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1. Auttaako nostalgia yksinäisyyden tunteessa?

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1. Auttaako nostalgia yksinäisyyden tunteessa?

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Miten pitkittynyt unettomuus vaikuttaa ihmisen hyvinvointiin?

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Auttaako Tetriksen pelaaminen psykologisista traumoista selviytymisessä?

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Ahdistaako maanantai ja näkyykö se kävelyssäsi?

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1. mistä ihmisten aivojen ylivertaisuus johtuu?

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1. mistä ihmisten aivojen ylivertaisuus johtuu?

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Miten ihmiset reagoivat valtasuhteisiin vankilaympäristössä, jossa ei ole täsmällisesti esitettyjä sääntöjä.

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Kyllä näkyy.

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Unettomuus vaikuttaa negatiivisesti aivoihin ja hyvinvointiin.

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syy voi löytyä pikkuaivoista

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Kyllä se auttaa

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kokeellinen tutkimusote

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Onko ihmisellä suurempi mahdollisuus tehdä jotain, jos siittä saa jotain palautetta esim. Jos on kaksi portaikkoa ja toisesta tulee jokin ääni, kuin toisesta ei tule mitään.

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kokeellinen tutkimus

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Ihmiset alkavat kohdella toisiaan epäoikeudenmukaisesti.

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Kyseessä on kokeellinen tutkimusote.

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Kokeellinen tutkimus

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Ihmiset valitsevat sen portaikon josta kuuluu ääntä.

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suurin osa kyllä

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Psykologiset testit, havainnointi, haastattelut, fysiologiset mittaukset ja lähdeaineiston tutkiminen

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kyllä se vaikuttaa

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Tutkivat ihmisten käyttäytymistä vankilaympäristössä kuuden päivän ajan.

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tutkivat ihmisten ja apinoiden otsalohkoja ja pikkuaivoja sekä jäljittivät aivojen kehityshistoriaa

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Valittiin vapaaehtoisia ja seurattiin heidän kävelyä maanantaisin ja heidän aivojen toimintaa seurattiin samalla.

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5. Nostalgiaa tuntevat olivat keskimäärin iloisempia kuin ne jotka eivät kokeneet nostalgiaa.

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5. Nostalgiaa tuntevat olivat keskimäärin iloisempia kuin ne jotka eivät kokeneet nostalgiaa.

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- elimistö kokee unen puutteen vaaratilanteena
- uni on välttämättömyys
- uni säätelee myös immuunijärjestelmän toimintaa

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kokeellinen tutkimus

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Kokeelliset tutkimukset
väestötutkimukset

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Kuvaileva tutkimus

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Ryhmä erilaisia ihmisiä joita yhdisti vain sukupuoli kerättiin yhteen ja jaettiin kahteen ryhmään. Toiset olivat auktoriteettejä eli opettajia ja toiset oppilaita. Opettajille annettiin tehtäväksi rankaista oppilasta sähköiskulla väärästä vastauksesta. Jokaisella vastauksella iskut voimistuivat.

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ihmisen ja apinan pikkuaivot erosivat toisistaan enemmän kuin ihmisen ja apinan otsalohkot, josta on ennen luultu ihmisen ylivertaisuuden johtuvan

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6. Tutkimus on loistavasti toteuttu ja luotettava taho on sen toteuttunat

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6. Tutkimus on loistavasti toteuttu ja luotettava taho on sen toteuttunat

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Tutkittiin ottavatko ihmiset portaat josta kuuluisi nuotteja

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65% ei vastustanut auktoriteettia vaan suorittivat voimmakkaimmatkin iskut

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7. Southamptonin yliopiston johtama tutkimus

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7. Southamptonin yliopiston johtama tutkimus

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Koe todisti, että melkein kuka tahansa kykenee julmaan sekä pahaan toimintaan lähimmäistään kohtaan, jos tähän annetaan valta ilman rajoja ja seurauksia.

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Ihmiset valitsivat portaikon josta kuului nuotteja

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Psykologiset testit ja fysiologiset mittaukset

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Tukimus oli tehty hyvin ja hauskasti.

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Artikkeli on luotettava, koska se pohjautuu tutkimukseen, jossa on hyödynnetty monia eri osa-alueita.

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Volkswagen

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The Piano Staircase

- The Fun Theory (initiative by Volkswagen)

"Can we get more people to choose the stairs by making it fun to do?"

Review by Vera Hendriks

The Piano Staircase is a project by The Fun Theory (which is an initiative of Volkswagen) from 2009. The objective of the project was initially to see if they could get people to choose the stairs over the escalator by making taking the stairs more fun to do.

This project transforms a plain staircase into a piano. These piano staircases are designed to make taking the stairs more fun and to encourage the people to walk up (or down) the stairs instead of taking the elevator or escalator. According to me the Piano Staircase project is part of the gamification issue.

Thanks to the project, 66% of the people who passed by at the original project site chose to take the stairs over the escalators. "Fun can obviously change behavior for the better." - Quote from YouTube video.

Walking up and down the stairs is a lot healthier as opposed to taking an escalator because it keeps you moving. The reason I like this project so much is because it is something I personally care about. Lately I have been trying to get my stamina up again and I have been trying to live a healthier lifestyle. I feel like it is hard to actually accomplish these things without putting a lot of effort in it, but small things like taking the stairs can already make a difference.

This is one of the contextual qualities of this project. For example, in the U.S.A. more than 2 out of 3 adults are considered overweight or obese.

We recently (29th of June 2016) had one of these piano staircases "installed" at Rotterdam Central Station, and for me it has worked really well so far. It is that last push you need to just take the stairs instead of the escalator and for me, personally, it can really lighten up my mood.

The artistic qualities are a little less obvious or present in this project. The stairs look more fun when they are decorated as a piano, but it is not necessarily focused on the creation of something from the imagination or focused on the aesthetics of the project. Personally, I absolutely love the way these stairs look as opposed to the average station (metro or train), it gives the stations a much friendlier appearance.

As for the participatory qualities, these are very high in this project. People are invited to actually walk on the project (/artwork) and to play with it. Apart from actually encouraging people to take part in the project (/artwork) it "raises awareness" for physical exercise as well.

The transformative qualities in this project are initially good in my opinion, but this is also one of the weaker aspects of this project. When you first encounter the Piano Stairs it is something new and fun and exciting, but when you have seen the Piano Stairs several times and after walking on them or using them a lot it can get boring. It will not be new and fun and exciting forever, and for some people (whose main concern is not being healthier or getting more exercise) this means that they will no longer care about it. Hence they start taking the escalators again.

A great opportunity is, in my opinion, the enthusiasm there is for this project on the internet and social media. I have seen a lot of people on social media asking for something like this project to be installed near where they live and personally, I would love to see more of these Piano Staircases as well, even if it is just to cheer me up while traveling.

In my opinion this project should be placed on the auto-relational side, somewhere between "completely auto-relational" and "the middle". The project was not made by the community or with the community. It was realized almost entirely be the designer (apart from the research, which included other people as well). The reason I dont think this project is completely auto-relational is because it can simply not exist without a community or participants using the project.

As for the other axis, I feel like this project should be placed on the digestive side. It does not conflict with ideals or any governmental issues. It is designed to encourage people to do something; get more exercise, and also to raise awareness for the problem that people don't move enough (which is why I haven't positioned my project all the way to the digestive side).

http://www.experientialdesignlandscapes.com/files/peeters-pt13.pdf

http://www.thefuntheory.com/piano-staircase

https://www.youtube.com/watch?v=2lXh2n0aPyw

http://creativity-online.com/work/volkswagen-fun-theory-piano-staircase/17522

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The Fun Theory (initiative by Volkswagen) "Can we get more people to choose the stairs by making it fun to do?" Review by Vera Hendriks The Piano Staircase is a project by The Fun Theory (which is an initiative of Volkswagen) from 2009.

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kokeeseen osallistui erittäin terveitä nuoria miehiä, jotka tavallisesti nukkuivat kahdeksan tuntia. Tutkimuksessa uniaika puolitettiin viiden vuorokauden ajaksi.

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Abstract

Lockdowns during the COVID-19 pandemic increased the risk for loneliness. We tested whether nostalgia counteracts loneliness via rises in happiness. We conducted surveys in China ( N = 1,546), the United States ( N = 1,572), and the United Kingdom ( N = 603). Although feeling lonely was associated with unhappiness, it was also associated with nostalgia, which in turn conduced to increased happiness. We complemented these findings with three experiments testing MTurk workers (Study 4, N = 209; Study 5, N = 196; Study 6, N = 190), where we manipulated nostalgia and assessed happiness. Nostalgia increased happiness immediately after the manipulation (Studies 4-6) and, following an induction booster, up to 2 days later (Studies 4-5). Nostalgia is a psychological resource that can be harnessed to raise happiness and help combat loneliness.

Since the COVID-19 outbreak, billions of people have been in lockdown, prevented from socializing with their social network. The pandemic-imposed lockdowns have been linked to psychological distress (e.g., unhappiness, depression, and anxiety; Rettie & Daniels, 2020; Xin et al., 2020; Zacher & Rudolph, 2020). In addition, lockdowns are associated with loneliness ( Armitage & Nellums, 2020; Enea et al., 2021). Loneliness (a) conduces to psychological distress (unhappiness, depression, and anxiety; Brodeur et al., 2020; Erzen & Çikrikci, 2018); (b) triggers cellular changes that result in chronic inflammation and weaken the immune system ( Cole et al., 2015), rendering lonely individuals vulnerable to viral infections much like COVID-19; and (c) is linked to morbidity (Holt-Lunstad et al., 2015).

As the pandemic has spurned "an epidemic of loneliness" (The Guardian, 2020b), finding ways to alleviate loneliness is of essence. Researchers have attempted to do so by fostering friendships or encouraging support from social networks ( Asher & Paquette, 2003; Bell, 1991). However, due to pandemic-necessitated lockdowns, such attempts are of limited range and value. Further, although virtual social networks may attenuate loneliness for some, they increase it for others ( Phu & Gow, 2019; Primack et al., 2019) while risking incivility ( Kim, 2020). Alternative strategies are needed that are easier to implement and more reliable. We propose such a strategy: drawing on one's reservoir of nostalgic memories.

Nostalgia entails sentimental longing for momentous events from one's past (e.g., birthdays, weddings, and graduations; Wildschut et al., 2006). Indeed, experiences that can later produce nostalgia are atypical, infrequent, and valued ( van Tilburg et al., 2019). The emotion is self-relevant ( van Tilburg et al., 2018), given that these events are personally meaningful ( Sedikides & Wildschut, 2018). It is also social, as the self is surrounded by close others ( Sedikides & Wildschut, 2019). Further, nostalgia is ambivalent but predominantly positive ( Leunissen et al., 2021): In nostalgic reverie, the individual feels warm and contented but also longs for valued moments ( Hepper et al., 2012). Nostalgia is experienced frequently (several times a week; Wildschut et al., 2006) and across ages ( Madoglou et al., 2017) or cultures ( Hepper et al., 2014).

Loneliness conduces to nostalgia. Lonelier participants were more nostalgic ( Abeyta et al., 2020; Zhou et al., 2008), and participants who were induced to feel lonely became more nostalgic ( Wildschut et al., 2006; Zhou et al., 2008). Moreover, nostalgia conduces to sociality. Nostalgia is positively associated with, and increases, social connectedness (sense of acceptance/belongingness; Sedikides & Wildschut, 2019; Wildschut et al., 2010). Relatedly, nostalgia is positively associated with, and augments, perceived social support ( Turner et al., 2013; Zhou et al., 2008). Further, social support constitutes a key source of happiness ( Chan & Lee, 2006; Siedlecki et al., 2014), and nostalgia contributes to happiness ( Hepper et al., 2021; Sedikides et al., 2016).

Together, the evidence indicates that (a) loneliness is positively associated with, or elicits, nostalgia ( Sedikides & Wildschut, 2019); (b) loneliness is negatively associated with, or decreases, happiness ( Cacioppo et al., 2006; Satici et al., 2016); and (c) nostalgia is positively related or conduces to happiness (eudaimonic well-being; Hepper et al., 2021; Sedikides et al., 2016) and can increase happiness (satisfaction with life; Cox et al., 2015). We propose an intervening variable model, known as statistical suppression or inconsistent mediation ( MacKinnon et al., 2000; Paulhus et al., 2004), to understand the relations among loneliness, nostalgia, and happiness. Here, the direct effect of a predictor is directionally opposite to its indirect effect via the intervening variable. When the indirect effect of the intervening variable is introduced in the model, the direct effect is strengthened (rather than weakened, as in consistent mediation models). In our case, the direct effect of loneliness on happiness will be negative: Loneliness will conduce to deficits in happiness. However, the indirect effect of loneliness on happiness via nostalgia will be positive: Loneliness will conduce to higher nostalgia, which will be associated with greater happiness.

We tested the model that nostalgia counteracts loneliness via increases in happiness in six studies conducted during the pandemic. In Studies 1-3, we examined the cross-sectional relations among loneliness, nostalgia, and happiness. We ran Study 1 in China when the number of new infections had leveled off. We conducted Studies 2 and 3 in the United States and United Kingdom, respectively, when infection cases were rising. We complemented these findings with three online experiments in Western countries when infections were rising. We examined the causal relation between nostalgia and happiness immediately and over a 2-day period (Studies 4-6). We summarized results with integrative data analyses (IDAs; Curran & Hussong, 2009), reporting them in Supplementary Material.

Our research makes several contributions to the literature. Studies 1-3 (which were part of larger surveys) are the first to include concurrently the measures of loneliness, nostalgia, and happiness and test for statistical suppression effects. Studies 4-6 provide experimental evidence for the nostalgia-happiness link, when prior experimental work has been concerned with the association between nostalgia and life satisfaction. Studies 4-6 test the effect of nostalgia on happiness. All studies were approved by the Institute of Psychology, Chinese Academy of Sciences's Institutional Review Board. The data and codes are available at OSF ( https://osf.io/u 5 rjb/) and the research protocol in Supplementary Material.

