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The History of Imperialism in Africa

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research paper about seasonal depression

Seasonality and symptoms of depression: a systematic review of the literature.

Affiliations.

• 1 Division of Mental and Physical Health, Norwegian Institute of Public Health, Bergen, Norway.
• 2 Department of Psychosocial Science, Faculty of Psychology, University of Bergen, Bergen, Norway.
• 3 Department of Psychological Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK.
• 4 Health Sciences Library, University of Ottawa, Ottawa, Ontario, Canada.
• 5 The Research Institute, Modum Bad Psychiatric Center, Vikersund, Norway.
• 6 Lovisenberg Diaconal Hospital, Oslo, Norway.
• 7 Innlandet hospital trust, Norway.
• 8 Department of Mental Health, Norwegian University of Science and Technology, Trondheim, Norway.
• 9 Department of Research and Innovation, Helse Fonna HF, Haugesund, Norway.
• 10 School of Epidemiology & Public Health, University of Ottawa, Ottawa, Canada.
• PMID: 31006406
• PMCID: PMC8061295
• DOI: 10.1017/S2045796019000209

Aims: Lay opinions and published papers alike suggest mood varies with the seasons, commonly framed as higher rates of depression mood in winter. Memory and confirmation bias may have influenced previous studies. We therefore systematically searched for and reviewed studies on the topic, but excluded study designs where explicit referrals to seasonality were included in questions, interviews or data collection.

Methods: Systematic literature search in Cochrane database, DARE, Medline, Embase, PsychINFO and CINAHL, reporting according to the PRISMA framework, and study quality assessment using the Newcastle-Ottawa scale. Two authors independently assessed each study for inclusion and quality assessment. Due to large heterogeneity, we used a descriptive review of the studies.

Results: Among the 41 included studies, there was great heterogeneity in regards to included symptoms and disorder definitions, operationalisation and measurement. We also observed important heterogeneity in how definitions of 'seasons' as well as study design, reporting and quality. This heterogeneity precluded meta-analysis and publication bias analysis. Thirteen of the studies suggested more depression in winter. The remaining studies suggested no seasonal pattern, seasonality outside winter, or inconclusive results.

Conclusions: The results of this review suggest that the research field of seasonal variations in mood disorders is fragmented, and important questions remain unanswered. There is some support for seasonal variation in clinical depression, but our results contest a general population shift towards lower mood and more sub-threshold symptoms at regular intervals throughout the year. We suggest future research on this issue should be aware of potential bias by design and take into account other biological and behavioural seasonal changes that may nullify or exacerbate any impact on mood.

Keywords: Admissions; antidepressants; depression; depressive symptoms; mood disorders; postpartum depression; seasonality; systematic review.

Publication types

• Systematic Review
• Seasonal Affective Disorder / psychology*
• Research article
• Open access
• Published: 26 November 2018

Implementing prevention of seasonal affective disorder from patients’ and physicians’ perspectives – a qualitative study

• Barbara Nussbaumer-Streit 1 , 2 ,
• Edda Pjrek 1 ,
• Christina Kien 2 ,
• Gerald Gartlehner 2 , 3 ,
• Lucie Bartova 1 ,
• Michaela-Elena Friedrich 1 ,
• Siegfried Kasper 1 &
• Dietmar Winkler 1  

BMC Psychiatry volume  18 , Article number:  372 ( 2018 ) Cite this article

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Seasonal affective disorder (SAD) is a seasonally recurrent type of major depression that has detrimental effects on patients’ lives during winter. Little is known about how it affects patients during summer and about patients’ and physicians’ perspectives on preventive SAD treatment. The aim of our study was to explore how SAD patients experience summers, what type of preventive treatment patients implement, which preventive treatment methods, if any, physicians recommend, and what factors facilitate or hinder implementation/recommendation of SAD prevention.

We conducted 15 semi-structured interviews, ten with adult patients with a history of SAD and five with physicians. Transcripts were analyzed by two researchers using an inductive thematic analysis approach.

One group of patients was able to enjoy summer and ignore thoughts of the upcoming winter. The other group feared the impending depressive episode in winter, and this fear negatively impacted these patients’ well-being during the summer. Preventive treatment was a relevant issue for all patients, and all but one person implemented SAD prevention during summer. We identified six factors that influenced patient use of preventive treatment of SAD. Four factors occur on an individual level ( knowledge about disease and preventive treatment options, experience with treatment in acute phase, acceptability of intervention, willingness to take responsibility for oneself ), one on an interpersonal level ( social and work environment ), and one on a structural level ( healthcare system ). All psychiatrists recommended some kind of preventive intervention, most commonly, lifestyle changes. Four factors influenced psychiatrists in recommending prevention of SAD ( patient expectations, disease history and stability, risk/benefit ratio, lack of evidence ).

Conclusions

Success in the implementation of SAD prevention does not solely depend on the willingness of the patients, but is also influenced by external factors. Raising awareness of SAD among general practitioners and low-level access to mental-health support could help patients find appropriate help sooner. To better guide the optimal treatment choice, comparative effectiveness research on treatments to prevent a new onset in patients with a history of SAD and clinical practice guidelines on SAD are needed.

Peer Review reports

Seasonal affective disorder (SAD) is a subtype of major depression that affects 2–8% of the total population in Europe [ 1 , 2 , 3 , 4 , 5 ]. It usually begins in fall/winter and remits in spring [ 6 , 7 , 8 ]. SAD is characterized by a high degree of persistence only resolving completely in one out of five patients after five to eleven years. In 22–42% of those affected, it persists with the seasonal pattern, and in 33–44% SAD turns into a non-seasonal major depression [ 9 , 10 ].

Depressive episodes negatively impact patients’ social as well as working lives [ 11 , 12 ]. In addition to depressive symptoms, most patients also experience hypersomnia, increased appetite often accompanied by weight gain, and extreme fatigue during winter months [ 13 ]. In summer, SAD patients are free of depressive symptoms. However, little is known whether or not the fear of upcoming depressive episodes impacts their well-being.

Light therapy is the first-choice treatment for acute SAD episodes and second-generation antidepressants are the second-choice treatment [ 14 , 15 , 16 ]. Other treatment options comprise agomelatine, melatonin, cognitive behavioral therapy, or lifestyle and diet changes [ 17 , 18 , 19 , 20 , 21 , 22 , 23 ]. The predictability of new depressive episodes in SAD patients provides a rationale for using these treatments preventively [ 24 ], beginning either in symptom-free summers or in fall when patients realize the first mild symptoms. A third approach to avoid the onset of a full-blown depression in the upcoming winter season is to continue acute treatment during summer.

Little guidance on the prevention of SAD exists. A German clinical practice guideline recommends starting light therapy in times of risk [ 25 ], while other guidelines do not provide specific recommendations for prevention of SAD [ 26 , 27 ]. Also, the evidence on efficacy and safety of preventive treatment in SAD patients is limited. A systematic review demonstrated that the preventive use of the antidepressant bupropion extended release (XL) reduced the number of patients developing a new depressive episode in the next winter by 44% compared to placebo [placebo: 27% vs. bupropion XL; 15%] [ 28 ]. A randomized controlled trial on psychotherapy showed that cognitive behavioral therapy led to 27% recurrence of SAD episodes in the following winters compared to 46% with light therapy [ 29 ]. A pilot study in 46 SAD patients, however, showed that preventive mindfulness-based cognitive therapy did not prevent recurrence of SAD better than “treatment as usual” when administered in a symptom-free time [ 30 ]. No evidence on preventive efficacy of other antidepressants [ 28 ] or other types of psychotherapy exists [ 31 ]. Systematic reviews on preventive light therapy [ 32 ], on agomelatine, and melatonin [ 33 ] were not able to draw valid conclusions on efficacy and safety of these preventive treatments either. Nevertheless, preventive treatment is common in clinical practice. A recent survey in German-speaking countries demonstrated that 81 out of 100 interviewed hospitals recommend preventive interventions to their SAD patients, most frequently, lifestyle changes and antidepressants, followed by psychotherapy and light therapy [ 34 ].

When evidence from clinical studies is scarce and guidance from clinical practice guidelines is unavailable, treatment choice should be heavily based on patient preferences and the clinical expertise of physicians. To our knowledge, no study has yet qualitatively explored patients’ and physicians’ perspectives on prevention of SAD.

The aims of our study were to investigate how patients with a history of winter-type SAD experience summers, what type of preventive treatments they implement, if any, and what facilitates or hinders the implementation of preventive treatment in symptom-free periods. In addition, we strove to identify factors that influence physicians in prescribing preventive treatment to SAD patients.

To understand what patients and physicians think about prevention of SAD and identify factors that influence the use and recommendation of interventions to prevent SAD, we interviewed both patients and physicians. The study was approved by and registered with the ethical review board of the Medical University of Vienna (EC No. 1586/2015). Throughout the manuscript, we adhere to the reporting guideline COREQ (COnsolidated criteria for REporting Qualitative research) for qualitative research [ 35 ].

Participants

We recruited adult patients from the register of the SAD outpatient clinic at the Vienna General Hospital. We started the selection of patients with the most recent registration entries. We checked whether patients fulfilled inclusion criteria (18 years or older, history of SAD) and used purposive sampling. We selected interviewees from different age groups, genders, and durations of SAD in order to ensure a broad sample base. We aimed for an even distribution of gender to gain similar insight into female and male experiences.

We sent an invitation letter containing written patient information to potential interviewees. One week later, we contacted the patients by phone and asked if they were willing to participate in our study. We continued to invite patients to participate in the study until we reached data saturation (no new topics emerged from the interviews). Overall, ten patients participated in the study; twelve invited persons declined to participate (ten had no interest or time, and two lived abroad).

For interviews with physicians, we recruited three psychiatrists working in a hospital in Vienna and one psychiatrist working in private practice. The only inclusion criterion for psychiatrists was working experience with SAD patients. To gain a broader perspective on the topic, we selected both men and women psychiatrists with different ages and whose number of years of work experience with SAD patients varied. To confirm the findings of patient interviews which revealed that general practitioners play an important role in SAD patient decisions to seek help, we consulted a general practitioner. We identified the general practitioner and the private practice psychiatrist through our professional network. All five contacted physicians agreed to participate in our study and signed an informed consent.

An experienced qualitative researcher conducted semi-structured interviews. To ensure that patients were free of depressive symptoms at the time of questioning, interview sessions were scheduled between April and August 2016. Patients chose the interview setting (their home, office at the clinic, café, or via telephone). The interviews with the three psychiatrists took place in the psychiatrists’ offices at the clinic. The general practitioner and the private practice psychiatrist were each interviewed by phone. Before each interview, we received a signed informed consent from each participant. To ensure anonymity, we coded patient identities with numbers. Interviews lasted 20 to 40 min, irrespective of interview mode (face-to-face or phone). An audio recording was made of each interview and destroyed after study use. All interviews were transcribed verbatim. The researcher also recorded field notes after each interview. Because the researcher and patient met for the first time at the interview, and the researcher was not involved in the care of the patients, patients could be assured that their interviews would not affect their treatment in any way. The researcher used an interview guide developed by the study team in order to answer the a priori defined research question. The first questions addressed patients’ characteristics and patients’ SAD history; physicians were asked about their experience with SAD patients. The main part of the patients’ interviews focused on: how they experience summers; what preventive measurements they implement, if any; and what facilitates or hinders them from implementing preventive interventions. Physicians were asked what motivates and/or keeps them from recommending preventive treatment to SAD patients.

Data analysis

We applied inductive thematic analysis as described by Braun & Clarke to identify, analyze, and report themes emerging from our data set – the interviews [ 36 ]. We chose thematic analysis because it focuses on the human experience similar to phenomenography [ 36 ]. First, we familiarized ourselves with the data and read and re-read the transcripts. Second, we assigned initial codes to the text. Third, we combined similar codes into subthemes and overarching themes. Fourth, we grouped themes into main categories. To facilitate the coding process, we used MAXQDA, Version 12.0 [ 37 ]. One experienced qualitative researcher performed the initial coding, grouping, and interpreting. As thematic analysis is an iterative process, the researcher discussed interim results (codes, subthemes, themes) and revised regularly with another researcher to corroborate findings.

