Validation of anti-aging drugs by treating age-related diseases Aging (Albany NY). 2009 March; 1(3): 281–288
Cancer Center, Ordway Research Institute, Albany, NY 12208, USA
Humans die from age-related diseases, which are deadly manifestations of the aging process. In order to extend life span, an anti-aging drug must delay age-related diseases. All together age-related diseases are the best biomarker of aging. Once a drug is used for treatment of any one chronic disease, its effect against other diseases (atherosclerosis, cancer, prostate enlargement, osteoporosis, insulin resistance, Alzheimer’s and Parkinson’s diseases, age-related macular degeneration) may be evaluated in the same group of patients. If the group is large, then the anti-aging effect could be validated in a couple of years. Startlingly, retrospective analysis of clinical and preclinical data reveals four potential anti-aging modalities.
Problem And Solution The discovery of anti-aging drugs is no longer a fantasy. Numerous genes for aging and longevity have been identified in diverse organisms, revealing potential targets for potential anti-aging drugs. But how could potential anti-aging drug be introduced to humans? There are two problems. First, the effect of anti-aging agents on human aging may require almost a lifetime to determine. Second, it is seemingly desirable to test anti-aging drugs in healthy individuals. However, all drugs have side effects. And, in healthy individuals, side effects would preclude clinical trials. How might these problems be solved? How could we validate anti-aging drugs in humans without life-long trials in healthy individuals?
The solution includes two steps. First, we must find an indication for a drug to treat at least one chronic disease. Then this drug could be tested in humans, not as an anti-aging drug, but as therapy for a particular disease. In fact this approach has been suggested for introduction of activators of sirtuins to the clinic. Second, we must find a biomarker of aging that absolutely predicts longevity. Then using this biomarker, the anti-aging effect could be evaluated in the same patients.
Disease-specific drugs versus anti-aging agents Slowing aging would delay all age-related diseases. If a drug is effective against one particular disease only, such a drug is not anti-aging. And current drugs are not anti-aging. For example, insulin compensates diabetes. Yet, insulin does not treat cancer. And vice versa chemotherapy may treat cancer but does not treat diabetes. So neither chemotherapy nor insulin is an anti-aging modality. Furthermore, both insulin and chemotherapy may accelerate aging.
From metformin and calorie restriction to rapamycin The underlying cause of age-related type II diabetes is insulin resistance. Insulin treatment does not ‘treat’ the cause, it just compensates for resistance. Unlike insulin, metformin, an oral anti-diabetic drug, restores insulin sensitivity in type diabetes type II. Remarkably, metformin decreases the incidence of breast cancer. Also, metformin is considered for cancer treatment and inhibits atherosclerosis in diabetic mice. Metformin is used to induce ovulation in patients with polycystic ovary syndrome (PCOS). Six months of 1700 mg/d metformin treatment improved fertility in anovulatory PCOS women. Given such effects on infertility, type II diabetes, cancer and atherosclerosis, it is plausible that metformin slows aging. In fact, it extends life span in rodents.
Calorie restriction (CR) extends life span from yeast and worms to rodents and perhaps humans. If we did not already know that CR slows aging, how might we figure that out based solely on clinical data? Unrestricted food consumption leads to obesity associated with diabetes, atherosclerosis, thrombosis, hypertension, cancer (especially breast, prostate and colon cancer), coronary heart disease, stroke, osteoporosis and Alzheimer’s disease. In other words, unrestricted eating in humans (ad libitum in rodents) accelerates most, if not all, diseases of aging. So we can conclude that CR delays all diseases of aging. This suggests that CR is an anti-aging modality. And it is known that CR extends life span in almost all organisms from yeast to mammals.
Numerous factors including insulin, glucose and amino acids activate the nutrient-sensing TOR (target of rapamycin) pathway. When the TOR pathway is activated, it acts via S6K to deplete the insulin-receptor-substrate (IRS1/2), causing insulin resistance. Metformin indirectly (by activating AMPK) inhibits TOR and thereby restores insulin sensitivity.
CR decreases levels of nutrients and insulin and thus de-activates TOR. It is possible that the anti-aging effects of CR and metformin are due to inhibition of the TOR pathway. Like CR, rapamycin decreases size of fat cells and animal weight. When rats (15 weeks old) were either treated 1 mg/kg rapamycin 3 times per week for 12 weeks, rapamycin decreased their weight. Mean adipocyte diameter was decreased from 36 μm to 25 μm. At the end of the study, mean body weight in the rapamycin-treated rats was 356 g instead of 507 g, in spite of comparable food intake. So rapamycin imitated CR. CR may also extend life span by activating sirtuins. Probably, sirtuins, AMPK and mTOR are linked in the common network. Genetic inhibition of the TOR pathway slows down aging in diverse organisms, including yeast, worms, flies and mice. If genetic inhibition of the TOR pathway slows aging, then rapamycin, a drug that inhibits TOR, must slow aging too. Once used for any indication, even unrelated to age-related diseases (such as renal transplantation, for instance), an anti-aging drug should slow down age-related diseases such as cancer, osteoporosis and atherosclerosis. Rapamycin is already used in renal transplant patients. If a drug is indicated to treat most age-related diseases, then this drug could be defined as an anti-aging drug. The probability that a non-anti-aging drug would have independent activities against all diseases is exceedingly low. Rapamycin analogs are approved to treat certain cancers. Based on preclinical data, rapamycin has been considered in such pathologies as obesity, atherosclerosis, cardiac hypertrophy, aortic aneurysm, osteoporosis, organ fibrosis (liver, renal, cardiac fibrosis), neurodegeneration, Alzheimer’s disease, Parkinson’s disease, psoriasis, skin scars and keloids, multiple sclerosis, arthritis, and renal hypertrophy in diabetes. In principle, life-extending effect of anti-aging drug might be limited by side effects. Although chronic administration of rapamycin is associated with some undesirable effects in transplant patients, they might be avoided by administrating rapamycin in pulses (for example, once a week). For example, chronic administration of rapamycin impairs wound healing. In theory, a pulse treatment might rejuvenate wound-healing cells. A single dose of rapamycin reverses insulin resistance, whereas chronic administration of rapamycin may precipitate diabetes in certain conditions. Clinical trials will be needed to determine benefits of pulse treatment with rapamycin. Alternatively, rapamycin can be combined with ‘complementary’ drugs. Thus, hyperlipidemia caused by rapamycin may deteriorate insulin-resistance. Yet, hyperlipidemia caused by rapamycin can be controlled by lipid-lowering drugs. A combination of rapamycin with resveratrol may be especially intriguing. Conclusion It was previously assumed that anti-aging drugs should be tested in healthy individuals. Ironically, the best biomarker of aging is the occurrence of age-related diseases. And this is how anti-aging drugs can be validated in the clinic (by showing that a putative anti-aging drug can prevent or delay the onset of all age-related diseases). Then such drugs could be approved for prevention of any particular age-related disease in healthy individuals. Thus, potential anti-aging drugs should be introduced to the clinical trials for therapy of a particular disease but be ultimately approved for prevention of all age-related diseases in healthy individuals. And this is synonymous to the approval of a drug as anti-aging.

