What's New?

The transcript is available at http://www.cushings-help.com/transcripts/jackieandsam2-9-2005.htm.

Cushing's Awareness Day. We are currently petitioning to have April 8 be declared as Cushing's Awareness day. This date was chosen because it was Dr. Harvey Cushing's Birthday.

Print out a sample letter to send to your congress person or senator or download it in Word format.

More information here

See what Jayne has done! She wrote to her representative and she's now in the Congressional Record. She has her first response and it's a fantastic one!

A new Message Board area is being added to discuss ideas for making Cushing's Awareness Day a reality. Please do what you can to help the cause! Thank you for helping to make this Cushing's Awareness Day a reality!

News:
We welcome your articles, letters to the editor, bios and Cushing's information. Submit a Story or Article to either the snailmail CUSH Newsletter or to an upcoming email newsletter at http://www.cushings-help.com/newsletter_story.htm Note: These articles are provided in furtherance of the mission of Cushing's Help and Support to help people with Cushing's or other endocrine problems, their friends and families through research, education, support, and advocacy. These news items are intended to serve as background concerning its subject for patient-physician discussions and discussions among Cushing's Help and Support Message Board Members. These articles contain information by authors and publishers that is subject to the Copyright Act of 1976, and "fair use doctrine" therein, effective on January 1, 1978 (17 U.S.C. § 101 et seq.). Cushing's Help and Support makes no representation that the information and any of the views or comments contained in these articles are completely accurate or current. Cushing's Help and Support takes no responsibility for any of the content.
Adrenal	Source: http://www.bpharmacysolutions.com/patient/articles/2005/0202-7.asp 02/02/2005 Adrenal Fatigue By Vicki Wade, R.Ph, Pharm. D.. Have you recently experienced a major stress in your life, be it illness, job, death, children, etc? After this stress, have you felt as though you just cannot seem to get yourself together, or at least back to where you used to be? Are you usually tired when you wake up, but still "too wired" to fall asleep at night? Is it hard for you to relax or to get exercise? Do you find that you get sick more often and take a long time to get well? If so, then you, like many other Americans may be experiencing symptoms of Adrenal Fatigue. Adrenal fatigue is not a new condition. People have been experiencing this condition for years. Although there is increasing physician awareness, many are not familiar with adrenal fatigue as a distinct syndrome. Because of this lack of knowledge, patients suffer because they are not properly diagnosed or treated. Adrenal fatigue is a condition in which the adrenal glands function at a sub-optimal level when patients are at rest, under stress, or in response to consistent, intermittent, or sporadic demands. The adrenal glands are two small glands that sit over the kidneys and are responsible for secreting over 50 different hormones - including epinephrine, cortisol, progesterone, DHEA, estrogen, and testosterone. Over the past century, adrenal fatigue has been recognized as Non-Addison's hypoadrenia, subclinical hypoadrenia, neurasthenia, adrenal neurasthenia, and adrenal apathy. Generally patients who present with adrenal fatigue can often be heard saying, "After______, I was never the same." The onset of adrenal fatigue often occurs because of financial pressures, infections, emotional stress, smoking, drugs, poor eating habits, sugar and white flour products, unemployment and several other stressors. After experiencing many of these events over a long period of time, the adrenal glands tend to produce less cortisol, the body's master stress hormone. Cortisol's main role in the body is to enable us to handle stress and maintain our immune systems. The adrenal gland's struggle to meet the high demands of cortisol production eventually leads to adrenal fatigue. Patients with adrenal fatigue have a distinct energy pattern. They are usually very fatigued in the morning, not really waking up until 10 AM, and will not usually feel fully awake until after a noon meal. They experience a diurnal lull in their cortisol (the stress hormone produced by the adrenal gland) and as a result, they feel low during the afternoon, generally around 2-4 PM. Patients generally begin to feel better after 6 PM; however, they are usually tired after 9 and in bed by 11 PM These patients find that they work best late at night or early in the morning. Some key signs and symptoms of adrenal fatigue include salt cravings, increased blood sugar under stress, increased PMS, perimenopausal, or menopausal symptoms under stress, mild depression, lack of energy, decreased ability to handle stress, muscle weakness, absent mindedness, decreased sex drive, mild constipation alternating with diarrhea, as well as many others. Although there no specific tests that will provide a true diagnosis of adrenal fatigue there are tests that may contribute to an assessment, such as a postural hypotension test, an AM cortisol test, or an ACTH stimulation test. It is customary for a physician to assess the adrenals together with thyroid tests to rule out insufficiency, which sometimes occurs in long-standing hypothyroidism. A single determination of plasma cortisol or 24-hour urinary free cortisol excretion is not useful and may be misleading in diagnosing adrenal insufficiency. However, if the patient is severely stressed or in shock, a single depressed plasma cortisol determination is highly suggestive. An elevated plasma ACTH level in association with a low plasma cortisol level is diagnostic. Treatment for adrenal fatigue is relatively simple. Lifestyle modifications can be initiated to treat this condition. Simple changes such as more laughter (increases the parasympathetic supply to the adrenals), small breaks to lie down, increased relaxation, regular meals, exercise (avoiding any highly competitive events), early bedtimes and sleeping until at least 9 AM whenever possible can all benefit those experiencing adrenal fatigue. A diet that would be conducive to treating adrenal fatigue includes one that combines unrefined carbohydrates (whole grains) with protein and oils (nuts and seeds) at most meals - olive, walnut, fiber, flax and high-quality fish oil. It is also important for patients to eat regular meals, chew food well, and eat by 10 AM and again for lunch. Patients should look to avoid any hydrogenated fats, caffeine, chocolate, white carbohydrates, and junk foods. Diets should have a heavy emphasis on vegetables. It may be of additional benefit that patients add salt to their diet, especially upon rising and at least a half-hour before their lowest energy point of the day. (Preferably, 1/8 to ½ teaspoonful of sea salt, Celtic salt, or sea salt w/ kelp powder added to an 8 oz glass of water). In adrenal fatigue, one should not follow the USDA's Food Guide Pyramid, as these patients tolerate fewer carbohydrates and need more protein. The addition of nutritional supplements may also offer additional benefits to patients experiencing adrenal fatigue. They should consider the addition of: Vitamin C 2,000-4,000 mg/day Sustained Release Vitamin E w/ mixed tocopherols 800 IU/day Vitamin B complex Niacin (125-150 mg/day)- as inositol hexaniacinate B-6 (150 mg/day) Pantothenic acid (1200-1500 mg/day) Magnesium citrate (400-1200 mg) Liquid trace minerals (zinc, manganese, selenium, chromium, molybdenum, copper, iodine)- calming effect If depression is present - Add SAM.e 200 mg bid; DL-Phenylalanine (DLPA) 500 mg bid Some herbal remedies that have been noted as possible therapies include Licorice, Ashwagandha, Maca, Siberian Ginseng, Korean Ginseng. Note: Licorice can and, if taken over time, does have a propensity to elevate blood pressure. It should not be used in persons with a history of hypertension, renal failure, or who current use digitalis preparations such as digoxin. Under the supervision of a physician hormone supplementation with DHEA, Pregnenolone, and Progesterone may also offer some benefits. There are several glandular extracts on the market that contain adrenal, hypothalamus, pituitary, thyroid, and gonadal that are also often recommended. Sometimes the initiation of hydrocortisone (Cortef®) may be necessary as a replacement hormone when cortisol is not being produced by the adrenals. While the initiation of corticosteroids, such as hydrocortisone may have quick and dramatic results, they can sometimes make the adrenals weaker rather than stronger. As a result, the initiation of hydrocortisone is usually a last resort. It is important to note that patients may have to undergo treatment for 6 month to 2 years. While a cortisol measurement may be helpful to confirm any thoughts or ideas that a patient may have decreased adrenal function, typically blood cortisol levels would be tested along with blood levels of potassium, and sodium. If the pituitary gland is the cause of adrenal failure electrolyte levels are usually normal. Practitioners usually pay attention to extremely low cortisol levels, which generally diagnoses Addison's disease - a condition in which the adrenal glands are completely depleted, also considered a medical emergency. If you think you may be experiencing adrenal fatigue or if you are unsure, feel free to contact Pete Hueseman, R.Ph., P.D. at 1-800-728-0288 or E.mail him directly at pharmacy@power-surge.com You can also your ask your questions of Pete at www.power-surge.com/asktheexperts.htm. Source:  http://www.poncacitynews.com/cgi-bin/LiveIQue.acgi$rec=63323?Lifestyle Valentine's Day Marks Expansion Of Newborn