What is S.A.D?
Seasonal affective disorder, appropriately referred to by the acronym "S.A.D", is a form of depression that occurs only during certain periods of the year. In some cases, an existing depression may become more severe during certain times of year. By far the most common and recognized form of seasonal affective disorder is "winter depression". This is characterized by recurrent episodes of depressed mood, over-sleeping or the urge to "hibernate", cravings for carbohydrate rich foods, and associated overeating and weight gain. Symptoms typically begin to appear in September and don't abate until spring comes around at the end of March or beginning of April. Since winter depression is the most common form of seasonal affective disorder and the type that almost everyone is familiar with, we will be concentrating on this and for simplicity will refer to it as SAD.
Like all forms of depressive illness, SAD can vary greatly in severity and can be a severely debilitating condition. Many sufferers can be perfectly healthy during the spring and summer months but unable to function during the winter. This leads to obvious problems with work and family life.
It is estimated that SAD affects 4-6% of the general population with a further 10-20% experiencing mild symptoms that don't meet the requirements for an official SAD diagnosis. The incidence is thought to be much higher than this in environmental illness sufferers, such as those with chronic fatigue syndrome. A study published in 1998 involving 110 CFS patients found that a large proportion had depressive symptoms, and that these, and the typical CFS symptoms not associated with depression, worsened during the winter months. The researchers concluded that SAD was present in a large subset of chronic fatigue syndrome patients and that CFS and SAD may share common causes. They suggest light therapy (one of the main treatment options for SAD) as an appropriate therapy for CFS patients who show seasonal changes in symptoms(1).
Women suffering from SAD outnumber men by 4 to 1 (2) and the risk of been affected by SAD appears to decrease with age (3). Of course this is if you are otherwise healthy. Suffering from environmental illness would appear to increase the risk of also suffering from SAD at any age.
A number of studies have found that the risk for SAD is greater the further north a person lives, although the evidence is not conclusive with other studies finding no significant connection between latitude and the number of people suffering from SAD. A major review of SAD research carried out in 1999 found that in both North America and Europe, there are more cases of SAD the further north you go. However, it was also found that North America has twice as many cases of SAD than does Europe, so other factors must also play a role (4).
The criteria for diagnosing all psychiatric conditions are laid out in The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). The manual describes SAD as a "specifier" for major depressive illness rather than as a separate mood disorder. This means that SAD is seen not as a condition in its own right but as a subset of major depressive or bipolar disorders. It should be noted that SAD is much more common as a form of major depression rather than bipolar disorder. Never the less, seasonal variations in symptoms do occur in those suffering from bipolar disorder.
Considering the above it would make sense to first look at the diagnostic criteria for major depressive disorder.
Making The Diagnosis of Major Depression
The DSM-IV states that "At least five of the following symptoms have been present during the same two-week period, nearly every day, and represent a change from previous functioning. At least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure."
The symptoms being:
- Depressed mood (or alternatively can be irritable mood in children and adolescents).
- Markedly diminished interest or pleasure in all, or almost all, activities.
- Significant weight loss when not dieting or weight gain or decrease or increase in appetite.
- Insomnia or hypersomnia.
- Psychomotor agitation or retardation.
- Fatigue or loss of energy.
- Feelings of worthlessness or excessive or inappropriate guilt.
- Diminished ability to think or concentrate, or indecisiveness.
- Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
As well as the symptom requirements, other diagnoses must be ruled out before major depression can be diagnosed. This is clarified in the following statements:
"The symptoms are not better accounted for by a mood disorder due to a general medical condition, a substance-induced mood disorder, or bereavement (normal reaction to the death of a loved one)."
"The symptoms are not better accounted for by a psychotic disorder like schizoaffective disorder."
Making The Diagnosis of Seasonal Affective Disorder
In addition to meeting the requirements for major depressive disorder (or bipolar disorder), the following must be true for a diagnosis of seasonal affective disorder to be made:
- Regular temporal relationship between the onset of major depressive episodes and a particular time of the year (unrelated to obvious season-related psychosocial stressors.
- Full remissions (or a change from depression to mania or hypomania) also occur at a characteristic time of the year.
- Two major depressive episodes meeting criteria A and B in last two years and no nonseasonal episodes in the same period.
- Seasonal major depressive episodes substantially outnumber the nonseasonal episodes over the individual's lifetime.
If all these criteria apply to you then you will be diagnosed as having SAD. Of course, as we have already mentioned, a large section of the population is affected by low mood and other symptoms during the winter months and may suffer from a mild version of SAD that doesn't meet the official diagnostic criteria.
What Causes SAD?
The cause or causes of SAD are not as clear cut as it may seem. Although it would appear to be a direct result of lack of sunlight in winter months, the exact mechanism by which this causes depressive symptoms has yet to be determined. There are of course a few leading theories that at least partially explain what is going on in patients suffering from SAD.
