Saffron effectively complements antidepressant medications

by Murdoch University

Credit: CC0 Public Domain

New research has shown that saffron may assist adults with depression when it is taken in conjunction with pharmaceutical antidepressants.

11 nov 2019--Murdoch University researchers Dr. Adrian Lopresti and Professor Peter Drummond, and UWA researcher Professor Sean Hood found greater reductions in depressive symptoms when adults with persistent depression, and currently taking a pharmaceutical antidepressant, complement their depression medication with saffron capsules.

Dr. Lopresti said that the trial was the largest of its kind to date and the first study looking at the effects of saffron as an add-on to pharmaceutical antidepressants. Previous research has only investigated the antidepressant effects of saffron as a stand-alone treatment.

"In our research, depressive symptoms decreased more in participants taking saffron compared with a placebo, with reductions of 41 and 21%, respectively on the clinician-rated scale," Dr. Lopresti said.

"In addition, improvements occurred in sleep quality, initiative and motivation, and interest and pleasure in activities."

Dr. Lopresti said that the study indicated that saffron could be used as a natural supplement given at the beginning of antidepressant treatment to increase its effectiveness and to possibly reduce potential adverse effects which are sometimes experienced when one is prescribed antidepressants.

"Saffron can be used at the outset in conjunction with antidepressants or it can be added to antidepressants if symptoms do not fully resolve," Dr. Lopresti said.

"At the moment, if pharmaceutical antidepressants aren't working the options are to increase the dose or to try a new antidepressant. This increases the likelihood of side effects. Now a new option is to take antidepressants and saffron together."

Background

• Participants in the survey were randomly allocated to one of two trial groups, one taking a placebo and one taking a standardized saffron extract.
• Participants were required to be physically healthy, aged 18–65 years and were taking a stable dose (at least eight weeks) of a single pharmaceutical antidepressant
• More research needs to be undertaken to replicate these findings and to determine the longer-term benefits of saffron in treating symptoms of depression.
• The findings do not mean the addition of saffron to cooking would necessarily promote antidepressant effects given the significant variance associated with the quality of saffron stigmas and the variability in extracts available on the market.
• This study was funded by the manufacturer of the saffron extract, Pharmactive Biotech Products SL. However, Pharmactive Biotech Products was not involved in the design of the research, analysis of data, or in the writing of the report.

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More information: Adrian L Lopresti et al. Efficacy of a standardised saffron extract (affron®) as an add-on to antidepressant medication for the treatment of persistent depressive symptoms in adults: A randomised, double-blind, placebo-controlled study, Journal of Psychopharmacology (2019). DOI: 10.1177/0269881119867703

Journal information: Journal of Psychopharmacology 

Provided by Murdoch University 

Combined use of antidepressants and painkillers linked to bleeding risk

Taking a combination of antidepressants and common painkillers is associated with an increased risk of bleeding soon after starting treatment, finds a study published in The BMJ this week.

19 july 2015--The researchers say their results may have been affected by other unmeasured or unknown factors and should be interpreted with caution. However, they suggest special attention is needed when patients use both these classes of drugs together.

Depression produces the greatest decrement in health of all common chronic conditions and depression in older people is an important public health problem.

But concern exists that antidepressants may interact with common painkillers called non-steroidal anti-inflammatory drugs (NSAIDs) to increase the risk of bleeding inside the skull (intracranial haemorrhage).

So a team of researchers based in Korea compared the risk of bleeding among patients treated with antidepressants with and without NSAIDs.

Using the Korean nationwide health insurance database, their study involved over four million people who were prescribed antidepressants for the first time between 2009 and 2013.

NSAID prescriptions were obtained and hospital records were used to identify time to first admission with intracranial haemorrhage within 30 days of a new prescription. Factors that could affect the results, such as age, sex, and use of other medications, were taken into account.

Compared with use of antidepressants alone, the team found that combined use of antidepressants and NSAIDs was associated with a substantially increased bleeding risk.

