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Woman Sleeping, Aletta Mes 2003
WOMEN'S PAGE - INDIVIDUATED DYSAUTOMANIA

this page: Birthstories:  - aletta & women's problemsBits and Pieces on topicArticles Menopause: Study aims to address hot flashes,




Birthstories:


Belinda - CGBD

I had 4 c-sections. The first one almost killed me and they did an emergency c-section because I was in danger of dying and killing my oldest child. My second child, I was told I had to have a c-section because I never went into labor with the first one so this is what I did again. The 3rd child was born exactly 12 months and 2 days later and since I hadn't had time to heal c-section again. The 4th child was born 12 months and 3 weeks later and c-section for the same reason the 3rd child was done that way. A year later I ended up having to have a partial hysterectomy because I hemmoraged when I had a period. I still have my ovaries. I have so much pain down there as I had said in a previous email to you. I don't have a clue if all the surgeries I have had is any reason for what is going on with me now or not. I had more surgeries then the ones I mentioned to you. I think 7 or 8 in all. I
Anne: - SDS/PAF
Pregnancies.  First I got eclampsia with from 5 months.  Spent the rest of the pregnancy in hospital UGH!  Extremely HIGH bp !!  Way over 200.  Went full time in those days too they didn't bring babies on as they do now for those that get it.  2nd pregnancy eclampsia again at 7 months.  2 months in hospital. 3rd pregnancy, no eclampsia but 6 weeks premmie birth, breech, and baby only lived 2 hours. I had severe haemorrhage from torn uterus. Surgery to repair uterus. Another time of coma, natural not induced as the later one. !   No facilities for premmies in those days as now!  4th pregnancy went like a dream.  Lorraine. 7 weeks premmie but she did well.  I did get a dislodged uterus. Had 7 Manchester repairs before they gave up and I had a hysterectomy!  Nowadays they would have done this much sooner!!
Aletta - SDS
My son was an eleven pound breech, two months overdue, preceded by three miscarriages.  I was in a come and go labour for a week when I had to be induced, broke water, nothing happened, then finally oxytosin.  Eight more hours of labour, he was delivered (assfirst) vaginally.  My daughter was born one month late, ten pounds, water never broke, finally went to ER when labour pains were 5 mins apart.  she was delivered on the first push, like a waterslide, water broke and baby born all very neatly.  I was physically very healthy and happy while pregnant and my epilepsy resolved.
I read somewhere with hereditary ataxias breech birth is not uncommon, and I was a post  mature breech myself.  So I thought it would be interesting to compare notes on that one since not one researcher seems to have collected data on various types of ataxias MSAs and the like in regard to women's reproductive organs, hormones etc.

So I think we women should collect up data among ourselves.

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aletta & Women's problems: 
 
