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Hormone Replacement Therapy Boca Raton – Hormone Doctor …

low hormone levels

Specializing in Hormone Replacement Therapy (HRT), Testosterone Replacement Therapy (TRT) and Human Growth Hormone Therapy (HGH), Elite HRToffers the most up to date treatment options available to optimize your physical and emotional health to the highest level possible, helping you to get your edge back.

Our fully personalized age management and wellness programs, incorporating Physician prescribed Hormone Replacement Therapy (HRT), wellness coaching and program monitoring will help to slow down and even reverse the signs and symptoms of aging so you can look and feel your absolute best at any age. How you look and feel as you age is entirely up to you, you can make the years to come the best years of your life. Take the first step toward a fitter, younger and healthier you. Our team of expert Physicians and wellness consultants are here to guide you every step of the way. Together, well help you to look better, feel younger and stay healthier.

Call us for a free private consultation, your call is completely confidential and no obligation is required, youll be glad you did. Prefer information via email? Submit your questions and concerns using one of our contact forms. One of our Physicians or wellness consultants will respond right away.

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Chris Wehr, M.D. – Orlando Bioidentical Doctor

Chris Wehr, M.D. Orlando Florida Bioidentical Doctor

Chris Wehr, M.D. of BodyLogicMD in Orlando Florida is an Anti-Aging Specialist who offers Preventative Medicine and Bioidentical Hormone Replacement Therapy for men and women in Orlando Florida. Doctor Wehr uses a combination of nutrition and fitness counseling, stress reduction techniques, pharmaceutical grade supplements, and Bioidentical Hormone Replacement Therapy to help his patients achieve optimal levels of health and wellness. Both men and women struggle with the symptoms of hormonal imbalance around midlife, which can create numerous physical and emotional symptoms. Bioidentical Hormone Replacement Therapy can help with general hormone balancing as well as alleviate the symptoms of more serious health conditions.

With over 20 years of experience working as a cardiothoracic surgeon, Dr. Wehr began searching for a way to offer more to his patients. This desire to connect with his patients on a deeper level and offer more comprehensive care for the whole person instigated Dr. Wehrs change of focus to Functional Medicine. His work with patients in the late stages of disease and those who were terminally ill left him wishing he could do more to help them before it was too late. However, his position as a surgeon only allowed him to treat symptoms that had already developed. Now as an Anti-Aging and Functional Medicine Specialist, Chris Wehr, M.D. has the opportunity to directly impact the health and future of thousands of people with the help he provides them today.

Doctor Wehr is an Orlando Bioidentical Hormone Replacement Therapy Expert with several impressive credentials. He is currently a member of the American Academy for Anti-Aging Medicine, a member of the National Board of Medical Examiners, and is Board Certified by the American Board of Thoracic Surgery. In addition, he has completed extensive post-graduate training through the fellowship in Anti-Aging and Regenerative Medicine and is a member of the American Association of Cycling Team Doctors. Doctor Wehr is an amateur cyclist himself.

Bioidentical Hormone Replacement Therapy in Orlando Florida can help men and women experience relief from a variety of symptoms and health conditions. If you deal with one or more of the issues described below, Bioidentical Hormone Replacement Therapy in Orlando with Chris Wehr, M.D. can help eliminate the symptoms and dramatically improve your quality of life.

Adrenal Fatigue

Even though adrenal fatigue is a common problem, traditional doctors often overlook or misdiagnose it. Your bodys adrenal glands produce cortisol, a hormone that enables you to manage stress from multiple sources. Aging, other hormone deficiencies, and prolonged stress can all make it impossible for your adrenal glands to manufacture enough cortisol. Indications that you may have adrenal fatigue include depression, inability to focus, food cravings, frequent minor illnesses, and chronic fatigue for which the condition is named. Balancing cortisol levels with Bioidentical Hormone Replacement Therapy helps to give you the energy you need while also relieving the other symptoms.

Andropause

Testosterone levels in men typically start falling in the early 30s, which leads to a condition called andropause a decade or so later. Some of the symptoms of the male equivalent of menopause include weight gain, depression, loss of muscle strength, erectile dysfunction, and body hair loss. Replenishing testosterone with bioidentical hormones restores balance and helps men feel more like their old selves again.

Hypothyroidism

Hypothyroidism is another common, yet frequently misdiagnosed, hormonal disorder. Some of its symptoms include weight gain, higher body fat percentage, cold intolerance, low blood pressure, lack of interest in sex, and general lethargy. Because a thyroid imbalance can potentially create dozens of symptoms, its essential to treat it with Bioidentical Hormone Replacement Therapy as soon as possible.

Hyperthyroidism

This condition happens when your bodys thyroid gland produces too many hormones rather than not enough. People with hyperthyroidism tend to feel highly anxious, lose weight quickly without dieting, experience panic attacks, and deal with frequent insomnia. Getting a proper diagnosis and following that immediately with Bioidentical Hormone Replacement Therapy can help you feel like youre on more of an even keel.

Insulin Resistance

Your body produces insulin in the pancreas to help maintain blood sugar balance. If you are pre-diabetic or have Type II diabetes, maintaining normal blood sugar levels becomes challenging. Bioidentical Hormone Replacement Therapy helps to replace the insulin that your body no longer makes on this own so you can manage this common, yet serious, metabolic disorder.

Symptoms of Menopause

Menopause occurs when a woman has gone an entire year without a menstrual period. Many women experience estrogen dominance when their progesterone levels start declining first. This can cause hot flashes, night sweats, irritability, depression, low libido, concentration problems, and several other symptoms. Bioidentical Hormone Replacement Therapy balances the affected hormones with natural ingredients so women can enjoy this changing season in their lives.

Symptoms of Perimenopause

Menstrual periods still exist but become increasingly irregular during the perimenopause years, which can last up to a decade for some women. The symptoms tend to be the same as during menopause. Additionally, the lack of estrogen and progesterone balance can cause issues such as uterine fibroids, endometriosis, and polycystic ovarian syndrome. Women can reduce their risk of these complications and get through perimenopause more comfortably with Bioidentical Hormone Replacement Therapy.

Dr. Chris Wehr offers men and women in the Orlando Florida area the opportunity to regain their health and experience a renewed optimism for life with Bioidentical Hormone Replacement Therapy and other natural treatment methods. Every patient receives an individualized compound of bioidentical hormones based on his or her symptoms, results of hormone testing, and therapy goals. Please contact Chris Wehr, M.D. at the Orlando BodyLogicMD clinic today to get started on your wellness journey.

Do you have questions about Bioidentical Hormones? Call Orlando Bioidentical Hormone Expert, Chris Wehr, M.D. at 800-775-4902 Ext. 617 to schedule a Bioidentical Hormones Consultation and takecharge of your wellness today!

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Hormone Replacement Therapy – WebMD

Is hormone therapy (HRT) making a comeback?

A few years ago, the use of hormone replacement therapy (HRT) looked like a medical mess. For decades, women were told that HRT — usually a combination of estrogen and progestin — was good for them during and after menopause. Then the 2002 results of the Women’s Health Initiative study seemed to show just the opposite: hormone replacement therapy actually had life-threatening risks such as heart attacks, strokes, and cancer.

“Women felt betrayed,” says Isaac Schiff, MD, chief of obstetrics and gynecology at Massachusetts General Hospital in Boston. “They were calling their doctors, saying, ‘How could you put me on this drug which causes heart attacks, strokes, and cancer?'”

Almost overnight, standard medical practice changed. Doctors stopped prescribing hormone replacement therapy and 65% of women on HRT quit, according to Schiff.

But some experts say hormone replacement therapy may be coming back. All along HRT remained an important treatment for menopause symptoms like hot flashes. And now, a number of recent studies show that hormone replacement therapy may have protective benefits for women who are early in menopause.

“I think we swung too positive on hormone therapy in the past and then we went too negative,” says Schiff, who is also chair of the American College of Obstetricians and Gynecologists Task Force on Hormone Therapy. “Now we’re trying to find a balance in between.”

“We’re definitely in a gray zone of uncertainty about hormone therapy,” says Jacques Rossouw, MD, project officer for the federal Women’s Health Initiative (WHI). “But when you’re uncertain, you have to err on the side of safety.”

While Rossouw concedes that new studies show some preventative benefit for younger women, he says any potential benefit is very slight. And, he notes, there is no evidence that any benefit would last if women kept taking hormones as they got older.

But increasing numbers of researchers say there should be a place for hormone replacement therapy as a preventive treatment for limited periods as it may help prevent disease in younger women around the age of menopause.

“We have evidence that hormone therapy can prevent heart disease, hip fractures, and osteoporosis, and that it cuts the risk of developing diabetes by 30% in younger women,” says Shelley R. Salpeter, MD, a clinical professor of medicine at Stanford University’s School of Medicine.

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Recommendation and review posted by sam

Corona California Bioidentical Doctor – Patricia Bogema, D.O.

Corona, California Bioidentical Hormone Replacement Therapy specialist, Patricia Bogema, D.O. at ReVitalize Health & Wellness Center is both certified and experienced in treating patients with Bioidentical Hormone Replacement Therapy. Doctor Bogema has been serving patients for over twelve years, and she has treated hundreds of patients experiencing the many symptoms and conditions related to hormonal imbalance, dominance or decline. Doctor Bogemas mission is to work as a team with her patients and guide them towards achieving peak levels of health. Taking a patient centered approach, Doctor Patricia Bogema endeavors to listen to her patients symptoms and customize a treatment regimen especially for them. Her unique process has allowed countless men and women to greatly improve their overall health.

By the time people come to Doctor Patricia Bogema they are ready to try something new. They are frustrated with traditional doctors treating their symptoms and not solving the root of their problems. Commonly, hormones become imbalanced with aging and stress, which can lead to numerous symptoms and conditions that greatly reduce the quality of life and overall vitality. Patricia Bogema, D.O. has helped many people permanently feel better through Bioidentical Hormone Replacement Therapy, and she can do the same for you.

One of the persistent myths that many patients believe is that only women experience hormonal changes as they age. While all women go through menopause, a large percentage of men also deal with symptoms brought on by the hormonal changes that come with aging. That is because a mans testicles naturally produce less testosterone as he gets older. The decrease starts as early as age 30, with the most noticeable symptoms starting in the mid 40s to early 50s. Coincidentally, this is the same age range that women are typically bothered the most by symptoms of menopause.

While normal aging is the most common reason for hormonal imbalance, it is not the only one. Stress, an unhealthy diet, certain illnesses, inadequate sleep, and poor lifestyle choices are also contributing factors. If you suspect that unbalanced hormones are causing your symptoms, it is important to schedule an evaluation with Doctor Bogema as soon as possible. The reason for the imbalance is not as important as determining the proper way to treat it.

When women stop producing estrogen and men slow down their production of testosterone, it seems obvious that restoring the balance they once had can make them feel better. However, most mainstream doctors fail to see the connection. They are trained to diagnose and treat disease. Since hormone imbalance is not an illness, they are at a loss for what to do. Doctor Bogema, on the other hand, introduces hormones into your body that are identical in cell structure and purpose to what it previously manufactured on its own. Within one month of starting treatment, you may notice improvement in some or all of these areas:

Doctor Patricia Bogema has used Bioidentical Hormone Replacement Therapy to help men and women prevent age related diseases and improve their general health. Often, patients come in to treat one symptom, and several others end up being alleviated, along with their chief complaint. Upon the initial visit, Doctor Bogema will test the levels of all major hormones in order to understand the full picture. After obtaining a detailed patient history and an analysis of the patients goals, Dr. Bogema will design a personalized treatment plan to address the patients health concerns. Doctor Bogema offers Bioidentical Hormone Replacement Therapy in the form of creams, injections, troches, and drops. Doctor Bogema offers patients continued support throughout the course of their Bioidentical Hormone Replacement Therapy programs. Men and women that are ready to experience life again and not just get through it can contact Patricia Bogema, D.O. at ReVitalize Health & Wellness Center in Corona, California today to schedule a Bioidentical Hormone consultation.

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Corona California Bioidentical Doctor – Patricia Bogema, D.O.

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Hypogonadism: MedlinePlus Medical Encyclopedia

Ali O, Donohoue PA. Hypofunction of the testes. In: Kliegman RM, Stanton BF, St. Geme JW III, et al., eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 577.

Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in adult men with androgen deficiency syndromes: An Endocrine Society Clinical Practice guideline. J Clin Endocrinol Metab. 2010;95:2536-59. PMID: 20525905 http://www.ncbi.nlm.nih.gov/pubmed/20525905

Kansra AR, Donohoue PA. Hypofunction of the ovaries. In: Kliegman RM, Stanton BF, St. Geme JW III, et al, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 580.

Swerdloff RS, Wang C. The testis and male sexual function. In: Goldman L, Schafer AI. Goldman’s Cecil Medicine. 24th ed. Philadelphia, PA: Elsevier Saunders; 2012:chap 242.

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Stem-cell therapy – Wikipedia, the free encyclopedia

This article is about the medical therapy. For the cell type, see Stem cell.

Stem-cell therapy is the use of stem cells to treat or prevent a disease or condition.

Bone marrow transplant is the most widely used stem-cell therapy, but some therapies derived from umbilical cord blood are also in use. Research is underway to develop various sources for stem cells, and to apply stem-cell treatments for neurodegenerative diseases and conditions such as diabetes, heart disease, and other conditions.

Stem-cell therapy has become controversial following developments such as the ability of scientists to isolate and culture embryonic stem cells, to create stem cells using somatic cell nuclear transfer and their use of techniques to create induced pluripotent stem cells. This controversy is often related to abortion politics and to human cloning. Additionally, efforts to market treatments based on transplant of stored umbilical cord blood have been controversial.

For over 30 years, bone marrow has been used to treat cancer patients with conditions such as leukaemia and lymphoma; this is the only form of stem-cell therapy that is widely practiced.[1][2][3] During chemotherapy, most growing cells are killed by the cytotoxic agents. These agents, however, cannot discriminate between the leukaemia or neoplastic cells, and the hematopoietic stem cells within the bone marrow. It is this side effect of conventional chemotherapy strategies that the stem-cell transplant attempts to reverse; a donor’s healthy bone marrow reintroduces functional stem cells to replace the cells lost in the host’s body during treatment. The transplanted cells also generate an immune response that helps to kill off the cancer cells; this process can go too far, however, leading to graft vs host disease, the most serious side effect of this treatment.[4]

Another stem-cell therapy called Prochymal, was conditionally approved in Canada in 2012 for the management of acute graft-vs-host disease in children who are unresponsive to steroids.[5] It is an allogenic stem therapy based on mesenchymal stem cells (MSCs) derived from the bone marrow of adult donors. MSCs are purified from the marrow, cultured and packaged, with up to 10,000 doses derived from a single donor. The doses are stored frozen until needed.[6]

The FDA has approved five hematopoietic stem-cell products derived from umbilical cord blood, for the treatment of blood and immunological diseases.[7]

In 2014, the European Medicines Agency recommended approval of Holoclar, a treatment involving stem cells, for use in the European Union. Holoclar is used for people with severe limbal stem cell deficiency due to burns in the eye.[8]

In March 2016 GlaxoSmithKline’s Strimvelis (GSK2696273) therapy for the treatment ADA-SCID was recommended for EU approval.[9]

Stem cells are being studied for a number of reasons. The molecules and exosomes released from stem cells are also being studied in a effort to make medications.[10]

Research has been conducted on the effects of stem cells on animal models of brain degeneration, such as in Parkinson’s, Amyotrophic lateral sclerosis, and Alzheimer’s disease.[11][12][13] There have been preliminary studies related to multiple sclerosis.[14][15]

Healthy adult brains contain neural stem cells which divide to maintain general stem-cell numbers, or become progenitor cells. In healthy adult laboratory animals, progenitor cells migrate within the brain and function primarily to maintain neuron populations for olfaction (the sense of smell). Pharmacological activation of endogenous neural stem cells has been reported to induce neuroprotection and behavioral recovery in adult rat models of neurological disorder.[16][17][18]

Stroke and traumatic brain injury lead to cell death, characterized by a loss of neurons and oligodendrocytes within the brain. A small clinical trial was underway in Scotland in 2013, in which stem cells were injected into the brains of stroke patients.[19]

Clinical and animal studies have been conducted into the use of stem cells in cases of spinal cord injury.[20][21][22]

The pioneering work[23] by Bodo-Eckehard Strauer has now been discredited by the identification of hundreds of factual contradictions.[24] Among several clinical trials that have reported that adult stem-cell therapy is safe and effective, powerful effects have been reported from only a few laboratories, but this has covered old[25] and recent[26] infarcts as well as heart failure not arising from myocardial infarction.[27] While initial animal studies demonstrated remarkable therapeutic effects,[28][29] later clinical trials achieved only modest, though statistically significant, improvements.[30][31] Possible reasons for this discrepancy are patient age,[32] timing of treatment[33] and the recent occurrence of a myocardial infarction.[34] It appears that these obstacles may be overcome by additional treatments which increase the effectiveness of the treatment[35] or by optimizing the methodology although these too can be controversial. Current studies vary greatly in cell-procuring techniques, cell types, cell-administration timing and procedures, and studied parameters, making it very difficult to make comparisons. Comparative studies are therefore currently needed.

