, peptide bioregulator (Vladonix®), peptide bioregulator (Thyreogen®), resveratrol, thymus, thyroid

Heart, arterial & blood (includes blood markers) Arteries (hard) Aminoguanidine, Bio-CUFF™, carnosine, resveratrol Blood pressure (high) Magnesium, Neo40®, potassium, propranolol, vinpocetine Calcium Peptide bioregulator (Bobothyrk®) Cholesterol (high) CoQ10, Gerovital-H3®, TRH, Xan-Pro™ Dilation (nitric-oxide) Deprenyl, Neo40®, Vielight® Fibrinogen Curcumin, TRH

Infections (also see immune system improvement, antibiotics & influenzas) 1st Line™, beta-glucans, fluconazole, silver Inflammation (reduction) Boluoke®, curcumin, Digestif®, PEO, pregnenolone, thymus Influenzas (also see anti-biotics, infections & immune system improvement) 1st Line™, beta-glucans, Injectable products Cerebrolysin®, Gerovital®, vitamin B12

General support CoQ10, PEO, peptide bioregulators (Chelohart® & Ventfort®), PQQ, vinpocetine

Insulin & glucose control (see diabetes)

Glucose (high) Acarbose, metformin, TRH

Intra-ear products Aldo-Spray™

Glycated end-products ACF228®, aminoguanidine, metformin

Intra-nasal products Desmopressin, GHRP6 (ReleasePro™), vasopressin, Vielight®

Heart pulse (irregular) ATP-Boost™, thyroid

Joints (also see bones & arthritis) Boluoke®, Novisyn®, PEO, peptide bioregulator (Sigumir®), pregnenolone, SAMe, thymus

Heavy metals (chelate) EDTA, zeolite Homocysteine TRH

Intestinal flora (see probiotics)

Kidney disorders (also see infections) Aminoguanidine, peptide bioregulator (Pielotak®) SAMe, TRH

Lipofuscin Centrophenoxine

Triglycerides Curcumin, PEO, TRH

Learning (also see memory & mental stimulants) Aniracetam, desmopressin, Hydergine®, piracetam, pramiracetam, vasopressin

Hepatitis (see liver and infections)

Libido (see sex)

Herpes (also see anti-biotics) 1st Line™, ACF228™, BHT, silver

Lipids (see blood disorders)

HIV (also see immune system improvement) 1st Line™, melatonin, naltrexone, thymus

Liver disorders (also see infections) CoQ10, idebenone, peptide bioregulator (Svetinorm®), pregnenolone, SAMe, silver

Plaques (clots) Boluoke®

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43

Longevity enhancement (significant lifespan increases seen in animal studies) Centrophenoxine, deprenyl, melatonin, peptide bioregulator (Endoluten®) vasopressin

Nitric Oxide release Neo40®, Nitric Oxide saliva test strips, Vielight®

Lou Gehrig’s disease (see ALS)

Osteoporosis (see bone problems)

Lungs ACF228™ Breathe-Easy, centrophenoxine, glutathione, peptide bioregulator (Taxorest®)

Pain relief (general) ATP-Boost™, Gerovital-H3®, memantine, milnacipran, nicergoline, oxytocin

Lupus Milnacipran, naltrexone

Parasites (see infections)

Lyme’s 1st Line™, beta-glucans, silver

Parkinson’s disease (see senile dementia)

Macular degeneration (see eyesight)

Pets (see animal use)

Malaria (see anti-biotics)

Photoaging (see skin problems)

Menopause (see HRT)

Ph balance (rebalancing) Symprove®

Mental stimulants (also see physical stimulants) Adrafinil, aniracetam, centrophenoxine, deprenyl, desmopressin, nicergoline, picamilone, piracetam, pramiracetam, vasopressin, Xan-Pro™

Physical energy improvement (also see mental stimulants) ATP-Boost™, carnosine, CoQ10, idebenone, Mito-Pro2™, NADH, oxaloacetate, PQQ, pregnenolone, SAMe

Memory (also see cognitive & senile dementia)

PMS (pre-menstrual syndrome) PEO, peptide bioregulator (Zhenoluten®), vinpocetine

General support PEO, picamilone, vinpocetine

Oral health care (see teeth & gums)