Since it is women's month or something, from one of my personal fav's, Florence Nightingale "I neither give, not take, excuses.", she spent the last twenty years ill in bed, the medical establishment said she was malingering (judging by her history/attitudes, I think she might have had MSA) - we share the same birth date - Epiphany 
All of us women get accused of malingering, infuriating.  There also never seem to be specific research papers for women.  I'd like to know how menopause will/will not complicate MSA and vise versa.  Impotence in men is considered a clear clue to MSA,  what about women, what happens to our reproductive system.  My estrogen is still normal and periods regular.  I have noticed I am slightly less ill in all regards during my period.  I've certainly not lost interest in sex (good men are just hard to come by).   Since the onset of MSA to the degree it was disabling I have also had cysts in my breasts, drained several times, went back to old country therapy of binding which does a fine job.  Each time cysts appear I am sicker.  I do tend to pass out during and after sex (I keep saying, no more marathons).  A husband can just get used to changes, but it would be very hard to explain to a new man (it's not you it's me).  During the screening process I now have to ask for first aid ticket.  As far as incontinence, this must also be different as women are structurally different.  I find retention is more of a problem as I do not feel and urge to go, I forget, overflow.  The tech doing an ultrasound last year remarked how large my bladder was, probably stretched beyond normal capacity, and I could not even feel the fullness unless I pressed down on my belly, then I need to go immediately.  What are the complications of having an overly stretched bladder? I'm still waiting to see a urologist but unless it becomes and emergency it could take another year because of the doctor shortage.  I'm very good at monitoring input output and what is normal and not, my health conscious parents made me very aware of it even as a child (clarity smell, thickness, frequency).  I've also had several times when my body produces no urine at all (nothing even when cathed), it builds up mostly in my abdomen, docs are slow to deal with this and I keep some of my mother's powerful diuretics handy, they work just a little. 
Women's Hospital has a department for studying ailment afflicting women, I'd rather see them study how women are treated differently in medicine, all their funding is strictly OB/GYN.  During the period of trying to establish a diagnosis most doctors (men and women alike) treated me much like a support system for a reproductive system.  If a man had my heart attack, he would have seen a cardiologist, I was never referred because women my age are not in the risk group.  Except for the day of my heart attack no cardiologist has been involved with  me.  A male friend who has high blood pressure and an irregular EKG sees one every six months.  My current doctors are not in that mind set, but it took a lot of digging to get to this point, where I had some support.  I've not been able to find a word equal to hysteria (hyster referring to the uterus) to apply to a male who malingers (John, Bill anyone).  I don't know how many times doctors told me I could not have Shy-Drager's because I was too young and not male, diagnosis by demographic.  When I found a lump on my breast, wow, did that get attention.  That puppy was incised and gone.  Threaten anything to do with reproductivity and it gets swift attention.  Fall on your head in the bathtub, fall and gash your elbow, you must be stressed and distracted, is it your period?  I've been told I'm lucky I'm a woman because men become impotent. Hey, being a staggering, speech slurring, incontinent woman ain't no picnic, not exactly catch of the week right now.  Boy, I'm kwetching aren't I. 

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Bits and Pieces on topic
 
Any ladies having surgery that are on Premarin or other hormone therapy, must stop this medication until two weeks after their surgery.  It can cause blood clots and other like problems. 
Anne (AU)
 
Another thing that has not been discussed much and that is the problem with monthly periods and what it does to the dehydration problem.  The system has to deplete one for the other and it has to create many more problems.  I have no idea what the answer is in how you go about trying to cope with it unless it would be something like birth control pills that would eliminate some of the trouble but would they create more problems.  I just really don't know.
Sally


I have been going down hill very noticeably since they have been insisting I go off the natural estrogen which started before I even went to California.  I even have been very depressed...I had been praying hard for some kind of way to slow all this down as is was pretty scary.

Then out of the blue, I get this call, "Hi Patty, this Randi, ( Dr. [Lady] Head of the research team that so loved me as well as all my symptoms.)  I said not too great.  Are you depressed?  Yes mega!  are you off the estrogen?  Yes.  Why? Because both Dr. B.L., who is working with her on my part of the Journal article, and the Dr. here insisted on it.  She said. "Get back on it now."  It is not a problem unless used in conjunction
with progesterone and will not only protect your heart and other organs, mostly slow down the brain deterioration. 
Please pass this important part on to those you know.  That was the reason for the rapid downhill for me. The depression is gone, but I will never regain what I have lost in walking, standing , hand coordination, brain loss, and so much more.....All of us with any form of ataxia NEED this.
Patty

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Articles
Estrogen Receptor Regulates Blood Flow in Brain,Rockefeller, Weill Cornell researchers find link between estrogen and brain structureMenopause: Study aims to address hot flashes,

Estrogen Receptor Regulates Blood Flow in Brain, 
UC Irvine Study Finds

May Result in Ways to Prevent Stroke, Brain Injury

Irvine, Calif., Oct. 23, 2001 -- A specific receptor for the sex hormone estrogen in the brain helps regulate pressure and blood flow there, a UC Irvine College of Medicine research team has found.

The receptor, which appears to influence certain genes' ability to produce nitric oxide and other chemicals that widen blood vessels, may be an effective target for new drugs to treat stroke and other injuries to the brain caused by high blood pressure.  The researchers' study, conducted on mice, appears in the November issue of the Journal of Applied Physiology.

Sue Duckles, professor of pharmacology, and her colleagues found that the receptor, called alpha-ER, regulated estrogen's ability to dilate blood vessels in the brain by raising levels of nitric oxide and another known dilator called prostacyclin.  By raising levels of nitric oxide and prostacyclin, estrogen could lower pressure in the brain's arteries.

