The Impact of Thiamine Treatment on Generalized Anxiety Disorder

Full-Text HTML XML Download Download as PDF (Size:209KB) PP. 439-443
DOI: 10.4236/ijcm.2011.24073    6,067 Downloads   14,623 Views   Citations


Objective: Patients with generalized anxiety disorder (GAD) are fearful. They constantly worried about minor matters, and they anticipate the worst. The GAD is diagnosed when a patient experiences excessive anxiety and worry for at least 6 months. The cause of GAD is unknown. In the present paper, we discuss patients with GAD who have low levels of thiamine in their bloods. We also discuss the role of thiamine in the pathogenesis and treatment of GAD. Methods: We examined 9 patients (6 males and 3 females) who met the DSM-IV-TR diagnostic criteria for GAD. These patients had no history of alcoholism. Their ages ranged from 57 to 83 years old (mean age –72.8 ± 2.9 years). All of the patients had low blood thiamine levels (mean –25.1 nmol/L ± 6.0 nmol/L; normal level—70 nmol/L - 180 nmol/L). Participants completed the Hamilton Anxiety Rating Scale (HARS) for anxiety before and after thiamine treatments. All of the patients received daily thiamine 100 mg intramuscularly. Results: Thiamine supplementation significantly improved HARS scores, increased both appetite and general well-being, and reduced fatigue in patients with GAD. Interestingly, these patients were able to discontinue taking anxiolytic and β-blocker medications. Conclusion: Parental thiamine significantly affects patients with GAD.

Cite this paper

K. Lương and L. Nguyễn, "The Impact of Thiamine Treatment on Generalized Anxiety Disorder," International Journal of Clinical Medicine, Vol. 2 No. 4, 2011, pp. 439-443. doi: 10.4236/ijcm.2011.24073.


