SSRIs

Antidepressant Use in Pregnancy

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A new mouse study investigated the impact of SSRIs on brain development.

  • A new mouse study found antidepressant use during pregnancy may influence brain development in utero.
  • Most antidepressants are safe to use during pregnancy, according to experts. Depending on the severity of mental illness, withholding medication can lead to more severe health risks.
  • Other treatments for depression include cognitive behavioral therapy, interpersonal psychotherapy, support groups, mindfulness, yoga, and exercise.

A new mouse study found taking antidepressants during pregnancy may affect brain development in utero and be a risk factor for developing mental health disorders later in life.

The findings were published February 16 inNature Communications.Trusted Source

Researchers examined the impact of a chemical called fluoxetine on mice.

Fluoxetine elevates the amount of serotonin in the brain and is typically used in selective serotonin reuptake inhibitors (SSRI) medications such as Prozac and Sarafem which are used to help treat depression and perinatal depression. The researchers looked at how serotonin influences prefrontal cortex development in a fetus – specifically, the effect of deficiency and surplus of serotonin on brain development in mice.

Results showed that serotonin not only impacts overall brain function but also impacts how individual connections between neurons change and adapt. This, in turn, affects the way the brain learns.

“This is certainly a fascinating scientific study on postnatal development in the mouse brain but how it applies to the human brain still remains a question,” said Dr. Michael Cackovic, maternal-fetal medicine physician at Bridgeport Hospital.

Cackovic wasn’t involved in the study.

Most brain development in humans occurs in the first two years of life and 90% before kindergarten so it would make sense that giving “pups” this medication early in life could potentially cause a problem, Cackovic explained.

SSRIs can transmit from parent to child in utero

Researchers looked at the effects of serotonin on the part of a developing brain called prefrontal cortex when it is exposed to fluoxetine.

Fluoxetine goes into the placenta but also into breast milk.

“All known SSRI medications readily pass through the placenta and enter the fetal circulation,” said Dr. Jay Gingrich, professor of developmental psychology at Columbia University Vagelos College of Physicians and Surgeons. “There are several studies that have examined the health and mental health outcomes of children exposed to SSRIs in utero. Because serotonin receptors and pathways are highly conserved through evolution (across distant species), there has been a presumption that findings in rodents may likely be relevant to human brain development.”

Gingrich continued: “This has been difficult to prove unequivocally, but several studies have found increased rates of depression, anxiety, and adjustment disorders in SSRI-exposed children as they age into adolescence. Other studies have found increased rates of autism, but most of those studies have not controlled for maternal mental health and several studies failed to find a similar linkage.”

The risk of exposure through breast milk is expected to be far lower than through placental passage and should not dissuade mothers from breastfeeding or resuming SSRI use during this period, he added.

These findings do not mean that people who wish to become pregnant should stop taking SSRIs immediately, according to experts.

“There is a tremendous amount of data that supports use of an SSRI during pregnancy when it is taken to help the person achieve remission or maintain remission of their depression and/or anxiety,” said Dr. Katherine Campbell, associate professor of obstetrics, reproductive sciences at Yale School of Medicine.

Campbell, who did not work on the study, did clarify that infants can have symptoms if their parent is on SSRIs while pregnant.

“When babies are born to parents who are on fluoxetine (or other SSRI), the baby can have withdrawal symptoms that can start after birth,” Campbell said. “Withdrawal symptoms can include irritability, jitteriness, and fast breathing. There are newer SSRIs on the market that cross the placenta and cross into breast milk in lower concentrations.”

Is it safe to take antidepressants during pregnancy?

While there may be risks in taking SSRIs while pregnant, there are also risks of experiencing mental health disorders. Experts point out that untreated mental illness has significant and well-established consequences to maternal and infant health.

For example, untreated depressionTrusted Source in pregnancy is associated with preterm birth, low birth weight and stillbirthTrusted Source.

“Antidepressants, and selective serotonin reuptake inhibitors (SSRIs) specifically, are the most studied class of medications in pregnancy and the clinical consensus based on the extensive literature (in human studies), is that they are generally safe to use in pregnancy and in lactation when medically indicated (with the exception of paroxetine, which is usually not prescribed or used in pregnancy due to equivocal evidence on possible minor cardiac malformations),” said Dr. Ariadna Forray, associate professor of psychiatry at Yale School of Medicine and Director at the Center for Wellbeing of Women and Mothers, Psychiatry; Yale Medical Director, ACCESS Mental Health for Moms.