We conducted 15 semi-structured interviews with ten patients and five physicians. We successfully created a diverse sample representing four female and six male SAD patients ranging between the ages of 20 to 60 years, with varying durations of the disease and differing living circumstances (see Table  1 ). The interviewed physicians represent two female and two male psychiatrists working in clinical or office-based settings as well as a male general practitioner, all with different degrees of experience in working with depressive patients (see Table 1 ).

First, we describe how patients experienced summers and which preventive treatments patients and physicians mentioned implementing/recommending. Then, we present the six identified factors that influenced patients to use, and the four factors that influenced physicians to recommend preventive interventions.

Patients’ experiences of summer

By the beginning of spring, patients experienced the end of a depressive episode, often as something quite sudden: “In March, April, it [the depression] cleared away as if by magic. It was just gone” (P_10). They perceived spring and summertime as positive contrasts to the depressive phase in fall/winter and felt clearly better during summer: “I feel good now. I am productive. I can cope with stress. That is how I imagine my life to be. I am motivated and able to cope with my private and professional life” (P_06).

However, while one group of patients managed to avoid any thought of a subsequent depressive episode during summer, the other group was worried about the onset of a new depressive episode throughout summer, and this negatively affected their well-being during symptom-free times, especially at the end of summer. One patient described the upcoming winter as a “sword of Damocles” (P_07). Another one said: “You cannot enjoy the sun that much because you think, ah, it is mid-August. In one or two months it will start again” (P_08) . In particular, those patients who had experienced more severe depressive episodes in previous winters already feared an upcoming episode in summer.

The severity of SAD differed strongly between interviewed patients. While some suffered from severe depression comprising suicidal thoughts and inability to participate actively in their social and professional life, others described their depressive episodes as mild. Despite different degrees of severity, all patients reported consequences to their professional and social lives. They felt a lack of drive and motivation. During depressive episodes, their performance at work dropped noticeably. Some were even unable to go to work at all. In addition, many interviewees had difficulties keeping up social contacts during winter. The concept of preventing the onset of a new depressive episode was relevant for all patients.

With the beginning of fall, some noticed signals like fatigue or lack of motivation as a sign that a new depressive episode was on the way: “There are signals. I don’t want to go out anymore, don’t want to meet people, and I am really tired. […] Usually I read the newspaper every day. As soon as I realize I haven’t read the newspaper for three days, I know – these are the first signs – I have to be alert” (P_05). For others the depressive episode came completely out of nowhere: “I always have the feeling as if I slip into this from one day to another. It hits me with surprise” (P_09).

Preventive treatment mentioned by interviewees

All patients except for one implemented, and all psychiatrists recommended, some kind of preventive intervention. The most common was lifestyle changes such as spending time outside, physical activity, or a balanced diet (see Table  2 ). Half of the patients came up with the idea of preventive interventions by themselves; the other half received specific recommendations from their physicians.

Factors influencing whether or not patients implement prevention of SAD

We identified six factors that influenced patients in their use of preventive treatment of SAD. Four acted on an individual, one on an interpersonal, and one on a structural level (see Table  3 ).

Knowledge about SAD and preventive treatment options

For patients who understood the mechanisms of SAD and the high rate of recurrence, it was easier to implement preventive treatment because they perceived it as reasonable. For them it made sense to substitute natural light with artificial light therapy in times when daylight hours decreased. They also wished for more information provided by physicians: “More information, more information – very important. In the end you are left alone with your problems […] more counseling by doctors would be nice ” (P_01).

However, patients often reported a lack of knowledge and awareness about SAD amongst their physicians, especially general practitioners. Upon noticing symptoms, most of the patients first consulted their general practitioners. However, none of the general practitioners consulted diagnosed SAD in the patients interviewed. Most of the general practitioners, in fact, refrained from referring the patients to a psychiatrist. Some interviewees felt that their general practitioners did not give serious consideration to their symptoms: “ If you go to a general practitioner in winter and tell him that you feel bad, he will say, ‘Well that is how it is in winter’” (P_08). Only one patient visited a general practitioner who was aware of SAD and advised the patient to visit a psychiatrist to be formally diagnosed. The general practitioner interviewed in this study also questioned the existence of SAD.

Another important influencing factor was knowledge about treatment options. If patients and physicians did not know about an intervention, this, of course, hindered them from using/recommending it. Most patients learned about different interventions from their psychiatrists or psychotherapists. As a barrier for not implementing any preventive treatment, one patient mentioned he was not aware that this was even an option: “ I understood that you cannot do anything about it because you cannot change the seasons ” (P_07).

Experience with treatment in acute phases of depression

The type of experiences patients had with diverse treatments during acute depressive phases strongly influenced their attitudes toward using those treatments for prevention. Those who experienced light therapy or antidepressants as effective and well tolerated treatments in acute depressive phases were more willing to use them for prevention. One patient explained: “I had the positive experience that drugs help me. And that is why I take them. As soon as I realize I’m not doing well, I’d better start right away” (P_05). Negative experiences (e.g. no effect, side effects), however, lead to negative attitudes toward the use of preventive treatment. If a treatment did not show an effect in an acute phase, patients did not consider it for preventive treatment, as one statement of a patient talking about light therapy illustrates: “If I had - I would have used it more intensively if I had noticed a change. I used it intensively in the beginning, but then I’ve used it less and less, after I did not notice any change” (P_10).

Acceptability of intervention

Perception of SAD being caused mainly by biological or psychological factors influenced patients’ acceptability of treatment options. For patients with a biological perception of SAD, medication or light therapy seemed adequate treatment options while psychotherapy did not. “So, I’m someone who tries to explain things chemically, that something is missing, synapses don’t work, and you can fix this with light therapy” (P_06). To those who had a psychological understanding of SAD, psychotherapy seemed to be an essential treatment option, and light therapy or antidepressants were perceived as useful additional interventions but not sufficient when applied alone: “I strongly believe that there is a connection between body and mind […] Light therapy only helps with symptoms […] I think my body will draw attention to something else with these symptoms” (P_07).

What patients believe about interventions also strongly influenced their willingness to use those interventions for prevention. Many patients expressed a general negative attitude toward antidepressants. Patients tried to get along without drugs for as long as possible. Reasons for a negative attitude toward antidepressants were a general antipathy toward drugs, including drug usage in other circumstances, and in mood-changing substances specifically, as these two patients described: “Before I take a pill for a headache, I try other things. I don’t want support from drugs. I look for alternatives” (P_02). “I am not a fan of drugs or pharmacological treatment because this only helps with symptoms not with the cause of the disease. That is why I try to change my lifestyle” (P_03).

The psychiatrists confirmed this finding. Psychiatrists reported their patients’ dislike of antidepressants and preferences for non-pharmacological treatment: “The majority of patients come to us and want light therapy. They have this expectation […] patients often simply don’t want drugs” (D_03).

Willingness to take responsibility for oneself

A major driver for implementing preventive treatment in symptom-free times was the willingness to take responsibility for oneself, which was linked to the degree of psychological strain, long-lasting experience of disease, and discipline.

Patients who suffered a high degree of psychological strain from depressive episodes were more willing to start preventive treatment in symptom-free times. Due to the seasonal change of SAD, they knew how life could be without depressive symptoms and how burdensome it feels during fall/winter. The greater the psychological strain patients suffered during fall/winter, the more motivated they were to take preventive actions in symptom-free times: “You know how bad you can feel in winter, and you learn from your experience. You know that you have to do something so that this doesn’t happen again. That is my motivation” (P_09) . One interviewed physician agreed: “This comes with high psychological strain. And they want to do something against these symptoms that they already know from the past winters” (D_01).

Those patients who reported their depression as mild during winter were less motivated to undertake preventive treatment: “I think I am at the beginning of my disease. I know how I feel when it gets worse. Well, I don’t have panic attacks, so I know that there are worse forms [of SAD]. That is not the case with me. Should it be worse this winter, I would need to think about it [preventive treatment]” (P_02).

Patients experienced with SAD seemed to succeed more in implementing preventive interventions. Those patients who have experience the seasonal pattern over the years, tried different treatment approaches to find what works best for them. They have learned to recognize small changes in their mood and to interpret them as signals for the next onset of depression: “In the meantime, I started to become more sensitive […] that was my learning over the last decades” (P_05); “I pay more attention to symptoms” (P_10). Regimens in which patients start treatment before the onset of symptoms, require patient experience and patient recognition of early signals: “When it became darker, I realized that symptoms were coming back, and then there was a point when it was nearly too late or at least it was critical, then I immediately went to the doctor and said, ‘Okay, I need medication’” (P_06). Preventive treatment also requires support from a psychiatrist who can give patients the freedom to decide when they subjectively feel it is necessary to begin treatment.

The less experienced SAD patients were still optimistic that the upcoming winter would be depression-free: “It got better in spring, and then I stopped treatment and thought, well, maybe next time it will not come back” (P_10). During the summer they tended to ignore the impending depression: “It doesn’t bother me at all in summer. Well, of course when it hits me in winter, it troubles me, but it’s not as if I already fear this phase in summer” (P_04). “In summer I just look toward the future. Everything is going to be brighter. No, there is nothing troubling me” (P_02).

The implementation of preventive treatment during times when people feel well requires patient discipline. Patients often struggled to enjoy summer and to ignore every thought of an impending depressive episode: “This is something you want to forget about. You don’t want to prepare for it because now, when you feel well, you want to enjoy it” (P_07). Patients who were able to successfully implement preventive treatments like lifestyle changes credited their success to self-discipline: “The older I got, the better it worked because I became more disciplined” (P_05). “That was my own internal process. I thought, I don’t want this anymore - to be lethargic all winter” (P_03). Physicians also believed that successful implementation of preventive treatment during summer depended on patient discipline: “Patients are often motivated to continue effective acute treatment to prevent the onset of new depressive phases, but then they don’t keep up with it” (D_03) .

Social and work environment

Factors in the social and work environment, such as compatibility with daily routines, or social support, were perceived as facilitators, or if lacking, as barriers in the implementation of preventive treatments.

Compatibility with daily routines: some patients experienced preventive treatments as easy to integrate in their daily routines, e.g. light therapy: “I could integrate it into my daily life. I have a desk job and sit in front of a computer. You only have to remind yourself to switch on the light” (P_07) . “It brought some structure into my life. I sat down, drank a cup of coffee, and looked into the light therapy device” (P_06) . Others reported difficulties in implementing preventive treatments, e.g. due to their work or private duties. One patient who works nightshifts said: “When I come home from a nightshift I would have to sit in front of a light therapy device, then I am awake again – that’s not working” (P_05). “For me it is not worth the effort” (P_04). “To be honest, the effort to sit in front of this lamp every day was time-consuming and a little bit difficult because of children and school and work” (P_08) . Physicians reported similar difficulties from their patients: “There are patients who have no desk job where they can install the lamp. I think this plays an important role” (D_01) .

Social support and understanding from family and friends were perceived as facilitators, especially in helping patients to maintain a structured and active lifestyle and to seek help from psychiatrists and psychotherapists.

Healthcare system

We also identified influencing factors on a structural level – the healthcare system. Access to treatments and reimbursement of their costs worked as facilitators in implementing prevention.

Access to treatment: patients described difficulties in finding the “right” psychotherapist for them: “Either you are lucky with your therapist or not […] if it fits – one cannot know in advance. You also don’t know if this will be better with the next therapist. And especially a patient suffering from depression will probably not think that the therapist might be the problem” (P_01). Also finding a therapist within a reasonable timeframe was challenging: “You have to wait up to a year and a half to get an appointment” (P_05). Others criticized the lack of access to support for SAD patients: “Why is there only one outpatient clinic for all the SAD patients in Austria?” (P_08). Patients reported that it was easier to find a suitable therapist within a timely fashion if they visited doctors/therapists in private practices: “My experience is that there is an extreme difference between the general health insurance system and the private system, especially in mental health” (P_10).

