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Mental health stigma remains a serious barrier to care, especially among Hispanic Americans. They may come to psychiatrists only after their illnesses are quite advanced and have seriously affected their functionality.

In this mental health minute, Agdel J. Hernandez-Colon, MD, talks about the challenges psychiatrists may face as they treat this underserved population. He offers advice on how to build a strong therapeutic alliance and provide culturally sensitive mental health education.

is the chairman of the department of psychiatry at Nuvance Health and its Residency Program Director.

How do you provide culturally sensitive care? 

Share comments with your colleagues by emailing 

. Comments may be shared online pending review and editing for style.

Seasonal Affective Disorder in Minority Populations

Blue light is getting blamed for everything from eye strain to cancer lately, but what does it do to our patients with depression and bipolar disorder. A lot, as you will see in this podcast, but it depends on what time of day it is shining.

, the Voice of Psychiatry. With thoughtful insights into the world of mental health, this podcast provides timely clinical commentary and practical cutting-edge pearls for you and your practice. We hope you enjoy.

I am Chris Aiken, the Mood Disorders Section Editor for 

, and I am Kellie Newsome, a psychiatric NP and the cohost of the 

: The biological clock is set by the daily rhythms of light and dark – morning sunrise and evening sunset. And this clock is so integral to bipolar disorder that you could almost rename it 

. Actually, patients prefer that name over bipolar disorder, and it gets to the heart of the problem. Bipolar is tightly linked to the genes that regulate the biological clock, and lithium actually 

 the clock by altering the expression of those genes.1 Many of the behavioral therapies for bipolar disorder, like dark therapy and social rhythm therapy, also work through the biological clock, helping patients to keep it running smoothly by regulating their exposure to light, darkness, and the timing of daily activities.

But bipolar is not the only mental illness that is linked to disrupted circadian rhythms. 

 is as well, though to a lesser extent – for example, rates of circadian rhythm disorders like the phase-delay night owl syndrome are more common in bipolar and unipolar, but they are about 20% less common in unipolar. And research is exploring circadian rhythm therapies in 

But while researching is advancing in the circadian direction, society is moving the other way. Indoor living and nocturnal light are dampening the natural signals that set the biological clock, and there is evidence that this is causing harm in our patients. In this podcast, we will explore those dangers, but first a little background on how light – and in particular blue light – set the biological clock.

 Light suppresses melatonin, but not just any light. It is the color that matters here, and blue light in the 460-480 nm range is particularly good at suppressing melatonin and promoting wakefulness. In the 1990s, a new photoreceptor called melanopsin was discovered that only responds to blue light, and it is this receptor that regulates melatonin production through the suprachiasmatic nucleus, the time-keeper of the biological clock.

What that means is that the body’s internal clock depends on strong shifts in blue-spectrum light at the bookends of the day: morning and night. High levels of evening blue light, and low levels in the morning, disrupt not just circadian rhythms but also the clock genes implicated in bipolar and other psychiatric disorders.

The main source of that blue light are electronic gadgets that were not available 20 years ago. Smart phones, LED screens, and energy-efficient bulbs emit a blue haze of light that is very different from the yellow starlight that we evolved under. This light may look white, like fluorescent bulbs, but white light has a lot of the blue wavelength within it. Distance also matters here. A cell phone close to your face emits about as much blue light as a large screen TV across the living room.

: The problem is not just psychiatric. Blue light is associated with physical health risks including obesity, diabetes, cancer, cardiovascular and neurologic diseases, gastrointestinal ulcers, and adverse reproductive outcomes.

 The American Medical Association released a 

 calling for reductions in nocturnal blue light, and psychiatry is catching on as well. The American Academy of Child and Adolescent Psychiatry updated their 

 in 2018. They no longer recommend night lights for anxious children and instead emphasize elimination of blue-light sources in the bedroom. Child psychiatrists in Canada have even 

: It is the young and old that are most vulnerable to these light changes, as we will see in the research here.

 But they are also the patients who are more likely to sleep with some lights on. So, if your patient needs a light at night – whether because of a childhood phobia or a fall risk – they can purchase amber nightlights that do not emit the blue wavelength.

: Psychiatric patients in general are more sensitive to the circadian disrupting effects of evening blue light, particularly patients with bipolar disorder. Melatonin is delayed, diminished, and more easily suppressed by blue light in these patients.

