神经科学与心理学2024nature.com
咖啡因抑制慢性睡眠限制下的大脑灰质反应
Caffeine suppresses cerebral grey matter responses to chronic sleep restriction
进阶 · 约 40 分钟读完前置知识：神经影像学基础、睡眠生理、随机对照试验与统计
导读
这项双盲随机对照研究让 36 名健康成人经历 5 天慢性睡眠限制（每天仅 5 小时卧床），一组每天摄入 300mg 咖啡因，另一组喝脱因咖啡，并用 MRI 追踪灰质变化。研究关注咖啡因能否缓解或加剧睡眠不足引起的灰质改变，以及这种影响是否取决于个体腺苷受体（ADORA2A 基因）的差异。
HN 关注点：咖啡因几乎是所有 HN 读者的日常摄入物，而它对睡眠和大脑的长期影响存在争议，评论焦点集中在咖啡因是否被社会低估了危害。
HN 评论精选
这几条评论里：质疑 1 补充 3
补充咖啡因因商业利益被美化，其危害被社会系统性低估
我爱咖啡因，但它是一种成瘾性、高利润的物质，所以广告和宣传它有健康益处的现象非常普遍。我不会惊讶于日常摄入咖啡因至少对健康有轻度危害。有些药物在我们的社会中获得了特殊地位，广告和游说扭曲了我们对这些药物的认知。我甚至在本帖中看到评论说，如果咖啡因对你有持久影响，那是你基因特殊、是你自己的问题，而不是药物的问题——这和关于酒精的叙事如出一辙。把它与那些无法做广告、无法游说的非法毒品所受的对待相比，很有意思。
ilaksh查看英文原文
I love my caffeine. But caffeine is an addictive, highly profitable substance. So advertising it and trying to promote it as somehow having real health benefits is widespread. I would not be surprised if routine consumption of caffeine was at least mildly detrimental to health. I think some drugs have managed to gain a special place in our society . Advertising and lobbying warps our perception of these drugs. I even saw a comment in this thread suggesting that if caffeine has a prolonged affect on you, then you have some unique genetics and it's essentially your problem, not the drug. Similar to the narrative about alcohol. It's interesting to compare that attitude to the way illegal drugs that can't advertise or lobby are viewed.
补充约半数人是咖啡因慢代谢者，咖啡因可能损害他们的睡眠
最近我了解到，一半的人是咖啡因慢代谢者，咖啡因在他们体内停留时间更长，可能会对睡眠产生负面影响。考虑到喝咖啡的人有多少，我认为受此影响的人非常多。
janpmz查看英文原文
Recently I've learned that half of the people are slow caffein metabolizers. The caffein stays longer in their system and it might negatively affect their sleep. Considering how many people drink coffee, I think a lot of people are affected by this.
质疑质疑研究结论：咖啡因是否反而加剧了睡眠限制下的灰质减少
我从摘要中得出'睡眠剥夺+咖啡因=灰质减少'的结论，这错了吗？（附摘要全文）
hu3查看英文原文
Am I wrong to conclude from the abstract that sleep deprivation + caffeine = reduction in grey matter? Abstract: > Evidence has shown that both sleep loss and daily caffeine intake can induce changes in grey matter (GM). Caffeine is frequently used to combat sleepiness and impaired performance caused by insufficient sleep. It is unclear (1) whether daily use of caffeine could prevent or exacerbate the GM alterations induced by 5-day sleep restriction (i.e. chronic sleep restriction, CSR), and (2) whether the potential impact on GM plasticity depends on individual differences in the availability of adenosine receptors, which are involved in mediating effects of caffeine on sleep and waking function. Thirty-six healthy adults participated in this double-blind, randomized, controlled study (age = 28.9 ± 5.2 y/; F:M = 15:21; habitual level of caffeine intake < 450 mg; 29 homozygous C/C allele carriers of rs5751876 of ADORA2A, an A2A adenosine receptor gene variant). Each participant underwent a 9-day laboratory visit consisting of one adaptation day, 2 baseline days (BL), 5-day sleep restriction (5 h time-in-bed), and a recovery day (REC) after an 8-h sleep opportunity. Nineteen participants received 300 mg caffeine in coffee through the 5 days of CSR (CAFF group), while 17 matched participants received decaffeinated coffee (DECAF group). We examined GM changes on the 2nd BL Day, 5th CSR Day, and REC Day using magnetic resonance imaging and voxel-based morphometry. Moreover, we used positron emission tomography with [18F]-CPFPX to quantify the baseline availability of A1 adenosine receptors (A1R) and its relation to the GM plasticity. The results from the voxel-wise multimodal whole-brain analysis on the Jacobian-modulated T1-weighted images controlled for variances of cerebral blood flow indicated a significant interaction effect between caffeine and CSR in four brain regions: (a) right temporal-occipital region, (b) right dorsomedial prefrontal cortex (DmPFC), (c) left dorsolateral prefrontal cortex (DLPFC), and (d) right thalamus. The post-hoc analyses on the signal intensity of these GM clusters indicated that, compared to BL, GM on the CSR day was increased in the DECAF group in all clusters but decreased in the thalamus, DmPFC, and DLPFC in the CAFF group. Furthermore, lower baseline subcortical A1R availability predicted a larger GM reduction in the CAFF group after CSR of all brain regions except for the thalamus. In conclusion, our data suggest an adaptive GM upregulation after 5-day CSR, while concomitant use of caffeine instead leads to a GM reduction. The lack of consistent association with individual A1R availability may suggest that CSR and caffeine affect thalamic GM plasticity predominantly by a different mechanism. Future studies on the role of adenosine A2A receptors in CSR-induced GM plasticity are warranted.
补充咖啡因摄入太普遍，导致人们难以察觉它对焦虑和睡眠质量的影响
任何有焦虑或睡眠问题的人都应该重新审视自己的咖啡因摄入。也许这些问题不是咖啡因引起的，但也许就是。我不认识多少不每天摄入咖啡因的人——在这种情况下，你根本无法判断你的焦虑、睡眠问题、疲惫、坏情绪是否由咖啡因造成。有人坚称晚餐后喝一杯浓缩咖啡照样'睡得很好'，但关键不是你能不能睡着，而是你的睡眠有多深、多具恢复性。
BossingAround查看英文原文
Anyone with anxiety or sleep issues should reexamine their caffeine usage. Maybe those problems do not stem from caffeine, but maybe they do. I don't know many people that do not consume caffeine regularly, at least once a day - in such cases, you cannot know whether your anxiety, sleep problems, general tiredness, bad moods, ... are or are not caused by one's caffeine consumption. Some people swear by drinking a shot of espresso right after dinner, claiming that they can "sleep just fine" (or that it even calms them). It's not whether you can or cannot fall asleep, it's how deep and restorative your sleep is that is important here.
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