Medically reviewed on Oct 1, 2018

Male hypogonadism is a condition in which the body doesn't produce enough testosterone the hormone that plays a key role in masculine growth and development during puberty or has an impaired ability to produce sperm or both.

You may be born with male hypogonadism, or it can develop later in life, often from injury or infection. The effects and what you can do about them depend on the cause and at what point in your life male hypogonadism occurs. Some types of male hypogonadism can be treated with testosterone replacement therapy.

Hypogonadism can begin during fetal development, before puberty or during adulthood. Signs and symptoms depend on when the condition develops.

If the body doesn't produce enough testosterone during fetal development, the result may be impaired growth of the external sex organs. Depending on when hypogonadism develops and how much testosterone is present, a child who is genetically male may be born with:

Male hypogonadism may delay puberty or cause incomplete or lack of normal development. It can cause:

In adult males, hypogonadism may alter certain masculine physical characteristics and impair normal reproductive function. Signs and symptoms may include:

Hypogonadism can also cause mental and emotional changes. As testosterone decreases, some men may experience symptoms similar to those of menopause in women. These may include:

See a doctor if you have any symptoms of male hypogonadism. Establishing the cause of hypogonadism is an important first step to getting appropriate treatment.

The male reproductive system makes, stores and moves sperm. Testicles produce sperm. Fluid from the seminal vesicles and prostate gland combine with sperm to make semen. The penis ejaculates semen during sexual intercourse.

Male hypogonadism means the testicles don't produce enough of the male sex hormone testosterone. There are two basic types of hypogonadism:

Either type of hypogonadism may be caused by an inherited (congenital) trait or something that happens later in life (acquired), such as an injury or an infection. At times, primary and secondary hypogonadism can occur together.

Common causes of primary hypogonadism include:

In secondary hypogonadism, the testicles are normal but function improperly due to a problem with the pituitary or hypothalamus. A number of conditions can cause secondary hypogonadism, including:

The rate at which testosterone declines varies greatly among men. As many as 30 percent of men older than 75 have a testosterone level that's below the normal range of testosterone in young men. Whether treatment is necessary remains a matter of debate.

The pituitary gland and the hypothalamus are situated within the brain and control hormone production.

Risk factors for hypogonadism include:

Hypogonadism can be inherited. If any of these risk factors are in your family health history, tell your doctor.

The complications of untreated hypogonadism differ depending on what age it first develops during fetal development, puberty or adulthood.

A baby may be born with:

Pubertal development can be delayed or incomplete, resulting in:

Complications may include:

Your doctor will conduct a physical exam during which he or she will note whether your sexual development, such as your pubic hair, muscle mass and size of your testes, is consistent with your age. Your doctor may test your blood level of testosterone if you have any of the signs or symptoms of hypogonadism.

Early detection in boys can help prevent problems from delayed puberty. Early diagnosis and treatment in men offer better protection against osteoporosis and other related conditions.

Doctors base a diagnosis of hypogonadism on symptoms and results of blood tests that measure testosterone levels. Because testosterone levels vary and are generally highest in the morning, blood testing is usually done early in the day, before 10 a.m.

If tests confirm you have low testosterone, further testing can determine if a testicular disorder or a pituitary abnormality is the cause. Based on specific signs and symptoms, additional studies can pinpoint the cause. These studies may include:

Testosterone testing also plays an important role in managing hypogonadism. This helps your doctor determine the right dosage of medication, both initially and over time.

Treatment for male hypogonadism depends on the cause and whether you're concerned about fertility.

Hormone replacement. For hypogonadism caused by testicular failure, doctors use male hormone replacement therapy (testosterone replacement therapy, or TRT). TRT can restore muscle strength and prevent bone loss. In addition, men receiving TRT may experience an increase in energy, sex drive, erectile function and sense of well-being.

If a pituitary problem is the cause, pituitary hormones may stimulate sperm production and restore fertility. Testosterone replacement therapy can be used if fertility isn't an issue. A pituitary tumor may require surgical removal, medication, radiation or the replacement of other hormones.

In boys, testosterone replacement therapy (TRT) can stimulate puberty and the development of secondary sex characteristics, such as increased muscle mass, beard and pubic hair growth, and growth of the penis. Pituitary hormones may be used to stimulate testicle growth. An initial low dose of testosterone with gradual increases may help to avoid adverse effects and more closely mimic the slow increase in testosterone that occurs during puberty.

Several testosterone delivery methods exist. Choosing a specific therapy depends on your preference of a particular delivery system, the side effects and the cost. Methods include:

Injection. Testosterone injections (testosterone cypionate, testosterone enanthate) are safe and effective. Injections are given in a muscle. Your symptoms might fluctuate between doses depending on the frequency of injections.

You or a family member can learn to give TRT injections at home. If you're uncomfortable giving yourself injections, a nurse or doctor can give the injections.

Testosterone undecanoate (Aveed), an injection recently approved by the Food and Drug Administration, is injected less frequently but must be administered by a health care provider and can have serious side effects.

Gel. There are several gel preparations available with different ways of applying them. Depending on the brand, you either rub testosterone gel into your skin on your upper arm or shoulder (AndroGel, Testim, Vogelxo), apply with an applicator under each armpit (Axiron) or pump on your front and inner thigh (Fortesta).

As the gel dries, your body absorbs testosterone through your skin. Gel application of testosterone replacement therapy appears to cause fewer skin reactions than patches do. Don't shower or bathe for several hours after a gel application, to be sure it gets absorbed.

A potential side effect of the gel is the possibility of transferring the medication to another person. Avoid skin-to-skin contact until the gel is completely dry or cover the area after an application.

Oral testosterone isn't recommended for long-term hormone replacement because it might cause liver problems.

Testosterone therapy carries various risks, including contributing to sleep apnea, stimulating noncancerous growth of the prostate, enlarging breasts, limiting sperm production, stimulating growth of existing prostate cancer and blood clots forming in the veins. Recent research also suggests testosterone therapy might increase your risk of a heart attack.

Reduce stress. Talk with your doctor about how you can reduce the anxiety and stress that often accompany these conditions. Many men benefit from psychological or family counseling.

Support groups can help people with hypogonadism and related conditions cope with similar situations and challenges. Helping your family understand the diagnosis of hypogonadism also is important.

Although you're likely to start by seeing your family doctor or general practitioner, you may need to consult a doctor who specializes in the hormone-producing glands (endocrinologist). If your primary care doctor suspects you have male hypogonadism, he or she may refer you to an endocrinologist. Or, you can ask for a referral.

The following information will help you prepare for your appointment, and understand what to expect from your doctor.

Preparing a list of questions for your doctor will help you make the most of your time together. For male hypogonadism, some basic questions to ask your doctor include:

Don't hesitate to ask other questions you have.

Examples of questions your doctor may ask, include:

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Overview

Hormone therapy for prostate cancer is treatment to stop the male hormone testosterone from reaching prostate cancer cells in your body. Hormone therapy for prostate cancer is also known as androgen deprivation therapy.

Most prostate cancer cells rely on testosterone to help them grow. Hormone therapy cuts off the supply of testosterone or stops testosterone from reaching the cancer cells, causing cancer cells to die or to grow more slowly.

Hormone therapy for prostate cancer may involve medications or possibly surgery to remove the testicles.

Hormone therapy for prostate cancer is used to stop your body from producing the male hormone testosterone, which fuels the growth of prostate cancer cells.

Your doctor may recommend hormone therapy for prostate cancer as an option at different times and for different reasons during your cancer treatment.

Hormone therapy can be used:

Side effects of hormone therapy for prostate cancer can include:

To minimize the side effects of hormone therapy medications, your doctor may recommend you take them only until prostate cancer responds to the treatment. You might need to resume these medications if the disease recurs or progresses.

Early research shows this intermittent dosing of hormone therapy medications may reduce the risk of side effects. However, additional studies are needed to determine the long-term survival benefits of intermittent therapy.

Your doctor might suggest intermittent dosing if:

As you consider hormone therapy for prostate cancer, discuss your options with your doctor. Approaches to hormone therapy for prostate cancer include:

LHRH agonist and antagonist medications stop your body from producing testosterone.

These medications are injected under your skin or into a muscle monthly, every three months or every six months. Or they can be placed as an implant under your skin that slowly releases medication over a longer period of time.

These medications include:

Testosterone levels may increase briefly (flare) for a few weeks after you receive an LHRH agonist. Degarelix is an exception that doesn't cause a testosterone flare.

Decreasing the risk of a flare is particularly important if you are experiencing pain or other symptoms due to cancer because an increase in testosterone can worsen those symptoms. To decrease the risk of a flare, your doctor might recommend you take an anti-androgen either before or along with an LHRH agonist.

Anti-androgens block testosterone from reaching cancer cells. These oral medications are usually prescribed along with an LHRH agonist or before taking an LHRH agonist.

Anti-androgens include:

You'll be given anesthetics to numb your groin area. The surgeon makes an incision in your groin and extracts the entire testicle through the opening, then repeats the procedure for your other testicle. Prosthetic testicles can be inserted if you choose.

All surgical procedures carry a risk of pain, bleeding and infection. Orchiectomy is usually performed as an outpatient procedure and doesn't require hospitalization. Typically, no additional hormone therapy is required after orchiectomy.

When prostate cancer persists or recurs despite hormone therapy, other medications can be used to block testosterone in the body. Each medication targets testosterone in the body in a different way.

These other medications include:

These other medications are generally reserved for men with advanced prostate cancer that no longer responds to other hormone therapy treatments.

Hormone therapy for prostate cancer doesn't cure the disease.

Almost all prostate cancers that require hormone therapy eventually recur or progress despite hormone therapy. But hormone therapy may manage prostate cancer by slowing its growth for months or years.

Our patients tell us that the quality of their interactions, our attention to detail and the efficiency of their visits mean health care like they've never experienced. See the stories of satisfied Mayo Clinic patients.

Aug. 15, 2017

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As the body ages, its only natural that some of its processes should break down. Humans become clumsier, stiffer, their reaction times slower, their senses duller. This is often due to the fact that nerves in the extremities grow less sensitive over time, transmitting messages to the brain more slowly and feeling less acutely a condition known as peripheral neuropathy or simply neuropathy.

While some of that is normal, especially in the golden years, neuropathy often manifests in people much too young in their 30s, 40s, or 50s as a result of a disease such as diabetes or autoimmune issues. Unfortunately, the condition can significantly hamper a persons quality of life, making mobility difficult and limiting everyday activities.

The good news? Neuropathy may have a cure, or at least a solid treatment, on the horizon. Stem cells show great promise for a wide variety of conditions, and nerve damage is the latest of these. To see how it can help, its important to understand what stem cell treatment is, what neuropathy is and what causes it, and how the former can address the latter.

In this article:

The body is made of trillions of tissue-specific cells, making up organs, skin, muscle, bone, nerves, and all other tissue. Some of these can renew indefinitely, such as blood cells. Others, however, cannot replace themselves: Once they have divided a certain number of times or become damaged, theyre dead for good. That goes for nerves and brain tissue, for example.

There is, however, an answer. The developing embryo uses stem cells, or master cells capable of differentiating into any kind of tissue in the human body, to transform one fertilized egg into a fully functional baby human. While adult humans lack these pluripotent stem cells that can transform into anything, they do have multipotent stem cells, which are tissue-specific master cells (such as blood cells).

By harvesting these multipotent stem cells from blood or fat tissue, scientists can induce the cells to become pluripotent, meaning theyre now capable of becomingany tissue in the human body. Essentially, researchers have figured out how to reverse-engineer adult stem cells to become all-powerful embryonic cells. This meansstem cells have a huge range of possible uses.

In other cases, multipotent stem cells alone are enough to heal some parts of the human bodysuch as nerves.

Peripheral neuropathymanifests in a number of ways. It causes pain, weakness, and tingling in affected areas, making it hard to lift objects, grasp items, walk competently, and more. Typically it affects the hands and feet most strongly, though it can also cause symptoms in the arms, legs, and face. Not only does it affect motor coordination,but it also makes it hard for the body to sense the environment, including temperature, pain, vibration, and touch.

A more serious manifestation of the disease is autonomic neuropathy, which influences more than the periphery of the body. It also messes with blood pressure, bladder and bowel function, digestion, sweating, and heart rate. Polyneuropathy is when the condition starts at the periphery of the body but gradually spreads inward.