Screening in Oklahoma Valentine's Day, Monday, Feb. 14, will have special relevance for Oklahoma families of newborns born that day and afterward. Effective that date, the Oklahoma State Department of Health will expand its newborn screening program to include screening for two additional disorders: cystic fibrosis and congenital adrenal hyperplasia. State public health officials say these tests and the provision of follow-up services to ensure treatment within the first weeks of life for affected newborns will help saves lives and prevent severe disability. To commemorate the expansion of the newborn screening program, selected public health officials and newborn screening program staff will be wearing a bright blue wristband on Valentine's Day that says, "Breathe." While the simple act of breathing is something most persons take for granted, it can be extremely difficult for someone living with cystic fibrosis (CF). Testing for CF in newborns will allow for early detection of the disorder so complications can be prevented or improved. Newborns will also be tested for congenital adrenal hyperplasia (CAH), a disorder that can lead to death if not treated within the first weeks of life. The addition of these two tests is an important step in moving Oklahoma toward meeting March of Dimes recommendations for uniform national newborn screening. In addition to funding the expansion of the newborn screening program to include CF and CAH screening, the State Board of Health has added a third test for implementation later this year. That test will be for the metabolic disorder medium-chain acyl coenzyme A dehydrogenase deficiency (MCAD). The Oklahoma State Department of Health has purchased new equipment to allow for MCAD testing as well as 30 other metabolic disorders. Oklahoma is one of nine states offering CF screening to all newborns, and is the 39th state to add CAH screening. Oklahoma's newborn screening program also screens for the disorders of phenylketonuria (PKU), congenital hypothyroidism, classic galactosemia, and sickle cell disease. In 2004, the Oklahoma State Department of Health screened more than 50,000 newborns for genetic disorders and identified 32 newborns with a disorder. Expanded screening is expected to identify 17 newborns with CF and two with CAH each year. In addition to screening, Oklahoma newborns identified with a disorder receive comprehensive follow-up program services to ensure optimal healthy outcomes, a unique service when compared to newborn screening efforts provided by other states. "The consequences of not detecting these conditions early are devastating. Without early detection and subsequent intervention, newborns may suffer profoundly, and for some of the disorders, there is a risk of death," said Pam King, director of Genetics. "The cost to screen an infant is far less than the cost of failing to promptly identify affected infants." Without the screening test, doctors are often unable to identify these disorders quickly. Failure to screen one affected infant can result in an odyssey of frequent hospital stays and invasive procedures trying to determine a diagnosis. Studies have shown costs for hospitalizations and diagnostic procedures can easily exceed $500,000 for one infant. The cost for disability services and in some cases institutionalization for profoundly affected infants who did not receive prompt treatment can exceed $1 million annually. "Even so, these costs are immeasurable when compared to the effect that the loss of an infant's life has on a family," said State Health Commissioner Dr. Michael Crutcher. "That's why we are indebted to the Board of Health and its many partners who were committed to improving the health of Oklahoma's children." Crutcher said expansion of the newborn screening program was successful due to diverse support from legislators, families and health care providers. "Enhancing newborn screening services is a way to prevent mental retardation, improve health, and save lives. When we improve the quality of life for our children, we also improve the quality of life for Oklahoma's future," Crutcher said. For more information about newborn screening services, contact Pam King, director of Genetics, Oklahoma State Department of Health, 405/271-6617. Published Friday, February 11, 2005 on page a5 Copyright ©1998-2005 The Ponca City News
Pituitary	Source: http://www.chicagotribune.com/technology/chi-0502130486feb13,1,7239751.story?coll=chi-techtopheds-hed&ctrack=1&cset=true QUALITIES OF LIFE HEALTH Beaming in on the brain New radiation system tackles tumors while bypassing nearby tissue By Marc Davis Special to the Tribune Published February 13, 2005 If it weren't for a unique method of removing residual brain tumor tissue, a treatment offered by Loyola University Health System, Craig Fedder might be blind. Fedder, who lives in Aurora, knew he had a serious problem when, driving home one evening after work in January 2003, he was suddenly stricken with double vision. "I was on the road, speeding along in the middle of traffic, when it happened," said the 60-year-old Fedder, training-development manager for the International Truck and Engine Co. in Warrenville. "I was really scared. I tried to drive with my hand over one eye. That didn't help. I thought I'd have an accident. I was lucky to make it home." Fedder sought medical attention, and eventually an MRI and CT scan revealed a 2.8-centimeter benign tumor on Fedder's pituitary gland. The tumor created pressure against nerves that control eye movement and caused his double vision. His tumor was removed in a traditional surgical procedure in March 2003 by Dr. Thomas Origitano, a neurosurgeon at Loyola University Chicago Stritch School of Medicine. But Fedder still had a problem. Microscopic residual tumor tissue remained in Fedder's brain and had to be removed or the tumor could grow back, causing a recurrence of his vision problems, Origitano explained. The usual method of tumor tissue removal is a monthlong course of external beam radiation. Although the treatment can be effective, the side effects can be rough: fatigue, nausea, time lost from work. Most dangerous, however, is the potential damage to brain tissue. "The danger of injury to adjacent [brain] tissue includes possible hearing loss, blindness, difficulty swallowing, even paralysis," said Dr. Bahman Emami, chairman of the department of radiation oncology at Loyola University Health System. In Fedder's case, the potential injury to his optic nerve, which was being pressured by the tumor, could cause permanent blindness. If his brain tumor tissue were removed in the traditional way, there was a chance of damaging the optic nerve. With Loyola's new Novalis system of radiation, however, the risk was substantially reduced, Emami said. "What's unique about this [Novalis] method is its ability to shape the radio beam to the contours of the tumor," Origitano explained. "This leaves as much healthy tissue as possible untouched. The patient's exposure to radiation is reduced, and side effects are not as severe. It's also now used as a surgical method which can treat smaller tumors, reduces treatment time and causes minimal bleeding. Patients recover more quickly and with fewer or less-troublesome aftereffects." Fedder was scheduled for a course of treatment using the Novalis system in early 2004 at the Loyola University Health System, Maywood. Loyola is the only Chicago-area medical facility using the system, Emami said. Before Fedder's treatment, a plastic mask was made of his face for use as a precision guide for aiming the beam. "They put a roll of plastic mesh over my face," Fedder said, describing the mask-making process. "It was warm and pliable and took an impression. It was not uncomfortable." The finished mask was attached with bolts to fixtures on both sides of Fedder's head that held it steady so that the radiation would target the same place every time. The computer recognized the face and made appropriate targeting adjustments after two X-ray images verified the exact position of the patient's head. The radiation machine then rotated around Fedder's head, dispensing a precise dose of radiation to a pinpoint target. The radiation is a stream of fast-moving subatomic particles generated by a linear accelerator, a machine that uses electricity to generate the high-energy radiation beam. Emami supervised the treatment. After the radiation, about a five-minute exposure, Fedder returned to work the same day. The whole thing took about 30 minutes, Fedder said. "That includes the time it took for me to get ready. After it, I didn't feel woozy, sick or tired." Only near the end of his 25 days of radiation--five days a week, with Saturday and Sunday off--did Fedder start to feel some fatigue. He also lost hair on his head in two small patches. "But I started to feel normal again pretty soon, and my hair grew back quickly," he said. The Novalis system is now being used for both initial brain tumor surgery and the radiation follow-up. The system may also soon be used to treat other types of tumors, including those of the breast and prostate, Origitano said. As for Fedder, "I feel great now," he said. "I have no eyesight problems, I see Dr. Origitano once a year and everything was covered by insurance. I feel pretty lucky." Copyright © 2005, Chicago Tribune
