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Archive for the ‘Hormone Physician’ Category

Windsor doctor penalized for ‘reckless’ narcotics prescribing – Windsor Star

Windsor Star
Windsor doctor penalized for 'reckless' narcotics prescribing
Windsor Star
She reported that Barnard was administering human growth hormone to help patients with weight loss, despite the fact its use for weight loss has been discredited and rejected by the medical community. The investigator also noted numerous examples of ...

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Windsor doctor penalized for 'reckless' narcotics prescribing - Windsor Star

‘Bathroom Bill’ is discrimination – Emporia Gazette

Current House Bill Text ColorSwatch/NoneStrokeStyle/$ID/SolidText ColorSwatch/NoneStrokeStyle/$ID/Solid$ID/NothingText ColorText Color$ID/NothingText ColorText Color2171 defines sex as the physical condition of being male or female, which is determined by a persons chromosomes, and is identified at birth by a persons anatomy as if this is always the case.

In the case of transgender children, this is not the case. This bills wording reveals major biological ignorance and discrimination against a handicap.

Usually, but not always, XY chromosomes produce a boy and XX produces a girl. However, a relatively high rate of babies are born XO: one X chromosome and no second X or a Y. This is called Turner syndrome. I have had at least six Turner syndrome students in my classrooms during my teaching career that I know of. Additional cases when chromosomes fail to separate normally produce individuals who are XXX, XXY, XYY, and XXXY, etc.

The bill states that sex is identified at birth. Not always. If a couple do not already know the sex of their child, the first announcement they await is its a boy or its a girl! But sometimes the delivering physician has to say Ill get back to you on that when the genital anatomy is ambiguous and not clearly either male or female. There are many causes for when the body does not follow normal development. Today, science understands most of them.

In the case of androgen insensitivity, a baby girl appears to have the external and internal anatomy of a girl, until they biopsy the gonadal tissues and discover internal testes! Testes produce testosterone that flows through the bloodstream and body tissues respond to the testosterone by developing male tissues. But in this case, the childs cells lack the receptors and ignore the testosterone. The child has XY chromosomes and testes but the childs body develops female.

Altogether there are five major factors that must align for normal sexual development: chromosomes, anatomy, hormones and brain development for gender and for sexual ideation. Most of us are very lucky to develop with all five of these in agreement. We inherit XY, have male anatomy, produce testosterone, feel comfortable in a more-or-less masculine role, and are sexually attracted to females after puberty. Or we inherit XX chromosomes, have female anatomy, produce estrogens (there are several), feel comfortable in a more-or-less feminine role, and are sexually attracted to males.

But some children are not as fortunate, and their chromosomes, anatomy, hormones, and brain development do not align. This is not uncommon. Taken in total, some form of sexual ambiguity is more common than all cases of Down syndrome and cystic fibrosis combined.

Forget the rest of the LGB alphabet. This is not about gay rights. The only group that is targeted by this legislation is transgender children. Usually by age 6, a childs brain develops a feeling of being either masculine or feminine. It is not learned. And at this age, it has nothing to do with sexual attraction.

For most of us, our feeling of being male or female will align with our anatomy. But for transgender children, this feeling of being masculine or feminine does not align with their birth anatomy. This is biological. It is not a choice. They will not decide to be a boy one day and a girl the next. These children will usually be facing hormone treatments and a series of reconstructive surgeries. But due to widespread ignorance among outside adults, some Kansas transgender children stay at home, homeschooled because of the discomfort they feel at school by the very same attitudes demonstrated in HB2171.

Masculinity or femininity is not something you learn or can change; it develops during the last trimester before birth. Dr. Dick Swaabs research team in the Netherlands was the first to clearly locate this brain difference over a decade ago.

This is a handicap, and HB2171 reflects an ignorance, indeed a cruel attitude toward those children whose brain development for gender identity does not match their birth anatomy.

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'Bathroom Bill' is discrimination - Emporia Gazette

People get test results, have more tests done at Live Healthy 2017 Health Fair – Grand Island Independent

AURORA Live Healthy 2017 Health Fair was supposedly a one-day event that drew a number of health care providers and visitors to the Ag Building at the Hamilton County Fairgrounds.

But some people prepared for the Saturday event well in advance by attending one of the three Memorial Health Clinics in January and February to get a low-cost blood draw, according to Tina Hunt, marketing director for Aurora Community Health. Hunt said people then could go to Saturdays health fair to pick up their results, or they could go to Memorial Healths online portal.

Its a big thing for people to pick up their results, Hunt said.

She provided a folder that showed blood draw test results for white and red blood counts.

The folder also provided explanations for what each test might possibly mean. For example, a low amount of red blood cells could indicate anemia.

The blood draw also included explanations for five cholesterol and triglycerides tests, including explanations of what each means and when it might be advisable to consult a physician.

Several tests look at both kidney and liver function.

Its a complete blood panel, but also we do TSH (thyroid stimulating hormone), Hunt said. Theres some extra thyroid functioning tests with it. People may want to do the extra A1C, which is for diabetes. And then we also have the PSA (prostate-specific antigen). Its really a complete panel plus.

Both the A1C and PSA tests came with an additional cost.

People could also schedule appointments to get three types of cardiovascular tests performed by the Bryan Health mobile screening unit. That was a popular attraction.

Bryan Health was not the only health-care provider from outside Aurora to be at Saturdays health fair. CHI Health St. Francis had a visually arresting booth that showed the health pink lung of a non-smoker next to a blackened, shriveled lung for a smoker.

The Central District Health Department, based in Grand Island, but covers Hall, Hamilton and Merrick counties, also had a booth in the Ag Building. Senior living and assisted-living centers near Aurora were also at the fair. There were booths for hospice care, message therapists and an organization that sells devices for older people living at home, for use in an emergency such as a fall.

But with Memorial Community Health acting as the host for its own event, it was no surprise they had the most booths.

We have 14 booths, Hunt said, who noted that those booths showed the full range of health care provided by Memorial Community Health, including:

Memorial Community Care, which provides long-term care.

The three Memorial Health Clinics, located in Aurora, Clay Center and Harvard.

East Park Villa, which provides assisted and independent living.

Memorial Community Health, the hospital.

Hunt said the health fair also allows Memorial Community Health to show off its many departments and services such as radiology, diabetes education and pulmonary rehab. She said pulmonary rehab is relatively new, with the pulmonary and respiratory therapist busy working with people who have COPD, chronic bronchitis and other respiratory ailments. She said people may be surprised at the broad range of surgeries performed at Memorial Community Health.

The health fair had a booth for its OB/GYN department. However, Hunt noted that Memorial Community Health also has a doula who provides information, as well as emotional and physical support to women before, during and after childbirth.

The health fair also included a couple fitness demonstrations and a yoga demonstration by Mardell Jasnoski.

Jasnoski said some people say they are not limber enough to do yoga but, she added, that is the very reason they should consider it. She said people can increase their flexibility through yoga.

Jasnoski said yoga also works helps people with deep breathing, as well as maintaining balance, which becomes increasingly important as people age.

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People get test results, have more tests done at Live Healthy 2017 Health Fair - Grand Island Independent

Colorado House panel rejects three GOP abortion bills – The Denver Post

Colorado House Democrats on Thursday beat backthree Republican-sponsoredabortion bills, the most restrictive of whichwould have made it a crime for a physician to perform anabortion in most cases.

The hearing stretched past midnight before the final bill was killed, with emotional testimony from dozens of people, including medical experts, activists on both sides and women who had had abortions and later regretted it.

The measures to impose new restrictions on abortion were debated a week after the Democrat-controlled House passed a resolution reaffirming its support for abortion rights in the state. None of the bills had much chance of passing, something abortion-rights advocatesreiteratedoften leading up to the vote.

These three bills are more of the old, tired attempts to interfere with womens health care, said Sarah Taylor-Nanista, a spokeswoman atPlanned Parenthood of the Rocky Mountains, in a statement.

The first to be rejected, House Bill 1086, would have required abortion doctors to tell patients about a hormone-boosting pill that backers say can reverse an abortion in progress, as long as its taken before misoprostol, the second drug taken in the course of a chemically induced abortion.

In a 2012 case study involving six women, four reportedly gave birth after using the drug. But several medical experts who testified at the hearing likened the bill tothe state endorsingbogus science, sayingthere are no peer-reviewed scientific studies backing the drug, and a number of medical groupsdispute its effectiveness.

The American Congress of Obstetricians and Gynecologistsdoesnt recommend its use, saying that simply not taking misoprostol is just as effective at preserving a pregnancy as the reversal drug.

Supporters of the billsaid it was vital that women considering an abortion were presented with all their options, while opponents decried what they called agovernment intrusion into the doctor-patient relationship.

This is an information measure it allows (a woman who has an abortion) to understand that after the first pill, theres still a chance that the pregnancy is viable, said state Rep. Dan Nordberg, R-Colorado Springs, one of the measures sponsors. This is simply informing her of the potential options no more, no less.

Why would we legislate the care a doctor provides a patient? countered Rep. Susan Lontine, D-Denver. politicians should stay out of the doctors office.

Another defeated measure, House Bill 1085, would have imposed new regulations on abortion clinics, requiring them to file detailed annual reports with the state and submit to regular inspections. It also would have required that clinics have certain advancedmedical equipment on hand, such as ultrasounds and resuscitation and life-supportmachines for infants.

Opponents likened it to a Texas law that was struck down by the Supreme Court for being too burdensome, forcing many abortion providers to close. Supporters disputed the comparison.

The third measure, House Bill 1108, echoes the personhood movement, which Colorado voters have rejected three timesat the ballot box.The bill would havemade it a felony for a physician to take an unborn life, defined as beginning at conception. It contains exceptions for cases in which a pregnant womanslife is in danger.

Democrats pointedly questioned the measures constitutionality, suggesting that passing the bill would subject the state to a costly legal challenge that it was likely to lose.

Do either one of you believe this bill is constitutional?State Rep. Daneya Esgar, D-Pueblo, at one point asked the bills two sponsors, Republican state Reps. Kim Ransom and Steve Humphrey.

Humphrey deflected the question, citing potential changes to the makeup of the Supreme Court: I believe the constitutionality of the Roe v. Wade decision is in big trouble.

If Supreme Court nominee Neil Gorsuch is confirmed, conservatives would likely still need at least another seat to hope for a reversal of the 1973 decision legalizing abortion. He would replace conservative Antonin Scalia, restoring the ideological split from much of the Obama era.

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Colorado House panel rejects three GOP abortion bills - The Denver Post

Dems defeat anti-choice bills – Pueblo Chieftain

In a House committee meeting that went past midnight Thursday, Democrats defeated three Republican-sponsored abortion bills, one of which would have criminalized abortion in most cases.

Democrats in the House Health, Insurance, & Environment Committee shot down the three bills, with Pueblo state Rep. Daneya Esgar, a Democrat asking two sponsors of the bills, Do either one of you believe this bill (House Bill 1108) is constitutional?

State Rep. Steve Humphrey answered, according to a Denver Post report, I believe the constitutionality of the Roe v. Wade decision is in big trouble.

Democrats said HB1108 echoes the personhood movement, which Colorado voters have rejected three times in general elections. The bill would have made it a felony for a physician to take an unborn life, defined as beginning at conception. It contains exceptions for cases in which a pregnant womans life is in danger.

Another rejected bill, HB1086, would have required abortion doctors to tell patients about a hormone-boosting pill that backers say can reverse an abortion in progress, as long as its taken before misoprostol, the second drug taken in the course of a chemically induced abortion.

Another measure, HB1085, would have imposed new regulations on abortion clinics, requiring them to file detailed annual reports with the state and submit to regular inspections. It also would have required that clinics have certain advanced medical equipment on hand, such as ultrasounds and resuscitation and life-support machines for infants.

In a press release, Republicans wrote, The outcome of todays votes is out of touch with the shifting public attitudes towards abortion, and in the four decades since the Roe v. Wade decision, scientific research has wholly disproved the long-held medical justifications for abortion.

Compiled by Peter Strescino from newspaper, wire and email sources.

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Dems defeat anti-choice bills - Pueblo Chieftain

Shed pounds to lower the risk – Times of India

Obesity is a serious problem across the world, with increasing risk of diabetes. Recently, there is change in the name of disease by the American Association of Clinical Endocrinologists (AACE), as ABCD- adiposity-based chronic disease. This indicates harmful effects of fatty tissues in the body, and its chronicity.

Previous two decades had seen tripling of obesity in developing countries, those who adopted western lifestyle. Population of the Middle East, Pacific Islands, Southeast Asia, India, and China are facing the greatest risk. As a result, the number of diabetic people in these countries are likely to increase from 84 million in 2000 to 228 million by 2030. Hence, in order to prevent the incidences of diabetes and other chronic diseases it is necessary to control obesity.

Modification of food, action in exercise, and reduction of at least 5% body weight decreases risk of diabetes by nearly 60%, following the same changes for around seven years decreases this risk by 40%. Benefits of weight loss in diabetes for glucose control are better in early diabetes stages than later. Thus, weight loss is essential and crucial step in managing diabetes. Although weight poses a burden on tissues, maintaining lost weight, bundled up with glucose levels, activity levels, will benefit in the long run.

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Shed pounds to lower the risk - Times of India

Human Growth Hormone – Rejuvalife Vitality Institute


Human growth hormone (HGH) is naturally produced by the pituitary gland, and acts as a catalyst for glandular secretions critical to maintaining a healthy body. It also fuels growth during childhood and adolescence, and continues to maintain organs, tissues, muscles, bone, and heart function throughout your life. Human growth hormone injections have been FDA-approved for treating poor growth in children, as well as medical disorders.

As early as the age of 40, HGH production begins declining. This decrease is more dramatic in people who have experienced a minor or traumatic brain injury, radiation, or surgery to the pituitary gland. Adults who have a deficiency of growth hormone, injections may be able to help.

The symptoms of declining HGH levels include:


Mental confusion


Cardiovascular problems

Decreased immunity

Human growth hormone replacement therapy has been shown to improve:

Increased bone density and muscle mass

Decrease in body fat

Improved mood

Improve the hearts ability to contract

Increased capacity to exercise

At Rejuvalife, we can help combat HGH deficiencies through an effective hormone replacement therapy plan. This hormone replacement plan can significantly improve the symptoms the deficiency. HGH therapy is administered by injection, as supplements taken orally will be digested by the stomach before the body can absorb it.

Take a look at our anti-aging procedures videos in our online video gallery.

Dr. Berger is a diplomat of the American Academy of Anti-Aging Medicine, and world-renowned for his age-defying results. As a leader in anti-aging, wellness and non-surgical cosmetic medicine, he possesses a unique combination of skills that make him a true specialist in his field.His techniques, for rejuvenating your health and appearance, effectively integrate Eastern philosophies with world-class Western medical technologies. With an artistic eye, a keen sense of aesthetics and his knowledge of science, Dr. Berger offers transformative results that will not only help you look great, but also help you feel your absolute best.

We understand that choosing a doctor or facility, for any treatment but especially anti-aging, can be a difficult decision. You can rest assured that with Dr. Berger and Rejuvalife, you are in good hands. He is dedicated to providing his patients with only the safest, most advanced, state-of-the-art treatment options.

Please contact Rejuvalife Vitality Institute using the form at the right side of the page or call (310) 276-4494 today to schedule your HGH consultation. Dr. Andre Berger serves patients in Beverly Hills and Los Angeles, California.

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Human Growth Hormone - Rejuvalife Vitality Institute

Doctor’s Tip: What is the safest cookware? – Glenwood Springs Post Independent

The current issue of the University of California, Berkeley Wellness Letter has a useful article about the pros and cons of various types of cookware. Here are some of the highlights:


Teflon, which prevents sticking, was discovered by a DuPont chemist in 1938. It is a brand name for polytetrafluoroethylene (PTFE), and other companies have developed other brands.

Fumes from heating PTFE-coated pots and pans to temperatures over 660 degrees can cause symptoms in humans and death in pet birds.

There is no evidence that ingesting PTFE flakes from old cookware causes cancer. However there are concerns about cancer and hormone disruption from another chemical, called PFOA, which until 2015 was used in the manufacturing of PTFE and which persists in our environment and our bodies.

The replacements for PFOA may not be any safer (we dont know yet). The nonprofit advocacy group Environmental Working Group advises consumers to avoid all nonstick cookware and kitchen utensils.

At the very least, avoid high temperatures with stick-free cookware, and replace it when it starts to deteriorate.


Aluminum cookware can scratch and stain easily and can give acidic food such as tomato sauce a bitter taste because aluminum leaches into the food.

In his book Power Foods For The Brain, Dr. Neal Barnard points out that there is still concern that aluminum ingestion may be linked to Alzheimers.

Ideally you should avoid aluminum cookware because you dont want to risk brain health.

If you do buy it, buy the anodized variety, which has a harder surface. However if labeled nonstick, it may contain PFTE-related compounds.

At the very least, avoid acid foods with aluminum cookware.


To maintain a cast-iron pan you have to rub oil on the surface, and a well-seasoned pan is fairly stick-free.

Iron leaches into acidic food.

Although we need some iron in our diet, we get plenty from what we eat (even if you are plant-based). Too much iron causes free radicals to form, which contribute to aging, cancer, heart disease and other health problems. According to Dr. Barnard, there is a link between high blood iron levels and Alzheimers.

Cast-iron cookware should be dried as soon as it is washed and should not be put in the dishwasher to avoid rusting (i.e. oxidation).


It is non-stick but contains no PTFE or PFOA, is heat-stable and flake-resistant.

It is therefore thought to be free of health and environmental concerns.

However, some products may use nanoparticle coatings, and the long-term health and environmental effects of nanoparticles are unknown.


Copper can leach into food, especially acidic foods such as tomatoes, unless its lined with stainless steel.

We need a small amount of copper in our diet, but too much causes health problems. Dr. Barnard talks in his book about evidence linking copper to Alzheimers, so its best to avoid copper cookware.


Stainless steel cookware does not react with food and doesnt rust.

Some has an inner core of copper or aluminum that helps food cook more uniformly, but this should not be a problem as long as the surface is stainless steel.


Pyrex is the best-known brand and was introduced over a century ago.

Glass is inert, does not react with food, and poses no known health or environmental problems.

So the bottom line is this: Avoid copper, aluminum and iron cookware for optimal health. Ideally use glass and stainless steel for cooking. Ceramic cookware is safe if it is not coated with nanoparticles, which have not been proven yet to be safe for us and for the environment. If sticking is a problem with these safe options, a small amount of oil rubbed on the surface solves that, but as per a previous health tip column, added oils cause several health problems and carcinogens form when oils reach their smoke point. So its better to use vegetable broth, water, wine or soy sauce to prevent sticking.

Dr. Feinsinger, who retired from Glenwood Medical Associates after 42 years as a family physician, now has a nonprofit Center For Prevention and Treatment of Disease Through Nutrition. He is available for free consultations about heart attack prevention and any other medical concerns. Call 970-379-5718 for an appointment. For questions about his columns, email him at

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Doctor's Tip: What is the safest cookware? - Glenwood Springs Post Independent

Nonbinary students confront surgery challenges – Yale Daily News (blog)

Britton O'Daly Feb 10, 2017

Staff Reporter

Brianna Loo

Though the Yale Health Plan extended insurance coverage to gender-affirming surgeries in 2013 in order to benefit gender-questioning students at Yale, Yale Healths current approval process for these surgeries can undermine care options for students who do not conform to a binary gender, according to two transgender students.

Yale Health follows the standard of care for transgender health and sex reassignment surgery, as defined by the World Professional Association for Transgender Health. According to WPATH standards, surgeons, prior to performing sex-reassignment surgery, must be confident that the referring mental health professional(s), and if applicable the physician who prescribes hormones, are competent in the assessment and treatment of gender dysphoria. Once gender dysphoria a condition in which ones psychological gender identity differs from ones biological sex has been documented by a mental health professional, the surgeon may then consult with the patient about an operation.

On the Yale Health Plan, Yale Mental Health operates as the gatekeeper between students and the required medical consultations for gender-affirmation surgery. Still, this system has attracted the criticism of Yale students who claim that the process favors students who identify as either trans man or trans woman over those who are gender nonconforming and therefore may not match Yales definition of gender dysphoria.

It was all tremendously emotionally draining, said a Yale alum who was refused a consultation under Yales health plan. I also had the sense that Yale had drawn out the process of rejecting me because I was about to graduate and lose health insurance and had not been forthright with me about how my application would be considered.

The former student, who identifies as trans, said they began their application for a sex-reassignment surgery consultation in spring 2016, but was ultimately rejected by a Yale Health committee that determined their request for surgery to be cosmetic. The committee also justified its rejection by arguing that the student had not been living as the opposite gender.

The alum told the News that Yale Healths decision perpetuates a false belief that only trans men or trans women require surgery and that other trans identities between the male and female binaries, like the anonymous students, are not legitimate. The committee never met the student in person, but grounded their judgment on letters written by the students psychiatrist and therapist.

The Directors Office of Yale Health referred all questions to Yales Office of Public Affairs & Communications, but Yale spokespeople did not respond to questions about the exact process by which Yale Health judges applications for consultation.

Yale, Brown, Cornell, Dartmouth, Harvard and Penn all cover transition-related medical expenses on their student health insurance. Princeton does not cover gender-affirming surgeries, but does offer hormone therapy to students. The fall 2015 Yale College Council Task Force on LGBTQ Resources also noted that Brown and Columbia are the only two Ivy League schools to offer gender-neutral rooming, a detail that trans students interviewed during the report identified as an area for change.

According to Maria Trumpler GRD 92, director of the Office of LGBTQ Resources, the coverage of sex-reassignment surgeries under the Yale Health Plan has significantly improved the lives of many Yale students. Still, she noted that the insurance plan is self-reflective and reviewed periodically by a committee to improve students medical care.

For several years theyve been discussing the issue, which is that there is not a particular gender identity that someone has to have to access hormones or surgery, said Trumpler. You do not have to identify as a transgender male or transgender female.

Still, the anonymous alum said they also ran into difficulties making a case for a consultation because mental health professionals typically assume patients have already decided they want to go through with the surgery prior to their first consultation. However, the alum in question wanted to talk to a medical professional about potential surgery before making an informed decision. Additionally, the former student told the News in an email that the committee member who communicated with them over the phone was unknowledgeable about the nuances of trans* experiences and at times offensive.

Isaac Amend 17, a staff columnist for the News, said that this type of decision from Yale Mental Health prevents gender nonconforming people from receiving much-needed treatment.

The medical establishment is prejudiced against nonbinary people, ignoring the fact that gender fluidity exists, Amend said. Doctors can propagate a notion of not being trans enough, which is toxic to the mental health of patients.

Amend added that there is a community of nonbinary or gender fluid students at Yale, and that he knows of students who have had to tell psychiatrists that they are more trans than they feel, out of a fear that the doctors will withhold treatment if they appear more gender fluid.

Laurence Bashford 18 and Kyle Ranieri 18, the respective 2017 and 2016 coordinators of the Yale LGBTQ Co-Op, said in a joint email to the News that there have been great steps made by the Yale administration to guarantee needed and deserved treatments to trans students within the student community.

