Tag: depression

Long Hours Worsen Depression Risk in New Doctors

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As work hours increase, new doctors are at greater risk of depression, according to a study in the New England Journal of Medicine. Working 90 or more hours a week was associated with changes in depression symptom scores three times larger than the change in depression symptoms among those working 40 to 45 hours a week.

Additionally, compared to those working normal hours, those working more hours had greater odds of scores equating to moderate to severe depression.

By means of advanced statistical methods, the researchers emulated a randomised clinical trial using data on more than 17 000 first-year medical residents, accounting for many other factors in the doctors’ personal and professional lives. Less than 5% met the criteria for moderate to severe depression.

They found a “dose response” effect between hours worked and depression symptoms, with an average symptom increase of 1.8 points on a standard scale for those working 40 to 45 hours, ranging up to 5.2 points for those working more than 90 hours. They conclude that, among all the stressors affecting physicians, working a large number of hours is a major contributor to depression.

The data come from the Intern Health Study, based at the Michigan Neuroscience Institute and the Eisenberg Family Depression Center. Each year, the study recruits new medical school graduates to take part in a year of tracking of their depressive symptoms, work hours, sleep and more while they complete the first year of residency, also called the intern year.

The impact of high numbers of work hours

Though the interns in the study reported a wide range of previous-week work hours, the most common work hour levels were between 65 to 80 hours per week.

The authors say their findings point to a clear need to further reduce the number of hours residents work each week on average.

“This analysis suggests strongly that reducing the average number of work hours would make a difference in the degree to which interns’ depressive symptoms increase over time, and reduce the number who develop diagnosable depression,” said Amy Bohnert, PhD, the study’s senior author and a professor at the U-M Medical School. “The key thing is to have people work fewer hours; you can more effectively deal with the stresses or frustrations of your job when you have more time to recover.”

Yu Fang, MSE, the study’s lead author and a research specialist at the Michigan Neuroscience Institute, notes that the number of hours is important, but so are the training opportunities that come from time spent in hospitals and clinics. “It is important to use the time spent at work for supervised learning opportunities, and not low-value clinical service tasks,” she says.

Source: Michigan Medicine – University of Michigan

Biological Changes in Mothers Experiencing Postpartum Depression

Woman with depression
Photo by Sydney Sims on Unsplash

Newly discovered biological changes in mothers who suffer postpartum depression may help explain the condition, yield long-sought treatments and let doctors identify those at risk even before their babies are born. The findings were published in Molecular Psychiatry.

Postpartum depression strikes up to 20% of new mothers, and roughly 20% of maternal deaths after childbirth are from suicide. Postpartum depression can cause anxiety and irritability, feelings of self-doubt and difficulty bonding with the baby, cognitive impairment, and interfering with sleeping and eating. For the child, maternal postpartum depression can lead to cognitive, emotional and social development problems.

Risk factors for postpartum depression are thought to include the mother’s age at childbirth, diabetes and prior history of mental health issues. But the new discovery suggests a previously unknown biological contributor: an impairment of the body’s ability to clean up old genetic material and other cellular debris.

“The finding that cells aren’t cleaning out old proteins and cellular debris, called autophagy, occurs before women develop depression symptoms, indicating that it could be part of the disease process,” explained Jennifer L. Payne, MD, director of the Reproductive Psychiatry Research Program at the University of Virginia School of Medicine. “There are several medications that promote autophagy in cells, so this finding might open the door to new treatments and to identification of women at risk of postpartum depression before they become ill.”

Understanding Postpartum Depression

Dr Payne and colleagues wanted to determine if ‘extracellular RNA communication’, a newly discovered form of communication among cells, might contribute to postpartum depression. Extracellular RNA communication is heightened during pregnancy and is critical in embryo implantation and in the body’s inflammatory response afterward.

The researchers analysed blood plasma samples from 14 research participants with and without postpartum depression, collected during and after their pregnancies. The researchers found that extracellular RNA communication in immune cells was altered extensively in women who suffered postpartum depression. Further, they determined that this “large and consistent” change significantly limited the women’s bodies’ ability to perform important cellular cleanup – suggesting a potential biological cause for their depression.

