Sermorelin – Improve hGH Therapy Safety With Peptides

hGH Replacement Therapy has been a popular Anti-Aging and performance enhancing treatment since as early as 1990, but unfortunately, use of hGH does not come without risks.

Sermorelin acetate has become a popular alternative as it enables you to obtain the benefits of hGH Therapy, without the associated risks.

This article looks more closely at Sermorelin injections as a hGH alternative.

To begin with, it is a good idea to have an understanding of what sermorelin acetate is and what role it plays when administered via injection. Scientifically sermorelin acetate is referred to as growth hormone releasing factor 129 NH2-acetate, this is because it is a peptide which contains the first 29 amino acids that make up growth hormone produced in our bodies.

This contributes to sermorelins function as a growth hormone secretagogue (a substance which causes another substance to be secreted Wikipedia) in this case, the substance whose secretion is promoted is growth hormone. For this reason, sermorelin is often also referred to as an hGH stimulator and is considered an excellent alternative to hGH.

One important thing to understand about Sermorelin is that it promotes healthy function of the pituitary (the gland responsible for our bodys production of hGH) during the aging process. This is a far cry from aggressive administration of hGH which can, in fact, negatively impact normal pituitary function.

There are many advantages of using sermorelin for hGH replacement therapy rather than hGH itself, both in terms of safety as well as accessibility and sermorelin price.

With regards to safety, it has long been known that administration of hGH is associated with a range of adverse side-effects. These include, but are not limited to, bone and tissue growth abnormalities, diabetes, heart disease and even cancer.

Add to this the possibility of overdose, a shutting down of normal growth hormone production and the possibility of a sudden reduction in response to hGH injections (a phenomenon known as Tachyphylaxis) and you may start to wonder if hGH is worth the risk.

Sermorelin on the other hand, has not been associated with the same long list of side-effects as hGH. Overdose is considered to be very difficult, if not impossible, and administration of sermorelin results in a release of growth hormone more in line with our bodys natural process rather than having consistently high levels as is the case with hGH injections.

Sermorelin peptides do not shut down the bodys own production of hGH but instead supports pituitary function and promotes natural production of hGH. For this reason, increased hGH production is noted for a period even after sermorelin therapy has stopped.

Check out this table comparing Peptide Therapy and hGH

Then there are the safety concerns surrounding use of hGH which arise from its status as a controlled substance. Legally doctors can only prescribe hGH for children with human growth hormone deficiency, medically diagnosed hGH deficiency in adults and individuals with HIV. This makes accessing hGH very difficult and has contributed to the illegal sale of hGH.

As with any illegally produced and purchased drug, the consumer has no way of knowing the quality of drug they are injecting into their body. At best, you may inject inert (and therefore useless) hGH, at worst a lethal cocktail of contamination produced in somebodies garage. And even if you do find what appears to be a reputable seller of hGH outside of the US, import it and you face the legal implications of importing a controlled substance.

Sermorelin, by comparison, is not governed by the same strict laws of medical use and this is largely due to its safety profile. For this reason, sermorelin is much more accessible and is commonly prescribed by doctors in anti-aging and wellness clinics in conjunction with other growth hormone releasing peptides such as GHRP-2 and GHRP-6.

Sermorelin is still a pharmaceutical and therefore a prescription is required to purchase it but there are legitimate online portals which match patients and doctors making it very easy for you to purchase sermorelin and have it delivered to your home.

Another distinct advantage of using sermorelin instead of hGH is cost. hGH typically costs $1000+ per month of treatment, sermorelin is a much more affordable option with 3 months treatment of sermorelin costing significantly less than just one month on hGH.

Check the Cost of 1 Month and 3 Months Supply of Sermorelin

Besides the obvious advantages of sermorelin injections detailed above, you may want to know how you can benefit from using this therapy. Perhaps the easiest way to understand the potential benefits of hGh replacement therapy is to look at the symptoms of hGH decline and the effect hGH replacement has on those symptoms. These are detailed below:

1. Changes in Body Composition

Changes in body composition due to decreasing levels of hGH are reflected by a decrease in lean body mass (muscle) and an increase in fat mass. Correcting hGH levels has been shown to reverse this state by improving muscle mass and reducing fat.

2. Bone Mineral Density

Research indicates that hGH deficiency in adults contributes to a reduction in bone density and therefore increased risk of osteoporosis. It has also been shown that hGH replacement therapy for greater than 12 months results in improved bone mineral density and hence, lower risk of osteoporosis.

3. Muscle Strength

Due to changes in body composition detailed above, muscle strength is understandably compromised. As hGH therapy corrects body composition and improves muscle mass, muscle strength also improves. The best results are gained after 12 months of hGH therapy.

4. Joint Health

By improving bone mineral density and increasing muscle mass and strength, hGH therapy can help to prevent joint deterioration that is a feature of arthritis. Optimal growth hormone levels are also essential for health of connective tissue such as the synovium found in joints.

5. Exercise Performance

Exercise performance is reduced in individuals with growth hormone deficiency. This appears to be partially due to reductions in bone density and muscle mass but also in part due to a reduction in oxygen uptake. hGH therapy for 6 months has been shown to improve exercise performance by improving muscle mass and also oxygen uptake

6. Heart Health

There is evidence of a greater risk of heart disease in individuals with growth hormone deficiency and it has been hypothesized that this is due to a greater propensity to develop premature atherosclerosis (a build-up of plaque inside the arteries which increases risk of heart attack and stroke). Growth hormone deficiency also results in changes in heart size and function. These changes have been demonstrated to be reversed after 6 months hGH therapy.

7. Metabolism

Growth hormone deficiency results in a reduced resting metabolism and replacement therapy reverses this decrease. hGH therapy has also been shown to increase protein synthesis, increase fat oxidation, normalize carbohydrate metabolism and reduce LDL (bad) cholesterol. These favorable effects on metabolism may in part explain some of the other benefits of hGH including improved hearth health and body composition.

8. Skin Thickness

A reduction in skin thickness and all-important skin collagen is another result of growth hormone deficiency. Both conditions are improved by hGH therapy.

9. Immune Function

Although adults with growth hormone deficiency are not normally considered to have a compromised immune system, there is some evidence to suggest that hGH therapy can help regulate immune function.

10. Libido

It has been demonstrated that people with growth hormone deficiency have more difficulty with sexual relationships and reportedly, lower energy levels. Many individuals have found an improvement in energy, libido and sexual performance following hGH therapy, some men even claiming an improvement in problems with premature ejaculation.

11. Quality of Life

Reduced psychological well-being has been reported in individuals with growth hormone deficiency and hGH replacement has resulted in improvements in mood, energy and general feelings of well-being.

As discussed, sermorelin peptides are a pharmaceutical product requiring prescription and purchase from a pharmacy.

There are online portals which can connect you with a physician who specializes in prescribing hGH therapy via phone/internet chat. You can then purchase and be sent the sermorelin via the mail.

This is all done in one easy order that includes the consultation with the prescribing doctor (via phone or internet chat), your hGH replacement therapy and ongoing support all in the upfront sermorelin price.

Beware of websites that offer sermorelin for sale without a prescription. Chances are you are not getting the real deal and could be jeopardizing your health.

Compare Available Sermorelin Programs Here

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Sermorelin - Improve hGH Therapy Safety With Peptides

Testosterone Replacement Therapy in Men | myVMC

Introduction to testosterone replacement therapy

Testosterone replacement therapy is a treatment in which additional testosterone is added to a mans body (e.g. by injecting medicines that contain testosterone), to increase the concentration of testosterone in his body. It is used to treat hypogonadism, a condition characterised by low levels of testosterone in the blood and clinical symptoms of testosterone deficiency (e.g. lack of body hair, excessive breast growth). Hypogonadism occurs when a mans testes do not produce enough testosterone, either because the testes are not working properly, or because the hypothalamus or pituitary glandin the brain are not working properly. The hypothalamus and pituitary glands produce hormones that stimulate testosterone production in the testes.

The aim of testosterone replacement therapy is to increase blood testosterone concentrations to normal levels. In doing so, it can also restore the mans sex drive and expression of male sex characteristics (e.g. deep voice, body hair).

Testosterone is one of the oldest marketed drugs and has been used in testosterone replacement therapy since the 1930s.

Testosterone replacement therapy is used to treat men who have received a definitive diagnosis of hypogonadism. In order to be diagnosed with hypogonadism, a man musthave both low blood concentrations of testosterone and clinical symptoms of deficiency (e.g. lack of body hair, breast growth). As most of the causes that underlie testosterone deficiency (e.g. testicular dysfunction) are untreatable, most men who commence testosterone replacement therapy must be treated for the rest of their lives. In men with reversible or age-related causes of testosterone deficiency, testosterone replacement therapy is not used.

Ageing men (> 40 years of age)

As men age, their testosterone levels naturally decrease in a process sometimes called andropause or male menopause. This can lead to clinical symptoms of testosterone deficiency and/or low blood testosterone levels. There is no evidence that testosterone replacement therapy is beneficial for these men.

For older men, treatments that address the conditions causing or worsening testosterone deficiency (e.g.obesity, diabetes, chronic illness) may be effective.

Chronic or transient illness or recent trauma

Testosterone replacement therapy is rarely beneficial where hypogonadism is caused by illness (e.g. diabetes) or trauma (e.g. injury to the testicles). In these cases, the illness or trauma causing testosterone deficiency should be treated.

Prostate or breast cancer

Testosterone replacement therapy is not used to treat men with breast or prostate cancer, because there is a hypothetical risk that treatment may stimulate the growth of these cancers.

Competitive athletes

Use of testosterone replacement therapy may lead to disqualification for professional athletes.

Others

Testosterone replacement therapy is not used to treat men with the following conditions:

Testosterone replacement therapy is not used totreat infertility, erectile dysfunction or non-specific symptoms.

Certain conditions require special consideration before testosterone replacement therapy is used. Tell your doctor if you have:

The goal of testosterone replacement therapy is to restore blood testosterone to normal levels. When used to treat men with hypogonadism, it may also result in other benefits, including:

Improvements in blood testosterone levels and libido generally occur within the first week of treatment, and other benefits usually occur within two months.

It is important to note that testosterone replacement therapy typically induces a strong placebo effect in the initial stages of therapy. This means that many men who are treated with testosterone notice an improvement (e.g. bettersex drive), not because of the testosterone-containing medication has improved their testosterone concentrations, but because of the psychological effect of taking it. In short, some men think testosterone therapy is working and then feel better, even though the treatment does not work. This may lead to confusion and dissatisfaction as the placebo effect of treatment diminishes.

Most adult men begin receiving replacement testosterone at a dose sufficient for restoring blood testosterone to normal levels in men aged < 40 years. In boys who have not yet reached puberty and elderly men, lower doses are usually used at the beginning to avoid excessive increases in libido or energy, which may be dangerous. Once treatment has started, the doctor will monitor the mans blood testosterone levels and symptoms, and may need to adjust the dose depending on how these change.

Testosterone can be administered in various ways, depending on the person. Most men will first receive treatment in the form of testosterone injections every two weeks. Men who cannot receive injections (e.g. those with bleeding disorders) will receive different modes of testosterone treatment. The doctor may also change the type of testosterone administered if the man is dissatisfied with thecurrenttreatment. A doctor will try to prescribe a type of testosterone therapy that suits the patient in terms of cost, response and convenience, and individuals should talk to their doctor if they have concerns about any aspects of treatment.

Injectable testosterone

Injectable testosterone is the standard and most cost-effective treatment option. It can be used in all men except those with bleeding disorders. The injection is an oil-based solution containing testosterone. It is administered by intramuscular injection. Once injected, the solution gradually releases testosterone into the bloodstream.

The standard starting dose is one injection containing 200250 mg of testosterone every 23 weeks. The dose may be reduced to as little as 100 mg in very young or old men. The quantity and frequency of the dose will be adjusted by the doctor, according to the response to treatment. Men who do not achieve adequate increases in blood testosterone may have the dose increased, while those who gain too much blood testosterone may have the dose reduced.

Testosterone injections which are administered every two weeks are known as short-acting injectable testosterones(e.g. Sustanon). While they are effective in increasing blood testosterone levels and often improve symptoms (e.g.libido, mood, energy), testosterone levels and symptoms tend to fluctuate between injections. Men using these injections may experience very high peaks intestosterone levels and a resulting increase in libido and energy in the period immediately following the injection, followed by a period of much lower blood testosterone. Long-acting injections of testosterone (e.g. Reandron), which are administered every 3 months, provide an alternative for men who experience the peaktrough effect.

Long-acting testosterone injections provide testosterone replacement for 1014 weeks.They areadministered by injection deep into the gluteal muscle. The testosterone is released gradually into the bloodstream.

For more information on long-acting testosterone injections, see testosterone undecanoate (Reandron).

Transdermal testosterone patches

Testosterone patches that adhere to the skin may also be suitable for long-term testosterone replacement therapy. However, the patches contain substances that increase the absorption of testosterone, and these cause skin irritation in up to 50% of men who use them. Some 10% of men stop using testosterone patches because of skin irritation. Men may also discontinue use because they find the patches cosmetically displeasing. They may find other transdermal methodsof administrationmore appropriate (e.g. gels, creams).

Most men require a single patch containing 5 mg of testosterone daily. The patch can be applied to the abdomen, upper arm or thigh, and should be left in place for 24 hours after application, when a new patch should be applied.

For more information on testosterone patchess, seetestosterone (Androderm).

Oral testosterone

Oral testosterone therapy (e.g. Andriol Testocaps) uses testosterone undecanoate, the only natural form of testosterone that can be absorbed when taken orally. It may be more expensive and less effective than other modes of testosterone replacement, and is therefore usually used by men who cannot use other forms of testosterone. Oral therapy may also be used to treat older men who are starting therapy, as treatment can be stopped quickly if they are diagnosed with prostate cancer.

The starting dose varies and may be as low as 40 mg daily, although men typically require 160240 mg a day, taken in 24 doses. The doctor will adjust the dose, depending on the response to treatment. Oral testosterone should be taken with food, as this increases the amount of testosterone absorbed by the body.

Testosterone implants

Testsosterone implants contain 800 mg of testosterone (usually in the form of four 200 mg pellets). They are implanted into the buttocks or abdomen, and provide testosterone replacement for around six months. Implants are replaced periodically, once symptoms of testosterone deficiency recur. Inserting the testosterone pellets is a minor surgical procedure, requiring local anaesthetic; this is the major limitation of this method of treatment. However, men using this form of testosterone replacement are usually satisfied with the method, and are more likely to continue being treated than men using other modes of testosterone replacement.

Testosterone implants are not safe for use by older men, who have an increased risk of prostate cancer. If prostate cancer is diagnosed, testosterone replacement must be stopped immediately, which cannot be done if an implant is being used. Implants are also unsuitable for young men with bleeding disorders. Another form of testosterone replacement must be used first, so that a doctor can be sure they will not have any negative reaction to testosterone, before starting this long-term mode of treatment.

For more information on testosterone implants, see testosterone(Testosterone Implants).

Testosterone gel

Testosterone gels (e.g. Testogel)contain 1% testosteronethat is absorbed through the skin. The gel is applied to the skin on the abdomen, shoulder or arm on a daily basis. The standard dose is 5 g (50 mg testosterone), although the dose may be increased to as much as 10 g daily in some men, while others will respond adequately to 2.5 g daily.

Care must be taken to ensure the gel does not come into contact with the skin of individuals other than the man being treated (e.g. sexual partners, children) for at least six hours following application, as this may cause testosterone to be transferred to the contacts skin and absorbed by their body. Absorbing testosterone may be dangerous for children and women, especially pregnant women.

For more information on testosterone gel, see testosterone (Testogel).

Testosterone cream

Andromen forte (testosterone) is a cream containing 5% testosterone. It is ideally applied to the skin of the scrotum on a daily basis. The cream can be applied to the skin of the torso, back, chest, arms and legs, although a higher dose might be required if these sites are used, as less testosterone is absorbed compared to if the cream is applied to the scrotum. The usual starting dose is 1 g of cream (5 mg testosterone), but a doctor may adjust the dose depending on how the man responds to the treatment.

As the causes of testosterone deficiency are typically irreversible, testosterone replacement therapy is usually lifelong. Men who use testosterone replacement therapywill be monitored throughout their treatment to assess their response.

To assess the mans response to treatment, levels of testosterone in his blood are usually measured three months after the start of treatment. Levels of luteinising hormone (LH) may also be measured three to six months after treatment starts, as low levels of LH indicate that the treatment is effective.

If blood tests show that testosterone replacement therapy has failed to adequately increase concentrations of testosterone in the mans blood, hypogonadism may not be the cause of the symptoms. In these cases, testosterone replacement therapy will be stopped and the doctor will start treating other conditions that may contribute to testosterone deficiency.

A doctor will monitor changes to symptoms of testosterone deficiency and side effects of the treatment. This monitoring usually occurs three and six months after treatment commences and annually thereafter. A doctor will typically examine a man for signs of:

Tests that will usually be conducted periodically include:

Testosterone replacement therapy may sometimes be combined with treatment using PDE-5 inhibitors, a medication used to treat erectile dysfunction, for men with both hypogonadism and erectile dysfunction. It should be noted, however, that testosterone deficiency is rarely associated with erectile dysfunction.

Effective testosterone therapy has numerous immediate and long term benefits. These include:

Physical

Sexual

Psychological

The side effects associated with testosterone replacement therapy are rare and vary depending on the age of the man being treated, his life circumstances and health condition. They include:

Testosterone replacement therapy increases the risk of some health conditions, including:

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Testosterone Replacement Therapy in Men | myVMC

Cell Therapy Conferences | Spain | Worldwide Events …

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Cell therapy market investigation gives information about generally accepted clinical and analytical methods that are currently in use for applying cell therapy techniques. It is mainly used mainly in clinics and hospitals. Analysis is done on those companies and products that are actively developing and marketing instrumentation, reagents, and supplies for cell therapy. The cell-based research markets was analysed for 2015, and projected to 2025.They analysed according to therapeutic categories, technologies and geographical areas. The largest expansion will be in diseases of the central nervous system, cancer and cardiovascular disorders. Skin and soft tissue repair as well as diabetes mellitus will be other major markets.

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Track-2 Cellular Therapy Technologies:

Cell therapy technologies overlap with those of gene therapy,immune therapy cancer vaccines, drug delivery, drug discovery, tissue engineering and regenerative medicine. The cellular therapy technologies and methods, which have already started to play a very important role in the practice of medicine. Cell treatments and immunotherapies are changing the substance of pharmaceutical, empowering specialists, doctors and researchers to address the side effects of a sickness, as well as its basic causes, basically educating the body to recuperate itself. The pace of current advancements in cell treatment and immunotherapy is promising, with a few scientists reporting remarkable clinical results.

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Track-3 Cell Therapy of Cardiovascular Disorders

Cardiovascular disease implies a range of disease entities whose therapeutic actions differ. Cell therapy is a 21st century approach which is used to treating the cardiovascular disease and now it is being applied worldwide. However, no concerted approach exists for defining the best treatment conditions.Cardio vascular disorders remains the number one cause of morbidity and mortality in the United States and Europe. In the United States alone, 1 million patients are suffering with myocardial infarction every year, with an associated mortality of 26% at 3 years.

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Track-4 Cell Therapy for Cancer

A number of cell and gene therapy strategies are being evaluated in patients suffering from cancer and these include manipulating cells to gain or lose function. Clinical trials of cell therapy for many different cancers are currently ongoing. The scientists has recently developed novel cancer therapies by combining both gene and cell therapies.Cancer therapeutics cannot cure cancer and yet in 2014, the overall market for Oncologic therapeutics stood at about $84.3 billion. Any drug that can treat a reasonable survival of more than five years for cancer patients can achieve a blockbuster status. Within oncologic therapeutics, immunotherapeutic drugs have increased worldwide acceptance, because they are targeted drugs targeting only cancer cells.

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Track-5 Cell Therapy for Neurological Disorders

New visions into the biology of neural stem cells (NSCs) have raised expectations for their use in the treatment of neurologic diseases. The truth is that the field is moving forward every year, well thought out clinical trials are being planned and undertaken, but to date none have shown a level of effectiveness that gives hope they may be useful as mainline therapies in 2013. With period, development will be made, but it is only by following the well-established methods of transformation from the laboratory to the clinic that this can happen. If such approaches are abandoned in the rush to get to clinic, then there is a real risk that the whole field will be derailed by a terrible result of an ill thought out treatment. If this were to happen then those treatments being advanced using sound scientific principles and which promise to be of a great use in the future, will instead be lost forever as the unproven, commercially driven cells of today confuse and kill the field. Cell therapy and gene transfer to the diseased or injured brain have provided the basis for the development of potentially powerful new therapeutic strategies for a broad spectrum of human neurological diseases.

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Track-6 Cell Science & Stem Cell Research:

Stem cell technology is the subject of much discussion and interest across the world. Newspapers and websites frequently report new discoveries, and this fast-paced field has been the focus of hope, excitement and sometimes controversy. Policy makers, regulators, researchers,clinicians and scientists are constantly debating the progress and potential applications of this exciting science. This Stem cell global strategic report will help us to understand unique product opportunities by stem cell type, derive more revenue from products sold to stem cell scientists, and identify new product growth opportunities before the competition. Use the Survey of Stem Cell Scientists & researchers to understand technical requirements, unmet needs, and purchasing preferences of stem cell researchers worldwide.

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Track-7 Cell Culture & Bioprocessing:

Getting cell therapy products onto the market as quickly as possible still remains a key driver in the improve of recombinant therapeutic proteins. Any such advance in bioprocessing is of particular interest to the industry if it considerably shortens the development timeline or improves the end product. In the monoclonal antibody (MAb) area, platform procedures have allowed companies to regulate on particular mammalian cell lines, transfection approaches, process conditions and also downstream processing to shorten the development timeline.

