CHICAGO – Hot flashes that bedevil many women in menopause might actually be a good thing, depending on when they strike, according to new data from a long-running government study.

Women who had hot flashes at the start of menopause but not later seemed to have a lower risk for heart attack and death than women who never had hot flashes or those whose symptoms persisted long after menopause began.

The research involved more than 60,000 women followed for an average of almost 10 years. It’s the first to examine timing of menopausal symptoms and subsequent risks for heart problems and deaths, said co-author Dr. JoAnn Manson, chief of preventive medicine at Harvard’s Brigham and Women’s Hospital.

Recent studies linked hot flashes with higher blood pressure and cholesterol levels, which could suggest a higher risk for heart problems, but the new research offers a more detailed look, Manson said.

Lead author Dr. Emily Szmuilowicz, an endocrinologist with Northwestern University’s medical school, said the results should reassure millions of women who experience hot flashes or night sweats, which are essentially hot flashes that can be bothersome enough to awaken women.

The results suggest “there may be a positive side” to having these annoying symptoms, Szmuilowicz said.

The study was released in the journal Menopause.

Dr. Elsa-Grace Giardina, a Columbia University specialist in women’s heart disease who was not involved in the study, said the research has several limitations and that more rigorous study is needed to prove the results.

Few women developed hot flashes long after menopause began, and for at least some, previous use of hormone pills may have increased their risks for heart problems, Giardina said.

But more than one third of the women with late-onset symptoms never used hormones, and Szmuilowicz said the researchers took past hormone use into consideration and still found timing of symptoms played a role.

Menopause occurs when women stop having periods and estrogen levels dwindle. Most women experience symptoms including hot flashes that can last for several years. But they don’t usually persist indefinitely or begin long after the beginning of menopause.

Hot flashes aren’t well studied but are thought to result from blood vessels dilating in response to the normal hormone fluctuations of menopause, Manson said. If they occur long after menopause begins, it could signal a blood vessel abnormality that could also affect the heart, she said.

The research involved 60,027 women from the ongoing Women’s Health Initiative observational study, examining disease risk factors and health outcomes and funded by the National Institutes of Health.

Women were in their early 60s on average, about 14 years past the start of menopause, when they answered questionnaires about their health, education history, and symptoms including hot flashes and night sweats. Cardiovascular problems and deaths were tracked during almost 10 years of follow-up.

More than one third, or almost 25,000 women, had early symptoms – hot flashes at the onset of menopause that had stopped before they enrolled. Just 1,391 had late symptoms – hot flashes at enrollment but not at the start of menopause.

About 2.5 percent of women with early symptoms had heart attacks, compared with 3.4 percent of women with no symptoms and 5.5 percent of those with late symptoms. also, about 6 percent of the early-symptom women died, versus 11 percent of the late-symptom group and 8 percent of the symptomless women. Women who had persistent hot flashes throughout menopause had risks similar to those without symptoms.

Giardina noted that high blood pressure, high cholesterol, diabetes and obesity – which all can contribute to heart problems – were more common among the late-symptom women.

But the researchers said they accounted for that and still found that timing of menopause symptoms played a role in later heart attacks and deaths.

Tags: life, health

CMHS Seminar to Focus on Treatment of Fibroids Santa Paula News Published:  December 24, 2010

Community Memorial Health System kicks off its 2011 seminar series with a free seminar on Tuesday, Jan. 11 focusing on the minimally invasive treatment of fibroids, benign tumors in a woman?s uterine smooth muscle.

Dr. Lois Barnes and Dr. Srisawai Pattamakom, Ventura obstetrician-gynecologists, will lead the seminar that will be held from 6 to 8 p.m. in Community Memorial Hospital?s eighth-floor Nichols Auditorium.

Drs. Barnes and Pattamakom will discuss symptoms of fibroids, which typically start in women in their 30s. Symptoms include heavy and prolonged periods, pain in the pelvis and during intercourse, and infertility. the seminar will delve into traditional treatments for fibroids and also provide information on alternative and minimally invasive procedures, including hysteroscopic myomectomy and robotically assisted laparoscopic myomectomy.

Dr. Barnes received her medical degree from the University of California at Davis and Dr. Pattamakom earned her medical degree from Northwestern University. both are active members of the Community Memorial Hospital medical staff.

Admission is free, but space is limited, so reservations are required. Call (805) 652-5436, or visit cmhshealth.org/rsvp.

Community Memorial Hospital is located at 147 N. Brent St. in Ventura.

Community Memorial Health System is a not-for-profit health system, which is comprised of Community Memorial Hospital, Ojai Valley Community Hospital, and nine family-practice health centers entitled Centers for Family Health. the health system is located in Ventura County, California.

Calcium activity in the brain plays an important role in the onset of Parkinson’s disease, according to a study in mice. The finding helps explain why common calcium-blocking drugs, such as those used to control blood pressure, appear to protect against the disease.

Damage to dopamine-releasing cells in a brain area called the substantia nigra (SN) is known to be involved in the onset of Parkinson’s disease. “Pacemaking” cells in this area release pulses of dopamine, a hormone crucial for movement and balance. so damage to these cells leads to the symptoms of Parkinson’s – such as tremors and stiffness.

A key question is why cells of the SN are so much more susceptible to damage than those in surrounding areas. Now it seems that calcium, which enters these cells to regulate their activity, is the culprit.

Jaime Guzman from Northwestern University in Chicago and colleagues compared the effect of calcium activity in two brain areas in mice – the pacemaking SN and a neighbouring area where there was no pacemaking activity.

Oxidative stress

They found that the calcium influx in the SN caused much higher levels of oxidative stress – pressure on cells to counteract the effects of molecules such as free radicals, that can damage proteins and DNA. Oxidative stress is thought to be the source of the cell damage that leads to Parkinson’s disease.

“Although calcium channels normally participate in pacemaking, they aren’t essential as other ion channels can pick up the slack,” says James Surmeier, who was part of the team. Treating mice that had Parkinson’s disease with calcium-channel-blocking drugs might therefore prevent cell damage without hindering essential pacemaking activity.

To investigate this possibility, the team used mice lacking a gene called DJ-1. The absence of this gene causes early onset Parkinson’s disease, and mice who lacked the gene showed much higher levels of damage to the dopamine-releasing cells of the SN than normal mice. When treated with drugs that block calcium channels, however, the degree of cell damage dropped to levels seen in other types of brain cells that are relatively resistant to oxidative stress.

The right drug

The findings explain why previous research conducted by Christoph Meier at University Hospital Basel in Switzerland showed that calcium-blocking hypertension drugs reduced the risk of Parkinson’s disease, while other types of drug used to treat high blood pressure did not.

“A lot seems to point towards a potential benefit of calcium-channel blockers in Parkinson’s disease,” says Meier, “but it’s too early to tell whether they help prevent the disease or could improve the situation of patients who already have a diagnosis.”

Surmeier is more confident. “We think that anyone at risk of developing Parkinson’s disease should benefit by the use of calcium blockers such as isradipine,” he says, as it appears that the dopamine-producing cells in the SN begin to disappear well before the onset of symptoms.

Isradipine is already in a phase II clinical trial for people with early stage Parkinson’s disease, and Surmeier is now planning to investigate more selective and potent drugs.

Journal reference:

Nature, DOI: 10.1038/nature09536

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