Disruption of Circadian Rhythms
One major theory for explaining SAD involves the circadian rhythms of the body. The term "circadian rhythm" describes the fact that bodily functions seem to follow a set pattern throughout the day as if the body is working to a set schedule or internal clock. It's thought that in SAD this internal clock is disrupted, leading to various biochemical abnormalities and associated symptoms. According to this theory, sunlight acts as a type of synchronizer of the circadian rhythms in humans, and exposure to light can shift these rhythms out of phase. What this means is that the SAD sufferers body may be producing hormones (such as cortisol) and neurotransmitters that promote wakefulness well into the early hours of the morning and then still be producing sleep inducing chemicals such as melatonin until midday. This results in the unlucky sufferer not being able to sleep until past midnight and then not being able to drag themselves out of bed until late morning or later, which is a common situation. It has been found that the timing of light exposure, rather than the amount of light exposure, may have the greatest influence over circadian rhythms, and hence SAD symptoms (5).
To further explain the enormous effect light exposure has on the physiology and functioning of the body, we need to take a closer look at the hormone melatonin. As light levels decrease in the evening, the pineal gland begins producing melatonin. Melatonin is a hormone whose main function is to induce sleep by traveling through the bloodstream and transmitting the sleep message to other body systems. In healthy individuals the secretion of melatonin peaks in the middle of the night during our deepest sleep. At dawn, sunlight shining into the eye triggers the pineal gland to switch off the production of melatonin, thus removing the desire to sleep. Since melatonin travels to all parts of the body in the blood, it has far-reaching effects, as all hormones do. During the hours of darkness and sleep, melatonin influences the secretion of hormones from the pituitary gland, often referred to as the "master gland" of the endocrine system. The pituitary then reduces hormone production from other important endocrine glands such as the thyroid and adrenals. These glands produce vital hormones such as thyroid hormone, cortisol, and adrenaline, which control metabolism and motivate us to action during our waking hours.
Researchers have found that this system is disrupted in people with SAD. When SAD patients were compared with healthy controls, it was found that the SAD patients had consistently higher daytime melatonin levels during the winter months (6). High daytime melatonin levels would be expected to produce the symptoms of excessive daytime sleepiness and the lack of motivation and desire to hibernate, that is seen in SAD sufferers. Other research has shown that taking melatonin supplements, which are available over-the-counter in the US, effectively "phase-shifts" the disrupted circadian rhythms (7). What this means is that if you have SAD and you tend to get to sleep past midnight and wake well into the morning or midday, if you take melatonin at say 9-10pm to induce sleep, your sleep cycle will be shifted back to normal and you will be able to wake earlier in the morning.
Another major theory explaining SAD involves disruption to the way the neurotransmitter serotonin works. Serotonin is an extremely important chemical messenger in the brain and its function has a major impact on mood. Low serotonin function is thought to result in a type of depression characterized by symptoms such as feelings of sadness, worthlessness, guilt, and suicidal thoughts.
The hypothesis regarding serotonergic dysfunction is based on the findings that serotonin levels vary significantly in normal humans across seasons with lowest levels in the winter months. The research that found high daytime levels of melatonin in SAD patients, also found that the serotonin levels of everybody tested, even the healthy volunteers, were lower in winter than in summer (6). The serotonergic dysfunction theory of SAD states, based on research findings, that the receptors on brain cells that are stimulated by serotonin are not functioning correctly, resulting in abnormal neuroendocrine responses and the symptoms experienced in SAD (2).
Serotonin production is also intimately connected with the "sleep" hormone melatonin whose levels we have already seen are abnormal in SAD. In fact, serotonin is actually converted into melatonin. This happens as light levels fall in the evening and the pineal gland signals for melatonin production to increase. In simplistic terms the actions of serotonin and melatonin are opposing with serotonin stimulating us during the daytime and melatonin inducing sleep at night. In SAD, we know that melatonin levels are higher than normal during the day, so sufferers experience sleepiness and other melatonin induced effects, and are also prone to serotonin deficiency symptoms such as negative emotional states.
As a result of the close relationship between serotonin and melatonin, the circadian rhythm and serotonergic dysfunction theories should probably be seen as complementary to each other rather than as totally distinct explanations for SAD.
An interesting area of SAD research has focused on genetics and how SAD affects families and populations both within countries and internationally. The issue of how susceptible different ethnic groups are to suffering from SAD has also been looked at.
One particular gene known as 5-HTTLPR has received a lot of attention from researchers as it has been found to be expressed differently in SAD patients (8). The 5-HTTLPR gene is involved with the function of serotonin (5-HT). Researchers have been careful to explain that this gene may not be the root cause of SAD but is certainly involved in the disease process and the production of symptoms. Other research has implicated the 5-HT2A gene, which is also involved with serotonin function. This gene they say is associated with the depressive symptoms of SAD but does not explain the seasonality of the disorder (9). Many of the genetic studies looking at particular genes have also looked patients families and found that, as with most mental illness, there is often a family history of mental health problems.
