Table of Content
When we discuss the effects of depression, we too often think exclusively about mood—about how a person “feels.” However, epidemiological, clinical, and economic research from recent decades proves beyond a doubt that depression is a disease of the entire organism and the entire lifespan. It destroys the heart, weakens the immune system, shortens life expectancy, destabilizes relationships, robs people of their jobs, and generates costs that the WHO and OECD measure in hundreds of billions of euros annually.
The effects of depression operate in a loop: somatic illness deepens depression, social isolation intensifies it, and the loss of work and finances becomes yet another risk factor for relapse. This article discusses all key areas of the effects of depression—mental, biological, social, and economic—with reference to current scientific research.
Suicide: The Most Severe Consequence of Depression
Suicide is the most dramatic result of untreated or insufficiently treated depression. The World Health Organization estimates that more than 720,000 people die by suicide globally each year, and in the 15–29 age group, suicide is a leading cause of death [1]. Depression is the most frequently identified mental disorder in psychological autopsy studies—the methodological standard for reconstructing risk factors in those who have taken their own lives. A meta-analysis by Favril et al. (2022), covering 72 studies, confirmed that mood disorders are the strongest risk factors for suicide [12].
In Poland, police data for 2024 indicate 4,845 suicide deaths and 14,980 suicide attempts. The increase in the under-18 group is particularly alarming, with 2,181 attempts recorded [3]. Risk is especially high during transitional phases: at the beginning of antidepressant treatment (when energy often returns faster than hope), following hospital discharge, and in the context of substance abuse [12].
CRISIS NUMBERS (UK/US/PL):
- UK: NHS 111 or Samaritans 116 123
- US: 988 Suicide & Crisis Lifeline
- PL: 116 123 (Adults) | 116 111 (Youth)
- Emergency: 112 / 911
Presuicidal Syndrome and “Ominous Calm”
Ringel’s concept of presuicidal syndrome (1976) identifies three elements: progressive constriction of perspective, inhibited aggression turned inward, and increasing suicidal fantasies [4]. While useful as a clinical framework, this is not a prognostic test; the absence of one element does not guarantee safety, nor does the presence of all three make the act inevitable.
“Ominous calm” is a clinically observed phenomenon where a patient, after a period of intense agitation, suddenly appears calmer. This may signal that a decision has been made—but it could also reflect a genuine therapeutic effect. In the early stages of antidepressant treatment, when physical energy returns before hopelessness lifts, the risk of impulsive action can be temporarily elevated. The WHO emphasizes that direct contact and asking plainly about suicidal thoughts has a protective effect [5].
How to Talk About Suicidal Thoughts
A safe conversation is based on: creating a quiet and private environment, asking specific questions (“Are you having thoughts of ending your life?”, “Do you have a plan?”, “Do you have access to the means?”), listening attentively without moralizing, and offering real help. When risk is high, it is crucial to stay with the person and secure the environment (restricting access to medication, alcohol, etc.).
Self-Harm and NSSI (Non-Suicidal Self-Injury)
Non-suicidal self-injury is a consequence of depression heavily marked by stigma and misinterpretation. Labels like “just attention-seeking” lead to the trivialization of symptoms and delayed help. In literature, NSSI is described as an emotion regulation strategy: reducing tension by shifting psychological pain to physical pain, regaining control, or acting as a form of self-punishment [7].
A meta-analysis by Ye et al. (2022) found that the co-occurrence of NSSI and suicide attempts is approximately 9.6%, with significantly higher rates in clinical populations [8]. A history of self-harm is a documented risk factor for later suicidal behavior. Treatment includes Dialectical Behavior Therapy (DBT), cognitive psychotherapy, and pharmacotherapy for the underlying depression.
Addiction and Depression: The Neurobiology of a Vicious Cycle
Depression and Substance Use Disorders (SUD) rarely have a one-way relationship. Many individuals turn to alcohol or other substances as a form of “self-medication” to temporarily reduce tension. At a neurobiological level, chronic use leads to deeper mood dysregulation and intensified anhedonia. Alcohol addiction and depression create a loop of mutual reinforcement [9].
A meta-analysis by Conner et al. (2019) found that the odds of suicidal behavior are approximately three times higher in individuals with Alcohol Use Disorder (AUD) compared to those without [10]. Treatment should be integrated—addressing depression and addiction simultaneously. Delaying depression treatment “until sobriety is achieved” lowers the effectiveness of both interventions.
Depression and the Cardiovascular System
A meta-analysis by Krittanawong et al. (2023), involving 26 studies and nearly 2 million people, found that depression is associated with a significantly higher risk of: stroke (HR 1.13), heart attack (HR 1.28), heart failure (HR 1.04), and overall cardiovascular disease (HR 1.16) [13]. A more recent meta-analysis (2025) confirmed that the prevalence of depression among cardiac patients is 20.8%, with Mendelian randomization showing a bidirectional, causal link [21].