Growth Hormone	Source: http://news.xinhuanet.com/english/2005-02/02/content_2538750.htm Dental surgery might become easier with new growth hormone injection technique Today, when dentists replace a tooth, they also have the complicated task (painful for the patient) of building a bone structure around the new tooth. They typically transfer excess bone material to the tooth from other areas of the patient's face. But some University of Michigan researchers may have found a better way. The scientist used gene therapy to inject a growth hormone into the mouths of lab mice, and the hormone coaxed bones into growing by themselves. LOS ANGELES, Feb. 2 (Xinhuanet) -- US Researchers have found that introducing a growth factor protein into a mouth wound, using gene therapy, helps generate bone around dental implants, according to a paper in the Molecular Therapy journal published on Tuesday. US Researchers have found that introducing a growth factor protein into a mouth wound, using gene therapy, helps generate bone around dental implants. (yahoo.com) For a patient with a sizable mouth wound, replacing a tooth means more than simply implanting a new one. The patient also needs the bone structure to anchor the new tooth in place. Such reconstructive surgery today involves either taking a bone graft from the patient's chin or jaw, which leaves a second wound needing to heal, or using donated bone from a tissue bank, which yields unpredictable results. A team of researchers at the University of Michigan led by Professor William Giannobile delivered the gene encoding for bone morphogenetic protein-7 (BMP-7) to large bone defects in rats, in an attempt to turn on the body's own bone growth mechanisms. The study showed that the animals produced nearly 50 percent more supporting bone around dental implants after getting BMP-7 treatment. BMP-7 is part of a family of proteins that regulates cartilage and bone formation. Recent studies have shown that BMPs are present in tooth development and periodontal repair. The Michigan study mixed BMP-7 genes with an inactivated virus in a gel-like carrier and injected it into wounds. Researchers said using a virus, with the harmful effects turned off, harnesses the virus' ability to enter into cells and use their genetic machinery. Once inside the cell, the viruses help BMP-7 genes get where they need to be in the host's cells to boost bone production. Gene expression producing BMP-7 proteins peaks after a week. The gene acts quickly to get bone growth started, then disappears within about 28 days. Scientists said a next step in this process could include looking for non-viral approaches to delivering gene therapy to the defect site. Alternatively, they could conduct the gene therapy outside the body using a tissue biopsy and then transplant the genetically modified cells back into the patient. But this would require two surgical procedures instead of one. "This study represents a proof-of-concept investigation. We are encouraged about the promise of this treatment," Giannobile said, adding that more work is necessary before the approach can be tested in humans.
Symptoms: Hirsuitism	Source: Yuma Sun - Yuma, AZ, USA http://sun.yumasun.com/artman/publish/articles/story_14728.php Tracking down the cause of women's facial hair BY PAUL G. DONOHUE, M.D. Feb 9, 2005 DEAR DR. DONOHUE: You recently wrote about a woman concerned with losing her hair. I have the opposite problem. I am 43 and have a mustache and goatee, and I must shave daily. The hair on my legs also grows rapidly. What are the treatments for this condition? -- D.S. ANSWER: Some of what I say applies only to premenstrual women, but most can be applied to women of all ages. Many women experience hair growth in places where it is a male feature -- the face, chin, neck or chest. Hair growth in those areas (and often robust leg-hair growth) depends on the influence of male hormones or on hair follicles that are extremely sensitive to low levels of male hormones. Tracking down the cause of the overly abundant supply of the hormone determines the proper treatment. One common condition is polycystic ovary syndrome, which, in its full expression, features large, cystic ovaries, menstrual irregularities, acne, infertility and the failure to ovulate. Male-pattern hair growth is another feature. Tumors of the ovary or adrenal gland that produce male hormones are a rare but other possible cause. So are thyroid gland disorders and a condition called the metabolic syndrome, in which blood pressure is elevated and blood sugar is high, as are blood triglycerides. However, the greatest number of women with the problem fall into the "idiopathic" category, meaning no cause can be found. Shaving is one solution. It doesn't make hair grow faster or thicker. Creme bleaches, chemical hair removers, electrolysis and laser treatments are other answers. Weight loss, when applicable, can lower male-hormone levels. Birth control pills are another way to blunt male-hormone action. So is the blood pressure medicine spironolactone. Vaniqa cream doesn't get rid of existing hair, but it prevents new hair growth.
Pain	Source: http://www.rd.com/content/openContent.do?contentId=14490 Oh, My Aching Back By Phyllis Schneider Back pain affects nearly half of all adults in any given year and at least two-thirds at some point in their lives. It's so prevalent that in the United States, back pain is second only to upper respiratory infections as the reason people visit their doctors. Unfortunately, many doctors don't have a clue about what causes back pain, so they order tests, which lead to unnecessary surgery for many people. But back pain usually doesn't signal a serious illness or condition, and in most cases, the pain will eventually go away with minimal treatment. Next time you feel the twinge of backache, here's what you need to know and do. Why It Hurts The mystery of back pain starts in your head, says Dennis C. Turk, Ph.D., a pain researcher at the University of Washington in Seattle. "Pain doesn't originate in the body but in the brain," he explains. "Let's say you strain your back. That information is transferred along nerve pathways to your brain, where it's interpreted as pain." And each person perceives that pain differently. Brain chemistry seems to play a role in pain perception. Recent research at Upstate Medical University in Syracuse, N.Y., found that chronic back pain triggered changes in several brain chemicals, most notably one involved in brain cell communication. According to principal investigator Igor D. Grachev, M.D., Ph.D., a neuroscientist, a reduction in this chemical resulted in increased feelings of pain. "This could explain why someone may feel intense pain when an MRI of the spine shows only a minor problem," he says. Low back pain can have many causes. It could be a pulled or strained muscle or ligament. It might be a herniated disk, which happens when tears in the outer part of a spinal disk release the jellylike substance that cushions the vertebra above and the one below. The cause might also be arthritis, osteoporosis, an infection of the spine, or physical trauma from a car accident or serious fall. Still another possibility is spinal stenosis, a condition in which bony overgrowths of the vertebrae narrow the spinal canal and hit nerve roots, notes Andrew J. Haig, M.D., director of the Spine Program at the University of Michigan in Ann Arbor. This condition is particularly common in people over 60. If you have pain, sometimes accompanied by numbness or tingling that radiates down the back of your leg and below the knee, the problem may be sciatica. "Sciatica is usually caused by a herniated disk pressing on nerve roots," Haig says, "but occasionally, it's the result of spinal stenosis." Although the potential causes are many, about 85 percent of the time no reason for the pain is ever found, Haig says. At best, diagnosis is often a guessing game. Some tantalizing new research, however, points to a genetic component in a small percentage of cases. To try to figure out what's going on, doctors may order X-rays, MRIs, or CT scans. But all too frequently these tests either don't pinpoint the cause of the pain or they find other back conditions that aren't related to the pain. "Studies have shown that an MRI or CT scan will show some 'problem' such as a herniated disk or spinal stenosis in one out of three people with absolutely no symptoms of back pain," Turk says. And when a test does show a spinal abnormality in someone with back pain, there's no guarantee that it's the cause of the pain. Too Many Tests "There's a tremendous problem with over-testing in this country," says John D. Loeser, M.D., a neurosurgeon at the University of Washington. Unfortunately, that over-testing may lead to unnecessary surgery. This is especially true for older people because of a misperception of what's "normal." "Radiologists tend to believe that 'normal' equals a picture of an 18-year-old's spine," he points out. "They label age-related changes that occur in almost everyone over 65 as 'abnormal.'" Does that mean testing is never called for? Of course not. Getting a picture of the spine is necessary for diagnosing low back pain in a person who has a history of cancer, a fever (which could indicate a spinal infection), or has undergone severe physical trauma. For others with low back pain, testing may be advisable if the pain fails to improve after four to six weeks of conservative treatment. Saying No to the Knife Surgeons perform approximately half a million back operations in the United States each year. Yet some experts suggest that an astonishing 95 to 98 percent of people with back pain do not require surgery. When is surgery appropriate? If people have failed to get better after a reasonable period of time or if they have sciatica, they should consider an operation, Loeser says. "But even in these instances, surgery may not be the best choice," he adds. "If you leave disk disease alone, most people will get better with nothing more than physical therapy and other conservative treatment. The problem is that if there's a lot of pain, some people simply can't or won't endure it. A surgical procedure can reduce the pain quickly." Nonsurgical Alternatives About one out of three people with back pain will improve substantially in