Intriguing facts have been discovered when researchers have looked at SAD in different populations. The general consensus appears to be that the further north you go (in the northern hemisphere), the greater the number of people there are suffering from SAD. As mentioned in the introduction, a major review of SAD research found that in both North America and Europe, there are more cases of SAD the further north you go. However, it was also found that North America has twice as many cases of SAD than does Europe (4). What this suggests is that the lower light levels at more northerly latitudes are indeed an important risk factor for SAD, but are not the only factor. Perhaps the higher incidence of SAD in North America can be attributed to greater racial diversity than is present in Europe or to other cultural and social factors.
Another piece of evidence suggesting a genetic predisposition to SAD comes from a study conducted at Columbia University, NY, in 2002. This study of 165 SAD patients found differences in symptoms experienced by sufferers of different races, and also the intriguing result that blue eyed people suffered less severe symptoms than those with darker eyes. The researchers stated that "lightly pigmented eyes, in particular, may serve to enhance photic input during winter and allay depressive symptoms in vulnerable populations" (10). Essentially, lighter eye colour allows more light to enter the eye and thus reduce susceptibility to SAD during the dark winter months.
These research findings lend some weight to the assumption that millions of years of evolution and adaptation to the environment have optimized human biochemical and physiological systems for living in equatorial conditions, where light is plentiful and of even intensity throughout the year. Humanity began its migration out of Africa only about 150,000 years ago. This relatively short evolutionary time-span may not have provided enough time for us to fully adapt to conditions in the more northerly areas of the globe that hundreds of millions of us now inhabit (11).
Although the exact mechanisms by which SAD occurs are not yet clear, the information presented in the theories above provides us with a basic understanding of the factors that contribute to the condition, and help direct treatment approaches (bright light therapy, antidepressants, nutrients, getting outside in the sun etc). It is likely that factors from all the theories discussed are involved with the illness. Further research should fill in the blanks in the coming years.
SAD in Environmental Illnesses
SAD itself could be described as an environmental illness, since lack of sunlight appears to be one of the most important factor in its development. Here however, we'll take a look at the relationship of SAD to the main environmental illnesses we focus on at The Environmental Illness Resource.
SAD appears to be common amongst chronic fatigue syndrome (CFS) and fibromyalgia sufferers. Dr. Jacob Teitelbaum, a CFS and fibromyalgia specialist, and author of best selling book 'From Fatigued to Fantastic', addresses the issue of SAD with his patients. Dr. Teitelbaum recommends using a 10,000 lux lightbox for 30-45 minutes every morning if his patients symptoms get worse during winter. He is the only physician to have had the effectiveness of his CFS and fibromyalgia treatment protocol proven by clinical studies (of the kind used to test effectiveness of new pharmaceutical drugs). Dr. Teitelbaum is not the only doctor treating CFS and fibromyalgia patients for SAD, it is common amongst environmentally aware physicians.
The instincts of Dr. Teitelbaum and others is backed up by research that we looked at earlier. If you recall, a study published in 1998 involving 110 CFS patients found that a large proportion had depressive symptoms, and that these, and the typical CFS symptoms not associated with depression, worsened during the winter months (1). Like Dr. Teitelbaum the researchers recommend bright light therapy to improve symptoms of both CFS and SAD during the winter months.
The results from a research study published in 2000 also found a link between multiple chemical sensitivity (MCS) and SAD. Two hundred and twenty-five subjects, including normal volunteers and patients with previously documented seasonal affective disorder (SAD), chronic fatigue syndrome (CFS), Cushing's syndrome, Addison's disease and obsessive-compulsive disorder (OCD), completed questionnaires describing their reactions to exposures to various chemicals. Patients with CFS, Addison's disease and SAD self-reported more sensitivity to chemical exposures than normal controls (12). The researchers suggest that these illnesses are linked to chemical sensitivity through the HPA-axis, the body's stress control system, as it is known to be dysfunctional in all of these conditions.
Anecdotal reports also suggest a link between SAD and MCS, and the author has also experienced this. It is often the case that people suffering from MCS also have problems with SAD. The interesting thing is that not only do SAD symptoms abate during the summer but the severity of their MCS symptoms also decreases. They may be able to tolerate larger amounts of chemicals, or reactions on exposure are less severe or prolonged, or both. This all suggests that serotonin is involved with both conditions. We've discussed serotonin's role in SAD, but it could also be involved in chemical sensitivity. A leading theory for MCS involves over-sensitivity of the limbic system in the brain. The limbic system is intimately involved with mood and emotions, and has high levels of serotonin. We could therefore hypothesize that disruption of serotonin function could result in both SAD and multiple chemical sensitivity.
Gut dysbiosis may also be connected to SAD by way of serotonin function. Serotonin is produced from the amino acid tryptophan which we get from protein foods. Unfortunately, it is known that if a gut dysbiosis condition is present, the unfriendly microorganisms such as bacteria and yeast can get hold of the tryptophan themselves before we have time to absorb it through our intestines (13). Without sufficient supply of tryptophan, susceptible individuals are likely to become deficient in serotonin, with the result being various forms of depression, including SAD (14).
There has been little research into a connection between autism and SAD but a report published in 1998 described 2 patients with learning disabilities who showed symptoms of SAD and responded to bright light therapy. The authors suggested more research was needed in this area (15).