Association of plasma calcium concentrations with alcohol craving: New data on potential pathways.

Recently, calcium was suggested to be the active moiety of acamprosate. We examined plasma calcium concentrations in association with severity of alcohol dependence and its interaction with regulating pathways and alcohol craving in alcohol-dependent patients. 47 inpatient alcohol-dependent patients undergoing detoxification treatment underwent laboratory testing, including calcium, sodium, liver enzymes as well as serum concentrations of calcitonin, parathyroid hormone and vitamin D. The psychometric dimension of craving was analyzed with the Obsessive Compulsive Drinking Scale (OCDS). The severity of withdrawal was measured with the Alcohol Dependence Scale (ADS) and with the Alcohol Dependence Scale for high-risk sample (ADS-HR). The main findings of our investigation are: a) a negative correlation of plasma calcium concentrations with alcohol craving in different dimensions of the OCDS; b) a negative correlation of plasma calcium concentrations with breath alcohol concentration; c) lowered calcitonin concentration in the high-risk sample of alcoholics; d) lowered plasma vitamin D concentrations in all alcoholic subjects. Our study adds further support for lowered plasma calcium concentrations in patients with high alcohol intake and especially in patients with increased craving as a risk factor for relapse. Lowered calcitonin concentrations in the high-risk sample and lowered vitamin D concentrations may mediate these effects. Calcium supplementation could be a useful intervention for decreasing craving and relapse in alcohol-dependent subjects.

Vitamin D insufficiency in a boy with obsessive-compulsive disorder.

Vitamin D deficiency not only causes low bone mass but also may lead to neuropsychiatric disorders. In the present case, vitamin D supplementation reduced obsessive-compulsive disorder (OCD) symptoms associated with streptococcal infection in a 7-year-old boy. Sudden onset of symptoms, including excessive hand washing and fear of touching anything, had occurred 1 month before presentation. Although there are few studies on a possible causal relationship between vitamin D and neuropsychiatric disorders, the present report; together with previous data, suggest an etiological role of vitamin D-related immune processes.

Serum selenium and plasma malondialdehyde levels and antioxidant enzyme activities in patients with obsessive-compulsive disorder.

There is mounting evidence indicating that reactive free radical species are involved in initiation and development of many different forms of human pathologies including psychiatric disorders. In the present study, we aimed to determine whether serum selenium (Se), antioxidant enzyme (glutathione peroxidase, GSH-Px, superoxide dismutase, SOD, and catalase, CAT) activities, and plasma malondialdehyde (MDA) levels, a product of lipid peroxidation, were associated with obsessive-compulsive disorder (OCD). The participants were 28 patients with OCD that were drug-free at least for a month and a control group (n=28) of healthy subjects, matched with respect to age and sex. In both groups, the levels of the erythrocyte MDA, GSH-Px, SOD, Se, and the CAT were measured. The levels of MDA and SOD were statistically significantly higher (p<0.01, p<0.05 respectively) in patients than controls. The activities of CAT, GSH-Px, and serum Se levels were statistically significantly lower (p<0.0001, p<0.001, and p<0.001 respectively) in patients than controls. There was a positive correlation in patients between plasma GSH-Px activity and Se concentration (r=52, p=0.001). However, in patients with OCD, CAT and SOD activities were significantly and negatively correlated with MDA levels (r=-0.45, p=0.017 for CAT and r=-0.54, p=0.020 for SOD). The study shows the presence of a significant relationship of OCD and oxidative stress, and consequently, an involvement of free radicals and of the antioxidant defence.

Magnesium influence on nicotine pharmacodependence and smoking.

