Alcohol and Alcoholism Advance Access originally published online on July 19, 2006
Alcohol and Alcoholism 2006 41(5):515-521; doi:10.1093/alcalc/agl056
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
THYROID FUNCTION IN EARLY AND LATE ALCOHOL WITHDRAWAL: RELATIONSHIP WITH AGGRESSION, FAMILY HISTORY, AND ONSET AGE OF ALCOHOLISM
Erciyes University School of Medicine, Department of Psychiatry, Talas Road, 38039-Kayseri, Turkey
* Author to whom correspondence should be addressed: Tel. and Fax: +90 352 4375702; E-mail: sozsoy{at}erciyes.edu.tr
(Received 28 February 2006; first review notified 27 April 2006; in revised form 26 June 2006; accepted 26 June 2006)
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
Aims: Thyroid dysfunction is a known finding in alcoholism. Most studies have reported the reduction in peripheral thyroid hormones in acute withdrawal and long-term abstinence periods of alcohol dependence. The aim of the present study was to investigate the alterations of free thyroid hormones in early and late withdrawal and their association with aggression, age of onset, and family history of alcoholism. Methods: Male inpatients (n = 39; mean age ± SD: 42.55 ± 8.02 years) in alcohol withdrawal were compared with healthy men (n = 28; mean age ± SD: 38.31 ± 9.26 years). Levels of free thyroxine (fT4), free triiodothyronine, (fT3) and thyrothrophin (TSH) were measured in early (first day) and late (28th day) withdrawal in the patients and only once in the controls. Results: In early withdrawal, levels of thyroid hormones did not differ from those in the controls. In late withdrawal, fT3 and fT4 levels (2.71 ± 0.56 and 10.80 ± 1.86 pg/ml) were lower than those of both controls (3.32 ± 0.41 and 11.95 ± 1.49 pg/ml, respectively, P < 0.05 in both cases) and patients in early withdrawal (3.18 ± 0.72 and 12.68 ± 2.50 pg/ml, respectively, P < 0.05 in both cases). Patients were divided into subgroups according to aggression level, onset age of alcoholism, and family history. While the high-aggression group had lower serum levels of fT3 and fT4 in late withdrawal (2.49 ± 0.41 and 10.44 ± 2.15 pg/ml) compared with those of controls (P < 0.05 in both cases), the low-aggression group only had lower serum levels of fT3 in late withdrawal (2.90 ± 0.62 pg/ml) compared with those of controls (P < 0.05). fT3 and fT4 values in the family history-negative group (2.67 ± 0.56 and 10.75 ± 1.88 pg/ml) were lower than those of controls in late withdrawal (P < 0.05 in both cases). Both fT3 and fT4 levels in late withdrawal (2.69 ± 0.54 and 10.83 ± 1.96 pg/ml) were decreased in early-onset group compared with those of controls (P < 0.05 in both cases). Conclusion: Decreased free thyroid hormone levels may be a result of heavy alcohol consumption or a trait marker of alcoholism, especially in high-aggressive, early-onset and family history-negative patients.
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
Alcohol dependence and withdrawal cause both peripheral thyroid hormone dysfunction and central hypothalamic–pituitary–thyroid (HPT) axis deregulation. Most studies have shown the reduction in peripheral thyroid hormones and/or blunted thyroid stimulating hormone (TSH) response to thyrotrophin-releasing hormone (TRH) in alcoholism (Valimaki et al., 1984
; Baumgartner et al., 1994). These abnormalities have been frequently observed during withdrawal (Geurts et al., 1981; Valimaki et al., 1984; Baumgartner et al., 1994; Heinz et al., 1996) and are also observed in some studies after several weeks or years of abstinence (Loosen et al., 1983; Dackis et al., 1984; Marchesi et al., 1992; Sudha et al., 1995). It is a controversial question whether these alterations are state or trait marker for alcohol dependence.
However, reports have varied between different studies. In early withdrawal (first day of the cessation of alcohol), total thyroxine (T4) concentration has been found to be normal (Majumdar et al., 1981; Rojdmark et al., 1984; Baumgartner et al., 1994) or decreased (Geurts et al., 1981; Dackis et al., 1984; Valimaki et al., 1984; Sudha et al., 1995; Heinz et al., 1996). In longitudinal studies, it has been reported that total T4 level has increased significantly 1 week (Heinz et al., 1996), 2 weeks (Geurts et al., 1981; Valimaki et al., 1984), or 3 weeks (Baumgartner et al., 1994) after alcohol cessation. Others have reported the continuation of decreased T4 level after 2 or 4 weeks, as well (Dackis et al., 1984; Sudha et al., 1995). In early and late withdrawal free T4 (fT4) has been found normal (Geurts et al., 1981; Pienaar et al., 1995), low (Baumgartner et al., 1994), or high (Valimaki et al., 1984).
