Of course, there are some women who have little interest in sex because they are depressed. That is an entirely different situation for them to unravel. It often can require the help of a mental health professional (preferably a sex therapist) to evaluate her situation and create the best path for her to take.

Women who use an antidepressant in the SSRI category (selective serotonin reuptake inhibitor) may sometimes find that their interest in sex (solitary or partnered) has decreased. In addition, there may also be negative impact upon their ability to get aroused or to reach orgasm. Not everyone experiences these difficulties, but enough do that whenever a women presents to me in my therapy practice with lowered sexual desire, I always ask about their use of antidepressant medication.

SSRIs are selective because they act only on the neurotransmitter serotonin. Normal levels of serotonin are required to regulate mood and other functions. Slowing the release of serotonin from the brain is thought to improve move and other functions. Benefit: Less side effects than other antidepressants Side effects include dry mouth, nausea, nervousness, insomnia, headache and sexual problems.

Sexual researchers are working on this very common problem. There is no ideal solution that works for most people (male or female).

Some women have had some success with using Viagra at the time they intend to be sexual in addition to their other medications. It works for some — for reasons that we do not yet fully comprehend — and not for others. Cialis and Levitra have not been explored as often in this manner, but my hunch is that they might offer a similar level of assistance.

If Wellbutrin (bupropion) has not been tried, it might be good to consider it either as a replacement to the SSRI or addition to it. It is a dopamine agonist and that has been found to be somewhat successful in treating women with sexual side effects due to antidepressants. Typically about 100 mg per day is used if it is added on. The woman’s prescribing physician would have to be consulted in order to do this. There is good evidence based, scientifically reviewed research on Wellbutrin use for this purpose.

Dostinex (cabergoline), also a dopamine agonist, has also been used, but I have less anecdotal evidence upon which to rely and no scientific research as yet.

In addition to those approaches, a woman with this difficulty (lowered sexual interest and the need to stay on the antidepressant) could speak to her prescribing physician. Robert Taylor Segraves and Richard Balon offer a number of SSRI “antidotes” that have some anecdotal support in “Sexual Pharmacology Fast Facts.” Among their suggestions are: Symmetrel (amantadine), Urecholine (bethanechol), bromocriptine, Periactin, (cyproheptadine), Kytril (granisetron), Claritin (loratadine), Prostigmin (neostigmine), phentolamine, Aphrodyne (yohimbine), and Ritalin (methylphenidate).

These antidepressants have a reportedly lower frequency of sexual dysfunction: Bupropion, Mirtazapine, Nefazodone, and Reboxetine. The SSRI antidepressants include: Celexa (citalopram), Lexapro (escitalopram), Prozac and Sarafem (fluoxetine), Luvox (fluvoxamine), Paxil (paroxetine), and Zoloft (sertraline). Paxil is a popular depression treatment drug prescribed to millions of people around the world. Paroxetine, which is an active ingredient in Paxil, is used for the treatment of depression and other emotional problems like anxiety.

There are several management strategies that can be tried, but each of these approaches has its limitations.

1. Waiting for spontaneous remission of symptoms or accommodation of symptoms.
2. Reducing the dose to the minimal that is effective.
3. Scheduling sexual activity around the dose.
4. Switching to another antidepressant with a lower frequency of sexual dysfunction.
5. Using other medications such as Viagra (sildenafil).
6. Take drug holidays with a doctor’s permission.
7. Addition of the mentioned “antidotes.”

As you can see, we are still very much in the try-and-see world with this problem. Pharmaceutical companies are well aware of these issues and will likely be tackling their own type of “solution.”

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The main motor symptoms are collectively called parkinsonism, or a “parkinsonian syndrome”. Parkinson’s disease is often defined as a parkinsonian syndrome that is idiopathic (having no known cause), although some atypical cases have a genetic origin. Many risk and protective factors have been investigated: the clearest evidence is for an increased risk of PD in people exposed to certain pesticides and a reduced risk in tobacco smokers. The pathology of the disease is characterized by the accumulation of a protein called alpha-synuclein into inclusions called Lewy bodies in neurons, and from insufficient formation and activity of dopamine produced in certain neurons of parts of the midbrain. Diagnosis of typical cases is mainly based on symptoms, with tests such as neuroimaging being used for confirmation.

Modern treatments are effective at managing the early motor symptoms of the disease, mainly through the use of levodopa and dopamine agonists. As the disease progresses and dopamine neurons continue to be lost, a point eventually arrives at which these drugs become ineffective at treating the symptoms and at the same time produce a complication called dyskinesia, marked by involuntary writhing movements. Diet and some forms of rehabilitation have shown some effectiveness at alleviating symptoms. Surgery and deep brain stimulation have been used to reduce motor symptoms as a last resort in severe cases where drugs are ineffective. Research directions include a search of new animal models of the disease and investigations of the potential usefulness of gene therapy, stem cell transplants and neuroprotective agents. Medications to treat non-movement-related symptoms of PD, such as sleep disturbances and emotional problems, also exist.

