• Malnutrition has long been researched and addressed in two distinct silos, focusing either on chronic 2 or acute undernutrition, energy inadequacy and micronutrient deficiencies, or on overweight, obesity 3 and dietary excess. The contemporary reality of the double burden of malnutrition is different, making it 4 impossible to separate these issues, but also indicating shared opportunities to address them. 5 • Malnutrition harms health throughout the life-course, but its emergence early in life has particularly 6 pernicious consequences. A variety of physiological mechanisms propagate effects of early-life 7 malnutrition across the life-course, while adolescent and adult malnutrition can transmit effects to the 8 next generation. 9 • Different forms of malnutrition can interact through the life-course and across generations. In some 10 settings, early stunting may predispose to a more central distribution of adiposity at later ages, while 11 the extent to which maternal obesity adversely affects early growth and development of the offspring 12 may be exacerbated if the mother herself was under-nourished in early life. 13 • Life-course exposure to the double burden of malnutrition (early undernutrition followed by later 14 overweight) increases the risk of non-communicable disease, by imposing a high metabolic load on a 15 depleted capacity for homeostasis. The health costs of adult obesity are therefore exacerbated among 16 those who previously experienced undernutrition. In women, life-course exposure to the double burden 17 of malnutrition increases the risk of childbirth complications. 18 • Exclusive and appropriate breast-feeding protects infants against all forms of malnutrition, and 19 protects mothers against diabetes and breast cancer, in part through healthy-weight benefits. However, 20 maternal obesity, diabetes and micronutrient deficiencies alter the biology of lactation, and should be 21 addressed to maximise the success of breast-feeding. 22 • Exposure to the double burden of malnutrition can only be fully understood in the context of broader 23 societal drivers acting across culture, behaviour and technology. Various groups are at high risk of the 24 double burden through elevated exposure to these drivers, often exacerbated by biological 25 susceptibility. 26 • Developmental responses to malnutrition in early life are shaped by ecological factors, such as 27 pathogen burden and extrinsic mortality risk. An evolutionary perspective, focusing on how our 28 biological plasticity was shaped in ancestral environments to promote survival and reproduction, may 29 help design interventions that promote linear growth and lean tissue accretion rather than excess 30 adiposity. 31 • Inter-generational cycles of malnutrition have proven difficult to disrupt through public health 32 interventions. Major societal shifts are required regarding nutrition and public health, in order to 33 implement comprehensive change that is sustained over decades, and scaled up into the entire global 34 food system.

Background: Previous research suggested that nutritionally stunted children may have increased risk of obesity, but little is known about potential underlying mechanisms. Objective: We sought to test the hypothesis that stunted children have a low metabolic rate and impaired fat oxidation relative to nonstunted children. Design: The subjects were 58 prepubertal boys and girls aged 8-11 y from the shantytowns of São Paulo, Brazil. Twenty-eight were stunted (height-for-age z score < Ϫ1.5) and 30 had similar weight-for-height but normal height (height-for-age z score > Ϫ1.5). Parents of children in the 2 groups had equivalent height and body mass index values. Fasting and postprandial energy expenditure, respiratory quotient (RQ), and substrate oxidation were measured with indirect calorimetry in a 3-d resident study in which all food was provided and body composition was measured with dual-energy X-ray absorptiometry. Results: Stunted children had normal resting energy expenditure relative to body composition compared with control children (4559 ± 90 and 4755 ± 86 kJ/d, respectively; P = 0.14) and had normal postprandial thermogenesis (2.4 ± 0.3% and 2.0 ± 0.3% of meal load, respectively; P = 0.42). However, fasting RQ was significantly higher in the stunted group (0.92 ± 0.009 compared with 0.89 ± 0.007; P = 0.04) and consequently, fasting fat oxidation was significantly lower (25 ± 2% compared with 34 ± 2% of energy expenditure; P < 0.01). Conclusions: Childhood nutritional stunting is associated with impaired fat oxidation, a factor that predicted obesity in other atrisk populations. This finding may help explain recent increases in body fatness and the prevalence of obesity among stunted adults and adolescents in developing countries.Am J Clin Nutr 2000;72:702-7.