Diabetic neuropathy is the most well-known incarnation of this disease. It is a result of high glucose and fat levels in the blood, which can damage nerves.Other causes include:

If the bad news is there are so many potential causes of neuropathy, the good news is stem cell treatments have the potential to address all of them.

In the case of neuropathy, stem cell treatment is simpler than in other conditions. Mesenchymal stem cells (certain types of multipotent stem cells) releaseneuroprotective and neuroregenerative factors, so when they are injected into the bloodstream they can begin to rebuild nerves and undo the damage caused by the disease. Also, because these stem cells replicate indefinitely, they will offer these benefits for the rest of the patients life.

The basic process is that scientists harvest these cells from the patient (autologous transplant) or from a donor (allogeneic transplant), then cultivate them until they reach certain levels before reinjecting them back into the patient. The stem cells, with the help of hormones and growth factors, seek out and repair the damage done by neuropathy.

The main risks to stem cell treatment include reaction to the injection. In an autologous transplant, the patient may react to the preservatives and other chemicals used by way of necessity. In an allogeneic transplant, the patient may exhibit an immune response to donor cells, or vice versa with the donor cells seeing the patients body as an invader and attacking it. All of the above reactions can prove minor or, on the other end of the spectrum, fatal.

The severity of the problem will, therefore, dictate whether or not it is worth moving forward. Note that those whodochoose to pursue the treatment often have extremely good results.

Unlike some other stem cell treatments, which remain in preliminary stages, stem cell therapy for neuropathy has thus far received serious attention. However, thesmall sample size and difficult conditions of clinical trialsmake it hard to say yet whether this treatment will become widespread or receive FDA approval.Other studies have demonstrated more significant resultsin the treatment of facial pain and may pave the way for future neuropathy treatments using stem cells.

For now, those suffering from neuropathy should seek the advice of a physician. If there are clinical trials available nearby, thats the place to start. Its possible to seek stem cell therapy through a clinic as well as through a clinical study or research institution, but make sure to research the provider thoroughly. With stem cells becoming such a relevantapproach to medical conditions of all kinds, its not safe to conclude that all providers are equally experienced or effective.

If you found this blog valuable, subscribe to BioInformants stem cell industry updates.

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Did this article address your concerns about neuropathy? Let us know in the comments section below.

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Stem Cell Therapy for Neuropathy: What Can We Expect

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Stability, Safety, And Security

We have a proven track record of financial security and stability, as well as price stability. CI is the only cryonics organization with no debt, no stockholders, and no landlords. We own our patient care facilities outright, and all of our member officers and directors donate their services voluntarily. We're one of the oldest cryonics organizations in existence -- and the only such organization that has never raised its prices, even in high-inflation times like the late 70s and early 80s. Adjusting for inflation, our prices have actually steadily declined, and we hope to continue that trend.

As members, each and every one of us has a vested interest in the long-term viability of our organization - our facilities, cryostats and finances are built to last into the future we're striving toward.

We have a flexible and rapid system of emergency patient care based on widely available networks of mortuary assistance. This means that in the critical early stages, we can bring qualified professionals to you throughout most of the world. In particular, London-based F.A. Albin & Sons funeral directors are trained, practiced, equipped, and prepared to fly a team anywhere in Europe on short notice to help European CI members, tourists or business travellers.

Our prices are lower than any other organization in fact, the most affordable prices anywhere in the world. This is in keeping with our membership philosophy to provide ourselves reliable cryonic services at a reasonable and affordable cost. If we were to raise prices, we'd only be charging ourselves more.

Our minimum whole-body suspension fee is $28,000. (For members at a distance, transportation costs and local help will be additional.) Our $28,000 fee is a one-time only payment, with no subsequent charges. It's easily funded by insurance or other means. (For last-minute cases, where the patient was not signed up beforehand, we ordinarily charge $35,000 rather than $28,000, if arrangements can be worked out at all.)

Does that lower fee mean lower quality patient care or services? Absolutely not. We believe that our non-profit status allows us to more successfully control costs. We believe that specific methods and research offered by alternative cryonics organizations differ only slightly from ours and that our procedures and policies give an equal or better chance for patient survival than competing organizations.

See for yourself. Read our FAQ and review "The CI Advantage." Remember, many CI members could afford the higher prices of other organizations for themselves and their families, but we've chosen CI because we know it's our best bet. And yours.

CI Membership

Details on joining the Cryonics Institute. We offer Annual (yearly) or Lifetime Membership options. Please note, ONLY members are eligible for the cryonics services provided by CI.

CI Membership Worldwide

The Cryonics Institute (CI) welcomes those living outside the United States to join us as as Members. We offer human cryopreservation, pet cryopreservation and tissue/DNA cryopreservation to CI Members around the world.

Membership Statistics

Details on CI's worldwide membership, including a breakdown by Country.

Cryopreservation Patient Details

A complete listing of patients curently in cryopreservation at CI's Michigan facility.

Human Cryostatis

CI's premier service is human cryopreservation, using state-of-the-art techniques and equipment to ensure optimal suspensions. CI only performs full-body suspensions, and at a fraction of the cost of other companies' "Neuro" (head only) suspensions.

DNA/Tissue Freezing

CI also offers DNA Preservation as a simpler and more economical cryopreservation option for members.

Pet Cryopreservation

Life-extension possibilities for beloved pets.

Memorabilia Storage

Secure perpetual storage for essential personal documents and keepsakes.

Optional Standby Service through Suspended Animation, Inc.

Third-Party Standby, Stabilization and Transport services are available to CI Members through an arrangement with SA inc.

Emergency Jewelry and Wallet Cards

Cryonics emergency necklaces and/or bracelets are available for Cryonics Institute (CI) Members who have made all the necessary arrangements to be cryopreserved by CI. These items include important information to help expedite local help in a cryonics emergency.

CI's state-of-the-art equipment ensures optimal cryonic suspensions.

Please see our extensive Resources Library for a deeper look into Cryonics and the Cryonics Institute. The library includes sample forms, internet links, equipment and procedure details and much more.

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Noticeable hair loss in women can be deeply distressing. Here are some medical treatments that may help.

About one-third of women experience hair loss (alopecia) at some time in their lives; among postmenopausal women, as many as two-thirds suffer hair thinning or bald spots. Hair loss in women often has a greater impact than hair loss does on men w, because it's less socially acceptable for them. Alopecia can severely affect a woman's emotional well-being and quality of life.

The main type of hair loss in women is the same as it is men. It's called androgenetic alopecia, or female (or male) pattern hair loss. In men, hair loss usually begins above the temples, and the receding hairline eventually forms a characteristic "M" shape; hair at the top of the head also thins, often progressing to baldness. In women, androgenetic alopecia begins with gradual thinning at the part line, followed by increasing diffuse hair loss radiating from the top of the head. A woman's hairline rarely recedes, and women rarely become bald.

There are many potential causes of hair loss in women , including medical conditions, medications, and physical or emotional stress. If you notice unusual hair loss of any kind, it's important to see your primary care provider or a dermatologist, to determine the cause and appropriate treatment. You may also want to ask your clinician for a referral to a therapist or support group to address emotional difficulties. Hair loss in women can be frustrating, but recent years have seen an increase in resources for coping with the problem.

Clinicians use the Ludwig Classification to describe female pattern hair loss. Type I is minimal thinning that can be camouflaged with hair styling techniques. Type II is characterized by decreased volume and noticeable widening of the mid-line part. Type III describes diffuse thinning, with a see-through appearance on the top of the scalp.

Almost every woman eventually develops some degree of female pattern hair loss. It can start any time after the onset of puberty, but women tend to first notice it around menopause, when hair loss typically increases. The risk rises with age, and it's higher for women with a history of hair loss on either side of the family.

As the name suggests, androgenetic alopecia involves the action of the hormones called androgens, which are essential for normal male sexual development and have other important functions in both sexes, including sex drive and regulation of hair growth. The condition may be inherited and involve several different genes. It can also result from an underlying endocrine condition, such as overproduction of androgen or an androgen-secreting tumor on the ovary, pituitary, or adrenal gland. In either case, the alopecia is likely related to increased androgen activity. But unlike androgenetic alopecia in men, in women the precise role of androgens is harder to determine. On the chance that an androgen-secreting tumor is involved, it's important to measure androgen levels in women with clear female pattern hair loss.

In either sex, hair loss from androgenetic alopecia occurs because of a genetically determined shortening of anagen, a hair's growing phase, and a lengthening of the time between the shedding of a hair and the start of a new anagen phase. (See "Life cycle of a hair.") That means it takes longer for hair to start growing back after it is shed in the course of the normal growth cycle. The hair follicle itself also changes, shrinking and producing a shorter, thinner hair shaft a process called "follicular miniaturization." As a result, thicker, pigmented, longer-lived "terminal" hairs are replaced by shorter, thinner, non-pigmented hairs called "vellus."

Each hair develops from a follicle a narrow pocket in the skin and goes through three phases of growth. Anagen (A), the active growth phase, lasts two to seven years. Catagen (B), the transition phase, lasts about two weeks. During this phase, the hair shaft moves upward toward the skin's surface, and the dermal papilla (the structure that nourishes cells that give rise to hair) begins to separate from the follicle. Telogen (C), the resting phase, lasts around three months and culminates in the shedding of the hair shaft.

A clinician diagnoses female pattern hair loss by taking a medical history and examining the scalp. She or he will observe the pattern of hair loss, check for signs of inflammation or infection, and possibly order blood tests to investigate other possible causes of hair loss, including hyperthyroidism, hypothyroidism, and iron deficiency. Unless there are signs of excess androgen activity (such as menstrual irregularities, acne, and unwanted hair growth), a hormonal evaluation is usually unnecessary.

Medications are the most common treatment for hair loss in women. They include the following:

Minoxidil (Rogaine, generic versions). This drug was initially introduced as a treatment for high blood pressure, but people who took it noticed that they were growing hair in places where they had lost it. Research studies confirmed that minoxidil applied directly to the scalp could stimulate hair growth. As a result of the studies, the FDA originally approved over-the-counter 2% minoxidil to treat hair loss in women. Since then a 5% solution has also become available when a stronger solution is need for a woman's hair loss.

Clearly, minoxidil is not a miracle drug. While it can produce some new growth of fine hair in some not all women, it can't restore the full density of the lost hair. It's not a quick fix, either for hair loss in women . You won't see results until you use the drug for at least two months. The effect often peaks at around four months, but it could take longer, so plan on a trial of six to 12 months. If minoxidil works for you, you'll need to keep using it to maintain those results. If you stop, you'll start to lose hair again.

How to use minoxidil: Be sure that your hair and scalp are dry. Using the dropper or spray pump that's provided with the over-the-counter solution, apply it twice daily to every area where your hair is thinning. Gently massage it into the scalp with your fingers so it can reach the hair follicles. Then air-dry your hair, wash your hands thoroughly, and wash off any solution that has dripped onto your forehead or face. Don't shampoo for at least four hours afterwards.

Some women find that the minoxidil solution leaves a deposit that dries and irritates their scalp. This irritation, called contact dermatitis, is probably caused not by the minoxidil itself, but rather by the alcohol that is included to facilitate drying.

Side effects and concerns: Minoxidil is safe, but it can have unpleasant side effects even apart from the alcohol-related skin irritation. Sometimes the new hair differs in color and texture from surrounding hair. Another risk is hypertrichosis excessive hair growth in the wrong places, such as the cheeks or forehead. (This problem is more likely with the stronger 5% solution.)

Because the patent on Rogaine (the brand-name version of minoxidil) has expired, many generic products are available. They all contain the same amount of minoxidil, but some include additional ingredients, such as herbal extracts, which might trigger allergic reactions.

Anti-androgens. Androgens include testosterone and other "male" hormones, which can accelerate hair loss in women. Some women who don't respond to minoxidil may benefit from the addition of the anti-androgen drug spironolactone (Aldactone) for treatment of androgenic alopecia. This is especially true for women with polycystic ovary syndrome (PCOS) because they tend to make excess androgens. Doctors will usually prescribe spironolactone together with an oral contraceptive for women of reproductive age. (A woman taking one of these drugs should not become pregnant because they can cause genital abnormalities in a male fetus.) Possible side effects include weight gain, loss of libido, depression, and fatigue.

Iron supplements. Iron deficiency could be a cause of hair loss in some women . Your doctor may test your blood iron level, particularly if you're a vegetarian, have a history of anemia, or have heavy menstrual bleeding. If you do have iron deficiency, you will need to take a supplement and it may stop your hair loss. However, if your iron level is normal, taking extra iron will only cause side effects, such as stomach upset and constipation.