They found no statistically meaningful differences in risk of bleeding between different types of antidepressant drugs, or with age. Being male was the most common factor for a higher risk of bleeding with combined use of antidepressants and NSAIDs.

"The addition of NSAIDs to antidepressant treatment increased the risk of intracranial haemorrhage within 30 days of the combination starting, especially in men," conclude the authors. "This result adds to evidence confirming the increase of risk with combination use of antidepressants and NSAIDs."

In an accompanying editorial, Dr Stewart Mercer at the University of Glasgow and colleagues at the University of Cambridge, say the results give some cause for concern.

They point out that both types of drug are widely used, and that co-morbidity of the conditions for which these drugs are used is very high - 65% of those with major depression also have chronic pain.

They urge family doctors to be extra vigilant in terms of prescribing behaviour and discussing the risks with patients, especially in deprived areas where "the combination of mental and physical problems (including chronic pain) is very common." And they say further research is required to extend the findings over longer time periods and in differing populations.

More information: Risk of intracranial haemorrhage in antidepressant users with concurrent use of non-steroidal anti-inflammatory drugs: nationwide propensity score matched study, The BMJ, www.bmj.com/cgi/doi/10.1136/bmj.h3517

Editorial: Risk of intracranial haemorrhage linked to co-treatment with antidepressants and NSAIDs, www.bmj.com/cgi/doi/10.1136/bmj.h3745 

Provided by British Medical Journal

Antidepressants alone are not enough

We should reconsider how we use antidepressants more effectively. The latest studies have shown that antidepressants restore the capacity of certain areas of the brain to repair abnormal neural pathways. According to neuroscientist Eero Castrén, the recipient of EUR 2.5 million of ERC funding, recovery requires redirection of these pathways through practice, rehabilitation or therapy.

23 feb 2013--This is a surprisingly blunt view, even for a respected neuroscientist such as Eero Castrén. After all, millions of people throughout the world have been prescribed antidepressants, and pharmaceutical companies have made a billion-dollar business out of selling them. Surely the system cannot be entirely wrong?

Recent studies suggest that this may be the case. Research on animal models demonstrates that antidepressants are not a cure as such. Rather, their role is to restore plasticity in the adult brain. Antidepressants reopen a window of brain plasticity, which allows the formation and adaptation of brain connections through the patient's own activities and observations, similarly to a young child whose brain and experiences about the world develop in response to environmental stimuli.   

Correcting abnormal pathways

When cerebral plasticity is reopened, problems caused by false connections in the brain can be addressed. Such problems can be manifested, for example, as phobias. Studies conducted on animal models by Professor Eero Castrén's research group at the University of Helsinki show that therapy helps to reduce fears for a time, but an antidepressant alone provides no relief. By combining the two, however, long-term effects can be achieved.

"Simply taking drugs is not enough. We must also show the brain what the desired connections should be," Professor Castrén of the Neuroscience Centre explains.

The need for both therapy and medical treatment may also explain why antidepressants sometimes seem to have no effect. If the patient's environment and situation remain unchanged, the drug-induced capacity of the brain to change will not make the patient feel better.

Reaching this point is the result of years of research. Scientists discovered as early as the 1960s that antidepressants affect neurotransmitters in the brain, such as serotonin. Later, antidepressants were found to increase neurotrophins and their ability to transmit signals in the brain. Only recently have scientists begun to explore the effects of drugs on plasticity of brain networks.

Enhancing the plasticity of the adult human brain through antidepressants has opened a whole new field of research for Eero Castrén. He has received a five-year grant of EUR 2.5 million from the European Research Council (ERC) to investigate mechanisms related to adult brain plasticity.

More information: Karpova, N. et al. Fear erasure in mice requires synergy between antidepressant drugs and extinction training. Science. 2011 Dec 23;334(6063):1731-4

Provided by University of Helsinki

Newer antidepressants not necessarily safest for older people

New generation antidepressants, known as selective serotonin reuptake inhibitors (SSRIs) are associated with an increased risk of several severe adverse outcomes in older people compared with older tricyclic antidepressants (TCAs), finds a study published on bmj.com today.

