One of the strengths of a biocultural perspective in anthropology is its broad approach to understanding human biology and health (Wiley and Allen 2008). Such a framework seems particularly appropriate when looking at the fascinating phenomenon of SUDS (Sudden Unexplained Death During Sleep). Though SUDS first appeared in the medical literature 1917 in the Philippines, where it is referred to as ‘bangungut’ (Guazon 1917), it was largely forgotten until the late 1970s when it regained notoriety as an important cause of mortality among Southeast Asian refugees in the United States, particularly among young men (Baron et al 1983).
Unlike the similar-sounding condition of SIDS (Sudden Infant Death Syndrome), SUDS has a completely different and more mysterious epidemiology and etiology. Although both conditions are sleep-related, the vast majority of SUDS cases are males (75-100% in various studies), young adults (average age of 30-34), with no previous history of health problems (Munger 1987). In addition, it appears to be largely concentrated among, if not exclusive to, persons of East and Southeast Asian origin. Family members who witnessed a SUDS case reported that victims had difficulty breathing, made groaning sounds, and were generally unresponsive. In short, it’s pretty bizarre. To solve the puzzle of SUDS, one needs to account for all of these factors (Asian, male, young adult, previously healthy, and during sleep).
At first, there was a tendency to view SUDS as a culture-bound syndrome, limited to persons of Hmong ethnicity. A new term, ‘Hmong Death Syndrome,’ was coined to describe the mysterious illness (Bliatout 1982; New Scientist 1982) before recognizing that other ethnic groups residing in both western and Asian countries were similarly afflicted, such as the Khmer, Lao, Khmu, Thai, Vietnamese, Filipinos, Japanese, and Guamanian Chamorros (Munger and Booton 1998; Tatsanavivat et al 1992). The focus on the Hmong was likely due to an American view of them as exotic newcomers from the highlands of Laos, but was also fed by Hmong animistic spiritual beliefs of the phenomenon (Fadiman 1998). Many persons of Hmong ethnicity have described being personally attacked and held down by a malevolent spirit during sleep (tsog tsuam), leaving them conscious but paralyzed (Adler 1995). Obviously, these attacks were not fatal.
What is interesting is that such experiences are found in many cultures, not just the Hmong. Al Cheyne at the University of Waterloo in Ontario has documented that the concept of being crushed by a ghost at night exists throughout the world (even the English word ‘nightmare’ may trace its origins to this), and that this may be related to a condition called sleep paralysis. In effect, sleep paralysis occurs when someone experiences a disconnect between waking and REM sleep (when muscle activity is suppressed), leaving a person conscious but unable to move voluntarily. However, while sleep paralysis appears to fit the nocturnal pattern of SUDS and the common cultural view of a being paralyzed by a ghost, it remains unclear why some of these cases would be fatal.
The immediate or proximate cause of death in SUDS has been determined to be ventricular fibrillation- a rapid, ineffective beating of the ventricles of the heart. By chance, three cases of SUDS attacks endured long enough to allow medical personnel to examine the victims while still alive, all of whom exhibited ventricular fibrillation (Otto et al 1984).
If ventricular fibrillation is the proximate cause of SUDS, the ultimate cause remains elusive. Hypotheses have ranged from genetics to infection to nutritional deficiencies to culture shock in newly adjusting refugees (Wong et al 1992). The notion of culture shock or psychological stress (while intriguing) never gained much traction, as it could not address important components of SUDS epidemiology, including why males were disproportionately affected, why individuals succumbed during sleep, and why refugees from regions other than Southeast Asia were not affected.
A genetic predisposition seems a necessary component for SUDS in order to account for its concentration in males from Asian populations, though it appears insufficient by itself. Instead, a complex interaction between genes and environmental factors may be in play. For the cases in the U.S., most fatalities occurred in refugees who had recently arrived (median length of time in the country was 4 years), with risk decreasing with time (CDC 1988). Furthermore, death rates from SUDS in the late 1980s were actually higher in refugee camps in Thailand than in the U.S. (Munger and Booton 1990), which was yet another strike against the culture shock hypothesis. In fact, while research continues in Asia, cases appear to have leveled off in the U.S. almost completely (or at least have not received much attention).
The biology of SUDS appears complex. Genetic studies have inquired whether there is a link between SUDS and cardiac sodium channel gene (SCN5A) mutations (Sangwatanaroj et al 2002), and whether it is linked to Brugada Syndrome, a fairly newly recognized condition with a similar electrocardiographic (ECG) profile and is also concentrated more in males (Brugada et al 1999). Brugada Syndrome has been described as being an autosomal dominant genetic condition, with a mutation traced to chromosome #3.
However, if SUDS and Brugada are in fact the same condition, some questions still remain. For one, why is sleep such an important factor in SUDS? (Brugada is not described as sleep-dependent.) Why are males vastly more likely to be affected if the condition has a simple autosomal inheritance? Is the suspected allele more common in Asian populations?
Most importantly, are there environmental variables that increase the risk for SUDS? Munger et al (1991) reported that ECG tests revealed that a prolonged QT heart interval (a specific measure of the heart’s electrical cycle) was found in 12% of the Thai camp refugees, 1.3% of Southeast Asian refugees in the U.S., and 0.5% of U.S. Blacks and Whites. QT intervals are normally lengthened during sleep, but an excessively prolonged interval may induce heart arrhythmias, including ventricular fibrillation. Munger and Booton (1990) suspected that a deficiency in thiamin (vitamin B-1) could lead to prolonged QT intervals. Perhaps substandard diets in refugee camps could help trigger the condition, partly explaining why rates were higher there and why rates have declined in the U.S. over time.
There is still much to be worked out regarding SUDS, given its complex epidemiology and biology. Anecdotally, I know Hmong individuals who described experiencing tsog tsuam/ sleep paralysis in the recent past, in both the U.S. and French Guiana. Fortunately, the fatalities have dropped considerably in the U.S., though they appear to remain steady in Asia. The mystery continues.
The above photo shows Hmong men in Huay Nam Khao refugee camp, praying for a peaceful life. From the Bangkok Post.
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