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presented a table full of Cushing's info at her local Health Fair In
you spend years searching for a diagnosis before finding one?
Medical detectives put Lenin under the microscope
New Study Shows Seditol™ Highly Effective For Improving Sleep and Reducing Fatigue.
Night eating syndrome is dark little secret of many.
Hemochromatosis -- the Celtic curse.
Disease (Dr. Gott).
ALD and Lorenzo's Oil.
inhibitors down-regulate oestrogen receptors in fat; possible contributor to fat
Laughter's Link to Health May Be in the Blood.
exempts injured workers from service-break PERS penalty.
and Ipsen Agree to Develop Sustained-Release Formulations of Recombinant Human
Medics are misreading CJD risk
Mecasermin Rinfabate for Growth Hormone Insensitivity Syndrome
Medical Hall of Fame Announces 2005 Inductees
‘Our dreams might just come true’
Still producing 'milk' two years after miscarriage?
Corticosteroid Treatment Effective for Children's Asthma
Upcoming Meetings in Tampa Bay, FL, DC Metro Area, New England, San Diego and Chicago; Local Meetings
new bios, three updates.
Read all about them below.
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
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!
Jayne presented a table full of Cushing's info at her local Health Fair In
Fredericksburg, VA. She plans to set up something similar at the NIH Health
and Wellness Fair May 15th.
More info here »
Double click on any photo to view full-sized.
A new Message Board area has been 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!
Did you spend years searching for a
diagnosis before finding one? Did you see doctor after doctor, desperately
looking for an answer to the question "what is wrong with me?" If so, your story
may be of interest for the new Discovery Health Channel series Mystery
- have spent months or years searching for a
- seen multiple doctors and gotten multiple
- have ultimately reached a diagnosis that
both you and your physician are satisfied with.
- The eventual diagnosis doesn't have to be
rare or complicated, but the "journey" to solving the mystery should be
If this situation sounds familiar to you, and
you are eager to tell your story, contact Timothy Hedden, (212) 627-6053 x443.
welcome your articles, letters to the editor, bios and Cushing's
Submit a Story or Article to either the snailmail CUSH Newsletter or to
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Medical detectives put Lenin under the microscope
Michael Woods, Medical Journal
Nashua Telegraph - Nashua, NH, USA
Published: Sunday, Mar. 20, 2005
Workers such as airline pilots, bus drivers and surgeons - who hold the lives of other people in their hands - are expected to take a break from work when they develop physical or mental illness that could affect their performance.
Heads of state who develop incapacitating illness sometimes ignore that basic rule of occupational medicine, even though their decisions can affect millions of people.
A long list of political leaders has stayed in power despite serious illnesses that may have lessened their ability to lead.
King George III of England, for instance, sometimes had to be put in a strait jacket and chained to a chair to control his insane outbursts. Former United States presidents Woodrow Wilson and Franklin D. Roosevelt had strokes that seemingly affected their judgment.
Former President John F. Kennedy looked tan and fit, but actually was taking a dozen medications a day for severe back pain, intestinal problems, Addison’s disease (a disorder of the adrenal glands) and other problems.
The newest addition to the list - Vladimir Illyich Lenin - may top them all in terms of the eventual toll in human life. Lenin founded the Bolshevik Party, which ushered the Soviet Union into existence. This year is the 81st anniversary of his death.
Lenin died at 53 on Jan. 21, 1924, after a long illness. In those final years, a political enemy named Joseph Stalin positioned himself to seize power after Lenin’s death. Stalin changed the country’s direction.
Historians rank Stalin among history’s greatest mass murderers. Through political purges, a contrived famine in the Ukraine and other acts, Stalin may have caused more than 12 million deaths.
A new study suggests that syphilis may have let power slip into Stalin’s grasp.
Rumors have circulated for decades that Lenin had syphilis, a sexually transmitted disease that can be fatal if not treated. The disease gradually spreads throughout the body and there was no effective treatment in Lenin’s day.
In the final stages, it damages the brain and blood vessels in ways that can lead to depression, lethargy, memory loss and strokes.
Until the Soviet Union’s collapse in 1991, however, medical records of Lenin’s illness and autopsy were secret. Since then, however, more and more information has leaked out, including recollections of doctors who treated Lenin and those present at the autopsy.
That information strongly supports the idea that Lenin died from syphilis that he caught decades earlier - and not from hardening of the arteries as the official Soviet accounts contended.
Researchers from the Be’er Sheva Mental Health Center in Israel now have analyzed the full body of information on Lenin’s illness. It included records of Lenin’s treatment by famous psychiatrists who treated only one disease - syphilis.
The researchers concluded that syphilis is the only explanation Lenin’s symptoms and the autopsy findings.
Lenin must have known his fate. What if he had stepped aside in favor of a trusted associate capable of dealing with Stalin?
Michael Woods is a medical writer for The Toledo Blade. Contact him at firstname.lastname@example.org.
New Study Shows Seditol™ Highly Effective For Improving Sleep and Reducing Fatigue
March 16, 2005 - Next Pharmaceuticals, Inc.
(Irvine, CA)– A new human study conducted by an independent contract research organization has clearly demonstrated that the natural ingredient Seditol™ is highly effective for ensuring a sound night’s sleep and allowing adults to wake up feeling refreshed. The study of forty-five adults, the second such study for Next Pharmaceuticals, reported the percentages of subjects that agreed with the following statements:
Helps ensure a sound night’s sleep: 91%
Allows you to wake up feeling refreshed: 89%
Reduces fatigue due to lack of sleep: 91%
Is gentle to your stomach: 96%
Has less side effects than other sleep aids: 87%
Gives me more energy during the day: 84%
Eighty-two percent (82%) of the subjects rated the product as “effective” in helping them fall asleep and 87% of the subjects reported that they fell asleep quickly. Eighty percent (80%) rated the product as effective in helping them sleep throughout the night. Eighty-seven percent (87%) of the subjects rated the product as effective in providing a restful sleep. Seventy-six percent (76%) of the subjects stated they felt “refreshed” after waking up and 84% rated the product as effective in relieving mild insomnia/sleeplessness.
Seditol™ is a blend of a patented extract of Magnolia officinalis (U.S. Patent No. US 6,582,735) and a proprietary extract of Ziziphus spinosa. “The exciting results of this study confirm the positive results we obtained from our first study.” says Bob Garrison, President and CEO of Next. “We believe Seditol™ can be highly effective for the 70 million Americans who have difficulty sleeping, because it addresses the primary cause of sleeplessness in otherwise healthy adults: an overactive hypothalamic-pituitary-adrenal axis due to unresolved stress. Plus, the pharmacology behind Seditol™ suggests that it is the natural choice for excessive body weight associated with less than adequate sleep.”
New research has shown a significant relationship with the amount of sleep a person gets and their weight/body mass index. A 2005 published paper showed that reduced amounts of sleep are associated with overweight and obese status. (Arch Intern Med, 2005;165:25-30) An explanation for these findings was published in two 2004 studies that demonstrated when people don’t get eight hours of sleep nightly there is an increase in stress hormones at night and an 18% reduction in the hormone leptin that normally helps control appetite, plus a 28% increase in the hormone ghrelin that increases appetite. (Ann Intern Med, 2004 Dec 7;141(11):846-50
Seditol™ is available to manufacturers of dietary supplements as a stand-alone product, or as an ingredient in combination formulas. Next Pharmaceuticals, Inc. is a research and development company that markets its patented or patent-pending ingredients to dietary supplement, food, and beverage companies focused on products for healthy living. For more information on Seditol™ or Next’s other ingredients, visit www.nextpharmaceuticals.com.
