antidepressant

Anti-depressants’ ‘link to diabetes’

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People prescribed anti-depressants should be aware they could be at increased risk of type 2 diabetes, say UK researchers.

The University of Southampton team looked at available medical studies and found evidence the two were linked.

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But there was no proof that one necessarily caused the other.

It may be that people taking anti-depressants put on weight which, in turn, increases their diabetes risk, the team told Diabetes Care journal.

Or the drugs themselves may interfere with blood sugar control.

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These findings fall short of being strong evidence that taking anti-depressants directly increases risk of type 2 diabetes”

Dr Matthew Hobbs of Diabetes UK

Their analysis of 22 studies involving thousands of patients on anti-depressants could not single out any class of drug or type of person as high risk.

Prof Richard Holt and colleagues say more research is needed to investigate what factors lie behind the findings.

And they say doctors should keep a closer check for early warning signs of diabetes in patients who have been prescribed these drugs.

With 46 million anti-depressant prescriptions a year in the UK, this potential increased risk is worrying, they say.

Prof Holt said: “Some of this may be coincidence but there’s a signal that people who are being treated with anti-depressants then have an increased risk of going on to develop diabetes.

“We need to think about screening and look at means to reduce that risk.”

Diabetes is easy to diagnose with a blood test, and Prof Holt says this ought to be part of a doctor’s consultation.

“Diabetes is potentially preventable by changing your diet and being more physically active.

“Physical activity is also good for your mental health so there’s a double reason to be thinking about lifestyle changes.”

Around three million people in the UK are thought to have diabetes, with most cases being type 2.

Dr Matthew Hobbs of Diabetes UK, said: “These findings fall short of being strong evidence that taking anti-depressants directly increases risk of type 2 diabetes. In this review, even the studies that did suggest a link showed only a small effect and just because two things tend to occur together, it doesn’t necessarily mean that one is causing the other.

“But what is clear is that some anti-depressants lead to weight gain and that putting on weight increases risk of type 2 diabetes. Anyone who is currently taking, or considering taking, anti-depressants and is concerned about this should discuss their concerns with their GP.”

Source: BBC

Antidepressants did not increase risk for bone loss in middle-aged women.

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Although previous studies have suggested selective serotonin reuptake inhibitors and tricyclic antidepressants have adverse effects on bone mineral density, a recent prospective study at five clinical centers in the United States demonstrates there is no increased risk for bone loss at the spine, total hip or femoral neck.

According to Susan J. Diem, MD, MPH,from the department of medicine and division of epidemiology and community health at the University of Minnesota in Minneapolis, and colleagues, these findings did not vary by level of depressive symptoms.

“Our findings should provide reassurance for women in midlife regarding the effects of selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs) on bone loss during the menopausal transition,” researchers wrote.

The study compared the annual BMD changes among community-dwelling women (aged 42 years and older) categorized as: nonusers (n=1,590), those taking SSRIs (n=311) or TCAs (n=71). All of the patients were enrolled in the Study of Women’s Health Across the Nation (SWAN), researchers wrote.

According to data, mean lumbar spine BMD decreased 0.68% per year in nonusers, 0.63% in SSRI users and 0.40% per year in TCA users, signaling no statistically significant increased rate of bone loss. Similarly, patients on SSRIs or TCAs displayed no significant bone loss at the total hip and femoral neck, researchers wrote.

In a secondary stratified analysis of depressive symptoms, Diem and colleagues reported no increase in the rate of bone loss among SSRI users or TCA users.

Source: Endocrine Today.

 

Use of antidepressants near delivery and risk of postpartum hemorrhage: cohort study of low income women in the United States.

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Abstract

Objective To determine whether use of serotonin or non-serotonin reuptake inhibitors near to delivery is associated with postpartum hemorrhage.

Design Cohort study.

Setting 2000-07 nationwide Medicaid data (Medicaid Analytic eXtract).