"We believe this study is among the first to show how estrogen affects arteries in the cerebral cortex," Duckles said.  "This receptor could help explain why women have fewer strokes than men before they reach menopause, and this knowledge may eventually lead to new treatments for stroke and other vascular disorders in the brain.  Future research may expand our understanding of how blood pressure is regulated elsewhere in the body."

Blood pressure is a major risk factor in stroke and other cardiovascular disease.  While the risk in women who have not reached menopause is lower than men, nearly 2 million women have a stroke each year.  About 93,000 of them die of it, according to the National Heart, Lung and Blood Institute.  In addition, about 10 percent of American women between the ages of 45 and 65 has heart disease; that proportion rises to 25 percent of women older than 65.  Of women older than 65, about half have high blood pressure.  Researchers suspect that a large reason for this rise is the diminishing levels of estrogen in older age.

Duckles and her colleagues found that estrogen treatment for one month resulted in elevated levels of nitric oxide synthase and cyclooxygenase-1, enzymes responsible for manufacturing the vasodilators, nitric oxide and prostacyclin.  Mice who had been bred without the alpha-ER receptor were less able to dilate blood vessels when they were given estrogen.  This led researchers to conclude that it was this receptor that controlled estrogen's actions on blood vessels in the brain.

Further, the receptor was located in the innermost layer of the blood vessel wall, known as the endothelium.  From there, it controlled the manufacture of enzymes that produce chemicals that dilate or constrict the vessels.

"Estrogen appears to control how genes produce at least some of the enzymes that affect dilation and pressure in vessels in the brain," Duckles said.  "While scientists knew that an estrogen receptor was at work, they didn't know which specific type played the most important role.  By identifying alpha-ER, we have brought this work closer to eventually identifying possible drugs that work on the receptor to increase blood flow."

The researchers now are exploring other enzymes and genes that may be controlling dilation and blood pressure and conducting more tests to determine what chemicals may best control the alpha-estrogen receptor.

Duckles' colleagues in the study included Greg Geary, Anne Marie McNeill, Jose Ospina and Diana Krause of UCI, and Kenneth Korach of the National Institute of Environmental Health Sciences in Research Triangle Park, N.C.  The National Heart, Lung and Blood Institute supported the study.

###

Copyright ©2003 The Regents of the University of California 

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"Rockefeller, Weill Cornell researchers find link between estrogen, brain structure changes"


Scientists at Rockefeller University and Weill Medical College of Cornell University have discovered how estrogen initiates physical changes in rodent brain cells that lead to increased learning and memory -- a finding, the researchers contend, that illustrates the likely value of the hormone to enhance brain functioning in women.

Their study, published in the March 15 issue of The Journal of Neuroscience, describes for the first time a chain of molecular events that is activated in the brain's primary memory center, called the hippocampus, when estrogen bathes neurons (nerve cells).

The study details how these nerve cells "grow in complexity" when exposed to estrogen, increasing connections among nerve cells in an area of the brain needed to store new memories, retrieve older ones and even recall location of an object or event in space.

A second study, published in the same journal by Weill Cornell Medical College scientists, led by Teresa Milner, Ph.D., in collaboration with Rockefeller University investigators, finds the same results in animal tissue experiments. Both the first study, at the test tube level, and the Milner tissue study were conducted simultaneously but independently, and serve as sort of "blind controls" in support of each other.

"We found a novel way in which estrogen affects neuronal structural remodeling in the hippocampus," says paper co-author Bruce S. McEwen, Ph.D., Professor and head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology at Rockefeller University.

"It shows us that estrogen plays an unsuspected role in primary biological processes involved in strengthening normal learning and memory function," says McEwen.

"We observed the neuronal structural remodeling at the subcellular level through electron microscopy," notes Milner, professor of neuroscience in the Division of Neurobiology at Weill Cornell. "We were able to visualize precise changes in protein distribution at the actual dendritic spines of the neurons." 

Findings from several previous studies have been mixed about whether estrogen replacement therapy bolsters brain functioning in postmenopausal women. McEwen says that the new study suggests some form of postmenopausal estrogen replacement may indeed be both helpful and neuroprotective.

