In 1990, we published a paper with his colleagues suggest that a particular genetic abnormality is linked to alcoholism (Blum et al. 1990). Unfortunately, it was often erroneously reported to have found the "alcoholism gene", which implies that there is a one-to-one relationship between a gene and a specific behavior. these interpretations are common readers may recall accounts of an "obesity gene" or a "personality gene." Needless to say, there is no such thing as a specific gene forAlcoholism, obesity, or a certain type of personality. However, it would be naive to say otherwise, that these aspects of human behavior are not associated with specific genes. Rather it is to understand how certain genes and behavioral traits are connected.
Over the past five years we have pursued the relationship between certain genes and various behavioral problems. In molecular genetics, the association refers to a statistically significant impacta genetic variant (an allele) among genetically related individuals with a particular disease or condition, compared with a control population. In the course of our
work, we found that the genetic anomaly previously found that alcoholism is associated with an increased frequency in people with other addictive disorders, compulsive or impulsive found. The list is long and remarkable, including alcoholism, drugs, smoking, compulsive overeating and obesity,Attention-deficit disorder, Tourette syndrome and compulsive gambling.
We believe that these diseases are a common biological substrate as a whole, a "hard-wired" system in the brain (consisting of cells and mediators), sees the joy in the process of re
warding certain behavior. Think of how people respond to the safety,
warmth and a full stomach. If these needs are threatened or not met, we experience discomfort and anxiety. Congenitalchemical imbalance, which could change the intercellular substance in the process of signal transmission in the brain re
ward a person's sense of well-being with anxiety, anger or desire for a substance that can alleviate the negative emotions out of the crowd. This chemical imbalance manifests as one or more behavior problems for which one of us (Blum) has coined the term "reward deficiency syndrome."
This syndrome includes a form of sensory deprivation of the brain's pleasure mechanisms. It may be manifestedin relatively mild or severe forms that follow are derived as a result of inability to reward the individual biochemical activities of daily living. We believe that we have found at least one genetic aberration that leads to a change in brain reward pathways. It is a variant of the gene for the D2 dopamine receptor, called the A1 allele. This is the same genetic variant, which we previously found to be associated with alcoholism. In this article weEvidence that the A1 allele is also associated with a spectrum of impulsive behavior, compulsive and addictive. The concept of a reward deficiency syndrome unites these disorders and may explain how simple genetic anomalies give rise to complex behaviors deviant.
The system of pleasure and reward in the brain was discovered by accident in 1954. The American psychologist James Olds was studying the rat brain process alarm, when he accidentally put the electrodes in aPart of the limbic system, a group of deep structures of the brain, which are generally believed to play a role in emotions. When the brain was wired so that the animal could stimulate this area by pressing a lever, Olds found that rats would press the lever almost nonstop, up to 5,000
times per hour. The animals would stimulate to sleep with the exclusion of everything else except. They would also bear the tremendous pain and discomfort for the chance to press the lever. Oldshad a gap in the limbic system, which led to a powerful reward for such animals.
Research on human volunteers have shown that electrical stimulation of certain areas of the brain (the medial hypothalamus) a sense of quasi-orgasmic sexual arousal (Olds and Olds 1969) produced. When some other areas were stimulated in the brain, has seen a kind of vertigo natural negative thoughts banned. These results show that a distinct pleasureneurological function, which is connected to a complex reward and reinforcement system (Hall, Bloom and Olds 1977).
In recent decades, research on the biological basis of chemical dependency may some brain regions and neurotransmitters involved in reward to be determined. In particular, it appears that dependence on alcohol, opiates and cocaine on a number of biochemical mechanisms (Cloninger 1983, Blum et al. 1989) is based. The neural circuitsdeep in the brain called the limbic system involved, and two regions of the nucleus accumbens and the globus pallidus appears to be critical in the expression of reward for people taking these drugs (Wise and Bozarth 1984). Although each substance of abuse appears to be different parts of the circuit to act, the end result is the same: dopamine in the nucleus accumbens and the hippocampus (Koob and Bloom 1988) was released. neurotransmitter dopamine seem to be the grand prize for theseAmplifier.
Although the system of neurotransmitters in the biology of reward is involved in complex, at least three other neurotransmitters known to be involved in several locations in the brain: serotonin in the hypothalamus, the enkephalins (opioid peptides) in the ventral tegmental area and nucleus accumbens, and inhibitory neurotransmitter GABA in the ventral tegmental area and nucleus accumbens (Stein and Belluz 1986, Blum 1989). Interestingly, the
glucose receptoris an important link between the serotonergic and the opioid peptides in the hypothalamus. An alternate pathway involves the release of noradrenaline prize in the hippocampus from neuronal fibers that originate in the locus coeruleus.
