Inflammation triggers chemical reactions in the body that can impact brain function and mood regulation. Studies have found that individuals with chronic inflammation are at a higher risk of developing depression.

Additionally, some people with depression show elevated levels of inflammatory markers in their blood. Recent scientific findings suggest that inflammatory molecules can disrupt the balance of neurotransmitters in the brain, such as serotonin and dopamine, which play a critical role in mood regulation.

Inflammation may also impair the growth and connectivity of brain cells, leading to changes in brain structure and function associated with depression. Monitoring your inflammatory markers can provide valuable insights into your health and potentially your mental well-being.

Convenient at-home lab tests for inflammation allow you to measure specific markers like C-reactive protein CRP or interleukin-6 IL-6 from the comfort of your home. Tracking these markers can help you measure underlying inflammation and make informed decisions about your well-being, including seeking appropriate treatment options.

Understanding and managing inflammation is crucial for promoting overall health. By adopting an anti-inflammatory lifestyle, such as consuming a balanced diet rich in fruits, vegetables, whole grains, and healthy fats, engaging in regular physical activity, managing stress effectively, and limiting exposure to toxins, you can help reduce chronic inflammation and potentially alleviate symptoms of depression.

Moreover, addressing inflammation not only might benefit your mental health but it may also lower the risk of developing chronic diseases such as cardiovascular conditions, diabetes, and autoimmune disorders. In conclusion, the surprising connection between inflammation and depression reveals an interplay between our physical and mental well-being.

For some people, chronic inflammation can contribute to the development or worsening of depression, emphasizing the importance of managing inflammation for mental health.

By adopting an anti-inflammatory lifestyle, including a balanced diet, regular exercise, stress management, and reducing exposure to toxins, individuals may be able to actively reduce chronic inflammation and potentially alleviate symptoms of depression. Monitoring inflammatory markers through at-home lab tests, allows for better understanding and personalized management of inflammation.

Recognizing the link between inflammation and depression empowers individuals to take proactive steps towards improved mental health and overall well-being. Hamzelou , J. Anti-inflammatory drugs can relieve symptoms of depression. Preidt , R. OCD May Be Linked to Inflammation in the Brain.

Salim , S. Inflammation in anxiety. Steinbaum , S. Inflammation Pictures for Women: Causes and Concerns With Pictures. Tynan , R. A comparative examination of the anti-inflammatory effects of SSRI and SNRI antidepressants on LPS stimulated microglia.

Weil , A. My interest in a DBH degree grew out of frustration and hope. On one hand, I grew frustrated with the quality of care my clients with intellectual and developmental disabilities were receiving. As members of a marginalized population who lack the skills to advocate for themselves, the clients I serve receive subpar medical care, mental health care, and behavioral health care.

On the other hand, as I learned more about the DBH program, a potential solution came into view. I believe this program will allow me to acquire the knowledge and skills to become a better advocate for my clients, and new job opportunities will open up in positions in which I will be able to make a bigger impact on a system level, thus improving quality of life for many clients.

A DBH degree will command interest and respect from other healthcare professionals who are evaluating their practices and noticing areas in which they are not being effective, namely the behavioral health side of the equation.

As we are learning in our first classes about the Biodyne Model, the Integrated Care Model is not widely accepted or known in the healthcare field, despite its proven track record.

I believe a DBH degree provides the necessary tool to change the landscape of healthcare provision by arming my passion for this topic with knowledge and concrete strategies.

As a Doctorate of Behavioral Health DBH student my vision for healthcare is to disrupt the current model, close gaps to care and create healthcare improvements. In the evolving world of healthcare I believe behavioral healthcare providers BCP are essential to the development of integrative healthcare.

Once I obtain a DBH degree, I know I will gain a leadership role and be able to add quality to the creation of integration efforts worldwide. I know I will graduate with the essential tools I need to stand at the forefront of integrated healthcare. I want to create healthcare improvements for marginalized populations that are typically underserved or forgotten.

As an individual of two minority groups; woman and African American, I am very passionate about helping reduce cultural, ethnic, social economic and geographic disparities within healthcare systems. Since beginning my studies at CGI, I have been awakened to how much I truly did not know and understand despite my specialty training in Social Work and behavioral health needs.

Services that I previously thought were quality and designed to meet the needs of special populations, I now believe to be woefully inadequate to serve the needs of the patients.

Patients cannot receive the best quality, efficient, and timely care they need and deserve within institutions that are not integrated. Institutions that continue to silo and do not encourage collaboration and integration are not focused on the needs of the patient.

