PEDIATRICS Vol. 108 No. 1 July 2001, pp. 218-219

Early Adiposity Rebound Is Not Associated With Energy or Fat Intake in Infancy

To the Editor.

Obesity is recognized to be the result of a positive energy balance, mainly attributable to excessive energy intake accounted for by a high contribution of dietary fat. This was our original hypothesis when we started a longitudinal study conducted in French children followed from infancy to age 8 years.¹ The aim of the study was to identify the causes of the early adiposity rebound recorded in most obese children. The adiposity rebound is the point at which the body mass index (BMI) increases after its nadir that takes place around the age of 6 years. An early adiposity rebound was found to be associated with higher BMI at adolescence and adulthood.^2-4 Recently, in a longitudinal study of children followed from birth to 5 years in the United Kingdom, Dorosty et al⁵ also investigated the factors associated with an early adiposity rebound.

First, neither of the 2 studies conducted in France or in the United Kingdom report an association between energy or fat intake in infancy and age at adiposity rebound. The specific value of longitudinal observations recorded during childhood is that children are often surveyed before obesity is established, in contrast with cross-sectional studies recording intakes in already obese individuals. In addition, in young children, underreporting is less probable than in later childhood and adulthood.⁶

Second, in the French study, an association was recorded between protein intake at age 2 years and age at adiposity rebound: the higher the percentage of protein in the diet, the earlier the adiposity rebound. This association was not found in the United Kingdom sample. However, the specific context of the short follow-up (5 years), while mean age at adiposity rebound is 6 years, probably did not allow a decisive assessment of the relationship between nutrient intake and age at adiposity rebound. It would be interesting to complete this analysis after a longer follow-up of the cohort.

The association found in the French study, between protein intake and an early adiposity rebound, led to the observation that in many countries, the infant diet is characterized by high intakes of protein (4 g/kg body weight/day) and by a generally inadequate nutrient balance, ie, a high protein (16% of total energy intake) and/or low fat diet (28%) by the age of 1 year.⁷ On the basis of the energy balance principle, such an association between a high protein-low fat diet and risk of obesity is unlikely. Hypotheses have been suggested, resting on the association between nutrient balance and hormonal status¹ and on a possible metabolic adaptation to low fat intakes in infancy, making the child unprepared to face a subsequent high fat diet later in life.⁸

Dorosty et al point out that they did not replicate our observation regarding protein intake. It should also be emphasized that they do confirm the lack of relationship between energy and fat intake recorded in early life and age at adiposity rebound. Thus, on the basis of present knowledge, it is unjustified to restrict fat intake in infants, a general practice evidenced by the low fat consumption in infants in many countries.⁷ Fat restriction is recommended in adults whose intakes are usually high, but it is not adapted to infants. Indeed, energy needs are high in infancy, the period of high rate of the myelinization of the nervous system. Human milk, the reference food, contains a low proportion of proteins (7%) and a high proportion of fat (50%).

The early adiposity rebound recorded in most obese children suggests that some determining events may have occurred early in life. Studies examining the composition of the diet early in life, in relation with age at adiposity rebound and the risk of obesity, deserve additional investigations.

Marie Françoise Rolland-Cachera, MD^*, Michele Deheeger, MD^*, and France Bellisle, MD
^* ISTNA-CNAM UMR Epidémiologie Nutritionnelle 5 rue du Vertbois 76003 Paris, France
 U341 INSERM and Service Nutrition Hôtel Dieu 1 place du Parvis Notre-Dame 75181 Paris Cedex 04-France

REFERENCES

1. Rolland-Cachera MF, Deheeger M, Akrout M, Bellisle F Influence of macronutrients on adiposity development: a follow up study of nutrition and growth from 10 months to 8 years of age. Int J Obes. 1995; 19:573-578 [Medline]
2. Rolland-Cachera MF, Deheeger M, Bellisle F, Sempé M, Guilloud-Bataille M, Patois E Adiposity rebound in children: a simple indicator for predicting obesity. Am J Clin Nutr. 1984; 39:129-135 [Abstract/Free Full Text]
3. Siervogel RM, Roche AF, Guo S, Mukherjee D, Chumlea WC Patterns of change in weight/stature² from 2 to 18 years: findings from long-term serial data for children in the Fels longitudinal growth study. Int J Obes. 1991; 15:479-485 [Medline]
4. Prokopec M, Bellisle F Adiposity in Czech children followed from one month of age to adulthood: analysis of individual BMI patterns. Ann Hum Biol. 1993; 20:517-525 [CrossRef][Medline]
5. Dorosty AR, Emmett PM, Cowin IS, Reilly JJ, and the ALSPAC Study team Factors associated with early adiposity rebound. Pediatrics. 2000; 105:1115-1118 [Abstract/Free Full Text]
6. Sichert-Hellert W, Kersting M, Schoch G Underreporting of energy intake in 1 to 18 years old German children and adolescents. Z Ernahrungswiss. 1998; 37:242-251 [CrossRef][Medline]
7. Rolland-Cachera MF, Deheeger M, Bellisle F Increasing prevalence of obesity among 18-year-old males in Sweden: evidence for early determinants. Acta Paediatr. 1999; 88:365-367 [CrossRef][Medline]
8. Rolland-Cachera MF. Obesity among children and adolescents: the importance of early nutrition. In: Johnston FE, Zemel B, and Eveleth, eds. Human Growth and Development. London, United Kingdom: Smith Gordon Publisher; 1999;245-258

In Reply.

