BackgroundGreen tea is a beverage with potential effects on cognitive dysfunction, as indicated by results of experimental studies. However, its effects in humans, especially at real-world (typical) consumption levels, are unclear.MethodsA double-blind, randomized controlled study was conducted to assess the effects of green tea consumption on cognitive dysfunction (Mini-Mental State Examination Japanese version (MMSE-J) score <28) in Japan. Participants were randomly allocated to the green tea or placebo group, and consumed either 2 g/day of green tea powder (containing 220.2 mg of catechins) or placebo powder (containing 0.0 mg of catechins), respectively, for 12 months. Cognitive function assessments were performed every 3 months using the MMSE-J and laboratory tests.ResultsThirty-three nursing home residents with cognitive dysfunction were enrolled (four men, 29 women; mean age ± SD, 84.8 ± 9.3; mean MMSE-J score ± SD, 15.8 ± 5.4), of whom 27 completed the study. Changes of MMSE-J score after 1 year of green tea consumption were not significantly different compared with that of the placebo group (−0.61 [−2.97, 1.74], least square mean (LSM) difference [95 % CI]; P = 0.59). However, levels of malondialdehyde-modified low-density lipoprotein (U/L), a marker of oxidative stress, was significantly lower in the green tea group (−22.93 [−44.13, −1.73], LSM difference [95 % CI]; P = 0.04).ConclusionsOur results suggest that 12 months green tea consumption may not significantly affect cognitive function assessed by MMSE-J, but prevent an increase of oxidative stress in the elderly population. Additional long-term controlled studies are needed to clarify the effects.Trial registration
UMIN000011668
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The frequently found mutations, C1058R and C1977S, were caused by founder effects. This result suggests that Tg mutations may provide a genetic basis for the cause of familial euthyroid goiter.
Purpose of developing the guidelines: The first guidelines for diagnosis and treatment of
21-hydroxylase deficiency (21-OHD) were published as a diagnostic handbook in Japan in
1989, with a focus on patients with severe disease. The “Guidelines for Treatment of
Congenital Adrenal Hyperplasia (21-Hydroxylase Deficiency) Found in Neonatal Mass
Screening (1999 revision)” published in 1999 were revised to include 21-OHD patients with
very mild or no clinical symptoms. Accumulation of cases and experience has subsequently
improved diagnosis and treatment of the disease. Based on these findings, the Mass
Screening Committee of the Japanese Society for Pediatric Endocrinology further revised
the guidelines for diagnosis and treatment. Target disease/conditions: 21-hydroxylase
deficiency. Users of the guidelines: Physician specialists in pediatric endocrinology,
pediatric specialists, referring pediatric practitioners, general physicians; and
patients.
Abstract.Purpose behind developing these guidelines: Over one decade ago, the “Guidelines for the
Treatment of Graves’ Disease with Antithyroid Drug, 2006” (Japan Thyroid Association
(JTA)) were published as the standard drug therapy protocol for Graves’ disease. The
“Guidelines for the Treatment of Childhood-Onset Graves’ Disease with Antithyroid Drug in
Japan, 2008” were published to provide guidance on the treatment of pediatric patients.
Based on new evidence, a revised version of the “Guidelines for the Treatment of Graves’
Disease with Antithyroid Drug, 2006” (JTA) was published in 2011, combined with the
“Handbook of Radioiodine Therapy for Graves’ Disease 2007” (JTA). Subsequently, newer
findings on pediatric Graves’ disease have been reported. Propylthiouracil (PTU)-induced
serious hepatopathy is an important problem in pediatric patients. The American Thyroid
Association’s guidelines suggest that, in principle, physicians must not administer PTU to
children. On the other hand, the “Guidelines for the Treatment of Graves’ Disease with
Antithyroid Drug, 2011” (JTA) state that radioiodine therapy is no longer considered a
“fundamental contraindication” in children. Therefore, the “Guidelines for the Treatment
of Childhood-Onset Graves’ Disease with Antithyroid Drug in Japan, 2008” required
revision.
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