DATE: May 28, 2025 at 08:00AM
SOURCE: PSYPOST.ORG

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TITLE: High caffeine intake linked to greater psychological distress in people with depression

URL: https://www.psypost.org/high-caffeine-intake-linked-to-greater-psychological-distress-in-people-with-depression/

A new study published in Complex Psychiatry has found that people with a history of depression who consume high amounts of caffeine tend to report higher levels of psychological distress. The researchers also found that certain genetic differences are associated with how much caffeine people drink and how sensitive they are to its effects. While caffeine use was not strongly linked to sleep satisfaction, people who said caffeine interfered with their sleep typically consumed less of it.

The study was designed to explore how caffeine consumption, sleep satisfaction, and psychological distress are connected in people with a history of depression, and whether genetic variants might explain some of these associations. Caffeine is the world’s most widely used psychoactive substance, often praised for its alertness-boosting effects.

But at higher doses, or in sensitive individuals, caffeine can increase anxiety and interfere with sleep. Although research has shown that moderate caffeine use may reduce the risk of developing depression in otherwise healthy individuals, less is known about its effects in people who have already been diagnosed or treated for depression.

“Caffeine is common, viewed as safe, and increasingly marketed toward and consumed by younger people,” said study author Harry McIntosh, a PhD student at the University of Queensland. “At the same time, mental health problems are on the rise and insomnia is an important symptom of a number of mental health disorders. We’re interested in caffeine consumption because it may be something that people suffering from mental health problems can change to improve their mental health and sleep.”

To explore these questions, the researchers used data from the Australian Genetics of Depression Study. Over 11,000 adults who had been diagnosed with or treated for depression completed detailed questionnaires about their caffeine consumption, sleep, and mental health. Of those, about 9,000 also provided DNA samples, allowing researchers to examine genetic differences previously linked to caffeine metabolism and sensitivity.

Caffeine consumption was measured by asking participants how many servings of caffeinated coffee, tea, soft drinks, and energy drinks they typically drank per day. Participants were grouped into low (0–2 drinks), medium (3–5 drinks), or high (6 or more drinks) caffeine consumers. Psychological distress was assessed using the Kessler Psychological Distress Scale, a commonly used measure of anxiety and depression symptoms. Sleep satisfaction was measured with a single question from the Insomnia Severity Index. Participants were also asked whether they felt caffeine interfered with their ability to sleep, which served as a proxy for caffeine sensitivity.

The researchers then used linear regression models to examine how caffeine use was related to distress and sleep satisfaction, adjusting for factors such as age, sex, body mass index, and other substance use (including alcohol, nicotine, and painkillers). They also looked at whether specific genetic variants were linked to caffeine intake and sensitivity.

The analysis found that participants who drank six or more caffeinated drinks per day scored higher on the psychological distress scale than those who consumed fewer drinks. For each additional caffeinated beverage consumed per day, participants’ distress scores increased by 0.2 points on a 50-point scale. While this is a small effect, it was statistically significant. People in the medium caffeine group (3–5 drinks per day) did not differ significantly from those in the low group, suggesting that only higher levels of consumption are linked to greater distress.

Interestingly, there was little evidence that caffeine consumption negatively affected sleep satisfaction in this group. Although those with higher caffeine intake reported slightly lower sleep satisfaction, the difference was small and did not remain statistically significant after correcting for multiple comparisons.

“We expected caffeine consumption to be associated with poorer sleep, which it wasn’t,” McIntosh told PsyPost.

Instead, caffeine sensitivity itself appeared to play a larger role. People who reported that caffeine interfered with their sleep were far less likely to drink large amounts of it. Each additional caffeinated drink consumed per day was associated with a 16% lower likelihood of reporting caffeine sensitivity. This suggests that people may naturally reduce their intake if they notice it disrupts their sleep.

“People naturally adjust how much caffeine they consume based on how they respond to it,” McIntosh said. “If caffeine was negatively impacting you, you’d probably reduce your intake accordingly, this could explain why caffeine was not associated with poor sleep quality.”