Forray was not involved in the study.

“The irony is that both untreated maternal depression and the use of antidepressants both increase the risk for anxiety and depressive disorders in the offspring in later life,” Gingrich said. “This conundrum is what has made it so difficult to discern whether SSRI use in pregnancy is a net positive to the child or whether we are exacerbating what trends were expected based on maternal history.”

Experts say if you are pregnant and taking SSRIs you can speak with your physician about whether or not it would make sense to stop taking the medication.

In many clinical scenarios, it is problematic to withhold medication treatment during pregnancy because of the severity of the mother’s symptoms.

“We have been working in this area for 20 years in attempt to provide a clearer risk-benefit profile to clinicians and their patients to help inform better decisions. This work is ongoing,” Gingrich added.

Other options to treat depression

There are various non-pharmacological interventions to help treat depression symptoms that people can explore after talking to their psychiatrist and physician if they want to avoid SSRIs.

“Evidence-based interventions include cognitive behavioral therapy and interpersonal psychotherapy,” said Forray. “Things like support groups, mindfulness, yoga and exercise can also be helpful additions to evidence-based treatments.”

In addition, “there are several effective psychotherapies for depression during pregnancy and in the post-partum period (IPT, CBT) and there are new non-SSRI medications specifically indicated for post-partum depression (e.g., Zurzuvae or zuranolone),” Gingrich explained. “The US needs to improve the availability and reimbursement of such non-pharmacologic therapies for patients in need. These are often barriers to obtaining appropriate psychotherapy for the expecting mother.”

Takeaway

According to a new mouse study, antidepressant use during pregnancy may affect brain development in utero. However, further research is needed.

The clinical consensus is that most antidepressants are safe to use during pregnancy, according to experts. It is important to note that withholding medication can pose greater health risks for the pregnant person and child.

Aside from medication, there are other ways to help treat symptoms of depression. These include cognitive behavioral therapy, interpersonal psychotherapy, support groups, mindfulness, yoga, and exercise.

Beyond SSRIs: How the Newest Antidepressants Work

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Antidepressants are medications that can help relieve depression symptoms, like fatigue and emotional numbness.

Several different kinds of antidepressants exist, but the most commonly prescribed are selective serotonin reuptake inhibitors (SSRIs).

Fluoxetine (Prozac) entered the market in 1988Trusted Source as the first SSRI, and for the next 30 years, many experts considered SSRIs the “modern” antidepressant.

In 2019, the Food and Drug Administration (FDA) approved two new antidepressants, brexanoloneTrusted Source and esketamineTrusted Source. There’s also been renewed interest in agomelatine, an antidepressant not currently available in the United States.

Read on to learn more about these new antidepressants, including how they compare to SSRIs, their side effects, and how to try them.

Brexanolone

In 2019, the FDA approved brexanolone (Zulresso) as the first drug specifically designed to treat moderate to severe postpartum depression (PPD).

Experts consider some SSRIs safe to take while pregnant or nursing, but these medications may not lead to much improvement for several weeksTrusted Source. When you have PPD, symptoms don’t just affect your own well-being — they can also have long-term effects on your bond with your baby.

Brexanolone, however, begins to take effect immediately. According to two randomized clinical trialsTrusted Source published in 2018, this medication can significantly reduce PPD symptoms — benefits that held when researchers followed up with participants 30 days after treatment.

How it works

Brexanolone raises brain levels of the neurotransmitter gamma aminobutyric acid (GABA).

In a nutshell, GABA dampens the chemical activity in your neurons, almost like a dimmer switch for certain cells.

Scientists aren’t sure exactly how brexanolone treats PPD symptoms, but one theoryTrusted Source suggests that with PPD, your GABA levels don’t recover quickly enough from pregnancy to manage your stress. Essentially, cortisol hormones rise unchecked, contributing to symptoms of depression. Brexanolone, then, may offer a “reset” by restoring your GABA levels.

You receive this medication as a one-time IV treatment over the course of 2 and a half daysTrusted Source. You’ll remain in your healthcare center for the entire 60-hour treatment for monitoring.