“Deficits in autophagy are thought to cause toxicity that may lead to the changes in the brain and body associated with depression,” Dr Payne said. “We have never fully understood the biological basis for postpartum depression, and this finding gets us closer to an understanding.”

Source: University of Virginia Health System

Depression Risk Increases with Greater Social Media Use

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A recent study published in the Journal of Affective Disorders Reports has found that young adults who use more social media are significantly more likely to develop depression within six months, regardless of personality type. 

“Previous research has linked the development of depression with numerous factors,” the authors noted. “However, the literature has been lacking in studies that focus on how various personality characteristics may interact with social media use and depression. This new study addressed these important research questions, finding strong and linear associations of depression across all personality traits.”

People with high agreeableness were found to be 49% less likely to become depressed than people with low agreeableness. Additionally, those with high neuroticism were twice as likely to develop depression than those with low neuroticism when using more than 300 minutes of social media per day. More importantly, for each personality trait, social media use was strongly associated with the development of depression.

A 2018 sample of 18–30 year old US adults was analysed with the Patient Health Questionnaire to measure depression. Social media was measured by asking participants how much daily time was spent using popular social media platforms, and personality was measured using the Big Five Inventory, which assessed openness, conscientiousness, extraversion, agreeableness and neuroticism. 

The authors suggest that problematic social comparison can enhance negative feelings of oneself and others, which could explain how risk of depression increases with increased social media use. Engaging primarily in negative content can also enhance these feelings. And lastly, engaging in more social media reduces opportunities for in-person interactions and activities outside of the home.

Depression has been noted as the leading cause of disability and mortality worldwide. This makes these findings even more pronounced for creating health interventions and prevention efforts.

“Findings from this study are important during a time of technology expansion and integration,” said author Renae Merrill said, a doctoral student when writing the paper. “Connecting to people virtually may increase the risk of miscommunication or misperception that leads to relationship difficulties and potential risk for developing mental health problems.” 

“People have innate emotional needs for social connection and understanding,” Merrill added. “For example, social media experiences can be improved by becoming more aware of our emotions and our connection with others in various life circumstances. This awareness helps improve relationship quality by simply reaching shared meaning and understanding through more effective communication and concern for others and ourselves. Despite our differences, we have the ability to create a culture of empathy and kindness.” 

Source: University of Arkansas

Genes and Environment Bridge Depression and Endocrine-metabolic Disorders

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While endocrine-metabolic disorders and depression are known to co-occur, genetic and environmental factors are known to underlie both. In a study examining the link, published in the American Journal of Psychiatry, analysis revealed the balance of genetic and environmental influences underlying the co-occurrence of depression for a range of endocrine-metabolic disorders.

It is known that there is elevated co-occurrence between endocrine-metabolic disorders and depression, but the relationship between them is still not well understood.

Familial aggregation

The authors identified 2.2 million individuals born in Sweden between 1973 and 1996, as well as their full and half siblings, and followed them up to age 40. A number of medical conditions were studied; depression and various endocrine-metabolic disorders, including three autoimmune diseases (autoimmune hypothyroidism, Graves’ disease, and type 1 diabetes) and three non-autoimmune disorders (type 2 diabetes, obesity, and polycystic ovary syndrome).

Individuals with endocrine-metabolic disorders had 1.4 to 3.5 times the risk of depression compared to people without these diagnoses. Full and half siblings of these individuals also showed some elevated risk for depression, suggesting that genetic and/or environmental risk factors shared between family members play a role in the co-occurrence of these mental and physical disorders.

Genetic and environmental contributions

By comparing pairs of full sibling (who share about half of their genes) to pairs of half siblings (who share about a quarter of their genes), it was possible to calculate the relative contribution of genetic and environmental factors to the co-occurrence of depression and various endocrine-metabolic disorders. 