Study 1

We examined the capacity of nostalgia to restore psychological homeostasis ( Folkman, 2008) by surveying a Chinese sample from March 8 to 14, 2020, when the infection's number had stabilized.

Participants

As an initial study, we estimated a small effect ( r = .10) for a two-tailed bivariate correlation test with power (1 − β) = .95 at α = .05. We aimed for a minimum N = 1,293. We recruited 1,549 Chinese participants via the online platform credamo.com in a nationwide survey (across 30 of the 34 provinces). We excluded three participants who reported an age < 18 years, resulting in 1,546 valid cases (763 women and 783 men; Myears = 28.43 and SDyears = 6.64).1

Method

We indexed loneliness as social isolation (whether participants lived alone for more than a week during the pandemic). Social isolation refers to an objective lack of social interactions, whereas loneliness refers to the subjective perception that one lacks meaningful social interactions. Although they are conceptually distinguishable ( Cornwell & Waite, 2009; Veazie et al., 2019), social isolation is a good proxy of loneliness ( Savikko et al., 2005).

We assessed loneliness with the item "During the outbreak, have you been living alone for more than a week?" (0 = no, 1 = yes). We assessed happiness with two items ( r = .763, p < .001; Spearman-Brown reliability coefficient = .866): "For the past week, how happy has your life been?" and "For the past week, how meaningful has your life been?" (1 = not at all and 7 = very much). We derived the first item from the Subjective Happiness Scale ( Lyubomirsky & Lepper, 1999) and added the second item to expand the constructs' scope to eudaimonic well-being ( Ryff, 1989). We assessed nostalgia with an established ( Hepper et al., 2012) three-item measure: "I feel quite nostalgic," "I have nostalgic feelings," and "I feel nostalgic" (1 = not at all and 7 = very much; α = .937).

Results and Discussion

We found that (a) lonely participants ( M = 5.03, 95% confidence interval [CI] [4.94, 5.12]) were less happy than nonlonely ones ( M = 5.17, 95% CI [5.07, 5.28]), F(1, 1544) = 4.18, p = .041, d = .106; (b) lonely participants ( M = 4.59, 95% CI [4.49, 4.69]) felt more nostalgic than nonlonely ones ( M = 4.22, 95% CI [4.10, 4.34]), F(1, 1544) = 21.66, p < .001, d = .242; and (c) nostalgia was positively associated with happiness ( r = .157, 95% CI [0.107, 0.206], p < .001; Table 1).

Correlations Among Variables in Study 1 (Chinese Sample).

We proceeded to test our model with mediational analyses. When we regressed happiness onto both loneliness (0 = nonlonely and 1 = lonely) and nostalgia, loneliness negatively predicted happiness, whereas nostalgia positively predicted happiness ( Figure 1, Panel A). Importantly, loneliness more strongly predicted decreases in happiness after nostalgia had been controlled for ( Paulhus et al., 2004). If it were not for nostalgia, loneliness would conduce more strongly to decreases in happiness. The indirect effect (denoted ab) of loneliness was supported by the bootstrapping method ( Hayes, 2018; PROCESS Model 4; 5,000 bootstraps). The 95% CI for the indirect effect did not include 0 ( ab = .055; 95% CI [0.028, 0.087]). Also, the 95% CI for the direct effect did not include 0 ( b = −.201; 95% CI [−0.340, −0.062]).

Study 2

We tested the replicability of Study 1 findings by surveying an American sample between April 3 and 12, 2020, when the infection's number was rising. We assessed loneliness and happiness differently than in Study 1.

Participants

We estimated a small effect ( r = .10) with power (1 − β) = .95 at α = .05, aiming for a minimum N = 1,293. We recruited 1,572 MTurk workers across all 50 states (921 women, 646 men, and five nonbinary; Myears = 41.06 and SDyears = 13.37).2,3

Method

We assessed loneliness with two items ( r = .458, p < .001; Spearman-Brown reliability coefficient = .628): "How isolated from the rest of the world did you feel in the past week?" (1 = not at all and 7 = very much) and "How lonely did you feel in the past week?" (1 = not at all lonely and 7 = very lonely). We adapted the first item from the Philadelphia Geriatric Center Morale Scale ( Lawton, 1975) and the second item from a loneliness scale suited for large surveys ( Hughes et al., 2004).

We assessed happiness with three items: "I consider myself as (1 = not a very happy person; 7 = a very happy person)," "Compared with my peers, I consider myself (1 = much less happy; 7 = much more happy)," and "I think my life is (1 = not meaningful at all; 7 = very meaningful)" at α = .879. We derived the first item, and adapted the second item, from the Subjective Happiness Scale ( Lyubomirsky & Lepper, 1999), whereas we added the third item to expand the construct's scope to eudaimonic well-being. We assessed nostalgia as in Study 1 (α = .976).

Results and Discussion

Loneliness was negatively associated with happiness ( r = −.184, 95% CI [−0.232, −0.135], p < .001) but positively associated with nostalgia ( r = .186, 95% CI [0.137, 0.234], p < .001). Nostalgia was positively associated with happiness ( r = .199, 95% CI [0.150, 0.247], p < .001; Table 2).

Correlations Among Variables in Study 2 (U.S. Sample).

When we regressed happiness onto both loneliness and nostalgia, loneliness negatively predicted happiness, whereas nostalgia positively predicted happiness ( Figure 1, Panel B). Crucially, loneliness predicted stronger reductions in happiness after nostalgia had been statistically controlled for. If it were not for nostalgia, loneliness would have further reduced happiness. The indirect effect of loneliness was supported by bootstrapping ( Hayes, 2018; PROCESS Model 4; 5,000 bootstraps). The 95% CI for the indirect effect did not include 0 ( ab = .035; 95% CI [0.023, 0.049]) and neither did the 95% CI for the direct effect ( b = −.181; 95% CI [−0.219, −0.143]). Study 1 results were replicated.

Study 3

As another replication, we surveyed a UK sample from April 20 to 21, 2020, when infections were ascendant.

Participants

Studies 1 and 2 demonstrated effect sizes among key variables between r = .118 and r = .199. We estimated a slightly larger effect ( r = .15) and aimed for power (1 − β) = .95 at α = .05, requiring N = 571. We recruited 603 participants via Prolific Academic (427 women, 174 man, and two nonbinary; Myears = 34.00 and SDyears = 11.28).4

Method

Participants completed the same measures of loneliness ( r = .400, p < .001; Spearman-Brown reliability coefficient = .571), happiness (α = .838), and nostalgia (α = .975) as in Study 2.

Results and Discussion

Loneliness was negatively linked to happiness ( r=−.404, 95% CI [−0.478, −0.331], p < .001) and positively linked to nostalgia ( r = .085, 95% CI [0.006, 0.165], p = .036). Nostalgia was positively linked to happiness ( r = .119, 95% CI [0.040, 0.199], p = .003; Table 3).

Correlations Among Variables in Study 3 (UK Sample).

We regressed happiness onto both loneliness and nostalgia. Loneliness negatively predicted happiness, whereas nostalgia positively predicted happiness ( Figure 1, Panel C). Further, loneliness predicted stronger reductions in happiness after nostalgia had been statistically controlled for. If it were not for nostalgia, loneliness would have decreased happiness to a greater extent. The indirect effect of loneliness was corroborated with the bootstrapping method ( Hayes, 2018; PROCESS Model 4; 5,000 bootstraps). The 95% CI for the indirect effect did not include 0 ( ab = .010; 95% CI [0.0002, 0.023]) and neither did the 95% CI for the direct effect ( b = −.329; 95% CI [−0.386, −0.272]). The Study 1 and 2 results were replicated.

Study 4

The results of the three cross-sectional studies converged in supporting our model across cultures. Loneliness during the pandemic was associated negatively with happiness but positively with nostalgia, and nostalgia counteracted loneliness via rises in happiness. These conclusions were reinforced by an IDA (see Supplementary Material).

Experimental evidence is congruent with the assumed directionality. The logic of experimental-causal-chain designs ( Spencer et al., 2005) dictates, and evidence indicates, that loneliness causes unhappiness ( Cacioppo et al., 2006), and loneliness causes nostalgia ( Wildschut et al., 2006). This logic also dictates that nostalgia causes happiness. However, experimental evidence for a causal connection between nostalgia and happiness is lacking, as the evidence is cross-sectional ( Hepper et al., 2021; Sedikides et al., 2016), with a daily diary study producing conflicting results ( Newman et al., 2020). An exception is an experiment ( Cox et al., 2015; Study 1), where the researchers induced nostalgia-through an internet blog that hosts notes to persons one has loved-and assessed satisfaction with life ( Diener et al., 1985; e.g., "So far I have gotten the important things I want in life").

We revisited the issue in Study 4. We asked whether nostalgia (induced differently than Cox et al., 2015) would lead to happiness (measured differently than Cox et al., 2015), especially in the time of a pandemic when national moods are tinged by stress, anxiety, and depression ( Montemurro, 2020; Qiu et al., 2020; Wang et al., 2020). Further, we asked, for the first time, whether experimentally induced nostalgia has delayed effects-up to 2 days-on happiness; that is, we had two measurement points, Time 1 and Time 2. Finally, we examined the impact of experimentally induced nostalgia on positive affect (PA) and negative affect (NA). Nostalgia typically increases PA but not necessarily NA ( Leunissen et al., 2021; but see Frankenbach et al., 2020). However, no work has examined the influence of nostalgia on PA (and NA) over a 2-day period. PA and NA, along with happiness, are often regarded as indicators of a global construct, well-being ( Martela & Sheldon, 2019). Happiness refers to a global appraisal of one's well-being, whereas PA refers to an affective appraisal of it ( DeNeve & Cooper, 1998; Lü et al., 2014). We conducted Study 4 between April 19 and 24, 2020, when infections were rising in all of participants' countries.

Participants

To calculate power, we relied on Cox et al.'s (2015) effect of induced nostalgia on satisfaction with life and PA. Those effect sizes equaled d = .57 and d = .58, respectively, and were our "best guess" for sample size determination in Studies 4-6. We estimated a medium effect size ( d = .50) and aimed for a minimum of N = 176 to achieve power (1 − β) = .95 at α = .05 (G*Power 3.1; Faul et al., 2009). We recruited 209 MTurk workers (126 men and 83 women; Myears = 36.06 and SDyears = 11.63). Here, and in Studies 5 and 6, the manipulation had similar effects on happiness and PA/NA at Time 1 among participants who continued to Time 2 versus did not (see Supplementary Material).

Method

We induced nostalgia with the Event Reflection Task ( Sedikides et al., 2015), randomly assigning participants to conditions (nostalgia n = 102 and control n = 107). Experimental participants read a definition of nostalgia ("sentimental longing for the past"; Pearsall, 1988, p. 1266), brought to mind a typical nostalgic event from their lives, and immersed themselves in the experience. Next, they listed four event-relevant key words, were allotted 3 min to write about the event, and were required to write at least 50 words. Control participants followed the same protocol but for an ordinary event. Subsequently, all participants completed a manipulation check ( Wildschut et al., 2006; e.g., "Right now, I am feeling quite nostalgic"; α = .917).

Participants completed a state version ("Right now...") of the same happiness measure as in Study 1 ( r = .716, p < .001; Spearman-Brown reliability coefficient = .834). Further, they completed the Positive and Negative Affect Schedule (PANAS; Watson et al., 1988), which comprised 10 PA adjectives (e.g., enthusiastic, proud) and 10 NA adjectives (e.g., distressed, upset). We formed PA (α = .932) and NA (α = .979) scores.

One or 2 days after the original assessment, we retested as many participants as possible after administering a nostalgia-induction booster ( n = 83). Experimental participants ( n = 47) read: "In our previous questionnaire, you were asked to recall a nostalgic event and write down a few keywords. Do you still remember the event? Please write it down in the blank space below." Control participants ( n = 36) read equivalent instructions for the ordinary event. Afterward, all participants completed the same manipulation check (α = .970), happiness measure ( r = .760, p < .001; Spearman-Brown reliability coefficient = .864), and PA (α = .942) and NA (α = .978) measures as at Time 1 ( Table 4).

Correlations Among Variables in Study 4.

Results and Discussion

To examine whether the magnitude of the nostalgia effect changed across time, we tested the Nostalgia (nostalgia vs. control) × Time (Time 1 vs. Time 2) interaction on the variables of interest. Of the 209 participants who completed the experiment at Time 1, 83 completed Time 2. Thus, treating time as a within-subject variable in a mixed analysis of variance would result in loss of Time 1 data for 126 (209 − 83) participants. To avoid this, we used hierarchical linear modeling, with time points nested within participants. We treated the participant-level intercept as a random effect and used a general Satterthwaite approximation for degrees of freedom (the same model specification was used in Studies 5 and 6). The Nostalgia × Time interactions were not significant: manipulation check: F(1, 107) = 0.29, p = .594, = .001; happiness: F(1, 102) = 0.06, p = .810, = .000; PA: F(1, 92.5) = 2.21, p = .140, = .005; NA: F(1, 84.9) = 0.46, p = .499, = .001.5 These results indicate that a booster sufficed to reinstate the beneficial effects of nostalgia on happiness and PA over time.

Study 5

We tested the replicability of Study 4 findings with minor measurement alterations. The study ran over 2 days (April 29, 2020 = Time 1; April 30, 2020 = Time 2) when infections were rising in all countries from which our participants originated.

Participants

Based on prior research ( Cox et al., 2015), we estimated a medium effect size ( d = .50) aiming for a minimum of N = 176 to achieve power (1 − β) = .95 at α = .05. We recruited 196 MTurk workers (103 men and 93 women; Myears = 39.16, SDyears = 14.33, and 1 unreported).

Method

We induced nostalgia as in Study 4 (nostalgia condition n = 99, control condition n = 97). Responses to the manipulation check cohered (α = .962). We next gathered the dependent measures. For generalizability purposes, we used another measure of happiness ( Kahneman & Deaton, 2010): "Right now, how much do you experience happiness?" "Right now, how much do you experience enjoyment?" and "How much do you want to smile or laugh right now?" (α = .859). Based on PANAS, we formed PA (α = .943) and NA (α = .979) composites.