In a normal person, these neurotransmitters
work together in a cascade of excitation or inhibition between complex stimuli and complex responses, leading to a feeling of comfort, the reward (Cloninger 1983, Stein and Belluz 1986, BlumAnd Koslowski 1990). In the cascade theory of reward, a disruption of these intercellular interactions results in anxiety, anger and other "bad feelings" or a desire for a substance that alleviates these negative emotions. Alcohol is known as norepinephrine in the limbic system activate circuits of a battery that contains intracellular serotonin, dopamine and opioid peptides. Alcohol may also act directly through the production of amine neuro that the interaction withopioid receptors or dopaminergic systems (Alvaksinen et al, 1984;. Blum and Kozlowski 1990). In the cascade theory can be rewarding, genetic anomalies, prolonged stress or long-term abuse of alcohol to a model of self-desire abnormal in both animals and humans.
Support for the cascade theory can be derived from a series of experiments on mice, strains of alcohol prefer
ring water. Compared with normal mice, serotonergic neurons less alcohol-prefer
ring ratshypothalamus, increased enkephalin in the hypothalamus (because less is released), plus the GABA neurons in the nucleus accumbens (inhibit the release of dopamine), a reduced supply of dopamine in the nucleus accumbens and a lower density of dopamine D2 receptors in some areas of the limbic system (Russell, Lanin and Taljaard 1988, McB
ride et al, 1990;. Zhou et al 1990, McB
ride et al .. 1993).
These studies suggest a cascade of four parts, where there is a reduction ofthe amount of dopamine in reward a key position, which was released in alcohol-prefer
ring rats. The administration of substances that increase the supply of serotonin in the synapses, or that directly stimulate the dopamine D2 receptors reduce the demand for alcohol (McBride et al. 1993). For example, D2 receptor agonists reduce alcohol consumption among rats that prefer alcohol, while the dopamine D2 receptor antagonists increase the consumption of alcohol in these inbred animals (Dyr et al. 1993).
Support for theCascade theory of alcoholism in humans in a number of clinical studies. have had as precursors of amino acids of some neurotransmitters (serotonin and dopamine) and a drug that promotes enkephalin alcoholic subjects experienced fewer people craving for alcohol, a lower incidence of stress, a greater likelihood of recovery and a reduction in interest rates relapse (Brown et al 1990;. Tractenberg and Blum 1988, Blum, Briggs and Tractenberg 1989). In addition,the idea that dopamine is the "final common pathway" for drugs such as cocaine, morphine and alcohol by more recent studies by Jordi Ortiz and his colleagues at Yale University School of Medicine and is supported by the University of Connecticut Health Center Services . These authors have shown that chronic use of cocaine, morphine or alcohol results in the biochemical adaptations in the limbic dopamine system. They suggest that these adjustments can lead to changes in earnings andfunctional properties of the dopaminergic system.
We believe that the biological substrates of reward that are behind the dependence on alcohol and other drugs also the basis of impulsive disorders, compulsive disorder and addiction in reward deficiency syndrome.
A change in one of the genes that are involved in the expression of molecules in the reward cascade might predispose an individual alcoholism. In fact, the evidence for a genetic basis for alcoholismaccumulated steadily over the past five decades. The first report is from studies on mice by American psychologist L. Myron in 1952. Myron noted that the selection, mice preferred alcohol to water. Gerald McLearn at the University of California at Berkeley took another step forward with the production of inbred mice (strain C57), which had a clear preference for alcohol. The alcohol-prefer
ring C57 strain bred for generations, probably was the firstclear sign that alcoholism is a genetic basis (McLearn and Rodgers 1959) did.
The first evidence that alcoholism has a genetic basis of human
trafficking came in 1972 when scientists at Washington University School of Medicine in St. Louis found that adopted children whose biological parents were alcoholics to have endured more a problem with alcohol as alcoholic parents (Schuckit, Goodwin and Winokur 1972). In 1973, Goodwin and Winokur, works for the PsykologiskInstitute in Copenhagen, studied 5,483 men in Denmark, which was adopted in early childhood. They found that children born of alcoholic fathers had become three
times more likely than children of fathers alcoholic drinks.
