Gene Therapy Method Using GAD2 Gene for Treatment of Eating Disorders Such as Anorexia Cross-Reference to Related Applications This application is a continuation-in-part of, and claims the benefit of U.S. Provisional Patent Application No. 60/555,029, filed on March 19, 2004. Background and Summary of the Invention The present invention relates to methods of and formulations for treating behavioural and nervous disorders such as anorexia and bulimia. More particularly, the present invention teaches methods and formulations for gene therapy using the GAD2 gene. While extreme obesity is thought to be the combined result of a variety of genetic and environmental factors, the GAD gene is the first gene implicated as a strong candidate gene in conditions of abnormal weight. The GAD2 gene codes for GAD65, an enzyme which increases production of the neurotransmitter GABA. When GABA interacts with another molecule, neuropeptide Y, in a specific part of the brain (the paraventricular nucleus of the hypothalamic), food intake is stimulated. While not limiting the present invention to its theoretical mechanistic aspects, it is believed that individuals with a more active form or a greater number of copies of the GAD gene, or more abundant GAD, accumulate a larger pool of GABA in the hypothalamus, and this explains why obese individuals overeat. GAD gene therapy is currently tested in treatment of both Parkinson's disease and epilepsy. While extreme obesity is thought to be the combined result of a variety of genetic and environmental factors, the GAD gene is the first gene implicated as a strong candidate gene in conditions of abnormal weight. The GAD2 gene codes for GAD65, an enzyme which increases production of the neurotransmitter GABA. When GABA interacts with another molecule, neuropeptide Y, in a specific part of the brain (the paraventricular nucleus of the hypothalamic), food intake is stimulated. GAD65 catalyses the formation of GABA from L-glutamate, and is expressed in both the central nervous system and in the insulin-producing cells of the pancreas. GABA is localized together with neuropeptide Y in nerve cells and is involved in the reaction of leptin in the hypothalamus (Ovesjό 2001). Increased activity of the GAD2 gene leads to increased levels of GAD65 and GABA. Together with neuropeptide Y, GABA stimulates appetite (Pu 1999). Dopaminergic nerve cells have previously been proposed to be involved in Parkinsons disease, behavioural disorders as well as eating disorders. Dopaminergic signals regulate the activity of the GAD2 gene and consequent production of GAD65 and GABA (Laprade 1999). A relationship thus exists between the dopamine system and GAD. Not only a central role of GAD65 in development of obesity but also a peripheral role can be envisaged. Each pancreatic insulin-producing beta cell contains approximately 3000 microvesicles containing GABA as a consequence of GAD65 activity. When GABA is released the release of insulin from beta cells and glucagon from alpha cells ceases (Rosman 1989). As insulin and glucagon have an anorexic effect in the brain, the GAD2 gene, being responsible for GABA and GAD65 production, also stimulates appetite in obese individuals (Niswender 2003). Previous studies have shown that obesity is associated with mutations in the leptin-melanocortin cascade (Clement 2002). Results from Frogeul's laboratory (see Meyre D, Boutin P, Tounian A, Deweirder M, Aout M, Jouret B, Heude B, Weill J, Tauber M, Tounian P, Froguel P. Glutamate Decarboxylase 2 (GAD2) a genetic link between low birth weight and subsequent development of obesity in children?, J. Clin. Endocrinol. Metab. 2005, hereby incorporated herein by reference) implicate the importance of the GAD2 gene in development of obesity, where GABA in neuropeptide Y nerve cells regulates the anorexic release of insulin from beta cells (Schwartz 2003). The treatment of eating disorders, dopamine related disorder including Parkinsons disease and behavioural diseases would benefit tremendously by new therapies. Summary of the Invention The present invention relates to the regulation of the abundance of GAD for treatment of neurological disease including Parkinson, behavioural disease, anxiety, including eating disorders. In particular the abundance of GAD is regulated using implantable pump systems for delivery of GAD or using GAD cDNA or in particular the GAD2 gene as a candidate gene for increasing GAD expression in relevant areas of the body. In some individuals the GAD2 gene is more active than in others. The reason for this may be that these individuals have more effective promoter sequences for the GAD2-gene which in turn leads to more GAD being produced. Greater GAD production in turn leads to more GABA, which together with neuropeptide Y in the paraventricular nucleus of the hypothalamus, stimulates appetite. Downregulation of the activity of the GAD2 gene may in turn lead to obese persons eating less. In fact, the bilateral injection of GAD2 antisense oligonucleotide into rat ventromedial hypothalamus decreases the GABA content and appetite. Accordingly, increased activity of the GAD2 gene may increase the GABA pool in the hypothalamus thus enhancing the GABA orexigenic effects. The GAD2 gene codes for GAD65, an enzyme which increases production