Some of the studies have found that total triiodothyronine (T3) level was normal in early and late withdrawal (Valimaki et al., 1984; Hermann et al., 2002). There have also been studies that report high levels in late withdrawal (Baumgartner et al., 1994; Pienaar et al., 1995; Sudha et al., 1995) or low levels in early withdrawal (Hegedüs et al., 1984; Agner et al., 1986) and after 2 years of abstinence (Loosen et al., 1983). Free T3(fT3) has been found to be reduced (Baumgartner et al., 1994) or normal (Pienaar et al., 1995; Heinz et al., 1996) in withdrawal.
It has also been claimed that thyroid functions are related to criminal behaviour and personality traits. It has been found that elevated T3 and lowered T4 levels were related to type II alcoholism, cluster B personality disorder, psychopathy, and criminality (Stalenheim et al., 1998). Stalenheim (2004) reported that criminal recidivists had higher serum T3 and lower free T4 levels than non-recidivists and controls, and the T3 levels in criminal recidivists correlated to psychopathy and aggression-related personality traits. He suggested that T3 has predictive validity of biological markers of psychopathy.
Possible causes of the inconsistent findings of thyroid hormone levels in alcoholism may be co-occurrence of some diseases such as depression or liver disease, influence of drugs, and different test-kits used. Not all studies have controlled these factors carefully. Methods of hormonal measurement have become more dependable in recent years.
The aim of the study was to investigate possible alterations in thyroid hormones during the early and late withdrawal periods and, if any, whether these alterations might be related to severity of aggression, age of alcoholism onset, and family history.
|
METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
Subjects
Male inpatients (n = 39; mean age ± SD: 42.55 ± 8.02 years, range: 20–55) who met the criteria for alcohol dependence and alcohol withdrawal (Diagnostic and Statistical Manual of Mental Disorders criteria, 4th edition, DSM-IV; American Psychiatric Association, 1994
) were included in the study. Two independent specialists in Psychiatry (E.E. and S.O.) diagnosed the patients. The patients were selected from the inpatient population of the Psychiatry Clinic of Erciyes University Medical School. They were in the first day of withdrawal when they were admitted to hospital for the programme of detoxification from alcohol. Exclusion criteria for patients were: (i) having any current or past psychiatric disease other than alcoholism, (ii) having substance use disorder except for alcohol or cigarette, (iii) having any significant medical and endocrine disorder, (vi) having a liver disease. Fourteen patients did not continue the study, because some had positive alcoholmeter scores, and others wanted to be discharged from the hospital and the study. Physically and mentally healthy men (n = 28; mean age ± SD: 38.31 ± 9.26 years, range: 20–55) who were recruited from volunteers and hospital staff members participated in the study as controls. Exclusion criteria for controls were the same as the criteria for patients, plus a history of alcohol or drug use disorders in either himself or his family.
The same psychiatrist selected the patients and controls and performed physical and psychiatric examinations and evaluated the biochemical laboratory tests results. Patients and controls were all smokers. The patients remained hospitalized for the full duration of the study and the same authors made the follow-up examinations (E.E. and S.O.).
This study was carried out in accordance with the Helsinki Declaration of the World Medical Association and was approved by the local Ethics Committee. Written informed consent was obtained from each patient after the description of the study.
During detoxification, patients received diazepam (mean dose ± SD: 40.83 ± 16.13 mg/day, range: 15–90) and multivitamins for up to 3 weeks. The patients did not take any additional drug or non-drug therapies.