Costs of treatment play a role, especially with light therapy and psychotherapy. The lack of coverage in health insurance plans for light therapy devices and psychotherapy treatments posed barriers for patients: “If the insurance doesn’t cover treatment costs - that is a problem. I am the sole breadwinner at home. I have to feed two adults and a child. I definitely couldn’t afford weekly therapy sessions for 300€ a month” (P_01) . Physicians also reported that the lack of health insurance coverage for certain treatments was problematic for many patients. On the other hand, when services were offered free of cost, insurance coverage acted as a facilitator: “I take part in a health promotion program. […] I can get psychological counseling without paying out of my own pocket” (P_05) .

Factors influencing psychiatrists in recommending prevention of SAD

Four factors that influenced psychiatrists in recommending prevention of SAD were identified (see Table  4 ). Because the general practitioner did not recommend preventive SAD treatment; results are based on the interviews conducted with the four psychiatrists.

Psychiatrists recommended preventive treatment only to patients with a long and stable history of SAD. Only if the onset of a new depressive episode was very likely did psychiatrists advise patients to start with a treatment such as antidepressants or light therapy before symptoms occurred: “In some patients, depressive episodes don’t return every season” (D_02) . “In my opinion, you have to consider if someone who might not develop a depressive episode should be treated without symptoms present” (D_01).

Patient expectations influence what physicians recommend to them. If patients are unwilling to take antidepressants or go to psychotherapy, doctors will not recommend these treatment options, even if such options would be effective in prevention or in acute phases of depression. Sometimes patients demand specific treatments and are not open to other possibilities their physicians might suggest: “The majority of people come to us and demand light therapy. If that is what they expect, it is hard to tell them that antidepressants are a good treatment option” (D_03).

When considering preventive treatment, physicians weigh risks and benefits. Because SAD preventive treatments are initiated during symptom-free times and a physician can never be certain that a depressive episode will indeed develop, SAD preventive treatments present a particular challenge and may expose patients to unnecessary risks. Light therapy is preferred over antidepressants because the risk for potential side effects might be smaller compared to antidepressants.

The main barrier in recommending preventive treatments, such as melatonin or vitamin D, was a lack of evidence: “It looks good, helps with sleeping problems, but as with antidepressants – I prefer to wait for study results” (D_04) . Psychiatrists extrapolated from acute treatment settings to preventive treatment but wished for valid evidence about efficacy and safety of preventive treatment.

To the best of our knowledge, this is the first qualitative study to explore patients’ and physicians’ perspectives on prevention of SAD and to identify factors that facilitate or hinder its implementation. By using thematic analysis we grouped the insights of the vast amount of information into factors that influence SAD prevention on an intrapersonal, interpersonal, and environmental level. This is in line with the ecological model of health behavior that argues that an individual’s health behavior is not solely affected by internal factors but also by other people and context factors [ 38 ]. The typical purpose of qualitative research is to gain an understanding of complex situations and real-world problems, especially, in areas which lack research efforts like patients’ and physicians’ perspective on SAD prevention [ 35 ].

Our study was the first to formally assess that preventing the onset of a new depressive episode in winter was a relevant issue for all SAD patients, whether the fear of the next upcoming depressive episode negatively impacted their wellbeing in summer, or not. This is in accordance with findings from a Swedish study exploring patients’ experiences with SAD in general [ 12 ], and underlines the need for preventive treatment. This need was also demonstrated in a recent survey that showed that preventive treatment is recommended by more than 80% of psychiatric hospitals in German-speaking countries [ 34 ].

Changing lifestyle, taking antidepressants, or starting light therapy and psychotherapy before the onset of depressive symptoms were preventive treatments implemented by the interviewed patients. This coincides with what psychiatrists reported as recommending most often for SAD prevention [ 34 ]. In our interviews, psychiatrists also reported a lack of evidence on prevention of SAD leading to high uncertainty and a need for comparative effectiveness studies on preventive treatment options for SAD. Consequently, psychiatrists relied more on patients’ preferences and values, indicating good shared decision-making. The identified barriers and facilitators on the individual level can support psychiatrists in the counselling process of their patients to find an individual suitable preventative treatment.

One major barrier patients encountered when searching for help, was that general practitioners did not recognize SAD symptoms. Consequently, SAD patients often remain mis- or underdiagnosed and continued to suffer from symptoms and functional disability. This is especially alarming considering that 60% of depression-related treatment is provided by general practitioners [ 39 ]. To ensure that patients receive the immediate care they need, general practitioners have to be aware of the symptoms, mechanisms, treatment and preventive options of SAD. In particular, patients who are lacking experience with SAD and have not learned to master their disease need support from physicians and therapists. Raising general awareness of SAD is important so those who experience it can recognize their symptoms and receive the necessary support in their social and working environment.

The inability of patients to integrate preventive treatments into their everyday working and social lives highlights the need for a broad range of treatment options that can better meet patient needs. On a structural level, a lack of access to treatments and coverage of costs pose barriers to treatment. Low-level access to and financial support for treatment of mental health problems is needed, especially for light therapy, which is recommended for clinical practice [ 25 ].

One limitation of our study is that we did not formally evaluate if patients still fulfilled diagnostic criteria for SAD, but relied on diagnoses documented in patient charts and on patient self-reports. However, since we were interested in experiences of SAD patients, it was essential that they had a history of SAD, which was confirmed by documented diagnoses. Second, we interviewed only a few psychiatrists, three of whom worked at the same institution. However, because the institution is specialized in the treatment of SAD patients, the psychiatrists selected have extensive experience with SAD patients. Although the initial research plan did not foresee an interview with a general practitioner, this component was added due to the amount of patients who reported their general practitioners as key persons in their search for help with SAD. Therefore, the interview guide was slightly adapted for the general practitioner interview. Third, patients were interviewed about past experiences and results could therefore be influenced by recall bias. Fourth, the method of interview differed for some interviewees. Two patients and two physicians preferred to be interviewed via phone due to logistical reasons. We cannot rule out that this affected the willingness to share personal experiences. However, the duration of the interviews via phone was comparable to the face-to-face interviews, the interviews followed the guiding questions, and no one listened to the conversation, ensuring a trustworthy atmosphere.

A special strength of our study is, that the researcher who conducted all patient interviews was in no way involved in the care provided to the patients and patients could be ensured that interview responses would not affect their treatment. This in turn, contributed to an atmosphere of trust and openness.

Raising awareness of SAD, its symptoms, and treatment options among general practitioners and in society is essential to help patients find appropriate support sooner.

Since prevention begins when patients still feel well, it costs them quite an effort to implement preventive interventions. Considering the high probability of the onset of a new depressive episode, it is important to enable SAD patients to implement prevention. Therefore, it is advisable to provide a broad range of treatment options that fit the practical needs of patients and allow them to integrate an intervention into their daily routines. Reimbursement of treatment costs, low-level access and short waiting times for psychotherapy (CBT) would be beneficial. To better guide the optimal treatment choice, comparative effectiveness research on treatments to prevent a new onset in patients with a history of SAD and clinical practice guidelines on SAD are needed.

Abbreviations

Number of interviewees

• Seasonal affective disorder

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Acknowledgements

We wish to thank all patients and physicians for their participation in the interviews. Furthermore we would like to thank Dawn Gartlehner for proofreading the final manuscript.

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

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BN and DW designed the study. EP and SK reviewed the protocol. BN collected the data. BN undertook the initial thematic analysis. Interim results were discussed regularly with CK. GG, CK, LB, and MF provided comments to the thematic analysis. BN wrote the initial draft of the manuscript. All authors helped critically revise the article and approved the final manuscript. The article is the authors’ original work, hasn’t received prior publication, and is not under consideration for publication elsewhere.

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The study was approved by and registered with the ethical review board of the Medical University of Vienna (EC No. 1586/2015). All interviewees read and signed the informed consent sheet before the interviews were conducted.

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Without any relevance to this work, Dr. Kasper received grants/research support, consulting fees and/or honoraria within the last three years from Angelini, AOP Orphan Pharmaceuticals AG, Celegne GmbH, Eli Lilly, Janssen-Cilag Pharma GmbH, KRKA-Pharma, Lundbeck A/S, Mundipharma, Neuraxpharm, Pfizer, Sanofi, Schwabe, Servier, Shire, Sumitomo Dainippon Pharma Co. Ltd., and Takeda.. Dr. Pjrek has received travel grants from AOP Orphan. Dr. Winkler received travel grants and/or speaker honoraria from Angelini, AOP Orphan, Bristol-Myers Squibb, Lundbeck, Pfizer, and Servier.

Barbara Nussbaumer-Streit, Christina Kien, Dr. Gerald Gartlehner, Dr. Michaela-Elena Friedrich, and Dr. Lucie Bartova have no conflict of interest.

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Nussbaumer-Streit, B., Pjrek, E., Kien, C. et al. Implementing prevention of seasonal affective disorder from patients’ and physicians’ perspectives – a qualitative study. BMC Psychiatry 18 , 372 (2018). https://doi.org/10.1186/s12888-018-1951-0

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This Winter, Pandemic May Intensify Seasonal Depression

• Katie O'Connor

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The COVID-19 pandemic and the accompanying stress may worsen seasonal affective disorder (SAD) for patients this winter, and SAD may worsen the course of COVID-19 for those patients who are infected.

This year, being outside has been a welcome reprieve for many Americans, allowing them to socialize safely with friends and family while escaping the confines of their homes. Yet as winter sets in and days shorten, experts fear the pandemic will exacerbate seasonal affective disorder (SAD) for a population that is already reporting alarmingly high rates of depression and anxiety.

“If overall depression rates are elevated, the risk of seasonal affective disorder may also be greater,” said Michael Thase, M.D., professor of psychiatry at the Perelman School of Medicine at the University of Pennsylvania.

For those individuals who have a tendency to feel low, moody, less motivated, and less excited by things that normally bring them joy around this time of year, then the other challenges that accompany the pandemic may further worsen those symptoms, Thase explained. “It’s both the negative and absence of the positive that make this pandemic so noxious from an anxiety and depression standpoint,” he said.

SAD is a form of depression, and it can become just as serious, causing the same symptoms as major depressive disorder such as fatigue, changes in mood, or loss of interest. About 5 percent of U.S. adults experience SAD, according to APA’s website, with the symptoms lasting about 40 percent of the year. The most difficult months tend to be January and February. Risk factors tend to be additive, Thase pointed out. Surveys have shown a significant jump in anxiety and depression since the pandemic began, which does not bode well for people who experience SAD in the winter months.

Teodor Postolache, M.D., and his colleagues have not only seasonal affective disorder as it presents in the fall and winter, but also trends in depression during the spring and spring peaks in suicide.

COVID-19’s biological underpinnings may also worsen SAD symptoms for some patients who have had the virus, hypothesized Teodor Postolache, M.D., professor of psychiatry at the University of Maryland School of Medicine. In a July 2020 viewpoint published in JAMA Psychiatry , Postolache and his colleagues pointed out that, as they noted in their previous published work, many infections that result in hospitalization such as COVID-19, “are predictively associated with suicide, and maximum behavioral effects can take more than 6 months postinfection to fully develop.” The COVID-19 virus may trigger priming in the immune cells in the brain, which could extenuate the individual’s vulnerability to mood disorders, Postolache told Psychiatric News .

Conversely, patients with SAD have elevated markers of immune activation, which could predispose them to a more severe and unremitting inflammatory response to the virus should they become infected, and thus a more severe and protracted course, Postolache explained.

“Once you have that additional vulnerability, you can see how the minute changes in someone’s life, plus the stressors that derive from not being able to function at your best academically, occupationally, or at home, may induce major mood episodes,” Postolache said. “My expectation is that COVID-19 is going to make things worse for patients with SAD, and SAD traits are going to make things worse for patients who have been infected with SARS-CoV-2.”

Additionally, during the fall and winter months, patients with SAD often crave carbohydrates, exercise less, gain weight, and have co-occurring metabolic abnormalities, which all represent risk factors for a severe course of COVID-19, Postolache pointed out.

There are three treatments for SAD that have been proven to work, Postolache said. Two are nonpharmacological, including light therapy and cognitive behavioral therapy. Pharmacological treatments can also be effective, and Postolache pointed to bupropion, which is the only FDA approved antidepressant for preventative and intermittent use in SAD patients.

