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.
This is a preview of subscription content, access via your institution.
Referenties
WHO. Global Strategy on Diet Physical Activity and Health. http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/index.html.
WHO. Global Alliance for the Prevention of Obesity and Related Chronic Disease. http://www.preventionalliance.net.
Haslam D, Rigby N. A long look at obesity. Lancet. 2010;376(9735): 85–6.
Gaulin SJC, Konner M. On the natural diet of primates, including humans. In: Wurtman RJ, Wurtman JJ, editors. Nutrition and the Brain. New York: Raven Press, 1977;1–86.
Reed KE. Early hominid evolution and ecological change through the African Plio-Pleistocene. J Hum Evol. 1997; 32(2- 3): 289–322.
Leonard WR, Robertson ML, Snodgrass JJ. Energetics and the evolution of brain size in early Homo. In: Roebroeks JWM, editor. Guts and Brains. An integrative approach to the hominin record. Leiden: Leiden University Press, 2007: 29–46.
Broadhurst CL, Cunnane SC, Crawford MA. Rift Valley lake fish and shellfish provided brain-specific nutrition for early Homo. Br J Nutr. 1998;79(1): 3–21.
Cordain L, Eaton SB, Miller JB, Mann N, Hill K. The paradoxical nature of hunter-gatherer diets: meat-based, yet nonatherogenic. Eur J Clin Nutr. 2002;56 Suppl 1:S42–S52.
Huang M-C, Brenna JT. On the relative efficacy of alinolenic acid and preformed docosahexanoic acid as substrates for tissue docohexanoate during perinatal development. In: Mostofsky DI, Yehuda S Jr, editors. Fatty acids: physiological and behavioral functions. Totowa, NJ: Humana Press, 2001: 99–113.
Carlson BA, Kingston JD. Docosahexaenoic acid, the aquatic diet, and hominin encephalization: difficulties in establishing evolutionary links. Am J Hum Biol. 2007;19(1): 132–41.
Leonard WR, Snodgrass JJ, Robertson ML. Effects of brain evolution on human nutrition and metabolism. Annu Rev Nutr. 2007;27: 311–27.
Cunnane SC, Crawford MA. Survival of the fattest: fat babies were the key to evolution of the large human brain. Comp Biochem Physiol A Mol Integr Physiol. 2003;136(1): 17–26.
Cordain L, Watkins BA, Mann NJ. Fatty acid composition and energy density of foods available to African hominids. Evolutionary implications for human brain development. World Rev Nutr Diet. 2001;90: 144–61.
Goren-Inbar N, Alperson N, Kislev ME, Simchoni O, Melamed Y, Ben-Nun A, et al. Evidence of hominin control of fire at Gesher Benot Ya’aqov, Israel. Science. 2004;304(5671): 725–7.
Carmody RN, Wrangham RW. The energetic significance of cooking. J Hum Evol. 2009;57(4): 379–91.
McDonald K. Ecological hypotheses for human brain evolution: evidence for skill and learning processes in the ethnographic literature on hunting. In: Roebroeks JWM, editor. Guts and Brains. An integrative approach to the hominin record. Leiden: Leiden University Press, 2007: 107–32.
Coward F, Gamble C. Big brains, small worlds: material culture and the evolution of the mind. Philos Trans R Soc Lond B Biol Sci. 2008;363(1499): 1969–79.
Guthrie RD. Haak and Steek-The tool that allowed hominins to colonize the African savanna and to fourish there. In Roebroeks JWM, editor. Guts and Brains. An integrative approach to the hominin record. Leiden: Leiden University Press, 2007: 133–64.
Speakman JR. A nonadaptive scenario explaining the genetic predisposition to obesity: the ‘predation release’ hypothesis. Cell Metab. 2007;6(1): 5–12.
Stringer C. Human evolution: Out of Ethiopia. Nature. 2003;423(6941): 692-3, 695.
Diamond J. Guns Germs and Steel. The fates of human societies. New York: W.W.Norton & Company Ltd, 1999.
Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr. 2000; 71(3): 682–92.
Cordain L, Watkins BA, Florant GL, Kelher M, Rogers L, Li Y. Fatty acid analysis of wild ruminant tissues: evolutionary implications for reducing diet-related chronic disease. Eur J Clin Nutr. 2002;56(3): 181–91.
Cohen MN. Health and the rise of civilisation. New Haven, Conn: Yale University Press, 1989.
Cohen MN. The significance of long-term changes in human diet and food economy. In: Harris M, Ross EB, editors. Food and Evolution: Toward a Theory of Human Food Habits. Philadelphia, PA: Temple University Press, 1987: 261–83.
Cassidy CM. Nutrition and health in agriculturalists and hunter-gatherers: a case study of two prehistoric populations. In: Jerome NW, Kandel RF, Pelto GH, editors. Nutritional Anthropology: Contemporary Approaches to Diet and Culture. Pleasantville, NY: Redgrave Publishing Co, 1980: 117–45.
Ruff CB, Trinkaus E, Holliday TW. Body mass and encephalization in Pleistocene Homo. Nature. 1997;387(6629): 173–6.
Haslam D. Obesity: a medical history. Obes Rev. 2007; 8 Suppl 1: 31–6.
O’Grada C. Markets and famines in pre-industrial Europe. Journal of Interdisciplinary History. 2005;36: 143–66.
Maddison A. The World Economy. Historical Statistics. Paris: OECD, 2003.
Food and Agricultural Organisation EaSDD. World Agriculture: towards 2015/2030. Summary Report. 2002.
Popkin BM, Gordon-Larsen P. The nutrition transition: worldwide obesity dynamics and their determinants. Int J Obes Relat Metab Disord. 2004;28 Suppl 3:S2–S9.
Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2): 341–54.
