Dietary intakes

A significant proportion (31 %) of our participants had a usual fat intake that fell outside the AMDR set at 30–40 %E for children aged 1–3 years. This proportion was at the lower end of those observed in representative groups of Canadian and US children of the same age (23–50 %E)⁽ Reference Butte, Fox and Briefel ^{24 –} Reference Troiano, Briefel and Carroll ^{27 )}. Also, in agreement with these studies, we found that more than a quarter of our participants (27·8 %) had a usual fat intake below the AMDR, with only a small proportion above the higher limit of the AMDR. According to the Institute of Medicine, there is no evidence that the macronutrient composition of the diet affects childhood growth if energy and protein requirements are met^{( 2 )}. This seems to be the case among our participants as only 1·4 % had a protein intake below the Estimated Average Requirement (H Turgeon O'Brien, D Gagné, É Vaissière et al., unpublished results). Moreover, the mean fat intake (32 %E) in the present study was in the range of values reported in a systematic review of fat and FA intakes of children and adolescents around the world (23–40 %E)⁽ Reference Harika, Cosgrove and Osendarp ^{28 )}. Mean usual intakes of SFA and MUFA were also similar to levels observed in a representative sample of 1–3-year-old Canadian children^{( 25 )}, whereas the usual intake of PUFA was slightly higher among our participants (4·5 %E v. 3·8 %E, respectively). Mean usual intakes of SFA and PUFA were also within the range observed by Harika et al. among children worldwide (1·0–15·2 %E and 3·5–9·7 %E, respectively)⁽ Reference Harika, Cosgrove and Osendarp ^{28 )}. When compared with a representative group of Inuit adults who participated in the Nunavik Inuit Health Study (NIHS), total fat and MUFA contributed a similar proportion to energy intake but PUFA contributed a slightly lower proportion to energy intake (4·5 %E v. 5 %E in NIHS, respectively)⁽ Reference Blanchet and Rochette ^{13 )}. In the same way, n-3 and n-6 PUFA usual dietary intakes of participants in the present study were almost half those in NIHS⁽ Reference Blanchet and Rochette ^{13 )}. However, our participants had the same median n-6:n-3 PUFA dietary intake ratio⁽ Reference Blanchet and Rochette ^{13 )}. The sum of dietary intakes of EPA + DHA (0·15 g/d) was similar to that observed in a group of 3–5-year-old Canadian children from Vancouver (0·14 g/d)⁽ Reference Innis, Vaghri and King ^{29 )} and within the range observed in children worldwide (0·05–0·15 g/d)⁽ Reference Harika, Cosgrove and Osendarp ^{28 )}. Concerning essential FA, the proportion of children with adequate usual intakes (>AI) of ALA and LA in the present study was lower than in Canadian children and Canadian Inuit adults (ALA: 40 %, 69 % and 75–90 %, respectively; LA: 5 %, 21 % and 2–29 %, respectively)^{( 30 –} Reference Kuhnlein, Receveur and Soueida ^{32 )}. Altogether, these results reiterate that Inuit pre-school children rely less on traditional foods than Inuit adults⁽ Reference Gagné, Blanchet and Lauzière ^{15 )} and indicate that their FA dietary intakes are similar to those of children worldwide.

Red-blood-cell fatty acid composition

RBC n-6 and n-3 PUFA were higher in our participants than in US children aged 1–11 years (30·11 %FA v. 24·93 %FA and 5·53 %FA v. 3·81 %FA, respectively)⁽ Reference Orton, Szabo and Clare-Salzler ^{7 )}. Although RBC PUFA composition of Danish adolescents was similar to that of our participants, the former had higher levels of LC-PUFA⁽ Reference Lauritzen, Harslof and Hellgren ^{8 )}. Canadian Inuit children living on Broughton Island (formerly in Northwest Territories, now in Nunavut) and aged 0–5 years in 1985 (n 13) had probably higher levels of n-3 LC-PUFA, although it is uncertain because concentrations of RBC FA were reported for phosphatidylcholine and phosphatidylethanolamine separately⁽ Reference Innis, Kuhnlein and Kinloch ^{17 )}.

