Archive for the ‘Hormone Clinic’ Category

The hormone melatonin appears to suppress the growth of breast cancer tumors, say researchers.

While treatments based on this key discovery are still years away, the results, published in the journal Genes and Cancer, offer a foundation forfuture research.

You can watch bears in the zoo, but you only understand bear behavior by seeing them in the wild, says coauthor David Arnosti, a biochemistry professor and director of the Gene Expression in Development and Disease Initiative at Michigan State University.

Similarly, understanding the expression of genes in their natural environment reveals how they interact in disease settings.

The brain manufactures melatonin only at night to regulate sleep cycles. Epidemiologists and experimentalists have speculated that the lack of melatonin, due in part to our sleep-deprived modern society, puts women at higher risk for breast cancer.

This newstudy shows that melatonin suppresses the growth of breast cancer stem cells, providing scientific proof to support the growing body of anecdotal evidence on sleep deprivation.

Before the team could test its theory, the scientists had to grow tumors from stem cells, known as mammospheres, a method perfected in the Michigan State laboratory of James Trosko.

The growth of these mammospheres was enhanced with chemicals known to fuel tumor growth, namely, the natural hormone estrogen, and estrogen-like chemical Bisphenol A, or BPA, found in many types of plastic food packages.

Melatonin treatment significantly decreased the number and size of mammospheres when compared with the control group.

Furthermore, when the cells were stimulated by estrogen or BPA and treated with melatonin at the same time, there was a greater reduction in the number and size of mammospheres.

This work establishes the principal by which cancer stem cell growth may be regulated by natural hormones, and provides an important new technique to screen chemicals for cancer-promoting effects, as well as identify potential new drugs for use in the clinic, Trosko says.

Additional researchers at Michigan State and from the Faculdade de Medicina de Sao Jose do Rio Preto in Brazil contributed to the work.

Want to find more Breast Cancer news? Follow Knowridge Science Report onFacebook.

News source: Michigan State University. The content is edited for length and style purposes. Figure legend: This Knowridge.com image is for illustrative purposes only.

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Is hormone melatonin the link between sleep and breast cancer? - Knowridge Science Report

O

UAGADOUGOU, Burkina Faso It was after dark when awoman and her husband arrived. They crossed the dirt road and entered the cement buildingin a western neighborhood ofthis sprawling West African capital.

He had a demand: Remove the metal rodsyouve put in my wifes arm.Hed heard rumors that the strange technological device was going to give her cancer, and itneeded to go.

The nurse on duty at the health clinic, Bernadette Nassa, was insistent. She explained that the tiny rods were there for a reason: They provided the womansbody with a hormone to keep her from having children. She needed to give her body rest before becoming pregnant again.Eventually, the husband relented.

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But, Nassa said, theres not always ahappyending. Shes seen womenwhose husbands insist on a divorce if their wife usescontraception.

Such encountersunderscore the difficultyof providingcontraceptive services and womenshealth care inOuagadougou and in other developing countries where reproductivehealth education is limited and husbands make many decisions for their wives.

Did gender bias derail a potential birth control option for men?

But since May, the clinic hashad a new partner: Pathfinder International, a nonprofit geared towardincreasing global access to reproductive health services. And soon many more clinics could receive their help. Pathfinder last month received a $10 million grant from theBill and Melinda Gates Foundation, based in part on the work theyve done in Burkina Faso, to study how tohelp women get access to contraception.

For instance,Nassas clinic is one of 84 in Burkina Faso that have received the tools to insert an intrauterine device, or IUD, from Pathfinder, according toDr. Bruno Ki, the organizations technical director in the country. Before that, theclinic didnt even have the basic specula and tongs used in gynecological exams. Since May, Nassaestimates, theclinic has performed 30 or 40 IUD insertions a month, and the devices remaineffective for up to 12 years.

Each morning, a hundred women crowd into Nassas small waiting room and spill out into the courtyard; she and her staff, just under a dozen, cant take care of all of them. Her cement clinic only has four rooms for patients, so one doubles as a birthing suite and a family planning consultation room.

Demand for the clinics services has soared since the government started subsidizing health care for new mothers and young children in April. Now, health care is free for womenfor six weeks after they give birth.

That makes for a crucial juncture for Nassa to intervene. Back-to-back births carry higher risks for both mother and baby, and non-hormonal methods of contraception, including IUDs, are safe to use while the woman is still breastfeeding.

If she comes in with her child, we can use that opportunity to chat with her about contraceptive methods before she gets pregnant again, Nassa said through a translator. She tells the women about all kinds of contraceptive methods, including IUDs.

Malaria kills a half-million Africans a year. Gene-edited mosquitoes might stop it

Pathfinder is also funding improvements at other health clinics around the city. It is building a cement incinerator for medical waste at a health clinic in Bangpoor, a poor neighborhood by the railroad tracks to Abidjan, where the current incinerator was nothing more than a brick fire pit in which a stack of papers smoldered next to a jumble of aluminum and a can of insecticide that had not yet exploded.

Meanwhile, the organization is working at a national level to change the countrys laws on abortion.

Abortion law is very restrictive in Burkina Faso, Ki said. In 2012, we [had] more than 105,000 unsafe abortions in Burkina Faso.

Currently, abortions are only legal if ordered by a judge, and only in four cases: rape, incest, if the mothers health is at risk, or if there is a high probability the child will be born with an incurable congenital disorder.

As a result, many women try to induce an abortion, with horrifying results. Ki has heard stories about women who stuck bleach pills into their vagina or drank soup laced with ground glass.

If the new statute is adopted, women would be able to receive an abortion if their mental health or social well-being is at risk. The legislature was supposed to vote on the changes in October, but never did, Ki said, and hes not sure when they will pick it up in the future.

If those at Pathfinder want their work to have a lasting impact, they know that it will have to involve changing the attitudes of husbands and mothers-in-law, who often exercise a lot of control over a womans choices.

A few years ago, Pathfinder completed a project where it educated mothers-in-law about the importance of contraception, convincing them to accompany their daughters-in-law to the health clinic. Ki said the project was successful: Pathfinder worked with local nongovernmental organizations to talk with hundreds of mothers-in-law, some of whom later accompanied their daughters-in-law to receive contraception.

And Nassa acknowledged that one of the reasons so many husbands abhor contraception is that their ideas are based on rumors; they rarely learn how implants, IUDs, or injections actually work.

And that can lead to confrontations like the one Nassa experienced with the angry husband last month.

Here in Africa, especially in Burkina Faso, a woman cannot take a decision by herself, she said through a translator. It is the men that decide.

Kate Sheridan contributed reporting.

Ike Swetlitz can be reached at ike.swetlitz@statnews.com Follow Ike on Twitter @ikeswetlitz

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In West Africa, clinics confront suspicion, and husbands, one IUD at a time - STAT

DEAR MAYO CLINIC: How is thyroid cancer treated? Does it always require taking out the thyroid? When is iodine treatment used, and how does that work?

Treatment for thyroid cancer usually involves removing all or part of the thyroid gland. In cases where thyroid cancer is advanced or aggressive, radioactive iodine treatment may be recommended after surgery to destroy any cancer cells that couldn't be removed during surgery. For very small papillary thyroid cancers (less than 1 centimeter in diameter and completely confined to the thyroid on ultrasound examination), it may be reasonable to avoid surgery and monitor them periodically without treatment. This is termed "surveillance" and requires annual imaging of the thyroid with high-quality ultrasound. These small thyroid cancers are low risk for progression, especially in persons over 60.

The thyroid is a butterfly-shaped gland located in the midline of your neck, about halfway between your Adam's apple and your breastbone. Your thyroid gland produces two main hormones: thyroxine, or T4, and triiodothyronine, or T3.

Thyroid hormones impact many cells within your body. They maintain the rate at which your body uses fats and carbohydrates, help control your body temperature, affect the working of your nervous system, and influence your heart rate. Your thyroid gland also produces calcitonin, a hormone that helps regulate the amount of calcium in your blood.

Thyroid cancer is not common in the U.S. When it is found, though, most cases can be cured. Surgery to remove all or most of the thyroid a procedure called a thyroidectomy is often the first step in treatment.

Thyroidectomy typically involves making an incision in the center of the neck to access the thyroid gland directly. In addition to removing the thyroid, the surgeon may remove lymph nodes near the thyroid gland if the cancer is known or suspected to be spreading outside the thyroid. Then, those lymph nodes will be checked for cancer cells. An ultrasound exam of the neck before surgery can help doctors determine if lymph node removal is necessary.

When thyroid cancer is found in its earliest stage, and the cancer is very small, it may only be necessary to remove one side, or lobe, of the thyroid, and leave the rest in place. In that situation, the thyroid still can function and produce hormones.

When the entire thyroid is removed, lifelong thyroid hormone therapy is required to replace the thyroid's natural hormones and regulate the body's metabolism. In addition to supplying the missing hormone the thyroid normally makes, this medication also suppresses the pituitary gland's production of thyroid-stimulating hormone, or TSH. That's useful, because there's a possibility that high TSH levels could foster the growth of any remaining cancer cells.

If thyroid cancer is found in its later stages, if it's a more aggressive form of cancer, or if it is cancer that has come back after earlier treatment, then radioactive iodine therapy may be recommended after the thyroid has been removed.

Radioactive iodine comes in a capsule or liquid that's swallowed. The therapy works because thyroid cells naturally absorb iodine. So when the medicine is taken up by any remaining thyroid cells or thyroid cancer, the radioactivity destroys those cells. Because the thyroid is the primary site where iodine is absorbed by the body, there's a low risk of harming other cells with this treatment. Afterward, the radioactive iodine leaves the body through urine.

If thyroid cancer is not cured with a combination of surgery and radioactive iodine therapy, then chemotherapy, external radiation therapy or other treatment may be necessary. Fortunately, surgery cures most cases of thyroid cancer, and the long-term outlook after the procedure is usually excellent. John Morris III, M.D., Endocrinology, Mayo Clinic, Rochester.

Mayo Clinic Q & A is an educational resource and doesnt replace regular medical care. Email a question to MayoClinicQ&A@mayo.edu. For more information, visit http://www.mayoclinic.org.

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Most cases of thyroid cancer are curable - Post-Bulletin

Gender dysphoria is one of few identities still deemed a health issue that requires diagnosis same-sex desire was removed from the Diagnostic and Statistical Manuel (DSM) in 1973. In order to medically transition and get safe access to hormones and other support, transgender people need to come out to a doctor and are often required to attend therapy.

In 2013 England's National Health Service's (NHS) changed protocol for gender dysphoria patients, asking general practitioners to refer to a gender clinic which can offer much needed services like hormone treatment, hair removal treatments, and family support groups. Yet, many GPs still refer first to a counselor who may have little to no experience with gender identity.

Gina Denham, a transgender police officer in England, is teaming up with the NHS to change that, according to Echo. It's her hope to provide trans patients in the area the support they need during transition, and get them access to one of the 7 designated NHS gender identity clinics in England.

One of the biggest barriers and potential cost to the NHS is our GPs sending our members to have counseling when they are meant to be referred to a gender clinic," Denham told Echo. "The GP just seems to ignore your request and sends you to counseling to try and cure you."

When she started to transition in 2014, Echo reports, Denham went to about 65 counseling sessions many of which were unnecessary.

Since then, Denham has become a champion for transgender rights in her community. Educating doctors is not her first project. In early 2016 Denham started a support group called Transpire for LGBTQ people in her neighborhood, which provides people the opportunity to both socialize with others who've had similar experiences and to engage in activist work. The Transpire group has helped educate medical professionals by working with the NHS on training materials.

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How This Police Officer Is Helping Trans Patients Get Better Care - Refinery29

When a woman becomes pregnant, many changes occur in her body. One of those changes is in the levels of various hormones produced by the body.

In the case of thyroid-stimulating hormone (TSH), pregnant women typically produce a lower level than normal (0.44.0 milli-international units per liter). Some international guidelines recommend levels be no higher than 2.5-3. milli-international units per liter during pregnancy. When their TSH levels rise above this, they may experience subclinical hypothyroidism, or mildly underactive thyroid, which can cause a number of health problems if left untreated.

Today, Mayo Clinic researchers report that one of those results could be pregnancy loss. Researchers further suggest a course of action that could positively impact as many as 15 of every 100 pregnancies. In a study published in The BMJ, they show that treating subclinical hypothyroidism (not quite the level that would be treated in a nonpregnant woman) can reduce pregnancy loss, especially for those with TSH levels on the upper end of normal or higher.

A recent analysis of 18 studies showed that pregnant women with untreated subclinical hypothyroidism are at higher risk for pregnancy loss, placental abruption, premature rupture of membranes, and neonatal death, said Dr. Spyridoula Maraka, an endocrinologist and lead author of the study. It seemed likely that treating subclinical hypothyroidism would reduce the chance of these deadly occurrences. But we know that treatment brings other risks, so we wanted to find the point at which benefits outweighed risks.

Using the OptumLabs Data Warehouse, Maraka and her team examined the health information of 5,405 pregnant women diagnosed with subclinical hypothyroidism. Of these, 843 women, with an average pretreatment TSH concentration of 4.8 milli-international units per liter, were treated with thyroid hormone. The remaining 4,562, with an average pretreatment TSH concentration of 3.3 milli-international units per liter, were not treated.

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Women's wellness: Understanding hypothyroidism and pregnancy - The Killeen Daily Herald

Amphetamine abuse is increasing internationally. While common sides effects of the drug include increased heart rate, headache, stomach pain, and mood changes, little is known about the drug's effect on the heart. Now, new research published in Heart Asia reports that using amphetamines recreationally may accelerate aging of the heart.