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The global cell line growth development in the market is segmented on the basis of products, types of cell lines used, the source of cell lines, applications, and geographies. The global cell line development market size was valued at USD 2.38 billion in 2014. The key growth drivers include the increasing demand for monoclonal antibodies, raising demand for effective cancer treatmentsand technical advancements introduced in this field. The global cell line growth market size was valued at USD 2.38 billion in 2014. Key growth drivers include the rising demand for monoclonal antibodies, raising demand for effective cancer therapeutics and technical advancements introduced in this field.

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Track-9 Tissue Science & Regenerative Medicine:

The Global Tissue Science & Regenerative Medicine Market is estimated to observe the highest development coming from the Tissue Engineering segment. By technology type, biomaterial segment presently holds the largest market share of global regenerative medicine market. However, Tissue Engineering segment is expected to be the fastest growing segment over the forecast period. In terms of value, the tissue engineering segment market is anticipated to increase at an outstanding CAGR of 17.5% over the forecast period of 2015-2019, to reach a market value of about US$ 1,070 Mn by 2019. Currently, it accounts for almost 13.2% of the total share of the global regenerative medicine market, which is expected to increase growth potentially by 2019 end.

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Track-10 Gene Therapy

Currently, the concept of gene therapy is being authorized by numerous pharmaceutical companies using clinical data, and there is a increasing interest among venture capitalists to discover the commercial potential of gene therapy. However, the development of the gene therapy market is largely needy on the regulatory environment, and on approvals from industry bodies. Currently, most gene therapy products are still in the clinical trials phase II and phase III, of which a common focuses on the treatment of oncology and heart diseases. The growing popularity of DNA vaccines has positively impacted the development of this market, and there is a high chance of cell and gene therapy being practiced in clinics in the next few years, as encouraging results are developing from the phase II/III trials. Gene therapies market will generate $204m in 2020, according to new visiongain analysis

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Track-11 Cancer Gene Therapy

Initially, scientists followed gene therapy for the administration of genetic material to treat genetic disorders, and it was soon adapted for cancer treatment. Approximately two-thirds of the clinical trials in gene therapy have been designed at the treatment of various types of cancers. Cancer Gene Therapy Marketsize was USD 805.5 million in 2015, with 20.7% CAGR estimation from 2016 to 2024; as per a new global strategic research report. Globally, increasing cancer prevalence will rise demand for gene therapy as the effective personalized treatment choice. According to WHO, cancer incidence is estimated to rise by 50% to reach 15 million by the end of this decade. This increase in number of patients needs this as a potential treatment approach addressing the growing global burden of the disease.

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Track-12 Diabetis Gene Therapy

Recent developments in the field of molecular and cell biology may allow for the growth of novel strategies for the therapy and cure of type 1 diabetes. In particular, it is now possible to predict restoration of insulin secretion by gene or cell-replacement therapy. Diabetes mellitus is growing globally affecting more than 180 million people worldwide . This is mostly type 2 diabetes and, because of the growth in the aging population and massive increase in prevalence of obesity, the incidence is likely to be more than doubled by 2030.

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Track-13 Vectors for Gene Therapy

According to the new research Global strategic report Gene Therapy Market Forecast to 2020, a major focus has been on the on-going clinical trials for the growth of innovative products using different vectors. Increasing number of clinical trials and availability of wide range of genes and vectors used in these trials will enable emergence of new therapy modalities to help make cancer a manageable disease. By the end of 2012, the expected number of clinical trials crossed 1,800 worldwide.

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9th International Conference onGenomicsand Pharmacogenomics, Chicago, USA, July 13-14, 2017; 7th International Conference onPlantGenomics, Bangkok, Thailand, July 03-05, 2017; 15th EuroBiotechnologyCongress, Valencia, Spain, June 05-07, 2017; 5th International Conference and Exhibition onCell and Gene Therapy,Madrid, Spain,Mar 2-3, 2017; 3rd International Conference & Exhibition onTissue Preservationand Bio banking,Baltimore, USA,June 29-30, 2017.

Track-14 Molecular Epigenetics

The global Epigenetic strategic research market was valued at an estimated$413.24 Millionin 2014. This market is expected to ncrease at a CAGR of 13.64% between 2014 and 2019 to reach$783.17 Millionin 2019. This Market is segmented mainly on the basis of products into enzymes; instruments and consumables; kits; and reagents. Each of these market is further divided into multiple product segments and sub-segments.

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International Conference on Animal and HumanCell Culture, Jackson Ville, USA, Sep 25-27, 2017; 14th Asia-PacificBiotechCongress,Beijing, China,April 10-12, 2017; 15thBiotechnologyCongress, Baltimore, USA, June 22-23, 2017; 3rd International Conference onSyntheticBiology, Munich, Germany,July 20-21, 2017; 5th International Conference and Exhibition on Cell and Gene Therapy,Madrid, Spain,Mar 2-3, 2017.

Track-15 Genetics & Genomic Medicine

The National Human Genome Research Institute describesgenomic medicine as"an developing medical discipline that mainly involves using genomic information about an individual as part of their clinical care (e.g., fordiagnostic or therapeutic decision-making) and the health outcomes and policy implications of that clinical use. Geographically, the global Genomic Medicine market is classified into different regions viz. North America, Latin America, Western Europe, Eastern Europe, Asia Pacific Excluding Japan (APEJ), Japan, Middle East and Africa (MEA). Owing to the presence of huge number of academic as well as research institutions in the United States. which are mainly working on genomic medicine to discover next-generation genomic medicines, North America region is expected to lead the global genomic market in terms of value during the forecast period. Also, the presence of several academies offering educational programs coupled with openings in scientific research in the North America and Europe is expected to have positive impact on the regional markets. The genetic & genomic medicine concept still in its nascent stage is yet to receive an drive from the emerging market which are anticipated to hold smaller shares in the global market.

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9th Annual Conference onStem Celland Regenerative Medicine ,Berlin, Germany,Aug 04-05, 2016; 2ndBiotechnologyWorld Convention,London,, UK,May 25-27, 2017; International Conference on Animal and HumanCell Culture, Jackson Ville, USA, Sep 25-27, 2017; 9th International Conference onCancerGenomics, Chicago, USA, May 29-31, 2017; 3rd International Conference onSyntheticBiology, Munich, Germany, July 20-21, 2017.

Track 16 Gene Therapy Commercialization

Themajor theme of this is whether gene therapy can attain commercial success by the early-to-mid 2020s, which types of gene therapy programs have the greatest likelihood of success, and what hurdles might stand in the way of clinical and commercial success of leading gene therapy programs. Asynchrony between the maturation of gene therapy technologies and capital investment in development-focused business models may have stalled the commercialization of gene therapy.

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Track 17 Gene Therapy for rare & Common Diseases

Gene therapy is a logical way to treat rare genetic disorders; and cure a single gene defect by introducing with a 'correct' gene. The first gene-therapy trials were conducted using patients with rare monogenetic disorders, but these are now outstripped by the clinical testing of gene therapeutics for more common conditions, for ex: cancer, AIDS and heart disease. This is partially due to a failure to achieve long-term gene expression with early vector systems, a critical condition for correcting many inborn genetic defects.

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6th International Conference onTissue Engineering &Regenerative Medicine, Baltimore, USA, Aug 20-22, 2017; 8th World Congress and Expo onCell &Stem Cell Research, Orlando, USA, March 20-22, 2017; 15thWorld Congress onBiotechnologyand Biotech Industries Meet,Rome, Italy,March 20-21, 2017; 2nd International Conference onGenetic Counselling andGenomic Medicine,Beijing, China,July 10-12, 2017; International Conference onClinical andMolecular Genetics, las vegas, USA, April 24-26, 2017.

Track 18 Gene Editing Technology

The genome editing market is expected to reach USD 5.54 billion by 2021 from USD 2.84 Billion in 2016, and it wil grow at a CAGR of 14.3% in the next five years (2016 to 2021). The growth of the overall market can be accredited to factors such as increasing government funding and growth in the number of genomics projects, high prevalence rate of infectious diseases and cancer among patients, technological advancements, increasing demand for synthetic genes, growing awareness about genomics, and increasing new product launches by industry players are expected to drive the market in the coming years. Rise in the production of genetically modified crops is also expected to increase the demand for genome editing.

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9th International Conference onGenomicsand Pharmacogenomics, Chicago, USA, July 13-14, 2017; 7th International Conference onPlantGenomics, Bangkok, Thailand, July 03-05, 2017; 15th EuroBiotechnologyCongress, Valencia, Spain, June 05-07, 2017; 5th International Conference and Exhibition onCell and Gene Therapy,Madrid, Spain,Mar 2-3, 2017; 3rd International Conference & Exhibition onTissue Preservationand Bio banking,Baltimore, USA,June 29-30, 2017.

Track 19 Cell & Gene Therapy Products

The Center for Biologics Evaluation and Research (CBER) controls cellular and gene therapy products and certain devices related to cell and gene therapy.In addition to regulatory oversight of clinical studies, it also provides proactive scientific and supervisory advice to medical and clinical researchers and manufacturers in the area of novel product development.

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International Conference on Animal and HumanCell Culture, Jackson Ville, USA, Sep 25-27, 2017; 14th Asia-PacificBiotechCongress,Beijing, China,April 10-12, 2017; 15thBiotechnologyCongress, Baltimore, USA, June 22-23, 2017; 3rd International Conference onSyntheticBiology, Munich, Germany,July 20-21, 2017; 5th International Conference and Exhibition on Cell and Gene Therapy,Madrid, Spain,Mar 2-3, 2017.

Track 20 Ethical Issues in Cell & Gene Therapy

The use of human embryos for research on embryonic stem (ES) cells is currently top on the ethical and political agenda in many countries. Notwithstanding the potential benefit of using human Embryonic Stem cells in the treatment of diseases, their use remains controversial because of their origin from early embryos.

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9th International Conference onGenomicsand Pharmacogenomics, Chicago, USA, July 13-14, 2017; 7th International Conference onPlantGenomics, Bangkok, Thailand, July 03-05, 2017; 15th EuroBiotechnologyCongress, Valencia, Spain, June 05-07, 2017; 5th International Conference and Exhibition onCell and Gene Therapy,Madrid, Spain,Mar 2-3, 2017; 3rd International Conference & Exhibition onTissue Preservationand Bio banking,Baltimore, USA,June 29-30, 2017.

Track 21 Regulatory & Safety Aspects of Cell & Gene Therapy

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Growth Hormone IGF-1 Cancer – Trans-D Tropin

Growth Hormone IGF-1 cancer

Rashid A Buttar D.O. Visiting Scientist, North Carolina State University As published in "Anti-Aging Medical Therapies, Volume 5"

ABSTRACT

The benefits of growth hormone (GH, also known as human growth hormone or hGH) have received increasing attention from not only the media but the medical profession as well, as a result of studies indicating GH may have the ability to restore a more youthful physiology and enhance the quality of life. However, there is controversy centered on the possibility that maintaining youthful GH levels may actually be harmful in the long run and may result in shortening life span by inducing cancer.

The first foundational objective essential to gaining an insight into these issues is to clearly understand the hypothalamic-pituitary axis. More often than not, we forget the physiological safety mechanisms designed within our systems to protect us. In this case, we refer to the negative inhibitory feedback loop designed to decrease or stop the release of endogenous GH when levels exceed the physiological range. This inhibitory feed back loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using growth hormone releasing hormone (GHRH) to increase endogenous GH as opposed to using exogenous GH.

This will lead to the discussion of why assessing increases in insulin-like growth factor type1 (IGF-1) as a marker of GH efficacy may not only be unreliable, but a compelling argument will be presented that the practice may be nothing more than the perpetuation of a medical myth. In fact, conclusive data from multiple sources showing that increases in IGF-1 are conducive to the propagation of oncogenesis will be presented and then supported by general physiological concepts, scientific observation and published research.

Finally, the inter-relationship of GH, GHRH, and IGF-1, as well as how each individual component correlates with incidence of cancer, will be thoroughly explained.

Keywords: Growth Hormo ne ; IGF-1; Cancer; Trans-D Tropin; Geref; GHRH analog

INTRODUCTION

The benefits of growth hormone (GH, also known as human growth hormone or hGH) have received increasing attention from not only the media but the medical profession as well, as a result of studies indicating GH may have the ability to restore a more youthful physiology and enhance the quality of life. However, there is controversy centered on the possibility that maintaining youthful GH levels may actually be harmful in the long run and may result in shortening life span by inducing cancer.

Intuitively, it is obvious that naturally occurring endogenous GH released within physiological parameters itself could not possibly cause cancer. The reasoning for this statement is actually quite simple because all mammalian species achieve the maximum level of GH levels when reaching late adolescence and young adulthood. If endogenous GH were actually a cause of cancer, then all mammalian species including man would have the highest incidence of cancer during late adolescence and young adulthood. However, as we all know, this is not what occurs.

So, what then causes cancer? The answer unfortunately, is more than a little involved. We know that a minimum of 75% of all cancers have been shown to have environmental etiologies. In addition, there are certain factors that predispose individuals to have a higher propensity to develop uncontrolled cellular proliferation and induce the suppression of apoptosis, leading to oncogenesis or the formation of cancer. In addition, we know that the incidence of cancer generally occurs later in life as opposed to late adolescence and young adulthood when we have the highest levels of GH.

The first foundational objective essential to gaining an insight into these issues is to clearly understand the hypothalamic-pituitary axis. More often than not, we forget the physiological safety mechanisms designed within our systems to protect us. In this case, we refer to the negative inhibitory feedback loop designed to decrease or stop the release of endogenous GH when levels exceed the physiological range. This inhibitory feed back loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using growth hormone releasing hormone (GHRH) to increase endogenous GH as opposed to using exogenous GH.

This will lead to the discussion of why assessing increases in insulin-like growth factor type1 (IGF-1) as a marker of GH efficacy may not only be unreliable, but a compelling argument will be presented that the practice may be nothing more than the perpetuation of a medical myth. In fact, conclusive data from multiple sources showing that increases in IGF-1 are conducive to the propagation of oncogenesis will be presented and then supported by published research. This conclusion is very well supported by scientific observation, clinical data, and published research, as well as being supported by general physiological concepts - all of which will be presented later in this chapter.

Finally, the inter-relationship between GH, GHRH, and IGF-1, as well as how each individual component correlates with incidence of cancer, will be thoroughly explained. It is important however, to first discuss the common characteristics of cancer and the various treatment options available so that all readers have the same foundational knowledge essential to understanding and conceptually comprehending the material being presented.

CANCER CHARACTERISTICS

The vast majority of cancers exhibit certain common characteristics including, but not limited to, uncontrolled cellular proliferation, suppression of apoptosis, and anaerobic metabolism. They also require a specific environmental state within the biological system. Cancer is also characterized as being an opportunistic process, inflammatory in nature, an obligate glucose feeder, and is associated at least in the early stages with a hyperinsulinemic state.

Despite the traditional methods of fighting cancer which include surgery, chemotherapy, and radiation, as well as the non-traditional treatments including nutrition, supplementation, herbs, lifestyle changes, detoxification, metabolism optimization, IV treatments, hyperthermia, immune modulation using peptides, insulin potentiation techniques, and the hundreds of other methods which can not be listed due to space constraints, the best defensive strategy against cancer remains maintaining a good offensive stance. What exactly do we mean by this statement? Remember, the process of oncogenesis begins not weeks or months before it manifests itself as cancer, but actually starts years before the cancer reaches a point where it can be diagnosed.

What this means is that it is essential to be proactive earlier in the game prior to the cancer being diagnosed. This strategy is most evident in the cardiovascular model where physicians intervene prior to the manifestation of heart disease, by managing hypertension and hypertriglyceridemia while encouraging life style changes such as reducing body fat, increasing exercise, and facilitating smoking cessation. Despite the trillions of dollars spent in the war against cancer, the mortality rate from cancer is secondary only to cardiac disease, with the incidence steadily rising. Therefore, the key to solving the issue of cancer, just as in cardiovascular disease, is prevention.

METHODS OF INCREASING GROWTH HORMONE

Extensive research to further the understanding of the aging process is currently being conducted at a number of leading institutions. Some of the findings from these studies show that as we age, GH levels steadily decline. The numerous potential benefits associated with GH treatments to stem this decline have generated an incredible plethora of products claiming to increase GH and IGF-1 levels. The studies necessary to validate these various anti-aging treatments as a result of this marketing surge unfortunately have not followed suit.

The answer that we seek as clinicians is how to effectively inhibit, or at least slow down the aging process and thus prevent the associated debilitating limitations, which are accepted by society as being inevitable as we grow older. The benefits of GH have increasingly received attention as a result of the ability of GH to restore a more youthful physiology and enhance the quality of life. However, controversy has centered on the possibility that maintaining youthful growth hormone levels may actually be harmful in the long run, actually shortening life span by promoting cancer. The topic of GH and cancer will be discussed in detail later but it is now becoming clear that in the quest for a longer life, we may possibly be hurting our patients by contributing to the increased incidence of cancer. We must be ever vigilant of the first rule of medicine as epitomized by Hippocrates, to Do No Harm.

Currently, there are only two clinically documented methods of increasing GH. The first method is by injecting recombinant, synthetic GH (a 198 amino acid peptide with a terminal end). There are a number of choices available to physicians who choose to pursue this method of increasing GH in their patients. The pitfalls of this choice will be clearly delineated. Tosimply summarize, the physiological safety mechanism, namely the negative, inhibitory feedback loop between the hypothalamus and pituitary is violated, leading to many potentially serious consequences.

The increased attention to the benefits attributed to GH has also given rise to hundreds of products that reportedly claim to increase GH levels. This second method of increasing GH levels is achieved by stimulating the pituitary to increase endogenous levels of GH. This technique of simulating the action of growth hormone releasing hormone (GHRH) has rapidly become a popular method, although the vast majority of products claiming to achieve these results have no scientific validity, having failed medical scrutiny.

The first foundational objective is to clearly understand the hypothalamic-pituitary axis (Figure 1). More often than not, we forget the physiological safety mechanisms designed within the biological system to protect us. In the case of GH, the reference is being made to the negative inhibitory feedback loop designed to decrease or stop the release of GH if the levels being released are beyond physiological range. This inhibitory feedback loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using GHRH manipulation to increase endogenous GH as opposed to simply injecting exogenous GH.

Although the GH injections and secretagogues (substances that cause the release of GH, including GHRH and other substances like GHRH) do offer many benefits to counteract the limitations associated with aging, the need for a safer and more effective modality of therapy has long been warranted. The necessity for a therapy offering a greater spectrum of results while providing an accelerated and rapid onset of subjective and objectively measurable efficacy, with a safer profile, a more efficient delivery mechanism, and an ease of administration leading to better patient compliance has led to the advent of many innovative and promising therapeutics. One among these has been uni que due to having created some interesting controversy as a result of going against the current fundamental understanding of the relationship between GH and IGF-1.

Figure 1. The hypothalamic-pituitary axis.

To date, there are only two GHRH analog products that have been clinically validated and scientifically studied. Both are available only via prescription. The first is Geref (NDC # 44087- 4010-1), which is marketed by Serono Laboratories, one of the largest producers of injectable growth hormone. Their product, Geref, is a 22 amino acid analog of GHRH, administered via subcutaneous injection. The second GHRH analog on the market is Trans-D Tropin (NDC # 65448-2115-1) marketed by a European company named Balance Dermaceuticals. Compared to Geref, Trans-D Tropin has the uniqueness of being the first and only GHRH analog that is administered transdermally (TD-GHRH-A). Trans-D Tropin is a polypeptide combinant, consisting of four different naturally conjugated amino acid sequences that are not recombinant in nature. Although not animal derived, these peptide combinants are also not synthetically sequenced. Rather, they are sequenced in a natural proprietary manner most easily explained as being as close to the in vivo process as we currently understand.

In an editorial review appearing in the Journal of Clinical Endocrinology (1999;50:547-556) Scott Chappel, PhD of Serono Laboratories wrote:

"Long-term stimulation of pituitary cells with GHRH will shift the GHRH/somatostatin tone by exogenous [injection] therapy to increase GHRH responsivity and pituitary GH stores. It is predicted that this therapy will reverse the chronic inhibitory state induced by long-term somatostatin domination and create an environment now responsive to the endogenous GHRH toneand allow for the normal [physiological] pulsatile GH release to reappear. This would produce a greater therapeutic benefit and a better safety profile compared with once daily injections of a bolus of recombinant GH...[the need for] repeated stimulation of GHRH receptors is required in a patient friendly formatefforts are ongoing"

From a long-term efficacy, safety, physiological, functional, and compliance standpoint, Trans-D Tropin (henceforth referred to as the trans-dermal GHRH analog or TD-GHRH-A in this chapter), appears to accomplish the goals that Chappel delineates. But some further interesting additional observations were noted during the clinical studies conducted on this TD-GHRH-A by the author, shedding light on a subject that is of great importance to any physician considering manipulation of their patient's hypothalamic-pituitary axis and vital for any patient who may be considering GH therapy as a treatment option.

It was during the initial clinical testing of this TD-GHRH-A, while undergoing the characteristic rigid scrutiny used for medical therapeutics, where the observation was made of IGF-1 deviating from the expected trend. Later, during subsequent clinical studies, the same observations were reproduced with findings being confirmed not only by other independently conducted studies but also found to be well documented within the published medical literature.

At the same time, other clinicians and researchers studying IGF-1 independent of the author, began observing and documenting similar findings. When these scientists began to report their findings starting in 1999, they enabled a greater understanding of the actual nature of IGF-1.

STUDY SHOWS INCREASED GROWTH HORMONE WITH DECREASED IGF-1

In 1998, we conducted a subjective study based upon the SF-36 patient outcome based research model, evaluating 30 patients taking the TD-GHRH-A. The study, which was published in published in the Journal of Integrative Medicine (2000;4:51-61), measured 22 subjective life style criteria and 5 objective criteria including overall strength, endurance, and IGF-1. Although every patient reported significant improvement in most criteria being monitored, a departure from the expected trend of IGF-1 was noted.