Safety and side effects

Like other drugs that affect GABA levels, brexanolone can cause sedation. Roughly 1 in 4 peopleTrusted Source experience sedation-related side effects in the first 24 hours of treatment.

You may feel:

  • extremely sleepy, even during the day
  • unfocused and distractible
  • dizzy or faint

Your care team will check on you every 2 hours for extreme symptoms like fainting. If you experience serious side effects, they’ll stop the infusion. Sedation-related symptoms should stop within 15 minutesTrusted Source after the IV infusion stops.

How to get a prescription

You can only receive this treatment from approved healthcare centers, and you’ll need a doctor’s referral to join the treatment program.

The treatment can cost up to $34,000Trusted Source, though health insurance can help offset some of the cost. Companies like Aetna and Cigna require pre-authorization, so you’ll want to make sure your insurance provider covers the treatment before you check in to your clinic.

Keep in mind, too, that most insurance companies only cover one round of treatment, as research has yet to explore the potential benefits of additional rounds of treatment.

The company that makes brexanolone also offers several financial assistance programs, which could be worth considering if the price tag puts it out of reach.

Esketamine

Esketamine (Spravato) is a chemical cousin of the anesthetic ketamine. The FDA approved esketamine in 2019 to treat treatment-resistant depression, or depression that persists after you try at least two different antidepressant treatments.

During clinical trials, doctors gave participants a nasal esketamine spray or a placebo spray. All participants also took an oral antidepressant they hadn’t tried before. Compared to people who took an oral antidepressant and used a placebo spray, those who used the esketamine spray reported greater symptom relief and longer symptom-free periodsTrusted Source.

How it works

Esketamine sets off a chain reaction of chemicals that ultimately raises your levels of brain-derived neurotrophic factor (BDNF). BDNF helps your neurons make new connections, which in turn enables you to form memories, learn new information, and develop different habits.

Depression typically involves low BDNF levels, and your brain may have difficulty adapting to changes. Esketamine helps restore BDNF levels, along with overall brain plasticity.

As with brexanolone, you have to take esketamine in the presence of a healthcare professional. Your doctor or clinician will give you a dose between 56–84 milligrams (mg), which you spray into your nostrils. You then relax in a chair for 2 hours. Your care team will monitor your blood pressure and heart rate during this time.

This medication works quickly, with many people noticing relief right away. Treatment requires multiple sessions, typically twice a week for the first 28 days and then spaced out over time. The effects usually last until your next dose.

Safety and side effects

In clinical trials, participants tended to report mild to moderate side effects. You may feel sleepy, dizzy, or a bit “out of it” during your treatment session. These side effects often go away within 90 minutes after you take your dose.

On rare occasions, people have reported more severe side effects like:

  • vomiting
  • anxiety and confusion
  • worsening depression or suicidal thoughts

Esketamine can also lead to significant increases in blood pressure during the treatment session, which is why you’ll need monitoring for 2 hours. If you have hypertension or another vascular condition, make sure to tell your doctor before receiving treatment.

How to get a prescription

You can only receive this treatment at an approved healthcare center, so you’ll need to ask your doctor or psychiatrist if you’d like to try esketamine.

The course of treatment instead depends on the severity of your symptoms — and how much you’re able to pay. As of 2021, a standard 56-mg dose of esketamine costs $590, and a large dose of 84 mg costs $885.

The initial month of therapy is often the most expensive since treatment guidelines recommend twice-weekly treatment for the first month. This first month can cost anywhere from $4,800 and $6,800 dollars.

To date, no official guidelines set an ideal length of treatment.

According to the company that produces Spravato, some insurance programs cover most of the cost of esketamine. You’ll only need to pay a $10 copay per session until you hit the benefits cap of $7,150 per year.

Agomelatine

Agomelatine (Valdoxan), an oral antidepressant, has been available in some other countries since 2009, though you can’t get this medication in the United States.

You take agomelatine as a 25-mg pill once a day at bedtime. If your depression symptoms don’t respond, a doctor may increase the dose to 50 mg per day.

Agomelatine may have particular benefit for depression that:

How it works

Agomelatine has two main effectsTrusted Source on your brain. It increases activity at melatonin nerve receptors, which helps you sleep. It also decreases activity at specific serotonin receptors and helps increase dopamine and norepinephrine in the frontal cortex.