Last Updated: 10:36 pm, Thursday, March 17th, 2005
Night eating syndrome is dark little secret of many
By Gannett News Service
Imagine a scenario where you get up in the morning with absolutely no hunger. You don’t eat.
As the day wears on, you drink a lot of coffee. You eat a light lunch or snack.
Come dinnertime you’re ravenous. You eat dinner.
But then you snack after dinner almost continuously right up to the time you go to bed. Your choices might include candy, cookies, potato chips or ice cream.
After falling asleep, you wake up and are convinced you can’t get back to sleep unless you eat something. You feel frantic. That’s when you steal into the kitchen and eat peanut butter right out of the jar.
This is the pattern day after day for people with night eating syndrome.
Dr. Albert J. Stunkard, a psychiatrist and director emeritus of the Weight and Eating Disorders Program in the Department of Psychiatry at the University of Pennsylvania Hospital, first described night eating syndrome with two colleagues in 1955.
Today the syndrome, which had remained a lesser-known disorder for years, is getting new attention because of its link to obesity and the current focus on overweight Americans, says Kelly C. Allison, a psychologist who is director of the night eating syndrome study at the University of Pennsylvania.
Night eating syndrome affects about 1 percent to 2 percent of the general population.
While you don’t have to be obese to have night eating syndrome, about 25 percent of people who are overweight by at least 100 pounds are thought to have night eating syndrome, according to several studies.
Both men and women are affected, with women representing about 60 percent of sufferers and men about 40 percent.
Research published last year in the International Journal of Eating Disorders indicated the syndrome might be a pathway to obesity.
An obese group and non-obese group with almost identical night eating behaviors were studied. The only difference that emerged was age. The non-obese were about 10 years younger, which led researchers to speculate that the night eating disorder would make them obese in time.
Those with night eating syndrome consume more than half of their daily food intake during and after dinner.
The foods of night eaters tend to be sugary and starchy.
“They’re eating chips and cookies,” says Cheryl Ades, a licensed clinical social worker in private practice in a center that treats eating disorders in Louisville, Ky. “They’re grabbing a pack of Reese’s.”
She says research shows night eaters are trying to relieve stress. The brain triggers a heavy preference for carbohydrates so the anxious mood of the person can be quieted.
Norwegian researchers found evidence the midnight raid on the refrigerator has more to do with the failure of the body to respond appropriately to stress than to a person’s appetite. The hypothalamus, pituitary and adrenal glands may be chronically overstimulated in people with night eating syndrome.
Allison says that in her night eating syndrome study group the usual age of onset is about 30, and for about three-fourths, there was a trigger event for the behavior.
“There was a stressful event — the loss of a job, difficult pregnancy, getting off drugs, alcohol or cigarettes. They calmed their stress or anxiety by eating.”
The University of Pennsylvania research has shown that the circadian cycle, 24-hour biological rhythm, for eating becomes disturbed in those with night eating syndrome, while their circadian cycle for sleeping does not.
Imagine that your body’s 24-hour cycle for eating and 24-hour cycle for sleeping were at odds with each other. This is the first disorder to be discovered in which the two biological rhythms have been dissociated, the researchers report.
The hope of experts studying night eating syndrome is that it will become more widely recognized as an eating disorder and that strategies of treatment and prevention can be developed.
Dear Dr. Gott
Posted on Mon, Mar. 14, 2005
By Peter H. Gott, M.D.
Dear Dr. Gott: I was hospitalized eight years ago because of lethargy, general weakness and signs of pigmentation. I was diagnosed with Addison's disease. I was prescribed cortisone and am now suffering from diabetes, which may be one side effect of the cortisone.
How can I get off this medication and, further, how do I bring the Addison's under complete control?
Dear Reader: Addison's disease is caused by a failure of the adrenal glands to manufacture and secrete vital chemicals, such as cortisone, that the body requires. The only treatment to avoid inevitable shock and death is to replace these chemicals with prescription pills.
As you know, excess cortisone can lead to diabetes. However, this shouldn't be a problem in patients with Addison's because the amount of the drug can be carefully controlled (using blood tests) so that only the necessary amount is administered.
Symptoms of Addison's include weakness, low blood pressure, skin pigmentation, diarrhea, dehydration and malaise. The diagnosis is made by blood tests, especially a test to measure serum cortisone after the adrenal glands have been stimulated by a medicine called ACTH.
On occasion, Addison's disease and diabetes may co-exist. Such a combination is challenging to treat because the diabetes may be exceptionally difficult to control with standard insulin therapy. Your doctor should address the issue of diabetes as a separate problem -- unless your blood tests show that your replacement therapy is excessive, in which case he should reduce the dosage.
You will need to take cortisone replacement therapy for the rest of your life. Don't stop it without your doctor's approval, because you could become dangerously ill.
Write to Dr. Gott c/o United Media, 200 Madison Ave., 4th fl., New York, N.Y. 10016.
The Medical Minute: Hemochromatosis -- the Celtic curse
Thursday, March 17, 2005
By John Messmer
Penn State Family and Community Medicine
Penn State Milton S. Hershey Medical Center
Penn State College of Medicine
March brings St. Patrick's Day, the traditional day to celebrate all things Irish. The 2000 census shows more than 10 percent of the U.S. population reporting Irish ancestry. In Pennsylvania, it's more than 16 percent. Many things are associated with Irish-Americans -- woolen goods, Celtic music, and Irish foods and drinks, but few people know the story of Celtic curse.
The Celtic curse refers to the disease of hereditary hemochromatosis, or HH. It is so-called because it is common in people of Celtic background: Irish, Scots, Welsh and British. Additionally, HH is one of the most common genetic diseases in the United States, occurring in one in 200 Caucasians with one in 10 being a carrier -- most, but not all of these having Celtic ancestry. By contrast, sickle cell anemia occurs in one in 500 African-Americans with one in 12 being carriers. Despite its prevalence, it remains relatively unknown, even among physicians.
HH causes iron to be absorbed even when it is not needed. Normally, people absorb a tiny amount of iron daily, just enough to replace what is lost from normal bodily functions. Women absorb more during their childbearing years to replace iron loss from menstrual blood. In hemochromatosis, iron continues to be absorbed excessively. Once the places where iron is normally stored are full, iron begins to be stored in the liver, heart, skin and other organs, damaging them. This can lead to heart failure and rhythm disorders, diabetes, cirrhosis and liver tumors. Untreated, it can be fatal.
HH is the result of genetic mutations, the most common ones called C282Y and H63D. The mutation is believed to have developed about 40,000 years ago in what is now Ireland to compensate for an iron-poor diet. At that time, it would have been beneficial.
The mutations are passed on from parents to children. The HH genes are recessive. That means the disease occurs only when two copies of the gene are present -- one from each parent. If only one copy is passed, the person is a carrier. The full-fledged disease is seen only in those with two copies. Carriers also can store too much iron, but they rarely have organ damage.
In the most common form of HH, males usually do not develop symptoms until after age 30, and women may not show problems until after menopause because they lose iron regularly during menses. Symptoms relate to the organs that become overloaded with iron and can include arthritis, liver disease, diabetes, thyroid deficiency, bronze skin color, impotence and adrenal gland abnormalities and such nonspecific symptoms as fatigue or aches.
The problem is actually easy to diagnose before any damage occurs by measuring iron levels in the blood. This is a different test than a blood count, the typical test for anemia. Having a normal blood count does not give any information about HH. Blood donor centers test for too little iron; passing the test does not say anything about having too much iron.