The observation of decreasing levels of IGF-1 prompted a second small study, this time to evaluate endogenous GH by drawing serum GH radioimmunoassays and comparing the response to changes measured in IGF-1. A total of 53 sets of serum GH levels were drawn before and after treatment, and analyzed using radioimmunoassays. IGF-1 levels were also collected at baseline and again at three weeks post treatment with the TD-GHRH-A.

Endogenous GH levels measured 90 minutes post treatment showed a 631.46% increase compared to baseline levels (Figure 2). The data was then re-evaluated using the first set of blood drawn and compared to the second set of blood drawn two weeks later in order to assess if changes in GH levels were only dose dependent or if the response were transitory in nature (Figure 3). There was also a concern that the response measured in GH would decrease after a few weeks due to desensitization or acclimatization to the TD-GHRH-A. The results were again diametrically opposed to what was expected. There was actually an improvement in GH release measured after two weeks of treatment with the TD-GHRH-A compared to first time usage. The results indicated an actual increase in sensitization or improvement in pituitary responsivity with continuous usage. This subject will be addressed in greater detail later in this chapter.

Figure 2. Effect of TD-GHRH treatment on endogenous growth hormone levels.

One of the criticisms when this data was presented was regarding the amount of change that was measured in GH levels. The increases in GH levels were felt to be insignificant since they were less than 5 ng/ml. However, the opposing argument questioned how an increase of greater than 600% within a two-week period could be considered insignificant. This argument can only be settled by defining what level of GH increase is necessary in order to achieve therapeutic benefit.

Endocrinology and physiology textbooks indicate that an absolute level of GH above 5 ng/ml is needed before efficacy can be attained. However, the "efficacy" being referred to is a "diagnostic" response (for purposes of diagnosis), not a "therapeutic" response. The "diagnostic" response would be defined as a change to elicit a response far beyond the normal physiological range by taxing and overloading the system. An example of this would be seen in the insulin and dopamine challenges done by endocrinologists to determine GH deficiency.

Figure 3. Comparison of growth hormone levels after initial treatment and after two weeks of treatment.

However, a "therapeutic" response would simply elicit a subtle response well within the normal physiological range in order to achieve a "therapeutic" effect. Although the average range of GH levels measured during this study was well below the 5 ng/ml level defining the diagnostic criteria, an increase in endogenous GH levels greater than 600% compared to baseline measurements is clinically and statistically significant. Furthermore, by keeping the levels of GH below 5 ng/ml, we experience a more physiological increase in endogenous GH as opposed to exceeding the physiological parameters achieved by exogenous, recombinant, injectable GH.

The interesting component of this study was the relationship of "increasing endogenous GH' to a concomitant measurable "decrease in IGF-1 levels' (ng/ml) on a consistent basis. TD-GHRH- A caused not only an increase in endogenous GH but also a decrease in IGF-1. If IGF-1 is an active metabolite of GH and is known to be converted in the liver from GH to one of the many growth factors responsible for normal growth, then why would IGF-1 levels decrease when the GH levels are increasing? Before discussing this important question, let's first discuss the data.

Figure 4. Serum IGF-1 levels at baseline and at three weeks post treatment with TD-GHRH-A

The IGF-1 levels reported in Figure 4 were drawn at baseline and three weeks post treatment with the TD-GHRH-A. There was over a 14% drop measured in IGF-1 levels in the males participating in the study. The female participants showed a greater drop in IGF-1 exceeding a 26% drop. The overall drop in IGF-1 was over a 20% decline in IGF-1 levels compared to baseline measurements over the three-week period. The evidence based on this study seemed to show an inverse correlation between IGF-1 and GH levels. Upon reviewing the published literature, it became clearly evident that IGF-1 and GH have at best, an unreliable correlation.

DOUBLE BLIND STUDY CONFIRMS DECREASING IGF-1

Eventually, the above mentioned data showing the increase in endogenous GH and decrease in IGF-1 became the pilot for a larger, more definitive study to determine not only the correlation between GH and IGF-1 but also to evaluate the effect the TD-GHRH-A had on cortisol, glucose, chemistry, and lipid parameters. The preliminary results of this multi-centered, double blind, placebo controlled, crossover study evaluating endogenous GH levels with serial GH radioimmunoassay levels after TD-GHRH-A administration showed some very interesting results and reinforced the earlier findings of the smaller previous studies.

The requirements for this study were stringent due to the transitory nature of serum GH so all data collection was tightly regulated in order to insure accuracy of the information collected. Patient selection criteria was simple, with age over 30 and non-gravid state being the only absolute exclusion criteria. The primary end point was eight weeks post treatment when the placebo group was scheduled to crossover into the treated group with the secondary endpoint being 16 weeks after the initiation of either treatment or placebo. The placebo (control) was completely indistinguishable from the TD-GHRH-A (treatment) with both utilizing the exact same carrier, with the same consistency, smell, color, and appearance, and with the packaging kept identical.

All control and treatment bottles were labeled with a numerical code and randomly distributed among the patient population selected for the study. The numerical codes facilitated the double blind component with supervising physicians unaware of which patients received placebo versus treatment . Study participants were scheduled for blood draws at very specific time intervals. If a study patient did not present as scheduled for blood draws, the patient was eliminated from the study. Out of 25 centers selected for participation, only eight centers completed the study, with 117 patients out of 317 patients reaching the stated endpoints without deviances from the testing schedule.

All study patients had blood drawn at specified intervals, starting with baseline GH radio- immunoassay levels as well as IGF-1, cortisol, lipid panels, and basic chemistry panels, followed immediately by administration of either the placebo in the control group or the TD-GHRH-A in the treated group. All study patients then had to have repeat blood draws at 30, 60, and 90 minutes after treatment administration. Each of these subsequent blood draws consisted of all the above mentioned serum parameters, with each set of blood draws obtained at a very specific weekly interval. If a study participant did not present at the specified time for a scheduled blood draw, they were eliminated from the study. This was the primary reason why only 117 patients completed the study.

The blood specimen analysis schedule for the treated group (on the TD-GHRH-A) was at the onset of the study, followed up again at the end of the second week, the fifth week and finally on the eighth week after study initiation. The blood specimen analysis schedule for the control group (on placebo) was at the onset of the study and then repeated at eight weeks after the initiation of the study. The blood specimens obtained during the second and fifth week blood draws in the placebo group were discarded, primarily due to the study's financial constraints but also because no significant change was anticipated in the placebo group. Only the start and the endpoint specimens, prior to the crossover point, were analyzed in the control (placebo) group. However, the blood had to be drawn in both placebo and treatment groups at the same time in order to preserve the double blind component of the study.

The percent change measured in endogenous GH levels as measured by GH radioimmunoassay in the 117 patients that completed the study were statistically significant. The change from the baseline blood draw to the blood drawn 90 minutes after the TD-GHRH-A treatment showed a 462.39% increase upon first time usage. At the end of two weeks after using the TD-GHRH-A, an increase of 815.59% in endogenous GH levels was noted, compared to baseline base line levels drawn 90 minutes earlier. By the fifth week, an increase of 1754.22% in endogenous GH was measured from baseline to 90 minutes post treatment with the TD-GHRH-A. However, by the eighth week, there was actually a drop in GH levels when compared to the fifth week, but overall, endogenous GH levels still increased over 609% over a 90 minute period compared to baseline.

The statistical analysis of the data was conducted by an independent source, showing a baseline mean of 0.295918367 with a 90-minute mean of 2.213636364 and a P value < 0.001. The baseline standard deviation was 0.464112 with the 90-minute standard deviation being 2.673173, establishing that the increase s in endogenous GH levels observed in this study were statistically significant. The most dramatic increases in endogenous GH release were measured between the 60 and 90 minute time periods post treatment, regardless of what weekly interval in the study the serum GH samples were drawn. All four time periods (initial baseline, second week, fifth week, and eighth week) clearly showed the time interval between 60 and 90 minutes as the most significant for endogenous GH release.

Figure 5. The change in endogenous growth hormone levels from baseline to 90 minutes after TD-GHRH-A treatment over an eight week period.

Although an increase in endogenous GH levels was clearly established, the decrease in GH levels at week eight compared to week five (Figure 5) was initially confusing. However, referring back to basic physiological principals, it became evident that there were only two possible postulates explaining the reason for a decrease in GH levels during the eight week of usage of the TD-GHRH-A.

The first possibility revolved around somatostatin. An increase of over 1750% in endogenous GH levels by the fifth week is a very significant increase. It would therefore logically follow that with such a tremendous increase in GH from baseline in such a short period, the negative inhibitory feedback loops would be initiated, causing the release of somatostatin from the hypothalamus in order to inhibit the release of GH by the pituitary. An increase in somatostatin (GH antagonist) would result in decreased levels of endogenous GH being released. This hypothesis based on clinical observation will be confirmed or refuted in future studies. The second postulate involves the issue of pituitary reserves. The pituitary gland holds only a limited amount of GH in store, releasing it in a pulsatile manner. Due to the effectiveness of the TD- GHRH-A, the pituitary reserves of GH may have been rapidly depleted and by the eight week, required additional time necessary for the pituitary to replenish its GH stores.

Figure 6. Serum cortisol levels obtained at baseline and 90-minutes after TD-GHRH-A administration.

As the possibilities were being entertained regarding the drop in GH observed at the eighth week compared to the fifth week in the TD-GHRH-A treated group, the placebo data was also being analyzed. The increase in GH in the treated group was measured at 1754 % at the fifth week interval but in the placebo group, although the blood was drawn, the samples were not analyzed as previously mentioned because the placebo group had the second and fifth weeks blood draws discarded. Therefore, a comparison of the fifth week data in the treated versus the placebo group could not be made. However, the data for the eighth week for both the treated group (on the TD-GHRH-A) and the control group (on placebo) were analyzed. Although this comparison did not allow for an explanation for the relative drop in GH from the fifth week to the eighth week in the treated group, it did give additional confirmation to previously conducted research unrelated to this study, further intriguing the study investigators.

The eighth week data for the treated group on the TD-GHRH-A showed 609.04 % increase in endogenous GH. However, surprisingly, the placebo group showed an increase of endogenous GH of 118.13% during the same time period. Although initially unexpected, this increase in GH in the placebo group validated previous research regarding the effect of diet and exercise on GH release. Life style modifications that all study patients were instructed to follow while participating in the study included a specific combination of aerobic and resistance exercise, as well as a high protein, low carbohydrate diet.

These findings validate some earlier independent studies showing that even without medical intervention, one can significantly increase endogenous GH levels by simple lifestyle modifications in diet and exercise. All patients in this study were crossed over into the treated group at the eighth week and subjectively followed for another eight weeks. Subjective improvements reported by patients were recorded in the form of a detailed questionnaire based upon the SF-36 patient outcome based research model, answered every two weeks by all study participants. Results correlated well with the objective data collected.

The most significant changes noted were in renal function, with bilirubin dropping 34.56% and creatinine dropping 22.23%. In addition, significant decreases were noted in serum glucose, serum cortisol and IGF-1 levels.

Figure 7. Percentage drop in serum cortisol levels over the 8-week study period.

Serum cortisol levels dropped significantly within a 90-minute interval on each consecutive blood draw (Figure 6). With the exception of a slight increase in baseline cortisol measured during the second week, all cortisol levels drawn decreased in a consistent manner. As depicted in Figure 7, cortisol levels not only dropped from baseline blood draw to the 90-minute blood draw during every occasion, but were also observed to consistently decrease throughout the study period as well. These changes in cortisol were significant for a number of reasons.

First, subjective improvements in attitude, depression, anxiety, sense of well being, ability to focus, concentration and ability to handle periods of stress were reported by a large number of patients participating in this study. These changes were reported later in the course of treatment, usually experienced by the third or fourth month of therapy. The steadily decreasing levels of cortisol correlate with the subjective response reported by patients in their patient self-assessment forms. Second, cortisol, being commonly referred to as the stress hormone, is known to have a significant inflammatory component and contributes to increased rate of aging. Reduction in any inflammatory component may have a substantial effect by reducing oxidative stress on the physiology and improving the "peak and trough" nature of cortisol, as opposed to chronically elevated levels. Reduction in serum cortisol levels was pronounced and consistent.

In addition, IGF-1 and serum Glucose levels were also noted to consistently drop (Figure 8).

Figure 8. Effect of TD-GHRH-A on serum IGF-1 and glucose levels.

The TD-GHRH-A appears to have a distinct "euglycemic" effect on serum glucose. Glucose level modulation was evidenced by glucose levels below 75 mg/dl trending up to approximately the 100 mg/dl levels while the levels above 150 mg/dl trending down to approximately the 110 mg/dl levels. Patients with Insulin-dependent diabetes mellitus (IDDM) experienced 50 to 70 mg/dl drops in serum glucose levels within 90 minutes after using the TD-GHRH-A. The IGF-1 levels were expected to drop based upon the earlier pilot study results, and were observed to drop on a consistent basis as expected.

Figure 9. Response in serum IGF-1 levels to TD-GHRH-A treatment.

The response in serum IGF-1 levels in the treated group showed a consistent and significant drop while on the TD-GHRH-A, dropping acutely within 90 minutes of administration of the TD- GHRH-A compared to baseline levels, and overall throughout the study period intervals as well. Despite endogenous GH levels increasing over 1750% by the 5 week, the mean serum IGF-1 t h levels dropped over 60 ng/ml in the treated group on the TD-GHRH-A. Figure 9 shows the consistently decreasing IGF-1 levels as the study progressed. This was the final indication that an increase in IGF-1 levels was not an appropriate method of monitoring efficacy of GH therapy.

In fact, an inverse correlation between IGF-1 and GH efficacy seemed to be established based on this data, which upon further review was well supported in published literature, current research, and in clinical observation. But further investigation revealed another component of IGF-1 that seemed to have been ignored despite extensive documentation in the medical literature. It was during this study and resulting subsequent inquiry into the IGF-1 controversy that led to the following observations, conclusions, and discovery regarding the correlation between IGF-1 and cancer. The evidence of this correlation is overwhelmingly clear and well supported.

THE NEW PARADIGM IN UNDERSTANDING IGF-1

IGF-1 insulin-like growth factor type is regarded as the most important metabolite of growth hormone, an anabolic hormone that promotes tissue growth. IGF-1 has a structure highly similar in morphology and function to that of insulin, while the receptor site of IGF-1 is indistinguishable from the insulin receptor site. Many of the effects attributed to IGF-1 are also attributable to, and overlap with, those of insulin.

Figure 10. Molecular Structure of IGF-1

The traditional view is that growth hormone is "translated" in the liver into IGF-1, and expresses its activity through IGF-1, even though it has been documented that low levels of IGF-1 are not a reliable indicator of growth hormone deficiency. Yet, many clinicians continue to use IGF-1 as a monitor of efficacy for GH treatment. The problem however is that numerous studies have shown IGF-1 to be modulated by factors completely independent from GH levels.

Many in the research arena have long felt that the chief culprits responsible for reducing life expectancy are likely to be excessive levels of insulin as well as IGF-1. In fact, excessive insulin and IGF-1 are precisely the type of pathological endocrine profiles that are observed in sedentary, obese patients. This has been reported in a number of studies, and recently confirmed in a massive National Institute of Aging study, which singled out low insulin as the best predictor of longevity in men.

All physicians treating patients with any modality used to manipulate growth hormone levels should make themselves familiar with the research on the extraordinary longevity of dwarf mice, which are deficient in IGF-1. Dr A Bartke, one of the chief investigators involved in the dwarf mouse research, was interviewed by Ivy Greenwell for the consumer oriented periodical LifeExtention Magazine (February 2001). When questioned regarding his opinion on the controversy of IGF-1, Bartke expressed that it is high IGF-1 that is likely to be harmful. Low IGF-1 correlates with longevity and is "virtually absent" from the serum of the long-lived dwarf mice according to Bartke. He stated that aiming at high IGF-1 levels might not be desirable not only in terms of life expectancy but also in those of cancer susceptibility as well. However, Bartke points out that the confusion regarding this issue is in great part, due to the difficulty and trouble with separating the effects of GH itself from those of its metabolites, specifically IGF-1. There is growing consensus that IGF-1 levels are indeed not related to GH levels. In a study published in the Journal of Metabolism Research (1999;10:576-579) , Inuki et al found that thyroid hormone modulates IGF-1 and IGF-BP3, without mediation by GH. Just a few months later, Janssen et al, published a study in the Journal of Clinical Endocrinology and Metabolism (2000:85:464-466), where the authors reported finding a direct relationship between serum levels of estradiol and IGF-1 levels, completely independent of GH levels.

Both these studies have set precedence in developing new strategies in treating cancer patients, which will be discussed in detail later in this chapter. However, before delving into the topic of IGF-1 and its relationship to cancer, it is important to review a few fundamental physiological concepts that may enhance the understanding of the nature of IGF-1.

Review of General Physiological Principals

When considering basic science physiological principals, the nature of IGF-1 becomes easier to understand and the controversy surrounding IGF-1 is removed. In order to accomplish this goal, the reader is asked to consider the following two questions and answer them before continuing to read. By answering these two questions, a logical explanation for the decrease in IGF-1 levels witnessed in the aforementioned studies will become self-evident.

Question 1: EXERCISE AND INSULIN SENSITIVITY Do sedentary people or athletes have lower glucose levels?

Exercise leads to an increase in insulin sensitivity. In other words, an increase in exercise leads to the body becoming more "sensitive" to the effects of insulin, thus requiring less insulin to accomplish the same task. The function of insulin is to drive glucose into the cell. Since exercise sensitizes the cells of the body to the effects of insulin, the body needs less insulin to drive the same amount of glucose into the cell. Thus, exercise leads to lower insulin levels by increasing insulin sensitivity.

There is also a higher efficiency in the use of glucose in individuals who exercise. This is due to a number of reasons. First, individuals who exercise have a higher metabolism because they have a greater lean body mass compared to sedentary individuals. Since it takes more energy (glucose) to maintain a greater lean body mass, i ndividuals who exercise have lower levels of circulating gl ucose. This is due to higher fuel consumption as a result of higher levels of activity, as well as a higher requirement to maintain an increased resting metabolism. The higher lean body mass plus higher levels of activity lead to more glucose usage.

Using a car as an analogy, an individual who exercises (exerciser) is like a racecar. The racecar (exerciser) has a larger engine (more lean body mass) and travels greater distances in a shorter period of time (more activity due to exercise), which leads to lower fuel levels due to increased consumption (lower glucose levels due to increased utilization). This in turn, reduces the need for a fuel injector that pushes fuel into the engine (insulin). A decrease in insulin requirements is referred to as becoming insulin sensitive.

This basic physiological concept is evidenced in clinical medicine every day. Individuals who exercise regularly have lower circulating glucose levels, and as a result require less insulin. The sedentary, obese, non-exercising patients have higher glucose levels, eventually having to increase their insulin requirements due to becoming insulin resistant. Insulin resistance is more commonly referred to as non insulin-dependent diabetes (NIDDM). Our obvious goal as clinicians should be to drive the physiology of our patients towards that of the exercising, athletic patient with lower insulin levels.

Question 2: EXERCISE AND YOUNGER PHYSIOLOGY Are people who exercise, biologically (physiologically) younger or older?

Exercise has always been considered a natural form of anti-aging or longevity therapy. From the study on the TD-GHRH-A, we know the placebo group was able to increase GH levels simply by lifestyle modifications including exercise. Other studies have also shown that exercise will increase GH. However, exercise will increase other hormones as well, including testosterone. In fact, exercise has been shown to improve the overall hormonal response within the entire biological system.

Exercise causes a decrease in blood pressure, heart rate, respiratory rate, and peripheral vascular resistance, making the system more efficient and allowing the "engine" to idle at a lower threshold. Exercise increases endorphin release, lean body mass, immunity, range of motion, endurance, stamina, libido, etc. These physiological changes induced by exercise are well established and extensively documented in the medical literature. All these responses are evidence of a younger physiology and are characteristics of younger individuals. Therefore, exercise leads to the physiology of a younger state. This is one of the primary reasons that exercise has long been recommended for better health.

EXPLANATION OF DECREASING IGF-1 LEVELS

The answers to our two questions at this point should be clear. The answer to the first question is that athletes have lower serum glucose levels secondary to an increase in insulin sensitivity. The answer to the second question is that exercise leads to a younger physiological age, i.e., increase in lean body mass, increase in insulin sensitivity (decrease in insulin levels), increase in GH, etc.

Now lets look at IGF-1 versus insulin. First, why is the molecule commonly referred to as IGF-1, named "Insulin-like growth factor type 1?" Insulin-like growth factor type 1 is just one of many growth factors. The polypeptide sequence of the general class of molecules referred to as IGF overall are very similar to the insulin molecule. The fact that IGF-1 is an acronym for "insulin-like growth factor type 1" should be the first indication that insulin and IGF-1 may be highly similar molecules. In fact, insulin and IGF-1 are extremely similar and have many of the same morphological characteristics, appearing to share many of the same properties and traits as one another much more so than the other insulin like growth factors

Figure 11. The Insulin-like growth factors, their receptors, and their binding proteins. SOURCE: The International Society for IGF Research website, http://www.igf-society.org

In Figure 11, note that the receptor site for insulin and the receptor site for IGF-1 are morphologically identical. Also note the significant difference in IGF-1 and insulin receptor sites compared to that of the IGF-2 receptor site. IGF-1 and insulin receptors appear to be completely interchangeable. Therefore, any molecule that binds to these receptor sites could also be interchangeable, indicating that insulin and IGF-1 should be able to interchangeably bind to either receptor site. All evidence indicates this theory to be correct with the findings appearing to be well confirmed on a clinical basis as well as confirmed within the didactic and research communities.

GENERAL PHYSIOLOGICAL PRINCIPALS

Based upon the answers to the two questions asked earlier, we can now support the conclusion that athletes have lower insulin levels and are biologically younger compared to their counterparts who do not exercise. As an example, a 79 year-old patient who exercises regularly is biologically younger than his 79 year-old sedentary counterparts. Based on this supposition, we can now logically conclude that exercise equates to a slowing down of the aging process or, a form of "anti-aging" therapy. Put another way, exercise promotes longevity.