Population 106 000 pregnant women aged 12-55 with a diagnosis of mood or anxiety disorder. Women were categorized into four mutually exclusive exposure groups according to pharmacy dispensing data: current (delivery date), recent (1-30 days before delivery date), past (1-5 months before delivery date), and no exposure (reference group).

Main outcome measures Risk of postpartum hemorrhage by timing of exposure and by serotonin or non-serotonin reuptake inhibitors, classes of antidepressant, and antidepressant types. Relative risks and 95% confidence intervals adjusted for delivery year, risk factors for postpartum hemorrhage, indicators of severity of mood/anxiety disorder, other indications for antidepressants, and other drugs. High dimensional propensity score (hdPS) methods were used to empirically identify and adjust for additional factors.

Results 12 710 (12%) women had current exposure to serotonin reuptake inhibitor monotherapy, and 1495 (1.4%) women had current exposure to non-serotonin reuptake inhibitor monotherapy. The risk of postpartum hemorrhage was 2.8% among women with mood/anxiety disorders but no exposure to antidepressants, 4.0% in the current users of serotonin reuptake inhibitors, 3.8% in the current users of non-serotonin reuptake inhibitors, 3.2% in the recent users of serotonin reuptake inhibitors, 3.1% in the recent users of non-serotonin reuptake inhibitors, 2.5% in the past users of serotonin reuptake inhibitors, and 3.4% in the past users of non-serotonin reuptake inhibitors. Compared with no exposure, women with current exposure to serotonin reuptake inhibitors had a 1.47-fold increased risk of postpartum hemorrhage (95% confidence interval 1.33 to 1.62) and women with current non-serotonin reuptake inhibitor exposure had a 1.39-fold increased risk (1.07 to 1.81). Results were similar with hdPS adjustment. Women with current exposure to serotonin reuptake inhibitors had an adjusted excess risk of 1.26% (0.90% to 1.62%), with a number needed to harm of 80, and for women with current exposure to non-serotonin reuptake inhibitors the excess risk was 1.03% (0.07% to 1.99%), with a number needed to harm of 97. For exposure to serotonin reuptake inhibitors the relative risk was 1.19 (1.03 to 1.38) for recent exposure and 0.93 (0.82 to 1.06) for past exposure; for non-serotonin reuptake inhibitors the figures were 1.17 (0.80 to 1.70) and 1.26 (1.00 to 1.59), respectively. Current exposure to selective serotonin reuptake inhibitor monotherapy was also associated with postpartum hemorrhage (1.42, 1.27 to 1.57), as was current serotonin norepinephrine (noradrenaline) reuptake inhibitor (1.90, 1.37 to 2.63) and tricyclic monotherapy (1.77, 0.90 to 3.47). All types of selective serotonin reuptake inhibitors available for analysis and venlafaxine, a serotonin norepinephrine reuptake inhibitor, were significantly associated with postpartum hemorrhage.

Conclusions Exposure to serotonin and non-serotonin reuptake inhibitors, including selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and tricyclics, close to the time of delivery was associated with a 1.4 to 1.9-fold increased risk for postpartum hemorrhage. While potential confounding by unmeasured factors cannot be ruled out, these findings suggest that patients treated with antidepressants during late pregnancy are more likely to experience postpartum hemorrhage.

Source: BMJ

 

Antidepressants Given Near Delivery Associated with More Postpartum Hemorrhage.

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Women exposed to antidepressants near the time of delivery show an increased risk for postpartum hemorrhage, according to a BMJ study.

Researchers analyzed Medicaid data on some 100,000 women with a diagnosis of mood or anxiety disorder. They used pharmacy dispensing data to characterize exposure, with “current exposure” defined as having a supply of antidepressant medicine on hand that overlapped with the delivery date.

Compared with nonexposed women (i.e., those having no drug supply within 5 months of the delivery date), those with current exposure showed a roughly 1.5-fold increased risk for postpartum hemorrhage. The authors calculate a number need to harm of 80 for patients on serotonin reuptake inhibitors and 97 for nonserotonin reuptake inhibitors.