“We don’t know as much as we’d like to know about SAD, but we know that it has to do with the circadian rhythm and a person’s natural biological clock,” said Aron Tendler, M.D., chief medical officer of BrainsWay. Those who are most susceptible to SAD are people who live in areas that receive significantly less sunlight during some parts of the year, such as Alaska, and those who already have been diagnosed with a mood disorder, he said. “People who might describe themselves as night owls might be more susceptible to SAD because they’re not getting the right amount of sunlight.”

Getting morning sunlight is best in the winter, Thase said, especially between 7 and 8 a.m. Evidence also suggests that light boxes can be beneficial for patients with SAD, allowing them to get the sunlight they need every day. Light boxes require only about 20 minutes a day and can improve SAD symptoms within a few weeks, according to APA’s website.

For psychiatrists who are expecting to see SAD emerge among their patients this winter, setting up a plan before the symptoms set in can be beneficial, Tendler said. They may want to set up scheduled virtual gatherings with friends, for example, or set a remind for themselves to reach out to loved ones or exercise. “Perfect is the enemy of good,” he said. “You don’t want patients saying things like, ‘I can’t exercise the way I want to, so I’m not even going to try.’ Exercising inside can have benefits, too.”

But just like other forms of depression, medication is an efficient treatment. “If you’ve tried exercise, social engagement, and the light box, then you may need to step up your level of intervention with medications,” Thase said.

Postolache emphasized that every patient is substantially different, both in regard to the pandemic and the accompanying stresses, but also in their vulnerability to SAD and responses to treatment. “When we think about SAD, we also have to perform differential diagnoses because many patients get depressed in the winter but don’t have SAD,” he said. “We have to think about one patient at a time.” ■

“Targetable Biological Mechanisms Implicated in Emergent Psychiatric Conditions Associated With SARS-CoV-2 Infection” is posted here .

The science behind seasonal depression

Seasonal affective disorder can occur in both winter and summer. here's why it happens, and how you might treat it..

When he moved from South Africa to New York City, Norman Rosenthal noticed he felt more depressed during the cold, short days of the city’s winters than he had in his home country.

“It was an illness hiding in plain sight because people said ‘well that’s how everyone feels in winter.’ They didn’t see it as treatable,” says Rosenthal, a psychiatrist at Georgetown Medical School. 

In 1984, he published the first paper to scientifically name the winter blues: Seasonal affective disorder (SAD), also called seasonal depression, was a type of depression brought on by the dark days of winter. 

Subsequent studies have found that this form of depression varies by geography, notably affecting those in northern latitudes more. And, surprisingly, about 10 percent of patients suffering from SAD have symptoms in the summertime instead. 

Whether in winter or summer, mental health experts say there are solutions to treat SAD. 

A bad mood versus a SAD mood

It’s normal for moods to fluctuate with seasons and even for people to feel a little more down in the winter, experts say, but those suffering from SAD experience the symptoms of clinical depression. 

“They’re exactly the same,” says Kelly Rohan , a psychologist at the University of Vermont who specialises in the disorder. 

“We would look for things like a persistently sad mood. Losing interest in things. Sleep changes. Significant eating or appetite change. Losing energy. Fatigue. Difficulty concentrating,” she says. 

At Yale’s Winter Depression Research Clinic , the most commonly reported symptoms of winter depression are hypersomnia—the desire to sleep more than usual—and an increased appetite, says Paul Desan, a psychiatrist and the clinic’s director. 

“It’s like human beings are trying to hibernate,” says Desan.

Most people begin experiencing symptoms in young adulthood, but SAD can begin at any stage of life. The condition also varies by sex. 

“About three times as many women as men get SAD for reasons we don’t understand,” says Desan. 

While SAD is typically diagnosed when patients meet the criteria for clinical depression, some patients fall just short of this official diagnosis. They’re instead diagnosed with “subsyndromal SAD,” a milder but still burdensome condition. 

Why does SAD happen? 

“It’s fairly accepted that the trigger is a short photoperiod—the number of hours from dawn to dusk,” says Rohan. “It’s the strongest predictor of when the symptoms begin.” 

But why, exactly, does less daylight seem to make some people clinically depressed? 

“That's the million-dollar question,” says Rohan. 

One leading theory is that the change in daylight disrupts our bodies’ release of melatonin, a hormone the brain releases every night to promote sleep. The process is part of our circadian rhythm, our innate biological clock dictating when we sleep and wake.

Our clocks are cued up by morning light, but as the supply of daylight dwindles in winter, melatonin may be released later and wear off later, the theory suggests. 

That means, “that alarm clock might be going off in the morning, but the body is still in a state of biological night,” says Rohan. 

Those diagnosed with SAD may be particularly sensitive to schedules that disrupt their circadian rhythm by beginning and ending at odd hours, like shift work, she adds.

Even given that theory, she says it’s still unclear why disrupted circadian rhythm can lead to depression, instead of just feeling fatigued. 

What about summertime depression? 

Rohan says a minority of people who experience SAD in the winter can become manic in the summer when the number of stimulating daylight hours increases. 

But still others experience a phenomenon called summer SAD, or when seasonal depression symptoms occur only in the summer—perhaps triggered by the heat and humidity. 

Instead of feeling lethargic, summer SAD patients more often feel irritable and agitated. 

( Learn more about why seasonal depression can happen in the summer .)

Scientists are studying whether temperatures rising as a result of climate change may harm mental health. A 2018 study of mood expressed on social media found depressive language increased with temperature. 

Is SAD a real condition? 

SAD is not without its sceptics. One study published in 2008 looked at rates of depression among populations in northern Norway, where there’s no sunlight at all for two months of every winter, and found no seasonal increase. 

Another study published in 2016 looked at a U.S. survey of just over 30,000 people. When asked to answer questions related to depression, there was no discernible spike related to season or latitude. 

Steven Lobello, a psychologist at Auburn University in Montgomery, Alabama, isn’t convinced SAD qualifies as a diagnosable mental disorder. He thinks previous studies done to measure rates of SAD have been too suggestive. Rather than calling people during the winter and asking them if they feel depressed, studies have asked people if they have ever felt depressed during winter—which many people believe they do. 

“If you ask questions of people in a way that allows them to know the nature of what you’re getting at, then I don't think you’re doing anything more than measuring that belief,” Lobello says. 

However, Rohan says these studies may not detect SAD because it’s relatively rare, representing about 10 percent of those diagnosed with clinical depression. 

“It’s like looking for a needle in a haystack and not finding needles and determining they don’t exist,” she says. 

Using light as therapy

For those who think they may be experiencing SAD, experts say a professional diagnosis is a crucial first step toward treatment. 

“People should really avoid self-diagnosis,” says Rohan. “Depression is a serious mental health problem, so it’s best to leave it to trained professionals.” 

Sitting in front of a bright box of light is one of the most common treatments for SAD. Experts say the key is to look for light boxes that provide light equalling 10,000 lux, a measure of brightness. 

“10,000 lux is like being outside on a summer day in July. It’s a lot of light,” says Desan. 

Be wary of the box’s size, he notes. A light box that’s too small can fail to deliver the adequate amount of light treatment. 

(His clinic’s website lists vetted boxes.) 

Experts recommend sitting in front of light boxes for about 30 minutes and usually first thing in the morning, to help signal to the body that it’s time to wake up. This treatment can improve mood the day it’s used. The only drawback to light boxes, notes Rohan, is that they only work on the day that you use them, so they need to be used daily. 

Talk therapy and lifestyle changes

One treatment that may have longer lasting benefits is Cognitive Behavioural Therapy (CBT), a form of talk therapy Rohan endorses for treating SAD. 

“Negative thinking tends to breed negative emotions, and we want to change those into slightly less negative, more neutral thoughts,” she says of the CBT approach. For example, “I hate winter,” might be reframed as, “winter isn’t my favourite season, but I still find things to enjoy.”

Finding wintertime hobbies may also help. 

“People with SAD often have hobbies and interests that are summer specific—growing gardens, beach going,” she says. Instead of hibernating under a blanket, she suggests those people find indoor hobbies to enjoy—knitting, joining a book club, or going to the gym, she suggests. 

Lifestyle changes can also be useful mental health tools, says Rosenthal. Exercising, learning ways to manage stress, or planning a sunny holiday during the winter can all help to boost your mood, he says. 

Whether using light or talk therapy, Rosenthal stresses that there’s no reason to not seek mental health treatment, even if symptoms are only present for a few months out of the year: “There are many, many strategies people can use that will help them thrive year-round.” 

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Seasonal affective disorder (SAD)

On this page, when to see a doctor, risk factors, complications.

Seasonal affective disorder (SAD) is a type of depression that's related to changes in seasons — seasonal affective disorder (SAD) begins and ends at about the same times every year. If you're like most people with SAD , your symptoms start in the fall and continue into the winter months, sapping your energy and making you feel moody. These symptoms often resolve during the spring and summer months. Less often, SAD causes depression in the spring or early summer and resolves during the fall or winter months.

Treatment for SAD may include light therapy (phototherapy), psychotherapy and medications.

Don't brush off that yearly feeling as simply a case of the "winter blues" or a seasonal funk that you have to tough out on your own. Take steps to keep your mood and motivation steady throughout the year.

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In most cases, seasonal affective disorder symptoms appear during late fall or early winter and go away during the sunnier days of spring and summer. Less commonly, people with the opposite pattern have symptoms that begin in spring or summer. In either case, symptoms may start out mild and become more severe as the season progresses.

Signs and symptoms of SAD may include:

• Feeling listless, sad or down most of the day, nearly every day
• Losing interest in activities you once enjoyed
• Having low energy and feeling sluggish
• Having problems with sleeping too much
• Experiencing carbohydrate cravings, overeating and weight gain
• Having difficulty concentrating
• Feeling hopeless, worthless or guilty
• Having thoughts of not wanting to live

Fall and winter SAD

Symptoms specific to winter-onset SAD , sometimes called winter depression, may include:

• Oversleeping
• Appetite changes, especially a craving for foods high in carbohydrates
• Weight gain
• Tiredness or low energy

Spring and summer SAD

Symptoms specific to summer-onset seasonal affective disorder, sometimes called summer depression, may include:

• Trouble sleeping (insomnia)
• Poor appetite
• Weight loss
• Agitation or anxiety
• Increased irritability

Seasonal changes and bipolar disorder

People who have bipolar disorder are at increased risk of seasonal affective disorder. In some people with bipolar disorder, episodes of mania may be linked to a specific season. For example, spring and summer can bring on symptoms of mania or a less intense form of mania (hypomania), anxiety, agitation and irritability. They may also experience depression during the fall and winter months.

It's normal to have some days when you feel down. But if you feel down for days at a time and you can't get motivated to do activities you normally enjoy, see your health care provider. This is especially important if your sleep patterns and appetite have changed, you turn to alcohol for comfort or relaxation, or you feel hopeless or think about suicide.

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The specific cause of seasonal affective disorder remains unknown. Some factors that may come into play include:

• Your biological clock (circadian rhythm). The reduced level of sunlight in fall and winter may cause winter-onset SAD . This decrease in sunlight may disrupt your body's internal clock and lead to feelings of depression.
• Serotonin levels. A drop in serotonin, a brain chemical (neurotransmitter) that affects mood, might play a role in SAD . Reduced sunlight can cause a drop in serotonin that may trigger depression.
• Melatonin levels. The change in season can disrupt the balance of the body's level of melatonin, which plays a role in sleep patterns and mood.

Seasonal affective disorder is diagnosed more often in women than in men. And SAD occurs more frequently in younger adults than in older adults.

Factors that may increase your risk of seasonal affective disorder include:

• Family history. People with SAD may be more likely to have blood relatives with SAD or another form of depression.
• Having major depression or bipolar disorder. Symptoms of depression may worsen seasonally if you have one of these conditions.
• Living far from the equator. SAD appears to be more common among people who live far north or south of the equator. This may be due to decreased sunlight during the winter and longer days during the summer months.
• Low level of vitamin D. Some vitamin D is produced in the skin when it's exposed to sunlight. Vitamin D can help to boost serotonin activity. Less sunlight and not getting enough vitamin D from foods and other sources may result in low levels of vitamin D in the body.