Imprinting (for later recall) Desmopressin, vasopressin

Premature ejaculation/ ejaculate (also see erectile dysfunction & sex-libido) Oxytocin

Medium-long term Hydergine®

Probiotics Symprove®

Short term Aniracetam, piracetam, pramiracetam

Prostate (also see cancer) DIM-Pro2™, dutasteride, finasteride, melatonin, peptide bioregulators (Chitomur® & Libidon®), Prostate-Pro2™

Speed of recall Centrophenoxine Methylation (conversion of one chemical into another inside the body) ATP-Boost™, Boluoke®, Mito-Pro2™, SAMe, Xan-Pro™ Migraines (also see pain relief) Nicergoline, memantine, picamilone, vitamin B12 Mitochondrial support ATP-Boost™, CoQ10, deprenyl, glutathione, Hydergine®, idebenone, Mito-Pro2™, NADH, oxaloacetate, PQQ, pregnenolone, SAMe Mtor inhibitors Curcumin, oxaloacetate, resveratrol Multiple Sclerosis (also see mitochondrial support) Melatonin, naltrexone, TRH Muscles (see sarcopenia) Nail condition Gerovital-H3®, PEO Narcolepsy (sleeping in the daytime) Adrafinil, melatonin, picamilone

Prolactin alteration Bromocriptine, cabergoline, GABOB PSA (prostate specific antigen- see prostate) Urination (frequent) Peptide bioregulator (Chitomur®), vasopressin RNA (see DNA support) Sarcopenia (muscle atrophy/ wastage) GHRP2, GHRP6, peptide bioregulator (Gotratix®), sermorelin Senile dementia (also see cognitive & memory) Alzheimer’s Centrophenoxine, curcumin, galantamine, Hydergine®, memantine, nicergoline General support Anacervix®, aniracetam, PEO, piracetam, pramiracetam, vinpocetine, Parkinson’s Bromocriptine, cabergoline, deprenyl, NADH, rasagiline Senility Gerovital-H3®

44

www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

Sex (libido, also see erectile dysfunction & premature ejaculation) Andro-Pro™, deprenyl, MSH, oxytocin Skin problems (also see herpes and tanning)

Sublingual products Oxytocin, sermorelin, TRH Sunburn (see skin problems)

Acne Beta-glucans

Syndrome X (metabolic syndrome) Aminoguanidine, ATP-Boost™, melatonin, metformin, Mito-Pro2™, PEO

Age (liver) spots Centrophenoxine

Tanning (darkening the coloration of skin) MSH

Anti-glycation Aminoguanidine, carnosine, Youth Gems® serum

Teeth & gum disorders Doxycycline, Min-Mouth™ mouthwash, NeyDent® toothpaste, silver, zeolite

Anti-oxidant Youth Gems® day cream

Telomeres (also see DNA support) Carnosine, PEO, peptide bioregulator (Endoluten®), TA65®

Cancer (non-melanoma) BEC5® Curaderm Cellulite Youth Gems® body milk Collagen Novisyn® Environmental Youth Gems® serum General support Gerovital-H3®, melatonin, PEO, thyroid Infections Silver, thymus

Testosterone & testes (also see fertility and prostate) Anastrozole, Andro-Pro™, DIM-Pro2™, melatonin, oxytocin, peptide bioregulator (Testoluten®), TRH, zinc Topical products BEC5®, beta-glucans, Can-C™ eyedrops, Esnatri™, progesterone, Retin-A®, silver, Youth Gems® Triglycerides (see blood disorders) Veterinarian (see animal use)

Moisturizer Youth Gems® day cream Psoriasis Beta-glucans Sun spots (keratosis) BEC5® Curaderm Wounds Silver Wrinkles Retin-A® Sleep disorders For less sleep Adrafinil, ATP-Boost™ For more sleep 5HTP, gabapentin, L-tryptophan, melatonin

Weight gain (muscle mass) Andro-Pro™, GABOB, GHRP6, sermorelin Weight loss (appetite suppressants and fat burners) 5HTP, acarbose, aminoguanidine, ATP-Boost™, DIMPro2™, galantamine, GHRP2, L-tryptophan, metformin, Mito-Pro2™, MSH2, thyroid, TRH, Xan-Pro™ Well-being (also see depression) 5HTP, aniracetam, ATP-Boost™, deprenyl, Gamalate®, Gerovital-H3®, L-tryptophan, melatonin, Mito-Pro2™, PEO, picamilone, piracetam, pramiracetam, SAMe, thymus, thyroid, zeolite

