Morris Martha Clare, Brockman John, Schneider Julie A, Wang Yamin, Bennett David A, Tangney Christy C, van de Rest Ondine
Section on Nutrition and Nutritional Epidemiology, Department of Internal Medicine, Rush University Medical Center, Chicago, Illinois.
Missouri University Research Reactor, Columbia.
JAMA. 2016 Feb 2;315(5):489-97. doi: 10.1001/jama.2015.19451.
Seafood consumption is promoted for its many health benefits even though its contamination by mercury, a known neurotoxin, is a growing concern.
To determine whether seafood consumption is correlated with increased brain mercury levels and also whether seafood consumption or brain mercury levels are correlated with brain neuropathologies.
DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional analyses of deceased participants in the Memory and Aging Project clinical neuropathological cohort study, 2004-2013. Participants resided in Chicago retirement communities and subsidized housing. The study included 286 autopsied brains of 554 deceased participants (51.6%). The mean (SD) age at death was 89.9 (6.1) years, 67% (193) were women, and the mean (SD) educational attainment was 14.6 (2.7) years.
Seafood intake was first measured by a food frequency questionnaire at a mean of 4.5 years before death.
Dementia-related pathologies assessed were Alzheimer disease, Lewy bodies, and the number of macroinfarcts and microinfarcts. Dietary consumption of seafood and n-3 fatty acids was annually assessed by a food frequency questionnaire in the years before death. Tissue concentrations of mercury and selenium were measured using instrumental neutron activation analyses.
Among the 286 autopsied brains of 544 participants, brain mercury levels were positively correlated with the number of seafood meals consumed per week (ρ = 0.16; P = .02). In models adjusted for age, sex, education, and total energy intake, seafood consumption (≥ 1 meal[s]/week) was significantly correlated with less Alzheimer disease pathology including lower density of neuritic plaques (β = -0.69 score units [95% CI, -1.34 to -0.04]), less severe and widespread neurofibrillary tangles (β = -0.77 score units [95% CI, -1.52 to -0.02]), and lower neuropathologically defined Alzheimer disease (β = -0.53 score units [95% CI, -0.96 to -0.10]) but only among apolipoprotein E (APOE ε4) carriers. Higher intake levels of α-linolenic acid (18:3 n-3) were correlated with lower odds of cerebral macroinfarctions (odds ratio for tertiles 3 vs 1, 0.51 [95% CI, 0.27 to 0.94]). Fish oil supplementation had no statistically significant correlation with any neuropathologic marker. Higher brain concentrations of mercury were not significantly correlated with increased levels of brain neuropathology.
In cross-sectional analyses, moderate seafood consumption was correlated with lesser Alzheimer disease neuropathology. Although seafood consumption was also correlated with higher brain levels of mercury, these levels were not correlated with brain neuropathology.
尽管汞这种已知的神经毒素对海鲜的污染日益引起关注，但由于海鲜对健康有诸多益处，所以仍提倡食用海鲜。
确定食用海鲜是否与大脑汞含量升高相关，以及食用海鲜或大脑汞含量是否与脑部神经病理学相关。
设计、地点和参与者：对2004年至2013年记忆与衰老项目临床神经病理学队列研究中的已故参与者进行横断面分析。参与者居住在芝加哥退休社区和保障性住房中。该研究包括554名已故参与者中286例经尸检的大脑（51.6%）。死亡时的平均（标准差）年龄为89.9（6.1）岁，67%（193例）为女性，平均（标准差）受教育年限为14.6（2.7）年。
海鲜摄入量首先通过食物频率问卷在死亡前平均4.5年时进行测量。
评估的与痴呆相关的病理学包括阿尔茨海默病、路易体以及大梗死灶和小梗死灶的数量。在死亡前几年通过食物频率问卷每年评估海鲜和n-3脂肪酸的饮食摄入量。使用仪器中子活化分析测量汞和硒的组织浓度。
在544名参与者的286例经尸检的大脑中，大脑汞含量与每周食用海鲜餐的次数呈正相关（ρ = 0.16；P = 0.02）。在根据年龄、性别、教育程度和总能量摄入进行调整的模型中，食用海鲜（≥1餐/周）与较少的阿尔茨海默病病理学显著相关，包括较低的神经炎性斑块密度（β = -0.69评分单位[95%置信区间，-1.34至-0.04]）、较轻且分布较广的神经原纤维缠结（β = -0.77评分单位[95%置信区间，-1.52至-0.02]）以及神经病理学定义的较低阿尔茨海默病（β = -0.53评分单位[95%置信区间，-0.96至-0.10]），但仅在载脂蛋白E（APOE ε4）携带者中如此。较高的α-亚麻酸（18:3 n-3）摄入量与较低的脑大梗死灶发生率相关（三分位数3与1相比的优势比，0.51[95%置信区间，0.27至0.94]）。补充鱼油与任何神经病理学标志物均无统计学显著相关性。大脑中较高的汞浓度与脑部神经病理学水平升高无显著相关性。
在横断面分析中，适度食用海鲜与较少的阿尔茨海默病神经病理学相关。尽管食用海鲜也与大脑中较高的汞含量相关，但这些含量与脑部神经病理学无关。
