Infancy may be a sensitive period regarding effects of sodium intake on future blood pressure (BP). This has only been demonstrated in one randomized trial of low sodium formulae with follow-up in adolescence in one-third of participants.
To prospectively assess associations between sodium intake in infancy and BP at 7 years in the Avon Longitudinal Study of Parents and Children (ALSPAC).
A total of 533 children with sodium data at 4 months and 710 children with sodium at 8 months.
0.4% of participants at 4 months and 73.0% at 8 months exceeded recommended levels for infant sodium intake. After minimal adjustment (child age, sex, energy), sodium intake at 4 months was positively associated with systolic blood pressure (SBP) at 7 years (β=0.54 mm Hg/mmol; 95% CI: 0.09, 0.98 mm Hg; P=0.02). This changed little following adjustment for confounders but attenuated after adjusting for breastfeeding. This association was not mediated by sodium intake at 7 years. Due to high sodium–potassium correlations, effects of sodium independent of potassium could not be estimated with reasonable precision. Sodium intake neither at 8 months nor at 7 years was associated with SBP at 7 years.
The association between sodium intake at 4 months and future SBP requires replication in studies that can control for effects of potassium before we can conclude that early infancy is a sensitive period with respect to effects of sodium on future BP. The majority of infants exceeded recommended levels of sodium intake at 8 months, and interventions to reduce sodium in infants' diets should be considered.
Observational studies have shown a positive association between sodium intake and blood pressure (BP) in adults (Frost et al., 1991; Law et al., 1991; Elliott et al., 1996). Additionally, lowering sodium intake in adults is associated with decreases in BP. However, although in some studies large effect sizes have been reported (Sacks et al., 2001), evidence from meta-analyses indicates that reductions in adult BP are generally small (Ebrahim and Davey Smith, 1998; Hooper et al., 2002).
There is some evidence that lowering sodium intake in infancy may have more marked long-term effects on BP (Lawlor and Davey Smith, 2005). In a trial of Dutch infants randomized to a low or normal sodium diet for the first 6 months of life, systolic blood pressure (SBP) at the end of the intervention period (at age 6 months) was 2.1 mm Hg (95% CI: 0.5, 3.7) lower in infants randomized to low sodium diets (Hofman et al., 1983). This difference in SBP increased to 3.6 mm Hg (95% CI: 0.5, 6.6) at 15 years (Geleijnse et al., 1997). Since strong tracking correlations are present from age 15 onwards, this effect would be expected to have a lasting impact on BP into adulthood (Lawlor and Davey Smith, 2005). This effect is also larger than the reported effects of salt reduction in adults. Meta-analyses report reductions in SBP of 1.1–1.3 mm Hg following sodium restriction interventions in normotensive adults (Hooper et al., 2002) and 2.9 mm Hg in hypertensive adults (Ebrahim and Davey Smith, 1998). Thus, infancy may be a sensitive period with respect to effects of dietary sodium on future BP (i.e. that negative effects of high sodium on BP may be more pronounced in relation to sodium intake in infancy than in adulthood). However, results from this earlier trial should be treated with some caution, as the long-term follow-up at age 15 was not planned at the time of the initial intervention and only one-third of the participants were traced at follow-up. As such, the effect of sodium intake in infancy on later BP requires further research.
The Avon Longitudinal Study of Parents and Children (ALSPAC) is a contemporary cohort that affords the possibility of investigating early dietary measures and later health in children. This study aimed to determine the relationship between sodium intake in infancy and BP in childhood in a subsample of children enrolled in ALSPAC on whom detailed nutritional intake in infancy and early childhood was prospectively collected.
ALSPAC is a prospective cohort study set in the south-west of England, which has the overall aim of investigating the health and development of children. A full description of the methodology is available elsewhere (www.alspac.bristol.ac.uk) (Golding et al., 2001). Briefly, pregnant women residing in three health districts located around the city of Bristol with an expected date of delivery between 1 April 1991 and 31 December 1992 were invited to take part in the study. Of 13 678 singleton, liveborn children, 1964 who were born in the last 6 months of the recruitment period were chosen at random to be invited to join the Children in Focus (CIF), study on whom detailed dietary information and growth patterns was collected repeatedly during infancy and early childhood. Data are available in 1394 singleton children from at least one CIF clinic. At 7 years of age, all children enrolled with ALSPAC, including those in CIF, were invited to the clinic for examination where a range of physiological measures, including BP, were obtained. The final analyses were carried out on children with complete information on all confounders: 533 children at 4 months and 710 at 8 months. Ethical approval for the study was obtained from the ALSPAC Law and Ethics Committee and from three Local Research Ethics Committees of the Health Districts covering the study area.