Smoking cessation 5HTP Spine issues (also see growth hormone) Novisyn®, peptide bioregulator (Sigumir®) Sports (see growth hormone, estrogen alteration, physical energy & testosterone) Stem Cells Stem Cell Worx® Stress (also see cortisol) 5HTP, GABOB, Gamalate®, Gerovital-H3®, L-tryptophan, melatonin, oxytocin, picamilone, phenytoin, pregnenolone, propranolol Stroke Anacervix®, aniracetam, Boluoke®, Hydergine®, idebenone, nicergoline, PEO, picamilone, piracetam, PQQ, pramiracetam, pregnenolone, vinpocetine Stomach (see digestive) www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

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A-Z INGREDIENT LIST The following list is intended to highlight the key ingredients in some products and cross reference them to the most relevant product brand names.

Note: Those products with the same name as the ingredients are not shown here as they are within the A-Z product list.

If you want this-

5HTP

Boron

Andro-Pro™

Acetyl-L-Carnitine (ALC)

ATP-Boost™, Vigor-Pro2™

Bromelain

Digestif®

Adenosine triphosphate (ATP)

ATP-Boost™

Buxamin (GABOB)

Gamalate®, Gamibetal®

Caffeine

Minox-Pro™

Aglomelatine

Valdoxan®

Calcium

Bone-Pro2™

Allicin (garlic)

EDTA-Pro™

Carboxymethylcellulose

Can-C™

Alpha lipoic acid (R-lipoic acid)

ATP-Boost™, Mito-Pro2™

Catalase

ACF228™

Aminexil

Dercos®

Chelation agents

Amino acids (includes di-peptides)

5HTP, ACF228™, ATPBoost™, carnosine, L-tryptophan, Mito-Pro2™

Carnosine, centrophenoxine, DMSA, EDTA-Pro™, zeolite

Choline

Centrophenoxine

Aminohydroxybutyric acid (GABOB)

Gamalate®, Gamibetal®

Chromium polynicotinate

ACF228™

Citrulline

Neo40®

Aminosyn

Hair-Pro™

Co-dergocrine mesilate

Hydergine®

Amygdalin

Laetrile

Coenzyme Q10

CoQ10, Mito-Pro2™

Anti-biotics

Ciproxin, doxycycline, penicillin, roxithromycin, tetracycline

Colloidal Silver

Silver

Colostrum

Stem Cell Worx®

Cortisol (cortisone)

Fludrocortisone, hydrocortisone

Cranberry extracts

Andro-Pro™

Creatine

Mito-Pro2™

Anti-depressants

46

look for:

5-hydroxy-tryptophan

Lithium, milnacipran, moclobemide, reboxetine, Stablon®, Valdoxan®, venlafaxine

Anti-oxidants

See free radical scavengers,

Cresote bush

ACF228®, Digestif®

Arginine

Mito-Pro2™

Cycloastragenol

TA65®

Arimidex®

Anastrozole

Cyclodextrin

Astragalus extracts

TA65®

CoQ10-SR™, Curcumin-SR™, resveratrol

Azelaic acid

Minox-Pro™

Dehydroepiandrosterone

DHEA

Azilect®

Rasagiline

Detox

Benzoic acid

Gerovital®

DIM-Pro2™, EDTA-Pro™, zeolite

Beta blocker

Propranolol

DHA (docosahexaenoic acid)

PEO-Pro™

Beta alistine

Carnosine, ACF228®, Can-C™, Can-C Plus™

Diapid®

Vasopressin

Beta glucan

BG-Cream™, BG-Pro™

Di-IndolylMethane (DIM)

ACF228™, DIM-Pro2™

bFGF

Hair-Pro™

Dilantin®

Phenytoin

BHT (butylhydroxytoluene)

ACF228™, BHT-Pro™

Blueberry extracts

Andro-Pro™

Borate

Andro-Pro™, Can-C™

DMAE (dimethylaminoeth- Centrophenoxine anol) DMSA (dimercaptosuccinic ACF228™, DMSA-Pro™ acid)

www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

DMSO (Dimethyl sulfoxide) Laetrile

Natural (animal): Armour® thyroid, ERFA® thyroid, Nature® thyroid, thymus, vasopressin