The results were a mix of these possibilities; the overlap between depression and non-autoimmune conditions was mainly explained by shared genetic influences, while environmental factors were predominantly involved in the association between depression and autoimmune disorders, particularly type 1 diabetes.

This indicates that the link between depression and different endocrine-metabolic disorders may be driven by different mechanisms. For example, shared biological mechanisms, such as immuno-inflammatory and metabolic dysregulations, may underlie the co-occurrence of depression and type 2 diabetes, obesity, and polycystic ovarian syndrome. In contrast, the absence of shared genetics in the association between type 1 diabetes and depression may reflect the existence of environmental factors influencing the risk of both conditions and/or a direct link between these conditions through mediating factors – eg, biological and psychosocial mechanisms connected to type 1 diabetes, including inflammation, cerebral damage, as well as stress of this lifelong condition that is often diagnosed early in life and that requires a complex management regime for both patients and their families.

“Our results underscore that clinicians should be aware of increased risks of depression in individuals with endocrine-metabolic disorders, and vice versa, and be vigilant for shared symptoms. This study also provides a useful foundation for future research aimed at identifying and targeting the biological mechanisms and modifiable risk factors underlying the co-presentation of endocrine-metabolic disorders and depression”, said Marica Leone, first author for the study.

Source: Karolinska Institutet

Unlocking the Complex Neurological Puzzle of Depression

Source: Pixabay

By studying the brains of fruit flies, which share similar mechanisms to human ones, scientists at Johannes Gutenberg University Mainz (JGU) are attempting to gain a better understanding of depression-like states and thus improve means of treating them. Their findings include the effect of Asian traditional medicine and its mode of preparation, and the effect of timing, such as getting a reward in the evening as opposed to other times of the day. The results were published recently in the journal Current Biology.

One aspect of their research “We have been looking at the effects of natural substances used in traditional Asian medicine, such as in Ayurveda, in our Drosophila fly model,” explained Professor Roland Strauss at JGU. “Some of these could have an anti-depressive potential or prophylactically strengthen resilience to chronic stress, so that a depression-like state might not even develop.”

The researchers intend to demonstrate efficacy, find optimal formulations, and isolate the active substances from the plant, which could lead to new drugs.

“In the Drosophila model we can pinpoint exactly where these substances are active because we are able to analyse the entire signalling chain,” Strauss pointed out. “Furthermore, every stage in the signalling pathway can also be proven.” The researchers subject the flies to a mild form of recurrent stress, such as irregular phases of vibration of the substrate. This treatment results in the development of a depression-like state (DLS) in the flies, ie, they move more slowly, do not stop to examine unexpectedly encountered sugar, and, unlike their more relaxed counterparts, are less willing to climb wide gaps. Whether or not the natural substances have an effect depends on the preparation of each natural substance, eg, whether it has been extracted with water or alcohol.

The research team has also discovered that if they reward the flies for 30 minutes on the evening of a stressful day, by offering them food with a higher sugar content than usual, or by activating the reward signalling pathway, this can prevent DLS developing. Flies have sugar receptors on their tarsi (the lower part of their legs) and their proboscis, while the end of the signalling pathway at which serotonin is released onto the mushroom body (equivalent to the human hippocampus) have also been located.

The researchers’ investigations showed that the pathway was considerably more complex than anticipated. Three different neurotransmitter systems have to be activated until the serotonin deficiency at the mushroom body, which is present in flies in a DLS, is compensated for by reward. One of these three systems is the dopaminergic system, which also signals reward in humans. Humans might obtain a reward through something other than sugar.

Boosting resilience by preventing depression

In addition, the researchers decided to look for resilience factors in the fly genome. The team intends to find out whether and how the genomes of flies that are able to better cope with stress differ from those that develop a DLS in response to exposure to recurrent mild stress. The hope is that in the future it will be possible to diagnose genetic susceptibility to depression in humans – and then treat this with the natural substances that are also being investigated during the project.