Conditions associated with motor impairment and other symptoms of Parkinson’s disease may need a variety of treatments.

Depression. Although depression is very common in PD, there have been surprisingly few controlled studies. Antidepressants used for PD include tricyclics, particularly amitriptyline (Elavil). Some studies have found that selective serotonin-reuptake inhibitors (SSRIs) — which include fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil) — may worsen symptoms of Parkinson’s. Doctors should monitor patients taking SSRIs.

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Of all the people who have Alzheimer’s disease, only about 5 percent develop symptoms before age 65. So if 4 million Americans have Alzheimer’s, at least 200,000 people have the early-onset form of the disease. Early-onset Alzheimer’s has been known to develop between ages 30 and 40, but that’s very uncommon. It’s more common to see someone in his or her 50s who has the disease.

It often runs in families. Many people with early-onset Alzheimer’s have a parent or grandparent who also developed Alzheimer’s at a younger age. A significant proportion of early-onset Alzheimer’s is linked to three genes.

These three genes are different from the APOE gene — the gene that can increase your risk of Alzheimer’s in general. The genetic path of inheritance is much stronger in early-onset Alzheimer’s. If you have a genetic mutation in one of those three genes — the APP, PSEN 1 or PSEN 2 — it would be common for you to develop Alzheimer’s before age 65.

Although there is no cure for Alzheimer’s disease, there are treatments that can help people cope with the symptoms.

A class of medications called cholinesterase inhibitors delays the worsening of symptoms for an average of 6 to 12 months for about half the people who take them. According to the Alzheimer’s Association, these medications work by supporting a neurotransmitter called acetylcholine. This chemical increases communication between nerve cells. It is thought that the breakdown of this communication may cause Alzheimer’s symptoms.

Brand names of this type of medication include Aricept (donepezil), Exelon (rivastigmine) and Razadyne (galantamine). Each medication is approved for specific stages of the disease, which range from mild to severe.

Another medication, called Namenda (memantine), works by supporting a different neurotransmitter, called glutamate. Namenda, approved in 2003, is the only medication in this class.

Paxil is an antidepressant from the class of drugs called SRI drugs. This stands for serotonin reuptake inhibitor drugs. They are generally well tolerated, but some patients experience difficulty sleeping, dry mouth and constipation.

Cognex is a relatively new drug, especially for the treatment of Alzheimer’s Dementia. Side effects are mainly liver and white cell depression. Trazadone is an antidepressant which is in a class of its own. It also works primarily through serotonin.

All of these medications have side effects that can be troubling. Nausea, dizziness, vomiting and liver damage are among them.

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Cognex is a relatively new drug, especially for the treatment of Alzheimer’s Dementia. Side effects are mainly liver and white cell depression. Trazadone is an antidepressant which is in a class of its own. It also works primarily through serotonin.

People should be very reluctant to combine Paxil and Trazadone since they both work through similar mechanisms. The only way to determine if the problem is his dementia or the drugs is to systematically stop one drug at a time. I’d start with the Trazadone.

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Despite the decline, however, suicide remains more common among young males than young females. For every one adolescent female (aged 15-19 years) who commits suicide in the UK, there are three adolescent males, the study revealed.

The research, which was carried out as part of the National Confidential Inquiry into Suicide and Homicide by People with Mental Illness, showed that there were 1,722 adolescent and juvenile deaths by suicide in the UK between 1997 and 2003, which represents 4% of all suicides in that time period. The majority of young people were aged 15-19 (93% of the sample), and overall, the most common methods of suicide were hanging, followed by self-poisoning.

“Between 1997 and 2003, we found that suicide rates fell significantly, although we can only speculate on what factors may have contributed to the decline,” said Dr Kirsten Windfuhr, from the Centre for Suicide Prevention at the University of Manchester. “Although changes to antidepressant prescribing may have been one factor contributing to changing suicide rates, it is likely that a combination of factors, both clinical and socio-economic, will have contributed to the decrease in suicide rates. Suicide is a rare event, and is, thankfully, rarer still among children and adolescents. However, it is still one of the leading causes of death among young people and continued monitoring of recent suicide trends is important.”

Over the seven year period, only 14% of young people who committed suicide were in contact with mental health services in the year prior to their death, compared to 26% in adults. Again, there was a marked difference between males and females, with 20% of young females in contact with mental health services compared to only 12% of young males.