The Mechanisms:
- Autonomic: Reduced heart rate variability (HRV), elevated sympathetic tone.
- Inflammatory: Elevated pro-inflammatory cytokines (IL-6, TNF-a, CRP) promoting atherosclerosis.
- Behavioral: Lower physical activity, smoking, irregular diet, low medication adherence.
- Metabolic: Insulin resistance and dyslipidemia.
For Clinicians: Every cardiac patient should be routinely screened for depression (using PHQ-2/PHQ-9). Untreated depression is an independent risk factor for cardiovascular mortality.
Depression, the Immune System, and Inflammation
Depression is associated with increased concentrations of inflammatory markers confirmed in numerous meta-analyses. Scassellati et al. (2024) indicate that inflammation may actively contribute to the pathogenesis of depression and a poorer response to treatment in treatment-resistant groups [A1]. The neuroimmunological model by Nusslock et al. (2024) explains how pro-inflammatory cytokines—by activating microglia and altering the sensitivity of reward and threat circuits—generate dysphoria and anhedonia [A2].
The concept of “immunometabolic depression” (Lamers et al., 2025) suggests that 20–30% of patients exhibit a specific profile: atypical energy symptoms (hypersomnia, increased appetite, fatigue), low-grade systemic inflammation, and metabolic disturbances. This subgroup responds poorly to standard antidepressants [A3].
Depression shortens life expectancy by 15–20 years—primarily due to somatic diseases, not just suicide [8B].
Other Somatic Effects: Diabetes, Pain, and Longevity
Type 2 diabetes and depression share a bidirectional link: the risk of depression in diabetics is roughly doubled, and depression in diabetics is associated with poorer glycemic control and a higher risk of complications [A4]. Chronic pain is both a cause and a consequence of depression: Aaron et al. (2025) document it as a strong predictor of persistent depression [A5].
Depression lowers the pain threshold through disturbances in the central modulation of nociception—descending pain-inhibitory pathways dependent on serotonin and norepinephrine are weakened. Dual reuptake inhibitors (SNRIs like venlafaxine or duloxetine) are used in both depression and pain syndromes specifically because of this shared mechanism.
Effects on the Workplace: Absenteeism and Presenteeism
Evans-Lacko et al. (2016) found that the costs of presenteeism (working while unwell) related to depression are 5–10 times higher than the costs of absenteeism. Annual costs per employee reach $5,524 in the US [22]. Employees with depression lose about 20% of total working time—81% of this loss results from presenteeism [23].
A longitudinal study showed that individuals with major depression or dystymia have a 12–15% rate of new unemployment over 6 months, compared to 2% in the control group and 3% for rheumatoid arthritis [28]. Investing in workplace depression treatment yields a return of 4–5 euros for every 1 euro spent (OECD 2025).
Economic Impact: European and Global Data
- Europe: The annual cost of depression is approximately €118 billion (1% of European GDP). It is the most expensive mental disorder in Europe, accounting for 33% of the total costs of mental health disorders [4a].
- Global: Losses due to mental disorders totaled $4.7 trillion in 2019 (OECD 2025).
- USA: The societal cost of major depression is $334 billion annually (38% healthcare, 34% productivity loss, 24% household income loss) [6a].
Depression and Relationships: Marriage and Social Isolation
A multi-national study by Kessler et al. across 19 countries found that major depressive disorder is one of the three disorders with the largest population-level contribution to the risk of divorce (OR 1.2–1.8) [39].
A Canadian longitudinal study by Byrne et al. (2009) found that a depressive episode doubles the risk of a relationship moving toward separation or divorce [36]. Conversely, separation increases the risk of a subsequent depressive episode. Social isolation is both a risk factor and a result: anhedonia and fatigue make maintaining relationships nearly impossible, which in turn reduces access to protective support and intensifies feelings of worthlessness [A8].
Daily Life: Cognitive Function
Depression impairs executive functions: concentration, working memory, planning, and decision-making. Residual cognitive deficits are observed in a significant portion of patients even after successful pharmacological treatment, which can hinder the return to work or school.
The WHO estimates that depression accounts for 6% of the total disease burden in Europe measured in DALYs (Disability-Adjusted Life Years) [4a]—more than many serious physical illnesses.
Intergenerational Impact: Children of Parents with Depression
Parental depression is one of the most strongly documented risk factors for emotional disorders in children.
The Mechanisms:
- Biological: Prenatal cortisol exposure programs the child’s HPA axis.
- Relational: A depressed parent may be less emotionally responsive and make less eye contact.
- Environmental: Marital tension and family instability.
Children of depressed parents have a 2–4 times higher risk of developing depression themselves. Treating parental depression is an investment in the mental health of the next generation.