Stem-cell therapy for treatment of myocardial infarction usually makes use of autologous bone-marrow stem cells (a specific type or all), however other types of adult stem cells may be used, such as adipose-derived stem cells.[36] Adult stem cell therapy for treating heart disease was commercially available in at least five continents as of 2007.[citation needed]

Possible mechanisms of recovery include:[11]

It may be possible to have adult bone-marrow cells differentiate into heart muscle cells.[11]

The first successful integration of human embryonic stem cell derived cardiomyocytes in guinea pigs (mouse hearts beat too fast) was reported in August 2012. The contraction strength was measured four weeks after the guinea pigs underwent simulated heart attacks and cell treatment. The cells contracted synchronously with the existing cells, but it is unknown if the positive results were produced mainly from paracrine as opposed to direct electromechanical effects from the human cells. Future work will focus on how to get the cells to engraft more strongly around the scar tissue. Whether treatments from embryonic or adult bone marrow stem cells will prove more effective remains to be seen.[37]

In 2013 the pioneering reports of powerful beneficial effects of autologous bone marrow stem cells on ventricular function were found to contain “hundreds” of discrepancies.[38] Critics report that of 48 reports there seemed to be just five underlying trials, and that in many cases whether they were randomized or merely observational accepter-versus-rejecter, was contradictory between reports of the same trial. One pair of reports of identical baseline characteristics and final results, was presented in two publications as, respectively, a 578 patient randomized trial and as a 391 patient observational study. Other reports required (impossible) negative standard deviations in subsets of patients, or contained fractional patients, negative NYHA classes. Overall there were many more patients published as having receiving stem cells in trials, than the number of stem cells processed in the hospital’s laboratory during that time. A university investigation, closed in 2012 without reporting, was reopened in July 2013.[39]

One of the most promising benefits of stem cell therapy is the potential for cardiac tissue regeneration to reverse the tissue loss underlying the development of heart failure after cardiac injury.[40]

Initially, the observed improvements were attributed to a transdifferentiation of BM-MSCs into cardiomyocyte-like cells.[28] Given the apparent inadequacy of unmodified stem cells for heart tissue regeneration, a more promising modern technique involves treating these cells to create cardiac progenitor cells before implantation to the injured area.[41]

The specificity of the human immune-cell repertoire is what allows the human body to defend itself from rapidly adapting antigens. However, the immune system is vulnerable to degradation upon the pathogenesis of disease, and because of the critical role that it plays in overall defense, its degradation is often fatal to the organism as a whole. Diseases of hematopoietic cells are diagnosed and classified via a subspecialty of pathology known as hematopathology. The specificity of the immune cells is what allows recognition of foreign antigens, causing further challenges in the treatment of immune disease. Identical matches between donor and recipient must be made for successful transplantation treatments, but matches are uncommon, even between first-degree relatives. Research using both hematopoietic adult stem cells and embryonic stem cells has provided insight into the possible mechanisms and methods of treatment for many of these ailments.[citation needed]

Fully mature human red blood cells may be generated ex vivo by hematopoietic stem cells (HSCs), which are precursors of red blood cells. In this process, HSCs are grown together with stromal cells, creating an environment that mimics the conditions of bone marrow, the natural site of red-blood-cell growth. Erythropoietin, a growth factor, is added, coaxing the stem cells to complete terminal differentiation into red blood cells.[42] Further research into this technique should have potential benefits to gene therapy, blood transfusion, and topical medicine.

In 2004, scientists at King’s College London discovered a way to cultivate a complete tooth in mice[43] and were able to grow bioengineered teeth stand-alone in the laboratory. Researchers are confident that the tooth regeneration technology can be used to grow live teeth in human patients.

In theory, stem cells taken from the patient could be coaxed in the lab turning into a tooth bud which, when implanted in the gums, will give rise to a new tooth, and would be expected to be grown in a time over three weeks.[44] It will fuse with the jawbone and release chemicals that encourage nerves and blood vessels to connect with it. The process is similar to what happens when humans grow their original adult teeth. Many challenges remain, however, before stem cells could be a choice for the replacement of missing teeth in the future.[45][46]

Research is ongoing in different fields, alligators which are polyphyodonts grow up to 50 times a successional tooth (a small replacement tooth) under each mature functional tooth for replacement once a year.[47]

Heller has reported success in re-growing cochlea hair cells with the use of embryonic stem cells.[48]

Since 2003, researchers have successfully transplanted corneal stem cells into damaged eyes to restore vision. “Sheets of retinal cells used by the team are harvested from aborted fetuses, which some people find objectionable.” When these sheets are transplanted over the damaged cornea, the stem cells stimulate renewed repair, eventually restore vision.[49] The latest such development was in June 2005, when researchers at the Queen Victoria Hospital of Sussex, England were able to restore the sight of forty patients using the same technique. The group, led by Sheraz Daya, was able to successfully use adult stem cells obtained from the patient, a relative, or even a cadaver. Further rounds of trials are ongoing.[50]

In April 2005, doctors in the UK transplanted corneal stem cells from an organ donor to the cornea of Deborah Catlyn, a woman who was blinded in one eye when acid was thrown in her eye at a nightclub. The cornea, which is the transparent window of the eye, is a particularly suitable site for transplants. In fact, the first successful human transplant was a cornea transplant. The absence of blood vessels within the cornea makes this area a relatively easy target for transplantation. The majority of corneal transplants carried out today are due to a degenerative disease called keratoconus.

The University Hospital of New Jersey reports that the success rate for growth of new cells from transplanted stem cells varies from 25 percent to 70 percent.[51]

In 2014, researchers demonstrated that stem cells collected as biopsies from donor human corneas can prevent scar formation without provoking a rejection response in mice with corneal damage.[52]

In January 2012, The Lancet published a paper by Steven Schwartz, at UCLA’s Jules Stein Eye Institute, reporting two women who had gone legally blind from macular degeneration had dramatic improvements in their vision after retinal injections of human embryonic stem cells.[53]

In June 2015, the Stem Cell Ophthalmology Treatment Study (SCOTS), the largest adult stem cell study in ophthalmology ( http://www.clinicaltrials.gov NCT # 01920867) published initial results on a patient with optic nerve disease who improved from 20/2000 to 20/40 following treatment with bone marrow derived stem cells.[54]

Diabetes patients lose the function of insulin-producing beta cells within the pancreas.[55] In recent experiments, scientists have been able to coax embryonic stem cell to turn into beta cells in the lab. In theory if the beta cell is transplanted successfully, they will be able to replace malfunctioning ones in a diabetic patient.[56]

Human embryonic stem cells may be grown in cell culture and stimulated to form insulin-producing cells that can be transplanted into the patient.

However, clinical success is highly dependent on the development of the following procedures:[11]

Clinical case reports in the treatment orthopaedic conditions have been reported. To date, the focus in the literature for musculoskeletal care appears to be on mesenchymal stem cells. Centeno et al. have published MRI evidence of increased cartilage and meniscus volume in individual human subjects.[57][58] The results of trials that include a large number of subjects, are yet to be published. However, a published safety study conducted in a group of 227 patients over a 3-4-year period shows adequate safety and minimal complications associated with mesenchymal cell transplantation.[59]

Wakitani has also published a small case series of nine defects in five knees involving surgical transplantation of mesenchymal stem cells with coverage of the treated chondral defects.[60]

Stem cells can also be used to stimulate the growth of human tissues. In an adult, wounded tissue is most often replaced by scar tissue, which is characterized in the skin by disorganized collagen structure, loss of hair follicles and irregular vascular structure. In the case of wounded fetal tissue, however, wounded tissue is replaced with normal tissue through the activity of stem cells.[61] A possible method for tissue regeneration in adults is to place adult stem cell “seeds” inside a tissue bed “soil” in a wound bed and allow the stem cells to stimulate differentiation in the tissue bed cells. This method elicits a regenerative response more similar to fetal wound-healing than adult scar tissue formation.[61] Researchers are still investigating different aspects of the “soil” tissue that are conducive to regeneration.[61]

Culture of human embryonic stem cells in mitotically inactivated porcine ovarian fibroblasts (POF) causes differentiation into germ cells (precursor cells of oocytes and spermatozoa), as evidenced by gene expression analysis.[62]

Human embryonic stem cells have been stimulated to form Spermatozoon-like cells, yet still slightly damaged or malformed.[63] It could potentially treat azoospermia.

In 2012, oogonial stem cells were isolated from adult mouse and human ovaries and demonstrated to be capable of forming mature oocytes.[64] These cells have the potential to treat infertility.

Destruction of the immune system by the HIV is driven by the loss of CD4+ T cells in the peripheral blood and lymphoid tissues. Viral entry into CD4+ cells is mediated by the interaction with a cellular chemokine receptor, the most common of which are CCR5 and CXCR4. Because subsequent viral replication requires cellular gene expression processes, activated CD4+ cells are the primary targets of productive HIV infection.[65] Recently scientists have been investigating an alternative approach to treating HIV-1/AIDS, based on the creation of a disease-resistant immune system through transplantation of autologous, gene-modified (HIV-1-resistant) hematopoietic stem and progenitor cells (GM-HSPC).[66]

On 23 January 2009, the US Food and Drug Administration gave clearance to Geron Corporation for the initiation of the first clinical trial of an embryonic stem-cell-based therapy on humans. The trial aimed evaluate the drug GRNOPC1, embryonic stem cell-derived oligodendrocyte progenitor cells, on patients with acute spinal cord injury. The trial was discontinued in November 2011 so that the company could focus on therapies in the “current environment of capital scarcity and uncertain economic conditions”.[67] In 2013 biotechnology and regenerative medicine company BioTime (NYSEMKT:BTX) acquired Geron’s stem cell assets in a stock transaction, with the aim of restarting the clinical trial.[68]

Scientists have reported that MSCs when transfused immediately within few hours post thawing may show reduced function or show decreased efficacy in treating diseases as compared to those MSCs which are in log phase of cell growth(fresh), so cryopreserved MSCs should be brought back into log phase of cell growth in invitro culture before these are administered for clinical trials or experimental therapies, re-culturing of MSCs will help in recovering from the shock the cells get during freezing and thawing. Various clinical trials on MSCs have failed which used cryopreserved product immediately post thaw as compared to those clinical trials which used fresh MSCs.[69]

There is widespread controversy over the use of human embryonic stem cells. This controversy primarily targets the techniques used to derive new embryonic stem cell lines, which often requires the destruction of the blastocyst. Opposition to the use of human embryonic stem cells in research is often based on philosophical, moral, or religious objections.[110] There is other stem cell research that does not involve the destruction of a human embryo, and such research involves adult stem cells, amniotic stem cells, and induced pluripotent stem cells.

Stem-cell research and treatment was practiced in the People’s Republic of China. The Ministry of Health of the People’s Republic of China has permitted the use of stem-cell therapy for conditions beyond those approved of in Western countries. The Western World has scrutinized China for its failed attempts to meet international documentation standards of these trials and procedures.[111]

State-funded companies based in the Shenzhen Hi-Tech Industrial Zone treat the symptoms of numerous disorders with adult stem-cell therapy. Development companies are currently focused on the treatment of neurodegenerative and cardiovascular disorders. The most radical successes of Chinese adult stem cell therapy have been in treating the brain. These therapies administer stem cells directly to the brain of patients with cerebral palsy, Alzheimer’s, and brain injuries.[citation needed]

Since 2008 many universities, centers and doctors tried a diversity of methods; in Lebanon proliferation for stem cell therapy, in-vivo and in-vitro techniques were used, Thus this country is considered the launching place of the Regentime[112] procedure. http://www.researchgate.net/publication/281712114_Treatment_of_Long_Standing_Multiple_Sclerosis_with_Regentime_Stem_Cell_Technique The regenerative medicine also took place in Jordan and Egypt.[citation needed]

Stem-cell treatment is currently being practiced at a clinical level in Mexico. An International Health Department Permit (COFEPRIS) is required. Authorized centers are found in Tijuana, Guadalajara and Cancun. Currently undergoing the approval process is Los Cabos. This permit allows the use of stem cell.[citation needed]

In 2005, South Korean scientists claimed to have generated stem cells that were tailored to match the recipient. Each of the 11 new stem cell lines was developed using somatic cell nuclear transfer (SCNT) technology. The resultant cells were thought to match the genetic material of the recipient, thus suggesting minimal to no cell rejection.[113]

As of 2013, Thailand still considers Hematopoietic stem cell transplants as experimental. Kampon Sriwatanakul began with a clinical trial in October 2013 with 20 patients. 10 are going to receive stem-cell therapy for Type-2 diabetes and the other 10 will receive stem-cell therapy for emphysema. Chotinantakul’s research is on Hematopoietic cells and their role for the hematopoietic system function in homeostasis and immune response.[114]

Today, Ukraine is permitted to perform clinical trials of stem-cell treatments (Order of the MH of Ukraine 630 “About carrying out clinical trials of stem cells”, 2008) for the treatment of these pathologies: pancreatic necrosis, cirrhosis, hepatitis, burn disease, diabetes, multiple sclerosis, critical lower limb ischemia. The first medical institution granted the right to conduct clinical trials became the “Institute of Cell Therapy”(Kiev).

Other countries where doctors did stem cells research, trials, manipulation, storage, therapy: Brazil, Cyprus, Germany, Italy, Israel, Japan, Pakistan, Philippines, Russia, Switzerland, Turkey, United Kingdom, India, and many others.

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Stem Cell 100 – Powerful Rejuvenation and Anti-Aging …

Stem Cell 100 is formulated to rejuvenate your body and slow the aging process to help you feel and function more like a young person. This can help you feel better, look younger and improve your health. Most of the cells in your body lose function with age. Everyone has special cells called adult stem cells which are needed to rejuvenate damaged and old tissues, but adult stem cells themselves are also aging. Until now there was not much you could do about it. Stem Cell 100 rejuvenates adult stem cells and their micro-environments. Stem Cell 100+ is a more advanced and faster acting version of Stem Cell 100.

Developed by experts in the anti-aging field, patent-pending Stem Cell 100 is the only supplement proven to double maximum lifespan of an animal model. No other product or therapy including caloric restriction even comes close.

SK of Santa Fe, NM

I have been using Stem Cell 100 for about one year. Initially I noticed a boost in energy level, which now remains steady-hence not noticed I have experienced no adverse effects from taking this product. I heartily recommend Stem Cell 100 and plan to continue on it.

Leslie

Stem Cell 100 has made a noticeable difference in me, including turning my gray hair back to its original color, which supposedly is impossible. The reversal of the gray hair to original color began a couple of months after starting the pill. After about 10 months, the gray hair is mostly gone. At the current rate of improvement, I expect my hair to completely be back to its original color within 1 to 2 months. I think my beard will take longer, but it was the first to gray. Also, my skin became smoother and younger looking. The skin and hair rely heavily on stem cells, and they seem to benefit strongly from this product. I’m so excited about telling people my results because there is nothing that can reverse the graying of hair. It will give me evidence that this supplement thing is really powerful. Unfortunately, I don’t have before and after pictures because I didn’t read any claims that the product would affect hair color. I would just say that I’m a person who totally believes that it does me no good to imagine things or interpret tings in a way favorable to what I want to believe. When I’m convinced enough to make a statement, you can count on it.

Joey of San Diego, CA

I am a 48 year old working woman. A friend of mine introduced me to Stem Cell 100. After taking Stem Cell 100 for about 4 months my anxiety level has really been diminished. Its a great supplement and I would recommend it to everyone!

Paul of San Diego, CA

I am an active 61 year old man in excellent health, but had experienced a serious drop in my energy level at the time I enrolled in a 4-month trial of Stem Cell 100. Within a month, my energy increased noticeably and I began to take to my physical activities (running, cycling) with a renewed enthusiasm and intensity level. My mood began to elevate steadily, and soon I had even lost those few stubborn pounds that had eluded me for years. I am very enthusiastic about Stem Cell 100. I look forward to continuing with the new, improved formulation, and would not hesitate to recommend it.

Mike, Texas

After taking the Stem Cell 100 for the last month my sinuses have also cleared, unplugging my ears for the first time since mid September.

Willie, California

As I was sprinting this morning around 6:00am I noticed that I was not hurting anymore! I have been having sore knees, ankles, hamstrings and back for the last couple of years. I usually just ran through it, but I noticed since I have been taking the Stem Cell 100 capsules for about 45 days now, those nagging pains are gone away!

Tom, Australia

Only after about 2-3 weeks of taking Stem Cell 100 my eye sight returned back to a level where I did not need glasses to work on my computer monitors. My eyes had always been good but had started to deteriorate about a year ago where 50% of the time I had to wear my glasses. I was shocked to find the improvement so quick. I found I was less stressed. No other changes to lifestyle yet a measureable difference. My fingers would sometimes get stiff in the mornings after long days on the keyboard. This stiffness disappeared. Some of my hair is getting darker. I have a full body of hair that had virtually all turned grey but I noticed that some of my hair was starting regrow brown – my original colour. I had some age spots in my left leg that are disappearing. Generally, I feel great.

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Harness the Power of Your Own Stem Cells

Millions of people suffer from chronic conditions of aging and disease. Based on international scientific studies in many academic and industry laboratories, there is new hope that many of the conditions afflicting mankind can some day be cured or greatly improved using stem cell regenerative medicine. Stem Cell 100 offers a way to receive some of the benefits of stem cell therapy today by improving the activity and effectiveness of your own adult stem cells.

Stem Cell 100 Helps to Support:

The statements above have not been reviewed by the FDA. Stem Cell 100 is not a preventive or treatment for any disease.