Procedures
Psychometric tests were performed on the eighth day of admission. The severity of clinical symptomatology of depression was assessed using the Montgomery–Asberg Depression Rating Scale (MADRS) (Montgomery and Asberg, 1979), and three patients who scored 
15 on MADRS were excluded. At the beginning 42 patients were included in the study. The Michigan Alcoholism Screen Test (MAST) (Selzer, 1971) was performed to assess the severity of alcoholism. Severity of withdrawal was evaluated using the Clinical Institute Withdrawal Assessment for Alcohol (CIWA-A) (Sullivan et al., 1991) each week, the treatment dosage and duration was adjusted according to this scale and clinical symptomatology. The Brown–Goodwin Assessment for Life History of Aggression (BG) (Brown et al., 1981) and the Buss–Durkee Inventory (Buss and Durkee, 1957) to measure the presence of aggressive tendencies were applied to patients and controls. BG involves questions about behavioural categories: discipline problems in the army and at work, assaults on people, property damage, incarceration due to assaultive behaviour and other crimes, and crimes that did not result in incarceration. Patients with a BG score of 8 were considered to be ‘high-aggressive patients’ (Buydens-Branchey and Branchey, 1992) (n = 17). The patients who had scores <8 in this scale were included in ‘low-aggression group’ (n = 22). According to presence of family alcoholism history, the patients were divided into two groups; family history-positive (regarding first-degree and second-degree relatives with alcoholism) (n = 17) and family history-negative (n = 22). Furthermore, the patients were also separated with respect to age of onset of alcoholism as follows; ‘early-onset’ (25 years or before) (n = 31) and ‘late-onset’ (after 25 years) (n = 8) (Varma et al., 1994; Wetterling et al., 2003).
Serum levels of fT3, fT4, and TSH were measured in the early (one day after cessation) withdrawal in all patients and late (28th day of alcohol cessation) withdrawal period in 25 patients and only once in the control subjects. Blood samples for thyroid hormones were taken with a catheter inserted into antecubital vein at 07:00 a.m. after an overnight fast. Separated serum was stored at –70°C until analysed. Serum fT3 and fT4 concentrations were analysed using radioimmunoassay (RIA) kits (RIAZENcoFT3 and RIAZENcoFT4, Belgium). Sensitivity values were 0.85 pg/ml for fT3, and 1.3 pg/ml for fT4. Intra-assay and inter-assay coefficients of variation were 2.7% for mean of 3.7 ± 0.1 pg/ml and 8.3% for mean of 3.6 ± 0.3 for fT3 and 3.7% for mean of 10.7 ± 0.4 pg/ml and 4.5% for mean of 11.1 ± 0.5 for fT4. Serum TSH concentration was analysed with immunoradiometric assay (IRMA) kits (BioSource TSH-IRMA, Belgium) with a sensitivity of 0.025 µIU/ml and intra-assay and inter-assay coefficients of variation 1.4% for mean of 1.82 ± 0.03 and 4.1% for mean of 1.34 ± 0.06, respectively. The coefficients of variation have been determined according to prospectus of the assay manufacturer.
Statistical analysis
The distributions of all the variables were checked by Kolmogorov–Smirnov test. If the variables had abnormal distribution or lower number of subjects, the comparisons were done with non-parametric tests. Parametric tests were performed in other conditions. Independent samples t-test and Mann–Whitney U-test were used to compare variables between groups. Paired samples t and Wilcoxon tests were carried out while comparing the variables within the groups. The same tests were performed to compare variables between and within the groups according to aggression level, onset age of alcoholism, and presence of family alcoholism history. Additionally, comparison of the distribution of these groups in relation to each other was analysed by using 
2-test. To investigate the relationships between hormonal values and clinical and demographical variables in patients, non-parametric Spearman's rank correlation test (for abnormal distribution variables) and Pearson's correlation test (for normal distribution variables) were performed.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
Evaluation of all patients
There were no significant differences in age between the patients and the controls. Patients' BG and Buss–Durkee scores were higher than those of the controls (Table 1).
|
No statistically significant difference was found between the thyroid hormones of the controls and patients in early withdrawal. Serum fT3 and fT4 levels were significantly lower in the patients in late withdrawal than those of the controls (t = 4.58, P < 0.05; t = 2.48, P < 0.05, respectively). But serum TSH values of the controls and patients in late withdrawal were similar. When alterations of hormone levels were investigated throughout the withdrawal in the patients, it was found that serum fT3 and fT4 levels decreased towards the late withdrawal (t = 2.11, P < 0.05; t = 3.47, P < 0.05, respectively) (Table 2).
|
Patients were divided into two groups in relation to aggression level, onset age of alcoholism, and presence of family alcoholism history. Cross tables (Tables 3–5) show the distribution of these groups in relation to each other. No statistically significant relationships were seen.