We are particularly wary of the fact that many important treatments for instance, laser hair treatment as part of the transitioning process are deemed unimportant or cosmetic and, so, are not available through regular University coverage, Bashford said.

The Yale Health Center was completed in 2010.

Contact Britton ODaly at

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Nonbinary students confront surgery challenges - Yale Daily News (blog)

Endocrine disease – Wikipedia

Endocrine diseases are disorders of the endocrine system. The branch of medicine associated with endocrine disorders is known as endocrinology.

Broadly speaking, endocrine disorders may be subdivided into three groups:[1]

Endocrine disorders are often quite complex, involving a mixed picture of hyposecretion and hypersecretion because of the feedback mechanisms involved in the endocrine system. For example, most forms of hyperthyroidism are associated with an excess of thyroid hormone and a low level of thyroid stimulating hormone.[2]

In endocrinology, medical emergencies include diabetic ketoacidosis, hyperosmolar hyperglycemic state, hypoglycemic coma, acute adrenocortical insufficiency, phaeochromocytoma crisis, hypercalcemic crisis, thyroid storm, myxoedema coma and pituitary apoplexy.[3]

Emergencies arising from decompensated pheochromocytomas or parathyroid adenomas are sometimes referred for emergency resection when aggressive medical therapies fail to control the patient's state, however the surgical risks are significant, especially blood pressure lability and the possibility of cardiovascular collapse after resection (due to a brutal drop in respectively catecholamines and calcium, which must be compensated with gradual normalization).[4][5] It remains debated when emergency surgery is appropriate as opposed to urgent or elective surgery after continued attempts to stabilize the patient, notably in view of newer and more efficient medications and protocols.[6][7][8]

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Endocrine disease - Wikipedia

What causes infertility and how can it be treated? – WRDW-TV

Wednesday, Feb. 8, 2017

(WRDW/WAGT) -- A new study with Occupational and Environmental Medicine shows work schedules and physically demanding jobs hurt women's fertility. However, what else causes infertility, how is it diagnosed, and how can it be treated?

Infertility can occur in either the male or female. Female infertility accounts for 50% or one-third of all infertility cases, and is a common problem with women between the ages of 15 and 44.

Causes of male infertility include varicocele (when veins become enlarged inside your scrotum), low or absent sperm count, sperm damage or certain diseases.

Female infertility is caused by a number of factors including age, a hormone imbalance, a tumor or cyst, eating disorders such as anorexia or bulimia, alcohol or drug use, thyroid gland problems, excess weight, stress, intense exercise that causes a significant loss in body fat, and extremely brief menstrual cycles. In addition, ovulation disorders, tubal blockage, uterine fibroids, and endometrial polyps can also cause female infertility.

In women, these tests could include a urinalysis or a blood test to check for infections or a hormone problem. A physician might also want to conduct a pelvic exam, breast exam, or an ultrasound of the reproductive organs.

In men, these tests would include looking at your medical history. A physician may also want to conduct a seminal analysis, a urinalysis, or an ultrasound of the reproductive organs.

In men, surgery and sperm retrieval techniques can be performed. Antibiotic treatment and hormone treatment can also treat infertility issues.

A physician may also recommend intrauterine insemination (a process where the sperm is washed and injected) or In Vitro Fertilization where eggs are collected and fertilized by sperm outside the body, and then inserted into a surrogate.

In women and men, this means taking steps to prevent sexually transmitted diseases, avoiding illicit drugs, avoid heavy or frequent alcohol use, avoid smoking, reduce stress, keeping your weight off, adopt good personal hygiene and health practices, and have annual checkups with your doctor once you're sexually active.

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What causes infertility and how can it be treated? - WRDW-TV

Veracyte (VCYT) Enters Agreement with Quest Diagnostics (DGX) to Expand Patient Access to GEC –

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Veracyte, Inc. (NASDAQ: VCYT) will extend access to its Afirma Gene Expression Classifier (GEC) through an agreement with Quest Diagnostics (NYSE: DGX), the world's leading provider of diagnostic information services. The agreement is intended to meet growing physician demand for innovative genomic testing services to improve thyroid cancer diagnosis.

The Afirma GEC is a laboratory-developed test that is widely ordered by physicians who perform fine needle aspiration (FNA) biopsies to evaluate thyroid nodules for potential cancer. Under the agreement, physician clients of Quest Diagnostics will be able to order the test on behalf of patients and refer patient specimens to Veracyte for genomic testing. Quest Diagnostics will make the service available through AmeriPath, the anatomic pathology business of Quest Diagnostics, for use on cytopathology results of these biopsies in cases when they are indeterminate (not clearly benign or malignant).

Veracyte currently makes the Afirma GEC available to physicians at institutions and community-practice settings throughout the country. Quest Diagnostic serves approximately half the physicians and hospitals in the United States, further broadening access to the Afirma GEC for patients who could benefit.

Quest Diagnostics is expected to begin offering the test to its customers nationally in the second quarter of 2017. Financial and other terms of the agreement were not disclosed.

"We are pleased to partner with Quest Diagnostics to further make the Afirma GEC available to physicians and their patients as our test increasingly becomes the new standard of care in thyroid cancer diagnosis," said Bonnie Anderson, Veracyte's chairman of the board, president and chief executive officer. "We believe Quest's leadership in innovation and quality and its extensive reach to endocrinologists and other physicians will enable us to further accelerate growth for the Afirma GEC."

Since launching the genomic test in 2011, Veracyte has performed over 65,000 Afirma GEC tests and estimates that the test has helped prevent more than 25,000 unnecessary thyroid surgeries. Such surgeries are invasive, costly and because they involve removal of all or part of the thyroid often render patients dependent on lifelong daily thyroid hormone replacement drugs. The Afirma GEC is supported by more than 20 published studies, including a clinical validation study published in The New England Journal of Medicine, and is recommended in leading clinical practice guidelines. The Afirma GEC is covered by Medicare and most leading private insurance companies, which collectively represent approximately 200 million Americans.

"Indeterminate thyroid nodules pose a significant challenge to physicians and patients, and many people have undergone unnecessary surgeries because it was difficult to rule out cancer in advance. It puts the physician and the patient in a difficult position," said Christopher C. Fikry, M.D., general manager, oncology, Quest Diagnostics. "The Afirma GEC is a terrific example of how diagnostic innovation can help replace uncertainty with clarity to promote better care and outcomes. We look forward to making it available through our already significant offering in cancer and endocrinology so that fewer people face the specter of unnecessary surgery and treatment."

About 15 to 30 percent of the more than 520,000 patients who undergo evaluation for potentially cancerous thyroid nodules in the United States each year receive an indeterminate result. Historically, most of these patients were directed to thyroid surgery for a definitive diagnosis. Following surgery, however, 70 to 80 percent of cases proved to be benign, meaning the surgery was unnecessary.

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Veracyte (VCYT) Enters Agreement with Quest Diagnostics (DGX) to Expand Patient Access to GEC -

Dear Dr. Roach: Elevated calcium level may signal excess hormone – Herald & Review

Dear Dr. Roach: I'm a healthy female in my mid-70s. I've taken the recommended calcium citrate with vitamin D for years, until about three months ago, when test results showed I have slightly higher than normal calcium levels. I stopped the calcium, but testing results were the same three months later. Since women have been advised to take calcium, especially as we age, this is quite a surprise.

A: Most of the calcium in the body is locked away in the bones. The body has several systems to carefully regulate the calcium level in the blood. The two most powerful of these are vitamin D and parathyroid hormone. Abnormalities in either of these can cause problems in blood calcium levels, which is very dangerous, because it can affect the muscles. A very low blood calcium level causes tetany, severe cramping and inability to move muscles normally (tetanus is an infectious disease that causes muscle cramps via an entirely different pathway).

With low calcium intake, blood calcium remains normal or near normal, but the calcium in the bones is depleted. That's why adequate calcium intake is important in the prevention and treatment of osteoporosis. Calcium through the diet is preferred to calcium via supplements, because supplements increase the risk of kidney stones and may increase the risk of heart disease.

High levels of blood calcium are more likely to be due to excess parathyroid hormone than high vitamin D (which is very uncommon). With the body systems working normally, excess dietary calcium is simply excreted by the kidneys.

Since the most likely cause for high calcium is an excess of parathyroid hormone, often made by a benign tumor of the parathyroid gland, your doctor should test your parathyroid hormone level.

The osteoporosis pamphlet furnishes details on calcium intake and how it affects bones. Readers can obtain a copy by writing: Dr. Roach, Book No. 1104, 628 Virginia Dr., Orlando, FL 32803. Enclose a check or money order (no cash) for $4.75 with the recipient's printed name address. Please allow four weeks for delivery.

Dear Dr. Roach:I read your recent column regarding Fosamax. I'm 55, female and recently have been diagnosed with osteoporosis. My left hip was at the -2.5 threshold for the diagnosis. My primary-care physician and gynecologist both are recommending Fosamax. With so much confusing information about this drug, I am questioning taking it. What is the alternative to taking Fosamax? Is there anything else I can do to increase my bone mass? Would you advise one of your family members to take Fosamax?

A:If there are no other treatable causes, such as low vitamin D or high parathyroid hormone levels, then I think Fosamax or another bisphosphonate is a good choice. There are others, but Fosamax has been well-studied. The recent critical column I wrote was about atypical femur fractures in women taking Fosamax and other similar medications for longer than three to five years without any re-evaluation of whether it is still needed.

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Dear Dr. Roach: Elevated calcium level may signal excess hormone - Herald & Review

Hospital adds doctors at Dove’s Landing – Oroville Mercury Register

Oroville >> Oroville Hospital has added two doctors to its Doves Landing facility, one of whom is an Oroville native.

Primary care physician Gladys Wyles is an Oroville native, who will be treating patients for a variety of conditions including hypertension, hyperlipidemia and diabetes.

She earned her bachelors degree in community medicine with an emphasis in hospital administration from Chico State University. She took pre-medicine classes at UC Davis before being accepted to medical school at the University of Minnesota.

After earning her medical degree, Dr. Wyles returned to UC Davis to complete her residency and internship in family medicine. She was the first rural track resident at UC Davis which allowed her to practice medicine in Oroville, Yuba City and Marysville while completing her training.

I always knew I wanted to give back to my local community, Dr. Wyles said in a press release. I chose family medicine because it allows you to touch on many aspects of health from dermatology to obstetrics. I enjoy the challenge of finding out what is happening with patients as well as figuring out how to manage their chronic health issues.

Also new to Doves Landing is endocrinology specialist Leena Singh, who focuses on treating disorders of the endocrine system related to hormone imbalances such as diabetes, osteoporosis and pituitary, thyroid and parathyroid conditions.

She has been a resident of Butte County since 2005.

After receiving her medical degree, Dr. Singh pursued a Ph.D. in pharmacology from Tufts University which furthered her knowledge of the use and effects of various medications on the body. This motivated her to specialize in endocrinology and she completed additional medical training with an internship and fellowship at the University of Massachusetts.

I have always been fascinated by the way hormones are released and interact with the bodys systems to function cohesively, Dr. Singh said. When these systems do not communicate properly or excessive levels of hormones are released, medical issues can arise. I enjoy working with patients to determine the best treatment options based on their endocrine disease.

The Doves Landing Multispecialty Practice is located at 2450 Oro Dam Blvd. For more information call 712-2171.


Hospital adds doctors at Dove's Landing - Oroville Mercury Register

Dr. Brian Irwin: BPH is a common but uncomfortable disorder – Conway Daily Sun

By Dr. Brian Irwin

Benign Prostatic Hyperplasia, also known as BPH, is an extremely common condition. It's also an extremely despised condition that results in significant discomfort and inconvenience for those who have to live with the disorder. One study showed that up to 90 percent of all men will develop symptomatic BPH by age 90.

What is a prostate anyway? The prostate is a male reproductive gland that resides deep in the pelvis. Its function is to produce the fluid that comprises a significant portion of ejaculate. The urethra, the "tube" through which we urinate, leaves the bladder, tunnels through the prostate gland and eventually runs to the end of the penis. Because the urethra courses through the prostate, enlargement of the prostate presents primarily with urinary symptoms.

Because the prostate is a reproductive organ, its function depends on male sex hormone levels. Unfortunately, over a man's lifetime the relentless exposure to circulating testosterone also causes the gland to slowly grow. Enlargement of the prostate over time eventually causes impingement on the prostatic urethra, leading to discomfort and symptomatic BPH.

Benign Prostatic Hyperplasia can present a number of ways. The most common symptoms are urinary hesitancy, weak urinary stream or post-urination dribbling. Because the symptoms stem from occlusion of the internal urethra, urinary retention (the inability to void), bladder stones or even urinary incontinence (from an overflowing bladder) can also be symptoms of BPH. In some cases, the presentation is as vague as more frequent nighttime urination, which can in turn delay the diagnosis of BPH for a number of years.

A careful physical exam and history by your primary health provider is necessary to diagnose BPH. While the history provided by the patient is most likely to reveal underlying BPH, your provider will likely also perform a digital exam of the prostate. The prostate itself is located adjacent to the front most wall of the rectum, so it can only be felt by performing a rectal exam. In addition to this exam, your provider may tap on your bladder to screen for urinary retention.

If you are diagnosed with BPH, there are treatment options for you. Two classes of medications exist that help relieve BPH. One class, which includes medications such as terazosin, acts on the muscular portion of the prostatic urethra, allows it to dilate and pass urine more easily. The other class of drugs works by blocking the conversion of a hormone called DHT to testosterone, which eventually leads to shrinkage of the prostate itself. Saw Palmetto, an herbal remedy, is another option that in my experience does seem to work for some patients; however, studies have failed to prove true efficacy when compared to placebo.

While these medications provide significant relief, many cases of BPH still progress to a more severe degree that requires a more aggressive treatment. In these cases, sometimes the only successful treatment is surgery on the prostate itself. Urologists have many options, from surgically cutting the occluded portion of the prostate, to laser vaporization of the hyperplastic prostate tissue. These procedures are feared by many men due to their anticipated discomfort or the potential complications. However they are generally considered very safe, very well tolerated and most patients are delighted with the results.

If you have symptoms suggestive of BPH, talk with your health-care provider. Early treatment not only makes your life more livable, but also delays progression of the condition and decreases the chance you'll need a more invasive procedure. By treating BPH early, you'll be more comfortable and your condition will be, in a sense, water over the dam.

Dr. Brian Irwin is a family physician at Tamworth Family Medicine, a division of Huggins Hospital.

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Dr. Brian Irwin: BPH is a common but uncomfortable disorder - Conway Daily Sun

Thyroid Disease Manager : Diagnosis and Treatment of Graves

Diagnosis of the classic form of Graves disease is easy and depends on the recognition of the cardinal features of the disease and confirmation by tests such as TSH and FTI. The differential diagnosis includes other types of thyrotoxicosis, such as that occurring in a nodular gland, accompanying certain tumors of the thyroid, or thyrotoxicosis factitia, and nontoxic goiter. Types of hypermetabolism that imitate symptoms of thyrotoxicosis must also enter the differential diagnosis. Examples are certain cases of pheochromocytoma, polycythemia, lymphoma, and the leukemias. Pulmonary disease, infection, parkinsonism, pregnancy, or nephritis may stimulate certain features of thyrotoxicosis. Treatment of Graves disease cannot yet be aimed at the cause because it is still unknown. One seeks to control thyrotoxicosis when that seems to be the major indication, or the ophthalmopathy when that aspect of the disease appears to be more urgent. The available forms of treatment, including surgery, drugs, and 131-I therapy, are reviewed. There is a difference of opinion as to which of these modalities is best, but to a large degree guidelines governing choice of therapy can be drawn. Antithyroid drugs are widely used for treatment on a long- term basis. About one-third of the patients undergoing long-term antithyroid therapy achieve permanent euthyroidism. Drugs are the preferred initial therapy in children and young adults. Subtotal thyroidectomy is a satisfactory form of therapy, if an excellent surgeon is available, but is less used in 2016. The combined use of antithyroid drugs and iodine makes it possible to prepare patients adequately before surgery, and operative mortality is approaching the vanishing point. Many young adults, are treated by surgery if antithyroid drug treatment fails. Currently, most endocrinologists consider RAI to be the best treatment for adults, and consider the associated hypothyroidism to be a minor problem. Evidence to date after well over five decades of experience indicates that the risk of late thyroid carcinoma must be near zero. The authors advise this therapy in most patients over age 40, and believe that it is not contraindicated above the age of about 15. Dosage is calculated on the basis of 131-I uptake and gland size. Most patients are cured by one treatment. Hypothyroidism.occurs with a fairly constant frequency for many years after therapy and may be unavoidable if cure of the disease is to be achieved by 131-I.. Many therapists accept this as an anticipated outcome of treatment. Thyrotoxicosis in children is best handled initially by antithyroid drug therapy. If this therapy does not result in a cure, surgery may be performed. Treatment with 131-I is accepted as an alternative form of treatment by some physicians, especially as age increase toward 15 years. Neonatal thyrotoxicosis is a rarity. Antithyroid drugs, propranolol and iodide may be required for several weeks until maternally-derived antibodies have been metabolized. The physician applying any of these forms of therapy to the control of thyrotoxicosis should also pay heed to the patients emotional needs, as well as to his or her requirements for rest, nutrition, and specific antithyroid medication. Consult our FREE web-book http://WWW.ENDOTEXT.ORG for complete coverage on this and related topics.

We note that there are currently available 2 very extensive Guidelines on Diagnosis and Treatment of Graves DiseaseThe 2016 ATA guideline (270 pages), and the AACE 2011 version on Hyperthyroidism and other Causes of Thyrotoxicosis (65 pages) Both are well worth reviewing.

The diagnosis of Graves disease is usually easily made. The combination of eye signs, goiter, and any of the characteristic symptoms and signs of hyperthyroidism forms a picture that can hardly escape recognition (Fig -1). It is only in the atypical cases, or with coexisting disease, or in mild or early disease, that the diagnosis may be in doubt. The symptoms and signs have been described in detail in the section on manifestations of Graves disease. For convenience, the classic findings from the history and physical examination are grouped together in Table 1a and 1b.These occur with sufficient regularity that clinical diagnosis can be reasonably accurate. Scoring the presence or absence and severity of particular symptoms and signs can provide a clinical diagnostic index almost as reliable a diagnostic measure as laboratory tests(1).

Occasionally diagnosis is not at all obvious.In patients severely ill with other disease, in elderly patients with apathetic hyperthyroidism, or when the presenting symptom is unusual, such as muscle weakness, or psychosis, the diagnosis depends on clinical alertness and laboratory tests.

The diagnosis of Graves Disease does not only depend on thyrotoxicosis. Ophthalmopathy, or pretibial myxedema may occasionally occur without goiter and thyrotoxicosis, or even with spontaneous hypothyroidism. While proper classification can be debated, these patients seem to represent one end of the spectrum of Graves Disease. Thus we are usually making two coincident diagnoses:1)- Is the patient hyperthyroid? and 2)- Is the cause of the problem Graves disease ?.

Family history of any thyroid disease, especially Graves disease

TSH and FT4 assay-Once the question of thyrotoxicosis has been raised, laboratory data are required to verify the diagnosis, help estimate the severity of the condition, and assist in planning therapy. A single test such as the TSH or estimate of FT4 (free T4) may be enough, but in view of the sources of error in all determinations, most clinicians prefer to assess two more or less independent measures of thyroid function. For this purpose, an assessment of FT4 and sensitive TSH are suitable. As an initial single test, a sensitive TSH assay may be most cost-effective and specific. TSH should be 0 .1 U/ml in significant thyrotoxicosis, although values of .1 .3 are seen in patients with mild illness, especially with smoldering toxic multinodular goiter in older patients(1.1). TSH can be low in some elderly patients without evidence of thyroid disease. TSH can be normal or elevated only if there are spurious test results from heterophile antibodies or other cause, or the thyrotoxicosis is TSH-driven, as in a pituitary TSH-secreting adenoma or pituitary resistance to thyroid hormone. Measurement of FT4 or FTI (Free thyroxine index)is also usually diagnostic.The degree of elevation of the FT4 above normal provides an estimate of the severity of the disease. During replacement therapy with thyroxine the range of both FTI and fT4 values tend to be about 20% above the normal range, possibly because only T4, rather than T4 and T3 from the thyroid, is providing the initial supply of hormone. Thus many patients will have an fT4 or FTI above normal when appropriately replaced and while TSH is in the normal range. Except for this, elevations of fT4 not due to thyrotoxicosis are unusual, and causes are given in Table 3.

Of course the Total T4 level may normally be as high as 16 or 20 g/dl in pregnancy, and can be elevated without thyrotoxicosis in patients with familial hyperthyroxinemia due to abnormal albumin, the presence of hereditary excess TBG, the presence of antibodies binding T4 , the thyroid hormone resistance syndrome, and other conditions listed in Table 3. The T4 level may be normal in thyrotoxic patients who have depressed serum levels of T4 -binding protein or because of severe illness, even though they are toxic. Thus, thyrotoxicosis may exist when the total T4 level is in the normal range. However measurement of FT4, FT3 (Free T3), or FTI (Free Thyroxine Index) usually obviates this source of error and is the best test. In the presence of typical symptoms, one measurement of suppressed TSH or elevated fT4 is sufficient to make a definite diagnosis, although it does not identify a cause. If the fT4 is normal, repetition is in order to rule out error, along with a second test such as serum FT3. And it should be noted that in much of Europe FT3 is the preferred test, rather than FT4, and serves very well.

A variety of methods for FT4 determination have become available, including commercial kits. Although these methods are usually reliable, assays using different kits do not always agree among themselves or with the determination of FT4 by dialysis. Usually T4 and T3 levels are both elevated in thyrotoxicosis, as is the FTI (Free Thyroxin Index), or an index constructed using the serum T3 and rT3U levels, and the newer measures of FT3.

T3 and FT3 ASSAY-The serumT3 level determined by RIA is almost always elevated in thyrotoxicosis and is a useful but not commonly needed secondary test. Usually the serum T3 test is interpreted directly without use of a correction for protein binding, since alterations of TBG affect T3 to a lesser extent than T4. Any confusion caused by alterations in binding proteins can be avoided by use of a FT3 assay or T3 index calculated as for the FTI. Generally the FT3 assay is as diagnostically effective as the FT4. In patients with severe illness and thyrotoxicosis, especially those with liver disease or malnutrition or who are taking steroids or propranolol, the serum T3 level may not be elevated, since peripheral deiodination of T4 to T3 is suppressed (T4 toxicosis). A normal T3 level has also been observed in thyrotoxicosis combined with diabetic ketoacidosis. Whether or not these patients actually have tissue hypermetabolism at the time their serum T3 is normal is not entirely certain. In these patients the rT3 level may be elevated. If the complicating illness subsides, the normal pattern of elevated T4 , FTI, and T3 levels may return(5,6). Elevated T4 levels with normal serum T3 levels are also found in patients with thyrotoxicosis produced by iodine ingestion(7).