I believe, as a DBH, I will disrupt the current healthcare system by promoting guaranteed health care for all as a right, not a privilege. I will advocate for a national , rather than state, licensing of providers.

This will allow clinicians medical , behavioral health , etc… to provide care across state lines using telem edicine. Finally, t he skills I have learned at Cummings Graduate Institute for Behavioral Health Studies allow me to identify healthcare delivery concerns , propose alternative interventions and cost — effective solutions and evaluate the ir return on investme nt.

I have always been proud of working in a hospital and delivering care, working as a multidisciplinary team member, and making a difference.

Preventative care can be part of service delivery from a hospital system; we should not rely only on public health programs to tackle social determinants of health. COVID is not only impacting mental health but also how we are delivering medical care. What does it all mean? Fortunately, the articles in this Special Report do an outstanding job of glossing our best current understandings, which are: What are these understandings?

There are plenty of other ways of getting depressed, or manic, or psychotic. Five Things to Know About Inflammation and Depression. Why Are Depressed Patients Inflamed? A New Path to Personalized Treatment in Psychiatry.

The author reports that he is a consultant for Novartis, Usona Institute, and Emory Healthcare. Wirtz PH1, von Känel R. Psychological stress, inflammation, and coronary heart disease. Curr Cardiol Rep. Miller AH1, Haroon E1, Felger JC1.

Therapeutic implications of brain-immune interactions: treatment in translation. Psychotherapy vs Pharmacotherapy for Depression in Heart Failure. Blue Light Blockers: A Behavior Therapy for Mania. The Week in Review: February Blue Light, Depression, and Bipolar Disorder.

The Week in Review: January February 2. Depression Research Roundup: February 2, Around the Practice. Between the Lines. Expert Perspectives. Case-Based Psych Perspectives.

Medical World News. Payer-Provider Perspective. Psychiatric Times. All Publications. Partner Perspectives. Job Board. Clinical Scales. Conference Coverage.

Psychological scientists have amassed a vast amount of empirical knowledge on the causes of and best treatments for mental disorders. Psychological scientists are leading the way in addressing the mental health issues resulting from traumatic events.

Chu University of Texas at Austin and colleagues wrote in a article. For example, in a study of 2, Singaporean adults ages 55 to 98 conducted by Rong Shi Shandong University and colleagues, participants had more ongoing symptoms of depression if their blood had higher levels of three proinflammatory cytokines: C-reactive protein CRP , interleukin-6 IL-6 , and tumor necrosis factor alpha TNF-α.

Blood levels of IL-6 and TNF-α also predicted which participants would become or still be depressed three and six years later. Until recently, most studies on inflammation and depression focused on between-person differences, allowing researchers to reach the conclusion that if one person has higher inflammation than another, they are likelier to have more symptoms of depression, Moriarity explained.

Now, studies that test within-person differences in inflammation are essential to understanding the causal relationship between inflammation and depression, as well as potential pathways for treatment.

The first of these studies, published in , focused on between-person differences in inflammation and depression. The researchers collected blood samples from American adolescents ages 12 to 20 years old at six points over a period of up to 31 months. While higher TNF-α levels predicted increased symptoms of depression at the next appointment for both males and females, higher IL-6 levels predicted increased depression in females, and higher IL-8 levels predicted decreased depression in males.

This suggests that sex-based differences in inflammatory responses could be part of the reason why females tend to experience higher rates of depression in adolescence, Moriarity and colleagues wrote in the Clinical Psychological Science article. Participants reported their depressive symptoms and had blood drawn at up to six appointments spaced approximately 1 year apart.

In this case, only TNF-α predicted depression. This could indicate that TNF-α is predictive of depression on a broader level, whereas other cytokines may be more closely related to specific symptoms or may require more time to build up in the body before influencing mental health outcomes, Moriarity and colleagues suggested.

Early adversity appears to be an important risk factor for increased inflammation because of how stress encourages unhealthy behaviors, according to Elizabeth B. Raposa University of California, Los Angeles and colleagues in a Psychological Science article.

The researchers explored this dynamic through a study of mother—child pairs who had previously participated in a longitudinal birth-cohort study in Queensland, Australia.

Raposa and colleagues then contacted the children again at 15, 20, and 21 years old to complete a survey about their depressive symptoms, health behaviors, and stress levels and later collected one blood sample from participants when they were 22 to 25 years old. By analyzing these data, the researchers found that adolescents raised in more adverse environments characterized by low income, harsh discipline, and parents reporting more mental health conditions, relationship conflict, and criminal behavior reported more symptoms of depression and chronic stress, were more likely to smoke, and had a higher body mass index BMI than adolescents raised in less stressful circumstances.