|
|
|
Effect of aggression
High-aggression and low-aggression groups of patients were evaluated separately. No difference was found between hormone levels of the high-aggression and low-aggression groups in early withdrawal. But in late withdrawal, serum fT3 level of patients was lower than that of controls in both low-aggression and high-aggression groups (Z = 2.05, P < 0.05; Z = 4.21, P < 0.05, respectively). Serum fT4 level was lower only in the high-aggression group (Z = 2.10, P < 0.05). When evaluated to check whether there was an alteration throughout the withdrawal, it was found that serum fT3 and fT4 levels reduced in late withdrawal only in the high-aggression group (Z = 1.96, P < 0.05; Z = 2.20, P < 0.05, respectively). In the low-aggression group, there was no significant difference between hormone levels in early and late withdrawals (Table 6).
|
Effect of age of onset
Early-onset and late-onset patients were compared with each other and with controls. There were significant differences between both groups in either early or late withdrawal. Although in early withdrawal hormone levels of both patient groups and controls were similar, in late withdrawal serum fT3 and fT4 levels of patients were lower than those of controls only in the early-onset patient group (t = 4.62, P < 0.05; t = 2.26, P < 0.05; respectively). When alteration of hormones levels during withdrawal was evaluated in early-onset and late-onset patients separately, fT3 and fT4 levels of early-onset patients had reduced in late withdrawal (t = 2.15, P < 0.05; t = 2.84, P < 0.05; respectively) (Table 7).
|
Effect of family history
In family history-positive group, only serum fT3 level in late withdrawal was lower than that of controls (Z = 2.60, P < 0.05). In family history-negative group, serum fT3 and fT4 levels in late withdrawal were lower than both those of controls (t = 4.43, P < 0.05; t = 2.33, P < 0.05; respectively) and those of patients in early withdrawal (t = 2.14, P < 0.05; t = 3.09, P < 0.05; respectively) (Table 8).
|
Correlations in patients
Severity of aggression got higher as onset of alcoholism got earlier (Buss–Durkee score was negatively correlated with onset age of alcoholism; r = –0.49, P < 0.01). There was a positive correlation between severity of alcoholism and aggression (MAST and Buss–Durkee score; r = 0.45, P < 0.05, MAST and BG score r = 0.39, P < 0.05). In early withdrawal, there was also a positive correlation between severity of withdrawal and Buss–Durkee score (r = 0.53, P < 0.005). Serum fT3 level fell as duration of alcohol use increased in late withdrawal (r = –0.32, P < 0.05). Serum fT3 level was not related to age (r = 0.02, P > 0.05). Severity of alcoholism (MAST score) and aggression (BG score) were negatively related to serum fT3 level in late withdrawal (r = –0.56, P < 0.05; r = –0.57, P < 0.05, respectively). Altogether, it seemed that intensity of alcoholism, duration of alcohol use, and severity of aggression affected thyroid hormone levels. However, there was no correlation between the severity of withdrawal symptoms (CIWA score) and thyroid hormones either in early withdrawal (r = –0.17, P = 0.37 for fT3, r = –0.15, P = 0.40 for fT4) or in late withdrawal (r = –0.49, P = 0.17 for fT3, r = –0.28, P = 0.46 for fT4).
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
The main results of the study are: (i) while fT3 and fT4 levels were normal in early withdrawal, they were lower in late withdrawal than those of both controls and patients in early withdrawal, (ii) in high-aggression patients, in early-onset patients, and in family history-negative patients, fT3 and fT4 levels in late withdrawal were lower compared with those of controls and patients in early withdrawal.
Decreased thyroid hormones might result from the damage to thyroid gland or from alterations in the HPT axis at the pituitary level caused by chronic alcohol intake. An ultrasound study has showed a significant reduction of the thyroid gland volume in alcohol-dependent patients (Hegedüs, 1984). A post-mortem autopsy study has found decreased thyroid volume in alcoholics, and this damage was associated with the duration of excessive alcohol intake and dose-dependent (Hegedüs et al., 1988). These studies suggest that alcohol may have a direct toxic effect on the thyroid gland. In addition, there are some studies reporting thyroid dysfunction in late withdrawal (20 days) (Sudha et al., 1995), as our study did, and during long-term abstinence (mean 5.8 ± 1.1 years) (Loosen et al., 1983).
