What makes you depressed

Personality — Some people may be more at risk of depression because of their personality, particularly if they have a tendency to worry a lot, have low self-esteem, are perfectionists, are sensitive to personal criticism, or are self-critical and negative. Drug and alcohol use — Drug and alcohol use can both lead to and result from depression. Many people with depression also have drug and alcohol problems. Over , Australians will experience depression and a substance use disorder at the same time, at some point in their lives.

Other pages in This Section What is mental health? Anxiety and depression checklist K10 Depression What causes depression? Signs and symptoms Types of depression Treatments for depression Who can assist Other sources of support Anxiety Suicide prevention Supporting someone Pregnancy and early parenthood Grief and loss Unemployment and mental health Drugs, alcohol and mental health.

Rather, many chemicals are involved, working both inside and outside nerve cells. There are millions, even billions, of chemical reactions that make up the dynamic system that is responsible for your mood, perceptions, and how you experience life. With this level of complexity, you can see how two people might have similar symptoms of depression, but the problem on the inside, and therefore what treatments will work best, may be entirely different.

Researchers have learned much about the biology of depression. They've identified genes that make individuals more vulnerable to low moods and influence how an individual responds to drug therapy. One day, these discoveries should lead to better, more individualized treatment see "From the lab to your medicine cabinet" , but that is likely to be years away.

And while researchers know more now than ever before about how the brain regulates mood, their understanding of the biology of depression is far from complete. What follows is an overview of the current understanding of the major factors believed to play a role in the causes of depression. Popular lore has it that emotions reside in the heart. Science, though, tracks the seat of your emotions to the brain.

Certain areas of the brain help regulate mood. Researchers believe that — more important than levels of specific brain chemicals — nerve cell connections, nerve cell growth, and the functioning of nerve circuits have a major impact on depression. Still, their understanding of the neurological underpinnings of mood is incomplete. Increasingly sophisticated forms of brain imaging — such as positron emission tomography PET , single-photon emission computed tomography SPECT , and functional magnetic resonance imaging fMRI — permit a much closer look at the working brain than was possible in the past.

An fMRI scan, for example, can track changes that take place when a region of the brain responds during various tasks. Use of this technology has led to a better understanding of which brain regions regulate mood and how other functions, such as memory, may be affected by depression. Areas that play a significant role in depression are the amygdala, the thalamus, and the hippocampus see Figure 1.

Research shows that the hippocampus is smaller in some depressed people. For example, in one fMRI study published in The Journal of Neuroscience , investigators studied 24 women who had a history of depression. The more bouts of depression a woman had, the smaller the hippocampus.

Stress, which plays a role in depression, may be a key factor here, since experts believe stress can suppress the production of new neurons nerve cells in the hippocampus. Researchers are exploring possible links between sluggish production of new neurons in the hippocampus and low moods.

An interesting fact about antidepressants supports this theory. These medications immediately boost the concentration of chemical messengers in the brain neurotransmitters. Yet people typically don't begin to feel better for several weeks or longer. Experts have long wondered why, if depression were primarily the result of low levels of neurotransmitters, people don't feel better as soon as levels of neurotransmitters increase.

The answer may be that mood only improves as nerves grow and form new connections, a process that takes weeks. In fact, animal studies have shown that antidepressants do spur the growth and enhanced branching of nerve cells in the hippocampus.

So, the theory holds, the real value of these medications may be in generating new neurons a process called neurogenesis , strengthening nerve cell connections, and improving the exchange of information between nerve circuits.

If that's the case, depression medications could be developed that specifically promote neurogenesis, with the hope that patients would see quicker results than with current treatments.

Amygdala: The amygdala is part of the limbic system, a group of structures deep in the brain that's associated with emotions such as anger, pleasure, sorrow, fear, and sexual arousal.

The amygdala is activated when a person recalls emotionally charged memories, such as a frightening situation. Activity in the amygdala is higher when a person is sad or clinically depressed. This increased activity continues even after recovery from depression. Thalamus: The thalamus receives most sensory information and relays it to the appropriate part of the cerebral cortex, which directs high-level functions such as speech, behavioral reactions, movement, thinking, and learning.

Some research suggests that bipolar disorder may result from problems in the thalamus, which helps link sensory input to pleasant and unpleasant feelings. Hippocampus: The hippocampus is part of the limbic system and has a central role in processing long-term memory and recollection.

Interplay between the hippocampus and the amygdala might account for the adage "once bitten, twice shy. The hippocampus is smaller in some depressed people, and research suggests that ongoing exposure to stress hormone impairs the growth of nerve cells in this part of the brain.

The ultimate goal in treating the biology of depression is to improve the brain's ability to regulate mood. We now know that neurotransmitters are not the only important part of the machinery. But let's not diminish their importance either.

