Obesity in Young Europeans: Genetic and Environmental In¯Uences

Obesity in young Europeans: genetic and environmental in¯uences

JA MartõÂnez*

Department Physiology and Nutrition, University of Navarra, Pamplona, Spain

Background: Nutrition, lifestyles and genetics are increasingly involved in the maintenance of health and the prevalence of several non-communicable diseases, such as cardiovascular illnesses, diabetes, cancer etc. In this context, obesity appears as a complex multi-factorial condition resulting from an imbalance between energy intake and expenditure, which has been associated with the genetic background (more than 50 genes have been located in the human gene map associated to obesity), but also with environmental forces such as reduced physical activity (more than 60% of Europeans spend more than 3 h sitting at work) and with the overconsumption of fat-rich and high energy yielding foods (fat oxidation is poorly regulated as compared with other fuel substrates). Subjects: Furthermore, subject selection was quota-controlled to make the sample nationally representative by various socio-demographic factors based on the most recent of®cial statistics (census data) in each member state. Overall, there were 15,239 subjects older than 15 y in the EU (17% of them were younger than 24 y old). Results: The obesity problem appears to be increasing rapidly in children and adolescents as well as in adults with an average rate of obese subjects of about 10% in the European Union, however several factors should be taken into consideration, such as the cut-off references, the age group and the conditions of the data collection when processing the information about obesity prevalence. Conclusions: Management of the increasing epidemic of obesity in young people must involve prevention strategies concerning nutritional education and physical activity programmes. Descriptors: obesity; adolescents; genes; dietary habits; exercise European Journal of Clinical Nutrition (2000) 54, Suppl 1, S56±S60