One day after the original assessment, participants ( n = 121) received a nostalgia-induction booster (nostalgia condition n = 60 and control condition n = 61) as in Study 4. Then, they completed the same manipulation check (α = .982), happiness measure (α = .916), and PA (α = .936) and NA (α = .963) measure as at Time 1 ( Table 5).

Correlations Among Variables in Study 5.

Results

We used hierarchical linear modeling to examine change in the nostalgia (vs. control) effect over time. None of the Nostalgia × Time interactions were significant-manipulation check: F(1, 152) = 3.33, p = .070, = .007; happiness: F(1, 138) = 0.01, p = .908, = .000; PA: F(1, 129) = 2.39, p = .125, = .006; NA: F(1, 122) = 1.06, p = .304, = .003.

Discussion

Study 5 replicated the Study 4 results with a different measure of happiness. The nostalgia-induction booster sufficed to reinstate nostalgia's beneficial effects over time (as in Study 4).

Study 6

In a partially preregistered experiment ( https://aspredicted.org/blind.php?x= 7 ff 8 ej), we tested the replicability of Study 4 and 5 findings in the absence of a nostalgia-induction booster. The study ran over 2 days (December 21, 2020 = Time 1; December 22, 2020 = Time 2) when infections were rising in all pertinent countries.

Participants

We estimated a medium effect size ( d = .50) aiming for a minimum of N = 210 to achieve power (1 − β) = .95 at α = .05. We recruited 209 U.S. MTurk workers (108 women and 101 men; M years = 38.34 and SD years = 11.22) but excluded 19 for failing to complete the manipulation, resulting in N = 190.

Method

We induced nostalgia as in Studies 4 and 5 (nostalgia condition n = 94 and control condition n = 96) and administered the same manipulation check (α = .929). We measured happiness (α = .876), and formed PA (α = .923) and NA (α = .980) composites, as in Study 5.

The day after, we recruited participants ( n = 136; nostalgia condition n = 74 and control condition n = 62) for the follow-up survey. With no mention of the nostalgic or ordinary event, we instructed them to complete the same manipulation check (α = .959), happiness measure (α = .890), and PA (α = .938) and NA (α = .977) measure as at Time 1 ( Table 6).

Correlations Among Variables in Study 6.

Results

We examined change in the nostalgia effect over time using hierarchical linear modeling. The Nostalgia × Time interaction was not significant for PA, F(1, 144) = 1.46, p = .228, = .004, or NA, F(1, 136) = 0.29, p = .589, = .001. However, the Nostalgia × Time interaction was significant for the manipulation check, F(1, 157) = 7.91, p = .006, = .018, and happiness, F(1, 150) = 4.99, p = .027, = .013. The effect of nostalgia on the manipulation check and happiness was significantly stronger at Time 1 than Time 2.

Discussion

Study 6 replicated the Study 4 and 5 Time 1 findings but not the Time 2 findings. In light of these results, it is prudent to conclude that the booster is important for producing the beneficial nostalgia effects at Time 2. However, we cannot definitively rule out the possibility that nostalgia's benefits may persist over time even in the absence of a booster. First, the failure to find significant effects on happiness and PA (and the manipulation check) at Time 2 may be due, in part, to reduced power stemming from attrition. All three effects were in the predicted direction, and, whereas the effects on the manipulation check and happiness were significantly smaller at Time 2, the effect size for PA was practically unchanged. Second, IDAs of Studies 4-6 (see Supplementary Material) revealed that (a) the magnitude of nostalgia effects at Time 2 did not vary significantly between studies (Nostalgia × Study interactions were not significant) and (b) the change in nostalgia effects from Time 1 to Time 2 did not vary significantly between studies (Nostalgia × Time × Study interactions were not significant). There was no evidence that diminution of nostalgia effects over time was significantly larger in Study 6 (when the booster was absent) than in Study 4 or Study 5 (when the booster was present).

General Discussion

Loneliness, a widespread psychological and societal problem ( Cacioppo, 2010; Haslam et al., 2018), is threatening to become an international health crisis during the pandemic ( Banerjee & Rai, 2020; Zandifar & Badrfam, 2020). Loneliness appears to have triggered a wave of nostalgia, from a surge in popularity of old-fashioned board games to social media trends like #MeAt20 and rebroadcasting of classic sporting events (The Guardian, 2020a). We theorized that nostalgia constitutes an antidote to loneliness. Nostalgia counters the negative aftermaths of loneliness (unhappiness), establishing a homeostatic correction.

We obtained support for our hypothesis in three surveys (Studies 1-3) conducted in three cultures (China, United States, United Kingdom) and at different stages of the pandemic (infections leveling off in China, rising in the United States/United Kingdom). Loneliness conduced to unhappiness but also to nostalgia. Nostalgia in turn elevated happiness, counteracting the adverse influence of loneliness. In three experiments, testing Western participants, nostalgia exerted a direct impact on happiness and PA. In two of them (Studies 4 and 5), following an induction booster, nostalgia heightened happiness and PA up to 2 days later. In Study 6, which did not involve a booster, the effect of nostalgia on Time 2 happiness and PA was in the predicted direction but nonsignificant, potentially due (at least in part) to reduced power stemming from attrition. Thus, an induction booster is sufficient to produce nostalgia's beneficial effects up to 2 days later, but more research is needed to determine whether it is necessary.

Our work enriched the literature. We proposed and supported empirically a suppression model involving the simultaneous operation of loneliness, nostalgia, and happiness. Also, we demonstrated that nostalgia can elevate happiness-all using varied methodological procedures and operationalizations of loneliness or happiness.

A possible limitation of our work is the small effect sizes. Yet, we obtained correlations that are typical of those reported in personality/social psychology ( Funder & Ozer, 2019; Gignac & Szodorai, 2016). More importantly, even small effect sizes can be meaningful and consequential ( Funder & Ozer, 2019). For example, nostalgia may increase appreciably happiness or help to counteract loneliness-at least in the short run-at the population level.

Another possible limitation concerns our use of cross-sectional mediation models, which has been criticized ( Maxwell & Cole, 2007; O'Laughlin et al., 2018). However, this criticism is largely inapplicable. First, we tested a specific theory, being interested in its empirical plausibility. Testing the cross-sectional mediation models was informative because it placed the theory at risk ( Anderson & Bushman, 1997; Fiedler et al., 2011)-a theory that has strong empirical grounding ( Sedikides et al., 2015). Second, we tested our theory by first assessing how nostalgia, via happiness, counters loneliness and then establishing the causal influence of nostalgia on happiness. An additional limitation is that we did not assess individual variation in fear of COVID-19 ( Ahorsu et al., 2020), a possible moderator of our findings.

Our findings have interventional implications, especially during the pandemic when social life is restricted. Nostalgia is easy to implement, as it can be self-initiated. Also, nostalgic engagement is mostly pleasurable ( Sedikides et al., 2015), and its effects likely sustained with some effort (Studies 4 and 5), although boosters may need to be frequent (e.g., two to three times a week, corresponding to the natural frequency of nostalgizing; Wildschut et al., 2006) and refer to diverse nostalgic experiences rather than repeat a single one ( Lyubomirsky, 2011). Such interventions can be cost- and time-effective. Nostalgia's potential can be harnessed to combat loneliness toward averting a downward spiral of declining mental health.

ORCID iDs
Xinyue Zhou https://orcid.org/0000-0001-5240-366X

Tiantian Mo https://orcid.org/0000-0001-8812-8938

Wanyue Li https://orcid.org/0000-0003-1924-0701

Notes

References

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Author Biographies

Xinyue Zhou is a professor of psychology and marketing at Zhejiang University, researching complex emotions.

Constantine Sedikides is a professor at the School of Psychology, University of Southampton, interested in self and identity.

Tiantian Mo is a PhD student at the School of Management, Zhejiang University, interested in consumer psychology.

Wanyue Li is a PhD student at the School of Management, Zhejiang University, interested in social perception and consumer behavior.

Emily K. Hong is a research fellow at the School of Psychology, University of Southampton, investigating self, identity, and emotion across time.

Tim Wildschut is a professor at the School of Psychology, University of Southampton, researching emotions, memories, and intergroup relations.

Handling Editor: Lisa Libby

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The Restorative Power of Nostalgia: Thwarting Loneliness by Raising Happiness During the COVID-19 Pandemic - Xinyue Zhou, Constantine Sedikides, Tiantian Mo, Wanyue Li, Emily K. Hong, Tim Wildschut, 2021

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Abstract Lockdowns during the COVID-19 pandemic increased the risk for loneliness. We tested whether nostalgia counteracts loneliness via rises in happiness. We conducted surveys in China ( N = 1,546), the United States ( N = 1,572), and the United Kingdom ( N = 603).

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Tetriksen pelaaminen auttaa traumoista selviytymisessä

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Toteutus ei onnistunut niin kuin piti mutta siitä saatiin luotettavaa ja tärkeää tietoa

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https://gspsy.fi/suomen-tunnetuimmat-psykologiset-tutkimukset/

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Ihmisen psyyke on kaiken toimintamme keskiössä. Yhden teorian mukaan kaikki mennyt muovaa meitä ja muokkaa käytöstämme, tietoisesti tai tiedostamattomasti, halusimme tai emme. Ihmisen psykologiaa tutkitaan monilla eri menetelmillä ja alaa on opiskeltu jo vuosisatojen ajan.

Eri psykologit ovat toteuttaneet erilaisia kokeita saadakseen paremman käsityksen ihmisen mielen toiminnasta. Aina ei kuitenkaan ole ollut kyse nykyaikana eettiseksi luokitellusta kokeesta ja nykyvinkkelistä katsottuna jotkin metodit ja menetelmät ovat olleet vähintäänkin arveluttaviksi luokiteltavia. Seuraavien rivien myötä esittelemme muutamia tunnetuimmista tutkimuksista, jotka ovat yliopistovuosilta tuttuja jokaiselle psykologiaa opiskelleelle.

Milgramin tottelevaisuuskoe

1960-luvulla mies nimeltä Stanley Milgram suoritti psykologisen kokeen, jota kutsuttiin Milgramin tottelevaisuuskokeeksi. Kyseessä on yksi sosiaalipsykologian keskustelluimmasta ja siteeratuimmasta kokeesta.

Koe toteutettiin seuraavasti: lehti-ilmoituksella kerättiin koehenkilöiksi suuri joukko ihmisiä eri ikäluokista, ammattiryhmistä ja sosioekonomisista ryhmistä. Yhdistävä tekijä oli ainoastaan sukupuoli, sillä kaikki kokeeseen osallistuneet henkilöt olivat miehiä. Miehet eivät tienneet ennen kokeeseen saapumista, minkälaisesta kokeesta oli kyse.

Vasta saapuessaan kokeeseen Yalen yliopistoon, he saivat selville kokeen toteutustavan. Laboratoriossa koehenkilö tapasi tutkijan sekä toisen "koehenkilön", joka todellisuudessa oli näyttelijä, mutta joka esiteltiin koehenkilölle toisena, itsensä kaltaisena lehti-ilmoitukseen vastanneena koehenkilönä.

Kyseisessä alkuasetelmassa kumpaisellekin koehenkilölle arvottiin roolit ja näyttelijäkoehenkilöstä tuli oppija ja lehti-ilmoitukseen vastanneesta henkilöstä opettaja. Oppijaksi päätynyt sidottiin sähkötuoliin ja opettajalle annettiin näyte sähköiskuista, joita oppijalle saatettaisiin antaa. Tämän jälkeen opettajaksi päätynyt vietiin iskugeneraattoriksi kutsutun laitteen ääreen.

Opettajan tuli lukea oppijalle lyhyitä tehtäviä ja oppijan tuli vastata niihin. Oppijan vastatessa väärin sai opettaja mahdollisuuden antaa oppijalle sähköiskun. Iskun voimakkuus nousi jokaisen väärän vastauksen myötä. Ensimmäinen isku oli 15 volttia, mutta nousi väärien vastausten myötä jopa kaksi kertaa Suomen sähköverkkoa kovempaan, 450 voltin iskuun.

Opettaja näki generaattorissa koko ajan selkeästi sen, mikä voimakkuus seuraavassa iskussa oli ja mikä sen voimakkuusaste oli. Viimeisimmissä iskuissa luki "vaara: vakava isku" ja yhdessä arvoituksellisesti vain "XXX". Osallistujille kerrottiin etukäteen, että voimakkaimmat iskut olisivat kivuliaita, mutta ne eivät aiheuttaisi todellista vaaraa.

Milgranin eettisestä näkökulmasta vähintäänkin arveluttavan kokeen ideana oli tietenkin nähdä, totteleeko kokeeseen osallistunut henkilö, joka uskoi antavansa sähköiskuja toiselle henkilölle. Tällainen käytös johtaa juurensa tottelevaisuuskasvatukseen, joka opettaa, että auktoriteettia on kuunneltava ja on toimittava, kuten käsketään.

Kokeen edetessä ja iskujen kovetessa valtaosa osallistujista alkoi epäröidä, eikä olisi halunnut antaa lisää iskuja, kannusti auktoriteetti antamaan iskuja edelleen. Vaikka viimeiset iskut olivat huomattavan voimakkaita ja mahdollisesti olisivat voineet tappaa toisen henkilön, käskyjen noudattaminen sai suurimman osan koehenkilöistä tottelemaan ja antamaan sähköiskun joka tapauksessa.

Kokeen historiallisesti tunnetuimmassa asemassa, jossa auktoriteetti ja sähköiskuja antanut henkilö olivat yhdessä huoneessa ja uhri puolestaan toisessa, osoitti, että peräti 65 % kokeeseen osallistuneista, absoluuttisina lukuina 26/40 henkilöä, ei vastustanut auktoriteettia, vaan suoritti omista tuntemuksistaan ja epäilyksistään huolimatta testin aina 450 voltin pisteeseen saakka.