Increasing melatonin levels can improve sleep-related issues. In a small 2018 study that included 24 young adults, researchers found that the more agomelatine shifted the participants’ circadian rhythms, the more their depression symptoms improved.

Experts don’t yet know exactly how decreasing serotonin fits into the picture.

That said, older animal research from 2014Trusted Source suggests boosting melatonin and decreasing serotonin binding to receptors simultaneously may help protect newly created neurons by shielding them from the damage caused by chronic stress.

Safety and side effects

Agomelatine may cause:

  • nausea and vomiting
  • constipation, stomach pain, and diarrhea
  • drowsiness or difficulty sleeping
  • headaches

But many people only experience mild side effects while taking agomelatine, which may partially explain the renewed interest in this antidepressant.

After all, if you don’t experience severe side effects, you’ll probably feel more inclined to continue taking the medication.

How agomelatine compares

A2018 reviewTrusted Sourceincluding 522 trials with a total of 116,477 participants compared 21 antidepressants.

When the review authors considered dropout rates specifically due to adverse reactions, they discovered all included antidepressants had a higher dropout rate than the placebo — except agomelatine.

Incidentally, researchers also listed agomelatine as one of seven most effective antidepressants among those studied.

With many antidepressants, you may experience flu-like symptoms if you suddenly stop taking the medication. This phenomenon, called discontinuation syndrome, doesn’t occur with agomelatine. You can easily stop even long-term agomelatine useTrusted Source.

So, you might wonder: If this medication works so well, what’s holding up approval in the United States?

Agomelatine does have the potential to cause one very severe side effect: liver toxicity. The medication raises the levels of liver amino acids called transaminases, causing liver damage for up to 4.6%Trusted Source of people who take it. People taking this medication need to have their liver function tested at weeks 3, 6, 12, and 24 of treatment.

Other antidepressants can have a similar impact on your liver, but at much lower ratesTrusted Source:

  • placebo: 2.1%
  • escitalopram (Lexapro): 1.4%
  • paroxetine (Paxil): 0.6%
  • fluoxetine (Prozac): 0.4%

How to get a prescription

Currently, you can’t get a prescription for agomelatine in the United States or Canada, as regulatory agencies have deemed the risk of liver injury too high to allow the drug on the market.

It’s possible that agomelatine could become more widely available in the future if researchers identify a way to minimize the risk of liver toxicity.

Doctors in Europe and Australia may prescribe this medication.

The bottom line

Brexanolone and esketamine appear to have the most benefit for postpartum depression and treatment-resistant depression, respectively. These medications also come with a high price tag that can make them harder to access.

Agomelatine can effectively treat a wider range of depression subtypes. But it also carries a risk of liver toxicity, and it hasn’t been approved for use in the United States.

To sum up, these medications likely won’t replace SSRIs as the first line of treatment for other types of depression anytime soon. Still, their existence opens up possibilities for future advances in depression treatment.

Using Ketamine to Find an Undiscovered Pathway in Depression

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Summary: Ketamine treatment leads to an increase in IGF-1, which, in turn, produces an antidepressant effect.

Source: Osaka Metropolitan University

For the 280 million people suffering from depression globally, relief cannot come fast enough. Monoaminergic antidepressants, including selective serotonin reuptake inhibitors (SSRIs) take weeks to months to take effect and do not work for more than one in three patients.

For patients diagnosed with treatment-resistant depression, or in immediate crisis, access to safe, effective, rapid-acting antidepressants can improve lives and decrease suicide.

One current possibility being investigated is ketamine, which can improve depression, even in treatment-resistant patients. Ketamine is an anesthetic used for over 50 years, but it has serious side-effects, including dependence, hallucinations, and delusions.

So, while preclinical studies have shown that a single dose of ketamine can have beneficial long-term effects on mental health and is only used to treat depression as a last resort.

There are good reasons to be cautious; in addition to the side-effects, the way ketamine alters brain chemistry is not fully understood. If the biological mechanisms in the brain that ketamine influences are discovered, new drugs could be developed to target the beneficial antidepressant effect specifically.

The study led by Professor Kondo demonstrated ketamine treatment led to an increase in insulin-like growth factor 1 (IGF-1), a known antidepressant brain molecule. However, they did not know if this was linked to previously discovered ketamine related antidepressant molecules like brain-derived neutrophic factor (BDNF).

