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zondag 29 december 2019

Broodje Aap Burp

In een Broodje Aap-kalender lees ik dat na het drinken van een glas bier de lever aan het werk om de alcohol af te breken. Echter kunnen Japanners sneller dronken worden.

Wat blijkt? Door een variatie in hun ADH-gen die bij Westerlingen nauwelijks voorkomt, zetten Japanners de alcohol sneller om in acetaldehyde. Door een mutatie van het ALDH-gen breekt de acetaldehyde niet afbreken. Zo ontstaat een grote hoeveelheid acetaldehyde in hun bloed en zijn ze na een paar biertjes al dronken... (zie de Broodje Aap Scheurkalender 2018).

Opname van alcohol in het lichaam
Als iemand alcoholhoudende drank drinkt gaat de alcohol via de slokdarm naar de maag. In de maag wordt alcohol in beperkte mate opgenomen (zo’n 20%). Als de maag vol is, gaat de absorptie van alcohol trager. Koolhydraatrijke maaltijden vertragen de absorptie van alcohol via de maagwand en vetrijke maaltijden vertragen de peristaltiek (samentrekkende bewegingen) in de maag. Beide soorten maaltijden zorgen dus voor een vertraagde opname van alcohol in het bloed1. Eiwitrijke maaltijden hebben minder effect op de snelheid van absorptie van alcohol in de maag2. In de dunne darm wordt het merendeel (80%) van de alcohol opgenomen in het bloed. (https://www.kennisinstituutbier.nl/gezondheid/gezondheid/metabolisme)

Alcoholopname
De alcohol die je op een gezellige avond drinkt, wordt vanuit het spijsverteringskanaal opgenomen in je bloed. In je maag wordt 10 tot 30 procent van de alcohol in het bloed opgenomen, de overige hoeveelheid in je dunne darm. Als je maag vol zit, duurt dit proces langer. Hoe hoger de alcoholconcentratie in je spijsverteringskanaal is, hoe sneller het wordt opgenomen.
De alcohol verspreidt zich door de gehele vetvrije massa van je lichaam (o.a. lichaamsvocht). Tien minuten na inname bereikt de alcohol je hersenen en je lever. De concentratie alcohol in je bloed, is afhankelijk van je lichaamsbouw. Hoe lichter iemand is, hoe hoger de concentratie zal zijn. Maar ook bij mensen die relatief veel lichaamsvet hebben, stijgt het alcoholgehalte in het bloed meer. Omdat mannen gemiddeld groter en zwaarder zijn en gemiddeld minder lichaamsvet (en dus meer lichaamsvocht) per kilo hebben dan vrouwen, hebben mannen een lager alcoholpercentage in hun bloed wanneer zij dezelfde hoeveelheid drinken als een vrouw. .... Alcohol wordt afgebroken in de lever, met behulp van twee enzymen. Het leverenzym alcohol dehydrogenase (A.D.H.) zet alcohol om in het giftige acetaldehyde, dat verantwoordelijk is voor de meeste schadelijke effecten van overmatig alcoholgebruik. Door een variatie in het ADH-gen, zetten Aziaten de alcohol honderd keer sneller om in acetaldehyde dan mensen met de Westerse variant. Vervolgens zet het enzym aldehyde dehydrogenase de acetaldehyde om in het onschadelijke acetaat (ook wel azijnzuur). Bij 30-50% van de Aziaten werkt dit enzym minder goed. Door deze twee genetische variaties, hebben zij hogere concentraties acetaldehyde in hun bloed, bij het drinken van dezelfde hoeveelheid alcohol. Dit leidt ertoe dat ze sneller dronken worden, met alle vervelende effecten die daarmee samenhangen, zoals hoofdpijn en braken. Je arme vriend kan er dus niets aan doen.
De totale hoeveelheid alcohol die het lichaam kan afbreken, wordt geschat op 7 gram alcohol per uur. Eén standaard glas alcohol bevat 10 gram alcohol, en het duurt dus 1 tot 1.5 uur voor dit is afgebroken. Als je drinktempo hoger ligt dan deze afbraaksnelheid, en daar zit je al snel aan, blijft het teveel aan alcohol in je bloed circuleren tot de lever in staat is om het af te breken.
(http://www.wrmmagazine.nl/aziaten-sneller-dronken/)

Afbraak van alcohol in het lichaam
De opname en afbraak van alcohol in het lichaam krijgt voorrang op andere voedingsstoffen. Het lichaam kan alcohol niet opslaan en ziet het als een potentieel toxische stof. Na opname in de maag en darmen gaat alcohol via het bloed naar de lever, waar het grootste deel van de alcohol wordt afgebroken (90-95%). Ook in de maag wordt al een kleine hoeveelheid alcohol afgebroken, maar deze hoeveelheid is verwaarloosbaar vergeleken met de lever (1-5%)3.