Source: Johannes Gutenberg Universitaet Mainz

Half of Moms of Autistic Children Have High Depressive Symptoms

Woman with depression
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About 50% of all mothers of children with autism spectrum disorder (ASD) had raised levels of depressive symptoms over 18 months, while rates were much lower (6% to 13.6%) for mothers with neurotypical children in the same period, according to a new study in Family Process.

Additionally, thought past studies suggest that having a parent with depression increases the child’s risk of mental health and behaviour problems, this study found something different.

“We found mothers’ higher symptoms of depression did NOT predict increases in children’s behaviour problems over time, including among families with a child with autism who experience a lot of stress,” said first author and UCSF Assistant Professor Danielle Roubinov. “That was surprising and good news.”

“Being the parent of a child with special needs is inherently challenging every day,” noted senior author UCSF Professor Elissa Epel. “It is a prototypical example of chronic stress, which is why we have been focusing on caregiving moms in our studies that examine effects of stress on health.”

“We already know from this sample that mothers with more depression tend to have signs of faster biological aging, such as lower levels of the anti-aging hormone klotho and older immune cells, on average,” added Prof Epel. “Here, we wanted to understand the impact of their depression on their child, and vice versa.”

A One-Way Street

Child behaviour problems predicted higher levels of maternal depression down the road, regardless of ASD status. The inverse effect was not seen, ie prior maternal depression didn’t predict later child behaviour problems.

Asst Prof Roubinov said that mothers of children with ASD need not feel guilty over their depressions impact on their children’s behaviours. “We hope these findings will reassure mothers that it’s both common to struggle with some depression in this high-stress situation of chronic caregiving, and that their depression likely isn’t making their child’s behavioural issues worse.”

Self-blame and guilt among parents of ASD children is common and predicts worsening depression and lower life satisfaction over time, the team’s past research shows.

In the current study, the researchers repeatedly measured maternal depression and children’s behaviour problems in 86 mother-child dyads across 18 months. Half of the mothers had children with ASD and half had neurotypical children. The children were aged 2–17 years old, with 75% being primary school age or younger.

Maternal depression was measured using the Inventory of Depressive Symptoms, a self-report scale completed by mothers. Child behaviour was measured through maternal report on the Child’s Challenging Behavior Scale, which focuses on externalising behaviours such as tantrums, aggression and defiance.

Few studies on maternal depression, child behaviour in ASD context

Bidirectional associations between maternal depression and child behaviour problems have been reported in prior research but few studies have examined these relationships in families with autism.

Families with autism tend to experience more marital conflict, lower relationship satisfaction, and many other challenges, said Ass Prof Roubinov, noting that a “stressful family environment may spill over onto family members” and changing their interactions. “We wanted to see whether the link between maternal and child mental health was different in the context of a high-stress family system, such as when a child has autism.”

Although the study acknowledged that families with a child with ASD experience high levels of stress, the authors were cautious to note that stress is not their only defining characteristic.

“Many mothers of children with autism also report high levels of emotional closeness and positive interactions with their children,” Asst Prof Roubinov said. “These are important experiences that supportive programs can build upon.”

The researchers offered mindfulness classes after the study to the participants to help manage parenting stress, and this improved their mental health.

It is important to experience and notice positive emotions and joy, despite having a more challenging life situation, said Prof Epel.

“Given the effects of chronic stress on health and mood, caregiving parents need extraordinary emotional support in addition to the special services for their child,” she said. “It’s as vital to provide support for parents’ mental health as it is for children’s mental health.”

Physicians should be on the lookout for parental distress and ready to offer resources for parents, especially for parents of special needs children, she said. The researchers said future studies should also look at associations between maternal depression and children’s internalising symptoms (eg, withdrawal, anxiety, emotional reactivity).

Source: University of California – San Francisco

No Evidence that Serotonin Imbalance Causes Depression

Depression, young man
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Decades of research has provided no clear evidence that serotonin levels or serotonin activity are responsible for depression, according to a major review of existing literature.

