Before the conventions, Sarah Palin caused a stir among the parents of children with Down Syndrome. My Leftist buddy Martin has a kid with Downs. Martin was moved by this Alaskan elected official’s seeking attention for the disability that his life revolved around. Martin seriously considered voting for McCain/Palin when Palin was picked as VP. Until he heard her speak.
I’ve not studied Down Syndrome. Still, in my explorations of autism, Down Syndrome kept emerging, but I did not swerve to explore its possible connection to the theory I was detailing. Several things do jump out. Those details suggest an evolutionary etiology for Down Syndrome. If supported, advocates like Sarah Palin that lambast evolutionary theory would be left advocating for advances within a discipline that she religiously combats.
Papers heavily support the thesis that Down Syndrome, in males and females, reveals extreme neoteny or maturational delay. Unlike in autism, where I posit males exhibit maturational delay and females maturational acceleration, all of those with Down Syndrome show extreme neoteny.
“Down syndrome individuals generally have retarded growth and maturational processes with retention of fetal development (”unfinished”) characteristics involving brain, face, and the 5th fingers. According to Waardenburg (1932) it was Blok in 1922, who first proposed a fetalization theory of Down Syndrome. From a palaeontological perspective all of these growth disturbances and developmental dysmaturities can be subsumed under the heading of neoteny. The concept of neoteny was coined by Kollmann in 1885 and refers to the retention of juvenile characters in the adult state, or to extention of fetal characteristics into childhood.” (Opitz, John M. & Gilbert-Barness, Enid F. (1990) Reflections on the Pathogenesis of Down Syndrome. American Journal of Medical Genetics 7: p. 44)
Most humans have 46 chromosomes. Chimpanzees have 48. A person with Down Syndrome has 47. The obvious question is whether those with Down Syndrome are transitional and when in our evolutionary past did the transition occur?
There is a higher incidence of autistic and Down Syndrome children being siblings than would be normally estimated.
A far higher number of Down children are left-handed than is the norm. My evolutionary theory posits we were all random-handed a hundred thousand years ago or so.
Older mothers are more likely to have a Down child. According to this blog’s thesis, the increased levels of testosterone in an older mother make her more likely to birth a son or daughter from an evolutionary past.
Several studies suggest that Down Syndrome reveals atavisms, or features characteristic of evolutionary progenitors.
Not supporting these ruminations is the fact that those with Down Syndrome are short in stature with unique physiological features. We have no ancestors of comparable stature or features in our archeological lineage. The physical handicaps are often profound. It’s hard to imagine a society of primitives with Down Syndrome characteristics surviving to procreate.
“Thus, with respect to (1) the fixation of a common pattern of major variability easily recognized in every race of humankind, (2) the invariable alteration of numerous morphometric traits and the abolition of family resemblance, (3) change in growth and of maturational characteristics with enhanced neoteny, (4) change in fertility, (5) appearance of a different behavioral phenotype, (6) change in chromosome number, and (7) changes in gene frequency —at least with respect to genes on chromosome 21 (Goodman, 1965; Rundle, 1973; Rundle and Sudell, 1973), we can only conclude that the occurrence of Down syndrome is akin to the process of speciation (albeit a sudden, rather than a gradual speciation). With respect to the relationship between speciation and chromosome abnormalities it is important to note that the types of chromosome rearrangements ‘that occur as polymorphosisms or as fixed permanent heterozygotes invariably involve meta- or submetacentric chromosomes. Those that distinguish species and serve to isolate those species involve telocentric or acrocentric chromosomes, which are self sterilizing.’ (John, 1981).” (Opitz, John M. & Gilbert-Barness, Enid F. (1990) Reflections on the Pathogenesis of Down Syndrome. American Journal of Medical Genetics 7: p. 45)
As an extreme example of neoteny, Down individuals are exaggerations of how our evolution might have occurred, without evidence of a dramatically expanded brain. It seems like Down Syndrome is some sort of alternative reality exhibition of how we could have evolved had our brains not grown at as fast a rate as they eventually achieved. The clues suggesting that Down Syndrome has an evolutionary etiology are powerful. Unlike autism, there is not a relatively clear hypothesis or picture of how exactly this occurred. Still, Sarah Palin, an aggressive, high-testosterone woman who gave birth to her Down child after 40, fits the thesis’s profile of the mother of an autistic child from the past.