 Circadian disruptions often trigger new episodes of mania and depression, such as shift work, seasonal changes, and travel across multiple time zones.

: Travel across time zones is only a problem with air travel, because the clock has time to adjust when you travel by land or sea unless you are driving at 300 miles per hour. And on average it only causes problems when patients travel across 2 or more time zones. Mania is more common with west to east travel, and depression more likely when travelling east to west. A simple rhyme can help you remember it – west is depressed – because travelling westbound can trigger depression.

: We can add nocturnal blue light and ambient bedroom light to that list of circadian disruptors. Evening use of smartphones delays and reduces melatonin secretion, and impairs sleep and cognition with a medium effect size (0.5), which means the effect should be noticeable to the casual observer.

 A viscous cycle is at play here, as evening-types (night owls) have a greater tendency to use electronics at night, and that use independently shifts circadian rhythms toward the evening type (phase delay).

 The evening chronotype is prominent in adolescents, and being a night owl is a risk factor for bipolar disorder, depression, and substance abuse.

Ambient bedroom light is also a problem, as it passes through the eyelids and suppresses melatonin during sleep. In controlled animal studies, ambient nocturnal light causes depression, impedes learning, and has detrimental effects on the brain. It lowers BDNF and shortens the dendritic spines that are essential for learning and cognition.

The circadian system is also involved in critical periods of brain development, and disruptions of light signals may play a role in the onset of psychiatric illnesses as well as their exacerbation.

 When mice are exposed to nocturnal dim light as infants, they grow up to have more anxiety as adults.

 Human studies have found a strong link between rapid flux of 

A study from Japan illustrates the problem for our patients.15 They followed 863 older adults for several years, carefully measuring how much light they were exposed to in their bedrooms. On follow up, the risk of depression was directly correlated with how much light they were exposed to in their bedrooms. Those who slept in pitch darkness had the lowest risk, but what is interesting is how little light was necessary to accomplish the shift: 5 lux – which is equivalent to a night light – was the cut off. Those who slept with at least 5 lux in their bedroom had double the risk of depression 2 years later.

That study was not controlled, although they attempted to control for confounders that might otherwise explain the association. But buried in the discussion was a sentence that struck me. The authors believed that the health risks of evening light are so well documented in animal and epidemiologic human studies that a controlled trial would be unethical in humans. In other words, we already know too much to learn anymore.

Instead, it is time for action, to educate our patients to follow the natural flow of day and night. That means bright light in the morning, low levels of blue light in the evening, and pitch dark in the bedroom. Those steps are not easy to follow in the modern world, and in a future podcast we will review new technologies that can ease those changes.

, and you can also catch us every Monday on the 

is the Mood Disorders Section Editor for 

 He has written several books on mood disorders, most recently

 with his cohost Kellie Newsome, PMH-NP. The author does not accept honoraria from pharmaceutical companies but receives royalties from PESI for

and is also a practicing psychiatric mental health nurse practitioner in Winston Salem, NC, at the Mood Treatment Center. Raised in Tasmania, Australia, Kellie moved to the United States in 1998.

Lithium and bipolar disorder: Impacts from molecular to behavioural circadian rhythms.

2. Charrier A, Olliac B, Roubertoux P, et al. 

Clock genes and altered sleep-wake rhythms: their role in the development of psychiatric disorders.

Suicide attempts in children and adolescents: The place of clock genes and early rhythm dysfunction.

Health consequences of electric lighting practices in the modern world: A report on the National Toxicology Program's workshop on shift work at night, artificial light at night, and circadian disruption.

Disruption of adolescents' circadian clock: The vicious circle of media use, exposure to light at night, sleep loss and risk behaviors.

The bipolarity of light and dark: A review on bipolar disorder and circadian cycles.

Circadian rhythm in bipolar disorder: A review of the literature.

Effects of smartphone use with and without blue light at night in healthy adults: A randomized, double-blind, cross-over, placebo-controlled comparison.

Outdoor light at night (LAN) is correlated with eveningness in adolescents.

10. Kivelä L, Papadopoulos MR, Antypa N. 

11. Bedrosian TA, Vaughn CA, Galan A, et al. 

Nocturnal light exposure impairs affective responses in a wavelength-dependent manner.

Clock genes control cortical critical period timing.

13. Borniger JC, McHenry ZD, Abi Salloum BA, et al. 

Exposure to dim light at night during early development increases adult anxiety-like responses.

Solar insolation in springtime influences age of onset of bipolar I disorder.

