Hero

Videos

Slideshows

Articles

Podcasts

Poll

Dr Drew Ramsey discusses the role of diet and nutrition in brain and mental health, promising areas of nutrition, and the importance of evidence-based treatment with food. Good nutrition is not a contest between zucchini and medications.



 is assistant clinical professor of psychiatry at Columbia University College of Physicians & Surgeons. His clinical work focuses on the treatment of depression and anxiety with a combination of psychotherapy, diet and lifestyle modification, and psychopharmacology. From 2005 to 2008, he directed the Audubon Continuing Day Treatment Program, a bi-lingual service for the severely mentally ill located in the Washington Heights area of Manhattan; a program of New York State Psychiatric Institute/Columbia Psychiatry.



is a board-certified psychiatrist and assistant professor in Clinical Psychiatry at Columbia University Medical Center and the New York State Psychiatric Institute. She serves as the medical director and team psychiatrist at ONTrackNY Washington Heights Community Service clinic. She completed her public psychiatry fellowship and adult psychiatry residency at Columbia University where she was a chief resident and co-organized the curriculum on racial/ethnic mental health disparities. In addition to her clinical work in the public sector, she also works in Columbia's psychiatric emergency room and has a private practice in Upper Manhattan. 

 is a fellow in consultation-liaison psychiatry at Columbia University Irving Medical Center with a part time private practice. She was formerly a chief resident at Columbia’s psychiatry residency program. Before medical training, she received an MS in Narrative Medicine, an interdisciplinary field that studies illness through a humanities lens. She is co-author of 

Conquering Lyme Disease: Science Bridges the Great Divide

 and has interests in medical education, psychotherapy, and medical humanities.

Thanks to Columbia University Department of Psychiatry for allowing us to present the Breakthrough Session podcast with experts in the field of psychiatry.

In this podcast, Drew Ramsey, MD, an nutritional expert and psychiatrist discusses the importance of diet and nutrition in mental health and wellness.

A Conversation With Drew Ramsey, MD, on Nutrition and Mental Health

Helen Flanders Dunbar, MD, PhD, recognized as the originator of psychosomatic medicine, was a clinician, writer, founder of the 

 As if that were not enough, she spent her professional life promoting the role of clergy in medicine and exploring accident proneness. Her work was also essential to the development of consultation liaison psychiatry.

 Her father was a mathematician, engineer, and patent attorney; her mother a genealogist; and her brother Francis earned an masters degree in botany at Stanford University. She too received a remarkable education At Bryn Mawr and Columbia she majored in mathematics and psychology. She then went on to earn 4 advanced degrees in 7 years. She attended the Yale Medical School in medicine and obstetrics. She wrote a doctoral thesis on Dante at Columbia University, while graduating magna cum laude from nearby Union Theological Seminary.

Her Episcopalian faith was a guiding light in her life, and she believed it should inform her medical practice. She worked closely with Anton Boisen, a clergyman inpatient at Westboro Mental Hospital, who was convinced that religion and psychiatry needed to be connected on a professional level. Together they trained ministers to work in medical settings.

In 1929, Dunbar broadened her medical and spiritual horizons by traveling to Europe. She met leading psychiatric figures of the day and visited Lourdes, the world’s most famous healing shrine in France, which had a profound spiritual effect.

She legally changed her name to Flanders Dunbar in 1938.

 It seems astonishing today that an accomplished woman had to change her name in an attempt to overcome the prevailing misogyny.

From 1930 to 1942, Dunbar was the medical director of the Council for Clinical Training of Theological Students and director of the Joint Committee on Religion and Medicine. During this time, she earned the soubriquet of “mother of holistic medicine” with her 1935 publication of 

Emotions and Bodily Changes: A Survey of Literature on Psychosomatic Interrelationships: 1910-1933

. In 1939, she became the first editor of the journal 

American psychosomatic medicine started in the 1930s. According to this school of thought, illnesses arose from the physiological effects of emotional stimuli. It was thought that certain psychodynamic patterns created typical illnesses, known as 

 Repressed (and forgotten) emotions emerged from the unconscious to target certain organs, producing psychosomatic disorders. Somatic dysfunctions thus arose from the patients’ emotional problems, which led practitioners of psychosomatic medicine to search for psychological profiles characteristic of specific syndromes. This expanded further to the belief that many diseases were psychogenic in origin and stressors, albeit undefined. Dunbar believed that having accidents was similar to the process by which other patients transformed psychological conflicts into somatic symptoms.