This shows a depressed looking woman
This discovery indicates that ketamine uses a previously unknown pathway that produces an antidepressant effect.

They confirmed IGF-1 produced an antidepressant effect then demonstrated that they could switch it off by blocking it with an IGF-1 neutralizing antibody.

After demonstrating they could switch off IGF-1, the researchers followed up with a separate experiment. Previous studies have shown that ketamine increases BDNF, a protein that promotes nerve growth, so the researchers wanted to check if IGF-1 and BDNF were working together or separately.

They tested whether IGF-1 and BDNF neutralizing antibodies blocked the other proteins antidepressant effect, they did not, leading the researchers to conclude that IGF-1 and BDNF work through their own independent pathways.

This discovery indicates that ketamine uses a previously unknown pathway that produces an antidepressant effect. The researchers hypothesized that the single dose of ketamine increases the level of IGF-1 in the brain, persistently changing prefrontal cortex nerves and causing them to increase their number of stable connections.

The link between ketamine and IGF-1 presents a brand-new direction for future studies investigating antidepressants that target IGF-1 directly.

IGF-1 release in the medial prefrontal cortex mediates the rapid and sustained antidepressant-like actions of ketamine

Ketamine, an N-methyl-D-aspartate receptor antagonist, exerts rapid and sustained antidepressant actions. Preclinical studies demonstrated that the release of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor in the medial prefrontal cortex (mPFC) is essential for the antidepressant-like effects of ketamine.

However, the role of other neurotrophic factors in the antidepressant-like effects of ketamine has not been fully investigated. Since the intra-mPFC infusion of insulin-like growth factor 1 (IGF-1) reportedly produced antidepressant-like effects, the present study examined the role of endogenous intra-mPFC IGF-1 signaling in the antidepressant-like actions of ketamine.

In vivo microdialysis showed that ketamine (10 and 30 mg/kg) significantly increased extracellular IGF-1 levels in the mPFC of male C57BL/6J mice for at least 5 h. Infusion of an IGF-1 neutralizing antibody (nAb; 160 ng/side) into the mPFC 15 min before or 2 h after ketamine injection blocked the antidepressant-like effects of ketamine in three different behavioral paradigms (forced swim, female urine sniffing, and novelty-suppressed feeding tests were conducted 1, 3 and 4 days post-ketamine, respectively).

The ketamine-like antidepressant-like actions of the intra-mPFC infusion of BDNF (100 ng/side) and IGF-1 (50 ng/side) respectively were not blocked by co-infused IGF-1 nAb and BDNF nAb (200 ng/side).

Moreover, intra-mPFC infusion of IGF-1 nAb 2 h post-ketamine blocked the antidepressant-like effects of ketamine in a murine lipopolysaccharide (LPS)-induced depression model. Intra-mPFC IGF-1 infusion also produced antidepressant-like effects in the LPS-challenged mice via mechanistic target of rapamycin complex 1 activation.

These results suggest that persistent release of IGF-1, independently of BDNF, in the mPFC is essential for the antidepressant-like actions of ketamine.

Magic Mushrooms Do The Opposite of Anti-Depressants, But That May Be Why They Work

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“I felt so much lighter, like something had been released.”

 

psychedelic therapy is going through something of a revival right now, and we may now know how one such hallucinogenic drug is seemingly able to alleviate symptoms of depression.

 

Psilocybin, the active compound in magic mushrooms, has long been known to deliver therapeutic effects to people with depression, and researchers think this is because the drug helps to revive emotional responsiveness in the brain.

What’s so remarkable is this kind of mechanism is actually the opposite effect of a major class of antidepressants used to treat the condition, called selective serotonin reuptake inhibitors (SSRIs).

“Psilocybin-assisted therapy might mitigate depression by increasing emotional connection,” neuroscientist Leor Roseman from Imperial College London explained to PsyPost.

“[T]his is unlike SSRI antidepressants which are criticised for creating in many people a general emotional blunting.”

The new study examined 20 patients diagnosed with moderate-to-severe treatment-resistant depression, to investigate what kinds of effects psilocybin would have on their brain activity and depressive symptoms.

A previous study by some of the same researchers had shown that the drug seems to ‘reset’ brain circuits in depressed people, with patient-reported benefits lasting up to five weeks after treatment.