In late 1980, proposed research on the inheritance of alcoholism, which may be important genetic differences between alcoholics and nonalcoholics (Cloninger, Bohman and Sigvardsson 1981, Goodwin 1979). One of us (Blum) and his colleagues suspect thatcould be the activity of chemical messengers in the brain reward pathways involved. In two years we compared eight genetic markers associated with various neurotransmitters (including serotonin, en
dogenous opioids, GABA, transferrin, acetylcholine, alcohol dehydrogenase and aldehyde dehydrogenase). In any case, we could not find a direct correlation between the genetic markers and alcoholism.
To examine the possibility of a genetic marker was the ninthOlivier Civelli Vollum Institute at the University of Oregon cloned and sequenced the gene for a form of D2 dopamine receptor. The D2 receptor is one of at least five physiologically distinct dopamine receptors (D1, D2, D3, D4 and D5) on the synaptic membrane of nerve cells in the brain (Sibley and Monsma 1992). Previous studies have shown that D2 receptors are expressed in neurons of the cerebral cortex and the limbic system, including the words nucleus accumbens, theAmygdala and hippocampus. Since they are the same areas of the brain (with the exception of the cerebral cortex) that are presumably involved in the reward cascade, are given the opportunity to work Civelli, a major candidate for molecular genetic aberrations to investigate among alcoholics.
The technique we used to distinguish between the D2 receptor gene in alcoholics and nonalcoholics is based on the detection of restriction fragments (RFLP).This approach involves the use of DNA-cutting enzymes (restriction endonucleases) that cut the DNA molecule at specific nucleotide sequences. If there are genetic differences between individuals using a restriction enzyme that cuts DNA, along various points (or almost) of a gene, the resulting fragments of their genes are different lengths. These different fragments, or polymorphisms, are detected with a labeled DNA probe in this case a short sequencethe D2 receptor gene binds to a complementary DNA sequence of the fragments. radioactive fragments of different lengths, a difference in the sequence of cleavage by restriction enzymes (Grandy et al. 1989) recognized.
The restriction enzyme (Taq 1) cuts the sequence of nucleotides in a place outside of the region coding for the D2 receptor gene. The result is the Taq 1A polymorphism. To date, there are four known Taq 1A allele, the alleles A1, A2, A3 and A4. The A3and A4 alleles are rare, while the A2 allele is found in almost 75 percent of the population and the A1 allele in about 25 percent of the population.
In 1990, we used the Taq Taq I enzyme polymorphism AI research in the DNA from the brains of deceased alcoholics and nonalcoholics to control the population. The results were striking: In our sample of 35 alcoholics, we found that 69 percent had the A1 allele and 31 percent had the A2 allele. In 35 nonalcoholics, we foundthat 20 percent had the A1 allele, and 80 percent had the A2 allele.
Since our 1990 study, some laboratories have failed to find a connection between the A1 allele and alcoholism. However, a review of their work that their samples are not severe forms of alcoholism, which in our opinion, defines a key differentiator. In our original study had more than 70 percent of alcoholic liver cirrhosis, a disease linked to serious and chronic alcoholism. In addition,studies do not adequately assess the negative control alcoholism, drug abuse and eliminate other related "reward behavior." In this context, Katherine Neiswanger and Shirley Hill, University of Pittsburgh recently found a strong association A1 allele and alcoholism, and suggested that the early failures were the result of poor assessment of a phenotype in the real control group (Neiswanger, Kaplan and Hill 1995). To date, 14 independent laboratories to determine that the supportA1 allele is a causative factor in severe forms of alcoholism, though perhaps not in milder forms (Blum and Noble 1994). These results show that the A1 allele of the dopamine D2 receptor gene is the only cause of severe alcoholism, but they are a strong indication that the A1 allele is involved with alcoholism.
Further evidence for the role of biology in alcoholism comes from efforts of electrophysiological markers that give a predisposition for the occasion, findAddiction. This label is the latency and amplitude of the positive of 300 milliseconds (P300) wave, an indicator of the overall supply of the brain caused by a specific stimulus, which produced a sound. It turns out that the differences are evident in the electrical activity of the brain in young children of alcoholic fathers. Their P300 waves are markedly reduced in amplitude compared to the P300 wave of the sons of alcoholic fathers. These results raised theWhether this deficit down from father to son, and this deficit would be if her son had been transferred to provide drug abuse in the future (Porjexa companion, Bihari and Kissin 1984).