Hair transplantation, a procedure used in the United States since the 1950s to treat androgenic alopecia, involves removing a strip of scalp from the back of the head and using it to fill in a bald patch. Today, 90% of hair-transplant surgeons use a technique called follicular unit transplantation, which was introduced in the mid-1990s.

During this procedure, surgeons remove a narrow strip of scalp and divide it into hundreds of tiny grafts, each containing just a few hairs. Each graft is planted in a slit in the scalp created by a blade or needle in the area of missing hair. Hair grows naturally this way, in small clusters of one to four follicles, called follicular units. As a result, the graft looks better than the larger "plugs" associated with hair transplants of yesteryear.

Disclaimer:

As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

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Bone Marrow (BM) contains hematopoietic stem/progenitor cells, which have the potential to self-renew, proliferate, and differentiate into multi-lineage blood cells. Multipotent, non-hematopoietic stem cells, such as mesenchymal stem cells, can be isolated from human BM as well. These non-hematopoietic, mesenchymal stem cells are capable of both self-renewal and differentiation into bone, cartilage, muscle, tendons, and fat. BM is drawn into a 60cc syringe containing heparin (80 U/mL of BM) from the posterior iliac crest, 25 mL/site, from a maximum of four sites.CustomizationLet us know how we can customize your product today Custom InquiryDonor CriteriaAge18-65 years oldWeight>= 130 lbsScreened before donationHIV (HIV 1 & 2 Ab)HBV (Surface Antigen HbsAg)HCV (HCVAb)Donation FrequencyMinimum 10 weeks between donationsDonors with any of the following will be excluded from donatingPregnancyHistory of heart, lung, liver, or kidney diseaseHistory of asthmaBlood and bleeding disorders including sickle cell diseaseNeurologic disordersAutoimmune disordersCancerDiabetesOther CriteriaMust be in general good healthMust have accessible hipsComplete Blood Count lab test must meet protocol specsRequired to sign procedure-specific consent form

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Whole Bone Marrow - AllCells.com

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Pellets

Estrogen and testosterone therapy by hormone pellet implantation is a safe and effective method of hormone therapy for both men and women. Hormone pellets deliver consistent, healthy levels of hormones for 3-4 months in women and 4-5 months in men. They avoid the fluctuations, or ups and downs, of hormone levels seen with every other method of delivery. Estrogen delivered by subcutaneous pellets, maintains the normal ratio of estradiol to estrone. This is important for optimal health and disease prevention. Hormone pellet therapy does not increase the risk of blood clots like conventional or synthetic hormone replacement therapy.

Pellet implantation has consistently proven more effective than oral, intramuscular, and topical hormone therapy with regard to bone density, sexual function, mood and cognitive function, urinary and vaginal complaints, breast health, lipid profiles, hormone ratios and metabolites. Pellet hormone therapy has been shown to be superior for relief of menopausal symptoms, maintenance of bone density, restoration of sleep patterns, and improvement in sex drive, libido, sexual response and performance.

To learn more, visit one of our hormone replacement clinics or please download our comprehensive brochure:

Blue Sky MD Pellets FAQ

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Have you had astem cell treatment and if so, what was your experience like? (Update, please also take our poll on stem cell therapy cost).

I really value the diversity of readers on this blog from all over the world. I know we have a lot of readerswho are patients and have had stem cell treatments. Every week I get emails from people asking about stem cell treatments and clinics.

I encourage you to weigh in here in the comments if you or a loved have had a stem cell treatment. What was itlike? If it was positive, why did you feel that way? Same if it was negative.

How much did you have to pay and did you think it was reasonable?

What condition were you hoping to improve?

How did you find out about the clinic and would you refer someone else to them?

Anything else youd like to share?Feel free to remain anonymous if you prefer.

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The pituitary gland produces growth hormones and releases them in bursts every three to five hours. The body normally regulates the amount which is produced and released. However, its possible for too much to be produced. Growth hormones are essential to promoting proper development in children, but what happens when there is too much growth hormone in a child?

Growth hormones are important influences on a childs height and development. While many children are shorter or taller than others due to genetics, some children may have a growth disorder.

Growth disorders affect the speed at which a child develops. Height, weight, and sexual development are just a few features which can be affected. Diseases or problems with the pituitary gland are the leading causes of growth disorders.

The pituitary gland is responsible for producing growth hormones. Too few can lead to poor growth in children, while too many can lead to a condition called gigantism.

Gigantism is a rare condition that usually occurs when a tumor grows on the pituitary gland, affecting the amount of growth hormones in a child. As a result, the childs body and organs grow extremely large for their age.

Excessive growth hormone symptoms are usually slow to form. Symptoms can be difficult to notice because children can develop in spurts or at different rates than their peers.

Symptoms of too much growth hormone in a child include:

Its important to treat gigantism because a child may experience delayed puberty, or their genitals may not fully develop.

Your doctor will be able to confirm whether a growth disorder is present through a combination of blood tests, CT or MRI, and study of serial photographs (photographs taken over the course of several years).

Treatment can stop or slow growth hormones from causing your child to grow larger than normal.

Stopping or slowing the production of growth hormones is not easy. Your doctor may need to use a combination of techniques to effectively treat your child.

Treating excess growth hormones in children is essential to ensuring that they live a long and healthy life.

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The problem with the embryonic stem cells are the many complications associated with them. Besides the ethical considerations, from a practical point of view, we are still a long way from being able to utilize these cells in a safe and consistent manner.

When using embryonic stem cells, you are inheriting any potential diseases that the baby may have. For instance, the baby may have a gene that increases susceptibility to cancer. In fact, the embryonic cells themselves may act as a tumor since there is no natural check on these cells. Furthermore, these cells are foreign materials to the body, and the body will react and attack these cells in an immune response. This can sometimes cause a serious medical condition called graft versus host disease. In that case, the patient may have to be placed on immunosuppressant drugslike an organ transplant patient. With our present technology, embryonic stem cells are not the answer. For those reasons, the FDA has put significant restrictions on the use of this type of cell in humans.

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The human genome is the complete set of instructions for building a human.

It is made up of 23 pair of chromosomes which each have somewhere between 500 5,000 individual genes, each of which are responsible for a particular trait hair color, eye color, etc. 22 of the chromosome pairs are the same in men and women, but the last set is the sex chromosome. Women have 2 X chromosomes (XX), while Men have an X and a Y (XY).When a baby is conceived the babys DNA comes from both the father and the mother. The egg contains a single set of 23 chromosomes and the sperm contains the other 23. When the sperm fertilizes the egg, the two sets of chromosomes combine to form a full set of DNA for the new little person. Interestingly, the gender of the baby is determined by the man. Sperm can carry either an X or a Y chromosome which will determine whether the baby will be a boy or a girl.

Genetic disorders can be divided into a few different categories. Numerical chromosomal abnormalities occur when a person receives an extra chromosome, which can cause various disorders such as Downs or Turners syndrome. Another thing that can happen is pieces of a gene can get deleted during duplication. Most of the time, large deletions cause severe enough disorders that dont enable an embryo to develop. However, some very small deletions, known as micro-deletions can lead to a variety of congenital defects including infertility. Microdeletions in the Y chromosome have a profound impact on sperm production and is a fairly common cause of infertility in men. Finally, mutations or trans-locations are disorders where parts of a gene form abnormally or get mixed up with other genes causing it to malfunction. This can cause disorders such as cystic fibrosis or sickle cell anemia. Sometimes these mutations can impact fertility.

As mentioned above, the most well-known of the numeric abnormalities is trisomy 21 or Downs Syndrome. This occurs when someone receives an extra copy of the 21st chromosome and happens in about 1 in every 700 births. It is also fairly common to have extra copies of either the X or the Y chromosome. Some women may have a an extra X resulting in a condition known as triple X. Men can receive either an extra X or an extra Y chromosome, resulting in XXY or XYY. Rarely, babies are born that are genetically female with two X chromosomes but present as males.

The most common genetic cause of male infertility is a condition known as Klinefelter Syndrome. About 1 in every 500 boys are born with an extra X chromosome in their genetic makeup XXY. This condition is known as Klinefelter Syndrome, and it has been shown to drastically reduce the mans fertility.

Microdeletions make up another large portion of the genetic causes of male infertility. Most of the time deletions occur on the Y chromosome.

The Y chromosome is by far the smallest chromosome and is primarily responsible for the creation of sperm and the development of tissue in the testicle. Because it is only passed from man to man via sperm, and sperm are continually being made by the body, it has a higher risk of mutating from one generation to the next when compared to the other genes. When a man has Y microdeletions, it is kind of like having a few bad sectors on a hard drive, it really doesnt affect anything EXCEPT trying to make sperm. Its estimated that somewhere around 10% of azoospermic men have these micro-deletions but the number could be bigger as it has been traditionally difficult and expensive to diagnose.

Another genetic disorder caused by microdeletions is Prader-Willi Syndrome. This syndrome is incredibly rare occurring once in every 25,000 births. It is caused by microdeletions on the 15th chromosome and is commonly diagnosed via genetic testing at birth. Like autism, Prader-Willi is a spectral disorder with a range of symptoms from mild to severe. The most common symptoms include hypgonadism, infertility, small hands and feet, and obesity stemming from an uncontrollable appetite.

Scientists estimate that there are around 2,300 genes involved in male reproduction. Each gene has several possible mutations, making it nearly impossible to isolate all genetic causes of infertility. The rise in genetic sequencing and other genetic testing techniques has dramatically increased our understanding of how genes impact our health and fertility. Here are some of the more common genetic mutations that can impact fertility.

Cystic Fibrosis is one of the most well known genetic mutation disorders. It occurs when there is a mutation in the CFTR gene (located on the 7th chromosome). This gene is responsible for helping your body regulate use of salt and over 1,200 mutations of the gene have been identified by scientists. Full blown CF occurs when an individual has two copies of a mutated gene, which happens about once in every 2,500 births. Thanks to modern medicine, CF patients are living longer, healthier lives and many are able to start families of their own. However, a hidden side-effect of CF is that it can often cause a natural vasectomy by preventing the formation of the vas deferens. Skilled urologists specialized in fertility are able to help men with CF become fathers.A lesser known fact about CF is 1 in 25 people carry one copy of the mutated gene. Some mutations specifically impact the formation of the vas deferens, so even men who dont have full blown CF may be genetic carriers with unexplained obstructive azoospermia. A skilled urologist should be able to detect the absence of the vas deferens during a physical evaluation and recommend genetic testing if a CF mutation is suspected.

Mutations in key genes involved with fetal development can prevent the testicles from descending. Other mutations can cause abnormal development of the ducts that connect the testicles to the body. Since sperm production is regulated by hormones, genetic problems with the endocrine system may also create conditions that are unfavorable for or preclude sperm production. Some of the known syndromes stemming from genetic mutations that affect male fertility include: Noonan Syndrome, Androgen Insensitivity Syndrome, Kallman Syndrome, Myotonic Dystrophy, and Kartageners Syndrome.

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CAR-T cell therapy is asa type of immunotherapy that teaches T cells to recognize and destroy cancer.CAR-T cell therapy has demonstrated promising results in a range of patients from young and old. In some patients, this can lead to the total elimination of the cancer. In others, there is a significant improvement of the disease.

For those who are facing cancer, it is important to answer the question What is CAR-T? This guide will answer the most common questions about CAR-T cell therapy for readers who want to understand this novel technology platform for treating cancer.

What you need to know about CAR-T therapy and its role in cancer treatment is described below.

CAR-T is pronounced phonetically, as car tee cell.CAR-T is named after a mythical creature called the chimera. A chimera is an animal made of different parts of different animals attached together.

With CAR-T cell therapy, apatientsTcells are modified within a laboratory, so that they they can find and attack cancer cells. Because CAR-T cells combine different parts from different sources, they are called chimera (meaning, blended or fused) antigen receptor T cells.

T cells are a type of white bloodcell that plays a central role in the immune response within humans.T cell that have been genetically altered into CAR-T cells function as living drugs when they are administered to patients.

To understand CAR-T cell therapy,a brief history of immunologymay prove helpful. An antigen is a foreign substance in the body, either a toxin or disease agent or unhealthy cell (as in cancer), that triggers an immune response. The body then produces white blood cells to attack the agent. It does this by binding to it with the use of antigen receptors on the surface of the white blood cells, or lymphocytes. Only then does the body produce antibodies to destroy the foreign or diseased agent.