They speculate that the effect could be partly explained by the effect of blocking serotonin reuptake in platelets, but the association with nonserotonin inhibiting drugs is “unexpected and should be confirmed.”

Soure: BMJ 

Is Ketamine the Next Big Depression Drug?

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ketamin

Ketamine, an anesthetic and illicit party drug, is emerging as a fast-acting antidepressant.

For 20 years Joan* quietly suffered from an unrelenting desire to commit suicide. She held down a job as a special-education teacher and helped care for her family in the northeastern U.S. Yet day after day she struggled through a crushing depression and felt neither joy nor pleasure. Except for the stream of psychiatrists recommending different antidepression treatments—all of which failed to provide relief—Joan kept her condition private. She says it was the fear of hurting her students or abandoning her father that kept her alive. “I really don’t know how I survived,” she says.

A few years ago Joan got a break. She came across a clinical trial for a drug called ketamine that had succeeded in treating patients with intractable major depressive disorder. She enlisted. Following one dose, she experienced her first reprieve from suicidal thoughts in two decades. She realized the drug was working while she was sitting outside on a pleasant day and noticed that the leaves on a tree looked bright green and that a spider was building a web. “It sounds crazy, but normally everything was clouded and gray,” she says. “Nothing stirred me.”

In Brief

Defeating Depression

  • Ketamine is an analgesic, an anesthetic and a hallucinogen—yet the drug also seems to alleviate depression.
    • More commonly known as a party drug, ketamine changes the neurotransmitter balance in the brain, thereby affecting consciousness.
    • Deciphering ketamine’s mechanism of action could pave the way for a new generation of antidepressants.

 

 

This article was originally published with the title A Trip Out of Depression.

Source: scientificamerican.com

 

 

 

 

Cognitive-Behavioral Therapy for Patients with Treatment-Resistant Depression.

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CBT added to antidepressant drugs was beneficial in primary care practices.

Primary care physicians (PCPs) often prescribe antidepressant medications, but only about a third of patients will respond fully to initial pharmacotherapy. When initial pharmacotherapy fails, options include dose escalation, changing agents, or psychotherapy. Brief cognitive-behavioral therapy (CBT) is effective for patients with previously untreated depression, but its role as second-line therapy, added to antidepressant medications, has not been studied well.

Researchers in the U.K. identified 469 depressed adults who had failed to respond to a minimum of 6 weeks of antidepressant therapy. Patients continued to receive usual care by their PCPs (including antidepressants) and were randomized to receive or to not receive 12 to 18 sessions of CBT delivered in or near their PCPs’ offices. Usual-care participants could be referred for counseling, CBT, or secondary care, when such treatment was deemed to be clinically appropriate.

After 6 months, significantly more patients in the CBT group than in the usual care–alone group (46% vs. 22%) reached the primary endpoint of 50% decline in depressive symptoms, as measured by the 63-point Beck Depression Inventory (BDI). Patients who received CBT also had significantly higher rates of remission (BDI <10) after 6 months. Differences in these outcomes remained significant after 12 months of follow-up.

Comment: This study will support the growing interest in integrating behavioral health services into primary care practices, where psychiatric and somatic morbidities commonly coexist and interact. New clinical and financial models will be required, but the payoff for patients’ health and productivity could be substantial.

Source:Journal Watch General Medicine

 

Selective serotonin reuptake inhibitors (SSRIs) for stroke recovery.

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Abstract

BACKGROUND:

Stroke is the major cause of adult disability. Selective serotonin reuptake inhibitors (SSRIs) have been used for many years to manage depression. Recently, small trials have demonstrated that SSRIs might improve recovery after stroke, even in people who are not depressed. Systematic reviews and meta-analyses are the least biased way to bring together data from several trials. Given the promising effect of SSRIs on stroke recovery seen in small trials, a systematic review and meta-analysis is needed.

OBJECTIVES:

To determine whether SSRIs improve recovery after stroke, and whether treatment with SSRIs was associated with adverse effects.