Screening for HH is done with a serum iron level and transferrin saturation and often a ferritin level. Transferrin is a protein that carries iron in the blood and ferritin is an iron storage protein. If the iron level is high and transferrin is more than 40 percent saturated or ferritin is higher than 200 or so, HH should be considered. If a doctor tells a patient that his or her iron is great or high enough that there is no need to worry about anemia, the patient should ask how high it is and whether he or she should be tested for hemochromatosis.
To diagnose HH, a blood sample is tested for the two more common DNA mutations. Until the DNA test was available, liver biopsy was needed to test for iron deposits. Biopsy is reserved for those who have developed cirrhosis of the liver to help determine if the cause is hemochromatosis.
People with one copy of the gene should avoid taking extra iron in vitamins and supplements and should avoid using iron cookware and extra vitamin C, which enhances iron absorption. A person with two copies of the gene has the disease and should begin a program of iron elimination. Treatment is through therapeutic phlebotomy. This is just like the process of donating blood -- a unit is removed as often as weekly if needed to reduce iron levels to normal. Treatment can be ordered by many types of medical specialists including a family physician.
The family of anyone with even one HH gene should consider testing even if they have no symptoms. Those with the disease will pass on one copy of the gene to each of their children. Carriers have a 50/50 chance of passing on a hemochromatosis gene to each child. Some advocate testing in childhood if one or both parents are known to carry the gene so the child's diet can be managed to keep iron levels under control.
Hereditary hemochromatosis is a fairly common disorder, but it's the luck o' the Irish to be able to diagnose and treat it effectively, especially if found early. This St. Patrick's Day, when a bit of the blarney leads to tales of leprechauns and shamrocks, remember the story of the Celtic curse.
Amy Buehler Stranges
ALD and Lorenzo's Oil
From Mary Kugler
Disease still not fully understood
The 1992 movie "Lorenzo's Oil" brought to the attention of the world a rare disorder called adrenoleukodystrophy (ALD). It is a progressive degenerative myelin disorder, meaning that myelin, the "insulation" around nerves, breaks down over time. Without myelin, nerves can't function normally, or at all. Unfortunately, the body can't grow replacement myelin, so the disorder is progressive--it gets worse over time.
What causes ALD? Who gets it?
ALD is an inherited genetic disorder linked to the X sex chromosome. Because of the way genetic inheritance works, only boys have the most severe form of ALD. The disorder leaves the body unable to break down big fat molecules, either ones the body makes itself or ones that enter the body through food. Recent research shows that this is most likely due to a carrier protein that fails to work correctly and carry the fat molecules to where they would be broken down.
The fat molecules build up and clog up cells, and hurt nerve cells in the brain and spinal cord.
Scientists now have a way of examining a woman's ALD gene to see if it's abnormal. This way, a woman who may have inherited an abnormal gene will know for certain whether or not she has it (is a carrier) and could pass it on to her children.
Do all boys with ALD die?
There are several forms that ALD can take. The most devastating type, what Lorenzo Odone has, is the childhood cerebral form, meaning that nerves in the brain are destroyed. About 35-40% of all cases of ALD are this type, which usually appears between 4 and 8 years of age in boys. These boys will become totally disabled in 6 months to 2 years, and will die sometime after.
ALD can also appear like multiple sclerosis, in that there is a gradual loss of function in the body but without the severe brain damage of the cerebral type. This second form is called adrenomyeloneuropathy (AMN), represents about 40-45% of all ALD cases, and affects men in their twenties or middle age.
Because adrenoleukodystrophy damages the adrenal glands, the disorder can begin as Addison's disease. This represents about 10% of all ALD cases, and affects males between 2 years of age and adulthood. Young men with this form usually also develop AMN by middle age. Boys diagnosed with Addison's disease are usually tested to see if ALD is at the root of the problem.
Can ALD be cured?
Unfortunately, there is as yet no complete cure for cerebral ALD. However, there are several methods being tried that seem to slow down the destruction of the disease. One method is the use of Lorenzo's oil and a very low fat diet. Unfortunately, Lorenzo's oil has not proven to be as effective as first thought. Researchers are still trying to understand the complex relationships among fats in the body, and how Lorenzo's oil could be further modified to be more effective.
A second treatment, being tested experimentally, is an anticholesterol drug called Lovastatin. Researchers aren't clear exactly why this drug seems to help, but are working on understanding the processes involved.
A third method for treating cerebral ALD is bone marrow transplant. The idea is to replace cells that have a defective ALD gene with cells that have a normal ALD gene and will break down fats.
As for adrenomyeloneuropathy (AMN), no treatment has yet been developed. If an adrenal disorder like Addison's disease is present, long-term hormone replacement provides treatment.
How is Lorenzo doing? Is he still surviving?
Lorenzo Odone turned 25 years old on May 29, 2003. He is "holding his own," said his father, Augusto Odone, in an interview with The Washington Post. "He looks healthy, but he hasn't recovered any functions in a big way," he added. Lorenzo can communicate by blinking his eyes and wiggling his fingers. Unfortunately his mother, Michaela (portrayed in the movie by Susan Sarandon), died June 10, 2000, of lung cancer.
Information for this article was taken from:
- GeneClinics (1999). X-Linked Adrenoleukodystrophy.
- Johns Hopkins Medical Institutions (Oct. 28, 1998). New test spots ALD carriers with near-perfect accuracy.
- King5.com (2000). 'Lorenzo's Oil' mother Michaela Odone dies. Reprinted from The Washington Post, June 11, 2000.
Protease inhibitors down-regulate
oestrogen receptors in fat; possible contributor to fat loss?
Protease inhibitors may reduce subcutaneous fat levels partly
through down-regulation of oestrogen receptors in fat tissue,
according to a report by Italian researchers published in the
March 25th edition of AIDS.
Some studies have shown women to be at higher risk of fat loss
than men, and the group from the universities of Padova and
Verona in Italy set out to determine whether this difference
might be explained through effects of antiretrovirals on
oestrogen receptor levels in adipose tissue.
Sex steroid hormones such as oestrogen play a role in the
differentiation of adipose cells and the consequent sex-related
distribution of fat throughout the body, giving rise to the
pear-shaped fat distribution seen in women and the apple-shaped
fat distribution seen in men as they age. If fewer receptors for
steroid hormones are present in fat, the normal distribution of
fat might be altered.
In this study, the researchers recruited 14 male HIV-positive
patients, six treatment-niave patients just beginning HAART and
eight switching from a protease inhibitor-containing regimen to
a PI-sparing regimen. Five of the switch group had lipodystrophy.
Metabolic, endocrinological and body fat measurements were
evaluated at the time of treatment initiation or switch, and
again six months later. Adipose tissue gene expression was also
evaluated by needle biopsy of abdominal subcutaneous fat at the
same time points.
Metabolic and body fat evaluation showed that patients with
lipodystrophy had significantly lower subcutaneous fat levels
and total body mass, but higher waist-to-hip ratio and visceral
adipose fat content as measured by DEXA scan. Lipodystrophic
patients also had higher total and LDL cholesterol levels, but
glucose and triglyceride levels did not differ between
lipodystrophic and non-lipodystrophic patients. Body fat
parameters did not change after six months of HAART or after a
switch of regimen.
Endocrinological analysis showed no significant difference in
levels of testosterone, free testosterone, estradiol,
progesterone, DHEAS, luteinising hormone (LH),
follicle-stimulating hormone (FSH), adrenocorticotrophic hormone
(ACTH) or urinary free cortisol.