"Even without estrogen, there are still plenty of synaptic connections in the hippocampus," McEwen says. "The study suggests that without estrogen, the connections that are there don't work as efficiently in storing and recalling certain types of memories, such as word lists, or remembering where something is in space," he said. "The hope is that an estrogen mimic could be developed that protects women not just against memory loss, but Alzheimer's disease, the consequences of stroke and other brain disorders." 

"Hormones like estrogens, which circulate in the bloodstream, are a major part of the communication system in the brain," McEwen concludes.

At its most fundamental, the study solves several neurobiological mysteries that were seemingly unrelated, says co-author Keith T. Akama, Ph.D., a postdoctoral researcher in McEwen's laboratory. It answers the question of why estrogen receptors, through which the hormone stimulates the cell, are located on the outer reaches of the neurons-- an observation that many researchers have been trying to explain --and it uncovers a functional role for protein synthesis that occurs far away from the cell body near the synapses. Protein synthesis is thought to be important in learning and memory.

"This marries two schools of neurobiology together," Akama says. "Much was known within those two separate investigative paths, but this experiment connected the dots," he says.

Estrogen at synapses

In earlier research with rodents, Milner, together with the McEwen laboratory, had demonstrated for the first time that estrogen receptors occur at the edges of nerve cells in the CA1 region of the hippocampus, far away from the cell's nucleus where most estrogen receptors are traditionally found. These receptors at the edges of the cells are found on structures known as "dendritic spines" -- the part of the cells that receives signals from other neurons in the central nervous system.

From a nerve cell, long tentacles called dendrites branch many times, extending out to reach other neurons. Dendritic branch points are covered with the nub- or bump-like spines, which are often the sites of synapses, junctions between neurons that pass chemical messages. When the spines are activated, they grow, or mature, into mushroom caps in order to make connections with the next neuron.

McEwen and many other scientists believe "plasticity," or the constant structural reshaping of synapses in forming new dendritic spines, encodes processes necessary to promote learning and memory.  These spines are diminished in the aged brain and are atrophied in Alzheimer's disease.   Furthermore, McEwen also believes that the formation of new spines may be a major way by which the brain protects itself from damage such as trauma and stroke. Plasticity also allows the brain to relearn skills that may have been lost to injury -- such as by stroke -- by rewiring important functions via alternate nervous system pathways.

Previous studies in mammals by McEwen and others showed that low estrogen levels reduced the animals' performance on learning and memory tests, but estrogen treatment reversed this negative effect, thus providing a link between estrogen and activity in the hippocampus. Human studies have also shown that the ability of women to remember word lists and other experimental tasks varies during a normal monthly estrous cycle, which is characterized by the ebb and flow of estrogen.

Further animal investigation revealed a dramatic decrease in dendritic spine density in rats whose ovaries were removed and thus were relatively low in blood estrogen levels; however, administering estrogen to the animals increased their spine formation. McEwen and his colleagues also found that the density of synapses and synaptic spines fluctuates during an animal's estrous cycle, increasing in response to estrogen.

This new study is the first to shed light on the precise molecular pathway by which estrogen increased the "plasticity" of neuronal spines. In the study, McEwen and Akama explored the question of how estrogen receptors influence growth of dendritic spines.

"We know how estrogen works genomically inside the cell's nucleus, how it turns on gene transcription, producing proteins, which are then shipped to where they are needed," says Akama. "But it is a long way from the nucleus to the synaptic ends of the neuron, where changes occur very rapidly, so estrogen has also found a way to work at edges of the nerve cell. We wanted to find out how."

Messenger RNA hanging out 

The researchers reasoned that an increase in the number of spines requires the translation, or synthesis, of new proteins, and they chose to investigate a key protein that has been found near estrogen receptors at the spine with undefined regulation of new protein synthesis.

That protein, postsynaptic density-95 (PSD-95), is a structural protein that researchers believe plays a critical role in building a synapse and maintaining plasticity. 

"A lot of researchers have looked at PSD-95, but it was not known to play any role with estrogen," says Akama. "Furthermore, no one knew how a neuron regulates PSD-95 production."

Through a series of test tube experiments, Akama and McEwen were able to delineate the molecular mechanisms by which estrogen might directly orchestrate such spine formation and development of synapses.