Obesity prevalence in young Europeans Comprehensive data about obesity rates in Europe come from the Monica study (WHO-Monica, 1989). A great Obesity, which has been de®ned as a body fat excess, variability both within and between countries has been occurs as a consequence of an imbalance in the energy reported in that study, which pointed out that about 15% equation, where calorie intake is higher than energy expen- of men and 22% women are obese, while other data reveal diture (MartõÂnez & FruÈhbeck, 1996). This pathological a prevalence of obesity in the range of 8 ± 20% for men and condition, which involves high economic costs and health 10 ± 25% in women (Seidell, 1995). complications, has been assessed by many different meth- An integrated recent overview of the global prevalence ods, although the BMI (weight=height2) is by far the most of obesity in the European Union can be obtained from a common tool to identify overweight (BMI 25 ± 30 kg=m2) survey completed between February and April 1997 under and obese (BMI>30 kg=m2) subjects in epidemiological the auspices of the IEFS (Dublin), which developed a studies (Bray, 1998). However, classifying obesity during questionnaire on body-weight and health (Gibney et al, adolescence has the complication that height and body 1997; MartõÂnez et al, 1999). One of the objectives of the composition are still changing (Friedman, 1997, Page & survey was to determine the proportion and socio-demo- Fox, 1998). Furthermore, differences in the age of the onset graphic characteristics of the obese population (self- of puberty may affect fat deposition (OMS=WHO, 1998). reported) in the EU. Subjects were asked to report their Traditionally, obesity therapy and management have own height and weight to calculate the body mass index been based upon dietary strategies, physical activity and (BMI, kg=m2) in order to estimate the extent of under- behavior programs, different pharmacological approaches weight, normal weight, overweight and obese throughout (anorectics, thermogenic agents, enzyme-blocking com- the EU. In this report, BMI was classi®ed as follows under- pounds, etc.) and surgical procedures (Aronne, 1998; weight <19.99, normal-weight 20 ± 24.99, over-weight Barlow & Dietz, 1998. Weiser et al, 1997), although 25 ± 29.99 and obese >30 (MartõÂnez et al, 1999). The increasing evidence suggests that prevention is a key national samples were weighted according to the propor- factor to successfully overcoming the growing `epidemic' tional size of the population of each country. of overweight and obese individuals in both developed and From the EU average results, it can be noted that almost developing societies (Jeffery, 1995, Gill, 1997). half of the EU population are within the normal weight range (MartõÂnez et al, 1998). The UK had the highest prevalence of obesity (12%), while the Italians, the *Correspondence: J Alfredo MartõÂnez, Department of Physiology and French and the Swedes have the lowest levels of obesity Nutrition, University of Navarra, c= Irunlarrea s=n, 31008-Pamplona (Navarra) Spain. (about 7%). The data concerning the occurrence of obesity E-mail: [email protected] (BMI>30) in young subjects (15 ± 24 y old) revealed a Obesity in young Europeans JA MartõÂnez S57 regional in¯uence (Figure 1), the values ranging between through the control of afferent mechanisms (leptin, nutri- 5.2% in Austria and 1% in Italy, as well as in young adults ents, etc.), the central nervous system (hypothalamic neuro- (25 ± 34 y old), where British (14.4%) and Italians (3.2%) transmitters) or efferent mechanisms (SNS, insulin etc.), showed the highest and the lowest rates of obesity pre- which may be affected by environmental in¯uences (Mar- valence, respectively. tõÂnez & FruÈhbeck, 1996; Hill & Peter, 1998). The genetic The lack of consistency between studies in children and epidemiology of human obesity tries to identify those traits, adolescents has been attributed to methodological reasons that are associated with the genotype and more affected by and classi®cation criteria, but also to genetic and societal external forces such as dietary habits and sedentary life- factors (Bray et al, 1998). In this context, the BMI is widely styles (Bouchard et al, 1998, Cowburn et al, 1997). In this used, despite some limitations (WHO Expert Committee, context, four types of the obesity phenotype can be dis- 1998, Page & Fox, 1998). Nevertheless, whatever