Information on all foods and drink, recorded in household measures, was obtained from CIF infants at 4 and 8 months of age (for a detailed description, see previous papers) (Noble and Emmett, 2001, 2006). Three-day diaries were used for dietary assessment at 8 months and 1-day diaries were used at 4 months, both completed by the main carer. Mothers of breastfed infants were asked to record each feed and the duration of each feed.
Weights of foods were allocated based on Ministry of Agriculture, Fisheries and Food Portion Sizes (Ministry of Agriculture FaF, 1993) and were also obtained from manufacturer's information, packaging and test weighing. Composite foods and recipes that did not have an equivalent in the food tables were broken into their components and allocated codes and weights appropriately. For breast milk, the number and duration of each feed was used to estimate the likely volume of milk using previously validated assumptions (Paul et al., 1988; Mills and Tyler, 1992). A feed lasting 10 min or longer was assumed to be 125 ml in volume at 4 months and 100 ml at 8 months. A proportion of this volume was taken if the feed was of shorter duration (i.e. 12.5 ml/min at 4 months and 10 ml/min at 8 months). We used McCance and Widdowson's food tables to obtain the sodium from breast milk (The Royal Society of Chemistry and MAFF, 1991a). Breast milk sodium levels were assumed to be the same for all women and equal to the mean sodium concentration for mature human milk (15 mg/100 ml) (The Royal Society of Chemistry and MAFF, 1991a).
Weights and food codes were entered into the computer software package Microdiet (University of Salford). Nutrient and food group information associated with each food code was obtained from McCance and Widdowson's The Composition of Foods, 5th edition (The Royal Society of Chemistry and MAFF, 1991a) and supplements (The Royal Society of Chemistry and MAFF, 1988, 1989, 1991b, 1992a, 1992b, 1995). The Microdiet program was used in conjunction with a nutrient database created using SAS (SAS Institute Inc., Cary, NC, USA). Dietary supplements were not included in this analysis (only a minority of infants in CIF were receiving supplements by 8 months) (Noble and Emmett, 2001).
Blood pressure measurement
Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured using a Dinamap 9301 Vital Signs Monitor. This device has been shown to be highly reliable with repeat measures, yielding correlation coefficients of 0.88 for SBP and 0.83 for DBP (Bolling, 1994). Compared with sphygmomanometers, BP values from the Dinamap instrument may be approximately 6–8 mm Hg greater for SBP and within 1 mm Hg difference for DBP (Bolling, 1994). Child-size cuffs were used for children with upper-arm circumferences of less than 18 cm and small adult cuffs for children with upper arm circumferences of 18 cm or more. Initial inflation was set to 130 mm Hg. Two readings of SBP and DBP were recorded and the mean for each measure was calculated. Current age of child at measurement was calculated from the date of clinic attendance and the child's date of birth.
We considered birth weight, gestational age, maternal smoking and familial socioeconomic position (maternal age at birth, family social class, maternal and paternal education, parity) as potential confounders, as they may influence infant feeding patterns and are associated with later BP (Lawlor and Davey Smith, 2005). We considered potassium intake, which has been shown to reduce BP (Whelton et al., 1997), to be a potential confounder and analysed energy-adjusted sodium intake rather than absolute sodium intake (Willett and Stampfer, 1998). We also considered breastfeeding to be a potential confounding factor, as this will influence infant sodium intake and is related to BP in ALSPAC (Martin et al., 2004). We also included sodium intake at 7 years as a possible mediator of the association between infant sodium intake and later BP.