Regarding possible alcohol impairment of the HPT axis at the level of pituitary or hypothalamus, some authors suggest that chronic alcohol consumption may cause an increase in TRH that might give rise to the downregulation of the pituitary TRH receptors and, in turn, to reduced TSH response to TRH and to decreased thyroid hormone level (Zoeller et al., 1996; Hermann et al., 2002).
The critical question in the present study is why the thyroid hormones are normal in early withdrawal (first day). Several previous studies have also reported normal free thyroid hormone levels in acute withdrawal (Geurts et al., 1981; Pienaar et al., 1995; Heinz et al., 1996). The cause of normal hormonal levels in early withdrawal may be transient norepinephrinergic overactivity during the acute withdrawal, since hyperactivity of norepinephrine leads thyroid hormones to increase (Linnoila et al., 1987; Turakulov and Burikhanov, 1993). Thus, thyroid hormones might increase temporarily to normal levels, owing to enhanced norepinephrinergic activity during the early withdrawal, and decrease again in late withdrawal. Indeed, some studies have found decreased thyroid hormones during active alcohol use in rats (Mason et al., 1988; Rasmussen, 2003). However, we cannot claim this explanation only from our results, because we did not measure hormone levels during the active alcohol consumption.
Another explanation for reduced thyroid hormones during the late alcohol withdrawal is that subclinical decrease in thyroid hormones may be a trait marker of alcohol dependence, i.e. it might exist before active alcohol use. Loosen et al. (1983) have found decreased thyroid values even years after alcohol cessation. Some studies have found that abnormal TSH response in the TRH test continues even some years after alcohol cessation (Marchesi et al., 1992; Loosen et al., 1983). Likewise, Casacchia et al. (1985) (abstinent from alcohol >20 days), Pienaar et al. (1995) (abstinent for 5–8 weeks) and Muller et al. (1989) (after several weeks of sobriety) have showed blunted TSH response to TRH as compared with that of healthy controls.
Opposed to the above findings are findings suggesting that reduced thyroid hormone level in alcoholics is a state marker limited to acute withdrawal, rather than a trait feature. Thyroid hormone levels were lower in acute withdrawal and returned to normal in late withdrawal in some studies (Geurts et al., 1981; Baumgartner et al., 1994; Heinz et al., 1996). In other studies, blunted TSH response to TRH has been found in acute withdrawal and disappeared during the first week of abstinence (Valimaki et al., 1984) or after >2 years of abstinence (Pienaar et al., 1995). Causes of differences between our finding and these literature findings might be that patient populations of these studies had less severity of alcoholism than our patient population.
Aggression
The other major result of our study is that fT3 and fT4 levels in late withdrawal were lower in high-aggression patients than those of healthy men. It seems that decrease of thyroid hormone levels might be a persistent feature especially in high-aggressive alcoholics.
Similar to Cloninger's type II patients, (Cloninger et al., 1981) high-aggression patients probably have a tendency to a more severe form of alcohol dependence and to consume the greater amount of alcohol. Therefore, thyroid dysfunction in high-aggressive patients may be a result of greater amounts of consumed alcohol. Indeed, thyroid dysfunction in alcoholics has been shown to be dose-dependent (Hegedüs et al., 1988), and patients with type II alcoholism have more disordered thyroid hormone status than pure alcohol dependents (Stalenheim et al., 1998). In addition, we found that there was a positive correlation between severity of alcoholism and aggression, and serum fT3 level reduced as severity of alcoholism and aggression increased. These findings support the idea that intensity of alcohol dependence is higher in aggressive alcoholics and that thyroid hypofunction may be a sequel of heavy alcohol consumption.
On the other hand, it may be that diminished thyroid hormone is related to aggression itself rather than alcohol. Lavender et al. (1987) showed that delinquent boys have significantly higher serum T3 levels than normal schoolboys. In a long-term follow-up study, serum T3 levels have been found significantly associated with criminality (Alm et al., 1996). High levels of fT3 have been reported in young patients with conduct disorder (Dimitrieva et al., 2001). These studies would seem to show that increased, rather than decreased, thyroid hormones may be associated with aggression. Nevertheless, Stalenheim et al. (1998, 2004) found that high serum T3 level and low serum T4 level were related to criminality, psychopathy, and antisocial behaviour. Therefore, it is difficult to advocate that decreased thyroid hormone is related to aggression from our data.