Bedroom light exposure at night and the incidence of depressive symptoms: a longitudinal study of the heijo-kyo cohort.

Blue light is associated with a host of physical health maladies, including obesity, diabetes, and cancer. But what does it do to patients with depression or bipolar disorder? 

Blue Light, Depression, and Bipolar Disorder

 Lamotrigine was launched for bipolar disorder in 2003, but it was a quiet launch, and since then a few myths have gathered around it as if to fill that vacuum. Today, we will address 4 of them.

, the voice of psychiatry. With thoughtful insights into the world of mental health, this podcast provides timely clinical commentary and practical cutting-edge pearls for you and your practice. We hope you enjoy it.

 On June 20, 2003, the world had its eyes on the United States’ invasion of Iraq. Some of us were following Martha Stewart’s indictment for insider trading, and quite a few were lining up at bookstores to be the first to buy the 5th installment in the Harry Potter series. But Russell Katz, MD, was busy at his desk on this day at the US Food and Drug Administration (FDA) headquarters, writing a letter to GlaxoSmithKline announcing the approval of their anticonvulsant lamotrigine in bipolar disorder. But the approval was not a slam-dunk. GlaxoSmithKline had submitted 12 trials, and only 2 of them were positive. Lamotrigine did not work in acute mania; it did not work in acute bipolar depression; and it did not work in rapid cycling.

But bipolar disorder (BD) is a chronic condition, and that is where the medication succeeded: in the maintenance phase.

The 2 positive studies looked at lamotrigine in the long term, over 1 and a half years. There, lamotrigine helped patients stay well about twice as long as a placebo.

 Katz knew that long-term studies like this were expensive and hard to come by, but for patients who have to stay on a mood stabilizer year after year it is this kind of data that matters most. So he gave it an indication for delaying new episodes of depression, hypomania, and mania in BD.

 And that is how lamotrigine was launched. But there are a lot of loose threads in that story that have tangled into myths, and today we are going to unravel 4 of them so you can use lamotrigine more effectively in practice.

 But first a warning. Lamotrigine is not a panacea. It works in BD, but it does not treat non-bipolar depression. There the studies are mixed: half positive, half negative. It has positive controlled trials in obsessive compulsive disorder, borderline personality disorder, and depersonalization disorder, but those studies are few and small.

 So do not start prescribing lamotrigine to every moody individual you see, because this medicine has one big risk that makes those uncharted adventures unwise: the potentially fatal rash of Stevens Johnson Syndrome.

That rash is part of the reason that lamotrigine had such a soft launch. Early on, the manufacturer decided not to market lamotrigine to primary care practices, and to minimize direct to consumer advertising. The decision may have hurt their quarterly profits, but it helped them stay in the market. You see, lamotrigine was nearly yanked off the market after its launch in epilepsy 10 years earlier. Back then, doctors were starting the drug at 100mg a day, which lead to an alarming rise in potentially fatal Stevens Johnson rashes. The medication only survived when the company was able to show that it could lower this risk through the slow titrations that we use today. Now that risk is around 1 in 3000.

GlaxoSmithKline was concerned that if they overhyped the drug, then clinicians with little experience in BD would prescribe it to every moody patient they saw, and if they overlooked the DSM in that way they might also overlook the titration instructions, causing a second flare of serious rashes that would cause the FDA to pull the plug again.

 And now let us get into those myths. There are 4 of them.

Myth #2: Lamotrigine does not treat acute episodes of bipolar depression

Myth #3: Lamotrigine is a weak mood stabilizer

Myth #4: It is a good idea to stop lamotrigine when a patient relapses, because it is probably not working

 This one is kind of true. Lamotrigine failed in the acute mania trials, and nothing that we have learned about this drug in the 25 years since suggests that it has any role in acute mania. But lamotrigine does help prevent mania, although it is better at preventing bipolar depression than it is at preventing mania. What that means in practice is that you should not rely on it as the sole maintenance medication in patients with a history of severe mania, but it may be used as monotherapy in bipolar II disorder, where the depressions are more common and the manic symptoms brief and mild.

In fact, many bipolar experts see good results in cyclothymic patients, who cycle frequently between mild depression, hypomania, and mixed states. That observation only supported by open-label studies, but hey – there are zero controlled medication trials in cyclothymic disorder so that is as good as it gets.