They are deeply involved in how nerve cells communicate with one another. And they are a component of brain function that we can often influence to good ends. Neurotransmitters are chemicals that relay messages from neuron to neuron. An antidepressant medication tends to increase the concentration of these substances in the spaces between neurons the synapses. In many cases, this shift appears to give the system enough of a nudge so that the brain can do its job better. How the system works.

If you trained a high-powered microscope on a slice of brain tissue, you might be able to see a loosely braided network of neurons that send and receive messages. While every cell in the body has the capacity to send and receive signals, neurons are specially designed for this function. Each neuron has a cell body containing the structures that any cell needs to thrive.

Stretching out from the cell body are short, branchlike fibers called dendrites and one longer, more prominent fiber called the axon. A combination of electrical and chemical signals allows communication within and between neurons. When a neuron becomes activated, it passes an electrical signal from the cell body down the axon to its end known as the axon terminal , where chemical messengers called neurotransmitters are stored. The signal releases certain neurotransmitters into the space between that neuron and the dendrite of a neighboring neuron.

That space is called a synapse. As the concentration of a neurotransmitter rises in the synapse, neurotransmitter molecules begin to bind with receptors embedded in the membranes of the two neurons see Figure 2.

If you have severe depression, you may be referred to a specialist mental health team for intensive specialist talking treatments and prescribed medicine.

Many people with depression benefit by making lifestyle changes, such as getting more exercise , cutting down on alcohol , giving up smoking and eating healthily. Reading a self-help book or joining a support group are also worthwhile. They can help you gain a better understanding about what causes you to feel depressed. Sharing your experiences with others in a similar situation can also be very supportive.

Our guide to care and support explains your options and where you can get support. Page last reviewed: 10 December Next review due: 10 December Overview - Clinical depression. Information: Coronavirus advice Get advice about coronavirus and looking after your mental wellbeing: Every Mind Matters: how to look after your mental wellbeing while staying at home Mind: Coronavirus and your wellbeing.

Information: Social care and support guide If you: need help with day-to-day living because of illness or disability care for someone regularly because they're ill, elderly or disabled — including family members Our guide to care and support explains your options and where you can get support. Cell and Tissue Research. Jaracz J. Overlapping chronic pain and depression: Pathophysiology and management.

Understanding Depression. October Exploring comorbidity within mental disorders among a Danish national population. JAMA Psychiatry. The link between thyroid function and depression. Journal of Thyroid Research. Childhood trauma and tts relation to chronic depression in adulthood. Depress Res Treat. Childhood trauma history is linked to abnormal brain connectivity in major depression.

The link between childhood trauma and depression: Insights from HPA axis studies in humans. Data Briefs - Number - December Household Population, December cdc. Poverty and common mental disorders in low and middle income countries: A systematic review. Soc Sci Med. Money and mental illness: A study of the relationship between poverty and serious psychological problems.

Community Ment Health J. Ali NA, Khoja A. Growing evidence for the impact of air pollution on depression. Ochsner Journal. Big Five aspects of personality interact to predict depression. Journal of Personality. Resilient people have lessons to offer, and USC researchers are listening. Published July 10, Correlation between cortisol level and serotonin uptake in patients with chronic stress and depression.

Intergenerational continuity in high-conflict family environments: Investigating a mediating depressive pathway. Dev Psychol. Guilt in bereavement: Its relationship with complicated grief and depression. International Journal of Psychology. Complicated grief as a disorder distinct from bereavement-related depression and anxiety: a replication study.

The American journal of psychiatry. Neural mechanisms of grief regulation. Biol Psychiatry. Boelen PA, van den Bout J. Complicated grief, depression, and anxiety as distinct postloss syndromes: a confirmatory factor analysis study. A systematic review: the influence of social media on depression, anxiety and psychological distress in adolescents. Int J Adolesc Youth. Psychosocial well-being and social media engagement: The mediating roles of social comparison orientation and fear of missing out.

New Media Soc. Online social media fatigue and psychological wellbeing—A study of compulsive use, fear of missing out, fatigue, anxiety and depression.

International Journal of Information Management. The causal effects of adolescent school bullying victimisation on later life outcomes. Published March Roles of cyberbullying, sleep, and physical activity in mediating the effects of social media use on mental health and wellbeing among young people in England: a secondary analysis of longitudinal data. August Real-world data and the patient perspective: the PROmise of social media?

BMC Medicine. Affective psychosis following Accutane isotretinoin treatment. Int Clin Psychopharmacol. Beta-blocker therapy and symptoms of depression, fatigue, and sexual dysfunction. Corticosteroids, depression and the role of serotonin. Rev Neurosci. Activation of central nervous system inflammatory pathways by interferon-alpha: relationship to monoamines and depression. Statins use and risk of depression: a systematic review and meta-analysis.

J Affect Disord.