A weather catastrophe such as the El Niño of 1997-1998, in effect, prolongs the seasons, thus making the Winter's SAD activity spill over into Spring. One scientific study's findings suggest that changes in atmospheric temperature played an important role the triggering of Spring-type SAD. Another study found that the depressive episodes of some people may be triggered at any time of the year if the weather is unusually dull, characterized by an unusually low light intensity.7 Other studies indicate that temperature change alone may bring about SAD.8 Other studies are in agreement that weather circumstances needed to induce SAD-type reactions include reduced sunshine, global radiation, length of daylight and temperature changes.9 Such conditions are typical of those fostered by El Niño. However, there is some controversy when analyzing winter depression with regard to cloud cover, rainfall or atmospheric pressure. But the data is clear that for some individuals subject to SAD there is a another trough of symptoms in March/April often equal in severity to that of November/December, and that in particularly inclement weather the trough can get deeper and longer. In some instances, SAD depression can extend - if weather conditions are severe and prolonged enough as is the case with this year's El Niño - right through the entire Spring!
In colder climates Winter SAD is a common condition that increases in prevalence and proportion to the number and darkness of overcast days.10 A random sample of nearly 300 Alaskans found that over 9.2% met diagnostic criteria for seasonal affective disorder, one of the highest figures yet reported.
These cyclic winter affective disorders occurred more often in women than men (ratio=3:2) and were more prevalent among residents who were younger than 40 years of age.11
One of the more reported clinical practices for SAD has been the use of light therapy, use of which seeks to correct the disturbance of circadian rhythm caused by desynchronization between the solar clock and the human biologic clock during seasons of short photoperiods. These include winter or extended periods of overcast, cloudy, or gloomy weather. Light therapy, also known as phototherapy, is thought to alter the production patterns of melatonin, the neurotransmitter serotonin, and the peptide neurohormone corticotropin releasing hormone (CRH) which together play a pathophysiological role when altered by Winter seasonal affective disorder.13 For some people phototherapy can help shorten SAD. However, the timing schedule of phototherapy remains controversial, the results are spotty, and therapy is both inconvenient and time consuming. Studies show that going outdoors can be more therapeutic than daylight-emulating artificial light.
ST. JOHN'S WORT
Also believed to be effective with SAD is St John's wort (hypericum extract). In one single-blind study 900 mg of St John's wort was given over the course of 4 weeks to two small groups suffering from SAD along with either bright light phototherapy or dim light therapy (placebo) for two hours each day. At the end of the study both groups were found to measure a significant reduction in the total score of the Hamilton Depression Rating Scale.13 There was no significant difference when bright light therapy was combined with St John's wort, compared to the situation without bright light therapy. St John's wort was well tolerated suggesting that St John's wort may be useful for SAD.15
MELATONIN NOT EFFECTIVE
Despite the theory behind phototherapy and data showing melatonin to be effective in the treatment of circadian-rhythm related sleep disturbances, studies have demonstrated that melatonin has little to no impact on the depressive symptoms of SAD.15 Light remains the therapy of choice despite its shortcomings. But recently scientists have identified the common feature of what they believe to be the root of the SAD problem: serotonin depletion,16 which is related to serotonin deficiency syndrome, a problem about which readers of this publication have heard much.
By the 1980s, scientists had firmed up their understanding of the causal connections between seasonal conditions, the cycles of mood and psychological health. In 1989, a study found that a serotonin-enhancing drug (D-fenfluramine, later of fen-phen infamy) was effective for the affective and appetitive symptoms of SAD.17 It was possible to say that carbohydrate craving was a kind of substance abuse because certain foods in that category could be eaten specifically for their serotonin-mediated psychotropic effects. This conclusion supported the idea that nutritional deficiencies could upturn the psychological cart and that there was a strong element of neuropsychopharmacological malfunctioning behind seasonal mood swings.
SEROTONIN AND SAD
Central serotonin pathways have been found to play an important role in the modulation of mood and behavioral impulsivity, and regulation of eating patterns, qualitatively and quantitatively. The many studies showing that the amino acids L-tryptophan and 5-hydroxytryptophan, and serotonin potentiating drugs relieve depression disorders suggest that brain serotonin influences pathophysiology. The tryptophans are precursors to the endogenous (inside the body) production of serotonin, the major inhibitory neurotransmitter in the brain. When tryptophan is taken along with carbohydrates the result is an increase in the plasma ratio of tryptophan to other large neutral amino acids, greater concomitant entry into the brain and increased serotonin synthesis. When those with SAD consume excessive carbohydrate intake their actions reflect a self-medication that temporarily relieves the vegetative symptoms via an increased central serotonergic activity.18
Using a tryptophan depletion test, it is possible to induce a rapid and substantial lowering of both total and free plasma tryptophan with consequent decreases in brain serotonin content and also cerebral serotonin function. When scientists used this test to measure health subjects with a genetic risk for affective disorder, their condition was worsened by induced tryptophan depletion.16 This indicates the relevance of altered brain serotonin function in the pathophysiology of affective disorders and strengthens the importance of serotonin to help prevent depressive states.