a week, and two out of three will feel better after seven weeks. So a wait-and-watch approach plus some simple pain-management strategies are the best course for most people, Haig says. But that doesn't mean taking to your bed, he adds. In spite of the once-prevailing belief that bed rest is the best therapy for an aching back, doctors now advise just the opposite. "When people are confined to bed, they lose muscle mass, coordination, and balance," Haig says. "For every week you spend in bed, you need six to eight weeks to regain lost muscle and get yourself back in shape." If you feel you must rest, don't stay in bed for more than a couple of days and even then try to get up periodically and move around. To reduce inflammation and pain, apply an ice pack for 20 to 30 minutes several times a day for the first day or two. After that, a heating pad set on low may offer some relief. Over-the-counter pain relievers such as acetaminophen, aspirin, or ibuprofen can also help. If you don't feel any improvement after a month, see your doctor or seek help from a center that specializes in treating back pain. These programs combine the techniques of several specialists. In many of them, a physiatrist (a physician who specializes in rehabilitation medicine) or other expert, such as an osteopath (whose training emphasizes musculoskeletal disorders), works with a physical therapist to develop an exercise regime that will stretch and strengthen the muscles and ligaments of the back and other parts of the body. In some cases doctors recommend antidepressants, even if the person isn't depressed. "Antidepressants seem to regulate the brain's neurotransmitters that control sensory perceptions," Haig explains. Anti-seizure medications may also relieve pain. "We don't know exactly why," Haig continues, "but when back pain becomes chronic, it cycles like a reverberating circuit in your brain, sending signals that say, 'I hurt, I hurt.' An anti-seizure drug may interrupt that cycle." But, he cautions, these and other drugs have side effects. "People need to understand that they have a choice to use or not use medicine for pain," he says. "No medicine cures all back pain. You and your doctor have to make a judgment based on the cost and side effects of a drug versus the amount of pain you're in." If you have pain, especially from sciatica, that's so severe it keeps you from exercising, you may benefit from an epidural cortisone injection, Haig says. "These have been used for 15 or 20 years to reduce the inflammation and swelling around nerve roots, but until recently, doctors weren't able to inject the cortisone in exactly the right place. Today, however, some doctors use fluoroscopes to locate the site of the inflammation, so the injections are more accurate." Although no research shows that these epidural cortisone injections cure back pain, and relief lasts only two or three months, that may be enough time to begin an exercise program and start benefiting from it. What Doesn't Work Some common treatments for back pain either don't work at all or provide minimal relief at best. Traction, for example, has been shown to be ineffective. And a recent large-scale study found that back braces and support belts (items often sold through mail-order health products catalogs and magazine ads) not only do not relieve pain or prevent injury but may actually increase the risk of damage. These devices tend to give their wearers a false sense of security, making them more likely to move incorrectly and put undue strain on their backs. Transcutaneous electrical nerve stimulation (TENS), a mild application of electrical current to the skin over the painful area, which attempts to block pain signals traveling to the brain, has also proved ineffective. On the other hand, a related procedure, percutaneous electrical nerve stimulation (PENS), in which acupuncture needles are used to deliver electricity, may offer some relief, according to preliminary research. Traditional acupuncture may relieve pain over the short term, but there's no evidence that the improvement lasts, according to Haig. The same goes for massage therapy. "We need careful research on both procedures," he says. "So far, the jury's still out." As for magnet therapy? "It's a complete scam," Loeser says. "Don't waste your money." Preventing Pain To reduce your risk of developing back pain or to prevent a recurrence, "Stay strong, flexible, and coordinated," Haig says. That means committing yourself to a program of stretching, aerobics, and strength training. Also, if you still smoke, quit. "Research shows that cigarette smoking is a significant risk factor for back pain," Haig notes. The way you sit or the mattress you sleep on may play some role in back pain, but not for reasons you might imagine. "There's no 'right' way to sit," Haig says. "What's important is that you are able to move around in your chair, to flex your back, and stretch your legs." An ideal chair has arms, provides support for your back (a lumbar cushion can be useful), and isn't so high that your legs dangle. While folklore holds that a hard mattress is better for a bad back, you can sleep on whatever kind of mattress feels best, Haig says. It's a matter of individual choice. One may like to sleep on their side with a pillow between her knees or on her back with a pillow under her knees. Pillows work for some but not for others. Ultimately, preventing back pain means staying active and exercising. And if you suffer from back pain, don't look to the experts for a quick fix. "Over the years, we've found that one of the major problems is that people with back pain have been misled into thinking that they can get rid of their symptoms if they find a smarter, better doctor," Loeser says. "But the truth is that they need to make themselves better."
Other Issues: Diabetes and Menopause	Source: http://www.forbes.com/business/feeds/ap/2005/02/09/ap1815905.html Associated Press DDAVP: Court Rules for Barr in Patent Suit 02.09.2005, 12:47 PM Barr Pharmaceuticals Inc. on Wednesday said a federal court rules in its favor in a lawsuit involving antidiuretic patents held by Ferring BV and Aventis Pharmaceuticals Inc. The generic drug maker said the District Court of Southern New York found that the patents for DDAVP tablets in doses of 0.1 milligrams and 0.2 milligrams are unenforceable and not infringed by a product made by the company's Barr Laboratories Inc. unit. The court's decision clears the way for the Food and Drug Administration to approve Barr's pending application to market a generic version of DDAVP, or desmopressin acetate. Barr said it is the first to file an abbreviated new drug application for the doses and has 180 days of exclusivity on the products. Barr filed the application in July 2002, and was sued Dec. 13, 2002 by Ferring and Aventis. Ferring manufactures DDAVP for Aventis, which markets the product in the United States. Barr filed for summary judgment in April 2004. DDAVP tablets had annual sales of $177 million last year. They are indicated as antidiuretic replacement therapy in the management of central diabetes insipidus - a disorder of the pituitary gland characterized by intense thirst and by the excretion of large amounts of urine - and for the management of the temporary excessive urination and thirst following head trauma or surgery in the pituitary region. They are also indicated for the management of primary nocturnal enuresis, or bed-wetting. Barr shares rose $1.07, or 2.3 percent, to $47.005 in midday trading on the New York Stock Exchange. Source: http://www.psychiatrictimes.com/showArticle.jhtml?articleId=60400124 Menopause and Mood Disturbance By Claudio N. Soares, M.D., Ph.D Psychiatric Times January 2005 Vol. XXII Issue 1 Gonadal steroids appear to affect brain systems known to mediate depression and anxiety on multiple levels (Leibenluft, 1999). The sexual dimorphism seen in hypothalamic-pituitary-adrenal (HPA) axis regulation and the response to stress observed in animal studies and in humans corroborate this observation. The impact of sex hormones on brain functioning has been associated with gender differences observed in the prevalence, outcome and response to treatment of mental disorders. It is noteworthy that such differences become more noticeable with the onset of puberty; young females undergoing physical and hormonal changes frequently report affective instability, as well as high levels of emotional distress. After puberty, gender proportions of depression and anxiety significantly change, with an increase in female to male ratio up to 2:1 to 3:1 (Born and Steiner, 2001; Kessler et al., 1994; Steiner, 1992). Some women seem to be particularly vulnerable for developing depression during periods of marked hormonal variability (i.e., premenstrual periods, puerperium and perimenopause) (Harlow et al., 2003, 1999; Soares et al., 2001b; Stewart and Boydell, 1993). Menopausal Transition and Mood The mechanism by which neuroregulatory changes modulate the transition to menopause is still largely unknown (Wise et al., 1996). Generally, perimenopause or menopause transition begins in a woman's 40s, with a mean age of 47.5 years and an average duration of four to eight years. Menopause usually occurs at a mean age of 51.2 years. Reproductive aging may occur as early as 10 years prior to menopause and is evidenced by a rising follicle-stimulating hormone (FSH) level in the early follicular phase of the cycle and a decrease in inhibin B. Therefore, for several years, women transitioning to menopause may face marked biological variability, with subsequent endocrinologic and clinical changes (e.g., irregular/anovulatory cycles, vasomotor symptoms). The interaction between these hormonal changes, the subsequent onset of menopause-related clinical symptoms, and the emergence of mood