Recreational amphetamine, commonly known as "ice," "speed," and ecstasy, is a central nervous system stimulant. Amphetamine sends the part of the nervous system that functions to accelerate heart rate, constrict blood vessels, raise blood pressure, and produce the "fight or flight" hormone adrenaline, into overdrive.

Given the effect of amphetamine on heart rate, blood vessels, and blood pressure, the abuse of stimulants is likely to have a stressful effect on the cardiovascular system over time. However, there have previously been few studies that explore these processes.

It is known that prolonged stimulant use causes premature aging of the skin. Following on from this knowledge, researchers from the University of Western Australia (UWA) aimed to find out whether amphetamine use prematurely ages the heart.

Albert Stuart Reece, associate professor of medicine at UWA, and collaborators measured levels of blood flow through the brachial artery in the upper arm, as well as the radial artery in the forearm, of 713 study participants.

Arteries harden as the body ages, and so the researchers aimed to assess the degree of artery stiffening in order to determine how the heart was aging in this population. The participants were in their 30s and 40s and attending a clinic for substance misuse.

The team used a standard blood pressure cuff on the upper arm of participants and a noninvasive monitoring system, called SphygmoCor, on the forearm to gather data.

SphygmoCor uses software that can calculate the biological vascular age of a person by matching the age, sex, and height of an individual with the extent of arterial stiffening.

The participants were divided into four groups depending on their drug use. There were 483 people who did not smoke, 107 people who did, 68 individuals who used the heroin substitute methadone, and 55 users of amphetamine.

Of the 66 times that the amphetamine group was monitored with the SphygmoCor, 94 percent of individuals had used the drug within the previous week, and almost half of the people in the group had used it the day before.

Findings indicated that compared with the people who smoked and used methadone, the cardiovascular system of the amphetamine users appeared to be aging at a much quicker rate.

These results remained significant when other known cardiovascular risk factors - such as weight, cholesterol levels, and the inflammation indicator C-reactive protein - were taken into consideration.

As exposure to amphetamine is often repetitive and prolonged, the heart is exposed to the effects of the stimulant on a behavioral, chronic, and long-term basis. "It is, therefore, conceivable that stimulant abusers do physiological and cardiovascular harm," says the team. They note that it is not clear to what extent the damage might be reversible.

The authors say that the results confirm their concerns that amphetamine abuse increases heart age. However, as the study is observational, no firm conclusion can be drawn regarding cause and effect.

The aging process suggests a power function over time, as many physiological processes begin to fail over the course of a lifespan progressively. However, the new findings suggest that stimulant abuse may accelerate the degeneration of the physiological systems. The authors write:

"If, as has been demonstrated, the damage from stimulant abuse is actually a power function of time, then this, in turn, implies that the gathering global stimulant epidemic carries a further message of urgency which has largely not been appreciated."

The team point to other research for a possible explanation for their findings. The research showed that amphetamine use interferes with stem cell functioning and normal cell division. Hence, amphetamines may both impede tissue repair and increase tissue injury, the authors conclude.

Learn how synthetic marijuana may have a variety of adverse health effects.

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Amphetamine use may 'speed up' heart aging - Medical News Today

Photo: Paul Chinn, The Chronicle

Heather Jacoby plays the piano with her 7-year-old daughter, Billie. Jacoby, who received lifesaving treatment at a Planned Parenthood facility, is upset by efforts to end federal funding for the organization.

Heather Jacoby plays the piano with her 7-year-old daughter, Billie. Jacoby, who received lifesaving treatment at a Planned Parenthood facility, is upset by efforts to end federal funding for the organization.

Heather Jacoby of Vacaville, shown with daughter Billie and dog Jazzie, says she was referred to Planned Parenthood by an emergency room doctor.

Heather Jacoby of Vacaville, shown with daughter Billie and dog Jazzie, says she was referred to Planned Parenthood by an emergency room doctor.

Nationwide Planned Parenthood protests energize patients, opponents

Damien Cox didnt have health insurance for most of his life. So when the transgender man began transitioning 11 years ago, he went to a Planned Parenthood clinic for hormone treatments.

Planned Parenthood isnt just a womans thing, said Cox, a 40-year-old Sunnyvale resident. Its a queer health issue and a trans health issue. It affects everybody.

Cox is among those voicing support for the nonprofit reproductive health organization at what could be a critical moment in its history. President Trump and his administration have threatened to eliminate federal funding for Planned Parenthood, because the services provided by the clinics include abortions.

On Saturday, the debate will crest with nationwide rallies including at clinics in San Francisco, Redwood City and Napa calling for the defunding of Planned Parenthood.

The whole issue would go away if they just didnt offer abortion services, said Monica Migliorino Miller, a Michigan resident who is part of a coalition of antiabortion groups that organized the demonstrations.

Supporters are planning counter-protests, arguing that a loss of funding would hurt an array of patients, and in particular low-income and minority communities. Planned Parenthoods services include prenatal care, testing and treatment for sexually transmitted infections, cancer and diabetes screenings and vaccinations.

In the fiscal year that ended in June 2015, Planned Parenthood received $553.7 million in Medicaid reimbursements and federal grant money, according to the groups latest annual report 43 percent of its total budget.

Under federal law, none of that money went toward abortion services, which make up 3 percent of all services provided, barring situations where a womans life was in danger or cases of incest and rape, said Gilda Gonzales, the interim chief executive of the organizations Northern California affiliate.

If the group was defunded, Gonzales said, 60 percent of Planned Parenthoods clientele would lose care provided under Medicaid and the Title X family planning program. The vast majority of patients in Northern California range from ages 20 to 35, are people of color and live below the poverty line, she said.

But opponents of abortion believe stripping all federal funding will help their cause. Vice President Mike Pence, speaking at the annual March for Life in Washington, D.C., on Jan. 27, said ending taxpayer abortions was a priority for the new administration.

At a GOP debate in Houston in February 2016, Trump pointed out that millions and millions of women cervical cancer, breast cancer are helped by Planned Parenthood. But he said, I would defund it because of the abortion factor, which they say is 3 percent. I dont know what percentage it is. They say its 3 percent. But I would defund it, because Im pro-life.

Republicans in both the House and Senate plan to introduce measures to end federal funding for Planned Parenthood and ban most abortions after 20 weeks of pregnancy, which Trump has pledged to sign.

While supporters of the group say the right to a safe abortion is critical, they are also working to bring more awareness to Planned Parenthoods other services. They include Nique Eagen, a 41-year-old Campbell resident, who will be among an expected 3,000 counter-protesters in San Jose.

For years, Eagen said she suffered through intense pain and nausea during her menstrual cycles, but didnt understand why.

I would get really, really sick, Eagen said. I was getting dehydrated. Id black out because I was losing too much blood.

After she lost her job in 2010, she sought care from Planned Parenthood and learned that the cause of her pain was ovarian cysts a problem that was solved by taking birth control, which keeps the cysts from growing, she said.

Heather Jacoby, a 31-year-old Vacaville resident, said she turned to Planned Parenthood when she ran out of other options.

Last summer, she was thrilled when she found out she was pregnant. But within weeks, she wound up in the emergency room due to severe pain, vomiting and blacking out. She had lost the baby and gone into septic shock.

I was carrying a dead fetus inside me for over six weeks. I felt hopeless, Jacoby said.

Jacoby didnt want an abortion but needed one to save her life. She had insurance, but said her primary care provider didnt immediately schedule the procedure. When she ended up in the emergency room, a doctor referred her to Planned Parenthood in Walnut Creek, she said.

I still remember the day because two of my good friends gave birth that day, Jacoby said. Before it started, I just started crying because this is the culmination of six weeks and I was so exhausted and I just remember the nurse (at Planned Parenthood) grabbed my hand and looked in my eyes and said, I got you.

Sarah Ravani is a San Francisco Chronicle staff writer. Email: sravani@sfchronicle.com Twitter: @SarRavani

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Nationwide Planned Parenthood protests energize patients, opponents - SFGate

By Molly Atchison | Opinion Editor

Editors Note: This is the thirdinstallment in a four-part series about gender transition and the issues surrounding it. For the personal safety of some of the individuals mentioned below, last names have been omitted.

Physical health is a multi-faceted issue that transgender people focus on once theyve determined that they want to begin their transition. Many health professionals point to the World Professional Association for Transgender Healths Standards of Care manual to give transitioning individuals a jumping off-point for research into sexual and physical health.

The first step in the transition process is to go through hormone therapy process, and the second step of the process is to commit to the sex-reassignment surgery.

For McLennan County junior Jessica, a transgender student attending Baylor University, beginning these transitions was not an easy decision to make.

I was praying and thinking about this decision for about a year before I began the process at all, Jessica said.

Hormone Treatment:

Jessica began her hormone therapy process almost a year ago. The Standards of Care manual states that hormone therapy is the administration of exogenous endocrine agents to induce feminizing or masculinizing changes.

In Fall of 2015, I began taking steps towards hormone therapy. I worried about the haters and the higher rate of suicide, but I kept pushing on until I got what I set out to achieve, Jessica said.

Testosterone and estrogen are two main hormones in the body. Every human has varying levels of testosterone and estrogen in their bodies, and the hormones will rise and fall naturally to maintain a healthy physical equilibrium. Both of these are the hormones that are supplemented in the transition process.

According to the Center of Excellence in Transgender Health, in a female-to-male transition, an individual will take testosterone supplements to help introduce general changes such as facial hair growth, deepening of the voice and redistribution of muscle and weight gain. This transformation happens over the course of 12 months, which is the general requirement to be eligible to receive the sex-reassignment surgery.

In contrast, the male-to-female transition can be administered with several different categories of estrogen supplements. According to the Center of Excellence in Transgender Health, these estrogen supplements aid in breast development, vocal shifting and the redistribution of fat and muscle on the body.

The Standards of Care manual says that the physical side effects of these therapies most commonly include decreased auto-immunity, lack of genital functioning and many other symptoms of raised or lowered increased levels of testosterone and estrogen. Other side effects include a higher risk of breast cancer in both types of patients, as well as other forms of cancer and genetic diseases, including heart disease and diabetes.

Sex-Reassignment surgery:

Now that Jessica is nearing the end of her initial hormone treatment, she awaits approval to continue to the sex-reassignment surgery.

The final step in the transition process is the sex-reassignment surgery. According to Transequality.org, sex-reassignment surgeries are Surgical procedures that change ones body to better reflect a persons gender identity.

For male-to-female patients, the Standards of Care manual cites two basic surgeries, the first being breast enhancement, and the second being a series of up to five smaller procedures to replace the existing male genitalia with female genitalia. Different doctors choose to use different techniques of genital conversion in the male-to-female transition.

In the same way, female-to-male patients go through a series of different surgeries, as is stated in the Standards of Care manual. They will undergo a surgery to remove the breasts, called a mastectomy, and then several surgeries that remove the female genitalia, and then phalloplasty that adheres a phallic implant in its place. One of the biggest differences between these surgeries is that with male-to-female transitions it is more common to use existing tissue to create the new genitalia, whereas in the female-to-male, fresh tissue is more commonly implanted.

There are many risks to undergoing such significant surgeries, which can be found online in the Standards of Care manual. I do fear the pain of recovery and the possibility of complications that any surgery could have, even as severe as death, Jessica said.

Health after surgery:

Along with risks during surgery, there are risks in the years following the surgery. However, the Center of Excellence for Transgender Health is one of the leading researchers in transgender health. Their guidelines have detailed lists of general and sexual health problems transgender people may face post-surgery including but not limited to Sexually Transmitted Diseases, blood pressure problems and reproductive health issues.

The Baylor Health Clinic also offers primary care services. Medical Director of Baylor Health Services Sharon Stern, M.D., said As primary care physicians and nurse practitioners, we care for the patients who come into the clinic. That means that we can do any testing and treatment of many infections, including sexually transmitted ones.

Stern acknowledges that the clinic, being a primary care clinic, does not directly identify or prescribe transgender treatments. However, the electronic medical records system the center allows healthcare professionals to make sure that the general medications they may be prescribing to a transgender individual will not counteract the hormone supplements they are taking.

If we had a patient present to us who was thinking of transitioning, we would most likely refer them to a counselor and an endocrine doctor who specializes in the type of specialized hormonal treatment necessary. We want to help all patients and we strive to never be judgmental. We want to help all Baylor students be healthy, she said.

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In Transition: Physical transitions can include hormone treatment, surgery - The Baylor Lariat

TheNational Institute of Diabetes and Digestive and Kidney Diseases, a part of the National Institutes of Health, has given out $41 milion in grants to four studies that will hopefully make the artificial pancreas a long-sought, fully automated, closed-loop system for insulin regulation a reality. Two of the studies are underway and two more are slotted to begin recruiting in the next two years.

Managing type 1 diabetes currently requires a constant juggling act between checking blood glucose levels frequently and delivering just the right amount of insulin while taking into account meals, physical activity, and other aspects of daily life, where a missed or wrong delivery could lead to potential complications, Dr. Andrew Bremer, the NIDDK program official overseeing the studies, said in a statement. Unifying the management of type 1 diabetes into a single, integrated system could lift so much of that burden.

A long-sought dream of diabetes technologists, an artificial pancreas would combine the functionality of an automated insulin pump and a continuous glucose monitor, automatically calculating dosages and delivering insulin based on readings from the CGM -- in essence replicating the behavior of a normally-functioning human pancreas, which regulates insulin in people without diabetes.