Take signs and symptoms of seasonal affective disorder seriously. As with other types of depression, SAD can get worse and lead to problems if it's not treated. These can include:

• Social withdrawal
• School or work problems
• Substance abuse
• Other mental health disorders such as anxiety or eating disorders
• Suicidal thoughts or behavior

There's no known way to prevent the development of seasonal affective disorder. However, if you take steps early on to manage symptoms, you may be able to prevent them from getting worse over time. You may be able to head off serious changes in mood, appetite and energy levels, as you can predict the time of the year in which these symptoms may start. Treatment can help prevent complications, especially if SAD is diagnosed and treated before symptoms get bad.

Some people find it helpful to begin treatment before symptoms would normally start in the fall or winter, and then continue treatment past the time symptoms would normally go away. Other people need continuous treatment to prevent symptoms from returning.

December 14, 2021

• Specifiers for depressive disorders: With seasonal pattern. In: Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th ed. American Psychiatric Association; 2013. https://dsm.psychiatryonline.org. Accessed July 15, 2021.
• Seasonal affective disorder. National Institute of Mental Health. https://www.nimh.nih.gov/health/publications/seasonal-affective-disorder/. Accessed July 15, 2021.
• Seasonal affective disorder (SAD). American Psychiatric Association. https://www.psychiatry.org/patients-families/depression/seasonal-affective-disorder. Accessed July 15, 2021.
• Seasonal affective disorder: More than the winter blues. American Psychological Association. https://www.apa.org/topics/depression/seasonal-affective-disorder. Accessed July 15, 2021.
• Major depressive disorder with a seasonal pattern. National Alliance on Mental Illness. https://www.nami.org/About-Mental-Illness/Mental-Health-Conditions/Depression/Major-Depressive-Disorder-with-a-Seasonal-Pattern. Accessed July 15, 2021.
• Galima SV, et al. Seasonal affective disorder: Common questions and answers. American Family Physician. 2020;102:668.
• Haller H, et al. Complementary therapies for clinical depression: An overview of systematic reviews. BMJ Open. 2019; doi:10.1136/bmjopen-2018-028527.
• Light therapy. Natural Medicines. https://naturalmedicines.therapeuticresearch.com. Accessed July 15, 2021.
• Seasonal affective disorder and complementary health approaches: What the science says. National Center for Complementary and Integrative Health. https://www.nccih.nih.gov/health/providers/digest/seasonal-affective-disorder-and-complementary-health-approaches-science. Accessed July 15, 2021.
• Safe use of complementary health products and practices. National Center for Complementary and Integrative Health. https://www.nccih.nih.gov/health/safety. Accessed July 19, 2021.
• Depression. National Institute of Mental Health. https://www.nimh.nih.gov/health/topics/depression/. Accessed July 19, 2021.
• Depression. National Institute of Mental Health. https://www.nimh.nih.gov/health/publications/depression/. Accessed July 19, 2021.
• Rosenthal SJ, et al. Seasonal effects on bipolar disorder: A closer look. Neuroscience and Biobehavioral Reviews. 2020; doi:10.1016/j.neubiorev.2020.05.017.
• Gitlin MJ. Antidepressants in bipolar depression: An enduring controversy. International Journal of Bipolar Disorders. 2018; doi:10.1186/s40345-018-0133-9.
• Sawchuk CN (expert opinion). Mayo Clinic. Sept. 2, 2021.
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Spring Allergy Season is Getting Worse. Here’s What to Know.

Experts explain how to tell if you have allergies, and how to find relief if you do.

By Nina Agrawal

Spring is here — and if you’re among the estimated one in four adults in the United States who suffer from seasonal allergies, your sneezing and scratching may have already started.

With climate change affecting temperatures and plant growth, you may need to be on the lookout earlier than ever before. It can be hard to distinguish allergy symptoms from those of a cold, but experts point to a few telltale signs.

Is allergy season getting worse?

Spring allergy seasons are beginning about 20 days earlier than they had, according to an analysis of pollen count data from 60 stations across North America from 1990 to 2018.

That shift can have significant health consequences, said William Anderegg, who is an author of the study and an associate professor of biology at the University of Utah. Other research has shown that very early onset of spring is associated with higher prevalence of allergic rhinitis, also known as hay fever. When people end up sick or in the hospital from uncontrolled allergy symptoms, he said, “it’s because they didn’t expect it, and didn’t have medications in hand.”

The researchers also found that pollen concentrations have risen about 20 percent nationwide since 1990, with Texas and the Midwest having the greatest increases. Warmer temperatures, higher concentrations of carbon dioxide and increased precipitation can all contribute to plants’ growing bigger and producing more pollen over longer periods of time, Dr. Anderegg said.

Dr. Gailen Marshall, chair of the allergy and immunology department at the University of Mississippi Medical Center, said that when he began practicing nearly 40 years ago, allergy seasons were confined to about eight weeks each. Tree pollen hit in the spring, grass pollen increased in spring and summer and ragweed pollen picked up in late summer and early fall.

Back then, people “could at least get some relief” between those cycles, said Dr. Marshall, who is also president of the American College of Allergy, Asthma and Immunology, a professional organization. “Now, these seasons end up becoming one long season.”

How can you tell whether it’s allergies or a cold?

Many people with nasal congestion or a runny nose may assume that they have a cold. Though allergy and cold symptoms can be similar, allergies often make the eyes, nose, throat, mouth or ears itchy, said Dr. Rita Kachru, chief of clinical allergy and immunology at UCLA Health. With allergies, the immune system mistakes a trigger, like pollen, for a harmful substance. When repeatedly exposed to that trigger, Dr. Kachru said, immune cells release chemicals, including histamine, that cause itchiness and inflammation.

Patients also often experience congestion and postnasal drip, or mucus dripping down the back of the throat. Some people may develop coughing, wheezing and shortness of breath.

With a viral infection, by contrast, you might have muscle fatigue, joint aches or a fever.

If your symptoms flare up every year around a certain season and last more than a week or two, then there is a good chance they’re being caused by allergies. A personal or family history of allergies, eczema or asthma can also be an important clue, doctors said.

What if I’ve never had allergies before?

Most people first develop symptoms in childhood or young adulthood. But several experts said it’s not uncommon for someone to have seasonal allergies for the first time as an adult.

Moving to a different part of the country and being exposed to different allergens may provoke a response, Dr. Kachru said.

New allergy symptoms in adulthood could also be “an inevitable consequence of really soaring pollen counts,” said Dr. Neeta Ogden, a New Jersey-based allergist.

The increase in winds associated with climate change could be distributing pollen farther, potentially exposing people to new varieties of it, said Dr. Mary Johnson, a research scientist at Harvard.

Research has also shown that hormones, including estrogen, progesterone and testosterone, can affect how allergic diseases develop.

Boys often have food allergies or eczema as babies and seasonal allergies or asthma in childhood but then have those conditions disappear when they hit puberty, Dr. Kachru said. But symptoms can return when they reach their 30s and 40s.

For some women, major hormonal shifts, including those that happen during puberty, pregnancy and menopause and while on birth control, can affect the onset and severity of allergy symptoms, Dr. Kachru said.

How do I manage the symptoms?

The first step is to reduce exposure. Keep your windows shut to prevent pollen from blowing into your home.

“The key is to prevent the outdoor allergens from becoming indoor allergens,” said Dr. William Reisacher, a professor of otolaryngology who treats allergies at Weill Cornell Medicine and New York-Presbyterian.

To help do so, take off the clothes you’ve worn outside when you get home and store them outside your bedroom. Then take a shower to rinse the pollen off your skin. Doctors recommend a saline nasal rinse to flush the pollen out of your nose. (If you make your own, be sure to use boiled, sterile or distilled water. )

Over-the-counter medications fall into two main categories: antihistamines and steroids. Both act on your immune system’s inflammatory response. Antihistamines are available as nasal sprays, eye drops and oral pills, including loratadine (Claritin), cetirizine (Zyrtec), levocetirizine (Xyzal) and fexofenadine (Allegra).

Steroids come as nasal sprays, including fluticasone (Flonase), budesonide (Benacort), triamcinolone (Nasacort) and mometasone (Nasonex).

If you have symptoms for the first time and aren’t sure how bad they’ll be or how long they’ll last, Dr. Kachru said, try an antihistamine to see if it helps.

If the symptoms persist, or you know that you get hit hard with allergy symptoms every spring, doctors recommend nasal sprays. Unlike antihistamines, which should be used only as needed, these steroids work best if you start using them a week or two before symptoms begin.

Doctors caution against using products with pseudoephedrine, such as Sudafed, for more than a day or two because they can increase heart rate and blood pressure. In 2020, a task force of physicians that issues guidelines for treating allergies recommended against using Benadryl to treat allergic rhinitis; doctors said it can have sedative effects and cause confusion.

If avoiding environmental triggers and taking medication don’t work for you, allergy shots or tablets that build your tolerance to allergens might help.

“It’s the only option available that actually makes the body less allergic,” Dr. Reisacher said.

A Guide to Surviving Allergy Season

For many people, springtime equals seasonal allergies. here is some guidance to deal with pollen-induced symptoms..

There are several steps you can take to prevent a bad allergy season. But you have to act early enough .

Studies suggest that allergens could play a role in mood disorders like depression and anxiety. Here’s what to know and how to get help if you need it.

The right products can go a long way in preventing allergy symptoms. Here are a few options for minimizing the allergens  around you.

Is your sneezing, sniffling and coughing a sign of allergies or a cold? There are some simple ways to tell what’s causing your symptoms .

When spring comes around, it can be difficult to know if fatigue is the result of allergies or something else. Here’s how to tell what’s making you tired .

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• v.9(31); 2021 Nov 6

Major depressive disorder: Validated treatments and future challenges

Rabie karrouri.

Department of Psychiatry, Moulay Ismaïl Military Hospital, Faculty of Medicine and Pharmacy, Sidi Mohamed Ben Abdellah University, Fez 30070, Morocco

Zakaria Hammani

Roukaya benjelloun.

Department of Psychiatry, Faculty of Medicine, Mohammed VI University of Health Sciences, Casablanca 20000, Morocco

Yassine Otheman

Department of Psychiatry, Moulay Ismaïl Military Hospital, Faculty of Medicine and Pharmacy, Sidi Mohamed Ben Abdellah University, Fez 30070, Morocco. [email protected]

Corresponding author: Yassine Otheman, MD, Associate Professor, Chief Doctor, Department of Psychiatry, Moulay Ismaïl Military Hospital, Faculty of Medicine and Pharmacy, Sidi Mohamed Ben Abdellah University, 1893, Km 2.2 road of Sidi Hrazem, Fez 30070, Morocco. [email protected]

Depression is a prevalent psychiatric disorder that often leads to poor quality of life and impaired functioning. Treatment during the acute phase of a major depressive episode aims to help the patient reach a remission state and eventually return to their baseline level of functioning. Pharmacotherapy, especially selective serotonin reuptake inhibitors antidepressants, remains the most frequent option for treating depression during the acute phase, while other promising pharmacological options are still competing for the attention of practitioners. Depression-focused psychotherapy is the second most common option for helping patients overcome the acute phase, maintain remission, and prevent relapses. Electroconvulsive therapy is the most effective somatic therapy for depression in some specific situations; meanwhile, other methods have limits, and their specific indications are still being studied. Combining medications, psychotherapy, and somatic therapies remains the most effective way to manage resistant forms of depression.

Core Tip: Depression is a persistent public health problem for which treatments must be codified and simplified to enhance current practice. Several therapies have been suggested worldwide, with varying levels of validity. This article explores effective and valid therapies for treating depression by addressing current and future research topics for different treatment categories.

INTRODUCTION

Depression is a common psychiatric disorder and a major contributor to the global burden of diseases. According to the World Health Organization, depression is the second-leading cause of disability in the world and is projected to rank first by 2030[ 1 ]. Depression is also associated with high rates of suicidal behavior and mortality[ 2 ].