T3 Toxicosis Since 1957, when the first patient with T3 thyrotoxicosis was identified, a number of patients have been detected who had clinical thyrotoxicosis, normal serum levels of T4 and TBG, and elevated concentrations of T3 and FT3[8]. Hollander et al [9] found that approximately 4% of patients with thyrotoxicosis in the New York area fit this category. These patients often have mild disease but otherwise have been indistinguishable clinically from others with thyrotoxicosis. Some have had the diffuse thyroid hyperplasia of Graves disease, others toxic nodular goiter, and still others thyrotoxicosis with hyperfunctioning adenomas. Interestingly, in Chile, a country with generalized iodine deficiency, 12.5% of thyrotoxic subjects fulfilled the criteria for T3 thyrotoxicosis [10]. Asymptomatic hypertriiodothyronemia is an occasional finding several months before the development of thyrotoxicosis with elevated T4 levels [11]. Since T4 is normally metabolized to T3, and the latter hormone is predominantly the hormone bound to nuclear receptors, it makes sense that elevation of T3 alone is already indicative of thyrotoxicosis.

Thyroid Isotope uptake-In patients with thyrotoxicosis the RAIU (Radioactive Iodine Uptake) at 24 hours is characteristically above normal. In the United States, which has had an increasing iodine supply in recent years, the upper limit of normal is now about 25% of the administered dose. This value is higher in areas of iodine deficiency and endemic goiter. The uptake value at a shorter time interval, for example 6 hours, is as valid a test and may be more useful in the infrequent cases having such a rapid isotope turnover that uptake has fallen to normal by 24 hours. If there is reason to suspect that thyroid isotope turnover is rapid, it is wise to do both a 6- and a 24-hour RAIU determination during the initial laboratory study. As noted below, rapid turnover of 131-I can seriously reduce the effectiveness of 131-I therapy. Similar studies can be done with 123-I and also technetium. Because of convenience, and since serum assays of thyroid hormones and TSH are reliable and readily available, the RAIU is now infrequently determined unless 131-I therapy is planned.. It is however useful in patients who are mildly thyrotoxic for factitia thyrotoxicosis, subacute thyroiditis and painless thyroiditis in whom RAIU is low, thus confirming thyrotoxicosis in the absence of elevated RAIU. This may include patients with brief symptom duration, small goiter, or lacking eye signs, absent family history, or negative antibody test result. Obviously other causes of a low RAIU test need to be considered and excluded. Tests measuring suppressibility of RAIU are of historical interest(13-15)

Thyroid IsotopeScanning-Isotope scanning of the thyroid has a limited role in the diagnosis of thyrotoxicosis. It is useful in patients in whom the thyroid is difficult to feel or in whom nodules (single or multiple) are present that require evaluation, or rarely to prove the function of ectopic thyroid tissue. Nodules may be incidental, or may be the source of thyrotoxicosis (toxic adenoma), or may contribute to the thyrotoxicosis that also arises from the rest of the gland. Scanning should usually be done with 123-I in this situation, in order to combine it with an RAIU measurement.

Thyroid Ultrasound- US exam of the thyroid is sometimes of value in diagnosis. For example, if a possible nodule is detected on physical exam. It also may confirm hypoechogenicity or intense vascularity of Graves disease if a color Doppler flow exam is done.

Antithyroid Antibodies Determination of antibody titers provides supporting evidence for Graves disease. More than 95% of patients have positive assays for TPO (thyroperoxidase or microsomal antigen), and about 50% have positive anti-thyroglobulin antibody assays. In thyroiditis the prevalence of positive TG antibody assays is higher. Positive assays prove that autoimmunity is present, and patients with causes of thyrotoxicosis other than Graves disease usually have negative assays. During therapy with antithyroid drugs the titers characteristically go down, and this change persists during remission. Titers tend to become more elevated after RAI treatment.

Antibodies to TSH-Receptor-Thyrotrophin receptor antibody (TRAb) assays have become readily available, and a positive result strongly supports the diagnosis of Graves disease(15.1). Determination of TRAb is not required for the diagnosis, but the implied specificity of a positive test provides security in diagnosis, and for this reason the assay is now widely used. The assay is valuable as another supporting fact in establishing the cause of exophthalmos, in the absence of thyrotoxicosis. High maternal levels suggest possible fetal or neonatal thyrotoxicosis. TRAb assays measure any antibody that binds to the TSH-R. Assays for Thyroid Stimulating Antibodies (TSAb,TSI) are less available, but are more specific for the diagnosis. Using current tests, both are positive in about 90% of patients with Graves disease who are thyrotoxic. Second generation assays becoming available use monoclonal anti-TSH-R antibodies and biosynthetic TSH-R in coated tube assays, are reported to reach 99% specificity and sensitivity(15.2,15.3,3). Although rarely required, serial assays are of interest in following a patients course during antithyroid drug therapy, and a decrease predicts probable remission(15.4).

Other Assays Rarely Used-General availability of assays that can reliably measure suppressed TSH has made this the gold standard to which other tests must be compared, and has effectively eliminated the need for most previously used ancillary tests. There are only rare causes of confusion in the TSH assay. Severe illness, dopamine and steroids, and hypopituitarism, can cause low TSH, but suppression below 0.1 /ml is uncommon and below 0.05 /ml is exceptional, except in thyrotoxicosis. Thyrotoxicosis is associated with normal or high TSH in patients with TSH producing pituitary tumors and selective pituitary resistance to thyroid hormone. If TSH, FT4, TRAb, and other tests noted above do not establish the diagnosis, it may be wise to do nothing further except to observe the course of events. In patients with significant thyroid hyperfunction, the symptoms and signs will become clearer, and the laboratory measurements will fall into line. Measurement of BMR, T3 suppression of RAIU, TRH testing, and clinical response to KI are of historical interest.

Graves disease must be differentiated from other conditions causing thyrotoxicosis. (Table -4).

Thyrotoxicosis factitia-Thyrotoxicosis may be caused by taking T4 or its analogs, most commonly due to administration of excessive replacement hormone by the patients physician. Hormone may be taken surreptitiously by the patient for weight loss or psychologic reasons. The typical findings are a normal or small thyroid gland, a low131-I uptake, a low serum TG, and, of course, a striking lack of response to antithyroid drug therapy. The problem can easily be confused with painless thyroiditis, but in thyrotoxicosis factitia, the gland is typically small.

Toxic nodular goiter is usually distinguished by careful physical examination and a history of goiter for many years before symptoms of hyperthyroidism developed. The thyrotoxicosis comes on insidiously, and often, in the older people usually afflicted, symptoms may be mild, or suggest another problem such as heart disease. The thyroid scan may be diagnostic, showing areas of increased and decreased isotope uptake. The results of assays for antithyroid antibodies, including TRAb, are usually negative. TMNG is typically produced by activating somatic mutations in TSH-R in one or more nodules, allowing them to enlarge and become functional even in the absence of TSH stimulation. (Interestingly, cats are well known to develop hyperthyroidism, with thyroid autonomy, often due to TSH-R gene mutations as seen in humans.(16))

Hyperfunctioning solitary adenoma is suggested on the physical finding of a palpable nodule in a otherwise normal gland, and is proved by a scintiscan demonstrating preferential radioisotope accumulation in the nodule. This type of adenoma must be differentiated from congenital absence of one of the lobes of the thyroid. Toxic nodules typically present in adults with gradually developing hyperthyroidism and a nodule > 3 cm in size. These nodules are usually caused by activating somatic mutations in the TSH-R, which endows them with mildly increased function, compared to normal tissue, even in the absence of TSH. These nodules are usually, but not always, monoclonal(17). In adults toxic nodules are very rarely malignant. Rarely, functioning thyroid carcinomas produce thyrotoxicosis. The diagnosis is made by the history, absence of the normal thyroid, and usually widespread functioning metastasis in lung or bones. Invasion of the gland by lymphoma has produced thyrotoxicosis, presumably due to thyroid destruction (18).

Thyrotoxicosis associated with subacute thyroiditis is usually mild and transient, and the patient lacks the physical findings of long-standing thyrotoxicosis. If thyrotoxicosis is found in conjunction with a painful goiter and low or absent 131-I uptake, this diagnosis is likely. Usually the erythrocyte sedimentation rate (ESR) and CRP are greatly elevated, and the leukocyte count may also be increased. Occasionally the goiter is non-tender. Antibody titers are low or negative. Many patients have the HLA-B35 antigen, indicating a genetic predisposition to the disease. The rare TSH secreting pituitary adenoma will be missed unless one measures the plasma TSH level, or until the enlargement is sufficient to produce deficiencies in other hormones, pressure symptoms, or expansion of the sella turcica(19). These patients have thyrotoxicosis with inappropriately elevated TSH levels and may/or may not secrete more TSH after TRH stimulation. The characteristic finding is a normal or elevated TSH, and an elevated TSH alpha subunit level in blood, measured by special RIA. TRAbs are not present. Exophthalmos, and antibodies of Graves disease are absent. Family history is sometimes positive for a similar condition. Demonstration of a suppressed TSH level excludes these rare cases.

The category of patients with thyrotoxicosis and inappropriately elevated TSH levels also includes the rare persons with pituitary T3 resistance as a part of the Resistance to Thyroid Hormone syndrome caused by TH Receptor mutations. The syndrome of Pituitary Thyroid Hormone Resistance is usually marked by mild thyrotoxicosis, mildly elevated TSH levels, absence of pituitary tumor, a generous response to TRH, no excess TSH alpha subunit secretion [19,20, 21],and by TSH suppression if large doses of T3 are administered. Final diagnosis depends on laboratory demonstration of a mutation in the TR gene, if possible. Hyperthyroidism caused by excess TRH secretion is a theoretical but unproven possibiity.

Administration of large amounts of iodide in medicines, for roentgenographic examinations, or in foods can occasionally precipitate thyrotoxicosis in patients with multinodular goiter or functioning adenomas. This history is important to consider since the illness may be self-limiting. Induction of thyrotoxicosis has also been observed in apparently normal individuals following prolonged exposure to organic iodide containing compounds such as antiseptic soaps and amiodarone. Amiodarone is of special importance since the clinical problem often is the presentation of thyrotoxicosis in a patient with serious cardiac disease including dysrythmia. Amodarone can induce thyrotoxicosis in patients without known prior thyroid disease, or with multinodular goiter. The illness appears to come in two forms. In one the RAIU may be low or normal. In the second variety , which appears to be more of a thyroiditis-like syndrome, the RAIU is very suppressed, and IL-6 may be elevated. In either case TSH is suppressed, FTI may be normal or elevated, but T3 is elevated if the patient is toxic. Antibodies are usually negative.

An increasingly recognized form of thyrotoxicosis is the syndrome described variously as painless thyroiditis, transient thyrotoxicosis, or hyperthyroiditis. Its hallmarks are self-limited thyrotoxicosis, small painless goiter, and low or zero RAIU(22,23). The patients usually have no eye signs, a negative family history, and often positive antibody titers. This condition is due to autoimmune thyroid disease, and is considered a variant of Hashimotos Thyroiditis. It occurs sporadically, usually in young adults. It frequently occurs 3 12 weeks after delivery, sometimes representing the effects of immunologic rebound from the immunosuppressive effects of pregnancy in patients with Hashimotos thyroiditis or prior Graves Disease, and is called Post Partum Thyroiditis(22-25). The course typically includes development of a painless goiter, mild to moderate thyrotoxicosis, no eye signs, remission of symptoms in 3 -20 weeks, and often a period of hypothyroidism before return to euthyroid function. The cycle may be repeated several times. Histologic examination shows chronic thyroiditis, but it is not typical of Hashimotos disease or subacute thyroiditis and may revert to normal after the attack(26). In most patients, the thyrotoxic episode occurs in the absence of circulating TSAb. This finding suggests that the pathogenesis is quite distinct from that in Graves disease. The thyrotoxicosis is caused by an inflammation-induced discharge of preformed hormone due to the thyroiditis. The T4/T3 ratio is higher than in typical Graves disease,and thyroid iodine stores are depleted. Since the thyrotoxicosis is due to an inflammatory process, therapy with antithyroid drugs or potassium iodide is usually to no avail, and RAI treatment of course cannot be given when RAIU is suppressed. Propranolol is usually helpful for symptoms. Glucocorticoids may be of help if the process often transient and mild requires some form of therapy. Propylthiouracil and/or ipodate can be used to decrease T4 to T3 conversion and will ameliorate the illness. Repeated episodes may be handled by surgery or by RAI therapy during a remission. Occasionally painless post-partum thyroiditis is followed by typical Graves Disease(27-29.1).

Hyperemisis gravidarum is frequently associated with elevated serum T4 , FTI, and variably elevated T3, and suppressed TSH. The abnormalities in thyroid function are caused by high levels of hCG. This molecule, or a closely related form, share enough homology with TSH so that it has about 1/1000 the thyroid stimulating activity of TSH, and can produce thyroid stimulation or thyrotoxicosis(29.12-29.14). It is typically self limited without specific treatment, disappears with termination of pregnancy, but may occasionally require anti-thyroid treatment temporarily or throughout pregnancy(29.3). Patients with minimal signs and symptoms, small or no goiter, and elevation of FTI up to 50 % above normal probably do not require treatment. Rarely those with goiter, moderate or severe clinical evidence of thyrotoxicosis, highly elevated T4 and T3 and suppressed TSH are best treated with antithyroid drugs. If antibodies are positive or eye signs are present, the picture is usually interpreted as a form of Graves disease. Familial severe hyperemesis gravidarum with fetal loss has been reported with an activating germline mutation in the TSH-R, which made it specifically more sensitive to activation by hCG(.29.2,29.3). Hyperthyroidism can be induced by hyperplacentosis, which is characterized by increased placental weight and circulating hCG levels higher than those in normal pregnancy(29.4). After hysterotomy, hCG levels declined in the one case reported and hyperthyroidism was corrected.

Congenital hyperthyroidism caused by a germ-line activating mutation in the TSH-R has recently been recognized . The mutations are usually single aminoacid transitions in the extracellular loops or transmembrane segments of the receptor trans-membrane domain. The diagnosis may be difficult to recognize in the absence of a family history. However the patients lack eye signs, and have negative assays for antibodies(29.2, 29.3)

Hydatidiform moles, choriocarcinomas, and rarely seminomas secrete vast amounts of hCG. hCG, with an alpha subunit identical to TSH , and beta subunit related to TSH , that binds to and activates the thyroid TSH receptor with about 1/1,000th the efficiency of TSH itself (Fig.-3)(30-33). Current evidence indicates that very elevated levels of native hCG or perhaps desialated hCG, cause the thyroid stimulation. Many patients have goiter or elevated thyroid hormone levels or both, but little evidence of thyrotoxicosis, whereas others are clearly thyrotoxic. Diagnosis rests on recognizing the tumor (typically during or after pregnancy) and measurement of hCG. Therapy is directed at the tumor.

Hyperthyroidism also is seen as one manifestation of autoimmune thyroid disease induced by interferon-alpha treatment of chronic hepatitis C. It can be self limiting, or severe enough to require cessation of IFN, or in some cases continue on after INF is stopped(33.1).

Hyperthyroidism also occurs during immune reconstitution seen after effective anti-viral therapy of patients with HIV(33.2), has occurred during recovery of low lymphocyte levels induced by therapy with CAMPATH in patients with Multiple sclerosis, has occurred after cessation of immune-suppressive treatment in patients with T1DM.

It should be remembered that thyrotoxicosis is today not only a clinical but also a laboratory diagnosis. Consistent elevation of the fT4 , and the T3 level, and suppressed TSH, or only suppression of TSH, can indicate that thyrotoxicosis is present even in the absence of clear-cut signs or symptoms These elevations themselves are a sufficient indication for therapy, especially in elderly patients with coincident cardiac disease(33a,b). Antithyroid drug treatment of patients with subclinical hyperthyroidism was found to result in a decrease in heart rate, decrease in number of atrial and ventricular premature beats, a reduction of the left ventricular mass index, and left ventricular posterior wall thickness, as well as a reduction in diastolic peak flow velocity. These changes are considered an argument for early treatment of subclinical hyperthyroidism. Subclinical hyperthyroidism may disappear or evolve into Graves hyperthyroidism, or when caused by MNG, persist for long periods unchanged. Individuals of any age with consistent suppression of TSH should be fully evaluated to determine if evidence of hyperthyroidism is present, or there is coincident disease that might be aggrevated by hyperthyroidism. SCH with TSH of 0.2-0.3.5 may not need treatment. Individuals with TSH at or below 0.1uU/ml most likely will require treatment by one of the methods described below.

Apathetic hyperthyroidism designates a thyrotoxic condition characterized by fatigue, apathy, listlessness, dull eyes, extreme weakness, often congestive heart failure, and low-grade fever.[ 34, 35] Often such patients have small goiters, modest tachycardia, occasionally cool and even dry skin, and few eye signs. The syndrome may, in some patients, represent an extreme degree of fatigue induced by long-standing thyrotoxicosis. Once the diagnosis is considered, standard laboratory tests should confirm or deny the presence of thyrotoxicosis even in the absence of classical symptoms and signs.

Other diagnostic problems Two common diagnostic problems involve (1) the question of hyperthyroidism in patients with goiter of another cause, and (2) mild neuroses such as anxiety, fatigue states, and neurasthenia. Most patients with goiter receive a battery of examinations to survey their thyroid function at some time. Usually these tests are done more for routine assessment than because there is serious concern over the possibility of thyrotoxicosis. In the absence of significant symptoms or signs of hyperthyroidism and ophthalmologic problems, a normal FTI or TSH determination is sufficiently reassuring to the physician and the patient. Of course, the most satisfactory conclusion of such a study is the identification of an alternate cause for enlargement of the thyroid. Some patients complain of fatigue and palpitations, weight loss, nervousness, irritability, and insomnia. These patients may demonstrate brisk reflex activity, tachycardia (especially during examinations), perspiration, and tremulousness. In the abscence of thyrotoxicosis, the hands are more often cool and damp rather than warm and erythematous. Serum TSH assay should be diagnostic.

Mild and temporary elevation of the FTI may occur if there is a transient depression of TBG production for example, when estrogen administration is omitted. This problem is occasionally seen in hospital practice, usually involving a middle-aged woman receiving estrogen medication that is discontinued when the patient is hospitalized. Estrogen withdrawal leads to decreased TBG levels and a transiently elevated FTI. After two to three weeks, both the T4 level and the FTI return to normal ( Table -3). In the differential diagnosis of heart disease, the possibility of thyrotoxicosis must always be considered. Some cases of thyrotoxicosis are missed because the symptoms are so conspicuously cardiac that the thyroid background is not perceived. This is especially true in patients with atrial fibrillation. Many disorders may on occasion show some of the features of hyperthyroidism or Graves disease. In malignant disease, especially lymphoma, weight loss, low grade fever, and weakness are often present. Parkinsonism in its milder forms may initially suggest thyroid disease. So also do the flushed countenance, bounding pulse, thyroid hypertrophy, and dyspnea of pregnancy. Patients with chronic pulmonary disease may have prominent eyes, tremor, tachycardia, weakness, and even goiter from therapeutic use of iodine. One should remember the weakness, fatigue, and jaundice of hepatitis and the puffy eyes of trichinosis and nephritis. Cirrhotic patients frequently have prominent eyes and lid lag, and the alcoholic patient with tremor, prominent eyes, and flushed face may be initially suspected of having thyrotoxicosis. Distinguishing between Graves disease with extreme myopathy and myopathies of other origin can be clinically difficult. The term chronic thyrotoxic myopathy is used to designate a condition characterized by weakness, fatigability, muscular atrophy, and weight loss usually associated with severe thyrotoxicosis. Occasionally fasciculations are seen. The electromyogram result may be abnormal. If the condition is truly of hyperthyroid origin, the thyroid function tests are abnormal and the muscular disorder is reversed when the thyrotoxicosis is relieved. Usually a consideration of the total clinical picture and assessment of TSH and FTI are sufficient to distinguish thyrotoxicosis from polymyositis, myasthenia gravis, or progressive muscular atrophy. True myasthenia gravis may coexist with Graves disease, in which case the myasthenia responds to neostigmine therapy. (The muscle weakness of hyperthyroidism may be slightly improved by neostigmine, but never relieved.) Occasionally electromyograms, muscle biopsy, neostigmine tests, and ACH-receptor antibody assays must be used to settle the problem.

No treatment is ideal and thus indicated in all patients ( 35.1).Three forms of primary therapy for Graves disease are in common use today: (1) destruction of the thyroid by 131-I; (2) blocking of hormone synthesis by antithyroid drugs; and (3) partial or total surgical ablation of the thyroid. Iodine alone as a form of treatment was widely used in the past, but is not used today because its benefits may be transient or incomplete and because more dependable methods became available. Iodine is primarily used now in conjunction with antithyroid drugs to prepare patients for surgical thyroidectomy when that plan of therapy has been chosen. There is, however, some revival of interest in use of iodine treatment as described subsequently. Roentgen irradiation was also used in the past, but is not currently [36]. Suppression of the autoimmune response is being attempted, and currently new treatments blocking the action of Thyroid Stimulating Immunoglobulins are being investigated.

Selection of therapy depends on a multiplicity of considerations [36.1]. Availability of a competent surgeon, for example, undue emotional concern about the hazards of 131-I irradiation, or the probability of adherence to a strict medical regimen might govern ones decision regarding one program of treatment as opposed to another. More than 90% of patients are satistactorly treated cumulating the effects of these treatment.(36.2) Fig. 2

Antithyroid drug therapy offers the opportunity to avoid induced damage to the thyroid (and parathyroids or recurrent nerves), as well as exposure to radiation and operation. In recent studies patients with thyroids under 40 gm weight, with low TRAb levels, and age over 40, were most likely to enter remission (in up to 80%) (36.3, 36.31). The difficulties are the requirement of adhering to a medical schedule for many months or years, frequent visits to the physician, occasional adverse reactions, and, most importantly, a disappointingly low permanent remission rate. Therapy with antithyroid drugs is used as the initial modality in most patients under age 18, in many adults through age 40, and in most pregnant women(36.31). Remission is most likely in young patients, with small thyroids, and mild disease. ATDs may be preferred in elderly patients, those with serious co-morbidities and who have been previously operated upon.

Iodine-131 therapy is quick, easy, moderatly expensive, avoids surgery, and is without significant risk in adults and probably teenagers. The larger doses required to give prompt and certain control generally induce hypothyroidism, and low doses are associated with a frequent requirement for retreatment or ancillary medical management over one to two years. 131-I is used as the primary therapy in most persons over age 40 and in most adults above age 21 if antithyroid drugs fail to control the disease. Treatment of children with 131-I is less common, as discussed later. It can be used in the elderly and those with co-morbidities with precautions.

Surgery, which was the main therapy until 1950, has been to a large extent replaced by 131-I treatment. As the high frequency of 131-I induced hypothyroidism became apparent, some revival of interest in thyroidectomy occurred. The major advantage of surgery is that definitive management is often obtained over an 8- to 12-week period, including preoperative medical control, and many patients are euthyroid after operation. Its well-known disadvantages include expense, surgery itself, and the risks of recurrent nerve and parathyroid damage, hypothyroidism, and recurrence. Nevertheless, if a skillful surgeon is available, surgical management may be used as the primary or secondary therapy in many young adults, as the secondary therapy in children poorly controlled on antithyroid drugs, in pregnant women requiring excessive doses of antithyroid drugs, in patients with significant exophthalmos, and in patients with coincident suspicious thyroid nodules. Early total thyroidectomy has been recommended for treating older, chronically ill patients with thyrotoxic storm if high-dose thionamide treatment, iopanoic acid, and glucocorticoids fail to improve the patients condition within 12 24 hours (36.4).