This time around, the team wanted to examine what impact psilocybin might have on the amygdala – the part of our brain that helps process emotional reactions, including fear – in addition to its effects on participants’ depression.

Before taking the drug, the participants underwent fMRI brain scans, then, in two separate sessions one week apart, they took doses of psilocybin, before again being scanned via fMRI the morning after receiving the second dose.

During the fMRI scans, the group were shown images of faces with either fearful, happy, or neutral expressions, and the researchers wanted to investigate what effect these faces had on the participants’ amygdala after taking psilocybin.

After the experiment, the majority of patients reported that the psilocybin had eased their depressive symptoms, with almost half the group still seeing benefits from the treatment five weeks later – in line with the kinds of benefits other depression studies using the drug have shown.

More intriguingly, the fMRI scans showed the drug heightened activity in the right amygdala, with increased responses to both fearful and happy faces – and the increases to fearful faces were predictive of clinical improvements in depressive symptoms one week after the experiment.

What’s striking is the alleviation of depression occurs from emotional receptivity being enhanced – the opposite of SSRI antidepressants.

“It has been proposed that decreased amygdala responsiveness to negative emotional stimuli under SSRIs is a key component of their therapeutic action,” the researchers explain, “but the present study’s findings suggest that this model does not extend to the therapeutic action of psilocybin for [treatment-resistant depression].”

The researchers don’t know for sure why that is, but after the experiment the patients reported “a greater willingness to accept all emotions post-treatment (including negative ones)” (original emphasis), whereas they felt their previous depression treatments worked to “reinforce emotional avoidance and disconnection.”

“I felt so much lighter, like something had been released, it was an emotional purging, the weight and anxiety and depression had been lifted,” one participant said.

“I have felt a sense of acceptance; more acceptance of agony, boredom, loneliness,” commented another.

“[A] willingness to try to accept the negative times – but also an appreciation of the wonderful times.”

The team acknowledges their study has a number of limitations, including a small sample size, and a lack of controls – including one for SSRIs.

But they say their next trial will try to address those shortcomings, as well as looking further into how this mysterious compound alleviates depression – while seemingly forcing people to confront their emotions, whether good or bad.

“I believe that psychedelics hold a potential to cure deep psychological wounds,” Roseman told PsyPost.

“[A]nd I believe that by investigating their neuropsychopharmacological mechanism, we can learn to understand this potential.”

Antidepressants Associated With Hyponatremia

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TAKE-HOME MESSAGE

  • A cohort of 638,352 people was evaluated from 1998 through 2012 to investigate the relationship between the use of antidepressants and the risk of hyponatremia. The incidence rate ratio for the association with hyponatremia after initiation of treatment was highest for citalopram (7.80) and lowest for mianserin (0.90). The incidence rate ratio for other agents were: clomipramine 4.93, duloxetine 2.05, venlafaxine 2.90, and mirtazapine 2.95.
  • Apart from mianserin, all antidepressant agents are associated with an increased risk of hyponatremia, with the highest risk seen with citalopram.

Antidepressants are associated with the development of several metabolic abnormalities. This study reports an association between antidepressants and the development of hyponatremia. With the wide use of antidepressants such as SSRIs and SNRIs, it is important to remember to monitor patients periodically on such medications for electrolyte disturbances, glucose intolerance, and lipid abnormalities. Elderly patients are especially at risk and may warrant closer monitoring as the use of other chronic medications and decreased renal clearance may further increase the risk for hyponatremia.

OBJECTIVE

To examine the association between classes of antidepressants and hyponatremia, and between specific antidepressants and hyponatremia.

DESIGN

Retrospective register-based cohort study using nationwide registers from 1998 to 2012.

SETTING

The North Denmark Region.

PARTICIPANTS

In total, 638 352 individuals were included.

PRIMARY AND SECONDARY OUTCOME MEASURES

Plasma sodium was obtained from the LABKA database. The primary outcome was hyponatremia defined as plasma sodium (p-sodium) below 135 mmol/L and secondary outcome was severe hyponatremia defined as p-sodium below 130 mmol/L. The association between use of specific antidepressants and hyponatremia was analysed using multivariable Poisson regression models.