Onset age
Similar to those of high-aggression patients, we found that patients with earlier onset of alcoholism had low free thyroid hormone levels in late withdrawal. It may be a result of toxic effect of long duration of alcohol consumption on the thyroid gland. Accordingly, we found also that serum fT3 level reduced as duration of alcohol use increased. Alcoholics with a long duration of disease show greater fibrosis in the thyroid gland than patients with a short history (Hegedüs et al., 1988). Sellman and Joyce (1992) found that patients with blunted TSH response to TRH were more likely to have had an earlier onset of alcoholism and to have had shorter alcoholic remissions in the past. It would seem that long duration of alcohol intake and/or early onset of alcoholism are related to dysfunction of thyroid rather than short duration of alcohol intake and/or late onset of alcoholism.
Family history
Little is known about how family alcoholism history influences thyroid functions in alcoholics or healthy people. In our study, family history-negative group had lower serum fT3 and fT4 levels in late withdrawal in comparison with those of controls. In the family history-positive group, only serum fT3 level in late withdrawal was lower than that of controls. It seems that hypofunction of thyroid is more obvious in family history-negative patients in the present study. Previous studies have reported a controversial result such that family history-positive young men did not differ from family history-negative group in their baseline levels of thyroid hormones (Garbutt et al., 1995), and blunted TSH response was not associated with family history of alcoholism in alcoholic men who had been abstinent for at least 4 weeks (Sellman and Joyce, 1992). Pienaar et al. (1995) reported that alcoholics abstinent for 5–8 weeks with family history of alcoholism had significantly lower TSH response levels than those without family history. Our finding that the family history-negative group had lower serum thyroid levels is not consistent with literature findings.
Effect of benzodiazepines. Our finding that thyroid hormones in late withdrawal were low might be due to benzodiazepine treatment. Balon et al. (1991) reported that treatment with diazepam led to decrease in T4 in panic disorder patients. Plasma T3 and T4 levels were low in clobazam, 1,5-benzodiazepine, treated male rats (Miyawaki et al., 2003). However, it was found that chronic alprazolam treatment caused an increase in T3 level in hamsters (Ottoweller et al., 1989). Thus, it is not clear whether benzodiazepines reduce thyroid hormones. In addition, at the late withdrawal time-point in our study, patients had not received diazepam for at least 1 week.
There are some limitations of this study. First, the small size of the subgroups may have led to some type-II statistical errors. Second, if we had carried out dynamic tests such as TSH response to TRH in place of or in addition to basal measurements we would have measured HPT axis activity more accurately. Finally, we could have measured the hormones during the active alcohol consumption as well and during a longer abstinence period.
In conclusion, chronic alcohol consumption may cause long-term thyroid dysfunction. This may be manifested as a subclinical hypothyroidism in clinical settings and may be related to the severity and duration of alcoholism, family history, and aggression tendency of the patient. Although decreased thyroid hormone levels seem to be a result of persistent effect of chronic alcohol use on thyroid gland, one cannot disregard the possibility that it may also be a trait marker of proneness to alcoholism. Further investigations are needed to determine the mechanisms responsible for thyroid dysfunction in alcoholism.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
Agner, T., Hagen, C., Nyboe-Andersen, B. et al. (1986) Pituitary thyroid function and thyrotrophin., prolactin and growth hormone responses to TRH in patients with chronic alcoholism. Acta Medica Scandinavica 220, 57–62.[Web of Science][Medline]
Alm, P., af Klinteberg, B., Humble, K. et al. (1996) Criminality and psychopathy as related to thyroid activity in former juvenile delinquents. Acta Psychiatrica Scandinavica 94, 112–117.[Web of Science][Medline]
American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders, 4th edn. American Psychiatric Press, Washington, DC.
Balon, R., Pohl, R., Yeragani, V. K. et al. (1991) The changes of thyroid hormone during pharmacological treatment of panic disorder patients. Progress in Neuropsychopharmacology and Biological Psychiatry 15, 595–600.
Baumgartner, A., Rommelspacher, H., Otto, M. et al. (1994) Hypothalamic pituitary thyroid (HPT) axis in chronic alcoholism. I. HPT axis in chronic alcoholics during withdrawal and after 3 weeks of abstinence. Alcoholism: Clinical and Experimental Research 18, 284–294.[CrossRef][Web of Science][Medline]
Brown, G. L., Ballenger, J. C., Minichiello, M. D. and Goodwin, F. K. (1981) Human aggression and its relationship to CSF 5-HIAA., MHPG and HVA. In Psychopharmacology of Aggression, Sandler, M. ed., pp. 131–147. Raven Press, New York.