Koe suoritettiin osittain uudelleen 45 vuotta myöhemmin, jolloin tulokset olivat huomattavan samansuuntaisia, kuin ensimmäisellä testikerralla. Se, ettei aikakauden muutokset tai sosiaalinen murros ollut juurikaan vaikuttanut toiminnan säätelyyn, auktoriteettiin suhtautumiseen tai tottelevaisuuteen, oli omassa lajissaan merkittävä löydös.

Uusintakokeesta ja sen tuloksista on julkaistu Santa Claran yliopistossa psykologian professorina työskentelevän Jerry M. Burgerin artikkeli American Psychologist -lehdessä tammikuussa 2009. Burger suoritti vuonna 2006 Milgrainin kokeeseen pohjautuvan uusintakokeen, jonka tulokset osoittivat, että tottelevaisuus oli lähes samaa luokkaa, kuin 45 vuotta aiemmin.

Stanfordin vankilakoe

Toinen erittäin laajasti tunnettu psykologinen koe on nimeltään Stanfordin vankilakoe. Tämä koe toteutettiin Kaliforniassa, Stanfordin yliopistossa tutkija Philip Zimbardon johdolla vuonna 1971. Kokeessa haluttiin tutkia sitä, miten ihmiset reagoivat valtasuhteisiin vankilaympäristössä, jossa ei ole täsmällisesti esitettyjä sääntöjä. Konstruoidussa asetelmassa mukana olevat henkilöt jaettiin vartijoihin ja vankeihin.

Kokeeseen valittiin 24 koehenkilöä, jotka olivat kaikki vapaaehtoisia miespuolisia opiskelijoita. Kaikki kokeeseen osallistujat oli ennen kokeeseen hyväksymistä testattu ja todettu henkisesti normaaleiksi yksilöiksi. Kaikki tulivat keskiluokkaisista ja koulutetuista perheistä eikä kenelläkään osallistuneista ei ollut taustalla mielenterveysongelmia eikä päihteiden väärinkäyttöä.

Kokeen alkaessa osallistujat jaettiin kahteen ryhmään. Toinen ryhmä edusti vankeja ja toinen joukko vanginvartioita. Osallistujat vietiin toteuttamaan koetta yliopiston kellariin, jossa olevaan laboratorioon oli rakennettu vankilan puitteet. Vangit puettiin vanginasuihin, jotka olivat keskenään identtisiä. Vartioille annettiin identtiset khakista tehdyt uniformut, aurinkolasit, kumipamppu sekä pilli.

Koe toteutettiin seuraavasti. Vartijoiden oli pidettävä vangit kurissa ja järjestyksessä ja huolehdittava siitä, että vangit käyttäytyisivät vartijoita kohtaan kunnioittavasti. Mitään erikoisempaa koulutusta tai ohjeistusta ei annettu lukuun ottamatta sitä, että väkivallankäyttö oli kielletty.

Kokeen oli määrä kestää peräti kaksi viikkoa, mutta ei kulunut kuin kuusi päivää, kun koe jouduttiin lopettamaan kesken. Keskeyttämistä vaati erityisesti opiskelija Christina Maslach, joka toimi kokeeseen osallistujien haastattelijana. Keskeytyksen syy oli se, että vartijat alkoivat kohdella vankeja alati kasvavalla julmuudella ja raakuudella.

Koetta on pidetty todisteena siitä, että lähes kuka tahansa meistä pystyy julmaan ja pahaan toimintaan lähimmäistään kohtaan, jos tähän annetaan rajoittamaton valta ilman seurauksia. Stanfordin vankilakoe on ollut heti toteuttamishetkestään lähtien kovan kritiikin kohteena epäeettisyytensä ja mahdollisesti myös epätieteellisyytensä takia. Näistä äärimmäisen räikeistä epäkohdista huolimatta koe puhututtaa vielä tänäkin päivänä.

Tästä huolimatta tämä jo lähes viisi vuosikymmentä sitten suoritettu koe on edelleen äärimmäisen tunnettu esimerkkitapaus, josta lähes jokainen vähääkään psykologiasta kiinnostunut on kuullut jossain yhteydessä. Stanfordin vankilakoe on hyvä osoitus siitä, että käytetyt metodit ja tutkimuksen validiustaso eivät välttämättä vaikuta siihen, jääkö se historiankirjoihin vai ei.

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Ihmisen psyyke on kaiken toimintamme keskiössä. Yhden teorian mukaan kaikki mennyt muovaa meitä ja muokkaa käytöstämme, tietoisesti tai tiedostamattomasti, halusimme tai emme. Ihmisen psykologiaa tutkitaan monilla eri menetelmillä ja alaa on opiskeltu jo vuosisatojen ajan. Eri psykologit ovat toteuttaneet erilaisia kokeita saadakseen paremman käsityksen ihmisen mielen toiminnasta.

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Tulos kertoi, että aivoilla on vaikutus ihmisten liikerataan ja, että ahdistuneet ihmiset kävelevät kallistuneemmin vasempaan suuntaan kuin oikeaan.

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Ihminen tottelee auktoriteettia ja toimii omien epäilysten vastaisesti. Tottelevaisuus ei ollut muuttunut 45 vuoteen kun testi tehtiin uudestaan. Tämä todistaa sen että kyse ei ole sosiaalinen ympäristö vaan ihmisen opittu tapa totella auktoriteettia.

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Tarja Stenberg ja hänen Helsingin yliopiston Helsinki Sleep Team- tutkimusryhmä

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Elimistö kokee unen puutteen vaaratilanteena.

Univaje aktivoi luonnollisen immuunijärjestelmän. Elimistössä syntyy lievä tulehdustila.

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Unella on paljon tärkeitä tehtäviä. Nukkuminen parantaa muistia, säätelee mielialaa ja huuhtoo kuona-aineita aivoista. Unen puute aiheuttaa tulehdustilan ja lisää monien sairauksien riskiä.

Makaamme karkeasti ottaen kolmasosan elämästämme paikallamme puolustuskyvyttöminä.

Kun nukkumista kuvailee näin, koko homma voi tuntua järjettömältä.

Nukkuessa tietoinen yhteys ympäröivään maailmaan on poikki. Emme havaitse ympäristössä mahdollisesti vaanivia vaaroja ja voi puolustautua niiltä. Emme myöskään pysty keräämään ravintoa tai lisääntymään - täyttämään muita hengissä säilymisen kannalta välttämättömiä tarpeita.

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Unitutkimus | Jatkuva tulehdustila, muistiongelmia ja tie muistisairauksiin - Näin pienikin univaje meihin vaikuttaa

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Unella on paljon tärkeitä tehtäviä. Nukkuminen parantaa muistia, säätelee mielialaa ja huuhtoo kuona-aineita aivoista. Unen puute aiheuttaa tulehdustilan ja lisää monien sairauksien riskiä. Makaamme karkeasti ottaen kolmasosan elämästämme paikallamme puolustuskyvyttöminä. Kun nukkumista kuvailee näin, koko homma voi tuntua järjettömältä. Nukkuessa tietoinen yhteys ympäröivään maailmaan on poikki.

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tutkimuksen linkki
https://www.nature.com/articles/srep24828

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Introduction

Short sleep duration, complaints of poor sleep quality and diagnosed sleep problems have in epidemiological studies been associated with metabolic disorders, which relate to low-grade chronic inflammation, including cardiovascular diseases, metabolic syndrome, obesity, and type 2 diabetes mellitus1,2,3,4. However, the functional pathways and molecules that mediate these effects are largely unknown.

Several previous studies have shown that experimental restriction of sleep to 4-5 h per night for 1-2 weeks activates immune responses, down-regulates gene pathways for macromolecular biosynthesis and metabolic processes8, and modifies glucose metabolism by inducing insulin resistance. However, the reported serum lipid levels, central factors in the pathogenesis of atherosclerosis, have shown only mild, inconsistent, or no effects, leaving open the question what specific metabolic modulations induced by sleep restriction could explain the increased association of restricted sleep to atherosclerosis, which is characterised by slow build-up of lipid plaques in the walls of the arteries, promoted by inflammatory responses and decrease in macrophage reverse cholesterol transport (RCT)15.

The duration of sleep restriction in previous studies has ranged from one to five days, which in the development of chronic diseases is a short period. In trying to understand the role of restricted sleep as a predisposing factor for such diseases, the key questions are: how do the short-term modifications in metabolism and inflammation develop when the duration of the sleep restriction is prolonged, and are these modifications such that could explain the association between restricted sleep and increased risk for e.g. atherosclerosis, as evidenced by the epidemiological studies?

The assessment of circulating lipid profiles using nuclear magnetic resonance (NMR) spectroscopy goes beyond the typically measured total lipids, like total cholesterol and triglycerides, and allows detailed characterization of many lipoprotein features at the subclass level, including the size of the particles, which are important in lipid physiology and pathophysiology16,17. Analysis of circulating lipid molecules based on mass spectrometry (MS), which gives an extensive profile of individual lipid molecules but does not quantify lipoprotein-related measures, has previously been applied in circadian research18,19,20,21. Recently one short-term sleep deprivation study22 and one partial sleep restriction study23 have applied MS-based lipid analyses in serum, while one study used NMR to assess urine metabolites in short-term sleep deprivation24, but NMR-based lipoprotein subclass analyses have not been used to analyse the effects of sleep loss. The assessment of the relationship between sleep/sleep insufficiency and metabolomics profiles in large epidemiological cohorts has not, to our knowledge, been reported before.

The short-term effects of insufficient sleep were assessed in a highly controlled experiment where a group of volunteers restricted their sleep to 4 hours per night during 5 days (sleep restriction, SR, N = 14 cases and N = 7 controls). The results focusing on the immunological effects at the level of gene expression, cytokines, and CRP have been previously published5. The putative longer-term effects were assessed in real-life conditions using two independent epidemiological cohorts (DILGOM25, N = 518, and Young Finns Study, YFS26, N = 2221), where the insufficiency of sleep was evaluated based on self-reported sleep parameters (subjective sleep insufficiency, SSI). Genome-wide transcriptome and NMR-based metabolome were obtained from all three samples, and mass spectrometry-based lipidome from the SR study participants (see flow of the analyses depicted in Supplementary Fig. S1).

Results

Subjective sleep insufficiency in epidemiological cohorts

Partial sleep loss was induced experimentally as 4 h sleep/night for 5 nights for 14 healthy young males in the SR study (including also 7 control subjects; total N = 21; age (mean ± s.d.) 23.2 ± 2.2 y, Supplementary Table S1)5. To study sleep loss in real life conditions, subjective feeling of insufficient sleep was assessed using questionnaire information in two epidemiological samples. In the DILGOM subsample with information of subjective sleep sufficiency and omics data (N = 472, 46% men, age (mean ± s.d.) 51.9 ± 13.8 y, Supplementary Table S1)25, we used the question "Do you, in your opinion, sleep enough?". The answer options were dichotomised, combining subjects reporting to sleep enough "almost always" (N = 168) or "often" (N = 218) to a phenotype of 'subjective sufficient sleep' (noSSI, N = 386). Subjects reporting to "seldom or almost never" (N = 86) sleep enough were considered as having 'subjective sleep insufficiency' (SSI, N = 86, 18.2%).

In the Cardiovascular Risk in Young Finns Study ("Young Finns Study", YFS; N = 2221, 55% men, age (mean ± s.d.) 37.7 ± 5.0 y, Supplementary Table S1) replication cohort26, sufficiency of sleep was assessed using two questions: one addressing self-reported sleep duration ("How many hours do you usually sleep per night?") and another on self-reported sleep need ("How many hours of sleep do you need per day to feel well rested?"). Subjective sleep duration was subtracted from subjective sleep need, and individuals sleeping more than an hour over their sleep need (N = 37, 1.7%) were excluded from further analyses. Remaining subjects were grouped into three groups based on their level of SSI: no (or only mild) SSI (sleep need - sleep duration = −1...0...1 h; N = 1825, 82.2%), moderate SSI (1.5-2 h; N = 304, 13.7%), and heavy SSI (>2 h; N = 55, 2.5%). Despite the differences in the questions and age groups, the overall prevalence of SSI (mSSI or hSSI), 16.2%, in the YFS sample was quite similar to the 18.2% found in the DILGOM. In accordance with these results, the prevalence of "sleep debt", using closely similar criterion as used in the YFS sample, has been earlier found to be 20% in 1004 French young adults27.

Gene expression in lipid pathways

Pathway analysis of differentially expressed genes

Gene expression profiles were analysed from peripheral blood mononuclear cells (PBMC) in the SR study (N = 9 cases, N = 4 controls)5 and whole blood in the DILGOM cohort (N = 472) using microarrays. Lipid-related pathways were enriched among transcripts down-regulated after 5 nights of experimental SR5. In the epidemiological DILGOM sample, linear regression was used to correlate RNA expression with SSI, adjusting for age and gender. Transcripts from 725 genes (2% of the total 35,420 transcripts analysed) had lower expression among subjects with SSI (N = 86) compared to subjects with no sleep complaints (N = 386) (pointwise P < 0.05). Enrichment of biological processes among these genes was analysed using DAVID Functional Annotation Clustering28. Five Gene Ontology (GO) clusters had enrichment scores >1.3 (referring to geometrical mean of the P values of the pathways <0.05) in subjects with SSI ( Supplementary Table S2).

The GO cluster 5 ("Lipid cluster", P = 0.045, Supplementary Table S2 and Supplementary Fig. S2) included 4/5 of the top pathways that were enriched among down-regulated genes in the SR study (permuted P < 0.001) reported previously ( Table 1)5. The Lipid cluster remained significant ( P  < 0.05) also after including BMI as a covariate in the explanatory model.

Table 1 Lipid pathways down-regulated in experimental sleep restriction (SR) and epidemiological subjective sleep insufficiency (SSI).

