Epidemiological and nutritional transition in Mexico: rapid increase of non-communicable chronic diseases and obesity
Juan A Rivera1 , Simo´n Barquera1,*, Fabricio Campirano1 , Ismael Campos1 , Margarita Safdie1 and Vı´ctor Tovar2
1 Centro de Investigacio´n en Nutricio´n y Salud, Instituto Nacional de Salud Pu´blica, Avenida Universidad 655 Col. Santa Marı´a Ahuacatitla´n, Cuernavaca, Morelos, Mexico, CP 62508: 2 Centro de Investigacio´n en Poblaciones, Instituto Nacional de Salud Pu´blica, Cuernavaca, Morelos, Mexico
Public Health Nutrition: 5(1A), 113–122
Abstract
Objective: The objective of this paper is to characterise the epidemiological and nutritional transition and their determinants in Mexico. Design: Age-adjusted standardised mortality rates (SMRs) due to acute myocardial infarction (AMI), diabetes mellitus and hypertension were calculated for 1980–1998. Changes in the prevalences of overweight and obesity in women and children and of dietary intake from 1988 to 1999 were also used in the analysis. Quantities of food groups purchased by adult equivalent (AE) and food expenditures away from home between 1984 and 1989 were used to assess trends. All information was analysed at the national and regional levels, and by urban and rural areas. Results: SMR for diabetes, AMI and hypertension increased dramatically parallel to obesity at the national and regional levels. Fat intake in women and the purchase of refined carbohydrates, including soda, also increased. Discussion: The results suggest that obesity is playing a role in the increased SMRs of diabetes, AMI and hypertension in Mexico. Total energy dietary intake and food purchase data could not explain the rise in the prevalence of obesity. The increases in fat intake and the purchase of refined carbohydrates may be risk factors for increased mortality. Information on physical activity was not available. Conclusion: SMRs due to diabetes, hypertension and AMI have increased dramatically in parallel with the prevalence of obesity; therefore actions should be taken for the prevention of obesity. Reliable information about food consumption and physical activity is required to assess their specific roles in the aetiology of obesity.
Keywords Diabetes mellitus Acute myocardial infarction Hypertension Obesity Dietary intake Mortality trends
Mexico is currently undergoing an epidemiological transition1–4 characterised as the retarded variant of the transition model4,5. Several studies have described a phenomenon of polarisation in the country, where the more developed industrial states (those in the north) have epidemiological profiles similar to those of developed countries and less developed states reflect pre-transitional epidemiological profiles2,3,6. This polarisation has been attributed to the uneven distribution of wealth, education, access to health services and overall quality of basic services between rich and poor families1–3; however, in recent years obesity, diabetes and other non-communicable chronic diseases (NCCDs) have been increasing among the poor7,8. Moreover, a growing number of studies are finding an association of low birth weight with obesity, diabetes and coronary heart disease in adults9–13. Access to inexpensive but high energy-dense foods is rising and physical activity is decreasing, since large numbers of people now live in urban areas and are engaged in less physical activity14,15. The objective of this paper is to characterise the epidemiological and nutritional transitions and their determinants in Mexico.
Methods
There were two types of information for this study: (1) datasets from national probabilistic surveys that were analysed specifically for this paper and (2) information that had been published. The sources of information are described below.
Trends of NCCD mortality in Mexico
Mortality rates for acute myocardial infarction (AMI), diabetes mellitus and hypertension were obtained from the National Institute of Informatics, Statistics and Geography (INEGI) using the International Classification of Diseases, version 9 (ICD-9) for the years 1980 to 199716 and version 10 (ICD-10) for 199817. AMI included causes 410 to 414 (ICD-9) in 1980–1997 and I20 to I25 (ICD-10) in 1998. Diabetes mellitus included cause 250 (ICD-9) in 1980–1997 and E10 to E14 (ICD-10) in 1998. Hypertension included causes 401 to 405 (ICD-9) in 1980–1987 and I10 to I15 (ICD-10) in 1998. The mortality rates were calculated using population estimates for Mexico provided by INEGI. Once crude mortality rates were obtained, they were age-adjusted according to the new World Health Organization (WHO) reference population to allow international comparisons18. In addition, the relative change from 1980 to 1998 was estimated for each year and compared across the selected mortality causes.