De afbraak van alcohol wordt schematisch weergegeven in figuur 1. De eerste stap van de afbraak van alcohol gebeurt door het enzym alcoholdehydrogenase (ADH). ADH zorgt voor de oxidatie van alcohol naar aceetaldehyde. Dit is een toxische stof die verantwoordelijk is voor sommige negatieve gevolgen van chronisch overmatige alcoholconsumptie, zoals de ontwikkeling van leverfibrose en -cirrose5,6. Aceetaldehyde wordt in de tweede stap omgezet naar het onschuldige acetaat onder invloed van aceetaldehyde dehydrogenase (ALDH). ADH en ALDH breken alcohol af door in twee stappen waterstofmoleculen te verwijderen (NAD tot NADH). NAD is een B-vitamine en heeft de rol van co-enzym in de omzetting van alcohol naar acetaat. NAD neemt de waterstofmoleculen aan die ADH en ALDH verwijderen1.Vervolgens wordt acetaat omgezet tot acetyl CoA of tot koolstofdioxide. Acetyl CoA wordt door het lichaam gebruikt om energie van te produceren via de citroenzuurcyclus. Als er teveel NADH en waterstofmoleculen ophopen in het lichaam, dan wordt de citroenzuurcyclus afgeremd en is het lichaam genoodzaakt om acetyl CoA op te slaan als vet in het lichaam1. (https://www.kennisinstituutbier.nl/gezondheid/gezondheid/metabolisme)

http://sites.dartmouth.edu/dujs/files//2009/11/zbeda_equation_cmyk.jpg


Alcohol dehydrogenase Alcohol dehydrogenases ( ADH ) ( EC 1.1.1.1 ) are a group of dehydrogenase enzymes that occur in many organisms and facilitate the interconversion between alcohols and aldehydes or ketones with the reduction of nicotinamide adenine dinucleotide (NAD + to NADH). In humans and many other animals, they serve to break down alcohols that otherwise are toxic, and they also participate in generation of useful aldehyde, ketone, or alcohol groups during biosynthesis of various metabolites. In yeast, plants, and many bacteria, some alcohol dehydrogenases catalyze the opposite reaction as part of fermentation to ensure a constant supply of NAD +. [Source: Wikipedia] (https://www.genenames.org/data/genegroup/#!/group/397)

Alcohol wordt opgenomen in de maag (20%) en in de darmen (80%) en via het bloed verspreid door het hele lichaam.
Alcohol komt 10 minuten na consumptie aan in de hersenen. Het heeft een verdovend effect op het centrale zenuwstelsel.
5% van de alcohol wordt direct uitgescheiden via adem, transpiratie en urine. 90-95% wordt door de lever afgebroken tot acetaat en uitgescheiden als water en koolzuur (CO2).
Bij de afbraak van alcohol spelen twee enzymen een rol; alcoholdehydrogenase (ADH) en aceetaldehydedehydrogenase (ALDH).
Het duurt ongeveer anderhalf uur voordat een standaard alcoholische consumptie (10 gram alcohol) is afgebroken en uitgescheiden. (https://www.kennisinstituutbier.nl/gezondheid/gezondheid/metabolisme)


Aldehydedehydrogenase (ALDH) is het enzym in het mitochondrium dat de afbraak van ethanal (aceetaldehyde) tot azijnzuur mogelijk maakt. Hierna wordt acetyl-CoA gevormd uit het azijnzuur en Coënzym A. Dit gaat de citroenzuurcyclus in waarna het afgebroken wordt tot koolstofdioxide en water.
Dit enzym is uiterst belangrijk, omdat het de giftige stof ethanal moet afbreken. Zonder dit enzym brengt onafgebroken ethanal schadelijke effecten toe aan het lichaam, waardoor de functionaliteit beperkt wordt.
Variant
Verder is het aangetoond dat een variant van dit enzym bij Oost-Aziatische individuen veel minder efficiënt is dan het normale enzym.[bron?] Dit zorgt ervoor dat grote hoeveelheden ethanal langdurig in het lichaam onafgebroken blijven, waardoor de toxische effecten voor ernstigere gevolgen zorgen. Mensen uit landen als Japan zijn meestal ook geen stevige drinkers, omdat ze de ethanal slecht kunnen verwerken. Dit verschijnsel verschilt echter van persoon tot persoon in verband met factoren als lichaamsgewicht. (https://nl.wikipedia.org/wiki/Aldehydedehydrogenase)

Wacht even, enzymen zijn toch geen genen???
De Aziatische variant mist op Wikipedia een bron?