method tinguished from an anatomical perspective: type I (excess is used to classify obesity, studies investigating obesity body mass or body fat), type II (excess subcutaneous during childhood and adolescence have generally reported abdominal fat or android), type III (excess abdominal a high prevalence of obesity, and that rates are on the visceral fat) and type IV (excess gluteo-femoral fat or increase (OMS=WHO,1998). In a survey carried out in the gynoid). USA, the prevalence of overweight people (de®ned by the Evidence for the relationships of genetic heritability or 85th percentile of weight-for height) among 5 ± 24-year-old transmission to the BMI or body fat phenotype have been rose approximately two-fold in two decades (Friedman, obtained by using many different research approaches 1997). A similar trend has been observed in Japan, where (Beales & Kopelman 1996; Chagnon et al, 1997; MartõÂnez, the rates of obese schoolchildren (>120% standard body 1999; Garcia et al, 1998) such as map location of obesity- weight (SBW)) aged 6 ± 14 y increased from 5% to 10% related Mendelian disorders, single gene mutations and between 1974 and 1993 (Kotani, 1997). Moreover, child- transgenic models of obesity in rodents and quantitative hood and adolescence obesity is already evident in some traits locus by crossbreeding experiments as well as developing countries. Thus, in a study concerning 6 ± 18-y- through association or linkage studies concerning candidate old male schoolchildren in Saudi Arabia, the prevalence of genes (family segregation, adoption and twin surveys). obesity was found to be 15.8% (Al-Nuaim et al, 1996), Thus at the end of the twentieth century, more than 50 while the prevalence of obesity among schoolchildren aged genes (ADBR3, LPL, UCP's, PPAR, Ob, LEPR, POMC, 6 ± 12 y in Thailand, as diagnosed by weight-for- etc.) have been related directly or indirectly to obesity height>120% of the reference, was about 15.6% (Mo- heritability (Chagnon et al, 1998), located in different loci suvan et al, 1993). of the human gene obesity map (Figure 2). From data currently available on the global prevalence of obesity during childhood compiled by the WHO Pro- gramme of Nutrition (WHO, 1990 and 1997), children were Sedentary habits and obesity classi®ed as obese when they exceeded the NCHS median weight-for-height plus two standard deviations or z-scores. Sedentary lifestyles are increasingly involved in the pre- However, some obese children under this criteria may valence of obesity (Taubes, 1998; Bar et al, 1998). Thus, actually have a higher relative weight due to stunting the process of modernization transport, labour-saving rather than as a result of excess adiposity (Popkin et al, devices, TV viewing etc has brought about a number of 1996). consequences affecting physical activity patterns that contribute to obesity (OMS=WHO, 1998; Goldblatt et al, 1995). In fact, the growing increase in the number of Gene in¯uences on obesity obese people in Europe appears to be associated with sedentarism (Prentice & Jebb, 1995; Seidell, 1995). Body weight and composition are conditioned by the Physical activity assessment has been carried out genetic background (Chagnon et al, 1998; Bray, 1997) through questionnaires and interviews by obtaining information about the period of time dedicated to sport, to watching television, to walking, or sitting down (Kriska & Carpesen, 1997). Using one of these methodological approaches, a survey about `Attitudes to physical activity exercise, body weight and health in the EU population' developed by the IEFS (MartõÂnez et al, 1998) showed that age is an important aspect affecting the number of hours spent sitting down at work (Figure 3A) and in leisure time (Figure 3B) as well as the time spent walking (Figure 3C). Furthermore, the proportion of individuals not participating in any sport increase with age, young subjects being more involved in exercise activities (Figure 3D). In general, it was found that young people (15 ± 34 y old) are more active then older subjects. Since increasing physical activity patterns are consid- ered a major modi®able factor affecting excessive body weigh gain, the implementation of prevention strategies, particularly in children and young subjects should be a key Figure 1 Prevalence of obesity in 15 ± 24 and 25 ± 34 y old young goal in reducing obesity rates (Bar et al, 1998; Barlow & Europeans. Dietz, 1998).