Recognizing that exercise creates a physiological situation that results in an increase in lean body mass, an increase in GH levels, an overall increase in hormonal levels, an increase in insulin sensitivity, a decrease in physiological age and a decrease in insulin levels, we can now understand why exercise equals "anti-aging". These physiological changes represent the goal all physicians desire to achieve in all their patients. These biological parameters are what doctors strive to accomplish, regardless of a patient seeking to simply optimize their health and live a longer life or facing a life threatening chronic illness such as diabetes, heart disease, or cancer.

If we recognize that all the above-mentioned desired physiological parameters are a consequence of exercise, then it would follow that as physicians, we would want to embrace any treatment modality for our patients that would recreate the same physiological parameters achieved by exercising, i.e., creating lower glucose levels, leading to insulin sensitivity and resulting in lower insulin levels as observed in young athletes. Conversely, we would want to refrain from any treatment modality that would oppose the effects of exercise, i.e., creating higher glucose levels, leading to insulin resistance and resulting in higher insulin levels as observed in sedentary, obese, diabetic patients. As previously discussed, the problem is that IGF-1 and insulin are very similar to one another morphologically. Even more importantly, IGF-1 and insulin receptor sites are virtually identical and interchangeable.

If lower insulin levels, such as those found in young athletes, are desirable from a longevity standpoint, then wouldn't we expect IGF-1 to also be lower in young athletes? The answer of course is "yes'. This is due to one simple reason that as a result of IGF-1 and insulin being morphologically identical, these two substances generally cannot be opposed in a normally functioning biological system. If IGF-1 is high, then the insulin levels will also be high.

IGF-1 should be lower in young athletes, just as insulin levels are lower in athletes. And in fact, this is exactly what is clinically observed! The same observation is noted when insulin begins to drop in individuals who begin to exercise. We tested this basic physiological principal and applied it clinically. The above conclusions were easily verified in a small clinical study, demonstrating IGF-1 to be demonstratively lower in athletes.

IGF-1 IN ATHLETES VS. SEDENTARY PATIENTS

In a small, outcome based study to assess IGF-1 levels in un-manipulated patients (patients who had no hormonal manipulation), the true nature of IGF-1 was clearly elucidated (Figure 12). The aged, inactive, obese subjects (sedentary group) had very high levels of IGF-1 when compared to the younger, active subjects (athletic group) who had levels as low as 88 ng/ml.

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Nanobiotechnology – Wikipedia

Nanobiotechnology, bionanotechnology, and nanobiology are terms that refer to the intersection of nanotechnology and biology.[1] Given that the subject is one that has only emerged very recently, bionanotechnology and nanobiotechnology serve as blanket terms for various related technologies.

This discipline helps to indicate the merger of biological research with various fields of nanotechnology. Concepts that are enhanced through nanobiology include: nanodevices (such as biological machines), nanoparticles, and nanoscale phenomena that occurs within the discipline of nanotechnology. This technical approach to biology allows scientists to imagine and create systems that can be used for biological research. Biologically inspired nanotechnology uses biological systems as the inspirations for technologies not yet created.[2] However, as with nanotechnology and biotechnology, bionanotechnology does have many potential ethical issues associated with it.

The most important objectives that are frequently found in nanobiology involve applying nanotools to relevant medical/biological problems and refining these applications. Developing new tools, such as peptoid nanosheets, for medical and biological purposes is another primary objective in nanotechnology. New nanotools are often made by refining the applications of the nanotools that are already being used. The imaging of native biomolecules, biological membranes, and tissues is also a major topic for the nanobiology researchers. Other topics concerning nanobiology include the use of cantilever array sensors and the application of nanophotonics for manipulating molecular processes in living cells.[3]

Recently, the use of microorganisms to synthesize functional nanoparticles has been of great interest. Microorganisms can change the oxidation state of metals. These microbial processes have opened up new opportunities for us to explore novel applications, for example, the biosynthesis of metal nanomaterials. In contrast to chemical and physical methods, microbial processes for synthesizing nanomaterials can be achieved in aqueous phase under gentle and environmentally benign conditions. This approach has become an attractive focus in current green bionanotechnology research towards sustainable development.[4]

The terms are often used interchangeably. When a distinction is intended, though, it is based on whether the focus is on applying biological ideas or on studying biology with nanotechnology. Bionanotechnology generally refers to the study of how the goals of nanotechnology can be guided by studying how biological "machines" work and adapting these biological motifs into improving existing nanotechnologies or creating new ones.[5][6] Nanobiotechnology, on the other hand, refers to the ways that nanotechnology is used to create devices to study biological systems.[7]

In other words, nanobiotechnology is essentially miniaturized biotechnology, whereas bionanotechnology is a specific application of nanotechnology. For example, DNA nanotechnology or cellular engineering would be classified as bionanotechnology because they involve working with biomolecules on the nanoscale. Conversely, many new medical technologies involving nanoparticles as delivery systems or as sensors would be examples of nanobiotechnology since they involve using nanotechnology to advance the goals of biology.

The definitions enumerated above will be utilized whenever a distinction between nanobio and bionano is made in this article. However, given the overlapping usage of the terms in modern parlance, individual technologies may need to be evaluated to determine which term is more fitting. As such, they are best discussed in parallel.

Most of the scientific concepts in bionanotechnology are derived from other fields. Biochemical principles that are used to understand the material properties of biological systems are central in bionanotechnology because those same principles are to be used to create new technologies. Material properties and applications studied in bionanoscience include mechanical properties(e.g. deformation, adhesion, failure), electrical/electronic (e.g. electromechanical stimulation, capacitors, energy storage/batteries), optical (e.g. absorption, luminescence, photochemistry), thermal (e.g. thermomutability, thermal management), biological (e.g. how cells interact with nanomaterials, molecular flaws/defects, biosensing, biological mechanisms s.a. mechanosensing), nanoscience of disease (e.g. genetic disease, cancer, organ/tissue failure), as well as computing (e.g. DNA computing)and agriculture(target delivery of pesticides, hormones and fertilizers.[8] The impact of bionanoscience, achieved through structural and mechanistic analyses of biological processes at nanoscale, is their translation into synthetic and technological applications through nanotechnology.

Nano-biotechnology takes most of its fundamentals from nanotechnology. Most of the devices designed for nano-biotechnological use are directly based on other existing nanotechnologies. Nano-biotechnology is often used to describe the overlapping multidisciplinary activities associated with biosensors, particularly where photonics, chemistry, biology, biophysics, nano-medicine, and engineering converge. Measurement in biology using wave guide techniques, such as dual polarization interferometry, are another example.

Applications of bionanotechnology are extremely widespread. Insofar as the distinction holds, nanobiotechnology is much more commonplace in that it simply provides more tools for the study of biology. Bionanotechnology, on the other hand, promises to recreate biological mechanisms and pathways in a form that is useful in other ways.

Nanomedicine is a field of medical science whose applications are increasing more and more thanks to nanorobots and biological machines, which constitute a very useful tool to develop this area of knowledge. In the past years, researchers have done many improvements in the different devices and systems required to develop nanorobots. This supposes a new way of treating and dealing with diseases such as cancer; thanks to nanorobots, side effects of chemotherapy have been controlled, reduced and even eliminated, so some years from now, cancer patients will be offered an alternative to treat this disease instead of chemotherapy, which causes secondary effects such as hair loss, fatigue or nausea killing not only cancerous cells but also the healthy ones. At a clinical level, cancer treatment with nanomedicine will consist on the supply of nanorobots to the patient through an injection that will seek for cancerous cells leaving untouched the healthy ones. Patients that will be treated through nanomedicine will not notice the presence of this nanomachines inside them; the only thing that is going to be noticeable is the progressive improvement of their health.[9]

Nanobiotechnology (sometimes referred to as nanobiology) is best described as helping modern medicine progress from treating symptoms to generating cures and regenerating biological tissues. Three American patients have received whole cultured bladders with the help of doctors who use nanobiology techniques in their practice. Also, it has been demonstrated in animal studies that a uterus can be grown outside the body and then placed in the body in order to produce a baby. Stem cell treatments have been used to fix diseases that are found in the human heart and are in clinical trials in the United States. There is also funding for research into allowing people to have new limbs without having to resort to prosthesis. Artificial proteins might also become available to manufacture without the need for harsh chemicals and expensive machines. It has even been surmised that by the year 2055, computers may be made out of biochemicals and organic salts.[10]

Another example of current nanobiotechnological research involves nanospheres coated with fluorescent polymers. Researchers are seeking to design polymers whose fluorescence is quenched when they encounter specific molecules. Different polymers would detect different metabolites. The polymer-coated spheres could become part of new biological assays, and the technology might someday lead to particles which could be introduced into the human body to track down metabolites associated with tumors and other health problems. Another example, from a different perspective, would be evaluation and therapy at the nanoscopic level, i.e. the treatment of Nanobacteria (25-200nm sized) as is done by NanoBiotech Pharma.

While nanobiology is in its infancy, there are a lot of promising methods that will rely on nanobiology in the future. Biological systems are inherently nano in scale; nanoscience must merge with biology in order to deliver biomacromolecules and molecular machines that are similar to nature. Controlling and mimicking the devices and processes that are constructed from molecules is a tremendous challenge to face the converging disciplines of nanotechnology.[11] All living things, including humans, can be considered to be nanofoundries. Natural evolution has optimized the "natural" form of nanobiology over millions of years. In the 21st century, humans have developed the technology to artificially tap into nanobiology. This process is best described as "organic merging with synthetic." Colonies of live neurons can live together on a biochip device; according to research from Dr. Gunther Gross at the University of North Texas. Self-assembling nanotubes have the ability to be used as a structural system. They would be composed together with rhodopsins; which would facilitate the optical computing process and help with the storage of biological materials. DNA (as the software for all living things) can be used as a structural proteomic system - a logical component for molecular computing. Ned Seeman - a researcher at New York University - along with other researchers are currently researching concepts that are similar to each other.[12]

DNA nanotechnology is one important example of bionanotechnology.[13] The utilization of the inherent properties of nucleic acids like DNA to create useful materials is a promising area of modern research. Another important area of research involves taking advantage of membrane properties to generate synthetic membranes. Proteins that self-assemble to generate functional materials could be used as a novel approach for the large-scale production of programmable nanomaterials. One example is the development of amyloids found in bacterial biofilms as engineered nanomaterials that can be programmed genetically to have different properties.[14]Protein folding studies provide a third important avenue of research, but one that has been largely inhibited by our inability to predict protein folding with a sufficiently high degree of accuracy. Given the myriad uses that biological systems have for proteins, though, research into understanding protein folding is of high importance and could prove fruitful for bionanotechnology in the future.

Lipid nanotechnology is another major area of research in bionanotechnology, where physico-chemical properties of lipids such as their antifouling and self-assembly is exploited to build nanodevices with applications in medicine and engineering.[15]

Meanwhile, nanotechnology application to biotechnology will also leave no field untouched by its groundbreaking scientific innovations for human wellness; the agricultural industry is no exception. Basically, nanomaterials are distinguished depending on the origin: natural, incidental and engineered nanoparticles. Among these, engineered nanoparticles have received wide attention in all fields of science, including medical, materials and agriculture technology with significant socio-economical growth. In the agriculture industry, engineered nanoparticles have been serving as nano carrier, containing herbicides, chemicals, or genes, which target particular plant parts to release their content.[16] Previously nanocapsules containing herbicides have been reported to effectively penetrate through cuticles and tissues, allowing the slow and constant release of the active substances. Likewise, other literature describes that nano-encapsulated slow release of fertilizers has also become a trend to save fertilizer consumption and to minimize environmental pollution through precision farming. These are only a few examples from numerous research works which might open up exciting opportunities for nanobiotechnology application in agriculture. Also, application of this kind of engineered nanoparticles to plants should be considered the level of amicability before it is employed in agriculture practices. Based on a thorough literature survey, it was understood that there is only limited authentic information available to explain the biological consequence of engineered nanoparticles on treated plants. Certain reports underline the phytotoxicity of various origin of engineered nanoparticles to the plant caused by the subject of concentrations and sizes . At the same time, however, an equal number of studies were reported with a positive outcome of nanoparticles, which facilitate growth promoting nature to treat plant.[17] In particular, compared to other nanoparticles, silver and gold nanoparticles based applications elicited beneficial results on various plant species with less and/or no toxicity.[18][19] Silver nanoparticles (AgNPs) treated leaves of Asparagus showed the increased content of ascorbate and chlorophyll. Similarly, AgNPs-treated common bean and corn has increased shoot and root length, leaf surface area, chlorophyll, carbohydrate and protein contents reported earlier.[20] The gold nanoparticle has been used to induce growth and seed yield in Brassica juncea.[21]

This field relies on a variety of research methods, including experimental tools (e.g. imaging, characterization via AFM/optical tweezers etc.), x-ray diffraction based tools, synthesis via self-assembly, characterization of self-assembly (using e.g. MP-SPR, DPI, recombinant DNA methods, etc.), theory (e.g. statistical mechanics, nanomechanics, etc.), as well as computational approaches (bottom-up multi-scale simulation, supercomputing).

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Transhuman – Wikipedia

Transhuman or trans-human is the concept of an intermediary form between human and posthuman.[1] In other words, a transhuman is a being that resembles a human in most respects but who has powers and abilities beyond those of standard humans.[2] These abilities might include improved intelligence, awareness, strength, or durability. Transhumans sometimes appear in science-fiction as cyborgs or genetically-enhanced humans.

The use of the term "transhuman" goes back to French philosopher Pierre Teilhard de Chardin, who wrote in his 1949 book The Future of Mankind:

Liberty: that is to say, the chance offered to every man (by removing obstacles and placing the appropriate means at his disposal) of 'trans-humanizing' himself by developing his potentialities to the fullest extent.[3]

And in a 1951 unpublished revision of the same book:

In consequence one is the less disposed to reject as unscientific the idea that the critical point of planetary Reflection, the fruit of socialization, far from being a mere spark in the darkness, represents our passage, by Translation or dematerialization, to another sphere of the Universe: not an ending of the ultra-human but its accession to some sort of trans-humanity at the ultimate heart of things.[4]

In 1957 book New Bottles for New Wine, English evolutionary biologist Julian Huxley wrote:

The human species can, if it wishes, transcend itself not just sporadically, an individual here in one way, an individual there in another way, but in its entirety, as humanity. We need a name for this new belief. Perhaps transhumanism will serve: man remaining man, but transcending himself, by realizing new possibilities of and for his human nature. "I believe in transhumanism": once there are enough people who can truly say that, the human species will be on the threshold of a new kind of existence, as different from ours as ours is from that of Peking man. It will at last be consciously fulfilling its real destiny.[5]

One of the first professors of futurology, FM-2030, who taught "new concepts of the Human" at The New School of New York City in the 1960s, used "transhuman" as shorthand for "transitional human". Calling transhumans the "earliest manifestation of new evolutionary beings", FM argued that signs of transhumans included physical and mental augmentations including prostheses, reconstructive surgery, intensive use of telecommunications, a cosmopolitan outlook and a globetrotting lifestyle, androgyny, mediated reproduction (such as in vitro fertilisation), absence of religious beliefs, and a rejection of traditional family values.[6]

FM-2030 used the concept of transhuman as an evolutionary transition, outside the confines of academia, in his contributing final chapter to the 1972 anthology Woman, Year 2000.[7] In the same year, American cryonics pioneer Robert Ettinger contributed to conceptualization of "transhumanity" in his book Man into Superman.[8] In 1982, American Natasha Vita-More authored a statement titled Transhumanist Arts Statement and outlined what she perceived as an emerging transhuman culture.[9]

Jacques Attali, writing in 2006, envisaged transhumans as an altruistic vanguard of the later 21st century:

Vanguard players (I shall call them transhumans) will run (they are already running) relational enterprises in which profit will be no more than a hindrance, not a final goal. Each of these transhumans will be altruistic, a citizen of the planet, at once nomadic and sedentary, his neighbor's equal in rights and obligations, hospitable and respectful of the world. Together, transhumans will give birth to planetary institutions and change the course of industrial enterprises.[10]

In March 2007, American physicist Gregory Cochran and paleoanthropologist John Hawks published a study, alongside other recent research on which it builds, which amounts to a radical reappraisal of traditional views, which tended to assume that humans have reached an evolutionary endpoint. Physical anthropologist Jeffrey McKee argued the new findings of accelerated evolution bear out predictions he made in a 2000 book The Riddled Chain. Based on computer models, he argued that evolution should speed up as a population grows because population growth creates more opportunities for new mutations; and the expanded population occupies new environmental niches, which would drive evolution in new directions. Whatever the implications of the recent findings, McKee concludes that they highlight a ubiquitous point about evolution: "every species is a transitional species".[11]

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Transhuman - Wikipedia

Healthy Living: 45 Tips To Live a Healthier Life

How healthy are you? Do you have a healthy diet? Do you exercise regularly? Do you drink at least 8 glasses of water a day? Do you get enough sleep every day?

Our body is our temple, and we need to take care of it to have a healthy life. Do you know that a shockingover 65% of Americans are either obese or overweight? Thats insane! Think of your body as your physical shell to take you through life.If you repeatedly abuse it with unhealthy food, your shell will wear out quickly. While you may look okay on the outside, on the inside, your arteries are getting clogged up with cholesteroland arterial plaque. Thats not a pretty sight!

Life is beautiful and you dont want to bog yourself down with unnecessary health problems. Today, your vital organs (kidney, heart, lungs, gall bladder, liver, stomach, intestines, etc) may be working well, but they may not be tomorrow. Dont take your good health today for granted. Take proper care of your body.

Good health isnt just about healthy eating and exercise it also includes having a positive mental health, healthy self-image and a healthy lifestyle.In this article, Ill share with you 45 tips to live a healthier life. Bookmark this article and save the tips, because they are going to be vital in living a healthier life.

Furthermore, drinking more water alone actually aids in losing weight. A Health.com study carried out among overweight/obese people showed that water drinkers lose 4.5 more pounds than a control group. The researchers believe that its because drinking more water helps fill your stomach, making you less hungry and less likely to overeat. I agree with that, and I have an added take thatyour body tries to retain whatever water you take when you dont take in enough water, leading to increase in weight. Whereas when you regularly drink water, your body knows that its going to get its supply of fluids, so it doesnt try to retain more water.

The amount of water we need is dependent on various factors such as the humidity, our physical activity, and your weight, but generally we need 2.7-3.7 litres of water intake!Since food intake contributes about20% of our fluid intake, that means we need to drink about 2.0-3.0 litres of water, or about 8-10 glasses (now you know how the 8 glasses recommendation came about!). One way to tell if youre hydrated your urine should be colorless or slightly yellow. If its not, youre not getting enough water! Other signs include: Dry lips, dry mouth and little urination. Go get some water first before you continue this article!

Which health tips are most applicable for you right now? These are timeless tips, so bookmark this article and integrate these tips into your life. Share these health tips with your family and friends too to help them stay healthy use your Twitter and Facebook via the buttons below.

If youre wondering why theres a healthy living post out of the blue, thats because well be having live a healthier life challenge come first Jan! Ill be posting the announcement post on 27 Dec, which will have the details of the challenge and sign up instructions. And to ensure that all of us start off 2011 with great health, vitality and goodness, the challenge is going to be 100% free! Yes, you got that right! Free, $0, nada, zilch!

Im personally super enthused about this and I cant wait to get started. Ill be posting more about the challenge in a couple of days time, so stay tuned!

Update Dec 27 10: The announcement post is up now! Sign up here!

Update Feb 11: The challenge is now over! Thanks to everyone whove taken part all 400 of you its been an amazing blast! Sign up for Personal Excellence newsletter to be in the loop of future challenges and also to receive life-time access of free, premium articles on how to live your best life.

Get the manifesto version of this article:[Manifesto] The Healthy Living Manifesto

Images: Fruits, Pink hearts, Legumes, Soda drinks, Home-prepared meal, Salad bar, Fruits, Salad, Woman brushing teeth

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KentuckyOne Health Healthy Lifestyle Centers

Promoting Wellness in Body, Mind and Spirit

The same health system that is Kentuckys leader in heart care, now provides medically supervised exercise, nutrition counseling, stress management and more to help you get healthy and stay healthy. Unlike other fitness programs, ours is backed by KentuckyOne Health, with a team of nurses, respiratory therapistsand exercise physiologists who work with your physician to prevent and treat heart disease, diabetes, cancer chronic lung conditions and obesity.

We team with you to create a health improvement and exercise plan tailored to your unique needs. Our wellness experts all nationally certified in their area of specialty offer services to support you on a path to healthy living. We offer three distinct programs to meet your needs:

Simply put, were your one stop for wellness. Best of all, you can join for not much more than the cost of a fitness club but with so much more.

For more information, please:

Louisville, Surrounding Counties: Call (502) 581-0110

Lexington, Surrounding Counties: Call (859) 313-4793

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5 Benefits of Healthy Habits

The impact of good health

You know that healthy habits, such as eating well, exercising, and avoiding harmful substances, make sense, but did you ever stop to think about why you practice them? A healthy habit is any behavior that benefits your physical, mental, and emotional health. These habits improve your overall well-being and make you feel good.

Healthy habits are hard to develop and often require changing your mindset. But if youre willing to make sacrifices to better your health, the impact can be far-reaching, regardless of your age, sex, or physical ability. Here are five benefits of a healthy lifestyle.

Eating right and exercising regularly can help you avoid excess weight gain and maintain a healthy weight. According to the Mayo Clinic, being physically active is essential to reaching your weight-loss goals. Even if youre not trying to lose weight, regular exercise can improve cardiovascular health, boost your immune system, and increase your energy level.

Plan for at least 150 minutes of moderate physical activity every week. If you cant devote this amount of time to exercise, look for simple ways to increase activity throughout the day. For example, try walking instead of driving, take the stairs instead of the elevator, or pace while youre talking on the phone.

Eating a balanced, calorie-managed diet can also help control weight. When you start the day with a healthy breakfast, you avoid becoming overly hungry later, which could send you running to get fast food before lunch.