Myth #2: Lamotrigine Does Treat Acute Episodes of Bipolar Depression

 Among the 12 trials on Katz’s desk, 5 of them are good candidates for the most disappointing trials in the history of psychiatry. These were the 5 controlled trials in acute bipolar depression, all funded by the manufacturer, and all of them failed. The trials were never published, but most psychiatrists knew about them when lamotrigine was released, and it gave some of us the impression that lamotrigine was a weak mood stabilizer that barely got approved for an indication that was not at the top of the list for doctors or patients.

But we have since learned that lamotrigine does treat acute depression, it just takes a little longer than faster options like the atypical antipsychotics. The problem is that the early studies only lasted 7 weeks, and lamotrigine requires a slow titration that takes 4 to 6 weeks to reach a therapeutic level. Later, lamotrigine did prove efficacious for acute bipolar depression in 2 independently funded randomized placebo-controlled trials.

 Wait a minute. You are saying the industry sponsored trials were all negative but the independent ones were positive? That is a first.

 Yes, and the difference is that the independently sponsored trials gave lamotrigine a little more time. They lasted 8 to 12 weeks instead of 7 weeks. Also, lamotrigine was used as augmentation in these trials – in 1 it augmented lithium and the other quetiapine – but I think lamotrigine can work as monotherapy in acute depression and the real difference here was the timespan.

 One reason we think it works as monotherapy is that John Geddes, MD, FRCPsych, Joseph Calabrese, MD, and Guy Goodwin, DPhil, reanalyzed the original 5 negative trials in an independently funded meta-analysis.

 They found that there was a positive signal in the original studies, but they were too small to detect it. When combined together, totaling 1072 participants, lamotrigine had a small effect, bringing about a meaningful response in 1 out of 11 participants. But hey, cariprazine got FDA approval in bipolar depression with the same number needed to treat, and lamotrigine’s efficacy only starts to build at that 7-week mark. If you use lamotrigine for acute depression, you will probably need to wait about a month and a half to see an effect, and, judging from the longer trials, those benefits are likely to keep building over the next 1 to 4 months.

A common strategy then is to start lamotrigine with a faster-acting agent like an atypical antipsychotic, and then slowly taper off the antipsychotic as lamotrigine starts to kick in. This gives you the best of both worlds: lamotrigine has excellent tolerability over the long term, with a low risk of weight gain, fatigue, cognitive problems, sexual dysfunction, or any of the long-term medical problems that show up in the warnings for antipsychotics.

 One risk we do not think about enough is stroke. Stroke is the #1 cause of death in bipolar disorder, and lamotrigine and lithium are the only mood stabilizers that do not increase the risk of stroke; all the others have some marks against them there.

 I am going to get on a soap box for a minute here and argue that bipolar is not a mental disorder. It’s a physical disorder, and not just because the brain is a physical organ. Heart disease starts 10 to 15 years earlier in individuals with BD, and you can even detect cardiovascular changes in teens with bipolar. Lifestyle may play a part, but I think about all that adrenaline pumping through the veins during mania and mixed states. This is a whole-body illness, and we ought to be thinking about long-term morbidity and mortality when choosing a mood stabilizer, not just relieving acute symptoms.

 is often criticized for promoting biological psychiatry through its black-box, symptom check-list approach. But to me, it is not biological enough. You could read the whole book and walk away with little sense that these mental illnesses are wrecking havoc on the heart, the gastrointestinal tract, the immunologic and neuroendocrine systems. You would never get that sense from reading Harrison’s textbook of internal medicine.

Myth #3: Lamotrigine Is a Weak Mood Stabilizer

 Yes, and that segues back to another myth about lamotrigine, which is that treatments that are slow to act are not strong ones. This is not how chronic diseases are approached in other medical specialties, which naturally take a long-term, disease-modifying view. You will never see a diabetes study that looks at change on a symptom check-list over 4 weeks. Or take hypertension. Clonidine lowers blood pressure right away, but most physicians prefer a thiazide for hypertension because it lowers the long-term risks of morbidity and mortality.

Individuals with bipolar disorder die 10 years earlier on average, and not from suicide. Kellie, can you read the top causes of death in bipolar disorder

Chronic obstructive pulmonary disease (COPD)

 Right, so if you can find a mood stabilizer that reduces those risks, or at least does not increase them, that is golden. Lamotrigine is neutral on all of them, and 

 most of them. Specifically, lithium lowers the risk of heart disease, 

 But we are getting a bit ahead of ourselves here. I mean, long-term medical risks are important when considering a mood stabilizer, but we also want something that prevents the episodes. Here we have an interesting finding from studies that have compared lithium and lamotrigine.