European Journal of Clinical Nutrition Obesity in young Europeans JA MartõÂnez S58

Figure 2 The human obesity gene map.

Figure 3 Patterns of physical activity in Europeans by measuring: (A) percentage of subjects sitting down for more than 3 h at work; (B) subjects sitting down more than 3 h in leisure time on a typical working day; (C) percentage of subjects walking less than 1 h=day; and (D) percentage of subjects not participating in any physical activity=sport.

Dietary habits and obesity fat-rich diet is a factor that may lead some people to obesity (Schutz, 1995), since it seems that the fat oxida- The overconsumption of high-energy yielding foods has tion and balance are poorly regulated as compared to been involved in the imbalance of the energy equation other fuel substrates such as protein and carbohydrates (MartõÂnez, 1996), despite the general interest in healthy (Scharauwen et al, 1997). Paradoxically, within areas of eating in the European population (Margetts et al, 1997). similar economic development, regional consumption of Furthermore, the fuel distribution appears to in¯uence fat and prevalence of obesity have not been positively body weight regulation. Thus, there are evidences that a correlated (Willett, 1998). Thus, within the United States

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Figure 4 Difference in glucose (A) and lipid oxidation (B) in lean young individuals fed on a formula with high content & carbohydrates (HC) or fat (HF). a substantial decline in fat=energy intake and frequent use Acknowledgements ÐThe IEFS (Dublin) and Directorate General V (EU of low-calorie food items have been associated with an Agreement 05 FO3) as well as Linea Especial (Nutrition and Obesity L97) increase in obesity rates, which could be explained by a are gratefully credited for ®nancial and scienti®c support. dramatic reduction in physical activity related energy expenditure (Tremblay & AlmeÂras, 1996; Heini and References Weinsier, 1997). Al-Nuaim AR, Bamgboye EA & Al-Herbish A (1996): The pattern of In this context, in an experimental trial concerning lean growth and obesity in Saudi Arabian male school children. Int. J. Obes. healthy young individuals (20 ± 27 y old), who were fed on Relat. Metabol. Disord. 20, 1000 ± 1005. two isocaloric liquid formulas with different macronutrient Aronne LJ (1998): Obesity. Med. Clin. North 82, 161 ± 181. composition: high fat (HF: 80% energy from lipids) and Bar OR, Foreyt J, Brownell KD, Dietz WH, Ravussin E, Salbe AD, high carbohydrate (HC: 80% energy from sugars), nutrient Schewenger S, Jeor S & Torun B (1998): Physical activity, genetic and nutritional considerations in childhood weight management. Med. Sci. oxidation was calculated with a computerized open-circuit Sports. Exerc. 30, 2 ± 10. calorimeter (Schutz, 1995), which showed that diet com- Barlow SE & Dietz WH (1998): Obesity evaluation and treatment: expert position may in¯uence body fat deposition, in addition to committee recommendations. Pediatrics 102, E29. the energy intake. Thus, post-prandial carbohydrate oxida- Beales PL & Kopelman PG (1996): Obesity genes. Clin. Endocrinol. 45, tion was higher with the HC than with HF formula and the 373 ± 378. Bouchard C, Perusse L, Rice T & Rao DC (1998): The genetics of human adjustment=matching between energy intake and energy obesity. In Handbook of Obesity, ed. Bouchard, G Bray, WPT James, expenditure was more accurate (Figure 4A and B). In pp. 157 ± 190. Basel: Marcel Dekker. contrast, the excess in energy intake led almost exclusively Bray GA (1997): Progress in understanding the genetics of obesity. J. Nutr. to an accumulation of body fat with the HF, despite an 127, 940S ± 942S. Bray A (1998): Classi®cation and evaluation of the overweight patient. initial increase in lipid oxidation at 30 min after the meal In Handbook of Obesity, ed. C Bouchard, G Bray, WPT James, intake (Labayen & MartõÂnez, 1998; Labayen et al 1999). pp 831 ± 851. Basel: Marcel Dekker. Finally, although energy balance was similar with both Bray GA, Bouchard C & James WPT (1998): Handbook of Obesity,pp meals, substrate balance was more adjusted with the HC 1084. Basel: Marcel Dekker. Chagnon YC, Perusse L & Bouchard C (1997): Familial aggregation of formula. All of this gives support to the hypothesis that obesity, candidate genes and quantitative trait loci. Curr. Opin. Lipido. energy supply from different nutrients may produce weight 8, 205 ± 211. changes that are not fully explained by the energy imbal- Chagnon YC, Perusse L & Bouchard C (1998): The human obesity gene ance, and that fat oxidation is less regulated than protein map: the 1997 update. Obes. Res. 6, 76 ± 92. and carbohydrate oxidation (Skov et al, 1998; Scharauwen Cowburn G, Hillsdwon M & Hankey CR (1997): Obesity management by life-style strategies. Br. Med. Bull. 53, 389 ± 408. et al, 1997). Friedman DS (1997): Secular increases in relative weight and adiposity among children over two decades: the Bogalusa Heart Study. Pediatrics 99, 420 ± 426. Conclusions Garcia F, Margareto J, Marti A, MartõÂnez JA & de Miguel C (1998): ExpresioÂn diferencial de genes en la obesidad inducida por la dieta en The obesity scaling trends all around the world should be ratas. Proc. SEB p 169 (Abstract). attributed to an interplay of several factors such as genetic Gibney MJ, Kearney M & Kearney MJ (1997): Methods used to conduct predisposition and different environmental in¯uences such as surveys on consumer attitudes to food, nutrition and health. Eur. J. Clin. dietary habits and physical activity patterns. Thus, the fat Nutr. 59, 53 ± 57. deposition variability appears to be dependent on genetic Gill TP (1997): Key issues in the prevention of obesity. Med. Bull. 53, 359 ± 388. components affecting both terms of the energy equation (food Goldblatt PB, Moore ME, & Stunkard AJ (1995): Social factors in obesity. intake and energy expenditure) by about 25 ± 40%, while JAMA 191, 1039 ± 1044. cultural factors contribute 30% and-non-communicable Heini AF & Weinsier RL (1997): Divergent trends in obesity and fat intake environmental factors about 40% (Bouchard et al, 1998; patterns: the American paradox. Am. J. Med. 192, 259 ± 264. Hill JO & Peter JC (1998): Environmental contributions to the obesity Orera, 1998). Management of the epidemic of obesity in epidemic. Science 280, 1371 ± 1374. young people must involve prevention strategies involving Jeffery RW (1995): Community programs for obesity prevention. Obes. nutritional education and physical activity programmes. Res. 3, 203S ± 208S.