The problem is T cells, the white blood cells responsible for destroying tumor cells,are not good enough at recognizing it. Therefore, in order to increase the patient immune levels, medical specialists take blood. From the blood, they harvest T cells and add extra antigen receptors to the surface of the cells. They inject those cells back into the patient via blood transfusion, where they multiply and can then attack cancer, either with or without the aid of additional therapies.

Specifically, the antigens can then recognize the protein CD-19, which forms on the surface of B cells, a type of blood cell that frequently becomes cancerous. By knowing which proteins to look for, the modified T cells can hunt them down, attack, and destroy them throughout the bloodstream.

CAR-T cells are defined as T-cells (immune cells) that have been modified to match markers present on the outside of cancer cells, allowing them to selectively find and attack them. To create CAR-T cells, physicians extract T-cells from a patient, genetically alter them, expand them in quantity, and re-infuse them to the patient so that the engineered CAR-T cell can selectively attack cancer cells.

The patient response is then monitored using a variety of tools.

There are four steps involved with the CAR-T cell therapy process.

These steps include:

The patient is then monitored by the attending physicians to document the therapeutic response.

Cancer is a silent killer. Too often, it has devastating results, because the cells in the human body are not adept at killingit. This is the case with T cells, human immune cells whose responsibility is to fight invasion and disease. These cells, also known as T lymphocytes a special type of white blood cell are not always able to recognize and eliminate cancer.A potential new solution may be CAR-T cell therapy.

As theCancer Treatment Centers of Americapoints to CAR-T treatment as a novel way to treat cancer, it could drastically alter the medical outlook for both children and adults. These patients would otherwise be without the possibility of a cure.

However, CAR-T immunotherapy is not a cure-all for every patient. For some, it only works for a short time before the cancer relapses. Other patients respond to it, but suffer such severe side effects that it does almost nothing to ease the symptoms. While researchers work furiously to determine why some treatments work on cancer cells and others do not, they still have not arrived at a firm answer.

During transport and until ready to administer at bedside CAR-T cells must be stored at least -150 Celsius. @SylvesterCancer is the only center in South Florida certified to treat patients with this novel #immunotherapy pic.twitter.com/1LKm6UHzd8

Sylvester Cancer (@SylvesterCancer) August 7, 2018

In 2017, two experimental CAR-T treatments received approval from the U.S. FDA with more in clinical trials:

Kymriah was approved by FDA in August 2017 to be used in children and adults with ALL. In May 2018, the FDA approved Kymriah for a second indication (diffuse large B-cell lymphoma). The second CAR-T product, Yescarta, was approved by FDA in October 2017 for patients with lymphoma.In August 2018, both Kymriah and Yescarta secured European regulatory approval. In September 2018, Health Canada made Kymriah the first CAR-T therapy to receive regulatory approval in Canada.

Numerous companies are also working to perfect the technology of CAR-T cells. Akron Biotechmodifies many types of cells for use in medical treatments.

CAR-T is a new technology. Not only is it expensive to manufacture antigens in a lab and attach them to T cells, it takes a long time and carries a number of different specifications in order for candidates to gain approval for the treatment. So, exactly which candidates can receive therapy?

Both treatment protocols modify T cells to help them recognize and attack diseased B cells in the blood. Patients with either leukemia or B-cell lymphoma may apply for the clinical trial at this time. However, they cannot do so without first trying at least two other cancer therapies of a more standard nature.

Currently, researchers are experimenting with CAR-T therapies for other types of cancers as well. These include leukemia and lymphoma subtypes, as well as non-blood-borne cancers. Its ability to fight solid tumors, or those that do not spread throughout blood or bone marrow, have thus far proven less than impressive.

Physicians make CAR-T cells via a careful process. First, the patient is set up in the hospital and prepped for a blood draw, followed by a long stay. Most patients are quite ill by the time they start CAR-T cell immunotherapy, necessitating they remain in the hospital until the completion of the treatment.

Doctors then take a patients blood and feed it into anapheresis machine. This device separates out the white blood cells, T cells included. Then it feeds the remaining blood back to the patient. This means they do not lose a lot of blood while physicians now have a healthy supply of cells to transform. Doctors then freeze the harvested cells and send them off to a lab.

Lab workers then take the collected T cells and introduce a gene that manufactures the chimeric antigen receptor into the DNA of each cell. Lab workers then grow millions of versions of these cells. Once they have enough, they harvest the cells, freeze them once more and deliver them back to the patient via transfusion.

Both these T cells, plus the ones subsequently manufactured by the patients body, can then bind to and attack the cancer cells.

Because transforming T cells is such a complex process, the treatment is typically a long one for the patient. From beginning to end, the transformation and reintroduction of cells may take up to 3 weeks. During that time, the patient is compromised even more than usual due to the reduction in their T cell population. Thats why they usually stay in the hospital during the entire process. This way, doctors can monitor them and make sure their immunity stays as robust as possible.

Before introducing the modified T cells to the patient, physicians typically give them a round of chemotherapy. This helps to weaken their immune system further, which reduces the chances that existing T cells will outnumber the new ones. Counterintuitively, by depressing the immune system in the short run, doctors give patients the best chance of engineered T cells multiplying and doing their job.

The transfusion itself is typically short and painless, lasting only about an hour. After staying in the hospital for monitoring, patients must come in regularly for a few weeks afterward.

The huge benefit of a treatment like this is the T cell modifications will last for life. Each time a bodys T cells encounter a toxin or disease agent and develop antigen receptors and antibodies to fight it, the person has that ability forever. That means patients who receive modified T cells now have the tools to fight their particular cancer for the remainder of their days.

This makes CAR-T cell therapy more than a treatment. For example, while chemotherapy and radiation are effective, their curative effects end when the treatment ends (or, more accurately, a few days or weeks after the last course). In contrast, modified T cells hang aroundforever, turning this type of immunotherapy into a living drug.

While CAR-T therapies are long-lasting, making them more affordable over a lifetime, it is expensive to access these therapies.Currently, Kymriah and Yescarta are offered at the following prices:

Moreover, possible side effects do exist. These include:

Finally, while the process is very beneficial to some patients, it is extremely time-consuming. Some question where it can actually serve the broader population, considering the necessary time and specialization required.

Do you need a visual look at how CAR-T therapy works? Watch this video from Associated Press.

CAR-T companies are on the rise, supported by growing investment flowing into CAR-T product development and landmark approvals of CAR-T cell therapies by the U.S. FDA, European Medicines Agency (EMA), and Health Canada.

Are you interested to know the identities of the companies developing CAR-T therapies worldwide?

For a limited-time, you can claim the Global Database of CAR-T Cell Therapy Companies and get the CAR-T Funding Brief ($49 value) for FREE:

Overall, T-cell therapy has proven a promising new treatment approach. As its manufacture, administration, and safety profile improve, it will become an important tool in the cancer treatment toolkit.

Do you know anyone in need of a cancer cure? What role could CAR-T therapy play in their treatment? Let us know in the comments below.

What is CAR-T Cell Therapy? | CAR-T Definition

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What is CAR-T Cell Therapy | CAR-T Definition | Bioinformant

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Some women release an enzyme that canbreak down the hormones from birth control, which may makethese contraceptive methods less effective in preventing pregnancy. (Credit: Image Point Fr/Shutterstock)

No form of birth control is 100 percent effective. Now, a new study provides an explanation for why a small number of women who use hormonalcontraceptive methods still become pregnant, even if they use them correctly.

A new study published in Obstetrics & Gynecologyexplains that somewomen have an uncommon genetic difference that makes hormonal contraception less effective for them.

In the paper, researchers at the University of Colorado School of Medicinesay that around5 percent of women carry a gene that makes their bodies produce an enzyme that breaks down the hormones in birth control faster than usual. The researchers think that the enzyme leaves women with hormone levels that may be too low to prevent pregnancy, particularly among users of low-dose contraceptives.

Hormonal contraceptive methods like the pill, implant or injection work by releasing synthetic versions of female hormones, usually estrogen and progestin, thatoverrides awomans monthly cycle andprevents ovulation. Receiving these hormones, ironically, tricks a womans body into thinking its pregnant, which stops the release of an egg each month. Thehormones also work to prevent pregnancy by thickening the mucus near the cervix, which preventssperm from reaching the egg.

To learn how a womans genetic makeup influences birth control hormones,the researchers examined 350 healthy women with a median age of 22.5 years old who had received a contraceptive implant. This long-lasting birth control device sits under the skin and delivers the hormones necessary toprevent ovulation.

The researchers found that around 5percent of women tested positive for agenetic variant, called CYP3A7*1C. And among these women, the researchers observed lower levels of birth control hormones in their system. Its thought thattheenzyme somehow interferes with the ovulation-suppressing effects of hormonal birth control.

Lead study author Aaron Lazorwitz said that the CYP3A7*1C gene normally shuts off during gestation, before a woman is ever born. But in some women that never happens and evidently impacts how they process steroid hormone-based drugs, like birth control.Better understanding genetic differences in medication effectiveness could be a game-changer in womens healthcare, Lazorwitz said.

The field of pharmacogenomics, looking at how genetics affects drugs, has been a hot topic in multiple areas of medicine [but] womens health research has unfortunately not focused much on this field to this point, he said. As we use the same types of hormonal medications for so many different treatments in womens health, the impact of genetics on these medications has huge potential to change how we take care of women.

According to the Centers for Disease Control and Prevention, 24 percent of women use a hormonal form of contraception like the pill or the implant. Lazorwitz said that many cases of birth control failure come down to user error such as missing a few pills. But, as this study shows, there arefactors outside of a womans controlthat can impact birth control effectiveness, and there are probably more to find, according to Lazorwitz.

We think that genetics is part of the equation, but there likely are other things we havent even considered yet, he said. This is just the first step in our work to try and figure out this complicated issue. Thankfully, we have extremely efficacious birth control methods like intrauterine devices and the [contraceptive] implant that we know work very well for the vast majority of women.

Lazorwitz said the findings likely apply to all forms of hormonal birth control such as the pill, implant or injection because the hormones used in these methods are similar and are processed similarly in the body. But future studies are needed to prove this.

The unintended pregnancy risk for women carrying this genetic variant cannot be quantified yet because its too early. Because the implant releases more than enough hormones needed to prevent pregnancy, Lazorwitz said the variant probably does not impact efficacy of the contraceptive implant. The researchers are more concerned that the genetic variant could affect the effectiveness of lower-dose hormonal methods, like the pill.

For now, Lazorwitz saidwomen should continue to work with their doctorsin finding the best birth control method for them.

We want to reassure women taking hormonal birth control that they dont need to go get genetic screening or anything like that at this time We hope that this kind of research will one day lead to enough information that we can develop some tools or screenings to help guide women on their individualized decision-making process in choosing a birth control method, he said.

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Hematopoietic stem cell transplantation (HSCT) is the new name for bone marrow transplantation.

The bone marrow is home to hematopoietic stem cells (HSCs), also called pluripotent stem cells because they can give rise to any cell your body requires at any given moment. These specialized cells play an essential role in replenishing our blood supply on a daily basis to maintain blood counts in a healthy host. These cells can be collected either by performing repeated bone marrow aspirations or by mobilizing HSCs into the circulation using special medications called cytokines (like GCSF, also called neupogen), and filtering them out of your blood using a highly specialized process called apheresis. After they are collected from your body, these stem cells can be preserved by storing them in a chemical called DMSO, and placing them in a freezer. Stem cell transplantation refers to a process whereby the patients HSCs are replaced by new cells (either from yourself [autologous] or someone else [allogeneic] that grow into a healthy hematopoietic system.

There are many types of HSCTs depending on the source of stem cells as described below:

Autologous Stem Cell Transplantation:

Autologous stem cell transplants are predicated on a simple concept: if a little chemotherapy has the potential to cure, than a lot could be even better. For lymphoma that has come back after conventional chemotherapy, this disease is not usually sensitive to lower doses of chemotherapy, so there is a need to consider higher doses. The challenge of course, is that higher doses of chemotherapy, while effective at treating the lymphoma, can also destroy all your bodys normal blood cells. Hence, after receiving high dose chemotherapy, there is a need to re-infuse your own normal stem cells, collected before you get the high dose therapy.