The genetic analysis offered further insight into why some people consume more caffeine than others. Several genetic variants were associated with differences in caffeine intake. For example, a variant near the AHR gene (rs4410790) was linked to increased caffeine use, while a variant near the CYP1A2 gene (rs2472297) was linked to lower consumption. These genes are involved in caffeine metabolism. People with faster metabolism may consume more caffeine to maintain the same level of alertness, while slower metabolizers may consume less.

A separate variant near the MMS22L/POU3F2 genes (rs34645063) was associated with a higher likelihood of reporting caffeine sensitivity. This finding is consistent with earlier research showing that this genetic region may be linked to both lower caffeine consumption and increased sensitivity.

Other variants in genes like ADORA2A—which encodes a receptor targeted by caffeine in the brain—were only weakly linked to consumption and did not remain significant after adjusting for multiple comparisons. Still, the results suggest that genetic differences play a role in shaping both how much caffeine people consume and how their bodies respond to it.

“Our work is focused on those diagnosed with depression,” McIntosh told PsyPost. “Higher caffeine consumption was associated with higher reported levels of current stress in people regardless of sleep quality. The effect size was not large but was statistically significant. However, we cannot assign a causal relationship because participants may increase caffeine consumption in response to symptoms of depression such as fatigue or lack of motivation. Common genetic variants play a sizeable role in how our body handles caffeine and were associated with consuming a larger or smaller number of caffeinated drinks each day.”

One of the main strengths of the study is its large sample size and inclusion of genetic data, which allowed researchers to detect even small effects. However, there are some limitations to consider. The data were cross-sectional, meaning they captured only one moment in time. This makes it difficult to determine cause and effect.

“Our data has only one timepoint and measures variables instead of controlling them experimentally, so we cannot use it to definitively state that caffeine is causing distress, or that people with higher stress are then choosing to consume more caffeine,” McIntosh noted.

Another caveat is that the study sample consisted entirely of people with a history of depression. This means the results may not apply to the general population, especially those without mental health conditions. Future research using more precise measures of caffeine intake and longitudinal designs could help clarify how these relationships unfold over time.

The study, “Caffeine Consumption, Psychological Distress, and Insomnia in a Cohort of Individuals with Depression,” was authored by Harry A. McIntosh, Aleah J. Borgas, Nisreen Aouira, Brittany L. Mitchell, Jacob J. Crouse, Sarah E. Medland, Ian B. Hickie, Naomi R. Wray, Nicholas G. Martin, Christel M. Middeldorp, and Enda M. Byrne.

URL: https://www.psypost.org/high-caffeine-intake-linked-to-greater-psychological-distress-in-people-with-depression/

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DATE: May 27, 2025 at 04:00PM
SOURCE: PSYPOST.ORG

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TITLE: Only a specific dose of psilocybin induces lasting antidepressant-like effects, study suggests

URL: https://www.psypost.org/only-a-specific-dose-of-psilocybin-induces-lasting-antidepressant-like-effects-study-suggests/

A new study published in Progress in Neuropsychopharmacology & Biological Psychiatry has found that a single moderate dose of psilocybin produces rapid and lasting antidepressant-like effects in rats, without the unwanted side effects seen at higher doses. The researchers showed that only an intermediate dose improved mood-related behaviors and social interaction while avoiding changes in body temperature, locomotion, and weight gain.

Psilocybin is the active ingredient in so-called magic mushrooms. It is a psychedelic compound that alters perception and consciousness and has attracted increasing interest as a potential treatment for depression, especially among individuals who have not responded to traditional antidepressants. Clinical trials have shown that even a single administration of psilocybin can lead to significant improvements in symptoms, sometimes lasting for weeks or months. However, because it can also produce strong hallucinogenic effects and other physiological changes, scientists are still working to determine the safest and most effective dosage.

In this new study, a team of researchers led by Lenka Seillier at Charles University in Prague aimed to better understand the relationship between psilocybin dose and its behavioral and physiological effects in an animal model. By testing a range of doses, they hoped to pinpoint the amount of psilocybin that produces therapeutic benefits while minimizing adverse outcomes.