 Lithium offers better prevention against the manic side, while lamotrigine works better against the depressive side, so combining the 2 makes sense. And one study did that – the LamLit trial – and confirmed that there are indeed additional benefits to combining the 2.

 And that is the long-term perspective that we need to take when choosing a mood stabilizer. This does not come naturally in psychiatry. If you work in a hospital, insurance is pressuring you to get the patient better quickly, so lamotrigine is not going to be your go-to agent. And if you work in an outpatient office, ask yourself: When was the last time a patient came in saying “I’d like a medication to prevent bipolar disorder”? In psychiatry, we treat suffering, and our patients want something that will work quickly.

Myth #4: It Is a Good Idea to Stop Lamotrigine When a Patient Relapses, Because It Is Probably not Working

 In the maintenance trials, lamotrigine delayed the time to a new episode by 197 days, about half a year, vs 86 days or 3 months for placebo. So it is about twice as effective as placebo, but it does not provide 100% protection (no mood stabilizer does). In practice, here is what I tell patients when starting it:

Lamotrigine’s going to have a slow build because you have to raise it slowly to prevent a serious rash. That means you’re going to feel better gradually over the next 1 to 2 months, but on the other hand you are not likely to have many side effects or medicated feelings. And that is a good thing because you are likely to need something long term to prevent mood problems, and this one does not have any major long-term risks. But keep in mind it is not going to prevent all mood episodes, but it will cut the rate of those episodes in half. So instead of having depression, say, every year, it may be every 2 years. But no medication does everything, and there is a lot you can do to raise those odds of success.

Then I talk about behavioral strategies for bipolar and depression. If you are interested in that, we have a separate podcast for patients that teaches these strategies. Search for 

 A common mistake is to stop lamotrigine when an episode returns, which is a bit like stopping blood pressure and cholesterol medications because a patient had a heart attack. Lamotrigine’s most robust effects are in prevention, and prevention is difficult to measure in psychiatry. You would need a before-and-after mood chart to confirm that the medication is lowering the frequency of episodes as it promises to do. Even then the work is difficult because so many other factors can make mood better or worse. What I look for is improvement in the first 3 to 6 months after starting lamotrigine. If a patient stops it, I watch for worsening over the next 3 to 6 months. And I also listen for something that I have heard a lot of patients say on this medication, particularly those with the frequent ups and downs of cyclothymic disorder.

 They say they still feel the same about whatever problems they were having in life, but the feelings are less overwhelming. They see things in perspective better. And that matches up with what we see in neuroimaging studies of lamotrigine. The 

 is less reactive to emotionally disturbing images, there is a rise in brain-strengthening 

 in the amygdala and frontal lobes. Overall, there are volumetric changes in 

, which react to emotional events, and the frontal lobes, which temper those emotions and help individuals see things in perspective.

 That sounds like something we could all use.

Hold it there! This medication is not for everyone, and those imaging studies were done in individuals with bipolar disorder.

 Always on your soapbox. We will be back with more practical updates on

is the Mood Disorders Section Editor for Psychiatric Times

1. Goodwin GM, Bowden CL, Calabrese JR, et al. 

A pooled analysis of 2 placebo-controlled 18-month trials of lamotrigine and lithium maintenance in bipolar I disorder.

Rechallenge with lamotrigine after a rash: a prospective case series and review of the literature.

4. Manning JS, Haykal RF, Connor PD, et al. 

Sustained remission with lamotrigine augmentation or monotherapy in female resistant depressives with mixed cyclothymic-dysthymic temperament.

5. Goldberg JF, Bowden CL, Calabrese JR. 

Six-month prospective life charting of mood symptoms with lamotrigine monotherapy versus placebo in rapid cycling bipolar disorder.

6. van der Loos ML, Mulder PG, Hartong EG, et al. 

Efficacy and safety of lamotrigine as add-on treatment to lithium in bipolar depression: a multicenter, double-blind, placebo-controlled trial.

7. Geddes JR, Gardiner A, Rendell J, et al. 

Comparative evaluation of quetiapine plus lamotrigine combination versus quetiapine monotherapy (and folic acid versus placebo) in bipolar depression (CEQUEL): a 2 × 2 factorial randomised trial.