———————

Can We Prevent Aging? — Tips From National Institute On Aging People are living longer. In 1970, the average life expectancy at birth was 70.8 years; in 2000, it was 76.9 years; and by 2030 it is estimated that the “oldest-old,” age 85 and older, could grow to 10 million people. Views on aging are also changing. It no longer necessarily means physical decline and illness— in the last two decades, the rate of disability among older people has declined dramatically. The National Institute on Aging (NIA), part of the Federal Government’s National Institutes of Health (NIH), investigates ways to support healthy aging and prevent or delay the onset of diseases that disproportionately affect us as we age. These studies may not only increase longevity, but may also promote what is known as “active life expectancy”—the time of advancing years free of disability.
Results from NIA-sponsored and other studies are likely to improve our understanding of the benefits and risks of antioxidants, calorie restriction, hormone supplements, and other interventions to promote healthy aging. This tip sheet provides an overview of what we know about these interventions and the research needed to learn more. Until we have a better understanding, it is a good idea to be skeptical of claims that any supplements can solve your age-related problems. Instead, focus on what is known to help promote healthy aging: healthy eating and physical activity. Antioxidants Antioxidants protect the body from the harmful effects of by-products, known as free radicals, made when the body changes oxygen and food into energy. The discovery of antioxidants raised hopes that people could slow aging simply by adding them to the diet. So far, studies of antioxidant-laden foods and supplements in humans have yielded little support for this premise. Further research, including large-scale epidemiological studies, might clarify whether dietary antioxidants can help people live longer, healthier lives. For now, however, the effectiveness of dietary antioxidant supplementation remains controversial. Calorie Restriction, Intermittent Fasting, and Resveratrol Scientists are discovering that what you eat, how frequently, and how much may have an effect on quality and years of life. Of particular interest has been calorie restriction, a diet that is lower by a specific percent of calories than the normal diet but includes all needed nutrients. Research in animals has shown calorie restriction of up to 40 percent fewer calories than normal to have an impressive effect on disease and markers of aging. It has been found to extend the life of protozoa (very small, one-celled organisms), yeast, fruit flies, mice, and rats, as well as other species. Calorie restriction studies with humans and other primates, such as monkeys, are ongoing. Early findings of the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy (CALERIE) study show that slightly overweight adults who cut their calorie consumption by 20 to 30 percent lowered their fasting insulin levels and core body temperature. Both of these changes correlate with increased longevity in animal models. Some studies in nonhuman primates have shown that calorie restriction reduces the incidence of certain diseases such as cancer. Other studies of the effects of calorie restriction on aging and disease in primates are ongoing and have not yet reached any conclusions. Even though calorie restriction appears to work in a variety of species, its effects on longevity are far from universal. Several animal models, including wild mice, show no lifespan extension by calorie restriction. In some strains of mice, calorie restriction even appears to shorten lifespan. Scientists do not know if long-term calorie restriction is safe or practical for humans. While a calorie-restricted diet may never be widely adopted for people, studying calorie restriction offers new insights into the aging process and biological mechanisms that could influence healthy aging. This research may also provide clues about how to prevent or delay diseases that become more prevalent with age and inform the development of treatments for such diseases. Some studies focus on identifying chemicals that somehow mimic calorie restriction’s benefits. Resveratrol, which is found naturally in foods like grapes and nuts, is one compound of interest. In one study, scientists compared two groups of overweight mice on a high-fat diet. One group of mice was given a high dose of resveratrol together with the high-fat diet. The overweight mice receiving resveratrol were healthier and lived longer than the overweight mice that did not get resveratrol. More research is needed before scientists know if a high dose of resveratrol would be safe for humans or even have the same effect as it had in mice. Scientists are also studying the effect of intermittent fasting or reduced meal frequency. In animal models, like mice, reduced meal frequency appears to have a protective effect on the brain and may also help with heart function and regulation of sugar content in the blood. However, the influence of intermittent fasting on human health and longevity is currently unclear. While research into calorie restriction and intermittent fasting continues, there is already plenty of research supporting the value of a healthy, balanced diet and physical activity to help delay or prevent age-related health problems. Hormones Hormones are chemical messengers that set in motion different processes to keep our bodies working properly. For example, they are involved in regulating our metabolism, immune function, sexual reproduction, and growth. Hormones are made by specialized groups of cells within the body’s glands. The glands—such as the pituitary, thyroid, adrenals, ovaries, and testes—release hormones into the body as