The researchers used 40 male Wistar rats and divided them into five groups. Each group received either a saline control injection or one of four psilocybin doses: 0.1, 0.32, 1.0, or 3.2 milligrams per kilogram of body weight. The study design included multiple behavioral tests to assess antidepressant-like effects, social interaction, and pleasure responses. They also monitored side effects such as changes in body temperature, movement, and weight gain. In addition, they examined whether psilocybin altered levels of brain-derived neurotrophic factor (BDNF), a protein involved in brain plasticity that is often linked to depression.

To assess antidepressant-like effects, the researchers used the forced swim test, a standard behavioral test in animal models of depression. In this task, less immobility and more active behaviors such as climbing are considered signs of a more hopeful or motivated behavioral state. They also used a sucrose preference test to evaluate sensitivity to reward and a social interaction test to measure sociability. Each test was repeated across several weeks to assess both immediate and long-term effects.

The researchers found that the 0.32 mg/kg dose of psilocybin had the strongest antidepressant-like effect. Rats that received this dose were more active in the forced swim test, spent more time engaging in social behavior, and showed a stronger preference for sweetened water—an indicator of heightened sensitivity to pleasure. Importantly, these effects were evident both shortly after treatment and weeks later, suggesting that the benefits were long-lasting.

Higher doses of psilocybin, by contrast, did not produce these same benefits. In fact, the rats that received 1.0 or 3.2 mg/kg showed no improvement in mood-related behaviors. These higher doses also led to adverse effects, including reduced locomotion, decreased body temperature, and lower body weight gain over time. The results suggest that these side effects may mask or interfere with potential antidepressant effects at higher doses.

The team also measured head-twitch responses, a behavior commonly used in rodents as a proxy for psychedelic effects in humans. The number of these responses followed an inverted U-shaped curve, peaking at the 0.32 mg/kg dose and declining at the higher doses, likely due to the overall suppression of movement caused by those doses.

In terms of biological effects, the researchers found that psilocybin increased levels of BDNF in the hippocampus and prefrontal cortex—two brain regions implicated in mood and depression. These increases occurred in a dose-dependent, linear fashion, meaning the more psilocybin the rats received, the higher the BDNF levels. However, this pattern did not align with the behavioral improvements, which only occurred at the moderate dose. This suggests that while BDNF may play a role in psilocybin’s effects, it is not the only factor at work and may not directly predict therapeutic outcomes.

The study highlights a narrow window of optimal dosing for psilocybin. At low doses, there was little effect. At moderate doses, the drug enhanced mood-related behavior without causing harmful physiological changes. But at high doses, the risk of side effects increased, and the benefits disappeared. This finding underscores the importance of dose selection in ongoing research and clinical applications.

As with any study, there are limitations. The study was conducted in healthy rats rather than animal models of depression, which may limit its generalizability. The researchers also note that they did not examine potential sex differences, which could be relevant for translating findings to human populations. Additionally, while they identified a mismatch between BDNF levels and behavioral outcomes, they did not investigate other molecular pathways that might help explain the observed effects.

Future studies could expand on this work by exploring how psilocybin affects rats with depression-like symptoms, whether similar effects are seen in female animals, and what other brain systems may contribute to the therapeutic effects. Investigating the role of specific serotonin receptors could also help clarify how different doses influence mood, perception, and physical responses.

The study, “Psilocybin has a narrow therapeutic window as an antidepressant treatment,” was authored by Lenka Seillier, Barbora Čechová, Alexandre Seillier, and Romana Šlamberová.

URL: https://www.psypost.org/only-a-specific-dose-of-psilocybin-induces-lasting-antidepressant-like-effects-study-suggests/

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DATE: May 24, 2025 at 10:00AM
SOURCE: PSYPOST.ORG

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TITLE: Bright light therapy linked to mood improvements and brain connectivity changes

URL: https://www.psypost.org/bright-light-therapy-linked-to-mood-improvements-and-brain-connectivity-changes/

A new neuroimaging study from China has found that an eight-week course of bright light therapy helped reduce depressive symptoms in individuals with subthreshold depression. The treatment also altered dynamic functional connectivity in several brain regions associated with mood regulation. The study was published in the Journal of Affective Disorders.

