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28个字说清楚阳明心学

Preventing Alzheimer Disease in Your Sleep?

RESEARCH

With an aging population and subsequent predicted increase in incidence of Alzheimer disease (AD), identifying early markers and interventions is on the fast track. Research from the University of Wisconsin suggests that assessment of sleep quality and amyloid burden in midlife can identify AD risk and provide a window for early intervention.1

Previous research has correlated sleep problems with amyloid burden in seniors but not persons in late middle age in whom symptoms of cognitive decline have yet to emerge. Animal studies suggest that sleep disruption disrupts amyloid clearance, which is greatest during sleep.

Alzheimer prevention©OcskayMark/Shutterstock The researchers reasoned that sleep quality could be a useful therapeutic target for AD prevention because methods exist for improving sleep. They studied 98 cognitively healthy adults participating in the Wisconsin Registry for Alzheimer’s Prevention, a longitudinal cohort of more than 1500 cognitively healthy adults who were aged 40 to 65 years at study entry. Only those participants who had positron emission tomography (PET) scans and had completed the Epworth Sleepiness Scale and the Medical Outcomes Study Sleep Scale were included in the study. The average age of the study cohort was 62 years.

Amyloid binding was averaged within the 8 bilateral brain regions for which amyloid deposition and AD have been correlated (the angular gyrus, anterior cingulate gyrus, posterior cingulate gyrus, frontal medial orbital gyrus, precuneus, supramarginal gyrus, middle temporal gyrus, and superior temporal gyrus). Multiple regression analyses were used to examine the extent to which sleep scores predicted regional amyloid burden.

After adjusting for covariates, poorer sleep was significantly associated (P < .05) with greater amyloid burden particularly in the angular gyrus, frontal medial orbital cortex, cingulate gyrus, and precuneus. Although amyloid burden was associated with reportage of inadequate sleep, it was not associated with the amount of sleep reported, symptoms of sleep-disordered breathing, trouble falling asleep, or Epworth Sleepiness Scale scores.

The sleep measure most consistently associated with increased amyloid burden was the perception of less adequate sleep. This measure was derived from questions that asked participants whether they believed they were getting the amount of sleep they needed and enough sleep to feel rested. Also, the researchers did not diagnostically assess for sleep disorders; they only questioned participants on whether they had symptoms, and pointed out that many other studies have found an association between sleep-disordered breathing and dementia, including AD.

The bottom line
The researchers concluded that poor sleep may be a risk factor for AD and that sleep quality is a potential early marker or target for prevention during midlife. According to them, early interventions to improve sleep quality and treat sleep disorders could potentially slow down or prevent progression of AD by reducing amyloid pathology. In addition, sleep characteristics affected by amyloid deposition may act as biomarkers of preclinical AD and be useful in diagnosis, prognosis, and treatment monitoring. Prospective longitudinal studies and randomized control trials will be needed for further exploration of this issue.

References

1. Sprecher KE, Bendlin BB, Racine AM, et al. Amyloid burden is associated with self-reported sleep in nondemented late middle-aged adults. Neurobiol Aging. 2015 May 14. [Epub ahead of print]

- See more at: http://www.psychiatrictimes.com/geriatric-psychiatry/preventing-alzheimer-disease-your-sleep?from=timeline&isappinstalled=0#sthash.wfQAPe5d.dpuf

Preventing Alzheimer Disease in Your Sleep?

RESEARCH

With an aging population and subsequent predicted increase in incidence of Alzheimer disease (AD), identifying early markers and interventions is on the fast track. Research from the University of Wisconsin suggests that assessment of sleep quality and amyloid burden in midlife can identify AD risk and provide a window for early intervention.1

Previous research has correlated sleep problems with amyloid burden in seniors but not persons in late middle age in whom symptoms of cognitive decline have yet to emerge. Animal studies suggest that sleep disruption disrupts amyloid clearance, which is greatest during sleep.

Alzheimer prevention©OcskayMark/Shutterstock The researchers reasoned that sleep quality could be a useful therapeutic target for AD prevention because methods exist for improving sleep. They studied 98 cognitively healthy adults participating in the Wisconsin Registry for Alzheimer’s Prevention, a longitudinal cohort of more than 1500 cognitively healthy adults who were aged 40 to 65 years at study entry. Only those participants who had positron emission tomography (PET) scans and had completed the Epworth Sleepiness Scale and the Medical Outcomes Study Sleep Scale were included in the study. The average age of the study cohort was 62 years.