Treatments administered during the acute phase of a major depressive episode aim to help the patient reach a remission state and eventually return to their baseline level of functioning[ 3 ]. Acute-phase treatment options include pharmacotherapy, depression-focused psychotherapy, combinations of medications and psychotherapy, and somatic therapies such as electroconvulsive therapy (ECT). Nevertheless, managing the acute phase of depression is only the first step in a long therapy process that aims to maintain remission and prevent relapses. In this article, we discuss various treatment options implemented by clinicians, highlighting the role that each option plays in actual psychiatric practice.

PHARMACOTHERAPY

While selective serotonin reuptake inhibitors (SSRIs) remain the gold-standard treatment for depression, new antidepressants are always being developed and tested. The ultimate goal is to discover a molecule that exhibits quick effectiveness with as few side effects as possible.

Daniel Bovet studied the structure of histamine (the causative agent in allergic responses) to find an antagonist, which was finally synthesized in 1937[ 4 ]. Since then, many researchers have studied the link between the structures and activities of different antihistaminic agents, contributing to the discovery of almost all antidepressants[ 5 ].

In the following subsections, we list the main classes of antidepressants in chronological order of apparition, highlighting the most widely used molecules in daily psychiatric practice.

Monoamine oxidase inhibitors

Iproniazid was the first drug defined as an antidepressant; it was later classified as a monoamine oxidase inhibitor (MAOI)[ 6 , 7 ]. Several other MAOIs have been introduced since 1957[ 8 ]. Due to their irreversible inhibition of monoamine oxidase, MOAIs have numerous side effects, such as hepatotoxicity and hypertensive crises, that can lead to lethal intracranial hemorrhages. Consequently, MAOIs have become less commonly used over time[ 9 ].

Trials have demonstrated that MAOIs’ efficacy is comparable to that of tricyclic antidepressants (TCAs)[ 10 , 11 ]. However, considering MAOIs’ drug interactions, dietary restrictions, and potentially dangerous side effects, they are now almost exclusively prescribed for patients who have not responded to several other pharmacotherapies, including TCAs[ 9 ]. Furthermore, MAOIs have demonstrated specific efficacy in treating depression with atypical features, such as reactive moods, reverse neuro-vegetative symptoms, and sensitivity to rejection[ 12 ].

MAOIs are also a potential therapeutic option when ECT is contraindicated[ 13 ]. MAOIs’ effectiveness is still unclear for treating depression in patients who are resistant to multiple sequential trials with SSRIs and serotonin-norepinephrine reuptake inhibitors (SNRIs)[ 14 ]. Nevertheless, psychiatrists’ use of MAOIs has declined over the years[ 15 , 16 ]. The use of MAOIs is generally restricted to patients who do not respond to other treatments.

The first TCA was discovered and released for clinical use in 1957 under the brand name Tofranil[ 5 , 17 ]. Since then, TCAs have remained among the most frequently prescribed drugs worldwide[ 9 ]. TCAs-such as amitriptyline, nortriptyline, protriptyline, imipramine, desipramine, doxepin, and trimipramine-are about as effective as other classes of antidepressants-including SSRIs, SNRIs, and MAOIs-in treating major depression[ 18 , 19 ].

However, some TCAs can be more effective than SSRIs when used to treat hospitalized patients[ 20 ]. This efficacy can be explained by the superiority of TCAs over SSRIs for patients with severe major depressive disorder (MDD) symptoms who require hospitalization[ 21 - 24 ]. However, no differences have been detected in outpatients who are considered less severely ill[ 18 , 20 ]. In most cases, TCAs should generally be reserved for situations when first-line drug treatments have failed[ 25 ].

In December 1987, a series of clinical studies confirmed that an SSRI called fluoxetine was as effective as TCAs for treating depression while causing fewer adverse effects[ 26 ]. After being released onto the market, its use expanded more quickly than that of any other psychotropic in history. In 1994, it was the second-best-selling drug in the world[ 7 ].

Currently available SSRIs include fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, and escitalopram. They have elicited different tolerance rates and side effects-mostly sexual and digestive (nausea and loss of appetite), as well as irritability, anxiety, insomnia, and headaches[ 27 ]. Nevertheless, SSRIs have a good tolerability profile[ 28 ].

In most systematic reviews and meta-analyses, SSRIs have demonstrated comparable efficacy to TCAs[ 18 , 19 , 29 ], and there is no significant evidence indicating the superiority of any other class or agent over SSRIs[ 29 - 31 ]. Furthermore, studies show no differences in efficacy among individual SSRIs[ 29 , 31 - 34 ]. Therefore, most guidelines currently recommend SSRIs as the first-line treatment for patients with major depression[ 25 ].

Norepinephrine reuptake inhibitors

Other monoamine (norepinephrine, serotonin, and dopamine) neurotransmitter reuptake inhibitors called SNRIs emerged during the 1990s to protect patients against the adverse effects of SSRIs[ 35 ]. Currently available SNRIs are venlafaxine, desvenlafaxine (the principal metabolite of venlafaxine), and duloxetine. The extended-release form of venlafaxine is the most commonly used drug in this class. Clinical guidelines commonly recommend prescribing SNRI to patients who do not respond to SSRIs[ 25 ].

In individual studies, venlafaxine and duloxetine are generally considered effective as SSRIs[ 36 ]. Also, venlafaxine’s efficacy is comparable to that of TCAs[ 37 , 38 ].

According to some meta-analyses, reboxetine (a selective noradrenaline reuptake inhibitor) seems less efficacious than SSRIs[ 39 ]. However, these findings could be due to the relatively poor tolerance of reboxetine[ 40 ].

Other antidepressants

Trazodone is the oldest medication of the so-called “other antidepressants” group that is still in wide use[ 41 , 42 ]. It has been shown to be an effective antidepressant in placebo-controlled research. However, in contemporary practice, it is much more likely to be used in low doses as a sedative-hypnotic than as an antidepressant[ 41 , 42 ].

Nefazodone’s structure is analogous to that of trazodone, though it has different pharmacological properties[ 43 ]. Its efficacy and overall tolerability are comparable to those of SSRIs, as indicated by comparative trials[ 43 ]. However, its use is associated with rare (but fatal) cases of clinical idiosyncratic hepatotoxicity[ 44 ].

Bupropion’s mechanism of action remains unclear, though it is classified as a norepinephrine and dopamine reuptake inhibitor[ 45 ]. It appears to have a more activating profile than SSRIs that are modestly superior to bupropion in patients with MDD[ 46 ]. However, for individuals with low to moderate levels of anxiety, the efficacy of bupropion in treating MDD is comparable to that of SSRIs[ 46 ]. Moreover, bupropion has a better tolerability profile than SSRIs, with minimal weight gain (or even leading to weight loss)[ 46 ]. In addition, bupropion is more likely than some SSRIs to improve symptoms of fatigue and sleepiness[ 47 ].

Mirtazapine and mianserin are tetracyclic compounds believed to increase the availability of serotonin or norepinephrine (or both), at least initially. Mirtazapine’s ability to antagonize serotoninergic subtypes receptors, <5-HT2A> and <5-HT2C>, could also increase norepinephrine and dopamine release in cortical regions[ 25 ]. Mirtazapine is about as effective as SSRIs[ 48 ].

Recently, drugs have been developed that block serotonin reuptake while affecting a variety of 5-HT receptor subtypes. The advantages of these agents ( e.g. , vilazodone and vortioxetine) over SSRIs are not fully clear. However, they appear to produce less sexual dysfunction and, in the specific case of vortioxetine, have particular benefits in depression-related cognitive impairment[ 49 ]. Indeed, vortioxetine is a very recent antidepressant with a multimodal mechanism that is thought to have a high affinity for serotonin transporters and 5-HT3, 5HT1A, 5HT7 receptors. Such a specific profile seems to indicate a level of efficacy to other antidepressants with a specific action on cognitive impairments[ 50 , 51 ].

In conclusion, no significant differences have been found between different classes of antidepressants in terms of their efficacy[ 52 ], though some drugs show some weak-to-moderate evidence indicating they are more effective than some other drugs[ 53 ]. Concerning the acceptability of these drugs, citalopram, escitalopram, fluoxetine, sertraline, and vortioxetine have been deemed more tolerable than other antidepressants, whereas amitriptyline, clomipramine, duloxetine, fluvoxamine, trazodone, and venlafaxine had the highest dropout rates[ 53 ] because of their more frequent and severe side effects. Nausea and vomiting were the most common reasons for treatment discontinuation; sexual dysfunction, sedation, priapism, and cardiotoxicity were also reported[ 31 , 41 ].

Ketamine and related molecules

In intravenous sub-anesthetic doses, ketamine has very quick effects on resistant unipolar (and, possibly, bipolar) depression and acute suicidal ideation[ 54 , 55 ]. The antidepressant effect of ketamine can persist for several days but eventually wanes. A few reports are have cited oral and intranasal formulations of ketamine for treatment-resistant depression[ 56 , 57 ], but there is still no data about the potential link between the onset of action and the route of administration.

Common adverse effects of ketamine include dizziness, neurotoxicity, cognitive dysfunction, blurred vision, psychosis, dissociation, urological dysfunction, restlessness, headache, nausea, vomiting, and cardiovascular symptoms[ 58 ]. Such adverse effects tend to be brief in acute, low-dose treatments[ 36 ], whereas prolonged exposure may predispose patients to neurotoxicity and drug dependence[ 56 ]. Lastly, since ketamine is associated with a higher risk of drug abuse and addiction, it cannot be recommended in daily clinical practice[ 59 , 60 ].

Ketamine is not a miracle drug, and many important factors still need to be defined, such as the most effective dose and the optimal administration route[ 61 , 62 ]. The current lack of guidelines about the therapeutic monitoring of ketamine treatment for depression further complicates the expanding use of this treatment[ 56 ]. Even though ketamine might never reach the market, it has stimulated research in the neurobiology of depression, including studies on potential fast and long-lasting antidepressants.

Ketamine has an active metabolite (hydroxynorketamine) that can produce rapid and sustained glutamatergic stimulation. It also seems to be free of many of the safety problems associated with ketamine and, thus, should be studied.

Research on the S-enantiomer of ketamine (S-ketamine, or esketamine, especially intranasal) could also be valuable, as it has a 3 to 4 times greater affinity than ketamine for the N-methyl-D-aspartate (NMDA) receptor[ 40 ]. It was approved by the United States Food and Drug Administration in March 2019 for treatment-resistant depression. However, current knowledge about the effects of prolonged esketamine therapy is still preliminary. In addition, regarding the potential risk of abuse, esketamine use must be carefully monitored[ 63 - 65 ].

Other glutamate receptor modulators have been evaluated in small studies as monotherapy agents or as adjuncts to other antidepressants. Examples include noncompetitive NMDA receptor antagonists (memantine, dextromethorphan/quinidi-ne, dextromethorphan/bupropion, and lanicemine), NR2B subunit-specific NMDA receptor antagonists (traxoprodil), NMDA receptor glycine site partial agonists (D-cycloserine, rapastinel), and metabotropic glutamate receptor antagonists (basimglurant, declogurant)[ 66 - 68 ] (Table ​ (Table1). 1 ).

Main classes of antidepressants with their date of approval, contributions, and disadvantages

NMDA: N-methyl-D-aspartate; SSRI: DSelective serotonin reuptake inhibitors; MDD: Major depressive disorder; MAOI: Monoamine oxidase inhibitor.

Perspectives

A purely neurotransmitter-based explanation for antidepressant drug action-especially serotonin-inhibiting drugs-is challenged by the significant percentage of patients who never achieve full remission[ 6 ] and the delayed clinical onset, which varies from two to four weeks. Moreover, studies show an acute increase in monoamines in the synaptic cleft immediately following treatment[ 69 ], even when the depletion of tryptophan (serotonin’s precursor) does not induce depressive-like behavior in healthy humans[ 70 , 71 ].

This finding shows that research on the pharmacological options for treating depression must go beyond monoaminergic neurotransmission systems. Research on the development of new antidepressants should explore several mechanisms of action on several types of receptors: Antagonism, inhibition of the reuptake of neurotransmitters, and modulators of glutamate receptors, as well as interactions with α-amino-3-acid receptors, hydroxy-5-methyl-4-isoxazolepropionic, brain-derived neurotrophic factor, tyrosine kinase B receptor (the mechanistic target of rapamycin), and glycogen synthase kinase-3[ 72 ].