Additionally, skipping breakfast can raise your blood sugar, which increases fat storage. Incorporate at least five servings of fruits and vegetables into your diet per day. These foods, which are low in calories and high in nutrients, help with weight control. Limit consumption of sugary beverages, such as sodas and fruit juices, and choose lean meats like fish and turkey.

Doing right by your body pays off for your mind as well. The Mayo Clinic notes that physical activity stimulates the production of endorphins. Endorphins are brain chemicals that leave you feeling happier and more relaxed. Eating a healthy diet as well as exercising can lead to a better physique. Youll feel better about your appearance, which can boost your confidence and self-esteem. Short-term benefits of exercise include decreased stress and improved cognitive function.

Its not just diet and exercise that lead to improved mood. Another healthy habit that leads to better mental health is making social connections. Whether its volunteering, joining a club, or attending a movie, communal activities help improve mood and mental functioning by keeping the mind active and serotonin levels balanced. Dont isolate yourself. Spend time with family or friends on a regular basis, if not every day. If theres physical distance between you and loved ones, use technology to stay connected. Pick up the phone or start a video chat.

Healthy habits help prevent certain health conditions, such as heart disease, stroke, and high blood pressure. If you take care of yourself, you can keep your cholesterol and blood pressure within a safe range. This keeps your blood flowing smoothly, decreasing your risk of cardiovascular diseases.

Regular physical activity and proper diet can also prevent or help you manage a wide range of health problems, including:

Make sure you schedule a physical exam every year. Your doctor will check your weight, heartbeat, and blood pressure, as well as take a urine and blood sample. This appointment can reveal a lot about your health. Its important to follow up with your doctor and listen to any recommendations to improve your health.

Weve all experienced a lethargic feeling after eating too much unhealthy food. When you eat a balanced diet your body receives the fuel it needs to manage your energy level. A healthy diet includes:

Regular physical exercise also improves muscle strength and boosts endurance, giving you more energy, says the Mayo Clinic. Exercise helps deliver oxygen and nutrients to your tissues and gets your cardiovascular system working more efficiently so that you have more energy to go about your daily activities. It also helps boost energy by promoting better sleep. This helps you fall asleep faster and get deeper sleep.

Insufficient sleep can trigger a variety of problems. Aside from feeling tired and sluggish, you may also feel irritable and moody if you dont get enough sleep. Whats more, poor sleep quality may be responsible for high blood pressure, diabetes, and heart disease, and it can also lower your life expectancy. To improve sleep quality, stick to a schedule where you wake up and go to bed at the same time every night. Reduce your caffeine intake, limit napping, and create a comfortable sleep environment. Turn off lights and the television, and maintain a cool room temperature.

When you practice healthy habits, you boost your chances of a longer life. The American Council on Exercise reported on an eight-year study of 13,000 people. The study showed that those who walked just 30 minutes each day significantly reduced their chances of dying prematurely, compared with those who exercised infrequently. Looking forward to more time with loved ones is reason enough to keep walking. Start with short five-minute walks and gradually increase the time until youre up to 30 minutes.

Bad habits are hard to break, but once you adopt a healthier lifestyle, you wont regret this decision. Healthy habits reduce the risk of certain diseases, improve your physical appearance and mental health, and give your energy level a much needed boost. You wont change your mindset and behavior overnight, so be patient and take it one day at a time.

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Self-care – Wikipedia

This article is about the maintenance of one's personal well-being and health. For a person's assessment of his/her own value and dignity, see Self-esteem.

In health care, self-care is any necessary human regulatory function which is under individual control, deliberate and self-initiated.[1]

Some place self-care on a continuum with health care providers at the opposite end to self-care.[2] In modern medicine, preventive medicine aligns most closely with self-care. A lack of adherence to medical advice and the onset of a mental disorder can make self-care difficult.[3] Self-care is seen as a partial solution to the global rise in health care costs placed on governments. The notion that self-care is a fundamental pillar of health and social care means it is an essential component of a modern health care system governed by regulations and statutes.[4]

Self-care is considered a primary form of care for patients with chronic conditions who make many day-to-day decisions, or self-manage, their illness.[5] Self-management is critical and self-management education complements traditional patient education in primary care to support patients to live the best possible quality of life with their chronic condition.[1][5] Self-care is learned, purposeful and continuous.[6] In philosophy, self-care refers to the care and cultivation of self in a comprehensive sense, focusing in particular on the soul and the knowledge of self.

There are a number of self-care requisites applicable to all humans across all ages and necessary to fundamental human needs.[6] For example, as humans we need to intake sufficient air, water and food; care also needs to be taken with the process of elimination and excrement. There must be a balance between rest and activity as well as between solitude and social activities.[6] The prevention and avoidance of human hazards and participation in social groups are also requisites. Maturity requires the autonomous performance of self-care duties.[7]

Self-care includes all health decisions people (as individuals or consumers) make for themselves and their families to ensure they are physically and mentally fit. Self-care includes exercising to maintain physical fitness and promote good mental health, as well as eating well, practicing good hygiene and avoiding health hazards such as smoking and drinking to prevent ill health. The personal responsibility for self-care in the context of preventative medicine was examined with a representative sample of the general public in a Citizens Jury, with the title: My health whose responsibility? A jury decides.[8]

The benefits of living a healthy lifestyle were analysed in the Caerphilly Heart Disease Study. Evidence showed a risk reduction in chronic diseases (including dementia and cognitive impairment) to be significantly associated with healthy lifestyles.[9]

Self-care is also taking care of minor ailments, long term conditions, or ones own health after discharge from secondary and tertiary health care. For instances of neck pain, for example, self-care is the recommended treatment.[10]

Patients who are better informed and more educated possess greater motivation for self-care.[2] Individuals conduct self-care and experts and professionals support self-care to enable individuals to undertake enhanced self-care. The recognition and evaluation of symptoms is a key aspect of self-care.[11] The main issues involved with self-care and the onset of illness are medically related such managing drug side effects, emotions and psychological issues, changes to lifestyle and knowledge acquisition to assist in decision-making.[2]

Self-care support has crucial enabling value and considerable scope in developing countries with an already overburdened health care system. But it also has an essential role to play in affluent countries where people are becoming more conscious about their health and want to have a greater role in taking care of themselves.

To enable people to do enhanced self-care, they can be supported in various ways and by different service providers.

Self-care support can include the following:

Self-care practices are shaped by what are seen as the proper lifestyle choices of local communities. Health-related self-care topics include;

A lack of self-care in terms of personal health, hygiene and living conditions is referred to as self-neglect. The use of caregivers and Personal Care Assistants may be needed. An aging population is seeking greater self-care knowledge primarily within families connections and with responsibility usually belonging to the mother.[7]

Michael Foucault understood the art of living (French art de vivre, Latin ars vivendi) and the care of self (French le souci de soi) to be central to philosophy. The third volume of his three-volume study The History of Sexuality is dedicated to this notion. For Foucault, the notion of care of self (epimeleia heautou) of Ancient Greek and Roman philosophy comprises an attitude towards the self, others and the world, as well as a certain form of attention. For Foucault, the pursuit of the care for one's own well-being also comprises self-knowledge (gnthi seauton).[16][17]

The self-care deficit nursing theory was developed by Dorothea Orem between 1959 and 2001. The positively viewed theory explores the use professional care and an orientation towards resources.[4] Under Orem's model self-care has limits when its possibilities have been exhausted therefore making professional care legitimate. These deficits in self-care are seen as shaping the best role a nurse may provide. There are two phases in Orem's self-care; the investigative and decision-making phase and the production phase.[18]

Self-care as health maintenance:

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Nanomedicine – Wikipedia

Nanomedicine is the medical application of nanotechnology.[1] Nanomedicine ranges from the medical applications of nanomaterials and biological devices, to nanoelectronic biosensors, and even possible future applications of molecular nanotechnology such as biological machines. Current problems for nanomedicine involve understanding the issues related to toxicity and environmental impact of nanoscale materials (materials whose structure is on the scale of nanometers, i.e. billionths of a meter).

Functionalities can be added to nanomaterials by interfacing them with biological molecules or structures. The size of nanomaterials is similar to that of most biological molecules and structures; therefore, nanomaterials can be useful for both in vivo and in vitro biomedical research and applications. Thus far, the integration of nanomaterials with biology has led to the development of diagnostic devices, contrast agents, analytical tools, physical therapy applications, and drug delivery vehicles.

Nanomedicine seeks to deliver a valuable set of research tools and clinically useful devices in the near future.[2][3] The National Nanotechnology Initiative expects new commercial applications in the pharmaceutical industry that may include advanced drug delivery systems, new therapies, and in vivo imaging.[4] Nanomedicine research is receiving funding from the US National Institutes of Health, including the funding in 2005 of a five-year plan to set up four nanomedicine centers.

Nanomedicine sales reached $16 billion in 2015, with a minimum of $3.8 billion in nanotechnology R&D being invested every year. Global funding for emerging nanotechnology increased by 45% per year in recent years, with product sales exceeding $1 trillion in 2013.[5] As the nanomedicine industry continues to grow, it is expected to have a significant impact on the economy.

Nanotechnology has provided the possibility of delivering drugs to specific cells using nanoparticles.

The overall drug consumption and side-effects may be lowered significantly by depositing the active agent in the morbid region only and in no higher dose than needed. Targeted drug delivery is intended to reduce the side effects of drugs with concomitant decreases in consumption and treatment expenses. Drug delivery focuses on maximizing bioavailability both at specific places in the body and over a period of time. This can potentially be achieved by molecular targeting by nanoengineered devices.[6][7] More than $65 billion are wasted each year due to poor bioavailability.[citation needed] A benefit of using nanoscale for medical technologies is that smaller devices are less invasive and can possibly be implanted inside the body, plus biochemical reaction times are much shorter. These devices are faster and more sensitive than typical drug delivery.[8] The efficacy of drug delivery through nanomedicine is largely based upon: a) efficient encapsulation of the drugs, b) successful delivery of drug to the targeted region of the body, and c) successful release of the drug.[citation needed]

Drug delivery systems, lipid- [9] or polymer-based nanoparticles,[10] can be designed to improve the pharmacokinetics and biodistribution of the drug.[11][12][13] However, the pharmacokinetics and pharmacodynamics of nanomedicine is highly variable among different patients.[14] When designed to avoid the body's defence mechanisms,[15] nanoparticles have beneficial properties that can be used to improve drug delivery. Complex drug delivery mechanisms are being developed, including the ability to get drugs through cell membranes and into cell cytoplasm. Triggered response is one way for drug molecules to be used more efficiently. Drugs are placed in the body and only activate on encountering a particular signal. For example, a drug with poor solubility will be replaced by a drug delivery system where both hydrophilic and hydrophobic environments exist, improving the solubility.[16] Drug delivery systems may also be able to prevent tissue damage through regulated drug release; reduce drug clearance rates; or lower the volume of distribution and reduce the effect on non-target tissue. However, the biodistribution of these nanoparticles is still imperfect due to the complex host's reactions to nano- and microsized materials[15] and the difficulty in targeting specific organs in the body. Nevertheless, a lot of work is still ongoing to optimize and better understand the potential and limitations of nanoparticulate systems. While advancement of research proves that targeting and distribution can be augmented by nanoparticles, the dangers of nanotoxicity become an important next step in further understanding of their medical uses.[17]

Nanoparticles can be used in combination therapy for decreasing antibiotic resistance or for their antimicrobial properties.[18][19][20] Nanoparticles might also used to circumvent multidrug resistance (MDR) mechanisms.[21]

Two forms of nanomedicine that have already been tested in mice and are awaiting human trials that will be using gold nanoshells to help diagnose and treat cancer,[22] and using liposomes as vaccine adjuvants and as vehicles for drug transport.[23][24] Similarly, drug detoxification is also another application for nanomedicine which has shown promising results in rats.[25] Advances in Lipid nanotechnology was also instrumental in engineering medical nanodevices and novel drug delivery systems as well as in developing sensing applications.[26] Another example can be found in dendrimers and nanoporous materials. Another example is to use block co-polymers, which form micelles for drug encapsulation.[10]

Polymeric nano-particles are a competing technology to lipidic (based mainly on Phospholipids) nano-particles. There is an additional risk of toxicity associated with polymers not widely studied or understood. The major advantages of polymers is stability, lower cost and predictable characterisation. However, in the patient's body this very stability (slow degradation) is a negative factor. Phospholipids on the other hand are membrane lipids (already present in the body and surrounding each cell), have a GRAS (Generally Recognised As Safe) status from FDA and are derived from natural sources without any complex chemistry involved. They are not metabolised but rather absorbed by the body and the degradation products are themselves nutrients (fats or micronutrients).[citation needed]

Protein and peptides exert multiple biological actions in the human body and they have been identified as showing great promise for treatment of various diseases and disorders. These macromolecules are called biopharmaceuticals. Targeted and/or controlled delivery of these biopharmaceuticals using nanomaterials like nanoparticles and Dendrimers is an emerging field called nanobiopharmaceutics, and these products are called nanobiopharmaceuticals.[citation needed]

Another highly efficient system for microRNA delivery for example are nanoparticles formed by the self-assembly of two different microRNAs deregulated in cancer.[27]

Another vision is based on small electromechanical systems; nanoelectromechanical systems are being investigated for the active release of drugs. Some potentially important applications include cancer treatment with iron nanoparticles or gold shells.Nanotechnology is also opening up new opportunities in implantable delivery systems, which are often preferable to the use of injectable drugs, because the latter frequently display first-order kinetics (the blood concentration goes up rapidly, but drops exponentially over time). This rapid rise may cause difficulties with toxicity, and drug efficacy can diminish as the drug concentration falls below the targeted range.[citation needed]

Some nanotechnology-based drugs that are commercially available or in human clinical trials include:

Existing and potential drug nanocarriers have been reviewed.[38][39][40][41]

Nanoparticles have high surface area to volume ratio. This allows for many functional groups to be attached to a nanoparticle, which can seek out and bind to certain tumor cells. Additionally, the small size of nanoparticles (10 to 100 nanometers), allows them to preferentially accumulate at tumor sites (because tumors lack an effective lymphatic drainage system).[42] Limitations to conventional cancer chemotherapy include drug resistance, lack of selectivity, and lack of solubility. Nanoparticles have the potential to overcome these problems.[43]

In photodynamic therapy, a particle is placed within the body and is illuminated with light from the outside. The light gets absorbed by the particle and if the particle is metal, energy from the light will heat the particle and surrounding tissue. Light may also be used to produce high energy oxygen molecules which will chemically react with and destroy most organic molecules that are next to them (like tumors). This therapy is appealing for many reasons. It does not leave a "toxic trail" of reactive molecules throughout the body (chemotherapy) because it is directed where only the light is shined and the particles exist. Photodynamic therapy has potential for a noninvasive procedure for dealing with diseases, growth and tumors. Kanzius RF therapy is one example of such therapy (nanoparticle hyperthermia) .[citation needed] Also, gold nanoparticles have the potential to join numerous therapeutic functions into a single platform, by targeting specific tumor cells, tissues and organs.[44][45]

In vivo imaging is another area where tools and devices are being developed. Using nanoparticle contrast agents, images such as ultrasound and MRI have a favorable distribution and improved contrast. This might be accomplished by self assembled biocompatible nanodevices that will detect, evaluate, treat and report to the clinical doctor automatically.[citation needed]

The small size of nanoparticles endows them with properties that can be very useful in oncology, particularly in imaging. Quantum dots (nanoparticles with quantum confinement properties, such as size-tunable light emission), when used in conjunction with MRI (magnetic resonance imaging), can produce exceptional images of tumor sites. Nanoparticles of cadmium selenide (quantum dots) glow when exposed to ultraviolet light. When injected, they seep into cancer tumors. The surgeon can see the glowing tumor, and use it as a guide for more accurate tumor removal.These nanoparticles are much brighter than organic dyes and only need one light source for excitation. This means that the use of fluorescent quantum dots could produce a higher contrast image and at a lower cost than today's organic dyes used as contrast media. The downside, however, is that quantum dots are usually made of quite toxic elements.[citation needed]

Tracking movement can help determine how well drugs are being distributed or how substances are metabolized. It is difficult to track a small group of cells throughout the body, so scientists used to dye the cells. These dyes needed to be excited by light of a certain wavelength in order for them to light up. While different color dyes absorb different frequencies of light, there was a need for as many light sources as cells. A way around this problem is with luminescent tags. These tags are quantum dots attached to proteins that penetrate cell membranes. The dots can be random in size, can be made of bio-inert material, and they demonstrate the nanoscale property that color is size-dependent. As a result, sizes are selected so that the frequency of light used to make a group of quantum dots fluoresce is an even multiple of the frequency required to make another group incandesce. Then both groups can be lit with a single light source. They have also found a way to insert nanoparticles[46] into the affected parts of the body so that those parts of the body will glow showing the tumor growth or shrinkage or also organ trouble.[47]

Nanotechnology-on-a-chip is one more dimension of lab-on-a-chip technology. Magnetic nanoparticles, bound to a suitable antibody, are used to label specific molecules, structures or microorganisms. Gold nanoparticles tagged with short segments of DNA can be used for detection of genetic sequence in a sample. Multicolor optical coding for biological assays has been achieved by embedding different-sized quantum dots into polymeric microbeads. Nanopore technology for analysis of nucleic acids converts strings of nucleotides directly into electronic signatures.[citation needed]

Sensor test chips containing thousands of nanowires, able to detect proteins and other biomarkers left behind by cancer cells, could enable the detection and diagnosis of cancer in the early stages from a few drops of a patient's blood.[48]Nanotechnology is helping to advance the use of arthroscopes, which are pencil-sized devices that are used in surgeries with lights and cameras so surgeons can do the surgeries with smaller incisions. The smaller the incisions the faster the healing time which is better for the patients. It is also helping to find a way to make an arthroscope smaller than a strand of hair.[49]

Research on nanoelectronics-based cancer diagnostics could lead to tests that can be done in pharmacies. The results promise to be highly accurate and the product promises to be inexpensive. They could take a very small amount of blood and detect cancer anywhere in the body in about five minutes, with a sensitivity that is a thousand times better than in a conventional laboratory test. These devices that are built with nanowires to detect cancer proteins; each nanowire detector is primed to be sensitive to a different cancer marker. The biggest advantage of the nanowire detectors is that they could test for anywhere from ten to one hundred similar medical conditions without adding cost to the testing device.[50] Nanotechnology has also helped to personalize oncology for the detection, diagnosis, and treatment of cancer. It is now able to be tailored to each individuals tumor for better performance. They have found ways that they will be able to target a specific part of the body that is being affected by cancer.[51]

Magnetic micro particles are proven research instruments for the separation of cells and proteins from complex media. The technology is available under the name Magnetic-activated cell sorting or Dynabeads among others. More recently it was shown in animal models that magnetic nanoparticles can be used for the removal of various noxious compounds including toxins, pathogens, and proteins from whole blood in an extracorporeal circuit similar to dialysis.[52][53] In contrast to dialysis, which works on the principle of the size related diffusion of solutes and ultrafiltration of fluid across a semi-permeable membrane, the purification with nanoparticles allows specific targeting of substances. Additionally larger compounds which are commonly not dialyzable can be removed.[citation needed]

The purification process is based on functionalized iron oxide or carbon coated metal nanoparticles with ferromagnetic or superparamagnetic properties.[54] Binding agents such as proteins,[53]antibodies,[52]antibiotics,[55] or synthetic ligands[56] are covalently linked to the particle surface. These binding agents are able to interact with target species forming an agglomerate. Applying an external magnetic field gradient allows exerting a force on the nanoparticles. Hence the particles can be separated from the bulk fluid, thereby cleaning it from the contaminants.[57][58]

The small size (< 100nm) and large surface area of functionalized nanomagnets leads to advantageous properties compared to hemoperfusion, which is a clinically used technique for the purification of blood and is based on surface adsorption. These advantages are high loading and accessibility of the binding agents, high selectivity towards the target compound, fast diffusion, small hydrodynamic resistance, and low dosage.[59]

This approach offers new therapeutic possibilities for the treatment of systemic infections such as sepsis by directly removing the pathogen. It can also be used to selectively remove cytokines or endotoxins[55] or for the dialysis of compounds which are not accessible by traditional dialysis methods. However the technology is still in a preclinical phase and first clinical trials are not expected before 2017.[60]

Nanotechnology may be used as part of tissue engineering to help reproduce or repair or reshape damaged tissue using suitable nanomaterial-based scaffolds and growth factors. Tissue engineering if successful may replace conventional treatments like organ transplants or artificial implants. Nanoparticles such as graphene, carbon nanotubes, molybdenum disulfide and tungsten disulfide are being used as reinforcing agents to fabricate mechanically strong biodegradable polymeric nanocomposites for bone tissue engineering applications. The addition of these nanoparticles in the polymer matrix at low concentrations (~0.2 weight%) leads to significant improvements in the compressive and flexural mechanical properties of polymeric nanocomposites.[61][62] Potentially, these nanocomposites may be used as a novel, mechanically strong, light weight composite as bone implants.[citation needed]

For example, a flesh welder was demonstrated to fuse two pieces of chicken meat into a single piece using a suspension of gold-coated nanoshells activated by an infrared laser. This could be used to weld arteries during surgery.[63] Another example is nanonephrology, the use of nanomedicine on the kidney.