Amyloid binding was averaged within the 8 bilateral brain regions for which amyloid deposition and AD have been correlated (the angular gyrus, anterior cingulate gyrus, posterior cingulate gyrus, frontal medial orbital gyrus, precuneus, supramarginal gyrus, middle temporal gyrus, and superior temporal gyrus). Multiple regression analyses were used to examine the extent to which sleep scores predicted regional amyloid burden.

After adjusting for covariates, poorer sleep was significantly associated (P < .05) with greater amyloid burden particularly in the angular gyrus, frontal medial orbital cortex, cingulate gyrus, and precuneus. Although amyloid burden was associated with reportage of inadequate sleep, it was not associated with the amount of sleep reported, symptoms of sleep-disordered breathing, trouble falling asleep, or Epworth Sleepiness Scale scores.

The sleep measure most consistently associated with increased amyloid burden was the perception of less adequate sleep. This measure was derived from questions that asked participants whether they believed they were getting the amount of sleep they needed and enough sleep to feel rested. Also, the researchers did not diagnostically assess for sleep disorders; they only questioned participants on whether they had symptoms, and pointed out that many other studies have found an association between sleep-disordered breathing and dementia, including AD.

The bottom line
The researchers concluded that poor sleep may be a risk factor for AD and that sleep quality is a potential early marker or target for prevention during midlife. According to them, early interventions to improve sleep quality and treat sleep disorders could potentially slow down or prevent progression of AD by reducing amyloid pathology. In addition, sleep characteristics affected by amyloid deposition may act as biomarkers of preclinical AD and be useful in diagnosis, prognosis, and treatment monitoring. Prospective longitudinal studies and randomized control trials will be needed for further exploration of this issue.

References

1. Sprecher KE, Bendlin BB, Racine AM, et al. Amyloid burden is associated with self-reported sleep in nondemented late middle-aged adults. Neurobiol Aging. 2015 May 14. [Epub ahead of print]

- See more at: http://www.psychiatrictimes.com/geriatric-psychiatry/preventing-alzheimer-disease-your-sleep?from=timeline&isappinstalled=0#sthash.wfQAPe5d.dpuf

Preventing Alzheimer Disease in Your Sleep?

RESEARCH

With an aging population and subsequent predicted increase in incidence of Alzheimer disease (AD), identifying early markers and interventions is on the fast track. Research from the University of Wisconsin suggests that assessment of sleep quality and amyloid burden in midlife can identify AD risk and provide a window for early intervention.1

Previous research has correlated sleep problems with amyloid burden in seniors but not persons in late middle age in whom symptoms of cognitive decline have yet to emerge. Animal studies suggest that sleep disruption disrupts amyloid clearance, which is greatest during sleep.

Alzheimer prevention©OcskayMark/Shutterstock The researchers reasoned that sleep quality could be a useful therapeutic target for AD prevention because methods exist for improving sleep. They studied 98 cognitively healthy adults participating in the Wisconsin Registry for Alzheimer’s Prevention, a longitudinal cohort of more than 1500 cognitively healthy adults who were aged 40 to 65 years at study entry. Only those participants who had positron emission tomography (PET) scans and had completed the Epworth Sleepiness Scale and the Medical Outcomes Study Sleep Scale were included in the study. The average age of the study cohort was 62 years.

Amyloid binding was averaged within the 8 bilateral brain regions for which amyloid deposition and AD have been correlated (the angular gyrus, anterior cingulate gyrus, posterior cingulate gyrus, frontal medial orbital gyrus, precuneus, supramarginal gyrus, middle temporal gyrus, and superior temporal gyrus). Multiple regression analyses were used to examine the extent to which sleep scores predicted regional amyloid burden.

After adjusting for covariates, poorer sleep was significantly associated (P < .05) with greater amyloid burden particularly in the angular gyrus, frontal medial orbital cortex, cingulate gyrus, and precuneus. Although amyloid burden was associated with reportage of inadequate sleep, it was not associated with the amount of sleep reported, symptoms of sleep-disordered breathing, trouble falling asleep, or Epworth Sleepiness Scale scores.