Tests
carried out since then have answered both questions. The alcoholic fathers had seen the same deficit in P300 wave of her sons and their children showed an increase in drug-seeking behaviors (including alcohol and nicotine) than children of nonalcoholic fathers. The children ofalcoholic father had an atypical neurocognitive profile (Whipple, Parker and Noble 1988). Now it seems that children with abnormal P300, rather than the abuse of drugs and tobacco in later years (Berman, Whipple, Fitch and Noble 1993).
Surprisingly, Noble and his colleagues found an association between the A1 allele and P300 wave latency in children of alcoholics (Noble et al. 1994). Two of us (Blum and Braverman) this work and observed a similarCorrelation between the A1 allele and a prolonged P300 latency in a neuropsychiatric population. Subjects who were homozygous for the A1 allele significantly prolonged P300 latency were compared with the A1/A2 and A2/A2
carriers.
Cocaine can bring intense, but temporary, pleasure to the user. The consequences are serious dependency and psychological and physiological damage. Various psychosocial theories have been developed to change the abuse of cocaine and other illicit drugs. UnlikeAlcoholism, which is growing empirical evidence implicated genetic factors, relatively little is known about the genetics of human cocaine addiction. However, recent studies suggest that hereditary factors are involved in the use and abuse of cocaine and other illicit drugs.
Studies of adopted children, for example, show that a biological background of alcohol problems among the parents provided a greater propensity for illegal drugs in children (Cadoret,Froughton, O'Gorman and Heywood 1986). Similarly, studies on family cocaine addiction, a high percentage of first and second grade, who have been diagnosed as alcoholics (Miller,
gold, Belkin and Klaher 1989, Wallace 1990).
Abnormal behavior, such as conduct disorder (in which children violated social norms and the rights of others) and antisocial personality (the adult equivalent behavior disorder) are often found to be associated with problems of alcohol and drugs. MoreThe researchers found that the inhumane behavior in children is a tendency for antisocial personality, abuse of alcohol and drug problems in later life provides. An analysis of 40 studies showed a strong positive correlation between the alcoholism and drug abuse, alcoholism and antisocial personality among and between drug abuse and antisocial personality (Schubert et al. 1988).
While there is little about the genetics of cocaine addiction is well known, numerous scientific dataeffects of cocaine on brain chemistry. The current thinking is that the system that uses dopamine in the brain an important role in the pleasurable effects of cocaine game. In animals, for example, is the main place where the cocaine effect of dopamine D2 receptor gene on chromosome 11 (Koob and Bloom 1988). Recently George Koob and his colleagues at the Scripps Research Institute in La Jolla, California, has found evidence that the dopamine D3 receptor gene is aprimary site of cocaine effects. The exact effect of cocaine on gene expression is not known. But we know that D2 receptors are decreased in chronic administration of cocaine, and this can cause severe craving for cocaine dreams and possibly (Volkow et al. 1993).
A recent study by Ernest Noble of the University of California at Los Angeles and Blum found that about 52 percent of cocaine addicts have the A1 allele of the dopamine D2 receptor gene, compared to only 21 percent ofnonaddicts. parental alcoholism and drug abuse, the power of cocaine by the addict (intranasal anti-cocaine "crack") are used, and early childhood deviant behavior, such as behavioral disorders: The prevalence of the A1 allele increases significantly with three risk factors. In fact, when the cocaine addict has three of these risk factors, the prevalence of A1 allele rose to 87 percent. These results suggest that childhood behavioral problems, a genetic predisposition to drug or signalAlcohol dependence (Noble et al. 1993).
A recent survey by the National Institute of Drug Abuse five independent studies have shown that the A1 allele is also poly drug use (Uhl, Blum, Noble and Smith 1993) attached. The A1 allele is an increase in the amount of money for drugs by polysubstance-dependent individuals (Comings et al. 1994) spent online.
Although not considered in the same light as the use of cocaine and other illicit drugs, smokingis another form of chemical dependency. Most attempts to quit smoking have withdrawal symptoms typical of other chemical dependency related. Although environmental factors important determinants of cigarette can be useful, there is strong evidence that the acquisition includes the habit of smoking and persistence of strong hereditary factors.