Neuro-electronic interfacing is a visionary goal dealing with the construction of nanodevices that will permit computers to be joined and linked to the nervous system. This idea requires the building of a molecular structure that will permit control and detection of nerve impulses by an external computer. A refuelable strategy implies energy is refilled continuously or periodically with external sonic, chemical, tethered, magnetic, or biological electrical sources, while a nonrefuelable strategy implies that all power is drawn from internal energy storage which would stop when all energy is drained. A nanoscale enzymatic biofuel cell for self-powered nanodevices have been developed that uses glucose from biofluids including human blood and watermelons.[64] One limitation to this innovation is the fact that electrical interference or leakage or overheating from power consumption is possible. The wiring of the structure is extremely difficult because they must be positioned precisely in the nervous system. The structures that will provide the interface must also be compatible with the body's immune system.[65]

Molecular nanotechnology is a speculative subfield of nanotechnology regarding the possibility of engineering molecular assemblers, machines which could re-order matter at a molecular or atomic scale. Nanomedicine would make use of these nanorobots, introduced into the body, to repair or detect damages and infections. Molecular nanotechnology is highly theoretical, seeking to anticipate what inventions nanotechnology might yield and to propose an agenda for future inquiry. The proposed elements of molecular nanotechnology, such as molecular assemblers and nanorobots are far beyond current capabilities.[1][65][66][67] Future advances in nanomedicine could give rise to life extension through the repair of many processes thought to be responsible for aging. K. Eric Drexler, one of the founders of nanotechnology, postulated cell repair machines, including ones operating within cells and utilizing as yet hypothetical molecular machines, in his 1986 book Engines of Creation, with the first technical discussion of medical nanorobots by Robert Freitas appearing in 1999.[1]Raymond Kurzweil, a futurist and transhumanist, stated in his book The Singularity Is Near that he believes that advanced medical nanorobotics could completely remedy the effects of aging by 2030.[68] According to Richard Feynman, it was his former graduate student and collaborator Albert Hibbs who originally suggested to him (circa 1959) the idea of a medical use for Feynman's theoretical micromachines (see nanotechnology). Hibbs suggested that certain repair machines might one day be reduced in size to the point that it would, in theory, be possible to (as Feynman put it) "swallow the doctor". The idea was incorporated into Feynman's 1959 essay There's Plenty of Room at the Bottom.[69]

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Diet Science by Dee and Michael McCaffrey on iTunes

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Diet Science is a fun 7 to 8 minute weekly program with insights and straight scoops on today's health and diet issues from Dee McCaffrey, CDC. Dee is an Organic Chemist who lost 100 pounds, nearly half her body weight, and has kept it off for 20 years by staying away from processed foods. She's the author of The Science of Skinny, released by Perseus June 2012, and The Science of Skinny Cookbook, which was released December 2014.

I love this podcast, and you should try it out, too! I am so tired of fad advice when it comes to nutrition and diet, and "Diet Science" is the opposite. I can't wait for each new episode. All of the information in this podcast is science-based, and will open your eyes to what you are really putting into your body. And, unlike many other podcasts, each episode contains worthwhile information, rather than a 'promo' for information you need to buy. Because of the new information I have found here, I am slowly guiding my family's diet to be more healthy. Right now we are experimenting with quinoa, and I look forward to trying flax oil next!

Great information presented in such a way even a "beginner" like me can understand it! "Mighty Dee" is a life-saver to me! Her podcasts have become my "bible" to healthy eating. There is so much information out there it gets so confusing just trying to figure out what and who to believe! As soon as you listen to ONE of Dee's podcasts you will become a "believer"! I have lost 15 pounds in 4 weeks using Dee's advice and guidelines. She has the education, the knowledge and personal experience and she willingly shares it all.

...and not those topics you are uninformed about. Your podcast on orthorexia demonstrated your lack of knowledge when it comes to eating disorders - and Michael's insensitivity towards people who suffer from this mental illness was disturbing. (Though he did "come around" towards the end of the episode.) Dee's comments clearly showed her ignorance of the topic, and were more damaging than helpful. Stick to what you "know" and do NOT dabble in content where you are uninformed/uneducated/unaware.

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Buy Sermorelin Injections | Buy Sermorelin Online

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Testosterone replacement therapy for older men

Clin Interv Aging. 2007 Dec; 2(4): 561566.

Published online 2007 Dec.

Geriatrics Research, Education, and Clinical Center, North Florida/South Georgia Veterans Health System, Gainesville, FL, USA

Despite intensive research on testosterone therapy for older men, important questions remain unanswered. The evidence clearly indicates that many older men display a partial androgen deficiency. In older men, low circulating testosterone is correlated with low muscle strength, with high adiposity, with insulin resistance and with poor cognitive performance. Testosterone replacement in older men has produced benefits, but not consistently so. The inconsistency may arise from differences in the dose and duration of testosterone treatment, as well as selection of the target population. Generally, studies reporting anabolic responses to testosterone have employed higher doses of testosterone for longer treatment periods and have targeted older men whose baseline circulating bioavailable testosterone levels were low. Most studies of testosterone replacement have reported anabolic that are modest compared to what can be achieved with resistance exercise training. However, several strategies currently under evaluation have the potential to produce greater anabolic effects and to do so in a safe manner. At this time, testosterone therapy can not be recommended for the general population of older men. Older men who are hypogonadal are at greater risk for the catabolic effects associated with a number of acute and chronic medical conditions. Future research is likely to reveal benefits of testosterone therapy for some of these special populations. Testosterone therapy produces a number of adverse effects, including worsening of sleep apnea, gynecomastia, polycythemia and elevation of PSA. Efficacy and adverse effects should be assessed frequently throughout the course of therapy.

Keywords: aging, testosterone, hypogonadism, physical function

In young adult men, the hypothalamic-pituitary-gonadal axis regulates the circulating concentration of testosterone. The hypothalamic pulse generator secretes a pulse of gonadotropin releasing hormone (GnRH) approximately every 90 minutes (Reyes-Fuentes and Veldhuis 1993). GnRH is secreted into the hypothalamic-pituitary portal circulation where it stimulates pituitary secretion of luteinizing hormone (LH) (Veldhuis et al 1990) into the systemic circulation. LH reaches the testes and promotes both tonic and episodic Leydig cell secretion of testosterone.

Nearly all of the testosterone circulating in the blood is bound to sex hormone-binding globulin (SHBG) or albumin. The affinity of SHBG for testosterone is about 1,000-fold higher than the affinity of albumin for testosterone (Pardridge et al 1985). Thus the combined free (1%2%) and albumin-bound fractions of testosterone are considered to be bioavailable (Manni et al 1985). Bioavailable testosterone in acts upon multiple target tissues and completes the feedback loop inhibiting GnRH and LH secretion.

The serum testosterone concentration displays both circadian and ultradian rhythms. The circadian rhythm results in peak testosterone serum concentrations during the early morning hours. In contrast, the ultradian rhythm has a cycle whereby the serum testosterone concentration fluctuates approximately every 90 minutes. This ultradian rhythm represents the burst-like secretory pattern of testosterone, which is superimposed on testosterones basal or tonic secretion.

In young adult health, the feedforward (GnRH stimulates LH which stimulates testosterone secretion) and feedback (free or bioavailable testosterone inhibits release of GnRH and LH) components of the hypothalamic-pituitary-gonadal axis maintain the serum total testosterone concentration within a normal range of 4501,000 ng/dL. The mean serum total testosterone concentration for healthy young adults approximates 650 ng/dL.

Unlike female menopause, the decline in testosterone serum concentration in men is gradual, and there is much inter-individual variability. Serum testosterone concentrations decline steadily after young adulthood, and by age of 80 years, the testosterone secretion rate decreases to approximately half that of a younger man (Tenover et al 1987; Mulligan et al 1995).

The decrease in bioavailable-testosterone appears to be greater than the decline in total testosterone with advancing age, due to an age-related increase in SHBG (Rubens et al 1974). The decline in testosterone with aging has been referred to by a variety of names including male menopause, climacteric, viropause, andropause, ADAM (androgen deficiency in aging men), or age-associated hypogonadism. Longitudinal studies confirm a decline in testosterone with aging, as has been reported earlier in cross-sectional studies (Morley et al 1997; Feldman et al 2002).

With age, changes that contribute to hypogonadism occur in both the hypothalamus and testes. The rise in LH following a decrease in testosterone is considerably blunted with age (Korenman et al 1990; Veldhuis et al 2001). This is likely due to failure of the hypothalamus to generate an appropriate burst of GnRH secretion (Veldhuis et al 1994; Mulligan et al 1999). The specific mechanism may be an age-related increased sensitivity of the hypothalamic-pituitary unit to the negative feedback effect of testosterone (Winters et al 1984). In older men, the decline in circulating testosterone also correlates with changes in the testes, specifically a decline in Leydig cell number (Neaves et al 1984), development of vacuolizations and lipofuscin within the Leydig cells, and decreased Leydig cell secretion of testosterone in response to provocative stimulation with human chorionic gonadotrophin (Harman and Tsitouras 1980).

The decline in bioavailable testosterone may be at least partially responsible for the decreased muscle mass, osteoporosis, mood disturbances, and frailty seen in older men (Nunez 1982).

The criteria for low testosterone are the same regardless of age. Symptomatic men with a total serum testosterone concentration less that 200 ng/dL are definitely hypogonadal, while those with a concentration between 200 and 300 ng/dL are probably hypogonadal. The prevalence of hypogonadism increases with advancing age; the odds ratio of hypogonadism is greater with each 10-year increase in age. Longitudinal studies in specific geographic areas of the United States and some small cross-sectional studies have demonstrated a decline in testosterone occurring as early as age 30, but usually testosterone levels remain within normal limits until men reach age 60 (Belanger et al 1994; Morley et al 1997). The prevalence of low serum total testosterone among men aged 45 years or older has been estimated to be 39% (Mulligan et al 2006). The prevalence of symptomatic hypogonadism is considerably lower, estimated as 6%12% in a group of men aged 4060 years in the report of the Massachusetts Male Aging Study (Araujo et al 2004).

Low serum testosterone concentration in older men is associated with depression (Shores et al 2005). However, most trials of testosterone replacement have not shown improvement in depression. Two small studies in younger hypogonadal men did show short term improvement in depression with testosterone supplementation, but this effect has not been reproduced in older men (Pope et al 2003). The age of onset of depression may also be a factor in response to testosterone. Perry et al (2002) reported that 6 weeks of testosterone treatment improved depression scores in men who had onset of depression after the age of 45 years, but not in men whose depression started at a younger age.

Higher bioavailable testosterone levels are associated with better performance in cognitive tests (Barett-Connor et al 2004). Short-term trials in healthy eugonadal older men have shown improvement in verbal and spatial memory (Cherrier et al 2001; Gray et al 2005). However, longer trials have produced mixed results. Haren et al (2005) reported no improvement in cognition or memory. In a recent study by Cherrier et al (2006), older men were treated for 6 weeks with testosterone at doses of 50, 100 or 300 mg/week. Interestingly, improvements in verbal and spatial memory were observed only with the intermediate dose.

Testosterone produces substantial anabolic effects in young and middle-aged hypogonadal men (Bhasin et al 2001). In contrast, the anabolic effects of testosterone replacement therapy in older men have been harder to demonstrate. Among the many published trials of testosterone in older men, some report strength gains and some do not. Only a few report strength gains that can be considered substantial in comparison to the benefits of resistance exercise training. In most cases, the studies reporting significant strength gains were performed in hypogonadal subjects and employed a higher dose of testosterone, for a longer duration.

In a recent report, Nair et al (2006) describe treating a group of hypogonadal men for 24 months with a transdermal testosterone at a dose of 35 mg/week and finding no increase in strength. However, 35 mg/week is less than a replacement dose and resulted in only a 30% increase in the circulating testosterone concentration. Studies by Brill et al (2002), Clague et al (1999), Kenny et al (2001), and Snyder et al (1999) also report small increases in strength. Brill et al treated older men for 1 month with 5 mg testosterone/day by patch and found an improvement in stair climb time, but no increase in strength. Clague et al treated men aged 60 or more with total T of 400 ng/dL or less were treated with 200 mg testosterone enanthate every two weeks by i.m. injection for 3 months and found no significant increase in strength. Kenny et al (2001) treated hypogonadal and low-normal older men with 5 mg testosterone/day by patch for 1 year and found a 38% increase in strength with testosterone, but surprisingly also a 27% increase with placebo, with no significant difference between the two groups. Snyder et al (1999) treated older hypogonadal and eugonadal men for 36 months with 6 mg testosterone/day by patch and found no increase in strength.

Several investigators have reported that testosterone caused moderate increases in strength; increases that are significant, but are still below than what can be obtained through resistance exercise training. Wang et al (2000) treated younger and older men (aged 1968) with total T of 300 ng/dL or less with a titrated dose of testosterone gel (equivalent of 5 to 10 mg per day) for 6 months found that the higher dose caused, a reduction in negative moods, a sizable increase in hematocrit (from 42 to 47), and modest increases in arm and leg strength. Sullivan et al (2005) conducted a 3-month study of low- or high-intensity resistance exercise training in men aged 65 or more, who were not hypogonadal (total T = 480 ng/dL or less). Some subjects also received a weekly i.m. injection of 100 mg testosterone enanthate. The addition of testosterone produced a trend toward greater increases overall, but the effect of testosterone appears to be substantial in the low-intensity training group. Considering that few men in the community will perform high-intensity training on their own, these results may indicate usefulness for testosterone therapy.

Three studies have reported substantial strength gains following testosterone treatment and all have employed doses of testosterone that are somewhat higher than replacement doses. Ferrando et al (2002) treated older hypogonadal and eugonadal men for 6 months with a biweekly injection of testosterone that was titrated to raises circulating testosterone into the normal range and resulted in an approximated doubling of circulating testosterone (from 300 to 600 ng/dL). Significant strength increases were observed, including a 15 kg increase in leg extension 1-RM strength. Page et al (2005) treated a group of older, hypogonadal men for 36 months with biweekly i.m. injections of 200 mg testosterone enanthate and found significant improvements in hand grip strength. However, the study that best demonstrates the dose dependence is that of Bhasin et al (2005). Both older and younger men were first made hypogonadal with luprolide and then treated for 5 months with testosterone enanthate at doses ranging from 25 mg to 600 mg/week. Higher doses of testosterone produced large increases in strength, including an increase of 50 kg in leg press 1-RM strength in older men receiving a dose of 300 mg/week. The doses of 300 and 600 mg/week produced a high incidence of adverse effects and a dose of 125 mg/week was considered to be the best trade-off of beneficial and adverse effects.

The dose of testosterone also appears to be critical in determining whether increases in bone mineral density are observed. Snyder et al (1999) treated older hypogonadal and eugonadal men for 36 months with 6 mg testosterone/day by patch and found that bone mineral density did not increase overall, but did do so in the group with the lowest pretreatment testosterone levels. However, Amory et al (2004) treated older hypogonadal men for 36 months with biweekly i.m. injections of 200 mg testosterone enanthate and obtained substantial increases in bone mineral density, 3%4% in the hip and a remarkable 10% in the lumbar spine.

The lower rate of heart disease in women has historically been attributed to the cardioprotective effects of estrogen. Presently, this position is being reexamined. The cardioprotective effects of estrogen have come into some question and there is emerging evidence that testosterone may have cardioprotective effects of its own. Swartz and Young (1987) have shown that older men with a low circulating testosterone, a higher fraction have previously suffered a myocardial infarction. Testosterone supplementation in hypogonadal men improves exercise tolerance and decreases exercise-associated ischemia in elderly patients with coronary artery disease and low (Malkin et al 2004) or low-normal (English et al 2000) testosterone. This protection may be secondary to a vasodilatory effect and/or higher pain threshold. The vasodilatory effect has been confirmed in animal models (English et al 2002). The beneficial effects are seen with both acute (Rosano et al 1999) and chronic (English et al 2000, 2002) testosterone administration, and also with low (Malkin et al 2004) and high (Rosano et al 1999) dose supplementation. However, none of these studies was long enough to show an effect on cardiovascular mortality.

Although there has been concern that testosterone therapy might adversely affect serum cholesterol and lipids, this concern has not been bourn out in controlled studies. Wang et al (2000) reported that treating hypogonadal men with testosterone gel (equivalent of 510 mg per day) for 6 months did not produce significant changes in LDL- or HDL-cholesterol. Whitsel et al (2001) performed a meta analysis of 19 studies involving administration of testosterone esters to older hypogonadal men and found that, on the whole, testosterone produces small, and probably offsetting, decreases in both HDL and LDL. An additional cardiac benefit of testosterone may be seen in the findings of Malkin et al (2004), who found that testosterone reduced circulating levels of tumor necrosis factor alpha and interleukin-1 beta, inflammatory cytokines that are elevated in heart failure.

Risks associated with testosterone replacement in elderly men include fluid retention, gynecomastia, worsening of sleep apnea, polycythemia and acceleration of benign or malignant prostatic disease (Matsumoto 2002). A high incidence of adverse effects was observed by Bhasin et al (2005) in treating older men with the very high doses of 300 and 600 mg/week.

Among these risks, the potential effects of testosterone on the prostate are of the greatest concern. These concerns stem from the known action of testosterone in accelerating active prostate cancer and from the high prevalence of early-stage prostate cancer in elderly men. While approximately 10% of men will develop clinically manifest prostate cancer in their lifetime and 3% will die of the disease, autopsy data show that 42% of men over the age of 60 have early-stage prostate cancer (Mikuz 1997). Clinical trials to date are not large enough or long enough to determine the potential effects of testosterone treatment on prostate cancer. Although Zitzmann et al (2003) have shown that replacement and slightly higher doses of testosterone produce a predictable and moderate degree of prostate enlargement, existing data do not indicate that testosterone promotes prostate cancer. Hajjar et al (1997) treated elderly men with a replacement dose of testosterone and found no increase in prostate cancer during a 2-year follow-up. Agarwal and Oefelein (2005) administered testosterone for 19 months to hypogonadal patients with a history of prostate cancer and prostatectomy, but whose recent PSA levels were low. Treatment significantly elevated circulating testosterone and improved quality of life without elevating PSA.

Patients should be evaluated one month after initiation of treatment and the dose should be increased if symptoms of hypogonadism have not improved. Rhoden and Morgentaler (2004) have reviewed the adverse effects and recommend the following monitoring. Safety monitoring should include sleep apnea, voiding symptoms, serum testosterone, PSA and hemoglobin or hematocrit and should be performed several times during the first year and yearly thereafter.

In response to concerns over the efficacy and risks of hormonal replacement in the elderly, the NIH commissioned an assessment by the Institute of Medicine (IOM). The IOM report states that there is insufficient evidence to conclude that testosterone treatment in older men has well established benefits. In addition, the IOM recommended that small and medium-sized trials be conducted to assess the efficacy of testosterone for treating muscle weakness, osteoporosis, sexual dysfunction, cognitive impairment and depression (Liverman and Blazer 2004). The IOM does not recommend prevention trials or trials for all hypogonadal older men. While we agree with these recommendations, at least two other avenues of exploration deserve attention.

First, while replacement doses of testosterone do not consistently produce substantial increases in strength, Page et al (2005) and Bhasin et al (2005) have shown that higher doses of testosterone do produce such increases. Higher doses of testosterone also produce more adverse effects, especially prostate effects. Strength, especially lower body strength, remains an important facto limiting the independence of older people. Currently, alternative strategies are being developed, aimed at stimulating the androgen receptor more powerfully, without producing added adverse effects. One such strategy is to administer a higher dose of testosterone with the addition of a 5-alpha reductase inhibitor to prevent the prostate symptoms. Another strategy is the use of selective androgen receptor modulators (SARMs), currently under development at several pharmaceutical firms.

A second avenue where more research is needed is testosterone therapy for special populations of men who are at risk for development of catabolic states and muscle wasting. Testosterone might be used to prevent disuse muscle atrophy following knee or hip replacement. A study by Amory et al (2002) suggests that treating men with testosterone before knee replacement surgery improved functional independence after. While these results were not dramatic, one limitation of the study is that testosterone therapy did not continue after surgery, ie, during the period of muscle atrophy. In addition, hypogonadism and muscle wasting are associated with a number of conditions that are more common in older men including COPD (Debigare et al 2003), coronary artery disease (Rosano et al 2006), glucocorticoid therapy (Salehian and Kejriwal 1999), and acute ischemic stoke (Jeppesen et al 1996). It is likely that in some cases, testosterone therapy may prevent catabolic/muscle wasting syndromes associated with these conditions.

In conclusion, while it is true that most studies of testosterone replacement in older men have not produced substantial increases in strength, testosterone therapy continues to hold promise for older men. Testosterone may be of greater use in special populations who are at risk for development of a catabolic state (eg, patients recovering from a long period of bed rest or joint replacement). In addition, there is promise that strategies will be developed to stimulate the testosterone pathway more robustly and to do so in a safe manner. If so, there may be indication for use of such therapy in a broader segment of the population of older men. In the meantime, truly hypogonadal men (those who are symptomatic men and have a serum testosterone concentration below 200 ng/dL) who have no contraindications to testosterone replacement therapy (eg, prostate cancer) may benefit from testosterone replacement regardless of whether they are 30 or 80 years of age.

Articles from Clinical Interventions in Aging are provided here courtesy of Dove Press

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Testosterone replacement therapy for older men

Paleo diet science and research – Robb Wolf

One of the most common questions we receive is what research is there on the Paleo Diet? Thats a great question and Id recommend thoroughly reading ALL of themateriallisted on this page if you have questions or curiosity about the Paleo Diet.

Prof. Loren Cordain has a remarkable number of peer reviewed papers on his site.

Prof. Staffan Lindeberg has conducted research on both free living hunter gatherers and in clinical settings.

The Protein Debate is a project we funded in which Prof. Loren Cordain debated China Study author T. Colin Campbell about the role of protein in degenerative disease.

We talk a lot about nutrition on this site but exercise is a key component of a healthylifestyle. Prof. Frank Booths paper is a phenomenal exploration of the importance of exercise and health.

Here is a list of some of the other studies that have been done in regards to a Paleo Diet:

Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis

Metabolic and physiologic effects from consuming a hunter-gatherer (Paleolithic)-type diet in type 2 diabetes.

Evolution of the diet from the paleolithic to today: progress or regress?

Evaluation of biological and clinical potential of paleolithic diet

Effects of a short-term intervention with a paleolithic diet in healthy volunteers

Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity.