“The low rate of service contact in young males is particularly interesting. Young men currently have the highest rates of suicide in the UK, and yet they are least likely to seek help,” said Windfuhr. “Further research is needed to identify the specific risk factors associated with young suicide, and a multi-agency approach including health, social and education services may be the most effective strategy for preventing suicide in young people. In particular, research should be focused on the barriers which prevent young males from seeking help.”

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Medline and the Cochrane Database were searched to identify RCTs of antidepressants for major depression approved by the Food and Drug Administration. Included studies enrolled outpatient participants aged 18-65, lasted 6-12 weeks, compared an antidepressant to placebo or another antidepressant and were published in English after 1985. Excluded trials enrolled inpatients, pregnant women and subjects with psychosis or mania.

Mixed-effects logistic regression models including study type (placebo-controlled or comparator) and study duration (6, 8 or 12 weeks) as fixed effects determined whether these factors affected response and remission rates. In the 90 trials analyzed, the odds of depression response (OR = 1.79, 95% CI = 1.45-2.17, p < 0.001) and remission (OR 1.53, 95% CI = 1.11-2.11, p < 0.001) were significantly higher in comparator relative to placebo-controlled trials. Trials lasting 8 (OR = 1.37, CI = 1.14-1.64, p = 0.001) and 12 (OR = 1.52, CI = 1.12-2.07, p = 0.008) weeks had significantly greater response rates than 6-week trials without differing themselves.

Response and remission rates to antidepressants are significantly affected by study type and duration. Clinicians and researchers must consider the study design when interpreting and designing RCTs of antidepressant medications, researchers urge.

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Whether the danger comes from depression, the drugs used to treat it, or something else, doctors are paying more attention to this association. During the 1990s, depression began to emerge as a possible cause of bone loss, rather than a result. Scientists studied women who didn’t have osteoporosis symptoms or even know they had the condition.

They found lower bone mineral density in those who were depressed. Moreover, the link was found in both younger women and women past menopause. Other studies have found a similar relationship, so investigators have been looking at hormones and brain chemicals potentially involved in both depression and bone loss.

Researchers working with an animal model found that depression triggers the release of noradrenaline, which interferes with bone-building cells. Moreover, they found that imipramine—a member of an older class of drugs called tricyclic antidepressants—reversed both depression and depression-induced bone loss.

It may be a long time before the depression-osteoporosis connection is fully clarified. In the meantime, Harvard Women’s Health Watch suggests that you continue taking an antidepressant if you already use one; depression is a serious illness that can have profound consequences. You may also want to talk to your doctor about getting a bone density test, and make sure you get adequate calcium.

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When a possible connection was suggested between teens who take antidepressant medications and a higher suicide rate, Hendricks Brown, professor and director of the Prevention Science and Methodology Group, USF College of Public Health, decided to investigate along with his colleague Robert Gibbons from the University of Illinois at Chicago.

Their study appears in the September 2007 issue of the American Journal of Psychiatry, titled “Early Evidence on the Effects of Regulated Suicidality Warnings on SSRI Prescriptions and Suicide in Children and Adolescents.” The researchers report findings contrary to earlier studies suggesting a link between antidepressants and suicidal thinking and behavior in youth.

“The overall effect of these newer antidepressants is very likely that they reduce suicide risk considerably,” Brown said. “Overall, the new antidepressants provide a large protective benefit. If there is any group of people who are adversely affected by taking these antidepressants, it has to be a very small group.”

The findings are compelling, especially in view of the FDA’s requirement in May for major black-box warnings to be placed on antidepressants for youth and young adults that advise of a potential suicide risk. The warnings, in turn, have led to a marked reduction in antidepressant use in adolescents and adults.

Suicide is the third leading cause of death in adolescents in this country, following only unintentional injuries and homicide. In real numbers, about 30,000 young people take their own lives in America each year.

These overwhelming figures, in addition to his own experiences with families who had lost loved ones to suicide, motivated Brown to devote enormous efforts to the study of teenage suicide prevention.

“People need to know if the antidepressant medication they are taking is increasing or decreasing their risk for suicide,” Brown said. “It would be bad if antidepressants were causing an increase in suicides, in which case the appropriate policy would be to restrict their use in adolescents. It would be even worse if FDA policies led to less treatment of depression and more suicides.”

Brown and his group examined different statistical approaches that might assess whether a widely used class of antidepressants known as selective serotonin reuptake inhibitors (i.e., Prozac, Zoloft, Paxil, Celexa) were causing more or less suicides in the teenage population.

The analysis was problematic because suicide occurs in one person out of 10,000 youth, but there were only a few thousand youth enrolled in all the clinical trials of antidepressants. And in none of these trials was there a suicide, either among those given an antidepressant, or those given an inactive placebo. There was no ability to compare rates because the number of subjects in the clinical trials was too small.