The four studies all vary from previous artificial pancreas studies in a few key ways. For one thing, they will each have 100 or more participants. For another, while previous studies looked at geographically co-located cohorts at summer camps for youth with diabetes or hotels near the study site, these studies will be conducted at multiple sites, remotely, allowing researchers to test the systems in natural, real-life contexts.

The studies will hopefully provide the data the FDA needs to clear a fully closed-loop system. Last year the FDA cleared Medtronic's artificial pancreas, but that was a hybrid system that still required patients to manually adjust insulin intake at mealtimes.

We wrote about one of the four studies when it began enrollment last year.The International Diabetes Closed Loop trial at the University of Virginia aims to enroll 240 adults with type 1 diabetes. The participants will come from 10 different clinical sites throughout the world including Mount Sinai Hospital in New York, Stanford University Hospital and the Mayo Clinic in the United States, as well as medical centers in France, Italy and the Netherlands. A Tandem insulin pump and Dexcom G5 sensor will be included as part of a blood glucose control system that combines the devices with a smartphone running TypeZeros closed loop algorithm app inControl.

The other study that has already begun recruiting isled by Dr. Roman Hovorka of the University of Cambridge in England. The 130-person study of teenagers, which looks at a system called FlorenceM using an Android smartphone and Medtronic devices, will be conducted at sites in California, Colorado, Connecticut, Minnesota, and two sites in the United Kingdom.

A third study is scheduled to begin recruiting this year. It's led by researchers from theInternational Diabetes Center in Minneapolis and the Moshe Phillip of Schneider Children's Medical Center in Petah Tikva, Israel and will include 100 youthsat sites in California, Connecticut, Florida, Massachusetts and Minnesota and abroad in Germany, Israel and Slovenia. It will compare the FDA-cleared hybrid system with a next-generation version of that system from Medtronic.

Finally, the fourth study will kick off in 2018, led by researchers in Boston from Massachusetts General Hospital and Boston University.The six-month study is a little different from the others -- it looks at a bionic pancreas system, with a dual-chamber pump to deliver both insulin and its counteracting hormone, glucagon, using tested algorithms for automated dual-hormone delivery. The study will include two sites in California and one each in Massachusetts, Michigan, Missouri, North Carolina, Ohio and Washington.

For many people with type 1 diabetes, the realization of a successful, fully automated artificial pancreas is a dearly held dream. It signifies a life freer from nightly wake-up calls to check blood glucose or deliver insulin, a life freer from dangerous swings of blood glucose, said NIDDK Director Dr. Griffin P. Rodgers. Nearly 100 years since the discovery of insulin, a successful artificial pancreas would mark another huge step toward better health for people with type 1 diabetes.

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Four NIH-backed projects aim to advance the artificial pancreas - MobiHealthNews

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A ribbon cutting ceremony will take place Wednesday, Feb. 8 at the Somerville campus of Robert Wood Johnson University Hospital. The Somerset County hospital is now the first in the entire state of New Jersey to open a family health center tailored to the LGBTQ community.

PROUD Family Health will offer services most important to LGBTQ New Jerseyans. In a recent press release, RWJUH president Michael Antoniades said, We recognized that the health care needs of the LGBTQIA community were not being met and in many cases, LGBTQIA individuals were traveling outside of New Jersey for their medical care. PROUD Family Health will offer them the care they need close to home.

A resource like this can be extremely beneficial to many New Jerseyans. It also sets a precedent for other New Jersey hospitals moving forward. The fact of the matter is the LGBTQ community has different priorities when it comes to healthcare.

I reached out to Christian Fuscarino, the Executive Director of New Jerseys largest civil rights organization, Garden State Equality, about this news. He had this to say:

Today we take an important step forward as a community and a state, with the opening of the first full service LGBT health clinic.

The PROUD Family Health Clinic at Robert Wood Johnson will provide medical care for children and adults, hormone therapy and monitoring, HIV care, referrals for specialty services, health education and counseling, and support groups for LGBT individuals and their family members.

Garden State Equality is proud to partner with RWJ on this project that makes New Jersey a national leader in the health care space.

Currently, operating hours will be on Mondays from 6 pm to 9 pm, although I would expect that to expand as demand increases. Medicare, Medicaid and most major insurance plans are accepted.

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Hospital in Somerset becomes first in NJ to open LGBTQ health center - New Jersey 101.5 FM Radio

The University of Nebraska-Lincoln campus got a little more trans-friendly on Feb. 1. The University Health Center opened a new clinic geared toward transgender and non-binary students, staff and faculty. After years of requests for the clinic, Dr. Jean Amoura will begin treatment for transgender patients at the university as an extension of her Nebraska Medicine practice in Omaha.

With easy access to a safe, affordable and knowledgeable clinic, trans students, faculty, and staff are now able to focus more on education, rather than whether or not they will have the care they need. It eliminates a concerning barrier, and it is validating for these individuals to have their needs recognized.

Over the past few years, there has been an increase in the amount of resources and services available to queer and trans individuals on campus. This includes other health services like LGBT-friendly counseling, with the option to see someone who has specialization in LGBT issues. There are also LGBT-centric social and community resources and organizations such as Spectrum and The Change, the LGBTQA+ Resource Center, a growing number of gender-inclusive housing options and numerous gender-inclusive bathrooms scattered around campus. Finally, there are opportunities for allies and queer people to be educated about queer issues, and there is also an LGBT-geared mentor program. As the campus continues to become more diverse, these various services become even more vital.

The Transgender Care Clinic is yet another massive step toward a more welcoming environment for queer and trans individuals at UNL. This should be an example to not only the rest of the universities in the Nebraska system, but also to universities across the nation. Currently, only 75 of all American colleges and universities cover both hormone treatment and gender-affirming surgeries under student health insurance.

Across the country, it is already incredibly difficult to find healthcare professionals who know how to treat transgender patients. Unfortunately, some insurance providers do not cover trans-related health services, and with the threat of the Affordable Care Act being repealed, queer and transgender patients face the risk of having even fewer options.

In Nebraska specifically, some health insurance providers can legally exclude transgender-specific services. In the case of discrimination from private health insurance providers, there is no protection for trans and queer folks, and Nebraska Medicaid does not cover transgender-related healthcare.

According to a Movement Advancement Project report, Nebraska ranks number three for the worst state for gender identity related policies, ranking up the most negative points in the category of healthcare and safety. As a nation, 52 percent of the queer and transgender population lives without LGBT-inclusive health insurance.

With such disparities in these services across the nation, and particularly in Nebraskas healthcare, the transgender health clinic on campus is a victory for some. While helping transgender Nebraskans, it also provides reliable care to out-of-state students who may or may not have inclusive healthcare in their home state. This simplifies the difficult process of finding a healthcare provider and professional willing to cover said treatments, while aiming to protect the wellbeing of those who use or need this type of care.

The next step for Nebraska as a state is to follow the footsteps of the university. With trans people experiencing dishearteningly high rates of depression, attempts of suicide and substance abuse, the need for healthcare designed for transgender people is always growing. Queer and trans people deserve to receive the healthcare they need. Ideally, Nebraska will take steps to provide that in the future.

Ellie Bruckner is a sophomore global studies major. Reach her at opinion@dailynebraskan.com or via @DNOpinion.

See the article here:
BRUCKNER: UNL a national model for trans, LGBT care - Daily Nebraskan

A study group from the Mayo Clinic found that thyroid hormone treatment of subclinical hypothyroidism during pregnancy was associated with a lower risk of pregnancy loss, but a higher risk for adverse pregnancy outcomes such as premature birth and gestational diabetes.

Subclinical hypothyroidism (hypothyroidism proven by laboratory results without clinical symptoms) affects around 15% of pregnant women. The recent regulatory changes in laboratory TSH (thyroid stimulating hormone an indicator of low thyroid hormone levels) threshold may have resulted in an overdiagnosis and overtreatment of hypothyroidism. A lower thyroid hormone level during pregnancy has been associated with adverse pregnancy outcomes such as pregnancy loss, placental abruption, premature rupture of membranes, and neonatal death.

An article was recently published in the British Medical Journal that analyzed data from the OptumLabs Data Warehouse database to assess the prevalence, effectiveness, and safety of thyroid hormone treatment of subclinical hypothyroidism among pregnant women. Researchers included 5405 pregnant women in the study with TSH 2.5-10mIU/L between 2010 and 2014. 15.6% received thyroid hormone treatment and the percentage of treated women increased each year. Comparing the treated and untreated groups, treated patients had a 38% lower risk of pregnancy loss, but higher odds of preterm delivery, gestational diabetes, and pre-eclampsia. However, the risk of pregnancy loss was only lower in treated women with higher TSH levels (meaning lower thyroid hormone levels) but not in women with lower TSH. Furthermore, the risk of gestational hypertension was higher among treated than untreated women with lower TSH levels.

In conclusion, it seems that thyroid hormone therapy of subclinical hypothyroidism lowers the risk of pregnancy loss, especially in patients with higher TSH levels, but is associated with a higher risk of adverse pregnancy outcomes. Further studies are needed to assess the safety of thyroid hormone treatment in pregnancy.

Written By: Dr. Fanni R. Eros

More here:
Thyroid Hormone Therapy for Subclinical Hypothyroidism in Pregnancy - Medical News Bulletin

A new video campaign is calling on the Alberta government to provide more funding to help transgender youth.

The only specialized, multi-disciplinary clinic in the province catering to transgender youth is at the Alberta Children's Hospital in Calgary and is only open one half-day each month as part of a pilot project.

The waiting list for the clinicis up to three years.

"We're hearing a lot of kids stuck in that long wait, and what we're hearing a lot of is desperation," said Amelia Newbert, who runs the Skipping Stone Foundation, the organization behind the video campaign.

The Metta Clinic at the children's hospital provides everything from mental health and psychiatric support, to hormone therapy and preparation for some surgeries for youth aged seven to 20.

Newbert, who is trans,says timing is key with kids.

"The reality of being forced to be exposed to a puberty that doesn't conform to your gender identity is profoundly damaging," she said.

That damagecan lead to an increase in problems such as self-harm, addiction and suicide, according to Newbert.

In thefirst video of the Skipping Stone campaign,Ace Peace, a 16-year-oldtransgenderboy, describes the desperation he felt watching his body change while he waited nine months to get into the clinic.

"When I came out as transgender everyone supported me. I was supported by family, friends and school. But it was still hell for me," he says.

"I was watching my body change in ways I didn't want to see it change. I felt like it was betraying me."

Speaking with the Calgary Eyeopeneron Tuesday morning,Peace said he was struggling at school andthe clinic provided much needed emotional support.

"They knew what to do, they knew what was going on, they knew the emotional impact that it had on me so they tried to get me on hormones as fast as they could," he said.

Pam Krause, whoruns the Calgary Sexual Health Centre, agrees it's important to offer support early.

"If you have to wait three years for something, for something that you know is your truth, Ithink that causes all kinds of difficulties for people. And the system is paying later on when people are having mental health problems," she said.

Alberta Health Services told CBC News that it continues to examine the pilot project, launched in 2014.

"AHS is currently gathering evidence and exploring best practices to determine the best approach to providing services to youth struggling with gender dysphoria," said an email fromJulie Kerr, the health authority'ssenior operating officer foraddictions andmental health in theCalgary zone.

"Any decisions on whether to expand the clinic will be evidence-based."

Alberta's health minister, Sarah Hoffman, said she understands the long delays are frustrating.

"While there are a number of health services that can support transgender youth in different parts of the province, having a designated service like the Metta Clinic has proven invaluable for many patients and families," she said by email.

Kerr said youth struggling with gender identity can find other programs and services in Alberta, including community mental health programs, crisis mental health, family physicians, edrocrinologyand psychiatry services.

More:
Transgender youth in Alberta need more than 1 part-time clinic, says new campaign - CBC.ca

Endocrinology Advisor

Risk of Pregnancy Loss in Subclinical Hypothyroidism Endocrinology Advisor Rozalina G McCoy, MD, from the Mayo Clinic in Rochester, Minnesota, and colleagues conducted the first national study to evaluate the effectiveness and safety of thyroid hormones for pregnant women with subclinical hypothyroidism. The study included ...

Read this article:
Risk of Pregnancy Loss in Subclinical Hypothyroidism - Endocrinology Advisor

NEW ALBANY Carla Copas, APN, is announced the grand opening of Finding Her Health, a new womens health care clinic located at 2708 Paoli Pike, Suite I, New Albany. A ribbon cutting ceremony will be held Feb. 8, at 10 a.m.

Copas specializes in Bio-Identical Hormone Replacement and has been prescribing this type of treatment to her patients with great success for 15 years. Formerly with OBGYN Associates of Southern Indiana, she is opening Finding Her Health to more fully utilize her skill and passion for a personalized approach to healthcare.

As an advanced practice registered nurse, I treat the whole person, not just the diagnosis or disease, Copas said in a news release. Unlike other healthcare offices where there are sometimes dozens of people in the waiting room and the providers see 30-40 patients a day that is one every 5-10 minutes, I take the time with each patient for education and understanding. Most of my patients have a time slot from 30 minutes to one hour. I provide same-day appointments and am available to my patients via secured email and answer within 24 hours.

Services available at Finding Her Health will include gynecology, STI testing and treatment, birth control options, hormone balance, well woman exams, treatment for UTIs, vaginal problems, painful intercourse, decreased libido, irregular menses, fertility, peri-menopause and menopause balance, prevention and other issues specific to womens health.