The ratio of n-6 to n-3 PUFA has been used as an indicator of dietary Westernization among Indigenous people, with higher ratios indicating lower consumption of traditional foods⁽ Reference Simopoulos ^{33 )}. In our study, we observed a high n-6:n-3 PUFA, confirming our previous observation on the dietary transition and the lower reliance upon traditional foods⁽ Reference Gagné, Blanchet and Lauzière ^{15 )}. Moreover, Zhou et al. suggested that a high DPA:EPA might be a novel indicator of a diet containing a larger proportion of land animals than of both fish and marine mammals⁽ Reference Zhou, Kubow and Egeland ^{6 )}. We observed a higher DPA:EPA than the ones reported by Zhou et al. in all the communities they surveyed, which would suggest that our participants may have consumed more land animals than fish and marine mammals. If we look more closely, we can see that this high ratio is explained by lower RBC EPA levels among our participants rather than higher levels of DPA. Therefore, this result seems to be more indicative of a low consumption of fish and marine mammals rather than of a high consumption of land animals. Indeed, when considering multiple indicators, we conclude that these young Inuit children eat a lower proportion of traditional food and more specifically a lower amount of fish and marine mammals than Inuit adults.

Multivariate models

In the regression models, we showed that breast-feeding status (never breast-fed/ever breast-fed/currently breast-fed) was positively associated with RBC n-3 and n-6 PUFA concentrations. This is in agreement with the positive association observed between breast-feeding duration and RBC DHA and EPA levels in Danish adolescents⁽ Reference Lauritzen, Harslof and Hellgren ^{8 )}. When replacing breast-feeding status by breast-feeding duration, we observed a positive and significant association with RBC n-3 PUFA but not with RBC n-6 PUFA. This result may suggest that breast-feeding duration may be indicative of a more traditional lifestyle containing more n-3 LC-PUFA than n-6 LC-PUFA after weaning⁽ Reference Kuhnlein, Chan and Leggee ^{34 )}.

In the model explaining RBC n-3 PUFA, dietary n-3 PUFA intake was not significantly associated. This is in agreement with Hoyos et al., who did not observe a significant association between n-3 PUFA dietary intake and plasma n-3 PUFA in 18- and 36-month-old Australian children⁽ Reference Hoyos, Almqvist and Garden ^{35 )}. On the contrary, we observed that the consumption of traditional foods during the 24 h dietary recall period was associated with higher RBC n-3 PUFA levels. This may suggest that having consumed a traditional food may be a better indicator of a traditional diet than n-3 PUFA or EPA + DHA dietary intakes when assessed with a 24 h dietary recall. Indeed, we have previously hypothesized that it might be harder to report traditional food serving sizes of young children as they are often served or taken by hand, one mouthful at a time, from a centre dish, with other family members (or child-care centre staff) participating in the service and that this could lead to misestimating traditional food intakes⁽ Reference Gagné, Blanchet and Lauzière ^{15 )}. The positive association between the consumption of traditional food and RBC n-3 PUFA is also in accordance with results from Lucas et al., who observed that intakes of most Inuit traditional foods (marine mammals, fish, land animals and game-bird eggs) were correlated with RBC n-3 LC-PUFA in Nunavik adults⁽ Reference Lucas, Proust and Blanchet ^{4 )}. Young et al. also reported a positive association between the consumption of traditional foods and plasma EPA and DHA among adults⁽ Reference Young, Gerrard and O'Neil ^{18 )}. In the present study, age also tended to be significantly associated with RBC n-3 PUFA levels and was significantly associated with RBC EPA+DHA, which is agreement with increased plasma n-3 LC-PUFA observed in 36- and 60-month-old children compared with the same children at age 24 months⁽ Reference Guerra, Demmelmair and Toschke ^{36 )}. Sex and infant formula status were not significantly associated with RBC n-3 PUFA. It has been hypothesized that intake of LA or n-6 PUFA may blunt the tissue incorporation of n-3 PUFA⁽ Reference Hoyos, Almqvist and Garden ^{35 ,} Reference Hibbeln, Nieminen and Blasbalg ^{37 )} but their intakes were not associated with RBC n-3 PUFA in our study. We did not observe any relationship between BMI-for-age Z-score and RBC n-3 PUFA levels; this differs from Burrows et al. who had suggested a role for n-3 LC-PUFA in the development of obesity as they observed lower levels of RBC EPA+DHA among obese Australian children compared with non-obese⁽ Reference Burrows, Collins and Garg ^{38 )}. As for RBC n-6 PUFA levels, they were positively associated with breast-feeding status as mentioned above and, as expected, with n-6 PUFA dietary intakes. In 18- and 36-month-old Australian children, dietary n-6 PUFA were also positively associated with plasma n-6 PUFA levels⁽ Reference Hoyos, Almqvist and Garden ^{35 )}. Age, sex and infant formula status were not associated with RBC n-6 PUFA concentrations.