 Their personality styles and neuroses translated into 

After 1939, Dunbar gave up academic commitments, drank heavily, alienated followers, and left the American Psychosomatic Society. On August 22, 1959, the publication day of her landmark book 

“A magnetic, charismatic woman with a disturbed and beautiful soul and an almost magical gift of insight and intuition,” said her daughter Marcia Dunbar Soule.

It is difficult to put it any better, only to reflect that the passage of time may vindicate the views Dunbar held.

The Exceptional Brain and How it Changed the World

. He is Clinical Associate Professor at the Graduate School of Medicine, Wollongong University and Research Fellow, History Department, Stellenbosch University, South Africa.

He is writing a biography of Helen Flanders Dunbar.

1. Ozarin L. A psychiatric pioneer remembered

. March 3, 2006. Accessed February 16, 2021.

2. Kemp HV. Biography of Helen Flanders Dunbar (1902-1959). 

https://www.apadivisions.org/division-35/about/heritage/helen-dunbar-biography

4. Powell RC. Emotionally, soulfully, spiritually ‘free to think and act’: the Helen Flanders Dunbar (1902–59) memorial lecture on psychosomatic medicine and pastoral care. 

5. Marcia Dunbar-Soule Dobson. Quoted in Stokes GA Dunbar, Helen Flanders. In: Sicherman B, Green CH, eds. 

Notable American Women: The Modern Period

. Harvard University Press; 1980: 210-212.

The rise and fall of a brilliant medical pioneer. 

Helen Flanders Dunbar: The Mother of Psychosomatic Medicine

A manic episode is a psychiatric condition characterized by the presence of elevated, expansive, or irritable mood; grandiosity; increased goal-directed activity; risk-taking behaviors; pressured speech; decreased need for sleep; racing thoughts; and distractibility. Most commonly, manic episodes occur because of an underlying primary bipolar disorder. However, manic episodes can occur as a result of multiple other causes, including general medical conditions, substance abuse, and medication side effects. One medication that has been hypothesized to precipitate manic episodes is the chemotherapy agent methotrexate.

Methotrexate is used in the treatment of multiple forms of 

 through folate antagonism; it is also used to treat multiple autoimmune conditions.

 Although there is very limited literature describing an association between methotrexate and the occurrence of manic episodes, there have been reported cases of manic episodes in patients with stable bipolar disorder following the administration of methotrexate.

 To date, however, there have been no reported cases of manic episodes precipitated by methotrexate in patients without an existing diagnosis of bipolar disorder.

This case report demonstrates the acute onset of mania in a patient with no history of 

, which putatively was precipitated by the use of intrathecal methotrexate in the treatment of acute lymphoblastic leukemia.

“Charlie” is an adolescent patient with a prior psychiatric history of attention-deficit/hyperactivity disorder (ADHD) and a medical history of acute lymphocytic leukemia (ALL). He had no prior history of affective or psychotic disorders. Family history was significant for depression in a maternal aunt, but there was no family history of bipolar disorder or psychosis. After the patient was diagnosed with high-risk ALL, he was started on induction chemotherapy. He completed a course of prednisone treatment and received a second dose of intrathecal methotrexate (IT MTX) a few days prior to presentation.

At that time, Charlie presented to the hospital with several days history of altered mental status in the form of irritability, elevated mood, poor sleep, pressured speech, grandiosity, 

Upon admission, computed tomography (CT) head without contrast, magnetic resonance imaging (MRI) brain with and without contrast, magnetic resonance angiography (MRA) head without contrast, and magnetic resonance venography (MRV) head with and without contrast were all unremarkable. Awake electroencephalogram (EEG) was normal. Labs including anti- hyroperoxidase (TPO), thyroid peroxidase antibody, paraneoplastic antibody panel, autoimmune encephalopathy panel, and N-methyl-D-aspartate (NMDA) receptor antibody (CSF and serum) were negative. Ammonia, ceruloplasmin, Vitamin B12, TSH, and T4 were normal.

After being evaluated by the psychiatric consult liaison (C-L) team, Charlie was started on olanzapine, which was titrated to 10 mg BID for treatment of acute manic and psychotic symptoms. During the following days, Charlie remained disorganized and delusional, so olanzapine was changed to haloperidol 1 mg BID. The next few days he was reported to be doing marginally better, with improved 

 and less pressured speech, though remained somewhat disorganized and delusional.