SEARCH METHODS:

We searched the Cochrane Stroke Group Trials Register (August 2011), Cochrane Depression Anxiety and Neurosis Group Trials Register (November 2011), Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2011, Issue 8), MEDLINE (from 1948 to August 2011), EMBASE (from 1980 to August 2011), CINAHL (from 1982 to August 2011), AMED (Allied and Complementary Medicine) (from 1985 to August 2011), PsycINFO (from 1967 to August 2011) and PsycBITE (Pyschological Database for Brain Impairment Treatment Efficacy) (March 2012). To identify further published, unpublished and ongoing trials we searched trials registers, pharmaceutical websites, reference lists, contacted experts and performed citation tracking of included studies.

SELECTION CRITERIA:

We included randomised controlled trials that recruited stroke survivors (ischaemic or haemorrhagic) at any time within the first year. The intervention was any SSRI, given at any dose, for any period. We excluded drugs with mixed pharmacological effects. The comparator was usual care or placebo. In order to be included, trials had to collect data on at least one of our primary (dependence and disability) or secondary (impairments, depression, anxiety, quality of life, fatigue, healthcare cost, death, adverse events and leaving the trial early) outcomes.

DATA COLLECTION AND ANALYSIS:

We extracted data on demographics, type of stroke, time since stroke, our primary and secondary outcomes, and sources of bias. For trials in English, two review authors independently extracted data. For Chinese papers, one review author extracted data. We used standardised mean differences (SMD) to estimate treatment effects for continuous variables, and risk ratios (RR) for dichotomous effects, with their 95% confidence intervals (CIs).

MAIN RESULTS:

We identified 56 completed trials of SSRI versus control, of which 52 trials (4059 participants) provided data for meta-analysis. There were statistically significant benefits of SSRI on both of the primary outcomes: RR for reducing dependency at the end of treatment was 0.81 (95% CI 0.68 to 0.97) based on one trial, and for disability score, the SMD was 0.91 (95% CI 0.60 to 1.22) (22 trials involving 1343 participants) with high heterogeneity between trials (I(2) = 87%; P < 0.0001). For neurological deficit, depression and anxiety, there were statistically significant benefits of SSRIs. For neurological deficit score, the SMD was -1.00 (95% CI -1.26 to -0.75) (29 trials involving 2011 participants) with high heterogeneity between trials (I(2) = 86%; P < 0.00001). For dichotomous depression scores, the RR was 0.43 (95% CI 0.24 to 0.77) (eight trials involving 771 participants) with high heterogeneity between trials (I(2) = 77%; P < 0.0001). For continuous depression scores, the SMD was -1.91 (95% CI -2.34 to -1.48) (39 trials involving 2728 participants) with high heterogeneity between trials (I(2) = 95%; P < 0.00001). For anxiety, the SMD was -0.77 (95% CI -1.52 to -0.02) (eight trials involving 413 participants) with high heterogeneity between trials (I(2) = 92%; P < 0.00001). There was no statistically significant benefit of SSRI on cognition, death, motor deficits and leaving the trial early. For cognition, the SMD was 0.32 (95% CI -0.23 to 0.86), (seven trials involving 425 participants) with high heterogeneity between trials (I(2) = 86%; P < 0.00001). The RR for death was 0.76 (95% CI 0.34 to 1.70) (46 trials involving 3344 participants) with no heterogeneity between trials (I(2) = 0%; P = 0.85). For motor deficits, the SMD was -0.33 (95% CI -1.22 to 0.56) (two trials involving 145 participants). The RR for leaving the trial early was 1.02 (95% CI 0.86 to 1.21) in favour of control, with no heterogeneity between trials. There was a non-significant excess of seizures (RR 2.67; 95% CI 0.61 to 11.63) (seven trials involving 444 participants), a non-significant excess of gastrointestinal side effects (RR 1.90; 95% CI 0.94 to 3.85) (14 trials involving 902 participants) and a non-significant excess of bleeding (RR 1.63; 95% CI 0.20 to 13.05) (two trials involving 249 participants) in those allocated SSRIs. Data were not available on quality of life, fatigue or healthcare costs.There was no clear evidence from subgroup analyses that one SSRI was consistently superior to another, or that time since stroke or depression at baseline had a major influence on effect sizes. Sensitivity analyses suggested that effect sizes were smaller when we excluded trials at high or unclear risk of bias.Only eight trials provided data on outcomes after treatment had been completed; the effect sizes were generally in favour of SSRIs but CIs were wide.