The use of your own stem cells, collected and frozen prior to the high dose therapy, is referred to as an autologous stem cell transplant. The most common indications for this kind of stem cell transplant are recurrent non-Hodgkin lymphoma and Hodgkin lymphoma. Typically, the patient undergoes chemotherapy to put their cancer into remission. At some point during their treatment they are assessed for HSCT that includes evaluation of the marrow to ensure healthy stem cells as well as adequate heart, lung and liver function. If they qualify then the stem cells are collected usually by apheresis.

In this process, stem cells that have been stimulated to divide and mobilized by medications (ex: GCSF or Neupogen) are filtered out of the circulation through an IV and stored for future use. Once the stem cells are collected, the patient undergoes further conditioning chemotherapy to destroy all cancer cells in their body. This kind of treatment can be toxic to stem cells and may result in long term inability to produce blood. The previously collected stem cells are infused back into the patient and after 7 to 10 days the blood counts recover and the patient can go home. Since these are the patients own cells there is no danger of graft rejection or graft versus host disease. The immune system may take up to a year to fully recover.

Allogeneic Stem Cell Transplantation:

Unlike autologous stem cell transplants, allogeneic stem cell transplants are predicated on the idea that if your immune system could not detect and destroy your lymphoma before it became obvious, then maybe an immune system from someone else (a sibling or an unrelated but matched person), can identify your lymphoma as foreign, and mount an immune response against it. The problem of course is that while the donor immune system, now transplanted and growing in a new host (that is the patient), can recognize the lymphoma as foreign (graft versus lymphoma effect, or GVL), it can also recognize the normal organs of the host as foreign, and mount a graft versus host (GVHD) response against your skin, lung, liver, and gastrointestinal tract. Drugs to suppress the immune system, called immunosuppressants, are often used to help control GVHD, but can obviously compromise some of the GVL effect as well. It is a double edge sword you want GVL without the GVHD, but unfortunately the two go and-in-hand. Indications for allogeneic stem cell transplant typically include acute myeloid leukemia, aggressive lymphomas, and stem cell disorders. A donor for a patient is defined by HLA typing of blood and tissues.

HLA stands for Human Leukocyte Antigen, and describes a series of proteins that exist on the surface of all cells in your body, and which is defined genetically. The degree of relatedness between individuals can be described by the similarities or differences in these genes that code for the HLA proteins, and are used to determine who might be a suitable donor for any given patient. The more closely related the individuals (say identical twins), the lower the risk of GVHD, but the lower the risk of GVL. The greater the difference in the HLA, the greater the risk of GVHD, but consequently, the greater the GVL benefit. Of course, if the toxicity of the GVHD is so great, producing increased mortality, then the GVL benefit becomes inconsequential. Thus, allogeneic transplanters walk a very fine line in assessing each patients individual risk and benefit with this type of transplant.

An HLA matched donor is needed for the host to allow the donor blood cells to engraft in the marrow, otherwise they will be rejected by the bodys immune system. The best donor, usually meaning the least degree of graft versus host disease (GVHD), is usually a sibling. Each person has about a 25% chance of having an HLA matched sibling donor. HLA matching is different from blood typing and can be done by a simple blood test or obtaining a swab from the inside of a persons mouth. Should no siblings be identified as a match, than a search is initiated to find an unrelated HLA match through the National Marrow Donor Program (NMDP). Once a match is identified, the patient is admitted to the hospital to receive conditioning chemotherapy and / or radiation therapy. At the end of this treatment, stem cells from the donor are infused into the patient and allowed to engraft. Even with an HLA matched donor there is a considerable risk of GVHD where the new grafted donor cells will attack the patients organs.

After the transplant, the patient is given immunosuppressive medications to prevent this condition, and is required to be on these for a considerable period of time.

Cord blood transplants:

Umbilical cord blood is an excellent source of stem cells and can be used as a source of stem cells in cases where an unrelated donor cannot be found. This has saved the lives of many patients. HSCT is a complicated process that requires a commitment from the patient and their families for the best outcome .You will be referred to a specialized center for HSCT where you will receive further details and education about the process.

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Bone Marrow Transplantation: Autologous and Allogeneic ...

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In January 2019, an international team of researchers led by Richard K. Burt, MD (Northwestern University, Chicago, IL) published results of the first randomized, control trial of bone marrow stem cell transplant (HSCT) in people with aggressive relapsing-remitting MS. They enrolled 110 people whose MS was not controlled by available disease-modifying therapies. Half received immunosuppressant therapy followed by hematopoietic (blood cell-producing) stem transplant. The other half were switched to a different disease-modifying therapy. Significantly fewer people experienced MS progression in the group that underwent HSCT, compared with the group who were switched to a different MS disease-modifying therapy. There were no deaths or life-threatening adverse events in either group. The investigators consider this study to be preliminary and recommend that further research is needed to confirm these findings and to determine longer-term outcomes and safety. Read the summary or read the abstract in JAMA.

In December 2018, Drs. John Moore, David Ma (St. Vincents Hospital, Darlinghurst, NSW, Australia) and colleagues reported results of a small clinical trial of HSCT conducted at a single medical center in Australia. This trial enrolled 35 people with relapsing-remitting MS or secondary progressive MS whose disease had not responded well to disease-modifying medications. There was no control group or blinding; all participants underwent the HSCT procedure. The team reported on results after following participants from 12 to 66 months after transplantation. After 12 months, 82% remained free of relapses, MRI-detected new or enlarging lesions, and progression (called Event-Free Survival or EFS). At two years after transplant, 65% of the group had EFS, and at three years 60%. EFS was better in those who had relapsing MS. Of 8 who experienced MS progression after transplantation, 2 had relapsing-remitting MS and 6 had secondary progressive MS. Twelve of thirteen whose disability scores improved after transplantation had relapsing-remitting MS.At this center, which has a long experience with bone marrow transplants, there were no transplant-related deaths. Many experienced complications expected from the chemotherapy cocktail (called BEAMS) used to deplete their bone marrow cells in preparation for the transplant. Read a summary or read the abstract in the JNNP.

In April 2017, researchers in Italy combined and analyzed results from 15 previously published studies of HSCT (Hematopoietic Stem Cell Transplantation) involving 764 people with various forms of MS. They found that overall, the procedure showed a significant benefit against disease activity and progression. Two years after transplantation, about 83% of all participants had not progressed; overall, studies involving more people with relapsing-remitting MS had lower progression rates. The pooled results showed an overall transplant-related mortality rate of 2.1%.There were fewer deaths in later studies as researchers gained more experience with the procedure. Read a summary of more details here or the abstract in Neurology

In February 2017, results of an international study were published. The study evaluated long-term outcomes from HSCT in 261 people with different forms of MS. The transplants took place between 1995 and 2006, with a follow-up period of up to 16 years. Several different transplant protocols were followed. After 5 years, 46% still had not experienced any progression or worsening of symptoms, including 73% of those with relapsing MS and 33% of those with secondary progressive MS. Eight deaths (2.8%) occurred within 100 days of the transplant. Most of these occurred during the early development of the procedure; improvements in patient selection and transplant techniques have significantly reduced the mortality. Those with the best outcomes tended to be younger, had relapsing MS, lower accumulation of disability and had used fewer MS therapies prior to the transplant procedure. Additional research is needed to better understand who might benefit from this procedure and how it compares to the benefits of powerful immune-modulating therapies now available. A phase 3 trial of HSCT is now in planning stages. The Society is engaged with the team planning the trial and is encouraging quick action to design and launch the trial.Read a summary of the results or the paper in JAMA Neurology

In February 2017, results were published from a multi-center, 5-year trial called theHALT MS Study. It tested HSCT in 24 people with MS and active relapsing-remitting disease that was not controlled by disease-modifying medications. Results suggest that after five years, 69.2% of participants experienced no new disease activity after the procedure and did not need disease-modifying therapies to control their disease. All participants experienced severe and/or life threatening adverse events. Most of these occurred within the first 30 days after transplant and were related to low white blood cell counts and infections. This trial, which was funded by the National Institutes of Health, is an important addition to research needed to determine whether this approach to stem cell transplantation is safe and effective in people with MS. A larger, phase 3 trial is in planning stages.Read a summary of the results or the paper in Neurology

In June 2016 researchers in Canada published results of a long-term HSCT trial involving 24 people with aggressive relapsing-remitting MS whose disease was not controlled with available therapies. Three years after the procedure, 70% remained free of disease activity, with no relapses, no new MRI-detected inflammatory brain lesions, and no signs of progression. None of the surviving participants experienced clinical relapses or required MS disease-modifying therapies to control their disease, and 40% experienced reductions in disability. One participant died and another required intensive hospital care for liver complications. All participants developed fevers, which were frequently associated with infections, and other toxicities.Read more about this study

In October 2015, researchers at the University of Genoa and other institutions in Italy reported on a small trial of HSCT in seven people with very active relapsing-remitting MS that was not controlled with MS disease-modifying therapy. They underwent a low-intensity lympho-ablative regimen in which the immune system was suppressed but not completely depleted before the stem cell transplant as an approach to reducing toxicity. The investigators did MRI scans (for 3 years) and clinical evaluations (for 5 years). They found dramatic reductions of MRI-detected inflammation after the procedure, but did not achieve complete absence of inflammation. After 5 years, two participants remained stable, one significantly improved, and four had mild disease progression. One experienced a relapse after treatment. No severe side effects occurred. The authors conclude that the low-intensity regimen they used was not sufficient to treat aggressive MS.Read an abstract from the paper(Multiple Sclerosis 2015 Oct;21(11):1423-30) In January 2015, doctors at Northwestern University published their10-year experience of treating people with HSCT. The report included 123 people with relapsing-remitting MS and 28 with secondary-progressive MS. Their method is nonmyeloblative HSCT, in which the immune system is suppressed but not completely depleted before the stem cell transplant. Individuals were followed from 6 months to 5 years, or an average of 2.5 years. The EDSS disability scores improved, compared to pretreatment, by one point or more in 64% of those followed out to year 4. Relapses and MRI-detected disease activity were also reduced. In evaluating which type of individuals benefited from the therapy, the doctors suggested that people with relapsing-remitting MS who had had MS for ten years or less showed improvements in their disability scores, whereas those with secondary-progressive MS or disease duration greater than ten years did not show improvements on their disability scores. They reported no treatment-related deaths or serious infections. ITP (immune-mediated thrombocytopenia), a potentially serious bleeding disorder, developed in 7 people, and thyroid disorders developed in 7 people.Read a summary of their resultsor thepaper in JAMA (Published onlineJanuary 20, 2015).

Ongoing Research in HSCTAdditional research is focusing on figuring out who might benefit from this procedure and how to reduce its risks. HSCTis being investigated in Canada, the United States, Europe and elsewhere. For example:

Dr. Richard Burt of Northwestern University in Chicago has recently begun a new phase 3 clinical trial at Northwestern to try to determine the optimal protocol for safety and benefit. Read more about this trial on clinicaltrials.gov A clinical trial is getting underway at medical centers in Denmark, Netherlands, Norway and Sweden. The trial is testing treatment with HSCT compared with alemtuzumab in people with active relapsing-remitting MS. Read more about this trial on clinicaltrials.gov

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Bone Marrow Stem Cell Transplant HSCT : National ...

Recommendation and review posted by Bethany Smith

Thyroid hormone is easy to take. Because it stays in your system for a long time, it can be taken just once a day, and this results in very stable levels of thyroid hormone in the blood stream. When thyroid hormone is used to treat hypothyroidism, the goal of treatment is to keep thyroid function within the same range as people without thyroid problems. Keeping the TSH level in the normal range does this. The best time to take thyroid hormone is probably first thing in the morning on an empty stomach. This is because food in the stomach can affect the absorption of thyroid hormone. However, the most important thing is to be consistent, and take your thyroid hormone at the same time, and in the same way, every day. If you are taking several other medications, you should discuss the timing of your thyroid hormone dose with your physician. Sometimes taking your thyroid hormone at night can make it simpler to prevent your thyroid hormone from interacting with food or other medications.

Do not stop your thyroid hormone without discussing this with your physician. Most thyroid problems are permanent, and therefore most patients require thyroid hormone for life. If you miss a dose of thyroid hormone, it is usually best to take the missed dose as soon as you remember. It is also safe to take two pills the next day; one in the morning and one in the evening. It is very important that your thyroid hormone and TSH levels are checked periodically, even if you are feeling fine, so that your dose of thyroid hormone can be adjusted if needed.