On day 9 of admission, Charlie received third IT MTX treatment. On the following day, he was very restless, making bizarre hand movements, pacing around the room, with pressured speech and tangential thoughts, and remained hyper-religious with delusions of grandeur. Following reassessment by the C-L team, he was started on sodium valproate and quetiapine in addition to haloperidol 1 mg BID. Total daily doses of sodium valproate and quetiapine were gradually titrated up to 1250 mg and 350 mg, respectively. Charlie could not tolerate further increases in quetiapine beyond 350 mg daily due to excessive sedation, and haloperidol was discontinued due to prolonged QTc. Lorazepam 1 mg TID was added for management of agitation and irritability.

During the following days, Charlie’s sleep started to improve with periods of lucid thoughts. He gradually became much calmer and redirectable, although remained occasionally delusional. As his mental status started to improve, quetiapine was decreased to 300 mg daily and lorazepam was decreased to 0.5 mg in the evening. Sodium valproate was continued at 1250 mg daily.

On day 16, Charlie received a fourth scheduled IT MTX treatment, with deterioration of mental status by the following day. He was noted to have more disorganized speech and delusional thoughts. Quetiapine was gradually titrated to 700 mg daily while sodium valproate was kept at 1250 mg daily.

Charlie showed marked improvement in mental status over the next few days of treatment, with less pressured speech and less disorganization. He continued to have tangential and racing thoughts but with much less intensity. Following stabilization, Charlie was discharged to home on a medication regimen that consisted of sodium valproate 1250 mg daily, quetiapine 700 mg daily, and lorazepam 0.5 mg TID.

After discharge, Charlie was followed by the psychiatric C-L team during outpatient visits to the Hem/Onc clinic. Five days after discharge, his thought process and behavior were noted to be much more organized. He continued to have some delusional thinking but was able to interact and engage in daily activities. Due to complaints of tiredness and increased sleep during the daytime, quetiapine was decreased to 500 mg daily and lorazepam was discontinued. Sodium valproate was continued at 1250 mg daily.

Twelve days following discharge, Charlie received fifth and last IT MTX treatment as scheduled. Six days after that, he was readmitted with acute manic and psychotic symptoms similar to the first admission. Following evaluation by psychiatry, Charlie was continued on sodium valproate 1250 mg daily, and quetiapine was increased to 600 mg daily. Due to elevated valproic acid (113.4 ug/mL, ref range 50-100 mcg/mL) and ammonia (97 umol/ L, ref range 11-32 umol/ L) levels, sodium valproate was subsequently decreased to 750 mg daily. During the following days, his behavior and mental status started to improve. After 6 days of hospitalization, the patient was discharged home on quetiapine 600 mg daily and sodium valproate 750 mg daily.

Seven days later, the patient presented at the outpatient clinic with markedly improved mental status and overall functioning. Sodium valproate 750 mg daily and quetiapine 500 mg daily were continued.

Given that Charlie presented with 4 episodes of severe manic symptoms with psychotic features after administration of intrathecal MTX, a causal association was assumed between the intrathecal MTX and development of these symptoms. After significant discussions between psychiatry and hem/onc, the decision was made to switch ALL treatment from IT MTX to intrathecal cytarabine/hydrocortisone (IT ARAC/HCZ) with oral MTX.

As a result, Charlie continued to present psychiatrically stable with no acute affective or 

. Psychotropic medications were gradually tapered off until they were discontinued 3 months after discharge. As per chart review, he remained psychiatrically stable over the next 2 years.

It is worth noting that Charlie received steroids in addition to IT MTX before the onset of first manic episode. No steroids, however, were given in combination with IT MTX prior to subsequent episodes. When treatment was switched to intrathecal steroid (IT ARAC/HCZ) with oral methotrexate, he remained psychiatrically stable with no further manic episodes reported.

In children with acute lymphoblastic leukemia, the addition of methotrexate to treatment protocols has been found to be beneficial in preventing central nervous system relapse.

 Methotrexate is a folate antagonist that is used for treating a variety of medical conditions including psoriasis, rheumatoid arthritis, and other 

Methotrexate inhibits dihydrofolate reductase (DHFR), the enzyme that reduces folic acid to tetrahydrofolic acid.

 The inhibition of DHFR by folate antagonists (methotrexate) results in a deficiency in the cellular pools of thymidylate and purines, and thus a decrease in nucleic acid synthesis. Therefore, methotrexate interferes with DNA synthesis, repair, and cellular replication. It also markedly interferes with transmethylation reactions, which are crucial for the formation of proteins, lipids, and also myelin, presumably leading to demyelination of nervous tissues.