Lamotrigine for treatment of bipolar depression: independent meta-analysis and meta-regression of individual patient data from five randomised trials.

Mood stabilisers and risk of stroke in bipolar disorder.

A deep dive into the history, side effects, and efficacy of a controversial drug. 

Four Myths About Lamotrigine

The first patient has been dosed in the second part of Seelos Therapeutics’ registrational study of their formulation of intranasal racemic ketamine (SLS-002) for acute suicidal ideation and behavior (ASIB) in patients with major depressive disorder (MDD).

“There is a significant unmet need within the MDD market for pharmacotherapies that can demonstrate rapid antidepressant effects, in particular for patients with severe MDD requiring hospitalization including those with ASIB. In part 1 of the study, SLS-002 showed significant improvement in depressive symptoms at 24 hours compared to placebo,” said Philippa Salter, Neurology Analyst at GlobalData.

If approved, SLS-002 would become the second product approved specifically for ASIB. The first product, Johnson & Johnson’s rapid-acting esketamine (Spravato), was approved for moderate-to-severe MDD patients with ASIB in 2020. Due to risk of sedation and disassociation, Spravato is only available through a restricted program.

“Although Spravato was a breakthrough treatment for ASIB, its high cost of therapy, and requirement for 2 hours of patient observation after administration will also limit its uptake,” Salter continued. “As a related compound, and with the same intranasal route of administration, it is possible that SLS-002 will face similar issues to Spravato. However, in a small, randomized trial intranasal ketamine caused minimal dissociative effects, which, if replicated in larger trials, would give SLS-002 an advantage over Spravato.”

Several fast-acting antidepressants are looking to enter the market, including the following late-stage products: Sage Therapeutics/Biogen’s 

. While these products are not specifically in development for ASIB, if they demonstrate strong efficacy for MDD, a label expansion could be sought in the future.

1. GlobalData. Seelos Therapeutics’ SLS-002 could be a strong competitior to Spravato for treatment of suicidal behavior, says GlobalData. News release. July 13, 2021. Accessed July 16, 2021. 

https://www.globaldata.com/seelos-therapeutics-sls-002-strong-competitior-spravato-treatment-suicidal-behavior-says-globaldata/

If approved, SLS-002 would be only the second approved product for ASIB. 

New Treatment for Acute Suicidal Ideation and Behavior

June is National Men’s Health Month, a good time to consider the unique mental health needs of men. In this edition of 

, Jonathan E. Alpert, MD, PhD discusses mood disorders and the surprising symptoms that male patients may present.

In this conversation, Alpert also covers:

1. The etiology of major depressive disorder in men and women

2. Common comorbidities to depression among men

3. How to build a therapeutic alliance with men and encourage adherence

4. Effective pharmacological and psychotherapeutic interventions for men and women

5. Future directions for scientific research on mood disorders, including their connections to autoimmune, cardiac, and thyroid conditions.

is the Dorothy and Marty Silverman Chair in in the department of Psychiatry and Behavioral Science, and professor of psychiatry, neuroscience, and pediatrics at Montefiore Medical Center and Albert Einstein College of Medicine.

Although depression is more prevalent among women, it may be more challenging to diagnose in men. This National Men’s Health Month, learn to recognize male depression’s symptoms and catch its comorbidities.  

What Makes Men’s Depression Different? 

is the Theodore J. Castele Professor of the History of Medicine and Associate Director of the Program in Medicine, Society, and Culture at Case Western Reserve University, Cleveland, Ohio. He holds secondary appointments in the Departments of Bioethics and Psychiatry. He earned degrees in history from Wesleyan (BA), Stanford (MA), and Johns Hopkins University (PhD); he also studied psychiatric epidemiology at Columbia University. He is the author of

 Imperial Bedlam: Institutions of Madness and Colonialism in Southwest Nigeria 

 Electroconvulsive Therapy in America: The Anatomy of a Medical Controversy 

 The Empire of Depression: A New History 

(Polity Books; 2020). His articles have appeared in journals including the

 Journal of the History of Medicine and Allied Sciences, Harvard Review of Psychiatry, Bulletin of the History of Medicine

Dr Sadowsky is a leading historian of psychiatry, and one I am proud to call him my teacher. As a psychiatry resident, I attended his lectures on history of psychiatry as part of our residency didactics and benefitted greatly from them. Sadowsky was 

 in 2017 by Greg Eghigian, PhD, about his book, 

Electroconvulsive Therapy in America: The Anatomy of a Medical Controversy

, an interview that is well worth revisiting. The present interview is about his new book 

. I admire Sadowsky for his ability to tackle complex and controversial issues with scholarly rigor and fair-minded appraisal, and I am delighted to have him participate in this series.