The sleep measure most consistently associated with increased amyloid burden was the perception of less adequate sleep. This measure was derived from questions that asked participants whether they believed they were getting the amount of sleep they needed and enough sleep to feel rested. Also, the researchers did not diagnostically assess for sleep disorders; they only questioned participants on whether they had symptoms, and pointed out that many other studies have found an association between sleep-disordered breathing and dementia, including AD.

The bottom line
The researchers concluded that poor sleep may be a risk factor for AD and that sleep quality is a potential early marker or target for prevention during midlife. According to them, early interventions to improve sleep quality and treat sleep disorders could potentially slow down or prevent progression of AD by reducing amyloid pathology. In addition, sleep characteristics affected by amyloid deposition may act as biomarkers of preclinical AD and be useful in diagnosis, prognosis, and treatment monitoring. Prospective longitudinal studies and randomized control trials will be needed for further exploration of this issue.

References

1. Sprecher KE, Bendlin BB, Racine AM, et al. Amyloid burden is associated with self-reported sleep in nondemented late middle-aged adults. Neurobiol Aging. 2015 May 14. [Epub ahead of print]

- See more at: http://www.psychiatrictimes.com/geriatric-psychiatry/preventing-alzheimer-disease-your-sleep?from=timeline&isappinstalled=0#sthash.wfQAPe5d.dpuf

28个字说清楚阳明心学

2015-08-12 悦网美文日赏

 

 

 
 

 

 

各位真爱好哇

今天熊猫君想酷一把

所以要跟你们聊聊心学

在我们的主题开始之前

熊猫君不得不提一本书

《知行合一王阳明》

 

 

至于不得不提的原因

就是这本书出第二部了

《知行合一王阳明2:四句话读懂阳明心学》

那么,究竟是哪四句呢

 

无善无恶心之体——世界观

 

图片关键词

理解这四句话,所有的困惑将变得清晰,所有的犹豫将变成果断。

 

王阳明说过这样的话:“在心体上不能遗留一个念头,有如眼中不能吹进一丁点灰尘。一丁点能有多少呢?它能使人满眼天昏地暗了。这个念头不仅是指私念,即便美好的念头也不能有一点。例如,眼中放入一些金玉屑,眼睛就不能睁开。”

 

我们于此可以知道,无善无恶就是本心最自然的状态,它是心的本体。

 

由于心即是理,心外无事、心外无物,心的本体是无善无恶,所以天地万物也应该无善无恶。这就是王阳明的世界观:天地万物无善无恶,我们对待天地万物的态度也应该是无善无恶。

 

故事:

 

下面这个故事极透彻地说明了这个观点。王阳明的弟子薛侃有一天在花园中除草时,付出了许多汗水,所以哀叹道:“为什么天地之间,善难培养,恶难铲除?!”

 

王阳明当时就在花园赏花,听到薛侃的叹息,立即察觉到传播心学世界观的机会来了,于是接口道:“你就没培养善,也没有铲除恶。”

 

薛侃莫名其妙,因为他劳碌了大半天,铲除了很多杂草,而且他经常浇灌花朵,这怎么能说是没有培养善,没有铲除恶呢!

 

王阳明发现了薛侃的疑惑,却没有继续深入这个话题,而是转到另外一个问题上去了:“你呀,如此看待善恶,因为从形体上着眼,错误在所难免。”

 

薛侃这回如堕云里雾里,更不知王老师的话是什么意思了。

 

王阳明马上解释说:“天生万物和花园里有花又有草一样。哪里有善恶之别?你想赏花,花就是善的,草就是恶的。可如有一天,你要在门前搞个草坪,草又是善的,草坪里的花就肯定被你当成恶的了。

 

这种‘善恶’都是由你的私意产生,所以就是错误的。”

 

薛侃吃惊地问:“这不就是无善无恶了吗?”

 

王阳明正色道:“天下任何事物本来就没有善恶,它之所以有善恶,全是你强加给它的。我问你,黄金是善还是恶?”

 

薛侃搓着手兴奋地说:“黄金是大大的好东西,当然是善的。”

 

王阳明问:“这要看黄金在什么地方。它在你手上,肯定是善的,可如果它在你胃里呢?”