Few mechanisms of precipitation of manic symptoms by methotrexate have been hypothesized. One possible cause is the interference of folate metabolism, as folic acid is used in the body to manufacture serotonin and dopamine neurotransmitters. Other postulations include interference in glutaminergic neurotransmission (increased release in glutamate and aspartate) by high levels of homocysteine and sulfur-containing amino acids, which is caused by the interference in folate metabolism.

 Glutaminergic neurotransmission is implicated in the pathophysiology of bipolar affective disorder and some studies report patients with manic episodes show elevated glutamate and glutamine.

Cytotoxic agents including methotrexate are potent neurotoxins. Although neurotoxicity has been observed with high dose oral or intrathecal methotrexate, to date there have been no published reports in the literature in which methotrexate precipitated a 

 in a patient with no prior history of bipolar disorder.

There are multiple drugs that are implicated in the development of manic symptoms, including antidepressants, steroids, levodopa, amphetamine, and phencyclidine, but methotrexate is not commonly implicated.

 In Charlie’s case, the contingency of the symptoms on methotrexate use and improvement on withdrawal of the drug and treatment of the manic episode suggest a causal relationship. 

ADHD has been genetically linked to bipolar disorder,

 and that may offer an explanation, at least in theory, about why this particular patient was more vulnerable to developing manic episodes.

In cases where mania is thought to be precipitated by IT MTX, we would recommend using an alternative medication or route of administration in addition to the use of psychotropic medications to manage the acute manic symptoms as appropriate.

To our knowledge, this is the first case report of acute onset mania in a patient with no prior personal or family history of bipolar disorder during IT MTX. It adds to the limited literature of methotrexate-induced mania in patients with previously stable bipolar disorder. Collectively, these reports contribute to the poorly understood relationship between bipolar disorder and treatment with cytotoxic agents, such as methotrexate.

is a child and adolescent psychiatrist, as well as an adjunct clinical assistant professor of psychiatry at Indiana University School of Medicine.

is an assistant professor at Emory University School of Medicine and is the Program Director for Emory’s Child and Adolescent Psychiatry Fellowship Program.

is the medical director for the psychiatry consultation-liaison service for Children’s Healthcare of Atlanta and adjunct assistant professor at Emory University School of Medicine.

is an assistant professor at Emory University School of Medicine.

1. Bedford Laboratories. Methotrexate for injection prescribing information. 2012. 

https://docs.boehringer-ingelheim.com/Prescribing%20Information/PIs/Ben%20Venue_Bedford%20Labs/55390-031-10%20MTX%2050MG/5539003110

2. Hariram J, Jegan Y. Contribution of methotrexate in precipitation of manic episode in bipolar affective disorder explored: a case report. 

3. Bührer C, Henze G, Hofmann J, et al. Central nervous system relapse prevention in 1165 standard-risk children with acute lymphoblastic leukemia in five BFM trials. 

4. Raimondi MV, Randazzo O, La Franca M, et al. DHFR inhibitors: reading the past for discovering novel anticancer agents. 

5. Vezmar S, Becker A, Bode U, Jaehde U. Biochemical and clinical aspects of methotrexate neurotoxicity. 

6. Sanacora G, Rothman DL, Mason G, Krystal JH. Clinical studies implementing glutamate neurotransmission in mood disorders. 

7. Michael N, Erfurth A, Ohrmann P, et al. Acute mania is accompanied by elevated glutamate/glutamine levels within the left dorsolateral prefrontal cortex. 

8. Ongür D, Jensen JE, Prescot AP, et al. Abnormal glutamatergic neurotransmission and neuronal-glial interactions in acute mania. 

9. Gigante AD, Bond DJ, Lafer B, et al. Brain glutamate levels measured by magnetic resonance spectroscopy in patients with bipolar disorder: a meta-analysis. 

10. Preda A, Shapiro B, Bienenfeld D. Substance-induced mood disorder. 

https://emedicine.medscape.com/article/286885-overview

11. Osser DN. ADHD in patients with bipolar disorder: genetics, diagnosis, and treatment. 

https://www.psychiatrictimes.com/view/adhd-bipolar-genetics-diagnosis-treatment

A case report and literature review of intrathecal methotrexate-induced mania.

 Can This Cancer Treatment Cause Manic Episodes?