Undernutrition is one of the most important public health problems, affecting more than 900 million individuals around the World. It is responsible for the highest mortality rate in children and has long-lasting physiologic effects, including an increased susceptibility to fat accumulation mostly in the central region of the body, lower fat oxidation, lower resting and postprandial energy expenditure, insulin resistance in adulthood, hypertension, dyslipidaemia and a reduced capacity for manual work, among other impairments. Marked changes in the function of the autonomic nervous system have been described in undernourished experimental animals. Some of these effects seem to be epigenetic, passing on to the next generation. Undernutrition in children has been linked to poor mental development and school achievement as well as behavioural abnormalities. However, there is still a debate in the literature regarding whether some of these effects are permanent or reversible. Stunted children who had experienced catch-up growth had verbal vocabulary and quantitative test scores that did not differ from children who were not stunted. Children treated before 6 years of age in day-hospitals and who recovered in weight and height have normal body compositions, bone mineral densities and insulin production and sensitivity.

The accuracy and precision of four different food intake assessment methods were evaluated in young and older women by comparing reported energy intakes with doubly labeled water measurements total energy expenditure (TEE). A study lasting 8 d was conducted in 10 young women aged 25.2+/-1.1 y (-x+/-SEM) and in 10 older women aged 74.0+/-1.4 y. Free-living TEE was measured over 7 d and food consumption was determined from weighed food intake data (7 d), a 24-h food recall (in duplicate), and two different food-frequency questionnaires [Fred Hutchinson Cancer Research Center (FHCRC)/Block and Willett, both in duplicate]. In addition, body composition was determined by using hydrodensitometry, and strenuous physical activity and the extent of dietary restraint were determined by questionnaire. In young women, 24-h recall gave mean energy intakes that were closest to measures of TEE (-0.34+/-3.71 MJ/d compared with TEE, P=0.178), and energy intakes by food-frequency questionnaires were the only intake data that correlated significantly with individual values for TEE (P<0.05). In older women, food-frequency questionnaires gave mean energy intakes that were closest to measured TEE (+0.53+/-2.95 MJ/d with the Willett questionnaire and -1.19+/-3.02 MJ/d with FHCRC/Block questionnaire). No energy intake data from this group correlated significantly with values for TEE. The 7-d weighed dietary intakes were significantly lower than measured TEE in both young and older women (-2.0 MJ/d in young and older women combined, P<0.001), and did not correlate significantly with values for TEE, although they did most closely mirror the mean difference in TEE between the young and older women (2.30 MJ/d for TEE and 2.11 MJ/d for 7-d weighed intake). These data suggest that none of the methods studied gave accurate estimates of the usual energy requirements of individual subjects. In addition, the results suggest that for some types of studies, simple methods for assessing group mean dietary intake may actually give more accurate information than weighed dietary intakes.

There is a fair amount of epidemiological evidence showing that nutritional stunting causes increased risks of obesity. Obesity is increasing dramatically not only in developed countries but also in developing countries, such as Brazil, especially among the poorer. The mere coexistence of undernutrition and obesity among poor people has a great impact, as the burden in the social, economic, and health care systems is remarkable. In addition, an increasing number of studies have shown that nutritional stunting causes a series of important long-lasting changes such as lower energy expenditure, higher susceptibility to the effects of high-fat diets, lower fat oxidation, and impaired regulation of food intake. These findings suggest that a broader and more detailed understanding of the long-lasting effects of early undernutrition, direct cause of nutritional stunting, is needed. Within this context, we present data of some physiological mechanisms that substantiate the association between previous undernutrition and future obesity.

