Age Differences in Vitamin A Intake Among Canadian Inuit
Background: Inuit traditional food provides ample amounts of preformed vitamin A. However, the dietary transition away from traditional food raises concerns regarding dietary adequacy. Vitamin A is an essential nutrient with inadequate and excessive exposures having adverse effects.
Objective: To evaluate total dietary vitamin A intake for Canadian lnuit from market food and traditional food sources and to evaluate retinol concentrations in liver and blubber.
Methods: Dietary surveys were conducted in 18 communities representing 5 Inuit regions, and traditional food items were evaluated for nutrient content.
Results: Among those 15-40 years of age, 68% of men and 60% of women had a dietary vitamin A intake below the estimated average requirement (EAR) for retinol activity equivalents (RAE)/day. Among those over 40 years of age, only 11 % of men and 1 5% of women had a dietary vitamin A intake below the EAR. Young Inuit men had a relative risk of 6.2 (95% Cl= 4.5-8.4), and young lnuit women had a relative risk of 4.0 (95% Cl= 3.1 5.0) for dietary inadequacy compared to the older lnuit men and women, respectively. The median retinol content of liver of ringed seal, caribou, and fish were comparable to levels observed in market food liver. Eiver was less frequently consumed by those 15-40 years of age than among older Inuit.
Discussion: Sub-optimal vitamin A intake is the predominant nutritional concern rather than excessive exposures. Public health education campaigns are needed to improve vitamin A intake among the younger generations of Inuit men and women.
Vitamin A is important for immune function, gene expression, reproduction and embryonic development, growth, and normal vision with both excessive and inadequate intakes having adverse health impacts. The developing fetus is particularly sensitive to suboptimal and excessive exposures.1-6 The term vitamin A includes preformed vitamin A found in foods of animal origin and the provitamin A carotenoids that are dietary precursors of retinol and are found in dark-green and yellow-orange fruits and vegetables.
Inuit traditional food includes liver and blubber which are rich in biologically active preformed vitamin A. However, the ongoing dietary transition away from traditional food to a greater reliance upon market food can introduce nutritional inadequacies in northern remote regions given market food preferences and the poor selection and availability of quality market food.7 Today, suboptimal vitamin A intake has been noted in many northern communities,8-10 and has been postulated to play a role in the high rate of infections and respiratory illness among Inuit children.”
The objectives of the current paper are to evaluate vitamin A intake among Canadian Inuit and report levels of vitamin A in liver and fat of species traditionally consumed in the Arctic.
Community representatives from all 39 communities in 5 Inuit regions selected 18 communities for the dietary surveys to achieve geographic representation (Figure 1). Research agreements were obtained with each community and interviews were conducted by locally trained interviewers in local language when needed.12-14 Random sampling of 10% of households in each community took place using household or utility lists. For small communities of 25 households or fewer, all households were selected for interview. Participation rate was greater than 70% in the communities. A 24- hour dietary recall questionnaire was administered in participants’ homes, and interviewers used locally available portion models. Interviewers were trained to probe participants using multiple pass techniques for selected items or times of the day.15 Participants were asked to keep a 7-day record of traditional food consumed and a 3-month traditional food frequency questionnaire was administered in summer (June-August) and winter (December-February). A total of 999 7-day dietary records and 1,875 24-hour recalls were collected. A second 24-hour recall was collected on a non-consecutive day for 17% of all study participants and for 20% of women 15-40 years of age. A total of 715 men and 909 women participated in the surveys conducted in 1998-1999.