04 aug 2011--The authors say the risks and benefits of different antidepressants should be carefully evaluated when prescribing these drugs to older people.

Depression is a common condition in older people, and antidepressants - particularly SSRIs - are widely used. Yet very little is known about the safety of these drugs in older people.

So a team of researchers at the Universities of Nottingham and East Anglia set out to investigate the association between antidepressant treatment and the risk of a number of potentially life threatening outcomes in older people.

They identified 60,746 UK patients aged 65 and over with a newly diagnosed episode of depression between 1996 and 2007. Many patients had other conditions, such as heart disease and diabetes, and were taking several medications.

Patients were tracked until the end of 2008. During this time, 54,038 (89%) received at least one prescription for an antidepressant: 55% of prescriptions were for SSRIs, 32% for TCAs, 0.2% for monoamine oxidase inhibitors (MAOIs), and 13.5% for other antidepressants.

Antidepressant use was then analysed against several adverse outcomes including all-cause mortality, attempted suicide or self harm, heart attack, stroke, falls, fractures, epilepsy or seizures, and hyponatraemia (high salt levels in the blood).

After adjusting for factors which could affect the results, including age, sex, severity of depression, other illnesses and use of other medications, the team found that SSRIs and drugs in the group of other antidepressants were associated with an increased risk of several adverse outcomes compared with TCAs.

SSRIs were associated with an increased risk of all-cause mortality, stroke, falls, fracture, epilepsy or seizures, and hyponatraemia compared with TCAs. The group of other antidepressants were associated with an increased risk of all-cause mortality, attempted suicide or self harm, stroke, fracture, and epilepsy or seizures.

Depressed patients who were not taking antidepressants at all had a 7% risk of dying (absolute risk of all-cause mortality) some time in the next year, while the comparable risks were 8.1% for those taking TCAs, 10.6% for SSRIs, and 11.4 % for the group of other antidepressants. For stroke, one-year risks were 2.3%, 2.6% and 3.0% (compared to 2.2% for those not on antidepressants) and for fracture they were 2.2%, 2.7% and 2.8% compared to 1.8%.

Among individual drugs, trazodone, mirtazapine and venlafaxine were associated with the highest risks for several outcomes.

Rates of most outcomes were highest in the first 28 days after starting an antidepressant, and also in the first 28 days after stopping.

The authors point out that TCAs were prescribed at lower doses than SSRIs and other antidepressant drugs, which they say "could in part explain our findings." They also warn that differences between patients prescribed different antidepressant drugs may account for some of the associations seen in the study and suggest that further research is needed to confirm these findings.

However, they conclude that the risks and benefits of different antidepressants should be carefully evaluated when prescribing these drugs to older people.

In an accompanying editorial, Professor Ian Hickie from the University of Sydney says that, despite some limitations, "the study has clear implications for more informed prescribing and enhanced clinical monitoring."

He adds: "Given the potential harms, the decision to prescribe for an older person with depression should not be taken lightly."

Provided by British Medical Journal

Antidepressants underused in the elderly: study

NEW YORK, 17 april 2009– The results of a postmortem toxicology study indicate that elderly people who commit suicide usually do not have antidepressant medications in their systems at the time of death.

Antidepressants were found in less than 1 in 4 victims overall, and in even fewer of those in the oldest age group, 85 years and older.

"Assuming that many of the suicide victims had clinically treatable depression, these findings implicate problems in the delivery of specific antidepressant pharmacologic treatment to the 'old-old'," Dr. Robert C. Abrams, from Weill Cornell Medical College, New York, and colleagues conclude in a report in the Journal of Clinical Psychiatry.

Their findings are based on a study of 255 suicide victims from New York City who were at least 65 years of age at the time of their death between 2001 and 2004.