Two recent surveys reporting trends in therapeutic choices made by thyroidologists have been published [37]. In Europe, most physicians tended to treat children and adults first with antithyroid drugs, and adults secondarily with 131-I or less frequently surgery. Surgery was selected as primary therapy for patients with large goiters. 131-I was selected as the primary treatment in older patients. Most therapists attempted to restore euthyroidism by use of 131-I or surgery. In the United States, 131-I is the initial modality of therapy selected by members of the American Thyroid Association for management of uncomplicated Graves disease in an adult woman [38]. Two-thirds of these clinicians attempt to give 131-I in a dosage calculated to produce euthyroidism, and one-third plan for thyroid ablation.

Introduction-In many thyroid clinics 131-I therapy is now used for most patients with Graves disease who are beyond the adolescent years. It is used in most patients who have had prior thyroid surgery, because the incidence of complications, such as hypoparathyroidism and recurrent nerve palsy, is especially high in this group if a second thyroidectomy is performed. Likewise, it is the therapy of choice for any patient who is a poor risk for surgery because of complicating disease. Surgery may be preferred in patients with significant ophthalmopathy, often combined with prednisone prophylaxis.

Treatment of children-The question of an age limit below which RAI should not be used frequently arises. With lengthening experience these limits have been lowered. Several studies with average follow-up periods of 12 15 years attest to the safety of 131-I therapy in adults [ 39- 41]. In two excellent studies treated persons showed no tendency to develop thyroid cancer, leukemia, or reproductive abnormalities, and their children had no increase in congenital defects or evidence of thyroid damage [ 42- 44]. Franklyn and co workers recently reported on a population based study of 7417 patients treated with 131-I for thyrotoxicosis in England [44.1]. They found an overall decrease in incidence of cancer mortality, but a specific increase in mortality from cancer of the small bowel (7 fold) and of the thyroid (3.25) fold. The absolute risk remains very low, and it is not possible to determine whether the association is related to the basic disease, or to radioiodine treatment. Although there is much less data on long term results in children, there is a increased use of this treatment in teenagers age 15-18, as discussed below. The epidemic of thyroid cancer apparently induced by radioactive iodine isotopes in infants and children living around Chernobyl suggests caution in use of 131-I in younger children. Since the possibility of a general induction of cancer by 131-I is of central concern, it is interesting to calculate the risk in children using the data presented by Rivkees et al (44.2) who are proponents of use of RAI for therapy in young children..The risk of death from any cancer due specifically to radiation exposure is noted by these authors to be 0.16%/rem for children, and the whole body radiation exposure from RAI treatment at age 10 to be 1.45 rem/mCi administered. Rivkees et al advise treatment with doses of RAI greater then 160 uCi/gram thyroid, to achieve a thyroidal radiation dose of at least 150Gy (about 15000 rads). Assuming a reasonable RAIU of 50% and gland size of 40 gm, the administered dose would thus be 40(gm) x 160uCi/gm x 2 (to account for 50% uptake) =12.8 mCi. Thus the long term cancer death risk would be 12.8 (mCi) x 1.45 rem (per mCi) x 0.16% (per rem) = 3%. For a dose of 15mCi the theoretical incremental risk of a later radiation-induced cancer mortality would be 4% at age 5, 2% at age 10, and 1% at age 15. Whether or not accepting a specific 2-4% risk of death from any cancer because of this treatment is of course a matter of judgment by the physician and family. However, this would seem to many persons to constitute a significant risk that might be avoided. We note that this is a thoretical risk, based on known effects of ioniing radiation to induce malignancies, but not so far proven in this setting.

Low 131-I uptake-Certain other findings may dictate the choice of therapy. Occasionally, the 131-I uptake is significantly blocked by prior iodine administration. The effect of iodide dissipates in a few days after stopping exposure, but it may take 3-12 weeks for the effect of amiodarone or IV contrast dyes to be lost. One may either wait for a few days to weeks until another 131-I tracer indicates that the uptake is in a treatable range or use an alternative therapeutic approach such as antithyroid drugs. Coincident nodule(s)-Sometimes a patient with thyrotoxicosis harbors a thyroid gland with a configuration suggesting the presence of a malignant neoplasm. These patients probably should have surgical exploration. While FNA may exclude malignancy, the safety of leaving a highly irradiated nodule in place for many years is not established. Currently few patients who will have RAI therapy are subjected to ultrasonagraphy or scintiscaning. However Stocker et al. found that 12% of Graves patients had cold defects on scan, and among these half were referred for surgery. Six of 22, representing 2% of all Graves patients, 15% of patients with cold nodules, 25% of patients with palpable nodules, and 27% of those going to surgery, had papillary cancer in the location corresponding to the cold defect. Of these patients, one had metastasis to bone and two required multiple treatments with radioiodine. They argue for evaluating patients with a thyroid scintigram and further diagnostic evaluation of cold defects(44.3). Certainly any patient with GD in whom a thyroid nodule is detected, deserves consideration for surgical treatment

Ophthalmopathy-131-I therapy causes an increase in titers of TSH-R Abs, and anti-TG or TPO antibodies, which reflects an activation of autoimmunity. It probably is due to release of thyroid antigens by cell damage, and possibly destruction of intrathyroidal T cells. Many thyroidologists are convinced that 131-I therapy can lead to exacerbation of infiltrative ophthalmopathy, perhaps because of this immunologic response. Tallstedt and associates published data indicating that 131-I therapy causes exacerbation of ophthalmopathy in nearly 25% of patients, while surgery is followed by this response in about half as many.The same group conducted a second randomized trial (44.3) with a follow-up of 4 yr. Patients with a recent diagnosis of Graves hyperthyroidism were randomized to treatment with iodine-131 (163 patients) or 18 months of medical treatment (150 patients). Early substitution with L-T4 was given in both groups.: Worsening or development of eye problems was significantly more common in the iodine-131 treatment group (63 patients; 38.7%) compared with the medical treatment group (32 patients; 21.3%) (P < 0.001). This adverse effect of RAI therapy has since been confirmed in multiple meta-analyses of randomized studies (44.4-44.7) Thus, as described below, patients with significant ophthalmopathy may receive corticosteroids along with131-I, or may be selected for surgical management. The indications and contraindications for 131-I therapy are given in Table 5.

There are two basically different goals in 131-I dose selection. The traditional approach has been to attempt to give the thyroid 1) sufficient radiation to return the patient to euthyroidism, but not induce hypothyroidism. An alternative approach is to intend to 2) induce hypothyroidism, or euthyroidism and avoid any possible return of hyperthyroidism.

BackgroundThe dosage initially was worked out by a trial-and-error method and by successive approximations. By 1950, the standard dose was 160 uCi 131-I per gram of estimated thyroid weight. Of course, estimating the weight of the thyroid gland by examination of the neck is an inexact procedure, but can now be made more accurate by use of ultrasound. Also, marked variation in radiation sensitivity no doubt exists and cannot be estimated at all. It was gratifying that in practice this dosage scheme worked well enough. In the early 1960s, it was recognized that a complication of RAI therapy was a high incidence of hypothyroidism. This reached 20 40% in the first year after therapy and increased about 2.5% per year, so that by 10 years 50 80% of patients had low function [45,46]. In an effort to reduce the incidence of late hypothyroidism, Hagen and colleagues reduced the quantity of 131-I to 0.08 mCi per gram of estimated gland weight [48]. No increase was reported in the number of patients requiring retreatment, and there was a substantial reduction in the incidence of hypothyroidism. Most of these patients were maintained on potassium iodide for several months after therapy, in order to ameliorate the thyrotoxicosis while the radioiodine had its effect [ 49, 50]. Patients previously treated with 131-I are sensitive to and generally easily controlled by KI. However KI often precipitates hypothyroidism in these patients, which may revert to hyperthyroidism when the KI is discontinued.

Over the years some effort was made to refine the calculation. Account was taken of uptake, half-life of the radioisotope in the thyroid, concentration per gram, and so on, but it is evident that the result in a given instance depends on factors that cannot be estimated precisely [47,]. One factor must be the tendency of the thyroid to return to normal if a dose of radiation is given that is large enough to make the gland approach, for a time, a normal functional state. In many patients, cure is associated with partial or total thyroid ablation. Although we, and many endocrinologists, attempt to scale the dose to the particular patient, some therapists believe it is futile, advocate giving up this attempt, and provide a standard dose giving up to 10000 rads to the thyroid(47.1). Leslie et al reported a comparison of fixed dose treatment and treatment adjusted for 24 hour RAIU, using low or high doses, and found no difference in outcome in either rate of control or induction of hypothyroidism on comparison of the methods. They favor the use of a fixed dose treatment with a single high or low dose (47.2).

Many attempts have been made to improve the therapeutic program by giving the RAI in smaller doses. Reinwein et al [51]. studied 334 patients several years after they had been treated with serial doses of less than 50 uCi 131-I per gram of estimated thyroid weight. One-third of these patients had increased levels of TSH, although they were clinically euthyroid. Only 3% were reported to be clinically hypothyroid.

Dosage adjustmentsmade to induce euthyroidism usually include a factor inc reassing with gland size, a standard dose in microCuries per gram, and a correction to account for 131-I uptake [52]. ALow Dose Protocol was designed to compensate for the apparent radiosensitivity of small glands and resistance of larger glands [53]. Using this approach, after one year, 10% of patients were hypothyroid, 60% are euthyroid, and 30% remained intrinsically toxic [53], although euthyroid by virtue of antithyroid drug treatment. At ten year follow-up, 40% were euthyroid and 60% hypothyroid. A problem with low-dose therapy is that about 25% of patients require a second treatment and 5% require a third. Although this approach reduces early hypothyroidism, it does so at a cost in time, money and patient convenience (Fig. 2). To answer these problems, patients can be re-treated, if need be, within six months, and propranolol and antithyroid drugs can be given between 131-I doses if needed. Unfortunately, experience shows that even low-dose 131-Itherapy is followed by a progressive development of hypothyroidism in up to 40 50% of patients ten years after therapy[ 54- 57].

Thyroid rads, avg.

Impressed by the need to retreat nearly a third of patients, a Moderate Dose Protocol was developed Table -6). This is a fairly conventional program with a mean dose of about 9 mCi. The 131-I dosage is related to gland weight and RAIU, and is increased as gland weight increases. The calculation used is as follows:

uCi given = (estimated thyroid weight in grams) X (uCi/g for appropriate weight from Table 6) / (fractional RAIU at 24 hours) (For readers who may find difficult the conversion of older units in Curies, rads, and rems to newer units of measurement, see Table -7.)

Thyroid rads, avg.

Probably it is wise to do uptakes and treatment using either capsules or liquid isotope for both events. Rini et al have reported that RAIU done with isotope in a capsule appears to give significantly lower values (25 30% lower) than when the isotope is administered in liquid form, and this can significantly influence the determination of the dosage given for therapy(57.1). Berg et al report using a relatively similar protocol (absorbed doses of 100-120 Gy) and that 93% of their patients required replacement therapy after 1-5 years [57.2]. Many studies have presented methods for more accurately delivering a specific radiation dose to the thyroid, and report curing up to 90% of patients, with low incidence of recurrence or hypothyroidism(57.3, 57.4). Franklyn and co-workers analyzed their data on treatment of 813 hyperthyroid patients with radioactive iodide and corroborate many of the previously recognized factors involved in response. Lower dose (in this case 5 mCi), male gender, goiters of medium or large size and severe hyperthyroidism were factors that were associated with failure to cure after one treatment. They suggest using higher fixed initial doses of radioiodine for treating such patients (58.2), as do Leslie et al(58.4). Santos et al (58.4) compared fixed doses of 10 and 15mCi and found no difference in outcome at 12 months post treatment. These authors suggest a standard 10mCi dose, with the larger dose reserved for larger glands.

Planned thyroid partial or complete ablation-All attempts to induce euthyroidism by a calculated moderate dose protocol end up with some patients hypothyroid, and others with persistent hyperthyroidism requiring further treatment. At this time many physicians giving 131-I therapy make no attempt to achieve euthyroidism, and instead use a dose sufficient to largely destroy the thyroid, followed by L- T4 replacement therapy [58]. For example, a dose is given that will result in 7-20 mCi retained at 24 hrs, which is intended to induce hypothyroidism, accepting that in some (or many) patients this will ablate the thyroid completely. A dose of 30 Mci was found to offer a slightly higher cure rate, not surprisingly, at one year than 15 Mci (95 vs 74% (58.1), They argue that this is realistic and preferable since it offers 1) near certainty of prompt control, 2) avoids any chance of persistent or recurrent disease, 3)there is no benefit in having residual thyroid tissue, and 4) hypothyroidism is inevitable in most patients given RAI. Probably many patients given this treatment do in fact have some residual thyroid tissue that is either heavily damaged or reduced in amount so that it can not produce normal amounts of hormone. So far there is no evidence, in adults, that this residual radiated tissue will develop malignant change. There is no certainty at this time that one approach is better than the other. It may be worth remembering that over 50% of patients given calculated moderate dose therapy remain euthyroid after ten years and can easily be surveyed at yearly intervals for hypothyroidism. When giving large doses of 131-I it is prudent to calculate the rads delivered to the gland (as above), which can reach 40-50,000rads. Such large doses of radiation can cause clinically significant radiation thyroiditis, and occasionally damage surrounding structures. And lastly, a speculation. Practitioners comment that the incidence of serious ophthalmopathy seems to be less that in former decades. Prompt diagnosis and therapy might contribute to such a change. Another factor could be the more common ablation of the thyroid during therapy for Graves disease, since this should over time reduce exposure of patients immune system to thyroid antigens.

Lithium with RAI therapy- Although rarely used, RAI combined with lithium is safe and more effective than RAI alone in the cure of hyperthyroidism due to Graves disease, probably because it it causes greater retention of RAI within the thyroid gland.. Bogazzi et al (58.5)reported a study combining lithium with RAI therapy. MMI treatment was withdrawn 5 days prior to treatment, Two hundred ninety-eight patients were treated with RAI plus lithium (900 mg/d for 12 d starting 5 days prior to 131-I treatment) and 353 with RAI alone. RAI dosage was 260mCi/g estimated thyroid weight, corrected for RAIU (done on lithium).. All patients receive prednisone 0.5mg/kg/day, beginning on day 7 after RAI, tapering over 2 months. Patients treated with RAI plus lithium had a higher cure rate (91.0%) than those treated with RAI alone (85.0%, P = 0.030). In addition, patients treated with RAI plus lithium were cured more rapidly (median 60 d) than those treated with RAI alone (median 90 d, P = 0.000). Treatment with lithium inhibited the serum FT4 increase seen after methimazole withdrawal and RAI therapy.

Pretreatment with antithyroid drugsPatients are often treated directly after diagnosis, without prior therapy with antithyroid drugs. This is safe and common in patients with mild hyperthyroidsm and especially those without eye problems. However often physicians give antithyroid drugs before 131-I treatment in order to deplete the gland of stored hormone and to restore the FTI to normal before 131-I therapy. This offers several benefits. The possibility of 131-I induced exacerbation of thyrotoxicosis is reduced, the patient recovers toward normal health, and there is time to reflect on the desired therapy and review any concerns about the use of radioisotope for therapy. If the patient has been on antithyroid drug, it is discontinued two days before RAIU and therapy. Patients can be treated while on antithyroid drug, but this reduces the dose retained, reduces the post-therapy increment in hormone levels, and reduces the cure rate, so seems illogical(58.6) . When antithyroid drugs are discontinued the patients disease may exacerbate, and this must be carefully followed. Beta blockers can be given in this interim, but there is no reason for a prolonged interval between stopping antithyroid drug, and 131-I therapy, unless there is uncertainty about the need for the treatment. Pretreatment with antithyroid drug does not appear in most studies to reduce the efficacy of 131-I treatment. [59] but the debate about the effect of antithyroid drug pretreatment on the efficacy of radioactive iodine therapy continues. In recent studies in which patients were on or off antithyroid therapy, which was discontinued four days, or 1-2 days before treatment, there was no effect on the efficacy of treatment at a one year endpoint (59.1,59.2, 59,3). In another study Bonnema et al found that PTU pretreatment , stopped 4 days prior to 131-I, reduced the efficacy of 131-I(59.6).

Pretreatment is usually optional but is logical in patients with large glands and severe hyperthyroidism. Antithyroid drug therapy does reduce the pretreatment levels of hormone and reduces the rise in thyroid hormone level that may occur after radioactive iodide treatment. This certainly could have a protective effect in individuals who have coincident serious illness such as coronary artery disease, or perhaps individuals who have very large thyroid glands (59.3). It is indicated in two circumstances. In patients with severe heart disease, an 131-I- induced exacerbation of thyrotoxicosis could be serious or fatal. Pretreatment may reduce exacerbation of eye disease (see below), and it does reduce the post-RAI increase in antibody titers(59.1,59.31). The treatment dose of 131-I is best given as soon as possible after the diagnostic RAIU in order to reduce the period in which thyrotoxicosis may exacerbate without treatment, and since any intake of iodine (from diet or medicines or tests) would alter uptake of the treatment dose (59.4), and 2 days seems sufficient.

Post 131-I treatment managementMany patients remain on beta-blockers but require no other treatment after 131-I therapy. Antithyroid drugs can be reinstituted after 5 ( or preferably 7 ) days, with minimal effect on retention of the treatment dose of 131-I.

Alternatively, one may prescribe antithyroid drug (typically 10 mg methimazole q8h) beginning one day after administration of 131-I and add KI (2 drops q8h) after the second dose of methimazole. KI is continued for two weeks, and antithyroid drug as needed. This promotes a rapid return to euthyroidism, but by preventing recirculation of 131-I it can lower the effectiveness of the treatment. This method has been employed in a large number of patients, and is especially useful in patients requiring rapid control- for example, with CHF. A typical response is shown in Fig -3. It also has provided the largest proportion of patients remaining euthyroid at 10 years after therapy, in comparison to other treatment protocols. Glinoer and Verelst also report successful use of this strategy [59.1]. As noted, antithyroid drugs may be given starting 7-10 days after RAI without significantly lowering the radiation dose delivered to the gland.

Treatment using 125-I was tried as an alternative to 131-I, because it might offer certain advantages [60]. 125-I is primarily a gamma ray emitter, but secondary low-energy electrons are produced that penetrate only a few microns, in contrast to the high-energy beta rays of 131-I. Thus, it might theoretically be possible to treat the cytoplasm of the thyroid cell with relatively little damage to the nucleus. Appropriate calculations indicated that the radiation dose to the nucleus could be perhaps one-third that to the cytoplasm, whereas this difference would not exist for 131-I. Extensive therapeutic trials have nonetheless failed to disclose any advantage thus far for 125I. Larger doses 10-20 mCi are required, increasing whole body radiation considerably [ 61, 62].

Doses of 131-I up to 33 mCi can be given to an outpatient basis, and this level is rarely exceeded in treatment of Graves disease. However patients must be given advice (written if possible) on precautions to be followed to prevent unneccessary or excessive exposure of other individuals by radiaactivity administered to the patient. For maximum safety, patients who have received 20 mCi should avoid extended time in public places for 1 day, maximize distance (6 feet) from children and pregnant women for 2 days, may return to work after 1 day, sleep in a separate (6-feet separation) bed from adults for 8 days, sleep in a separate bed from pregnant partners, infant, or child for 20 days, and avoid contact with body fluids (saliva, urine) for at least one week. Lower therapeutic doses require proportionally more moderate precautions. The basic NRC rule is that patients may be released from hospital when (1) the 131I measured dose rate is 7mrem/hr at 1m, or (2) when the expected total dose another person would receive is unlikely to exceed 500mrem (5mSv). Written precaution instructions are required If 100mrem (1mSv) may be exceeded in any person. This topic is well covered in articles by Sisson et al ( andLiu et al (62.1).

If adequate treatment has been given, the T4 level falls progressively, beginning in one to three weeks.. Labeled thyroid hormones, iodotyrosines, and iodoproteins appear in the circulation [63,63.1]. TG is released, starting immediately after therapy. Another iodoprotein, which seems to be an iodinated albumin, is also found in plasma. This compound is similar or identical to a quantitatively insignificant secretion product of the normal gland. It comprises up to 15% or more of the circulating serum 131-I in thyrotoxic patients [64]. It is heavily labeled after 131-I therapy, and its proportional secretion is probably increased by the radiation. Iodotyrosine present in the serum may represent leakage from the thyroid gland, or may be derived from peripheral metabolism of TG or iodoalbumin released from the thyroid.

The return to the euthyroid state usually requires at least two months, and often the declining function of the gland proceeds gradually over six months to a year. For this reason, it is logical to avoid retreating a patient before six months have elapsed unless there is no evidence of control of the disease. While awaiting the response to131-I the symptoms may be controlled by propranolol, antithyroid drugs, or iodide. Hypothyroidism develops transiently in 10 20% of patients, but thyroid function returns to normal in most of these patients in a period ranging from three to six months. These patients rarely become toxic again. Others develop permanent hypothyroidism and require replacement therapy. It is advantageous to give the thyroid adequate time to recover function spontaneously before starting permanent replacement therapy. This can be difficult for the patient unless partial T4 replacement is given. Unfortunately, one of the common side effects of treating hyperthyroidism is weight gain, averaging about 20 lbs through four years after treatment (64.1).

Patients may develop transient increases in FTI and T3 at 2-4 months after treatment [63.1], sometimes associated with enlargement of the thyroid. This may represent an inflammatory or immune response to the irradiationinduced thyroid damage, and the course may change rapidly with a dramatic drop to hypothyroidism in the 4-5th month.

Hypothyroidism may ultimately be inescapable after any amount of radiation that is sufficient to reduce the function of the hyperplastic thyroid to normal [65]. Many apparently euthyroid patients (as many as half) have elevated serum levels of TSH long after 131-I therapy, with normal plasma hormone levels [66]. An elevated TSH level with a low normal T4level is an indicator of changes progressing toward hypothyroidism [67]. The hypothyroidism is doubtless also related to the continued autoimmune attack on thyroid cells. Hypofunction is a common end stage of Graves disease independent of 131-I use; it occurs spontaneously as first noted in 1895(!) [68] and in patients treated only with antithyroid drugs [69]. Just as after surgery, the development of hypothyroidism is correlated positively with the presence of antithyroid antibodies.

During the rapid development of postradiation hypothyroidism, the typical symptoms of depressed metabolism are evident, but two rather unusual features also occur. The patients may have marked aching and stiffness of joints and muscles. They may also develop severe centrally located and persistent headache. The headache responds rapidly to thyroid hormone therapy. Hair loss can also be dramatic at this time.