Evaluation of biological and clinical potential of paleolithic diet

Effects of a short-term intervention with a paleolithic diet in healthy volunteers

Long-term effects of a Palaeolithic-type diet in obese postmenopausal women: a 2-year randomized trial

If you want to find more, PUBMED is one of the largest repositories of humanlearningin existence. Put in asearchterm like Paleo Diet or Hunter Gatherer and get ready to learn! And check out Scientific Research 101 if you need a tutorial on how to read research studies.

Paleodiet.com is full of paleo diet goodness.

I hear thisGooglething might catch on.

Calcium

Acid Basebalance

Fatty acids(including omega 3s and 6s) My rough recommendation on fish oil supplementation is 2-4g per day.

What about thefructose/glucosecontent of fruits?

What aboutKetosis? Dr. Mike Eades has a fantastic blog and here is an amazing primer on Ketosis:Metabolism & Ketosis. What about ketosis and exercise? Here is a great piece detailing both anthropological data and modern laboratory data on the subject:Ketogenic diets and physical performance. The bottom line? No glycogen, no glycolytic activity!

Are beansgood for you?No.

See more here:
Paleo diet science and research - Robb Wolf

BodyLogicMD – Hormone Replacement Therapy for Men

Hormone therapy programs aren't only for women. Men experience a more gradual loss of hormones, mainly testosterone. The result is andropause, known as the "male menopause." Andropause can make daily life feel like an uphill battle, and because men are living longer, more active lives they are seeking and finding relief from the serious symptoms of hormone imbalance with bioidentical hormone replacement therapy for men.

The signs of andropause and related hormonal issues include:

This personalized, medically supervised program includes natural HRT for men, as well as customized fitness and nutrition programs for millions of men suffering from hormonal imbalance. These expert bioidentical hormone doctors provide a natural treatment for the symptoms of andropause, helping men regain their health and confidence.

Hormonal imbalances in men are at the root of many chronic health problems and can increase the risk of serious disease. BodyLogicMD affiliated physicians have developed customized hormone replacement therapy for men that has proven successful in supporting men's health and a healthy hormonal balance.

Individual male hormone replacement treatment programs includes:

To determine your hormonal needs, BodyLogicMD affiliated physicians thoroughly evaluate your symptoms using state-of-the-art diagnostic tests, such as, saliva, urine and/or blood tests to determine your hormone levels and your unique bioidentical hormonal needs. After starting bioidentical hormone therapy, your physician will monitor and re-evaluate your hormone levels, meeting with you, to insure that they are maintained at their optimum balance.

Read about Bioidentical Hormones For Women

CONTACT A PHYSICIAN

CLICK HERE

HORMONE BALANCE QUIZ Take it now!

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BodyLogicMD - Hormone Replacement Therapy for Men

Low-T (Low Testosterone) Quiz on MedicineNet

Q:Testosterone is a chemical found only in men.

The correct answer is: False

Explanation:

Testosterone is a steroid hormone which is made in the testes in males and in the ovaries in women (a minimal amount is also made in the adrenal glands).

The correct answer is: False

Explanation:

Menopause itself does not seem to play a role in a reduction of testosterone levels in women. With advancing age, in both men and women, the body produces decreasing amounts of testosterone over time.

The correct answer is: Men

Explanation:

Testosterone is the most important hormone in men. While it helps to maintain sex drive, sperm production, pubic hair and body hair, testosterone is also responsible for maintaining muscles and bones.

When testosterone production is low in men, sexual dysfunction is a common complaint; but other nonspecific symptoms such as depression, mood changes, weight gain, or fatigue, have been reported.

The correct answer is: DAll of the above

Explanation:

An upsurge in media attention regarding the so-called "male menopause" has left many men rushing to their doctor to treat symptoms they believe may be related to low levels of testosterone. The thought behind the concept of male menopause is that the decline in testosterone levels that occurs as men age may produce a characteristic and potentially treatable set of symptoms. Male menopause is also commonly referred to as low-T, andropause, or its medical name, late-onset hypogonadism.

The correct answer is: DAll of the above

Explanation:

Low levels of testosterone in men can affect a man in the following ways: - Loss of sexual interest and function - Erection problems - Increased breast size - Hot flashes - Problems with memory and concentration - Mood problems such as irritability and depression - Smaller and softer testicles - Loss of muscle strength and weakened bones

Symptoms of low testosterone levels in women include: - Hot flashes - Irritability - Loss of sexual desire - Sleep disturbances - Loss of muscle mass - Decreased bone density (osteoporosis)

The correct answer is: BThe brain

Explanation:

Testosterone production is regulated by hormones released from the brain. The hypothalamus and pituitary gland, located in the brain, produce hormonal signals that ultimately result in the production of testosterone. These hormones travel through the bloodstream to activate the sex organs in both men and women.

The correct answer is: False

Explanation:

In men, low testosterone levels in the body can be supplemented by hormone replacement with testosterone. Testosterone replacement therapy can be prescribed as an intramuscular injection usually given on a biweekly basis; as a patch or gel placed on the skin, or as putty that is applied to the gums of the mouth. Each of the treatments has its risks and benefits. The decision as to which form of testosterone to use depends upon the clinical situation. Discussions between the patient and health care professional often helps decide which medication to use.

In the United States there are currently no preparations that are FDA approved for testosterone replacement for women.

The correct answer is: CDiabetes

Explanation:

Men with diabetes are more likely to have low testosterone. Moreover, men with low testosterone are more likely to develop diabetes later. Testosterone helps the body's tissues take up more blood sugar in response to insulin. Men with low testosterone more often have insulin resistance.

Note: Scientists aren't sure whether diabetes causes low testosterone, or the other way around. Still, a link between diabetes and low testosterone is well established.

The correct answer is: BObese

Explanation:

Research has shown that nearly 40% of obese men over age 45 have a low testosterone blood levels. Men with very low testosterone also are more likely to become obese. Losing weight through exercise can increase testosterone levels. Testosterone supplements in men with low testosterone also can slightly reduce obesity.

The correct answer is: False

Explanation:

For a reasonably healthy man, having no interest in sex is not normal. As a man ages, it is natural for him to have less interest in sex than when he was younger. A gradual decrease of testosterone is normal as a man ages, but it is not normal for a healthy, older man, to have no interest in sex.

A man of any age who has lost interest in sex should have a frank conversation with a doctor.

The correct answer is: False

Explanation:

Many people with low testosterone have no symptoms. Only a blood test can determine a person's testosterone levels. The Endocrine Society considers 300 to 1,200 nanograms per deciliter (ng/dL) normal, and that less than 300 is low. Doctors usually use a blood test and a number of symptoms to make a diagnosis and to determine whether treatment is needed.

The correct answer is: False

Explanation:

From puberty, when a boy starts to grow a beard and pubic hair, testosterone affects hair growth in men. But it doesn't affect growth on all parts of the body the same way. Low testosterone can cause you to lose body or facial hair, but it doesn't cause male pattern baldness. Genetics have more to do with male pattern baldness.

The correct answer is: CAlcoholism

Explanation:

Alcohol is directly toxic to the testicles where testosterone is produced, and it seems to affect the release of other hormones related to men's sexual function and fertility. Shrunken testicles are a common sign of low testosterone in alcoholic men with liver disease, as well as lower libido and sexual potency. Enlarged breasts are common in heavy drinkers because alcohol may help convert testosterone into the female hormone estrogen.

The correct answer is: True

Explanation:

Up to 9 out of 10 men who have symptoms of low testosterone may not seek treatment. They may attribute their symptoms to other conditions or think their symptoms are a normal part of aging. Guys, if you have symptoms and believe they are having an impact on your quality of life and well-being, talk to your doctor.

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Sources:

MedicineNet. Low Testosterone (Low T). <http://www.medicinenet.com/low_testosterone/article.htm>

womenshealth.gov. Men's Health. <http://www.womenshealth.gov/mens-health/sexual-health-for-men/sexual-problems.cfm#low>

MedicineNet. Male Menopause: Fact or Fiction? <http://www.medicinenet.com/script/main/art.asp?articlekey=119561>

WebMD. Low Testosterone and Your Health. <http://men.webmd.com/what-low-testosterone-can-mean-your-health>

WebMD. Quiz: The Truth About Testosterone. <http://www.webmd.com/sex-relationships/low-testosterone-8/rm-quiz-truth-testosterone>

This tool does not provide medical advice. See additional information:

THIS TOOL DOES NOT PROVIDE MEDICAL ADVICE. It is intended for general informational purposes only and does not address individual circumstances. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. Never ignore professional medical advice in seeking treatment because of something you have read on the MedicineNet Site. If you think you may have a medical emergency, immediately call your doctor or dial 911.

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Low-T (Low Testosterone) Quiz on MedicineNet

Low T (Low Testosterone)

Don't Let Low Testosterone (LowT) Get You Down. Fight Back, Intelligently!

Testosterone levels start declining around the age of 30 by 1 to 2 % per year. By the age of 45, the average mans testosterone levels have started dropping precipitously. By the age of 80, most men have less than 20% of the testosterone they had when they were in their 30s. This process of declining testosterone is often referred to as Andropause (or male menopause), and because it takes place gradually over decades, the symptoms of Low T often go unnoticed for a long period of time.

Not only does normal aging cause a decrease in testosterone levels, there are quite a number of other causes of Low T that affect many men. Among these are: stress and various medications. In addition, the following can also cause Low T: alcoholism, cirrhosis of the liver, cancer treatments such as chemotherapy and radiation, pituitary dysfunction, chronic kidney failure, too much iron, testicular damage or infection, AIDS and other chronic diseases.

Another way to increase your testosterone levels is to do it naturally. Thousands of men (especially in Asia) use a rain forest herb that naturally causes their body to produce its own testosterone. Because testosterone is produced by the body rather than coming from an outside source, there are no negative side effects using this method. It has also been found to be a very cost-effective approach to resolving the problem of Low T.

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Low T (Low Testosterone)

Transhumanism, medical technology and slippery slopes

J Med Ethics. 2006 Sep; 32(9): 513518.

M J McNamee, S D Edwards, Centre for Philosophy, Humanities and Law in Healthcare, School of Health Science, University of Wales, Swansea, UK

Correspondence to: Dr Mike McNamee Centre for Philosophy, Humanities and Law in Healthcare, School of Health Science, University of Wales, Swansea SA2 8PP, UK; m.j.mcnamee@swansea.ac.uk

Received 2005 Jul 28; Accepted 2005 Nov 10.

In this article, transhumanism is considered to be a quasimedical ideology that seeks to promote a variety of therapeutic and humanenhancing aims. Moderate conceptions are distinguished from strong conceptions of transhumanism and the strong conceptions were found to be more problematic than the moderate ones. A particular critique of Bostrm's defence of transhumanism is presented. Various forms of slippery slope arguments that may be used for and against transhumanism are discussed and one particular criticism, moral arbitrariness, that undermines both weak and strong transhumanism is highlighted.

No less a figure than Francis Fukuyama1 recently labelled transhumanism as the world's most dangerous idea. Such an eyecatching condemnation almost certainly denotes an issue worthy of serious consideration, especially given the centrality of biomedical technology to its aims. In this article, we consider transhumanism as an ideology that seeks to evangelise its humanenhancing aims. Given that transhumanism covers a broad range of ideas, we distinguish moderate conceptions from strong ones and find the strong conceptions more problematic than the moderate ones. We also offer a critique of Bostrm's2 position published in this journal. We discuss various forms of slippery slope arguments that may be used for and against transhumanism and highlight one particular criticism, moral arbitrariness, which undermines both forms of transhumanism.

At the beginning of the 21st century, we find ourselves in strange times; facts and fantasy find their way together in ethics, medicine and philosophy journals and websites.2,3,4 Key sites of contestation include the very idea of human nature, the place of embodiment within medical ethics and, more specifically, the systematic reflections on the place of medical and other technologies in conceptions of the good life. A reflection of this situation is captured by Dyens5 who writes,

What we are witnessing today is the very convergence of environments, systems, bodies, and ontology toward and into the intelligent matter. We can no longer speak of the human condition or even of the posthuman condition. We must now refer to the intelligent condition.

We wish to evaluate the contents of such dialogue and to discuss, if not the death of human nature, then at least its dislocation and derogation in the thinkers who label themselves transhumanists.

One difficulty for critics of transhumanism is that a wide range of views fall under its label.6 Not merely are there idiosyncrasies of individual academics, but there does not seem to exist an absolutely agreed on definition of transhumanism. One can find not only substantial differences between key authors2,3,4,7,8 and the disparate disciplinary nuances of their exhortations, but also subtle variations of its chief representatives in the offerings of people. It is to be expected that any ideology transforms over time and not least of all in response to internal and external criticism. Yet, the transhumanism critic faces a further problem of identifying a robust target that stays still sufficiently long to locate it properly in these webdriven days without constructing a straw man to knock over with the slightest philosophical breeze. For the purposes of targeting a sufficiently substantial target, we identify the writings of one of its clearest and intellectually robust proponents, the Oxford philosopher and cofounder of the World Transhumanist Association , Nick Bostrm,2 who has written recently in these pages of transhumanism's desire to make good the halfbaked project3 that is human nature.

Before specifically evaluating Bostrm's position, it is best first to offer a global definition for transhumanism and then to locate it among the range of views that fall under the heading. One of the most celebrated advocates of transhumanism is Max More, whose website reads no more gods, nor more faith, no more timid holding back. The future belongs to posthumanity.8 We will have a clearer idea then of the kinds of position transhumanism stands in direct opposition to. Specifically, More8 asserts,

Transhumanism is a blanket term given to the school of thought that refuses to accept traditional human limitations such as death, disease and other biological frailties. Transhumans are typically interested in a variety of futurist topics, including space migration, mind uploading and cryonic suspension. Transhumans are also extremely interested in more immediate subjects such as bio and nanotechnology, computers and neurology. Transhumans deplore the standard paradigms that attempt to render our world comfortable at the sake of human fulfilment.8

Strong transhumanism advocates see themselves engaged in a project, the purpose of which is to overcome the limits of human nature. Whether this is the foundational claim, or merely the central claim, is not clear. These limitationsone may describe them simply as features of human nature, as the idea of labelling them as limitations is itself to take up a negative stance towards themconcern appearance, human sensory capacities, intelligence, lifespan and vulnerability to harm. According to the extreme transhumanism programme, technology can be used to vastly enhance a person's intelligence; to tailor their appearance to what they desire; to lengthen their lifespan, perhaps to immortality; and to reduce vastly their vulnerability to harm. This can be done by exploitation of various kinds of technology, including genetic engineering, cybernetics, computation and nanotechnology. Whether technology will continue to progress sufficiently, and sufficiently predictably, is of course quite another matter.

Advocates of transhumanism argue that recruitment or deployment of these various types of technology can produce people who are intelligent and immortal, but who are not members of the species Homo sapiens. Their species type will be ambiguousfor example, if they are cyborgs (part human, part machine)or, if they are wholly machines, they will lack any common genetic features with human beings. A legion of labels covers this possibility; we find in Dyen's5 recently translated book a variety of cultural bodies, perhaps the most extreme being cyberpunks:

...a profound misalignment between existence and its manifestation. This misalignment produces bodies so transformed, so dissociated, and so asynchronized, that their only outcome is gross mutation. Cyberpunk bodies are horrible, strange and mysterious (think of Alien, Robocop, Terminator, etc.), for they have no real attachment to any biological structure. (p 75)

Perhaps a reasonable claim is encapsulated in the idea that such entities will be posthuman. The extent to which posthuman might be synonymous with transhumanism is not clear. Extreme transhumanists strongly support such developments.

At the other end of transhumanism is a much less radical project, which is simply the project to use technology to enhance human characteristicsfor example, beauty, lifespan and resistance to disease. In this less extreme project, there is no necessary aspiration to shed human nature or human genetic constitution, just to augment it with technology where possible and where desired by the person.

At present it seems to be a movement based mostly in North America, although there are some adherents from the UK. Among its most intellectually sophisticated proponents is Nick Bostrm. Perhaps the most outspoken supporters of transhumanism are people who see it simply as an issue of free choice. It may simply be the case that moderate transhumanists are libertarians at the core. In that case, transhumanism merely supplies an overt technological dimension to libertarianism. If certain technological developments are possible, which they as competent choosers desire, then they should not be prevented from acquiring the technologically driven enhancements they desire. One obvious line of criticism here may be in relation to the inequality that necessarily arises with respect to scarce goods and services distributed by market mechanisms.9 We will elaborate this point in the Transhumanism and slippery slopes section.

So, one group of people for the transhumanism project sees it simply as a way of improving their own life by their own standards of what counts as an improvement. For example, they may choose to purchase an intervention, which will make them more intelligent or even extend their life by 200years. (Of course it is not selfevident that everyone would regard this as an improvement.) A less vociferous group sees the transhumanism project as not so much bound to the expansion of autonomy (notwithstanding our criticism that will necessarily be effected only in the sphere of economic consumer choice) as one that has the potential to improve the quality of life for humans in general. For this group, the relationship between transhumanism and the general good is what makes transhumanism worthy of support. For the other group, the worth of transhumanism is in its connection with their own conception of what is good for them, with the extension of their personal life choices.

Of the many points for transhumanism, we note three. Firstly, transhumanism seems to facilitate two aims that have commanded much support. The use of technology to improve humans is something we pretty much take for granted. Much good has been achieved with lowlevel technology in the promotion of public health. The construction of sewage systems, clean water supplies, etc, is all work to facilitate this aim and is surely good work, work which aims at, and in this case achieves, a good. Moreover, a large portion of the modern biomedical enterprise is another example of a project that aims at generating this good too.

Secondly, proponents of transhumanism say it presents an opportunity to plan the future development of human beings, the species Homo sapiens. Instead of this being left to the evolutionary process and its exploitation of random mutations, transhumanism presents a hitherto unavailable option: tailoring the development of human beings to an ideal blueprint. Precisely whose ideal gets blueprinted is a point that we deal with later.

Thirdly, in the spirit of work in ethics that makes use of a technical idea of personhood, the view that moral status is independent of membership of a particular species (or indeed any biological species), transhumanism presents a way in which moral status can be shown to be bound to intellectual capacity rather than to human embodiment as such or human vulnerability in the capacity of embodiment (Harris, 1985).9a

Critics point to consequences of transhumanism, which they find unpalatable. One possible consequence feared by some commentators is that, in effect, transhumanism will lead to the existence of two distinct types of being, the human and the posthuman. The human may be incapable of breeding with the posthuman and will be seen as having a much lower moral standing. Given that, as Buchanan et al9 note, much moral progress, in the West at least, is founded on the category of the human in terms of rights claims, if we no longer have a common humanity, what rights, if any, ought to be enjoyed by transhumans? This can be viewed either as a criticism (we poor humans are no longer at the top of the evolutionary tree) or simply as a critical concern that invites further argumentation. We shall return to this idea in the final section, by way of identifying a deeper problem with the openendedness of transhumanism that builds on this recognition.

In the same vein, critics may argue that transhumanism will increase inequalities between the rich and the poor. The rich can afford to make use of transhumanism, but the poor will not be able to. Indeed, we may come to think of such people as deficient, failing to achieve a new heightened level of normal functioning.9 In the opposing direction, critical observers may say that transhumanism is, in reality, an irrelevance, as very few will be able to use the technological developments even if they ever manifest themselves. A further possibility is that transhumanism could lead to the extinction of humans and posthumans, for things are just as likely to turn out for the worse as for the better (eg, those for precautionary principle).

One of the deeper philosophical objections comes from a very traditional source. Like all such utopian visions, transhumanism rests on some conception of good. So just as humanism is founded on the idea that humans are the measure of all things and that their fulfilment is to be found in the powers of reason extolled and extended in culture and education, so too transhumanism has a vision of the good, albeit one loosely shared. For one group of transhumanists, the good is the expansion of personal choice. Given that autonomy is so widely valued, why not remove the barriers to enhanced autonomy by various technological interventions? Theological critics especially, but not exclusively, object to what they see as the imperialising of autonomy. Elshtain10 lists the three c's: choice, consent and control. These, she asserts, are the dominant motifs of modern American culture. And there is, of course, an army of communitarians (Bellah et al,10a MacIntyre,10b Sandel,10c Taylor10d and Walzer10e) ready to provide support in general moral and political matters to this line of criticism. One extension of this line of transhumanism thinking is to align the valorisation of autonomy with economic rationality, for we may as well be motivated by economic concerns as by moral ones where the market is concerned. As noted earlier, only a small minority may be able to access this technology (despite Bostrm's naive disclaimer for democratic transhumanism), so the technology necessary for transhumanist transformations is unlikely to be prioritised in the context of artificially scarce public health resources. One other population attracted to transhumanism will be the elite sports world, fuelled by the media commercialisation complexwhere mere mortals will get no more than a glimpse of the transhuman in competitive physical contexts. There may be something of a doublebinding character to this consumerism. The poor, at once removed from the possibility of such augmentation, pay (per view) for the pleasure of their envy.

If we argue against the idea that the good cannot be equated with what people choose simpliciter, it does not follow that we need to reject the requisite medical technology outright. Against the more moderate transhumanists, who see transhumanism as an opportunity to enhance the general quality of life for humans, it is nevertheless true that their position presupposes some conception of the good. What kind of traits is best engineered into humans: disease resistance or parabolic hearing? And unsurprisingly, transhumanists disagree about precisely what objective goods to select for installation into humans or posthumans.

Some radical critics of transhumanism see it as a threat to morality itself.1,11 This is because they see morality as necessarily connected to the kind of vulnerability that accompanies human nature. Think of the idea of human rights and the power this has had in voicing concern about the plight of especially vulnerable human beings. As noted earlier a transhumanist may be thought to be beyond humanity and as neither enjoying its rights nor its obligations. Why would a transhuman be moved by appeals to human solidarity? Once the prospect of posthumanism emerges, the whole of morality is thus threatened because the existence of human nature itself is under threat.

One further objection voiced by Habermas11 is that interfering with the process of human conception, and by implication human constitution, deprives humans of the naturalness which so far has been a part of the takenforgranted background of our selfunderstanding as a species and Getting used to having human life biotechnologically at the disposal of our contingent preferences cannot help but change our normative selfunderstanding (p 72).