Toxicology results available for 162 victims revealed the presence of antidepressant medication in only about 23 percent of cases.

By age group, rates of antidepressant detection were 22.0 percent in subjects 65 to 74 years of age, 26.8 percent in those 75 to 84 years, and just 16.7 percent in those 85 years and older.

There was some evidence that many had been using anti-anxiety drugs, hypnotics and painkillers in lieu of antidepressants.

SOURCE: Journal of Clinical Psychiatry, March 2009.

Response rates to antidepressants differ among English- and Spanish-speaking Hispanics

LA BioMed study suggests additional treatment may be necessary

TORRANCE , 05 nov 2008--In the first-ever study of its kind, a team led by researchers at Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) report in November's Psychiatric Services journal that Spanish-speaking Hispanics took longer to respond to medication for depression and were less likely to go into remission than English-speaking Hispanics.
Using data from the nation's largest real-world clinical study of depression, the researchers found the Spanish-speaking participants in the study were older and were more likely to be women than the English speakers. The Spanish speakers also had less education and lower income, more medical issues and were more likely than English speakers to be seen in primary care than psychiatric clinics.
"Once we adjusted for these differences in their socioeconomic status, both groups responded about the same to medication for depression," said Ira Lesser, M.D., a LA BioMed investigator who authored the report. "These results are important for clinicians and patients to be aware that Spanish-speaking Hispanics with depression who come from lower social economic groups may need more than medication for depression."
Funded by the National Institute of Mental Health, the study surveyed the treatment records of 195 Spanish-speaking and English-speaking Hispanics who had sought care at the Los Angeles and San Diego sites from among the more than 4,000 patients who participated in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, the nation's largest real-world study of depression.
"Hispanics are the nation's largest ethnic minority and its fastest-growing population group," said Dr. Lesser. "As clinicians ourselves, we always are seeking information on the best treatments for our patients, taking into account the differences among them."
Hispanics comprise about 15% of the U.S. population, and 40% are born outside the country. In the 2000 Census, 32% of Hispanic respondents who said they spoke Spanish at home also said they spoke English "not well" or "not at all." Depression is the nation's most prevalent psychiatric disorder, with approximately 16 out of 100 Americans suffering from it at some point in their lives.
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About LA BioMed
Founded 56 years ago, LA BioMed is one of the country's largest not-for-profit independent biomedical research institutes. It conducts biomedical research, trains young scientists and provides community services, including childhood immunization, nutrition assistance and anti-gang violence programs. The institute's researchers conduct studies in such areas as cardiovascular disease, emerging infections, cancer, diabetes, kidney disease, dermatology, reproductive health, vaccine development, respiratory disorders, inherited illnesses and neonatology.
LA BioMed is an independent institute that is academically affiliated with the David Geffen School of Medicine at UCLA. The institute is located on the campus of Harbor-UCLA Medical Center near Torrance. It contributes to Los Angeles County's economic viability while inventing the future of health care through its ground-breaking research, its training of the scientists of tomorrow and its service to the local community. Please visit our website at www.LABioMed.org