Im excited about this new venture. Opening this clinic will provide a unique opportunity for me to help women in all walks of life, Copas said. At Finding Her Health, no matter what a womans age or medical situation, I want to help guide my patients to feeling the best they have ever felt.

The public is invited to attend the ribbon cutting ceremony to meet Copas and tour the new office. For more information, visit http://www.findingherhealth.com or Facebook/findingherhealth.

Read more here:
Public invited to women's clinic opening in New Albany - Evening News and Tribune

After a massive mess up with the NHS recently (a long story) I finally managed to get my AMH (Anti-Mullerian hormones) tested last week at a private clinic.

Facts and Figures

Im sure lots of you are already too familiar with the meaning of AMH, but just incase you are unfamiliar here is a bit more information from Lane Fertility Magazine:

Anti Mullerian Hormones (AMH)

Many physicians and researchers believe that the best blood test to assess the supply of follicles in a womans ovaries is Anti-Mullerian Hormone (AMH), also known as Mullerian Inhibiting Substance (MIS). In females, this hormone is secreted by a particular group of cells in the follicles called granulosa cells. Thus, the more follicles there are in the ovaries, the greater the amount of AMH in the blood. Conversely, the fewer follicles there are in the ovaries, the lower the amount of AMH in the blood. Therefore, AMH is a reflection of the number of follicles in both ovaries. With time, as women become older, the level of AMH will naturally decrease.

This graph was interesting about how AMH levels decline with age, read more about it atFertility Associates.

The ranges used in the U.K. and U.S. should be as follows:

U.K.

U.S.

AMH Blood Level

Interpretation

AMH Blood Level

Interpretation

>68pmol/L

High

Over 3.0 ng/ml

High (often PCOS)

22 40pmol/L

Satisfactory

Over 1.0 ng/ml

Normal

3.1 22pmol/L

Low

0.7 0.9 ng/ml

Low Normal Range

0 3.1pmol/L

Very Low

0.3 0.6 ng/ml

Low

Note:Reference range formerly in g/L(conversion g/L pmol/L = 7.14)

Less than 0.3 ng/ml

Very Low

I also found a great conversion chart, which was very useful as different information/labs seems to use different units of measurement.

Confusion

Once again there is quite a lot of differing opinions about AMH. On my mission to source information I have found out that:

Can you imagine my surprise when I discovered that (once again) there are differing opinions and inconsistencies in the facts? Detect a hint of sarcasm? Sorry, I just couldnt resist! Once again my search for clear cut facts was in vain another grey area in this mixed up IF world.

My Results

My result came back as 8 pmol/L, in the low fertility bracket. My first reaction was to be upset (of course), but the nurse kindly explained that it isnt too bad; it is age related and lots can be done with an AMH of that level especially if I have been pregnant before. Also that it is more about quality, not quantity.

I also had a go at converting my result into ng/ml (as per the U.S. figures). I know, I know, before you say it, this is probably the wrong thing to do. They probably use different methods of testing, blah blah blah. But I couldnt resist, I was grasping at straws. And the result? 1.12 ng/ml which puts me in the normal range. Do I believe this? Im not sure, but I do like the sound of normal much more than low fertility.

So, yet again an emotional roller-coaster (albeit a small one this time) began:

What can I do about it? Nothing! Absolutely nothing! It frustrates me that time is my enemy and Im feeling the sense of urgency more than ever. But its not like Hubby and I havent been trying for the last two years what more can we do?

Your AMH Levels

Id love to hear what your AMH levels were and what you have been told about it. And Im sure there are plenty of others out there who are just as confused as I am about all this. Please comment, and lets get to the bottom of this!

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Originally posted here:
Worrying about Anti Mullerian Hormones? | Baby Hopeful

PRL Available structures PDB Ortholog search: PDBe RCSB List of PDB id codes

1RW5, 2Q98, 3D48, 3EW3, 3MZG, 3N06, 3N0P, 3NCB, 3NCC, 3NCE, 3NCF, 3NPZ

Prolactin (PRL), also known as luteotropic hormone or luteotropin, is a protein that in humans is best known for its role in enabling mammals, usually females, to produce milk. It is influential in over 300 separate processes in various vertebrates.[4] Prolactin is secreted from the pituitary gland in response to eating, mating, estrogen treatment, ovulation and nursing. Prolactin is secreted in pulses in between these events. Prolactin plays an essential role in metabolism, regulation of the immune system and pancreatic development.

Discovered in non-human animals around 1930 by Oscar Riddle[5] and confirmed in humans in 1970 by Henry Friesen[6] prolactin is a peptide hormone, encoded by the PRL gene.[7]

It is associated with human milk production. In fish it is thought to be related to control of water and salt balance. Prolactin also acts in a cytokine-like manner and as an important regulator of the immune system. It has important cell cycle-related functions as a growth-, differentiating- and anti-apoptotic factor. As a growth factor, binding to cytokine-like receptors, it influences hematopoiesis, angiogenesis and is involved in the regulation of blood clotting through several pathways. The hormone acts in endocrine, autocrine and paracrine manner through the prolactin receptor and a large number of cytokine receptors.[4]

Pituitary prolactin secretion is regulated by endocrine neurons in the hypothalamus. The most important ones are the neurosecretory tuberoinfundibulum (TIDA) neurons of the arcuate nucleus that secrete dopamine (aka Prolactin Inhibitory Hormone) to act on the D2 receptors of lactotrophs, causing inhibition of prolactin secretion. Thyrotropin-releasing factor (thyrotropin-releasing hormone) has a stimulatory effect on prolactin release, however prolactin is the only adenohypophyseal hormone whose principal control is inhibitory.

Several variants and forms are known per species. Many fish have variants prolactin A and prolactin B. Most vertebrates including humans also have the closely related somatolactin. In humans, three smaller (4, 16 and 22kDa) and several larger (so called big and big-big) variants exist.[not verified in body]

Prolactin has a wide variety of effects. It stimulates the mammary glands to produce milk (lactation): increased serum concentrations of prolactin during pregnancy cause enlargement of the mammary glands and prepare for milk production, which normally starts when the levels of progesterone fall by the end of pregnancy and a suckling stimulus is present. Sometimes, newborns (males as well as females) secrete a milky substance from their nipples known as witch's milk. This is in part caused by maternal prolactin and other hormones. Prolactin plays an important role in maternal behavior.[8]

Prolactin provides the body with sexual gratification after sexual acts: The hormone counteracts the effect of dopamine, which is linked to sexual arousal. This is thought to cause the sexual refractory period. The amount of prolactin can be an indicator for the amount of sexual satisfaction and relaxation. Unusually high amounts are suspected to be responsible for impotence and loss of libido (see hyperprolactinemia symptoms).

Elevated levels of prolactin decrease the levels of sex hormones estrogen in women and testosterone in men.[9] The effects of mildly elevated levels of prolactin are much more variable, in women, substantially increasing or decreasing estrogen levels.

Prolactin is sometimes classified as a gonadotropin[10] although in humans it has only a weak luteotropic effect while the effect of suppressing classical gonadotropic hormones is more important.[11] Prolactin within the normal reference ranges can act as a weak gonadotropin, but at the same time suppresses GnRH secretion. The exact mechanism by which it inhibits GnRH is poorly understood. Although expression of prolactin receptors (PRL-R) have been demonstrated in rat hypothalamus, the same has not been observed in GnRH neurons.[12] Physiologic levels of prolactin in males enhance luteinizing hormone-receptors in Leydig cells, resulting in testosterone secretion, which leads to spermatogenesis.[13]

Prolactin also stimulates proliferation of oligodendrocyte precursor cells. These cells differentiate into oligodendrocytes, the cells responsible for the formation of myelin coatings on axons in the central nervous system.[14]

Other actions include contributing to pulmonary surfactant synthesis of the fetal lungs at the end of the pregnancy and immune tolerance of the fetus by the maternal organism during pregnancy. Prolactin delays hair regrowth in mice.[15] Prolactin promotes neurogenesis in maternal and fetal brains.[16][17]

In humans, prolactin is produced at least in the anterior pituitary, decidua, myometrium, breast, lymphocytes, leukocytes and prostate.[18][19]

Pituitary PRL is controlled by the Pit-1 transcription factor that binds to the prolactin gene at several sites. Ultimately dopamine, extrapituitary PRL is controlled by a superdistal promoter and apparently unaffected by dopamine.[19] The thyrotropin-releasing hormone and the vasoactive intestinal peptide stimulate the secretion of prolactin in experimental settings, however their physiological influence is unclear. The main stimulus for prolactin secretion is suckling, the effect of which is neuronally mediated.[20] A key regulator of prolactin production is estrogens that enhance growth of prolactin-producing cells and stimulate prolactin production directly, as well as suppressing dopamine.

In decidual cells and in lymphocytes the distal promoter and thus prolactin expression is stimulated by cAMP. Responsivness to cAMP is mediated by an imperfect cAMPresponsive element and two CAAT/enhancer binding proteins (C/EBP).[19]Progesterone upregulates prolactin synthesis in the endometrium and decreases it in myometrium and breast glandular tissue.[21] Breast and other tissues may express the Pit-1 promoter in addition to the distal promoter.

Extrapituitary production of prolactin is thought to be special to humans and primates and may serve mostly tissue specific paracrine and autocrine purposes. It has been hypothesized that in vertebrates such as mice a similar tissue specific effect is achieved by a large family of prolactin-like proteins controlled by at least 26 paralogous PRL genes not present in primates.[19]

Vasoactive intestinal peptide and peptide histidine isoleucine help to regulate prolactin secretion in humans, but the functions of these hormones in birds can be quite different.[22]

Prolactin follows diurnal and ovulatory cycles. Prolactin levels peak during REM sleep and in the early morning. Many mammals experience a seasonal cycle.

During pregnancy, high circulating concentrations of estrogen and progesterone increase prolactin levels by 10- to 20-fold. Estrogen and progesterone inhibit the stimulatory effects of prolactin on milk production. The abrupt drop of estrogen and progesterone levels following delivery allow prolactinwhich temporarily remains highto induce lactation.[verification needed]

Sucking on the nipple offsets the fall in prolactin as the internal stimulus for them is removed. The sucking activates mechanoreceptors in and around the nipple. These signals are carried by nerve fibers through the spinal cord to the hypothalamus, where changes in the electrical activity of neurons that regulate the pituitary gland increase prolactin secretion. The suckling stimulus also triggers the release of oxytocin from the posterior pituitary gland, which triggers milk let-down: Prolactin controls milk production (lactogenesis) but not the milk-ejection reflex; the rise in prolactin fills the breast with milk in preparation for the next feed.

In usual circumstances, in the absence of galactorrhea, lactation ceases within one or two weeks following the end of breastfeeding.

Compared to un-mated males, fathers and expectant fathers have increased prolactin concentrations.[23]

Levels can rise after exercise, high-protein meals,[24]sexual intercourse, breast examination,[24] minor surgical procedures,[25] following epileptic seizures[26] or due to physical or emotional stress.[24][27] In a study on female volunteers under hypnosis, prolactin surges resulted from the evocation, with rage, of humiliating experiences, but not from the fantasy of nursing.[27]

Prolactin levels have also been found to rise with use of the drug MDMA (Ecstasy), leading to speculation that prolactin may have a role in the post-orgasmic state as well as decreased sexual desire.[28]

Hypersecretion is more common than hyposecretion. Hyperprolactinemia is the most frequent abnormality of the anterior pituitary tumors, termed prolactinomas. Prolactinomas may disrupt the hypothalamic-pituitary-gonadal axis as prolactin tends to suppress the secretion of GnRH from the hypothalamus and in turn decreases the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, therefore disrupting the ovulatory cycle.[29] Such hormonal changes may manifest as amenorrhea and infertility in females as well as impotence in males. Inappropriate lactation (galactorrhoea) is another important clinical sign of prolactinomas.

The structure of prolactin is similar to that of growth hormone and placental lactogen. The molecule is folded due to the activity of three disulfide bonds. Significant heterogeneity of the molecule has been described, thus bioassays and immunoassays can give different results due to differing glycosylation, phosphorylationsandulfation, as well as degradation. The non-glycosylated form of prolactin is the dominant form at is secreted by the pituitary gland.

The three different sizes of prolactin are:

The levels of larger ones are somewhat higher during the early postpartum period.[33]

Prolactin receptors are present in the mammillary glands, ovaries, pituitary glands, heart, lung, thymus, spleen, liver, pancreas, kidney, adrenal gland, uterus, skeletal muscle, skin and areas of the central nervous system.[34] When prolactin binds to the receptor, it causes it to dimerize with another prolactin receptor. This results in the activation of Janus kinase 2, a tyrosine kinase that initiates the JAK-STAT pathway. Activation also results in the activation of mitogen-activated protein kinases and Src kinase.[34]

Human prolactin receptors are insensitive to mouse prolactin.[35]

Prolactin levels may be checked as part of a sex hormone workup, as elevated prolactin secretion can suppress the secretion of FSH and GnRH, leading to hypogonadism and sometimes causing erectile dysfunction.