[1] [1] R. C. Kessler, N. Brandenburg, M. Lane, P. Roy-Byrne, P. D. Stang, D. J. Stein and H. U. Wittchen, “Rethinking the Duration Requirement for Generalized Anxiety Disorder: Evidence from the National Comorbidity Survey Replication,” Psychological Medicine, Vol. 35, No. 7, 2005, pp. 1073-1082. doi:10.1017/S0033291705004538
[2] R. M. Carter, H. U. Wittchen, H. Pfister and R. C. Kessler, “One-Year Prevalence of Subthreshold and Threshold DSM-IV Generalized Anxiety Disorder in a Nationally Representative Sample,” Depression and Anxiety, Vol. 13, No. 2, 2001, pp. 78-88.
[3] M. A. Buist-Bouwman, R. De Graaf, W. A. Vollebergh, J. Alonso, R. Bruffaerts, J. Ormel and ESEMeD/MHEDEA 2000 Investigators, “Functional Disability of Mental Disorders and Comparison with Physical Disorders: A Study among the General Population of Six European Countries,” Acta Psychiatrica Scandinavica, Vol. 113, No. 6, 2006, pp. 492-500.
[4] R. C. Kessler, P. E. Greenberg, K. D. Mickelson, L. M. Meneades and P. S. Wang, “The Effects of Chronic Medical Conditions on Work Loss and Work Cutback,” Journal of Occupational and Environmental Medicine, Vol. 43, No. 3, 2001, 218-225.
[5] C. L. Woodman, R. Noyes Jr., D. W. Black, S. Schlosserand and S. J. Yagla, “A 5-Year Follow-Up Study of Generalized Anxiety Disorder and Panic Disorder,” Journal of Nervous & Mental Disease, Vol. 187, No. 1, 1999, pp. 3-9. doi:10.1097/00005053-199901000-00002
[6] K. A. Yonkers, M. G. Warshaw, A. O. Massion and M. B. Keller, “Phenomenology and Course of Generalised Anxiety Disorder,” The British Journal of Psychiatry, Vol. 168, 1996, pp. 308-313. doi:10.1192/bjp.168.3.308
[7] M. D. De Bellis, B. J. Casey, R. E. Dahl, B. Birmaher, D. E. Williamson, K. M. Thomas, D. A. Axelson, K. Frustaci, A. M. Boring, J. Hall and N. D. Ryan, “A Pilot Study of Amygdala Volumes in Pediatric Generalized Anxiety Disorder,” Biological Psychiatry, Vol. 48, No. 1, 2000, pp. 51-57. doi:10.1016/S0006-3223(00)00835-0
[8] C. Ferrarese, I. Appollonio, M. Frigo, M. Perego, R. Piolti, M. Trabucchi and L. Frattola, “Decreased Density of Benzodiazepine Receptors in Lymphocytes of Anxious Patients: Reversal after Chronic Diazepam Treatment,” Acta Psychiatrica Scandinavica, Vol. 82, No. 2, 1990, pp. 169-173. doi:10.1111/j.1600-0447.1990.tb01376.x
[9] S. Sevy, G. N. Papadimitriou, D. W. Surmont, S. Goldman and J. Mendlewicz, “Noradrenergic Function in Generalized Anxiety Disorder, Major Depressive Disorder, and Healthy Subjects,” Biological Psychiatry, Vol. 25, No. 2, 1989, pp. 141-152. doi:10.1016/0006-3223(89)90158-3
[10] M. Germine, A. W. Goddard, S. W. Woods, D. S. Charney and G. R. Heninger, “Anger and Anxiety Responses to m-Chlorophenylpiperazine in Generalized Anxiety Disorder,” Biological Psychiatry, Vol. 32, No. 5, 1992, pp. 457-461. doi:10.1016/0006-3223(92)90133-K
[11] K. S. Kendler, M. C. Neale, R. C. Kessler, A. C. Heath and L. J. Eaves, “Generalized Anxiety Disorder in Women. A Population-Based Twin Study,” Archives of General Psychiatry, Vol. 49, No. 4, 1992, pp. 267-272.
[12] S. N. Young, “Clinical Nutrition: 3. The Fuzzy Boundary between Nutrition and Psychopharmacology,” Canadian Medical Association Journal, Vol. 166, No. 2, 2002, pp. 205-209.
[13] R. J. Wurtman, D. O’Rourke and J. J. Wurtman, “Nutrient Imbalances in Depressive Disorders. Possible Brain Mechanisms,” Annals of the New York Academy of Sciences, Vol. 575, 1989, pp. 75-82. doi:10.1111/j.1749-6632.1989.tb53234.x
[14] L. Vognar and J. Stoukides, “Low Plasma Thiamin Levels in Cognitively Impaired Elderly Patients Presenting with Acute Behavioral Disturbances,”Journal of the American Geriatrics Society, Vol. 57, No. 11, 2009, pp. 2166-2168. doi:10.1111/j.1532-5415.2009.02542.x
[15] M. Hamilton, “The Assessment of Anxiety States by Rating,” British Journal of Medical Psychology, Vol. 32, No. 1, 1959, pp. 50-55. doi:10.1111/j.2044-8341.1959.tb00467.x
[16] A. Torvik, “Two Types of Brain Lesions in Wernicke’s Encephalopathy,” Neuropathology and Applied Neurobiology, Vol. 11, No. 3, 1985, pp. 179-190. doi:10.1111/j.1365-2990.1985.tb00016.x