Buss, A. H. and Durkee, A. (1957) An inventory for assessing different kinds of hostility. Journal of Consulting and Clinical Psychology 21, 343–349.
Buydens-Branchey, L. and Branchey, M. H. (1992) Cortisol in alcoholics with a disordered aggression control. Psychoneuroendocrinology 17, 45–54.[CrossRef][Web of Science][Medline]
Casacchia, M., Rossi, A. and Stratta, P. (1985) Thyrotrophin releasing hormone test in recently abstinent alcoholics. Psychiatry Research 16, 249–251.[CrossRef][Web of Science][Medline]
Cloninger, C. R., Bohman, M., and Sigvardsson, S. (1981) Inheritance of alcohol abuse. Cross-fostering analysis of adopted men. Archives of General Psychiatry 38, 861–868.
Dackis, C. A., Bailey, J., Pottash, A. L. et al. (1984) Specificity of the DST and the TRH test for major depression in alcoholics. American Journal of Psychiatry 141, 680–683.
Dimitrieva, T. N., Oades, R. D., Hauffa, B. P. et al. (2001) Dehydroepiandrosterone sulphate and corticotropin levels are high in young male patients with conduct disorder: comparisons for growth factors, thyroid and gonadal hormones. Neuropsychobiology 43, 134–140.[CrossRef][Web of Science][Medline]
Garbutt, J. C., Miller, L. P., Mundle, L. et al. (1995) Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in young men at high or low risk for alcoholism. Alcoholism: Clinical and Experimental Research 19, 1133–1140.
Geurts, J., Demeester Mirkine, N., Glinoer, D. et al. (1981) Alterations in circulating thyroid hormones and thyroxine binding globulin in chronic alcoholism. Clinical Endocrinology 14, 113–118.[Medline]
Hegedüs, L. (1984) Decreased thyroid gland volume in alcoholic cirrhosis of the liver. The Journal of Clinical Endocrinology and Metabolism 58, 930–933.
Hegedüs, L., Rasmussen, N., Ravn, V. et al. (1988) Independent effects of liver disease and chronic alcoholism on thyroid function and size: the possibility of a toxic effect of alcohol on the thyroid gland. Metabolism: Clinical and Experimental 37, 229–233.[Web of Science]
Heinz, A., Bauer, M., Kuhn, S. et al. (1996) Long-term observation of the hypothalamic-pituitary-thyroid (HPT) axis in alcohol-dependent patients. Acta Psychiatrica Scandinavica 93, 470–476.[Web of Science][Medline]
Hermann, D., Heinz, A. and Mann, K. (2002) Dysregulation of the hypothalamic-pituitary-thyroid axis in alcoholism. Addiction 97, 1369–1381.[CrossRef][Web of Science][Medline]
Levander, S., Mattson, A., Schalling, D. and Dalteg, A. (1987) Psychoendocrine patterns within a group of male juvenile delinquents as related to early psychosocial stress, diagnostic classification, and follow-up data. In Psychopathology: An Interactional Perspective, Magnusson, D. and Öhman, A. eds, pp. 235–252. Academic Press, Orlando.
Linnoila, M., Mefford, I., Nutt, D. et al. (1987) NIH conference. Alcohol withdrawal and noradrenergic function. Annals of Internal Medicine 107, 875–889.
Loosen, P. T., Wilson, I. C., Dew, B. W. and Tipermas, A. (1983) Thyrotrophin-releasing hormone (TRH) in abstinent alcoholic men. American Journal of Psychiatry 140, 1145–1149.
Majumdar, S. K., Shaw, G. K. and Thomson, A. D. (1981) Thyroid status in chronic alcoholics. Drug and Alcohol Dependence 7, 81–84.[CrossRef][Web of Science][Medline]
Marchesi, C., De Risio, C., Campanini, G. et al. (1992) TRH test in alcoholics: relationship of the endocrine results with neuroradiological and neuropsychological findings. Alcohol and Alcoholism 27, 531–537.
Mason, G. A., Stanley, D. A., Walker, C. H. et al. (1988) Chronic alcohol ingestion decreases pituitary-thyroid axis measures in Fischer-344 rats. Alcoholism: Clinical and Experimental Research 12, 731–734.