Of particular importance to studies in identical twins, which means that if one twin smokes to smoke the others are likely to show. This isis not the case with fraternal twins. In a twin study examines Dorit Carmella Stanford Research Institute and its staff in a national sample of male twins who were veterans of World War II. A unique aspect of this study is that the twins were interviewed twice, 1967-1968 and again 16 years later. This is a study of possible genetic factors in all aspects of smoking initiation, maintenance and removal. In general, what happens to an identical twin has happened toothers, including the long-term patterns of smoking smoke, the smoke and then. The absence of these similarities in a control group of dizygotic twins suggests a strong component of smoking behavior biogenetic (Swan et al. 1990).
Animal studies have suggested that the dopaminergic pathways of the brain may be involved. For example, administration of nicotine to rodents metabolism of dopamine in reward centers of the brain interferes in excess ofThe administration of alcohol.
examined in this context, one of us (to come) and his colleagues, the frequency of A1 allele in a population of Caucasian smokers. These smokers do not abuse alcohol or other drugs, but had at least one failed attempt to quit smoking. It was discovered that 48 percent of smokers carried the A1 allele. The higher prevalence of A1 allele had age of onset of smoking, the greater the amount of smoke and the majority wasthe difficulties, wanted to learn how to quit smoking. In another sample of Caucasian smokers and nonsmokers, found Noble and his colleagues found that the higher prevalence of A1 allele in smokers, less for those who had stopped smoking and the lowest among those who had never smoked (Noble et al. 1994).
Obesity is a disease that comes in many forms. have believed that once primarily environmental, it is now both genetic and environmental components. In a SwedishAdoption of study, for example, the weight of adult adoptees strongly correlated with body mass index of biological parents and the body mass index of adoptive parents. The links to both genetic and environmental factors have been dramatic. Other studies of twins and adopted indicate that heredity is an important factor for the development of obesity in childhood environment has little or no control. Moreover, the distribution of body fat have been foundhave inherited items. The legacy of subcutaneous fat distribution is genetically separable from the body fat stored in other subjects (with the viscera in the abdomen, for example). It was suggested that there is no evidence of single and multiple-gene abnormalities (Bouchard, 1995).
Given the complex range of metabolic pathways contribute to overeating and obesity, it is not surprising that a number were affected by neurochemical deficiencies. In reality, at least three of theseThe genes were found: one with the production of cholesterol, a place with the transport of fat and one for the production of insulin (Bouchard, 1995). The ob gene and its product range of the protein leptin in regulating feeding behavior of long-term (Zhang et al. 1994) associated with it. Finally, a further protein, glucagon-like peptide 1 (GLP-1) must be in the regulation of feeding behavior in the short term in question (Turton et al. 1996). The relationship between leptin and GLP-1 is unknown.The OB gene may be involved in the choice of animal fats, but do not seem to be the intake of carbohydrates that are regulated by the dopaminergic system. It 'possible that the ob gene is functionally the opioid systems are involved in peptodergic reward.
Whatever the relationship between these systems, the complexity of the compulsive eating disorders suggests that more than one defective gene is involved. In fact, the relationship between overeating compulsive drug and alcoholThe dependence is well documented (Krahn 1991, Newman and
gold, 1992). Studies show that neurochemical pleasure-seeking behavior is a common denominator of addiction to alcohol, drugs and carbohydrates (Blum et al. 1990). Alcohol, drugs and all carbohydrates cause the release of dopamine in the primary sector of the brain reward, the nucleus accumbens. Although the precise location and the specific properties like the induction of alcohol, drugs and food are still to be discussed, there are generalAgreement that work through the dopaminergic pathways of the brain. Other studies suggest that at least three other neurotransmitters serotonin, GABA and opioid peptides.
Variants of the dopamine D2 receptor gene appear to be risk factors for obesity. The A1 allele was in 45 percent of obese 19 percent of non-obese subjects (Noble, Noble and Ritchie 1994) in comparison. In addition, the A1 allele is not a series of metabolic and other relatedcardiovascular risks, including cholesterol and high blood
pressure. In contrast, when the profile of subjects included factors such as obesity of the parents preferred a later onset of obesity and carbohydrates, increase the prevalence of A1 allele at 85 percent. More recently, another study found a significant association between genetic variants of the D2 receptor and obesity (Comings et al. 1993).
There is also an increased prevalence of the A1 allele in obese subjectsthe grave by an alcohol and drug dependence (Blum et al. 1996a). were found for obesity, alcoholism and drug addiction in a patient, the incidence of allele A1 at 82 percent. In contrast, the allele has an incidence of zero percent in non-obese patients who can not addicts and do not have a family history of drug abuse. The presence of variants of the D2 dopamine receptor gene increases the risk of obesity and related behaviors.