Help Rejuvenate Your Body by Boosting Your Own Stem Cells

As a child, we are protected from the ravages of aging and can rapidly recover from injury or illness because of the ability of the young regenerative stem cells of children have a superior ability to repair and regenerate most damaged tissues. As we age, our stem cell populations become depleted and/or slowly lose their capacity to repair. Moreover, the micro-environment (i.e. niches) around stem cells becomes less nurturing with age, so cell turnover and repair are further reduced. This natural progression occurs so slowly that we are barely aware of it, but we start to notice the body changes in our 20s, 30s, 40s, and especially after 50 years of age. Stem Cell 100 helps adults regain their youthful regenerative potential by stabilizing stem cell function.

Stem Cell 100 works differently than other stem cell products on the market

You may have seen a number of products that are advertised as stimulating or enhancing the number of stem cells. Each person only has a limited number of stem cells so using them up faster may not be a good strategy. Stem Cell 100 is about improving the effectiveness and longevity of your stem cells as well as preserving the stem cell micro-environment. That should be the goal of any effective stem cell therapy and is what Stem Cell 100 is designed to do and what other stem cell products cannot do.

Stem Cell 100 Extends Drosophila (Fruit Fly) Lifespan

In extensive laboratory testing Stem Cell 100 greatly extended both the average and maximum lifespan of Drosophila fruit flies. The study (see Charts below) included three cages of Drosophila fruit flies that were treated with Stem Cell 100 (Cages T1 to T3) and three cages which were untreated controls (Cages C1 to C3). Each cage started with 500 fruit flies including 250 males and 250 females. The experiment showed that median lifespan more than doubled with a 123% increase. While fruit flies are not people they are more like us than you might think. Drosophila have a heart and circulatory system, and the most common cause of death is heart failure. Like humans and other mammals (e.g. mice), it is difficult to increase their lifespan significantly. These observed results outperform every lifespan enhancing treatment ever tested – including experiments using genetic modification and dietary restriction.

The longest living fruit fly receiving Stem Cell 100 lived 89 days compared to the longest living untreated control which lived 48 days. It is possible that the single longest living fruit fly lived longer for other reasons such as genetic mutation, however, there were many others that lived almost as long so it was not just an aberation. The oldest 5% of the treated fruit flies lived 77% longer than the oldest 5% of the control group. It is also important that the study showed an improved ability of the fruit flies to survive stress and illness at all ages not just during old age. Even after the first few days of the study there were already more of the Stem Cell 100 treated fruit flies alive that survived youth than the control group of untreated fruit flies. For additional information about the study please go to our Longevity page.

Supplement Facts

Stem Cell 100 is a Patent-Pending Life Code Nutraceutical. All Life Code products are nutraceutical grade and provide the best of science along with the balance of nature.

All Life Code products are nutraceutical grade and provide the best of science along with the balance of nature.

Click label to enlarge

Stem Cell 100 Plus+ is a more powerful and faster acting version of Stem Cell 100.

Click label to enlarge

Serving Size: One type O capsule

Servings Per Container: 60 Capsules

Recommended Use: Typical usage of Stem Cell 100 is two capsules per day, preferably at meal times. While both capsules can be taken at the same time, it is preferable to separate the two capsules by at least 4 hours. Since Stem Cell 100 is a potent formulation, do not take more than three capsules per day. One capsule per day may be sufficient for those below 110 pounds.

Recommended Users: Anyone from ages 22 and up could benefit from Stem Cell 100. Those in their 20s and 30s will like the boost in endurance during sports or exercise, while older users will notice better energy and general health with the potential for some weight loss.

Active Ingredients in Stem Cell 100: There are ten herbal components that make up the patent-pending combination in Stem Cell 100. The herbal components are highly extracted natural herbs that are standardized for active components that promote adult stem cells and lower inflammation:

1) Polysaccharides, flavonoids, and astragalosides extracted from Astragalus membranaceus, which has many positive effects on stem cells and the cardiovascular and immune systems.

2) Proprietary natural bilberry flavonoids and other compounds from a stabilized nutraceutical grade medicinal Vaccinium extract. Activate metabolic PPARS and helps produce healthy levels of cholesterol and silent inflammation. Also has anti-fungal and anti-viral activity.

3) Flavonoids and oligo-proanthocyanidins (OPCs) extracted from Pine Bark, which greatly reduce oxidative stress, DNA damage, and inflammation.

4) L-Theanine, which is a natural amino acid from Camellia sinesis that reduces mental stress and inflammation while improving cognition and protecting brain cells from ischemic or toxic injury.

5) Pterocarpus Marsupium, which contains two stable resveratrol analogs which promote stem cells, lower inflammation, and stabilized metabolism.

6) Polygonum Multiflorium stem stem is a popular Chinese herbal tonic that fights premature aging and promotes youthfulness. Polygonum is reported to enhance fertility by improving sperm count in men and egg vitality in women. Polygonum is also widely used in Asia to strengthen muscle and is thus used by many athletes as an essential tonic for providing strength and stamina to the body. Modern research has supported Polygonum multiflorium stem in that animal studies have proven that it can extend lifespan and improve the quality of life. Polygonum appears to protect the liver and brain against damage, perhaps by improving immune and cardiovascular health. The stem sections of Polygonum multiflorium are also calming to the nervous system and promote sounder sleep. Life Code uses a proprietary Polygonum multiflorium stem extract.

7) Schisandra Berry is used by many Chinese women to preserve their youthful beauty. For thousands of years, Schisandra has been prized as an antiaging tonic that increases stamina and mental clarity, while fighting stress and fatigue. In Chinese traditional medicine, Schisandra berry has been used for liver disorders and to enhance resistance to infection and promote skin health and better sleep. Schisandra berry is classified as an adaptogen, which can stimulate the central nervous system, increase brain efficiency, improve reflexes, and enhance endurance. Modern research indicates that Schisandra berry extracts have a protective effect on the liver and promote immunity. A double-blind human trial suggested that Schisandra berry may help patients with viral hepatitis, which is very prevalent in China. Recent work indicates that the liver is protected by the enhanced production of glutathione peroxidase, which helps detoxify the liver. Life Code uses a proprietary Schisandra berry extract.

8) Fo-Ti Root (aka He-Shou-Wu) is one of the most widely used Chinese herbal medicines to restore blood, kidney, liver, and cardiovascular health. Fo-Ti is claimed to have powerful rejuvenating effects on the brain, endocrine glands, the immune system, and sexual vigor. Legend has it that Professor Li Chung Yun took daily doses of Fo-Ti to live to be 256 and is said to have outlived 23 wives and spawned 11 generations of descendents before his death in 1933. While it is unlikely that he really lived to such an old age there is scientific support for Fo-Ti as beneficial for health and longevity. Like the Indian Keno bark, Fo-ti contains resveratrol analogs and likely acts by various mechanism, which includes liver detoxification and protection of skin from UVB radiation. Life CodeTM uses a proprietary Fo-Ti root extract.

9 ) Camellia sinensis has many bioactive polyphenols including the potent epigallocatechin-3-gallate (EGCG). A 2006 Japanese study published in the Journal of the American Medical Association reports that adults aged 40 to 79 years of age who drank an average of 5 or more cups of tea per day had a significantly lower risk of dying from all causes (23% lower for females and 12% lower for males). The study tracked more than 40,000 adults for up to 11 years and found dramatically lower rates of cardiovascular disease and strokes in those drinking 5 or more cups of tea. Many studies have found that adults drinking 3 or more cups of tea per day have significantly less cancer. Other studies have found that green tea helps protect against age-related cognitive decline, kidney disease, periodontal disease, and type 2 diabetes. Green tea also promotes visceral fat loss and higher endurance levels. Summarizing all of the thousands of studies on tea and tea polyphenols that have been published, it can be concluded that tea polyphenols preserve health and youth. This conclusion is backed up by gene studies showing that tea polyphenols decrease insulin-like growth factor-1 (IGF-1), which is a highly conserved genetic pathway that has been strongly linked to aging in yeast, worms, mice, and humans. If everyone could drink 4 to 5 cups of green tea each day, they could enjoy these important health benefits, but for most people drinking that much green tea can disturb their sleep patterns. Life Code uses a nutraceutical grade green tea extract that has 98% polyphenols and 50% ESCG that provides the polyphenol and ESCG equivalent of 4 to 5 cups of green tea with only 2% of the caffeine. Thus, most or all of the benefits of green tea are provided without concerns about disturbing sleep.

10) Drynaria Rhizome is used extensively in traditional Chinese medicine as an effective herb for healing bones, ligaments, tendons, and lower back problems. Eastern martial art practitioners have used Drynaria for thousands of years to help in recovering from sprains, bruises, and stress fractures. Drynaria has also helped in many cases of bleeding gums and tinnitus (ringing in the ears). The active components of Drynaria protect bone forming cells by enhancing calcium absorption and other mechanisms. Drynaria is also reported to act as a kidney tonic and to promote hair growth and wound healing. Life Code uses a proprietary Drynaria rhizome extract.

Active Ingredients in Stem Cell 100+ There are 11 herbal extracts in Stem Cell 100+ along with two nutraceutical grade vitamins Methyl Folate (5-MTHF) and Methyl B12 that are bioavailable vitamin supplements that are highly potent but rarely found. The highly extracted natural herbs are standardized for active components that promote adult stem cells and lower inflammation and have been tested as a synergistic herbal formulation with the proper dosage of each component:

1) Polysaccharides, flavonoids, and astragalosides extracted from Astragalus membranaceus, which has many positive effects on stem cells and the cardiovascular and immune systems. Astragalus has been used for thousands of years in Traditional Chinese Medicine (TCM) to promote cardiovascular and immune health. Astragalus is also known as a primary stimulator of Qi (Life Force). Life Code uses a high quality proprietary TCM extract that tested highest in our longevity experiments.

2) Proprietary natural bilberry flavonoids and other compounds from a stabilized nutraceutical grade medicinal Vaccinium extract. Activate metabolic PPARS and helps produce healthy levels of cholesterol and silent inflammation. Also has anti-fungal and anti-viral activity.

3) Flavonoids and oligo-proanthocyanidins (OPCs) extracted from Pine Bark, which promote the vascular system and reduce oxidative stress, DNA damage, and inflammation.

4) L-Theanine, which is a natural amino acid from Camellia sinesis that reduces mental stress and inflammation while improving cognition and protecting brain cells from ischemic or toxic injury. Life Code tested supplement with Mass Spec to verify high purity.

5) Genistein, which is an isoflavone phytoestrogen, activates telomerase, metabolic PPARs, autophagy (cell waste disposal), and smooth muscles. It also inhibits DNA methylation and the carbohydrate transporter GLUT1. Life Code tested supplement with Mass Spec to verify high purity.

6) Harataki Extract (aka Terminalia chebula) contains rejuvenating tannin flavonoids that have doubled human cell longevity in culture while maintaining telomere length. In Traditional Indian Medicine, Harataki has been used to treat skin disorders and heart disease, among many other uses.

7) Two stable resveratrol analogs from extracts of Pterocarpus Marsupium, which promote stem cells, less silent inflammation, and better metabolism. Life Code uses a highly purified proprietary source that is only available to Indian doctors. Life Code does not recommend taking resveratrol supplements or synthetic analogs, as these supplements are inherently unstable.

8) He-Shou-Wu is one of the most widely used Chinese herbal medicines to restore blood, kidney, liver, and cardiovascular health. He-Shou-Wu is claimed to have powerful rejuvenating effects on the brain, endocrine glands, the immune system, and sexual vigor. Legend has it that Professor Li Chung Yun took daily doses to live to 256 years and is said to have outlived 23 wives and spawned 11 generations of descendants before his death in 1933. While it is unlikely that he really lived to such an old age, there is scientific support for He-Shou-Wu as beneficial for health and longevity. Life Code uses a proprietary TCM He-Shou-Wu root extract.

9) Schisandra Berry is used by many Chinese women to preserve their youthful beauty. For thousands of years, Schisandra has been prized as an antiaging tonic that increases stamina and mental clarity, while fighting stress and fatigue. In TCM, Schisandra berry has been used for liver disorders and to enhance resistance to infection and promote skin health and better sleep. Schisandra berry is classified as an adaptogen, which can stimulate the central nervous system, increase brain efficiency, improve reflexes, and enhance endurance. Life Code uses a proprietary TCM extract.

10) Drynaria Rhizome is used extensively in TCM as an effective herb for healing bones, ligaments, tendons, and lower back problems. Eastern martial art practitioners have used Drynaria for thousands of years to help in recovering from sprains, bruises, and stress fractures. The active components of Drynaria protect bone forming cells by enhancing calcium absorption and other mechanisms. Drynaria is also reported to act as a kidney tonic and to promote hair growth and wound healing. Life Code uses a proprietary TCM Drynaria rhizome extract.

11) BioPerine is a proprietary brand of peperine extracted from black pepper. BioPerine has been shown to enhance bioavailability of herbal extracts. Piperine has been shown in rats to have cognitive enhancing effects and to help control silent inflammation.

Safety: The extracts in Stem Cell 100 and Stem Cell 100+ are nutraceutical grade and have been individually tested in both animals and humans without significant safety issues. Those with pre-existing conditions of diabetes or hypertension should coordinate this product with your doctor, as lower blood glucose or reduced blood pressure can result from taking the recommended dose of this product.

Warnings: may lower glucose and/or blood pressure in some individuals. The supplement is not recommended for pregnant, lactating, or hypoglycemic individuals.

References

1. Yu, Q., Y.S. Bai, and J. Lin, [Effect of astragalus injection combined with mesenchymal stem cells transplantation for repairing the Spinal cord injury in rats]. Zhongguo Zhong Xi Yi Jie He Za Zhi, 2010. 30(4): p. 393-7.

2. Xu, C.J., et al., [Effect of astragalus polysaccharides on the proliferation and ultrastructure of dog bone marrow stem cells induced into osteoblasts in vitro]. Hua Xi Kou Qiang Yi Xue Za Zhi, 2007. 25(5): p. 432-6.

3. Xu, C.J., et al., [Effects of astragalus polysaccharides-chitosan/polylactic acid scaffolds and bone marrow stem cells on repairing supra-alveolar periodontal defects in dogs]. Zhong Nan Da Xue Xue Bao Yi Xue Ban, 2006. 31(4): p. 512-7.

4. Zhu, X. and B. Zhu, [Effect of Astragalus membranaceus injection on megakaryocyte hematopoiesis in anemic mice]. Hua Xi Yi Ke Da Xue Xue Bao, 2001. 32(4): p. 590-2.

5. Qiu, L.H., X.J. Xie, and B.Q. Zhang, Astragaloside IV improves homocysteine-induced acute phase endothelial dysfunction via antioxidation. Biol Pharm Bull, 2010. 33(4): p. 641-6.

6. Araghi-Niknam, M., et al., Pine bark extract reduces platelet aggregation. Integr Med, 2000. 2(2): p. 73-77.

7. Rohdewald, P., A review of the French maritime pine bark extract (Pycnogenol), a herbal medication with a diverse clinical pharmacology. Int J Clin Pharmacol Ther, 2002. 40(4): p. 158-68.

8. Koch, R., Comparative study of Venostasin and Pycnogenol in chronic venous insufficiency. Phytother Res, 2002. 16 Suppl 1: p. S1-5.

9. Rimando, A.M., et al., Pterostilbene, a new agonist for the peroxisome proliferator-activated receptor alpha-isoform, lowers plasma lipoproteins and cholesterol in hypercholesterolemic hamsters. J Agric Food Chem, 2005. 53(9): p. 3403-7.

10. Manickam, M., et al., Antihyperglycemic activity of phenolics from Pterocarpus marsupium. J Nat Prod, 1997. 60(6): p. 609-10.

11. Grover, J.K., V. Vats, and S.S. Yadav, Pterocarpus marsupium extract (Vijayasar) prevented the alteration in metabolic patterns induced in the normal rat by feeding an adequate diet containing fructose as sole carbohydrate. Diabetes Obes Metab, 2005. 7(4): p. 414-20.

12. Mao, X.Q., et al., Astragalus polysaccharide reduces hepatic endoplasmic reticulum stress and restores glucose homeostasis in a diabetic KKAy mouse model. Acta Pharmacol Sin, 2007. 28(12): p. 1947-56.

13. Schafer, A. and P. Hogger, Oligomeric procyanidins of French maritime pine bark extract (Pycnogenol) effectively inhibit alpha-glucosidase. Diabetes Res Clin Pract, 2007. 77(1): p. 41-6.

14. Kwak, C.J., et al., Antihypertensive effect of French maritime pine bark extract (Flavangenol): possible involvement of endothelial nitric oxide-dependent vasorelaxation. J Hypertens, 2009. 27(1): p. 92-101.

15. Xue, B., et al., Effect of total flavonoid fraction of Astragalus complanatus R.Brown on angiotensin II-induced portal-vein contraction in hypertensive rats. Phytomedicine, 2008.

16. Mizuno, C.S., et al., Design, synthesis, biological evaluation and docking studies of pterostilbene analogs inside PPARalpha. Bioorg Med Chem, 2008. 16(7): p. 3800-8.

17. Sato, M., et al., Dietary pine bark extract reduces atherosclerotic lesion development in male ApoE-deficient mice by lowering the serum cholesterol level. Biosci Biotechnol Biochem, 2009. 73(6): p. 1314-7.

18. Kimura, Y. and M. Sumiyoshi, French Maritime Pine Bark (Pinus maritima Lam.) Extract (Flavangenol) Prevents Chronic UVB Radiation-induced Skin Damage and Carcinogenesis in Melanin-possessing Hairless Mice. Photochem Photobiol, 2010.

19. Pavlou, P., et al., In-vivo data on the influence of tobacco smoke and UV light on murine skin. Toxicol Ind Health, 2009. 25(4-5): p. 231-9.