The common pathways in the experimental SR study and the DILGOM sample were: Cholesterol transport, Sterol transport (both P = 0.048), Cholesterol homeostasis and Sterol homeostasis (both with a borderline significance of P = 0.052) ( Table 1). The genes contributing to these GO pathways in the DILGOM sample were ATP-binding cassette, sub-family G, member 1 (ABCG1), caveolin 1 (CAV1), Niemann-Pick disease, type C1 (NPC1), and Niemann-Pick disease, type C1, gene-like 1 (NPC1L1), while in the experimental SR study they were ABCA1 and NPC1. All genes and pathways of the Lipid cluster are shown in Supplementary Fig. S2.

Gene expression replication

Gene expression was measured in the YFS replication sample (N = 1407) from whole blood using Illumina microarrays to evaluate whether the expression of the genes found in the down-regulated pathways in DILGOM (ABCG1, CAV1, NPC1, and NPC1L1) was lower in subjects with SSI also in this sample. The ABCG1 finding replicated ( P  < 0.05) in this cohort, supporting the suppressive effect of subjective sleep loss on this cholesterol transporter.

Serum lipids and lipoproteins

NMR metabolomics

Next, we examined whether the transcriptional changes were reflected in the serum lipid and lipoprotein profiles using NMR-based metabolomics analyses. This high-throughput method provides concentration information for over 200 metabolic measures, including different sized VLDL, IDL, LDL, and HDL particles, various fatty acids, amino acids, and small molecule energy metabolites29.

Concentration of lipoprotein particles and their components

In the SR study (N = 14 cases, 6 controls), the number of small, medium, and large LDL particles ( P after correction <0.01) as well as small VLDL particles ( P < 0.05) was decreased after SR compared to BL, while there were no changes in the number of small and medium size HDL particles ( Fig. 1A, Supplementary Table S3). Large HDL particles showed a trend of increase during SR ( P before correction for multiple testing <0.05, not significant after correction). These changes were also reflected by changes in LDL/VLDL structural protein apoB-100. ApoB-100 levels decreased ( P  < 0.005) whereas apoA-I (major structural protein in HDL) levels did not change.

Changes in lipoprotein particles in ( A) experimental sleep restriction (SR) and ( B) epidemiological subjective sleep insufficiency (SSI). Concentration differences of different sized very low density (VLDL), intermediate density (IDL), low density (LDL), and high density (HDL) lipoprotein particles. ( A) Experimental SR compared to baseline (BL, normalised to 1) (* P < 0.05, paired t test; N = 14). ( B) DILGOM subjects with SSI compared to subjects without SSI (noSSI, normalised to 1) (*pointwise P  < 0.05, linear modelling adjusting for sex and age; N = 414).

In the DILGOM sample (N = 414), the number of serum large HDL particles was lower among individuals with SSI (pointwise P < 0.05). SSI had an independent association to large HDL concentration also after adding BMI as a covariate in the model ( P < 0.05). There was no significant difference in the levels of any of the LDL or VLDL subclasses, although there was a consistent trend for increase in both LDL and VLDL particles of all sizes ( Fig. 1B, Supplementary Table S3).

The lower number of large HDL particles in subjects with SSI replicated ( P < 0.005) in the YFS sample (N = 2077) ( Fig. 2). In this sample, number of XL HDL was also lower ( P < 0.005). No differences were observed in small or medium HDLs. For the epidemiological samples, age and gender were adjusted for in the linear regression model. The decrease in large HDL was independently associated with SSI ( P  < 0.01) also when probable self-reported obstructive sleep apnoea (OSA) was included in the model.

Large (L) and extra-large (XL) HDL decreased with increasing level of subjective sleep insufficiency (SSI) ( P < 0.005; N = 2077), whereas the expression of interleukin 1 β (IL1B) and toll-like receptor 4 (TLR4) genes was higher in subjects with SSI ( P < 0.005 and P  < 0.05, respectively; N = 1407). NoSSI = no or only mild SSI, mSSI = moderate SSI, hSSI = heavy SSI. HDL graphs represent mean ± s.e.m. concentrations in serum. Gene expression is shown relative to the mean expression in the noSSI group (relative mean ± s.e.m.). Effect of SSI on HDL concentrations and gene expression was modelled with linear regression adjusting for age and sex.

Mass spectrometric measurements

In the SR study (N = 14 cases, N = 7 controls), molecular lipids were further analysed with MS-based lipidomics. Altogether 20 lipids were increased after SR in the sleep-deprived cases as compared to the controls ( Supplementary Table S4). The increased lipids comprised mostly polyunsaturated phosphatidylethanolamines (PE) and phosphatidylcholines (PC) ( P < 0.05; Supplementary Table S4).

Network analysis on experimental SR

The findings from the SR study suggested that cholesterol transport had declined and inflammation increased. An important transcriptional regulator of the RCT is the nuclear liver X receptor (LXR) signalling, which promotes RCT and decreases inflammation. We thus hypothesized that decrease in LXR activity could be mediating the effects of sleep restriction on the immune system and metabolism ( Fig. 3, Table 2). Alternatively, the activity of lipid transfer proteins could be changed. To study these hypotheses and the associations between the observed changes, we selected relevant immunological, metabolic, and sleep variables measured in the experimental SR study (listed in Supplementary Table S5), including the parameters where changes had been detected also in the epidemiological cohorts, and performed a dependency network analysis ( Supplementary Fig. S3).

( A) Proposed model to explain the findings. 1 Sleep loss activates inflammatory responses through toll-like receptors (TLR)5 2 suppressing liver X receptor (LXR) activity33,34,35. 3 Decreased LXR activity leads to decreased reverse cholesterol transport (RCT) and synthesis of fatty acids (FA) and triglycerides (TG), and increased immunological activation30,31,32. (Red arrows showing increase, green arrows decrease.) ( B) The figure summarises our findings from transcriptomics and NMR metabolomics in experimental (E) sleep restriction (SR; N = 21), and in the DILGOM epidemiological cohort (D; N = 518) and Young Finns Study replication cohort (Y; N = 2221) subjects with subjective sleep insufficiency (SSI). Numbers 1 and 3 refer to the locations in the model proposed in Fig. 3A.(a) Up-regulation of TLR and other inflammatory genes/gene pathways in SR reported in5. Pathway analysis for up-regulated genes in subjects with SSI in DILGOM confirmed up-regulation of B-cell activation, lymphocyte activation, and immune system development ( P < 0.05) also at epidemiological level. Individual genes showed only non-significant trends for higher expression in SSI. (b)TLR4 and several inflammation-related genes had higher expression among subjects with SSI in the replication sample Young Finns Study. (c) Increase in proinflammatory cytokines IL-1b and TNF-a assessed by in vitro stimulation of white blood cells and reported in7.(d) Higher expression of genes encoding for proinflammatory cytokines at epidemiological level in subjects with SSI. (e) Down-regulation of genes/gene pathways of reverse cholesterol transport assessed with transcriptomics and reported in the present publication. Concentrations of large HDL in serum measured using NMR metabolomics. (f) Acetyl-CoA carboxylase (ACC), the rate-limiting enzyme of FA synthesis, was down-regulated in SR and DILGOM SSI. No major differences were observed in the expression of other FA and TG synthesis genes in SR or SSI.(g) FA and TG measured with NMR metabolomics in experimental SR and DILGOM. Paired t tests used for comparing SR to BL, and linear regression used for modelling the effect of SSI on gene expression or lipid concentration, adjusting for age and sex. See abbreviations in Table 2.

Table 2 Variables in Fig. 3B.

Immunological parameters

Inflammation suppresses LXR activity via toll-like receptors (TLR). We have earlier shown that the gene coding for TLR4 was up-regulated in our 5 nights' SR protocol5. Also proinflammatory cytokines interleukin 1β (IL-1b) and tumour necrosis factor α (TNF-a) have been shown to suppress LXR activity36 ( Fig. 3), and these cytokines have been consistently shown to increase in experimental sleep restriction7,37. We observed higher expression of the gene encoding for TNF-a in free-living individuals with SSI in the DILGOM sample (pointwise P < 0.05), and genes encoding for both IL-1b and TNF-a in the Young Finns replication sample ( P < 0.005 and P < 0.05, respectively) ( Figs 2 and 3). In addition to the cytokines, up-regulation of inflammation-related genes encoding for TLR4 ( Fig. 2), MyD88 (an essential signal transducer in the IL-1 and TLR pathways), inducible prostaglandin endoperoxide synthase (cyclooxygenase 2, PTGS2), and Fas cell surface death receptor (FAS) - observed in the experimental SR study - replicated in the YFS sample ( Fig. 3). Increased inflammation could be further augmented through decreased LXR activity30.

Dependency network analysis

In order to distinguish direct and indirect interactions of these immune, metabolic and sleep variables, we utilised undirected Gaussian graphical model where the variables are connected if and only if their partial correlation is significantly non-zero (using FDR multiple testing for the selection of edges) to visualise the dependencies as a network38.

The lipids that were increased after SR associated to several immunological parameters ( Supplementary Fig. S3; P < 0.05 for all associations shown in the figure). The correlation analysis revealed significant positive associations with PE(38:3), PE(38:5e), PE(36:2e), ChoE(16:1) and B-cells. PE(38:3) was further negatively correlated with TNF-a, which was positively correlated with interleukins 18 and 1 and interferon-γ (IFNG). LXRA associated positively with B cells and TLR8, and negatively with ABCA1, NRIP1 and LXRB. TLR4 had a strong negative association with NPC1 and ABCA1 ( Supplementary Fig. S3), as would be expected if LXR activity was decreased.

In the control subjects ( Supplementary Fig. S4), the associations between the variables were fewer and weaker than in the experimental group. Particularly, scarce associations between the lipids and the immunological variables were observed. As the networks are baseline-corrected, they show the changes occurring between baseline and sleep restriction timepoint. As the control group was not subjected to any treatment (besides staying in the laboratory) between these timepoints, it was expected that no major changes would be detected.

Lipid transfer protein and enzyme activities in SR

Lipid transfer proteins comprise the two key regulators of serum lipid balance between lipoproteins. However, we did not find significant changes in the activity of cholesterol ester transfer protein (CETP) or phospholipid transfer protein (PLTP) in the experimental SR study. Furthermore, no changes were observed in the activity of lecithin-cholesterol acyltransferase (LCAT), the enzyme converting HDL unesterified cholesterol to cholesteryl ester, or the atheroprotective enzyme paraoxonase 1 (PON1) linked to antioxidative properties of HDL particles.

Discussion

The main finding of the present study was that restriction of sleep either experimentally or in natural living conditions modified lipoprotein metabolism and immune responses. The changes were detected at the level of transcriptome as well as in the circulating lipid profile. The transcriptional changes - the down-regulation of reverse cholesterol transport-related gene pathways - were similar in the relatively short term exposure of the experimental sleep restriction and in the epidemiological cohorts among subjects reporting insufficient sleep. Interestingly, the lipoprotein profile showed decreased LDL in experimental SR, resembling LDL changes in acute-phase response39, but in epidemiological SSI large HDL was decreased. Decrease in HDL has been regarded as one important risk factor for cardiovascular diseases40.

The classical view on the relationship between serum lipid levels and risk for cardiovascular events, formulated based on the findings of the Framingham study41 and since confirmed by many epidemiological studies, states that serum high LDL and low HDL cholesterol level is a risk combination for cardiovascular events42. These findings have encouraged efforts to develop treatments with the aim of either to lower LDL levels (e.g. statins) or increase HDL levels (e.g. CETP inhibitors and niacin). Particularly the latter approach has been a disappointment: pharmacological increase of serum HDL levels has not affected the risk of cardiovascular diseases42, indicating that the mere serum HDL cholesterol concentration is not a sufficient metrics to explain its epidemiologically verified cardioprotective effect. HDL can protect against atherosclerosis by multiple mechanisms, including the ability to efflux cholesterol from endothelial macrophages (macrophage reverse cholesterol transport)43, or through anti-inflammatory44, antioxidative45 and antiapoptotic46 pathways. A newly discovered regulation by microRNAs adds to the complexity of the task to discover mechanisms that explain the relationship between HDL and cardiovascular disease (CVD) risks47. Moreover, modulations in HDL particle composition can transform it to dysfunctional and, through this modulation, increase the risk of CVD40.

Combining the knowledge of the epidemiologically verified increased risk for CVD associated with the low HDL/high LDL lipid profile and short/insufficient sleep, we expected to measure such lipid profiles in SR and in persons with SSI. This prediction did not prove quite correct. In SR we measured, using the NMR metabolomics, decreased levels of LDL while we found no significant changes in HDL levels. In the SSI subjects we found decreased HDL levels but not significant differences in LDL levels. The one week experimental SR may have been too short to affect the number of HDL particles, while in the epidemiological samples, the number of large HDL particles was lower among those who reported insufficient sleep. Since the nature of conditions that induce insufficient sleep is often persistent48,49,50,51, we argue that the SSI subjects reporting insufficient sleep had been exposed to insufficient sleep for a longer period than those in the five day experimental sleep restriction study. We propose that the lipid profile is modulated in the course of exposure to insufficient sleep from low LDL levels at early phase of sleep insufficiency to low HDL levels upon longer exposure. However, in a cross-sectional study we cannot provide direct evidence on the duration of SSI for those who reported it. The low LDL concentration in the SR may have been induced by the inflammation, particularly by the activation of the acute phase response, induced by the sleep restriction5.

While some previous gene expression studies have indicated that cholesterol/lipid metabolism is regulated by sleep-wake cycle and sleep restriction could modify it, detailed characterization of lipid profiles has remained scarce. It has been shown that serum triglyceride levels decreased following restriction of sleep to 4 hours on 5 consecutive nights12, and also that myeloperoxidase-modified LDL particles increased under similar conditions13. In a recent study, no changes in blood total cholesterol, LDL, HDL, or triglycerides were found after sleep restriction to 4 hours on 5 nights14. Two recent studies have measured lipid profiles in human blood samples using mass spectrometry analysis after polar and non-polar extraction of the samples after a short term (24 h) total sleep restriction22 and a partial sleep restriction for five days23. In both studies, the majority of the altered, identified species, consisted of lipid species (including phospholipids, sphingolipids, acylcarnitides and phosphatidylcholines). In the acute SR study22, only increases in lipid levels were observed after the deprivation period, while in the partial SR study23 also declines were recorded. In the present SR study, all significant changes from BL to SR, measured using the mass spectrometry technique, were increases, mainly in phosphatidyl ethanolamides, phophatidyl cholines, triglycerides and cholesterol esters. In spite of some discrepancies in the results, possibly explained by different extraction and other methods and/or differences in the experimental arrangements, these three independent studies point out that restriction of sleep, either acutely or partially for a longer period, significantly affects serum lipid levels, as measured using mass spectrometry. In the present study, also NMR spectroscopy measurement was able to track changes in lipid profiles under conditions of restricted sleep, further confirming that this condition modifies lipid metabolism.