In patients developing hypothyroidism rapidly, the plasma T4 level and FTI accurately reflect the metabolic state. However, it should be noted that the TSH response may be suppressed for weeks or months by prior thyrotoxicosis; thus, the TSH level may not accurately reflect hypothyroidism in these persons and should not be used in preference to the FTI or FT4.

If permanent hypothyroidism develops, the patient is given replacement hormone therapy and is impressed with the necessity of taking the medication for the remainder of his or her life. Thyroid hormone replacement is not obligatory for those who develop only temporary hypothyroidism, although it is possible that patients in this group should receive replacement hormone, for their glands have been severely damaged and they are likely to develop hypothyroidism at a later date. Perhaps these thyroids, under prolonged TSH stimulation, may tend to develop adenomatous or malignant changes, but this has not been observed. Many middle-aged women gain weight excessively after radioactive iodide treatment of hyperthyroidism. Usually such patients are on what is presumed to be appropriate T4 replacement therapy. Tigas et al note that such weight gain is less common after ablative therapy for thyroid cancer, in which case larger doses of thyroxine are generally prescribed. Thus they question whether the excessive weight gain after radioactive iodide treatment of Graves disease is due to the fact that insufficient thyroid hormone is being provided, even though TSH is within the normal range. They suggest that restoration of serum TSH to the reference range by T4 alone may not constitute adequate hormone replacement [ 69a}. We noted above that the correct reference range for TT4 and FT4, when the patient is on replacement T4, should be 20% higher than normal.

Permanent replacement therapy (regardless of the degree of thyroid destruction) for children who receive 131-I has a better theoretical basis. In these cases, it is advisable to prevent TSH stimulation of the thyroid and so mitigate any possible tendency toward carcinoma formation.

Exacerbation of thyrotoxicosis-During the period immediately after therapy, there may be a transient elevation of the T4 or T3 level [70], but usually the T4 level falls progressively toward normal. Among treated hyperthyroid patients with Graves disease, only rare exacerbations of the disease are seen. These patients may have cardiac problems such as worsening angina pectoris, congestive heart failure, or disturbances of rhythm such as atrial fibrillation or even ventricular tachycardia. Radiation-induced thyroid storm and even death have unfortunately been reported [71- 73]. These untoward events argue for pretreatment of selected patients who have other serious illness, especially cardiac disease, with antithyroid drugs prior to 131-I therapy.

The immediate side effects of 131-I therapy are typically minimal. As noted above, transient exacerbation of thyrotoxicosis can occur, and apparent thyroid storm has been induced within a day (or days) after 131-I therapy. A few patients develop mild pain and tenderness over the thyroid and, rarely, dysphagia. Some patients develop temporary hair loss, but this condition occurs two to three months after therapy rather than at two to three weeks, as occurs after ordinary radiation epilation. Hair loss also occurs after surgical therapy, so that it is a metabolic rather than a radiation effect. If the loss of hair is due to the change in metabolic status, it generally recovers in a few weeks or months. However hair thinning, patchy alopecia, and total alopecia, are all associated with Graves Disease, probably as another auto-immune processes. In this situation the prognosis for recovery is less certain, and occasionally some other therapy for the hair loss (such as steroids) is indicated. Permanent hypoparathyroidism has been reported very rarely as a complication of RAI therapy for heart disease and thyrotoxicosis[ 74- 76]. Patients treated for hyperthyroidism with 131-I received approximately 39 microGy/MBq administered (about 0.144rad/mCi) of combined beta and gamma radiation to the testes. This is reported to cause no significant changes in FSH. Nevertheless, testosterone declines transiently for several months, but there is no variation in sperm motility or % abnormal forms (76.1). Long term studies of patients after RAI treatment by Franklyn et al (76.2) show a slight increase in mortality which appears to be related to cardiovascular disease, possibly related to periods of hypothyroidism.

Worsening of ophthalmopathy after RAIIn contrast to the experience with antithyroid drugs or surgery, antithyroid antibodies including TSAb levels increase after RAI [ 77, 78]. (Fig. 11-4, above). Coincident with this condition, exophthalmos may be worsened [79].(Fig. 11-5, below). This change is most likely an immunologic reaction to discharged thyroid antigens.The relationship of radiation therapy to exacerbation of exophthalmos has beem questioned], but much recent data indicates that there is a definite correlation[ 79, 80, 80.1, 80.2, 80.3]. Many therapists consider bad eyes to be a relative contraindication to RAI. Induction of hypothyroidism, with elevation of TSH, may contribute to worsening of ophthalmopathy. This offers support for early induction of T4 replacement (80.3). Pretreatment with antithyroid drugs has been used empirically in an attempt to prevent this complication. Its benefit, if any, may be related to an immunosuppressive effect of PTU, described below. Treatment with methimazole before and for three months after I-131 therapy has been shown to help prevent the treatment-induced rise in TSH-R antibodies which is otherwise seen[81].

Prophylaxis with prednisone after 131-I helps prevent exacerbation of exophthalmos, and this approach is now the standard approach in patients who have significant exophthalmos at the time of treatment [ 82, 82.1]. (Fig. 6, below) The recommended dose is 30 mg/day for one month, tapering then over 2-3 months. Of course prednisone or other measures can be instituted at the time of any worsening of ophthalmopathy. In this instance doses of 30-60 mg/day are employed, and usually are required over several months. While treatment with prednisone helps prevent eye problems, it does not appear to reduce the effectiveness of RAI in controlling the hyperthyroidism(82.2). Thyroidectomy, with total removal of the gland, should be considered for patients with serious active eye disease. Operative removal of the thyroid is followed by gradual diminution is TSH-R antibodies.(82.3 ), and as shown by Tallstedt is associated with a lower incidence of worsening eye problems than is initial RAI treatment. Several studies document better outcomes of ophthalmopathy in patients with GD who have total thyroidectomy vs those treated by other means(82.4, 82.5, 82.6).

Failure of 131-I to cure thyrotoxicosis occurs occasionally even after 2 or 3 treatments, and rarely 4 or 5 therapies are given. The reason for this failure is usually not clear. The radiation effect may occur slowly. A large store of hormone in a large gland may be one cause of a slow response. Occasional glands having an extremely rapid turnover of 131-I requiring such high doses of the isotope that surgery is preferable to continued 131-I therapy and its attendant whole body radiation. If a patient fails to respond to one or two doses of 131-I, it is important to consider that rapid turnover may reduce the effective radiation dose. Turnover can easily be estimated by measuring RAIU at 4, 12, 24, and 48 hours, or longer. The usual combined physical and biological half-time of 131-I retention is about 6 days. This may be reduced to 1 or 2 days in some cases, especially in patients who have had prior therapy or subtotal thyroidectomy. If this rapid release of 131-I is found, and 131-I therapy is desired, the total dose given must be increased to compensate for rapid release. A rough guide to this increment is as follows:

Increased dose = usual dose X ( (usual half time of 6 days) / (observed half time of X days) )

Most successfully treated glands return to a normal or cosmetically satisfactory size. Some large glands remain large, and in that sense may constitute a treatment failure. In such a situation secondary thyroidectomy could be done, but it is rarely required in practice.

Long term care- Patients who have been treated with RAI should continue under the care of a physician who is interested in their thyroid problem for the remainder of their lives. The first follow-up visit should be made six to eight weeks after therapy. By this time, it will often be found that the patient has already experienced considerable improvement and has begun to gain weight. The frequency of subsequent visits will depend on the progress of the patient. Symptoms of hypothyroidism, if they develop, are usually not encountered until after two to four months, but one of the unfortunate facts of RAI therapy is that hypothyroidism may occur almost any time after the initial response.

In the early days of RAI treatment for Graves disease, only patients over 45 years of age were selected for treatment because of the fear of ill effects of radiation. This age limit was gradually lowered, and some clinics, after experience extending over nearly 40 years, have now abandoned most age limitation. The major fear has been concern for induction of neoplasia, as well as the possibility that 131-I might induce undesirable mutations in the germ cells that would appear in later generations.

See the original post here:
Thyroid Disease Manager : Diagnosis and Treatment of Graves

Medicine – Wikipedia

Medicine (British English i; American English i) is the science and practice of the diagnosis, treatment, and prevention of disease.[1][2] The word medicine is derived from Latin medicus, meaning "a physician".[3][4] Medicine encompasses a variety of health care practices evolved to maintain and restore health by the prevention and treatment of illness. Contemporary medicine applies biomedical sciences, biomedical research, genetics, and medical technology to diagnose, treat, and prevent injury and disease, typically through pharmaceuticals or surgery, but also through therapies as diverse as psychotherapy, external splints and traction, medical devices, biologics, and ionizing radiation, amongst others.[5]

Medicine has existed for thousands of years, during most of which it was an art (an area of skill and knowledge) frequently having connections to the religious and philosophical beliefs of local culture. For example, a medicine man would apply herbs and say prayers for healing, or an ancient philosopher and physician would apply bloodletting according to the theories of humorism. In recent centuries, since the advent of modern science, most medicine has become a combination of art and science (both basic and applied, under the umbrella of medical science). While stitching technique for sutures is an art learned through practice, the knowledge of what happens at the cellular and molecular level in the tissues being stitched arises through science.

Prescientific forms of medicine are now known as traditional medicine and folk medicine. They remain commonly used with or instead of scientific medicine and are thus called alternative medicine. For example, evidence on the effectiveness of acupuncture is "variable and inconsistent" for any condition,[6] but is generally safe when done by an appropriately trained practitioner.[7] In contrast, treatments outside the bounds of safety and efficacy are termed quackery.

Medical availability and clinical practice varies across the world due to regional differences in culture and technology. Modern scientific medicine is highly developed in the Western world, while in developing countries such as parts of Africa or Asia, the population may rely more heavily on traditional medicine with limited evidence and efficacy and no required formal training for practitioners.[8] Even in the developed world however, evidence-based medicine is not universally used in clinical practice; for example, a 2007 survey of literature reviews found that about 49% of the interventions lacked sufficient evidence to support either benefit or harm.[9]

In modern clinical practice, doctors personally assess patients in order to diagnose, treat, and prevent disease using clinical judgment. The doctor-patient relationship typically begins an interaction with an examination of the patient's medical history and medical record, followed by a medical interview[10] and a physical examination. Basic diagnostic medical devices (e.g. stethoscope, tongue depressor) are typically used. After examination for signs and interviewing for symptoms, the doctor may order medical tests (e.g. blood tests), take a biopsy, or prescribe pharmaceutical drugs or other therapies. Differential diagnosis methods help to rule out conditions based on the information provided. During the encounter, properly informing the patient of all relevant facts is an important part of the relationship and the development of trust. The medical encounter is then documented in the medical record, which is a legal document in many jurisdictions.[11] Follow-ups may be shorter but follow the same general procedure, and specialists follow a similar process. The diagnosis and treatment may take only a few minutes or a few weeks depending upon the complexity of the issue.

The components of the medical interview[10] and encounter are:

The physical examination is the examination of the patient for medical signs of disease, which are objective and observable, in contrast to symptoms which are volunteered by the patient and not necessarily objectively observable.[12] The healthcare provider uses the senses of sight, hearing, touch, and sometimes smell (e.g., in infection, uremia, diabetic ketoacidosis). Four actions are the basis of physical examination: inspection, palpation (feel), percussion (tap to determine resonance characteristics), and auscultation (listen), generally in that order although auscultation occurs prior to percussion and palpation for abdominal assessments.[13]

The clinical examination involves the study of:

It is to likely focus on areas of interest highlighted in the medical history and may not include everything listed above.

The treatment plan may include ordering additional medical laboratory tests and medical imaging studies, starting therapy, referral to a specialist, or watchful observation. Follow-up may be advised. Depending upon the health insurance plan and the managed care system, various forms of "utilization review", such as prior authorization of tests, may place barriers on accessing expensive services.[14]

The medical decision-making (MDM) process involves analysis and synthesis of all the above data to come up with a list of possible diagnoses (the differential diagnoses), along with an idea of what needs to be done to obtain a definitive diagnosis that would explain the patient's problem.

On subsequent visits, the process may be repeated in an abbreviated manner to obtain any new history, symptoms, physical findings, and lab or imaging results or specialist consultations.

Contemporary medicine is in general conducted within health care systems. Legal, credentialing and financing frameworks are established by individual governments, augmented on occasion by international organizations, such as churches. The characteristics of any given health care system have significant impact on the way medical care is provided.

From ancient times, Christian emphasis on practical charity gave rise to the development of systematic nursing and hospitals and the Catholic Church today remains the largest non-government provider of medical services in the world.[15] Advanced industrial countries (with the exception of the United States)[16][17] and many developing countries provide medical services through a system of universal health care that aims to guarantee care for all through a single-payer health care system, or compulsory private or co-operative health insurance. This is intended to ensure that the entire population has access to medical care on the basis of need rather than ability to pay. Delivery may be via private medical practices or by state-owned hospitals and clinics, or by charities, most commonly by a combination of all three.

Most tribal societies provide no guarantee of healthcare for the population as a whole. In such societies, healthcare is available to those that can afford to pay for it or have self-insured it (either directly or as part of an employment contract) or who may be covered by care financed by the government or tribe directly.

Transparency of information is another factor defining a delivery system. Access to information on conditions, treatments, quality, and pricing greatly affects the choice by patients/consumers and, therefore, the incentives of medical professionals. While the US healthcare system has come under fire for lack of openness,[18] new legislation may encourage greater openness. There is a perceived tension between the need for transparency on the one hand and such issues as patient confidentiality and the possible exploitation of information for commercial gain on the other.

Provision of medical care is classified into primary, secondary, and tertiary care categories.

Primary care medical services are provided by physicians, physician assistants, nurse practitioners, or other health professionals who have first contact with a patient seeking medical treatment or care. These occur in physician offices, clinics, nursing homes, schools, home visits, and other places close to patients. About 90% of medical visits can be treated by the primary care provider. These include treatment of acute and chronic illnesses, preventive care and health education for all ages and both sexes.

Secondary care medical services are provided by medical specialists in their offices or clinics or at local community hospitals for a patient referred by a primary care provider who first diagnosed or treated the patient. Referrals are made for those patients who required the expertise or procedures performed by specialists. These include both ambulatory care and inpatient services, emergency rooms, intensive care medicine, surgery services, physical therapy, labor and delivery, endoscopy units, diagnostic laboratory and medical imaging services, hospice centers, etc. Some primary care providers may also take care of hospitalized patients and deliver babies in a secondary care setting.

Tertiary care medical services are provided by specialist hospitals or regional centers equipped with diagnostic and treatment facilities not generally available at local hospitals. These include trauma centers, burn treatment centers, advanced neonatology unit services, organ transplants, high-risk pregnancy, radiation oncology, etc.

Modern medical care also depends on information still delivered in many health care settings on paper records, but increasingly nowadays by electronic means.

In low-income countries, modern healthcare is often too expensive for the average person. International healthcare policy researchers have advocated that "user fees" be removed in these areas to ensure access, although even after removal, significant costs and barriers remain.[19]

Working together as an interdisciplinary team, many highly trained health professionals besides medical practitioners are involved in the delivery of modern health care. Examples include: nurses, emergency medical technicians and paramedics, laboratory scientists, pharmacists, podiatrists, physiotherapists, respiratory therapists, speech therapists, occupational therapists, radiographers, dietitians, and bioengineers, surgeons, surgeon's assistant, surgical technologist.

The scope and sciences underpinning human medicine overlap many other fields. Dentistry, while considered by some a separate discipline from medicine, is a medical field.

A patient admitted to the hospital is usually under the care of a specific team based on their main presenting problem, e.g., the Cardiology team, who then may interact with other specialties, e.g., surgical, radiology, to help diagnose or treat the main problem or any subsequent complications/developments.

Physicians have many specializations and subspecializations into certain branches of medicine, which are listed below. There are variations from country to country regarding which specialties certain subspecialties are in.

The main branches of medicine are:

In the broadest meaning of "medicine", there are many different specialties. In the UK, most specialities have their own body or college, which have its own entrance examination. These are collectively known as the Royal Colleges, although not all currently use the term "Royal". The development of a speciality is often driven by new technology (such as the development of effective anaesthetics) or ways of working (such as emergency departments); the new specialty leads to the formation of a unifying body of doctors and the prestige of administering their own examination.

Within medical circles, specialities usually fit into one of two broad categories: "Medicine" and "Surgery." "Medicine" refers to the practice of non-operative medicine, and most of its subspecialties require preliminary training in Internal Medicine. In the UK, this was traditionally evidenced by passing the examination for the Membership of the Royal College of Physicians (MRCP) or the equivalent college in Scotland or Ireland. "Surgery" refers to the practice of operative medicine, and most subspecialties in this area require preliminary training in General Surgery, which in the UK leads to membership of the Royal College of Surgeons of England (MRCS). At present, some specialties of medicine do not fit easily into either of these categories, such as radiology, pathology, or anesthesia. Most of these have branched from one or other of the two camps above; for example anaesthesia developed first as a faculty of the Royal College of Surgeons (for which MRCS/FRCS would have been required) before becoming the Royal College of Anaesthetists and membership of the college is attained by sitting for the examination of the Fellowship of the Royal College of Anesthetists (FRCA).

Surgery is an ancient medical specialty that uses operative manual and instrumental techniques on a patient to investigate and/or treat a pathological condition such as disease or injury, to help improve bodily function or appearance or to repair unwanted ruptured areas (for example, a perforated ear drum). Surgeons must also manage pre-operative, post-operative, and potential surgical candidates on the hospital wards. Surgery has many sub-specialties, including general surgery, ophthalmic surgery, cardiovascular surgery, colorectal surgery, neurosurgery, oral and maxillofacial surgery, oncologic surgery, orthopedic surgery, otolaryngology, plastic surgery, podiatric surgery, transplant surgery, trauma surgery, urology, vascular surgery, and pediatric surgery. In some centers, anesthesiology is part of the division of surgery (for historical and logistical reasons), although it is not a surgical discipline. Other medical specialties may employ surgical procedures, such as ophthalmology and dermatology, but are not considered surgical sub-specialties per se.

Surgical training in the U.S. requires a minimum of five years of residency after medical school. Sub-specialties of surgery often require seven or more years. In addition, fellowships can last an additional one to three years. Because post-residency fellowships can be competitive, many trainees devote two additional years to research. Thus in some cases surgical training will not finish until more than a decade after medical school. Furthermore, surgical training can be very difficult and time-consuming.

Internal medicine is the medical specialty dealing with the prevention, diagnosis, and treatment of adult diseases. According to some sources, an emphasis on internal structures is implied.[20] In North America, specialists in internal medicine are commonly called "internists." Elsewhere, especially in Commonwealth nations, such specialists are often called physicians.[21] These terms, internist or physician (in the narrow sense, common outside North America), generally exclude practitioners of gynecology and obstetrics, pathology, psychiatry, and especially surgery and its subspecialities.

Because their patients are often seriously ill or require complex investigations, internists do much of their work in hospitals. Formerly, many internists were not subspecialized; such general physicians would see any complex nonsurgical problem; this style of practice has become much less common. In modern urban practice, most internists are subspecialists: that is, they generally limit their medical practice to problems of one organ system or to one particular area of medical knowledge. For example, gastroenterologists and nephrologists specialize respectively in diseases of the gut and the kidneys.[22]

In the Commonwealth of Nations and some other countries, specialist pediatricians and geriatricians are also described as specialist physicians (or internists) who have subspecialized by age of patient rather than by organ system. Elsewhere, especially in North America, general pediatrics is often a form of Primary care.

There are many subspecialities (or subdisciplines) of internal medicine:

Training in internal medicine (as opposed to surgical training), varies considerably across the world: see the articles on Medical education and Physician for more details. In North America, it requires at least three years of residency training after medical school, which can then be followed by a one- to three-year fellowship in the subspecialties listed above. In general, resident work hours in medicine are less than those in surgery, averaging about 60 hours per week in the USA. This difference does not apply in the UK where all doctors are now required by law to work less than 48 hours per week on average.

The followings are some major medical specialties that do not directly fit into any of the above-mentioned groups.

Some interdisciplinary sub-specialties of medicine include:

Medical education and training varies around the world. It typically involves entry level education at a university medical school, followed by a period of supervised practice or internship, and/or residency. This can be followed by postgraduate vocational training. A variety of teaching methods have been employed in medical education, still itself a focus of active research. In Canada and the United States of America, a Doctor of Medicine degree, often abbreviated M.D., or a Doctor of Osteopathic Medicine degree, often abbreviated as D.O. and unique to the United States, must be completed in and delivered from a recognized university.

Since knowledge, techniques, and medical technology continue to evolve at a rapid rate, many regulatory authorities require continuing medical education. Medical practitioners upgrade their knowledge in various ways, including medical journals, seminars, conferences, and online programs.

In most countries, it is a legal requirement for a medical doctor to be licensed or registered. In general, this entails a medical degree from a university and accreditation by a medical board or an equivalent national organization, which may ask the applicant to pass exams. This restricts the considerable legal authority of the medical profession to physicians that are trained and qualified by national standards. It is also intended as an assurance to patients and as a safeguard against charlatans that practice inadequate medicine for personal gain. While the laws generally require medical doctors to be trained in "evidence based", Western, or Hippocratic Medicine, they are not intended to discourage different paradigms of health.

In the European Union, the profession of doctor of medicine is regulated. A profession is said to be regulated when access and exercise is subject to the possession of a specific professional qualification. The regulated professions database contains a list of regulated professions for doctor of medicine in the EU member states, EEA countries and Switzerland. This list is covered by the Directive 2005/36/EC.

Doctors who are negligent or intentionally harmful in their care of patients can face charges of medical malpractice and be subject to civil, criminal, or professional sanctions.

Medical ethics is a system of moral principles that apply values and judgments to the practice of medicine. As a scholarly discipline, medical ethics encompasses its practical application in clinical settings as well as work on its history, philosophy, theology, and sociology. Six of the values that commonly apply to medical ethics discussions are:

Values such as these do not give answers as to how to handle a particular situation, but provide a useful framework for understanding conflicts. When moral values are in conflict, the result may be an ethical dilemma or crisis. Sometimes, no good solution to a dilemma in medical ethics exists, and occasionally, the values of the medical community (i.e., the hospital and its staff) conflict with the values of the individual patient, family, or larger non-medical community. Conflicts can also arise between health care providers, or among family members. For example, some argue that the principles of autonomy and beneficence clash when patients refuse blood transfusions, considering them life-saving; and truth-telling was not emphasized to a large extent before the HIV era.

Prehistoric medicine incorporated plants (herbalism), animal parts, and minerals. In many cases these materials were used ritually as magical substances by priests, shamans, or medicine men. Well-known spiritual systems include animism (the notion of inanimate objects having spirits), spiritualism (an appeal to gods or communion with ancestor spirits); shamanism (the vesting of an individual with mystic powers); and divination (magically obtaining the truth). The field of medical anthropology examines the ways in which culture and society are organized around or impacted by issues of health, health care and related issues.

Early records on medicine have been discovered from ancient Egyptian medicine, Babylonian Medicine, Ayurvedic medicine (in the Indian subcontinent), classical Chinese medicine (predecessor to the modern traditional Chinese Medicine), and ancient Greek medicine and Roman medicine.