symptoms and cognitive deficits constitute a complex puzzle. Epidemiological studies have shown mixed results with respect to the association between depression and menopause (McKinlay, 1996; Porter et al., 1996). Initial data obtained in 1994 from a cross-sectional population survey of 2,103 women from the Netherlands were compared to data from the same population obtained three and one-half years later (range=2.8 to 4.7 years) (Maartens et al., 2002). By using a cutoff score of 12 on the Edinburgh Depression scale (EDS) to define presence of depression, the investigators found a significant association between the transition from pre- to perimenopause (mainly based on menstrual history) and a higher increase in EDS scores (odds ratio=1.8, 95% confidence interval=1.1-3.3). Other independent factors contributing significantly to an increase in depressive symptoms over time included prior depression, financial problems, unemployment, transition from peri- to postmenopause and death of a partner. A prospective study by Freeman et al. (2004) also found an increased likelihood of depressive symptoms during transition to menopause and a decreased likelihood after menopause, after adjusting for other predictors of depression. The Harvard Study of Moods and Cycles is an ongoing community-based, prospective study designed to explore some of the characteristics involving the association between depression and ovarian failure. After screening more than 4,000 premenopausal women (ages=36-44), subgroups of women with (n=332) and without (n=644) history of depression were enrolled for prospective assessments of serum hormone levels, menstrual characteristics and standardized psychiatric evaluations (Harlow et al., 2003). Findings of this study demonstrated that women with a history of depression (assessed by standardized psychiatric interview--Structured Clinical Interview for DSM-IV [SCID]) are more likely to develop greater hormonal fluctuations (serum levels of FSH, luteinizing hormone [LH] or estradiol [E2]) over time, even while still being premenopausal, than women without depression. In addition, women with a history of depression are more likely to present with symptoms that characterize an earlier transition to menopause (menstrual irregularities, presence of hot flushes and night sweats) (Harlow et al., 2003). More recent findings derived from the Harvard Study of Moods and Cycles also suggest that women approaching menopause (i.e., presenting with irregular cycles and significant vasomotor symptoms) are at significantly greater risk for developing depressive symptoms, even in the absence of prior episodes of depression (Soares, 2003). This putative association could consolidate the view of an existing intrinsic connection between disrupted hormone milieu and brain functioning. A study of more than 500 pre-, peri- and postmenopausal women in a primary care clinic demonstrated that marital disruption and unemployment, as well as somatic symptoms and past history of depression, may influence the likelihood of depressive symptoms in this population, regardless of menopausal status (Joffe et al., 2002). The presence of severe hot flushes, however, was a risk factor for depression only among perimenopausal women, even though hot flushes occurred in all three menopausal groups. This correlation between hot flushes and depression corroborates one of the physiological theories commonly employed to explain the occurrence of depressive symptoms among menopausal women--the so-called domino effect (Campbell and Whitehead, 1977). This theory proposes that the discomfort caused by night sweats and hot flushes provokes physical changes (e.g., sleep disturbance) and, consequently, affects mood stability. Hence, investigators have speculated that the capacity of estrogen to improve mood is secondary to providing relief of somatic menopausal symptoms and normalization of sleep. Despite accumulating evidence that hormonal fluctuations exert a psychological destabilizing action during certain reproductive cycle-related events, clinical studies have also demonstrated that sex hormones may in fact help to prevent or even treat depressive symptoms. This correlation has already been shown in studies that examined the effects of treatment with estradiol for premenstrual depressive symptoms (Smith et al., 1995) and during puerperium (Ahokas et al., 2001; Gregoire et al., 1996). Double-blind, placebo-controlled studies have shown significant antidepressant benefit with the use of transdermal estradiol in perimenopausal women suffering from major depressive disorder, dysthymia or minor depression (Schmidt et al., 2000; Soares et al., 2001a). Results obtained with the use of estradiol for postmenopausal depressed women were less promising (Cohen et al., 2003). Transdermal testosterone, on the other hand, has been shown to be efficacious for the treatment of psychological distress and decreased libido in some surgically induced menopausal women (Shifren et al., 2000). These were mostly small studies, so larger studies are needed to corroborate these promising findings. Hormones and the Brain The complex interactions between estrogens and brain functioning have gained greater understanding over the last decade (Joffe and Cohen, 1998). The distribution of various E2 receptors (named and E2 receptors, to date) in different brain regions (such as the medial amygdala, hippocampus and limbic system) and their distinct up- or downregulation by estradiol contribute to the complexity of estrogen's effects on the central nervous system (Genazzani et al., 1997; Maggi and Perez, 1985; Silva et al., 2001; Woolley, 1999). Estrogens interact with membrane and nuclear receptors. Through nuclear receptors, they act as transcription factors regulating the expression of targeted genes. In addition, estrogens affect membrane receptors by possibly modulating the synthesis, release and metabolism of monamines (McEwen and Alves, 1999; Stahl, 2001). Estrogens exert an agonist effect on serotonergic activity by increasing the number of serotonergic receptors and the transport and uptake of the neurotransmitter. They also increase synthesis of serotonin, upregulate 5-HT1 receptors, downregulate 5-HT2 receptors and decrease monoamine oxidase activity (Halbreich and Kahn, 2001). Estrogens appear to increase noradrenergic (NA) activity by increasing NA turnover, decreasing NA reuptake, and decreasing the number and sensitivity of dopamine D2 receptors (Garlow et al., 1999). Lastly, estrogens induce new dendritic spine formation and synapses in hippocampal neurons, and they regulate neurotropic factors and neuropeptides (e.g., neuropeptide Y [NPY] and corticotropin-releasing hormone [CRH]). Estrogen availability may also modulate the binding affinity of 5-HT receptors, as shown in animal models (Bethea et al., 2002) and neuroimaging clinical studies (Kugaya et al., 2003). Estrogen Therapy Estrogens are available in many preparations: transdermal patches and creams, oral tablets, intranasal or sublingual formulations, injections, and subdermal implants (Ramachandran and Fleisher, 2000; Stahl, 2001). Most data on the efficacy and safety of estrogens in the United States have been based on studies using oral conjugated estrogens. Differences in the pharmacokinetic aspects of estrogen preparations may contribute to the lack of consistency across studies regarding the effect of estrogen treatment on mood (Halbreich and Kahn, 2001). Treatment studies of transdermal estradiol for perimenopausal depression (randomized, placebo-controlled studies, 50 g/day or 100 g/day) have shown positive results (Schmidt et al., 2000; Soares et al., 2001a). Most estrogen trials that failed to detect an antidepressant efficacy in comparison with placebo used either oral preparations of conjugated equine estrogen or piperazine sulfate estrone (Coope et al., 1975; Strickler et al., 1977; Thomson and Oswald, 1977). The use of transdermal estradiol (50 g/day) showed superior efficacy compared to placebo in 34 perimenopausal women with major and minor depression, in the presence or absence of hot flushes (Schmidt et al., 2000). These findings corroborate the idea that the effects of estrogen on mood and on vasomotor symptoms, the latter possibly resulting from hypothalamic thermoregulatory dysfunction, are independent. Similar results were found in a larger sample of perimenopausal women suffering from depressive disorders (mostly major depression) who were treated with transdermal estradiol (100 µg/day) or placebo (Soares et al., 2001a). In this study, most women were able to sustain an antidepressant benefit after a four-week washout period, despite the re-emergence of vasomotor symptoms, again suggesting the existence of independent effects of estradiol on mood and vasomotor symptoms. Studies on postmenopausal subpopulations have shown less compelling evidence of estrogen's antidepressant efficacy. Negative results have been reported when conjugated estrogen (George et al., 1973) or estrogen sulfate (Coppen et al., 1977) were given to surgically induced menopausal women. In addition, the use of transdermal estradiol (50 µg/day) in postmenopausal women did not show superior efficacy when compared with placebo for the treatment of depressive symptoms (Saletu et al., 1995). Antidepressant benefit of estrogen for postmenopausal women appears to be limited even when examined in open clinical trials (Cohen et al., 2003). It is possible that postmenopausal women would require a higher dose and/or prolonged treatment with E2 to obtain a satisfactory antidepressant response to estrogen treatment, possibly due to the altered sensitivity of their estrogen receptors. Also, it is possible that perimenopausal women with depression are uniquely responsive to the mood-enhancing effects of E2. Studies of the efficacy