Ji Hyun Baek1, Eun-Suk Kang2, Maurizio Fava3, David Mischoulon3, Andrew A Nierenberg4, Dongsoo Lee5, Jung-Yoon Heo5, Hong Jin Jeon6. 1. Department of Psychiatry, Depression Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea; Bipolar Clinic and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, USA. 2. Department of Laboratory Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 3. Depression Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, USA. 4. Depression Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, USA; Bipolar Clinic and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, USA. 5. Department of Psychiatry, Depression Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 6. Department of Psychiatry, Depression Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea; Samsung Advanced Institute for Health Sciences & Technology (SAIHST), Seoul, Republic of Korea; Bipolar Clinic and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, USA. Electronic address: jeonhj@skku.edu.
Abstract
BACKGROUND: Thyroid dysfunction and elevated thyroid stimulating hormone (TSH) are common in patients with depression. TSH might exert its function in the brain through blood levels of brain-derived neurotrophic factor (BDNF). BDNF decreases during depressed states and normalize after treatment. The gap is that the association between TSH and BDNF in patients with major depressive disorder (MDD) is unknown. METHODS: We studied 105 subjects ≥18 years of age with MDD and measured serum, plasma, and platelet BDNF at baseline, 1 month and 3 months during antidepressant treatment. Other baseline measurements included hypothalamic-pituitary-thyroid axis hormones such as TSH, triiodothyronine (T3) and thyroxine (T4); hypothalamic-pituitary-adrenal (HPA) axis hormones and hypothalamic-pituitary-gonadal (HPG) axis hormones and prolactin. RESULTS: Linear mixed model effect analyses revealed that baseline TSH level was negatively associated with changes of serum BDNF from baseline to 3 months (F=7.58, p=0.007) after adjusting for age, sex, and body mass index, but was not associated with plasma and platelet BDNF. In contrast, T3 and T4, HPA axis hormones, HPG axis hormones, and prolactin were not associated with serum, plasma, or platelet BDNF levels. Patients in the highest quartile of TSH showed significantly lower serum BDNF than in the other quartiles (F=4.54, p=0.038), but no significant differences were found based on T3 and T4 levels. LIMITATIONS: TSH was only measured at baseline. CONCLUSIONS: Higher TSH is associated with lower baseline and reduced the increase of serum BDNF levels during antidepressant treatment in patients with MDD.
BACKGROUND:Thyroid dysfunction and elevated thyroid stimulating hormone (TSH) are common in patients with depression. TSH might exert its function in the brain through blood levels of brain-derived neurotrophic factor (BDNF). BDNF decreases during depressed states and normalize after treatment. The gap is that the association between TSH and BDNF in patients with major depressive disorder (MDD) is unknown. METHODS: We studied 105 subjects ≥18 years of age with MDD and measured serum, plasma, and platelet BDNF at baseline, 1 month and 3 months during antidepressant treatment. Other baseline measurements included hypothalamic-pituitary-thyroid axis hormones such as TSH, triiodothyronine (T3) and thyroxine (T4); hypothalamic-pituitary-adrenal (HPA) axis hormones and hypothalamic-pituitary-gonadal (HPG) axis hormones and prolactin. RESULTS: Linear mixed model effect analyses revealed that baseline TSH level was negatively associated with changes of serum BDNF from baseline to 3 months (F=7.58, p=0.007) after adjusting for age, sex, and body mass index, but was not associated with plasma and platelet BDNF. In contrast, T3 and T4, HPA axis hormones, HPG axis hormones, and prolactin were not associated with serum, plasma, or platelet BDNF levels. Patients in the highest quartile of TSH showed significantly lower serum BDNF than in the other quartiles (F=4.54, p=0.038), but no significant differences were found based on T3 and T4 levels. LIMITATIONS: TSH was only measured at baseline. CONCLUSIONS: Higher TSH is associated with lower baseline and reduced the increase of serum BDNF levels during antidepressant treatment in patients with MDD.
Authors: Honglei Yin; Hanga Galfalvy; Spiro P Pantazatos; Yung-Yu Huang; Gorazd B Rosoklija; Andrew J Dwork; Ainsley Burke; Victoria Arango; Maria A Oquendo; J John Mann Journal: Depress Anxiety Date: 2016-03-31 Impact factor: 6.505