needed to stimulate, regulate, and control the function of other tissues and organs involved in biological processes. We cannot survive without hormones. As children, hormones help us grow up. In our teenage years, they drive puberty. As we get older, some hormone levels naturally decline. But what does that mean? Scientists do not know exactly. In order to learn more, NIA investigates how administering hormones to older people affects frailty and function. Many of these studies focus on hormones that naturally decline with age, including: Despite research thus far, there are still many unknowns about the risks and benefits of MHT. For instance, because women in their early 50’s were only a small part of the WHI, scientists do not yet know if certain risks are applicable to younger women who use estrogen drugs to relieve their symptoms during the menopausal transition. You may also have heard about a relatively new approach to hormone therapy for women— “bioidentical hormones.” These are hormones derived from plants, such as soy or yams, that have identical chemical structures to hormones produced by the human body. The term “bioidentical hormones” is now also being applied to the practice of compounding or combining hormones such as estrogen and progesterone, theoretically based on a woman’s individual hormonal needs. Large clinical trials of these compounded hormones have not been done, and many bioidentical hormones that are available without a prescription are not regulated or approved for safety and efficacy by the FDA. FDA-regulated bioidentical hormones, such as estradiol and progesterone, are available by prescription for women considering MHT. For middle-age and older women, the decision to take hormones is far more complex and difficult than ever before. Questions about MHT remain. Would using a different estrogen and/or progestin or different dose change the risks? Would the results be different if the hormones were given as a patch or cream, rather than a pill? Would taking progestin less often be as effective and safe? Does starting MHT around the time of menopause, compared to years later, change the risks? Can we predict which women will benefit or be harmed by using MHT? As these and other questions are addressed by research, women should continue to review the pros and cons of MHT with their doctors and assess their personal risks and benefits to make an informed decision about whether or not this therapy is right for them. NIA has additional free information on menopausal hormone therapy. DHEA Dehydroepiandrosterone, or DHEA, is made from cholesterol by the adrenal glands, which sit on top of each kidney. It is converted by the body into two other important hormones: testosterone and estrogen. For most people, DHEA production peaks in the mid-20’s and then gradually declines with age. The effects of this decline, including its role in the aging process, are unclear. Even so, some proponents claim that over-the-counter DHEA supplements can improve energy and strength and boost immunity. Claims are also made that supplements increase muscle and decrease fat. To date, there is no conclusive scientific evidence that DHEA supplements have any of these benefits. The conversion of naturally produced DHEA into estrogen and testosterone is highly individualized. There is no way to predict who will make more or less of these hormones. Having an excess of testosterone or estrogen in your body could be risky. Scientists do not yet know the effects of long-term (defined as over 1 year) use of DHEA supplements. Early indications are that these supplements, even when taken briefly, may have detrimental effects on the body, including liver damage. But the picture is not clear. Two short-term studies showed that taking DHEA supplements has no harmful effects on blood, prostate, or liver function. However, these studies were too small to lead to broader conclusions about the safety or efficacy of DHEA supplementation. Researchers are working to find more definite answers about DHEA’s effects on aging, muscles, and the immune system. In the meantime, if you are thinking about taking DHEA supplements, be aware that the effects are not fully known and might turn out to cause more harm than good. Many Questions, Seeking Answers NIA supports research that seeks to learn more about aging and the risks and benefits of potential interventions such as antioxidants, calorie restriction, hormone therapies, and supplements. These studies take time. A great deal of basic animal and clinical research is yet to be done. And, because research is an incremental process, results can move knowledge forward, but it can also take scientists back to basics. Although one goal of NIA research is to determine whether these interventions improve the health of older people, have no effect, or are harmful, don’t be surprised if the results of these studies open the door to more questions. Until more is known about antioxidants, resveratrol, and hormone supplements, consumers should view these types of supplements with a good deal of caution and doubt. Despite what advertisements on television, the internet, and magazines may claim, there are no specific therapies proven to prevent aging. Some harmful side effects already have been discovered; additional research may uncover others. People with genuine deficiencies in specific hormones should consult their doctors about appropriate treatments. Talk with your doctor if you are interested in any form of hormone therapy or “anti-aging” approaches beyond a healthy diet and physical activity. Meanwhile, people who choose to take any hormone supplement without a doctor’s supervision should be aware that these supplements appear to have few clear-cut benefits for healthy individuals and no proven influence on the aging process.