20. Ni, Z., Y. Mu, and O. Gulati, Treatment of melasma with Pycnogenol. Phytother Res, 2002. 16(6): p. 567-71.

21. Bito, T., et al., Pine bark extract pycnogenol downregulates IFN-gamma-induced adhesion of T cells to human keratinocytes by inhibiting inducible ICAM-1 expression. Free Radic Biol Med, 2000. 28(2): p. 219-27.

22. Rihn, B., et al., From ancient remedies to modern therapeutics: pine bark uses in skin disorders revisited. Phytother Res, 2001. 15(1): p. 76-8.

23. Saliou, C., et al., Solar ultraviolet-induced erythema in human skin and nuclear factor-kappa-B-dependent gene expression in keratinocytes are modulated by a French maritime pine bark extract. Free Radic Biol Med, 2001. 30(2): p. 154-60.

24. Van Wijk, E.P., R. Van Wijk, and S. Bosman, Using ultra-weak photon emission to determine the effect of oligomeric proanthocyanidins on oxidative stress of human skin. J Photochem Photobiol B, 2010. 98(3): p. 199-206.

25. Haskell, C.F., et al., The effects of L-theanine, caffeine and their combination on cognition and mood. Biol Psychol, 2008. 77(2): p. 113-22.

26. Owen, G.N., et al., The combined effects of L-theanine and caffeine on cognitive performance and mood. Nutr Neurosci, 2008. 11(4): p. 193-8.

27. Yamada, T., et al., Effects of theanine, a unique amino acid in tea leaves, on memory in a rat behavioral test. Biosci Biotechnol Biochem, 2008. 72(5): p. 1356-9.

28. Jia, R.Z., et al., [Neuroprotective effects of Astragulus membranaceus on hypoxia-ischemia brain damage in neonatal rat hippocampus]. Zhongguo Zhong Yao Za Zhi, 2003. 28(12): p. 1174-7.

29. Nathan, P.J., et al., The neuropharmacology of L-theanine(N-ethyl-L-glutamine): a possible neuroprotective and cognitive enhancing agent. J Herb Pharmacother, 2006. 6(2): p. 21-30.

30. Nobre, A.C., A. Rao, and G.N. Owen, L-theanine, a natural constituent in tea, and its effect on mental state. Asia Pac J Clin Nutr, 2008. 17 Suppl 1: p. 167-8.

31. Murakami, S., et al., Effects of oral supplementation with cystine and theanine on the immune function of athletes in endurance exercise: randomized, double-blind, placebo-controlled trial. Biosci Biotechnol Biochem, 2009. 73(4): p. 817-21.

32. Kawada, S., et al., Cystine and theanine supplementation restores high-intensity resistance exercise-induced attenuation of natural killer cell activity in well-trained men. J Strength Cond Res, 2010. 24(3): p. 846-51.

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Stem Cell 100 – Powerful Rejuvenation and Anti-Aging …

Recommendation and review posted by sam

Human chorionic gonadotropin – Wikipedia, the free …

Human chorionic gonadotropin (hCG) is a hormone produced by the embryo after implantation.[1][2] The presence of hCG is detected in some pregnancy tests (HCG pregnancy strip tests). Some cancerous tumors produce this hormone; therefore, elevated levels measured when the patient is not pregnant can lead to a cancer diagnosis and, if high enough, paraneoplastic syndromes. However, it is not known whether this production is a contributing cause or an effect of carcinogenesis. The pituitary analog of hCG, known as luteinizing hormone (LH), is produced in the pituitary gland of males and females of all ages.[1][3]

Regarding endogenous forms of hCG, there are various ways to categorize and measure them, including total hCG, C-terminal peptide total hCG, intact hCG, free -subunit hCG, -core fragment hCG, hyperglycosylated hCG, nicked hCG, alpha hCG, and pituitary hCG. Regarding pharmaceutical preparations of hCG from animal or synthetic sources, there are many gonadotropin preparations, some of which are medically justified and others of which are of a quack nature. As of December 6, 2011[update], the United States FDA has prohibited the sale of “homeopathic” and over-the-counter hCG diet products and declared them fraudulent and illegal.[4][5][6]

Human chorionic gonadotropin is a glycoprotein composed of 237 amino acids with a molecular mass of 25.7 kDa.[7]

It is heterodimeric, with an (alpha) subunit identical to that of luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), and (beta) subunit that is unique to hCG.

The two subunits create a small hydrophobic core surrounded by a high surface area-to-volume ratio: 2.8 times that of a sphere. The vast majority of the outer amino acids are hydrophilic.[7]

Human chorionic gonadotropin interacts with the LHCG receptor of the ovary and promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to secrete the hormone progesterone during the first trimester. Progesterone enriches the uterus with a thick lining of blood vessels and capillaries so that it can sustain the growing fetus[citation needed].

Due to its highly negative charge, hCG may repel the immune cells of the mother, protecting the fetus during the first trimester[citation needed]. It has also been hypothesized that hCG may be a placental link for the development of local maternal immunotolerance[citation needed]. For example, hCG-treated endometrial cells induce an increase in T cell apoptosis (dissolution of T cells). These results suggest that hCG may be a link in the development of peritrophoblastic immune tolerance, and may facilitate the trophoblast invasion, which is known to expedite fetal development in the endometrium.[10] It has also been suggested that hCG levels are linked to the severity of morning sickness or Hyperemesis gravidarum in pregnant women.[11]

Because of its similarity to LH, hCG can also be used clinically to induce ovulation in the ovaries as well as testosterone production in the testes. As the most abundant biological source is women who are presently pregnant, some organizations collect urine from pregnant women to extract hCG for use in fertility treatment.[12][13]

Human chorionic gonadotropin also plays a role in cellular differentiation/proliferation and may activate apoptosis.[14]

Naturally, it is produced in the human placenta by the syncytiotrophoblast.

Like other gonadotropins, it can be extracted from the urine of pregnant women or produced from cultures of genetically modified cells using recombinant DNA technology.

In Pregnyl, Follutein, Profasi, Choragon and Novarel, it is extracted from the urine of pregnant women. In Ovidrel, it is produced with recombinant DNA technology.[15]

Regarding endogenous forms of hCG, there are various ways to categorize and measure them, including total hCG, C-terminal peptide total hCG, intact hCG, free -subunit hCG, -core fragment hCG, hyperglycosylated hCG, nicked hCG, alpha hCG, and pituitary hCG.

Regarding pharmaceutical preparations of hCG from animal or synthetic sources, there are many gonadotropin preparations, some of which are medically justified and others of which are of a quack nature.

Blood or urine tests measure hCG. These can be pregnancy tests. hCG-positive indicates an implanted blastocyst and mammalian embryogenesis. These can be done to diagnose and monitor germ cell tumors and gestational trophoblastic diseases.

Concentrations are commonly reported in thousandth international units per milliliter (mIU/ml). The international unit of hCG was originally established in 1938 and has been redefined in 1964 and in 1980.[16] At the present time, 1 international unit is equal to approximately 2.351012 moles,[17] or about 6108 grams.[18]

Most tests employ a monoclonal antibody, which is specific to the -subunit of hCG (-hCG). This procedure is employed to ensure that tests do not make false positives by confusing hCG with LH and FSH. (The latter two are always present at varying levels in the body, whereas the presence of hCG almost always indicates pregnancy.)

Many hCG immunoassays are based on the sandwich principle, which uses antibodies to hCG labeled with an enzyme or a conventional or luminescent dye. Pregnancy urine dipstick tests are based on the lateral flow technique.

The following is a list of serum hCG levels. (LMP is the last menstrual period dated from the first day of your last period.) The levels grow exponentially after conception and implantation.

The ability to quantitate the hCG level is useful in the monitoring germ cell and trophoblastic tumors, follow-up care after miscarriage, and in diagnosis of and follow-up care after treatment of ectopic pregnancy. The lack of a visible fetus on vaginal ultrasound after the hCG levels have reached 1500 mIU/ml is strongly indicative of an ectopic pregnancy.[21] Still, even an hCG over 2000 IU/l does not necessarily exclude the presence of a viable intrauterine pregnancy in such cases.[22]

As pregnancy tests, quantitative blood tests and the most sensitive urine tests usually detect hCG between 6 and 12 days after ovulation.[23] However, it must be taken into account that total hCG levels may vary in a very wide range within the first 4 weeks of gestation, leading to false results during this period.[24] A rise of 35% over 48 hours is proposed as the minimal rise consistent with a viable intrauterine pregnancy.[22]

Gestational trophoblastic disease like hydatidiform moles (“molar pregnancy”) or choriocarcinoma may produce high levels of hCG (due to the presence of syncytialtrophoblasts- part of the villi that make up the placenta) despite the absence of an embryo. This, as well as several other conditions, can lead to elevated hCG readings in the absence of pregnancy.

hCG levels are also a component of the triple test, a screening test for certain fetal chromosomal abnormalities/birth defects.

A study of 32 normal pregnancies came to the result a gestational sac of 13mm was detected at a mean hCG level of 1150 UI/l (range 800-1500), a yolk sac was detected at a mean level of 6000 UI/l (range 4500-7500) and fetal heartbeat was visible at a mean hCG level of 10,000 UI/l (range 8650-12,200).[25]

Human chorionic gonadotropin can be used as a tumor marker,[26] as its subunit is secreted by some cancers including seminoma, choriocarcinoma, germ cell tumors, hydatidiform mole formation, teratoma with elements of choriocarcinoma, and islet cell tumor. For this reason a positive result in males can be a test for testicular cancer. The normal range for men is between 0-5 mIU/mL. Combined with alpha-fetoprotein, -HCG is an excellent tumor marker for the monitoring of germ cell tumors.[citation needed]

Human chorionic gonadotropin is extensively used parenterally for final maturation induction in lieu of luteinizing hormone. In the presence of one or more mature ovarian follicles, ovulation can be triggered by the administration of HCG. As ovulation will happen between 38 and 40 hours after a single HCG injection,[27] procedures can be scheduled to take advantage of this time sequence,[28] such as intrauterine insemination or sexual intercourse. Also, patients that undergo IVF, in general, receive HCG to trigger the ovulation process, but have an oocyte retrieval performed at about 34 to 36 hours after injection by, a few hours before the eggs actually would be released from the ovary.

As HCG supports the corpus luteum, administration of HCG is used in certain circumstances to enhance the production of progesterone.

In the male, HCG injections are used to stimulate the Leydig cells to synthesize testosterone. The intratesticular testosterone is necessary for spermatogenesis from the sertoli cells. Typical uses for HCG in men include hypogonadism and fertility treatment.

Several vaccines against human chorionic gonadotropin (hCG) for the prevention of pregnancy are currently in clinical trials.[29]

In the case of female patients who want to be treated with HCG Pregnyl:[30] a) Since infertile female patients who undergo medically assisted reproduction (especially those who need in vitro fertilization), are known to often be suffering from tubal abnormalities, after a treatment with this drug they might experience many more ectopic pregnancies. This is why early ultrasound confirmation at the beginning of a pregnancy (to see whether the pregnancy is intrauterine or not) is crucial. – Pregnancies that have occurred after a treatment with this medicine are submitted to a higher risk of multiplets. – Female patients who have thrombosis, severe obesity or thrombophilia should not be prescribed this medicine as they have a higher risk of arterial or venous thromboembolic events after or during a treatment with HCG Pregnyl. b)Female patients who have been treated with this medicine are usually more prone to pregnancy losses.

In the case of male patients: A prolonged treatment with HCG Pregnyl is known to regularly lead to increased production of androgen. Therefore: Patients who are suffering from overt or latent cardiac failure, hypertension, renal dysfunction, migraines or epilepsy might not be allowed to start using this medicine or may require a lower dose of HCG Pregnyl. Also this medicine should be used with extreme caution in the treatment of prepubescent teenagers in order to reduce the risk of precocious sexual development or premature epiphyseal closure. This type of patients’ skeletal maturation should be closely and regularly monitored.

Both male and female patients who have the following medical conditions must not start a treatment with HCG Pregnyl: (1) Hypersensitivity to this medicine or to any of its main ingredients. (2) Known or possible androgen-dependent tumors for example male breast carcinoma or prostatic carcinoma.

In the world of performance-enhancing drugs, HCG is increasingly used in combination with various anabolic androgenic steroid (AAS) cycles. As a result, HCG is included in some sports’ illegal drug lists.

When exogenous AAS are put into the male body, natural negative-feedback loops cause the body to shut down its own production of testosterone via shutdown of the hypothalamic-pituitary-gonadal axis (HPGA). This causes testicular atrophy, among other things. HCG is commonly used during and after steroid cycles to maintain and restore testicular size as well as normal testosterone production.[31]

High levels of AASs, that mimic the body’s natural testosterone, trigger the hypothalamus to shut down its production of gonadotropin-releasing hormone (GnRH) from the hypothalamus. Without GnRH, the pituitary gland stops releasing luteinizing hormone (LH). LH normally travels from the pituitary via the blood stream to the testes, where it triggers the production and release of testosterone. Without LH, the testes shut down their production of testosterone.[32] In males, HCG helps restore and maintain testosterone production in the testes by mimicking LH and triggering the production and release of testosterone.

If HCG is used for too long and in too high a dose, the resulting rise in natural testosterone would eventually inhibit its own production via negative feedback on the hypothalamus and pituitary gland.[citation needed]

Professional athletes who have tested positive for HCG have been temporarily banned from their sport, including a 50-game ban from MLB for Manny Ramirez in 2009[33] and a 4-game ban from the NFL for Brian Cushing for a positive urine test for HCG.Mixed Martial Arts fighter Dennis Siver was fined $19,800 and suspended 9 months for being tested positive after his bout at UFC 168.[35]

British endocrinologist Albert T. W. Simeons proposed HCG as an adjunct to an ultra-low-calorie weight-loss diet (fewer than 500 calories).[36] Simeons, while studying pregnant women in India on a calorie-deficient diet, and “fat boys” with pituitary problems (Frlich’s syndrome) treated with low-dose HCG, observed that both lost fat rather than lean (muscle) tissue.[36] He reasoned that HCG must be programming the hypothalamus to do this in the former cases in order to protect the developing fetus by promoting mobilization and consumption of abnormal, excessive adipose deposits. Simeons in 1954 published a book entitled Pounds and Inches, designed to combat obesity. Simeons, practicing at Salvator Mundi International Hospital in Rome, Italy, recommended low-dose daily HCG injections (125IU) in combination with a customized ultra-low-calorie (500 cal/day, high-protein, low-carbohydrate/fat) diet, which was supposed to result in a loss of adipose tissue without loss of lean tissue.[36]

Simeons’ results were not reproduced by other researchers and in 1976 in response to complaints the FDA required Simeons and others to include the following disclaimer on all advertisements:[37]

These weight reduction treatments include the injection of HCG, a drug which has not been approved by the Food and Drug Administration as safe and effective in the treatment of obesity or weight control. There is no substantial evidence that HCG increases weight loss beyond that resulting from caloric restriction, that it causes a more attractive or “normal” distribution of fat, or that it decreases the hunger and discomfort associated with calorie-restrictive diets.

1976 FDA-mandated disclaimer for HCG diet advertisements

There was a resurgence of interest in the “HCG diet” following promotion by Kevin Trudeau who was later banned from making HCG diet weight-loss claims by the U.S. Federal Trade Commission and eventually jailed over such claims.[38]

While not specifically cited here, review studies refuting the HCG diet have been published in the Journal of the American Medical Association and the American Journal of Clinical Nutrition,[39] concluded that HCG is not more effective as a weight-loss aid than dietary restriction alone.[40]

A meta analysis found that studies supporting HCG for weight loss were of poor methodological quality and concluded that “there is no scientific evidence that HCG is effective in the treatment of obesity; it does not bring about weight-loss or fat-redistribution, nor does it reduce hunger or induce a feeling of well-being”.[41]

There is no scientific evidence that HCG is effective in the treatment of obesity. The meta-analysis found insufficient evidence supporting the claims that HCG is effective in altering fat-distribution, hunger reduction or in inducing a feeling of well-being. The authors stated the use of HCG should be regarded as an inappropriate therapy for weight reduction In the authors opinion, Pharmacists and physicians should be alert on the use of HCG for Simeons therapy. The results of this meta-analysis support a firm standpoint against this improper indication. Restraints on physicians practicing this therapy can be based on our findings.

According to the American Society of Bariatric Physicians, no new clinical trials have been published since the definitive 1995 meta-analysis.[42]

The scientific consensus is that any weight loss reported by individuals on an “HCG diet” may be attributed entirely to the fact that such diets prescribe calorie intake of between 500 and 1,000 calories per day, substantially below recommended levels for an adult, to the point that this may risk health effects associated with malnutrition.[43]

Controversy about, and shortages[44] of, injected HCG for weight loss have led to substantial Internet promotion of “homeopathic HCG” for weight control. The ingredients in these products are often obscure, but if prepared from true HCG via homeopathic dilution, they contain either no HCG at all or only trace amounts. Moreover, it is highly unlikely that oral HCG is bioavailable due to the fact that digestive protease enzymes and hepatic metabolism renders peptide-based molecules (such as insulin and human growth hormone) biologically inert. HCG can likely only enter the bloodstream through injection.

