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Anxiety Medications That Cause Weight Gain
Many anxiety and antidepressant medications, such as paroxetine, escitalopram, and duloxetine, may cause weight gain. But weight gain isn't guaranteed and shouldn't stop you from seeking treatment with medication.
Finding the right treatment if you have anxiety, which often includes medication, may be challenging.
While anxiety medications are very effective in managing symptoms of anxiety, some may lead to weight gain.
If you're unsure about anxiety medicationThe benefits of anxiety medications often outweigh the risks. Talk with a healthcare professional to find the most effective anxiety treatment for you, with the fewest side effects.
Anxiety may cause a loss of appetite if left untreated. Once you start anxiety medications, your appetite may return, or your metabolism may decrease. This may cause you to eat more, and you might see an increase in weight.
However, not everyone taking anxiety medications will gain weight. The weight you may gain may be modest and temporary with proper management strategies.
Anxiety medications aren't the only medications that may cause weight gain. Those also used to treat depression, which sometimes overlaps with anxiety treatment, and other mood stabilizers may lead to weight gain.
Anxiety and antidepressant medications
A review of 27 studies from 2008 to 2019 found that people gained 5% of their weight on average while taking antidepressants.
According to a 2018 research review carried out in Canada, antidepressants and anxiety medications that may lead to weight gain include:
In particular, paroxetine, escitalopram, and duloxetine are antidepressants most likely to potentially cause weight gain compared to other antidepressants, according to a 2-year 2024 observational cohort study.
More research, however, is needed as some medications were found to cause both weight gain and weight loss:
Though weight gain is commonly listed as a side effect of many anxiety and antidepressant medications, your response may vary. If you do gain weight, the amount may be modest.
Talk with your prescriber before you stop taking your anxiety medication. They may have you taper off or switch medications if you're not seeing improvements in symptoms.
Antipsychotic medications and mood stabilizers
Besides anxiety and antidepressant medications, other medications used to treat mental conditions may contribute to weight gain, including antipsychotics and other mood stabilizers. This may include:
A study of 395 records from psychiatry outpatient clinics between May 2016 and August 2021 found that those on antipsychotics alone experienced weight gain. Those who also took metformin, a diabetes treatment, were less likely to see weight gain.
Taking an anxiety medication doesn't guarantee weight gain. But you can make lifestyle changes to prevent or limit weight gain and maintain a moderate weight while on anxiety medication.
You can try (or keep up, if you already do these):
Talk with a healthcare professional if you're concerned about weight gain from anxiety medications.
A registered dietitian may also help you develop an eating plan that works with your anxiety treatment and other health conditions you may be managing.
Many psychiatric medications, including those used to treat anxiety, list weight gain as a possible side effect. But this doesn't mean you will experience weight gain, and if you do, the amount may be modest.
Speak with a healthcare professional if you're concerned about weight gain from anxiety medications. You can also try monitoring your weight during treatment, keeping active, and eating mindfully.
Antidepressants May Act In Gut To Reduce Depression And Anxiety
Most of us have experienced the effects of moods and emotions on our gastrointestinal tract, from "butterflies" in the stomach caused by nervousness to a loss of appetite when we're feeling blue.
A new study in animals suggests that targeting antidepressant medications to cells in the gut could not only be an effective treatment of mood disorders like depression and anxiety but may also cause fewer cognitive, gastrointestinal, and behavioral side effects for patients and their children than current treatments.
"Antidepressants like Prozac and Zoloft that raise serotonin levels are important first-line treatments and help many patients but can sometimes cause side effects that patients can't tolerate. Our study suggests that restricting the drugs to interact only with intestinal cells could avoid these issues," says Mark Ansorge, associate professor of clinical neurobiology at Columbia University Vagelos College of Physicians and Surgeons, who co-led the study with Kara Margolis, Director of the NYU Pain Research Center and an associate professor of molecular pathobiology in the NYU College of Dentistry.
For pregnant mothers, antidepressants that raise serotonin (called selective serotonin reuptake inhibitors, or SSRIs) present a unique problem, because the drugs cross the placenta and have been associated with mood, cognitive, and gastrointestinal problems later in childhood.
"But not treating a pregnant person's depression also comes with risks to their children," Ansorge says. "An SSRI that selectively raises serotonin in the intestine could be a better alternative."
How do SSRI antidepressants work?
For more than 30 years, SSRIs have been the first-line pharmacological treatments for anxiety and depression. They are also commonly prescribed to treat gastrointestinal issues that co-occur with these mood disorders.
SSRIs boost serotonin signaling, and the drug's effects on mood are thought to stem from increased serotonin signaling in the brain, where serotonin helps to relay messages.
Serotonin is also produced outside the brain, largely in cells that line the intestines. "In fact, 90% of our bodies' serotonin is in the gut," says Margolis, who is also an associate professor of pediatrics and cell biology at NYU Grossman School of Medicine. SSRIs therefore increase serotonin signaling not just in the brain but also in the gut, raising the possibility that increasing serotonin signaling in the gut may impact gut-brain communication and ultimately mood.
The researchers tested this possibility in mice using a combination of genetic engineering, surgery, and pharmaceuticals.