Published in Molecular Psychiatry, this new umbrella review is an overview of existing meta-analyses and systematic reviews. It suggests that depression is not likely to be caused by a chemical imbalance. It also calls into question what antidepressants do: most antidepressants are selective serotonin reuptake inhibitors (SSRIs), whose mechanism of action was supposedly to correct abnormally low serotonin levels. But there is no other accepted pharmacological mechanism by which antidepressants affect the symptoms of depression.

Lead author Professor Joanna Moncrieff, at University College London said: “It is always difficult to prove a negative, but I think we can safely say that after a vast amount of research conducted over several decades, there is no convincing evidence that depression is caused by serotonin abnormalities, particularly by lower levels or reduced activity of serotonin.

“The popularity of the ‘chemical imbalance’ theory of depression has coincided with a huge increase in the use of antidepressants. Prescriptions for antidepressants have risen dramatically since the 1990s, with one in six adults in England and 2% of teenagers now being prescribed an antidepressant in a given year.

“Many people take antidepressants because they have been led to believe their depression has a biochemical cause, but this new research suggests this belief is not grounded in evidence.”

The umbrella review aimed to capture all relevant studies, encompassing tens of thousands of participants, that have been published in the most important fields of research on serotonin and depression.

Research that compared levels of serotonin and its breakdown products in the blood or brain fluids found no difference between participants diagnosed with depression and healthy controls.

Research on serotonin receptors and the serotonin transporter, the protein targeted by most antidepressants, found weak and inconsistent evidence suggestive of higher levels of serotonin activity in people with depression. However, the researchers say the findings are likely explained by the use of antidepressants among people diagnosed with depression, since such effects were not reliably ruled out.

Some studies artificially lowered serotonin levels were by depriving participant’s diets of the necessary amino acid. These studies have been cited as demonstrating that a serotonin deficiency is linked to depression. A meta-analysis conducted in 2007 and a sample of recent studies found that lowering serotonin in this way did not produce depression in hundreds of healthy volunteers, however. There was very weak evidence in a small subgroup of people with a family history of depression, but this only involved 75 participants, and more recent evidence was inconclusive.

Very large studies involving tens of thousands of patients looked at gene variation, including the gene for the serotonin transporter, and found no difference between people with depression and healthy controls. These studies also examined stressful life events, and found these to strongly increase people’s risk of becoming depressed. A famous early study found a relationship between stressful events, the type of serotonin transporter gene a person had and the chance of depression. But larger, more comprehensive studies suggest this was a false finding.

These findings together led the authors to conclude that there is “no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations.”

The researchers say their findings are important as studies show that as many as 85–90% of the public believes that depression is caused by low serotonin or a chemical imbalance. A growing number of scientists and professional bodies are recognising the chemical imbalance framing as an over-simplification. Evidence also suggests that believing that low mood is caused by a chemical imbalance leads to pessimism about recovery, and the possibility of managing moods without medical help. This is important because most people will at some point in their lives meet criteria for anxiety or depression.

A large meta-analysis provided evidence that people who used antidepressants actually had lower levels of serotonin in their blood. The researchers concluded that some evidence was consistent with the possibility that long-term antidepressant use reduces serotonin concentrations. The researchers say this may imply that the increase in serotonin that some antidepressants produce in the short term could lead to compensatory changes in the brain that produce the opposite effect in the long term.

Though antidepressants’ efficacies was not examined, the authors encourage looking into treatments such psychotherapy, alongside other practices such as exercise or mindfulness, or addressing underlying contributors such as poverty, stress and loneliness.

Professor Moncrieff said: “Our view is that patients should not be told that depression is caused by low serotonin or by a chemical imbalance, and they should not be led to believe that antidepressants work by targeting these unproven abnormalities. We do not understand what antidepressants are doing to the brain exactly, and giving people this sort of misinformation prevents them from making an informed decision about whether to take antidepressants or not.”

Co-author Dr Mark Horowitz said: “I had been taught that depression was caused by low serotonin in my psychiatry training and had even taught this to students in my own lectures. Being involved in this research was eye-opening and feels like everything I thought I knew has been flipped upside down.

“One interesting aspect in the studies we examined was how strong an effect adverse life events played in depression, suggesting low mood is a response to people’s lives and cannot be boiled down to a simple chemical equation.”