 

薛侃摇头道:“那这就是恶的了。”

 

王阳明又问:“粪便是善的还是恶的?”

 

薛侃肯定地回答:“那玩意儿肯定是恶的。”

 

王阳明笑了:“粪便可以让庄稼生长,在老农心中,它就是善的。

 

所以说,天下的万事万物哪里有善恶之分?都是人强行加到它上面的。同样是一座大山,旅游的人就认为它是善的,有急事要翻越它的人就认为是恶的。同样一个人,在朋友心中是善的,而到了他的敌人心中,他就是十恶不赦的。”

 

有善有恶意之动——人生观

 

 

图片关键词

 

人人皆有良知,为何有人会流芳千古,有人则遗臭万年?为何有人出类拔萃,有人却碌碌无为?为何有人是善人,而有人就成了恶人?

 

这些问题的答案很简单:他们的人生观出了问题。用王阳明的话讲就是:他们的心,失去了本体。所谓失去本体,其实就是良知被遮蔽,不能正常工作了。所以王阳明说,有善有恶意之动。良知一旦被遮蔽,所发出的意(念头)就有了善恶,而有了善恶之后,又不肯为善去恶,所以人生观就有了善恶。

 

良知是如何被遮蔽的呢?

 

王阳明的结论是:习气所染。

 

习气就是我们身处的社会,王阳明不无遗憾地说,由于不是每个人都自动自发地去致良知,所以由众人组成的这个社会不是真诚恻怛的,而是充满了客套和虚伪。

 

故事:

 

他曾在一次讲学间隙对弟子们说:“人人胸中都有个圣人,只是不自信,又不肯努力,所以埋没了这位圣人。”

 

弟子们唯唯。

 

王阳明看着一位弟子说:“你胸中有个圣人。”

 

这名弟子马上站起,慌张得很:“不敢。”

 

王阳明叫他坐下,笑着说:“众人皆有,你怎么就没有?天下万事都可谦虚,唯独这事不可谦虚。”

 

该弟子笑着接受。

 

王阳明扫视众弟子,先诵了自己的一首诗:“个个人心有仲尼,自将闻见苦遮迷。而今指与真头面,只是良知更莫疑。”

 

然后他又语重心长地注解道:“人皆有良知,圣人之学,就是致此良知。自然而致的是圣人,勉强而致的是贤人,不肯致的是愚人。虽是愚人,只要他肯致良知,就和圣人无异。此良知所以为圣愚之同具备,而皆可为尧舜者,以此也。”

 

知善知恶是良知——价值观

 

 

图片关键词

 

如果我们用现代心理学来描述“良知”,就是这样的:当我们面对一个情境时,它不会导致我们的直接反应,而会不由自主地产生一个快速评价思维,这个评价思维不是深思熟虑或理性推理的结果,而是自动闪现,迅如闪电,如你所知,这个评价思维就是良知。

 

比如得到一笔确凿的不义之财,我们最先出现的是对这份不义之财的是非评价,而不是行为、情绪和生理上的反应,这个是非评价就是良知。它先天而来,自动自发,不受你控制。

 

通俗而言就是,良知,是人与生俱来的道德与智慧的直觉(直观)力,或是直觉(直观)的道德力和智慧力。见父自然知孝是道德,何尝又不是智慧?见强凌弱所以义愤填膺,因为我们判断这是错的,这是智慧,何尝又不是道德?

 

王阳明对“良知”的推崇几乎无以复加,他说:“乾坤由我在,安用他求为?千圣皆过影,良知乃吾师。”他又说,“良知是造化的精灵。这些精灵,生天生地,成鬼成帝,皆从此出。”他还说,“良知学是千古圣贤相传的一点真骨血,譬之如行舟得舵,平澜浅滩无不如意,虽遇巅风逆浪,舵柄在手,可免没溺之患。”

 

这些对良知的赞美之词大有“良知在手,天下我有”的意味,良知真的无所不能吗?

 

故事:

 

1509年,也就是王阳明龙场悟道的第二年,其名气已大震于贵州。省会贵阳主管教育的行政长官席书慕名前来拜会王阳明,听了几句后,就问他:“请问朱熹和陆九渊有什么不同?”