The United States Food and Drug Administration has stated that over-the-counter products containing HCG are fraudulent and ineffective for weight loss. They are also not protected as homeopathic drugs and have been deemed illegal substances.[45][46] HCG itself is classified as a prescription drug in the United States and it has not been approved for over-the-counter sales by the FDA as a weight loss product or for any other purposes, and therefore neither HCG in its pure form nor any preparations containing HCG may be sold legally in the country except by prescription.[4] In December 2011, FDA and FTC started to take actions to pull unapproved HCG products from the market.[4] In the aftermath, some suppliers started to switch to “hormone-free” versions of their weight loss products, where the hormone is replaced with an unproven mixture of free amino acids[47] or where radionics is used to transfer the “energy” to the final product.

In order to induce a stronger immune response, some versions of human chorionic gonadotropin based anti-fertility vaccines were designed as conjugates of the subunit of HCG covalently linked to tetanus toxoid.[29][48] It has been alleged that a non-conguated tetanus vaccine used in developing countries is laced with a human chorionic gonadotropin based anti-fertility drug[49] and is distributed as a means of mass sterilization.[50] This charge has been vigorously denied by the World Health Organization (WHO) and UNICEF.[51] Others have argued that a hCG laced vaccine could not be used for sterilization since the effects of the anti-fertility vaccines are reversible (requiring booster doses to maintain immunity) and a non-conjugated vaccine is likely to be ineffective.[52][53] Finally, independent testing of the tetanus vaccine by Kenyas health authorities has revealed no traces of the human chorionic gonadotropin hormone.[54]

PDB gallery

1hcn: STRUCTURE OF HUMAN CHORIONIC GONADOTROPIN AT 2.6 ANGSTROMS RESOLUTION FROM MAD ANALYSIS OF THE SELENOMETHIONYL PROTEIN

1hrp: CRYSTAL STRUCTURE OF HUMAN CHORIONIC GONADOTROPIN

1qfw: TERNARY COMPLEX OF HUMAN CHORIONIC GONADOTROPIN WITH FV ANTI ALPHA SUBUNIT AND FV ANTI BETA SUBUNIT

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Recommendation and review posted by sam

Diagnosis of Hypogonadism: Clinical Assessments and …

Rev Urol. 2004; 6(Suppl 6): S3S8.

Auxilium Pharmaceuticals, Inc., Norristown, PA

Hypogonadism can be of hypothalamic-pituitary origin or of testicular origin, or a combination of both, which is increasingly common in the aging male population. In the postpubertal male, testosterone replacement therapy can be used to treat the signs and symptoms of low testosterone, which include loss of libido, erectile dysfunction, diminished intellectual capacity, depression, lethargy, osteoporosis, loss of muscle mass and strength, and some regression of secondary sexual characteristics. Before initiation of testosterone replacement therapy, an examination of the prostate and assessment of prostate symptoms should be performed, and both the hematocrit and lipid profile should be measured. Absolute contraindications to testosterone replacement therapy are prostate or breast cancer, a hematocrit of 55% or greater, or sensitivity to the testosterone formulation.

Key words: Hypogonadism, Testosterone replacement therapy, Serum hormone-binding globulin, Luteinizing hormone, Follicle-stimulating hormone

Hypogonadism is a lack of testosterone in male patients and can be of central (hypothalamic or pituitary) or testicular origin, or a combination of both. Hypogonadism in male patients with testicular failure due to genetic disorders (eg, Klinefelters syndrome), orchitis, trauma, radiation, chemotherapy, or undescended testes, is known as hypergonadotropic hypogonadism or primary hypogonadism. Hypogonadism in male patients with gonadotropin deficiency or dysfunction as a result of disease or damage to the hypothalamic-pituitary axis is known as hypogonadotropic hypogonadism, central hypogonadism, or secondary hypogonadism. This might be due to Kallmanns syndrome, tumor, trauma, radiation, sarcoidosis, or tuberculosis. In addition, men older than 50 years might have low testosterone levels with functional abnormalities at multiple levels of the hypothalamic-pituitary-testicular axis.1,2,3

The prevalence of hypogonadism has increased in recent years. It has been reported that 12%, 19%, 28%, and 49% of men greater than 50, 60, 70, or 80 years of age, respectively, fit the criteria of hypogonadism.4

During puberty, testosterone is required for the development of male secondary sexual characteristics, stimulation of sexual behavior and function, and initiation of sperm production.5,6 In adult males, testosterone is involved in maintaining muscle mass and strength, fat distribution, bone mass, red blood cell production, male hair pattern, libido and potency, and spermatogenesis.13,5,6

In men, the major gonadal steroid hormone is testosterone. Testosterone circulates in 3 major forms: unbound, or free, testosterone; tightly bound testosterone, which is bound to sex hormone-binding globulin (SHBG); and weakly bound testosterone, which is bound to albumin. Only free and weakly bound testosterone is bioavailable or able to bind to the androgen receptor.2,3

In males, serum testosterone levels show a circadian variation, with the highest levels in the morning and lowest levels in the late afternoon. In young men, the variation in testosterone levels is approximately 35%. Although the normal range for serum testosterone might vary between different laboratories, the normal range for early morning total testosterone in healthy adult males is approximately 300 ng/dL to 1000 ng/dL.7,8

To determine whether a patient is testosterone deficient, a clinician must consider clinical signs and symptoms in conjunction with laboratory values. The initial clinical picture will vary depending on the age of the patient at the onset of the disorder.

In the normal male, the start of puberty is apparent by enlargement of the testes and the appearance of pubic hair, followed by the appearance of auxiliary and facial hair. At puberty there is also increased penile length and the onset of spermatogenesis. If signs of puberty are not evident in boys by 14 years of age, a workup for delayed puberty is warranted.

In the prepubertal age group, hypogonadism might be either primary hypogonadism or secondary hypogonadism. To differentiate primary from secondary hypogonadism, early morning luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels must be obtained. Because LH and FSH are secreted during the early morning at the beginning of puberty, it is necessary to measure these hormones in the early morning (8:0010:00 AM). Primary hypogonadism is associated with low levels of testosterone and high-normal to high levels of LH and FSH. Secondary hypogonadism is associated with low levels of testosterone and normal to low levels of LH and FSH.5,6

The signs and symptoms of low testosterone in postpubertal adult males can be more difficult to diagnose and might include loss of libido, erectile dysfunction, diminished intellectual capacity, depression, lethargy, osteoporosis, loss of muscle mass and strength, and some regression of secondary sexual characteristics.13 At the initial visit, the first objective is to distinguish between primary gonadal failure, in which low testosterone is accompanied by increased FSH and increased LH, and hypothalamic-pituitary disorders (secondary hypogonadism), with low testosterone and low to normal FSH and LH levels.

Initial laboratory testing should include early morning (8:0010:00 AM) measurement of serum testosterone, prolactin, FSH, and LH levels. For the diagnosis of primary hypogonadism, FSH measurement is particularly important because FSH has a longer half life, is more sensitive, and demonstrates less variability than LH.2,3

The aging male patient can present with signs and symptoms of low testosterone, including loss of libido, erectile dysfunction, diminished intellectual capacity, depression, lethargy, osteoporosis, and loss of muscle mass and strength.13 At the initial visit, laboratory testing should include early morning (8:0010:00 AM) measurement of serum testosterone. In elderly men, testosterone levels decrease between 15% and 20% over the course of 24 hours.8

Total testosterone levels might be normal with hypogonadism if the SHBG levels are increased.79 Levels of SHBG increase with age, causing a decrease in bioavailable testosterone.9 If testosterone levels are low-normal but the clinical symptoms and signs indicate hypogonadism, measurement of serum total testosterone levels should be repeated and an SHBG level should be determined. With the total testosterone and SHBG levels, a bioavailable testosterone value can be calculated. A bioavailable testosterone calculator is available at http://www.issam.ch/freetesto.htm.

It is usually not necessary to determine FSH or LH levels in the aging male.

It is well accepted that testosterone levels should be measured in the early morning, when they are at their peak level. However, in community practice the choice of which testosterone parameter to measure is still debatable.

Total testosterone assay is widely available and inexpensive to perform. Although the ranges and methods vary, physicians can consult their local laboratories for the applicable values in their clinical practice. Total testosterone values, however, must be interpreted carefully in the aging male because SHBG levels might be elevated. If the total testosterone level is normal in the aging male presenting signs of hypogonadism, the clinician can measure free testosterone or measure SHBG and calculate bioavailable testosterone.9

Free testosterone can be measured by equilibrium dialysis or ultrafiltration, which are difficult to perform and largely unavailable but reliable. In contrast, the radioimmunoassay for free testosterone is widely available but unreliable. Because total testosterone and SHBG assays are readily available and cheap, calculating bioavailable testosterone might be a good compromise. Whichever method is chosen, if the early morning testosterone level is at or below the lower limit of normal for the individual laboratory, then a repeat measurement of the early morning testosterone level should be performed to confirm the result. Because testosterone is secreted in a pulsatile fashion, it is important to obtain 2 early morning testosterone levels.

In selected patients, FSH, LH, and prolactin can be measured. If the FSH and LH levels are raised, this suggests a primary testicular cause, and if levels are low or normal, a hypothalamic or pituitary cause should be considered. A raised prolactin level suggests that further investigation of the pituitary gland should be undertaken.1,2

The clinical signs and symptoms of hypogonadism will vary depending on whether the patient presents before or after puberty. Depending on the age of the patient, the degree of pubertal development is important for establishing the differential diagnosis.

Boys aged 14 years or older should be suspected of being hypogonadal if on examination they have underdeveloped testes, lack of penile enlargement, and absence of pubic, auxiliary, and facial hair.

In patients with primary hypogonadism, history might reveal the cause for primary testicular failure, such as familial autoimmune disease, physical trauma to the testes, or trauma to the testes caused by radiation, chemotherapy, or infection.

A karyotype should be obtained to diagnose chromosomal abnormalities, such as Klinefelters syndrome, and a physical examination will reveal small or absent testes resulting from anorchia, Noonans syndrome, or other testicular disorders.

Hypothalamic or pituitary deficiency might be transitory or permanent. Transient secondary hypogonadism might be related to malnutrition or stress states and can be diagnosed by physical examination and evaluation of the patients growth chart. If permanent hypothalamic or pituitary hormone deficiency is suspected, serum levels of pituitary hormones and magnetic resonance imaging of the brain and pituitary should be obtained to screen for hypothalamic or pituitary disease.

If both physical examination and serum chemistry tests are normal, then by exclusion a diagnosis of constitutional pubertal delay must be considered.

To establish a diagnosis of hypogonadism, it is important to take a careful history to determine whether there have been major medical problems, toxic exposure, concomitant drug therapy that might cause hypogonadism, or fertility problems.

Low libido, impotence, fatigue, impaired concentration, and sexual dysfunction are important clinical problems that might not be raised by the patient in the clinic. Therefore, these symptoms need to be asked about specifically if hypogonadism is suspected.13

Formal assessment of intellectual changes, mood, and cognitive changes can be performed. Changes in lean body mass will be apparent from the medical history and examination, as will changes in hair, skin, and fat distribution. Decreases in bone mineral density might be apparent from a history of recent fractures but can only be confirmed by dual energy x-ray absorptiometry (DEXA).1

Physical examination should include testicular examination, including size and consistency. The distribution and amount of body hair should also be noted. Penile size is not affected by postpubertal testosterone deficiency. An assessment of the prostate by digital rectal examination (DRE) should be performed and a prostate-specific antigen (PSA) value obtained.3

To establish a diagnosis of hypogonadism in the aging male, it is important to assess the patient carefully for signs and symptoms. Low libido, impotence, fatigue, impaired concentration, and sexual dysfunction are important clinical problems that might not be raised by the patient in the clinic, especially by an aging patient. Therefore, as with the younger postpubertal patient, these symptoms need to be asked about specifically if hypogonadism is suspected.1,2 As with the postpubertal patient (see previous section), changes in intellectual functioning; mood; lean body mass; and hair, skin, and fat distribution should all be assessed, and DEXA can be used to confirm decreases in bone mineral density.1

In older patients, an important part of the physical examination includes an assessment of the prostate by DRE and PSA assay. In addition, an assessment of prostate-related symptoms should be undertaken. The presence of gynecomastia or carcinoma of the breast are important physical findings.

In cases of primary and permanent secondary hypogonadism diagnosed in the prepubertal male, life long testosterone treatment is needed. The usual treatment is initiation of therapy with small doses of testosterone (50100 mg IM) every 3 to 4 weeks at the appropriate psychosocial stage in development. When a final adult height is thought to have been obtained, the adult dose of testosterone replacement is inaugurated.

In the postpubertal period, once the diagnosis of testosterone deficiency has been made, replacement therapy should be considered in light of the clinical signs and symptoms in conjunction with the laboratory values. The objective of testosterone replacement therapy is to normalize serum testosterone and maintain the level within the eugonadal state. In addition, treatment objectives might include improving sexual dysfunction, intellectual capacity, depression, and lethargy; maintaining bone mineral density and possibly reducing fracture risk; increasing muscle mass and strength; and enhancing the quality of life.13,9

Although the normal range for serum testosterone might vary between different laboratories, the normal range for early morning testosterone in male adults is approximately 300 ng/dL to 1000 ng/dL.7 An early morning total serum testosterone level of less than 300 ng/dL clearly indicates hypogonadism, and under most circumstances benefit will be derived from testosterone replacement therapy. A healthy male adult patient with a serum testosterone level greater than 400 ng/dL is unlikely to be testosterone deficient, and therefore clinical judgment should be exercised if he has symptoms suggestive of testosterone deficiency.

There are some absolute contraindications to testosterone replacement therapy. These include prostate cancer, which must be assessed by history and clinical examination. If on DRE the prostate is enlarged or if the PSA level is greater than 4.0 ng/mL, biopsy of the prostate should be undertaken to confirm a diagnosis of prostate cancer or benign prostatic hyperplasia (BPH).3

An existing or prior history of breast cancer is also an absolute contraindication to testosterone replacement therapy. Testosterone therapy is known to increase the hematocrit, and therefore a pre-existing hematocrit of 55% or greater is an absolute contraindication to replacement therapy.

Sensitivity to any of the ingredients in the testosterone formulation would also be an absolute contraindication. Relative contraindications include an increased hematocrit, untreated sleep apnea, severe obstructive symptoms of BPH, and advanced congestive cardiac failure.2,3

The goal of replacement therapy is to maintain testosterone in the normal physiological range; therefore, a combination of clinical and biochemical measures should be monitored 6 to 12 weeks after initiating therapy. In most cases, an early morning serum total testosterone level is adequate to determine whether dosage adjustment is necessary. However, patients receiving injections of testosterone enanthate or cypionate every 2 weeks will require an earlier measurement of serum testosterone at 1 to 2 weeks after commencement of therapy.3

Examination of the prostate should be performed routinely, although the exact frequency after initiation of testosterone replacement is still debatable. Digital rectal examination of the prostate and PSA assay should be performed before initiation of therapy, along with an assessment of prostate-related symptoms. In elderly men, a DRE and PSA assay should be performed at 3 and 6 months after commencing testosterone therapy and then annually thereafter.3 A high PSA level should be further evaluated with a highly specific PSA assay, if available. A patient should be referred to a urologist if his PSA level increases over time or if he has a PSA level greater than 4.0 ng/mL.3

It is known that testosterone stimulates bone marrow production of erythrocytes, which might result in an increased hematocrit in some men, and therefore this should be checked at the same time as the PSA level.2,3

Lipid disturbances in testosterone-treated male patients are generally not a problem because the ratio of high-density lipoprotein to total cholesterol usually remains constant. An initial lipid profile should be performed before therapy, and a follow-up profile should be obtained after 6 to 12 months of therapy and annually thereafter.3

Hypogonadism can be of hypothalamic-pituitary origin or of testicular origin, or a combination of both, which is increasingly common in the aging male population. It can be easily diagnosed with measurement of the early morning serum total testosterone level, which should be repeated if the value is low. Follicle-stimulating hormone, LH, and prolactin might also need to be measured. If the clinical signs and symptoms suggest hypogonadism but the serum testosterone level is near normal, then assay of serum testosterone should be repeated in conjunction with SHBG because serum testosterone might be normal in the presence of hypogonadism if the SHBG level is raised, which commonly occurs in elderly male patients.

Before initiation of testosterone replacement therapy, an examination of the prostate, including DRE, PSA assay, and assessment of prostate symptoms should be undertaken, and both the hematocrit and lipid profile should be measured. There are few absolute contraindications to testosterone replacement therapy other than prostate or breast cancer, a hematocrit of 55% or greater, or sensitivity to the testosterone formulation. Monitoring of the prostate (assessed with DRE and PSA assay) and hematocrit and lipid profile should be repeated during testosterone replacement therapy.

The benefits of testosterone replacement therapy may include restoring metabolic parameters to the eugonadal state; improving psychosexual function and intellectual capacity, including depression and lethargy; maintaining bone mineral density and reducing bone fractures; improving muscle mass and strength; and enhancing quality of life.

Hypogonadism is a lack of testosterone in male patients and can be of central (hypothalamic or pituitary) or testicular origin, or a combination of both.

Boys ages 14 years or older should be suspected of being hypogonadal if on examination they have underdeveloped testes, a lack of penile enlargement, and an absence of pubic, auxiliary, and facial hair.

In pre- and postpubertal male patients, primary hypogonadism is associated with low levels of testosterone and high-normal to high levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH); secondary hypogonadism is associated with low levels of testosterone and normal to low levels of LH and FSH.

In the aging male patient, signs and symptoms of hypogonadism can include loss of libido, erectile dysfunction, diminished intellectual capacity, depression, lethargy, osteoporosis, and loss of muscle mass and strength.