Treating depression in the context of any other medical disorder can challenge our usual approaches and frustrate our efforts to reach good outcomes. Not surprisingly, this is especially true for patients with depression and 

 (CHD). For example, how should we screen for CHD risks in our patients with recurrent depression? Does it matter which came first, the depression or the heart disease? What is next for patients who do not respond to the second or third antidepressant trial? How does relapse prevention for depression in patients with CHD differ from relapse prevention in those with depression alone?

Psychiatric epidemiology over the past 10 years has given us some useful guideposts for approaching patients with comorbid depression and CHD.

 Psychosocial factors, especially recurrent depressive symptoms, severe mental illness, and high numbers of adverse childhood experiences, contribute substantially to both the onset and progression of CHD.

 is as strong as that of the traditional CHD risk factors, such as 

 Since there is no single cause of CHD, it is helpful to consider psychosocial risk factors among the many contributing influences that determine the course of CHD. The more effectively these psychosocial factors are managed, the fewer hurdles patients will face.

The large number of psychosocial risk factors for CHD represent the 

 of autonomic imbalance, hypothalamic-pituitary-adrenal axis dysregulation, and/or low grade inflammation.

 Each of these pathways reflects chronic dysregulation of the stress response system.

 High risk health behaviors common in depression, such as 

, physical inactivity, and high-carbohydrate diets, add to this dysregulation process.

 Effective treatment of depression in patients at risk for CHD includes reducing these early indicators of metabolic syndrome.

Patients with depression and elevated cardiac risk factors can often be 

 in their 30s and 40s, a prime opportunity for preventive interventions in the context of depression treatment and relapse prevention.

, psychiatrists can play an essential role, offering both early identification of CHD risks and behavioral interventions for CHD risk reduction.

The most robust psychosocial interventions for CHD are intensive lifestyle medicine programs

 Psychiatrists can motivate patients with depression to engage in and sustain these behavior changes.

summarizes the pathways by which depression leads to adverse cardiac outcomes, and it suggests a framework for approaching common dilemmas in assessment and treatment.

“Norma,” a 34-year-old single Black woman comes to see you after her third panic attack on the job as a high school history teacher. She is most concerned about the cat calls and notes passed around by 3 senior athletes insinuating she is gay, which she finds threatening and humiliating. She scores 18 on the Patient Health Questionnaire-9 (PHQ 9). Her history reveals at least 2 other episodes of depression lasting several months at ages 18 and 23, both of which resolved without treatment.

Psychiatrists should consider these important questions as they move forward with such a case (

 More digging may illuminate underlying and complicating issues that need to be consider to develop a successful treatment plan.

 The interrelationship and how one disorder impacts the other is an important consideration in understanding the issues at hand and implementing a treatment plan.

The preceding questions should lead to this important query. Based on the issues uncovered, it should become obvious which 

 symptoms should be monitored to ensure a successful outcome.

Do we keep treatment simple, ie, treat her with sertraline, and see what happens? Or do we dig and look for potential complications? Norma’s blood pressure is 135/90, and her resting heart rate is 88, both of which she attributes to her being nervous about the appointment. Further probing reveals she has had high blood pressure readings at 2 gynecology visits for birth control pills in the past 2 years, but it has never been addressed. Her BMI is 29, and her mother developed 

 at age 46. A metabolic panel ordered at your first visit confirms she has high low-density lipoprotein and, therefore, metabolic syndrome (3 of 5 risk factors for CHD).

On her second visit, you press Norma to return to her gynecologist or establish a relationship with a primary care clinician. In addition to a trial of 

, you devote some of each monthly appointment to helping her understand how untreated depression accelerates the development of common risk factors for heart disease. At first, she is alarmed. But eventually Norma is motivated to walk to work instead of riding the bus and give up sweetened drinks, 2 behavior changes that are good for her limbic system as well as her heart.

In most individuals the age of onset for depression appears to precede the age of onset for CHD by about 30 years. But Norma’s case reminds us that the underlying processes for each illness may begin much closer in time for many individuals. These 2 illnesses, recurrent depression and CHD, may be 

 by shared genetic vulnerabilities to stress.

 The bidirectional relationship between depression and CHD—each illness raises the risks for the other—means that we should always suspect that in a given patient the occurrence of 1 illness may accelerate the development of the other. It is also safe to assume that effective treatment of either illness facilitates the treatment or prevention of the other illness. For psychiatrists, this translates into the necessity of effective collaborations with primary care clinicians and cardiologists. It is easier to reverse the course of cardiac risk factors when treated early, compared to reversing them after the first heart attack.