Efficacy Overstated for Antidepressants

By Crystal Phend
PORTLAND, Ore., Jan. 16 -- Publication bias may have cast the benefit of antidepressant medications in a better light than deserved, researchers said.A third of FDA-registered antidepressant trials were never published, found Erick H. Turner, M.D., of the Oregon Health and Science University and Portland VA Medical Center, and colleagues in a meta-analysis.Because unpublished studies were almost twice as likely to have negative findings as those that were published, effect sizes in the literature were artificially inflated by 11% to 69% for individual drugs and by 32% overall, they reported in the Jan. 17 issue of the New England Journal of Medicine.
"By altering the apparent risk-benefit ratio of drugs," they said, "selective publication can lead doctors to make inappropriate prescribing decisions that may not be in the best interest of their patients and, thus, the public health."
Studies have raised concerns about selective publication of safety issues with selective serotonin-reuptake inhibitors for depression in children, the researchers said.
To see whether these issues have an impact on efficacy as well, the researchers analyzed all phase II and III clinical-trial programs for 12 antidepressant agents approved by the FDA from 1987 through 2004.
They gathered hard copies of the FDA's statistical and medical reviews from Freedom of Information Act requests for eight older drugs. Reviews of the four newer antidepressants were available on an FDA Web site.
The researchers searched the literature for all FDA-registered randomized, double-blind, placebo-controlled studies of short-term antidepressant use, then contacted each drug sponsor's medical-information department if no publications were found.
Overall, 31% of the studies -- 23 of 74 -- were unpublished.
Sample size did not appear to be a factor in publication. Unreported trials were not substantially or significantly smaller than those that were published (median 146 patients versus 153, P=0.29).
However, outcome did appear to be a factor. Positive studies were about 11.7 times more likely to be published than negative or questionable studies (P<0.001).
All but one of the 38 trials deemed by the FDA as positive were published, whereas among the 49% of trials that were either negative (24 studies) or questionable (12), only three were published as not positive while the majority were not published (61%).
This publication bias resulted in 94% (95% confidence interval: 84% to 99%) of published studies appearing to have positive results, whereas according to the FDA, only 51% of trials done (95% CI: 39% to 63%) had positive results.
"Not only were positive results more likely to be published," Dr. Turner and colleagues said, "but studies that were not positive, in our opinion, were often published in a way that conveyed a positive outcome."
Published methods in 15% of studies were different than those prespecified to the FDA.
In every case, the study failed its protocol-specified primary outcome but its authors highlighted another positive finding as if it were the primary outcome. In nine cases, the nonsignificant pre-specified primary outcomes were omitted entirely.
The publication bias also had an impact on effect-sizes for the antidepressants, both overall (P=0.012) and individually (P<0.001).
Although the efficacy of antidepressants remained significant regardless of whether unpublished studies were considered, the overall mean weighted effect-size dropped from 0.41 (95% CI: 0.36 to 0.45) to 0.31 (95% CI: 0.27 to 0.35) when the unpublished studies were included.
The findings were limited by restriction to industry-sponsored trials registered with the FDA and to issues of efficacy rather than "real-world" effectiveness, the researchers noted.
And because papers covering multiple studies -- such as those bundling a negative study with a positive study -- were excluded, some studies that were technically published may have been counted as unpublished, they added.
The study was not designed to determine why the publication bias occurred, Dr. Turner said. However, it could have been because the researchers or pharmaceutical companies failed to submit manuscripts, because journal editors and reviewers rejected the studies, or both, he said.
"Perhaps the physician might be slightly less enthusiastic about prescribing them, realizing there are many trials where there was not a positive outcome," Dr. Turner concluded.
Dr. Turner reported having served as a medical reviewer for the FDA. No other potential conflict of interest relevant to this article was reported.
Primary source: New England Journal of MedicineSource reference:Turner EH, et al "Selective publication of antidepressant trials and its influence on apparent efficacy" N Engl J Med 2008; 358: 252-60.

Antidepressant Use and Suicide: Reassuring Findings

Two studies in the American Journal of Psychiatry offer some reassurance about antidepressant therapy and suicide risk.
The first, done in a large prepaid health plan, examined insurance claims for antidepressants or psychotherapy for new episodes of depression. Claims were also examined for evidence of suicide attempts in the 90 days before and the 180 days after the start of therapy. Suicide attempts were highest in the month before therapy began, fell significantly during the first month of treatment, and declined steadily thereafter. This pattern held for treatment with antidepressants or psychotherapy. And although suicide attempt rates were higher in adolescents and young adults, the time patterns remained the same.
The second study examined Veterans Administration records of some 225,000 patients with new depression. Suicide attempt rates were lower among those treated with antidepressants, especially SSRIs or tricyclics, than among those who didn't receive drug therapy. Again, rates were higher before treatment than after.
An editorialist writes that while the studies do not prove that therapy reduces risk, they support the conclusion that "it is much more likely that suicidal behavior leads to treatment than that treatment leads to suicidal behavior."
Writing in Journal Watch Psychiatry, Joel Yager comments: "These association studies do not preclude the fact that a minority of younger patients may well experience an increase in suicidal ideation and perturbation when they start antidepressant medications and bear close follow-up during treatment initiation."