of the neurotransmitter GABA. When GABA interacts with another molecule, neuropeptide Y, in a specific part of the brain (the paraventricular nucleus of the hypothalamic), food intake is stimulated. Accordingly, the present invention recognizes that individuals with a more active form or a greater number of copies of the GAD gene accumulate a larger pool of GABA in the hypothalamus, and this explains why obese individuals overeat. Accordingly, the present invention is conversely applied to increase appetite in anorexic individuals or individuals with other eating disorders where an increase in appetite may be therapeutic. In the present invention, the GAD2 gene is inserted with a strong promoter, such as in an adenoassociated virus, and this is in turn administered into the paraventricular nucleus and other areas of the hypothalamus of anorexic individuals. The anorectic individual would then be cured. Also, as partly disclosed in US Published Patent Application No. 20020028212 (Geoffroy-95; hereby incorporated herein by reference), according to the present invention, means and formulations are provided for GAD- based treatments of neurological, behavioural, Glutamate/GABA and dopamine related disorders including eating disorders by means of regulating the abundancy of GAD in relevant parts of the body. As examples not intended to limit the scope of the invention are mentioned implantable pumps for delivery of GAD-formulations into the Cerebral Spinal Fluid or into other body compartments, DNA-guns for delivery of GAD cDNA or vectors such as Adeno Associated Viruses for delivery of the GAD 2 gene. Accordingly, the invention includes a method for an eating disorder comprising grafting donor cells into the central nervous system of a subject, said subject or donor cells treated so as to minimize graft rejection, said donor cells genetically modified by insertion of at least one transgene encoding a product or products which directly or indirectly affect the cells into said cells to produce functional molecules in a sufficient amount to ameliorate said defective, diseased or damaged cells in the central nervous system. The invention also includes a method of treating a patient suffering from obsessive-compulsive disorder, said method comprising the provision for such a patient a pharmaceutical agent comprising cotinine or a pharmaceutically acceptable salt thereof in a dosage between about 0.5 mg/kg to 100 mg/kg body weight per day for alleviating, in a human in need of such treatment, at least one of the symptoms of obsessive-compulsive disorder. Also according to the present invention, there is a method of treating a patient suffering from anorexia or bulimia, said method comprising the provision for such a patient with a a pharmaceutical agent comprising cotinine or a pharmaceutically acceptable salt thereof in a dosage between about 0.5 mg/kg to 100 mg/kg body weight per day for alleviating, in a human in need of such treatment, at least one of the symptoms of anorexia or bulimia. The pharmaceutical agent or said salt may be selected from the group consisting of a tablet or capsule, a transdermal delivery system, a chewing gum, an interocular insert, an inhaler and an aqueous solution of cotinine. As the present invention relates to methods of treatment of eating disorders such as anorexia using methods and formulations for gene therapy using the GAD2 gene, this method may be practiced using known gene therapy techniques as they may be applied to GAD2. These techniques and reagents are described in U.S. Provisional Patent Application No. 60/415,494, filed on October 2, 2002 and its corresponding U.S. Patent Application Serial No. 10/677,767 filed October 2, 2003, and U.S. Provisional Patent Application Serial No. 60/478,392, filed June 13, 2003, as well as, for instance, Boutin, et al. "GAD2 on Chromosome 10p12 is a Candidate Gene for Human Obesity" PLoS Biology, Vol. 1 , Issue 3, pp 001-011 (2003), all of which are incorporated herein by reference. The present invention also includes a method of treating a patient suffering from at least one of the diseases selected from the group: anorexia, bulimia, anxiety, obesity, neurological disease, behavioural diseases, Parkinsons disease, ALS, MS, Glutamate/GABA related disorders, the method in which a gene coding for a GAD protein is administered to said patient. Also part of the present invention is a GAD-based medicament for the treatment of at least one of the diseases from the group: anorexia, bulimia, anxiety, obesity, neurological disease, behavioural diseases, Parkinsons disease, ALS, MS, Glutamate/GABA related disorders, wherein the medicament comprises a GAD protein. The carrier may be selected from any of the group Cerebral Spinal Liquid derived media; and HAS. The present invention also includes a method for administering an effective dose of a GAD-based medicament where the GAD-formulation is delivered into CSF or bloodstream by means of an implantable pump. The impantable pump may be any of those known and used in the art. The invention also includes an implantable pump for delivery of GAD-based formulations. Such an implantable pump for delivery of GAD- based formulations typically will be capable of delivering between 1 femtoliter and 1 microliter medicament per hour.