The results from the gene expression pathways were more consistent than those of the lipid profiles. The cholesterol pathways that were down-regulated in SR and SSI included members of the ATP-binding cassette families A and G (ABCA1 and ABCG1). ABCA1 and ABCG1 facilitate the efflux of free cholesterol and phospholipids from macrophage-foam cells to HDL particles. Of all cholesterol carried by HDL, the proportion originating from peripheral macrophages is low compared to liver (75%) and intestine (20%) produced HDL. However, this route of removal of cholesterol (macrophage RCT) has been regarded as an important (but not only) component in retaining cholesterol balance in arterial endothelium43. Since ABCA1 and ABCG1 work in tandem to facilitate cholesterol removal from the macrophages54, the reduction in their expression would implicate a reduced potential of these monocyte-derived macrophages to egress cholesterol to HDL acceptors55. ABCA1 deficiency in Tangier disease leads to very low or absent HDL levels and larger VLDL particles56. Since the relationship between cholesterol transporter expression in white blood cells and serum HDL concentration is far from simple, it is difficult to evaluate how the observed expression changes were reflected to the flow of cholesterol from macrophages to liver and finally feces (RCT), particularly as the activities of the enzymes/transporters modulating HDL pool (CETP, PLTP, LCAT, PON1) measured in the SR study were not affected by. However, it can be noted that the observed expression changes in the cholesterol transport-related genes are compatible with those in down-regulation of LXR activity39,57 ( Fig. 3).

Caveolin-1 (CAV1) is found in caveolae, cholesterol-rich membrane lipid formations that are involved in cholesterol traffic and homeostasis58 and regulation of inflammation59 among other functions. CAV1 has been proposed to participate in the regulation of cholesterol efflux to HDL60,61, possibly in interaction with ABCG161. Some other studies have not found an effect62,63, and the overall effect of CAV1 on cholesterol efflux is complex61. The observed decrease in CAV1 expression may add to the view that reverse cholesterol transport from macrophages is compromised by insufficient sleep.

Previous studies indicate that the immune system is activated during experimental sleep restriction, and in persons who in epidemiological studies report short sleep duration (reviewed in64,65). We have earlier shown that cytokine (interleukins IL-1b, IL-6 and IL-17) release as response to in vitro immunological challenge is increased after sleep restriction, as well as serum acute phase protein CRP7. At gene expression level, the activation included increases in expression of toll-like receptors, NF-kB signalling pathway and interleukin-8 production pathways5.

Many acute conditions, including surgical trauma, myocardial infarction and inflammation, induce the systemic acute phase reaction (APR), with acute phase protein production in the liver as an integral part of the host defence response. In addition to changes in protein synthesis, also lipid metabolism undergoes significant modifications in APR66,67. Metabolic modifications aim at optimization of the defence, and would return to baseline level after the need for defence has disappeared68. However, if the inflammation-sustaining condition continues, as presumably in the epidemiological SSI groups of the present study, the metabolic modifications may develop further and become chronic39,68. Moreover, the modifications differ according to the nature of the event that aroused the reaction, e.g. surgical trauma and infection66,68. Decreases in HDL and LDL cholesterol, as well as RCT, belong to the metabolic adaptations found in APR during inflammatory attack67. While cytokines (including IL-1b, IL-6 and TNF-a) are central regulators of the APR, recent research suggests that an important part of the metabolic regulation in APR is channelled via nuclear receptors, including LXR, PPAR and LHR-1 ³⁹. Thus both the down-regulation of RCT pathway and up-regulation of the inflammatory pathways could result from a decrease of LXR activity ( Fig. 3).

Methodological issues

To evaluate sleep in the epidemiological samples, we used subjective evaluation of sleep insufficiency, instead of sleep duration. While sleep duration as a measure of sleep has many advantages, in evaluation of sleep insufficiency it has one considerable disadvantage: it cannot differentiate sleep insufficiency-inducing short sleep from natural short sleep69.

In epidemiological studies sleep duration and self-reported sleep insufficiency have shown independent effects on cardiovascular outcomes (including hypertension, cholesterol level and cardiac events)70 and performance71. Thus, although the correlation of short sleep duration and subjective sleep insufficiency is usually high (in the present study, P = 2.5E-10 and β = −0.5 h in DILGOM, and P = 4.9E-93 and β = −0.5 h in YFS, Supplementary Fig. S5), these variables may represent partly overlapping, but separate physiological entities69,70. In epidemiological studies, a question addressing sleep need and/or subjective feeling of sleep insufficiency may help to separate natural short sleepers from those that don't get enough sleep.

While the participants of the experimental study were carefully screened not to have any (sleep) disorders, the participants in the epidemiological studies reported different medical conditions, including sleep apnoea, which is known to be associated to both insufficient sleep and cardiovascular diseases. The evaluation of the potential effects of OSA on our results revealed that although the subjects reporting symptoms of OSA reported also more sleep insufficiency, OSA did not explain the difference in HDL, as SSI was independently associated to lower level of large HDL.

The main regulation of metabolism takes place in other tissues (e.g. liver, pancreas) than blood cells, which were used in the gene expression analyses. Thus it is unclear to which extent the results reflect changes in the actual metabolic processes. An additional source of variation lies in the differences in age and gender between the populations studied. The effects of these factors have been addressed by including them in the linear models used for statistical analyses.

Sleep loss is often accompanied with circadian misalignment, also known to cause changes in the regulation of the immune system and metabolism and associate to cardiovascular diseases72,73. In our experimental SR study, the modest delay (16 min) in circadian rhythm, measured in the morning salivary cortisol peak, is unlikely to significantly modulate the results, but the effect cannot be entirely ruled out.

In real life, people frequently experience consecutive cycles of sleep restriction and recovery sleep (e.g., shift workers, people working extended days). Often recovery sleep between two periods of sleep restriction remains incomplete and induces a carry-over effect74. In the SR experiment, participants were subjected to only one cycle. From this perspective, the results of the SR study may underestimate what actually happens to the cholesterol metabolism of sleep-restricted individuals in real life.

We propose that sleep restriction arouses a host defence response that shares features with APR aroused by trauma and infection. These responses modulate lipid metabolism, possibly through LXRs, and in the long run may contribute to the increased risk of cardiovascular diseases.

Conclusion

Sleep restriction-induced decrease in expression of genes in pathways related to reverse cholesterol transport from macrophages, in combination with inflammatory activation, may at least partly explain the increased risk for cardiovascular diseases established in epidemiological studies for persons with short/insufficient sleep.

Methods

Samples

Experimental sleep restriction

An experimental schedule simulating a working week with restricted sleep was executed at the Brain and Work Research Centre of the Finnish Institute of Occupational Health (FIOH). We have earlier reported changes observed in glucose metabolism75, cytokines, white blood cell subpopulations, and C-reactive protein7, leukocyte gene expression5, as well as cognitive performance76 from this SR experiment. Study participants were men (N = 21; age 19-29 years; mean ± s.d. 23.2 ± 2.2 years; Supplementary Table S1) with regular sleep wake cycle that was checked by wrist-worn actigraphy and sleep diaries during 1-2 weeks prior to the study. In the sleep laboratory, the participants were randomly allocated to the experimental group ("cases"; N = 14) or the control group ("controls", N = 8) ( Supplementary Fig. S1). Cases spent the first two nights 8 h/night in bed (baseline, BL; from 23:00 h to 07:00 h), followed by five nights of 4 h/night in bed (sleep restriction, SR; from 03:00 h to 07:00 h). Controls spent 8 h in bed every night. One control subject was excluded after the EEG analysis as he had been sleeping less than 6 h/night during the experiment. Total sleep duration in the cases (N = 14) decreased from 7 h 22 min ± 20 min in BL to 3 h 54 min ± 5 min in SR, while it remained relatively constant, 7 h 19 min ± 16 min to 7 h 26 min ± 17 min at the same timepoints, in the controls (N = 7).

During waking, main activities of the participants included training and testing of memory and motor tasks simulating office work tasks. These tests were conducted during the day at 10:00-12:30 and 14:30-15:40, and during the sleep restriction at 00:30-01:40. In the test room the illumination ranged from 150 to 400 lux and in the living room from 350 to 600 lux. Physical exercise or leaving the sleep laboratory was not allowed during the experiment. Polygraphy was measured continuously and EEG scored according to the Rechtschaffen-Kales manual75,77. EEG data from the previous night before morning blood sample-taking for timepoints BL and SR were included in the dependency network analysis.

Prestudy mean (±s.d.) body mass index (BMI) was 23.2 (±2.4) for controls and 23.5 (±2.6) for cases. Standardised meals based on the Finnish nutrition recommendations for 18-30 years old normal-weighted men with low activity78 were eaten at fixed times throughout the experiment: breakfast at 08:00 h (600 kcal), lunch at 12:30 h (800 kcal), dinner at 18:30 h (700 kcal); snacks at 15:30 h (300 kcal) and 21:30 h (200 kcal). In addition, cases ate a piece of fruit (apple or orange) at 00:30 h (50 kcal) which did not exceed the estimated increase of energy expenditure during the SR79. No caffeine, alcohol, or tobacco was allowed during the experiment. Blood samples were collected at BL and SR timepoints at 7.30 h after fasting overnight.

Saliva cortisol was assessed 10 times per day during the experiment, and only a modest, 16 min on average, delay in the circadian phase measured by the morning peak of cortisol (from mean ± s.d. 07:39 ± 0:14 in BL to 07:55 ± 0:11 in SR) was observed in the sleep-deprived cases75. No changes in the overall cortisol concentration in SR compared to BL was observed7.

The DILGOM cohort

The Dietary Lifestyle and Genetic determinants of Obesity and Metabolic Syndrome (DILGOM) study was originally performed as an extension of the FINRISK 2007 study (N = 7993; age 25-74 years; from five geographical areas in Finland). The national, cross-sectional FINRISK surveys have been carried out every 5 years since 1972 to assess the risk factors of chronic diseases (e.g. CVD, diabetes, obesity, cancer) and health behaviour in the working age population in Finland. The aim of the DILGOM study (N = 5024) was to characterise risk factors for metabolic and cardiovascular diseases in the Finnish population both at the epidemiological and at the genetic level25. In addition to questionnaire data on health and lifestyle, a blood sample was drawn after at least 10 h of overnight fasting for genetic and biomedical analyses. Time of sampling varied from 7:11 a.m. to 11:31 a.m., with mean 8:56 a.m. (±s.d. 58 min).

NMR metabolomics and genome-wide gene expression were measured for a subsample from Helsinki metropolitan area (N = 518, age 25-74 years, 54% females, Supplementary Table S1, Supplementary Fig. S1)80. For the present study, these measures were correlated with a question probing subjective feeling of insufficient sleep. The question was "Do you, in your opinion, sleep enough?", and it had four answer options: 1) "Yes, almost always" (N = 168), 2) "Yes, often" (N = 218), 3) "Seldom or almost never" (N = 86), and 4) "I cannot say" (N = 46). Answer 4 was excluded, and answers 1-3 (N = 472) were dichotomised combining 1 and 2 to a phenotype of 'subjective sufficient sleep' (noSSI, N = 386) and comparing this to 3, 'subjective sleep insufficiency' (SSI, N = 86). Habitual sleep duration was assessed with the question "How many hours, on average, do you sleep per night?" with a free entry answer in hours.

The Young Finns Study (YFS) cohort

The Cardiovascular Risk in Young Finns Study ("Young Finns Study", YFS) is a Finnish prospective multi-centre cohort26. It aims to study cardiovascular risk factors in children and adolescents (aged 3, 6, 9, 12, 15 and 18 at baseline). The study participants were randomly selected in 5 centres in Finland. The baseline study was conducted in 1980 (N = 3596). Sleep parameters were assessed with a questionnaire in 2007 when the study subjects were 30 to 45 years of age ( Supplementary Table S1, Supplementary Fig. S1). Blood samples were collected after overnight fasting (97.4% of the subjects reported to have fasted overnight before the sample taking as requested and 1.3% not to have, while no information on fasting was obtained for 1.4%). The mean time of sampling was 9:46 a.m. (±s.d. 1:38).

In this cohort, subjective sleep insufficiency was assessed using two questions. Subjects reported their habitual sleep duration on a 10-level scale (≤5 h, 6 h, 6.5 h, 7 h, 7.5 h, 8 h, 8.5 h, 9 h, 9.5 h, or ≥10 h). They also evaluated their subjective sleep need ("How many hours of sleep do you need per day to feel well rested?") on the same scale. A measure of subjective sleep insufficiency for each subject was formed by subtracting the sleep duration from the sleep need. Subjects (N = 2221 with SSI data) were grouped into three groups based on their level of SSI: no (or only mild) SSI (sleep need - sleep length = −1...0...1 h; N = 1825), moderate SSI (1.5-2 h; N = 304), and heavy SSI (>2 h; N = 55). Subjects sleeping more than 1 h over their subjective sleep need (N = 37) were not included in the analyses. Correlation of sleep insufficiency with sleep duration is shown in Supplementary Fig. S5).

Possible self-reported OSA was estimated using questions addressing the frequency and quality of snoring, as described earlier81. The questions used were "How often do you snore?", "What does your snoring sound like?", and "Have you noticed (or have others noticed) respiratory pauses when you sleep?". Self-reported probable OSA was diagnosed if snoring was frequent (at least 3-5 nights per week) and either of the following was true: a) snoring was loud and irregular, with occasional respiratory pauses and/or stertorous breathing, or b) respiratory pauses at least 1-2 nights per week. The prevalence of probable self-reported OSA in the YFS sample using these criteria was 5%.