European Journal of Clinical Nutrition Obesity in young Europeans JA MartõÂnez S60 Kotani K (1997): Two decades or annual medical examinations in Popkin BM, Richards MK & Monteiro CA (1996): Stunting is associated Japanese obese children: do obese children grow into obese adults? with overweight in children of our nations that are undergoing the Int. J. Obes. Metabol. Disord. 21, 912 ± 921. nutrition transition. J. Nutr. 126, 3009 ± 3016. Kriska AM & Caspersen CJ (1997): Introduction to a collection of physical Prentice AM & Jebb S (1995): Obesity in Britain: gluttony or sloth. Br. activity questionnaires. Med. Sci. Sport. Exerc. 29, S5 ± S9. Med. J. 311, 437 ± 439. Labayen I & MartõÂnez JA (1998): DistribucioÂn de macronutrientes de la Scharauwen PD, Van Marken Lichtenbelt W, Saris W & Westerperp K dieta y regulacioÂn del peso y composicioÂn corporal. Nutr y Obes. 2, 23 ± 31. (1997): Changes in fat oxidation in response to a high-fat diet. Am. J. Labayen I, Forga L, MartõÂnez JA (1999): Nutrient oxidation and metabolic Clin. Nutr. 66, 276 ± 282. rate as affected by meals containing different proportions of carbohy- Schutz Y, (1995): Macronutrients and energy balance and obesity. Meta- drates and fat. Eur. J. Nutr. 38, 158 ± 166. bolism 44, 7 ± 11. Margetts BM, MartõÂnez JA, Saba A, Holm M & Kearney M (1997): Seidell JC (1995): Obesity in Europe Ð Scaling a epidemic. Int. J. Obesity De®nitions of healthy eating: a pan-EU survey. Eur. J. Clin. Nutr. 51, 19, S1 ± S4. S23 ± S29. Skov AR, Toubro S, Raben A & Astrup A (1998): A method to achieve MartõÂnez JA (1996): NutricioÂn, metabolismo y obesidad: avances y nuevas control of dietary macronutrient composition in ad libitum diets con- perspectivas. San Sebastian: Universidad del PaõÂs Vasco. sumed by free-living subjects. Eur. J. Clin. Nutr. 51, 667 ± 672. MartõÂnez JA (1999): Determinates geneÂticos de la obesidad. In: Proc. Taubes B (1998): As obesity rates rise, experts struggle to explain why? Symp. Int. Obesidad. Chile: PAHO=OMS (in press). Science 280, 1367 ± 1368. MartõÂnez JA & FruÈhbeck G (1996): Regulation of energy balance and Tremblay A & AlmeÂras N (1996): Physical activity, macronutrient balance adiposity:amodelwithnewapproaches.J.Physiol.Biochem.52,255 ± 258. and body weight control. In: Progress in Obesity Research, pp 207 ± MartõÂnez JA, Kearney JM, Kafatos A, Paquet S & MartõÂnez-GonzaÂlez MA 212. London: Libbey. (1999): Variables independently associated with self-reported obesity Weiser M, Frishman WM, Michaelson MA & Aben Ma (1997): The (BMI>30 kg=m2) in the European Union population. Public Health pharmacological approach to the treatment of obesity. J. Clin. Pharmac. Nutr. 2, 125 ± 134. 37, 453 ± 473. Mo-suvan L, Junjana C & Puctaiboon A (1993): Increasing obesity in school WHO (1990): Diet nutrition and the prevention of chronic diseases. children is a transitional society and the effect of the weight control Report of a WHO Study Group. WHO Technical Report Series no. program. Southeast Asian J. Trop. Med. Public Health 24, 590 ± 594. 797. Geneva: World Health Organization. OMS=WHO (1998): Obesity. Preventing and managing the global epi- WHO (1997): Global Database on Child Growth and Malnutrition. demic. Geneva: World Health Organization. Geneva: WHO=NUT. Orera J (1998): Aspectos geneÂticos de la obesidad. In Obesidad, ed. B WHO Expert Committee (1998): Physical status: the use and interpreta- Moreno, S Monereo, J Alvarez, pp 51 ± 68. Madrid: Aula MeÂdica. tion of anthropometry. Geneva: WHO. Page A & Fox KR (1998): Is body composition important in young WHO-Monica (1989): Project: risk factors. Int. J. Epidemiol. 18, S46 ± S56. people's weight management decision-making? Int. J. Obes. Relat. Willett WC (1998): Is dietary fat a major determinant of body fat? Am. J. Metab. Disord. 22, 186 ± 192. Clin. Nutr. 67, 556S ± 562S.

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