In 1985 I first produced my hypothesis that sudden infant death syndrome (SIDS) results from underproduction of the adrenal hormone, dehydroepiandrosterone (DHEA) during sleep. I think DHEA is necessary for proper growth, development, and activation of all tissues of the body, including all parts of the brain. My 1985, theory of sleep says that sleep occurs when DHEA is reduced at night. In normal sleep, enough DHEA is still produced to properly activate the brainstem so that cardiopulmonary functions continue, but the upper brain is reduced to unconsciousness. I deduced that SIDS may be due to underproduction of DHEA sufficient to maintain brainstem function in infants who succumb to SIDS. Also, at my internet page is my explanation of migraine headaches and epilepsy in which I describe the connection of blood pressure with DHEA. I suggest that levels of DHEA directly and positively affect blood pressure.

I have found some new research that directly connects these two ideas and produces further support of my explanation of SIDS. (These are reproduced below.) It was reported in the American Journal of Hypertension 1998; 11: 532, that DHEA sulfate (the blood source of DHEA) declines during sleep and that blood pressure declines in proportion to DHEA in human subjects. A study of blood pressure in mice reported that blood pressure dropped directly parallel to the sequential stages of sleep (J. Appl. Physiol. 1998; 85: 366). A hospital study of a child who died of SIDS indicated that the child exhibited a number of symptoms including low blood pressure (Arch. Dis. Child. 1998; 78: 481). These reports support my hypothesis that SIDS may represent underproduction of DHEA during sleep in infants who succumb to SIDS.

Am. J. Hypertens. 1998 May; 11(5): 532-538
"Relationship between blood pressure variability and serum dehydroepiandrosterone sulfate levels"
Barna I., Feher T., de Chatel R.

"Decreased diurnal blood pressure variability and low dehydroepiandrosterone sulfate (DHEAS) levels are important predictors of cardiovascular morbidity and mortality. The aim of the study was to determine the relationship between DHEAS levels and diurnal blood pressure variability in normotensive subjects and in patients with essential hypertension of both genders. An ambulatory blood pressure monitor (ABPM), Meditech O2 device and radioimmunoassay were used for ambulatory blood pressure monitoring and the determination of DHEAS levels, respectively. A close correlation (P < 0.001) was found between the diurnal indices and plasma DHEAS levels of the 387 subjects (86 normotensive and 301 hypertensive patients) participating in the study. Decreased plasma DHEAS levels were associated in both genders, and in both normotensive and hypertensive patients with significantly (P < 0.001) lower diurnal indices. There was a close correlation (P < 0.001) between the age-related decrease in plasma DHEAS levels and diurnal indices in both genders. Systolic and diastolic blood pressure variability changed parallel to plasma DHEAS levels in both genders, whether hypertension was present or not. Additional investigations are needed to find out whether reduced DHEAS levels play a role in decreased diurnal indices or whether both can be traced back to one and the same cause"

Arch. Dis. Child. 1998 May; 78(5): 481-483
"Neurocardiogenic syncope: a model for SIDS"
Ledwidge M., Fox G., Matthews T.

"A 5 1/2 month old male infant who had suffered three acute life threatening episodes was admitted for overnight sleep studies but was found dead after their completion while still in hospital. A necropsy classified the cause of death as sudden infant death syndrome (SIDS). The sleep studies had shown no periods of apnoea (> 20 seconds) or bradycardia (< 90 beats/min), and a rapid response to nasal occlusion (5 seconds). However, autonomic function during sleep was poor, with reduced heart rate variability (6 beats/min v control 24 beats/min, SD 6.2) and postural hypotension (a 12-14% fall in resting systolic blood pressure) associated with a fall in heart rate when tilted to a vertical position. Postural hypotension with bradycardia occurs in adults with unexplained syncopal episodes and is called a neurocardiac reflex. It involves poor vasomotor tone with peripheral pooling of blood, a consequent reduction in central venous return and cardiac distension, and in some individuals a neurally mediated bradycardia, as seen in this infant, rather than the expected tachycardia. A progressive bradycardia is the predominant mechanism of death seen in SIDS infants dying on cardiorespiratory monitors at home. This case suggests that a neurocardiac reflex occurs in infants, may have been involved in this infant's death, and deserves further study in the context of SIDS."

J. Appl. Physiol. 1998 Jul; 85(1):366-371
"Effect of sleep/wake state on arterial blood pressure in genetically identical mice"
Schaub C.D., Tankersley C., Schwartz A.R., Smith P.L., Robotham J.L., O'Donnell C.P.

"Genetic determinants may contribute to the large variability in arterial blood pressure responses to changes in sleep/wake state in humans. In this study, we developed techniques to examine the relationship between sleep/wake state and mean arterial pressure (MAP) in unrestrained, genetically identical mice (C57BL/6J; n = 9). The left common carotid artery was catheterized, and arterial blood gases were analyzed 24-48 h postsurgery to verify normal respiratory and metabolic function. The animals were then allowed to cycle naturally through sleep/wake states over a 3- to 4-h period while continuous polysomnography and arterial pressure measurements were made. The MAP decreased from quiet wakefulness to non-rapid-eye-movement sleep (9.8 +/- 1.3 mmHg; P < 0.001) and further decreased from non-rapid-eye-movement to rapid-eye-movement sleep (9.7 +/- 1.8 mmHg; P < 0.001). We conclude that the inbred strain of C57BL/6J mice exhibits significant and consistent changes in MAP related to sleep/wake state. Future studies can compare responses in this strain of mice with those in other inbred or transgenic mice to determine whether specific genes regulate arterial blood pressure responses to sleep/wake state."