 

朱熹创建理学、陆九渊奠基心学,两个截然不同的人物。王阳明却戳了戳自己胸口说:“都是一样的心。”

 

显然,席书问的不是这个,王阳明也没给他机会继续问别的,急转直下大谈特谈自己体悟的“格物致知”。席书渐渐听得入了港,热情邀请王阳明到贵阳讲学。

 

王阳明欣然同意。席书临行前问道:“您讲课的主题是什么?”

 

“知行合一!”

 

席书一愣:“知行本是两件事,怎么能合一?”

 

王阳明摆出一副惊骇的样子:“知行就是一回事,我说‘合’都欠妥了。”

 

席书更是大惑,王阳明马上和他讲起“知行合一”的真谛来,这个真谛就记载于《传习录・卷上》中。

 

徐爱和席书一样,也不能理解“知行合一”,于是向王阳明请教。王阳明说:“空谈理论,你理解起来很麻烦,你举个例子吧。”

 

徐爱说:“例子很多,比如大家明知对父母应该孝顺,对兄长应该尊敬,但往往不能孝、不能敬,可见知与行分明是两码事。”

 

王阳明道:“这种人是被私欲遮蔽了,所以知行分为两截。《大学》中有两句话叫‘如好好色’‘如恶恶臭’,说的就是知行合一的问题。”

 

徐爱眉头紧皱,表示不明白。

 

王阳明解释道:“见好色是知,喜好色是行。在见到好色时马上就喜好它了,不是在见了好色之后才起一个念头去喜好。闻到恶臭是知,讨厌恶臭是行。闻到恶臭时就开始讨厌了,不是在闻到恶臭之后才起一个念头去讨厌。”

 

为善去恶是格物——方法论

 

 

图片关键词

 

王阳明的弟子陆澄有个困惑,当然也是我们的困惑。他问:“静坐用功,觉得此心异常强大,甚至想着如果我们遇到某某事,必能轻松解决。可一遇事就蒙了,真是烦躁。”

 

王阳明针对此症,对陆澄说:“人须在事上磨练做功夫,乃有益。

 

事上磨练,通俗而言,就是要参与社会实践,在纷繁复杂的具体事务中锻造自己的心理素质,做到动静皆定,泰山崩于前而色不变,麋鹿兴于左而目不瞬,以此沉着冷静,正确应对,最后就进入“不动心”境界。

 

事上磨练就是存天理、去人欲,就是让自己的喜怒哀乐恰到好处,不可过分,这就是“和”,就是良知本体。我们事上磨练,就是要到人情事变上去练心,喜怒哀乐是人情,富贵、贫贱、患难、生死是事变,事变也只是在人情里,只要能在人情事变上致良知,那就是最好的练心,自然是最好的事上练。

 

故事:

 

有一位地方官常去听王阳明的心学讲座,每次都听得津津有味,偶尔会呈恍然大悟之态,眉飞色舞。月余后,他却深表起遗憾来:“您讲得真精彩,可是我不能每天都来听,身为官员,好多政事缠绕,不能抽出太多时间来修行啊。”

 

王阳明接口道:“我什么时候让你放弃工作来修行?”

 

该官员吃了一小惊:“难道在工作中也可以修行?”

 

“工作即修行!”王阳明斩钉截铁地回道。

 

“我愚昧得很,”该官员既迷惑又惊奇,“难道您让我一边工作一边温习您的学说?”

 

王阳明说:“心学不是悬空的,只有把它和实践相结合,才是它最好的归宿。我常说去事上磨练就是因此。你要断案,就从断案这件事上学习心学。例如,当你判案时,要有一颗无善无恶的心,不能因为对方的无礼而恼怒;不能因为对方言语婉转而高兴;不能因为厌恶对方的请托而存心整治他;不能因为同情对方的哀求而屈意宽容他;不能因为自己的事务烦冗而随意草率结案;不能因为别人的诋毁和陷害而随别人的意愿去处理。这里所讲的一切情况都是私,唯有你自己清楚。这就是良知,良知就是自己知道而别人不知道。你必须认真省察克治,心中万不可有丝毫偏离而枉人是非,这就是致良知了。如果抛开事物去修行,反而处处落空,得不到心学的真谛。”

 

该官员恍然大悟,心灵满载而归。

图片关键词

 

 
 

 

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