Psychopathological and nutritional correlates of plasma homovanillic acid in adolescents with anorexia nervosa

Variability of Plasma Homovanillic Acid Over 13 Months in Patients with Schizophrenia; Relationship with the Clinical Response and the Wisconsin Card Sort Test

“…measurements vary together or that the peripheral contribution remains relatively stable [17]. Moreover, various authors have found a relationship between the pHVA levels and the severity of certain psychiatric and neurological pathologies [18][19][20][21][22]. Overall, these results suggest that, under controlled conditions, this plasma metabolite may well reflect changes which occur in cerebral dopaminergic activity, especially when measured in response to pharmacological stimuli.…”

Compulsivity in anorexia nervosa: a transdiagnostic concept

“…Evidence of decreased DA activity following chronic drug use has led to the suggestion that this deficiency in DA may cause an increase in the compulsion to seek further drug reward to order to increase deficient DA levels, with repetition of this behavior leading to a dependence on the substance (Fineberg et al, 2010). In contrast, individuals recovered from AN have increased binding of DA D2/D3 receptors in the anterior VS while currently ill AN patients has shown increased levels of the DA metabolite homovanillic acid (HVA) in cerebrospinal fluid (Castro-Fornieles et al, 2008). The increased DA receptor binding in recovered AN patients contrasts with the reduced striatal DA binding found in those with substance abuse (Volkow et al, 2009, 2012a), which is paralleled by those with BN (Broft et al, 2012), and obesity (Kenny, 2011).…”

Catechol-O-methyltransferase genotype modifies executive functioning and prefrontal functional connectivity in women with anorexia nervosa

“…Cognitive performance measured by the WCST in the underweight women with anorexia nervosa was consistent with the U-shaped curve as the effect of the COMT polymorphism, as previously observed in situations characterized by increased PFC dopaminergic activity. 30,31 There is growing evidence of a dysfunction of dopaminergic systems in patients with anorexia nervosa, 1,32 although published data mainly refer to subcortical functioning. Patients with anorexia nervosa display increased D2/D3 receptor binding in the ventral striatum, alteration of reward-related processes, reduced cerebrospinal fluid concentrations of the DA metabolite homo vanillic acid, and altered growth hormone response to apomorphine stimulation.…”

“…Patients with anorexia nervosa display increased D2/D3 receptor binding in the ventral striatum, alteration of reward-related processes, reduced cerebrospinal fluid concentrations of the DA metabolite homo vanillic acid, and altered growth hormone response to apomorphine stimulation. 32 However, the effects of the COMT genotype are usually appreciable only on PFC function, probably because of the presence of more efficient DA transporters in subcortical areas. 33 Decreased motivation, compulsive exercising and loss of appetitive responses are considered to be a consequence of dopaminergic dysfunction, although the biological mechanisms underlying these symptoms are not clear.…”

“…33 Decreased motivation, compulsive exercising and loss of appetitive responses are considered to be a consequence of dopaminergic dysfunction, although the biological mechanisms underlying these symptoms are not clear. Some form of DA dysregulation occurs in both the acute stage of anorexia nervosa 32 and in patients who have recovered from the illness, 34,35 but clinical characteristics, such as low motivation and compulsive exercise, typically tend to exacerbate with weight loss.…”