Limitations

When interpreting the present results, one ought to keep in mind the limits of the study. First, to estimate usual dietary intakes, SIDE requires that individuals must be independent. This was not always true in the present study as some siblings were recruited. Unfortunately, this information was not collected, preventing us from adjusting for this variable. Also, as reported elsewhere⁽ Reference Gagné, Blanchet and Lauzière ^{15 )}, children in the present study had a lower energy intake compared with a representative group of Canadian children of the same age group participating in the 2004 Canadian Community Health Survey (CCHS). Even though parents in the CCHS were believed to have overestimated the dietary intakes of their children^{( 39 )}, there is a possibility that energy intake was under-reported in our participants and this could have increased the prevalence of inadequate nutrient intakes in our study⁽ Reference Gibson ^{40 )}. Moreover, we may have induced a selection bias since children included in the present analyses (i.e. those with a complete set of variables) represent 68·2 % of enrolled participants.

Another limit of our study includes the use of a 24 h dietary recall to estimate FA dietary intakes. The 24 h dietary recall method is a simple, rapid and well-established tool to assess the average intake of groups⁽ Reference Willett ^{41 )}. We collected a second recall for a significant proportion of the children to improve the accuracy of individual intake estimates and take intra-individual variability into account. However, in multivariate models, we had to use only the first 24 h dietary recall because we did not have enough recalls per children to represent usual dietary intakes on an individual basis. For example, sixty-four recalls per adults are necessary to estimate individual usual intakes of total fat⁽ Reference Basiotis, Welsh and Cronin ^{42 )}. Therefore dietary intakes included in regression models may not represent the usual intakes of children. Moreover, our results also depend on the Canadian Nutrient File for data analysis^{( 20 )} which has its own limits. Indeed, the version used did not cover all foods for n-3 and n-6 PUFA, and there might be more variation among wild animals resulting in higher or lower dietary intakes than estimated by the Canadian Nutrient File. Furthermore, a measure of dietary intakes covering a longer period of time would have been optimal to compare with exposure reflected by the RBC FA concentrations. The fact that we used a 24 h dietary recall could have lowered the strength of the relationships between dietary intakes and RBC levels, especially for n-3 LC-PUFA. However, using an FFQ covering a longer period of time was difficult with our population as some children had only commenced eating solids during the last 12 months, which was the period covered by the FFQ; limiting our capacity to use it. The uncertainty in the present study is therefore presumed to be mainly related to the dietary assessment, while assessment of RBC membranes reflects the general intake over the lifespan of RBC, or ∼120 d⁽ Reference Arab ^{3 ,} Reference Hodson, Skeaff and Fielding ^{43 )}. Still, FA in RBC membranes are under the control of both genetic and other modifying factors such as disease and nutritional status, although RBC PUFA respond to differences in dietary intake more so than do RBC SFA⁽ Reference Arab ^{3 ,} Reference Hodson, Skeaff and Fielding ^{43 )}.