Prolactin levels may be of some use in distinguishing epileptic seizures from psychogenic non-epileptic seizures. The serum prolactin level usually rises following an epileptic seizure.[36]

The serum concentration of prolactin can be given in mass concentration (g/L or ng/mL), molar concentration (nmol/L or pmol/L) or in international units (typically mIU/L). The current IU is calibrated against the third International Standard for Prolactin, IS 84/500.[37][38] Reference ampoules of IS 84/500 contain 2.5g of lyophilized human prolactin[39] and have been assigned an activity of .053 International Units.[37][38] Measurements that are calibrated against the current international standard can be converted into mass units using this ratio of grams to IUs;[40] prolactin concentrations expressed in mIU/L can be converted to g/L by dividing by 21.2. Previous standards use other ratios.[41][42][43][44]

The first International Reference Preparation (or IRP) of human Prolactin for Immunoassay was established in 1978 (75/504 1st IRP for human Prolactin) at a time when purified human prolactin was in short supply.[40][41] Previous standards relied on prolactin from animal sources.[44] Purified human prolactin was scarce, heterogeneous, unstable and difficult to characterize. A preparation labelled 81/541 was distributed by the WHO Expert Committee on Biological Standardization without official status and given the assigned value of 50 mIU/ampoule based on an earlier collaborative study.[40][42] It was determined that this preparation behaved anomalously in certain immunoassays and was not suitable as an IS.[40]

Three different human pituitary extracts containing prolactin were subsequently obtained as candidates for an IS. These were distributed into ampoules coded 83/562, 83/573 and 84/500.[37][38][40][43] Collaborative studies involving 20 different laboratories found little difference between these three preparations. 83/562 appeared to be the most stable. This preparation was largely free of dimers and polymers of prolactin. On the basis of these investigations 83/562 was established as the Second IS for human Prolactin.[43] Once stocks of these ampoules were depleted, 84/500 was established as the Third IS for human Prolactin.[37][40]

General guidelines for diagnosing prolactin excess (hyperprolactinemia) define the upper threshold of normal prolactin at 25g/L for women and 20g/L for men.[34] Similarly, guidelines for diagnosing prolactin deficiency (hypoprolactinemia) are defined as prolactin levels below 3g/L in women[45][46] and 5g/L in men.[47][48][49] However, different assays and methods for measuring prolactin are employed by different laboratories and as such the serum reference range for prolactin is often determined by the laboratory performing the measurement.[34][50] Furthermore, prolactin levels also vary factors including age,[51] sex,[51]menstrual cycle stage[51] and pregnancy.[51] The circumstances surrounding a given prolactin measurement (assay, patient condition, etc.) must therefore be considered before the measurement can be accurately interpreted.[34]

The following chart illustrates the variations seen in normal prolactin measurements across different populations. Prolactin values were obtained from specific control groups of varying sizes using the IMMULITE assay.[51]

The following table illustrates variability in reference ranges of serum prolactin between some commonly used assay methods (as of 2008), using a control group of healthy health care professionals (53 males, age 2064 years, median 28 years; 97 females, age 1959 years, median 29 years) in Essex, England:[50]

An example usage of table above is, if using the Centaur assay to estimate prolactin values in g/L for females, the mean is 7.92g/L and the reference range is 3.3516.4g/L.

Hyperprolactinaemia, or excess serum prolactin, is associated with hypoestrogenism, anovulatory infertility, oligomenorrhoea, amenorrhoea, unexpected lactation and loss of libido in women and erectile dysfunction and loss of libido in men.[53]

Hypoprolactinemia, or serum prolactin deficiency, is associated with ovarian dysfunction in women,[45][46] and arteriogenic erectile dysfunction, premature ejaculation,[47]oligozoospermia, asthenospermia, hypofunction of seminal vesicles and hypoandrogenism[48] in men. In one study, normal sperm characteristics were restored when prolactin levels were raised to normal values in hypoprolactinemic men.[49]

Hypoprolactinemia can result from hypopituitarism, excessive dopaminergic action in the tuberoinfundibular pathway and ingestion of D2 receptor agonists such as bromocriptine.

While there is evidence that women who smoke tend to breast feed for shorter periods, there is a wide variation of breast-feeding rates in women who do smoke. This suggest that psychosocial factors rather than physiological mechanisms (e.g., nicotine suppressing prolactin levels) are responsible for the lower rates of breast feeding in women who do smoke.[54][55]

Prolactin is available commercially for use in animals, but not in humans.[56] It is used to stimulate lactation in animals.[56] The biological half-life of prolactin in humans is around 1520 minutes.[57] The D2 receptor is involved in the regulation of prolactin secretion, and agonists of the receptor such as bromocriptine and cabergoline decrease prolactin levels while antagonists of the receptor such as domperidone, metoclopramide, haloperidol, risperidone, and sulpiride increase prolactin levels.[58] D2 receptor antagonists like domperidone, metoclopramide, and sulpiride are used as galactogogues to increase prolatin secretion and induce lactation in humans.[59]

See more here:
Prolactin - Wikipedia

If you are feeling out of balance, tired and overwhelmed, or your quality of life is being compromised by the symptoms of aging, don't despair. Your body and hormones are simply trying to give you a wake-up call. There is plenty you can do to feel energetic, vibrant and healthy again.

The medical team at Westcoast Women's Clinic are specially trained hormone physicians and experts in helping women achieve optimal health and wellness during their midlife years, which can range from their late-30s to mid-60s.

We also offer programs for Young Women and Male patients to optimize hormone health.

Our Comprehensive Hormone Health Program includes state-of-the-art hormone testing, bioidentical hormone therapy, mind/body medicine, nutritional supplements and lifestyle modifications. Every treatment program is fully customized, from the bioidentical hormones to the physical, emotional and spiritual recommendations, to help ensure individual success.

Our Hormone Health program is an effective way to manage:

Link:
West Coast Womens Clinic - Vancouver Womens Health Clinic

Personalized Solutions For Wellness & Vitality

Hormones control everything in your body. At any age, our hormones can begin to decrease causing low energylevels, fatigue, trouble sleeping, trouble losing weight, mood swings, depression and low libido. Our providers haveover 100 years of combined clinical experience specializing in Bioidentical Hormone Replacement Therapy and Medical Weight LossPrograms.

Do you experience hormone imbalance symptoms such as:

Have you been informed by your doctor that you have normal blood test results or that its all in your head? We want you to have the energy and ability to experience life to its fullness. Natural Bio Healths focus is to help each patient gain control of their individual health. Dont wait this is the first step to getting your life back!

Congratulations on taking charge of your health! The first step is a phone consultation with a wellness consultant who will guide you through the process of becoming part of the Natural Bio Health Family and to schedule your appointment.

Continue reading here:
Medical Weight Loss | Endocrinology & Hormone Replacement

What is natural hormone replacment and why consider it an option for you?

Natural hormones are biologically identical to the hormones your body makes. Meaning, the chemical structures of the hormones are identical to those synthesized in your ovaries and other areas of the body. The body sees Prempro and Premarin and considers them foreign substances, but it recognizes bioidentical hormones as familiar and responds to them in natural ways.

Dosages are customized to each patient. One size does not fit all. Each patient is put on a dose specifically chosen according toindividualhormone levels, symptoms, genetic profile, stress level, and overall health assessment.

Since the product is compounded at special pharmacies, any dose of any hormone can be added, subtracted, and adjusted as appropriate. This is individualized hormone replacement therapy, which takes into account the fact that all women and men are not the same.

There are multiple modalities of administering natural hormones: creams, gels, sublingual drops, injections, capsules, hormone pellet implants.

All the benefits of hormone replacement therapymood, sex drive, heart, brain, bone density, and cancer protectionapply to natural hormone replacement without clinical evidence of the well documented side effects of the chemicalized, horse urine, conjuguated estrogens contained in conventional hormone replacement therapy (HRT).

What is the difference between bioidentical and chemical/synthetic hormones?

Premarin/Prempro

1.) Mixture of horse urine-based, chemicalized synthetic estrogens (equilin, equilinin, etc.) plus additives and coatings, which are also synthetic.

2). Can remain in the body for as long as 13 weeks.

3.) Potency of synthetic estrogen is approximately 200 times that of natural estrogen.

4.) Contains higher percentage of more aggressive types of estrogen.

5.) One-size-fits-all dosing.

Natural/Bioidentical HRT

1.) Bioidentical replaces instead of substituting an unfamiliar chemical.

2.) Eliminated from the body in a matter of hours, not weeks.

3.) Potency is same or even less than estrogen levels in ovulating women.

4.) Customized treatment program.

5.) Physiologic doses used.

6.) All of the bodys other hormones are evaluated and treated simultaneously, to keep natural balance intact (DHEA, cortisol, testosterone, progesterone, thyroid hormones, insulin, etc.)

7.) Diet /nutrition, exercise, stress control, digestion, and detox are equally important parts of treatment.

Latest Research

Its not the estrogen you take that causes breast cancer , but the estrogen you make. We now know that estrogen converts into other forms (metabolites), which determine the ultimate effects of estrogen on your body.

It appears to be the metabolites of estrogen that determine the risk of developing breast cancer. (Metabolite: The product of the chemical changes a substance undergoes in the tissues.)

There are three signifcant metabolites of estrogen that determine cancer risk:

The first is 2-hydroxy estrone (good for you). It does not stimulate cell division and it attaches to estrogen cell receptors and blocks attachment of more aggressive estrogens.

The second is 16-hydroxy estrone (bad for you). This one strongly attaches to receptors and stimulated DNA synthesis and cell replication. It binds permanently to receptors, while other estrogens attach briefly and are released.

The third metabolite is 4-hydroxy estrone (also bad). May directly damage DNA and can cause mutations that are carcinogenic.

Equine estrogens (Premarin, Prempro) promote metabolism of the 4-hydroxy estrones, causing mutagenic damage (cancer potential) five times more rapidly than human 4-hydroxy estrones.

Too high (or low) doses of ANY type of hormone (hormone imbalance) will cause undesirable sideeffects. Natural HRT is prescribed at the lowest effective doses, and treatment is followed with regular lab tests (blood, saliva, urine), uterine ultrasounds, breast exams, mammograms/thermograms, pap smears, and regular visits to the physicians office.

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Hormone Replacement Therapy | Born Clinic

National Guideline Clearinghouse

The National Guideline Clearinghouse (NGC), an AHRQ initiative, is a publicly available database of evidence-based clinical practice guidelines and related documents. Updated weekly with new content, the NGC provides physicians and other health professionals, health care providers, health plans, integrated delivery systems, purchasers, and others an accessible mechanism for obtaining objective, detailed information on clinical practice guidelines and to further their dissemination, implementation, and use.

Created in 1984, the U.S. Preventive Services Task Force (USPSTF or Task Force) is an independent group of national experts in prevention and evidence-based medicine that works to improve the health of all Americans by making evidence-based recommendations about clinical preventive services such as screenings, counseling services, or preventive medications. The USPSTF is made up of 16 volunteer members who come from the fields of preventive medicine and primary care, including internal medicine, family medicine, pediatrics, behavioral health, obstetrics/gynecology, and nursing. All members volunteer their time to serve on the USPSTF, and most are practicing clinicians.

The Guide to Clinical Preventive Services includes U.S. Preventive Services Task Force (USPSTF) recommendations on screening, counseling, and preventive medication topics and includes clinical considerations for each topic. This new pocket guide is an authoritative source for making decisions about preventive services.

Between 1992 and 1996, the Agency for Health Care Policy and Research (now the Agency for Healthcare Research and Quality) sponsored development of a series of 19 clinical practice guidelines. These guideline products are no longer viewed as guidance for current medical practice, and are provided for archival purposes only.

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Clinical Guidelines and Recommendations | Agency for ...

We Are Magnet

UT Southwestern has achieved Magnet designation, the highest honor bestowed by the American Nurses Credentialing Center (ANCC).

We've brought the leading-edge therapies and world-class care of UT Southwestern to Richardson/Plano, Las Colinas, and the Park Cities.

Clinical Center at Las Colinas The Las Colinas Obstetrics/Gynecology Clinic is a full-service practice, treating the full range of obstetric and gynecologic conditions.

Clinical Center at Park Cities The Clinical Center at Park Cities features cardiology, general internal medicine, obstetric/gynecologic, and rheumatology services.

Clinical Center at Richardson/Plano The Clinical Center at Richardson/Plano features behavioral health, cancer, neurology, obstetric/gynecologic, primary care, sports medicine, and urology services.

UT Southwestern Medical Center is honored frequently for the quality of our care and the significance of our discoveries. Some of our recent awards include the Press Ganey Beacon of Excellence Award for patient satisfaction and the National Research Consultants' Five Star National Excellence Award.

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UT Southwestern, Dallas, Texas - UTSW Medicine (Patient ...

If you are sick and tired of being sick and tired, feel yourself gaining more weight, confused about supplements and bioidentical hormones, or lost your libido then you may want to contact the top hormone replacement clinic in the area. Many of us suffer from insomnia, weight gain, wrinkling of skin, fatigue, thinning of hair, hot flashes, night sweats, loss of muscle tone and increased body fat, and have risk factors for heart disease. Our experienced bio identical hormone doctors specialize in the field of bioidentical hormones, functional and regenerative medicine with a proven track record of success.

I am eternally grateful for Healthy Aging Medical Centers. Once my hormone levels were optimized it was like I got my life back. At 55 years old, my mood improved, my sex life returned and I had energy to give to my family again. I realized it wasnt a red corvette I needed, it was testosterone and thyroid! Now my wife is on the program and she no longer has hot flashes and chases me around the house. Thank you Healthy Aging Medical Centers!.

S.W.

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Hormone Replacement Clinic in NJ | Healthy Aging Medical ...

Melatonin, chemically N-acetyl-5-methoxy tryptamine,[1] is a substance found in animals, plants, fungi, and bacteria. In animals, it is a hormone that anticipates the daily onset of darkness;[2] however in other organisms, it may have different functions. Likewise, the synthesis of melatonin in animals differs from that in other organisms.