Identifying the cellular targets of rapid-acting agents like ketamine could help practitioners develop more effective antidepressant molecules by revealing other receptors involved in gamma-aminobutyric acid regulation and glutamate transmission[ 73 ].

PSYCHOTHERAPY

Psychotherapeutic interventions are widely used to treat and prevent most psychiatric disorders. Such interventions are common in cases of depression, psychosocial difficulties, interpersonal problems, and intra-psychic conflicts. The specific psychotherapy approach chosen for any given case depends on the patient’s preference, as well as on the clinician’s background and availability[ 74 ] . Psychotherapy for patients with depression strengthens the therapeutic alliance and enables the patient to monitor their mood, improve their functioning, understand their symptoms better, and master the practical tools they need to cope with stressful events[ 75 ]. The following subsections briefly describe psychotherapeutic interventions that have been designed specifically for patients with depression.

Overview of psychotherapy in depression

Depression-focused psychotherapy is typically considered the initial treatment method for mild to moderate MDD. Based on significant clinical evidence, two specific psychotherapeutic methods are recommended: Cognitive-behavioral therapy (CBT) and interpersonal therapy (IPT). Supportive therapy (ST) and psychoeducational intervention (PEI) have also been recommended, those the evidence supporting these methods s not as strong. In more cases of severe depression, ST and PEI are used only to augment pharmacological treatments.

After remission, CBT, PEI, and mindfulness-based cognitive therapy (MBCT) are proposed to maintain and prevent depression. However, when psychotherapy has been effective during the initial phases of a depressive episode, it should be continued to maintain remission and prevent relapses while reducing the frequency of sessions[ 25 , 75 , 76 ].

Specific and intensive psychotherapeutic support is recommended for patients with chronic depression because of high rates of comorbidity with personality disorders, early trauma, and attachment deficits. The European Psychiatric Association recommends using the Cognitive Behavioral Analysis System of Psychotherapy (CBASP) for treating chronic depression and utilizing specific approaches suited to each patient’s preferences[ 77 ]. All these therapeutic options are summarized in Figure ​ Figure1 1 .

Overview of psychotherapy in different clinical situations of depression. MDD: Major depressive disorder; CBT: Cognitive-behavioral therapy; IPT: Interpersonal therapy; ST: Supportive therapy; PEI: Psycho-educational intervention; MBCT: Mindfulness based cognitive therapy; SIPS: Specific and intensive psychotherapeutic support; CBASP: Cognitive Behavioral Analysis System of Psychotherapy.

Structured psychotherapies

Cognitive and behavioral therapies: Based on robust evidence, CBT is one of the most well-documented and validated psychotherapeutic methods available. Interventional strategies are based on modifying dysfunctional behaviors and cognitions[ 77 ]. CBT targets depressed patients’ irrational beliefs and distorted cognitions that perpetuate depressive symptoms by challenging and reversing them[ 3 ]. Thus, CBT is a well-known effective treatment method for MDD[ 78 ] and has been recommended in most guidelines as a first-line treatment[ 79 - 81 ].

However, the effectiveness of CBT depends on patient’s capacity to observe and change their own beliefs and behaviors. Some simple techniques were developed to overcome this issue, especially in primary care management. Behavioral activation is one such technique, consisting of integrating pleasant activities into daily life to increase the number and intensity of the positive interactions that the patient has with their environment[ 82 , 83 ].

Acceptance and commitment therapy is another form of CBT. This type of therapy, which is based on functional contextualism, can help patients accept and adjusting to persistent problems. It appears to be effective in reducing depressive symptoms and preventing relapses[ 77 , 84 ].

Another form of CBT is computerized CBT (CCBT), implemented via a computer with a CD-ROM, DVD, or online CCBT, allowing patients to benefit from this therapy under conditions of reduced mobility, remoteness, confinement, or quarantine[ 79 ] .

CCBT and guided bibliotherapy based on CBT could be considered for self-motivated patients with mild to moderate major depression or as a complementary treatment to pharmacotherapy[ 25 ]. CBT is also recommended for patients with resistant depression in combination with antidepressants[ 85 ].

Schema therapy is another CBT-derived therapy that can be used in patients who have failed classical CBT, like patients with personality disorder comorbidity. Schema therapy is about as effective as CBT for treating depression[ 86 ]. In adolescent patients with depression, CBT is also a recommended option with plenty of evidence from multiple trials. Meanwhile, it remains the first-line treatment in children despite mixed findings across trials[ 87 ] . CBT is also a promising option for elderly depressed patients, though substantial evidence is still lacking because of the limited data on the subject[ 88 ] .

IPT: The goal of IPT is to identify the triggers of depressive symptoms or episodes. These triggers may include losses, social isolation, or difficulties in social interactions. The role of the intervention is to facilitate mourning (in the case of bereavement), help the patient recognize their own affect, and resolve social interaction dysfunction by building their social skills and social supports[ 89 ]. IPT, like CBT, is a first-line treatment for mild to moderate major depressive episodes in adults; it is also a well-established intervention for adolescents with depression[ 25 ] .

Problem-solving therapy: The problem-solving therapy (PST) approach combines cognitive and interpersonal elements, focusing on negative assessments of situations and problem-solving strategies. PST has been used in different clinical situations, like preventing depression among the elderly and treating patients with mild depressive symptoms, especially in primary care. Despite its small effect sizes, PST is comparable to other psychotherapeutic methods used to treat depression[ 88 , 90 ].

Marital and family therapy: Marital and family therapy (MFT) is effective in treating some aspects of depression. Family therapy has also been used to treat severe forms of depression associated with medications and hospitalization[ 91 ]. Marital and family problems can make people more vulnerable to depression, and MFT addresses these issues[ 92 ]. Marital therapy includes both members of the couple, as depression is considered in an interpersonal context in such cases. Some of the goals of this therapy are to facilitate communication and resolve different types of marital conflict. Family therapy uses similar principles as other forms of therapy while involving all family members and considering depression within the context of pathological family dynamics[ 93 ].

ST: Although ST is not as well-structured or well-evaluated as CBT or IPT, it is still commonly used to support depressed patients. In addition to sympathetic listening and expressing concern for the patient’s problems, ST requires emotionally attuned listening, empathic paraphrasing, explaining the nature of the patient’s suffering, and reassuring and encouraging them. These practices allow the patient to ventilate and accept their feelings, increase their self-esteem, and enhance their adaptive coping skills[ 94 ].

Psychodynamic therapy: Psychodynamic therapy encompasses a range of brief to long-term psychological interventions derived from psychoanalytic theories. This type of therapy focuses on intrapsychic conflicts related to shame, repressed impulses, problems in early childhood with one’s emotional caretakers that lead to low self-esteem and poor emotional self-regulation[ 93 , 95 ]. Psychodynamic therapy’s efficacy in the acute phase of MDD is well-established compared to other forms of psychotherapy.

Group therapy: The application of group therapy (GT) to MDD remains limited. Some data support the efficacy of specific types of GT inspired by CBT and IPT[ 96 - 98 ]. Group CBT for patients with subthreshold depression is an effective post-depressive-symptomatology treatment but not during the follow-up period[ 99 ]. Supportive GT and group CBT reduce depressive symptoms[ 96 ], especially in patients with common comorbid conditions[ 100 ]. However, studies are still lacking in this domain.

MBCT: MBCT is a relatively recent technique that combines elements of CBT with mindfulness-based stress reduction[ 101 ]. Studies have shown that eight weeks of MBCT treatment during remission reduces relapse. Thus, it is a potential alternative to reduce, or even stop, antidepressant treatment without increasing the risk of depressive recurrence, especially for patients at a high risk of relapse ( i.e. , patients with more than two previous episodes and patients who have experienced childhood abuse or trauma)[ 102 ].

Other psycho-interventions

Psycho-education: This type of intervention educates depressed patients and (with their permission) family members involved in the patient’s life about depression symptoms and management. This education should be provided in a language that the patient understands. Issues such as misperceptions about medication, treatment duration, the risk of relapse, and prodromes of depression should be addressed. Moreover, patients should be encouraged to maintain healthy lifestyles and enhance their social skills to prevent depression and boost their overall mental health. Many studies have highlighted the role of psycho-education in improving the clinical course, treatment adherence, and psychosocial functioning in patients with depression[ 103 ].

Physical exercise: Most guidelines for treating depression, including the National Institute for Health and Care Excellence, the American Psychiatric Association, and the Royal Australian and New Zealand College of Psychiatrists, recommend that depressed patients perform regular physical activity to alleviate symptoms and prevent relapses[ 104 ] . Exercise also promotes improvements in one’s quality of life in general[ 105 ] . However, exercise is considered an adjunct to other anti-depressive treatments[ 25 ] .

Although psychotherapy is effective for treating depression and improving patients’ quality of life, its direct actions against depressive symptoms are not fully understood[ 106 ]. Identifying factors ( e.g. , interpersonal variables) linked to treatment responses can help therapists choose the right therapeutic strategy for each patient and guide research to modify existing therapies and develop new ones[ 107 ].

Since depression is a primary care problematic, simplifying psychotherapy procedures will increase the use of psychological interventions for depression, especially in general practice. Brief forms (six to eight sessions) of CBT and PST have already shown their effectiveness for treating depression[ 108 ]. Nevertheless, simpler solutions must be made available to practitioners to help them manage and prevent depression.

SOMATIC TREATMENTS

In many situations, depression can also be managed via somatic treatments. ECT is the most well-known treatment for resistant depression, and solid evidence supports its effectiveness and safety. In recent decades, various innovative techniques have been proposed, such as repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation (tDCS), vagus nerve stimulation (VNS), deep brain stimulation (DBS), and magnetic seizure therapy, with varying efficiency levels[ 109 ].

ECT is arguably the most effective treatment modality in psychiatry, and its superiority over pharmacotherapy for major unipolar depression is widely supported[ 110 ]. ECT reduces the number of hospital readmissions and lightens the burden of depression, leading to a better quality of life[ 111 , 112 ].

Moreover, ECT is considered safe[ 113 ]. Advances in anesthesia and ECT techniques have decreased complications related to ECT while also improving cognitive outcomes and patient satisfaction.

However, the stigma surrounding ECT limits its use. Most misconceptions date back to early ECT techniques (when it was performed without muscle relaxants or anesthesia). Nevertheless, some people still consider ECT as the last option for treating depression, even though most studies indicate that ECT is more beneficial in patients with fewer pharmacological treatments[ 114 - 116 ].

ECT is typically recommended for patients with severe and psychotic depression, a high risk of suicide, or Parkinson’s disease, as well as pregnant patients[ 117 - 119 ]. The maintenance ECT also appears to prevent relapses[ 120 ]. The current practice of ECT continues to improve as protocols become more advanced, mainly owing to bioinformatics, and as more research is carried out in this domain[ 121 - 125 ].

This method, which is a type of biological stimulation that affects brain metabolism and neuronal electrical activity, has been widely used in research on depression[ 126 ]. Recent literature shows a significant difference between rTMS and fictitious stimulation regarding its improvements in depressive symptoms[ 127 ]. Preliminary research has revealed synergistic ( e.g. , rTMS/quetiapine) and antagonizing ( e.g. , rTMS/cannabinoid receptor (CB1) antagonist) interactions between neuro-modulation and pharmacotherapy[ 128 ]. Treatments combining rTMS and antidepressants are significantly more effective than placebo conditions, with mild side effects and good acceptability[ 129 ]. Although these results are encouraging, they remain inconsistent due to differences in rTMS treatment frequencies, parameters, and stimulation sites[ 129 ]. Therefore, clinical trials with large sample sizes are needed to specify which factors promote favorable therapeutic responses. Also, additional preclinical research should investigate the synergistic effects of other pharmacological molecules and guide integrated approaches (rTMS plus pharmacotherapy).

