karppaus.infon arkistoitu foorumi

Cambridgen yliopiston johtama tutkimus on saanut selville, että 24 tunnin säännöllinen paastoaminen saattaa madaltaa riskiä sairastua muun muassa kakkostyypin diabetekseen ja Alzheimerin tautiin. Vuorokauden kestävä paasto voi Cell Reports -tiedejulkaisussa julkaistun tutkimuksen mukaan hillitä kehon haitallista tulehdusvastetta. Tutkimustuloksista uutisoi The Times.

Tutkimuksen mukaan näin pitkä paastoaminen tehostaa arakidonihappona tunnetun rasvahapon tuotantoa elimistössä. Kyseinen rasvahappo rampauttaa kehon haitallista tulehdusreaktiota ruokkivan NLRP3–inflammasomi-valkuaisaineen toimintaa.


TUTKIJAPIIREISSÄ on jo pitkään uumoiltu, että ihmiskeho ei ole varsinaisesti soveltunut nykyaikaisiin ruokailutottumuksiin, joita värittää usein välipalojen napostelu pitkin päivää. Sen sijaan pidemmät välit ruokailuissa näyttäisivät sopivan ihmiskeholle paremmin, viimeaikaiset tutkimustulokset antavat ymmärtää. Näyttäisi myös siltä, että pidemmät välit ruokailuissa antaisivat ihmiskeholle aikaa korjautua solutasolla.

Jos verensokeria nostattaa pitkin päivää vähän väliä napostelemalla, ei keho ehdi välttämättä toteuttaa tarvittavia korjaustoimia napostelun häiritessä prosesseja.

Kun elimistön puolustusjärjestelmä kytkeytyy päälle, käynnistyy elimistössä tulehdusreaktio, jonka puitteissa elimistö valmistautuu puolustamaan itseään ja korjaamaan vaurioita. Pitkittynyt tulehdusreaktio ei ole kuitenkaan hyvä asia. Nykytiedon mukaan pitkään jatkuva kehon tulehdusvaste on haitaksi terveydelle ja on myös monien elintapasairauksien taustalla.

”Haluamme ymmärtää paremmin kroonisen tulehdusreaktion roolin monissa sairauksissa ja erityisesti juuri sen roolin, joka inflammasomilla on niissä. Viime vuosina on käynyt yhä selvemmäksi, että NLRP3-inflammasomi näyttelee hyvin tärkeää roolia monissa länsimaissa yleisissä sairauksissa, kuten lihavuudessa, valtimonkovettumataudissa, Alzheimerin taudissa ja Parkinsonin taudissa”, kertoo uutta tutkimusta johtanut Cambridgen yliopiston professori Clare Bryant yliopiston tiedotteessa.

BRYANTIN johtamassa tutkimuksessa 21 vapaaehtoista söi kokeen alussa 500 kalorin aterian ja paastosi sitten vuorokauden ajan. Paaston päätyttyä he söivät uudestaan 500 kalorin aterian.


Tiimi havaitsi, että 24 tunnin paasto lisäsi arakidonihapon tuotantoa. Kyseessä on omega-6-rasvahappo, joka toimii muun muassa solukalvojen perusaineosana. Paaston päätyttyä hapon tuotanto laski heti.

Havainnon tehtyään Bryant testasi kollegoineen laboratoriossa arakidonihapon vaikutuksia immuunisoluissa. Tutkijat havaitsivat, että arakidonihappo hillitsi haitallisia tulehdusreaktioita käynnistävien ja ruokkivien NLRP3–inflammasomi-valkuaisaineiden toimintaa. Näin ollen vaikuttaisi siltä, että pitkät, säännölliset paastot voivat ehkä purra kehon haitallisiin kroonisiin tulehdusreaktioihin, jotka ovat monien länsimaissa yleisten elintapasairauksien taustalla.

”Havainto antaa mahdollisen vastauksen siihen, miten ruokavalion muuttaminen paastoamalla voi suojata meitä terveydelle haitallisilta tulehdusreaktioilta, jotka ovat monien, länsimaisen korkeakalorisen ruokavalion aikaansaamien sairauksien taustalla. On kuitenkin liian aikaista sanoa, suojaako paastoaminen esimerkiksi Alzheimerin tai Parkinsonin taudilta, koska arakidonihapon vaikutukset ovat lyhytaikaisia”, Bryant sanoo tiedotteessa.