AUTHORS’ CONCLUSIONS:

SSRIs appeared to improve dependence, disability, neurological impairment, anxiety and depression after stroke, but there was heterogeneity between trials and methodological limitations in a substantial proportion of the trials. Large, well-designed trials are now needed to determine whether SSRIs should be given routinely to patients with stroke.

Source: PubMed

 

Psychotropic Drug Use Associated with Increased Risk for Car Crashes .

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Antidepressants, benzodiazepines, and so-called “Z-drugs” such as zolpidem (Ambien) and zaleplon (Sonata) are associated with increased risk for motor vehicle accidents, according to a case-control study in the British Journal of Clinical Pharmacology.

Using registry and claims data from Taiwan, researchers assessed use of psychotropic drugs among 5200 people who were drivers during motor vehicle accidents and 31,000 matched controls who were not in accidents.

Relative to nonusers, the risk for motor vehicle accidents was higher among patients who had taken the following classes of drugs within the previous month: antidepressants (adjusted odds ratio, 1.73), benzodiazepines (1.56), and Z-drugs (1.42), but not antipsychotics. Even relatively low doses of antidepressants and benzodiazepines conferred increased risks.

The authors conclude that clinicians should “choose safer, alternative treatments and advise patients not to drive, especially while taking medications, to minimize the risk of causing [traffic accidents] under the influence of psychotropic medications.”

Source: British Journal of Clinical Pharmacology

Antidepressants: Another weapon against chronic pain

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Some of the more effective and commonly used medications for chronic pain are drugs that were developed to control other conditions. Antidepressants are a mainstay in the treatment of many chronic pain conditions — even when depression isn’t a factor.

Tricyclics used most often

Tricyclic antidepressants are the most common type used for pain. They include:

  • Amitriptyline
  • Imipramine (Tofranil)
  • Clomipramine (Anafranil)
  • Nortriptyline (Pamelor)
  • Desipramine (Norpramin)
  • Doxepin (Sinequan)

Types of pain relieved

Tricyclic antidepressants seem to work best for pain caused by:

  • Nerve damage from diabetes (diabetic neuropathy)
  • Nerve damage from shingles (postherpetic neuralgia)
  • Tension headache
  • Migraine
  • Fibromyalgia
  • Low back pain

The painkilling mechanism of these drugs is still not fully understood. Tricyclic antidepressants may increase neurotransmitters in the spinal cord that reduce pain signals. But they don’t work immediately. You may have to take a tricyclic antidepressant for several weeks before it starts reducing your pain.

Side effects usually mild

Side effects of tricyclic antidepressants may include:

  • Drowsiness
  • Dry mouth
  • Constipation
  • Weight gain
  • Difficulty with urination
  • Changes in blood pressure

To reduce or prevent side effects, your doctor will likely start you at a low dose and slowly increase the amount. Most people are able to take tricyclic antidepressants, particularly in low doses, with only mild side effects. The doses that are effective for pain are typically lower than the doses used for depression.

Other antidepressants that may help

Drugs such as venlafaxine (Effexor) and duloxetine (Cymbalta) can relieve many of the same types of painful conditions that are eased by tricyclic antidepressants. Known as serotonin and norepinephrine reuptake inhibitors (SNRIs), these drugs don’t work quite as well as tricyclic antidepressants, but they also don’t produce as many side effects.

Selective serotonin reuptake inhibitors (SSRIs) such as paroxetine (Paxil) and fluoxetine (Prozac) don’t appear to help relieve pain on their own. However, fluoxetine appears to boost the painkilling effects of some tricyclic antidepressants.