———————

First stop, diabetes. Next stop: the very process of aging.

In a study scheduled to be published tomorrow in Nature, Sirtris Pharmaceuticals researchers successfully treated diabetic mice with a compound that activates

=============
Article Content:

Searching for Fountain of Youth in a Pill
By Brandon Keim

First stop, diabetes. Next stop: the very process of aging.

In a study scheduled to be published tomorrow in Nature, Sirtris Pharmaceuticals researchers successfully treated diabetic mice with a compound that activates an enzyme linked to the body’s most fundamental metabolic processes. Though preliminary, the results add momentum to a body of research that sees seemingly-disparate diseases, from diabetes to cancer, as manifestations of a single fundamental problem: age-related cellular breakdown. Slow that breakdown, and perhaps you can slow aging itself. It won’t ever stop, but it might not be attended by physical and mental failure.

“This is a watershed moment,” said Sirtris CEO Christoph Westphal. “It looks like you can control the proteins controlling the aging process with orally available drugs.”

The enzyme targeted in the Nature paper, called SIRT1, is believed to be stimulated by calorie-restricted diets, which are linked to longevity increases in primates and humans. Another SIRT1 activator, the grape leaf compound resveratrol, has increased lab animal lifespans and been used to treat diabetes and obesity in mice.

Thousands of people already practice caloric restriction, which requires incredible discipline and may cause unwanted metabolic changes. Thousands more take resveratrol, though the effects have yet to be rigorously studied. They’re willing to turn themselves into human guinea pigs or near-emaciated waifs because the benefits are so tantalizing. In the last few decades, some scientists and doctors have suggested that a range of lethal conditions have the same root: cellular deterioration that progresses with age.