of estrogen as an adjunctive therapy for major depression in postmenopausal women have had mixed results. Retrospective analyses of older women have shown greater improvement in depressive symptoms among those who received fluoxetine (Prozac) plus hormone therapy, which may include estrogen preparations, progestogens or both, than those receiving the antidepressant alone (Amsterdam et al., 1999; Schneider et al., 1997). However, in these studies, women were not randomly assigned to hormone therapy, which might have contributed to a selection bias. A similar study with sertraline (Zoloft) did find a positive effect of hormone therapy augmentation (Schneider et al., 1998). A pooled analysis of women treated with venlafaxine (Effexor) with or without concomitant use of hormone therapy for depression found no evidence suggesting a significant change in efficacy associated with hormone therapy use (Entsuah et al., 2001). However, that concomitant use of hormone therapy could maximize some of the benefits obtained with the selective serotonin reuptake inhibitors in perimenopausal women, particularly in promoting greater well-being (Soares et al., 2003). The Women's Health Initiative Study, a randomized, controlled, primary prevention trial (planned duration, 8.5 years), randomly assigned 16,608 postmenopausal women 50 to 79 years of age (mean age=63 years) with an intact uterus at baseline to receive estrogen plus progestin (0.625 mg/day of conjugated equine estrogen [CEE] plus 2.5 mg/day of medroxyprogesterone acetate [MPA]; n=8,506) or placebo (n=8,102). The primary outcome measure was coronary heart disease, with invasive breast cancer as the primary adverse outcome. Other measures included cases of stroke, pulmonary embolism, endometrial cancer, colorectal cancer and hip fracture. In May 2002, the trial was stopped by recommendation of the data and safety monitoring board, as the overall health risks associated with combined estrogen plus progestin had exceeded the benefits (Rossouw et al., 2002). In February 2004, the estrogen alone arm (or placebo), including postmenopausal women with hysterectomy, was also stopped because the burden of incident disease events was showing similar impact on both groups and, therefore, would not result in any significant benefit (Anderson et al., 2004). Lastly, although not specifically designed to examine the benefits of hormone therapy for psychological symptoms, mood or cognition, the Women's Health Initiative Study also reported the impact of estrogen (plus progestin) on quality of life, including questions on general health, vitality, mental health, depressive symptoms and sexual satisfaction. At three years, there were no significant benefits in terms of any quality-of-life outcomes (Hays et al., 2003). The results from this study should be carefully interpreted. In fact, various menopause societies have expressed their concerns about the generalization of its findings; investigators and seasoned clinicians have pointed out that some of these results were a "direct consequence of unsuitable population selection [e.g., older, postmenopausal women], terribly wide inclusion criteria [e.g., subjects with various pre-existing medical conditions], lack of adequate assessments [e.g., lack of adequate assessment for menopause-related somatic symptoms, and the incongruous treatment choice [CEE + MPA]" (Notelovitz, 2003). The main criticism, however, relies on the fact that this study was designed essentially to examine the impact of a specific hormone formulation (CEE + MPA) on the relative risk for developing coronary heart disease, cancer or fractures in older, postmenopausal women. The study was not designed to address the impact/safety of using CEE + MPA (or any other hormone preparation) for the management of menopause-related somatic and/or psychological complaints in younger, perimenopausal women--for example, for the treatment of hot flushes and depressive symptoms in this population. Clinicians and health care professionals should continue to consider many factors when advising treatment choices for women approaching menopause or for those who are postmenopausal. It has been speculated that hormone therapy discontinuation could increase the risk for mood instability, anxiety and insomnia, especially in women with a past history of these symptoms. The Women's Health Initiative study yielded data only on the use of conjugated estrogens and medroxyprogesterone; long-term data on other hormone therapy regimens are sparse and certainly overdue. As already seen with various antidepressants, hormonal therapies differ with respect to absorption, metabolism and bioavailability. Nonetheless, in the absence of more data, we cannot ensure the safety of switching patients to another hormone combination. Moreover, clinicians and health care professionals should continue to weigh the risks and contraindications for using short- or long-term estrogen/progestin preparations, particularly in light of updated data on the impact of such treatments for the risk of developing new thromboembolic events, breast cancer or endometrial cancer. Androgens might have important neuroprotective properties (Wolf and Kirschbaum, 1999), as well as an essential role in the organization or programming of brain circuits (Rubinow and Schmidt, 1996). Androgens are produced by the adrenal glands and ovaries in women, and they include testosterone, androstenedione, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S). The latter two are adrenal steroids and are available in higher concentrations than other androgens (Morrison, 1997). The impact of testosterone on mood and behavior in women has been well described. Depressive symptoms and anxiety, as well as decreased libido, have been described among postmenopausal women who present with decreased testosterone, particularly after oophorectomy; however, testosterone supplementation has been shown to alleviate these symptoms (Sherwin and Gelfand, 1985). Shifren and colleagues (2000) examined the impact of transdermal testosterone in 75 surgically induced postmenopausal women (ages 31 to 56). They received patches containing 150 g or 300 g of testosterone or placebo for 12 weeks. All participants received concomitant treatment with oral conjugated estrogens. When compared with placebo, women who received testosterone reported greater psychological well-being and a significant improvement in mood and anxiety. Treatment with testosterone was well tolerated without significant occurrence of acne or hirsutism. Conclusions There is accumulating evidence suggesting a complex interaction between sex hormones and brain functioning. The transition to menopause serves as an interesting model for the understanding of this interaction and its implication for the development of mood disturbances during the menopausal years. The extent to which the use of hormone interventions (particularly estrogen and testosterone preparations) may help to improve treatment outcomes among women who present with depressive symptoms or cognitive decline is still debatable given the methodological limitations of the existing data. Antidepressants, mood stabilizers and psychotherapy will continue to be well-established treatments for mood disturbances. It is plausible, however, that subgroups of menopausal women will benefit from the combined use of hormonal and nonhormonal strategies. The search for an improved quality of life for our female patients will certainly stimulate further studies to define strategies for ameliorating depressive symptoms with fewer side effects. Psychiatrists and other health care professionals should, therefore, be aware of the accumulating data on the psychotropic effects of sex hormones. Dr. Soares is assistant professor of psychiatry at Harvard Medical School and is associate director for research at Massachusetts General Hospital Center for Women's Mental Health. References Ahokas A, Kaukoranta J, Wahlbeck K, Aito M (2001), Estrogen deficiency in severe postpartum depression: successful treatment with sublingual physiologic 17beta-estradiol: a preliminary study. J Clin Psychiatry 62(5):332-336 [see comment]. Amsterdam J, Garcia-Espana F, Fawcett J et al. (1999), Fluoxetine efficacy in menopausal women with and without estrogen replacement. J Affect Disord 55(1):11-17. Anderson GL, Limacher M, Assaf AR et al. (2004), Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women's Health Initiative randomized controlled trial. JAMA 291(14):1701-1712 [see comments]. Bethea CL, Lu NZ, Gundlah C, Streicher JM (2002), Diverse actions of ovarian steroids in the serotonin neural system. Front Neuroendocrinol 23(1):41-100. Born L, Steiner M (2001), The relationship between menarche and depression in adolescence. CNS Spectrums 6(2):126-138. Campbell S, Whitehead M (1977), Oestrogen therapy and the menopausal syndrome. Clin Obstet Gynaecol 4(1):31-47. Cohen LS, Soares CN, Poitras JR et al. (2003), Short-term use of estradiol for depression in perimenopausal and postmenopausal women: a preliminary report. Am J Psychiatry 160(8):1519-1522. Coope J, Thomson JM, Poller L (1975), Effects of "natural oestrogen" replacement therapy on menopausal symptoms and blood clotting. Br Med J 4(5989):139-143. Coppen A, Bishop M, Beard RJ (1977), Effects of piperazine oestrone sulphate on plasma tryptophan, oestrogens, gonadotrophins and psychological functioning in women following hysterectomy. Curr Med Res Opin 4:29-36. Entsuah AR, Huang H, Thase ME (2001), Response and remission rates in different subpopulations with major depressive disorder administered venlafaxine, selective serotonin reuptake inhibitors, or placebo. J Clin Psychiatry 62(11):869-877. Freeman EW, Sammel MD, Liu L et al. (2004), Hormones and menopausal status as predictors of depression in women in transition to