Geographic location
Age-adjusted standardised mortality rate (SMR) data are also presented by four regions to allow comparisons with the Mexican Nutrition Survey and the National Chronic Diseases Survey, which were representative of four regions constructed on the basis of common characteristics, such as development and per capita income19. The states included in each region are: North (Baja California, Baja California Sur, Coahuila, Chihuahua, Durango, Nuevo Leo´n, Sonora, Sinaloa, Tamaulipas and Zacatecas), Central (Aguascalientes, Colima, Guanajuato, Hidalgo, Jalisco, Me´xico, Michoaca´n, Nayarit, Queretaro, San Luis Potosı´ and Tlaxcala), Mexico City and South (Campeche, Chiapas, Guerrero, Morelos, Oaxaca, Puebla, Quintana Roo, Tabasco, Veracruz and Yucata´n). Data were also analysed by rural (population equal to or less than 15 000) or urban location (population more than 15 000). All data were weighted for the analysis using the corresponding expansion factors provided by INEGI.
Discussion
An increasing trend in SMRs from diabetes mellitus, AMI and hypertension was observed during the 19-year study period. The increases observed were considerable, ranging from 53% to 62%, relative to the SMR in 1980. One possibility is that increases observed are explained by improvements in the quality of the deaths registry system in Mexico. In 1980, medical doctors certified 86% of total deaths, while in 1998 this figure increased to 96.8%29. Illdefined causes decreased from 6.7% in 1980 to 2.0% in 199229. Thus, it is possible that at least part of the sharp increases was due to improvements in the quality of the registry system. However, the relatively small magnitude of the increase in certifications by medical doctors and of the decrease in ill-defined causes of death relative to the increases in mortality for the three causes studied suggest that improvements in the registry system do not account for a significant part of the increases in mortality observed. This claim is further substantiated by the decline or lack of change in mortality rates for several other causes of death during the study period. For example, mortality rates due to accidents have decreased by about half during the period, deaths due to liver disease decreased by 28%, and neonatal mortality remained constant30. As shown in Fig. 1, SMRs for cirrhosis and vascular cerebral disease decreased during the study period. Further support for the mortality findings is the morbidity information presented, which shows high prevalences of diabetes, hypertension and hypercholesterolaemia. Moreover, preliminary data of diabetes mortality in 1999 confirms the high SMR found in 1998, suggesting that the sharp increase observed from 1997 to 1998 seems to be real. Our conclusion is that important increases in SMR for the three causes studied actually took place.
Epidemiological studies indicate that the three causes of death are of multiple aetiologies and result from a variety of risk factors. Heredity plays a role in all, but the three causes of death share common risk factors such as obesity, inadequate dietary intakes (high energy, fat, cholesterol and carbohydrates intake) and physical inactivity.
Overweight and obesity increased dramatically during the last decade by 78%. This increase is consistent with the increases in mortality for the three causes considered, for which obesity is a risk factor. Moreover, obesity rates parallel mortality rates in the four regions studied. The highest prevalences of overweight and obesity in 1984 were found in the North and in Mexico City, coincident with the highest SMRs during the first half of the 1980s in these regions. The changes in overweight and obesity in women from 1980 to 1999 were larger for the South and Centre, which is consistent with the largest increases in SMR in the same regions. Comparisons of trends in obesity and SMRs for the NCCDs suggest that overweight and obesity are playing an important role in the aetiology of these NCCDs in Mexico.