Systematic symptom monitoring for depression is especially helpful in the context of physical illnesses symptoms that overlap with depressive symptoms. Serial assessments of depressive symptoms with a PHQ-9 or similar measure improves the efficiency of antidepressant treatment trials. It also charts the relationship between depressive symptoms and the target physical measures of CHD. For example, effective treatment of Norma’s panic attacks and depression may reduce her resting heart rate and her need for antihypertensive medication, or it may not. Serial monitoring of both targets is the most efficient way to establish the relationship between these dimensions of the 2 illnesses.

Choosing a treatment option can be guided by a few considerations, such as previous responses, side effects, and genetic drug 

 profiles. In the absence of any evidence pointing to or from a specific strategy, the serotonin reuptake inhibitors (SSRIs) sertraline and 

 have the broadest research base from clinical trials of antidepressants in patients with CHD, are well tolerated, and have the fewest clinically relevant drug interactions.

 There is also some evidence that SSRIs may provide a protective anti-inflammatory effect in patients with major depression.

 Serotonin-norepinephrine reuptake inhibitors (

) are second tier choices only because of their smaller research base. The atypical antidepressant mirtazapine carries a heavier risk for metabolic burden, while bupropion may be a first choice for patients who smoke or those who need to avoid potential sexual side effects. Tricyclic antidepressants, because of their lethality in overdose, should be reserved for patients with malabsorption, since blood levels in tricyclics follow a linear dose-response relationship. Their use requires attention to the potential risks of arrhythmias and postural hypotension.

Two areas of drug interactions between antidepressants and CHD medications deserve consideration for special monitoring: anticoagulation and arrhythmias. In some patients, SSRIs may augment the effects of anticoagulants in a clinically significant way. International Normalized Ratio (INR) monitoring provides the best way to adjust the proper doses of both sets of medications. In a similar way, SSRIs may prolong the 

 (QTc) in a clinically significant way for some patients on antiarrhythmic medications. Citalopram carries a black box warning about its potential for QTc prolongation. Regular electrocardiogram monitoring provides the standard measure for adjusting these doses or determining when a medication switch is necessary.

Studies of response rates to standard antidepressant treatment trials of both medications and psychotherapies have shown mixed results.15 Psychiatrists can expect to see a disproportionate number of nonresponders and partial responders referred by primary care physicians and cardiologists. Here is where a familiarity with standard approaches to 

 can serve us well. After revisiting the accuracy of our 2 primary diagnoses (major depression and CHD), it helps to scour the terrain for any missed comorbid diagnoses, medical or psychiatric, that could undermine the current treatment efforts. On the psychiatric side of the street, the most commonly missed comorbid conditions include attention-deficit/hyperactivity disorder, anxiety disorders, and substance use disorders. On the medical side, unrecognized or inadequately managed chronic pain and sleep disorders are common disrupters of treatment efforts. Effective management of these comorbid conditions often turns a partial responder into a full responder to antidepressant treatments.

The role of daily self-management plans in the treatment of complex comorbid disorders is often overlooked by psychiatrists. For example, exercise has been shown to be as effective for the treatment of major depression as 

 yet formal exercise regimens are not a common element of treatment plans for patients with depression. Careful attention to structured, daily self-management plans that address both the depression and the CHD can often turn a partial responder into a responder within months. The intensity of the self-management plan needed to achieve a remission of the depression may require a care manager or a health coach in the early stages of exploring what works and sustaining the habit of practicing the plan.

For almost all patients with complex comorbid chronic disorders, many of whom only partially respond to initial treatments, combined treatment plans that include a course of psychotherapy, care management, and stepped care focused on achieving remission from depression is an investment that brings returns for many years.

The relief and sense of emancipation that comes with 

 invites patient and psychiatrist alike to count our victories and overlook the risks for relapse. Although we have achieved our primary goal of relieving suffering, it is also important to prevent future suffering, and there is no better time to prevent relapse than in the wake of a depressive episode. Given that the risks of recurrence for depression are magnified by CHD, and the consequences of a recurrence are more severe when the management of CHD is undermined by a depressive episode, the stakes are high to prevent a relapse in the months and years that follow a recovery from depression. Relapse prevention plans are essential, not extra, especially for patients with comorbid CHD.

Effective relapse prevention plans should include a list of maintenance treatment plans,

, a monitoring measure, and predetermined early steps to respond to warning signs. This information should be shared in writing with the patient and the relevant clinicians, and documented in the patient’s chart. Periodic check-ins, if only through brief phone appointments at 6- or 12-month intervals, can verify those plans that are working, and identify those that are not.