SAWAYA, ANA L, GERALD DALLAL, GISELA SOLYMOS, MARIAHDESOUSA, MARIAL-, SUSANB ROBERTSAND DIRCE M SIGULEM. Obesity andmalnutritionin a shantytown populationin the city of SIioPaulo,Brazil. Obes Res. 1995;3(supp12):107~-115~. To investigatethe prevalence of obesity and malnutrition inthe poor Brazilianpopulationweconducted asurveyon the socioeconomic and nutritional status of 535 families (comprising2 411 individuals)livinginshantytownsinthe cityofSIioPaulo. Therewas a30% prevalenceofmalnutrition in the children, with chronic malnutrition as the mostpredominantproblem. Theprevalenceofobesitywas 6.4% in boys and 8.7% in girls. Overweight and obesity associated with stunting was found in 5.8% of boys and 6.8% girls. Adolescents showed a higher prevalence of malnutrition when weight-for-age distribution was used (boys 46.4%, girls 40.2%), but a right deviation in the distributionwas observedwith anincreaseinobesity and adecreaseof malnutritionwasobsered (obesity was 21% ingirlsand8.8% inboys;malnutritionwas 15.5% inboys and 12.6% in girls) when the weight-for-height adjustmentwasmade. Stuntingwas themost predominanttype of malnutrition in both sexes. Obesity associated with stuntingwas morecommon than obesitywithout stunting, bothin younger children and adolescents. Adults had a higher prevalence of obesity than malnutrition according to both the Metropolitan Life Insurance tables (1.7% of undernutrition, 16.7% of overweight , and 14.1% of obesity) and Body Mass Index (8.5% of undernutrition, 21.9% of overweight, and 14.6% of obesity). There was an increase in the percentage of obese children when at least one adult in the family was obese and an increased percentage of malnourished children when undernour- ishedadultswerepresentinthefamily. Obesity amongthe adults of the family decreased the occurrence of malnutrition among the children. In 9% of families there was a coexistenceofobesity intheadults andmalnutritioninthe children. These results demonstrate a coexistence of malnutrition and obesity in poor urban Braziliancommunities.

The aim of the present study was to analyse the changes in body composition of stunted children during a follow-up period and to test the hypothesis of a tendency to accumulate body fat as a consequence of undernutrition early in life. We selected fifty boys and girls aged 11 to 15, who were residents of slums in Sao Paulo, Brazil. Twenty were stunted (S) and thirty had normal stature (NS). The children's nutritional status and body composition were assessed through anthropometry and dual-energy X-ray absorptiometry, at the beginning of the present study and after 3 years, and changes in lean mass (LM and LM%) and fat mass (FM and FM%) were calculated. Stunted boys accumulated more body fat (FM%: S=1.62%, NS=-3.40%; P=0.003) and gained less lean mass (LM%: S=-1.46, NS=3.21%; P=0.004). Stunted girls gained less lean mass (S=7.87 kg, NS=11.96 kg; P=0.032) and had significantly higher values of FM% at follow-up when compared with their baseline values (P=0.008), whereas non-stunted girls had a non-significant difference in FM% over time (P=0.386). These findings are important to understand the factors involved in the increased prevalence of overweight and obesity among poor populations, which appear to be associated with hunger during infancy and/or childhood.

Obesity is the nutritional disorder which has shown the greatest increase in prevalence, even in those countries in which deficiency diseases represent a severe public health problem. The goal of the present study was to analyse the anthropometric profile of a community living in the outskirts of Maceió, capital of Alagoas (northeastern Brazil), and to investigate the hypothesis of a coexistence of undernutrition and obesity in a very low-income population. The survey was conducted on 315 families (1247 individuals). Among the children (aged < or =10 years), the prevalence of wasting, stunting and wasting plus stunting was 3.8, 8.3 and 8.7 % respectively. Wasting (10.2 %) was the most prevalent form of undernutrition among adolescents; nonetheless, a higher frequency of stunting (11 %) and overweight-obesity (5.5 %) was seen specifically in girls, in agreement with trends found in other studies. Adults exhibited a high prevalence of overweight-obesity (25 %), but stunting was also present (22 %). Of the stunted individuals, 30 % were overweight-obese and 16.3 % were underweight. There were eighty-six families with at least one parent who was underweight (27 %) and 104 families with at least one parent who was overweight (33 %). Underweight and overweight-obesity were both present in ninety-six households (30 %). These results may indicate that better living conditions in urban areas in a population 'adapted' to chronic famine might increase the susceptibility to obesity. Considering the harm caused by the cumulative effect of these two conditions (undernutrition in childhood and obesity in adult life) there is a clear need for new studies to uncover the determinant factors so that preventive measures can be implemented.