Energy intake in women did not increase between 1988 and 1999 as expected, given the increase in obesity. It is well known that 24-hour recall, the technique employed in both surveys, underestimates energy intake. The degree to which energy intake is underestimated is influenced by factors that changed between 1988 and 1999. For example, we have documented that obese women tend to underestimate their intake to a greater extent than non-obese women31. The larger proportion of obese women in 1999 relative to 1988 suggests a higher degree of underreporting in 1999. We suspected that more women consumed food out of their homes in 1999 than in 1988. It is well known that underreporting is higher when food is consumed out of home. However, we found that food expenditure away from home did not increase during the study period. Despite the possible higher underestimation of intakes in 1999, fat intake increased substantially during the decade, both in absolute terms and relative to total energy intake. This is an important finding, given the role of fat intake as a risk factor for some NCCDs and obesity. In addition to dietary intake data, we obtained quantities of food purchased by food groups using expenditure data from 1984 to 1998. The only quantities of food groups that were higher for Mexico City and the North in 1984 (at the time when SMRs for NCCDs and obesity were clearly higher in these two regions) were sugars and refined carbohydrates, which were 20–30% above the quantities reported for the Centre and South. Mexico City also reported higher quantities of meat, poultry and eggs, which contain foods that are high in saturated fatty acids and cholesterol; however, Mexico City also reported the highest quantities of fruits, vegetables and legumes, which include foods that are considered protective for several NCCDs.
To explain the changes in SMRs for NCCDs and obesity during the study period, the changes in quantities of food purchased during the period were analysed. The only food group with increased quantities purchased was sugar and refined carbohydrates. Soda, a component of that group, showed a substantial increase. However, comparisons among regions show similar or larger changes in Mexico City and the North (the regions with the smallest change in SMR and obesity) relative to those observed in the Centre and South (the regions with the highest change in SMR and obesity). Therefore, the findings do not support attributing a role in explaining the changes in obesity observed to sugar and refined carbohydrates. One limitation of the food expenditure data used to construct quantities purchased is that, although questions are asked in the surveys to account for expenditures outside the home, no questions directed at identifying the particular foods purchased outside the home were made. Therefore, the expenditure data clearly underestimate all food consumed at work, at school or in the street. Results using food expenditure data indicate that food expenditures away from home not only did not increase from 1988 to 1998, but actually dropped. These results suggest that energy and macronutrient intake out of the home did not increase during the study period. Unfortunately, we do not have information regarding the specific foods purchased away from home. Although unlikely, it could be possible that people spent less money but purchased larger amounts of cheaper foods. Therefore,we cannot be conclusive about the changes of energy and nutrient intake away from home using only food expenditure data.
We conclude that food expenditure data do not explain the increases in obesity observed during the period. However, the increasing trends in the quantities of sugars and refined carbohydrates purchased, and more particularly the purchase quantities of soda, could be associated with the increased mortality from NCCDs, and therefore should be considered a sign of caution. It is recommended that food policy and nutrition specialists should monitor the trends closely .
Taken together, energy dietary intake of women and quantities of food purchased per adult equivalent do not seem to explain the changes observed in obesity. However, higher fat dietary intakes may be partially responsible for the increases in obesity and NCCDs.
One limitation of the study is that we do not have reliable information about other lifestyle risk factors for NCCDs. For example, reduced physical activity may be an important factor that has not been considered in our analysis. We suspect that physical activity has declined over time in recent years, as a result of urbanisation, increased availability of motorised transportation and more sedentary occupations. Unfortunately, we do not have information at this time to confirm our suspicions. Neither have other risk factors, such as smoking, been considered to explain the causes of death studied. Finally, mortality from these diseases can be reduced through adequate medical attention. Therefore, part of the differences in mortality rates among regions in Mexico may be due to differences in coverage and quality of medical attention, which has not been considered in this analysis.