Continue reading here:
Thyroid Hormone Treatment | American Thyroid Association

Recommendation and review posted by Bethany Smith

Gene therapy is a technology aimed at correcting or fixing a gene that may be defective. This exciting and potentially transformative area of research is focused on the development of potential treatments for monogenic diseases, or diseases that are caused by a defect in one gene.

The technology involves the introduction of genetic material (DNA or RNA) into the body, often through delivering a corrected copy of a gene to a patients cells to compensate for a defective one, using a viral vector.

The technology involves the introduction of genetic material (DNA or RNA) into the body, often through delivering a corrected copy of a gene to a patients cells to compensate for a defective one, using a viral vector.

Viral vectors can be developed using adeno-associated virus (AAV), a naturally occurring virus which has been adapted for gene therapy use. Its ability to deliver genetic material to a wide range of tissues makes AAV vectors useful for transferring therapeutic genes into target cells. Gene therapy research holds tremendous promise in leading to the possible development of highly-specialized, potentially one-time delivery treatments for patients suffering from rare, monogenic diseases.

Pfizer aims to build an industry-leading gene therapy platform with a strategy focused on establishing a transformational portfolio through in-house capabilities, and enhancing those capabilities through strategic collaborations, as well as potential licensing and M&A activities.

We're working to access the most effective vector designs available to build a robust clinical stage portfolio, and employing a scalable manufacturing approach, proprietary cell lines and sophisticated analytics to support clinical development.

In addition, we're collaborating with some of the foremost experts in this field, through collaborations with Spark Therapeutics, Inc., on a potentially transformative gene therapy treatment for hemophilia B, which received Breakthrough Therapy designation from the US Food and Drug Administration, and 4D Molecular Therapeutics to discover and develop targeted next-generation AAV vectors for cardiac disease.

Gene therapy holds the promise of bringing true disease modification for patients suffering from devastating diseases, a promise were working to seeing become a reality in the years to come.

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What is Gene Therapy? | Pfizer: One of the world's premier ...

Recommendation and review posted by Bethany Smith

The CMTA Is Accelerating Research Through Gene Therapy

The CMTA looks forward to a time when doctors are able to use genetic therapies to treat the root cause of CMT rather than prescribing medications or recommending surgery. We are already envisioning the possibilities that gene therapy holds for our community of 2.8 million people worldwide living with CMT. In fact, were leading the pursuit to explore gene therapy in CMT by expanding our Strategy to Accelerate Research (STAR) program and our STAR Advisory Board.

At the CMTA, we are already envisioning the possibilities that gene therapy holds for our community of 2.8 million people worldwide living with CMT. John Svaren, PhD, Chair, CMTA Scientific Advisory Board

Given the increased feasibility and applicability of gene therapy to CMT, the CMTA hosted a Gene Therapy Workshop in 2018. In response to invitations from CMTA board member Dr. Steven Scherer, more than 20 of the top gene therapy experts gathered for the inaugural CMT-centered workshop on gene therapy. This meeting included experts who have worked in related genetic and neuromuscular disease areas, as well as clinicians and scientists spearheading efforts toward gene therapy for CMT2D and CMT4J.

Building on this meeting, the CMTA is assembling the best experts to formulate gene therapy strategies for CMT2 and CMT1 subtypes. Four gene therapy experts, Beverly Davidson, PhD, at the University of Pennsylvania, Kleopas Kleopa, MD, at the Cyprus Institute of Neurology & Genetics, Scott Harper, PhD, at the Ohio State University School of Medicine, and Steven Gray, PhD, at the University of Texas Southwestern Medical Center have now joined the Scientific Advisory Board of the CMTA. Dr. Davidson is an acknowledged leader in the gene therapy field, and her extensive experience includes both academic research and commercial translation gene therapy approaches. Dr. Kleopa has shown proof of concept that gene therapy works in two mouse models of CMT: CMT1X and CMT4C. This strategy can capitalize on the CMT animal models that have been developed and characterized with CMTA support. Dr. Harper is collaborating with Robert Burgess, PhD, at the Jackson Laboratory to develop a gene therapy vector to be used in a treatment for CMT2D. Dr. Grays core expertise is in Adeno-Associated Virus (AAV) gene therapy vector engineering, followed by optimizing approaches to deliver a gene to the nervous system, with application to CMT4J.

Our genes dictate many of our personal characteristics; however, mutations in genes cause genetic diseases, such as CMT. Scientists have been working for decades to modify or replace faulty genes with healthy ones to treat, cure or prevent disease. Fortunately, we are seeing significant progress on these efforts to provide gene therapy options for CMT. In fact, recent studies have provided an effective gene therapy for spinal muscular atrophy (SMA), a devastating disorder that affects the same motor neurons that are affected by CMT.

Sometimes the whole gene is duplicated, as in CMT1A, where a chromosome segment around the PMP22 gene is present in three copies instead of two. Alternatively, a part of a gene is defective or missing from birth, causing many of the other known forms of CMT. Any of these variations can disrupt the structure of the protein that is encoded by the affected gene, causing cellular problems that ultimately lead to disease.

In gene therapy, scientists can do one of several things depending on the problem with the gene. The simplest form of gene therapy is to simply provide a correct copy of the gene, which is the basis of the gene therapy for SMA. In variations of this approach, genes that are causing problems can be suppressed. One example of this was the recent demonstration that antisense oligonucleotides can be used to improve the neuropathy in rodent models of CMT1A. In addition, the exciting new field of genome editing using CRISPR technology has now made it possible to correct disease-causing mutations, and collaborative projects have already been initiated with leaders in this field

In order to insert new genes directly into cells, scientists use a vehicle called a vector that is genetically engineered to deliver the correct version of the gene. For example, viruses have a natural ability to deliver genetic material into cells, and therefore, can be used as vectors. While some viruses cause disease, virus vectors are highly modified to remove their ability to cause disease so that they can be safely used to carry therapeutic genes into human cells.

Gene therapy can be used to modify cells inside or outside the body. When its done inside the body, a doctor will inject the vector carrying the gene directly into the part of the body that has defective cells.

Before a company can market a gene therapy product for use in humans, the gene therapy product has to be tested for safety and effectiveness so that the Food and Drug Administration (FDA) can evaluate whether the risks of the therapy are acceptable in light of its potential benefits. Gene therapies have begun to receive FDA approval, and many gene therapies are in clinical trials.

At the CMTA, we believe gene therapy holds the promise to provide effective therapies for people living with CMT. As we continue to make great strides in this area, the CMTA is committed to helping speed the development of gene therapy approaches by investing in the most promising and groundbreaking gene therapy treatments that have the potential to benefit our community.

We are members of the National Organization for Rare Disorders (NORD), and they have put together a six-minute video to help answer questions frequently asked about gene therapy. We think this video will help you better understand the basics of gene therapy.

See the article here:
STAR Gene Therapy | Charcot-Marie-Tooth Association

Recommendation and review posted by Bethany Smith

Testosterone is a hormone that is present in both men and women. Testosterone is the androgenic hormone primarily responsible for normal growth and development of male sex and reproductive organs, including the penis, testicles, scrotum, prostate, and seminal vesicles. It facilitates the development of secondary male sex characteristics such as musculature, bone mass, fat distribution, hair patterns, laryngeal enlargement, and vocal chord thickening. Additionally, normal testosterone levels maintain energy level, healthy mood, fertility, and sexual desire.

The number of men diagnosed with hypogonadism, commonly referred to as Low T has grown dramatically in recent years due to an increasing awareness of the importance of hormones in a mans health and well being. Research shows that about 1 out of 4 men over the age of 30 may have low testosterone. Circulating testosterone levels decline progressively with age, starting in the second and third decade of life. Testing for testosterone deficiency requires a comprehensive understanding of the intricacies of hormone balance before one makes a commitment to what may be lifelong therapy.

Low Libido

Gaining fat around the middle

If you have any of these common symptoms, it is recommended you have a proper and thorough set of labs drawnto help determine if you havehypogonadism.

Testosterone replacement therapy is essential for men with hypogonadism. In these men, full replacement of testosterone is necessary. The amount of total testosterone in men can range from 300 to 1100 ng/ml, while the range for free testosterone is 50 to 250 ng/ml. It is more accurate to utilize free testosterone levels instead of total T levels.

Because the range is so broad, testosterone optimization must be individualized. In general, Dr. Rob aims to provide the lowest dose of testosterone that relieves symptoms and causes the man to be in the optimized zone. All while monitoring testosterone and its by-products for any potential unwanted side effects. There are several delivery method options and Dr. Rob presents the pros and cons of each before a mutually agreed upon delivery method is instituted.

It is also important to note that men should not be started on testosterone replacement without a careful endocrine evaluation to determine the cause of the low testosterone. Serious conditions including pituitary tumors can present with low testosterone.

Women have testosterone too

Men have 10 to 20 times higher levels of testosterone than women. Nonetheless, even this small amount of testosterone in women is important for maintaining sexual function, and healthy bladder and vaginal function.

When used in small physiologic doses with monitoring of testosterone blood levels, testosterone in women is well tolerated. High doses must be avoided as they can cause facial hair, loss of scalp hair, deepening of voice, and acne. Just like men, womenshould not be started on testosterone replacement without a careful endocrine evaluation to determine if it will provide a health benefit.

ReNue Healthis located conveniently in Springboro, Ohio with easy access from Dayton International Airport, Cincinnati International Airport or the adjacent Wright Brothers Private Airport (MGY) for those travelling by private aviation.Click here for directions and contact information.

Only one visit is necessary to perform a comprehensive history, interview, and education. Follow up evaluations, adjustments and balancing of hormones are done by phone or written communications and a return visit to Dr. Rob is not necessary. Ongoing testing and adjustment is mandatory and performed through a laboratory convenient to your home.

Its that nagging feeling that something does not feel quite right and you cant put your finger on it. Youre a busy person and your own health is the last thing you have time to think about, but think again!

To learn how the ReNue Health Opportunity may help restore your youth and vitality, simply call937-350-5527or visit us online atwww.renuehealth.com

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Testosterone Replacement Therapy For Men - Renue Health

Recommendation and review posted by Bethany Smith

In Boston, scientists are working at the frontier of genetic research in an attempt to cure Macular Degeneration, the leading cause of blindness in the U.S., an enormous task.

Rajendra Kumar-Singh: There are about 3 billion nucleotides in the human genome and just 1 small mistake is sufficient to cause a problem. And when that problem occurs it can lead to inherited retinal degeneration.

Dean Bok: The promises of gene therapy at this point in time are tremendous. In principal, one can replace a bad gene with a good one. Its easier to replace a gene thats recessive, where you need two bad ones in order to produce the disease, and thats where weve had success. The challenge is for genes that are dominant. You need to get rid of the bad guys before the good guys can do their work.

Rajendra Kumar-Singh: Because the source of inherited retinal degeneration is DNA, it makes sense to be able to deliver normal DNA to correct the defect and hence gene therapy is going to be a key player in trying to develop novel therapies for these inherited retinal degeneration.

Narrator: (Animation) An imbalance in the complement system, which helps to fight many diseases, can cause holes or, macs, to form in the macula. A protein called cd59 normally helps prevent this from occurring. At Tufts University they are seeking a way to increase this protein in people with macular degeneration.

Rajendra Kumar-Singh: We plan to express the same protein but at higher levels on the cells that are normally getting damaged in AMD and theoretically we hope to be able to prevent the formation of these macs on these cells. When we use gene therapy we are in fact putting back in a normal version of the gene, such as the protein that is produced from that is now normal and allows the cell to revert to a normal, healthy looking or healthy functioning cell. We can potentially inject just once directly into the eye and that may serve as a therapeutic for the lifetime of the patient whether it be dry AMD or wet AMD. Science is all about solving problems and I would love to be the one to be able to solve this problem and provide some sort of therapies to people who otherwise might potentially go blind. And I think Ill have fulfilled my role as a scientist if I can achieve that.

Rajendra Kumar-Singh, PhD, Professor of Ophthalmology and NeuroscienceTufts University

Dean Bok, Phd, Distinguished Professor of Neurobiology and OphthalmologyUCLA

See the article here:
Gene Therapy to Treat Macular Degeneration - AMDF

Recommendation and review posted by Bethany Smith

In the race for the most potent CAR T-cell therapy, there is a big interest to the issue of purity and composition of the final cell product. In this post, Ill try to summarize the current knowledge about defined CAR T-cell products, based on two clinical studies, published this week.