Suicide Findings Question Link to Antidepressants

By NICHOLAS BAKALAR
Two large new studies in The American Journal of Psychiatry suggest that treatment of depression, either with psychotherapy or drugs, reduces the risk of suicide attempts in all age groups, especially during the first months of treatment. The findings raise further questions about possible links between antidepressant drugs and suicide.
In 2005, the Food and Drug Administration, faced with evidence from controlled studies, mandated a “black box” notification on all antidepressant drugs, warning that their use in children and adolescents could increase the risk of suicide. In May, after reviewing controlled data from all age groups, the F.D.A. required an updated version to include a warning about suicide risk in young adults 18 to 24.
The studies the F.D.A. analyzed, in which patients were followed closely and matched to controls, are considered the most direct way to analyze results. The two new studies were based on retrospective reviews of medical records.
In one, researchers led by Dr. Gregory E. Simon, a psychiatrist with the Center for Health Studies in Seattle, reviewed the records of 109,356 people being treated for depression in a large prepaid health plan serving 500,000 people in Washington State and northern Idaho. They found that suicide attempts were most common in the month before treatment began, declined sharply in the month after it began, and tapered off in the following six months. All treatments — psychotherapy, medication or both — showed the same pattern, suggesting that treating depression reduced suicide risk regardless of technique.
The authors acknowledged that they had no way to assess the severity of illness either before or after starting treatment, and that about a third of patients dropped out of treatment within a few weeks, two factors that may have influenced the results. Dr. Simon has received research grants and consulting fees from pharmaceutical companies.
Dr. David Shaffer, a professor of pediatrics and psychiatry at Columbia who was not involved in the study, said the results should prove reassuring to people taking antidepressants. “The study provided no evidence that starting an antidepressant increases the likelihood of a suicide attempt,” he said. “Starting treatment, regardless of which kind, seems to reduce suicide attempts.”
The second study was led by Robert D. Gibbons, director of the Center for Health Statistics at the University of Illinois at Chicago. Using medical data from the Veterans Health Administration, researchers found that among 226,866 adults with depression, the overall rate of suicide attempts after beginning treatment with a selective serotonin reuptake inhibitor, or S.S.R.I., was about one-third the rate of those who received no antidepressant at all. This was true for men 18 to 25 as well as for older adults.
“The V.A. has a very good electronic medical record system, so this is likely to be reliable data,” said Dr. Nada Stotland, a professor of psychiatry at Rush Medical College in Chicago. “That makes these results even more powerful.” Dr. Stotland had no part in the study.
The risk of suicide attempt was significantly higher before S.S.R.I. treatment than immediately after starting it, a finding that coincides with that of the Simon study. The scientists acknowledged that their patients were almost all men, and that they did not include any suicide attempts that did not result in contact with the Veterans Health Administration medical records system. One of the six authors has been a paid adviser to pharmaceutical companies.
The authors of both papers worried that extending the boxed warning to young adults might discourage people from seeking effective treatment. “The F.D.A. didn’t say anything wrong in the warning,” Dr. Simon said. “I am 100 percent in support of the message that we need better follow-up care. But my concern is that the warning may scare people away from treatment.”
Dr. Gibbons expressed similar concerns. “These two studies clearly show that the greatest risk for suicide is depression,” he said. “Failure to treat depression, either using pharmacotherapy or psychotherapy, will lead to dramatic increases in the rate of serious suicide attempts and completions in the U.S. and in the world.”

