BackgroundOver the last two decades, antidepressant prescribing in the UK has increased considerably, due to an increased number of people staying on antidepressants for longer. Even when treatment is no longer clinically indicated, qualitative research suggests many people continue due to a fear of depressive relapse or antidepressant withdrawal symptoms. The quantitative effects of peoples’ beliefs and attitudes towards long-term antidepressant use remain relatively unexplored.ObjectivesTo determine the extent to which beliefs and attitudes towards antidepressant treatment are associated with intentions to stop or continue long-term use; and whether intentions translate into actual discontinuation.MethodsA questionnaire survey formed the main component of an embedded mixed-methods study. Twenty general practices posted questionnaires to adults aged over 18 receiving continuous antidepressant prescriptions for over two years. Outcomes and explanatory variables were determined using an extended model of the Theory of Planned Behaviour, conducting exploratory descriptive and regression analyses. The primary outcome was participants’ intentions to discontinue antidepressants. The secondary outcome of behaviour change was determined by any change in antidepressant dosage at six months.Results277 people were surveyed from 20 practices, with 10 years median antidepressant duration. Mean questionnaire scores for intention and subjective norms towards starting to come off antidepressants were low, and 85% of participants declared that continuing their antidepressant was necessary. Prescribing outcomes retrieved from 175 participants’ medical records six months after they completed the survey found 86% had not changed their antidepressant, 9% reduced the dose, only 1% discontinued their antidepressant, and 4% increased the dose. All Theory of Planned Behaviour constructs and concerns were associated with intentions, with more favourable attitudes towards stopping and subjective norms having the strongest associations towards intentions to discontinue antidepressant use.ConclusionGiven few intentions to stop taking antidepressants, patients should be made more aware of the importance of ongoing antidepressant monitoring and review from their primary care practitioners. This would promote discussion to support an attitudinal change and initiation of antidepressant tapering where appropriate.

Europeans use of antidepressants more than doubles in 20 years.

Use of antidepressants increased by nearly two and a half times between 2000 and 2020 in 18 European countries, Organisation for Economic Cooperation and Development (OECD) data shows.

Link to an article from Future Care Capital.

The idea that depression is the result of abnormalities in brain chemicals, particularly serotonin (5-hydroxytryptamine or 5-HT), has been influential for decades, and provides an important justification for the use of antidepressants.

The below review suggests that the huge research effort based on the serotonin hypothesis has not produced convincing evidence of a biochemical basis to depression. This is consistent with research on many other biological markers. We suggest it is time to acknowledge that the serotonin theory of depression is not empirically substantiated.

Link to a systematic review from Molecular Psychiatry.

Analysis: Depression is probably not caused by a chemical imbalance in the brain.

Link to a document about SSRI antidepressants.

We conclude that it is impossible to say that taking SSRI antidepressants is worthwhile, or even completely safe. People need all this information to make informed decisions about whether or not to take antidepressants.

Link to an article from UCL News.

Antidepressants are not associated with improved quality of life in the long run, study finds.

Over time, using antidepressants is not associated with significantly better health-related quality of life, compared to people with depression who do not take the drugs, according to a new study.

Link to an article from Science Daily.

Data Visualisations.

A link to a Markdown document with code chunks and two basic scatter plots, using data from census.csv.

The following spreadsheets are edited versions of the original data as uploaded (census.csv).

Using data from only Sweden from 2007 to 2017, using two age groups: 5-9 years old and 10-19 years old.

Group 1: 5-9 years old. A link to an edited spreadsheet and bar chart.

https://www.googleapis.com/download/storage/v1/b/kaggle-user-content/o/inbox%2F13231939%2Fd1666bcda386fb8a6577d6c2bafe7b29%2FScreenshot%202023-08-16%2014.06.40.png?generation=1692191292935092&alt=media" alt="">

Group 2: 10-19 years old. A link to an edited spreadsheet and bar chart.

https://www.googleapis.com/download/storage/v1/b/kaggle-user-content/o/inbox%2F13231939%2Fab165fd25b2a97d9bb135e52466755f4%2FScreenshot%202023-08-16%2014.08.46.png?generation=1692191417619734&alt=media" alt="">

As the data from Sweden shows, a lot of 5-19 year old children and adolescents were prescribed antidepressants between 2007-2017. With a noticeable uptrend in the numbers of users in the 5-9 year old, children's age group.

Can you eat foods to boost Serotonin levels ?

Tryptophan is an essential amino acid that cannot be produced by the human body and must be obtained through your diet, primarily from animal or plant based protein sources.

Tryptophan plays a role in the production of serotonin, a mood stabiliser, melatonin, which helps regulate sleep patterns, niacin or vitamin B-3, and nicotinamide also known as vitamin B-3 - signs of severe niacin deficiency include depression.

Tryptophan has the lowest concentration in the body of any amino acid, yet, it is vital for a wide variety of metabolic functions that affect your mood, cognition, and behaviour.

Link to an article from WebMD about Tryptophan.

Foods that are high in Tryptophan. Link

Vegetarian & Vegan foods high in Tryptophan. Link

The determinants of mental health and well being are largely about the society we live in, rather than medical.

[Link](https://research.senedd.wales/research-articles/poverty-and-mental-health-it-s-a-two-way-street/#:~:text=Poverty%20is%20clearly%20linked%20with,and%20anxiety%2C%...

BackgroundIn vitro and animal studies have suggested that trazodone, a licensed antidepressant, may protect against dementia. However, no studies have been conducted to assess the effect of trazodone on dementia in humans. This electronic health records study assessed the association between trazodone use and the risk of developing dementia in clinical practice.Methods and findingsThe Health Improvement Network (THIN), an archive of anonymised medical and prescribing records from primary care practices in the United Kingdom, contains records of over 15 million patients. We assessed patients from THIN aged ≥50 years who received at least two consecutive prescriptions for an antidepressant between January 2000 and January 2017. We compared the risk of dementia among patients who were prescribed trazodone to that of patients with similar baseline characteristics prescribed other antidepressants, using a Cox regression model with 1:5 propensity score matching. Patients prescribed trazodone who met the inclusion criteria (n = 4,716; 59.2% female) were older (mean age 70.9 ± 13.1 versus 65.6 ± 11.4 years) and were more likely than those prescribed other antidepressants (n = 420,280; 59.7% female) to have cerebrovascular disease and use anxiolytic or antipsychotic drugs. After propensity score matching, 4,596 users of trazadone and 22,980 users of other antidepressants were analysed. The median time to dementia diagnosis for people prescribed trazodone was 1.8 years (interquartile range [IQR] = 0.5–5.0 years). Incidence of dementia among patients taking trazodone was higher than in matched users of other antidepressants (1.8 versus 1.1 per 100 person-years), with a hazard ratio (HR) of 1.80 (95% confidence interval [CI] 1.56–2.09; p < 0.001). However, our results do not suggest a causal association. When we restricted the control group to users of mirtazapine only in a sensitivity analysis, the findings were very similar to the results of the main analysis. The main limitation of our study is the possibility of indication bias, because people in the prodromal stage of dementia might be preferentially prescribed trazodone. Due to the observational nature of this study, we cannot rule out residual confounding.ConclusionsIn this study of UK population-based electronic health records, we found no association between trazodone use and a reduced risk of dementia compared with other antidepressants. These results suggest that the clinical use of trazodone is not associated with a reduced risk of dementia.