Related Research Topic: Childhood Adversity. Interestingly, research suggests that although early adversity may make people uniquely susceptible to social stress, people from low-income families may also be uniquely receptive to the buffering effects of social support. In a Psychological Science study , Neha A.

John-Henderson University of Pittsburgh and colleagues took salivary samples from 63 undergraduate students before and after they discussed a negative experience from their past with a confederate pretending to be another participant. The IL-6 levels in the saliva of students who described themselves as having grown up in households with higher socioeconomic status SES remained the same regardless of how interested or disinterested the confederate pretended to be in their story.

John-Henderson, N. Socioeconomic status and social support: Social support reduces inflammatory reactivity for individuals whose early-life socioeconomic status was low.

Psychological Science, 26 10 , — When the confederate behaved in a disinterested manner by refusing to make eye contact and sighing with boredom, the IL-6 levels of these students spiked.

Students from low- and high-SES backgrounds exhibited the same inflammatory response to a socially supportive confederate, but low-SES participants had significantly stronger IL-6 responses to the unsupportive and control conditions. People raised with access to more resources tend to think more independently, the researchers wrote, so it follows that they would be less sensitive to social support.

The exact relationship between social behavior and inflammation may differ across cultures. In a Psychological Science article , for example, APS Fellow and Past-President Shinobu Kitayama University of Michigan and colleagues compared how negative emotions influenced the health risk factors, including inflammation, of 1, American and Japanese adults.

Drawing on surveys about how each participant expressed and suppressed feelings of anger, Kitayama and colleagues found that Americans who expressed more anger had more health risks—including increased levels of IL-6 and CRP in addition to higher blood pressure and cholesterol—than their more serene peers.

This is consistent with the prevailing notion that anger is bad for your cardiovascular health, Kitayama explained to the Observer.

By contrast, Japanese participants who expressed anger more frequently had fewer health risk factors than those who did so less often. This could be because of differences in when anger is expressed across cultures, Kitayama and colleagues suggested.

In more individualist Western cultures like that in the United States, people with lower status, who generally have worse health outcomes, may be more likely to express anger in response to not being able to achieve their goals, the researchers explained.

In more interdependent cultures like that in Japan, on the other hand, anger is perceived as more socially disruptive and undesirable, meaning that only those with high social status, who have better health outcomes, can afford to express it. The social-signal-transduction theory of depression provides one explanation for how social stress contributes to a cycle of inflammation and increased risk of depression, Annelise A.

Madison The Ohio State University said in an interview with the Observer. Maintaining elevated levels of inflammation consumes a lot of metabolic resources, Madison continued, resulting in a number of symptoms of depression intended to help conserve energy, including anhedonia, hypersomnia, and low mood.

This dynamic was evident in a pair of Psychological Science studies Madison and colleagues conducted with 38 married couples and a group of 79 breast cancer survivors. In both cases, participants reported their symptoms of depression and stress levels and had their blood drawn before completing a stressful social task.

For the couples, the task entailed discussing an ongoing problem in their relationship; the breast cancer survivors were required to give a speech.

The researchers then took two additional blood samples from each participant over the next several hours. When the married couples returned for their second appointment, participants who reported experiencing more interpersonal stress in their daily lives and had a greater increase in IL-6 in response to the social-stress task during their first visit were more likely to report increased symptoms of depression at their second visit.

Similarly, all breast cancer survivors who reported receiving less social support in their daily lives during their first visit reported an increase in depression at their second appointment.

This was particularly pronounced among participants whose TNF-α levels increased more during the social-stress task. In a Psychological Science study of people with early-stage breast cancer, Andrew W. Manigault University of California, Los Angeles and colleagues found that participants with higher levels of CRP were more likely to become depressed over the month study period.

However, this was only true when they reported high levels of cancer-related stress and few psychosocial resources such as close social relationships, optimism, high self-esteem, mindfulness, and a sense of control over their lives with which to combat it.

When participants reported having more psychosocial resources to draw on, increased stress was less likely to increase their symptoms of depression, and the effects of inflammation on depression were also reduced. These and other psychosocial sources of resilience could help explain why many people do not become depressed in response to deeply stressful events.

They could also provide a path forward for people who do, Manigault and colleagues wrote. Inflammation and stress do appear to fuel a range of mental and physical maladies, but research on the mind—body connection suggests that the cycle can be broken. Feedback on this article?