Ethanol is metabolized mainly by 2 major enzymes: alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Genetic variations of genes encoding the 2 enzymes are very common among East Asians but relatively rare for most other populations. Facial flushing and other physical discomforts after alcohol drinking triggered by accumulation of acetaldehyde through defective genes for ADH and ALDH have been reported. Approximately 40% of East Asians (Chinese, Japanese, and Korean) show facial flushing after drinking alcohol, known as "Asian flush," which is characterized by adverse reactions on alcohol drinking in individuals possessing the fasting metabolizing alleles for ADH, ADH1B*2, and ADH1C*1, and the null allele for ALDH and ALDH2*2. Alcoholism is determined not only by the genetic deficiency but also by behaviors that involve complex interactions between genetic and sociocultural factors.  (https://www.ncbi.nlm.nih.gov/pubmed/25271825)

Alcohol flush reaction is a condition in which a person develops flushes or blotches associated with erythema on the face, neck, shoulders, and in some cases, the entire body after consuming alcoholic beverages. The reaction is the result of an accumulation of acetaldehyde, a metabolic byproduct of the catabolic metabolism of alcohol, and is caused by an acetaldehyde dehydrogenase deficiency.[3]
This syndrome has been associated with an increased risk of esophageal cancer in those who drink.[1][4] It has also been associated with lower than average rates of alcoholism, possibly due to its association with adverse effects after drinking alcohol.[5]
Approximately 36% of East Asians (Chinese, Japanese, and Koreans) show characteristic physiological responses to drinking alcohol that includes facial flushing, nausea, headaches and a fast heart rate.[2][1][3] ... Around 80% of East Asians (less common in Southeast Asia and the Indian subcontinent) have a variant of the gene coding for the enzyme alcohol dehydrogenase called ADH1B, whereas almost all Chinese, Japanese, and Korean people have a variant of the gene called ADH1C.[11] These varients result in the alcohol dehydrogenase enzyme converting alcohol to toxic acetaldehyde at a higher efficiency than other gene variants (40- to 100-fold in case of ADH1B).[5]
In about 50% of East Asians, the increased acetaldehyde accumulation is worsened by another gene variant, the mitochondrial ALDH2 allele, which results in a less functional acetaldehyde dehydrogenase enzyme, responsible for the breakdown of acetaldehyde.[11] The result is that affected people may be better at metabolizing alcohol, often not feeling the alcohol "buzz" to the same extent as others, but show far more acetaldehyde-based side effects while drinking alcohol.
Genetics... Alcohol flush reaction is best known as a condition that is experienced by people of East Asian descent. According to the analysis by HapMap project, the rs671 allele of the ALDH2 responsible for the flush reaction is rare among Europeans and Sub-Saharan Africans. 30% to 50% of people of Chinese, Japanese, and Korean ancestry have at least one ALDH2 allele.[12] The rs671 form of ALDH2, which accounts for most incidents of alcohol flush reaction worldwide, is native to East Asia and most common in southeastern China. It most likely originated among Han Chinese in central China,[13] ... Since the mutation is a genetic issue, there is currently no cure for the flush reaction. Prevention would include not drinking alcohol. (https://en.wikipedia.org/wiki/Alcohol_flush_reaction)