O’Keefe JH, Vogel R, Lavie CJ, Cordain L. Achieving Huntergatherer Fitness in the 21(st) Century: Back to the Future. Am J Med. 2010;123(12): 1082–6.
Haslam DW, James WP. Obesity. Lancet. 2005;366(9492): 1197–209.
van Marken Lichtenbelt WD, Vanhommerig JW, Smulders NM, Drossaerts JM, Kemerink GJ, Bouvy ND, et al. Coldactivated brown adipose tissue in healthy men. N Engl J Med. 2009;360(15): 1500–8.
Cypess AM, Lehman S, Williams G, Tal I, Rodman D, Goldfne AB, et al. Identifcation and importance of brown adipose tissue in adult humans. N Engl J Med. 2009;360(15): 1509–17.
Diamond J. The double puzzle of diabetes. Nature. 2003;423(6940): 599–602.
Daniel M, Rowley KG, McDermott R, Mylvaganam A, O’Dea K. Diabetes incidence in an Australian aboriginal population. An 8-year follow-up study. Diabetes Care. 1999;22(12): 1993–8.
Ebbesson SO, Schraer CD, Risica PM, Adler AI, Ebbesson L, Mayer AM, et al. Diabetes and impaired glucose tolerance in three Alaskan Eskimo populations. The Alaska-Siberia Project. Diabetes Care. 1998;21(4): 563–9.
O’Dea K. Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes. 1984;33(6): 596–603.
Neel JV. Diabetes mellitus: a ‘thrifty’ genotype rendered detrimental by ‘progress’? Am J Hum Genet. 1962;14: 353–62.
Vallence-Owen J, Lilley MD. Insulin antagonism in the plasma of obese diabetic and prediabetics. Lancet. 1961;1(7181): 806–7.
Neel JV, Weder AB, Julius S. Type II diabetes, essential hypertension, and obesity as ‘syndromes of impaired genetic homeostasis’: the ‘thrifty genotype’ hypothesis enters the 21st century. Perspect Biol Med. 1998;42(1): 44–74.
Maes HH, Neale MC, Eaves LJ. Genetic and environmental factors in relative body weight and human adiposity. Behav Genet. 1997;27(4): 325–51.
O’Rahilly S. Human genetics illuminates the paths to metabolic disease. Nature. 2009;462(7271): 307–14.
McCarthy MI. Genomics, type 2 diabetes, and obesity. N Engl J Med. 2010;363(24): 2339–50.
O’Rahilly S, Farooqi IS. Genetics of obesity. Philos Trans R Soc Lond B Biol Sci. 2006;361(1471): 1095–105.
Staiger H, Machicao F, Fritsche A, Haring HU. Pathomechanisms of type 2 diabetes genes. Endocr Rev. 2009;30(6): 557–85.
Stumvoll M, Goldstein BJ, van Haeften TW. Type 2 diabetes: principles of pathogenesis and therapy. Lancet. 2005;365(9467): 1333–46.
Walley AJ, Asher JE, Froguel P. The genetic contribution to non-syndromic human obesity. Nat Rev Genet. 2009;10(7): 431–42.
Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ. Weight in infancy and death from ischaemic heart disease. Lancet. 1989;2(8663): 577–80.
Jackson AA, Burdge GC, Lillycrop KA. Diet, nutrition and modulation of genomic expression in fetal origins of adult disease. World Rev Nutr Diet. 2010;101: 56–72.
Jaenisch R, Bird A. Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals. Nat Genet. 2003;33 Suppl: 245–54.
Heerwagen MJ, Miller MR, Barbour LA, Friedman JE. Maternal obesity and fetal metabolic programming: a fertile epigenetic soil. Am J Physiol Regul Integr Comp Physiol. 2010;299(3):R711–R722.
Stein AD, Kahn HS, Rundle A, Zybert PA, van der Pal-de Bruin, Lumey LH. Anthropometric measures in middle age after exposure to famine during gestation: evidence from the Dutch famine. Am J Clin Nutr. 2007;85(3): 869–76.
Hult M, Tornhammar P, Ueda P, Chima C, Bonamy AK, Ozumba B, et al. Hypertension, diabetes and overweight: looming legacies of the Biafran famine. PLoS One. 2010;5(10):e1358–2.
DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am. 2004;88(4): 787-835, ix.
Pereira S, Marliss EB, Morais JA, Chevalier S, Gougeon R. Insulin resistance of protein metabolism in type 2 diabetes. Diabetes. 2008;57(1): 56–63.
Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120(16): 1640–45.
Lahiry P, Pollex RL, Hegele RA. Uncloaking the genetic determinants of metabolic syndrome. J Nutrigenet Nutrigenomics. 2008;1(3): 118–25.
Colagiuri S, Brand MJ. The ‘carnivore connection’–evolutionary aspects of insulin resistance. Eur J Clin Nutr. 2002;56 Suppl 1:S30–S35.
Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM. Diabetologia. 1994;37(12): 1280–6.
Galic S, Oakhill JS, Steinberg GR. Adipose tissue as an endocrine organ. Mol Cell Endocrinol. 2010;316(2): 129–39.
Pasquali R, Patton L, Gambineri A. Obesity and infertility. Curr Opin Endocrinol Diabetes Obes. 2007;14(6): 482–7.
Author information
Authors and Affiliations
Corresponding author
Additional information
In: Neth J Med. 2011 Apr;69(4):159-66.
Afdeling interne geneeskunde, Universitair Medisch Centrum Leiden
Correspondentie:
Hanno Pijl Afdeling interne geneeskunde Universitair Medisch Centrum Leiden tel.: +31 (0)71 526 37 38
h.pijl@lumc.nl
About this article
Cite this article
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
Published:
Issue Date:
DOI: https://doi.org/10.1007/s12467-011-0126-0