Email apsobserver psychologicalscience. org or login to comment. Interested in writing for us? Read our contributor guidelines. Chu, A. Inflammation and depression: A public health perspective. Brain, Behavior, and Immunity , 95 , 1—3.

Psychological Science , 26 10 , — Kitayama, S. Expression of anger and ill health in two cultures: An examination of inflammation and cardiovascular risk.

Psychological Science , 26 2 , — Madison, A. Frequent interpersonal stress and inflammatory reactivity predict depressive-symptom increases: Two tests of the social-signal-transduction theory of depression. Psychological Science , 33 1 , — Manigault, A. Psychosocial resilience to inflammation-associated depression: A prospective study of breast-cancer survivors.

Psychological Science , 33 8 , — Moriarity, D. Bidirectional associations between inflammatory biomarkers and depressive symptoms in adolescents: Potential causal relationships. Clinical Psychological Science , 8 4 , — Inflammatory proteins predict change in depressive symptoms in male and female adolescents.

Clinical Psychological Science , 7 4 , — Raposa, E. A developmental pathway from early life stress to inflammation: The role of negative health behaviors. Psychological Science , 25 6 , — Shi, R. Psychoneuroendocrinology , , Article Shields, G.

Inflammation, self-regulation, and health: An immunologic model of self-regulatory failure. In the 21st century, however, it has become clear that they are deeply interconnected and talk to each other all the time.

Medical minds are now opening up to the idea that inflammation could be as widely and deeply implicated in brain and mind disorders as it is in bodily disorders.

Advances in treatment of multiple sclerosis have shown the way. Many of the new medicines for MS were designed and proven to protect patients from brain damage caused by their own immune systems.

The reasonably well-informed hope — and I emphasise those words at this stage — is that targeting brain inflammation could lead to breakthroughs in prevention and treatment of depression, dementia and psychosis on a par with the proven impact of immunological medicines for arthritis, cancer and MS.

Indeed, a drug originally licensed for multiple sclerosis is already being tried as a possible immune treatment for schizophrenia. Is that hope realistic for depression? It is beyond reasonable doubt that inflammation and depression are correlated with each other — or comorbid , to use some unlovable but important medical jargon.

The key scientific questions are about causation, not correlation. Does inflammation cause depression? And, if so, how? One experiment that scientists have designed to tackle these questions is to do two functional MRI brain scans, one before and one after an inflammatory response has been deliberately provoked by the injection of typhoid vaccine.

A recent meta-analysis reviewed data from 14 independent versions of this experiment. On average, the data showed a robust effect of inflammation on brain activity. These results confirmed that bodily inflammation can cause changes in how the brain works.

Encouragingly, they also localised the effect of inflammation to particular parts of the brain that were already known to be involved in depression and many other psychiatric disorders. If inflammation can cause depression then anti-inflammatory drugs should work as antidepressants.

Several studies have reviewed clinical trial data on thousands of patients treated with anti-inflammatory drugs for arthritis and other bodily disorders that are commonly associated with depressive symptoms. Overall, patients treated with anti-inflammatory drugs, rather than a placebo, had significantly improved mental health scores.

However, there is a caveat. The largest and most rigorous of these studies were designed to test drug effects on physical health and that makes it difficult to interpret the results too strongly as proof of beneficial effects on mental health.

The next step is to run studies designed from the outset to test new anti-inflammatory drugs as antidepressants, or to test existing antidepressants for anti-inflammatory effects. We should be looking for ways to match the choice of treatment to the cause of psychiatric symptoms on a more personalised basis.

And using blood tests to measure inflammation could help us to make those choices. For example, a consortium funded by the Wellcome Trust has just started a trial of a new anti-inflammatory drug for depression.

It is one of the first antidepressant trials ever to use blood tests to screen for inflammation in potential participants. If the blood tests show no evidence of inflammation then patients will not be recruited into the trial, because if they are not inflamed, there is no reason to think they will benefit from anti-inflammatory treatment.

An alternative example might be ketamine, a form of which has just been licensed in the UK for treatment of depression. In future, we might use blood tests or biomarkers of inflammation to predict which depressed people are most likely to benefit from ketamine.

The therapeutic scope of these new insights is potentially bigger than depression or drugs. There is also interest in the role of diet, obesity, stress, gum disease, the gut microbiome and other risk factors in low-grade inflammation that could be controlled without drugs.

There are now dozens of studies measuring the anti-inflammatory effects of psychological interventions, such as meditation or mindfulness, or lifestyle management programmes, diets or exercise regimes.