e may contribute to behavioral or mental health problems prior to obvious cognitive decline. This gap can make it more difficult to determine the age of onset issue.
Genes and developmental disabilities
The number of genetic syndromes is growing in conjunction with the development of new genetic techniques. 30 years ago genetic testing usually meant chromosome testing and linkage studies. Nowadays we can obtain genome wide scans, florescence in situ hybridization, and microarrays that hone in on single nucleotide polymorphisms, copy number variants and the structure of specific genes (18). Recent breakthroughs in Fragile X research have opened another doorway with the discovery that mglut5 antagonists appear to reverse both molecular and cognitive/behavioral features of Fragile X (18, 19). There is growing research in epigenetics that point to changes in genes regulation due to trauma or faulty parenting. These findings challenge genetic determinism and force us to rethink nature-nurture arguments in terms of a newer understanding of gene–environment interactions.
Behavioral phenotypes are patterns of cognition and behavior associated with specific genetic disorders. Examples include: gaze aversion and anxiety in Fragile X (20); hyperphagia and binge eating in Prader Willi syndrome (21); personality traits linked to Trisomy 21 (22); increased risk for schizophrenia in 22q deletion (Velocardiofacial syndrome) (23); and epilepsy, dysmorphologies, hypotonia, and autism in 15q11.2-13 duplications (24). Many behavioral phenotypes bear some resemblance to temperamental features of affected individuals. Others seem more like prodromal primary psychiatric disorders (18). Unfortunately, there are too many genetic and neuroanatomical “smoking guns” for polygenic disorders like psychosis, bipolar disorder/schizophrenia, autism, and epilepsy in patients with IDD. This observation suggests that we are dealing with complex disorders and reinforces the idea that many syndromes are related to disruptions in pathways rather than specific lesions or related to single neurotransmitter abnormalities.
The most commonly neglected component of the biopsychosocial model is the role played by socio-cultural forces in dual diagnosis. Over the past three centuries, attitudes and values about individuals with IDD changed dramatically. These changes impact the social risk factors on the epidemiology, availability and types of habilitation and treatment services for those with IDD and mental disorders. In industrialized societies, urbanization and changing modes of living and working placed new occupational and educational demands that changed the niche occupied by individuals with ID. For example, many individuals with IDD now live in a society where there are fewer less technologically demanding jobs (requiring basic skill sets) and these jobs are often subject to increasing competition. These social changes are complicated by smaller families, greater geographic mobility and the problem of isolation from traditional sources of family support. Today families rely upon “professional services” to fill this void (8).
These social and cultural changes are redefining our sense of community. Historically, attitudes such as relative pessimism by medical providers about a lack of effective interventions and prognosis; marginalization and socio-economic segregation of individuals and their families; and lack of community-based resources contributed to out-of-home residential placement. Governmental actions focused mainly on developing programs that eventually became large custodial institutions (25). As an outgrowth of the Civil and Human Rights movement and numerous lawsuits, there is a shift to community care, inclusion, freedom of choice, active treatment and protection from various forms of restraint. But these changes are quite vulnerable to economic downturns; legislative battles ensue over cost-effectiveness instead of treatment efficacy. Unfortunately, there has been a resurgence of ambivalence about placing group homes in residential neighborhoods 