Antidepressants weaken bones in elderly: studies

By Will DunhamMon Jun 25, 5:47 PM ET
Two studies published on Monday added to the growing evidence that the most popular class of drugs taken to treat depression may contribute to fragile bones in elderly people.
The research focused on a class of antidepressant drugs called selective serotonin reuptake inhibitors. Millions of people, including many elderly, take these drugs, known as SSRIs, which include Eli Lilly and Co's Prozac, known generically as fluoxetine.
Two teams of researchers found that older men and women taking SSRIs had more bone loss than those not taking the drugs, which account for more than 60 percent of U.S. antidepressant drug prescriptions. A drop in bone mass can lead to osteoporosis and bone fractures.
A team led by Dr. Susan Diem of the University of Minnesota tracked 2,722 women, average age 78, including 198 SSRI users. They measured their bone mineral density five years apart.
Those taking the antidepressants experienced a density decrease at the hip of 0.82 percent per year, compared to 0.47 percent per year among those not taking them, the study found.
"We found that SSRI use was associated with increased rates of bone loss in this group of older women," Diem said in a telephone interview.
"But our research cannot definitively determine whether the SSRIs are the cause of the increased rates of the bone loss or whether the increased rate is due to other differences between SSRI users and nonusers," Diem added.
Diem noted, for example, that users of these drugs may be less physically active than people not using the drugs.
"I don't want people stopping their antidepressants for these results. These are all preliminary findings," Diem said. "However, I think our findings suggest that this area needs to be further looked at."
In the second study, researchers led by Dr. Elizabeth Haney of Oregon Health & Sciences University in Portland tracked 5,995 men, average age 74, including 160 who used SSRIs. Bone mineral density at the hip was 3.9 percent lower among SSRI users and 5.9 percent lower in the spine in than men not taking antidepressants, the study found.
Haney's team compared other antidepressants and found no apparent effects on hip or spine density measurements between men who took tricyclic antidepressants or a third type of antidepressant called trazodone and those who took no antidepressants.
The studies, published in the journal Archives of Internal Medicine, did not look at fracture risk.
But another study by researchers from McGill University in Montreal, published in January, found that older adults taking these drugs had double the risk of a bone fracture compared to those not taking the drugs.
SSRIs inhibit a protein that transports serotonin, a chemical messenger involved in sleep and mood. The protein has been discovered in bone as well, raising the possibility these drugs may affect bone strength, the researchers said.

Sex and Antidepressants

Question
I have a patient who reported sexual side effects before with selective serotonin reuptake inhibitors (SSRIs). I started her on bupropion (Wellbutrin XL), but discontinued it because the patient could not tolerate headache for 2 weeks. I thought they would pass but they did not. Any suggestions about what I should do next?
Response from Michael E. Thase, MD Professor of Psychiatry, University of Pittsburgh Medical Center; Chief, Division of Adult Academic Psychiatry, Western Psychiatric Institute and Clinic, Pittsburgh, Pennsylvania
About 1 in 3 patients treated with SSRIs or serotonin-norepinephrine reuptake inhibitors (SNRIs) experience significant sexual dysfunction.[1] Because this side effect can sometimes lessen with the passage of time, a "wait-and-see" approach is often initially prudent. When the sexual side effect persists across a number of weeks, therapeutic action is generally necessary. Options include reducing the dose of the offending medication, adding a second medication with "antidote-like" effects, and switching to an alternate medication with a lower likelihood of sexual side effects.[2]
Let's assume in the case described that dose reduction of the SSRI was attempted and resulted in a decrease in symptomatic benefit and the treating clinician opted to switch to bupropion. This is normally the best choice with respect to reversal of the SSRI-induced sexual dysfunction (ie, bupropion has about the same risk of causing sexual side effects as an inert placebo).[3] However, bupropion, classified as a norepinephrine-dopamine reuptake inhibitor, is mechanistically unrelated to SSRIs and there are the possibilities of different side effect issues and/or lack of response. In this particular case, headache has emerged as an unacceptable side effect during bupropion therapy.