menopause. Arch Gen Psychiatry 61(1):62-70. Garlow S, Musselman D, Nemeroff C (1999), The neurochemistry of mood disorders: clinical studies. In: Neurobiology of Mental Illness, Charney DS, Nestler EJ, Bunney B, eds. New York: Oxford University Press, pp348-364. Genazzani AR, Lucchesi A, Stomati M et al. (1997), Effects of sex steroid hormones on the neuroendocrine system. Eur J Contracept Reprod Health Care 2(1):63-69. George GC, Utian WH, Beaumont PJ, Beardwood CJ (1973), Effect of exogenous oestrogens on minor psychiatric symptoms in postmenopausal women. S Afr Med J 47(49):2387-2388. Gregoire AJ, Kumar R, Everitt B et al. (1996), Transdermal oestrogen for treatment of severe postnatal depression. Lancet 347(9006):930-933 [see comment]. Halbreich U, Kahn LS (2001), Role of estrogen in the aetiology and treatment of mood disorders. CNS Drugs 15(10):797-817. Harlow BL, Cohen LS, Otto MW et al. (1999), Prevalence and predictors of depressive symptoms in older premenopausal women: the Harvard Study of Moods and Cycles. Arch Gen Psychiatry 56(5):418-424 [see comment]. Harlow BL, Wise LA, Otto MW et al. (2003), Depression and its influence on reproductive endocrine and menstrual cycle markers associated with perimenopause: the Harvard Study of Moods and Cycles. Arch Gen Psychiatry 60(1):29-36. Hays J, Ockene JK, Brunner RL et al. (2003), Effects of estrogen plus progestin on health-related quality of life. N Engl J Med 348(19):1839-1854 [see comments]. Joffe H, Cohen LS (1998), Estrogen, serotonin, and mood disturbance: where is the therapeutic bridge? Biol Psychiatry 44(9):798-811. Joffe H, Hall JE, Soares CN et al. (2002), Vasomotor symptoms are associated with depression in perimenopausal women seeking primary care. Menopause 9(6):392-398 [see comment]. Kessler RC, McGonagle KA, Zhao S et al. (1994), Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry 51(1):8-19. Kugaya A, Epperson CN, Zoghbi S et al. (2003), Increase in prefrontal cortex serotonin 2A receptors following estrogen treatment in postmenopausal women. Am J Psychiatry 160(8):1522-1524. Leibenluft E (1999), Foreward. In: Gender Differences in Mood and Anxiety Disorders: From Bench to Bedside, Leibenluft E, ed. Washington, D.C.: American Psychiatric Press. Maartens LW, Knottnerus JA, Pop VJ (2002), Menopausal transition and increased depressive symptomatology: a community based prospective study. Maturitas 42(3):195-200. Maggi A, Perez J (1985), Role of female gonadal hormones in the CNS: clinical and experimental aspects. Life Sci 37(10):893-906. McEwen BS, Alves SE (1999), Estrogen actions in the central nervous system. Endocr Rev 20(3):279-307. McKinlay SM (1996), The normal menopause transition: an overview. Maturitas 23(2):137-145. Morrison MF (1997), Androgens in the elderly: will androgen replacement therapy improve mood, cognition, and quality of life in aging men and women. Psychopharmacol Bull 33(2):293-296. Notelovitz M (2003), The clinical practice impact of the Women's Health Initiative: political vs biologic correctness. Maturitas 44(1):3-9. Porter M, Penney GC, Russell D et al. (1996), A population based survey of women's experience of the menopause. Br J Obstet Gynaecol 103(10):1025-1028. Ramachandran C, Fleisher D (2000), Transdermal delivery of drugs for the treatment of bone diseases. Adv Drug Deliv Rev 42(3):197-223. Rossouw JE, Anderson GL, Prentice RL et al. (2002), Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women's Health Initiative randomized controlled trial. JAMA 288(3):321-333 [see comments]. Rubinow DR, Schmidt PJ (1996), Androgens, brain, and behavior. Am J Psychiatry 153(8):974-984. Saletu B, Brandstatter N, Metka M et al. (1995), Double-blind, placebo-controlled, hormonal, syndromal and EEG mapping studies with transdermal oestradiol therapy in menopausal depression. Psychopharmacology (Berl) 122(4):321-329. Schmidt PJ, Nieman L, Danaceau MA et al. (2000), Estrogen replacement in perimenopause-related depression: a preliminary report. Am J Obstet Gynecol 183(2):414-420. Schneider LS, Small GW, Clary CM (1998), Estrogen replacement therapy status and antidepressant response to sertraline. NR426. Presented at the 151st Annual Meeting of the American Psychiatric Association. Toronto; June 2. Schneider LS, Small GW, Hamilton SH et al. (1997), Estrogen replacement and response to fluoxetine in a multicenter geriatric depression trial. Fluoxetine Collaborative Study Group. Am J Geriatr Psychiatry 5(2):97-106. Sherwin BB, Gelfand MM (1985), Sex steroids and affect in the surgical menopause: a double-blind, cross-over study. Psychoneuroendocrinology 10(3):325-335. Shifren JL, Braunstein GD, Simon JA et al. (2000), Transdermal testosterone treatment in women with impaired sexual function after oophorectomy. N Engl J Med 343(10):682-688 [see comments]. Silva I, Mor G, Naftolin F (2001), Estrogen and the aging brain. Maturitas 38(1):95-100; discussion 100-101. Smith RN, Studd JW, Zamblera D, Holland EF (1995), A randomised comparison over 8 months of 100 micrograms and 200 micrograms twice weekly doses of transdermal oestradiol in the treatment of severe premenstrual syndrome. Br J Obstet Gynaecol 102(6):475-484. Soares CN (2003), Sex, hormones and depression: the impact of sex steroids on mood across the reproductive life cycle. Industry-supported symposium 41B. Presented at the 156th Annual Meeting of the American Psychiatric Association. San Francisco; May 20. Soares CN, Almeida OP, Joffe H, Cohen LS (2001a), Efficacy of estradiol for the treatment of depressive disorders in perimenopausal women: a double-blind, randomized, placebo-controlled trial. Arch Gen Psychiatry 58(6):529-534 [see comments]. Soares CN, Cohen LS, Otto MW, Harlow BL (2001b), Characteristics of women with premenstrual dysphoric disorder (PMDD) who did or did not report history of depression: a preliminary report from the Harvard Study of Moods and Cycles. J Womens Health Gend Based Med 10(9):873-878. Soares CN, Poitras JR, Prouty J et al. (2003), Efficacy of citalopram as a monotherapy or as an adjunctive treatment to estrogen therapy for perimenopausal and postmenopausal women with depression and vasomotor symptoms. J Clin Psychiatry 64(4):473-479. Stahl SM (2001), Sex and psychopharmacology: is natural estrogen a psychotropic drug in women? Arch Gen Psychiatry 58(6):537-538 [comment]. Steiner M (1992), Female-specific mood disorders. Clin Obstet Gynecol 35(3):599-611. Stewart DE, Boydell KM (1993), Psychologic distress during menopause: associations across the reproductive life cycle. Int J Psychiatry Med 23(2):157-162. Strickler RC, Borth R, Cecutti A et al. (1977), The role of oestrogen replacement in the climacteric syndrome. Psychol Med 7(4):631-639. Thomson J, Oswald I (1977), Effect of oestrogen on the sleep, mood, and anxiety of menopausal women. Br Med J 2(6098):1317-1319. Wise PM, Krajnak KM, Kashon ML (1996), Menopause: the aging of multiple pacemakers. Science 273(5271):67-70 [see comment]. Wolf OT, Kirschbaum C (1999), Actions of dehydroepiandrosterone and its sulfate in the central nervous system: effects on cognition and emotion in animals and humans. Brain Res Brain Res Rev 30(3):264-288. Woolley CS (1999), Effects of estrogen in the CNS. Curr Opin Neurobiol 9(3):349-354.
Steroids	Source: http://www.fdaadvisorycommittee.com/FDC/AdvisoryCommittee/ Committees/Dermatologic+and+Ophthalmic+Drugs/ 032405_TopCortico/032405_TopCorticoA.htm Topical Corticosteroid Rx-To-OTC Switch Safety Data Will Be Topic Of Joint Cmte. Meeting Safety data needed for prescription-to-over-the-counter switches of topical corticosteroid products will be discussed at a joint meeting of FDA’s Nonprescription Drugs and Dermatologic & Ophthalmic Drugs Advisory Committees on March 24. The committees will focus particularly on the database to evaluate the potential for hypothalamic, pituitary, adrenal (HPA) and growth suppression and other systemic and local adverse events. The potential for HPA axis and growth suppression with topical corticosteroids is considered a potential stumbling block for the Rx-to-OTC switch of topical corticosteroids. Studies on various corticosteroids indicate use of the drugs can slow children’s growth. Data are not yet available on whether the impact is reversible. The development of a risk management program for topical corticosteroids to prevent hypothalamic pituitary axis suppression in pediatric patients being treated for atopic dermatitis was discussed by FDA’s Pediatric Subcommittee of its Anti-Infective Drugs Advisory Committee at an Oct. 29, 2003 meeting. The subcommittee recommended a boxed warning be added to topical corticosteroids concerning the HPA axis suppression risk. Other recommendations by the advisory committee included additional studies to determine risk, patient package inserts, “Dear Health Care Provider” letters and provider educational programs. While HPA axis suppression from topical steroid use will often resolve without consequence, FDA has noted that “pediatric patients who are suppressed from topical steroid use and experience a significant physiologic stress (such as trauma, surgery, or serious infection) may have life-threatening complications from their suppression (including death) which are preventable if the suppression is recognized and treated appropriately with stress doses of glucocorticoids." On March 23, the Nonprescription Drugs Advisory Committee will consider microbiologic surrogate endpoints for demonstrating the effectiveness of antiseptic products in health care settings. To watch a live or archived webcast of this meeting, click here. To arrange for live videoconferencing or to order videotapes & DVDs, email webcasthelp@elsevier.com or call 800-627-8171. This meeting will be held March 24, 2005 at the Hilton in Gaithersburg, Md. beginning at 8 a.m. Posted: Friday, February 11, 2005