More specifically, many scientists point to deterioration of mitochondria, the organelle power plants present in every cell of the human body. As mitochondria generate chemical energy — and help cells communicate, differentiate and grow – they spew out DNA-damaging free radicals. Over time, the mitochondria wear down; tissues malfunction and fail. The picture’s still hazy, the cause-and-effect not clear, but scientists have found evidence of mitochondrial degeneration in cancer, Parkinson’s disease, Alzheimer’s disease, diabetes, heart disease and a plethora of other conditions.

As described in the Nature paper, diabetic mice given Sirtris’ compound had improved insulin sensitivity and and lower blood glucose levels — and their mitochondria worked better, too. Rejuvenated mitochondria have also been observed in earlier studies of resveratrol’s therapeutic and longevity-enhancing effects.

It’s too soon to apply the results to people with diabetes, much less to people hoping to evade the ravages of dementia and debilitation — but the possibility is there. “Mechanistically, it’s fair to think that this will work in the biggest killers of western society. It’s one of the few approaches that could help with multiple diseases,” said Westphal.

He’s careful to point out that barely a tenth of all drugs survive from testing to approval, and the compound described in Nature isn’t even in Phase I trials. He’s also quick to distance Sirtris from off-label claims; this compound, as well as a resveratrol derivative currently in Phase I trials, are both aimed squarely at diabetes, and won’t be marketed as anything more.

But if people are willing to push ahead of science by taking resveratrol or practicing caloric restriction, they’ll certainly push to use a SIRT1-activating diabetes drug for other conditions. Neither is Sirtris the only player: every major pharmaceutical company, said Westphal, is pursuing research on the seven sirtuin enzymes. SIRT1 is but one of these, and all are linked to cellular regulation. “We’re trying to emphasize how many years and how much risk is involved,” he said. “But we’re at a different stage than we were five or ten years ago. There are people trying to develop drugs that target the aging process.”

———————

source: www.vanuatumedical.com
As we age, a non-enzymatic reaction between sugars in the blood and amino groups in our body’s proteins, fats, and DNA, produces compounds called advanced glycation end-products (appropriately called AGEs). AGEs bond to one another, creating crosslinks between proteins that disrupt normal cellular activity. By stiffening collagen and elastin (the key proteins of the extracellular matrix in all tissues), AGEs promote high blood pressure, atherosclerosis, and heart failure. In the kidneys, AGEs target nephrons, the filtering units that remove wastes from the blood.
Not only do AGEs wreak havoc on extracellular matrix proteins, they also activate AGE receptors (called RAGEs) on cells throughout the body. RAGEs trigger the release of a wide variety of compounds involved in inflammation and the creation of stiff fibrous tissue, compromising function in the heart, blood vessels, kidneys and brain.
In addition to chronological aging, AGE formation is greatly increased by high blood sugar levels and plays a central role in all diabetes-related disease complications.
AGE accumulation is also accelerated by insulin resistance, high cholesterol, smoking, and a diet lacking in vitamin, mineral and antioxidant-rich fruits and vegetables. In fact, a diet made up of highly processed foods, especially foods processed at high heat, is loaded with AGEs, which our bodies absorb from the food.
Fortunately, test tube, animal and human studies demonstrate that AGE crosslinks can be effectively—and safely—broken by ALT-711 (alagebrium), preventing and reversing AGE-related pathology. In diabetic animals, ALT-711 has been shown to reduce the body’s load of AGEs, promoting AGE excretion in the urine, and to improve the heart muscle’s pumping ability, decrease stiffness in the aorta (the artery through which blood flows into the body from the heart), decrease proteinuria (protein in the urine, a sign of kidney damage), reverse ED (erectile dysfunction) and extend survival.
In men who still had high blood pressure (systolic blood pressure >140 mmHg, diastolic blood pressure <90 mmHg or pulse pressure >60 mmHg), even after treatment with antihypertensive drugs, ALT-711 (210 mg twice daily for 8 weeks) decreased arterial stiffness by 37% and reduced blood pressure by an average of 6.8 mmHg. The men’s blood flow (measured by flow-mediated dilation) increased from an average of 4.6 to 7.1, plus levels of a number of compounds that indicate blood vessel damage and thickening greatly decreased.
When given to elderly patients (mean age 71) with diastolic heart failure, ALT-711 (420 mg/day for a period of 16 weeks) significantly decreased left ventricular mass (the major pumping chamber on the left side of the heart). Patients’ quality of life increased almost 25% as measured by the Minnesota Living with Heart Failure assay.
Other recent studies indicate that ALT-711’s multiple benefits are related not only to its ability to break AGE-related crosslinks, but also to its effects on cell receptors (RAGE), which result in lowered oxidative stress (free radical damage) and diminished pro-fibrotic cytokine production.
In Phase 2 clinical trials involving approximately 800 patients, ALT-711 has been found to be so safe and well-tolerated that it produced fewer side effects than placebo!
For all of us as we grow older, but especially for those with diabetes, metabolic syndrome or cardiovascular disease, ALT-711 (alagebrium) offers effective, safe therapy for the prevention, retardation, and reversal of the diseases of AGE-ing.
REFERENCES
Pizzorno L, ALT-711 – Effective New Anti-Aging Therapy, Smart Publications http://www.smart-publications.com
Pizzorno L, ALT-711: Cross Link Breaker Delivers Effective Anti-AGE-ing Therapy, http://www.lmreview.com/#AGEs
Author: dragon web profit