In animals, melatonin is involved in the entrainment (synchronization) of the circadian rhythms of physiological functions including sleep timing, blood pressure regulation, seasonal reproduction, and many others.[3] Many of melatonin's biological effects in animals are produced through activation of melatonin receptors,[4] while others are due to its role as a pervasive and powerful antioxidant,[5] with a particular role in the protection of nuclear and mitochondrial DNA.[6]

It is used as a medication for insomnia, however, scientific evidence is insufficient to demonstrate a benefit in this area.[7] Melatonin is sold over-the-counter in the United States and Canada. In other countries, it may require a prescription or it may be unavailable.

Melatonin has shown promise in treating sleep-wake cycle disorders in children with underlying neurodevelopment difficulties.[8][9] As add-on to antihypertensive therapy, prolonged-release melatonin has improved blood pressure control in people with nocturnal hypertension.[10]

People with circadian rhythm sleep disorders may use oral melatonin to help entrain (biologically synchronize in the correct phase) to the environmental light-dark cycle. Melatonin reduces sleep onset latency to a greater extent in people with delayed sleep phase disorder than in people with insomnia.[11]

Melatonin has been studied for insomnia in the elderly.[12][13][14] Prolonged-release melatonin has shown good results in treating insomnia in older adults.[15] Short-term treatment (up to three months) of prolonged-release melatonin was found to be effective and safe in improving sleep latency, sleep quality, and daytime alertness.[16]

Evidence for use of melatonin as a treatment for insomnia is, as of 2015, insufficient;[7] low-quality evidence indicates it may speed the onset of sleep by 6 minutes.[7] A 2004 review found "no evidence that melatonin had an effect on sleep onset latency or sleep efficiency" in shift work or jet lag, while it did decrease sleep onset latency in people with a primary sleep disorder and it increased sleep efficiency in people with a secondary sleep disorder.[11] A later review[17] found minimal evidence for efficacy in shift work.

Melatonin is known to aid in reducing the effects of jet lag, especially in eastward travel, by promoting the necessary reset of the body's sleep-wake phase. If the timing is not correct, however, it can instead delay adaption.[18]

Melatonin appears also to have limited use against the sleep problems of people who work rotating or night shifts.[17]

Tentative evidence shows melatonin may help reduce some types of headaches including cluster headaches.[19]

A 2013 review by the National Cancer Institutes found evidence for use to be inconclusive.[20] A 2005 review of unblinded clinical trials found a reduced rate of death, but that blinded and independently conducted randomized controlled trials are needed.[21]

Melatonin presence in the gallbladder has many protective properties, such as converting cholesterol to bile, preventing oxidative stress, and increasing the mobility of gallstones from the gallbladder.[22]

Both animal[23] and human[24][25] studies have shown melatonin to protect against radiation-induced cellular damage. Melatonin and its metabolites protect organisms from oxidative stress by scavenging reactive oxygen species which are generated during exposure.[26] Nearly 70% of biological damage caused by ionizing radiation is estimated to be attributable to the creation of free radicals, especially the hydroxyl radical that attacks DNA, proteins, and cellular membranes. Melatonin has been described as a broadly protective, readily available, and orally self-administered antioxidant that is without major known side effects.[27]

Tentative evidence of benefit exists for treating tinnitus.[28]

Melatonin might improve sleep in autistic people.[29] Children with autism have abnormal melatonin pathways and below-average physiological levels of melatonin.[30][31] Melatonin supplementation has been shown to improve sleep duration, sleep onset latency, and night-time awakenings.[30][32][33] However, many studies on melatonin and autism rely on self-reported levels of improvement and more rigorous research is needed.

While the packaging of melatonin often warns against use in people under 18 years of age, available studies suggest that melatonin is an efficacious and safe treatment for insomnia in people with ADHD. However, larger and longer studies are needed to establish long-term safety and optimal dosing.[34]

Melatonin in comparison to placebo is effective for reducing preoperative anxiety in adults when given as premedication. It may be just as effective as standard treatment with midazolam in reducing preoperative anxiety. Melatonin may also reduce postoperative anxiety (measured 6 hours after surgery) when compared to placebo.[35]

Some supplemental melatonin users report an increase in vivid dreaming. Extremely high doses of melatonin increased REM sleep time and dream activity in people both with and without narcolepsy.[36]

Melatonin appears to cause very few side effects as tested in the short term, up to three months, at low doses. Two systematic reviews found no adverse effects of exogenous melatonin in several clinical trials and comparative trials found the adverse effects headaches, dizziness, nausea, and drowsiness were reported about equally for both melatonin and placebo.[37][38] Prolonged-release melatonin is safe with long-term use of up to 12 months.[39]

Melatonin can cause nausea, next-day grogginess, and irritability.[40] In the elderly, it can cause reduced blood flow and hypothermia.[41] In autoimmune disorders, evidence is conflicting whether melatonin supplementation may ameliorate or exacerbate symptoms due to immunomodulation.[42][43]

Melatonin can lower follicle-stimulating hormone levels.[44] Effects of melatonin on human reproduction remain unclear,[45] although it was with some effect tried as a contraceptive in the 1990s.[46]

Anticoagulants and other substances are known to interact with melatonin.[47]

In animals, the primary function is regulation of day-night cycles. Human infants' melatonin levels become regular in about the third month after birth, with the highest levels measured between midnight and 8:00 am.[48] Human melatonin production decreases as a person ages.[49] Also, as children become teenagers, the nightly schedule of melatonin release is delayed, leading to later sleeping and waking times.[50]

Besides its function as synchronizer of the biological clock, melatonin is a powerful free-radical scavenger and wide-spectrum antioxidant as discovered in 1993.[51] In many less-complex life forms, this is its only known function.[26] Melatonin is an antioxidant that can easily cross cell membranes[52] and the bloodbrain barrier.[5][53] This antioxidant is a direct scavenger of radical oxygen and nitrogen species including OH, O2, and NO.[54][55] Melatonin works with other antioxidants to improve the overall effectiveness of each antioxidant.[55] Melatonin has been proven to be twice as active as vitamin E, believed to be the most effective lipophilic antioxidant.[56] An important characteristic of melatonin that distinguishes it from other classic radical scavengers is that its metabolites are also scavengers in what is referred to as the cascade reaction.[26] Also different from other classic antioxidants, such as vitamin C and vitamin E, melatonin has amphiphilic properties. When compared to synthetic, mitochondrial-targeted antioxidants (MitoQ and MitoE), melatonin proved to be a comparable protector against mitochondrial oxidative stress.[57]

While it is known that melatonin interacts with the immune system,[58][59] the details of those interactions are unclear. Antiinflammatory effect seems to be the most relevant and most documented in the literature.[60] There have been few trials designed to judge the effectiveness of melatonin in disease treatment. Most existing data are based on small, incomplete clinical trials. Any positive immunological effect is thought to be the result of melatonin acting on high-affinity receptors (MT1 and MT2) expressed in immunocompetent cells. In preclinical studies, melatonin may enhance cytokine production,[61] and by doing this, counteract acquired immunodeficiences. Some studies also suggest that melatonin might be useful fighting infectious disease[62] including viral, such as HIV, and bacterial infections, and potentially in the treatment of cancer.

In rheumatoid arthritis patients, melatonin production has been found increased when compared to age-matched healthy controls.[63][relevant? discuss]

In vitro, melatonin can form complexes with cadmium and other metals.[64]

Biosynthesis of melatonin occurs through hydroxylation, decarboxylation, acetylation and a methylation starting with L-tryptophan. [65] L-tryptophan is produced in the shikimate pathway from chorismate or is acquired from protein catabolism. First L-tryptophan is hydroxylated on the indole ring by tryptophan hydroxylase. The intermediate is decarboxylated by PLP and 5-hydroxy-L-tryptophan to produce serotonin also known as 5-hydroxytryptamine. Serotonin acts as a neurotransmitter on its own, but is also converted into N-acetyl-serotonin by serotonin N-acetyl transferase and acetyl-CoA. Hydroxyindole O-methyl transferase and SAM convert N-acetyl-serotonin into melatonin through methylation of the hydroxyl group.

In bacteria, protists, fungi, and plants, melatonin is synthesized indirectly with tryptophan as an intermediate product of the shikimic acid pathway. In these cells, synthesis starts with d-erythrose-4-phosphate and phosphoenolpyruvate, and in photosynthetic cells with carbon dioxide. The rest of the reactions are similar, but with slight variations in the last two enzymes.[66][67]

In order to hydroxylate L-tryptophan, the cofactor tetrahydrobiopterin must first react with oxygen and the active site iron of tryptophan hydroxylase. This mechanism is not well understood, but two mechanisms have been proposed:

1. A slow transfer of one electron from the pterin to O2 could produce a superoxide which could recombine with the pterin radical to give 4a-peroxypterin. 4a-peroxypterin could then react with the active site iron (II) to form an iron-peroxypterin intermediate or directly transfer an oxygen atom to the iron.

2. O2 could react with the active site iron (II) first, producing iron (III) superoxide which could then react with the pterin to form an iron-peroxypterin intermediate.

Iron (IV) oxide from the iron-peroxypterin intermediate is selectively attacked by a double bond to give a carbocation at the C5 position of the indole ring. A 1,2-shift of the hydrogen and then a loss of one of the two hydrogen atoms on C5 reestablishes aromaticity to furnish 5-hydroxy-L-tryptophan. [68]

A decarboxylase with cofactor pyridoxal phosphate (PLP) removes CO2 from 5-hydroxy-L-tryptophan to produce 5-hydroxytryptamine. [69] PLP forms an imine with the amino acid derivative. The amine on the pyridine is protonated and acts as an electron sink, breaking the C-C bond and releasing CO2. Protonation of the amine from tryptophan restores the aromaticity of the pyridine ring and then imine is hydrolyzed to produce 5-hydroxytryptamine and PLP. [70]

It has been proposed that His122 of serotonin N-acetyl transferase is the catalytic residue that deprotonates the primary amine of 5-hydroxytryptamine, which allows the lone pair on the amine to attack acetyl-CoA, forming a tetraherdral intermediate. The thiol from coenzyme A serves as a good leaving group when attacked by a general base to give N-acetyl-serotonin.[71]

N-acetyl-serotonin is methylated at the hydroxyl position by S-adenosyl methionine (SAM) to produce S-adenosyl homocysteine (SAH) and melatonin.[72][73]

In vertebrates, melatonin secretion is regulated by norepinephrine. Norepinephrine elevates the intracellular cAMP concentration via beta-adrenergic receptors and activates the cAMP-dependent protein kinase A (PKA). PKA phosphorylates the penultimate enzyme, the arylalkylamine N-acetyltransferase (AANAT). On exposure to (day)light, noradrenergic stimulation stops and the protein is immediately destroyed by proteasomal proteolysis.[74] Production of melatonin is again started in the evening at the point called the dim-light melatonin onset.

Blue light, principally around 460 to 480nm, suppresses melatonin,[75] proportional to the light intensity and length of exposure. Until recent history, humans in temperate climates were exposed to few hours of (blue) daylight in the winter; their fires gave predominantly yellow light.[citation needed] The incandescent light bulb widely used in the 20th century produced relatively little blue light.[76] Light containing only wavelengths greater than 530nm does not suppress melatonin in bright-light conditions.[77] Wearing glasses that block blue light in the hours before bedtime may decrease melatonin loss. Use of blue-blocking goggles the last hours before bedtime has also been advised for people who need to adjust to an earlier bedtime, as melatonin promotes sleepiness.[78]

When used several hours before sleep according to the phase response curve for melatonin in humans, small amounts (0.3mg[79]) of melatonin shift the circadian clock earlier, thus promoting earlier sleep onset and morning awakening.[80] In humans, 90% of orally administered exogenous melatonin is cleared in a single passage through the liver, a small amount is excreted in urine, and a small amount is found in saliva.[11]

In vertebrates, melatonin is produced in darkness, thus usually at night, by the pineal gland, a small endocrine gland[81] located in the center of the brain but outside the bloodbrain barrier. Light/dark information reaches the suprachiasmatic nuclei from retinal photosensitive ganglion cells of the eyes[82][83] rather than the melatonin signal (as was once postulated). Known as "the hormone of darkness", the onset of melatonin at dusk promotes activity in nocturnal (night-active) animals and sleep in diurnal ones including humans.

Many animals use the variation in duration of melatonin production each day as a seasonal clock.[84] In animals including humans,[85] the profile of melatonin synthesis and secretion is affected by the variable duration of night in summer as compared to winter. The change in duration of secretion thus serves as a biological signal for the organization of daylength-dependent (photoperiodic) seasonal functions such as reproduction, behavior, coat growth, and camouflage coloring in seasonal animals.[85] In seasonal breeders that do not have long gestation periods and that mate during longer daylight hours, the melatonin signal controls the seasonal variation in their sexual physiology, and similar physiological effects can be induced by exogenous melatonin in animals including mynah birds[86] and hamsters.[87] Melatonin can suppress libido by inhibiting secretion of luteinizing hormone and follicle-stimulating hormone from the anterior pituitary gland, especially in mammals that have a breeding season when daylight hours are long. The reproduction of long-day breeders is repressed by melatonin and the reproduction of short-day breeders is stimulated by melatonin.

During the night, melatonin regulates leptin, lowering its levels.