FEBRUARY 27, 2024
Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting



Highlights
•In fasting compared to fed subjects, plasma IL-1β is lower and arachidonic acid (AA) is higher
•Exogenous AA impairs NLRP3 inflammasome activity in human and mouse macrophages
•AA inhibits phospholipase C and reduces JNK stimulation and hence NLRP3 activity

Summary
Elevated interleukin (IL)-1β levels, NLRP3 inflammasome activity, and systemic inflammation are hallmarks of chronic metabolic inflammatory syndromes, but the mechanistic basis for this is unclear. Here, we show that levels of plasma IL-1β are lower in fasting compared to fed subjects, while the lipid arachidonic acid (AA) is elevated. Lipid profiling of NLRP3-stimulated mouse macrophages shows enhanced AA production and an NLRP3-dependent eicosanoid signature. Inhibition of cyclooxygenase by nonsteroidal anti-inflammatory drugs decreases eicosanoid, but not AA, production. It also reduces both IL-1β and IL-18 production in response to NLRP3 activation. AA inhibits NLRP3 inflammasome activity in human and mouse macrophages. Mechanistically, AA inhibits phospholipase C activity to reduce JNK1 stimulation and hence NLRP3 activity. These data show that AA is an important physiological regulator of the NLRP3 inflammasome and explains why fasting reduces systemic inflammation and also suggests a mechanism to explain how nonsteroidal anti-inflammatory drugs work.

Scientists identify how fasting may protect against inflammation
Intermittent fasting conceptual image showing a plate of food to represent a clock
Cambridge scientists may have discovered a new way in which fasting helps reduce inflammation – a potentially damaging side-effect of the body’s immune system that underlies a number of chronic diseases.

Our work adds to a growing amount of scientific literature that points to the health benefits of calorie restriction
Clare Bryant
In research published in Cell Reports, the team describes how fasting raises levels of a chemical in the blood known as arachidonic acid, which inhibits inflammation. The researchers say it may also help explain some of the beneficial effects of drugs such as aspirin.

Scientists have known for some time that our diet – particular a high-calorie Western diet – can increase our risk of diseases including obesity, type 2 diabetes and heart disease, which are linked to chronic inflammation in the body.

Inflammation is our body’s natural response to injury or infection, but this process can be triggered by other mechanisms, including by the so-called ‘inflammasome’, which acts like an alarm within our body’s cells, triggering inflammation to help protect our body when it senses damage. But the inflammasome can trigger inflammation in unintentional ways – one of its functions is to destroy unwanted cells, which can result in the release of the cell’s contents into the body, where they trigger inflammation.

Professor Clare Bryant from the Department of Medicine at the University of Cambridge said: “We’re very interested in trying to understand the causes of chronic inflammation in the context of many human diseases, and in particular the role of the inflammasome.

“What's become apparent over recent years is that one inflammasome in particular – the NLRP3 inflammasome – is very important in a number of major diseases such as obesity and atherosclerosis, but also in diseases like Alzheimer's and Parkinson's disease, many of the diseases of older age people, particularly in the Western world.”

Fasting can help reduce inflammation, but the reason why has not been clear. To help answer this question, a team led by Professor Bryant and colleagues at the University of Cambridge and National Institute for Health in the USA studied blood samples from a group of 21 volunteers, who ate a 500kcal meal then fasted for 24 hours before consuming a second 500kcal meal.

The team found that restricting calorie intake increased levels of a lipid known as arachidonic acid. Lipids are molecules that play important roles in our bodies, such as storing energy and transmitting information between cells. As soon as individuals ate a meal again, levels of arachidonic acid dropped.

When the researchers studied arachidonic acid’s effect in immune cells cultured in the lab, they found that it turns down the activity of the NLRP3 inflammasome. This surprised the team as arachidonic acid was previously thought to be linked with increased levels of inflammation, not decreased.

Professor Bryant, a Fellow of Queens’ College, Cambridge, added: “This provides a potential explanation for how changing our diet – in particular by fasting – protects us from inflammation, especially the damaging form that underpins many diseases related to a Western high calorie diet.

“It’s too early to say whether fasting protects against diseases like Alzheimer's and Parkinson's disease as the effects of arachidonic acid are only short-lived, but our work adds to a growing amount of scientific literature that points to the health benefits of calorie restriction. It suggests that regular fasting over a long period could help reduce the chronic inflammation we associate with these conditions. It's certainly an attractive idea.”

The findings also hint at one mechanism whereby a high calorie diet might increase the risk of these diseases. Studies have shown that some patients that have a high fat diet have increased levels of inflammasome activity.

“There could be a yin and yang effect going on here, whereby too much of the wrong thing is increasing your inflammasome activity and too little is decreasing it,” said Professor Bryant. “Arachidonic acid could be one way in which this is happening.”

The researchers say the discovery may also offer clues to an unexpected way in which so-called non-steroidal anti-inflammatory drugs such as aspirin work. Normally, arachidonic acid is rapidly broken down in the body, but aspirin stops this process, which can lead to an increase in levels of arachidonic acid, which in turn reduce inflammasome activity and hence inflammation.

Professor Bryant said: “It’s important to stress that aspirin should not be taken to reduce risk of long terms diseases without medical guidance as it can have side-effects such as stomach bleeds if taken over a long period.”

Ja kun karpatessa saa syödä sitä eläinperäistä rasvaa! Ja paastotessa kun käytetään sitä omaa eläinperäistä varastorasvaa.