We followed the magnesium effect (Magne B(6)R, Sanofi-Synthelabo) with internal administration in 53 adult neurotic smoking patients (more than 10 cigarettes/day) of both genders admitted into psychiatric hospital. The nicotine dependence was assessed by the Fagerstrom test, initially and after 28 days of magnesium intake. Plasmatic magnesium level was determined before any therapy and at 28 days. All patients received benzodiazepines during the trial. Our data show that patients that received magnesium therapy showed a significant decrease in the number of cigarettes smoked and Fagerstrom test after 4 weeks [Fagerstrom score 7.93 +/- 0.17 before magnesium therapy versus 6.78 +/- 0.18 (P < 0.05) after 28 days of magnesium therapy]. In the group of smokers who did not receive magnesium, the Fagerstrom score did not change significantly [Fagerstrom score 7.48 +/- 0.22 initial versus 7.24 +/- 0.19 after 28 days]. Magnesium supplementation raised plasmatic levels (17.2 +/- 1.2 mg/L before versus 26.1 +/- 1.6 mg/L after 28 days of magnesium intake, P < 0.01). The results suggest that this cation might be a useful adjuvant in treatment of nicotine pharmacodependence.

Hypothalamic digoxin deficiency in obsessive compulsive disorder and la Tourette's syndrome.

The isoprenoid pathway related cascade was assessed in 15 patients with obsessive compulsive disorder (OCD) and la Tourette's syndrome (TS). The pathway was also assessed in right hemispheric dominant, left hemispheric dominant, and bihemispheric dominant individuals to assess whether hemispheric dominance has any correlation with these disease states. The levels of serum digoxin, HMG CoA reductase activity, and dolichol were found to be decreased in OCD and la Tourette's syndrome as well as in left hemispheric dominant individuals with a corresponding increase in RBC Na(+)-K+ ATPase activity, serum ubiquinone, and magnesium levels. There was an increase in tyrosine and its catabolites, and a reduction in tryptophan and its catabolites in the serum. The total and individual glycosaminoglycan (GAG) fractions, carbohydrate residues of glycoproteins, and the concentration of glycolipids decreased in the serum. The activity of GAG degrading enzymes and glycohydrolases were decreased. The RBC membrane glycoconjugates were increased while the membrane cholesterol:phospholipid ratio was decreased. The activity of free radical scavenging enzymes increased while the concentration of free radicals decreased significantly. On the other hand, there was hyperdigoxinemia and the reverse biochemical patterns in those with right hemispheric dominance. Membrane Na(+)-K+ ATPase stimulation can result in decreased intracellular Ca2+ and increased magnesium levels. Increased levels of dopamine can lead to a tic syndrome, while reduced levels of serotonin and increased dopamine can both lead to obsessive compulsive disorder. Decrease in fucose and sialo-ligands, increased immunosuppressive morphine levels, decreased T-cell calcineurin signal transduction related to decreased intracellular calcium, reduced free radical production, and altered presentation of bacterial glycoconjugate antigens can lead to a hypoimmune response and recurrent respiratory infection in OCD patients. OCD and la Tourette's syndrome are associated with left hemispheric chemical dominance.

Tryptophan depletion in patients with obsessive-compulsive disorder who respond to serotonin reuptake inhibitors.

METHODS: The effects of short-term tryptophan depletion were examined in 15 patients with DSM-III-R obsessive-compulsive disorder who had demonstrated symptom reduction following treatment with serotonin reuptake inhibitors. Patients received a 24-hour, low-tryptophan (160-mg/d) diet followed the next morning by a drink of 15 amino acids. A double-blind, placebo-controlled cross-over design was used. RESULTS: The diet and the amino acid drink reduced free plasma tryptophan levels by a mean of 84% 5 hours later. Short-term tryptophan depletion did not significantly change mean ratings of obsessions and compulsions. In contrast, mean depression ratings were significantly increased with tryptophan depletion compared with the control (tryptophan-supplemented) testing. CONCLUSION: Maintenance of serotonin reuptake inhibitor-induced improvement of obsessive and compulsive symptoms, unlike remission of depressive symptoms, may not depend on ongoing short-term availability of serotonin.