Pathological gambling in which an-In particular, the act of risking money or goods as "payments" obsessive-occurs with a rate below two percent in the general population. Even if the employee is more socially acceptable behavior, gambling has many similarities with alcohol and drug abuse. Physicians have noted the similarity between the state of euphoria caused the player and the "high" of cocaine addict or substance abuser. pathological gamblers express clearNostalgia for the "feel" of gambling, but to develop tolerance to them to take greater risks and larger bets to reach a level of excitement you want to, and experience withdrawal-like symptoms (anxiety and irritability) when "Action is available (Volberg and Steadman, 1988). There is actually a typical course of progression through four stages of the syndrome of compulsive gambling: winning, losing, do not despair and without hope of a series of unusual that another addictive behavior.
Could the dopamine in the membranes of the brain are involved with gambling? A recent study of Caucasian pathological gamblers found that 50.9 percent of the A1 allele of the dopamine D2 receptor (Comings et al. 1996b) carried out. The most serious is the problem of play, the more likely it was that each institution has been A1 allele. Finally, in a population of men with drug problems, the pathological gamblers and the incidence A1 allele were increased to 76 percent.
This disease is most common in school-age children who are at least four times more frequently than the symptoms of young girls to find expression. These children have difficulty applying themselves to tasks that require mental effort, is easily distracted, have difficulty in sitting still without restless and impulsive, they may blurt out answers in class or can not wait for their turn. Although normal children occasionally exhibit these symptoms,attention deficit disorder is diagnosed when the behavior of the persistence and severity of the child hinders social development and education.
Early speculation about the causes of attention deficit disorder on potential sources of stress within the child's family, including marital problems, poor education, psychiatric disorders, alcoholism or drug abuse focus. Has gradually become clear, however, that the stress in the family can not explain the incidence of the disease. It 's timedoubt that the disease has a genetic basis.
The proof of this idea comes from inheritance patterns in families of children with the disease, and studies of identical twins. For example, consider the cases where they are bred full brothers and half brothers (who have only half the genetic identity of whole blood) and in the same family environment. If behavioral problems have been subject to attention deficit disorder "learned" in the family, then the frequency ofthe disease should be the same for others full as it is for brothers. In fact half-siblings of children with attention deficit disorder significantly lower incidence of the disease in full siblings (Lopez 1965) have. In another study, researchers found that if one identical twin had attention deficit disorder, there was a 100 percent chance that the others also had the disorder. In contrast, the frequency of concordance between dizygotic twins, only 17 percent. ThisResult was supported by two other independent studies of identical twins (Willerman 1973). Finally found one of us (to come) and his staff was that the A1 allele of the dopamine D2 receptor gene in 49 percent of children with attention deficit disorder, compared to only 27 percent of controls (Comings et al. 1991).
Tourette Syndrome: In some recent work of others has linked attention deficit disorder with another impulsive disorder. More than 100 years before the FrenchNeurologists Giles de la Tourette described a condition that is characterized by compulsive swearing, multiple muscle tics and loud noises. He found that the disease occurs mainly in children aged 7 to 10 years to be with boys affected more often than girls. Tourette proposal that could be inherited.
In the early 1980s, a study by us (coming soon) and his colleagues 246 families in which at least one family member had Tourette's disease. The study showedthat almost all cases of Tourette syndrome gene (the Comings et al. 1991) are. Subsequent studies also found that there is a high incidence of impulsive, compulsive, addictive, mood and anxiety disorders on both sides of the affected person Family (coming and coming 1987). The A1 allele has been shown in a recent report implied that nearly 45 percent of people diagnosed with Tourette's disorder performed aberrant gene (Comings et al. 1991). In addition, the A1 allele had the highestIncidence in people who had the most serious of the disease.
As mentioned above, Tourette's syndrome seems strictly for attention deficit disorder are related. In studies of the two diseases, it was found that 50 to 80 percent of people with Tourette syndrome also had attention deficit disorder. In addition, an increase in the number of relatives of people with Tourette's disorder and disturbance in attention (Knell and Comings 1993) had. Now it seemsthat Tourette syndrome is a complex disease, attention deficit disorder, conduct disorder, obsessive compulsive disorders and addiction and related diseases may include others. The close link between these disorders, one of us (to come) is to propose that Tourette syndrome is a severe form of attention deficit disorder (coming and coming 1989, Comings 1995).
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