Treating depression in people with CHD can be tricky and pose complicated dilemmas. It is reassuring to remember that, in spite of all the dilemmas, guidelines to treat these patients boil down to a simple maxim: what is good for the brain is good for the heart.

is professor emeritus of psychiatry and family medicine in the Department of Psychiatry and Behavioral Neuroscience and Department of Family and Community Medicine at the University of Cincinnati.

is a research fellow in psychiatry in the Department of Psychiatry at Massachusetts General Hospital.

1. Rosengren A, Hawken S, Ounpuu S, et al. 

Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): case-control study

2. Galatzer-Levy IR, Bonanno GA. Optimism and death: predicting the course and consequences of depression trajectories in response to heart attack. 

3. Thayer JF, Yamamoto SS, Brosschot JF. 

The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors

4. Wulsin L, Herman J, Thayer JF. Stress, autonomic imbalance, and the prediction of metabolic risk: a model and a proposal for research. 

5. Huffman JC, Celano CM, Beach SR, et al. Depression and cardiac disease: epidemiology, mechanisms, and diagnosis. 

Insights into causal pathways for ischemic heart disease: adverse childhood experiences study

7. Brown DW, Balluz LS, Heath GW, et al. Associations between recommended levels of physical activity and health-related quality of life. Findings from the 2001 Behavioral Risk Factor Surveillance System (BRFSS) survey. 

8. Weissman MM, Pilowsky DJ, Wickramaratne PJ, et al. Remissions in maternal depression and child psychopathology: a STAR*D-child report. 

9. Jagannathan R, Patel SA, Ali MK, Narayan KMV. 

Global updates on cardiovascular disease mortality trends and attribution of traditional risk factors

10. Silberman A, Banthia R, Estay IS, et al. The effectiveness and efficacy of an intensive cardiac rehabilitation program in 24 sites. 

11. Razavi M, Fournier S, Shepard DS, et al. Effects of lifestyle modification programs on cardiac risk factors. 

12. McCaffery JM, Frasure-Smith N, Dubé MP, et al. 

Common genetic vulnerability to depressive symptoms and coronary artery disease: a review and development of candidate genes related to inflammation and serotonin

13. Sun Q, Townsend MK, Okereke OI, et al. Physical activity at midlife in relation to successful survival in women at age 70 years or older. 

14. Lachman ME, Teshale S, Agrigoroaei S. Midlife as a pivotal period in the life course: balancing growth and decline at the crossroads of youth and old age. 

15. Zambrano J, Celano CM, Januzzi JL, et al. Psychiatric and psychological interventions for depression in patients with heart disease: a scoping review. 

16. Wang L, Wang R, Liu L, et al. Effects of SSRIs on peripheral inflammatory markers in patients with major depressive disorder: a systematic review and meta-analysis. 

17. Marshall JB, Forker AD. Cardiovascular effects of tricyclic antidepressant drugs: therapeutic usage, overdose, and management of complications. 

18. Blumenthal JA, Smith PJ, Hoffman BM. Is exercise a viable treatment for depression? 

How does relapse prevention for depression in patients with coronary heart disease differ from relapse prevention in those with depression alone? That question and more answered.

Treatment Dilemmas in Depression and Coronary Heart Disease

In 2018 the United States National Survey on Drug Use and Health estimated that 164.8 million individuals aged 12 or older (60.2% of the US population) were 

 Of those 164.8 million, 139.8 million individuals drank alcohol, 58.8 million used a tobacco product, and 31.9 million used an illicit drug.

 Furthermore, the data reveals that 1 in 5 (~19.4%) individuals aged 12 and older took an illicit drug in the last year.

More granular examinations reveal that illicit drug activity was primarily driven by marijuana/cannabis use, with 43.5 million past-year users. The second most commonly used illicit drug was prescription pain relievers, often opioid-based, misused by 3.6 million individuals aged 12 years or older.

 Given widespread substance abuse, it is critical to be aware of both the cardiovascular risks that these substances pose and the challenges associated with managing cardiovascular complications.

World-wide, alcohol abuse is estimated to be 1 of the 4 most common, non-communicable diseases that is both 

 The widespread use of alcohol can be attributed to the globalization of its production and marketing, and its relative ease of access. Often, moderate alcohol consumption has been thought to lower risk of cardiovascular and all-cause mortality. The culmination of data suggests a half- to 1-standard drink (7 to14 grams pure ethanol) per day for women and 1 to 2 standard drinks for men (14 to 28 grams pure ethanol) can lead to roughly an 17-18% reduction in all-cause mortality.