Conclusions
SMRs due to diabetes, hypertension and AMI have increased dramatically in parallel with an increase in obesity. The association of overweight and obesity with mortality rates among regions at baseline, as well as their parallel evolution over time, suggests that overweight and obesity are playing an important role in the increasing trends observed in these three NCCDs. Overweight and obesity should, therefore, be considered public health problems and actions should be taken for their prevention and control. We were unable to consistently relate the changes in overweight, obesity or mortality from NCCDs with the total energy intake or food quantities purchased by adult equivalent. An increase in fat intake is evident from the dietary intake data, suggesting that increases in fat intake may explain the rise in overweight and obesity as well as mortality. However, the results are not supported by the changes in quantities of food purchased, probably due to methodological problems; therefore, the evidence is not conclusive. An increase in the purchase of sugars and refined carbohydrates, particularly soda, is worrisome and may be related to the increases in mortality due to NCCDs. Other factors such as changes in physical activity, which are not considered in the analysis, may explain the increment in the prevalence of overweight and obesity. Reliable information about food consumption and physical activity is required in order to assess their specific roles in the aetiology of obesity. Acknowledgements We would like to acknowledge Eric Monterrubio for his help in the configuration of the income–expenditure databases, Luis Va´zquez Segovia for his assistance in the analysis and interpretation of the food expenditure databases, Drs. Steffano Bertotzi and Paul Gertler for their advice in the adjustment and interpretation of food expenditure data.
References
1 Cha´vez A, De Cha´vez M, Rolda´n A, Bermejo S, Avila A, Madrigal H. The Food and Nutrition Situation in Mexico: A Food Consumption, Nutritional Status and Applied Programs Tendencies Report from 1960 to 1990, 1st ed. Mexico City: Editorial Pax, Mexico, 1996.
2 Hernandez-Diaz S, Peterson K, Dixit S, Hernandez-Prado B, Parra S, Barquera S, Sepu´lveda J, Rivera J. Association of maternal short stature with stunting in Mexican children: common genes vs common environment. Eur. J. Clin. Nutr. 1999; 53: 938–45.
3 Frenk J, Frejka T, Bobadilla JL, Stern C, Lozano M, Sepu´lveda J, et al. The epidemiologic transition in Latin America [in Spanish]. Boletin de la Oficina Sanitaria Panamericana 1991; 111(6): 485–96.
4 Omran AR. The epidemiologic transition. A theory of the epidemiology of population change. Milbank Mem. Fund Quart. 1971; 49(4): 509–38.
5 Omran AR. The epidemiologic transition theory. A preliminary update. J. Trop. Pediatr. 1983; 29: 305–16.
6 Bobadilla J, Frenk J, Lozano R, Frejka T, Stern C. The epidemiologic transition and health priorities. In: Jamison D, ed. Disease Control Priorities in Developing Countries. New York: Oxford University Press, 1993.
7 Drewnowski A, Popkin BM. The nutrition transition: new trends in the global diet. Nutr. Rev. 1997; 55(2): 31–43.
8 Pen˜a M, Bacallao J. Obesity and poverty: an emerging problem in the Americas. In: Pen˜a MaBJ, ed. Obesity and Poverty: A New Public Health Challenge. PAHO Scientific Publication No. 576. Washington, DC: Pan American Health Organization, 2000; 132.
9 Barker DJ. The intrauterine environment and adult cardiovascular disease. Ciba Foundation Symp. 1991; 156: 3–10.
10 Barker DJ. Fetal growth and adult disease. Br. J. Obstet. Gynaecol. 1992; 99(4): 275–6.
11 Barker DJ, Hales CN, Fall CH, Osmond C, Phipps K, Clark PM. Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. Diabetologia 1993; 36(1): 62–7.
12 Barker DJ, Martyn CN, Osmond C, Hales CN, Fall CH. Growth in utero and serum cholesterol concentrations in adult life. BMJ 1993; 307(6918): 1524–7.
13 Phillips DI, Hirst S, Clark PM, Hales CN, Osmond C. Fetal growth and insulin secretion in adult life. Diabetologia 1994; 37(6): 592–6.