Until its identification in plants in 1987, melatonin was for decades thought to be primarily an animal neurohormone. When melatonin was identified in coffee extracts in the 1970s, it was believed to be a byproduct of the extraction process. Subsequently, however, melatonin has been found in all plants that have been investigated. It is present in all the different parts of plants, including leaves, stems, roots, fruits, and seeds in varying proportions.[88][89] Melatonin concentrations differ not only among plant species, but also between varieties of the same species depending on the agronomic growing conditions, varying from picograms to several micrograms per gram.[90][67] Notably high melatonin concentrations have been measured in popular beverages such as coffee, tea, wine, and beer, and crops including corn, rice, wheat, barley, and oats.[89] Melatonin is a poor direct antioxidant, it is, however, a highly efficient direct free radical scavenger and indirect antioxidant due to its ability to stimulate antioxidant enzymes.[91][92][93] Thus, melatonin in the human diet is believed to confer a number of beneficial health-related effects.[89][90][94] In some common foods and beverages, including coffee[89] and walnuts,[95] the concentration of melatonin has been estimated or measured to be sufficiently high to raise the blood level of melatonin above daytime baseline values.

Although a role for melatonin as a plant hormone has not been clearly established, its involvement in processes such as growth and photosynthesis is well established. Only limited evidence of endogenous circadian rhythms in melatonin levels has been demonstrated in some plant species and no membrane-bound receptors analogous to those known in animals have been described. Rather, melatonin performs important roles in plants as a growth regulator, as well as environmental stress protector. It is synthesized in plants when they are exposed to both biological stresses, for example, fungal infection, and nonbiological stresses such as extremes of temperature, toxins, increased soil salinity, drought, etc.[67][93][96]

Melatonin is categorized by the US Food and Drug Administration (FDA) as a dietary supplement, and is sold over-the-counter in both the US and Canada.[97] The FDA regulations applying to medications are not applicable to melatonin.[3] However, new FDA rules required that by June 2010, all production of dietary supplements must comply with "current good manufacturing practices" (cGMP) and be manufactured with "controls that result in a consistent product free of contamination, with accurate labeling."[98] The industry has also been required to report to the FDA "all serious dietary supplement related adverse events", and the FDA has (within the cGMP guidelines) begun enforcement of that requirement.[99]

As melatonin may cause harm in combination with certain medications or in the case of certain disorders, a doctor or pharmacist should be consulted before making a decision to take melatonin.[18]

In many countries, melatonin is recognized as a neurohormone and it cannot be sold over-the-counter.[100]

Melatonin has been reported in foods including cherries to about 0.1713.46ng/g,[101] bananas and grapes, rice and cereals, herbs, plums,[102] olive oil, wine[103] and beer. When birds ingest melatonin-rich plant feed, such as rice, the melatonin binds to melatonin receptors in their brains.[104] When humans consume foods rich in melatonin such as banana, pineapple and orange, the blood levels of melatonin increase significantly.[105]

As reported in the New York Times in May 2011,[106] beverages and snacks containing melatonin are sold in grocery stores, convenience stores, and clubs. The FDA is considering whether these food products can continue to be sold with the label "dietary supplements". On 13 January 2010, it issued a warning letter to Innovative Beverage, creators of several beverages marketed as drinks, stating that melatonin is not approved as a food additive because it is not generally recognized as safe.[107]

Melatonin was first discovered in connection to the mechanism by which some amphibians and reptiles change the color of their skin.[108][109] As early as 1917, Carey Pratt McCord and Floyd P. Allen discovered that feeding extract of the pineal glands of cows lightened tadpole skin by contracting the dark epidermal melanophores.[110][111]

In 1958, dermatology professor Aaron B. Lerner and colleagues at Yale University, in the hope that a substance from the pineal might be useful in treating skin diseases, isolated the hormone from bovine pineal gland extracts and named it melatonin.[112] In the mid-70s Lynch et al. demonstrated[113] that the production of melatonin exhibits a circadian rhythm in human pineal glands.

The discovery that melatonin is an antioxidant was made in 1993.[114] The first patent for its use as a low-dose sleep aid was granted to Richard Wurtman at MIT in 1995.[115] Around the same time, the hormone got a lot of press as a possible treatment for many illnesses.[116]The New England Journal of Medicine editorialized in 2000: "With these recent careful and precise observations in blind persons, the true potential of melatonin is becoming evident, and the importance of the timing of treatment is becoming clear."[117]

Immediate-release melatonin is not tightly regulated in countries where it is available as an over-the-counter medication. It is available in doses from less than half a milligram to 5mg or more. Immediate-release formulations cause blood levels of melatonin to reach their peak in about an hour. The hormone may be administered orally, as capsules, tablets, or liquids. It is also available for use sublingually, or as transdermal patches.

Formerly, melatonin was derived from animal pineal tissue, such as bovine. It is now synthetic and does not carry a risk of contamination or the means of transmitting infectious material.[3][118]

Melatonin is available as a prolonged-release prescription drug. It releases melatonin gradually over 810 hours, intended to mimic the body's internal secretion profile.

In June 2007, the European Medicines Agency approved UK-based Neurim Pharmaceuticals' prolonged-release melatonin medication Circadin for marketing throughout the EU.[119] The drug is a prolonged-release melatonin, 2mg, for patients aged 55 and older, as monotherapy for the short-term treatment (up to 13 weeks) of primary insomnia characterized by poor quality of sleep.[120][121]

Other countries' agencies that subsequently approved the drug include:

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Melatonin - Wikipedia, the free encyclopedia

Ageing, also spelled aging, is the process of becoming older. The term refers especially to human beings, many animals, and fungi, whereas for example bacteria, perennial plants and some simple animals are potentially immortal. In the broader sense, ageing can refer to single cells within an organism which have ceased dividing (cellular senescence) or to the population of a species (population ageing).

In humans, ageing represents the accumulation of changes in a human being over time,[1] encompassing physical, psychological, and social change. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. Ageing is among the greatest known risk factors for most human diseases:[2] of the roughly 150,000 people who die each day across the globe, about two thirds die from age-related causes.

The causes of ageing are unknown; current theories are assigned to the damage concept, whereby the accumulation of damage (such as DNA breaks or oxidised DNA) may cause biological systems to fail, or to the programmed ageing concept, whereby internal processes (such as DNA telomere shortening) may cause ageing. Programmed ageing should not be confused with programmed cell death (apoptosis).

The discovery, in 1934, that calorie restriction can extend lifespan by 50% in rats has motivated research into delaying and preventing ageing.

Human beings and members of other species, especially animals, necessarily experience ageing and mortality. Fungi, too, can age.[3] In contrast, many species can be considered immortal: for example, bacteria fission to produce daughter cells, strawberry plants grow runners to produce clones of themselves, and animals in the genus Hydra have a regenerative ability with which they avoid dying of old age.

Early life forms on Earth, starting at least 3.7 billion years ago,[4] were single-celled organisms. Such single-celled organisms (prokaryotes, protozoans, algae) multiply by fissioning into daughter cells, thus do not age and are innately immortal.[5][6]

Ageing and mortality of the individual organism became possible with the evolution of sexual reproduction,[7] which occurred with the emergence of the fungal/animal kingdoms approximately a billion years ago, and with the evolution of flowering plants 160 million years ago. The sexual organism could henceforth pass on some of its genetic material to produce new individuals and itself could become disposable with regards to the survival of its species.[7] This classic biological idea has however been perturbed recently by the discovery that the bacterium E. coli may split into distinguishable daughter cells, which opens the theoretical possibility of "age classes" among bacteria.[8]

Even within humans and other mortal species, there are cells with the potential for immortality: cancer cells which have lost the ability to die when maintained in cell culture such as the HeLa cell line,[9] and specific stem cells such as germ cells (producing ova and spermatozoa).[10] In artificial cloning, adult cells can be rejuvenated back to embryonic status and then used to grow a new tissue or animal without ageing.[11] Normal human cells however die after about 50 cell divisions in laboratory culture (the Hayflick Limit, discovered by Leonard Hayflick in 1961).[9]

A number of characteristic ageing symptoms are experienced by a majority or by a significant proportion of humans during their lifetimes.

Dementia becomes more common with age.[31] About 3% of people between the ages of 6574 have dementia, 19% between 75 and 84 and nearly half of those over 85 years of age.[32] The spectrum includes mild cognitive impairment and the neurodegenerative diseases of Alzheimer's disease, cerebrovascular disease, Parkinson's disease and Lou Gehrig's disease. Furthermore, many types of memory may decline with ageing, but not semantic memory or general knowledge such as vocabulary definitions, which typically increases or remains steady until late adulthood[33] (see Ageing brain). Intelligence may decline with age, though the rate may vary depending on the type and may in fact remain steady throughout most of the lifespan, dropping suddenly only as people near the end of their lives. Individual variations in rate of cognitive decline may therefore be explained in terms of people having different lengths of life.[34] There might be changes to the brain: after 20 years of age there may be a 10% reduction each decade in the total length of the brain's myelinated axons.[35][36]

Age can result in visual impairment, whereby non-verbal communication is reduced,[37] which can lead to isolation and possible depression. Macular degeneration causes vision loss and increases with age, affecting nearly 12% of those above the age of 80.[38] This degeneration is caused by systemic changes in the circulation of waste products and by growth of abnormal vessels around the retina.[39]

A distinction can be made between "proximal ageing" (age-based effects that come about because of factors in the recent past) and "distal ageing" (age-based differences that can be traced back to a cause early in person's life, such as childhood poliomyelitis).[34]

Ageing is among the greatest known risk factors for most human diseases.[2] Of the roughly 150,000 people who die each day across the globe, about two thirds100,000 per daydie from age-related causes. In industrialised nations, the proportion is higher, reaching 90%.[40][41][42]

At present, researchers are only just beginning to understand the biological basis of ageing even in relatively simple and short-lived organisms such as yeast.[43] Less still is known about mammalian ageing, in part due to the much longer lives in even small mammals such as the mouse (around 3 years). A primary model organism for studying ageing is the nematode C. elegans, thanks to its short lifespan of 23 weeks, the ability to easily perform genetic manipulations or suppress gene activity with RNA interference, and other factors.[44] Most known mutations and RNA interference targets that extend lifespan were first discovered in C. elegans.[45]

Factors that are proposed to influence biological ageing[46] fall into two main categories, programmed and damage-related. Programmed factors follow a biological timetable, perhaps a continuation of the one that regulates childhood growth and development. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair and defence responses. Damage-related factors include internal and environmental assaults to living organisms that induce cumulative damage at various levels.[47]

There are three main metabolic pathways which can influence the rate of ageing:

It is likely that most of these pathways affect ageing separately, because targeting them simultaneously leads to additive increases in lifespan.[49]

The rate of ageing varies substantially across different species, and this, to a large extent, is genetically based. For example, numerous perennial plants ranging from strawberries and potatoes to willow trees typically produce clones of themselves by vegetative reproduction and are thus potentially immortal, while annual plants such as wheat and watermelons die each year and reproduce by sexual reproduction. In 2008 it was discovered that inactivation of only two genes in the annual plant Arabidopsis thaliana leads to its conversion into a potentially immortal perennial plant.[50]

Clonal immortality apart, there are certain species whose individual lifespans stand out among Earth's life-forms, including the bristlecone pine at 5062 years[51] (however Hayflick states that the bristlecone pine has no cells older than 30 years), invertebrates like the hard clam (known as quahog in New England) at 508 years,[52] the Greenland shark at 400 years,[53] fish like the sturgeon and the rockfish, and the sea anemone[54] and lobster.[55][56] Such organisms are sometimes said to exhibit negligible senescence.[57] The genetic aspect has also been demonstrated in studies of human centenarians.

In laboratory settings, researchers have demonstrated that selected alterations in specific genes can extend lifespan quite substantially in yeast and roundworms, less so in fruit flies and less again in mice. Some of the targeted genes have homologues across species and in some cases have been associated with human longevity.[58]

Caloric restriction substantially affects lifespan in many animals, including the ability to delay or prevent many age-related diseases.[99] Typically, this involves caloric intake of 6070% of what an ad libitum animal would consume, while still maintaining proper nutrient intake.[99] In rodents, this has been shown to increase lifespan by up to 50%;[100] similar effects occur for yeast and Drosophila.[99] No lifespan data exist for humans on a calorie-restricted diet,[72] but several reports support protection from age-related diseases.[101][102] Two major ongoing studies on rhesus monkeys initially revealed disparate results; while one study, by the University of Wisconsin, showed that caloric restriction does extend lifespan,[103] the second study, by the National Institute on Ageing (NIA), found no effects of caloric restriction on longevity.[104] Both studies nevertheless showed improvement in a number of health parameters. Notwithstanding the similarly low calorie intake, the diet composition differed between the two studies (notably a high sucrose content in the Wisconsin study), and the monkeys have different origins (India, China), initially suggesting that genetics and dietary composition, not merely a decrease in calories, are factors in longevity.[72] However, in a comparative analysis in 2014, the Wisconsin researchers found that the allegedly non-starved NIA control monkeys in fact are moderately underweight when compared with other monkey populations, and argued this was due to the NIA's apportioned feeding protocol in contrast to Wisconsin's truly unrestricted ad libitum feeding protocol. [105] They conclude that moderate calorie restriction rather than extreme calorie restriction is sufficient to produce the observed health and longevity benefits in the studied rhesus monkeys.[106]

In his book How and Why We Age, Hayflick says that caloric restriction may not be effective in humans, citing data from the Baltimore Longitudinal Study of Aging which shows that being thin does not favour longevity.[need quotation to verify][107] Similarly, it is sometimes claimed that moderate obesity in later life may improve survival, but newer research has identified confounding factors such as weight loss due to terminal disease. Once these factors are accounted for, the optimal body weight above age 65 corresponds to a leaner body mass index of 23 to 27.[108]