: I suppose some folks, on hearing the title of your new book, may reflexively think, “What…another book about depression? Don’t we have enough of those already?” In your opinion, why was a new history of depression needed?

: Interestingly, not many of the books about depression are histories. Take 

The Noonday Demon: An Atlas of Depression 

 I think it is great, but it has only a single chapter on history, and it is a brief account. In addition, with a few exceptions, most of the history books are focused on antidepressants, but many other treatments have important histories—psychodynamic psychotherapy, cognitive behavioral therapy (CBT), electroconvulsive therapy (ECT), and the many approaches that were taken prior to the 20th century, for example.

A couple of long, detailed histories of depression barely mention ECT. This is weird. I know 

—my book about ECT is also about that controversy. However, whatever you think about ECT, many psychiatrists consider it among the best treatments psychiatry has for serious affective disorder. Imagine for a moment a medical historian in another specialty writing a long history of a particular ailment, and then only briefly noting a treatment many doctors say is among the most effective! Previous histories of depression have also been a bit weak on psychoanalysis, which is a strong interest of mine.

Little existing historiography of depression focused on patient experiences and self-representations. This is not an easy area to research, because a lot of depression treatment takes place in private office practice, a confidential setting, and documentation is not really publicly available. I would have liked to do more, but I hope I pushed the field a little in that direction. I want to add immediately that some historical and other critical studies of psychiatry see patient voices as only a way to criticize psychiatry. It is important to document patient complaints, but some critics of psychiatry go to tortuous lengths to deny any therapeutic benefits. Honoring patient voices also means seeing that many feel helped by treatment.

I also wanted to draw attention to the politics of inequality. Like so many other illnesses, depression hits different populations to different extents. Solomon drew attention to this, but most of the historical work on depression restricts inquiry to the gender ratio, which is an important axis, but not the only one. Class, 

 status, for example, also matter for depression, and I hope future historians will develop this further.

Finally, I wanted to make the story more global, less focused entirely on the West, and especially the United States, although I do give the United States a lot of attention. Anthropologists and global mental health workers have looked at the wider world, but historians really have not done so for depression. I would like to have gone further here, too, and I hope others will.

: What I love about your book is that it does not settle for easy answers. It embraces the uncertainty, ambiguity, contradictions, and flux inherent in the very subject matter. One of the difficulties with studying depression is it’s a fluid entity, with variations across both time and space. Is depression the same today as it was in the 17th century when Robert Burton wrote 

? Is depression the same thing in the United States and, say, Nigeria? These are obviously thorny issues. Can you elaborate on the approach you take to address this? How can we tell a coherent history of something if we are having a hard time pinning down what that something is?

: The various illness categories—or, as it may be in some contexts, conceptions that are not illness categories—are already included in a long-running discussion of the comparability of diagnostic categories and sickness experience across time and space. The discussion is a story itself.

Most of the illness states I compare have a core feature, which is excessive sadness or blue mood, in whatever that particular context considers excessive. But some definitions of depressive illness consider this a common, but not necessary, feature for diagnosis. As you know, DSM-5 does not require depressed mood as a necessary criterion for major depressive disorder (MDD), provided there is loss of interest and 4 other symptoms. I draw (lightly) on the concept of family resemblances Ludwig Wittgenstein, PhD: Things do not need precise overlaps to have similarities that justify 

 For all the imperfections of the DSM, I think if you look at the menu of symptoms for MDD, they do form a constellation of related signs of suffering that have been clumped together in disparate contexts.

Overemphasizing cultural differences has its own risks. I show in chapter 1 the idea that African societies had little or no depression had roots in some frankly racist ideas. Universalizing labels can be a form of cultural imperialism, but overinsistence on difference forecloses possibilities for meaningful comparisons. And some who think depression is a purely modern or Western illness might be surprised at how many cultures, across time and space, have had some conception of excessive sadness as a malady.

Chiara Thuminger, PhD, is a great historian of madness with whom I am collaborating on a new project.

She has set forth 4 principles for comparisons 

1. The human mind is biological, a part of a shared evolutionary heritage, so you can expect some measure of universality.