 However, there are reasons to be skeptical of this data. Lower-risk drinkers may appear healthier than abstainers due to the fact that the abstainers are not drinking due to pre-existing medical conditions or disease(s) caused by prior excessive alcohol use. When adjusting for these factors, it appears the benefit may dissipate.

 The association between excessive drinking and various forms of cardiovascular disease is well defined, and an increased death rate has been observed with consumption of 2.5 drink/day in women or 4 drink/day in men.

The cardiovascular complications of alcohol can be divided into acute and chronic effects (

). It is also important to be aware many individuals who use alcohol abuse other substances and have additional risk factors that contribute to cardiovascular disease (

 The potential mechanism leading to hypertension include endothelial dysfunction, vasoconstriction, sympathetic activation, and activation of the renin-angiotensin-aldosterone system (RAAS). Furthermore, alcohol use may contribute to secondary causes of hypertension, including sleep apnea and renal atrophy.

 A multi-national meta-analysis has demonstrated a linear relationship between alcohol consumption and hypertension, with a risk factor that is 1.7 times higher with use of 50 grams/daily, and 2.5 times higher at 100 grams/daily.

 Management options include abstinence and use of RAAS inhibitors.1 In fact, blood pressure reductions of 7.2mmHg has been seen with up to 1 month of abstinence.

Binge drinking and/or heavy alcohol consumption has been linked to the development of a variety of acute cardiac arrhythmias, with atrial fibrillation (AF) being the most common.

 Mechanistically, alcohol may lead to direct autonomic effects as well as atrial remodeling overtime. In addition, as with hypertension, alcohol impacts other secondary risk factors for AF like obesity, electrolyte abnormalities, or sleep apnea.

 The key means of AF prevention is reducing or limiting alcohol consumption, but if AF occurs, the risk/benefit of anticoagulation should be considered. The adoption of a rate or rhythm control strategy should be considered too.

Regular, heavy alcohol use can lead to alcoholic cardiomyopathy (ACM), which accounts for 33% of all cases of non-ischemic cardiomyopathy, characterized by dilation and impaired contraction of 1 or both ventricles.

 The free radical generation accompanying alcohol use, along with activation of the RAAS and sympathetic nervous system, is thought to lead to ACM. After abstinence, patients who develop ACM and subsequent heart failure with reduced ejection fraction should be managed with guideline director medical therapy, including RAAS inhibitors, beta-blockers, and diuretics.

Cannabis, or marijuana, is increasingly used both recreationally and therapeutically 

 Particularly, the major chemical compounds excreting these effects are D-9-tetrahydrocannabinol (THC) and cannabidiol (CBD). While the benefits of cannabis are numerous, few of them are cardiovascular-related, and cannabis’ true risk to the cardiovascular system is poorly understood. In terms of adverse cardiovascular consequences, THC appears to impart most of the negative impact, but larger and longer-term outcomes are lacking.

 Mechanistically, THC stimulates the sympathetic nervous system while concurrently inhibiting the parasympathetic nervous system, leading to increased heart rate and elevated blood pressure, which effects myocardial oxygen demand (

). Furthermore, it appears THC can lead to platelet activation and overtime associated endothelial dysfunction and oxidative stress. In addition, impurities in cannabis products can induce or exacerbate these effects.

Given this cardiovascular milieu, it is prudent to understand the short- and long-term outcomes; however, this collection of existing outcomes data is limited to due to its short-term nature. It is observational and retrospective, and it suffers from recall bias, lack of exposure determination, and the given age of the data may not reflect 

Some commonly used drugs and narcotics have serious cardiovascular effects.

Psychosomatics

A Conversation With Drew Ramsey, MD, on Nutrition and Mental Health

Helen Flanders Dunbar: The Mother of Psychosomatic Medicine

Can This Cancer Treatment Cause Manic Episodes?

Treatment Dilemmas in Depression and Coronary Heart Disease

The Cardiovascular Consequences of Drug Use

The ABCs of Cardiac Screening and Electrocardiography

Positivism and Heart Health: Issues for Psychiatrists

Recognize and Treat Traumatic Brain Injury

Understanding the QTc

Care of Youth Hospitalized With Somatic Symptom and Related Disorders