Low dose of caffeine enhances the efficacy of antidepressants in major depressive disorder and the underlying neural substrates

Liu, Qingshan; Deng, Ronghai; Fan, Yu-Yan; Li, Keqin; Meng, Fanggang; Li, Xueli; Li, Rui

doi:10.1002/mnfr.201600910

Cited by 28 publications

(18 citation statements)

References 59 publications

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“…Randomized controlled studies show that better sleep hygiene 8,9 , physical activity interventions 10 , as well as mindfulness meditation 11,12 can all benefit depressed patients. Evidence for efficacy also exists for dietary interventions that focus on reducing processed fats and sugars and moderating caffeine intake [13][14][15][16][17] . Unfortunately, not all interventions work for all depressed patients.…”

Section: Introductionmentioning

confidence: 99%

Personalized machine learning of depressed mood using wearables

et al. 2021

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Depression is a multifaceted illness with large interindividual variability in clinical response to treatment. In the era of digital medicine and precision therapeutics, new personalized treatment approaches are warranted for depression. Here, we use a combination of longitudinal ecological momentary assessments of depression, neurocognitive sampling synchronized with electroencephalography, and lifestyle data from wearables to generate individualized predictions of depressed mood over a 1-month time period. This study, thus, develops a systematic pipeline for N-of-1 personalized modeling of depression using multiple modalities of data. In the models, we integrate seven types of supervised machine learning (ML) approaches for each individual, including ensemble learning and regression-based methods. All models were verified using fourfold nested cross-validation. The best-fit as benchmarked by the lowest mean absolute percentage error, was obtained by a different type of ML model for each individual, demonstrating that there is no one-size-fits-all strategy. The voting regressor, which is a composite strategy across ML models, was best performing on-average across subjects. However, the individually selected best-fit models still showed significantly less error than the voting regressor performance across subjects. For each individual’s best-fit personalized model, we further extracted top-feature predictors using Shapley statistics. Shapley values revealed distinct feature determinants of depression over time for each person ranging from co-morbid anxiety, to physical exercise, diet, momentary stress and breathing performance, sleep times, and neurocognition. In future, these personalized features can serve as targets for a personalized ML-guided, multimodal treatment strategy for depression.

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Section: Introductionmentioning

confidence: 99%

Personalized machine learning of depressed mood using wearables

et al. 2021

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“…28 Moreover, there reported that chronic supplementation with low dose of caffeine produced rapid antidepressant action in patients treated with the selective serotonin reuptake inhibitor (SSRI) escitalopram. 29 Furthermore, adult neurogenesis has been newly defined as a novel mechanism responsible for the antidepressive effect of caffeine, in view of its improving effect on neuron cell proliferation in DG of sleep-deprived rats. 30 Considering the reported modulating effects of caffeine on neuroinflammation in vivo and in vitro, 31,32 we proposed that there might be a certain connection between the effects of caffeine on hippocampal neurogenesis and microglia activation.…”

Section: Introductionmentioning

confidence: 99%

New insights into the effects of caffeine on adult hippocampal neurogenesis in stressed mice: Inhibition of CORT‐induced microglia activation

et al. 2020

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Chronic stress-evoked depression has been implied to associate with the decline of adult hippocampal neurogenesis. Caffeine has been known to combat stress-evoked depression. Herein, we aim to investigate whether the protective effect of caffeine on depression is related with improving adult hippocampus neurogenesis and explore the mechanisms. Mouse chronic water immersion restraint stress (CWIRS) model, corticosterone (CORT)-established cell stress model, a coculture system containing CORT-treated BV-2 cells and hippocampal neural stem cells (NSCs) were utilized. Results showed that CWIRS caused obvious depressive-like disorders, abnormal 5-HT signaling, and elevated-plasma CORT levels. Notably, microglia activationevoked brain inflammation and inhibited neurogenesis were also observed in the hippocampus of stressed mice. In comparison, intragastric administration of caffeine (10 and 20 mg/kg, 28 days) significantly reverted CWIRS-induced depressive behaviors, neurogenesis recession and microglia activation in the hippocampus. Further evidences from both in vivo and in vitro mechanistic experiments demonstrated that | 10999 MAO et Al.

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“…Of note, recent clinical study indicated beneficial effects of caffeine in terms of augmenting antidepressant treatment. A 2-week supplementation with a low dose of caffeine (60 mg/day) enhanced the efficacy of treatment with a selective serotonin reuptake inhibitor (SSRI), escitalopram (Liu et al 2017). Since in the present study no increases in the spontaneous locomotor activity were found, the results indicate an antidepressant-like activity of low, ineffective doses of agomelatine or mianserin administered together with caffeine.…”

Section: Discussionmentioning

confidence: 99%

Withdrawal of caffeine after its chronic administration modifies the antidepressant-like activity of atypical antidepressants in mice. Changes in cortical expression of Comt, Slc6a15 and Adora1 genes

et al. 2018

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RationaleDepressed patients often present increased consumption of caffeine.ObjectivesWe aimed to investigate the effects of chronic treatment with caffeine (5 mg/kg, twice daily for 14 days) on the activity of single, ineffective doses of agomelatine (20 mg/kg) or mianserin (10 mg/kg) given on day 15 alone or simultaneously with caffeine.MethodsWe used the forced swim test (FST), tail suspension test (TST), and locomotor activity test in mice and quantitative real-time PCR analysis of the selected genes in the cerebral cortex (Cx).ResultsThere were no changes in the immobility time between mice that received saline and caffeine for 14 days. Administration of agomelatine or mianserin on day 15 did not produce an antidepressant-like effect, but such effect was observed after administration of agomelatine or mianserin simultaneously with caffeine on day 15, in both mice that received saline and caffeine for 14 days. In mice treated with caffeine for 14 days, joint administration of agomelatine or mianserin and caffeine on day 15 decreased solute carrier family 6, member 15 (Slc6a15), messenger RNA (mRNA) level in the Cx, compared to the group which received only the respective antidepressant on this day. Moreover, in mice treated with caffeine for 14 days, joint administration of mianserin and caffeine on day 15 decreased adenosine A1 receptor (Adora1) and catechol-O-methyltransferase (Comt) mRNA level in the Cx, compared to the group which received mianserin without caffeine on this day.ConclusionsWithdrawal of caffeine after its chronic intake can modify the activity of antidepressants. Adora1, Slc6a15, and Comt may be involved in the antidepressant-like effect observed after joint administration of caffeine and mianserin or agomelatine, following chronic treatment with caffeine.

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Low dose of caffeine enhances the efficacy of antidepressants in major depressive disorder and the underlying neural substrates

Abstract: These findings indicated the potential benefits of further implications of supplementary administration of caffeine to reverse the development of depression and enhance the outcome of antidepressants treatment in major depressive disorder.

Cited by 28 publications

References 59 publications

Personalized machine learning of depressed mood using wearables

Personalized machine learning of depressed mood using wearables

New insights into the effects of caffeine on adult hippocampal neurogenesis in stressed mice: Inhibition of CORT‐induced microglia activation

Withdrawal of caffeine after its chronic administration modifies the antidepressant-like activity of atypical antidepressants in mice. Changes in cortical expression of Comt, Slc6a15 and Adora1 genes

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