For aging men, laboratory testing should include early morning (8:0010:00 AM) measurement of serum testosterone; levels less than 300 ng/dL clearly indicate hypogonadism, and under most circumstances benefit will be derived from testosterone replacement therapy.

Before initiation of testosterone replacement therapy, an examination of the prostate and assessment of prostate symptoms should be performed, and both the hematocrit and lipid profile should be measured.

There are few absolute contraindications to testosterone replacement therapy other than prostate or breast cancer, a hematocrit of 55% or greater, or sensitivity to the testosterone formulation.

1. AACE Hypogonadism Task Force. Endocr Pract. 2002;8:439456.

5. Griffin JE, Wilson JD. Endocrinology & Metabolism. 15th Ed. Vol. 335. New York, NY: McGraw Hill; 2001. Disorders of the testes. Harrisons principles of internal medicine; pp. 21432154.

6. Beers MH, Berkow R, editors. The Merck Manual of Diagnosis and Therapy. 17th ed. New York, NY: John Wiley & Sons; 1999.

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Diagnosis of Hypogonadism: Clinical Assessments and …

Recommendation and review posted by simmons

Genetics and Cancer | American Cancer Society

Some types of cancer run in certain families, but most cancers are not clearly linked to the genes we inherit from our parents. Gene changes that start in a single cell over the course of a person’s life cause most cancers. In this section you can learn more about the complex links between genes and cancer.

Cancer is such a common disease that it is no surprise that many families have at least a few members who have had cancer. Sometimes, certain types of cancer seem to run in some families. But only a small portion of all cancers are inherited. This document focuses on those cancers.

Advances in genetics and molecular biology have improved our knowledge of the inner workings of cells, the basic building blocks of the body. Here we review how cells can change during a persons life to become cancer, how certain types of changes can build on inherited gene changes to speed up the development of cancer, and how this information can help us better prevent and treat cancer.

Genetic testing can be useful for people with certain types of cancer that seem to run in their families, but these tests aren’t recommended for everyone. Here we offer basic information to help you understand what genetic testing is and how it is used in cancer.

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Genetics and Cancer | American Cancer Society

Recommendation and review posted by sam

Directory of Innovative Anti-Aging Doctors, Health And …

The directory of Innovative Doctors and Health Practitioners is a worldwide listing of anti-aging doctors and other medical professionals who practice or have expressed interest in all aspects of preventive medicine (such as heart attack and stroke prevention), hormone replacement therapy, nutrition and dietary supplements, and other areas of alternative and complementary medicine. Invariably, they welcome individuals who choose to be involved in their own health care.

Provided to you by Extension, the directory of Innovative Doctors and Health Practitioners facilitates the location of anti-aging doctors and health practitioners who are open to alternatives to allopathic medicine. Conveniently organized geographically, the listing can be used to find a doctor by areaa handy feature for those who are traveling or are simply seeking out anti-aging doctors or health practitioners at home. The directory of Innovative Doctors and Health Practitioners is especially useful for those on a life extension program that includes the use of dietary supplements and hormones, as the listed physicians and health practitioners would likely be more suited to evaluate such a program than more conventional doctors.

While prevention, nutrition and longevity are important to the physicians and health practitioners listed, each of them has their own approach to health and wellness. So be sure to clarify the reason for your visit, as well as your goals in seeking out such treatment when scheduling your appointment.

ALABAMA ALASKA AMERICAN SAMOA ARIZONA ARKANSAS ARMED FORCES AMERICAS ARMED FORCES EUROPE ARMED FORCES PACIFIC CALIFORNIA COLORADO CONNECTICUT DELAWARE DISTRICT OF COLUMBIA FLORIDA GEORGIA GUAM HAWAII IDAHO ILLINOIS INDIANA IOWA KANSAS KENTUCKY LOUISIANA MAINE MARSHALL ISLANDS MARYLAND MASSACHUSETTS MICHIGAN MICRONESIA FED STATES MINNESOTA MISSISSIPPI MISSOURI MONTANA NEBRASKA NEVADA NEW HAMPSHIRE NEW JERSEY NEW MEXICO NEW SOUTH WALES NEW YORK NORTH CAROLINA NORTH DAKOTA NORTHERN MARIANA ISLANDS OHIO OKLAHOMA OREGON PALAU PENNSYLVANIA PLEASE SELECT PUERTO RICO RHODE ISLAND SOUTH AUSTRALIA SOUTH CAROLINA SOUTH DAKOTA TASMANIA TENNESSEE TEXAS UTAH VERMONT VICTORIA VIRGIN ISLANDS VIRGINIA WASHINGTON WEST VIRGINIA WISCONSIN WYOMING

DISCLAIMER: Inclusion in the directory of Innovative Doctors and Health and Wellness Practitioners does not constitute endorsement by Life Extension, nor are these physicians or other health practitioners affiliated with Life Extension. All physicians and health practitioners who appear on this list do so on the sole basis of their own expression of interest in the fields of health and wellness, longevity, or preventive medicine. Life Extension has not verified the competence, professional credentials, business practices or validity of the expressed interests of these physicians and health practitioners. Life Extension makes no recommendation of any physician or health practitioner on this list and makes no suggestion that any such physician or health practitioner will cure or prevent any disease, reduce anyone’s rate of aging or extend anyone’s life. Those consulting a physician or other health practitioner on this list should approach the consultation exactly as they would with any other unknown physician or health practitioner. Listings are periodically updated. However, physicians and health practitioners are not obligated to notify Life Extension should they relocate or retire. Life Extension relies in great part on feedback, which determines the continued eligibility of the physicians and health practitioners listed. Please contact Life Extension if you have any comments concerning any of the physicians or other health practitioners on this list.

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Directory of Innovative Anti-Aging Doctors, Health And …

Recommendation and review posted by Bethany Smith

Autologous mesenchymal stem cells produce concordant …

RATIONALE:

Although accumulating data support the efficacy of intramyocardial cell-based therapy to improve left ventricular (LV) function in patients with chronic ischemic cardiomyopathy undergoing CABG, the underlying mechanism and impact of cell injection site remain controversial. Mesenchymal stem cells (MSCs) improve LV structure and function through several effects including reducing fibrosis, neoangiogenesis, and neomyogenesis.

To test the hypothesis that the impact on cardiac structure and function after intramyocardial injections of autologous MSCs results from a concordance of prorecovery phenotypic effects.

Six patients were injected with autologous MSCs into akinetic/hypokinetic myocardial territories not receiving bypass graft for clinical reasons. MRI was used to measure scar, perfusion, wall thickness, and contractility at baseline, at 3, 6, and 18 months and to compare structural and functional recovery in regions that received MSC injections alone, revascularization alone, or neither. A composite score of MRI variables was used to assess concordance of antifibrotic effects, perfusion, and contraction at different regions. After 18 months, subjects receiving MSCs exhibited increased LV ejection fraction (+9.4 1.7%, P=0.0002) and decreased scar mass (-47.5 8.1%; P

Intramyocardial injection of autologous MSCs into akinetic yet nonrevascularized segments produces comprehensive regional functional restitution, which in turn drives improvement in global LV function. These findings, although inconclusive because of lack of placebo group, have important therapeutic and mechanistic hypothesis-generating implications.

http://clinicaltrials.gov/show/NCT00587990. Unique identifier: NCT00587990.

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Autologous mesenchymal stem cells produce concordant …

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Genome Therapy of Myotonic Dystrophy Type 1 iPS Cells for …

Myotonic dystrophy type 1 (DM1) is caused by expanded Cytosine-Thymine-Guanine (CTG) repeats in the 3′-untranslated region (3′ UTR) of the Dystrophia myotonica protein kinase (DMPK) gene, for which there is no effective therapy. The objective of this study is to develop genome therapy in human DM1 induced pluripotent stem (iPS) cells to eliminate mutant transcripts and reverse the phenotypes for developing autologous stem cell therapy. The general approach involves targeted insertion of polyA signals (PASs) upstream of DMPK CTG repeats, which will lead to premature termination of transcription and elimination of toxic mutant transcripts. Insertion of PASs was mediated by homologous recombination triggered by site-specific transcription activator-like effector nuclease (TALEN)-induced double-strand break. We found genome-treated DM1 iPS cells continue to maintain pluripotency. The insertion of PASs led to elimination of mutant transcripts and complete disappearance of nuclear RNA foci and reversal of aberrant splicing in linear-differentiated neural stem cells, cardiomyocytes, and teratoma tissues. In conclusion, genome therapy by insertion of PASs upstream of the expanded DMPK CTG repeats prevented the production of toxic mutant transcripts and reversal of phenotypes in DM1 iPS cells and their progeny. These genetically-treated iPS cells will have broad clinical application in developing autologous stem cell therapy for DM1.Molecular Therapy (2016); doi:10.1038/mt.2016.97.

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Genome Therapy of Myotonic Dystrophy Type 1 iPS Cells for …

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HIV and Testosterone Deficiency – verywell.com

Testosterone deficiency is frequently seen in both men and women with HIV. Endocrine abnormalities, which can affect testosterone production, have long been recognized as a complication of HIV since the earliest days of the pandemic (although it has generally been associated with late stage disease).

However, recent research has shown that nearly one out of every five men with HIV has documented testosterone deficiency, irrespective of CD4 count, viral load, or treatment status.

Similarly, testosterone deficiency is seen in one in four HIV-positive women, most often in the context of severe, unexplained weight loss (HIV wasting).

Testosterone is the steroid hormone which is central to the development of the testes (testicles) and prostate in men as well as the promotion of secondary male sexual characteristics (e.g., lean muscle mass, bone mass, hair growth). Testosterone is also important to women in maintaining normal muscle and bone mass, although at levels around 10% less than men.

In both men and women, testosterone is essential to a person’s overall health and well-being, contributing to an individual’s strength, energy levels, and libido.

By contrast, testosterone depletion is associated with:

Testosterone deficiency in men with HIV is largely associated with an endocrine abnormality called male hypogonadism in which the function of the male gonads (testes) is impaired, resulting in the diminished production of sex hormones beyond what would be expected of a man’s specific age.

In the general population, hypogonadism is known to occur in about one in 25 men between the ages of 30 and 50, increasing to one in 14 between the ages of 50 to 79. By contrast, the incidence among men with HIV is as much as five times greater.

Hypogonadism can be caused by either a defect in the testes themselves (primary) or a dysfunction occurring outside of the testes (secondary). In adult males with HIV:

Hypogonadism can also be caused by childhood mumps or the abuse of anabolic steroids. HIV medications have not been shown to contribute to hypogonadism.

Hypogonadism in adult males is characterized by low serum (blood) testosterone levels, as well as one or several of following symptoms:

Diagnosis is made by measuring the amount of testosterone in the blood, of which there are three different subtypes. When a test is performed, the results will reveal both a person’s total testosterone (all subtypes) and one of the three subtypes called free testosterone.

Free testosterone is simply a type of testosterone to which no protein is attached, allowing it enter cells and activate receptors that other subtypes can’t. It is considered the most accurate measure of testosterone deficiency, despite representing only 2-3% of the total population. On its own, total testosterone is considered less accurate since results can appear normal if other non-free subtypes are elevated.

Testing should be performed early in the morning since levels can fluctuate by up to 20% during the course of a day. “Normal” levels are simply those within the reference range of the lab. These ranges can vary, but, for illustrative purposes, are roughly between

However, an assessment of “normal” cannot be made by numbers alone. Testosterone levels tend to drop by about 1-2% every year after the age of 40. Therefore, what may be “normal” for a 60-year-old male won’t be the same for a 30-year-old. Assessments need to be made on an individual basis with your treating doctor.

If a diagnosis of hypogonadism is confirmed, testosterone replacement therapy may be indicated. Intramuscular testosterone injections are usually recommended, which offer low side effects if physiological doses are used and adjusted by the treating doctor. FDA-approved options include Depo-testosterone (testosterone cypionate) and Delatestryl (testosterone enanthate).

On average, injections are given every two to four weeks. To avoid the effects of fluctuating testosterone levelswhich can cause sometimes dramatic swings in mood, energy, and sexual functionlower doses and shorter dosing intervals are often used.

Side effects of treatment can include:

Testosterone replacement therapy can also cause the acceleration of pre-existing prostate cancer. Because of this, a patient’s prostate-specific antigen (PSA) levels will be tested and monitored during the course of therapy.

All told, intramuscular injections offer a cost-effective option for treating hypogonadism, with associative increases in alertness, well-being, libido, lean muscle mass, and erection ability. Disadvantages include regular doctor’s visits and dosing administration.

Oral, transdermal, and topical gel agents are also available, and may be applicable in certain cases. Discuss these with your doctor.

In women, testosterone is produced in the ovaries and adrenal glands. As with men, it is an important hormone for maintaining normal muscle and bone mass, as well as energy, strength, and libido.

While hypogonadism is far less common in women with HIV, it can occur and is most often in the context of HIV wasting and advanced disease. The implementation of ART can reverse wasting and the hypogonadal state in many cases.

There are currently no fixed guidelines for the treatment of female hypogonadism, and treatment options are limited. Hormone replacement therapy (HRT) may be appropriate for some, while the short-term use of testosterone may improve sex drive, lean muscle mass, and energy levels.

However, data is still incomplete on the use of testosterone to treat hypogonadism in pre-menopausal women with HIV. Speak with your health care provider about possible side effects. Testosterone is not recommended for women who are pregnant or wish to become pregnant.

Rietschel, P.; Corcoran, C.; Stanley T.; et al. “Prevalence of hypogonadism among men with weight loss related to human immunodeficiency virus infection who were receiving highly active antiretroviral therapy.” Clinical Infectious Diseases. November 2, 2000; 31(5):1240-1244.

Hugh Jones, T. “Late Onset Hypogonadism.” British Medical Journal. February 13, 2009; 338:b352.

Huang, J.; Wilkie, S.; Dolan, S.; et al. “Reduced testosterone levels in human immunodeficiency virus-infected women with weight loss and low weight.” Clinical Infectious Diseases. January 28, 2003; 36(4):499-506.

Grinspoon, S. “The Use of Androgens in HIV-Infected Men and Women.” Physicians Research Network Notebook. March 2005.

Kalyani, R.; Gavini, S.; and Dobs. A. “Male Hypogonadism in systemic disease.” Endocrinology Metabolism Clinics of North America Journal. June 2007; 36(2):333-48.

Carnegie, C. “Diagnosis of Hypogonadism: Clinical Assessment and Laboratory Tests.” Review in Urology. 2004; 6(6):s3-8.

Kumar, P.; Kumar, N.; Patidar, A.; et al. “Male Hypogonadism: Symptoms and treatment.” Journal of Advanced Pharmacological Technology and Research. July-September 2010; 1(3): 297-302.

Mylonakis, E.; Koutkia, P.; and Grinspoon, S. “Diagnosis and treatment of androgen deficiency in human immunodeficiency virus-infected men and women.” Clinical Infectious Diseases. September 15, 2001; 33(6):857-64.

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HIV and Testosterone Deficiency – verywell.com

Recommendation and review posted by Bethany Smith

Hypogonadism – Definition, Causes, Symptoms and Treatment

Hypogonadism is a medical term for a defect of the reproductive system which results in lack of function of the gonads (ovaries or testes).

Hypogonadism may occur if the hypothalamic-pituitary-gonadal axis is interrupted at any level. Hypergonadotropic hypogonadism (primary hypogonadism) results if the gonad does not produce the amount of steroid sufficient to suppress secretion of LH and FSH at normal levels. Hypogonadism resulting from defects of the gonads is traditionally referred to as primary hypogonadism. Examples include Klinefelter syndrome and Turner syndrome. Hypogonadism resulting from hypothalamic or pituitary defects are termed secondary hypogonadism or central hypogonadism (referring to the central nervous system). Hypogonadism can affect men of any age, from fetal development, through puberty and adulthood. Hypogonadism is one of the main causes of male infertility. It is estimated that 13 million men in the United States alone are affected by hypogonadism. Hypogonadism is caused by deficient testosterone secretion by the testes. The two basic types of male hypogonadism are Primary and Secondary.

Hypogonadism Primary, also known as primary testicular failure, originates from an abnormality in the testicles. Hypogonadism may be induced by chronic use of anabolic/androgenic steroids (AAS). The Secondary type of hypogonadism is caused by defects in the pituitary gland connected to the brain that controls hormone production. If chemical messages from the pituitary gland to the testicles aren’t sent, impaired testicular function occurs. This condition can be a result from defects in development of the pituitary gland, certain inflammatory diseases, and the use of certain drugs used in the treatment of psychiatric disorders and gastroesophageal reflux disease. Mental and emotional changes can also accompany hypogonadism. As testosterone decreases, some men may experience signs and symptoms similar to those of menopause in women. These may include hot flashes, decreased drive, irritability, depression and fatigue.

Hypogonadism is most often treated by replacement of the appropriate hormones.

Gonadotropin or GnRH replacement is offered to the patient when fertility is desired. Oral testosterone is no longer used in the U.S. because it is broken down in the liver and rendered inactive. In boys, testosterone replacement therapy (TRT) can stimulate puberty and the development of secondary characteristics, such as increased muscle mass, beard and pubic hair growth. Also available is a topical 1% testosterone gel. It is applied once daily to clean, dry skin of the shoulders, upper arms, or abdomen. Another alternative is testosterone patches. The testosterone may be mixed with the adhesive with a new patch applied daily to a different site; this system leaves a sticky residue but causes little skin irritation. Injections of pituitary hormone may be used to help male patients produce sperm. In others, surgery and radiation therapy may be needed. In adult men, TRT can restore function and muscle strength and prevent bone loss.