D-pantethine

Can-C Plus™

Dr. Dean’s recommendations

Acarbose, centrophenoxine, CurcuminSR™, Hydergine®, metformin, piracetam, Xan-Pro™

Dr. Pierpaoli’s recommendations

Melatonin, TRH

Dr. Wright’s recommendations

DHEA, Esnatri™, progesterone

Ebixa®

Memantine

EDTA (ethylene diamine tetraacetic acid)

EDTA-Pro™

HRT (hormone replacement therapy for women)

DHEA, Esnatri™, melatonin, progesterone

Eldepryl®

Deprenyl

Hair-Pro™, Novisyn®

Electrolytes

Volt-Pro™

Hyaluronic acid (hyaluronan)

Enzymes

Boluoke®

Hy-Pro™

EPA (eicosapentaenoic acid)

PEO-Pro™

Hydergine (ergoloid mesylates)

IGF-1 (LR3)

Ergoloid mesylate

Hydergine®, nicergoline

IGF-1 (insulin like growth factor one) Indol-3-Carbinol (I3C)

DIM

Iodide/ Iodine Ixel® Ketoconazole L-arginine L-carnitine L-carnosine

ACF228™, Iodine-Pro™ Milnacipran Nizoral® Mito-Pro2™ Mito-Pro2™ Carnosine, ACF228®, Can-C™, Can-C Plus™ Neo40® Can-C Plus™ Digestif® ATP-Boost™, Mito-Pro2™

Estrogens (estradiol, estriol, Esnatri™ estrone) Finasteride

Hair-Pro™

Florinef®

Fludrocortisone

Folic acid (folate)

ACF228™, DIM-Pro2™§

Free radical scavengers

ACF228™, ATP-Boost™, BHT, glutathione, idebenone, melatonin, Mito-Pro2™, pyritinol

Fructoborate

Andro-Pro™

Fucoidan

Stem Cell Worx®

GABA (gamma-aminohydroxybutyric acid)

Gamalate®, picamilone

GABOB

Gamalate®, Gamibetal®

GHRP6

Release-Pro™

Ginseng

Youth Gems®

Glucophage®

Metformin

Glutathione

ACF228®, ACG

Glycerine (glycerin)

Can-C™

Glycosides

BEC5 Curaderm®

Hawthorne Berry (crataegus)

Neo40®

HGH (human growth hormone/ somatropin)

GABOB, GHRP2, GHRP6, sermorelin

Hormones (includes Bio-identical: Aldosterone, hormonal support supple- DHEA, Esnatri™, melatonin, ments) MSH, oxytocin, pregnenolone, progesterone, TRH

Synthetic: Desmopressin, Eutirox® thyroid, fludrocortisone, hydrocortisone, T3-Pro™ Supporting agents: DIMPro2™, GHRP2, GHRP6, peptide bioregulators, SAMe, sermorelin

L-citrulline L-histidine Licorice Lipoic acid (includes R-lipoic acid) L-methione Lucidril® Lumbrokinase Magnesium

Malic Acid Manganese Mastic Meclofenoxane Melanocyte stimulating hormone Mild Silver Protein Milk protein Minerals (general) Minoxidil N-acetylcarnosine N-acetylcysteine Namenda®

ACF228™, Can-C Plus™ Centrophenoxine Boluoke® Andro-Pro™, Bone-Pro2™, Digestif®, Gamalate®, Magnesium-Pro™, Mito-Pro2™ EDTA-Pro™ Mito-Pro2™ Digestif® Centrophenoxine MSH2 Silver Bone-Pro2™ Min-Mouth™ (mouthwash), Volt-Pro™ Minox-Pro™ Can-C™ ACF228™, Can-C™ Plus Memantine

www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

47

Neurontin® Nettle root extract Niacin (nicotinate, niacinamide, vitamin B3) Nicotinamide adenine dinucleotide Nootropil®/ Nootropyl® Nordihydroguaiaretic acid (NDGA) Omega 3 (DHA) Omega 6 (linoleic acid, GLA) Omega 9 (oleic acid) Oxythiocynate (OCSN) Parent Essential Oils (PEO) PABA (para-aminobenzoic acid) Panthenol (pantothenic acid) PCPA (paarachlorophenoxyacetic acid) Pepermint Oil Peptides