Anti-Aging Skin Care Web Site: http://www.antiagingskincarebeauty.com

Emai: dragonwebprofit@antiagingskincarebeauty.com

———————

source: www.waaam.net
A comprehensive program to reform and advance healthcare in the United States, The A4M Twelve-Point Actionable Healthcare Plan: A Blueprint for A Low Cost, High Yield Wellness Model of Healthcare by 2012 has garnered support from 35 professional medical organizations and educational institutions and was developed with invaluable input from the 24,000 physician, health practitioner, and scientist members of the American Academy of Anti-Aging Medicine (A4M; www.worldhealth.net) who represent 110 nations worldwide.
We unveil an innovative, technology-based fix to healthcare with the potential to:
the underlying philosophy of healthcare in this nation must be reformed in revolutionary new ways. In place of the disease-based approach that treats people after they exhibit signs of illness, we submit that it is time for the nation to adopt a wellness-oriented model to healthcare. Such a model stresses very early detection of illness and promotes disease prevention, yielding opportunities for the best prognoses and economical treatments. As reported by the Congressional Budget Office, up to one-third of this nation’s healthcare spending – more than 0 billion – does not improve Americans’ health outcomes.
To compound the issue of healthcare reform, the United States is a driving force in a trend of unprecedented global aging. The average age of the world’s population is increasing at an unprecedented rate. The number of people worldwide ages 65+ was 506 million as of midyear 2008; by 2040, that number will hit 1.3 billion. Thus, in just over 30 years, the proportion of older people will double from 7% to 14% of the total world population. In the United States, men and women ages 65+ represented 12.4% of the population in the year 2000, with that age bracket projected to swell to stand at 20% of the population by 2030. In 2007 in the United States, six major diseases among Americans ages 65+ resulted in medical and lost productivity costs of more than 6 billion. In the coming years, the cases of these six diseases, namely – chronic lung disease, ischemic heart disease, stroke, lung cancer, pneumonia and gastrointestinal illness – are expected to surge as the population ages, potentially sending the costs of age-related diseases skyrocketing. Steps to prepare the nation to address the social, economic, and personal ramifications of a graying society now, are urgently necessary.
The A4M Twelve-Point Actionable Healthcare Plan: A Blueprint for A Low Cost, High Yield Wellness Model of Healthcare by 2012 provides the following practicable “here and now” solutions to reform and advance healthcare in the United States, while addressing the challenges of global aging:
Point Point Item Projected Extension in Healthspan, Lifespan: ADDITIONAL YEARS PER PERSON Projected Savings to Healthcare System: US $ DOLLARS I Point of Care (POC) Laboratory Testing 2 .75 Billion II Biomarkers of Aging and Health Measurement 5 9.5 Billion III Free Biannual Comprehensive Metabolic Testing 3 4.6 Billion IV 24/7 Telemedicine Consultation Access 3 0 Billion V Aging Intervention Drugs 3 .2 Billion VI Stem Cells, Nanotechnology, Genetic Engineering 4-12 7.1 Billion VII Personalized Genetic Testing and Nutrigenomics 2 2.3 Billion VIII Free/Subsidized Access to Gym, Spa, Detoxification, and Physical Rehabilitation Facilities 2 .4 Billion IX Online Electronic Database on Aging Intervention 5 .4 Trillion X Free Online Medical Education XI The World Center for Anti-Aging Medicine XII The Leisure Class TOTAL IMPACT, Points 1 though 12 29+ years .64 Trillion Author: dragon web profit

Anti-Aging Skin Care Web Site: http://www.antiagingskincarebeauty.com

Emai: dragonwebprofit@antiagingskincarebeauty.com

———————