Treatment for Hypogonadism

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Hypogonadism – Definition, Causes, Symptoms and Treatment

Recommendation and review posted by Bethany Smith

Hypogonadism – UT Medical Center

Definition

Hypogonadism occurs when the body’s sex glands produce little or no hormones. In men, these glands (gonads) are the testes. In women, these glands are the ovaries.

Gonadal deficiency

The cause of hypogonadism can be primary or central. In primary hypogonadism, the ovaries or testes themselves do not function properly. Causes of primary hypogonadism include:

The most common genetic disorders that cause primary hypogonadism are Turner syndrome (in women) and Klinefelter syndrome (in men).

If you already have other autoimmune disorders you may be at higher risk of autoimmune damage to the gonads. These can include disorders that affect the liver and adrenal and thyroid glands as well as type 1 diabetes.

In central hypogonadism, the centers in the brain that control the gonads (hypothalamus and pituitary) do not function properly. Causes of central hypogonadism include:

A genetic cause of central hypogonadism is Kallmann syndrome. Many people with this condition also have a decreased sense of smell.

Girls who have hypogonadism will not begin menstruating. Hypogonadism can affect their breast development and height. If hypogonadism occurs after puberty, symptoms in women include:

In boys, hypogonadism affects muscle, beard, genital and voice development. It also leads to growth problems. In men the symptoms are:

If a pituitary or other brain tumor is present (central hypogonadism), there may be:

The most common tumors affecting the pituitary are craniopharyngioma in children and prolactinoma adenomas in adults.

You may need to have tests to check:

Other tests may include:

Sometimes imaging tests are needed, such as a sonogram of the ovaries. If pituitary disease is suspected, an MRI or CT scan of the brain may be done.

You may need to take hormone-based medicines. Estrogen and progesterone are used for girls and women. The medicines comes come in the form of a pill or skin patch. Testosterone is used for boys and men. The medicine can be given as a skin patch, skin gel, a solution applied to the armpit, a patch applied to the upper gum, or by injection.

For women who have not had their uterus removed, combination treatment with estrogen and progesterone may decrease the chance of developing endometrial cancer. Women with hypogonadism who have low sex drive may also be prescribed low-dose testosterone.

In some women, injections or pills can be used to stimulate ovulation. Injections of pituitary hormone may be used to help men produce sperm. Other people may need surgery and radiation therapy.

Many forms of hypogonadism are treatable and have a good outlook.

In women, hypogonadism may cause infertility. Menopause is a form of hypogonadism that occurs naturally and can cause hot flashes, vaginal dryness, and irritability as a woman’s estrogen levels fall. The risk of osteoporosis and heart disease increase after menopause.

Some women with hypogonadism take estrogen therapy, especially those who have early menopause. But long-term used of hormone therapy can increase the risk of breast cancer, blood clots and heart disease. Women should talk with their health care provider about the risks and benefits of hormone replacement therapy with your doctor.

In men, hypogonadism results in loss of sex drive and may cause:

Men normally have lower testosterone as they age. However, the decline in hormone levels is not as dramatic as it is in women.

Talk to your health care provider if you notice:

Both men and women should call their provider if they have headaches or vision problems.

Maintain normal body weight and healthy eating habits may help in some cases. Other causes may not be preventable.

Ali O, Donohoue PA. Hypofunction of the testes. In: Kliegman RM, Stanton BF, St. Geme JW III, et al., eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 577.

Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in adult men with androgen deficiency syndromes: An Endocrine Society Clinical Practice guideline. J Clin Endocrinol Metab. 2010;95:2536-59. PMID: 20525905 http://www.ncbi.nlm.nih.gov/pubmed/20525905

Kansra AR, Donohoue PA. Hypofunction of the ovaries. In: Kliegman RM, Stanton BF, St. Geme JW III, et al, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 580.

Swerdloff RS, Wang C. The testis and male sexual function. In: Goldman L, Schafer AI. Goldman’s Cecil Medicine. 24th ed. Philadelphia, PA: Elsevier Saunders; 2012:chap 242.

Review Date: 10/25/2014 Reviewed By: Brent Wisse, MD, Associate Professor of Medicine, Division of Metabolism, Endocrinology & Nutrition, University of Washington School of Medicine, Seattle, WA. Also reviewed by David Zieve, MD, MHA, Isla Ogilvie, PhD, and the A.D.A.M. Editorial team.

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Hypogonadism – UT Medical Center

Recommendation and review posted by Bethany Smith

Lipocine – Hypogonadism

Testosterone levels in men decline with age, at a rate of about 1% per year beginning at about 40 years old.3 Epidemiological studies have determined that total testosterone follows an age-related decline with mean serum concentration at the age of 75 years approximately two thirds that at 25 years.4

According to reports, approximately 74% of chronic opioid users5, 50% of AIDS patients6, 52% of obese men7, 50% of diabetic men7,8 have low testosterone.

Other causes of lowered testosterone levels include: injury, infection, or loss of the testicles; chemotherapyor radiation treatment for cancer; genetic abnormalities such as Klinefelter’s Syndrome (extra X chromosome); hemochromatosis(too much iron in the body); dysfunction of the pituitary gland; inflammatory diseases such as sarcoidosis (a condition that causes inflammation of the lungs); chronic illness; chronic kidney failure; liver cirrhosis; stress; and, alcoholism.

3Feldman HA, et al. J. Clin Endocrinol Metab 2002; 87 (2):589-98 4Myers et al. Rev Urol 2003; 5 (4) 216-226 5Daniell HW., J Pain. 2002; 3:377-384 6Dobs AS. Baillires Clin Endocrinol Metab. 1998; 12:379-390 7Mulligan T, et al. Int J Clin Pract. 2006;60:762-769 8Bodie J, et al. J Urol. 2003;169:22622264 9Jackson JA et al., AM. J. Med. Sci. 1992,304 (1) 4-8

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Lipocine – Hypogonadism

Recommendation and review posted by simmons

Hypogonadism – Risks, Symptoms and Leading Causes | Treato

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Recommendation and review posted by Bethany Smith

Hypogonadism diagnosis – history – Endobible

Loss of gonadal function of any cause. Diagnosis requires testing of sex hormone and gonadotropin levels. This section includes absent or delayed puberty, primary testicular failure, premature ovarian failure, and secondary hypogonadotropic hypogonadism.

Detailed history,including pubertal development,is mandatory in all patients as this may reduce the list of differential diagnoses considerably.

Specific lines of questioning are indicated according to the exact problem, as below.

The list of differential diagnoses will be different in a patient with multiple medical problems or an obvious congenital condition.

Serious systemic illness of any cause is associated with pubertal delay. Specific conditions associated with abnormal pubertal develoment include the intersex disorders, pseudopseudohypoparathyroidism, Cushing’s syndrome andcongenital hypothyroidism.

Pubertal delay is defined by theabsence of thelarche by age 13, or menarche by age 16.

Assess thetiming ofpuberty in as much detail as possible: timing of secondary hair development, breast development and menarche in females, increase in testicular and penile volume, early morning erections and voice breaking in males.

Loss of secondary sexual characteristics such as body hair,and aninability to build new muscle mayoccur withgonadotropin deficiency of any cause.

Weight loss may indicate the development of hypopituitarism or hyperthyroidism. Hypogonadotropic hypogonadism may also occur with Cushing’s syndrome and in obesity.

Tall stature and a feminine or ‘eunucoid’ body shape may be associated with absent puberty in males.

Gynaecomastia may indicate gonadotropin deficiency but in the absence of other symptoms other causes should be considered. Gynaecomastia occurring in conjunction with weight loss should alert to the possibility of malignancy and other systemic diseases.

Absent libido occurs with primary hypogonadism.

New onset loss of libido may be associated with hypogonadism though may be multifactorial.

This may indicate sex hormone deficiency.

Differential diagnoses differ between primary and secondary amenorrhoea.

For secondary amenorrhoea or oligomenorrhoea, specifically assess for symptoms ofpolycystic ovarian syndromeas well as hyperprolactinaemia and thyroid dysfunction below.

Previous pregnancies may help define the duration of disease.

Amenorrhoea and breast swelling are signs of early pregnancy which may not be noticed in the oligomenorrhoeic patient.

Post partum haemorrhage leading to Sheehans syndrome as a cause of hypopituitarism is possible if the patient was unable to breast feed and developed secondary amenorrhoea.

Frequency of shaving varies widely but is usually constant within an individual adult.

Loss of early morning erections is usually important though erectile dysfunction is frequently multifactorial. Symptoms of erectile dysfunction may not be forthcoming unless specifically asked about.

These are all causes of gonadal failure, though orchitis is frequently asymptomatic.

Maldescent may be associated with gonadal dysfunction as well as an increased risk of malignancy.

Hyperprolactinaemia of any cause usually causes hypogonadotropic hypogonadism.

Ask about headache, visual disturbance, breast swelling and galactorrhoea.

Hypothyroidism is a common cause ofdelayed puberty.

Also ask whether the patient hasdeveloped increased sweating, palpitations, tremor, weight loss or diarrhoea, as thyrotoxicosis may also cause gynaecomastia andoligomenorrhoea.

Patients presenting with infertility can on rare occasion befound to havehypopituitarism.

Anorexia nervosa and very low BMI of any cause may cause hypothalamic dysfunction.

Soyacontains large amounts of phytoestrogens which may interfere with the hypothalamic-pituitary-gonadal axis and may be associated with reversible gyncecomastia.

Steroids also interact with the hypothalamic-pituitary-gonadal axis and may occasionally be found in preparations thought by the patient to be ‘natural’ or ‘herbal’.

Excessive exercise may lead to hypothalamic dysfunction.

Various agents associated with hypogonadism are listed below (although it is not exhaustive):

Opiates and recreational drugs, for examplediamorphine, morphine sulphate,heroin, marijuana and alcohol.

Steroids, for examplehydrocortisone, beclamethasone, fluticasone interfere with the hypothalamo-pituitary axis.

Exogenous testosterone,for exampleused forfitness, body building or other sports, will alsoenhance estrogen synthesis.

Estrogens and drugs with estrogen-like activity, such as diethylstilbestrol anddigoxin will also cause gynaecomastia in some cases.

Phenytoin alsoenhances estrogen synthesis, as dogonadotropins.

A range of drugs can inhibit testosterone synthesis or action, includingketoconazole, metronidazole, alkylating agents,spironolactone, cimetidine, flutamide, finasteride, and etomidate.

Other agentssuch asmethyldopa,tricyclic antidepressants, diazepam, penicillamine, omeprazole, phenothiazines, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors have all been reported as causing gynaecomastia, though themechanisms underlying this are unclear.

Patients may not report anosmia unless specifically questioned. Kallmanns syndrome is typified by anosmia and hypogonadotropic hypogonadism.

Dental aplasia, cleft palate and dental malalignment requiring orthodontic treatment may not be obvious and are associated with Kallmanns syndrome.

Congenital abnormalities of the urogenital system may occur with Kallmanns and Turners syndromes.

Specifically ask if any family members, for example cousins,have had late or absent puberty,infertility or simply never had children.

Ask also if any family members have had dental or palatal problems, kidney abnormalities or anosmia which might suggest a family history of Kallmanns syndrome.

Congenital hypothyroidism is associated with delayed puberty.

Hypothyroidismis also associated with Turner’s syndrome.

These may be associated with Turner’s syndrome.

Deafness may be associated with Turner’s syndrome.

Patients with Klinefelter’s syndrome have an increased incidence of psychiatric problems.

Multiple congenital conditions includeabnormalities of sexual development. Examples includepseudopseudohypoparathyroidism, Russell Silver syndrome, congenital hypothyroidism.

Specificdisorders of sexual development may also be encountered: congenital adrenal hyperplasia,androgen insensitivity syndrome, 5-alpha reductase deficiency, aromatase deficiency, gonadal dysgenesis, Kallmann’s syndrome, Turner’s syndrome, Klinefelter’s syndrome, and other rarer conditions.

Loss of acuity or failing vision at night are worrying features suggesting optic nerve involvement.

Visual field loss, for examplehomonymous hemianopia,is common indicating chiasmal impingement.

It is worth specifically asking whether patients drive and, if so, whether they have had trouble noticing street signs on either side of the road as this may be the first instance in which field loss is noticed.

Assess for red flag symptoms: headaches present on waking, whichworsen on coughing or leaning forward, are more suggestive of increased intracranial pressure.

Headaches or lancing pain across one section of the head or face only are more suggestive of cranial nerve involvement particularly with disease in the cavernous sinus.

Vague symptoms of tiredness, nausea and dizziness may indicate the development of hypopituitarism with ACTH or TSH deficiency.

Diabetes insipidusis uncommon with intrinsic pituitary disease and suggests para sellar pathology.

Pituitary metastases are common and may be the first presentation of malignant disease.

Ask specifically about change of bowel habit, new prostatic symptoms andbreast lumps.

Ask the patient whetherthere has been a change in their weight or body shape. New bruising, redness, acne, hirsuitism, oligomenorrhoea, diabetes, hypertension, depression, osteoporosisor muscle weakness are all associated with Cushing’s syndrome, which leads to pubertal delay and hypogonadotropic hypogonadism.

A detailed history of gynaecomastia will help elucidate likely causes.

Peripubertal breast swelling is common and usually requires no treatment. Long standing obesity may be associated with bilateral non-glandular breast swelling. Sudden onset and unilateral gynaecomastia should alert to the possibility of breast cancer.

Sudden onset and unilateral gynaecomastia should alert to the possibility of breast cancer.

Changes in the skin, nipple or unilateral discharge is highly suspicious for breast cancer.

Bilateral galactorrhoea is suggestive of elevated prolatin.

Weight loss and malaise occur with hypopituitarism but may indicate malignancy.

Hyperthyroidism may be associated with gynaecomastia: ask about sweating, palpitations, tremor, weight loss ordiarrhoea.

Hypothyroidism may be associated with delayed puberty.

Cirrhosis, haemachromatosis and congestive cardiac failure are frequently associated with gynaecomastia.

Various agents associated with hypogonadism are listed below (although it is not exhaustive):

Opiates and recreational drugs, for examplediamorphine, morphine sulphate,heroin, marijuana and alcohol.

Steroids, for examplehydrocortisone, beclamethasone, fluticasone interfere with the hypothalamo-pituitary axis.

Exogenous testosterone,for exampleused forfitness, body building or other sports -will alsoenhance estrogen synthesis.

Estrogens and drugs with estrogen-like activity, such as diethylstilbestrol anddigoxin will also cause gynaecomastia in some cases.

Phenytoin alsoenhances estrogen synthesis, as dogonadotropins.

A range of drugs can inhibit testosterone synthesis or action, includingketoconazole, metronidazole, alkylating agents,spironolactone, cimetidine, flutamide, finasteride, and etomidate.

Other agentssuch asmethyldopa,tricyclic antidepressants, diazepam, penicillamine, omeprazole, phenothiazines, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors have all been reported as causing gynaecomastia, though themechanisms underlying this are unclear.

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Hypogonadism diagnosis – history – Endobible

Recommendation and review posted by Bethany Smith

Testosterone Deficiency, Hypogonadism | Froedtert Hospital …

Male hypogonadism is a deficiency of testosterone in men. About 5 percent to 6 percent of men experience male hypogonadism, and the condition becomes more common as a man ages.

Hypogonadism may be congenital or may be acquired as the result of aging, disease, drugs or other factors. Symptoms include low sperm count, decreased libido, erectile dysfunction, fatigue, sleep disturbances and depression.

In primary hypogonadism, the testes fail to make testosterone because of infection or injury to the testes. Common causes of testicular dysfunction include cancer treatment, excessive alcohol consumption, Klinefelter syndrome, mumps orchitis and autoimmune disorders.

In secondary hypogonadism, which is more common, the hypothalamus or the pituitary gland fails to produce enough hormones. These hormones are needed to trigger the testes to produce testosterone. Secondary hypogonadism can be caused by Kallmann syndrome, pituitary or hypothalamic tumors or disorders, obesity, diabetes and Prader-Willi syndrome.

Following a complete medical history and physical, tests will be done to measure the man’s testosterone level. Because testosterone levels naturally fall off during the day, a testosterone blood test is done between 7:00 am and 10:00 am.

If the test shows a low testosterone level, additional tests may be ordered to check for a pituitary gland disorder. A blood test to check serum follicle-stimulating hormone (FSH), luteinizing hormone (LH) and prolactin levels can help determine the cause. If needed, specialized testing may be performed in the Endocrine Diagnostic Unit, based at Froedtert Hospital.

Other tests may be used to measure sperm count, check for testicle or gland tumors, or identify a genetic (congenital) cause.

For men with primary hypogonadism, treatment typically involves lifelong testosterone replacement therapy. Options for replacement therapy include:

Too much testosterone can place a man at a higher risk for blood clots. As with any hormonal therapy, its important to monitor patients as treatment progresses. Men receiving hormone replacement therapy are seen for blood tests and a prostate exam at one, three and six months after beginning treatment. They continue to be seen every six months.

Secondary hypogonadism is treated by addressing the root cause – a disorder with the hypothalamus or pituitary gland.

Treatment may also be needed for conditions related to hypogonadism, including:

Infertility related to secondary hypogonadism may respond to hormonal replacement therapy. Infertility related to primary hypogonadism, however, does not respond to hormonal therapy. In these cases, a man and his partner can be referred to the Reproductive Medicine Center for help conceiving a child.

