Human behavior is a loosely defined foundation for individuality, generally considered to be influenced and developed by the environment.

However, recent molecular studies have exposed genetic factors that suggest a more biological origin for behavior. Gene segments in the genome of humans and other animals have been identified and associated with particular behavioral traits. Is it possible that the presence or absence of even a single gene may predispose one to alcoholism, increased irritability, or enhanced intelligence? Clearly exploration of the nature versus nurture argument with regard to genetic predisposition has social, political, and legal significance.

Employing "behavior" as the experimental variant requires identification of intrinsic behavioral characteristics that may be very difficult to define. Intelligence is

considered an expression of behavior, yet the delineation of what makes an individual intelligent has been highly debated. Does IQ determine intelligence? Or is

economic success indicative of intelligence? Once an experimenter is comfortable with his proposed definition for a behavior, the characteristic must be reliably and validly measured. However, if the relationship between, for example, intelligence and IQ is not clear, then assigning parameters for levels of intelligence will be even more challenging (1).

Genetically influenced traits tend to be polygenic in character, involving many genes acting in concert to produce a certain response. Therefore, association of one gene with one behavior is usually only partially conclusive. Behavior depends on the interaction of multiple gene sequences with environmental influences. These multiple gene systems are referred to as "quantitative trait loci" (QTL), reflecting their ability to quantitatively distribute phenotypic characteristics. The recently completed human genome sequence has greatly assisted the detection of QTLs and polymorphisms (2). It must also be emphasized that genes do not directly dictate action, but rather are mediated by the proteins that they code for. It is necessary to examine not only the genes but also the assortment of proteins responsible for expression of particular traits (3)It is anticipated that detailed analysis of the human genome will contribute to understandings about gene protein and behavior may be more accurately described. Effective behavioral genetic research requires investigation of families and populations, rather than individuals. Environmental factors influencing populations must also be considered. The heritability patterns of a behavior are compared with a control population experiencing similar environmental factors. A theoretical formula the interaction of the two (4). However, research has determined that environmental influences tend to disengage behavioral traits among family members rather factors during later maturation. Recent genetic-behavioral findings support an opposite conclusion. It appears that the influence of certain genetic traits actually experiences contributing to one's unique behavioral profile. to account for variability is frequently employed: total phenotypic variability of a specific trait equals the genetic component plus the environmental component plus than unify them. Furthermore, traditional belief asserted that genetic influences were critical only in infancy and early childhood, being superceded by environmental intensify through adolescence (5). Despite attempts to eliminate variability between studied populations, it is virtually impossible to account for the myriad of social

organization and transcription, and hence regulatory elements that control expression. By utilizing genomic and proteomic tools, the relationship between gene/

There are several existing indications that support biologically-based behavioral characteristics. Behavior tends to be species specific; varying species of birds utilize different methods for mating and feeding. Behaviors also reproduce themselves in successive generations, or "breed true." This is particularly evident in artificial selection for traits in domestic animals. However, behaviors do change when exposed to altered biological processes. For example, expression of undesirable social manifestations in mental illnesses is commonly controlled with drugs that alter brain chemistry (1).

Behaviors such as mental illness are also found to run in families. In fact, nearly all of the studied behaviors are found to be more heritable than common physical diseases (2). The incidence of schizophrenia in the general population is relatively low, but the siblings of schizophrenics are about 10 times more likely to suffer study investigated the incidence of schizophrenia among fraternal and identical twin populations. Identical twins, who essentially possess identical genomes, maintained a 46 percent rate of tandem schizophrenia. The rate for fraternal twins, however, was only slightly higher than that of non-twin siblings, at an incidence of 14 percent. The exact location of the schizophrenia gene (or genes) has not yet been verified (5). , humans have old genes in a new environment. Our species evolved to sustain a hunting-gathering lifestyle with frequent famine and mandatory physical activity for survival. Food is made readily available in our society, and many children are become increasingly less physically active. Unfortunately, the genes governing metabolism have not changed to accommodate this indulgent, inactive lifestyle. It has been estimated that genetics contributes to about 40 percent of obesity are influencing behavior. A rare genetically based neurodevelopment disorder, Williams Syndrome (WS), may provide the most compelling evidence for parallel functional networks within the brain, as well as expose how these functions are influenced by genetic processes during neurodevelopment. WS is caused by a micro-deletion on the long arm of chromosome 7 (7q.11.23) with an incidence of 1 in 20,000 live births. This deletion encompasses a 1.5 mega base chromosomal segment, coding for an estimated 17 genes, and is thought to occur by unequal recombination during meiosis. The deleted segment includes elastin (ELN) and four genes that are from the disorder, while the average incidence among children of schizophrenics is about 13 percent. Risks of subsequent generations are comparatively lower. A

variance, while over 200 genes and gene markers for obesity have been identified (8). This is a classic example of how both environmental and biological factors

understood to be highly expressed in the brain (FZD9, STXIA, LIMK1, CYLN2) (9). .