Professor Moncrieff added: “Thousands of people suffer from side effects of antidepressants, including the severe withdrawal effects that can occur when people try to stop them, yet prescription rates continue to rise. We believe this situation has been driven partly by the false belief that depression is due to a chemical imbalance. It is high time to inform the public that this belief is not grounded in science.”  

Source: EurekAlert!

High Doses of Vitamin B6 Slightly Reduce Anxiety and Depression

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University of Reading scientists have shown that taking high doses of Vitamin B6 reduces feelings of anxiety and depression to a small degree. Study participants reported feeling less anxious and depressed after taking the supplements every day for a month. 

The study, published in Human Psychopharmacology: Clinical and Experimental, demonstrates that certain supplements thought to modify levels of activity in the brain could be useful for preventing or treating mood disorders. 

The study’s lead author, Dr David Field, explained: “The functioning of the brain relies on a delicate balance between the excitatory neurons that carry information around and inhibitory ones, which prevent runaway activity. Recent theories have connected mood disorders and some other neuropsychiatric conditions with a disturbance of this balance, often in the direction of raised levels of brain activity. Vitamin B6 helps the body produce a specific chemical messenger that inhibits impulses in the brain, and our study links this calming effect with reduced anxiety among the participants.” 

While previous studies have produced evidence that multivitamins or Marmite can reduce stress levels, few studies have been carried out into which particular vitamins contained within them drive this effect. The new study focused on the potential role of Vitamins B6, which is known to increase the body’s production of GABA (Gamma-Aminobutyric Acid), the primary inhibitory neurotransmitter. 

In the current trial, more than 300 participants were randomised to either Vitamin B6 or B12 supplements far above the recommended daily intake (about 50 times higher) or placebo, and took one a day with food for a month. Vitamin B12 had little effect compared to placebo, but Vitamin B6 was found to have a significant effect. Raised levels of GABA among participants who had taken Vitamin B6 supplements were confirmed by visual tests carried out at the end of the trial, supporting the hypothesis that B6 was responsible for the reduction in anxiety. Subtle but harmless changes in visual performance were detected, consistent with controlled levels of brain activity. 

Dr Field notes that, while many foods contain Vitamin B6, “the high doses used in this trial suggest that supplements would be necessary to have a positive effect on mood. It is important to acknowledge that this research is at an early stage and the effect of Vitamin B6 on anxiety in our study was quite small compared to what you would expect from medication. However, nutrition-based interventions produce far fewer unpleasant side effects than drugs, and so in the future people might prefer them as an intervention. 

“To make this a realistic choice, further research is needed to identify other nutrition-based interventions that benefit mental wellbeing, allowing different dietary interventions to be combined in future to provide greater results. One potential option would be to combine Vitamin B6 supplements with talking therapies such as Cognitive Behavioural Therapy to boost their effect.”

Source: University of Reading

Why Depression Treatments May Have Different Efficacy for Women

Woman with depression
Photo by Sydney Sims on Unsplash

It is not clear why women experience higher rates of depression than men, complicating treatments that are already prone to failure. Research exploring the reasons behind this found a difference in a part of the brain associated with motivation, social interactions and reward. The researchers’ findings were published in the journal Biological Psychiatry.

The study set out to understand how a specific part of the brain, the nucleus accumbens, is affected during depression. The nucleus accumbens is important for motivation, response to rewarding experiences and social interactions – all of which are affected by depression.

Brain drawing
The nucleus accumbens (represented in blue) is a part of the brain that controls motivation. Researchers from UC Davis compared samples of the nucleus accumbens in mice and humans to find clues to how this part of the brain is affected by stress and depression in males and females.

Previous analyses within the nucleus accumbens showed that different genes were turned on or off in women, but not in men diagnosed with depression. These changes could have caused symptoms of depression, or alternatively, the experience of being depressed could have changed the brain. To differentiate between these possibilities, the researchers studied mice that had experienced negative social interactions, which induce stronger depression-related behavior in females than males.