Summary: Table of the Effects of Depression
| Area | Main Effects | Key Data / Source |
| Suicide Risk | Most common disorder in suicide autopsies | 720k deaths/yr globally [1]; 4,845 in PL 2024 [3] |
| Self-Harm (NSSI) | Emotion regulation; risk factor for suicide | NSSI + Attempt co-occurrence: ~9.6% [8] |
| Addiction | Self-medication; vicious cycle | AUD = 3x higher suicide risk [10] |
| Heart Disease | Higher risk of MI (HR 1.28), stroke (HR 1.13) | Krittanawong et al., Am J Med 2023 [13] |
| Immune System | Elevated inflammation (IL-6, CRP); weak immunity | Scassellati 2024; Lamers 2025 [A1, A3] |
| Diabetes & Pain | 2x higher T2DM risk; lower pain threshold | Aaron et al., JAMA Net Open 2025 [A5] |
| Life Expectancy | Reduction by 15–20 years | EBC/PMC 2023 [8B] |
| Work: Absenteeism | 12–15% new unemployment in 6 months | PMC 2017 [28] |
| Work: Presenteeism | 5–10x costlier than absenteeism | Evans-Lacko et al. 2016 [22] |
| Economic Impact | €118 billion/yr in Europe (1% GDP) | Sobocki 2006 [4a]; OECD 2025 [6a] |
| Relationships | Doubles risk of separation/divorce | Kessler et al. [39]; Byrne 2009 [36] |
| Impact on Children | 2–4x higher depression risk for offspring | Hellyer et al. 2025 [11B] |
| Cognitive Function | Deficits in attention, memory, executive function | WHO DALY: 6% burden in Europe [4a] |
Bibliography and Sources
[1] WHO. Suicide – Fact sheet (2025). who.int/news-room/fact-sheets/detail/suicide
[2] Isometsä E.T. Suicides in Mood Disorders. Front. Psychiatry 2020.
[3] Sąd Rejonowy dla Warszawy-Woli. Prewencja samobójstw (dane Policji 2024).
[4] Ringel E. The presuicidal syndrome. Suicide Life Threat Behav. 1976.
[4a] Sobocki P. et al. Cost of Depression in Europe. J. Ment. Health Policy Econ. 2006;9(2):87–98.
[5] WHO. Preventing suicide: a resource for media professionals (2023).
[6] Ustawa z 19 sierpnia 1994 r. o ochronie zdrowia psychicznego.
[6a] OECD (2025). Mental Health Promotion and Prevention: Best Practices in Public Health.
[7] Halicka J. et al. Non-suicidal self-injury (NSSI) and suicidal (przegląd).
[8] Ye Z. et al. Meta-analysis of co-occurrence of NSSI and suicide attempt. Front. Psychiatry 2022.
[8B] Europejski Parlament. BRIEFING EPRS: Mental Health in the EU 2023.
[9] PsychDB. Substance/Medication-Induced Depressive Disorder (DSM-5).
[10] Conner K.R. et al. Suicidal Behavior: Links Between AUD and Alcohol. Curr. Opin. Psychol. 2019.
[11] Cucu A. et al. Cost of Depression in Romania. Int. J. Environ. Res. Public Health 2023.
[11B] Hellyer E. et al. Postpartum depression beyond 12 months. Wiley 2025.
[12] Favril L. et al. Risk factors for suicide: meta-analysis of psychological autopsies. EBMH 2022.
[13] Krittanawong C. et al. Association of Depression and CVD. Am. J. Med. 2023;136:881–895.
[21] Shen W. et al. CVD and depression: meta-analysis and Mendelian randomization. Mol. Psychiatry 2025.
[22] Evans-Lacko S. et al. Global workplace productivity and depression. Soc. Psychiatry 2016.
[23] Gopal S. et al. Work productivity loss among employees with depression. PMC/Psychiatr. Serv.
[28] Liao K. et al. Unemployment and depression. Psychiatr. Serv. PMC 2024.
[36] Byrne M. et al. Major depression and marital disruption is bidirectional. PubMed 2009.
[37/40] Torvik F.A. et al. Mental distress predicts divorce over 16 years: the HUNT study. BMC 2015.
[39] Kessler R.C. et al. Multinational study of mental disorders, marriage, and divorce. PMC 2011.
[A1] Scassellati C. et al. Inflammation and depression. Brain Behav. Immun. Health 2024.
[A2] Nusslock R. et al. Neuroimmune network model of depression. J. Child Psychol. Psychiatry 2024.
[A3] Lamers F. et al. Immuno-metabolic depression. Lancet Psychiatry/PMC 2025.
[A4] Frontiers in Public Health (2024). Depressive symptoms and life expectancy.
[A5] Aaron S.F. et al. Depression and chronic pain outcomes. JAMA Network Open 2025.
[A8] Li X. et al. Social isolation and depression risk. PMC 2023.