TRYPTOPHAN AND 5-HYDROXYTRYPTOPHAN
Because the production and utilization of serotonin appears to be central to alleviating the symptoms of SAD, and because carbohydrate craving is also symptomatic to this syndrome, it appears as if SAD may be viewed as a dietary deficiency with special seasonal considerations given to the Winter months or to other periods of sunshine deprivation. Other special winter dietary considerations have been identified throughout history, not the least of which is vitamin C deficiency (scurvy) which has traditionally been more of a problem in winter, when ascorbate concentrations decline in food and the availability of citrus fruit becomes scarce. Energy requirements also vary according to season and activity levels and we also know that stressor conditions can increase the utilization of noradrenaline and dopamine and thus upset the balance with other neurotransmitters such as serotonin.21
Based on the serotonin connection to SAD it stands to reason that 5-hydroxytryptophan (5-HTP) - related to tryptophan and much closer to serotonin (5-HTP is the immediate precursor to serotonin) on the metabolic pathway - would be useful because it is a superior serotonin producer. Indeed, in one study, after 5-HTP was administered orally at 200 mg/d to 26 depressed patients, serum cortisol levels were significantly higher compared with controls.22 Serum cortisol increase has been found to correlate positively with tests to measure affective disorder and to indicate improvement.
A double-blind study examined the effect of 200 mg oral doses of 5-HTP in ten depressed patients with SAD and ten controls. Before administration of 5-HTP, data disclosed those with SAD had significantly higher basal levels of serum prolactin and a trend toward higher basal levels of serum compared with controls. After administration of 5-HTP, the cortisol level significantly increased and the prolactin level significantly decreased.23 High levels of prolactin have been shown to reflect many depressive states.
The scientific literature on 5-HTP appears to make it an extremely valuable dietary aid to insure support for a wide spectrum of functional benefits [see back issues of this publication]. There is a large variety of literature on the use of this serotonin precursor for conditions associated with serotonin deficiency.24-29
FAT LOSS TOO
Scientific observation has also shown 5-HTP to be associated with diminished appetite, decreased food intake, and weight loss in obese subjects. In one double-blind study, 20 obese people were given either 5-HTP (900 mg/d) or a placebo for two consecutive 6-week periods. Significant weight loss resulted along with reduced carbohydrate intake with continuous levels of satisfaction (satiety) reported.51
When 5-HTP was administered to 26 healthy, non-depressed subjects marked mood elevation was observed and the subjects reported feeling happier.52-53 The authors remarked at how the improved mood changes seemed to increase rather than plateau over the course time during which 5-HTP effects were measured.
Another study followed 247 subjects who fasted on a very-low calorie diet for a 2-year period using a considerably smaller amount of 5-HTP (15 mg/d) along with other nutrients thought to be of value as part of a weight control program.54 Those chosen for the study were particularly unable to either acheive their desired target weight or maintain it.
The results included considerable decreases in food craving (70% for males and 63% for females) as well as a significant decreases in binge eating (66% for females and 41% for males). Those taking the 5-HTP formulation saw the amount of excess fat decline by half for men and women alike. At the follow up after the fast, those taking the 5-HTP-containing formulation were found to regain only about 15% of the weight lost vs about 42% for the control group.
Recently famed thermogenic researcher Astrup has also found that a particular regimen helps prevent regaining weight lost through dieting. The report followed 41 women and 2 men who were obese (with a body mass idex of 27-40) but otherwise healthy on two different weight regimes, one of which was very low calorie and the other a conventional diet.55 To induce fat burning both groups were given 20 mg of ephedrine and 200 mg caffeine three times daily and followed for one year. The low-calorie group achieved its weight loss goal of about 30 lbs, on average, in eight weeks while the conventional diet group took 17 weeks to lose on average 30 lbs.
Following the weight loss, the subjects entered a 6 to 12 month period of weight maintenance at which the very low calorie group was found to have regained less than 2 lbs for a loss maintenance of nearly 98%. The conventional diet group - surprise! - regained, on average, about 9 lbs for a loss maintenance of 70%. Then another 6 month period followed and the subjects were again measured. The conventional/slow loss group was found to have regained 25 lbs while the very low calorie/fast loss group regained only 12 lbs. Also at follow up, 65% of the very low calorie/fast loss group vs 40% of the conventional/slow loss group has maintained a weight loss greater than 12 lbs.
These data suggest that the rate of initial weight loss has no effect on weight maintenance contrary to the "famine mechanism" that cautions about rapid weight loss for purposes of health. Tripping the cellular setting for famine-level (slower) metabolism explains the yo-yo syndrome in dieting where weight loss is gained back faster and then some. However, this study may indicate that ephedrine and caffeine may allow a person to lose weight faster without setting off metabolic alarms. The subjects in the fast weight loss group lost a little more than 3 lbs per week while the slower group lost a little under 2 lbs per week. Nonetheless, we still think it is best to work with a physician when attempting to lose more than 10% of your body weight.
Whether El Niño or any bad weather you may encounter gets you down (in spirit) or up (in weight) or both, it's a good time to decide to do something about it. Whether you're SAD, pre-SAD, or post-SAD, it's possible to get out of the cycles of mood shift and uncontrolled cravings. Wouldn't you rather be happy than SAD?
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