We recently reported no evidence of any association between timing of adiposity rebound and dietary intake in a representative, contemporary sample of 889 children in the United Kingdom.¹ Since publication we have analyzed dietary data from the cohort at age 43 months, with the same conclusions. Our study was the largest investigation of the influences on timing of the adiposity rebound to date. The contemporary nature of the study was also important because of the secular trend to earlier adiposity rebound.^2,3

Dr Rolland-Cachera and colleagues⁴ are satisfied with the validity of our conclusions in relation to energy and fat intake, but not protein intake. In particular, they suggest that the duration of follow-up (to age 5) might have limited our ability to test the hypothesis that protein intake influences timing of adiposity rebound. We contend that our study design was sufficient to draw such inferences for the following reasons. First, the sample size allowed us to identify children defined as having "very early" and "early" rebound in much greater numbers than in any previous study. Second, the dietary intake methodology used was both more accurate and more precise than the previous study, which suggested a possible role for protein in timing of adiposity rebound. These design issues meant that the power to detect any influence of nutrient intake was greater than in any previous study. Finally, children in our study who had experienced adiposity rebound did so in the mid-1990s, much later than in previous investigations. Many had experienced adiposity rebound before age 5. This probably reflects the secular trend to earlier rebound and the dramatic increase in childhood obesity recently observed in the United Kingdom,⁵ even in young children.⁶

In our view, the statement that "mean age of rebound is age 6"⁴ describes smaller, more selected samples of children studied in the past when adiposity rebound typically occurred later. Although descriptive studies of contemporary samples are required to adequately define the distribution of timing of adiposity rebound, there is little doubt that adiposity rebound occurs earlier than in the past.

We agree with Dr Rolland-Cachera and colleagues that additional studies of the influences on timing of adiposity rebound are necessary, particularly in view of the importance of this event to long-term obesity risk.⁷ It is widely accepted that the key to obesity prevention is the identification of modifiable risk factors.⁸ Early adiposity rebound is clearly a risk factor for later obesity, and the secular trend to earlier rebound encourages our belief that it must be influenced by environmental factors that are potentially modifiable. Additional study of possible influences on adiposity rebound, which we did not measure (eg, energy expenditure, physical activity), might be profitable.

John J. Reilly
Ahmad Dorosty
University of Glasgow
Department of Nutrition
Yorkhill NHS Trust
Glasgow G3 8SJ Scotland

Pauline M. Emmett
Unit of Paediatric and Perinatal Epidemiology
Institute of Child Health
University of Bristol
Bristol, United Kingdom

REFERENCES

1. Dorosty AR, Emmett PM, Cowin IS, Reilly JJ, and the ALSPAC Study Team Factors associated with early adiposity rebound. Pediatrics. 2000; 105:1115-1118
2. Cole TJ, Freeman JV, Preece MA Body mass index reference curves for the UK. 1990. Arch Dis Child. 1995; 73:25-29 [Abstract/Free Full Text]
3. Rolland-Cachera MF. Obesity among adolescents: evidence for the importance of early nutrition. In: Johnston FE, Zemel B, Eveleth PB, eds. Human Growth and Development. London, United Kingdom: Smith Gordon; 1999;245-258
4. Rolland-Cachera MF, Deheeger M, Bellisle F Early adiposity rebound is not associated with energy or fat intake in infancy [letter]. Pediatrics. 2001; 108:000-000
5. Reilly JJ, Dorosty AR, Emmett PM Prevalence of overweight and obesity in British children. Br Med J. 1999; 319:1039 [Free Full Text]
6. Reilly JJ, Dorosty AR Epidemic of obesity in UK children. Lancet. 1999; 354:1874-1875 [CrossRef][Medline]
7. Whitaker RC, Pepe MS, Wright JA, et al. Early adiposity rebound and risk of adult obesity. Pediatrics. 1998;101:(3). URL: http://www.pediatrics.org/cgi/content/full/101/3/e5
8. Dietz WH Birth weight, socioeconomic status, and adult adiposity among African Americans. Am J Clin Nutr. 2000; 72:335-336 [Free Full Text]