Given those limitations, Brown used several data sources where depressed individuals were treated differently with different classes of antidepressants or no medication, and he examined the rates of suicide along with the rates of antidepressant prescriptions at the county level. He also looked at the reports of suicide detailed by U.S. doctors after medication use.

Brown found that suicide attempts were dramatically lowered once antidepressant medication began, indicating an overall benefit of these newer medications. Also, very few people who died from suicide had been taking antidepressants.

He also found consistent reductions in suicide across counties as well as across countries during the time when there was increased use of antidepressants. Now that the overall level of antidepressants have decreased since the FDA warnings, there is very early evidence of an upturn in youth suicides.

“With the FDA warnings there has been a rapid lowering of antidepressant prescriptions, and there has been a corresponding increase in youth suicides” noted Brown. “We found similar results in the Netherlands once the warning was broadcast there as well.”

Brown said sometimes health policy decisions are made on limited information, and it may be that the FDA warnings about suicide in youth treated with antidepressants could have unintended consequences of placing more youth at risk. The FDA is now reviewing policy decisions in the light of these data and at some point may withdraw or revise its warning.

Brown’s other work involves some of the first rigorous evaluations of additional therapies and corresponding successes of teenage suicide prevention, including community-based prevention plans. One such program, Sources of Strength, was developed in North Dakota and appears to be very helpful for rural, under-served communities and Native-American communities.

“There are valuable treatments available and ways that people can cope and thrive with adversity, rather than just survive in this world,” Brown said. “There are ways for people who have suicidal thoughts and attempts to get help.”

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Fibromyalgia syndrome (FMS), which consists of chronic widespread pain and tenderness, with other symptoms including fatigue and sleep difficulties, has an estimated prevalence of 0.5 percent to 5.8 percent in North America and Europe. “Patients with FMS experience disability and reduced health-related quality of life (HRQOL). Fibromyalgia syndrome is also associated with high direct and indirect disease-related costs. Effective treatment of FMS is therefore necessary for medical and economic reasons,” the authors write.

Winfried Häuser, M.D., of Klinikum Saarbrücken, Saarbrücken, Germany, and colleagues conducted a meta-analysis to evaluate the effects of treatment with antidepressants on FMS-related symptoms. The researchers identified 18 randomized controlled trials, involving 1,427 participants, for inclusion in the study.

Overall, there was strong evidence for a reduction of pain, fatigue and depressed mood and improved sleep and HRQOL with the use of antidepressants by patients with FMS.

The researchers found large effect sizes of tricyclic and tetracyclic antidepressants (TCAs) for reducing pain, fatigue, and sleep disturbances; small effect sizes of selective serotonin reuptake inhibitors (SSRIs) for reducing pain; small effect sizes of serotonin and noradrenaline reuptake inhibitors (SNRIs) for reducing pain, sleep disturbances, and depressed mood; and small effect sizes of monoamine oxidase inhibitors (MAOIs) for reducing pain.

“Before treatment is initiated, [accompanying] diseases related to potential adverse effects of the drugs and patients’ preferences should be considered. Goals of pharmacological therapy should be defined (no cure, but possible symptom reduction). Since evidence for a long-term effect of antidepressants in FMS is still lacking, their effects should be re-evaluated at regular intervals to determine whether benefits outweigh adverse effects,” the authors write. “The identification of patient characteristics associated with positive and negative therapeutic outcomes are needed to better target antidepressant therapy for FMS.”

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Researchers compared birth outcomes among babies born to 329 women who took selective serotonin reuptake inhibitors (SSRIs) during pregnancy, 4,902 women who had a history of psychiatric illness but did not take SSRIs during pregnancy and 51,770 women with no history of mental illness.

Compared with women who had no history of mental illness, those who took SSRIs during pregnancy gave birth an average of five days earlier and had double the risk for preterm delivery. Babies of mothers who took SSRIs during pregnancy were significantly more likely than infants in the other two groups to have a five-minute Apgar score of seven or lower (seven is the general indicator of good infant health) or to be admitted to the neonatal intensive care unit. Exposure to SSRIs did not affect birth weight or head circumference.

The researchers also found that SSRI-exposed infants admitted to the neonatal intensive care unit had symptoms including seizures, jitteriness, infections, respiratory problems and jaundice that may have been caused by withdrawal from SSRIs or adverse effects from them.

The findings appear in the October issue of Archives of Pediatrics & Adolescent Medicine.

“The study justifies increased awareness to the possible effects of intrauterine exposure to antidepressants,” the researchers concluded. “However, treatment of depression during pregnancy may be warranted, and future studies need to distinguish between individual SSRIs to find the safest medication.”

It’s estimated that more than 10 percent of pregnant women have depression. The authors noted that SSRIs have been shown to cross the placenta and be present in the umbilical cord blood of infants whose mothers took the drugs during pregnancy.

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