2. The mind and mental life are not confined to the brain, but involve other parts of the body.

3. Mind and brain are situated in and shaped by culture, so universality will always be limited.

4. Every individual has an irreducible quality, uniqueness.

I think these are great principles to keep in mind.

: You are clearly dissatisfied with a lot of popular critiques of depression. You write, “One thing this book is not is a long lament on the overdiagnosis of depression, and the turning of life’s normal suffering into a medical problem.” Tell us more about your dissatisfaction with this line of criticism.

: Many people look at the high numbers of individuals with a depression diagnosis compared with previous times and take it as self-evident that we are overdiagnosing. It is not. Rising diagnosis rates is a valid reason for concern about overdiagnosis, but it is not proof. In 1950, much of psychiatry was concerned that we were underdiagnosing depression, so from that perspective, we may be finding a lot that we had been missing. We should at least consider the upside: More diagnosis means that more individuals who could use professional help are getting it.

As for medicating the normal pain of living, we should keep in mind that getting treatment for depression, whether in psychotherapy or with antidepressants, does not protect anyone from suffering, although one hopes it is reduced. Life remains hard. And many patients with depression welcome sadness as a relief from feelings of deadness or numbness inside.

In the book, I offer some defense of antidepressants against their most severe critics. But I also think we are probably overreliant on antidepressants. I think the benefits of psychotherapy, particularly long-term insight-oriented therapy, have become underrated in the antidepressant era.

Still, why some advocates of psychotherapy are so adamantly and categorically opposed to any medication use, or to any suggestion of a biological component to depression, is a mystery to me. I have read many hardline critiques of biological and pharmaceutical psychiatry that are focused on whether the evidence for efficacy is robust, or questioning the philosophical underpinnings of the enterprise, or worried about adverse effects, or indicting the pharmaceutical industry. The thoughtful challenges have reinforced my view that we are overreliant on drugs, at least for some populations. Other critiques have struck me as dogma masquerading as critique. But even the smartest of them have not convinced me that antidepressants are worthless, a claim several important voices have made.

The biology of depression is incompletely known, and much of it may remain permanently elusive. However, the idea that depression is purely psychological is, I think, implausible. Yet, so is the view that depression is purely biological. The dichotomy itself is the problem. Mark Solms, PhD, said that mind and brain are 2 ways of looking at the same thing. I find this more helpful. I do not understand how something could affect either the mind or the brain independently of the other. That is not a coherent idea.

I am getting away from your question a little, but it is an important point. Proponents of a life history emphasis in etiology sometimes take it as self-evident that if trauma or neglect is the cause, the better solution must be psychotherapeutic, as opposed to somatic. Psychotherapy might be the better treatment, but it is not self-evident just from the etiology. And the reverse: Individuals who lean toward more organic theories of etiology—genes, brain chemistry—sometimes take it as self-evident that the better solution must be something more physical, like a drug or ECT. Again, this could be true, but it is far from self-evident. In any event, I think monocausal approaches to etiology are misguided.

: You write at one point, “The growing interest in depression led more people, both professional and lay, to learn to label problems as depression, which was a growing idiom of distress before the advent of antidepressants . . . The medications, though, provided new incentives for multiple actors—pharmaceutical companies, doctors, patients, and patient’s families—to identify cases of depression.”

 I suspect you would have been writing a very different history of depression if antidepressant medications had not been developed, or if their use had continued to be severely restricted due to tolerability.

A curious thing, however, is that anxiety disorders are more common in the general community than depressive disorders, and antidepressants such as selective serotonin reuptake inhibitors (SSRIs) are not just antidepressants but also antianxiety medications. We could perhaps imagine an alternative history in which anxiety was the idiom of distress, SSRIs had been marketed as antianxiety rather than antidepressant, and you would perhaps be writing a book about the empire of anxiety, and the continuous historical links between melancholia and anxiety! Is it merely an accident of history that we ended up in the age of depression rather than the age of anxiety?

: Cross-cultural study has shown that the separation of anxiety and depression is a convention of Western psychiatry (which is rapidly becoming a global or cosmopolitan psychiatry, with both good and bad effects). Many healing systems around the world assume anxiety and depression are aspects of a single thing. And even in the West, the separation is somewhat new, a Kraepelinian innovation.

Is depression the same today as it was in the 17th century? Is it the same thing in Nigeria as it is in the United States? One of the foremost historians of psychiatry weighs in. 

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