What is defined product and why it is important?We can roughly divide CAR T-cell products on bulk T-cell or crude and defined composition. Crude CART products are not purified and contain: different ratios of CD4/CD8 T-cells and their subsets, other than T- contaminating cells and non-CAR cells. Defined composition products could be the following:

There are few good reasons for development of defined CART products:

The later is single most important reason, which begs the question Will defined CAR T-cell products deliver superior therapeutic benefit? As of today, vast majority of CART developers manufacture crude cell products. Manufacturing process usually does not include sorting of T-cells on day 0 or purification of T-cells/ CAR+ cells in-process or on a harvest day. Most of developers release final CAR T-cell product with CD3+ cells >80-90%, highly variable CD4/CD8 ratio and % of CAR+ cells.

Preclinical dataAt least one group of researchers have done a lot of experimental and clinical work on defined composition of CAR T-cell products. Defined product/ process development has been done by Michael Jensen lab, initially at City of Hope and then further adapted and modified at Fred Hutchinson Cancer Center and Seattle Childrens Hospital. Stanly Riddells lab from Hutch did a lot of experimental work to demonstrate potential value of defined CAR T-cell product. All together they have tried all versions of defined composition CAR T-cell products, mentioned above. One of recent and the most comprehensive studies by Riddells lab, showed that (1) combination of both CD4 and CD8 T-cells has superior therapeutic potency and (2) naive CD4 cells and central memory (T-CM) CD8 T-cell subsets were the most potent in vivo. Long-term persistence of human memory T-cells was demonstrated by Riddell and Jensen earlier in mouse and primate models. Importance of CD4+CD8 combo rather than use of potent cytotoxic CD8+ cells alone was also demonstrated in numerous studies (check here, here and here). Therefore, experimental studies created a strong rational for favoring T-CM, naive T-cells (T-N) and CD4+CD8 combo in adoptive cell therapy trials.

Feasibility of manufacturing defined T-CM CAR T-cell productBefore I get to the first clinical results, Id like to look at manufacturing process of defined CAR T-cell product. Jensen started with purified CD8 T-CM or CD4 + CD8 T-CM manufacturing process, which described in details here. It includes sequential 2-step CliniMACS procedure for negative selection of CD14/CD45RA/CD4 or CD14/CD45RA-negative cells, positive selection for CD62L (marker of T-CM) and culture with IL2/IL15 for up to 30 days in bags. After two CliniMACS procedures, cell recovery was as low as 0.4% (in contrast to expected 1.4%). If input cell number was usually 5 billions PBMCs, average output cell number before starting a culture was ~19 millions. T-CM recovery efficiency was 26%. Even though, they typically started culture from 7-15 millions of CD8 T-CM cells, generation of ~3 billions of cells in 3-6 weeks was feasible. This manufacturing process was used in 2 clinical trials: NHL1 and NHL2.

In the modified manufacturing process, designed for NCT01865617 trial, included CliniMACS selection of CD4+ bulk population and 2-step CD8 T-CM (see above) or CD8 bulk selection with 2 parallel 15-20 days cultures and mixing CD4:CD8 as 1:1 before infusion. Importantly, CAR+ cells were selected before infusion by a marker (EGFRt). Interestingly, either CD8 T-CM purified on day 0 or CD8 bulk cells yielded only ~40-50% of CD8+/CAR+ cells with T-CM phenotype (CD45RA-CD62L+).Now, feasibility of manufacturing in NCT01865617. 16/30 (53%) patients have passed threshold of 20 T-CM cells/ ul in screening assay for feasibility of manufacturing. From selected products, T-CM were successfully manufactured in all, but 1 cases. 3 out of 30 infused products were not formulated as 1:1 (10%), due to lack of expansion.Id summarize some of my thoughts of defined CAR T-cell product manufacturing feasibility as the following:

Clinical outcomes of using defined CAR T-cell productsResults of 3 clinical trials (NCT01318317, NCT01815749, NCT01318317), using defined CAR T-cell products have been published so far (here and here). However, the therapeutic benefit of using defined versus crude CAR T-cell product remains unclear. Ideally, defined CAR T-cells should be compared with crude product within one trial settings, because even for the same conditions, clinical protocols are very very different between sites. Also, ideally, CD8 bulk vs. CD T-CM or CD8 alone vs. CD8+CD4 combo should be compared within one trial in exactly the same settings. Unfortunately, none of these ideal comparison conditions were met in 3 published trials, mentioned above.

Even though, it seem like CD4 + CD8 T-CM combo performed better in NHL2 trial (75% progression-free survival at 1-year) than CD8 T-CM alone in NHL1 (50% progression-free survival at 1-year), the difference is not significant, due to low number of patients (n=8 in each trial). On top of it, different CAR vectors were used between these trials, culture duration was shorter and CD25+ T-regs were depleted in NHL2 trial manufacturing protocol. So, data cannot be compared. If we look at results of other CAR T-cell lymphoma trials (narrowing to DLBCL), City of Hope results are not much better than reported from other centers (for example, from Penn). CD8 T-CM persistence was not beneficial, compare to data from other centers. Two excerpts from the study, which demonstrate that assessment of defined CAR T-cell product benefit is impossible:

CD19-CAR T cell activity is difficult to assess by disease response, since 9/16 patients were in CR at start of study, and HSCT can also produce CRs.Thus, a T cell product derived from central-memory enrichment as described in these studies, does not persist longer than what is observed in trials with conventional bulk T cells transduced with CARs bearing CD28 co-stimulatory domains.

Now, moving to B-ALL study, published this week in JCI. First of all, B-ALL is not the best condition to assess a difference by clinical outcome between crude and defined CAR T-cell products, because response rate is too high (close to 90%) across the centers no matter what. The authors about outcome:

The 93% remission rate by flow cytometry and 86% MRD-negative CR rate in our study compares very favorably to that reported by others in which CART cells of undefined composition were manufactured using CD19 CARs that incorporate either a 4-1BB costimulatory domain (children and young adults, 79%) or a CD28 costimulatory domain (adults, 75%; children and young adults, 60%) (1-4)

What about persistence? Theoretically, based on experimental work, CD8 T-CM should have superior long-term persistence. But it was not the case. The study showed persistence only at 1 month time point. What about relapses? Maybe application of T-CM will reduce the rate of relapses? No, 9/30 patients in the study relapsed, half of them (5/9) received CD8 T-CM product. Clinical outcome was significantly improved in the study after implementation of different conditioning regiment (with fludarabine). This change significantly complicates and even make impossible data comparison between CD8 bulk and CD8 T-CM groups:

The high overall rate of BM remission of 93% by flow cytometry in this study and differences in lymphodepletion regimens and infused cell doses do not allow comparison of the efficacy of CART cell products manufactured from CD8+ TCM cells or from bulk CD8+ T cells. Analysis of differences in long-term persistence of cell products that were selected for CD8+ TCM or bulk CD8+ T cells in our study was further complicated by our findings that immune-mediated rejection of CART cells occurs in some patients, which may provide an explanation for the loss of CART cells observed in a subset of patients in other studies

To conclude: Despite the strong experimental evidence and very attractive idea behind of defined CAR T-cell products, it is too early to conclude about their therapeutic benefit and superior potency. With greater number of patients and technical improvements in manufacturing (more efficient clinical cell sorting, IL7+IL15 in culture and other), potential benefit of defined CAR T-cell product may become more obvious. Such benefits as dropping a therapeutic dose, better correlation between dose and in vivo expansion dynamics, decreasing donor variability in manufacturing, we can see today already.

Tagged as:CART, cell product, manufacturing

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Crude versus defined CAR T-cell therapy product

Recommendation and review posted by Bethany Smith

In our society, we think of anxious behavior as being a disadvantage. But that's because, for the most part, we live in a nutrient-rich, low-danger environment. In the rat equivalent to our world, the relaxed rat lives a comfortable life. It is likely to reach a high social standing, and it doesn't have to worry about where its next meal is coming from. An anxious rat, on the other hand, doesn't do so well. It is more likely to have a low social standing and suffer from diabetes and heart disease.

In another environment, however, the tables turn. The anxious, guarded behavior of the low-nurtured rat is an advantage in an environment where food is scarce and danger is high. The low nurtured rat is more likely to keep a low profile and respond quickly to stress. In the same environment, a relaxed rat might be a little too relaxed. It may be more likely to let down its guard and be eaten by a predator.

More here:
Lick Your Rats - Genetics

Recommendation and review posted by Bethany Smith

Studies show that people who eat the most fruits and vegetables enjoy healthier and longer lives, but getting the recommended five servings a day is difficult for even the healthiest diets. That's why we created Life Extension Mix, a daily supplement that provides all the high-potency vitamins and minerals needed to form the cornerstone of a comprehensive health maintenance program.

Benefits at a Glance:

Our formula saves time and money by combining the most important nutrients including unique vegetable, fruit, and botanical extracts into one product, eliminating the need to take dozens of separate supplements.

More facts about Life Extension Mix

Life Extension Mix is a state-of-the-art multi-nutrient formula jam-packed with the purest and most potent forms of vitamins, minerals, amino acids, and unique vegetable, fruit, and botanical extracts. In every daily dose of Life Extension Mix, you'll get an extensive array of nutrients:

Bioactive quercetin phytosome

Life Extension Mix contains 5 mg of quercetin that has been integrated into a phytosome. A phytosome is a phospholipid sphere that encases a botanical compound, aiding in its absorption and making it more bioavailable: this quercetin is up to 50 times more bioavailable than standard quercetin. Quercetin supports cellular health, endothelial health, and healthy immune function.

Delphinidins

Found in dark red fruits, delphinidins are potent anthocyanin compounds that activate the production of nitric oxide, promoting vascular relaxation and blood pressure support.14 They can also help inhibit inflammatory factors58 and glycation,9 support immune health, and help maintain healthy blood sugar levels within normal range.

Pyridoxal 5'-phosphate

Glycation is a normal part of the aging process that can affect your health.1014 To help inhibit glycation, each daily dose of Life Extension Mix provides 100 mg of pyridoxal 5'-phosphate a metabolically active B6 that has been shown to help inhibit glycation reactions.15-17

Standardized pomegranate extract

Pomegranate supports healthy cardiovascular function32-37 and DNA structure in prostate cells.18-23 Our pomegranate extract is standardized to provide the biologically active punicalagins that are so unique to this fruit. These punicalagins are 100% water-soluble, have a remarkable 95% absorption rate,24 and are highly potent at inhibiting free radicals.25

Blueberry extracts

Blueberry anthocyanin compounds help inhibit free radicals, while blueberry's other active constituents promote healthy lipid and glucose levels for those already within normal range.26-29 Even more exciting: these blueberry constituents may help protect DNA structure.30-34 Life Extension Mix features the wild blueberry extract packed with active blueberry constituents.

Standardized green tea extract

In recent years, the active polyphenol compounds in green tea have been found to help inhibit LDL oxidation, neuronal peroxidation, and help maintain healthy DNA structure.35-44 Life Extension Mix's daily dose contains 325 mg of a decaffeinated green tea extract standardized to provide 98% of the active polyphenols that scientists attribute to green tea's multiple health benefits.

Standardized vegetable extracts

Life Extension Mix offers a wide array of vegetable extracts, including 8 mg of luteolin, a flavonoid found in parsley, basil, celery, and other foods. Luteolin has been shown to inhibit DNA oxidation45 and to inhibit excess levels of cytokines such as interleukin-4 and interleukin-13.46

Our formula features a concentrated broccoli mixture with standardized extracts of sulforaphane and glucosinolates, compounds attributed to broccoli's detoxification, DNA,47-50 and other health benefits,51-71 as well as chlorophyll.72-83A daily dose also provides 200 mg of calcium D-glucarate (supplying 175 mg of D-glucarate), a phytonutrient found in grapefruit, apples, oranges, broccoli, and Brussels sprouts. D-glucarate supports detoxification processes.84-86

Life Extension Mix also contains lutein and lycopene. Lutein, an extract found in in leafy greens such as kale and spinach, has been shown to help maintain critical pigments in the eye macula.87 Lycopene from tomatoes helps to maintain DNA structure and protect against LDL oxidation.88-98

Standardized fruit extracts

In addition to our standardized pomegranate and wild blueberry extracts, Life Extension Mix also features fruit extracts such as bilberry, grape seed, and citrus bioflavonoids to promote healthy circulation help maintain healthy DNA.