In Egypt, Imhotep (3rd millennium BC) is the first physician in history known by name. The oldest Egyptian medical text is the Kahun Gynaecological Papyrus from around 2000 BCE, which describes gynaecological diseases. The Edwin Smith Papyrus dating back to 1600 BCE is an early work on surgery, while the Ebers Papyrus dating back to 1500 BCE is akin to a textbook on medicine.[24]

In China, archaeological evidence of medicine in Chinese dates back to the Bronze Age Shang Dynasty, based on seeds for herbalism and tools presumed to have been used for surgery.[25] The Huangdi Neijing, the progenitor of Chinese medicine, is a medical text written beginning in the 2nd century BCE and compiled in the 3rd century.[26]

In India, the surgeon Sushruta described numerous surgical operations, including the earliest forms of plastic surgery.[27][dubious discuss][28][29] Earliest records of dedicated hospitals come from Mihintale in Sri Lanka where evidence of dedicated medicinal treatment facilities for patients are found.[30][31]

In Greece, the Greek physician Hippocrates, the "father of western medicine",[32][33] laid the foundation for a rational approach to medicine. Hippocrates introduced the Hippocratic Oath for physicians, which is still relevant and in use today, and was the first to categorize illnesses as acute, chronic, endemic and epidemic, and use terms such as, "exacerbation, relapse, resolution, crisis, paroxysm, peak, and convalescence".[34][35] The Greek physician Galen was also one of the greatest surgeons of the ancient world and performed many audacious operations, including brain and eye surgeries. After the fall of the Western Roman Empire and the onset of the Early Middle Ages, the Greek tradition of medicine went into decline in Western Europe, although it continued uninterrupted in the Eastern Roman (Byzantine) Empire.

Most of our knowledge of ancient Hebrew medicine during the 1stmillenniumBC comes from the Torah, i.e.the Five Books of Moses, which contain various health related laws and rituals. The Hebrew contribution to the development of modern medicine started in the Byzantine Era, with the physician Asaph the Jew.[36]

After 750 CE, the Muslim world had the works of Hippocrates, Galen and Sushruta translated into Arabic, and Islamic physicians engaged in some significant medical research. Notable Islamic medical pioneers include the Persian polymath, Avicenna, who, along with Imhotep and Hippocrates, has also been called the "father of medicine".[37] He wrote The Canon of Medicine, considered one of the most famous books in the history of medicine.[38] Others include Abulcasis,[39]Avenzoar,[40]Ibn al-Nafis,[41] and Averroes.[42]Rhazes[43] was one of the first to question the Greek theory of humorism, which nevertheless remained influential in both medieval Western and medieval Islamic medicine.[44]Al-Risalah al-Dhahabiah by Ali al-Ridha, the eighth Imam of Shia Muslims, is revered as the most precious Islamic literature in the Science of Medicine.[45] The Persian Bimaristan hospitals were an early example of public hospitals.[46][47]

In Europe, Charlemagne decreed that a hospital should be attached to each cathedral and monastery and the historian Geoffrey Blainey likened the activities of the Catholic Church in health care during the Middle Ages to an early version of a welfare state: "It conducted hospitals for the old and orphanages for the young; hospices for the sick of all ages; places for the lepers; and hostels or inns where pilgrims could buy a cheap bed and meal". It supplied food to the population during famine and distributed food to the poor. This welfare system the church funded through collecting taxes on a large scale and possessing large farmlands and estates. The Benedictine order was noted for setting up hospitals and infirmaries in their monasteries, growing medical herbs and becoming the chief medical care givers of their districts, as at the great Abbey of Cluny. The Church also established a network of cathedral schools and universities where medicine was studied. The Schola Medica Salernitana in Salerno, looking to the learning of Greek and Arab physicians, grew to be the finest medical school in Medieval Europe.[48]

However, the fourteenth and fifteenth century Black Death devastated both the Middle East and Europe, and it has even been argued that Western Europe was generally more effective in recovering from the pandemic than the Middle East.[49] In the early modern period, important early figures in medicine and anatomy emerged in Europe, including Gabriele Falloppio and William Harvey.

The major shift in medical thinking was the gradual rejection, especially during the Black Death in the 14th and 15th centuries, of what may be called the 'traditional authority' approach to science and medicine. This was the notion that because some prominent person in the past said something must be so, then that was the way it was, and anything one observed to the contrary was an anomaly (which was paralleled by a similar shift in European society in general see Copernicus's rejection of Ptolemy's theories on astronomy). Physicians like Vesalius improved upon or disproved some of the theories from the past. The main tomes used both by medicine students and expert physicians were Materia Medica and Pharmacopoeia.

Andreas Vesalius was the author of De humani corporis fabrica, an important book on human anatomy.[50] Bacteria and microorganisms were first observed with a microscope by Antonie van Leeuwenhoek in 1676, initiating the scientific field microbiology.[51] Independently from Ibn al-Nafis, Michael Servetus rediscovered the pulmonary circulation, but this discovery did not reach the public because it was written down for the first time in the "Manuscript of Paris"[52] in 1546, and later published in the theological work for which he paid with his life in 1553. Later this was described by Renaldus Columbus and Andrea Cesalpino. Herman Boerhaave is sometimes referred to as a "father of physiology" due to his exemplary teaching in Leiden and textbook 'Institutiones medicae' (1708). Pierre Fauchard has been called "the father of modern dentistry".[53]

Veterinary medicine was, for the first time, truly separated from human medicine in 1761, when the French veterinarian Claude Bourgelat founded the world's first veterinary school in Lyon, France. Before this, medical doctors treated both humans and other animals.

Modern scientific biomedical research (where results are testable and reproducible) began to replace early Western traditions based on herbalism, the Greek "four humours" and other such pre-modern notions. The modern era really began with Edward Jenner's discovery of the smallpox vaccine at the end of the 18th century (inspired by the method of inoculation earlier practiced in Asia), Robert Koch's discoveries around 1880 of the transmission of disease by bacteria, and then the discovery of antibiotics around 1900.

The post-18th century modernity period brought more groundbreaking researchers from Europe. From Germany and Austria, doctors Rudolf Virchow, Wilhelm Conrad Rntgen, Karl Landsteiner and Otto Loewi made notable contributions. In the United Kingdom, Alexander Fleming, Joseph Lister, Francis Crick and Florence Nightingale are considered important. Spanish doctor Santiago Ramn y Cajal is considered the father of modern neuroscience.

From New Zealand and Australia came Maurice Wilkins, Howard Florey, and Frank Macfarlane Burnet.

In the United States, William Williams Keen, William Coley, James D. Watson, Italy (Salvador Luria), Switzerland (Alexandre Yersin), Japan (Kitasato Shibasabur), and France (Jean-Martin Charcot, Claude Bernard, Paul Broca) and others did significant work. Russian Nikolai Korotkov also did significant work, as did Sir William Osler and Harvey Cushing.

As science and technology developed, medicine became more reliant upon medications. Throughout history and in Europe right until the late 18th century, not only animal and plant products were used as medicine, but also human body parts and fluids.[54]Pharmacology developed in part from herbalism and some drugs are still derived from plants (atropine, ephedrine, warfarin, aspirin, digoxin, vinca alkaloids, taxol, hyoscine, etc.).[55]Vaccines were discovered by Edward Jenner and Louis Pasteur.

The first antibiotic was arsphenamine (Salvarsan) discovered by Paul Ehrlich in 1908 after he observed that bacteria took up toxic dyes that human cells did not. The first major class of antibiotics was the sulfa drugs, derived by German chemists originally from azo dyes.

Pharmacology has become increasingly sophisticated; modern biotechnology allows drugs targeted towards specific physiological processes to be developed, sometimes designed for compatibility with the body to reduce side-effects. Genomics and knowledge of human genetics is having some influence on medicine, as the causative genes of most monogenic genetic disorders have now been identified, and the development of techniques in molecular biology and genetics are influencing medical technology, practice and decision-making.

Evidence-based medicine is a contemporary movement to establish the most effective algorithms of practice (ways of doing things) through the use of systematic reviews and meta-analysis. The movement is facilitated by modern global information science, which allows as much of the available evidence as possible to be collected and analyzed according to standard protocols that are then disseminated to healthcare providers. The Cochrane Collaboration leads this movement. A 2001 review of 160 Cochrane systematic reviews revealed that, according to two readers, 21.3% of the reviews concluded insufficient evidence, 20% concluded evidence of no effect, and 22.5% concluded positive effect.[56]

Traditional medicine (also known as indigenous or folk medicine) comprises knowledge systems that developed over generations within various societies before the era of modern medicine. The World Health Organization (WHO) defines traditional medicine as "the sum total of the knowledge, skills, and practices based on the theories, beliefs, and experiences indigenous to different cultures, whether explicable or not, used in the maintenance of health as well as in the prevention, diagnosis, improvement or treatment of physical and mental illness."[57]

In some Asian and African countries, up to 80% of the population relies on traditional medicine for their primary health care needs. When adopted outside of its traditional culture, traditional medicine is often called alternative medicine.[57] Practices known as traditional medicines include Ayurveda, Siddha medicine, Unani, ancient Iranian medicine, Irani, Islamic medicine, traditional Chinese medicine, traditional Korean medicine, acupuncture, Muti, If, and traditional African medicine.

The WHO notes however that "inappropriate use of traditional medicines or practices can have negative or dangerous effects" and that "further research is needed to ascertain the efficacy and safety" of several of the practices and medicinal plants used by traditional medicine systems.[57] The line between alternative medicine and quackery is a contentious subject.

Traditional medicine may include formalized aspects of folk medicine, that is to say longstanding remedies passed on and practised by lay people. Folk medicine consists of the healing practices and ideas of body physiology and health preservation known to some in a culture, transmitted informally as general knowledge, and practiced or applied by anyone in the culture having prior experience.[58] Folk medicine may also be referred to as traditional medicine, alternative medicine, indigenous medicine, or natural medicine. These terms are often considered interchangeable, even though some authors may prefer one or the other because of certain overtones they may be willing to highlight. In fact, out of these terms perhaps only indigenous medicine and traditional medicine have the same meaning as folk medicine, while the others should be understood rather in a modern or modernized context.[59]

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Steroid – Wikipedia

This article is about the family of polycyclic chemical compounds. For the drugs, also used as performance-enhancing substances, see Anabolic steroid. For the scientific journal, see Steroids (journal).

A steroid is an organic compound with four rings arranged in a specific configuration. Examples include the dietary lipid cholesterol, the sex hormones estradiol and testosterone[2]:1019 and the anti-inflammatory drug dexamethasone.[3] Steroids have two principal biological functions: certain steroids (such as cholesterol) are important components of cell membranes which alter membrane fluidity, and many steroids are signaling molecules which activate steroid hormone receptors.

The steroid core structure is composed of seventeen carbon atoms, bonded in four "fused" rings: three six-member cyclohexane rings (rings A, B and C in the first illustration) and one five-member cyclopentane ring (the D ring). Steroids vary by the functional groups attached to this four-ring core and by the oxidation state of the rings. Sterols are forms of steroids with a hydroxyl group at position three and a skeleton derived from cholestane.[1]:1785f[4] They can also vary more markedly by changes to the ring structure (for example, ring scissions which produce secosteroids such as vitamin D3).

Hundreds of steroids are found in plants, animals and fungi. All steroids are manufactured in cells from the sterols lanosterol (animals and fungi) or cycloartenol (plants). Lanosterol and cycloartenol are derived from the cyclization of the triterpene squalene.[5]

Space-filling representation

Ball-and-stick representation

Gonane, also known as steran or cyclopentaperhydrophenanthrene, the simplest steroid and the nucleus of all steroids and sterols,[6][7] is composed of seventeen carbon atoms in carbon-carbon bonds forming four fused rings in a three-dimensional shape. The three cyclohexane rings (A, B, and C in the first illustration) form the skeleton of a perhydro derivative of phenanthrene. The D ring has a cyclopentane structure. When the two methyl groups and eight carbon side chains (at C-17, as shown for cholesterol) are present, the steroid is said to have a cholestane framework. The two common 5 and 5 stereoisomeric forms of steroids exist because of differences in the side of the largely planar ring system where the hydrogen (H) atom at carbon-5 is attached, which results in a change in steroid A-ring conformation.

Examples of steroid structures are:

In addition to the ring scissions (cleavages), expansions and contractions (cleavage and reclosing to a larger or smaller rings)all variations in the carbon-carbon bond frameworksteroids can also vary:

For instance, sterols such as cholesterol and lanosterol have an hydroxyl group attached at position C-3, while testosterone and progesterone have a carbonyl (oxo substituent) at C-3; of these, lanosterol alone has two methyl groups at C-4 and cholesterol (with a C-5 to C-6 double bond) differs from testosterone and progesterone (which have a C-4 to C-5 double bond).

The following are some common categories of steroids. In eukaryotes, steroids are found in fungi, animals, and plants. Fungal steroids include the ergosterols.

Animal steroids include compounds of vertebrate and insect origin, the latter including ecdysteroids such as ecdysterone (controlling molting in some species). Vertebrate examples include the steroid hormones and cholesterol; the latter is a structural component of cell membranes which helps determine the fluidity of cell membranes and is a principal constituent of plaque (implicated in atherosclerosis). Steroid hormones include:

Plant steroids include steroidal alkaloids found in Solanaceae,[8] the phytosterols, and the brassinosteroids (which include several plant hormones). In prokaryotes, biosynthetic pathways exist for the tetracyclic steroid framework (e.g. in mycobacteria)[9] where its origin from eukaryotes is conjectured[10] and the more-common pentacyclic triterpinoid hopanoid framework.[11]

Steroids can be classified based on their chemical composition.[12] One example of how MeSH performs this classification is available at the Wikipedia MeSH catalog. Examples of this classification include:

The gonane (steroid nucleus) is the parent 17-carbon tetracyclic hydrocarbon molecule with no alkyl sidechains.[13]

Secosteroids (Latin seco, "to cut") are a subclass of steroidal compounds resulting, biosynthetically or conceptually, from scission (cleavage) of parent steroid rings (generally one of the four). Major secosteroid subclasses are defined by the steroid carbon atoms where this scission has taken place. For instance, the prototypical secosteroid cholecalciferol, vitamin D3 (shown), is in the 9,10-secosteroid subclass and derives from the cleavage of carbon atoms C-9 and C-10 of the steroid B-ring; 5,6-secosteroids and 13,14-steroids are similar.[14]

Norsteroids (nor-, L. norma; "normal" in chemistry, indicating carbon removal)[15] and homosteroids (homo-, Greek homos; "same", indicating carbon addition) are structural subclasses of steroids formed from biosynthetic steps. The former involves enzymic ring expansion-contraction reactions, and the latter is accomplished (biomimetically) or (more frequently) through ring closures of acyclic precursors with more (or fewer) ring atoms than the parent steroid framework.[16]

Combinations of these ring alterations are known in nature. For instance, ewes who graze on corn lily ingest cyclopamine (shown) and veratramine, two of a sub-family of steroids where the C- and D-rings are contracted and expanded respectively via a biosynthetic migration of the original C-13 atom. Ingestion of these C-nor-D-homosteroids results in birth defects in lambs: cyclopia from cyclopamine and leg deformity from veratramine.[17] A further C-nor-D-homosteroid (nakiterpiosin) is excreted by Okinawan cyanobacteriosponges Terpios hoshinota leading to coral mortality from black coral disease.[18] Nakiterpiosin-type steroids are active against the signaling pathway involving the smoothened and hedgehog proteins, a pathway which is hyperactive in a number of cancers.

Steroids and their metabolites often function as signalling molecules (the most notable examples are steroid hormones), and steroids and phospholipids are components of cell membranes. Steroids such as cholesterol decrease membrane fluidity.[19] Similar to lipids, steroids are highly concentrated energy stores. However, they are not typically sources of energy; in mammals, they are normally metabolized and excreted.

Steroids play critical roles in a number of disorders, including malignancies like Prostate Cancer, where steroid production inside and outside the tumour promotes cancer cell aggressiveness.[20]

Two classes of drugs target the mevalonate pathway: statins (used to reduce elevated cholesterol levels) and bisphosphonates (used to treat a number of bone-degenerative diseases).

The hundreds of steroids found in animals, fungi, and plants are made from lanosterol (in animals and fungi; see examples above) or cycloartenol (in plants). Lanosterol and cycloartenol derive from cyclization of the triterpenoid squalene.[5]

Steroid biosynthesis is an anabolic pathway which produces steroids from simple precursors. A unique biosynthetic pathway is followed in animals (compared to many other organisms), making the pathway a common target for antibiotics and other anti-infection drugs. Steroid metabolism in humans is also the target of cholesterol-lowering drugs, such as statins.

In humans and other animals the biosynthesis of steroids follows the mevalonate pathway, which uses acetyl-CoA as building blocks for dimethylallyl pyrophosphate (DMAPP) and isopentenyl pyrophosphate (IPP).[21][bettersourceneeded] In subsequent steps DMAPP and IPP join to form geranyl pyrophosphate (GPP), which synthesizes the steroid lanosterol. Modifications of lanosterol into other steroids are classified as steroidogenesis transformations.

The mevalonate pathway (also called HMG-CoA reductase pathway) begins with acetyl-CoA and ends with dimethylallyl pyrophosphate (DMAPP) and isopentenyl pyrophosphate (IPP).

DMAPP and IPP donate isoprene units, which are assembled and modified to form terpenes and isoprenoids[22] (a large class of lipids, which include the carotenoids and form the largest class of plant natural products.[23] Here, the isoprene units are joined to make squalene and folded into a set of rings to make lanosterol.[24]

Lanosterol can then be converted into other steroids, such as cholesterol and ergosterol.[24][25]

Steroidogenesis is the biological process by which steroids are generated from cholesterol and changed into other steroids.[27] The pathways of steroidogenesis differ among species. The major classes of steroid hormones, with prominent members and examples of related functions, are:

Human steroidogenesis occurs in a number of locations:

In plants and bacteria, the non-mevalonate pathway uses pyruvate and glyceraldehyde 3-phosphate as substrates.[22][30]

During diseases pathways otherwise not significant in healthy humans can become utilized. For example, in one form of congenital adrenal hyperplasia an deficiency in the 21-hydroxylase enzymatic pathway leads to an excess of 17-Hydroxyprogesterone (17-OHP) this pathological excess of 17-OHP in turn may be converted to dihydrotestosterone (DHT, a potent androgen) through among others 17,20 Lyase (a member of the cytochrome P450 family of enzymes), 5-Reductase and 3-Hydroxysteroid dehydrogenase.[31]

Steroids are primarily oxidized by cytochrome P450 oxidase enzymes, such as CYP3A4. These reactions introduce oxygen into the steroid ring, allowing the cholesterol to be broken up by other enzymes into bile acids.[32] These acids can then be eliminated by secretion from the liver in bile.[33] The expression of the oxidase gene can be upregulated by the steroid sensor PXR when there is a high blood concentration of steroids.[34] Steroid hormones, lacking the side chain of cholesterol and bile acids, are typically hydroxylated at various ring positions or oxidized at the 17 position, conjugated with sulfate or glucuronic acid and excreted in the urine.[35]

Steroid isolation, depending on context, is the isolation of chemical matter required for chemical structure elucidation, derivitzation or degradation chemistry, biological testing, and other research needs (generally milligrams to grams, but often more[36] or the isolation of "analytical quantities" of the substance of interest (where the focus is on identifying and quantifying the substance (for example, in biological tissue or fluid). The amount isolated depends on the analytical method, but is generally less than one microgram.[37][pageneeded] The methods of isolation to achieve the two scales of product are distinct, but include extraction, precipitation, adsorption, chromatography, and crystallization. In both cases, the isolated substance is purified to chemical homogeneity; combined separation and analytical methods, such as LC-MS, are chosen to be "orthogonal"achieving their separations based on distinct modes of interaction between substance and isolating matrixto detect a single species in the pure sample. Structure determination refers to the methods to determine the chemical structure of an isolated pure steroid, using an evolving array of chemical and physical methods which have included NMR and small-molecule crystallography.[2]:1019Methods of analysis overlap both of the above areas, emphasizing analytical methods to determining if a steroid is present in a mixture and determining its quantity.[37]

Microbial catabolism of phytosterol side chains yields C-19 steroids, C-22 steroids, and 17-ketosteroids (i.e. precursors to adrenocortical hormones and contraceptives).[38][39][40][41] The addition and modification of functional groups is key when producing the wide variety of medications available within this chemical classification. These modifications are performed using conventional organic synthesis and/or biotransformation techniques.[42][43]

The semisynthesis of steroids often begins from precursors such as cholesterol,[41]phytosterols,[40] or sapogenins.[44] The efforts of Syntex, a company involved in the Mexican barbasco trade, used Dioscorea mexicana to produce the sapogenin diosgenin in the early days of the synthetic steroid pharmaceutical industry.[36]

Some steroidal hormones are economically obtained only by total synthesis from petrochemicals (e.g. 13-alkyl steroids).[41] For example, the pharmaceutical Norgestrel begins from Methoxy-1-tetralone, a petrochemical derived from phenol.

A number of Nobel Prizes have been awarded for steroid research, including:

Steroid signaling



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DIM for Hormone Balance –

DIM (diindolylmethane), is a food-based compound found in cruciferous vegetables like broccoli, cabbage, cauliflower and Brussels sprouts.Studies have shown that it has the ability to reduce the risk of certain cancers, especiallythose influenced by excessive estrogen levels, such as breast, uterine and prostate. DIM can also stimulatefat breakdown and encourage an increase in muscle mass. I can attest, through my own personal experience supplementing with DIM as well as that of quite a few clients (both male and female), that DIM effectively modulates estrogen metabolism helping to do away with uncomfortable symptoms of PMS, perimenopause and prostate issues.

The following excerpt comes from Dr. Scott Rollins, MD, founder and Medical Director at the Integrative Medicine Center of Western Colorado ( Thisis a very well-written and comprehensive account of the effects of DIM and how to best use this supplement to make the most out of its incredible benefits:

Lower your risk of cancer, help lose weight and build muscle all remarkable benefits of a simple food supplement called DIM. For men or women, DIM is something to consider as part of an overall supplement program.

DIM, or diindolylmethane, is a plant based compound found in cruciferous vegetables, such as brussel sprouts,cabbage, broccoli and cauliflower. DIM has been shown in studies to reduce the risk of certain cancers, especiallythose driven by abnormally high estrogen levels, such as breast, uterus and prostate cancer. DIM can also stimulate the breakdown of fat while encouraging muscle development.

Estrogen hormones are naturally found in men and women and have many benefits such as preserving artery healthand brain function while fighting oxidative free radical damage. Higher estrogen levels found in women cause thefemale body shape with breast and hip development. Many women are estrogen dominant however, meaning theyhave too much estrogen accumulating in the body for the complementary progesterone to balance.

Natural estrogen dominance occurs as women near menopause, starting even ten years prior to menopause, where theyoften dont make as much progesterone to balance their estrogen. Symptoms such breast pain, water retention, heavypainful menstrual cycles, or irritable anxious moods are typical bothersome symptoms. Estrogens over-stimulation ofbreasts and uterus tissue can lead to breast cysts or adenomas and uterine growths both unpleasant and potentiallydangerous physical outcomes are too often accompanied by worrisome mammograms and hysterectomies.