Pimagedine Pomegranate extracts Potassium Prasterone Propionyl-L-carnitine Probiotics Procaine (Novocain®) Pygeum africanum Pyroloquinoline quinone Quercetin Red clover herb extracts Reminyl® Resveratrol Retinolic acid (tretinoin) Ribonucleic acids (RNA) Salicylic acid S-Adenosyl-L-Methionine Saw palmetto (Serena Repens) Selenium

Seligiline

48

Gabapentin Prostate-Pro2™ Picamilone, Xan-Pro™

Silver

NADH, PQQ

Thiocynates Thyroids

Solasodine glycosides

Piracetam ACF228™, Digestif® PEO-Pro™ PEO-Pro™ PEO-Pro™ 1st Line™ PEO-Pro™ Gerovital® Mito-Pro2™ Centrophenoxine Min-Mouth™ mouth rinse Cerebrolysin®, GHRP2, GHRP6, peptide bioregulators, sermorelin, TRH, Youth Gems® Aminoguanidine Andro-Pro™ Gerovital®, Potassium-Pro™ DHEA Vigor-Pro2™ Symprove® Gerovital® Prostate-Pro2™ PQQ Digestif® Prostate-Pro2™ Galantamine Resveratrol-SR™, Stem Cell Worx® Retin-A®, Retirides® Cerebrolysin®, NeyDent® toothpaste BEC5 Curaderm®, Sol Answer™ SAMe MinSaw™, Prostate-Pro2™

Thyrotropin releasing hormone Tribulus terrestris TRX Turmeric

ACS®, Min-Mouth™ mouth rinse BEC5 Curaderm®, Sol-Answer™ 1st Line™ Natural brands: Armour®, ERFA®, Nature® Synthetic brands: Eutirox® (T4), T3-Pro® (T3) Supporting agents: Peptide bioregulator (Thyreogen®) TRH Andro-Pro™ Hair-Pro™ Curcumin

Ubiquinone, ubiquinol

CoQ10

VEGF Vincamine Vinpocetine Vitamin B1 (thiamine) Vitamin B2 (riboflavin) Vitamin B3 (niacin, niacinamide) Vitamin B6 (pyridoxal, pyridoxine)

Hair-Pro™ Anacervix® Vin-Pro™ Mito-Pro2™ Mito-Pro2™ Mito-Pro2™, Picamilone, Xan-Pro™ ACF228™, Andro-Pro™, DIM-Pro2™, Gamalate®, pyridoxamine DIM-Pro2™, Neo40® Laetrile Digestif®, MinSaw™, Neo40® Can-C Plus™, DIM-Pro2™, Prostate-Pro2™ Bone-Pro2™

Vitamin B12 (cobalamin) Vitamin B17 Vitamin C (ascorbic acid) Vitamin E (tocopherols) Vitamin K2 (menatretrenone) Yohimbine Zeolite Zinc

ACF228™, DIM-Pro2™, MZS™, Prostate-Pro2™, Selenium-Pro™, Thym-Uvocal® Deprenyl

www.antiaging-systems.com • Order hotline: 1-866-800-4677 • e-mail: ias@antiaging-systems.com

Vigor-Pro2™ ACZ® Andro-Pro™, Can-C Plus™, Mito-Pro2™, MZS™, Thym-Uvocal®, Zinc-Pro™

OUR NEW LOOK WEBSITE

WE’ VE GONE GREEN! After several months of work overhauling the IAS website in 2015, we are pleased to announce its refresh and update in January 2016. There is a new color and look and it’s a mobile friendly site with drop-down menus making navigation easier, helping you to find what you need faster.