Gene expression analysis did show differences in gene expression
however. Individuals with lipodystrophy had significantly lower
baseline levels of ER(beta) messenger RNA (a gene that encodes
steroid hormone receptors and which is more commonly expressed
in subcutaneous fat), and these levels rose significantly in all
switch group patients six months after switching from a
PI-containing regimen, whilst falling significantly in
treatment-naïve individuals after six months of HAART.
“As sex steroid hormone levels did not significantly change in
our patients during HAART, the modulation of ER(beta) expression
did not seem to be a consequence of abnormal hormone levels”,
the researchers note.
“Our findings suggest a role for this receptor in HIV-associated
lipodystrophy, opening the avenue to investigations on selective
oestrogen receptor modulators for the management of this
Barzon L et al. Do oestrogen receptors play a role in the
pathogenesis of HIV-associated lipodystrophy? AIDS 19:
Laughter's Link to Health May Be in the Blood
By Rob Stein
Washington Post Staff Writer
Monday, March 14, 2005; Page A10
According to the Bible, "a merry heart doeth good like a medicine." Now, modern science may be validating that Old Testament proverb -- a good laugh may actually help fend off heart attacks and strokes.
"We believe laughing is good for your health," said Michael Miller of the University of Maryland School of Medicine in Baltimore, who led the research. "And we think we have evidence to show why that's the case."
A growing body of other evidence has suggested that negative emotions, particularly depression and stress, can be harmful, making people more prone to illness, more likely to experience suffering from their ailments and less likely to recover as quickly, or at all. One recent study even found sudden emotional shock can trigger life-threatening heart symptoms that many doctors mistake for a classic heart attack. Miller himself, along with his colleagues, had done a study that found people who have a negative reaction to social situations tend to be more prone to heart disease.
But far less has been done to examine whether positive emotions can reduce the risk and complications of illness.
"The focus is always on the negative aspects," he said. "We thought, 'Why not look at the opposite?' "
So they decided to examine the ability of blood vessels to expand -- known as vasodilation. Poor vasodilation can increase the risk of heart attacks and strokes by making the passageways prone to being blocked, cutting off vital blood flow.
The researchers asked 20 healthy men and women to watch clips of two movies -- either the violent opening battle scene in the 1998 film "Saving Private Ryan" or a humorous scene from a comedy, such as the 1996 "Kingpin."
The researchers tested the subjects' vasodilation, before and after the movie, by constricting and releasing an artery in their arms with a blood pressure cuff and then using ultrasound to measure how the blood vessels were functioning.
The researchers discovered striking differences depending on which movie the volunteers had watched. Blood flow was significantly reduced in 14 of the 20 volunteers who saw the stressful film. In contrast, blood flow markedly increased in 19 of the 20 volunteers after watching the funny movie, the researchers reported last week at a meeting of the American College of Cardiology in Orlando.
Overall, blood flow decreased by about 35 percent after experiencing stress but increased 22 percent after laughter -- an improvement equivalent to that produced by a 15- to 30-minute workout.
"It was a pretty dramatic difference," Miller said.
Previous research has indicated that stress hormones may be the primary culprit by which negative emotions harm health. When a person is under stress, the body pumps out hormones such as adrenalin and cortisol. That is designed to prime the body for a fight or a flight, but the hormones can have detrimental effects on the body, including suppressing the immune system and constricting blood vessels.
Miller and his colleagues hypothesize that laughter may have a contrasting effect, causing the body to release other natural chemicals known as endorphins -- pleasure-producing agents best known for producing the "runner's high" -- that may counteract the effects of stress hormones and cause blood vessels to dilate.
The researchers acknowledge they are still a long way from proving their hypothesis or fully understanding the process, but they say the theory makes sense.
"Conceivably, when you laugh you send a signal to the brain to release these endorphins, and these may activate receptors to release other chemicals, perhaps including nitric oxide, which is known to enhance blood vessel dilation," Miller said.
Laughter may also use similar mechanisms to help boost the immune system and reduce the amount of inflammation in the body, which has been linked to an increased risk of a host of health problems, said Lee Berk, an associate professor of health promotion and education who studies laughter at Loma Linda University in California.
"Laughter is not dissimilar from exercise," Berk said. "It's not going to cure someone from stage three cancer, but in terms of prevention it does make sense. In a sense, we have our own apothecary on our shoulders. Positive emotions such as laughter affect your biology."
Other researchers said the findings add new insight into the interplay of emotions and health.
"This is just the latest example of the importance of the mind-body relationship," said Herbert Benson, who studies emotions and health at Harvard Medical School. "This shows that we have to look not only towards how to reduce stress but how we can elicit positive feelings, as well."
Heart specialists agreed.
"We've known that there's an association between state of mind and cardiovascular health," said Stuart Seides, associate director of cardiology at Washington Hospital Center. "This type of study gives us a peek into the mechanism."
Robert Provine, a University of Maryland psychologist who also studies laughter, was somewhat more cautious. It remains unclear whether the act of laughter was really at work in the movie-watching volunteers, since the researchers did not actually measure how much they laughed, he said.
"The results could be the result of just the act of watching the movie. Or maybe it's just the act of engaging in something interesting that doesn't cause stress," Provine said.
Miller acknowledged he has no way to know for sure that laughing per se produced the effect he measured.
"Is it laughing or just feeling good? We don't know at this time. But clearly laughter is an active process, and probably a good belly laugh will be better than just smiling. I think this active process helps release endorphins," he said.
Provine, despite his doubts about the study, is all for laughter.
"I strongly recommend laughter, based on the fact that a life of laughter is better than one without it," Provine said. "It feels better when you do it."
Miller envisions a time when doctors might recommend that everyone get 15 to 20 minutes of laughter a day in the same way they recommend at least 30 minutes of daily exercise.
"Wouldn't it be ironic if it turns out that laughing 15 to 20 minutes a day would be added as part of overall good health habits, like running?" Miller asked.
He added that he would not recommend that people replace their daily trips to the gym with a Marx Brothers movie, but they could consider adding activities that make them laugh.
"There's no downside that I know of to laughing," Miller said. "Based on these results, I am happy to recommend laughing to my patients."
Bill exempts injured workers from service-break PERS penalty
All who leave for six to 12 months return to lower-tier benefits
Statesman Journal (Salem, OR)
March 21, 2005
After surviving a life-threatening brain tumor, David Beranek hopes to regain enough stamina to reclaim his McKay High School teaching job.
With help from the Legislature, the Keizer resident might be able to reclaim his former pension plan as well.
Beranek, 44, is one of tens of thousands of Oregon public employees who lost their rights to top-tier benefits of the Public Employees Retirement System because of a little-discussed provision enacted in 2003. Public employees who leave PERS-covered jobs for six to 12 months return under the lower-tier pension benefits offered to new employees.
For Beranek and others ensnared by the "break-in-service" provision, that means a lower guaranteed pension and several more years of work before reaching retirement age.
It's a "double whammy hitting me," Beranek said. "I won't possibly be able to work all the number of years I'll need to work to be able to afford retirement."
Beranek, off work since June 2003, said that he only has strength to be out of bed for two to four hours per day. He usually only leaves home for church and doctors' appointments.
Out of concern for people like Beranek, Gov. Ted Kulongoski's administration is asking the 2005 Legislature to approve two changes to the break-in-service rules. Senate Bill 105 would exempt people who leave their jobs because of injury and disease. Senate Bill 188 would exempt seasonal workers.
Others are hopeful
Mason Young hopes the Legislature will go beyond those bills and aid others harmed by the break-in-service provision.
Young, 42, is one of 318 school custodians laid off by Portland Public Schools in 2002. The school district replaced the custodians with a private company, which hires people with disabilities who work for lower pay.