14 Anon. Urbanization and public health. WHO Chronicle 1967; 21(10): 428–35.
15 Popkin BM. The nutrition transition in low-income countries: an emerging crisis. Nutr. Rev. 1994; 52(9): 285–98.
16 Pan American Health Organization (PAHO)/World Health Organization (WHO). International Classification of Diseases, Revision 9 (ICD-9). Washington, DC: PAHO/WHO, 1978.
17 World Health Organization (WHO). International Statistical Classification of Diseases and Related Health Problems, ICD- 10. Geneva: WHO, 1992.
18 World Health Organization (WHO). World Health Statistics Annual. Geneva: WHO, 1999.
19 Sepu´lveda-Amor J, Lezana MA, Tapia-Conyer R, Valdespino JL, Madrigal H, Kumate J. Nutritional status of pre-school children and women in Mexico: results of a probabilistic national survey [in Spanish]. Gaceta Medica de Mexico 1990; 126(3): 207–24.
20 Secretarı´a de Salud, Direccio´n de Epidemiologı´a. Encuesta Nacional de Enfermedades Cro´nicas. Mexico DF: Secretarı´a de Salud, Direccio´n de Epidemiologı´a, 1993.
21 World Health Organization (WHO). Obesity. Preventing andManaging the Global Epidemic. Report of a WHO Consultation on Obesity, June. Geneva: WHO, 1997.
22 National Center for Health Statistics (NCHS)/Centers for Disease Control (CDC). NCHS Growth Curves for Children, birth–18 y. Series 11, 165. DHEW Publication (PHS) 78 1650. Washington, DC: US Government Printing Office, 1978.
23 Food and Nutrition Board Commission of Life Sciences, National Research Council. Recommended Dietary Allowances, 10th ed. Washington, DC: Subcommittee on the 10th edition of the RDAs, 1989.
24 SPSS, Inc. SPSS for Windows, Release 10.0.0. Chicago, IL: SPSS Inc., 1999.
25 Rivera J, Long K, Go´nzalez-Cossı´o T, Parra S, Rivera M, Rosado J. Nutricio´n y Salud: Un Menu´ para la Familia. Cuadernos de Salud. Problemas Pretransicionales. Mexico: Secretarı´a de Salud, 1994.
26 Instituto Nacional de Salud Pu´blica (INSP). Encuesta Nacional de Nutricio´n 1999. Tomo I. Nin˜os Menores de 5 an˜os. Cuernavaca Morelos: INSP, 2000.
27 Rivera-Dommarco J, Shamah T, Villalpando-Herna´ndez S, Gonza´lez de Cossı´o T, Herna´ndez-Prado B, Sepu´lveda J. Encuesta Nacional de Nutricio´n 1999. Estado Nutricio en Nin˜os y Mujeres en Me´xico. Cuernavaca Morelos: Instituo Nacional de Salvd Pu´blica, 2001.
28 Flores M, Melgar H, Cortes C, Rivera M, Rivera J, Sepulveda J. Consumo de energı´a y nutrimentos en mujeres mexicanas en edad reproductiva. Salud Pu´ blica de Me´xico 1998; 40: 161–71.
29 Cuadernos de Salud. La Mortalidad en Me´xico: Registro, Estructura y Tendencias, 1st ed. Mexico: Secretarı´a de Salud, 1994.
30 Secretarı´a de Salud. Mortalidad 1998. Contexto Actual y Aspectos Relevantes. Perfiles Estadı´sticos No. 13. Mexico: Direccio´n General de Estadı´stica e Informa´tica, 1999.
31 Campirano F, Barquera S, Rivera J, Herna´ndez-Prado B, Flo´res-Lo´pez ML, Monterrubio E. Estimation of energy under-reporting in obese and non-obese Mexican women using different equations: analysis of the Mexican National Nutrition Survey. Ann. Nutr. Metab 2001; 45(Suppl. 1): 146.
Full Text
ليست هناك تعليقات:
إرسال تعليق