It wouldn't be December 22 without the 'Guardian UK' doing its obligatory 'Druids-at-Stonehenge-Winter-Solstice story.'
But, millions of people who suffer from Seasonal Affective Disorder (SAD) across the world are celebrating December 22 for another reason: daylight is now increasing...and, with increased daylight comes decreased symptoms of SAD.
By now, most are familiar with the symptoms: difficulty getting out of bed, afternoon slumps, voracious carb cravings and social withdrawal.
But what exactly is it about reduced daylight that triggers SAD's daisy chain of misery?
Researchers have identified two major theories to explain the physiological triggers and mechanisms of SAD: the circadian rhythm theory and the serotonergic dysfunction theory. Of additional interest is some of the genetic investigation of SAD: a growing consensus of researchers are pointing to the 5-HTTLPR gene as some kind of regulator, not only to SAD, but to any serotonin production-related symptom.
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Research now suggests that SAD has a genetic component. Simply put, low-sunlight is not an equal opportunity depressant. Some genetic groups are more affected by SAD than others. Specifically, the 5-HTTLPR gene has been found to be expressed differently in SAD patients.
One major theory for explaining SAD involves the circadian rhythms of the body. In effect, reduced daylight causes a 'phase shift' of the body's circadian rhythms which affects when and how much melatonin is produced. During sleep, melatonin acts affects the amount of hormones secreted by the body's 'master gland' -- the pituitary gland. The result is a cascade of symptoms common to SAD.
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.
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