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Seasonal Affective Disorder Study

Seasonal Affective Disorder Study - Introduction

In the early 1980s, Herb Kern, a research engineer, who thought that his annual cycle of depression might be caused by the shorter and duller daylight hours in winter, approached doctors working at the National Institute for Mental Health in Bethesda, USA. They proposed a treatment where he was exposed to light, equivalent to summer sunlight, for several hours each day. By the fourth day his symptoms had virtually disappeared (Lewy et al 1982). This was the start of our acknowledging the condition that has come to be known as Seasonal Affective Disorder (SAD).

Seasonal Affective Disorder (SAD), or recurrent winter depression, is now considered a clinical subtype of major depression. The criteria for Seasonal Affective Disorder (SAD), or "winter seasonal pattern", in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, which are similar to other definitions of Seasonal Affective Disorder, specify a recurrent pattern of major depressive episodes during winter and remission of Seasonal Affective Disorder (SAD) symptoms during summer, in the absence of seasonal psychosocial stressors.

Much of the interest in Seasonal Affective Disorder (SAD) has been stimulated by its response to exposure to bright artificial light. Clinical consensus guidelines have recommended SAD light therapy as a first-line treatment for Seasonal Affective Disorder (Lam & Levitt, 1999). Although light therapy may be regarded as a radical intervention for depression, in the case of Seasonal Affective Disorder (SAD) the use of SAD lights is rather common sense.

Human beings are influenced by light. Light determines our sleep/wake cycle. In most animals and humans, the desire to sleep is brought on by the secretion of a hormone called melatonin. In the evening the pineal gland reacts to the diminishing levels of daylight and begins producing melatonin. melatonin is then released into the blood and flows through the body making us drowsy. Its secretion peaks in the middle of the night during our heaviest hours of sleep. In the morning, bright light shining into the eye reaches the pineal gland, which reacts by switching off the production of melatonin, thus removing the desire to sleep.

The pineal gland communicates with the rest of the hormonal system. Consequently melatonin production also influences the functioning of other parts of the body. During darkness and sleep, melatonin modifies the secretion of hormones from organs such as the pituitary gland, the "master gland" of the hormonal system. The pituitary in turn regulates the secretion of hormones controlling growth, milk production, egg and sperm production. It also regulates the action of the thyroid gland, which is concerned with metabolism, and the adrenal glands, which control excretion of the body's waste. Further, it has been shown that light also effects levels of serotonin and dopamine neurotransmitters. The latter are connected with the Limbic system and the hypothalamus, which effects mood, emotion and autonomic systems, such as digestion. Therefore, fluctuations in light and darkness according to the seasons of the year influence rhythms of growth, reproduction and activity in animals and humans alike, and are the root of Seasonal Affective Disorder (SAD).

Statistics show that despite living and working in closed structures, our bodies still respond to the external environment and to its seasonal variability in duration and intensity. Studies have shown that growth rates in children are affected by the seasons. For example, surveys carried out in Germany, Sweden and Scotland show that height and weight increase is more predominant in the spring and early summer (Smyth, 1990). In many countries the rate of conception peaks in the summer when the hours of daylight are longest. In numerous trials the seasons have been seen to influence the timing and duration of sleep, pain threshold, alertness, eating habits, mood, the onset of menstruation and sexual activity.

It is generally assumed that millions of years of evolution and adaptation have optimised human biochemical and physiological systems for function and survival under equatorial environmental conditions. Modern humans began their migration out of Africa only about 150,000 years ago. Little change in our "equatorial" systems might have been expected over this relatively short evolutionary time-span. Susceptibility to seasonal changes in mood and behaviour (that are found to extremes in Seasonal Affective Disorder) may reflect a genetic predisposition to an insufficient adaptation to temperate and high latitudes (Sher, 2000).

Unfortunately, research has not yet been able to find a definitive aetiology for Seasonal Affective Disorder (Lam & Levitan, 2000; Lee et al 1998a; Mersch et al 1999; Sato 1997). Hormonal dispositions can explain perceived phenomena, yet, the systems involved are too complex to fully understand and thus predict cause and affect. Recent research has shown that Seasonal Affective Disorder (SAD) may be due to retinal sensitivity (Lee et al 1997), though more work needs to be done in this area.

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