Young was lucky enough to land another PERS job in the Beaverton School District. But it took 16 months in a state mired in a recession. Under the pension plan adopted by the 2003 Legislature for newly hired employees, he will have to wait five more years until reaching retirement age.
"Oh, man, that's really going to hurt, having to work another five to six years," Young said. "I'm going to have 34, 35 years in the system before I can retire."
His ultimate pension also is likely to be lower, though it's not clear by how much.
"They just take and pull the rug out from under you," Young said.
Grant Walker was one of the few Portland custodians who landed another PERS job before six months passed. He thinks the break-in-service rule was unfair to his co-workers, who were laid off in the middle of a recession.
"If you're lucky enough to find a PERS job, you shouldn't have to be penalized for something that's way above and beyond your control," Walker said.
New plan gets support
Rep. Greg Macpherson, D-Lake Oswego, helped craft the Oregon Public Service Retirement Plan for new employees. He said it still is generous compared with many other retirement plans.
The new plan guarantees workers a pension equalling 45 percent of their final salary if they work 30 years. Workers also get individual accounts, amassed from 6 percent of their salary set aside each year, known as the "employee contribution." Once Social Security benefits kick in, many public employees might still retire with pensions approaching their salary while working.
"I think that's a very good result for them," Macpherson said. "I would not apologize for it."
Most custodians in the private sector get no pension plan outside Social Security, he said.
But workers covered by the Oregon Public Service Retirement Plan must work longer than the previous generation of public employees.
Tier 1 PERS members hired before 1996 can retire at 58, or as soon as they work 30 years, regardless of age. Normal retirement age went up to 60 under the Tier 2 plan for new hires adopted in 1995 . The normal retirement age rose to 65, or 58 once workers log 30 years, under the Oregon Public Service Retirement Plan adopted in 2003.
After leaving their PERS jobs for more than six to 12 months, people like Beranek and Young must work an extra five to seven years to qualify for regular retirement.
Decision widens gap
Last week's Oregon Supreme Court decision widened the gap between the new and old plans. The court reinstated the most generous benefit for Tier 1 members: guaranteed 8 percent annual investment earnings on their regular accounts, even when PERS investments lose money. That will enable more Tier 1 workers to benefit from the Money Match option, which has served to drive up pensions in recent years.
Macpherson and PERS Executive Director Paul Cleary said that it's appropriate for the Legislature to consider some exemptions from break-in-service rules for situations that weren't anticipated when the law was crafted in 2003.
"Some of the employers did recognize that the break-in-service (rules) did create a number of difficult situations," Cleary said.
Government employers appear more sympathetic to exemptions for injury and disease than other circumstances. That's because the main reason for the 2003 change was to rein in costs of the pension system, which still faces a long-term shortfall of more than $6 billion.
It's unclear where to draw the line when 8 percent to 10 percent of the PERS work force turns over each year, Cleary said.
Other groups of people harmed by the break-in-service rules are young families, especially mothers who want to stay at home for a while to be with their babies, and Mormons called to two-year missionary stints.
A coalition led by public employees has filed suit against the break-in-service rules in Multnomah County. That suit hasn't gone to trial yet.
"If we could fix the break-in-service (rules) through legislation, we'd probably drop the lawsuit," said Mary Botkin, a lobbyist for the American Federation of State, County and Municipal Employees.
Aside from worrying about his pension, Beranek is focusing on regaining his strength. He desperately wants to return to the classroom, where he was an award-winning Spanish teacher.
He shed the weight he gained because of a tumor on his pituitary gland. He lost the "buffalo hump" on his shoulders that is another symptom of Cushing's disease.
"My body on the outside looks normal," he said.
But living on his wife's salary and a $479 monthly disability check has been a strain. He's hoping to get well enough to return to McKay in 18 months.
slaw@StatesmanJournal.com or (503) 399-6615
Genentech and Ipsen Agree to Develop Sustained-Release Formulations of Recombinant Human Growth Hormone
SOUTH SAN FRANCISCO, Calif. and PARIS, March 21 /PRNewswire-FirstCall/ --
Genentech, Inc. (NYSE: DNA) and Ipsen today announced the recent execution of
a collaborative research and development (R&D) agreement to develop
sustained-release formulations of Genentech's recombinant human growth hormone
[somatropin (rDNA origin)].
This R&D collaboration is in addition to and supplements a previous
agreement signed in 2002 whereby Ipsen gained exclusive rights to market
NutropinAq(TM) Pen throughout Europe and the rest of the world, excluding
North America and Japan. Nutropin AQ Pen(R) for use with the Nutropin AQ
Pen(R) cartridge was cleared for marketing by the U.S. Food and Drug
Administration in April 2002 and obtained marketing authorization under the
trade name NutropinAq Pen from the European Medicines Agency in March 2004.
Ipsen has already launched NutropinAq Pen in 12 European countries.
"We at Ipsen are proud to bring our expertise in sustained-release
technology to this new collaboration with Genentech," said Mr. Jean-Luc
Belingard, president and chief executive officer of the Ipsen Group. "Our
common objective is to develop sustained-release formulations of recombinant
human growth hormone to meet the needs of pediatric and adult growth hormone
deficiency (GHD) patients."
"Genentech has a 20 year heritage of exploring new product options for
growth hormone delivery to patients," said Joseph S. McCracken, Genentech's
vice president of Business Development. "We value our collaboration with
Ipsen and their experience with novel sustained release technology."
About Nutropin AQ
Nutropin AQ [somatropin (rDNA origin) injection] is produced using
recombinant DNA technology and has the same amino acid sequence as human
growth hormone produced naturally in the human body. It is marketed as
NutropinAq in Austria, Denmark, Finland, France, Germany, Ireland, the
Netherlands, Norway, Sweden, Portugal, Spain and the United Kingdom. Other
regulatory reviews are underway in Europe and worldwide, excluding North
America and Japan.
Nutropin AQ is supplied as 10 mg of sterile liquid somatropin per
cartridge for exclusive use with the Nutropin AQ Pen, a simple, convenient,
easy-to-use device for subcutaneous injection. Nutropin AQ is approved for
the treatment of GHD in children and adults, for the long-term treatment of
short stature in children with Turner syndrome and the treatment of growth
failure in chronic renal insufficiency patients prior to transplantation.
Nutropin AQ Safety Information
Growth hormone should not be initiated to treat patients with acute
critical illness due to complications following open heart or abdominal
surgery, multiple accidental trauma, or to patients having acute respiratory
Nutropin AQ should not be used for growth promotion in pediatric patients
with closed epiphyses. Nutropin AQ should not be used in patients with active
neoplasia. Growth hormone therapy should be discontinued if evidence of
Growth hormone is contraindicated in patients with Prader-Willi syndrome
who are severely obese or have severe respiratory impairment. Unless patients
with Prader-Willi syndrome also have a diagnosis of growth hormone deficiency,
Nutropin AQ is not indicated for the long-term treatment of pediatric patients
who have growth failure due to genetically confirmed Prader-Willi syndrome.
Genentech is a leading biotechnology company that discovers, develops,
manufactures and commercializes biotherapeutics for significant unmet medical
needs. A considerable number of the currently approved biotechnology products
originated from, or are based on, Genentech science. Genentech manufactures
and commercializes multiple biotechnology products directly in the United
States, and receives royalties or other income from companies that are
licensed to market its products outside of the United States. The company has
headquarters in South San Francisco, California and is traded on the New York
Stock Exchange under the symbol DNA. For additional information about the
company, please visit http://www.gene.com .
