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ELECTRONIC ARTICLE: Warren G. Guntheroth and Philip S. Spiers The Triple Risk Hypotheses in Sudden Infant Death Syndrome Pediatrics 2002; 110: e64 [Abstract] [Full text] [PDF]

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Gender: a missing factor in the triple risk models for SIDS

David T. Mage   (27 November 2002)

Gender: a missing factor in the triple risk models for SIDS 27 November 2002
David T. Mage, Environmental Scientist Temple University Send letter to journal: Re: Gender: a missing factor in the triple risk models for SIDS david.mage{at}temple.edu David T. Mage	Guntheroth and Spiers (2002) do not note that all the triple-risk models they cite are without specific gender-dependent risk factors, so they cannot predict the global 50% male excess of SIDS per 1000 live births of each gender [e.g., USA, 57,624 male, 37,880 female, male fraction = 0.603 (CDC, 2002); Albania, 151 male, 94 female, male fraction = 0.616 (Godo et al., 2002)]. Consequently any triple-risk hypothesis to explain SIDS that only has gender-independent risk factors must be incomplete (Mage and Donner, 1996; 2002). The authors also discuss triple-risk models for SIDS in relation to the form of the SIDS age distribution and uncritically accept a 2- parameter lognormal model for the SIDS age distribution to describe it (Raring, 1975). But they present it as a paradigm of a triple-risk “multifactorial causation” for SIDS which by definition must contain 3 or more adjustable age-parameters, at least one for each of the three independent risk factor that varies with age. By definition (Hahn and Shapiro, 1967), any probability distribution for a SIDS risk factor, P(x) at age x, must satisfy the integral (Int) condition, Int [P(x) dx] = 1 (0 < x < infinity). (1) Raring's lognormal model for the SIDS age distribution has two adjustable parameters, with the age appearing in the denominator as 1/x (Aitchison and Brown, 1972). Because it would go to infinity at birth as x goes to zero, a risk factor with only an age term of 1/x would violate Equation 1. However, the numerator of the lognormal distribution has another age term in a negative exponential function of the logarithm of the age squared, that goes to zero faster than the denominator as x goes to zero. Thus, it must be part of the same risk factor with the 1/x term which leads to P(x) = 0 at birth. Therefore this lognormal model with only two independent terms involving age may apply to a single risk factor for SIDS that rises rapidly from zero at birth and then falls slowly towards zero with age, without any upper age limit, and thus it cannot be a product of three independent risk factors. The authors correctly noted that Raring’s lognormal model for SIDS ages plots as a straight line on probability paper, but did not recognize that such a line incorrectly predicts SIDS can occur at any age throughout life. Had they done so the lognormal age model could have been rejected immediately on its face because no valid SIDS age model should predict SIDS occurring beyond infancy into adulthood. For any probability model to represent a “triple- risk” it would require at least three age parameters, one or more for each of the three hypothesized independent risk distributions that all must satisfy Equation 1. The authors are apparently unaware that this antinomy of irreconcilable contradiction between a two-parameter SIDS age model and a triple-risk SIDS causation model can be resolved by use of a Johnson SB model to describe the age distribution (Johnson, 1949; Hahn and Shapiro, 1967). The SB probability model for SIDS ages has four adjustable parameters that allow for modeling of three age-dependent risk factors satisfying Equation 1, that together may lead to a fatal cerebral anoxia. They might vary as increasing with age (e.g., risk of infection), decreasing with age (e.g., risk of neurological prematurity), and rising and falling with age (e.g., risk of infant anemia as adult hemoglobin slowly replaces rapidly depleted fetal hemoglobin), and together they predict zero SIDS beyond an age of 3.5 years(Mage, 1996; 2001). In conclusion, a gender-related risk factor needs to be added to the triple-risk models the authors discussed in order to predict the 50% preponderance of male SIDS in the global data base, and the 2-parameter lognormal distribution is an invalid model for the SIDS age distribution. References: Aitchison J, Brown JAC. The Lognormal Distribution, Cambridge, Cambridge University Press, 1972: 8. CDC. Infant mortality data, 1979-1998, http://wonder.cdc.gov, Accessed November 10, 2002. Godo A, Pano A, Veveca E, Kuli Gj, Caushi N, Cenko F. Osservazioni epidemiologici sulla SIDS in Albania (in Italian). Abstract, The Seventh SIDS International Conference, Firenze, August 31 - September 4, 2002., Conference Handbook, 14-15. Guntheroth WG, Spiers PS. The triple risk hypotheses in sudden infant death syndrome. Pediatrics 2002; 110: e64. Hahn GJ, Shapiro SS. Statistical Models in Engineering, New York, John Wiley, 1967: 33, 213. Johnson, NL. Systems of frequency curves generated by methods of translation. Biometrika 1949; 36: 149 - 182. Mage DT. A probability model for the age distribution of SIDS. Journal of Sudden Infant Death Syndrome and Infant Mortality 1996; 1: 13- 32 (1996). Mage DT, Donner M. A genetic basis for the sudden infant death syndrome sex ratio. Medical Hypotheses 1997; 48: 137-142. Mage DT. Antinomy and the SB model for SIDS. Epidemiology. 2001; 12: 471. Mage DT, Donner M. Is SIDS an X-linked recessive condition? A four- factor risk model. Abstract, The Seventh SIDS International Conference, Firenze, August 31 - September 4, 2002., Conference Handbook, p. 122. Raring RH. Crib Death: Scourge of Infants - Shame of Society. Hicksville NY: Exposition Press; 1975: 93-97.