They found that in a neuronal cell line, estrogen binding to its receptor led to a series of signaling switches that resulted in PSD-95 protein translation. These switches involves rapid activation of an enzyme called Akt, a common intermediate in signaling pathways, which subsequently disinhibits 4E-BP1 (eukaryotic initiation factor-4E binding protein 1) to allow new protein synthesis. 

"PSD-95 mRNA is hanging out near the spines and was not being translated because it had a big, inhibiting protein complex bound to it," says Akama. "Phosphorylation of 4E-BP1 disrupts this binding and when estrogen stimulates this release of 4E-BP1, new PSD-95 proteins were rapidly synthesized. More PSD-95 protein translated immediately at the spine increases spine maturation and synaptic formation. All this action is occurring far away from the nucleus, way off in the dendrite, without estrogen traveling back and forth down to the nucleus.

"In addition to the genomic mechanisms initiated within the nucleus, we have shown another way that estrogen can regulate dendritic function, and this gives us hope that selective agents can be developed that work through these signal pathways.

The study was funded by grants from the National Institutes of Health and the Ares-Serono Foundation. 

Founded by John D. Rockefeller in 1901, The Rockefeller University was this nation's first biomedical research university. Today it is internationally renowned for research and graduate education in the biomedical sciences, chemistry, bioinformatics and physics. A total of 22 scientists associated with the university have received the Nobel Prize in medicine and physiology or chemistry, 18 Rockefeller scientists have received Lasker Awards, five have been named MacArthur Fellows, and 11 have garnered the National Medal of Science. More than a third of the current faculty are elected members of the National Academy of Sciences. 

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Menopause: Study aims to address hot flashes, 
February 25, 2003

More than 50% of women entering into menopause know the feeling all too well.  That sudden rush of uncomfortable and often embarrassing heat that seems to take over your body, causing your heart to race and your skin to redden.

To control hot flashes in the past, women used estrogen replacement therapy during this natural stage of menopause.  However, recent concerns about the safety of estrogen use have left many women looking for alternatives.

Breast cancer oncologists at the University of Michigan (U-M) Comprehensive Cancer Center have been searching for another way to treat hot flashes - by studying a popular drug type used for the treatment of depression.

The search for an alternative treatment for patients who suffer from hot flashes and have a history of breast cancer has been going on for several years by investigators who are now at the U-M Cancer Center.

"In the breast cancer field, we've been concerned for years about giving estrogen replacement therapy to women who have a history of breast cancer," said Daniel F. Hayes, MD, clinical director of the breast oncology program at the U-M Cancer Center.  U-M breast cancer oncologists knew that the use of estrogen increased the risk of a woman developing certain forms of cancer, including breast cancer.

Although the exact triggers for hot flashes are not completely understood, experts do know that they are a result of a decrease in the female hormone estrogen during menopause. It's believed that estrogen production affects the part of the brain that controls the body's temperature.  The body's  thermostat prevents us from overheating or freezing in various environments.

"With menopause, there's a lack of estrogen that causes this thermostat to become irregular, which causes women to be substantially sensitive to temperature changes that would normally not bring about a sudden change in the body's temperature," explained Hayes.

That's why estrogen replacement therapy had previously been so successful in treating hot flashes.  Estrogen helps reduce the incident of hot flashes almost completely in 80-90% of women.

But with concern over the safety of estrogen replacement therapy, especially for women who have had breast cancer, it became important to find a safer, nonhormonal treatment.

In a step toward finding an alternative treatment for hot flashes, experts from several different centers have discovered that a class of drugs used to treat depression may be an effective treatment.  The drugs, called selective serotonin re-uptake inhibitors (SSRI), work well because with depression and hot flashes, serotonin, a major neurotransmitters found in the synapses of the brain, isn't functioning correctly.

Several SSRI drugs, such as Prozac, Paxil, and Effixor, decrease hot flashes in about 50% of women.  So, while SSRI drugs are not as effective as estrogen, they appear to perform better than a placebo.

For women who don't want to take drugs, there are still other options to help control hot flashes such as soy.  However, Hayes warned that soy does contain a weaker estrogen-like product and there is little known about its effects.

This article was prepared by Cancer Weekly editors from staff and other reports. 

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