Ipsen in Endocrinology and Drug Delivery Technology
Endocrinology is one of the therapeutic areas targeted by Ipsen. Ipsen
endocrinology sales are driven by its somatostatin analog (Somatuline(R) and
Somatuline(R) Autogel(R)) mainly indicated in the treatment of acromegaly and
Among Ipsen R&D programs in endocrinology & metabolic diseases, two major
molecules are under clinical development:
-- BIM51077 (Glucagon Like Peptide-1 analogue), in phase II clinical
development intended for the treatment of Type 2 diabetes;
-- BIM44058 in Phase I clinical development intended for the treatment of
severe osteoporosis and bone fractures.
Regarding drug delivery technology, Ipsen is one of the world leaders in
the production of sustained-release systems with two peptides, triptorelin
(Decapeptyl(R)) and lanreotide (Somatuline(R) and Somatuline(R) Autogel(R)).
Present in over 110 countries, with a total staff of nearly 4,000, Ipsen
recorded sales of Euro 737.2 million in 2003, a third of which originated
outside the five major countries in Western Europe (France, Germany, Italy,
Spain and the United Kingdom). The Group develops products in three targeted
therapeutic areas: oncology, endocrinology and neuromuscular disorders, and
is also engaged in developing certain biological derived products. Ipsen is
currently marketing more than 20 products, both to specialists working in its
targeted therapeutic areas and in therapeutic areas related to the Group's
history. In 2003, 18.5% of Ipsen's turnover was invested in Research and
Development, carried out through an international network of about 615 people
from 4 centres: Paris, Boston, Barcelona and London. Ipsen's Internet website
CONTACT: media, Edward Lang, +1-650-467-8606, or investors,
Diane Schrick, +1-650-225-1599, both for Genentech; or Didier Veron,
+33 (0) 1 44 30 42 15, for Ipsen.
SOURCE Genentech, Inc.
Web Site: http://www.gene.com
Medics are misreading CJD risk
By Jennifer Cooke
March 14, 2005
A misinterpretation of infection-control guidelines has led to some surgeons, dentists and hospitals refusing or deferring patients whose previous medical regime has put them at small risk of a fatal brain disease.
The patients who need surgery or elective procedures to improve or monitor their health feel they are mistakenly treated as being at "high risk" rather than at "low risk" of contracting the lethal Creutzfeldt-Jakob Disease, and that finance and insurance take priority over their well-being because cleaning expensive surgical instruments to the required standard to neutralise the CJD agent can destroy the instruments.
The instruments, some of which cost tens of thousands of dollars, must be treated either with longer and higher temperature surgical autoclaving - after use on high-risk tissue such as the brain or spine - or destroyed or quarantined for exclusive use on an individual patient.
The national co-ordinator of the CJD Support Group Network, Suzanne Solvyns, said problems have occurred because some medical professionals have mistakenly treated procedures on patients with low infectivity tissue as the more dangerous high-infectivity tissue.
A Sydney woman told the Herald she had been "treated like a leper" three times in the past three years by different surgeons and hospitals operating in the eastern suburbs - most recently by a gastroenterologist who refused to treat her and referred her for an alternative procedure and to an infectious diseases specialist.
Other cases include a woman from Canberra - already prepped for a gall bladder removal at a hospital that had known of her hHG injections for months - who was sent home after an infection-control nurse read her medical history.
A Queensland man had his public dental surgery postponed - just as the procedure was starting - when he belatedly told the dentist of his hGH treatment.
The latest guidelines state that people regarded at "low" risk of acquiring CJD include those recipients of cadaver-derived human pituitary hormone drugs, but that it is only high-risk tissue such as the brain and spine that requires the quarantining of equipment until CJD is either confirmed - when the instruments must be destroyed - or ruled out, which then allows the instruments to be re-used.
Mrs Solvyns said these patients were not in any high-risk group.
"Low infectivity tissue only needs normal sterilisation and that's what's causing the stress to recipients. "It's almost like they won't believe the guidelines - or the experts," she said.
A spokeswoman for the Department of Health and Ageing, Kay McNiece, said yesterday: "The department was very disappointed to find that in some cases doctors are misreading the infection-control guidelines which very clearly spell out what precautions are needed, but also what precautions aren't required."
Mecasermin Rinfabate for Growth Hormone Insensitivity Syndrome
Mar 11, 2005, 07:12
Mecasermin rinfabate is a proprietary delivery composition of insulin-like growth factor I (IGF-I). The novel compound is administered as a subcutaneous injection, which can restore IGF-I levels to physiologically relevant levels.
By Akanksha, Pharmacology Correspondent,
Insmed Incorporated announced today that the Company has received the acceptance to file notification from the U.S. Food and Drug Administration (FDA) for the New Drug Application (NDA) for its drug candidate SomatoKine (mecasermin rinfabate), a novel once-daily IGF-I therapy for the treatment of growth hormone insensitivity syndrome (GHIS).It is expected that the FDA will take action on the application no later than November 3, 2005.
The FDA previously granted mecasermin rinfabate, an IGF-I therapy, orphan drug designation, a designation conferred upon investigational products for diseases that affect fewer than 200,000 patients in the United States. Products with orphan drug designation that are the first to be approved for a specific indication have seven years market exclusivity within the United States.
Mecasermin rinfabate is a proprietary delivery composition of insulin-like growth factor I (IGF-I). The novel compound is administered as a subcutaneous injection, which can restore IGF-I levels to physiologically relevant levels.
On July 20, Insmed provided the top-line results from a six-month data analysis of the pivotal Phase III GHIS clinical trial showing a statistically significant increase (p less than 0.0001) in height velocity in children receiving mecasermin rinfabate as a once-daily injection.
In diabetic subjects, administration of mecasermin rinfabate demonstrated a significant improvement in blood sugar control and a significant reduction in daily insulin use.
Following severe burn injury, in both children and adults, administration of mecasermin rinfabate demonstrated a significant improvement in muscle protein synthesis and a significant reduction in the inflammatory response associated with the trauma.
In recovery from hip fractures, administration of mecasermin rinfabate demonstrated a significant improvement in functional recovery and bone mineral density.
Canadian Medical Hall of Fame Announces 2005 Inductees
LONDON, March 10 /CNW Telbec/ - The Canadian Medical Hall of Fame (CMHF)
announced its 2005 Inductees today. The five Inductees - luminaries of
medicine - forever changed the country's health care landscape through their
innovation and dedication to advancing the well-being of people everywhere.
- Dr. David Hubel Co-winner of the 1981 Nobel Prize in Medicine
for his ground-breaking research of the visual
cortex, the part of the brain involved in
vision. His discoveries have advanced the
understanding of brain development following
birth, and emphasized the importance of
treating strabismus - a condition in which the
eyes are crossed - at an early age.
- Dr. John McEachern (1873-1947) Identified the value of a national
cancer care strategy in the 1930's. Founding
President of the Canadian Society for the
Control of Cancer, the forerunner of the
Canadian Cancer Society. He was also a strong
advocate for the Canadian Medical Association,
and led the movement to federate the CMA with
provincial medical associations in 1938.
- Dr. Ian McWhinney A founder of modern Family Medicine in Canada,
credited with defining the discipline as a
distinct field of medicine. A world-renowned
medical educator, his approach to health care
is a basic model used in training family
doctors. He established the Centre for Studies
in Family Medicine, which is regarded as a
premier medical research centre in Canada.
- Dr. Anthony Pawson International leader in biomedical research.
His discoveries have greatly enhanced the
understanding of the way cells "communicate"
with each other, and how this communication
breaks down in diseases such as cancer, heart
disease, and immune system deficiencies. This
research has led to the development of new
cancer treatment drugs.