[17] K. G. Baker, A. J. Harding, G. M. Halliday, J. J. Kril and C. G. Harper, “Neuronal Loss in Functional Zones of the Cerebellum of Chronic Alcoholics with and without Wernicke’s Encephalopathy,” Neuroscience, Vol. 91, No. 2, 1999, pp. 429-438.
[18] P. Ruenwongsa and S. Pattanavibag, “Impairment of Acetylcholine Synthesis in Deficient Rats Developed by Prolonged Tea Consumption,” Life Sciences, Vol. 34, No. 4, 1984, pp. 365- 370.doi:10.1016/0024-3205(84)90625-8
[19] C. V. Vorhees, D. E. Schmidt and R. J. Barrett, “Effects of Pyrithiamin on acetylcholine Levels and Utilization in Rat Brain,” Brain Research Bulletin, Vol. 3, No. 5, 1978, pp. 493-496. doi:10.1016/0361-9230(78)90078-3
[20] R. G. Mair, C. D. Anderson, P. J. Langlais and W. J. McEntee, “Thiamine Deficiency Depletes Cortical Norepinephrine and Impairs Learning Processes in the Rat,” Brain Research, Vol. 360, No. 1-2, 1985, pp. 273-284. doi:10.1016/0006-8993(85)91243-0
[21] K. J. Meador, M. E. Nichols, P. Franke, M. W. Durkin, R. L. Oberzan, E. E. Moore and D. W. Loring, “Evidence for a Central Cholinergic Effect of High-Dose Thiamine,” Annals of Neurology, Vol. 34, No. 5, 1993, pp. 724-726. doi:10.1002/ana.410340516
[22] L. L. Barclay, G. E. Gibson and J. P. Blass, “Impairment of Behavior and Acetylcholine Metabolism in Thiamine Deficiency,” Journal of Pharmacology and Experimental Therapeutics, Vol. 217, 1981, pp. 537-543.
[23] G. Freund and W. E. Ballinger Jr., “Loss of Muscarinic and Benzodiazepine Neuroreceptors from Hippocampus of Alcohol Abusers,” Alcohol, Vol. 6, No. 1, 1989, pp. 23-31.
[24] G. Freund and W.E. Ballinger Jr., “Loss of Muscarinic Cholinergic Receptors from Temporal Cortex of Alcohol Abusers,” Metabolic Brain Disease, Vol. 4, No. 2, 1989, pp. 121-141. doi:10.1007/BF00999390
[25] O. G. Cameron, C. B. Smith, M. A. Lee, P. J. Hollingsworth, E. M. Hill and G. C. Curtis, “Adrenergic Status in Anxiety Disorders: Platelet Alpha 2-Adrenergic Receptor Binding, Blood Pressure, Pulse, and Plasma Catecholamines in Panic and Generalized Anxiety Disorder Patients and in Normal Subjects,” Biological Psychiatry, Vol. 28, No. 1, 1990, pp. 3-20. doi:10.1016/0006-3223(90)90427-4
[26] J. L. Abelson, D. Glitz, O. G. Cameron, M. A. Lee, M. Bronzo and G. C. Curtis, “Blunted Growth Hormone Response to Clonidine in Patients with Generalized Anxiety Disorder,” Archives of General Psychiatry, Vol. 48, No. 2, 1991, pp. 157-162.
[27] T. Shimizu, H. Hoshino, S. Nishi, S. Nozaki and Y. Watanabe, “Anti-Fatigue Effect of Dicethiamine Hydrochloride Is Likely Associated with Excellent Absorbability and High Transformability in Tissues as a Vitamin B1,” European Journal of Pharmacology, Vol. 635, No. 1-3, 2010, pp. 117-123. doi:10.1016/j.ejphar.2010.02.053
[28] O. Van Reeth, “Pharmacologic and Therapeutic Features of Sulbutiamine,” Drugs Today (Barc), Vol. 35, No. 3, 1999, pp. 187-192.
[29] O. Kreisler, E. Liebert and M. K. Horwitt, “Psychiatric Observations on Induced Vitamin B Complex Deficiency in Psychotic Patients,” American Journal of Psychiatry, Vol. 105, No. 2, 1948, pp. 107-110.
[30] G. D. Mishra, S. A. McNaughton, M. A. O’Connell, C. J. Prynne and D. Kuh, “Intake of B Vitamins in Childhood and Adult Life in Relation to Psychological Distress among Women in a British Birth Cohort,” Public Health Nutrition, Vol. 12, No. 2, 2009, pp. 166-174. doi:10.1017/S1368980008002413
[31] Y. D. Bakhai and S. Muqtadir, “Thiamine Deficiency and Psychosis,” American Journal of Psychiatry, Vol. 144, No. 5, 1987, pp. 687-688.
[32] I.G. Gontzea, V. Gorcea and F. Popescu, “Biochemichal Assessment of Thiamin Status in Patients with Neurosis,” Nutrition and Metabolism, Vol. 19, No. 3-4, 1975, pp. 53- 157.
[33] D. Benton, J. Fordy and J. Haller, “The Impact of Long-Term Vitamin Supplementation on Cognitive Functioning,” Psychopharmacology, Vol. 117, No. 3, 1995, pp. 298-305.