Increasing intestinal serotonin reduces anxiety, depressive behaviors in mice
To determine if targeting serotonin in the gut can affect mood, the researchers engineered mice to amplify serotonin signaling in the gut -- which mimicked an SSRI delivered selectively to the gut. They found that animals with increased serotonin signaling in the gut displayed fewer anxiety and depressive-like behaviors than their unaffected littermates.
"These results suggest that SSRIs produce therapeutic effects by working directly in the gut," Ansorge says.
The animals also displayed none of the cognitive or gastrointestinal side effects commonly seen in patients taking SSRIs or in mice with increased serotonin signaling throughout their entire bodies.
"Based on what we know about interactions between the brain and gut, we expected to see some effect. But to see enhanced serotonin signaling in the gut epithelium produce such robust antidepressant and anxiety-relieving effects without noticeable side effects was surprising even to us," Ansorge says.
"There may be an advantage to targeting antidepressants selectively to the gut epithelium," adds Margolis. "Systemic treatment may not be necessary for eliciting the drugs' benefits."
The researchers also found that the vagus nerve was necessary for the gut's antidepressant and anxiety-relieving effects. The vagus nerve has long been known for its critical role in brain/gut communication, but mostly for top-down communication from the brain to the gut. Here the researchers found the other direction to be critical, with vagus nerve signaling from the gut to the brain.
A better antidepressant option during pregnancy?
SSRI treatment poses challenges in pregnancy, because some studies have found that exposure in utero may negatively affect the development of mood, behavior, and cognition later in childhood. Ansorge's previous research in animals has found similar results, identifying behavioral changes in offspring exposed only briefly to SSRIs during development.
The new study adds to the evidence that in utero exposure to serotonin-targeting antidepressants has negative effects on children. The researchers looked at more than 400 mothers and babies and found that children exposed to such antidepressants were 3 times more likely to develop constipation in their first year of life.
Ansorge and Margolis caution that pregnant people currently taking SSRIs should not discontinue their treatment based on these and other findings. "Maternal depression and anxiety can have many unwanted effects on fetal and child development and must thus be treated and monitored adequately to the benefit of both mother and child," says Ansorge.
The researchers are now working to develop a selective SSRI that targets the gut, which could be a better option for treating depression and anxiety especially in pregnant women.
"Our findings indicate that we may be able to treat a mother's depression or anxiety effectively without exposing the child," Ansorge says, "and we are working on drug delivery technology that will hopefully help us achieve that."
Ketamine Treatment Shows Promise For Treatment-Resistant Depression
In past trials, ketamine intravenous treatment has shown promise, with 64% of depression patients in trials experiencing major symptom relief.
Ketamine intravenous treatment (KIT) may be more effective than traditional medication management for those with treatment resistant depression (TRD), helping reduce symptoms and improve responses to treatment, according to new a study published in the 2025 issue of Psychiatry Research.
Nearly 3 million Americans have TRD, a condition where two or more antidepressants don't improve your depression symptoms. TRD often leads to disability and higher suicide risk —30% of TRD patients have attempted suicide compared to 15% with regular depression and 1.8% of the general population, according to the study.
In past trials, KIT treatment has shown promise, with 64% of patients in trials experiencing major symptom relief. However, many of these previous trials have struggled to find consistent results due to small sample sizes and varied methods across clinics.
KIT is commonly used in community clinics, but there's little research on its effects for complex TRD patients in controlled, standardized settings.
To explore this area in depth, researchers aimed to compare depression symptom changes in patients receiving standardized KIT versus those using traditional medication management in a large healthcare system.
Using electronic health records, depression symptoms were tracked in 143 adults observing 9-item Patient Health Questionnaire (PHQ-9) scores over six weeks.
Participants 18 and older were Kaiser Permanente members receiving KIT or medication management from 2018 to 2022. Patients with schizophrenia, neurocognitive impairment, pregnancy, incomplete data or insurance loss were excluded. Researchers expected KIT to show better results but noted that complex psychiatric issues might impact outcomes.
It was found that patients receiving KIT for TRD were 72% more likely to experience a significant improvement in symptoms (a 50% or greater reduction in PHQ-9 scores) compared to those receiving standard medication management.
On average, the KIT group's depression scores dropped by 2.25 points more than the medication management group.
However, rates of full remission were low (8% for KIT, 5% for medication management) and not statistically different between groups.
Even though there were some improvements, the remission rates for KIT were lower than in previous studies. This could be due to participants having more severe depression, symptoms were measured after treatment and the treatment was given in a controlled setting.
KIT's effects only last about 20 days, and the lack of follow-up treatments could have also affected the results.
Participants with higher depression levels, anxiety and personality disorders had worse outcomes.
However, there was no clear link between BMI and how well the treatment worked, which is similar other studies.
Because this study's findings align with prior research, it reinforces the efficacy of KIT in addressing TRD.
In addition, the study used a standardized treatment protocol across five sites, ensuring consistency in the data. The study also highlighted the challenges of treating these patients in real-life situations.
Researchers suggest that doctors treating patients with severe depression, anxiety or personality disorders should consider combining treatments and setting realistic expectations for improvement. Since BMI didn't affect how well patients responded to KIT, it was also recommended doctors shouldn't prioritize obese patients for this therapy.
Future research should include larger studies with higher KIT doses, longer follow-ups and more precise tools for measuring results to better understand KIT's effects and potential benefits, researchers add.
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