Miyawaki, I., Moriyasu, M., Funabashi, H. et al. (2003) Mechanism of clobazam-induced thyroidal oncogenesis in male rats. Toxicology Letters 145, 291–301.[CrossRef][Web of Science][Medline]
Montgomery, S. A. and Asberg, M. (1979) A new depression scale designed to be sensitive to change American Journal of Psychiatry 134, 382–389.
Muller, N., Hoehe, M., Klein, H. E. et al. (1989) Endocrinological studies in alcoholics during withdrawal and after abstinence. Psychoneuroendocrinology 14, 113–123.[CrossRef][Web of Science][Medline]
Ottenweller, J. E., Tapp, W. N. and Natelson, B. H. (1989). Effects of alprazolam treatment on plasma concentrations of glucocorticoids, thyroid hormones, and testosterone in cardiomyopathic hamsters. Psychopharmacology 98, 369–371.[CrossRef][Medline]
Pienaar, W. P., Roberts, M. C., Emsley, R. A. et al. (1995) The thyrotrophin releasing hormone stimulation test in alcoholism. Alcohol and Alcoholism 30, 661–667.
Rasmussen, D. D. (2003) Chronic daily ethanol and withdrawal: 5. Diurnal effects on plasma thyroid hormone levels. Endocrine 22, 329–334.[CrossRef][Web of Science][Medline]
Rojdmark, S., Adner, N., Andersson, D. E. et al. (1984) Prolactin and thyrotrophin responses to thyrotrophin-releasing hormone and metoclopramide in men with chronic alcoholism. Journal of Clinical Endocrinology and Metabolism 59, 595–600.
Sellman, J. D. and Joyce P. R. (1992) The clinical significance of the thyrotrophin-releasing hormone test in alcoholic men. The Australian and New Zealand Journal of Psychiatry 26, 577–585.[Web of Science][Medline]
Selzer, M. L. (1971) The Michigan Alcoholism Screening Test: The quest for a new diagnostic instrument. American Journal of Psychiatry 127, 1653–1658.
Stalenheim, E. G., von Knorring, L. and Wide, L. (1998) Serum levels of thyroid hormones as biological markers in a Swedish forensic psychiatric population. Biological Psychiatry 43, 755–761.[CrossRef][Web of Science][Medline]
Stalenheim, E. G. (2004) Long-term validity of biological markers of psychopathy and criminal recidivism: follow-up 6–8 years after forensic psychiatric investigation. Psychiatry Research 121, 281–291.[CrossRef][Web of Science][Medline]
Sudha, S., Balasubramanian, K., Arunakaran, J. et al. (1995) Preliminary study of androgen., thyroid and adrenal status in alcoholic men during deaddiction. The Indian Journal of Medical Research 101, 268–272.[Web of Science][Medline]
Sullivan, J. T., Swift, R. M. and Lewis, D. C. (1991) Benzodiazepine requirements during alcohol withdrawal syndrome: clinical implications of using a standardized withdrawal scale. Journal of Clinical Psychopharmacology 11, 291–295.[Web of Science][Medline]
Turakulov, Ia. Kh. and Burikhanov, R. B. (1993) Role of norepinephrine in the regulation of thyroid gland functional activity in rabbits. Problemy Endokrinologii 39, 45–48.
Valimaki, M., Pelkonen, R., Harkonen, M. et al. (1984) Hormonal changes in noncirrhotic male alcoholics during ethanol withdrawal. Alcohol and Alcoholism 19, 235–242.
Varma, V. K., Basu, D., Malhotra, A. et al. (1994) Corelates of early- and late-onset alcohol dependence. Addictive Behaviors 19, 609–619.[CrossRef][Web of Science][Medline]
Wetterling, T., Veltrup, C., John, U. et al. (2003) Late onset alcoholism. European Psychiatry: The Journal of the Association of European Psychiatrists 18, 112–118.
Zoeller, R. T., Fletcher, D. L., Simonyl, A. et al. (1996) Chronic ethanol treatment reduces the responsiveness of the hypothalamic-pituitary-thyroid axis to central stimulation. Alcoholism: Clinical and Experimental Research 20, 954–960.[Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  G. A. Barclay, J. Barbour, S. Stewart, C. P. Day, and E. Gilvarry Adverse physical effects of alcohol misuse Advan. Psychiatr. Treat., March 1, 2008; 14(2): 139 - 151. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||