Measures

Expression microarrays

DILGOM cohort

Genome-wide gene expression analysis was performed for 518 individuals ( Supplementary Fig. S1). Gene expression was detected and data processed as described in80. Briefly, peripheral blood total RNA was extracted with PAXgene Blood RNA Kit (Qiagen GmbH, Hilden, Germany). RNA quantity and quality was evaluated with 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA, USA). 200 ng of total RNA from each sample was used for production of biotinylated cRNA with Ambion Illumina TotalPrep RNA Amplification Kit (Applied Biosystems, Foster City, CA, USA). 750 ng of biotinylated cRNA was hybridised onto Illumina HumanHT-12 Expression BeadChips (Illumina Inc., San Diego, CA, USA). Biotinylated cRNA preparation and hybridization onto BeadChip were done in duplicates for each sample.

Statistical analysis. All arrays were quantile normalised at the strip-level. Technical replicates were combined via a bead-count weighted average, and replicates with Pearson's correlation coefficient <0.94 or Spearman's rank correlation coefficient <0.60 were removed from further analysis. 472 subjects with gene expression and sleep sufficiency data were included in the final analysis. 35,420 probes were analysed.

Subjects were grouped into two groups (SSI, noSSI) based on their report of subjective sleep insufficiency. Linear regression was used to correlate RNA expression with SSI, adjusting for age and gender (R version 2.14).

Young Finns Study cohort

Genome-wide gene expression was detected using Illumina microarrays as described in82. Briefly, 2.5 ml of whole blood was collected to a PAXgene Blood RNA Tubes (PreAnalytix, Hombrechtikon, Switzerland) after fasting overnight. RNA was isolated with PAXgene Blood RNA Kit (Qiagen) with DNase Set according to manufactures instructions using the QiaCube.

The concentrations and purity of the RNA samples were evaluated spectrophotometrically with NanoDrop (BioPhotomer, Eppendorf, Wesseling-Berzdorf, Germany). Samples were considered pure, if the 260/280 ratio was 1.8-2.2. The RNA isolating process was validated by analysing the integrity of RNA with the RNA 6000 Nano Chip Kit (Agilent).

The expression levels were analysed with an Illumina HumanHT-12 version 4 Expression BeadChip (Illumina Inc.) containing 47,231 expression and 770 control probes. In brief, 200 ng of RNA was reverse-transcribed into cDNA and biotin-UTP-labelled using the Illumina TotalPrep RNA Amplification Kit (Ambion); 1500 ng of cDNA was then hybridised to the Illumina HumanHT-12 v4 Expression BeadChip. The BeadChips were scanned with the Illumina iScan system.

Statistical analysis. Raw Illumina probe data was exported from GenomeStudio and analysed in R ( http://www.r-project.org/) using the Bioconductor ( http://www.bioconductor.org/) packages. The expression data was processed using nonparametric background correction, followed by quantile normalization with control and expression probes, using the neqc function in the limma package and log2 transformation. The expression analysis was successful for 1650 subjects.

Subjects were grouped into three groups based on their level of subjective sleep insufficiency (noSSI, moderate SSI, heavy SSI; N = 1407). Linear regression was used to correlate RNA expression with SSI, adjusting for age and gender (R version 2.14).

Pathway analysis

The genes with differing expression levels in the SSI group compared to subjects satisfied with their sleep amount ( P < 0.05) in the DILGOM cohort were further analysed with Database for Annotation, Visualization and Integrated Discovery (DAVID) pathway analysis (DAVID Bioinformatics Resources 6.7, NIAID/NIH, http://david.abcc.ncifcrf.gov/home.jsp). Illumina probe IDs were converted to DAVID IDs using Gene ID Conversion Tool, removing all redundancies in the original IDs. DAVID Functional Annotation Tool was used for identifying enriched biological processes among the genes with lower or higher expression in the SSI group (analysed separately; N genes 725 and 734, respectively) compared to the whole human genome28. Gene Ontology (GO) Biological Process annotations were used and pathways with less than 3 genes from our gene list were excluded. Other than this, default parameters were used in the analysis. Considering the hierarchical nature of GO annotations, the GO pathways were grouped using DAVID Functional Annotation Clustering. Medium classification stringency and other default parameters were used.

NMR spectroscopy

The NMR-based analyses provide absolute quantification of multiple serum metabolites, including lipoprotein subclass distribution, fatty acids, and various small molecules including amino acids and glycolysis precursors ( Supplementary Table S3). The lipoprotein subclasses were classified as follows: chylomicrons and extremely large VLDL particles (average particle diameter at least 75 nm); five different VLDL subclasses: very large VLDL (average particle diameter of 64.0 nm), large VLDL (53.5 nm), medium VLDL (44.5 nm), small VLDL (36.8 nm), and very small VLDL (31.3 nm); intermediate-density lipoprotein (IDL) (28.6 nm); three LDL subclasses: large LDL (25.5 nm), medium LDL (23.0 nm), and small LDL (18.7 nm); and four HDL subclasses: very large HDL (14.3 nm), large HDL (12.1 nm), medium HDL (10.9 nm), and small HDL (8.7 nm). The NMR-based metabolite profiling has previously been used in various epidemiological and genetic studies and details of the method have been described.

Statistical analysis. The concentrations of 135 serum metabolites were assessed with NMR spectroscopy from serum samples of the experimental SR study and the epidemiological cohorts. In the SR study, SR timepoint was compared to BL with paired t tests. Hierarchical clustering analysis using principal components revealed that the 135 metabolites cluster into 21 clusters that explain 95% of the variance. P values from the t tests were corrected with the amount of clusters (N = 21).

In the epidemiological samples DILGOM and YFS, linear regression was used to correlate NMR metabolites with SSI, adjusting for age and gender (R version 3.0), similarly as was done in the gene expression analysis. In the YFS sample, the analyses were run also with self-reported probable OSA added in the model.

Mass spectrometry

Lipidomic analyses were performed on serum samples from the experimental SR study at VTT Technical Research Centre of Finland. Ultra Performance Liquid Chromatography (UPLC) coupled to electrospray ionization quadrupole time-of-flight mass spectrometry (QTOFMS) was used with the established protocol87. Data was processed using the MZmine 2 software88. The data was normalised using internal standards representative of each class of lipid present in the samples. A total of 530 lipids were detected and 330 identified.

Statistical analysis. BL-normalised values of the lipids in the SR timepoint were compared between cases and controls using t tests.

Lipid transfer protein and enzyme activity assays

CETP activity was analysed as the transfer/exchange of radiolabelled [14C]cholesteryl oleate between exogenously added human LDL and HDL2, as described in89. PLTP activity was assessed with phosphatidylcholine liposomes following an earlier reported protocol90. Liquid scintillation counting was used to detect radioactivity in HDL as a measure of transfer activity. LCAT activity was assessed by measuring cholesterol esterification activity using exogenous [ ³H]cholesterol-labelled HDL proteoliposome discs as the substrate91. Serum PON1 activity was measured using spectroscopy method and Paraoxon (diethyl-p-nitrophenyl phosphate; Sigma) as the substrate92.

Statistical analysis. The activities in the SR timepoint were compared to their BL using first 2-way repeated measures ANOVA with group (case vs control) and timepoint (BL vs SR) (R version 3.0), and then with paired t tests between the two timepoints.

Dependency network analysis

Partial correlation network analysis using the undirected Gaussian graphical model (Genenet package38) was performed on baseline-normalised data for cases and controls separately, by using the log2 of the ratio between the SR and BL timepoints. Unlike the pairwise measures of associations such as Pearson correlation coefficient, partial correlation provides a stronger criterion for dependency by adjusting for confounding effects, and thus removing spurious associations to a large extent. This is particularly favourable for an integration of multiple layers of information as in our study, because it inherently filters out false positives by discovering only direct interactions with high confidence.

52 variables from the SR study were selected for the network analysis and are listed in Supplementary Table S5. The eleven lipid molecular species included in the network analysis were those lipids that showed differences ( t test, P  < 0.05) between cases and controls at SR timepoint for BL-normalised data. The sleep variable data used were those from the previous night before the blood sampling (second night of BL and fifth night of SR).

In these networks non-missing edges denote non-zero partial correlations ( P < 0.05) between pairs of variables and thus imply direct interactions. The edge width is proportional to strength of dependency. The node colour corresponds to the significance and direction of regulation comparing cases versus controls. The yED graphical editor93 was used for network´s visualization.

Study approval

This study was conducted according to the Declaration of Helsinki principles, and written informed consent was obtained from all participants. The experimental sleep restriction study protocol and the FINRISK 2007 study including the DILGOM subsample were approved by the coordinating ethics committee of the Hospital District of Helsinki. The Cardiovascular Risk in Young Finns Study was approved by the ethics committees of University Hospitals of Turku, Helsinki, Tampere, Kuopio, and Oulu.

Additional Information

Data availability: The gene expression data has been deposited to the ArrayExpress database (accession numbers E-MEXP-3936 and E-TABM-1036 for the experimental and epidemiological data sets, respectively)

How to cite this article: Aho, V. et al. Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses. Sci. Rep. 6, 24828; doi: 10.1038/srep24828 (2016).

Acknowledgements

We thank Päivi Pöhö and Helena Simolin for their contribution to the MS lipidomics analyses, and others who have contributed to the laboratory analyses. The expert technical assistance in the statistical analyses by Ville Aalto and Irina Lisinen is gratefully acknowledged. We also thank all the study subjects. The authors gratefully acknowledge support for this work from the EU (LSHM-CT-2005-518189 and QLK6-CT-2000-00499), Finska Läkaresällskapet, the Finnish Work Environment Fund, Yrjö Jahnsson Foundation, Orion Research Foundation, and Jenny and Antti Wihuri Foundation (to VA), the Finnish Foundation for Cardiovascular Research (to HMO and VO), the Liv och Hälsa Foundation, the Magnus Ehrnrooth Foundation, and the Diabetes Research Foundation (to VO), the Sigrid Juselius Foundation (to VO and TP), Helsinki University Central Hospital research funds (TYH6254 to TP), the Carlos III Health Institute of the Spanish Ministry of Health (Sara Borrell postdoctoral contract to IBP), and the Academy of Finland (118065 for DILGOM, 138201 to MiHi, 283045 to JK, 139635 to VS, 137870 to PS, 257545 to MJ, 250114 to MO, and 137575 to TPH). The quantitative serum NMR metabolomics platform and its development and applications have been supported by the Academy of Finland, TEKES - the Finnish Funding Agency for Technology and Innovation, the Sigrid Juselius Foundation, the Novo Nordisk Foundation, the Finnish Diabetes Research Foundation, and the strategic and infrastructural research funding from the University of Oulu, Finland, as well as by the British Heart Foundation, the Welcome Trust, and the Medical Research Council, UK. The Young Finns Study has been financially supported by the Academy of Finland (grants 134309 (Eye), 126925, 121584, 124282, 129378 (Salve), 117797 (Gendi), and 41071 (Skidi)), the Social Insurance Institution of Finland, Kuopio, Tampere and Turku University Hospital Medical Funds, Juho Vainio Foundation, Sigrid Juselius Foundation, Paavo Nurmi Foundation, Finnish Foundation of Cardiovascular Research and Finnish Cultural Foundation, Tampere Tuberculosis Foundation, Emil Aaltonen Foundation, and Yrjö Jahnsson Foundation. The funders had no role in study design, data collection or analysis, decision to publish, or preparation of the manuscript.

Author information

Author notes

Vilma Aho and Hanna M. Ollila: These authors contributed equally to this work.

Affiliations

1. Department of Physiology, Faculty of Medicine, University of Helsinki, Finland

Vilma Aho, Hanna M. Ollila & Tarja Porkka-Heiskanen

2. Genomics and Biomarkers unit and Institute for Molecular Medicine FIMM, National Institute for Health and Welfare, Helsinki, Finland

Hanna M. Ollila, Johannes Kettunen, Matti Jauhiainen & Tiina Paunio

3. Department of Psychiatry, University of Helsinki and Helsinki University Hospital, Finland

Hanna M. Ollila & Tiina Paunio

4. Stanford University Center for Sleep Sciences, Palo Alto, CA, USA

Hanna M. Ollila

5. Department of Chronic Disease Prevention, Population Studies Unit, National Institute for Health and Welfare, Turku, Finland

Erkki Kronholm

6. VTT Technical Research Centre of Finland, Espoo, Finland

Isabel Bondia-Pons, Mika Hilvo, Tuulia Hyötyläinen & Matej Orešič

7. Steno Diabetes Center A/S, Gentofte, Denmark

Isabel Bondia-Pons, Tuulia Hyötyläinen & Matej Orešič

8. Computational Medicine, Institute of Health Sciences, University of Oulu, Oulu, Finland

Pasi Soininen, Antti J. Kangas, Johannes Kettunen & Mika Ala-Korpela

9. NMR Metabolomics Laboratory, School of Pharmacy, University of Eastern Finland, Kuopio, Finland

Pasi Soininen, Johannes Kettunen & Mika Ala-Korpela

10. Department of Clinical Chemistry, Fimlab Laboratories, and University of Tampere, School of Medicine, Tampere, Finland

Ilkka Seppälä, Emma Raitoharju & Terho Lehtimäki

11. Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland

Mervi Oikonen & Olli T. Raitakari

12. Department of Clinical Physiology, University of Tampere and Tampere University Hospital, Tampere, Finland

Mika Kähönen

13. Department of Medicine, and Division of Medicine, University of Turku, Turku University Hospital, Turku, Finland

Jorma S.A. Viikari

14. Brain and Work Research Centre, Finnish Institute of Occupational Health, Helsinki, Finland

Mikko Härmä & Mikael Sallinen

15. Agora Center, University of Jyväskylä, Jyväskylä, Finland

Mikael Sallinen

16. Minerva Foundation Institute for Medical Research, Helsinki, Finland

Vesa M. Olkkonen

17. Institute of Biomedicine, Anatomy, University of Helsinki, Finland

Vesa M. Olkkonen

18. Unit of Excellence for Immunotoxicology, Finnish Institute of Occupational Health, Helsinki, Finland

Harri Alenius

19. Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland

Veikko Salomaa

20. Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Turku, Finland

Olli T. Raitakari

21. Oulu University Hospital, Oulu, Finland

Mika Ala-Korpela

22. Computational Medicine, School of Social and Community Medicine & Medical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom

Mika Ala-Korpela

Contributions

Conceived and designed the experiments: T.P.-H., M.H., M.S., M.K., T.L., O.T.R. and V.S., Performed the experiments: V.A., H.M.O., P.S., A.J.K. and E.R. Analysed the data: V.A., H.M.O., E.K., I.B.-P. and Mi.Hi. Conceived, designed and performed the NMR analyses: P.S., A.J.K. and M.A.K. Contributed data/reagents/materials/analysis tools: I.S., E.R., M.K., T.L., J.S.A.V., V.S., Ma.Or. and O.T.R. Wrote the paper: V.A., H.M.O. and T.P.-H. Provided expertise for data analysis and interpretation, commented the paper: E.K., I.S., E.R., J.K., M.K., T.L., T.H., J.S.A.V., V.S., V.M.O., H.A., M.J., T.P., Ma.Or., M.A.K., Mi.Ha., O.T.R. and Me.Oi.