Our unique formula is fortified with maqui berry and tart cherry for their antioxidant benefits for heart health as well as muscle and joint function support.99-118 It also includes a customized blend of blackberry, cranberry, plum, elderberry, persimmon, cherry, and other fruits that studies indicate provide multiple favorable effects on the body.

Numerous studies have pointed toward the many benefits of olive polyphenols, and Life Extension Mix contains an olive extract standardized to provide polyphenols like hydroxytyrosol that have been shown to help inhibit LDL oxidation, free radicals, and promote healthy cell membranes.119-131

Sesame seed lignan extract

Sesame lignans promote healthy levels of gamma tocopherol,132,133 enhance the beneficial effects of fish oils, and helping to maintain already-normal cholesterol/LDL levels.134-143 Life Extension Mix provides 10 mg of a sesame lignan extract to supply the direct benefits of the lignans and to augment the effects of vitamin E174 and other nutrients such as gamma-linolenic acid (GLA).

Nutrients to maintain healthy blood glucose levels

Chromium, magnesium, and biotin help maintain healthy blood sugar for those already within normal range.145-156 In addition to highly absorbable forms of magnesium and biotin, Life Extension Mix contains 500 mcg of Crominex 3+, a biologically active chromium complex. Studies on the benefits of chromium supplementation show that doses exceeding 200 mcg a day are required for optimal effects.157-159

High-potency vitamin D3

Researchers today are concerned that many people are not supplementing with enough vitamin D, a critical nutrient for maintaining bone density and healthy cell division.160-167 Currently, most experts in the field believe that intakes of between 1,000 and 10,000 IU for adults will lead to a more healthy level of serum 25(OH)D, at approximately 50-80 ng/mL.168-170

Each daily dose of Life Extension Mix provides 2,000 IU of vitamin D3. What's more, this formula contains only 500 IU of preformed vitamin A. Preformed (not beta-carotene) vitamin A may interfere with the benefits of vitamin D, yet most multivitamins contain between 5,000 and 25,000 IU of preformed vitamin A.171

Cyanidin-3-glucoside (C3G)

Life Extension Mix contains 1.25 mg of C3G to support eye health. Found in blackberries and black currants, this potent compound promotes healthy levels of rhodopsin a compound that absorbs light in the retina and enhance night vision.172-176

In one study, just 50 mg of a berry extract concentrate containing C3G helped aging individuals see better in the darkness after 30 minutes.177 Bioavailable C3G also supports other body functions,178-191 has potent antioxidant properties,192,193 and supports endothelial cell health.194,195

5-MTHF (5-methyltetrahydrofolate)

Folate helps maintain homocysteine levels within the normal range. One dose of our formula contains 400 mcg of the bioactive 5-MTHF form of folate, which is up to 7 times more bioavailable than ordinary folic acid.

Selenium and Apigenin

Life Extension Mix contains three potent forms of selenium (SelenoExcell, Se-methyl-selenocysteine, and sodium selenite). Also newly included is apigenin, a powerful bioflavonoid found in many vegetables and fruits which boosts cell protection.

Why choose Life Extension Mix?

The ingredients in Life Extension Mix are based on over 35 years of clinical research, and we've selected the purest and most potent forms of plant extracts, vitamins, minerals, and other nutrients for maximum absorption. Discover the extensive benefits of Life Extension Mix!

See more here:
Life Extension Mix, 360 capsules | Life Extension

Recommendation and review posted by Bethany Smith

Pluripotent stem cells are master cells. Theyre able to make cells from all three basic body layers, so they can potentially produce any cell or tissue the body needs to repair itself. This master property is called pluripotency. Like all stem cells, pluripotent stem cells are also able to self-renew, meaning they can perpetually create more copies of themselves.

There are several types of pluripotent stem cells, including embryonic stem cells. At Childrens Hospital Boston, we use the broader term because pluripotent stem cells can come from different sources, and each method creates a cell with slightly different properties.

But all of them are able to differentiate, or mature, into the three primary groups of cells that form a human being:

Right now, its not clear which type or types of pluripotent stem cells will ultimately be used to create cells for treatment, but all of them are valuable for research purposes, and each type has unique lessons to teach scientists. Scientists are just beginning to understand the subtle differences between the different kinds of pluripotent stem cells, and studying all of them offers the greatest chance of success in using them to help patients.

Types of pluripotent stem cells:

All four types of pluripotent stem cells are being actively studied at Childrens.

Induced pluripotent cells (iPS cells):Scientists have discovered ways to take an ordinary cell, such as a skin cell, and reprogram it by introducing several genes that convert it into a pluripotent cell. These genetically reprogrammed cells are known as induced pluripotent cells, or iPS cells. The Stem Cell Program at Childrens Hospital Boston was one of the first three labs to do this in human cells, an accomplishment cited as the Breakthrough of the Year in 2008 by the journal Science.

iPS cells offer great therapeutic potential. Because they come from a patients own cells, they are genetically matched to that patient, so they can eliminate tissue matching and tissue rejection problems that currently hinder successful cell and tissue transplantation. iPS cells are also a valuable research tool for understanding how different diseases develop.

Because iPS cells are derived from skin or other body cells, some people feel that genetic reprogramming is more ethical than deriving embryonic stem cells from embryos or eggs. However, this process must be carefully controlled and tested for safety before its used to create treatments. In animal studies, some of the genes and the viruses used to introduce them have been observed to cause cancer. More research is also needed to make the process of creating iPS cells more efficient.

iPS cells are of great interest at Childrens, and the lab of George Q. Daley, MD, PhD, Director of Stem Cell Transplantation Program, reported creating 10 disease-specific iPS lines, the start of a growing repository of iPS cell lines.

Embryonic stem cells:Scientists use embryonic stem cell as a general term for pluripotent stem cells that are made using embryos or eggs, rather than for cells genetically reprogrammed from the body. There are several types of embryonic stem cells:

1. True embryonic stem cell (ES cells)These are perhaps the best-known type of pluripotent stem cell, made from unused embryos that are donated by couples who have undergone in vitro fertilization (IVF). The IVF process, in which the egg and sperm are brought together in a lab dish, frequently generates more embryos than a couple needs to achieve a pregnancy.

These unused embryos are sometimes frozen for future use, sometimes made available to other couples undergoing fertility treatment, and sometimes simply discarded, but some couples choose to donate them to science. For details on how theyre turned into stem cells, visit our page How do we get pluripotent stem cells?

Pluripotent stem cells made from embryos are generic and arent genetically matched to a particular patient, so are unlikely to be used to create cells for treatment. Instead, they are used to advance our knowledge of how stem cells behave and differentiate.

2. Stem cells made by somatic cell nuclear transfer (ntES cells)The term somatic cell nuclear transfer (SCNT) means, literally, transferring the nucleus (which contains all of a cells genetic instructions) from a somatic cellany cell of the bodyto another cell, in this case an egg cell. This type of pluripotent stem cell, sometimes called an ntES cell, has only been made successfully in lower animals. To make ntES cells in human patients, an egg donor would be needed, as well as a cell from the patient (typically a skin cell).

The process of transferring a different nucleus into the egg reprograms it to a pluripotent state, reactivating the full set of genes for making all the tissues of the body. The egg is then allowed to develop in the lab for several days, and pluripotent stem cells are derived from it. (Read more in How do we get pluripotent stem cells?)

Like iPS cells, ntES cells match the patient genetically. If created successfully in humans, and if proven safe, ntES cells could completely eliminate tissue matching and tissue rejection problems. For this reason, they are actively being researched at Childrens.

3. Stem cells from unfertilized eggs (parthenogenetic embryonic stem cells)Through chemical treatments, unfertilized eggs can be tricked into developing into embryos without being fertilized by sperm, a process called parthenogenesis. The embryos are allowed to develop in the lab for several days, and then pluripotent stem cells can be derived from them (for more, see How do we get pluripotent stem cells?)

If this technique is proven safe, a woman might be able to donate her own eggs to create pluripotent stem cells matching her genetically that in turn could be used to make cells that wouldnt be rejected by her immune system.

Through careful genetic typing, it might also be possible to use pES cells to create treatments for patients beyond the egg donor herself, by creating master banks of cells matched to different tissue types. In 2006, working with mice, Childrens researchers were the first to demonstrate the potential feasibility of this approach. (For details, see Turning pluripotent stem cells into treatment).

Because pES cells can be made more easily and more efficiently than ntES cells, they could potentially be ready for clinical use sooner. However, more needs to be known about their safety. Concerns have been raised that tissues derived from them might not function normally.

Read more about pluripotent stem cells by following these links:

Read the original:
Pluripotent Stem Cells 101 Boston Children's Hospital

Recommendation and review posted by Bethany Smith

A popular hormone clinic that was accused in a lawsuit in September of causing a patients death by giving him too much testosterone has been accused in another complaint of prescribing a diet drug banned by the federal government.

In a suit filed Friday in Jefferson Circuit Court, Cindy Kinder-Benge and her husband Mark allege that a nurse at 25 Again gave her human chorionic gonadotropin, or HCG, for weight loss, without disclosing that it is ineffective for that purpose.

In a consumer update headlined HCG Diet Products Are Illegal, the U.S. Food & Drug Administration saidthe hormone is not approved and there is no evidence that it produces weight loss.

The latest suit alleges that a nurse at 25 Agains New Albany clinic provided HCG in conjunction with a 700-calorie-a-day diet, which the FDA says can be dangerous and potentially fatal.

The suitsays "multiple peer-reviewed, prospective, randomized, clinical trials dating back to 1976 have concluded that HCG is ineffective for weight loss and should not be prescribed for that purpose. This information was not shared with the plaintiff."

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Ted Ennenbach, who owns 25 Again, also known as Body Shapes Medical, said in an email that the company "promotes health" anddoes not "endorse or use" either homeopathic HCG or 700-calorie diets. He said he was out of town and hadn't seen the suit and couldn't confirm whetherKinder-Benge was a patient.

The lawsuit follows other legal trouble for the clinic. In the suit filed in September, MelanieLester said the clinic repeatedly administered testosterone to her husband David, even thoughhis levels of it were normal, eventually causing his death from a heart attack.

Two other widows have sued nurse practitioner Karla King, who previously worked in Owensboro, alleging she also gave excessive testosterone to their husbands, who had normal levels of the male hormone, resulting in their deaths.King has denied negligence.

In her complaint Friday, Kinder-Bengesaid she saw ads on TV in which the clinic said its hormone treatments could resolve symptoms of menopause, such as hot flashes, and cause weight loss. She signed up for treatment at an annual rate of $2,388 plus an additional $209 for HCG.

She said blood work showed she had normal thyroid levels but a nurse nonetheless gave her additionalthyroid that caused her to experience severe chest pain and weakness due to her heart racing.

The clinic allegedly continued to tell her she needed extra thyroid, which she took for 22 months.

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From August: Why are nurses fleeing a controversial Louisville hormone treatment clinic 25 Again?

The lawsuit alleges a co-worker had to take her to BaptistHealth Floyd, where she was diagnosed as suffering from atrial fibrillation, an irregular heartbeat that can lead to blood clots, stroke, heart failure and other heart-related complications

Last September, despite being on medication to control her irregular heartbeat, she had chest pains again and hadto be returned by ambulance to the hospital, where she was intubated, placed on a ventilator and spent several days in the intensive care unit, according to the suit.

It asks for unspecified damages for negligence, fraud, lack of informed consent and violations of consumer-protection laws.

The suit,Lesters and the Owensboro complaints werefiled by attorney Ronald Johnson, who says 25 Again prescribes and administers hormones to patients when they are not clinically indicated, do not provide any benefit, and expose patients to risk of harm and death.

The Kentucky Board of Medical Licensure in June prohibited 25 Agains then-medical director, Elizabeth Bates, from practicing hormone medicine after finding her practice violated acceptable and prevailing standards of medicine.

But the agency did not ban others from the practice.

Ennenbach has said the clinic provides safe care to thousands of satisfied patients.

It is a sponsor of University of Louisville mens basketball and advertises heavily on sports talk radio, promising that patients will look younger, feel healthier and feel 25 again.

Andrew Wolfson: 502-582-7189; awolfson@courier-journal.com; Twitter: @adwolfson. Support strong local journalism by subscribing today: http://www.courier-journal.com/andreww.

Read or Share this story: https://www.courier-journal.com/story/news/local/2019/03/04/hormone-clinic-25-again-faces-another-lawsuit-banned-diet-drug/3031906002/

Original post:
Louisville hormone clinic 25 Again sued over diet drug

Recommendation and review posted by Bethany Smith