Some women have estrogen dominance throughout their life for various reasons, such as low thyroid, high cortisol,exposure to environmental estrogen-like chemicals, or impaired detoxification pathways for estrogen.

Men often suffer from estrogen overload as well. With normal aging our testosterone levels drop as the conversion toestrogen increases, leading to a falling ratio of testosterone to estrogen. Higher estrogen levels in men lead to weightgain, loss of muscle mass, feminization of the body, further decreases in already falling testosterone levels, andincrease the risk of diseases such as heart disease and prostate cancer. The enzyme that normally converts testosteroneto estrogen is most abundant in fat, so as men put on weight the cycle of falling testosterone and rising estrogen simply picks up steam!

There are two main pathways in the liver for our estrogen to be normally metabolized and excreted. One pathwayleads to very good metabolites called 2-hydroxy estrogens. The other pathway leads to bad metabolites called 4 or 16-hydroxy estrogens. DIM stimulates the favorable 2-hydroxy pathway for estrogen metabolism and this is how DIMworks to improve our health.DIM is not a hormone, nor is it a hormone replacement. It is a plant compound that will improve our hormonebalance. By improving the metabolism of our natural estrogens DIM will help lower high levels of estrogen in thebody. This alone can help remedy estrogen dominant conditions and restore a healthy estrogen/testosterone ratio inmen and women.The favorable 2-hydroxy metabolites promoted by DIM are potent anti-oxidants and help prevent muscle breakdownafter exercise, as evidenced by female athletes having less muscle tissue breakdown after intense exercise than men.By reducing the estrogen dominance and also reducing the accumulation of cancer-promoting 4/16-hydroxymetabolites DIM can help lower the risk of cancer.The 2-hydroxy metabolites help increase the active testosterone levels in men and women by displacing inactiveprotein-bound testosterone to its active free portion. This leads to significant improvements in the ability to buildmuscle and enjoy the benefits of testosterone including better mood, increased stamina, endurance, sex drive anderectile function.The accumulation of fat around the belly, hips and buttocks is partly due to excess estrogen levels combined withfalling testosterone levels. DIM will help lower excess estrogen and promote the fat-burning 2-hydroxy metabolites.This can help you achieve a leaner body with less body fat.

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Hormonal Imbalance Anxiety a Precursor to Other Health …

Leslie Carol Botha: I originally posted this article in 2009. Thought it was well-written then and still think so. However, in the past two weeks readers of my blog have dug back into the HHH archives and have commented on their own hormonal anxiety so I decided to repost it in June 2012. Now 288 posts later it appears that hormone imbalance has become a silent epidemic affecting women of all ages.

Hormone imbalance -in the form of estrogen dominance which can cause hormone-related anxiety, insomnia, weight gain, emotional rage, phobias, and diabetes is due to the plastics in our environment. throw out all of your plastic water bottles they contain high amounts of estrogen mimickers, AND DO NOT MICROWAVE IN PLASTIC. Estrogen mimickers are found in food, household chemicals and our water supply from the high amounts of synthetic estrogen being excreted into the water streams from synthetic birth control and HRT. I kid you not. There have been plenty of articles about fishing changing their sex because of excreted hormones.

Lastly we are now 3 to 4 generations into synthetic hormone suppression, i.e., birth control (pills, IUDs implants, injections, rings, and patches). All of the estrogen is being built up in the body and passed in-utero to the fetus. So you will note many young women who have posted comments about hormone imbalance too. This is sad. We are upsetting the hormone chemical balance in the body. Women are suffering. And if we do not correct the imbalance it will only get worse. Such is the nature of not taking care of our health.

I believe that most women experience hormonal anxiety in one form or another. Unfortunately, the medical and psychiatric professions are quick to diagnosis and label with syndromes and then proceed to treat with drugs.

Now we know that source of this misdiagnosis is, in most cases hormone imbalance it can be corrected through nutritional supplementation, and hormone balancing. Most women are estrogen dependent. I have been recommending Progessence Plus that contains a wild yam extract infused with essential oils that repair the DNA and clear off the receptor sites on our cells so that the natural progesterone can be absorbed into the cell and not remain in fatty tissue of the body. By Shelly Mcrae, eHow Editor


Everyone experiences anxiety at one point or another, such as before an important test in school, an important presentation at work, during the holidays or when experiencing a crisis of any kind. Anxiety in these instances help you stay alert, focus on tasks at hand or make quick decisions.

But when anxiety turns into an ongoing sense of apprehension, or begins to manifest as debilitating fear, it may be due to personality disorder or a hormonal imbalance. Its important to determine the cause of your anxiety and determine how to treat it.

When these fears and paranoid thoughts manifest themselves and then fade within 30 minutes or so, it is referred to as a panic attack. You may be so overwhelmed by the mental and physical symptoms that you feel unable to go on and instead try to escape, literally going home or someplace you feel safe. In such cases, you may have a personality disorder.

In cases in which hormonal imbalances are the root cause, as opposed to a personality disorder, the anxiety may not be so severe as to be labeled a panic attack. Rather, it more closely resembles mood swings or depression. But rather than feeling sad or irritable, you feel apprehension and uneasiness.

Anxiety induced by hormonal imbalances, such as estrogen dominance in which the level of the hormone progesterone is very low, differs from those panic attacks associated with personality disorders such as bipolar or obsessive-compulsive disorders. But there are also similarities. Determining the root cause of the anxiety can determine which treatment is appropriate.

The inability to control the onslaught of negative thoughts is symptomatic in both panic attacks and anxiety. Anxiety, though, may be more consistent and you may display fewer physical symptoms. You may feel that it is all in your head.

The sense of anxiety may not be as exaggerated as for those suffering from personality disorders. Instead, you may feel uneasy in social situations, be reluctant to make decisions or continually worry over problems that are relatively minor.

But your anxiety may not be limited to the more subtle form. In cases of severe hormonal imbalance, you may suffer full-blown panic attacks in which fear, though irrational, overwhelms your reasoning. You may be unable to explain why you are reacting to a simple incident as if it were a life crisis.

One of the characteristics of both panic attack and anxiety due to hormonal imbalances is the levels of cortisol in the system. Cortisol is the chemical released by the adrenals that activates the fight or flight response.The hypothalamic-pituitary-adrenal (HPA) axis is the hormonal system that controls your mood. If you suffer from a hormonal imbalance, this system may go into overdrive. The result is that your body and mind will believe a threatening situation exists, which in turn results in feelings of apprehension, fear and dread.

Treatments for hormonal imbalance range from basic lifestyle changes to replacement hormone therapy. Bioidentical hormones, which are naturally occurring hormones found in plants and synthesized for human consumption, are a common treatment when anxiety is one of the symptoms of hormonal imbalance.

In the case of severe panic attacks, such medications as benzodiazepines and antidepressants may be necessary to control the attacks. These are common treatments for personality disorders. (I DO NOT AGREE WITH THIS STATEMENT. LB.)

Left untreated, mild anxiety can worsen, resulting in debilitating behavior patterns due to unwarranted fear. Whether the underlying cause is personality disorder or hormonal imbalance, effective treatment is available.

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Endocrinology – Wikipedia

Endocrinology (from Greek , endon, "within"; , krn, "to separate"; and -, -logia) is a branch of biology and medicine dealing with the endocrine system, its diseases, and its specific secretions known as hormones. It is also concerned with the integration of developmental events proliferation, growth, and differentiation, and the psychological or behavioral activities of metabolism, growth and development, tissue function, sleep, digestion, respiration, excretion, mood, stress, lactation, movement, reproduction, and sensory perception caused by hormones. Specializations include behavioral endocrinology[1][2][3] and comparative endocrinology.

The endocrine system consists of several glands, all in different parts of the body, that secrete hormones directly into the blood rather than into a duct system. Hormones have many different functions and modes of action; one hormone may have several effects on different target organs, and, conversely, one target organ may be affected by more than one hormone.

Examples of amine hormones

Endocrinology is the study of the endocrine system in the human body. This is a system of glands which secrete hormones. Hormones are chemicals which affect the actions of different organ systems in the body. Examples include thyroid hormone, growth hormone, and insulin. The endocrine system involves a number of feedback mechanisms, so that often one hormone (such as thyroid stimulating hormone) will control the action or release of another secondary hormone (such as thyroid hormone). If there is too much of the secondary hormone, it may provide negative feedback to the primary hormone, maintaining homeostasis.

In the original 1902 definition by Bayliss and Starling (see below), they specified that, to be classified as a hormone, a chemical must be produced by an organ, be released (in small amounts) into the blood, and be transported by the blood to a distant organ to exert its specific function. This definition holds for most "classical" hormones, but there are also paracrine mechanisms (chemical communication between cells within a tissue or organ), autocrine signals (a chemical that acts on the same cell), and intracrine signals (a chemical that acts within the same cell).[4] A neuroendocrine signal is a "classical" hormone that is released into the blood by a neurosecretory neuron (see article on neuroendocrinology).

Examples of steroid hormones

Griffin and Ojeda identify three different classes of hormone based on their chemical composition:[5]

Amines, such as norepinephrine, epinephrine, and dopamine (catecholamines), are derived from single amino acids, in this case tyrosine. Thyroid hormones such as 3,5,3-triiodothyronine (T3) and 3,5,3,5-tetraiodothyronine (thyroxine, T4) make up a subset of this class because they derive from the combination of two iodinated tyrosine amino acid residues.

Peptide hormones and protein hormones consist of three (in the case of thyrotropin-releasing hormone) to more than 200 (in the case of follicle-stimulating hormone) amino acid residues and can have a molecular mass as large as 30,000 grams per mole. All hormones secreted by the pituitary gland are peptide hormones, as are leptin from adipocytes, ghrelin from the stomach, and insulin from the pancreas.

Steroid hormones are converted from their parent compound, cholesterol. Mammalian steroid hormones can be grouped into five groups by the receptors to which they bind: glucocorticoids, mineralocorticoids, androgens, estrogens, and progestogens. Some forms of vitamin D, such as calcitriol, are steroid-like and bind to homologous receptors, but lack the characteristic fused ring structure of true steroids.

Although every organ system secretes and responds to hormones (including the brain, lungs, heart, intestine, skin, and the kidney), the clinical specialty of endocrinology focuses primarily on the endocrine organs, meaning the organs whose primary function is hormone secretion. These organs include the pituitary, thyroid, adrenals, ovaries, testes, and pancreas.

An endocrinologist is a physician who specializes in treating disorders of the endocrine system, such as diabetes, hyperthyroidism, and many others (see list of diseases below).

The medical specialty of endocrinology involves the diagnostic evaluation of a wide variety of symptoms and variations and the long-term management of disorders of deficiency or excess of one or more hormones.

The diagnosis and treatment of endocrine diseases are guided by laboratory tests to a greater extent than for most specialties. Many diseases are investigated through excitation/stimulation or inhibition/suppression testing. This might involve injection with a stimulating agent to test the function of an endocrine organ. Blood is then sampled to assess the changes of the relevant hormones or metabolites. An endocrinologist needs extensive knowledge of clinical chemistry and biochemistry to understand the uses and limitations of the investigations.

A second important aspect of the practice of endocrinology is distinguishing human variation from disease. Atypical patterns of physical development and abnormal test results must be assessed as indicative of disease or not. Diagnostic imaging of endocrine organs may reveal incidental findings called incidentalomas, which may or may not represent disease.

Endocrinology involves caring for the person as well as the disease. Most endocrine disorders are chronic diseases that need lifelong care. Some of the most common endocrine diseases include diabetes mellitus, hypothyroidism and the metabolic syndrome. Care of diabetes, obesity and other chronic diseases necessitates understanding the patient at the personal and social level as well as the molecular, and the physicianpatient relationship can be an important therapeutic process.

Apart from treating patients, many endocrinologists are involved in clinical science and medical research, teaching, and hospital management.

Endocrinologists are specialists of internal medicine or pediatrics. Reproductive endocrinologists deal primarily with problems of fertility and menstrual functionoften training first in obstetrics. Most qualify as an internist, pediatrician, or gynecologist for a few years before specializing, depending on the local training system. In the U.S. and Canada, training for board certification in internal medicine, pediatrics, or gynecology after medical school is called residency. Further formal training to subspecialize in adult, pediatric, or reproductive endocrinology is called a fellowship. Typical training for a North American endocrinologist involves 4 years of college, 4 years of medical school, 3 years of residency, and 2 years of fellowship. In the US, adult endocrinologists are board certified by the American Board of Internal Medicine (ABIM) or the American Osteopathic Board of Internal Medicine (AOBIM) in Endocrinology, Diabetes and Metabolism.

Endocrinology also involves study of the diseases of the endocrine system. These diseases may relate to too little or too much secretion of a hormone, too little or too much action of a hormone, or problems with receiving the hormone.

Because endocrinology encompasses so many conditions and diseases, there are many organizations that provide education to patients and the public. The Hormone Foundation is the public education affiliate of The Endocrine Society and provides information on all endocrine-related conditions. Other educational organizations that focus on one or more endocrine-related conditions include the American Diabetes Association, Human Growth Foundation, American Menopause Foundation, Inc., and Thyroid Foundation of America.

In North America the principal professional organizations of endocrinologists include The Endocrine Society,[6] the American Association of Clinical Endocrinologists,[7] the American Diabetes Association,[8] the Lawson Wilkins Pediatric Endocrine Society,[9] and the American Thyroid Association.[10]

In the United Kingdom, the Society for Endocrinology[11] and the British Society for Paediatric Endocrinology and Diabetes[12] are the main professional organisations. The European Society for Paediatric Endocrinology[13] is the largest international professional association dedicated solely to paediatric endocrinology. There are numerous similar associations around the world.

The earliest study of endocrinology began in China.[14] The Chinese were isolating sex and pituitary hormones from human urine and using them for medicinal purposes by 200 BCE.[14] They used many complex methods, such as sublimation of steroid hormones.[14] Another method specified by Chinese textsthe earliest dating to 1110specified the use of saponin (from the beans of Gleditschia sinensis) to extract hormones, but gypsum (containing calcium sulfate) was also known to have been used.[14]

Although most of the relevant tissues and endocrine glands had been identified by early anatomists, a more humoral approach to understanding biological function and disease was favoured by the ancient Greek and Roman thinkers such as Aristotle, Hippocrates, Lucretius, Celsus, and Galen, according to Freeman et al.,[15] and these theories held sway until the advent of germ theory, physiology, and organ basis of pathology in the 19th century.

In 1849, Arnold Berthold noted that castrated cockerels did not develop combs and wattles or exhibit overtly male behaviour.[16] He found that replacement of testes back into the abdominal cavity of the same bird or another castrated bird resulted in normal behavioural and morphological development, and he concluded (erroneously) that the testes secreted a substance that "conditioned" the blood that, in turn, acted on the body of the cockerel. In fact, one of two other things could have been true: that the testes modified or activated a constituent of the blood or that the testes removed an inhibitory factor from the blood. It was not proven that the testes released a substance that engenders male characteristics until it was shown that the extract of testes could replace their function in castrated animals. Pure, crystalline testosterone was isolated in 1935.[17]

The Graves' disease was named after Irish doctor Robert James Graves,[18] who described a case of goiter with exophthalmos in 1835. The German Karl Adolph von Basedow also independently reported the same constellation of symptoms in 1840, while earlier reports of the disease were also published by the Italians Giuseppe Flajani and Antonio Giuseppe Testa, in 1802 and 1810 respectively,[19] and by the English physician Caleb Hillier Parry (a friend of Edward Jenner) in the late 18th century.[20]Thomas Addison was first to describe Addison's disease in 1849.[21]

In 1902 William Bayliss and Ernest Starling performed an experiment in which they observed that acid instilled into the duodenum caused the pancreas to begin secretion, even after they had removed all nervous connections between the two.[22] The same response could be produced by injecting extract of jejunum mucosa into the jugular vein, showing that some factor in the mucosa was responsible. They named this substance "secretin" and coined the term hormone for chemicals that act in this way.

Joseph von Mering and Oskar Minkowski made the observation in 1889 that removing the pancreas surgically led to an increase in blood sugar, followed by a coma and eventual deathsymptoms of diabetes mellitus. In 1922, Banting and Best realized that homogenizing the pancreas and injecting the derived extract reversed this condition.[23] The hormone responsible, insulin, was not discovered until Frederick Sanger sequenced it in 1953.

Neurohormones were first identified by Otto Loewi in 1921.[24] He incubated a frog's heart (innervated with its vagus nerve attached) in a saline bath, and left in the solution for some time. The solution was then used to bathe a non-innervated second heart. If the vagus nerve on the first heart was stimulated, negative inotropic (beat amplitude) and chronotropic (beat rate) activity were seen in both hearts. This did not occur in either heart if the vagus nerve was not stimulated. The vagus nerve was adding something to the saline solution. The effect could be blocked using atropine, a known inhibitor to heart vagal nerve stimulation. Clearly, something was being secreted by the vagus nerve and affecting the heart. The "vagusstuff" (as Loewi called it) causing the myotropic (muscle enhancing) effects was later identified to be acetylcholine and norepinephrine. Loewi won the Nobel Prize for his discovery.

Recent work in endocrinology focuses on the molecular mechanisms responsible for triggering the effects of hormones. The first example of such work being done was in 1962 by Earl Sutherland. Sutherland investigated whether hormones enter cells to evoke action, or stayed outside of cells. He studied norepinephrine, which acts on the liver to convert glycogen into glucose via the activation of the phosphorylase enzyme. He homogenized the liver into a membrane fraction and soluble fraction (phosphorylase is soluble), added norepinephrine to the membrane fraction, extracted its soluble products, and added them to the first soluble fraction. Phosphorylase activated, indicating that norepinephrine's target receptor was on the cell membrane, not located intracellularly. He later identified the compound as cyclic AMP (cAMP) and with his discovery created the concept of second-messenger-mediated pathways. He, like Loewi, won the Nobel Prize for his groundbreaking work in endocrinology.[25]

Read more here:
Endocrinology - Wikipedia

Bioidentical Hormones: Dr. John R. Lee’s Three Rules for BHRT

Use a sprinkle of common sense and a dash of logic.

by John R. Lee, M.D.

The recent Lancet publication of the Million Women Study (MWS) removes any lingering doubt that there's something wrong with conventional HRT (see Million Woman Study in the UK, Published in The Lancet, Gives New Insight into HRT and Breast Cancer for details). Why would supplemental estrogen and a progestin (e.g. not real progesterone) increase a woman's risk of breast cancer by 30 percent or more? Other studies found that these same synthetic HRT hormones increase one's risk of heart disease and blood clots (strokes), and do nothing to prevent Alzheimer's disease. When you pass through puberty and your sex hormones surge, they don't make you sickthey cause your body to mature into adulthood and be healthy. But, the hormones used in conventional HRT are somehow not rightthey are killing women by the tens of thousands.

The question iswhere do we go from here? My answer iswe go back to the basics and find out where our mistake is. I have some ideas on that.

Over the years I have adopted a simple set of three rules covering hormone supplementation. When these rules are followed, women have a decreased risk of breast cancer, heart attacks, or strokes. They are much less likely to get fat, or have poor sleep, or short term memory loss, fibrocystic breasts, mood disorders or libido problems. And the rules are not complicated.

Rule 1. Give hormones only to those who are truly deficient in them.

The first rule is common sense. We don't give insulin to someone unless we have good evidence that they need it. The same is true of thyroid, cortisol and all our hormones. Yet, conventional physicians routinely prescribe estrogen or other sex hormones without ever testing for hormone deficiency. Conventional medicine assumes that women after menopause are estrogen-deficient. This assumption is false. Twenty-five years ago I reviewed the literature on hormone levels before and after menopause, and all authorities agreed that over two-thirds (66 percent) of women up to age 80 continue to make all the estrogen they need. Since then, the evidence has become stronger. Even with ovaries removed, women make estrogen, primarily by an aromatase enzyme in body fat and breasts that converts an adrenal hormone, androstenedione, into estrone. Women with plenty of body fat may make more estrogen after menopause than skinny women make before menopause.

Breast cancer specialists are so concerned about all the estrogen women make after menopause that they now use drugs to block the aromatase enzyme. Consider the irony: some conventional physicians are prescribing estrogens to treat a presumed hormone deficiency in postmenopausal women, while others are prescribing drugs that block estrogen production in postmenopausal women.

How does one determine if estrogen deficiency exists? Any woman still having monthly periods has plenty of estrogen. Vaginal dryness and vaginal mucosal atrophy, on the other hand, are clear signs of estrogen deficiency. Lacking these signs, the best test is the saliva hormone assay. With new and better technology, saliva hormone testing has become accurate and reliable. As might be expected, we have learned that hormone levels differ between individuals; what is normal for one person is not necessarily normal for another. Further, one must be aware that hormones work within a complex network of other hormones and metabolic mediators, something like different musicians in an orchestra. To interpret a hormone s level, one must consider not only its absolute level but also its relative ratios with other hormones that include not only estradiol, progesterone and testosterone, but cortisol and thyroid as well.

For example, in healthy women without breast cancer, we find that the saliva progesterone level routinely is 200 to 300 times greater than the saliva estradiol level. In women with breast cancer, the saliva progesterone/estradiol ratio is considerably less than 200 to 1. As more investigators become more familiar with saliva hormone tests, I believe these various ratios will become more and more useful in monitoring hormone supplements.

Serum or plasma blood tests for steroid hormones should be abandonedthe results so obtained are essentially irrelevant. Steroid hormones are extremely lipophilic (fat-loving) and are not soluble in serum. Steroid hormones carry their message to cells by leaving the blood flow at capillaries to enter cells where they bond with specific hormone receptors in order to convey their message to the cells. These are called free hormones. When eventually they circulate through the liver, they become protein-bound (enveloped by specific globulins or albumin), a process that not only seriously impedes their bioavailability but also makes them water soluble, thus facilitating their excretion in urine. Measuring the concentration of these non-bioavailable forms in urine or serum is irrelevant since it provides no clue as to the concentration of the more clinically significant free (bioavailable) hormone in the blood stream.

When circulating through saliva glands, the free nonprotein-bound steroid hormone diffuses easily from blood capillaries into the saliva gland and then into saliva. Protein-bound, non-bioavailable hormones do not pass into or through the saliva gland. Thus, saliva testing is far superior to serum or urine testing in measuring bioavailable hormone levels.

Serum testing is fine for glucose and proteins but not for measuring free steroid hormones. Fifty years of blood tests have led to the great confusion that now befuddles conventional medicine in regard to steroid hormone supplementation.

Rule 2. Use bioidentical hormones rather than synthetic hormones.