“These high-throughput analyses are very informative for understanding long-lasting effects of stress on the brain. In our rodent model, negative social interactions changed gene expression patterns in female mice that mirrored patterns observed in women with depression,” said study leader Alexia Williams, a doctoral researcher. “This is exciting because women are understudied in this field, and this finding allowed me to focus my attention on the relevance of these data for women’s health.”

After identifying similar molecular changes in the brains of mice and humans, researchers chose one gene, regulator of g protein signaling-2, or Rgs2, to manipulate. This gene controls the expression of a protein that regulates neurotransmitter receptors that are targeted by antidepressant medications such as Prozac and Zoloft. “In humans, less stable versions of the Rgs2 protein are associated with increased risk of depression, so we were curious to see whether increasing Rgs2 in the nucleus accumbens could reduce depression-related behaviorus,” said Professor Brian Trainor, senior author on the study.

When the researchers experimentally increased Rgs2 protein in the nucleus accumbens of the mice, they effectively reversed the effects of stress on these female mice, noting that social approach and preferences for preferred foods increased to levels observed in females that did not experience any stress.

“These results highlight a molecular mechanism contributing to the lack of motivation often observed in depressed patients. Reduced function of proteins like Rgs2 may contribute to symptoms that are difficult to treat in those struggling with mental illnesses,” Williams said.

Findings from basic science studies such as this one may guide the development of pharmacotherapies to effectively treat individuals suffering from depression, the researchers said.

“Our hope is that by doing studies such as these, which focus on elucidating mechanisms of specific symptoms of complex mental illnesses, we will bring science one step closer to developing new treatments for those in need,” said Williams.

Source: UC Davis

IBD and Depression is a Two-way Street

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While irritable bowel disease (IBD) and depression are known to occur together, scientists report a clinical overlap of these conditions in the Journal of Gastroenterology and Hepatology, implying the existence of a two-way relationship. Patients diagnosed with IBD were nine times as likely to develop depression than the general population. Their siblings who did not suffer from IBD were almost two times as likely to develop depression.

Conversely, patients with depression were two times as likely to develop IBD, and their siblings without depression were more than one and a half times as likely to develop IBD.

“This research reveals a clinical overlap between both conditions, and is the first study to investigate the two-way association between IBD and depression in siblings,” said Bing Zhang, MD, a gastroenterologist with Keck Medicine and co-lead author of the study.

The researchers drew on the data of more than 20 million people from Taiwan’s National Health Insurance Research Database. For 11 years, they tracked patients with either IBD or depression and their siblings without either condition, comparing onset of depression or IBD with a control group of people without either condition, but with similar age, sex and socioeconomic status.

Zhang hypothesises that many factors may contribute to the bidirectional nature of the disorders, including environmental stressors, the gut microbiome and genetics.

“The finding that people with IBD are more prone to depression makes sense because IBD causes constant gastrointestinal symptoms that can be very disruptive to a patient’s life,” he said. “And the elevated depression risk among siblings of IBD patients may reflect caregiver fatigue if the siblings have a role in caring for the patient.”

What surprised researchers was that patients with depression were prone to IBD. Zhang speculates that this discovery may have to do with what is known as the gut-brain axis, a scientifically established connection between the gastrointestinal system and the central nervous system, which consists of the spinal cord and the brain.

For example, he said, inflammation of the brain, which plays a role in depression, may be linked to the inflammation of the gastrointestinal tract, a hallmark of IBD.

The researchers are not sure why siblings of patients with depression are more likely to be diagnosed with IBD. Zhang surmises that there may be a shared genetic susceptibility for either disease that presents differently in family members.

Zhang hopes that the study findings will encourage health care professionals to take both family history and the relationship between gastrointestinal and mood disorders into consideration when evaluating or treating patients with either IBD or depression.

Through more research and better understanding of the gut-brain axis, he envisions leveraging the newfound connection between the conditions to improve the prevention, diagnosis and treatment of IBD and mental disorders.

Source: University of Southern California – Health Sciences