Seasonal Affective Disorder
Phototherapy
Color Therapy
Melatonin
Seasons
Melatonin sensitivity to dim white light in affective disorders. (1/73)
Both dim and bright light has been shown to suppress the nocturnal secretion of the pineal hormone melatonin. Early reports suggests that an abnormal response to light occurs in patients with bipolar affective disorder, where as patients with major depressive disorder respond similarly to controls. It has been suggested that this abnormal sensitivity of the melatonin response to light could be a trait marker of bipolar affective disorder. However reports lack consistency. Hence, we investigated the melatonin suppression by dim light (200 lux) in patients with bipolar affective disorder, seasonal affective disorder and major depressive disorder. Results suggest that a supersensitive melatonin suppression to light in bipolar affective disorder (p < .005), and seasonal affective disorder (p < .05), whereas patients with major depressive disorder display similar suppression to controls. The supersensitivity may be a mechanism where by phase-delayed rhythms, are resynchronised to a new circadian position. Conversely, an abnormality may exist in the pathway from the retina to the suprachiamatic nucleus. (+info)Influence of sleep-wake and circadian rhythm disturbances in psychiatric disorders. (2/73)
Recent evidence shows that the temporal alignment between the sleep-wake cycle and the circadian pacemaker affects self-assessment of mood in healthy subjects. Despite the differences in affective state between healthy subjects and patients with psychiatric disorders, these results have implications for analyzing diurnal variation of mood in unipolar and bipolar affective disorders and sleep disturbances in other major psychiatric conditions such as chronic schizophrenia. In a good proportion of patients with depression, mood often improves over the course of the day; an extension of waking often has an antidepressant effect. Sleep deprivation has been described as a treatment for depression for more than 30 years, and approximately 50% to 60% of patients with depression respond to this approach, especially those patients who report that their mood improves over the course of the day. The mechanisms by which sleep deprivation exerts its antidepressant effects are still controversial, but a reduction in rapid eye movement sleep (REM sleep), sleep pressure and slow-wave sleep (SWS), or a circadian phase disturbance, have been proposed. Although several studies support each of these hypotheses, none is sufficient to explain all observations reported to date. Unfortunately, the disturbed sleep-wake cycle or behavioural activities of depressed patients often explain several of the abnormalities reported in the diurnal rhythms of these patients. Thus, protocols that specifically manipulate the sleep-wake cycle to unmask the expression of the endogenous circadian pacemaker are greatly needed. In chronic schizophrenia, significant disturbances in sleep continuity, REM sleep, and SWS have been consistently reported. These disturbances are different from those observed in depression, especially with regard to REM sleep. Circadian phase abnormalities in schizophrenic patients have also been reported. Future research is expected to clarify the nature of these abnormalities. (+info)Pathophysiology of seasonal affective disorder: a review. (3/73)
The study of the pathophysiology of seasonal affective disorder (SAD, also known as winter depression) has historically been intimately linked to investigations into the mechanisms of action of light therapy. This paper reviews the studies on the pathophysiology of SAD with emphasis on circadian, neurotransmitter, and genetic hypotheses. There is substantial evidence for circadian phase shift and serotonergic hypotheses, but conflicting results may indicate that SAD is a biologically heterogeneous condition. Recent progress in defining the molecular mechanisms of the human circadian clock and retinal phototransduction of light will provide important new directions for future studies of the etiology and pathophysiology of SAD. (+info)Light therapy for seasonal affective disorder in primary care: randomised controlled trial. (4/73)
BACKGROUND: Studies of light therapy have not been conducted previously in primary care. AIMS: To evaluate light therapy in primary care. METHOD: Fifty-seven participants with seasonal affective disorder were randomly allocated to 4 weeks of bright white or dim red light. Baseline expectations for treatment were assessed. Outcome was assessed with the Structured Interview Guide for the Hamilton Depression Scale, Seasonal Affective Disorder Version. RESULTS: Both groups showed decreases in symptom scores of more than 40%. There were no differences in proportions of responders in either group, regardless of the remission criteria applied, with around 60% (74% white light, 57% red light) meeting broad criteria for response and 31% (30% white light, 33% red light) meeting strict criteria. There were no differences in treatment expectations. CONCLUSIONS: Primary care patients with seasonal affective disorder improve after light therapy, but bright white light is not associated with greater improvements. (+info)Variability in the 5-HT(2A) receptor gene is associated with seasonal pattern in major depression. (5/73)