The second rule is also just common sense. The message of steroid hormones to target tissue cells requires bonding of the hormone with specific unique receptors in the cells. The bonding of a hormone to its receptor is determined by its molecular configuration, like a key is for a lock. Synthetic hormone molecules and molecules from different species (e.g. Premarin, which is from horses) differ in molecular configuration from endogenous (made in the body) hormones. From studies of petrochemical xenohormones, we learn that substitute synthetic hormones differ in their activity at the receptor level. In some cases, they will activate the receptor in a manner similar to the natural hormone, but in other cases the synthetic hormone will have no effect or will block the receptor completely. Thus, hormones that are not bioidentical do not provide the same total physiologic activity as the hormones they are intended to replace, and all will provoke undesirable side effects not found with the human hormone. Human insulin, for example, is preferable to pig insulin. Sex hormones identical to human (bioidentical) hormones have been available for over 50 years.

Pharmaceutical companies, however, prefer synthetic hormones. Synthetic hormones (not found in nature) can be patented, whereas real (natural, bioidentical) hormones can not. Patented drugs are more profitable than non-patented drugs. Sex hormone prescription sales have made billions of dollars for pharmaceutical companies Thus is women's health sacrificed for commercial profit.

Rule 3. Use only in dosages that provide normal physiologic tissue levels.

The third rule is a bit more complicated. Everyone would agree, I think, that dosages of hormone supplements should restore normal physiologic levels. The question ishow do you define normal physiologic levels? Hormones do not work by just floating around in circulating blood; they work by slipping out of blood capillaries to enter cells that have the proper receptors in them. As explained above, protein-bound hormones are unable to leave blood vessels and bond with intracellular receptors. They are non-bioavailable. But they are water-soluble, and thus found in serum, whereas the free bioavailable hormone is lipophilic and not water soluble, thus not likely to be found in serum. Serum tests do not help you measure the free, bioavailable form of the hormone. The answer is saliva testing.

It is quite simple to measure the change in saliva hormone levels when hormone supplementation is given. If more physicians did that, they would find that their usual estrogen dosages create estrogen levels 8 to 10 times greater than found in normal healthy people, and that progesterone levels are not raised by giving supplements of synthetic progestin such as medroxyprogesterone acetate (MPA).

Further, saliva levels (and not serum levels) of progesterone will clearly demonstrate excellent absorption of progesterone from transdermal creams. Transdermal progesterone enters the bloodstream fully bioavailable (i.e., without being protein-bound). The progesterone increase is readily apparent in saliva testing, whereas serum will show little or no change. In fact, any rise of serum progesterone after transdermal progesterone dosing is most often a sign of excessive progesterone dosage. Saliva testing helps determine optimal dosages of supplemented steroid hormones, something that serum testing cannot do.

It is important to note that conventional HRT violates all three of these rules for rational use of supplemental steroid hormones.

A 10-year French study of HRT using a low-dose estradiol patch plus oral progesterone shows no increased risk of breast cancer, strokes or heart attacks. Hormone replacement therapy is a laudable goal, but it must be done correctly. HRT based on correcting hormone deficiency and restoring proper physiologic balanced tissue levels, is proposed as a more sane, successful and safe technique.

Other Factors

Hormone imbalance is not the only cause of breast cancer, strokes, and heart attacks. Other risk factors of importance include the following:

Men share these risks equally with women. Hormone imbalance and exposure to these risk factors in men leads to earlier heart attacks, lower sperm counts and higher prostate cancer risk.


Conventional hormone replacement therapy (HRT) composed of either estrone or estradiol, with or without progestins (excluding progesterone) carries an unacceptable risk of breast cancer, heart attacks and strokes. I propose a more rational HRT using bioidentical hormones in dosages based on true needs as determined by saliva testing. In addition to proper hormone balancing, other important risk factors are described, all of which are potentially correctable. Combining hormone balancing with correction of other environmental and lifestyle factors is our best hope for reducing the present risks of breast cancer, strokes and heart attacks.

A much broader discussion of all these factors can be found in the updated and revised edition of What Your Doctor May Not Tell You About Menopause and What Your Doctor May Not Tell You About Breast Cancer.

More here:
Bioidentical Hormones: Dr. John R. Lee's Three Rules for BHRT

Man vs. Estrogen: It’s Not Just A Woman Thing! | Seasons …

Posted by Dr. Nathan Goodyear on June 5, 2012 45 Comments

Nathan Goodyear, M.D.

Testosterone is the defining hormone of a man.Estrogen is the defining hormone of a woman.

So when we talk about estrogen, its that word men whisper in secret when the women in their lives seem a little hormonal, right? When people find out that my wife and I have 3 daughters, the resulting comment is usually, Wow, thats a lot of estrogen in your household! (Thankfully, I have a son, too, who helps balance the estrogen to testosterone ratio at our house!)

Im sorry to burst your bubble, guys, but estrogen is not exclusive to women. We make estrogen, too.In fact, some of us make aLOTof estrogen. Too much, in fact. And it creates some serious problems.

But before we talk about estrogen, we need to talk about testosterone.Testosterone levels in American men are at an all-time low! There are four major reasons for that: stress, weight, endogenous estrogens, and xenoestrogens. In this post, Ill address three of those stress, weight, and endogenous estrogen.

So lets get started learning four important facts about testosterone, estrogen, and men!

What problems do high estrogen levels create in men?

1. High estrogen = low testosterone.One of the primary causes of low testosterone is a high estrogen level.Estrogens can be endogenous (produced by your body) or exogenous (from the environment, also known as xenoestrogens).Estradiol and Estrone (two of the three kinds of estrogen produced by your body) feed back to the hypothalamus and pituitary and shut off testosterone production.

2. High estrogen = inflammation.Not only do high estrogen levels decrease testosterone in men, they also increaseinflammation. And this is VERY significant.Inflammation, just like stress, is a biochemical process.

Inflammation is the natural result of the immune system.Remember the last time you got a paper cut? It was incredibly painful, probably red, warm and swollen, allcardinal symptoms of inflammation.Inflammation, in the right setting, is actually the body protecting itself. However, when the immune system becomesimbalancedorchronically activated, the immune system causes damage through inflammation. For example, chronically activated immune cells in the brain (glial cells) play a pivotal role in the development of Alzheimers, Parkinsons, and Multiple Sclerosis.

Inflammation is a SERIOUS issue.Chronic inflammation has been linked to many of the chronic diseases of aging: Type II Diabetes, obesity, hypertension, and cancer.In fact, a new term has been coined to describe inflammation arising from the gut which results in many of the above listed disease states metabolic endotoxemia.

Weve established that high estrogen levels are bad for men, shutting down testosterone production and causing chronic inflammation leading to disease.

What causes high estrogen levels in men?

1. High aromatase activity = high estrogen.First, high endogenous estrogen levels in men come fromhigh aromatase activity.Aromataseis the enzyme that converts androstenedione and testosterone into estrone and estradiol respectively. Aromatase is present in many different tissues. But in men aromatase is highly concentrated in thatmid-life bulge.

Unfortunately, aromatase activity in menincreasesas we age due to stress, weight gain, and inflammation. None of us are going to get away from aging (its right there with death and taxes). And who do you know that has NO stress? (Remember, it is estimated that 90% of doctor visits are stress-related.) Typically, as we age we gain weight and have more inflammation.

That age-related tire around the mid-section is more than just unsightly. It is a hormone and inflammation-producing organ.Remember metabolic endotoxemia, the disease-producing state I mentioned earlier? Metabolic endotoxemia is inflammation arising from the GI system whichcausesobesity and then turns right around andproducesinflammation. Its a vicious cycle! And guess what is concentrated in fat? If you guessed aromatase activity, then you are absolutely correct. Aromatase activity in men accounts for80%of estrogen production.

Hormones are not just about numbers, but balance and metabolism as well (readmy recent post on the topic).

2. Overdosage of testosterone = high estrogen.As mentioned earlier, testosterone levels in men are at an all-time low. And the mass solution for this problem with most physicians is to increase testosterone without evaluating or treating the underlying causes for low testosterone. Unfortunately, this complicates the entire low testosterone problem. Overdosage of testosterone increases estrogen production.

What? You mean you can dose too high on testosterone? Yes, andmost of the patients I see who are being treated with testosterone have been, in fact,overdosed.

In fact, at Seasons Wellness Clinic and Seasons of Farragut, we have seen many men must donate blood due to excess production of hemoglobin and hematocrit, a by-product of testosterone overdosage. A 20-22 year old male normally produces5-10 mgdaily of testosterone. It is during this age range that men are at their physical peak of testosterone production. For me, this was during my college football years.

Does it make sense for 40-and-up men currently taking testosterone, that they didnotneed to donate blood monthly during their peak years of natural testosterone production, but are currently required to donate blood regularly with their current regimen of testosterone? Of course not. So, if you didnt have to donate blood with your peak testosterone production in your 20s, you shouldnt have to donate with testosterone therapy in your 40s and beyond either. Something is wrong here, right?

Thestartingdosage for one of the most highly-prescribed androgen gels is1 gram daily.Men, we didnt need 1 gram of testosterone in our early 20s, and we dont need it in our 30s and beyond.

80% of a mans Estrogen production occurs from aromatase activity, and aromatase activity increases as we age. So high doses of testosterone dont make sense. Doctors are just throwing fuel on the fire with these massive doses. More is not better if its too much, even when it is something your body needs.

Then, there is the delivery of testosterone therapy. The bodys natural testosterone secretion follows a normal diurnal rhythm. Testosterone is known to be greatest in early morning and lowest in the evening. But with many prescribing testosterone therapy today, it is very common to get weekly testosterone shots or testosterone pellets. This method of delivery does NOT follow the bodys natural rhythm. The shots and pellets delivery method of testosterone produce supra physiologic (abnormal) peaks. If the purpose of hormone therapy is to return the body to normal levels, then that objective can never be reached with this type of testosterone therapy.

The effects of Testosterone to estrogen conversion in men and women are different. Thats certainly no surprise. In men, high aromatase activity and conversion of testosterone to estrogen has been linked to elevatedCRP,fibrinogen, andIL-6.

Are these important?CRPis one of the best indicators of future cardiovascular disease/events (heart attacks and strokes), and is associated with metabolic syndrome. And yes, it is more predictive than even a high cholesterol level. Fibrinogen is another marker of inflammation that has been associated with cardiovascular disease and systemic inflammation. IL-6 is an inflammatory cytokine (immune signal) that has been implicated in increased aromatase activity (conversion of testosterone to estrogen) and at the same time is the result of increased testosterone to estrogen activity.

So, whats the big deal?The studies are not 100% conclusive, but it is clear thatinflammation increases the testosterone to estrogen conversionthrough increasedaromataseactivity. And the increased estrogen conversion is associated with increased inflammation in men. Itsa vicious cycle that will lead to disease states such asinsulin resistance, hypertension, prostatitis, cardiovascular disease, autoimmune disease,andcancer,to name a few.

You may be thinking, Is the testosterone I need leading me to disease?

The answer is, Yes, it sure can.If your testosterone therapy includes prescription of supra physiologic levels of testosterone, lack of follow-up on hormone levels, and no effort to balance hormones and metabolism, then yes, it sure can.

Is there a safe and effective way to balance hormones, lower estrogen and increase testosterone for men?

Effectively administering hormone therapy requires the following:

At Seasons of Farragut, Nan Sprouse and I are fellowship-trained (or completing fellowship training) specifically in the areas of hormone therapy and wellness-based medicine.

Our patient experience begins with an initial consultation to evaluate symptoms and develop an evaluation plan.

The next step is testing.In the case of hormone imbalance, we evaluate hormones withstate-of-the-arthormone testing via saliva, not just blood. As stated in a 2006 article, plasma levels of estradiol do not necessarily reflect tissue-level activity. Saliva has been shown to reveal the active hormone inside the cell at the site of action.

After initial testing and a therapy program, hormone levels are re-evaluated to ensure the progression of treatment and necessary changes are made to the treatment program. Testing and follow-up are key to proper balance of hormones (read myrecent post). At Seasons of Farragut, our approach to treatment and therapy is fully supported in the scientific research literature, and were happy to share that research with you if youd like to educate yourself.

The way estrogens aremetabolizedplays an equally pivotol role in hormone risk and effect. At Seasons of Farragut, our system of testing, evaluating, and monitoring is the only way to ensure that testosterone therapy for men is raising the testosterone and DHT levels instead of all being converted to estrogen. Hormone therapy is safe, but for it to work effectively, it must be properly evaluated, dosed, followed, and re-evaluated.

If you have questions or comments, please post them below and Ill respond as soon as possible. What is your experience with testosterone therapy? How has your physician tested and re-evaluated your therapy program?

For more information about the Seasons approach to wellness or to schedule an appointment, please contact our office at (865) 675-WELL (9355).

Filed under Bioidentical Hormone Replacement Therapy, Bioidentical Hormone Replacement Therapy, Cancer, Etcetera, From The Doctor's Desk, Heart Health, Hormone Balance, Hormone Balance, Hormone Symphony, Hormone Symphony, Men's Health, Mind Tagged with BHRT, bioidentical hormones, Conditions and Diseases, DHEA, Diabetes, Diabetes Mellitus Type 2, estrogen, Heart disease, Hormone, Hormone Balance, Hormone Imbalance, stress, Symptom

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Man vs. Estrogen: It's Not Just A Woman Thing! | Seasons ...

The Physician Assistant Life – Essay

by Stephen Pasquini PA-C

After reading a number of questions about acceptance into PA programs a prevailing theme has emerged.

Many international physicians stated that their interest in becoming PAs stems from dissatisfaction with the hours or volume of patients they are seeing in their own practices in their native countries.

So, what is my advice?

That you make an honest, soul-searching assessment of what it is you are seeking.

If you have a prevailing feeling that your MD is a superior credential and that you will be functioning as an "MD Surrogate" in the US, then perhaps you don't fully understand the concept of a PA/supervising MD team.

Every good PA knows very well our limits in scope of practice which have served us and our physician mentors very well for over 40 years.

We aren't, and never will be physicians!

Nor will you, if you practice as a PA within your scope of practice.

You may also want to investigate why you believe that coming to the United States to become a PA will ensure that your hours will be regular, predictable and better than what you have now.

Your hours will depend completely on the medical practice or hospital which hires you.

Expecting that as a PA you will have it easier than you have it as an MD may be a false assumption.

Many PAs work very long, grueling hours in emergency rooms, critical care, hospitals, public health facilities, family health care, community clinics and countless other fields in addition to volunteer work on their own time.

The person who inquired about coming to a US PA program because PAs in Canada are still new and not well respected might do well to step back for perspective.

PAs in the US are the single most serially tested group of medical providers in the world.

We are currently changing a decades-old requirement for national board certification exams every six years to maintain our treasured "C" on our credential, indicating board certification.

But if you look closely at the environment which mandated our test schedule it reveals that we have been regularly asked to "prove" our knowledge, skills, and trustworthiness for those same decades.

Each of us went through some version of facing the "newness" question about what is a PA and scrutiny and occasional rejection by physicians, nurses, and patients.

And most of us will tell you the struggle to prove ourselves is hard.

And at one time it may have been necessary.

But now, for most situations, when you join a medical practice, your patients already know what a PA is and how we function with their physicians.

In Canada, your PA profession, though in comparative infancy to the US, needs great people to choose it, build its competence and support its growth rather than abandon it and go to already proven territory.

If you believe in rigorous academic and clinical training then wouldn't you want to be in the vanguard in Canada demanding that rigor?

I treasure my life and work as a PA in California and Florida.

Anyone fortunate enough to come here as an immigrant looking for anopportunity to serve in the medical corps is warmly welcomed and will be honored by our ranks.

But when you choose this path to PA make sure you are seeing the good with the challengingand accepting that part of being in medical care.

Every place in the world demands a near total commitment of time and the humility to be comfortable caring for impoverished people, people of every cultural and ethnic background, just as you are doing wherever you currently live.

Your challenges are the same as ours in that regard.

The United States PA programs are unparalleled in preparing a workforce to address the overwhelming problem of inadequate access to health care.

But we may not be a panacea for overworked, over-scheduled and feeling unappreciated, at times.

Sincerely, and with good wishes for your success,

- Martie Lynch BS, PA-C

Today's post comes to us via the comments section and was written by physician assistant Margie Lynch, PA-C .

I receive many comments and emails from internationally trained doctors looking for career options here in the United States.

In fact, as an undergraduate, while working in the campus health clinic, I had the privilege of being trained by a foreign medical doctor from India who had transitioned to a laboratory tech in the United States.

The truth is, in many instances, a foreign medical degree is non-transferable and the barriers to practice prevent many highly skilled, well-intentioned international providers from coming to the United States. And like the MD I worked with, their skills and training may go to waste. This is a shame sad there are many clinics and hospitals in the US that would benefit from culturally competent bilingual practitioners.

And like the MD I worked with, their skills and training may go to waste. This is a shame sad there are many clinics and hospitals in the US that would benefit from culturally competent bilingual practitioners.

This is a shame as there are many clinics and hospitals in the US that would benefit from culturally competent, highly skilled, bilingual practitioners.

According to this NY Times Article, the United States already faces a shortage of physicians in many parts of the country, especially in specialties where foreign-trained physicians are most likely to practice, like primary care. And that shortage has gotten exponentially worse since the passage of the affordable healthcare act in 2014.

For years the United States has been training too few doctors to meet its own needs, in part because of industry-set limits on the number of medical school slots available. Today about one in four physicians practicing in the United States were trained abroad, a figure that includes a substantial number of American citizens who could not get into medical school at home and studied in places like the Caribbean.

But immigrant doctors, no matter how experienced and well trained, must run a long, costly and confusing gantlet before they can actually practice here.

The process usually starts with an application to a private nonprofit organization that verifies medical school transcripts and diplomas. Among other requirements, foreign doctors must prove they speak English; pass three separate steps of the United States Medical Licensing Examination; get American recommendation letters, usually obtained after volunteering or working in a hospital, clinic or research organization; and be permanent residents or receive a work visa (which often requires them to return to their home country after their training).

The biggest challenge is that an immigrant physician must win one of the coveted slots in Americas medical residency system, the step that seems to be the tightest bottleneck.

That residency, which typically involves grueling 80-hour workweeks, is required even if a doctor previously did a residency in a country with an advanced medical system, like Britain or Japan. The only exception is for doctors who did their residencies in Canada.

The whole process can consume upward of a decade for those lucky few who make it through.

The counterargument for making it easier for foreign physicians to practice in the United States aside from concerns about quality controls is that doing so will draw more physicians from poor countries. These places often have paid for their doctors medical training with public funds, on the assumption that those doctors will stay.

According to one study, about one in 10 doctors trained in India have left that country, and the figure is close to one in three for Ghana. (Many of those moved to Europe or other developed nations other than the United States.)

No one knows exactly how many immigrant doctors are in the United States and not practicing, but some other data points provide a clue. Each year the Educational Commission for Foreign Medical Graduates, a private nonprofit, clears about 8,000 immigrant doctors (not including the American citizens who go to medical school abroad) to apply for the national residency match system. Normally about 3,000 of them successfully match to a residency slot, mostly filling less desired residencies in community hospitals, unpopular locations and in less lucrative specialties like primary care.

In the United States, some foreign doctors work as waiters or taxi drivers while they try to work through the licensing process.

Is PA a reasonable alternative to foreign trained medical providers whose skills we desperately need here in the United States?

And just how many PA schools are eagerly opening their doors to these practitioners?

This, my friends, is a topic for another blog post.

Feel free to share your thoughts in the comments section down below.


-Stephen Pasquini PA-C

Are you or someone you know a foreign trained doctor or medical provider looking to practice as a PA in the US? Here are some useful resources from the internets:

by Stephen Pasquini PA-C

Welcome to episode 41of the FREE Audio PANCE and PANRE Physician Assistant Board Review Podcast.

Join me as Icover 10 PANCE and PANRE board review questions from the Academy course content following the NCCPA content blueprint.

This week we will be taking a break from topic specific board review and covering 10 generalboard review questions.

Below you will find an interactive exam to complement the podcast.

I hope you enjoy this free audio component to the examination portion of this site. The full genitourinary boardreview includes over 72 GUspecific questions andis available to all members of the PANCE and PANRE Academy.

If you can't see the audio player click here to listen to the full episode.

1. A mother brings her 6-year-old boy for evaluation of school behavior problems. She says the teacher told her that the boy does not pay attention in class, that he gets up and runs around the room when the rest of the children are listening to a story, and that he seems to be easily distracted by events outside or in the hall. He refuses to remain in his seat during class, and occasionally sits under his desk or crawls around under a table. The teacher told the mother this behavior is interfering with the child's ability to function in the classroom and to learn. The mother states that she has noticed some of these behaviors at home, including his inability to watch his favorite cartoon program all the way through. Which of the following is the most likely diagnosis?

Click here to see the answer

Answer: D. Attention deficit hyperactivity disorder

Attention deficit hyperactivity disorder is characterized by inattention, including increased distractibility and difficulty sustaining attention; poor impulse control and decreased self-inhibitory capacity; and motor over activity and motor restlessness, which are pervasive and interfere with the individual's ability to function under normal circumstances.


2. Which of the following is the treatment of choice for a torus (buckle) fracture involving the distal radius?

A. Open reduction and internal fixation B. Ace wrap or anterior splinting C. Closed reduction and casting D. Corticosteroid injection followed by splinting

Click here to see the answer

Answer:B. Ace wrap or anterior splinting

Atorus or buckle fracture occurs after a minor fall on the hand. These fractures are very stable and are not as painful as unstable fractures. They heal uneventfully in 3-4 weeks.

3. Which of the following can be used to treat chronic bacterial prostatitis?

A. Penicillin B. Cephalexin (Keflex) C. Nitrofurantoin (Macrobid) D. Levofloxacin (Levaquin)

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Chronic bacterial prostatitis (Type II prostatitis) can be difficult to treat and requires the use of fluoroquinolones or trimethoprim-sulfamethoxazole, both of which penetrate the prostate.

4. A 25 year-old male with history of syncope presents for evaluation. The patient admits to intermittent episodes ofrapid heart beating that resolve spontaneously. 12 Lead EKG shows delta waves and a short PR interval. Which ofthe following is the treatment of choice in this patient?

A. Radiofrequency catheter ablation B. Verapamil (Calan) C. Percutaneous coronary intervention D. Digoxin (Lanoxin)

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Answer:A. Radiofrequency catheter ablation

Radiofrequency catheter ablation is the treatment of choice on patients with accessory pathways, such as Wolff-Parkinson-White Syndrome.


5. Which of the following pathophysiological processes is associated with chronic bronchitis?

A. Destruction of the lung parenchyma B. Mucous gland enlargement and goblet cell hyperplasia C. Smooth muscle hypertrophy in the large airways D. Increased mucus adhesion secondary to reduction in the salt and water content of the mucus

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Chronic bronchitis results from the enlargement of mucous glands and goblet cell hypertrophy in the large airways.


6. Which of the following dietary substances interact with monoamine oxidase-inhibitor antidepressant drugs?

A. Lysine B. Glycine C. Tyramine D. Phenylalanine

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Answer:C. Tyramine

Monoamine oxidase inhibitors are associated with serious food/drug and drug/drug interactions. Patient must restrict intake of foods having a high tyramine content to avoid serious reactions. Tyramine is a precursor to norepinephrine.


Lysine, glycine, and phenylalanine are not known to interact with MAO inhibitors.

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The Physician Assistant Life - Essay