Corresponding author

Correspondence to Tarja Porkka-Heiskanen.

Ethics declarations

Competing interests

PS, AJK and MAK are shareholders of Brainshake Ltd. ( http://www.brainshake.fi), a startup company offering NMR-based metabolite profiling. VO is a Board Member in Medix Biochemica Ltd. (Kauniainen, Finland).

Supplementary information

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Aho, V., Ollila, H., Kronholm, E. et al. Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses. Sci Rep 6, 24828 (2016). https://doi.org/10.1038/srep24828
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Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses - Scientific Reports

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Sleep loss and insufficient sleep are risk factors for cardiometabolic diseases, but data on how insufficient sleep contributes to these diseases are scarce. These questions were addressed using two approaches: an experimental, partial sleep restriction study (14 cases and 7 control subjects) with objective verification of sleep amount, and two independent epidemiological cohorts (altogether 2739 individuals) with questions of sleep insufficiency.

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https://gspsy.fi/suomen-tunnetuimmat-psykologiset-tutkimukset/ tekijä: Stanley Milgram

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Ihmisen psyyke on kaiken toimintamme keskiössä. Yhden teorian mukaan kaikki mennyt muovaa meitä ja muokkaa käytöstämme, tietoisesti tai tiedostamattomasti, halusimme tai emme. Ihmisen psykologiaa tutkitaan monilla eri menetelmillä ja alaa on opiskeltu jo vuosisatojen ajan.

Eri psykologit ovat toteuttaneet erilaisia kokeita saadakseen paremman käsityksen ihmisen mielen toiminnasta. Aina ei kuitenkaan ole ollut kyse nykyaikana eettiseksi luokitellusta kokeesta ja nykyvinkkelistä katsottuna jotkin metodit ja menetelmät ovat olleet vähintäänkin arveluttaviksi luokiteltavia. Seuraavien rivien myötä esittelemme muutamia tunnetuimmista tutkimuksista, jotka ovat yliopistovuosilta tuttuja jokaiselle psykologiaa opiskelleelle.

Milgramin tottelevaisuuskoe

1960-luvulla mies nimeltä Stanley Milgram suoritti psykologisen kokeen, jota kutsuttiin Milgramin tottelevaisuuskokeeksi. Kyseessä on yksi sosiaalipsykologian keskustelluimmasta ja siteeratuimmasta kokeesta.

Koe toteutettiin seuraavasti: lehti-ilmoituksella kerättiin koehenkilöiksi suuri joukko ihmisiä eri ikäluokista, ammattiryhmistä ja sosioekonomisista ryhmistä. Yhdistävä tekijä oli ainoastaan sukupuoli, sillä kaikki kokeeseen osallistuneet henkilöt olivat miehiä. Miehet eivät tienneet ennen kokeeseen saapumista, minkälaisesta kokeesta oli kyse.

Vasta saapuessaan kokeeseen Yalen yliopistoon, he saivat selville kokeen toteutustavan. Laboratoriossa koehenkilö tapasi tutkijan sekä toisen "koehenkilön", joka todellisuudessa oli näyttelijä, mutta joka esiteltiin koehenkilölle toisena, itsensä kaltaisena lehti-ilmoitukseen vastanneena koehenkilönä.

Kyseisessä alkuasetelmassa kumpaisellekin koehenkilölle arvottiin roolit ja näyttelijäkoehenkilöstä tuli oppija ja lehti-ilmoitukseen vastanneesta henkilöstä opettaja. Oppijaksi päätynyt sidottiin sähkötuoliin ja opettajalle annettiin näyte sähköiskuista, joita oppijalle saatettaisiin antaa. Tämän jälkeen opettajaksi päätynyt vietiin iskugeneraattoriksi kutsutun laitteen ääreen.

Opettajan tuli lukea oppijalle lyhyitä tehtäviä ja oppijan tuli vastata niihin. Oppijan vastatessa väärin sai opettaja mahdollisuuden antaa oppijalle sähköiskun. Iskun voimakkuus nousi jokaisen väärän vastauksen myötä. Ensimmäinen isku oli 15 volttia, mutta nousi väärien vastausten myötä jopa kaksi kertaa Suomen sähköverkkoa kovempaan, 450 voltin iskuun.

Opettaja näki generaattorissa koko ajan selkeästi sen, mikä voimakkuus seuraavassa iskussa oli ja mikä sen voimakkuusaste oli. Viimeisimmissä iskuissa luki "vaara: vakava isku" ja yhdessä arvoituksellisesti vain "XXX". Osallistujille kerrottiin etukäteen, että voimakkaimmat iskut olisivat kivuliaita, mutta ne eivät aiheuttaisi todellista vaaraa.

Milgranin eettisestä näkökulmasta vähintäänkin arveluttavan kokeen ideana oli tietenkin nähdä, totteleeko kokeeseen osallistunut henkilö, joka uskoi antavansa sähköiskuja toiselle henkilölle. Tällainen käytös johtaa juurensa tottelevaisuuskasvatukseen, joka opettaa, että auktoriteettia on kuunneltava ja on toimittava, kuten käsketään.

Kokeen edetessä ja iskujen kovetessa valtaosa osallistujista alkoi epäröidä, eikä olisi halunnut antaa lisää iskuja, kannusti auktoriteetti antamaan iskuja edelleen. Vaikka viimeiset iskut olivat huomattavan voimakkaita ja mahdollisesti olisivat voineet tappaa toisen henkilön, käskyjen noudattaminen sai suurimman osan koehenkilöistä tottelemaan ja antamaan sähköiskun joka tapauksessa.

Kokeen historiallisesti tunnetuimmassa asemassa, jossa auktoriteetti ja sähköiskuja antanut henkilö olivat yhdessä huoneessa ja uhri puolestaan toisessa, osoitti, että peräti 65 % kokeeseen osallistuneista, absoluuttisina lukuina 26/40 henkilöä, ei vastustanut auktoriteettia, vaan suoritti omista tuntemuksistaan ja epäilyksistään huolimatta testin aina 450 voltin pisteeseen saakka.

Koe suoritettiin osittain uudelleen 45 vuotta myöhemmin, jolloin tulokset olivat huomattavan samansuuntaisia, kuin ensimmäisellä testikerralla. Se, ettei aikakauden muutokset tai sosiaalinen murros ollut juurikaan vaikuttanut toiminnan säätelyyn, auktoriteettiin suhtautumiseen tai tottelevaisuuteen, oli omassa lajissaan merkittävä löydös.

Uusintakokeesta ja sen tuloksista on julkaistu Santa Claran yliopistossa psykologian professorina työskentelevän Jerry M. Burgerin artikkeli American Psychologist -lehdessä tammikuussa 2009. Burger suoritti vuonna 2006 Milgrainin kokeeseen pohjautuvan uusintakokeen, jonka tulokset osoittivat, että tottelevaisuus oli lähes samaa luokkaa, kuin 45 vuotta aiemmin.

Stanfordin vankilakoe

Toinen erittäin laajasti tunnettu psykologinen koe on nimeltään Stanfordin vankilakoe. Tämä koe toteutettiin Kaliforniassa, Stanfordin yliopistossa tutkija Philip Zimbardon johdolla vuonna 1971. Kokeessa haluttiin tutkia sitä, miten ihmiset reagoivat valtasuhteisiin vankilaympäristössä, jossa ei ole täsmällisesti esitettyjä sääntöjä. Konstruoidussa asetelmassa mukana olevat henkilöt jaettiin vartijoihin ja vankeihin.

Kokeeseen valittiin 24 koehenkilöä, jotka olivat kaikki vapaaehtoisia miespuolisia opiskelijoita. Kaikki kokeeseen osallistujat oli ennen kokeeseen hyväksymistä testattu ja todettu henkisesti normaaleiksi yksilöiksi. Kaikki tulivat keskiluokkaisista ja koulutetuista perheistä eikä kenelläkään osallistuneista ei ollut taustalla mielenterveysongelmia eikä päihteiden väärinkäyttöä.

Kokeen alkaessa osallistujat jaettiin kahteen ryhmään. Toinen ryhmä edusti vankeja ja toinen joukko vanginvartioita. Osallistujat vietiin toteuttamaan koetta yliopiston kellariin, jossa olevaan laboratorioon oli rakennettu vankilan puitteet. Vangit puettiin vanginasuihin, jotka olivat keskenään identtisiä. Vartioille annettiin identtiset khakista tehdyt uniformut, aurinkolasit, kumipamppu sekä pilli.

Koe toteutettiin seuraavasti. Vartijoiden oli pidettävä vangit kurissa ja järjestyksessä ja huolehdittava siitä, että vangit käyttäytyisivät vartijoita kohtaan kunnioittavasti. Mitään erikoisempaa koulutusta tai ohjeistusta ei annettu lukuun ottamatta sitä, että väkivallankäyttö oli kielletty.

Kokeen oli määrä kestää peräti kaksi viikkoa, mutta ei kulunut kuin kuusi päivää, kun koe jouduttiin lopettamaan kesken. Keskeyttämistä vaati erityisesti opiskelija Christina Maslach, joka toimi kokeeseen osallistujien haastattelijana. Keskeytyksen syy oli se, että vartijat alkoivat kohdella vankeja alati kasvavalla julmuudella ja raakuudella.

Koetta on pidetty todisteena siitä, että lähes kuka tahansa meistä pystyy julmaan ja pahaan toimintaan lähimmäistään kohtaan, jos tähän annetaan rajoittamaton valta ilman seurauksia. Stanfordin vankilakoe on ollut heti toteuttamishetkestään lähtien kovan kritiikin kohteena epäeettisyytensä ja mahdollisesti myös epätieteellisyytensä takia. Näistä äärimmäisen räikeistä epäkohdista huolimatta koe puhututtaa vielä tänäkin päivänä.

Tästä huolimatta tämä jo lähes viisi vuosikymmentä sitten suoritettu koe on edelleen äärimmäisen tunnettu esimerkkitapaus, josta lähes jokainen vähääkään psykologiasta kiinnostunut on kuullut jossain yhteydessä. Stanfordin vankilakoe on hyvä osoitus siitä, että käytetyt metodit ja tutkimuksen validiustaso eivät välttämättä vaikuta siihen, jääkö se historiankirjoihin vai ei.

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Ihmisen psyyke on kaiken toimintamme keskiössä. Yhden teorian mukaan kaikki mennyt muovaa meitä ja muokkaa käytöstämme, tietoisesti tai tiedostamattomasti, halusimme tai emme. Ihmisen psykologiaa tutkitaan monilla eri menetelmillä ja alaa on opiskeltu jo vuosisatojen ajan. Eri psykologit ovat toteuttaneet erilaisia kokeita saadakseen paremman käsityksen ihmisen mielen toiminnasta.

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tämä tutkimus oli perusteellisesti tehty, mutta oltaisi voitu saada vielä laajempi koekohderyhmä.

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Tutkimus oli tehty hyvin ja tulokset oli selkeästi merkitty.

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Kirsi Heikkisen uutisessa olevan tutkimuksen tekijät olivat Elaine Guevara ja hänen ryhmänsä.

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https://www.hs.fi/tiede/art-2000008361710.html

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Aivotutkimus | Syy ihmisaivojen ylivertaisuuteen voi löytyä pikkuaivoista, tutkijat uskovat

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Selitystä fiksuuteemme on etsitty väärästä paikasta.

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tutkittu eri osa-alueilla, sekä tulokset on merkitty selkeästi

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HS Pinja Päivänen

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Klassisen pulmapelin ja muiden yhtä intensiivisten tietokonepelien naputtaminen voi tutkijoiden mukaan tarjota apua esimerkiksi traumaperäisestä stressihäiriöstä toipumiseen.

Tetriksen pelaaminen voi helpottaa psykologisista traumoista selviytymistä, selviää brittiläisen kognitiotieteen yksikön tutkimuksesta.

Klassisen pulmapelin ja muiden yhtä intensiivisten tietokonepelien naputtaminen voi tutkijoiden mukaan tarjota apua esimerkiksi traumaperäisestä stressihäiriöstä toipumiseen.

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Klassisen pulmapelin ja muiden yhtä intensiivisten tietokonepelien naputtaminen voi tutkijoiden mukaan tarjota apua esimerkiksi traumaperäisestä stressihäiriöstä toipumiseen. Tetriksen pelaaminen voi helpottaa psykologisista traumoista selviytymistä, selviää brittiläisen kognitiotieteen yksikön tutkimuksesta. Klassisen pulmapelin ja muiden yhtä intensiivisten tietokonepelien naputtaminen voi tutkijoiden mukaan tarjota apua esimerkiksi traumaperäisestä stressihäiriöstä toipumiseen.