- Dr. Hans Selye (1907-1982) Scientist, endocrinologist and
Nobel prize nominee. "Father" of the field of
stress who discovered the biological stress
response. His initial, and yet one of his
greatest, discoveries was that stress affected
the endocrine, gastrointestinal and immune
systems through the brain's release of factors
and of hormones, inducing the production of
adrenal steroids, which he subsequently named
-corticoids--. He demonstrated the role of
stress in illness and the interaction between
the mind and the body, initiating the era of
The Inductees were selected by an independent committee of leaders from
the medical sciences community.
"When I graduated from McGill Medical School in 1951, over a half century
ago, I could not have imagined that I would ever qualify for such an honour as
to be elected to the Canadian Medical Hall of Fame. My fellow medical students
would have been equally astonished! I believe I owe any abilities I may have
had in scientific research to my training in high school, college and medical
school in Montreal, and am forever grateful for that," says 2005 Inductee
Dr. David Hubel.
"It is a great honour to be named to The Canadian Medical Hall of Fame as
a Builder in Medicine. I came to London in 1968 and, like many others, have
worked to advance the discipline of Family Medicine. To attain all that has
been achieved has taken dedication by many people. I feel that I represent
them all," says 2005 Inductee Dr. Ian McWhinney.
The Canadian Medical Hall of Fame will formally induct the five incoming
Laureates on September 22, 2005 at the Shaw Convention Centre in Edmonton,
"True to its tradition, the CMHF recognizes the outstanding achievements
of biomedical scientists whose work has, or will, significantly improve our
lives and by health professionals whose leadership and dedication have greatly
contributed to health care, and our health care system," says Dr. Claude Roy,
Chair of the CMHF.
The Canadian Medical Hall of Fame celebrates discovery and innovation in
medical science with the goal of raising awareness of Canada's rich medical
history. Through educational programs, The Canadian Medical Hall of Fame
encourages young people to pursue careers in the health sciences, fostering
future generations of medical heroes.
Biographies and pictures of the 2005 inductees are available on The
Canadian Medical Hall of Fame website: www.cdnmedhall.org
For further information: Jan Sims, Communications Coordinator,
(519) 488-2003, Fax: (519) 488-2999, email@example.com;
a href="http://www.cdnmedhall.org" target="_blank">www.cdnmedhall.org
‘Our dreams might just come true’
Published: Sunday, Mar. 13, 2005
My parents realized around 1970 that I wasn’t growing. After lots of testing, Dr. Hans Bode started me off on human growth hormone (the same drug some athletes are using for performance enhancement.) In my case, three shots administered weekly by my dad caused me to grow an astonishing 10 inches over eight years.
The pituitary is the “master gland” and also controls other hormones. So I had to take medication to replace the hormones my body was not producing. I took a daily pill (Synthroid) and a monthly injection of testosterone. Over the years I’d been told by several doctors and my urologist that I would never be able to have children . . . but I remembered Dr. Bode’s words, “Come see me if you want to have kids.”
I lost touch with Bode over the years - he moved to Australia. I really never thought much about it, I focused more on the mountains and hiking pursuits. But one day among the high peaks in Colorado I met and fell in love with Anne, who would become my wife.
I was up front with her on the first or second date, so she knew that I would never be able to father a child. This was hard, but she hung around anyway. I remember her telling me how much she wanted to be a mom. At times I thought I was less of a man. Just a few months before we were married, a friend told her about Dr. William Crowley at Mass General Hospital’s Reproductive Unit.
I made an appointment at the busy clinic for late January 2003. Anne and I were married on Jan. 4. We eagerly looked forward to meeting with the doctors. The day arrived and we were ushered into the small waiting room overlooking Fruit Street across from the hospital. I was nervous. We were introduced to Dr. Nelly Pitteloud, who was positive and upbeat.
She said there would need to be some tests. (When I was 9 or 10 I’d gone though a bunch of tests to see if I would respond to growth hormone, so I knew what to expect.) We were also introduced to Andrew Dwyer, the unit’s nurse practitioner and clinical research coordinator. I would need to have a weekly blood draw for now.
As I boarded the elevator that day, I was filled with lots of doubt. It seemed
like a lot of tests, not much fun at all.
In early spring I had an appointment with a pediatric surgeon who performed a biopsy to find out if there were germ cells in my testes, which are necessary for developing fertility. Sitting in the waiting room surrounded by fish-painted walls, toys and kids waiting to be operated on was pretty weird. I got some strange looks from parents, too. You may be wondering why a grown man would need to have a biopsy done by a pediatric surgeon. With my disease (pituitary deficiency), my testes were undeveloped. So the doctor needed to specialize in surgery on children.
After I woke up, the surgeon was pretty negative about the results. She called to make sure I was OK that night; she said it didn’t look good, but she’d give the results to Dr. Pitteloud and Crowley.
So when I got the call a few days later from Pitteloud, I wasn’t holding out much hope. She was positive as always and said we would go ahead and begin treatment. There weren’t many germ cells, but she thought there were enough to try. They began in June 2003 by prescribing a drug called Profasi, which is a hormone called hCG that’s used to stimulate the reproductive organs. I gave myself a shot every other day. Weekly blood tests continued, shipped in a freezer pack to Dwyer.
When we met Crowley that spring, he was concerned about my adrenal glands because an MRI had shown that my pituitary gland was there but wasn’t attached to the stalk that connects it to the brain. The pituitary uses the stalk like a telephone wire to send messages to the brain: “more hormone!”
He asked me: “How do you have the energy to hike mountains if your adrenal glands aren’t working?” I always had plenty of energy, sometimes doing 15- or 20-mile trips over multiple peaks. Could it have been the monthly testosterone injections? After 20 years of regular testosterone injections, I stopped taking them in January 2003 to prepare for the tests. In May of that year, I barely made it to the north summit of Mount Hancock in the White Mountains. I had no energy at all.
At that time, Dwyer, the nurse practitioner, invited me to an overnight test at Mass General. They took frequent blood samples to measure LH (a reproductive hormone produced by the pituitary) for 12 hours as I slept through the night. Normally the LH looks like a mountain range with peaks and valleys. My results showed a flat line. Cortisol levels were also tested. Cortisol is a steroid hormone that is extremely important to your health; mine were OK.
They agreed that my monthly testosterone steroid injections had compensated for the fact that I didn’t have any LH coming from my pituitary. This finally answered why my energy levels were so low that spring.
That same summer I was prescribed a new drug called Gonal/f (FSH), also to be injected. I was able to mix it in the same syringe as the hCG hormone I was taking, so I didn’t have to poke too many holes in myself. The doctors explained that the two drugs would work together to induce puberty. Imagine, puberty at 43 years old?
Gonal/f, another hormone produced by the pituitary and important for reproduction, is extremely expensive. We were fortunate that our insurance covered it. One of the funny side effects from 10 months of treatment was that my hair (which had been thinning badly) started to grow back. Evidently the change in my hormones had temporarily halted my hair loss! Unfortunately it didn’t last.
I noticed on a strenuous hike up a rock slide in November that my energy was back to normal. I had other symptoms of “puberty” also, the folks at the reproductive unit told us what to expect. The shots continued, I got real good at mixing and injecting and was faithful to it. Time passed and this became routine. Everyone was happy with the progress.
We went to Africa in the summer of 2004 on a short-term mission trip. We were able to carry our supplies and I continued treatment. I had no problems with lack of energy on our climb of Mount Kilimanjaro.