This technique delivers weak currents to the brain via electrodes placed on the scalp[ 130 ]. It is easy to use, safe, and tolerable[ 131 ]. The tDCS technique significantly outperforms the simulator in terms of the rate of response and remission[ 132 ]. However, its effect remains lower than that of antidepressants[ 133 ] and rTMS[ 134 ]. It can be used as a complementary intervention or as monotherapy to reduce depressive symptoms in unipolar or bipolar depression patients[ 135 ]. The antidepressant effects of tDCS may involve long-term neuroplastic changes that continue to occur even after the acute phase of treatment, which explains its delayed efficacy[ 135 ].

Recently, neurophysiological studies have shown that the clinical effects of tDCS do not have a direct linear relationship with the dose of stimulation[ 136 ]. tDCS, as a relatively simple and portable technology, is well-suited for remote supervised treatment and assessment at home, thus facilitating long treatment durations[ 136 ].

Since the optimal clinical effects of tDCS are delayed, future clinical trials should use longer evaluation periods and aim to identify responsive patients using algorithms[ 137 ].

VNS is a therapeutic method that has been used for the last sixteen years to treat resistant unilateral or bipolar depression. However, despite several clinical studies attesting to its favorable benefit-risk ratio and its approval by the Food Drug Administration in 2005, it is not used very often[ 138 ].

VNS involves the implantation of a pacemaker under the collarbone that is connected to an electrode surrounding the left vagus nerve. The left vagus nerve is preferred because it exposes the patient to fewer potential adverse cardiac effects. Indeed, most cardiac afferent fibers originate from the right vagus nerve[ 139 ]. Since the turn of the century, numerous studies have demonstrated the efficacy of VNS in resistant depression[ 140 - 142 ].

However, only one randomized, double-blind, controlled trial comparing VNS with usual medical treatment has been conducted over a short period of 10 wk[ 141 ]. Moreover, the results of this study did not indicate that the combination of VNS with typical medical treatments was better than the typical medical treatment on its own.

However, VNS has demonstrated progressively increasing improvements in depressive symptoms, with significant positive outcomes observed after six to 12 mo; these benefits can last for up to two years[ 143 ].

More long-term studies are needed to fully determine the predictors of the correct response.

According to the literature, DBS of the subgenual cingulate white matter (Brodmann area = BA 25) elicited a clinical response in 60% of resistant depression patients after six months and clinical remission in 35% of patients, with benefits maintained for over 12 mo[ 144 ]. The stimulation of other targets, in particular the nucleus accumbens, to treat resistant depression has gained interest recently. Behavioral effects indicate the quick and favorable impact of stimulation on anhedonia, with significant effects on mood appearing as early as week one after treatment begins[ 145 ].

Magnetic seizure therapy

Magnetic seizure therapy involves inducing a therapeutic seizure by applying magnetic stimulation to the brain while the patient is under anesthesia. This technique is still being investigated as a viable alternative to ECT to treat many psychiatric disorders. Evidence supporting its effectiveness on depressive symptoms continues to grow, and it appears to induce fewer neurocognitive effects than ECT[ 146 , 147 ].

Luxtherapy (phototherapy)

The first description of reduced depression symptoms due to intense light exposure was presented in 1984[ 148 ]. Optimal improvements were obtained with bright light exposure of 2500 Lux for two hours per day, with morning exposure shown to be superior to evening exposure[ 149 ].

A review and meta-analysis[ 150 ] showed that more intense (but shorter) exposures (10000 Lux for half an hour per day or 6000 Lux for 1.5 h per day) have the same efficacy. Importantly, this treatment method is effective both for those with seasonal and non-seasonal depression. Benefits of phototherapy related to sleep deprivation and drug treatments have also been reported[ 151 ].

Neuro-modulation treatments offer a range of treatment options for patients with depression. ECT remains the most documented and effective method in this category[ 151 ]. rTMS is an interesting technique as well, as it offers a well-tolerated profile[ 85 ], while tDCS offers encouraging but varying results that depend on the study’s design and the techniques used[ 130 ].

More investigations are needed to specify which indications are the best for each method according to the clinical and biological profiles of patients. The uses of such methods are expanding, probably, with their efficiency increasing when they are tailored to the patient. Furthermore, somatic interventions for depression need to be regularly assessed and integrated into psychiatrists’ therapeutic arsenals.

Treating depression is still a significant challenge. Finding the best option for each patient is the best way to obtaining short- and long-term effectiveness. The three principal methods available to caregivers are antidepressants, specifically structured psychotherapies, and somatic approaches. Research on depression pharmacotherapy continues to examine new molecules implicated in gamma-aminobutyric acid regulation and glutamate transmission. Also, efforts to personalize and simplify psychotherapeutic interventions are ongoing. Protocols using somatic interventions need to be studied in more depth, and their indications must be specified. ECT is the only somatic treatment with confirmed indications for certain forms of depression. Combinations of medications, psychotherapy, and somatic therapies remain the most effective ways to manage resistant forms of depression.

Conflict-of-interest statement: All authors declare that they have no conflict of interest related to this article.

Manuscript source: Invited manuscript

Peer-review started: March 31, 2021

First decision: June 5, 2021

Article in press: October 11, 2021

Specialty type: Medicine, research and experimental

Country/Territory of origin: Morocco

Peer-review report’s scientific quality classification

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P-Reviewer: Narumiya K S-Editor: Fan JR L-Editor: A P-Editor: Fan JR

Contributor Information

Rabie Karrouri, Department of Psychiatry, Moulay Ismaïl Military Hospital, Faculty of Medicine and Pharmacy, Sidi Mohamed Ben Abdellah University, Fez 30070, Morocco.

Zakaria Hammani, Department of Psychiatry, Moulay Ismaïl Military Hospital, Faculty of Medicine and Pharmacy, Sidi Mohamed Ben Abdellah University, Fez 30070, Morocco.

Roukaya Benjelloun, Department of Psychiatry, Faculty of Medicine, Mohammed VI University of Health Sciences, Casablanca 20000, Morocco.

Yassine Otheman, Department of Psychiatry, Moulay Ismaïl Military Hospital, Faculty of Medicine and Pharmacy, Sidi Mohamed Ben Abdellah University, Fez 30070, Morocco. [email protected] .

The results of this review suggest that the research field of seasonal variations in mood disorders is fragmented, and important questions remain unanswered. ... We used a broad search strategy and selected the subset of papers on depression and depressive symptoms during the full-text paper review. The following databases were accessed as part ...

Seasonal affective disorder or SAD is a recurrent major depressive disorder with a seasonal pattern usually beginning in fall and continuing into winter months. A subsyndromal type of SAD, or S-SAD, is commonly known as "winter blues.". Less often, SAD causes depression in the spring or early summer. Symptoms center on sad mood and low energy.

Abstract. Since the first description of Seasonal Affective Disorder (SAD) by Rosenthal et al. in the 1980s, treatment with daily administration of light, or Bright Light Therapy (BLT), has been proven effective and is now recognized as a first-line therapeutic modality. More recently, studies aimed at understanding the pathophysiology of SAD ...

Background Seasonal Affective Disorder is a recurrent depressive disorder which usually begins in the fall/winter and enters into remission in the spring/summer, although in some cases may occur in the summer with remission in the autumn-winter. In this study the authors evaluated the association between seasonal changes in mood and behavior with psychiatric disturbance. Method Descriptive ...

Seasonal Affective Disorder / psychology*. Seasons. The results of this review suggest that the research field of seasonal variations in mood disorders is fragmented, and important questions remain unanswered. There is some support for seasonal variation in clinical depression, but our results contest a general population shift towards lower ...

Seasonal affective disorder (SAD) is a seasonally recurrent type of major depression that has detrimental effects on patients' lives during winter. Little is known about how it affects patients during summer and about patients' and physicians' perspectives on preventive SAD treatment. The aim of our study was to explore how SAD patients experience summers, what type of preventive ...

Seasonal affective disorder or SAD is a recurrent major depressive disorder with a seasonal pattern usually beginning in fall and continuing into winter months. A subsyndromal type of SAD, or S-SAD, is commonly known as "winter blues." Less often, SAD causes depression in the spring or early summer. Symptoms center on sad mood and low energy.Those most at risk are female, are younger, live ...

1. Introduction. Seasonal Affective Disorder (SAD) of the winter subtype is identified by recurrent depressive episodes that correspond with winter months and remit during the spring, for at least 2 consecutive years (Rosenthal et al., 1984).Despite the abundance of previous research on seasonality of depression, the existence of a seasonal pattern remains debated among experts.

Introduction. Seasonal affective disorder or SAD is defined in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) as a type of recurrent major depressive disorder with a seasonal pattern [Citation 1].This type of depression occurs during a specific time of year, with the onset of symptoms for winter-pattern SAD, the predominant subtype and focus of this study ...

1. Introduction. Rosenthal's seminal description of Seasonal Affective Disorder confirmed a place in modern psychiatric thinking for hypotheses linking affective state and light (Rosenthal et al., 1984).In the intervening decades, accumulating evidence ranging in scope from the basic neurosciences (Ciarleglio et al., 2011) to population-based observational studies (Magnusson, 2000), has ...

Despite the abundance of previous research on seasonality of depression, the existence of a seasonal pattern remains debated among experts. Various population based studies have failed to identify the expected seasonal pattern, notably, two population based analyses conducted by researchers in the United States and Norway (Hansen et al., 2011 ...

Seasonal affective disorder, also known as SAD, is more than just the winter blues. It is a type of depression that lasts for a season, typically the winter months, and goes away during the rest of the year. Symptoms of SAD are the same as those of depression. They can vary in severity and often interfere with personal relationships.

Abstract. Seasonal affective disorder or SAD is a recurrent major depressive disorder with a seasonal pattern usually beginning in fall and continuing into winter months. A subsyndromal type of ...

Seasonal depressive disorder is a condition known to occur to a small part of the United States population. It is also called seasonal affective disorder.[1] It is dominant in areas known to experience lower sunlight levels at certain times of the year, most commonly at the change of seasons, particularly in late fall and continuing into winter, but it can also happen in the spring and summer.

SAD is a form of depression, and it can become just as serious, causing the same symptoms as major depressive disorder such as fatigue, changes in mood, or loss of interest. About 5 percent of U.S. adults experience SAD, according to APA's website, with the symptoms lasting about 40 percent of the year. The most difficult months tend to be ...

In 1984, he published the first paper to scientifically name the winter blues: Seasonal affective disorder (SAD), also called seasonal depression, was a type of depression brought on by the dark days of winter. Subsequent studies have found that this form of depression varies by geography, notably affecting those in northern latitudes more.

Discussion. This analysis confirms the existence of seasonal variability in depressive symptoms in the Canadian household population. The lack of association for respondents scoring 10+ fails to confirm that major depressive episodes (as opposed to subsyndromal ones included in the 5+ group) have a seasonal pattern.

Research on seasonal affective disorder ... An Overview of Assessment and Treatment Approaches. Depression Research and Treatment, 2015: 178564. doi: 10.1155/2015/178564. ... paper or report: APA.

Seasonal affective disorder (SAD) is a type of depression that's related to changes in seasons — seasonal affective disorder (SAD) begins and ends at about the same times every year. If you're like most people with SAD, your symptoms start in the fall and continue into the winter months, sapping your energy and making you feel moody. These ...

Mindfulness-based cognitive therapy (MBCT) is a well-known, effective treatment in the prevention of relapse in Major Depression Disorder (MDD). However, a recent study in people with Seasonal Affective Disorder (SAD) showed that MBCT given in spring was ineffective in preventing a next depressive episode. To test the hypothesis that people ...

Spring allergy seasons are beginning about 20 days earlier than they had, according to an analysis of pollen count data from 60 stations across North America from 1990 to 2018. That shift can have ...

Method. We conducted prospective summer followup of community adults who, the winter before, were diagnosed with Major Depression, Recurrent with Seasonal Pattern on the Structured Clinical Interview for DSM-IV Axis I Disorders, developed a current SAD episode on the Structured Interview Guide for the Hamilton Rating Scale for Depression—Seasonal Affective Disorder Version (SIGH-SAD), and ...

Depression is a prevalent psychiatric disorder that often leads to poor quality of life and impaired functioning. Treatment during the acute phase of a major depressive episode aims to help the patient reach a remission state and eventually return to their baseline level of functioning. Pharmacotherapy, especially selective serotonin reuptake ...

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