Subthreshold depression refers to the presence of depressive symptoms that are clinically relevant but do not meet the full diagnostic criteria for major depressive disorder. Individuals with subthreshold depression may experience persistent sadness, fatigue, sleep disturbances, or concentration problems, but with fewer symptoms or a shorter duration than required for a formal diagnosis.

Despite being “subthreshold,” the condition can impair daily functioning and reduce quality of life. It is also linked to an increased risk of developing major depression in the future. Subthreshold depression is common—especially among adolescents, older adults, and individuals with chronic illnesses—and it often goes undiagnosed and untreated because the symptoms are perceived as mild or situational. However, research shows that even mild depressive symptoms can negatively affect social relationships, job performance, and physical health.

Study author Guixian Tang and his colleagues aimed to examine the effects of bright light therapy on both depressive symptoms and brain function in individuals with subthreshold depression. Bright light therapy involves exposure to artificial light that mimics natural sunlight and is commonly used to regulate circadian rhythms and improve mood. While it is best known as a treatment for seasonal affective disorder, it has also shown benefits for non-seasonal depression, sleep disorders, and circadian rhythm disruptions. The authors hypothesized that it might also be effective for subthreshold depression.

The study involved 95 students from Jinan University in China. Participants were between 18 and 28 years old, ethnically Han Chinese, and right-handed. They were included in the study if they had a mild, nonseasonal depressive symptom profile, with scores meeting specific thresholds on two established depression measures.

Participants were randomly assigned to one of two groups. One group received bright light therapy: daily 30-minute exposure to a 5000 lux light box before noon for eight weeks. The placebo group used an identical-looking device that emitted only a dim light (less than 5 lux).

Before and after the treatment period, participants completed standardized assessments of depression (the Hamilton Depression Rating Scale and the Center for Epidemiologic Studies Depression Scale) and anxiety (the Hamilton Anxiety Scale). They also underwent resting-state functional magnetic resonance imaging (rs-fMRI) scans, with a focus on dynamic functional connectivity in the cingulate cortex—a brain region involved in emotional regulation.

The results showed that participants who received bright light therapy had significantly greater reductions in depressive symptoms than those in the placebo group. Neuroimaging data revealed that bright light therapy led to increased dynamic functional connectivity between:

• The right supracallosal anterior cingulate cortex and the right temporal pole,
•

• The left middle cingulate cortex and the right insula,
•

• The left supracallosal anterior cingulate cortex and the pons.
•

Conversely, the therapy decreased dynamic connectivity between the right supracallosal anterior cingulate cortex and the right middle frontal gyrus.

Importantly, increases in connectivity between the right supracallosal anterior cingulate cortex and the right temporal pole were positively associated with reductions in depressive symptoms, suggesting a link between brain network changes and mood improvement.

“BLT [bright light therapy] alleviates depressive symptoms and changes the CC dFC [cingulate cortex dynamic functional connectivity] variability in StD [subthreshold depression], and pre-treatment dFC variability of the CC could be used as a biomarker for improved BLT treatment in StD. Furthermore, dFC changes with specific neurotransmitter systems after BLT may underline the antidepressant mechanisms of BLT.”, study authors concluded.

The study sheds light on the effects of bright light treatment on subthreshold depression. However, the study was conducted on a small group of university students. Results on larger groups and groups that include older individuals might differ.

The paper “Effects of bright light therapy on cingulate cortex dynamic functional connectivity and neurotransmitter activity in young adults with subthreshold depression” was authored by Guixian Tang, Pan Chen, Guanmao Chen, Zibin Yang, Wenhao Ma, Hong Yan, Ting Su, Yuan Zhang, Shu Zhang, Zhangzhang Qi, Wenjie Fang, Lijun Jiang, Qian Tao, and Ying Wang.

URL: https://www.psypost.org/bright-light-therapy-linked-to-mood-improvements-and-brain-connectivity-changes/

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