The 102-T/C polymorphism of the 5-HT(2A) receptor gene was analysed in 159 patients with major depression and 164 unrelated and healthy controls using a case-control design. Allele and genotype frequencies did not differ between cases and controls. No differences according to sex, age of onset, melancholia, suicidal behaviour or family history of psychiatric illness were found. However, genotype distributions significantly differed between patients with seasonal pattern in their episodes (MDS) and patients with no seasonal pattern (N-MDS) (chi(2) = 10.63; P = 0.004). A seasonal pattern was 7.57 times more frequent in 102C-allele carriers than in 102T homozygous (95.1% of patients MDS carried 102C-allele vs 72% of patients N-MDS (chi(2) = 9.45, df=1, P = 0.002; OR = 7.57 (95% CI: 1.65--48.08)). These results suggest that variation in the 5-HT2A receptor gene may play a role in the development of major depression with seasonal pattern and support the existence of a genetic and etiological heterogeneity underlying the diagnosis of major depression. (+info)Seasonal affective disorder: prevalence, detection and current treatment in North Wales. (6/73)
BACKGROUND: There is a paucity of information concerning the prevalence and detection of seasonal affective disorder (SAD) in UK populations. AIMS: To determine the prevalence, detection and current treatment of SAD within a general population sample. METHOD: The study was conducted in conjunction with the Outcomes of Depression International Network (ODIN) project, a large European study of depression. At the North Wales arm of the project, 1999 adults were randomly selected from a health authority database and screened by post for SAD with the Seasonal Patterns Assessment Questionnaire (SPAQ). Those scoring above cut-off were offered diagnostic interview, after which diagnosis of SAD according to DSM-IV criteria could be made. RESULTS: The prevalence rate of SAD was calculated to be 2.4% (95% CII.4-1.3). The majority of identified cases had not previously received a diagnosis of SAD from their general practitioner, although over half had been diagnosed with other forms of depression and had been prescribed antidepressant medication. CONCLUSIONS: Although SAD was found to be common in this general population sample it appeared to be largely underdiagnosed and/or misdiagnosed. (+info)Early response to light therapy partially predicts long-term antidepressant effects in patients with seasonal affective disorder. (7/73)
OBJECTIVE: To determine if the antidepressant effect of 1 hour of light therapy is predictive of the response after 1 and 2 weeks of treatment in patients with seasonal affective disorder (SAD). PATIENTS: Twelve patients with SAD. SETTING: National Institutes of Health Clinical Center, Bethesda, Md. INTERVENTIONS: Light therapy for 2 weeks. OUTCOME MEASURES: Scores on the Seasonal Affective Disorder Version of the Hamilton Depression Rating Scale (SIGH-SAD) on 4 occasions (before and after 1 hour of light therapy and after 1 and 2 weeks of therapy) in the winter when the patients were depressed. Change on typical and atypical depressive scores at these time points were compared. RESULTS: Improvement of atypical depressive symptoms after 1 hour of light therapy positively correlated with improvement after 2 weeks of therapy. CONCLUSION: In patients with SAD, the early response to light therapy may predict some aspects of long-term response to light therapy, but these results should be treated with caution until replicated. (+info)Effects of alpha-methyl-para-tyrosine-induced catecholamine depletion in patients with seasonal affective disorder in summer remission. (8/73)
Noradrenergic and dopaminergic mechanisms have been proposed for the pathophysiology of seasonal affective disorder (SAD). We investigated the effects of catecholamine depletion using alpha-methyl-para-tyrosine (AMPT), an inhibitor of tyrosine hydroxylase, in patients with SAD in natural summer remission. Nine drug-free patients with SAD by DSM-IV criteria, in summer remission for at least eight weeks, completed a double-blind, crossover study. Behavioral ratings and serum HVA and MHPG levels were obtained for 3-day sessions during which patients took AMPT or an active control drug, diphenhydramine. The active AMPT session significantly reduced serum levels of HVA and MHPG compared with the control diphenhydramine session. The AMPT session resulted in higher depression ratings with all nine patients having significant clinical relapse, compared with two patients during the diphenhydramine session. All patients returned to baseline scores after drug discontinuation. Catecholamine depletion results in significant clinical relapse in patients with SAD in the untreated, summer-remitted state. AMPT-induced depressive relapse may be a trait marker for SAD, and/or brain catecholamines may play a direct role in the pathogenesis of SAD. (+info)Seasonal Affective Disorder (SAD) is not specifically defined in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DS-5), which is used by mental health professionals to diagnose mental conditions. However, it is classified as a recurrent major depressive disorder with a seasonal pattern.
According to the DSM-5, a seasonal pattern is defined as: "There has been a regular temporal relationship between the onset of major depressive episodes in major depressive disorder and a particular time of the year (e.g., always starts in fall or winter)." This means that someone with SAD experiences depressive symptoms during specific seasons, most commonly in late fall or winter, but in some cases, also in spring or summer.