The liver metabolises alcohol (ethanol) in two steps: in the first step, an enzyme (Alcohol Dehydrogenase; ADH) turns the toxic alcohol into another toxic substance, called acetaldehyde. The second step takes care of the toxic acetaldehyde by turning it into acetate, which is safe for the body. This last step is facilitated by the enzyme Aldehyde Dehydrogenase (ALDH).  In people from Asian descent, it’s this particular enzyme they lack
This is caused by a gene variant of the alleles responsible for the enzyme ALDH. Most people carry the ADH1B*1, ADH1C*2 or ALDH2*1 gene that codes for ALDH, but around half of the Asian people carry at least one of the ADH1B*2, ADH1C*1 or ALDH2*2 genes that code for inactive ALDH. Consequently, the acetaldehyde will not be metabolized in acetate and thereby rapidly accumulates in the body, causing redness of the skin, often referred to as “Asian flush”. Besides this, it can cause nausea, headache and even hangovers.
These consequences of the acetaldehyde build-up are the least concerning. Recent studies by Akira Yokoyama and colleagues in Japan showed that the alcohol-related acetaldehyde build-up can even cause esophageal cancer. Yokoyama compared East-Asian people with and without the inactive ALDH-gene. The study showed that the participants with the inactive ALDH-gene are 6-10 times more likely to develop esophageal cancer in comparison with the ones from the active ALDH-gene group. ... In summary, around 50% of the Asian people have inactive ALDH, which causes problems when drinking alcohol. These problems include the so-called Asian flush, nausea, headache, hangovers and even esophageal cancer. So next time you have Asian people over, go easy on the bottle, don’t laugh at them when they turn red or vomit, give some advice instead.(https://www.libcblog.nl/articles/alcohol-intolerance-asian-friends)

Written on May 1, 2014 by Hsin-Yu Chang and Alex Mitchell
Do you have friends that cannot handle alcoholic drinks? Just half a pint of beer or a few sips of wine, and their faces turn red, possibly with some hangover symptoms, such as headaches and nausea? You may envy their cheap night out, but wonder why these people cannot tolerate alcohol as you do. The phenomenon is called ‘alcohol flush reaction’, also known as ‘Asian flush syndrome’, due to its association with the Asian population. It is a condition caused by the accumulation of acetaldehyde, a metabolic byproduct of the catabolic metabolism of alcohol.... Normally, during the alcohol metabolic process, ethanol is converted to acetaldehyde by an alcohol dehydrogenase enzyme, called ADH1B, and then broken down to acetic acid by an aldehyde dehydrogenase enzyme (ALDH).
In humans, there are nineteen identified ALDH genes (ALDH1-19). Most Europeans have normal copy of the ALDH2 gene, whilst approximately 30-50% of East Asians carry an allele (ALDH2*2) that results in the synthesis of a less efficient enzyme [1].
ALDH2 forms homotetramers. Each subunit in the tetramer consists of three domains - the catalytic domain, the coenzyme-binding domain and the oligomerisation domain. The low activity of ALDH2*2 is the result of a substitution of lysine for glutamate at position 487 (Glu487) of the 500-amino-acid mature enzyme [2]. The Glu487 links the coenzyme-binding site to the active site, which creates a stable structural scaffold contributing to catalysis (Figure 1). In the ALDH2*2 apoenzyme, the presence of a lysine at residue 487 disturbs the hydrogen bonds and causes disruptions of the αG helix structure [3]. This reduces affinity for the coenzyme and lowers the rate of the metabolic process [3].
As a result of this mutation, acetaldehyde accumulates whenever alcohol is consumed. Unfortunately, acetaldehyde is a DNA damaging agent that can cause cancer [4], and a higher risk of ALDH2-deficient drinkers developing esophageal cancer has been shown by several studies [4,5,6]. A knock out mouse model also links ethanol consumption with higher risk of acetaldehyde toxicity in ALDH2 deficient individuals [7]. But whilst the outlook seems to be dim and gloomy for the ALDH2*2 drinkers, on the bright side, they are less likely to suffer alcohol addiction problems [8]. In fact, there is a drug called disulfiram that causes symptoms similar to Asian flush syndrome that is used to treat alcoholism.... We may not yet understand the reason why the ALDH2 deficiency is widespread in Asian populations. However, research can help us understand more about the relationship between ALDH2, cancers and alcoholism, as well potentially uncovering the safe number of alcohol units that ALDH2*2 individuals can consume.
So before you encourage your friends to have another glass of wine or a pint of beer, you may need to check if they have the Asian flush symptoms, or even review their ALDH2 phenotype! (https://proteinswebteam.github.io/interpro-blog/2014/05/01/Dionysian-mysteries-the-aldehyde-dehydrogenase-(ALDH)-family/)

Okee, dus het zijn dus wel genen en inderdaad hebben Aziaten een mutatie waardoor ze slechter alcohol afbreken en daardoor dus eerder dronken worden.

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