[34] J. Brozek and W. O. Caster, “Psychologic Effects of Thiamine Restriction and Deprivation in Normal Young Men,” American Journal of Clinical Nutrition, Vol. 5, No. 2, 1957, pp. 109-120.
[35] L. J. Smidt, F. M. Cremin, L. E. Grivetti and A. J. Clifford, “Influence of Thiamin Supplementation on the Health and General Well-Being of an Elderly Irish Population with Marginal Thiamin Deficiency,” Journal of Gerontology, Vol. 46, No. 1, 1991, pp. M16-M22.
[36] H. Heseker, W. Kuebler, J. Westenhoefer and V. Pudel, “Psychische Ver?derungen als Frühzeichen einer suboptitalen Vitaminversorgung,” Ern?hrungsumschau, Vol. 37, 1990, pp. 87-94.
[37] I. R. Bell, J. S. Edman, F. D. Morrow, D. W. Marby, G. Perrone, H. L. Kayne, M. Greenwald and J. O. Cole, “Vitamin B1, B2, and B6 Augmentation of Tricyclic Antidepressant Treatment in Geriatric Depression with Cognitive Dysfunction,” American Journal of Clinical Nutrition, Vol. 11, No. 2, 1992, pp. 159-163.
[38] D. Lonsdale and R. J. Shamberger, “Red Cell Transketolase as an Indicator of Nutritional Deficiency,” American Journal of Clinical Nutrition, Vol. 33, No. 2, 1980, pp. 205-211.
[39] T. J. Wilkinson, H. C. Hanger, J. Elmslie, P. M. George and R. Sainsbury, “The Response to Treatment of Subclinical Thiamine Deficiency in the Elderly,” American Journal of Clinical Nutrition, Vol. 66, No. 4, 1997, pp. 925-928.
[40] D. Benton, R. Griffiths and J. Haller, “Thiamine Supplementation Mood and Cognitive Functioning,” Psycho- pharmacology (Berl), Vol. 129, No. 1, 1997, pp. 66-71.
[41] R. A. Baum and F. L. Iber, “Thiamin-the Interaction of Aging, Alcoholism, and Malabsorption in Various Populations,” World Review of Nutrition & Dietetics, Vol. 44, 1984, pp. 85-116.
[42] K. Schaller and H. Holler, “Thiamine Absorption in Rat. II. Intestinal Alkaline Phosphatase Activity and Thiamine Absorption from Rat Small Intestines in-vitro and in-vivo,” International Journal for Vitamin and Nutrition Research, Vol. 45, No. 1, 1975, pp. 30-38.
[43] G. Rindi, V. Ricci, G. Gastaldi and C. Patrini, “Intestinal Alkaline Phosphatase Can Transphosphorylate during Intestinal Transport in the Rats,” Archives of Physiology and Biochemistry, Vol. 103, No. 1, 1995, pp. 33-38. doi:10.3109/13813459509007560
[44] K. V. Q. Luong and L. T. H. Nguyen, “Adult Hypophosphatasia and a Low Level of red Blood Cell Thiamine Pyrophosphate,” Annals of Nutrition and Metabolism, Vol. 49, No. 2, 2005, pp. 107-109. doi:10.1159/000084743
[45] P. H?hn, H. Gabbert and R. Wagner, “Differentiation and Aging of the Rat Intestinal Mucosa. II. Morphological, Enzyme Histochemical and Disc Electrophoretic Aspects of the Aging of the Small Intestinal Mucosa,” Mechanisms of Ageing and Development, Vol. 7, 1978, pp. 217- 226. doi:10.1016/0047-6374(78)90068-4
[46] I. Jang, K. Jung and J. Cho, “Influence of Age on Duo-Denal Brush Border Membrane and Specific Activities of Brush Border Membrane Enzymes in Wistar Rats,” Experimental Animals, Vol. 49, No. 4, 2000, pp. 281-287.
[47] T. E. Friedman, T. C. Kmieckiak, P. K. Keegan and B. B. Sheft, “The Absorption, Destruction, and Excreyion of Orally Administered Thiamine by Human Subjects,” Gastroenterology, Vol. 11, 1948, pp. 100-114.
[48] A. B. Morrison and J. A. Campbell, “Vitamin Absorption Studies. I. Factors Influencing the Excretion of Oral Test Doses of Thiamine and Riboflavin by Human Subjects,” Journal of Nutrition, Vol. 72, 1960, pp. 435-440.
[49] H. Baker, O. Frank and S. P. Jaslow, “Oral versus Intramuscular Vitamin Supplement for Hypovitaminosis in the Elderly,” Journal of the American Geriatrics Society, Vol. 28, No. 1, 1980, pp. 42-45.
[50] T. Sasaki, T. Yukizane, H. Atsuta, H. Ishikawa, T. Yoshiike, T. Takeuchi, K. Oshima, N. Yamamoto, A. Kurumaji and T. Nishikawa, “A Case of Thiamine Deficiency with Psychotic Symptoms-Blood Concentration of Thiamine and Response to Therapy,” in Japanese, Seishin Shinkeigaku Zasshi, Vol. 112, No. 2, 2010, pp. 97-110.

comments powered by Disqus

Copyright © 2017 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.