The symptoms of SAD may include:
* Feeling depressed most of the day, nearly every day
* Losing interest in activities you once enjoyed
* Having low energy
* Having problems sleeping
* Experiencing changes in appetite or weight
* Feeling sluggish or agitated
* Having difficulty concentrating
* Feeling hopeless, worthless or guilty
* Having thoughts of death or suicide
These symptoms must be more severe than just feeling "blue" or having a bad day. They also must cause significant distress or impairment in social, occupational, or other important areas of functioning. Additionally, the symptoms must not be due to substance use or another medical condition.
Phototherapy is a medical treatment that involves the use of light to manage or improve certain conditions. It can be delivered in various forms, such as natural light exposure or artificial light sources, including lasers, light-emitting diodes (LEDs), or fluorescent lamps. The wavelength and intensity of light are carefully controlled to achieve specific therapeutic effects.
Phototherapy is most commonly used for newborns with jaundice to help break down bilirubin in the skin, reducing its levels in the bloodstream. This type of phototherapy is called bilirubin lights or bili lights.
In dermatology, phototherapy can be applied to treat various skin conditions like psoriasis, eczema, vitiligo, and acne. Narrowband ultraviolet B (UVB) therapy, PUVA (psoralen plus UVA), and blue or red light therapies are some examples of dermatological phototherapies.
Phototherapy can also be used to alleviate symptoms of seasonal affective disorder (SAD) and other mood disorders by exposing patients to bright artificial light, which helps regulate their circadian rhythms and improve their mood. This form of phototherapy is called light therapy or bright light therapy.
It's essential to consult a healthcare professional before starting any phototherapy treatment, as inappropriate use can lead to adverse effects.
Color therapy, also known as chromotherapy, is a complementary medicine practice that uses color and light to balance energy in the body, mind, and spirit with the goal of promoting physical and emotional health and well-being. It is based on the idea that different colors correspond to the seven main chakras or energy centers in the body and can help to balance, heal, and restore these centers.
In color therapy, various colors are used to treat different conditions. For example, red is thought to stimulate and energize, while blue is considered calming and soothing. Practitioners may use colored lights, colored fabrics, or other tools to expose the body to specific colors. Some practitioners also incorporate color therapy into other forms of healing, such as massage or acupuncture.
It's important to note that there is limited scientific evidence to support the use of color therapy for specific medical conditions. While some people report feeling better after receiving color therapy, it should not be used as a substitute for conventional medical care. If you are considering trying color therapy, it is a good idea to discuss it with your healthcare provider first.
Melatonin is a hormone that is produced by the pineal gland in the brain. It helps regulate sleep-wake cycles and is often referred to as the "hormone of darkness" because its production is stimulated by darkness and inhibited by light. Melatonin plays a key role in synchronizing the circadian rhythm, the body's internal clock that regulates various biological processes over a 24-hour period.
Melatonin is primarily released at night, and its levels in the blood can rise and fall in response to changes in light and darkness in an individual's environment. Supplementing with melatonin has been found to be helpful in treating sleep disorders such as insomnia, jet lag, and delayed sleep phase syndrome. It may also have other benefits, including antioxidant properties and potential uses in the treatment of certain neurological conditions.
It is important to note that while melatonin supplements are available over-the-counter in many countries, they should still be used under the guidance of a healthcare professional, as their use can have potential side effects and interactions with other medications.
I'm sorry for any confusion, but "seasons" is not a term that has a medical definition. Seasons refer to the four divisions of the year (spring, summer, autumn or fall, and winter) based on the position of the earth in its orbit around the sun. If you have any questions related to health or medicine, I'd be happy to try to help answer those!
A circadian rhythm is a roughly 24-hour biological cycle that regulates various physiological and behavioral processes in living organisms. It is driven by the body's internal clock, which is primarily located in the suprachiasmatic nucleus (SCN) of the hypothalamus in the brain.
The circadian rhythm controls many aspects of human physiology, including sleep-wake cycles, hormone secretion, body temperature, and metabolism. It helps to synchronize these processes with the external environment, particularly the day-night cycle caused by the rotation of the Earth.
Disruptions to the circadian rhythm can have negative effects on health, leading to conditions such as insomnia, sleep disorders, depression, bipolar disorder, and even increased risk of chronic diseases like cancer, diabetes, and cardiovascular disease. Factors that can disrupt the circadian rhythm include shift work, jet lag, irregular sleep schedules, and exposure to artificial light at night.