At initial enrolment with ALSPAC, mothers provided their date of birth, which was used to calculate maternal age at childbirth. Infant gestational age was estimated using date of delivery, mother's last menstrual period and in some cases early ultrasounds. Infant sex and birth weight were obtained from obstetric records and/or birth notifications. Information on number of previous pregnancies (live or stillborn) was gathered from a questionnaire at 18-weeks gestation. In a questionnaire at 32 weeks, mothers recorded their own and their partner's highest education level, which was collapsed into none/CSE (Certificate of Secondary education; national school exams at 16 years), vocational, O level (national school exams at 16 years, higher than CSE), A level (national school exams at 18 years) or degree. Mothers also recorded their occupation and their partner's occupation, which were used to allocate them to the Office and Population Censuses and Surveys social categories (OPCS, 1991) (I, II, III non-manual, III manual, IV and V, where I is the highest (professional) category and V (unskilled manual worker) is the lowest. A single variable (head of household social class) was derived from the highest social class of both partners. Breastfeeding information was collected from questionnaires sent to mothers at 6 months from which categories of exclusive, partial or never breastfed by the third month were derived. Responses for tobacco and cigarette use in the 18- and 32-week questionnaire provided information on smoking in the first and third trimesters. These were combined to create a variable for any smoking during pregnancy.
Correlation coefficients were calculated for sodium, potassium and energy, at 4 and 8 months. Linearity of relationships between sodium, BP and confounders was assessed from means or prevalence of confounders per quarter of sodium intake and BP. Means are presented for continuous confounders and prevalence for categorical confounders that have been collapsed into binary variables. Multiple linear regression was used to investigate the relationship between sodium intake and BP, with cumulative adjustments for confounders. Our primary analyses was of energy-adjusted sodium intake (adjusting for energy in all models) with secondary analyses using the sodium/potassium ratio and absolute sodium intake. Statistical analysis was conducted using STATA version 9.
Children included in this analysis (N=745 total) were compared with those in CIF not included owing to missing data on BP, sodium intake or confounders (N=649). Mothers of children not included in our analysis were more likely to be younger and to have smoked during pregnancy and were less likely to have breastfed their child, to have a degree and to have a partner with a degree compared to mothers of children included in the analyses. Children not included for analysis were also more likely to have come from a family of manual social class. No differences between those included and excluded for analysis were observed for SBP, DBP, birth weight, gestational age, sex or maternal parity.
Sodium intake at 4 months ranged from 3.1 to 19.2 mmol/day with a geometric mean of 7.2 mmol/day (6.0, 8.8, interquartile range; IQR). Sodium intake at 8 months ranged from 3.5 to 116.6 mmol/day with a geometric mean of 23.1 mmol/day (16.0, 32.6, IQR). Only two infants (0.4%) at 4 months exceeded current UK Department of Health recommendations for infant sodium intake (<1 g salt/day or 17 mmol/day sodium, for infants <1 year) (Department of Heath, 2006). However, at 8 months, 510 (73.0%) infants exceeded these recommended levels.
At 4 months, 257 (48.2%) infants were being breastfed (46 exclusively breastfed) and 467 (87.6%) had mixed feeding (any type of milk and solids). By contrast at 8 months, 186 (26.2%) infants were being breastfed, with all infants at this age on mixed feeding. The proportion of daily sodium intake due to breastfeeding at 4 months (median and IQR) was 0% (0, 82.6) for all 533 infants and 83.4% (56.9, 97.9) in the 257 exclusively and non-exclusively breastfed infants. At 8 months, the proportion of daily sodium intake due to breastfeeding (median and IQR) was 0% (0, 1.8) for all 710 infants and 9.5% (5.0, 17.1) in the 186 breastfeeding infants. Detailed information on types of food and drinks consumed in the CIF cohort at 4 and 8 months are available elsewhere (Noble, 2001,2006; Emmett, 2000).
Mean SBP at 7 years in children assessed at 4 and/or 8 months was 98.4 mm Hg (9.4 s.d.) and mean DBP was 56.4 mm Hg (6.7 s.d.). Correlations were high between sodium, potassium and energy at 4 months, and also at 8 months (Table 1). However, correlations between specific dietary variables across time in infancy were weak or modest. In particular, sodium intake at 4 months was only weakly correlated with sodium intake at 8 months. Sodium intake at 7 years was also weakly correlated with sodium intake at 4 months (r=0.17, P<0.001) and sodium intake at 8 months (r=0.08, P=0.05).