Alternatively, the benefits of dietary restriction can also be found by changing the macro nutrient profile to reduce protein intake without any changes to calorie level, resulting in similar increases in longevity.[109][110] Dietary protein restriction not only inhibits mTOR activity but also IGF-1, two mechanisms implicated in ageing.[70] Specifically, reducing leucine intake is sufficient to inhibit mTOR activity, achievable through reducing animal food consumption.[111][112]

The Mediterranean diet is credited with lowering the risk of heart disease and early death.[113][114] The major contributors to mortality risk reduction appear to be a higher consumption of vegetables, fish, fruits, nuts and monounsaturated fatty acids, i.e., olive oil.[115]

The amount of sleep has an impact on mortality. People who live the longest report sleeping for six to seven hours each night.[116][117] Lack of sleep (<5 hours) more than doubles the risk of death from cardiovascular disease, but too much sleep (>9 hours) is associated with a doubling of the risk of death, though not primarily from cardiovascular disease.[118] Sleeping more than 7 to 8 hours per day has been consistently associated with increased mortality, though the cause is probably other factors such as depression and socioeconomic status, which would correlate statistically.[119] Sleep monitoring of hunter-gatherer tribes from Africa and from South America has shown similar sleep patterns across continents: their average sleeping duration is 6.4 hours (with a summer/winter difference of 1 hour), afternoon naps (siestas) are uncommon, and insomnia is very rare (tenfold less than in industrial societies).[120]

Physical exercise may increase life expectancy.[121] People who participate in moderate to high levels of physical exercise have a lower mortality rate compared to individuals who are not physically active.[122] Moderate levels of exercise have been correlated with preventing aging and improving quality of life by reducing inflammatory potential.[123] The majority of the benefits from exercise are achieved with around 3500 metabolic equivalent (MET) minutes per week.[124] For example, climbing stairs 10 minutes, vacuuming 15 minutes, gardening 20 minutes, running 20 minutes, and walking or bicycling for 25 minutes on a daily basis would together achieve about 3000 MET minutes a week.[124]

Avoidance of chronic stress (as opposed to acute stress) is associated with a slower loss of telomeres in most but not all studies,[125][126] and with decreased cortisol levels. A chronically high cortisol level compromises the immune system, causes cardiac damage/arterosclerosis and is associated with facial ageing, and the latter in turn is a marker for increased morbidity and mortality.[127][128] Stress can be countered by social connection, spirituality, and (for men more clearly than for women) married life, all of which are associated with longevity.[129][130][131]

The following drugs and interventions have been shown to retard or reverse the biological effects of ageing in animal models, but none has yet been proven to do so in humans.

Evidence in both animals and humans suggests that resveratrol may be a caloric restriction mimetic.[132]

As of 2015 metformin was under study for its potential effect on slowing ageing in the worm C.elegans and the cricket.[133] Its effect on otherwise healthy humans is unknown.[133]

Rapamycin was first shown to extend lifespan in eukaryotes in 2006 by Powers et al. who showed a dose-responsive effect of rapamycin on lifespan extension in yeast cells.[134] In a 2009 study, the lifespans of mice fed rapamycin were increased between 28 and 38% from the beginning of treatment, or 9 to 14% in total increased maximum lifespan. Of particular note, the treatment began in mice aged 20 months, the equivalent of 60 human years.[135] Rapamycin has subsequently been shown to extend mouse lifespan in several separate experiments,[136][137] and is now being tested for this purpose in nonhuman primates (the marmoset monkey).[138]

Cancer geneticist Ronald A. DePinho and his colleagues published research in mice where telomerase activity was first genetically removed. Then, after the mice had prematurely aged, they restored telomerase activity by reactivating the telomerase gene. As a result, the mice were rejuvenated: Shrivelled testes grew back to normal and the animals regained their fertility. Other organs, such as the spleen, liver, intestines and brain, recuperated from their degenerated state. "[The finding] offers the possibility that normal human ageing could be slowed by reawakening the enzyme in cells where it has stopped working" says Ronald DePinho. However, activating telomerase in humans could potentially encourage the growth of tumours.[139]

Most known genetic interventions in C. elegans increase lifespan by 1.5 to 2.5-fold. As of 2009[update], the record for lifespan extension in C. elegans is a single-gene mutation which increases adult survival by tenfold.[45] The strong conservation of some of the mechanisms of ageing discovered in model organisms imply that they may be useful in the enhancement of human survival. However, the benefits may not be proportional; longevity gains are typically greater in C. elegans than fruit flies, and greater in fruit flies than in mammals. One explanation for this is that mammals, being much longer-lived, already have many traits which promote lifespan.[45]

Some research effort is directed to slow ageing and extend healthy lifespan.[140][141][142]

The US National Institute on Aging currently funds an intervention testing programme, whereby investigators nominate compounds (based on specific molecular ageing theories) to have evaluated with respect to their effects on lifespan and age-related biomarkers in outbred mice.[143] Previous age-related testing in mammals has proved largely irreproducible, because of small numbers of animals and lax mouse husbandry conditions.[citation needed] The intervention testing programme aims to address this by conducting parallel experiments at three internationally recognised mouse ageing-centres, the Barshop Institute at UTHSCSA, the University of Michigan at Ann Arbor and the Jackson Laboratory.

Several companies and organisations, such as Google Calico, Human Longevity, Craig Venter, Gero,[144]SENS Research Foundation, and Science for Life Extension in Russia,[145] declared stopping or delaying ageing as their goal.

Prizes for extending lifespan and slowing ageing in mammals exist. The Methuselah Foundation offers the Mprize. Recently, the $1 Million Palo Alto Longevity Prize was launched. It is a research incentive prize to encourage teams from all over the world to compete in an all-out effort to "hack the code" that regulates our health and lifespan. It was founded by Joon Yun.[146][147][148][149][150]

Different cultures express age in different ways. The age of an adult human is commonly measured in whole years since the day of birth. Arbitrary divisions set to mark periods of life may include: juvenile (via infancy, childhood, preadolescence, adolescence), early adulthood, middle adulthood, and late adulthood. More casual terms may include "teenagers," "tweens," "twentysomething", "thirtysomething", etc. as well as "vicenarian", "tricenarian", "quadragenarian", etc.

Most legal systems define a specific age for when an individual is allowed or obliged to do particular activities. These age specifications include voting age, drinking age, age of consent, age of majority, age of criminal responsibility, marriageable age, age of candidacy, and mandatory retirement age. Admission to a movie for instance, may depend on age according to a motion picture rating system. A bus fare might be discounted for the young or old. Each nation, government and non-governmental organisation has different ways of classifying age. In other words, chronological ageing may be distinguished from "social ageing" (cultural age-expectations of how people should act as they grow older) and "biological ageing" (an organism's physical state as it ages).[151]

In a UNFPA report about ageing in the 21st century, it highlighted the need to "Develop a new rights-based culture of ageing and a change of mindset and societal attitudes towards ageing and older persons, from welfare recipients to active, contributing members of society."[152] UNFPA said that this "requires, among others, working towards the development of international human rights instruments and their translation into national laws and regulations and affirmative measures that challenge age discrimination and recognise older people as autonomous subjects."[152] Older persons make contributions to society including caregiving and volunteering. For example, "A study of Bolivian migrants who [had] moved to Spain found that 69% left their children at home, usually with grandparents. In rural China, grandparents care for 38% of children aged under five whose parents have gone to work in cities."[152]

Population ageing is the increase in the number and proportion of older people in society. Population ageing has three possible causes: migration, longer life expectancy (decreased death rate) and decreased birth rate. Ageing has a significant impact on society. Young people tend to have fewer legal privileges (if they are below the age of majority), they are more likely to push for political and social change, to develop and adopt new technologies, and to need education. Older people have different requirements from society and government, and frequently have differing values as well, such as for property and pension rights.[153]

In the 21st century, one of the most significant population trends is ageing.[154] Currently, over 11% of the world's current population are people aged 60 and older and the United Nations Population Fund (UNFPA) estimates that by 2050 that number will rise to approximately 22%.[152] Ageing has occurred due to development which has enabled better nutrition, sanitation, health care, education and economic well-being. Consequently, fertility rates have continued to decline and life expectancy have risen. Life expectancy at birth is over 80 now in 33 countries. Ageing is a "global phenomenon," that is occurring fastest in developing countries, including those with large youth populations, and poses social and economic challenges to the work which can be overcome with "the right set of policies to equip individuals, families and societies to address these challenges and to reap its benefits."[155]

As life expectancy rises and birth rates decline in developed countries, the median age rises accordingly. According to the United Nations, this process is taking place in nearly every country in the world.[156] A rising median age can have significant social and economic implications, as the workforce gets progressively older and the number of old workers and retirees grows relative to the number of young workers. Older people generally incur more health-related costs than do younger people in the workplace and can also cost more in worker's compensation and pension liabilities.[157] In most developed countries an older workforce is somewhat inevitable. In the United States for instance, the Bureau of Labor Statistics estimates that one in four American workers will be 55 or older by 2020.[157]

Among the most urgent concerns of older persons worldwide is income security. This poses challenges for governments with ageing populations to ensure investments in pension systems continues in order to provide economic independence and reduce poverty in old age. These challenges vary for developing and developed countries. UNFPA stated that, "Sustainability of these systems is of particular concern, particularly in developed countries, while social protection and old-age pension coverage remain a challenge for developing countries, where a large proportion of the labour force is found in the informal sector."[152]

The global economic crisis has increased financial pressure to ensure economic security and access to health care in old age. In order to elevate this pressure "social protection floors must be implemented in order to guarantee income security and access to essential health and social services for all older persons and provide a safety net that contributes to the postponement of disability and prevention of impoverishment in old age."[152]

It has been argued that population ageing has undermined economic development.[158] Evidence suggests that pensions, while making a difference to the well-being of older persons, also benefit entire families especially in times of crisis when there may be a shortage or loss of employment within households. A study by the Australian Government in 2003 estimated that "women between the ages of 65 and 74 years contribute A$16 billion per year in unpaid caregiving and voluntary work. Similarly, men in the same age group contributed A$10 billion per year."[152]

Due to increasing share of the elderly in the population, health care expenditures will continue to grow relative to the economy in coming decades. This has been considered as a negative phenomenon and effective strategies like labour productivity enhancement should be considered to deal with negative consequences of ageing.[159]

In the field of sociology and mental health, ageing is seen in five different views: ageing as maturity, ageing as decline, ageing as a life-cycle event, ageing as generation, and ageing as survival.[160] Positive correlates with ageing often include economics, employment, marriage, children, education, and sense of control, as well as many others. The social science of ageing includes disengagement theory, activity theory, selectivity theory, and continuity theory. Retirement, a common transition faced by the elderly, may have both positive and negative consequences.[161] As cyborgs currently are on the rise some theorists argue there is a need to develop new definitions of ageing and for instance a bio-techno-social definition of ageing has been suggested.[162]

With age inevitable biological changes occur that increase the risk of illness and disability. UNFPA states that,[155]

"A life-cycle approach to health care one that starts early, continues through the reproductive years and lasts into old age is essential for the physical and emotional well-being of older persons, and, indeed, all people. Public policies and programmes should additionally address the needs of older impoverished people who cannot afford health care."

Many societies in Western Europe and Japan have ageing populations. While the effects on society are complex, there is a concern about the impact on health care demand. The large number of suggestions in the literature for specific interventions to cope with the expected increase in demand for long-term care in ageing societies can be organised under four headings: improve system performance; redesign service delivery; support informal caregivers; and shift demographic parameters.[163]

However, the annual growth in national health spending is not mainly due to increasing demand from ageing populations, but rather has been driven by rising incomes, costly new medical technology, a shortage of health care workers and informational asymmetries between providers and patients.[164] A number of health problems become more prevalent as people get older. These include mental health problems as well as physical health problems, especially dementia.

It has been estimated that population ageing only explains 0.2 percentage points of the annual growth rate in medical spending of 4.3% since 1970. In addition, certain reforms to the Medicare system in the United States decreased elderly spending on home health care by 12.5% per year between 1996 and 2000.[165]

Positive self-perception of health has been correlated with higher well-being and reduced mortality in the elderly.[166][167] Various reasons have been proposed for this association; people who are objectively healthy may naturally rate their health better than that of their ill counterparts, though this link has been observed even in studies which have controlled for socioeconomic status, psychological functioning and health status.[168] This finding is generally stronger for men than women,[167] though this relationship is not universal across all studies and may only be true in some circumstances.[168]

As people age, subjective health remains relatively stable, even though objective health worsens.[169] In fact, perceived health improves with age when objective health is controlled in the equation.[170] This phenomenon is known as the "paradox of ageing." This may be a result of social comparison;[171] for instance, the older people get, the more they may consider themselves in better health than their same-aged peers.[172] Elderly people often associate their functional and physical decline with the normal ageing process.[173][174]

The concept of successful ageing can be traced back to the 1950s and was popularised in the 1980s. Traditional definitions of successful ageing have emphasised absence of physical and cognitive disabilities.[175] In their 1987 article, Rowe and Kahn characterised successful ageing as involving three components: a) freedom from disease and disability, b) high cognitive and physical functioning, and c) social and productive engagement.[176]

The ancient Greek dramatist Euripides (5th century BC) describes the multiply-headed mythological monster Hydra as having a regenerative capacity which makes it immortal, which is the historical background to the name of the biological genus Hydra. The Book of Job (c. 6th century BC) describes human lifespan as inherently limited and makes a comparison with the innate immortality that a felled tree may have when undergoing vegetative regeneration.[177]

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