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Umbilical cord biomarkers in autism determination “Autism is commonly thought to be the combined result of both genetic predisposition and an environmental trigger.” In the urgent search to elucidate the etiology of autism, care must be taken to distinguish between correlation and causation. Many hypotheses have been proposed to explain the origin of this disease, but none has been insightful enough to resolve this enigma convincingly. In most cases, emphasis has been placed on the coexistence of unusual phenomena in affected individuals. These include gross mutations, oxidative stress, and exposure to specific toxins, drugs and pollutants, among others [1] . Autism is commonly thought to be the combined result of both genetic predisposition and an environmental trigger. No report thus far has identified the same, specific hereditary promoter and situational catalyst in the majority of autistic cases studied. Thus, it would seem that essentially all of the published proposals are describing a correlation of autism and a comorbid attribute, both of which may be the product of a third causative agent. The cofactor would be a related sign but not necessarily the unique driving force underlying the universal etiology of this disease. Given this shortcoming, diagnostic medicine is consequently dependent on identifiable biomarkers, most or all of which are comorbid but questionably causative with autism. For example, many SNPs (e.g., CDH9 and SEMA5A) have been identified, coexisting with autism in some affected patients [2] . Finding such a genetic/environmental combination typically has an odds ratio
Umbilical cord biomarkers in autism determination “Autism is commonly thought to be the combined result of both genetic predisposition and an environmental trigger.” In the urgent search to elucidate the etiology of autism, care must be taken to distinguish between correlation and causation. Many hypotheses have been proposed to explain the origin of this disease, but none has been insightful enough to resolve this enigma convincingly. In most cases, emphasis has been placed on the coexistence of unusual phenomena in affected individuals. These include gross mutations, oxidative stress, and exposure to specific toxins, drugs and pollutants, among others [1] . Autism is commonly thought to be the combined result of both genetic predisposition and an environmental trigger. No report thus far has identified the same, specific hereditary promoter and situational catalyst in the majority of autistic cases studied. Thus, it would seem that essentially all of the published proposals are describing a correlation of autism and a comorbid attribute, both of which may be the product of a third causative agent. The cofactor would be a related sign but not necessarily the unique driving force underlying the universal etiology of this disease. Given this shortcoming, diagnostic medicine is consequently dependent on identifiable biomarkers, most or all of which are comorbid but questionably causative with autism. For example, many SNPs (e.g., CDH9 and SEMA5A) have been identified, coexisting with autism in some affected patients [2] . Finding such a genetic/environmental combination typically has an odds ratio