Lynne Clemens, Secretary of CUSH Org is be the person responsible for the creation of this register. If you have any questions you may contact her at lynnecush@comcast.net. You do not have to be a member of CUSH to fill out this questionnaire, as long as you are a Cushing’s patient. We do not believe that the world has an accurate accounting of Cushing’s patients. The only way to authenticate accuracy is with actual numbers. Your help will be appreciated. Thank you."

April 1-2, 2005, Human Growth Foundation Annual Conference, Safety Harbor (Tampa Bay), FL. Families concerned about their child's growth and adults who wish to learn more about growth hormone deficiency from endocrinologists and other knowledgeable professionals. More info here »

Easter Weekend, 2005, April 26, 2005, Meeting in DC Metro Area More info here »

Spring 2005, (date TBA), Meeting in New England More info here »

May 15, 2005, 11 a.m. to 3:00 p.m., NIH Share the Health: Health and Fitness Expo More info here »

June 4-7, 2005, ENDO 2005, San Diego. Mainly for physicians, but patients may attend. More info here.

July 21-24, 2005, MAGIC Foundation Convention, Chicago, O'Hare Marriott. For Growth Hormone patients and their families. More info here »

More upcoming local meetings are listed here »

Sign up for notification of local meetings. You need not be a CUSH member to participate.

The new chatroom is available through http://www.cushings-help.com/chatroom.htm. Since this is our own room, you won't need to go into another area after first logging in. You'll be right there!

The very first time you go in, you will have to register for this chat. Although you may use your user name and password from the message boards, you will still need to register those before being allowed into the room.

This room is always open, and has convenient links so that you can get needed information while you're chatting.