In October, Dwyer said it was time for another test. So, after 17 months of treatment, it had come to this. On Dec. 17, we got incredible news. My sperm count had gone from zero to 1.2 million/milliliter (actually 20-million/milliliter is considered normal, but you don’t need that number to be fertile.)
Andrew told us at our latest appointment. “This is why we do what we do; your story makes it all worthwhile.”
So now we would begin the process to become pregnant. I can’t begin to tell you the different feelings that I’ve experienced through this long process; once it seemed like there was no end to all this, and no hope. But now we feel like our dreams might just come true and we’ll be hearing the pattering of little footsteps coming down the hall real soon.
Our heartfelt thanks to the people at the reproductive unit at Mass General. You’ve given us a chance for our dreams to come true. Thanks also to Andrew Dwyer for contributing to this article.
Jim Lombard lives in Sandown.
Still producing 'milk' two years after miscarriage?
Dr Sharmaine Mitchell
Monday, March 21, 2005
I had a miscarriage in 2003 and until this day whenever I squeeze my breast I see some watery substance like milk coming out; but it is not white like the real breast milk. The pregnancy was three-months-old. Could it be that I'm still producing breast milk?
Another query I have is that I am feeling a pain in my left side. I went to see the doctor once and she said that it was a bladder infection and I was treated for that. But I am still feeling the pain, even as I type, and it's really hurting me. What do you think could cause this pain?
Elevated prolactin level is usually the underlying cause of inappropriate lactation. Prolactin is a hormone produced by the pituitary gland in the brain. Excessive production of prolactin may be due to enlargement of the gland. There may be a slight enlargement resulting in a microadenoma or excessive enlargement resulting in a macroadenoma.
When the gland is significantly enlarged, this may result in visual disturbances because of compression of the optic nerve to the eyes. Additionally, some drugs may also stimulate prolactin secretion, thus causing milk production which is unrelated to pregnancy. These drugs include antipsychotics (used to treat some psychiatric disorders, such as schizophrenia), antidepressants, antihypertensives such as Reserpine and methyldopa, anti-anxiety agents and other drugs such as estrogen and phenobarbitone.
It is not impossible to have milk in the breast secondary to pregnancy loss at three months' gestation. It is, however, important for you to be examined and have your prolactin level done. High prolactin levels can also contribute to suppression of ovulation and subsequent infertility. The treatment of this condition is usually very effective and quite simple. You should avoid squeezing the breast, as excessive stimulation may cause the milk production to continue. If the milk secretion becomes excessive and fertility is desired, then either bromocriptine (Parlodel) or Dopergin tablets are usually effective in decreasing the prolactin level and suppressing the milk production.
Regarding your other concern, the pain that you experience in your left side may be as a result of one several conditions. An ovarian cyst or an inflamed fallopian tube is quite possible. You need to be examined by your gynaecologist and probably have a pelvic ultrasound done to confirm the underlying cause.
Dr Sharmaine Mitchell is an obstetrician and gynaecologist. Email your health queries to Dr Mitchell at firstname.lastname@example.org or write to Dear Dr Mitchell, c/o all woman, Jamaica Observer, 40-42 1/2 Beechwood Avenue, Kgn 5.
Corticosteroid Treatment Effective for Children's Asthma
By Amanda Gardner
SATURDAY, March 19 (HealthDay News) -- New studies are confirming the benefit of treating young asthmatic children with inhaled corticosteroids.
"It's not new information, but it backs up what we know," said allergy expert Dr. Clifford Bassett, a clinical assistant professor of medicine at the State University of New York. "It's viable as a long-term treatment." A pharmacological corticosteroid is a hormone similar to those produced by the adrenal cortex, such as cortisol and aldosterone. These hormones have been shown to be effective in in combating asthma.
The studies were presented Saturday at the annual meeting of the American Academy of Allergy, Asthma and Immunology in San Antonio.
According to background information, the proportion of American children with asthma has grown from 3.6 percent to 6.2 percent. Children under the age of 5 have the highest rate of hospitalization from the disease.
"Asthma in young children results in significant morbidity," said Dr. Kevin Murphy, lead author of one of the studies and a clinical professor of pediatrics at the University of Nebraska Medical Center in Omaha. "It's the No. 1 chronic disease in children."
Murphy's study was a retrospective analysis of 11,407 children under 5 years old who had been diagnosed with asthma and were taking medication for their condition.
Those who were given inhaled corticosteroids first (before any other medication) had fewer emergency room visits than those who were prescribed the therapy first or second: 25 percent of the kids who got inhaled corticosteroids first had an emergency room visit or a hospital stay at least once during a year vs. 29 percent of those who had the drug prescribed second and 41 percent of those who had it prescribed third.
"The earlier you get it, the better," Murphy said. "This should encourage people to think about early intervention."
A second study looked at 1,974 children 5 to 10 years old who were randomized to receive either budesonide, an inhaled corticosteroid, once a day or a placebo. All the participants also took their regular asthma medications.
Use of budesonide earlier reduced the risk of an exacerbation by 40 percent. These children also had less of a need to use their other mediation (12 percent versus 23 percent).
"When we added budesonide, we saw a significant decrease in asthma," said Dr. Albert Sheffer, chairman of the study safety committee and a clinical professor of medicine at Harvard Medical School in Boston.
Children taking budesonide, however, did have slowed growth, Sheffer added, but they caught up after five years.
The frequency of other side effects was similar in both groups.
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Annie's right adrenal gland was removed 3 years ago.
Christine had an MRI of her pituitary gland which showed a
lesion, but her doctor still can't say if she has Cushing's or not.
Diane had pituitary surgery Sept 21, 2004.
Jill's Father died following a triple bypass surgery. He had
Addison's Disease but was without steroids for 22 hours.
Johnna (Johnni) is not yet diagnosed. She saw Sam's and Jackie's Mystery
Diagnosis show on Discovery Health.
Kaelynn possibly has iatrogenic Cushing's from a Depo Provera
Currently in Frankfurt Germany but will be moving back to
Colorado Springs, CO.
is not yet diagnosed.
Mindy is not yet diagnosed.
Hilliard Ohio, a sub-community of Columbus.
Nancy is not yet diagnosed.
Rosemary is not yet diagnosed with Cushing's but she has had
endometriosis and is diagnosed bipolar.
is not yet diagnosed.
Steve had transphenoidal surgery on Feb. 7, 2004 at UVa with
is not yet diagnosed.
• If you've been diagnosed with Cushing's, please
participate in the
Cushing's Register »
The information you provide will be used to create a register
and will be shared with the medical world. It would not be used
for other purposes without your expressed permission. Note:
This information will not be sold or shared with other
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
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."
|The Cushing's Store|
| for all kinds of Cushing's Labeled clothing, coffee mugs, totebags and much more. Great for your endo or Secret Someone.|
CUSH can always use funds to help us all, by spreading the word and helping others. What can *you* do to help CUSH?
|Upcoming Conventions, Meetings and Seminars:|
March 26, 2005,
Noon Meeting in DC Metro Area at Stromboli Restaurant, 7023 Wisconsin,
Bethesda MD, 301 986-1980. More info here »
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 »
2005, (date TBA), Meeting in New England More info here »
May 3, 2005, 6:30 – 8:00 P.M., Chicago, Illinois
Greater Chicago Pituitary Support Group: QUARTERLY MEETING,
Topic: "Management of Prolactinomas"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, OHare 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.
|Please join us in the Chat
Room TONIGHT at 9 PM Eastern.
The chatroom is available through http://www.cushings-help.com/chatroom.htm.
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.
I hope to see you tonight!
Cushing's Help and Support at
Cushing's Message Boards at
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