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Association between the Polar T3 Syndrome and the Winter-Over Syndrome in Antarctica

LAWRENCE A. PALINKAS, Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, California 92093-0807 

H. LESTER REED and NHAN DO, Department of Medicine, Madigan Army Medical Center, Tacoma, Washington 98431

The austral winter in Antarctica has long been associated with reports of depression, irritability, aggressive behavior, insomnia, difficulty in concentration and memory, absentmindedness, and the occurrence of mild fugue states known as "long-eye" or the "antarctic stare" (Palmai 1963; Palinkas, Cravalho, and Browner 1995). During the 1989 winter season at McMurdo Station, for instance, 64.1 percent of the winter-over crew members interviewed reported some problem with sleep over the winter; 62.1 percent reported feeling depressed; 47.6 percent reported feeling more irritable than usual; and 51.5 percent reported difficulty with concentration or memory (Palinkas 1992). Collectively, these symptoms are referred to as the "Winter-Over Syndrome" (Strange and Youngman 1971).

Despite decades of research, the etiology of the Winter-Over Syndrome has not been clearly identified. In many instances, these symptoms can be attributed to characteristics of the social environment, including the absence of face-to-face social interaction and support associated with the prolonged isolation from family and friends (Palinkas 1992), the absence of social stimulation and opportunities to disengage from stressful social situations associated with the experience of confinement with the same small group of individuals, and increased work demands at certain times of the winter season (Palinkas et al. in press). On the other hand, the role of certain environmental factors including the lack of environmental stimulation and prolonged exposure to cold temperatures and constant darkness is suggested by the observation that winter-over personnel experience a significant increase in the prevalence of subsyndromal seasonal affective disorder (S-SAD) during the austral winter and that this increase appears to be associated with increasing latitude and, hence, exposure to prolonged darkness (Palinkas, Houseal, and Rosenthal 1996).

Alterations in thyroid hormone functions similar to those reported by Reed and colleagues during the austral winter in Antarctica (Reed et al. 1986) are also known to be associated with increased depressive symptomatology and disruption of cognitive performance (Gold, Pottash, and Extein 1981). Known as the Polar T3 Syndrome, these alterations share many of the same characteristics of subclinical hypothyroidism (SCH), including elevated thyrotropin-stimulating hormone (TSH) levels and/or enhanced TSH response to thyrotropin-releasing hormone (TRH) stimulation. Subclinical hypothyroidism is found in 8 to 17 percent of depressed patients vs. 5 percent of the general population (Haggerty and Prange 1995).

The Polar T3 Syndrome is also associated with a significant reduction in serum total triiodothyronine (T3) and free T3, and a 12 percent reduction in thyroxin (T4) (Reed et al. 1986). Individuals with low normal T4 values experience more memory loss than those with high normal T4 values (Zach and Ackerman 1988). Studies have also found improved memory in patients with SCH following T4 treatment (Nystrom et al. 1988). These results support the hypothesis that the cognitive and affective symptoms characteristic of the Winter-Over Syndrome are a state of relative central nervous system hypothyroidism accompanied by systemic euthyroidism (Jackson 1996). The T3 receptor is widely distributed throughout the central nervous system, suggesting that thyroid hormones are necessary for normal brain function. Some evidence suggests that these hormones may have synaptic as well as nuclear actions (Haggerty and Prange 1995). A reduction in levels of T3 and T4 in the brain resulting from the increased energy requirements of the Polar T3 Syndrome could conceivably affect adrenergic neurotransmission. On the other hand, T3 in the brain is normally derived by conversion locally from T4 due to the effect of brain Type II 5'-deiodinase. Any mechanism that inhibits this enzyme, such as an increase in cortisol due to stress, could result in functional brain hypothyroidism (Jackson 1996). A TSH-driven increase of circulating thyroid hormones typically occurs in euthyroid individuals in the face of depression and other stress states; an increase in thyroid hormone favors recovery from depression (Haggerty and Prange 1995).

Longitudinal assessments of thyroid function, cognitive performance, and depressive symptoms are essential to identifying the causal nature of the relationship between the Polar T3 Syndrome and the Winter-Over Syndrome if, in fact, such an association exists. Over the past year, 16 members of the winter-over crew at McMurdo Station participated in a randomized clinical trial to determine if changes in thyroid function characteristic of the Polar T3 Syndrome were associated with changes in mood and memory characteristic of the Winter-Over Syndrome. This association was assessed in two ways:

A preliminary analysis of the data collected during the past year and presented in the figure suggests an increase in Center for Epidemiologic Studies-Depression (CES-D) scores in the 1996-1997 study cohort from baseline (September) to mid-January, followed by a gradual decline through May and a second increase in midwinter (June and July). This second increase was not observed in the Profile of Mood States (POMS) depression (D) scores. Mean POMS scores of tension-anxiety (TA) and fatigue (F) declined during the austral summer and most of the winter, followed by an increase during the last two months of winter. Mean POMS anger (A) scores increased during the austral summer, decreased during the first few months of winter, and increased again at the end of winter. Mean POMS confusion (C) and vigor (V) scores remained relatively stable throughout the study period. Analyses are underway to determine if these patterns correspond to changes in thyroid function and metabolic regulation and if they are affected by thyroxine supplementation.

This work was supported by National Science Foundation grant OPP 94-18466. The author wishes to acknowledge the contributions of Kathleen Reedy, Sam Case, Mark Staudacher, and Nancy Finney to this study.


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