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Obesitas: evolutie van een symptoom van overvloed

Hoe voedsel ons bestaan heeft vormgegeven

Samenvatting

In dit artikel wordt de evolutionaire achtergrond geschetst van de ongekende obesitasepidemie die in de vorige eeuw ontstaan is. Zo’n twee miljoen jaar geleden bracht een klimaatverandering in de habitat van onze primatenvoorouders voedingsaanpassingen op gang die maakten dat onze hersenen konden groeien. Een verschuiving in eetgewoonten voornamelijk gebaseerd op koolhydraten naar eetgewoonten op basis van vis en vlees verschafte voldoende brandstof en bouwstenen om encefalisatie mogelijk te maken. Tegelijkertijd kan insulineresistentie zijn ontstaan als middel om het gevaar van cerebrale hypoglycemie (in het licht van de afgenomen inname van koolhydraten) af te wenden. De daaruit voortvloeiende cognitieve vermogens maakten controle over vuur en de vervaardiging van gereedschappen mogelijk, waardoor voedsel nog meer energie ging opleveren en verdediging tegen roofdieren makkelijker werd. Die laatste ontwikkeling verlichtte de selectieve druk om een optimaal lichaamsgewicht te handhaven, een druk die aangestuurd werd door de predatie van te zware individuen. Willekeurige mutaties die maakten dat het lichaamsgewicht kon toenemen, hebben zich sindsdien via genetische ‘drift’ in de menselijke genenpool verspreid. Ook heeft (seizoensgebonden) voedselonzekerheid in jager-verzamelaargemeenschappen aangezet tot de evolutie van zuinigheidsgenen die tot optimalisatie leidden van de absorptie van voedingsstoffen en de opslag van energie in tijden van voedselaanbod. Door de agrarische en industriële revoluties is onze habitat snel veranderd: vrijwel onbeperkte voorraden van (geraffineerde) voedingsmiddelen en mechanische vervanging van fysieke inspanning stuwen de energiebalans omhoog, vooral bij diegenen onder ons die nog altijd zijn aangepast aan vroegere leefomstandigheden, dat wil zeggen mensen met zuinigheidsgenen en ontbrekende (genetische) bescherming tegen gewichtstoename. Intra-uteriene epigenetische mechanismen versterken potentieel de invloed van deze genen op de aanleg voor obesitas.

Summary

This paper delineates the evolutionary background of the unprecedented epidemic of obesity that has evolved over the last century. Some two million years ago, a change of climate in the habitat of our primate ancestors triggered dietary adaptations which allowed our brain to grow. A shift from principally carbohydrate- based to fish- and meat-based eating habits provided sufficient fuel and building blocks to facilitate encephalisation. Insulin resistance may have evolved simultaneously as a means to avert the danger of hypoglycaemia to the brain (in view of the reduction of carbohydrate intake). Ensuing cognitive capacities enabled the control of fire and the manufacturing of tools, which increased energy yield from food even further and eased the defence against predators. The latter development relieved the selective pressure to maintain an upper level of bodyweight (driven by predation of overweight individuals). Since then, random mutations allowing bodyweight to increase spread in the human gene pool by genetic drift. Also, (seasonal) food insecurity in hunter-gatherer societies spurred the evolution of thrifty genes to maximise nutrient intake and energy storage when food was available. The agricultural and industrial revolutions rapidly changed our habitat: virtually unlimited stocks of (refined) foodstuffs and mechanical substitutes of physical efforts push up energy balance, particularly in those of us who are still adapted to former environmental conditions: i.e. who carry thrifty genes and lack (genetic) protection against weight gain. Intrauterine epigenetic mechanisms potentially reinforce the impact of these genes on the propensity to grow obese.

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Correspondence to Hanno Pijl.

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In: Neth J Med. 2011 Apr;69(4):159-66.

Afdeling interne geneeskunde, Universitair Medisch Centrum Leiden

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Hanno Pijl Afdeling interne geneeskunde Universitair Medisch Centrum Leiden tel.: +31 (0)71 526 37 38

h.pijl@lumc.nl

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Pijl, H. Obesitas: evolutie van een symptoom van overvloed. NED. TIJDSCHR. DIABET. 9, 175–184 (2011). https://doi.org/10.1007/s12467-011-0126-0

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  • DOI: https://doi.org/10.1007/s12467-011-0126-0