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Testosterone Deficiency, Hypogonadism | Froedtert Hospital …

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Hypogonadism and Hypogonadism Resources – What is …

Early symptoms of low testosterone in men include low libido (sex drive). As levels become very low, sexual dysfunction (also called “erectile dysfunction (ED)” or “impotence”) often develops. Other signs and symptoms of low testosterone may include depression, fatigue, osteoporosis, loss of muscle mass, an increase in abdominal fat, development of breast tissue (gynecomastia) and infertility.

Symptoms of low testosterone in women may include low libido (sex drive), sexual dysfunction, fatigue, loss of muscle mass, an increase in body fat and bone loss.

Pituitary Symptoms

There are many causes of low testosterone. These can be differentiated with hormone testing. Pituitary dysfunction is one cause of low testosterone and can result from compression of the pituitary gland by a large pituitary tumor. In addition, excess hormone secretion by a pituitary tumor can cause low testosterone either directly or indirectly. For example, elevated prolactin, cortisol or GH levels can cause low testosterone. Testosterone levels normalize with treatment of the tumor in some, but not all, cases. There are other causes of low testosterone that are not related to pituitary tumors. These include anabolic steroid use (for body building or athletic enhancement), obesity, depression, and testicular failure.

Research Studies

The complications of low testosterone in men include infertility, sexual dysfunction, osteoporosis, loss of muscle mass, depression and fatigue.

Research Studies

You’re likely to start by seeing your family doctor or a general practitioner. However, in some cases when you call to set up an appointment, you may be referred immediately to an endocrinologist, a doctor who specializes in endocrine (hormonal) disorders.

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Appointments

Testosterone levels can be measured directly. An endocrinologist can test for causes of low testosterone, including elevated prolactin levels. Sometimes other blood tests are indicated to make the diagnosis or determine the cause, including free testosterone, sex hormone binding globulin, leutinizing hormone (LH) or evaluation for Cushing’s disease or acromegaly.

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If the underlying cause of the low testosterone can be determined and corrected, testosterone levels often rise to normal levels. Medical treatment to lower prolactin levels from a prolactinoma often results in normalization of testosterone level. In addition, resection of large nonfunctioning pituitary tumors that are causing low testosteorne by compressing the pituitary gland results in restoration of normal testosterone levels in approximately 50% of cases. Cure of acromegaly or Cushing’s disease also often results in normalization of testosterone levels. In patients for whom the cause cannot be determined or addressed, testosterone replacement therapy can be prescribed by an endocrinologist with expertise in this area. There are a number of different preparations available, including gels, creams, patches, and injections. Your endocrinologist can discuss the pros and cons of the different options with you. S/he will also check lab results to make sure it is safe to prescribe the medication and that your testosterone levels on the medication are appropriate. If bone density does not improve when testosterone has been normalized, additional medications may be necessary.

There are no FDA-approved testosterone preparations for women, who make 10 to 20 times less testosterone than men and therefore need much lower replacement doses than men.

Appointments

Research is ongoing in the Neuroendocrine Unit on the effects of low testosterone and testosterone treatment in both men and women.

Research Studies

Originally posted here:
Hypogonadism and Hypogonadism Resources – What is …

Recommendation and review posted by simmons

How Cells Work | HowStuffWorks

At a microscopic level, we are all composed of cells. Look at yourself in a mirror — what you see is about 10 trillion cells divided into about 200 different types. Our muscles are made of muscle cells, our livers of liver cells, and there are even very specialized types of cells that make the enamel for our teeth or the clear lenses in our eyes!

If you want to understand how your body works, you need to understand cells. Everything from reproduction to infections to repairing a broken bone happens down at the cellular level. If you want to understand new frontiers like biotechnology and genetic engineering, you need to understand cells as well.

Anyone who reads the paper or any of the scientific magazines (Scientific American, Discover, Popular Science) is aware that genes are BIG news these days. Here are some of the terms you commonly see:

Gene science and genetics are rapidly changing the face of medicine, agriculture and even the legal system!

In this article, we’ll delve down to the molecular level to completely understand how cells work. We’ll look at the simplest cells possible: bacteria cells. By understanding how bacteria work, you can understand the basic mechanisms of all of the cells in your body. This is a fascinating topic both because of its very personal nature and the fact that it makes these news stories so much clearer and easier to understand. Also, once you understand how cells work, you will be able to answer other related questions like these:

All of these questions have obvious answers once you understand how cells work — so let’s get started!

Original post:
How Cells Work | HowStuffWorks

Recommendation and review posted by Bethany Smith

Gene Therapy in Sheep May Bring Hope to Adults With Tay …

For 26 years, doctors could not piece together the medical puzzle of Stewart Altman’s symptoms — as a child growing up on Long Island, he was uncoordinated and slurred his speech. Later, as a volunteer fireman, he kept falling down and had trouble climbing the ladders.

It seemed unrelated at the time, but his older sister, who had a history of psychological symptoms, was hospitalized in a mental institution. Her psychiatrist suspected a physical disorder and consulted a geneticist who eventually connected the dots.

In 1978, Altman and his sister Roslyn Vaccaro were given a stunning diagnosis: Tay-Sachs — an inherited neurological disease that typically affects babies, killing them between the ages of 3 and 5. Only several hundred cases exist in the United States.

Altman, now 58, has a non-fatal, adult form of the disease, late onset Tay-Sachs (LOTS), and depends on his wife and a service dog to perform most daily tasks.

“I am devastated,” Altman said of the disease that has robbed him of much of his speech and muscle strength, confining him to a wheelchair. “But the alternative is much worse.”

His sister died in 2000 after battling LOTS-related bipolar disorder and schizophrenia — which occurs in 50 to 60 percent of all adult cases — and Altman and his wife raised her two sons.

Now scientists are hopeful that gene therapy may help late-onset patients like Altman and look forward to human trials.

Tay-Sachs is caused by gene mutation results in the absence or insufficient levels of the enzyme, hexosamindase A or Hex A. Without it, a fatty substance or lipids accumulates in the cells, mostly in the brain. It comes in three forms: infantile, juvenile or adult onset.

Doctors say there can be great variations in the presentation of Tay-Sachs, even in the same family with the same mutations. Babies born with Tay-Sachs appear normal at first, but by 3 or 4 years old, their nerve cells deteriorate and they eventually die. Those with LOTS can live a long life, but, like Altman, are progressively disabled.

The story of Tay-Sachs is a miraculous one. It was first identified in the late 1800s by British ophthalmologist Warren Tay and New York neurologist Bernard Sachs, who noticed the disease was prevalent in Jews of Eastern European origin.

In the 1970s and 1980s, when genetic testing became available, synagogues launched public education campaigns encouraging prospective parents to be tested, and the disease was virtually eliminated in those of Jewish ancestry.

Now, mostly non-Jews, though their risk is not as great, are among the 100 American children who have the disease, according to the National Tay-Sachs and Allied Diseases Association (NTSAD), which leads the fight for a cure.

Altman’s speech is difficult to understand, so his wife Lorrie said her husband of 37 years wanted the public to know, “it’s not just an infant’s disease.”

“Tay-Sachs is also in the general population and people don’t know,” she said. “He thinks we need to get the word out. One in 250 Americans carries the gene.”

French Canadians, Louisiana Cajuns and even those of English-Irish ancestry have a greater chance of carrying the recessive gene that causes the disease.

Tay-Sachs is an autosomal recessive disorder, which means each parent must carry the gene. Their children have a 25 percent chance of developing Tay-Sachs, 50 percent chance of being a carrier and a 25 percent chance of being free of that recessive gene.

Altman was born in 1952, before genetic testing was available. Both his parents were carriers of the recessive gene that causes Tay-Sachs and both he and sister were stricken with the mildest form of the disease. Two of their brothers were unaffected, although one is a carrier.

The Massapequa, N.Y., couple have two healthy sons, who are carriers, but whose wives are not, and four healthy grandchildren.

For years, Altman was able to get around with a walker until he had to drop out of a clinical trial for a new drug because of debilitating side effects. After that, he said he lost 40 pounds and so much muscle that he could no longer stand on his own.

“Between the two of us we handle it and we lead kind of a normal life,” said Lorrie. “But we have no idea what the future will bring.”

Altman works at Nassau University Medical Center in the security monitoring department. He raises funds for about 11 different non-profit organizations, including NTSAD, and has given presentations to the Boy Scouts and senior citizens.

Much of the public work has now ended, as his speech has become more incomprehensible because the degeneration of the nerves that control his respiratory muscles.

“Stewart has a good way of just living in the moment,” said his wife, who met Altman in college. “But the worst part for him is his speech. He is such a social, outgoing person.”

He has faced discrimination along the way, especially after leaving a Manhattan engineering job because he couldn’t climb the subway stairs.

“He has such a hard time getting a job — it was devastating,” said Lorrie Altman. “On paper, he looked so good, but his speech was terrible. He has a college degree and isn’t stupid, but all people see is the wheelchair.”

Doctors say that many with the milder adult form of Tay-Sachs can lead full lives, despite their disability. And science is getting closer to finding treatments for this devastating disease.

Dr. Edwin Kolodny, former department chair and now professor of neurology at New York University School of Medicine, has been a leader in the field for 30 years. He first helped identify the role of the enzyme Hex-A and later tested more than 30,000 young adults in the 1970s and 1980s.

Today, he and others are involved in the promising gene therapy studies involving first mice, then cats and now sheep. Injecting genes into the brains of Jacob lambs has doubled their life span.

Clinical trials on humans are set to begin as soon as researchers can raise another $700,000 — in addition to a grant from the National Institutes of Health — to manufacture the vectors required to insert the genes into the body.

“It seems like every parent in the world would like to be part of the trial,” said Kolodny. “And there are reasons to think there will be success here, especially for children who have a slightly later onset and not the classic form Tay-Sachs.”

In the past, infantile Tay-Sachs has seen most of the medical attention. “These children have zero quality of life,” he said.

Those with mild mutations, like Altman, who have 5 to 10 percent of Hex A enzyme activity, “sometimes lead full lives,” according to Kolodny. “Intellectually, most of their cognitive function is retained. We have patients who are lawyers and accountants.”

Pre-conception testing is still the gold standard for fighting the disease. “If your parents don’t have the same recessive genes, you are home free,” he said.

Those identified as at risk for having a child with Tay-Sachs can decide to adopt or conceive through in vitro fertilization, where geneticists can test the embryos before implantation to ensure the child will be disease-free.

Doctors can also do prenatal genetic testing and if the fetus is affected, the decision is up to the parents whether or not they want to terminate the pregnancy. “Three out of four times, they are reassured they have a normal child,” said Kolodny.

Doctors say such testing — at a cost of around $100 — should be done routinely for 18 autosomal recessive disorders, including the gene for cystic fibrosis, which occurs in one in 20 caucasians, said Kolodny. Even with advances in Tay-Sachs testing in the Jewish community, public education must continue.

“The problem is each generation forgets what happened in the prior generation — the grandmothers die out, ” said Kolodny. “We need to educate health care professionals. Each new group of students graduating from medical school isn’t prepared to ask the right questions.”

Susan Kahn, NTSAD’s executive director, who is involved in fundraising for research, agrees that along with a fight for a cure, genetic testing is critical.

“When there is a genetic disease, it’s not just about that person, there is a whole implication for the rest of the family and how they deal with it,” she said.

Stewart Altman sits on the association’s board of directors and is a tireless crusader for a cure.

“He’s got some disabilities that make it difficult for him to do certain things, but of all the board members asking for money to support, he is probably the boldest in our group,” said Kahn. “He does have a lot of limitations, but he is still very energetic and wants to do something important. Not everyone responds with the same attitude.”

His wife Lorrie backed that up with a laugh. “He is persistent,” she said. “He carries these little envelopes around and will ask anyone he meets for a donation. It’s almost embarrassing. He’s not afraid to ask.”

Link:
Gene Therapy in Sheep May Bring Hope to Adults With Tay …

Recommendation and review posted by Bethany Smith

Hypogonadism – Medscape Reference

Morbidity for men and women with hypogonadism includes infertility and an increased risk of osteoporosis; there is no increase in mortality.

Hypogonadotropic hypogonadism (see the image below) is one of several types of hypogonadism.

History

Considerations in the evaluation of males with hypogonadism include the following:

For postpubertal males, the rate of beard growth, libido and sexual function, muscle strength, and energy levels

Possible causes of acquired testicular failure (eg, mumps orchitis, trauma, radiation exposure of the head or testes, and chemotherapy)

Drugs that may interrupt testicular function: Including agents that interfere with testosterone synthesis, such as spironolactone, cyproterone, marijuana, heroin, and methadone

Considerations in the evaluation of females with hypogonadism include the following:

Signs associated with Turner syndrome (eg, lymphedema, cardiac or renal congenital anomalies, and short growth pattern)

Age of menarche

Physical examination

Considerations in the physical examination of males with hypogonadism include the following:

Evaluation of the testes: This is the most important feature of the physical examination; determine whether both testes are palpable, their position in the scrotum, and their consistency; testes size can be quantitated by comparison with testicular models (orchidometer), or their length and width may be measured

Examination of the genitalia for hypospadias

Examination of the scrotum to see if it is completely fused

Evaluation of the extent of virilization

Staging of puberty: Use the Tanner criteria for genitalia, pubic hair, and axillary hair

Examination for signs of Klinefelter syndrome (eg, tall stature, especially if the legs are disproportionately long, gynecomastia, small or soft testes, and a eunuchoid body habitus)

Considerations in the physical examination of females with hypogonadism include the following:

Examination of the genitalia is important

Determination of the extent of androgenization: May be adrenal or ovarian in origin and is demonstrated in pubic and axillary hair

Determination of the extent of estrogenization: As evidenced by breast development and maturation of the vaginal mucosa

Examination for signs of Turner syndrome (eg, short stature, webbing of the neck [such as pterygium colli], a highly arched palate, short fourth metacarpals, widely spaced nipples, or multiple pigmented nevi)

See Clinical Presentation for more detail.

The following studies may be indicated in males with hypogonadism:

Follicle-stimulating hormone (FSH) levels

Luteinizing hormone (LH) levels

Prolactin levels

Testosterone levels

Thyroid function

Seminal fluid examination

Karyotyping

Testicular biopsy

For males after puberty, the Guidelines of the Endocrine Society[2] require that the diagnosis of hypogonadism be based on symptoms and signs of hypogonadism plus the presence of a low testosterone level measured on at least 2 occasions.

The following studies may be indicated in females with hypogonadism:

Additional tests in the evaluation of patients with hypogonadism include the following:

Adrenocorticotropic hormone (ACTH) stimulation testing: In patients in whom a form of congenital adrenal hyperplasia is suspected, adrenal steroid synthesis is best evaluated by performing a cosyntropin (ACTH 1-24) stimulation test

Luteinizing-hormone releasing hormone (LHRH) stimulation testing: To distinguish between true hypogonadotropic hypogonadism and constitutional delay in growth and maturation

Testicular tissue testing: If the testes are not palpable and if it is not certain whether any testicular tissue is present, administering human chorionic gonadotropin (hCG) and measuring testosterone response may be helpful

See Workup for more detail.

Hormonal replacement

The simplest and most successful treatment for males and females with either hypergonadotropic or hypogonadotropic hypogonadism is replacement of sex steroids, but the therapy does not confer fertility or, in men, stimulate testicular growth.

When fertility is desired, an alternative therapy for men with hypogonadotropic hypogonadism is administration of pulsatile LHRH or injections of hCG and FSH. (In patients with hypergonadotropic hypogonadism, fertility is not possible.)

In a 6-year European study of men being treated for hypogonadism, long-term transdermal testosterone treatment did not increase prostate-specific antigen (PSA) levels or influence prostate cancer risk.[3, 4]

Investigators used data from a 5-year, open-label extension of a 1-year trial of a transdermal testosterone patch (Testopatch) in men with hypogonadism. Study subjects wore two 60 cm2 patches, each of which delivered 2.4 mg of testosterone per day. More than 90% of patients had PSA concentrations below 2 ng/mL during the 6-year study, and no prostate cancer was found in patients over the course of the trial.

See Treatment and Medication for more detail.

Read more:
Hypogonadism – Medscape Reference

Recommendation and review posted by Bethany Smith

Male Hypogonadism – Genitourinary Disorders – Merck …

By Irvin H. Hirsch, MD

NOTE: This is the Professional Version. CONSUMERS: Click here for the Consumer Version

NOTE: This is the Professional Version. DOCTORS: Click here for the Consumer Version

Hypogonadism is defined as testosterone deficiency with associated symptoms or signs, deficiency of spermatozoa production, or both. It may result from a disorder of the testes (primary hypogonadism) or of the hypothalamic-pituitary axis (secondary hypogonadism). Both may be congenital or acquired as the result of aging, disease, drugs, or other factors. Additionally, a number of congenital enzyme deficiencies cause varying degrees of target organ androgen resistance. Diagnosis is confirmed by hormone levels. Treatment varies with etiology but typically includes gonadotropin-releasing hormone, gonadotropin, or testosterone replacement.

DELATESTRYL

No US brand name

ZOLADEX

ALDACTONE

REGLAN

TAGAMET

NIZORAL

LUPRON

OZURDEX

NOTE: This is the Professional Version. CONSUMERS: Click here for the Consumer Version

NOTE: This is the Professional Version. DOCTORS: Click here for the Consumer Version

View post:
Male Hypogonadism – Genitourinary Disorders – Merck …

Recommendation and review posted by simmons


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