Here’s a quick breakdown of what you can find at:

www.antiaging-systems.com SHOP All Products » Search by A-Z » Search by Ingredients » New Products » Special Offers PRODUCT CATEGORIES » Books » Diagnostics » Hormones » Medicines » Nutrition » Peptides » Smart Drugs » Topicals » Others INFO Health Conditions » Search via cross-reference list Aging Matters™ magazine » Download all the back issues

Articles » View all our professional and referenced materials Videos » See the complete list here, also includes audio files Ward Dean, M.D. » Read Dr. Dean’s answers Calendar of events » What’s happening around the World Books » Publication reviews Blog » Read and join our Blog SUBSCRIBE » Get your Aging Matters™ magazine TESTIMONIALS » From both professionals and public CONTACT » IAS phone, fax and email

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49

TESTIMONIALS NICE COMMENTS FROM NICE PEOPLE

Dr. Aubrey De Grey “IAS has shown great vision and

Garry Gordon, MD, DO, MD (H)

Jonathan Wright, M.D.

“I am a 77 year old Physician

“Every adult has the right to take

Nicholas Perricone, M.D. “IAS is an outstanding resource

leadership, as an organisation

who has practiced medicine

care of his or her own personal

for the finest, most up-to-

focused mainly on the

for nearly half a century.

health as he or she chooses.

date news and information

provision of contemporary

My antiaging research has

In the 20th and 21st centuries,

on healthy aging. They also

medical interventions against

permitted me to overcome

this universal human right

offer products of the highest

aging, and in also supporting

serious health problems.

has been nearly obliterated

integrity and efficacy. In fact,

the SENS Foundation’s efforts

Everyone can do this, but it

by an ocean of nanny-state

IAS is the world’s greatest

to hasten the development of

requires specialized knowledge

regulation and deliberate

source (often the only source)

much more powerful future

and the highest quality

suppression of information by

for the most cutting edge and

interventions.”

products. IAS is a vital link in

bureaucracies, with hidden

advanced nutrients to ensure

my antiaging program because

and not-so-hidden agendas.

optimum health span and maximum life span.”

they continually provide both

International Antiaging

accurate information AND the

Systems is a beacon of useful

high quality products we all

health care information and

require, if we are to achieve

a literal island of freedom of

our maximum intended

health care product choice in

useful lifespan.”

our otherwise un-free health care world.”

Thierry Hertoghe, M.D.

“IAS is one of the pioneering societies in antiaging medicine...”

Thierry Hertoghe, M.D.

“IAS has a history of making throughout the world crucial, but difficultly accessible medications available to patients. IAS is one of the pioneering societies in antiaging medicine that has

See all professional and public testimonials at: www.antiaging-systems.com/content/11-testimonials

50

www.antiaging-systems.com // Order hotline: 1-866-800-4677 // e-mail: ias@antiaging-systems.com

helped this new medical specialty move forward.”

PAYMENT OPTIONS ACROSS THE IA S WEBS ITES…

PAYMENT OPTIONS AND CONTACT DETAILS The IAS Group offers a wide range of payment options to make the completion of your order as easy as possible.

Payment options for www.antiaging-systems.com:

Other sites in the IAS Group www.antiaging-nutrition.com, www.iasjapan.com, www.antiaging-peptides.com, www.antiaginghormones.com and www.antiaging-nootropics.com accept the following method of payments:

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WEBSITES www.antiaging-systems.com www.antiaging-nutrition.com www.antiaging-nootropics.com www.antiaging-peptides.com www.antiaging-hormones.com www.IASjapan.com

(all of our products in one place; English language) (our nutritional products; English language) (our smart drugs and nutrients; English language) (our peptide bioregulators; English language) (our hormones; English language) (our nutritional products; Japanese language)

EMAIL ias@antiaging-systems.com iasjapan@antiaging-systems.com

(English language) (Japanese language)

PHONE USA: 1-866-800-4677 (orders only) Japan: 050-553-29606 UK: 0208-123-2106 ROW: +44-208-123-2106

1-415-992-5563 (enquiries)

Please note: Our customer care team is available from 9am till 6pm GMT Monday-Friday.

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MAIL Unfortunately personal checks and money orders cannot be accepted at this time.

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51

PIRAPRO

™

The original nootropic

PIRAPRO™

CONTAINS PIRACETAM

100X 800MG TABLETS $19.99

BUY 4 OR MORE FOR ONLY $14.99* (SAVE 25% PER BOX) *Offer valid until June 30th 2016

*Restrictions may apply in some countries. All information is educational and does not replace your physician’s advice and is subject to IAS terms and conditions which may change without notice.