On this account, our selfunderstanding would include, for example, our essential vulnerability to disease, ageing and death. Suppose the strong transhumanism project is realised. We are no longer thus vulnerable: immortality is a real prospect. Nevertheless, conceptual caution must be exercised hereeven transhumanists will be susceptible in the manner that Hobbes12 noted. Even the strongest are vulnerable in their sleep. But the kind of vulnerability transhumanism seeks to overcome is of the internal kind (not Hobbes's external threats). We are reminded of Woody Allen's famous remark that he wanted to become immortal, not by doing great deeds but simply by not dying. This will result in a radical change in our selfunderstanding, which has inescapably normative elements to it that need to be challenged. Most radically, this change in selfunderstanding may take the form of a change in what we view as a good life. Hitherto a human life, this would have been assumed to be finite. Transhumanists suggest that even now this may change with appropriate technology and the right motivation.

Do the changes in selfunderstanding presented by transhumanists (and genetic manipulation) necessarily have to represent a change for the worse? As discussed earlier, it may be that the technology that generates the possibility of transhumanism can be used for the good of humansfor example, to promote immunity to disease or to increase quality of life. Is there really an intrinsic connection between acquisition of the capacity to bring about transhumanism and moral decline? Perhaps Habermas's point is that moral decline is simply more likely to occur once radical enhancement technologies are adopted as a practice that is not intrinsically evil or morally objectionable. But how can this be known in advance? This raises the spectre of slippery slope arguments.

But before we discuss such slopes, let us note that the kind of approach (whether characterised as closedminded or sceptical) Bostrm seems to dislike is one he calls speculative. He dismisses as speculative the idea that offspring may think themselves lesser beings, commodifications of their parents' egoistic desires (or some such). None the less, having pointed out the lack of epistemological standing of such speculation, he invites us to his own apparently more congenial position:

We might speculate, instead, that germline enhancements will lead to more love and parental dedication. Some mothers and fathers might find it easier to love a child who, thanks to enhancements, is bright, beautiful, healthy, and happy. The practice of germline enhancement might lead to better treatment of people with disabilities, because a general demystification of the genetic contributions to human traits could make it clearer that people with disabilities are not to blame for their disabilities and a decreased incidence of some disabilities could lead to more assistance being available for the remaining affected people to enable them to live full, unrestricted lives through various technological and social supports. Speculating about possible psychological or cultural effects of germline engineering can therefore cut both ways. Good consequences no less than bad ones are possible. In the absence of sound arguments for the view that the negative consequences would predominate, such speculations provide no reason against moving forward with the technology. Ruminations over hypothetical side effects may serve to make us aware of things that could go wrong so that we can be on the lookout for untoward developments. By being aware of the perils in advance, we will be in a better position to take preventive countermeasures. (Bostrm, 2003, p 498)

Following Bostrm's3 speculation then, what grounds for hope exist? Beyond speculation, what kinds of arguments does Bostrm offer? Well, most people may think that the burden of proof should fall to the transhumanists. Not so, according to Bostrm. Assuming the likely enormous benefits, he turns the tables on this intuitionnot by argument but by skilful rhetorical speculation. We quote for accuracy of representation (emphasis added):

Only after a fair comparison of the risks with the likely positive consequences can any conclusion based on a costbenefit analysis be reached. In the case of germline enhancements, the potential gains are enormous. Only rarely, however, are the potential gains discussed, perhaps because they are too obvious to be of much theoretical interest. By contrast, uncovering subtle and nontrivial ways in which manipulating our genome could undermine deep values is philosophically a lot more challenging. But if we think about it, we recognize that the promise of genetic enhancements is anything but insignificant. Being free from severe genetic diseases would be good, as would having a mind that can learn more quickly, or having a more robust immune system. Healthier, wittier, happier people may be able to reach new levels culturally. To achieve a significant enhancement of human capacities would be to embark on the transhuman journey of exploration of some of the modes of being that are not accessible to us as we are currently constituted, possibly to discover and to instantiate important new values. On an even more basic level, genetic engineering holds great potential for alleviating unnecessary human suffering. Every day that the introduction of effective human genetic enhancement is delayed is a day of lost individual and cultural potential, and a day of torment for many unfortunate sufferers of diseases that could have been prevented. Seen in this light, proponents of a ban or a moratorium on human genetic modification must take on a heavy burden of proof in order to have the balance of reason tilt in their favor. (Bostrom,3 pp 4989).

Now one way in which such a balance of reason may be had is in the idea of a slippery slope argument. We now turn to that.

A proper assessment of transhumanism requires consideration of the objection that acceptance of the main claims of transhumanism will place us on a slippery slope. Yet, paradoxically, both proponents and detractors of transhumanism may exploit slippery slope arguments in support of their position. It is necessary therefore to set out the various arguments that fall under this title so that we can better characterise arguments for and against transhumanism. We shall therefore examine three such attempts13,14,15 but argue that the arbitrary slippery slope15 may undermine all versions of transhumanists, although not every enhancement proposed by them.

Schauer13 offers the following essentialist analysis of slippery slope arguments. A pure slippery slope is one where a particular act, seemingly innocuous when taken in isolation, may yet lead to a future host of similar but increasingly pernicious events. Abortion and euthanasia are classic candidates for slippery slope arguments in public discussion and policy making. Against this, however, there is no reason to suppose that the future events (acts or policies) down the slope need to display similaritiesindeed we may propose that they will lead to a whole range of different, although equally unwished for, consequences. The vast array of enhancements proposed by transhumanists would not be captured under this conception of a slippery slope because of their heterogeneity. Moreover, as Sternglantz16 notes, Schauer undermines his case when arguing that greater linguistic precision undermines the slippery slope and that indirect consequences often bolster slippery slope arguments. It is as if the slippery slopes would cease in a world with greater linguistic precision or when applied only to direct consequences. These views do not find support in the later literature. Schauer does, however, identify three nonslippery slope arguments where the advocate's aim is (a) to show that the bottom of a proposed slope has been arrived at; (b) to show that a principle is excessively broad; (c) to highlight how granting authority to X will make it more likely that an undesirable outcome will be achieved. Clearly (a) cannot properly be called a slippery slope argument in itself, while (b) and (c) often have some role in slippery slope arguments.

The excessive breadth principle can be subsumed under Bernard Williams's distinction between slippery slope arguments with (a) horrible results and (b) arbitrary results. According to Williams, the nature of the bottom of the slope allows us to determine which category a particular argument falls under. Clearly, the most common form is the slippery slope to a horrible result argument. Walton14 goes further in distinguishing three types: (a) thin end of the wedge or precedent arguments; (b) Sorites arguments; and (c) dominoeffect arguments. Importantly, these arguments may be used both by antagonists and also by advocates of transhumanism. We shall consider the advocates of transhumanism first.

In the thin end of the wedge slippery slopes, allowing P will set a precedent that will allow further precedents (Pn) taken to an unspecified problematic terminus. Is it necessary that the end point has to be bad? Of course this is the typical linguistic meaning of the phrase slippery slopes. Nevertheless, we may turn the tables here and argue that [the] slopes may be viewed positively too.17 Perhaps a new phrase will be required to capture ineluctable slides (ascents?) to such end points. This would be somewhat analogous to the ideas of vicious and virtuous cycles. So transhumanists could argue that, once the artificial generation of life through technologies of in vitro fertilisation was thought permissible, the slope was foreseeable, and transhumanists are doing no more than extending that lifecreating and fashioning impulse.

In Sorites arguments, the inability to draw clear distinctions has the effect that allowing P will not allow us to consistently deny Pn. This slope follows the form of the Sorites paradox, where taking a grain of sand from a heap does not prevent our recognising or describing the heap as such, even though it is not identical with its former state. At the heart of the problem with such arguments is the idea of conceptual vagueness. Yet the logical distinctions used by philosophers are often inapplicable in the real world.15,18 Transhumanists may well seize on this vagueness and apply a Sorites argument as follows: as therapeutic interventions are currently morally permissible, and there is no clear distinction between treatment and enhancement, enhancement interventions are morally permissible too. They may ask whether we can really distinguish categorically between the added functionality of certain prosthetic devices and sonar senses.

In dominoeffect arguments, the domino conception of the slippery slope, we have what others often refer to as a causal slippery slope.19 Once P is allowed, a causal chain will be effected allowing Pn and so on to follow, which will precipitate increasingly bad consequences.

In what ways can slippery slope arguments be used against transhumanism? What is wrong with transhumanism? Or, better, is there a point at which we can say transhumanism is objectionable? One particular strategy adopted by proponents of transhumanism falls clearly under the aspect of the thin end of the wedge conception of the slippery slope. Although some aspects of their ideology seem aimed at unqualified goods, there seems to be no limit to the aspirations of transhumanism as they cite the powers of other animals and substances as potential modifications for the transhumanist. Although we can admire the sonic capacities of the bat, the elastic strength of lizards' tongues and the endurability of Kevlar in contrast with traditional construction materials used in the body, their transplantation into humans is, to coin Kass's celebrated label, repugnant (Kass, 1997).19a

Although not all transhumanists would support such extreme enhancements (if that is indeed what they are), less radical advocates use justifications that are based on therapeutic lines up front with the more Promethean aims less explicitly advertised. We can find many examples of this manoeuvre. Take, for example, the Cognitive Enhancement Research Institute in California. Prominently displayed on its website front page (http://www.ceri.com/) we read, Do you know somebody with Alzheimer's disease? Click to see the latest research breakthrough. The mode is simple: treatment by front entrance, enhancement by the back door. Borgmann,20 in his discussion of the uses of technology in modern society, observed precisely this argumentative strategy more than 20years ago:

The main goal of these programs seems to be the domination of nature. But we must be more precise. The desire to dominate does not just spring from a lust of power, from sheer human imperialism. It is from the start connected with the aim of liberating humanity from disease, hunger, and toil and enriching life with learning, art and athletics.

Who would want to deny the powers of viral diseases that can be genetically treated? Would we want to draw the line at the transplantation of nonhuman capacities (sonar path finding)? Or at in vivo fibre optic communications backbone or antidegeneration powers? (These would have to be nonhuman by hypothesis). Or should we consider the scope of technological enhancements that one chief transhumanist, Natasha Vita More21, propounds:

A transhuman is an evolutionary stage from being exclusively biological to becoming postbiological. Postbiological means a continuous shedding of our biology and merging with machines. () The body, as we transform ourselves over time, will take on different types of appearances and designs and materials. ()

For hiking a mountain, I'd like extended leg strength, stamina, a skinsheath to protect me from damaging environmental aspects, selfmoisturizing, cooldown capability, extended hearing and augmented vision (Network of sonar sensors depicts data through solid mass and map images onto visual field. Overlay window shifts spectrum frequencies. Visual scratch pad relays mental ideas to visual recognition bots. Global Satellite interface at microzoom range).

For a party, I'd like an eclectic look a glistening bronze skin with emerald green highlights, enhanced height to tower above other people, a sophisticated internal sound system so that I could alter the music to suit my own taste, memory enhance device, emotionalselect for feelgood people so I wouldn't get dragged into anyone's inappropriate conversations. And parabolic hearing so that I could listen in on conversations across the room if the one I was currently in started winding down.

Notwithstanding the difficulty of bringing together transhumanism under one movement, the sheer variety of proposals merely contained within Vita More's catalogue means that we cannot determinately point to a precise station at which we can say, Here, this is the end we said things would naturally progress to. But does this pose a problem? Well, it certainly makes it difficult to specify exactly a horrible result that is supposed to be at the bottom of the slope. Equally, it is extremely difficult to say that if we allow precedent X, it will allow practices Y or Z to follow as it is not clear how these practices Y or Z are (if at all) connected with the precedent X. So it is not clear that a form of precedentsetting slippery slope can be strictly used in every case against transhumanism, although it may be applicable in some.

Nevertheless, we contend, in contrast with Bostrm that the burden of proof would fall to the transhumanist. Consider in this light, a Soritestype slope. The transhumanist would have to show how the relationship between the therapeutic practices and the enhancements are indeed transitive. We know night from day without being able to specify exactly when this occurs. So simply because we cannot determine a precise distinction between, say, genetic treatments G1, G2 and G3, and transhumanism enhancements T1, T2 and so on, it does not follow that there are no important moral distinctions between G1 and T20. According to Williams,15 this kind of indeterminacy arises because of the conceptual vagueness of certain terms. Yet, the indeterminacy of so open a predicate heap is not equally true of therapy or enhancement. The latitude they permit is nowhere near so wide.

Instead of objecting to Pn on the grounds that Pn is morally objectionable (ie, to depict a horrible result), we may instead, after Williams, object that the slide from P to Pn is simply morally arbitrary, when it ought not to be. Here, we may say, without specifying a horrible result, that it would be difficult to know what, in principle, can ever be objected to. And this is, quite literally, what is troublesome. It seems to us that this criticism applies to all categories of transhumanism, although not necessarily to all enhancements proposed by them. Clearly, the somewhat loose identity of the movementand the variations between strong and moderate versionsmakes it difficult to sustain this argument unequivocally. Still the transhumanist may be justified in asking, What is wrong with arbitrariness? Let us consider one brief example. In aspects of our lives, as a widely shared intuition, we may think that in the absence of good reasons, we ought not to discriminate among people arbitrarily. Healthcare may be considered to be precisely one such case. Given the everincreasing demand for public healthcare services and products, it may be argued that access to them typically ought to be governed by publicly disputable criteria such as clinical need or potential benefit, as opposed to individual choices of an arbitrary or subjective nature. And nothing in transhumanism seems to allow for such objective dispute, let alone prioritisation. Of course, transhumanists such as More find no such disquietude. His phrase No more timidity is a typical token of transhumanist slogans. We applaud advances in therapeutic medical technologies such as those from new genetically based organ regeneration to more familiar prosthetic devices. Here the ends of the interventions are clearly medically defined and the means regulated closely. This is what prevents transhumanists from adopting a Soritestype slippery slope. But in the absence of a telos, of clearly and substantively specified ends (beyond the mere banner of enhancement), we suggest that the public, medical professionals and bioethicists alike ought to resist the potentially openended transformations of human nature. For if all transformations are in principle enchancements, then surely none are. The very application of the word may become redundant. Thus it seems that one strong argument against transhumanism generallythe arbitrary slippery slopepresents a challenge to transhumanism, to show that all of what are described as transhumanist enhancements are imbued with positive normative force and are not merely technological extensions of libertarianism, whose conception of the good is merely an extension of individual choice and consumption.

Already, we have seen the misuse of a host of therapeutically designed drugs used by nontherapeutic populations for enhancements. Consider the nontherapeutic use of human growth hormone in nonclinical populations. Such is the present perception of height as a positional good in society that Cuttler et al22 report that the proportion of doctors who recommended human growth hormone treatment of short nongrowth hormone deficient children ranged from 1% to 74%. This is despite its contrary indication in professional literature, such as that of the Pediatric Endocrine Society, and considerable doubt about its efficacy.23,24 Moreover, evidence supports the view that recreational body builders will use the technology, given the evidence of their use or misuse of steroids and other biotechnological products.25,26 Finally, in the sphere of elite sport, which so valorises embodied capacities that may be found elsewhere in greater degree, precision and sophistication in the animal kingdom or in the computer laboratory, biomedical enhancers may latch onto the genetically determined capacities and adopt or adapt them for their own commercially driven ends.

The arguments and examples presented here do no more than to warn us of the enhancement ideologies, such as transhumanism, which seek to predicate their futuristic agendas on the bedrock of medical technological progress aimed at therapeutic ends and are secondarily extended to loosely defined enhancement ends. In discussion and in bioethical literatures, the future of genetic engineering is often challenged by slippery slope arguments that lead policy and practice to a horrible result. Instead of pointing to the undesirability of the ends to which transhumanism leads, we have pointed out the failure to specify their telos beyond the slogans of overcoming timidity or Bostrm's3 exhortation that the passive acceptance of ageing is an example of reckless and dangerous barriers to urgently needed action in the biomedical sphere.

We propose that greater care be taken to distinguish the slippery slope arguments that are used in the emotionally loaded exhortations of transhumanism to come to a more judicious perspective on the technologically driven agenda for biomedical enhancement. Perhaps we would do better to consider those other alltoohuman frailties such as violent aggression, wanton selfharming and so on, before we turn too readily to the richer imaginations of biomedical technologists.

Competing interests: None.

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21. Vita More N. Who are transhumans? http://www.transhumanist.biz/interviews.htm, 2000 (accessed 7 Apr 2006)

25. Grace F, Baker J S, Davies B. Anabolic androgenic steroid (AAS) use in recreational gym users. J Subst Use 20016189195.195

Continued here:
Transhumanism, medical technology and slippery slopes

Transhumanism Australia

[Update 2016.06.20] -Treat ageing as a disease - let's spread the word on election day!

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[Update 2016.05.21]- Triple H FM radio interview with transhumanist and Science Party Candidate for Berowra, Brendan Clarke!

[Update 2016.05.18] - Matt Barrie Supports Science Party

[Update 2016.05.10]- Podcast with Questionable Content - AI For Prime Minister!

[Update 2016.05.05]- Coverage of Zoltan Istvan and the Transhumanist Partyby Vocativ!

[Update 2016.04.27]- Transhumanism Australia Update blog is up!Science Party Candidates, Design Workshops, Biohackers, Effective Altruism and More!

[Update 2016.04.09]- "CRISPR: A Genetic Cut and Paste Tool" from The Verge

[Update 2016.03.21]- Blog update is up! Future Day, Biohack+Ethereum, Basic Income and More!

[Update 2016.03.20] - The Tiny Key To Ageing

[Update 2016.03.18]- Dr Brian Greene in Sydney, Luna Park During Q&A

[Update 2016.03.12]- Real Future: Meet Zoltan Istvan, the Transhumanist Running For President (Episode 5)

Cleaned up homepage and moved old stuff to Archives

[Update 2016.3.01]- Happy Future Day! The videos from the Sydney event are up!

[Update 2016.02.26] - Transhumanism Australia on Vice AU!

[Update 2016.02.25]- Zoltan on The Feed - SBS 2!

[Update 2016.01.26] - New AI blog on Sightings from the Edge: Artificial Intelligence - January 2016. See our page dedicated to AI

[Update 2016.01.23] - How Will You Die? (Unless We Do Something About It)

Sign the petition to deem ageing as a disease.

[Update 2016.01.10]- Update to our page onAutomation. Enjoy!

[Update 2016.01.06] - Podcast with Questionable Content onSimulated Transhuman Overlords!

[Update 2016.01.02] -We've started uploading videos on our Facebook page and YouTube channel!

[Update 2015.12.31] - Zoltan's 2015 wrap up!

[Update 2015.12.30] -Join the chat group on Slack for all transhumanists around the world! If you haven't received an invite already, send an email to info@transhumanism.com.au

[Update 2015.11.29] -Check out our new page onTranshumanism in pop culture!

[Update 2015.11.09]

Join us in signing this petition to deem ageing as a disease!

[Update 2015.10.17]Transhumanist Leandro Brun joins Sunday Night Safran on Triple J radio! (Skip to 43:45)

INTRO

Welcome to the official site shared by Transhumanism Australia - the nonprofit organisation, and Transhumanist Party Australia - the Australian political organisation.

TRANSHUMANISM

Transhumanism(abbreviated as H+ or h+) is an international cultural and intellectual movement with an eventual goal of fundamentally transforming the human condition by developing and making widely available technologies to greatly enhance human intellectual, physical, and psychological capacities.

Transhumanismis a positive philosophy about the future based in optimism, rational thinking and the application of science and technology to improve the human condition. We seek to live longer, stay healthier, and become smarter and even more physically fit. We want to develop tools and technologies to help ourselves and others do the same.

Here's a well designed FAQ on What Is Transhumanism.

TRANSHUMANISM AUSTRALIA

Transhumanism in Australia is a nonprofit organisation dedicated to our communities which educate and invest in scientific research and technologies enhancing the human biological condition.

Get involved with the Transhumanist movement today!

For a timeline of Transhumanism throughout history, check out the coverage by The Verge.

TRANSHUMANIST PARTY AUSTRALIA (TPAU)

TPAU is an Australian political organisation dedicated to putting science, health, and technology at the forefront of the Australian political agenda.

TPAU aims to uphold the energy and political might of millions of transhumanist advocates around the world who desire to usescience and technology to significantly improve our lives.

The co-founders of TPAU arelisted here. Join ourFacebook groupto meet our existing TPAU admins and the transhumanist community in Australia!

Our party's core ideas and goals can be found in theTranshumanistDeclaration.The Transhumanist Party in the United States wasfoundedby futurist and philosopherZoltan Istvanon October 7, 2014 as a nonprofit organisation. Istvan manages the party and is its 2016 US Presidential candidate.

Check out thecalendarfor a list of upcoming events, and please considervolunteering for the partyormaking a donation.

Together we can vastly improve Australia through effective policy and investment in science, health and technology. Help us create a better future for all Australians.

Become a member today!

Find out more about us belowand get to know our team.

TPAU is not currently registered with the AEC. We have an alliance with theScience Partyto pool our votes and therefore contribute to shaping the policies of the Science Party. The Science Party's values are aligned with ours and you can find out about their policieshere.

Please support us by clicking on the sponsored ad below or throughout the website, or by making a donation!

GLOBAL NETWORK OF TRANSHUMANISTS

Transhumanist Party Globalis an organisation co-founded byAmon TwymanandZoltan Istvan,dedicated to supporting Transhumanist Parties around the world and encouraging effective cooperation between them.

H+Pedia is a wiki for a single source of truth on all things transhumanism, created by Chris Monteiro and David Wood

2045 Initiative

MAKING TRANSHUMANISM MAINSTREAM

Transhumanism is becoming more and more popular every day, and we hope to desensitise the term itself so that people can understand what the movement is about. Here's a video fromRhett & LinkfromGood Mythical Morningthat did a great job of this:

More here:
Transhumanism Australia