RESULTS

An event of hyponatremia occurred in 72 509 individuals and 11.36% (n=6476) of these events happened during treatment with antidepressants. Incidence rate ratios and CIs for the association with hyponatremia in the first p-sodium measured after initiation of treatment were for citalopram 7.8 (CI 7.42 to 8.20); clomipramine 4.93 (CI 2.72 to 8.94); duloxetine 2.05 (CI 1.44 to 292); venlafaxine 2.90 (CI 2.43 to 3.46); mirtazapine 2.95 (CI 2.71 to 3.21); and mianserin 0.90 (CI 0.71 to 1.14).

CONCLUSIONS

All antidepressants except mianserin are associated with hyponatremia. The association is strongest with citalopram and lowest with duloxetine, venlafaxine and mirtazapine.

SSRIs make patients lose feelings of love

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Patients who regularly take serotonin reuptake inhibitors, or SSRIs, can lose feelings of love and attachment, according to the results of a new study.

Researchers found that men’s feelings of love in particular tend to be more affected than women’s when taking SSRIs, drugs which work mainly through the serotonin system. By contrast, drugs that are called tricyclic antidepressants, which have less of an effect on the serotonin system, seems to affect women’s feelings of love and attachment more than men’s, the scientists found.

“The good news is that there are a variety of agents for treating depression, ” said study author Dr. Hagop S. Akiskal, a distinguished professor of psychiatry at the University of California, San Diego. Except that none of them are really very good, but more on that in a moment.

In the new study, researchers compared the effects of SSRIs and tricyclic antidepressants on the love lives of 192 study participants who had been diagnosed with depression — 123 women and 69 men — with a mean age of 41. The study also included 13 people who were homosexual. All study participants told researchers that they had been in loving relationships for between seven months and 26 years.

“Indeed, our subjects were those who could be properly considered smitten by love,” Akiskal told Live Science.

Fewer feelings of love, emotional attachment

According to an abstract of the study:

The results showed that SSRIs had a significant impact on the feelings of love and attachment towards the partner especially in men, while women taking TCAs complained of more sexual side effects than men. These data were supported also by the detection of a significant interaction between drug and sex on the “Love” and “Sex” domains.

The present findings, while demonstrating a dimorphic effect of antidepressants on some component of loving relationships, need to be deepened in future studies.

Study participants filled out a questionnaire that measured their feelings of love, attachment and sexual attraction to their partners for the duration of their relationship. As part of the questionnaire, participants addressed HOW their feelings had changed after they began taking antidepressants, in comparison to before they began taking them.

When researchers measured the results from all study participants, they found those taking SSRIs were more likely to say that they were less at ease with sharing the thoughts and feelings of their partners, and were less hopeful that their love for their mate would last forever, compared with those taking tricyclics.

In addition, researchers found that the men in the study who were taking SSRIs reported that they were not as likely to ask their partners for advice or help, or to take care of their partners, compared with women who had been taking SSRIs.

By contrast, women who had been taking the tricyclics reported being more likely to complain about disturbances in their sex life than men who had been taking similar medications.

The researchers said they were motivated to conduct the study after having carried out previous research with people in romantic relationships, and those who were suffering from obsessive compulsive disorder found that “serotonin function was more deviant in a state of romantic love, than in obsessive compulsive disorder,” said Akiskal.

He added that it is important that patients who are suffering depression communicate very openly with care providers about how they are feeling.

“Certainly, a physician should always inquire whether there is any impairment in the love life during depressive illness, because the loss of sexual desire and sexual feelings are common manifestations of depressive illness itself,” he said.

Taking any antidepressant is risky and dangerous

The study was published in the September issue of the Journal of Affective Disorders.

As for antidepressants in general, their use has increased dramatically worldwide over the past year, with many people using them just to get by in daily life, the Seattle Post-Intelligencer reports:

Antidepressants and painkillers rank among the most commonly prescribed drugs in the United States today. In 2011, the Centers for Disease Control and Prevention (CDC) National Center for Health Statistics published a report that identified about 11 percent of the American public as antidepressant users, a 400 percent increase since the 1980s when previous surveys were taken.

As regular readers of Natural News know, however, there are many more inherently dangerous risks to taking antidepressants, and especially SSRIs, than any potential benefit.

Sources:

http://www.foxnews.com

http://www.jad-journal.com

http://www.livescience.com

http://blog.seattlepi.com

http://science.naturalnews.com