Compared with children in lower quarters of sodium intake at 4 months, children in the highest quarter had a higher birth weight, higher energy and potassium intake at 4 months, were more likely to be male, had a higher prevalence of mothers with non-degree education and were less likely to have been breastfed (Table 2). Similar associations were observed with sodium intake at 8 months, except no association was observed for breastfeeding (Table 2). None of the confounders was strongly associated with SBP (Table 3) or DBP (data not shown).
After minimal adjustment (child age and sex), energy-adjusted sodium intake at 4 months was positively associated with SBP at 7 years (Table 4). Adjusting for all confounders had little effect on the regression coefficient (Models 2–5). Sodium intake at 7 years (adjusted for age, sex and energy) was not associated with SBP at 7 years (β=0.03 mm Hg/mmol; 95% CI −0.01, 0.06; P=0.2) and including sodium intake at 7 years as a potential mediator did not reduce the association (Model 6). Sodium intake at 8 months was not associated with SBP at 7 years in any of Models 1–6 (Table 4). DBP was not associated with sodium intake at either 4 or 8 months.
When absolute sodium intake was analysed (i.e. with no adjustment for energy intake), the same pattern of results was observed (e.g. for sodium intake at 4 months: β=0.39; 95% CI 0.05, 0.73; P=0.03 for Model 1 and β=0.34; 95% CI –0.05, 0.72; P=0.09 for Model 6). Adjusting for potassium attenuated the association between sodium intake at 4 months and later SBP; however, there was evidence of multicollinearity when potassium, energy and sodium were all included in the same model. The variance inflation factors (VIFs) were 3.6 for potassium and 3.2 for energy, and although it has been suggested that VIFs above 10 are of concern (Armitage and Berry, 1994), the standard errors for the regression coefficients increased markedly from 0.18 (sodium only) to 0.31 (sodium, potassium and energy, both fully adjusted), making their interpretation difficult. Additionally, although the sodium/potassium ratio at 4 months was positively associated with SBP at 7 years, confidence intervals were wide indicating that this association could not be precisely estimated in this study (Table 5).
In simple age- and sex-adjusted models, potassium at 4 months was positively associated with later SBP and there was no association between potassium at 8 months and SBP (mean difference per 1 s.d. potassium=0.89 mm Hg, 95% CI: 0.09–1.69, P=0.03 at 4 months and β=0.12 mm Hg/s.d., 95% CI: −0.59 to 0.83, P=0.7 at 8 months). There was no association between SBP at 7 years and energy intake at either 4 or 8 months (β=0.31 mm Hg/s.d., 95% CI −0.49 to 1.12, P=0.4 at 4 months and β=0.39, 95% CI −0.32 to 1.10, P=0.3 at 8 months, both age- and sex-adjusted). When analyses were performed separately for boys and girls, no differences were detected in the associations between BP and sodium intake (P for interaction ⩾0.3 for all).
Among these children who were born in the United Kingdom in the early 1990s, very few (0.4%) were exceeding current UK Department of Health recommendations for infant sodium intake at 4 months, but the majority (73.0%) were exceeding these levels at 8 months (Department of Heath, 2006). It is not clear which foods constitute the main sources of higher sodium intake in infants. Preliminary analyses by one of the authors of determinants of sodium intake in CIF infants indicate that variations in sodium are not principally attributable to any particular types of food (DA Lawlor, in preparation).
The median (IQR) value for the proportion of dietary sodium intake attributable to breast milk was 0% (0, 82.6) at 4 months and 0% (0, 1.8) at 8 months. Furthermore, 87.6% of infants at 4 months (100% at 8 months) were being given solids. This suggests that variation in sodium intake is at least in part related to variations in diet and weaning practices and not simply due to a greater volume of breast milk or formula.
Similar effect sizes are observed between our study and the earlier Dutch trial (Geleijnse et al., 1997). In the Dutch trial, a difference in sodium intake of 8.8 mmol between the randomized groups corresponded to an increase in SBP at 15 years of 3.6 mm Hg in children randomized to the higher sodium group for the first 6 months of life. In our cohort, an increase in energy-adjusted sodium intake at 4 months of 9 mmol per day was associated with an increase in SBP at 7 years of 4.0 mm Hg, adjusted for all confounders.
Three trials have reported that sodium intake in infancy is not associated with later BP in infancy and childhood. One trial was of pre-term infants with intervention implemented in the early postpartum weeks only. No differences in BP were observed at 18 months (Lucas et al., 1988) or at 8 years (Singhal et al., 2001). In the other two trials, differences in BP were not detected at 6 months in one trial (Pomeranz et al., 2002) nor at 8 months and 8 years of age in the other trial (Whitten and Stewart, 1980). However, these studies may have been insufficiently powered to detect such effects (N=27 (Whitten and Stewart, 1980) and N=58 (Pomeranz et al., 2002)).
The association between sodium intake at 4 months and later SBP, found in this study, may simply be a chance finding. However, it is also possible that early infancy may represent a sensitive period in relation to effects of sodium on later BP since, before the age of 4 months, infants are less efficient at excreting excess sodium and healthy infants only begin to excrete an excessive sodium load at around 4 months (Fleischer Michaelsen et al., 2003).
Although we were unable to adjust for potassium in this study, administration of oral potassium in adults actually lowers the BP (Whelton et al., 1997). This suggests that potassium intake may not be the driving factor behind the association of higher infant sodium intake and increased BP. However, effects of infant potassium intake on later BP have not been studied previously and potassium intake in infancy was in fact positively associated with SBP at 7 years in this cohort.
The gold standard for the measurement of sodium is 24-h urinary sodium. However, this method is difficult to implement in infants (requires urine extraction from diapers) and is not feasible in population studies. A review conducted by one of the authors (DA Lawlor, in preparation) indicates that at present there are no validation studies for assessment of infant sodium intake using diet diaries by comparison with 24-h urinary sodium. However, in adults, diet diaries provide better estimates of average sodium intake than food frequency questionnaires, which have largely been the instrument of choice in population-based studies (Day et al., 2001).
Our assessment of breast milk sodium assumes similar concentrations for all women. This is reasonable, as the time points at which they were assessed in this study were at times of mature breast milk production when there is little within or between individual variation in breast milk (Koo and Gupta, 1982; Hazebroek and Hofman, 1983). Any measurement error in breast milk assessment would be expected to affect the 4-month intake more than the 8-month intake, due to the higher proportion of sodium attributable to breast milk at 4 months. However, any measurement error will be non-differential with respect to the child's BP and therefore would be expected to bias results towards the null.
Adjusting for breastfeeding resulted in a slight attenuation of the association between sodium intake at 4 months and later BP, suggesting that a small proportion of the observed association may be related to breastfeeding patterns. This is likely to be owing to the fact that breastfeeding is associated with lower BP (Martin et al., 2005), and that infants who had higher sodium intake at 4 months in this cohort were less likely to have been breastfed.
In conclusion, we have found that at 8 months of age, a large proportion of participants in this cohort of children born in the early 1990s were exceeding the maximum recommended intake for sodium in infancy. We found some evidence that greater sodium intake in infancy is associated with elevated BP in later life; however, this was found for sodium intake at 4 months only despite almost all infants at this age consuming below the maximum recommended intake. Further studies are required to confirm this finding before one could conclude that infancy is a sensitive period with respect to the effect of dietary sodium intake on later BP.
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We are extremely grateful to all the families who took part in this study, the midwives for their help in recruiting them and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. The UK Medical Research Council, the Wellcome Trust and the University of Bristol provide core support for ALSPAC. Marie-Jo Brion is jointly funded by the Overseas Research Students Awards Scheme and the University of Bristol. Debbie A Lawlor is supported by a UK Department of Health Career Scientist Award. None of us had any financial or personal interest in any of the companies or organizations sponsoring this research. Contents of this article represent the views of the authors and not necessarily those of the funding bodies or anyone else listed in these acknowledgements.
Guarantor: M-J Brion and DA Lawlor.
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Brion, M., Ness, A., Davey Smith, G. et al. Sodium intake in infancy and blood pressure at 7 years: findings from the Avon Longitudinal Study of Parents and Children. Eur J Clin Nutr 62, 1162–1169 (2008). https://doi.org/10.1038/sj.ejcn.1602837
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