Retinol Activity Equivalents (RAE) were calculated based upon new Dietary Reference Intakes (DRI) and procedures for analysis developed by the National Academy of Sciences, Institute of Medicine and Health Canada.16 Is Also, an update of the carotenoid content of US foods was used to compute the RAE of the market food items.19 The market food data were combined with the Centre for Indigenous Peoples’ Nutrition and Environment’s (CINE) traditional food nutrient composition database. The market food database was derived from the University of California Mini-list using existing US data,20 and adjusted to include Canadian food items and nutrient fortification levels using the Canadian Nutrient file.21 Retinol was measured in selected traditional food (liver and blubber) using a methodology that is described elsewhere.13,22
We used Software for Intake Distribution Estimation (SIDE) developed by Iowa State University to obtain estimates of usual nutrient intake distributions based upon observed intake. SAS version 8.0 was used to run the SIDE software which is in SAS syntax.23 SIDE transforms observed nutrient intakes, where the transformed data represent the distribution of the population’s usual nutrient intakes. Inter- and intraperson variability was examined by two age groups, 15-40 and greater than 40 years of age, for men and women separately. The usual intake of vitamin A was assessed for adequacy using the estimated average requirement (EAR), where the proportion falling below the EAR indicates prevalence of intakes below the requirement.17 The tolerable upper intake level (UL) was used to evaluate the extent of usual daily intakes above the UL which reflects potential risk of adverse effects from excessive intakes. Plantbased sources of carotenoids were excluded in calculating the percent above the UL of 3,000 g/day of preformed vitamin A for adults.6 The EAR is 500 RAE/day for females and 625 RAE/day for males.6 Analyses were conducted on participants after excluding individuals reporting
Figure 1. Participating Inuit regions
Figure 2. Usual Vitamin A intake by gender and age group: Canadian Inuit
RAE intake varied by gender and age group (Figure 2). For male and female Inuit greater than 40 years of age, 85% of females and 89% of males had dietary intake above the EAR. In contrast, for Inuit aged 15-40, 60% of females and 68% of males fell below the EAR. Young Inuit men had a relative risk of 6.2 (95% CI= 4.5-8.4), and young Inuit women had a relative risk of 4.0 (95% CI= 3.1-5.0) for dietary inadequacy compared to the older Inuit men and women, respectively (Table I). Exclusion of those in the lowest 10th percentile of energy intake, increased the median energy intake by an average of 124 kcal in each age and sex group: for example among men, median energy intake increased from 2,161 to 2,288 kcal and from 1,951 to 2,077 for those aged 15-40 and those >40 years of age, respectively. These data indicate that underreporting still exists in our data, but that it is unlikely to account for the large differences observed in the distribution of vitamin A intake between older and younger Inuit.
Relative Risks for Usual Retinol Activity Equivalent (RAE) Intake Falling Below the Estimated Average Requirement (EAR) by Gender and Age: Canadian Inuit
Percent Reporting Liver Consumption in the Three-month Food Frequency Questionnaire by Age, Gender, Season and Species: Canadian Inuit
Traditional Food Sources of Vitamin A
In examination of the UL, 7% of men over 40 years of age, but no women and no men under 40 years of age had a preformed vitamin A intake above the UL. For the men over 40 years of age, the upper 99th percentile of intake was 5,090 pg of preformed vitamin A.
Vitamin supplement use was reported by 5.1% of all survey respondents and 8.6% of women of reproductive age. The average beta carotene and vitamin A content of supplements were 1,821 IU and 3,268 IU, respectively. If we assume that 8.6% of women aged 15-40 with dietary intakes below the EAR regularly took a vitamin supplement, the percent falling below the EAR would be reduced from 60% to 54.8%.
The 7-day food diary records indicated that the majority of survey respondents consumed liver relatively infrequently: 1.1% and 2.0% for women and men aged 15-40 years, respectively, and 2.7% among those over 40 years of age. In contrast, the 3-month FFQ showed a somewhat higher proportion of respondents indicated liver consumption at least once a month. For the summer months, 9% of young women reported consuming caribou liver, 9% char, 2% fowl, and 19% ringe\d seal liver, whereas for older Inuit women, summer liver consumption was more frequently reported: 14% for caribou, 21% for char, 10% for fowl, and 34% for ringed seal liver (X^sup 2^-tests, p≤0.05 for Char, fowl, and ringed seal) (Table II). Similar differences were observed in liver consumption between younger and older women during the winter season. Likewise, for men, older Inuit more frequently reported consuming liver than younger men. Also, young men and women reported similar liver consumption frequencies with the exception that men consumed significantly more ringed seal liver in summer months than women (X^sup 2^-test, p≤0.05). Whale liver consumption was not reported and kidney consumption was rarely reported.
Median retinol concentrations were 5,486 g/100 g for ringed seal liver and 9,636 g/100 g for caribou (Table III). These traditional food liver tissue levels are comparable to those observed in market food liver24 and lower than Beluga and Narwhal whale (36,000 and 30,000 g/100 g) measured in a Greenlandic study.25 Beluga blubber contained average (median) retinol in concentrations of 1,360 g/100 g and narwhal blubber contained average retinol concentrations of 1,890 g/100 g. The Baffin region reported the most traditional food consumption: the percent of total RAE intake from market food ranged from 69% in Baffin, to 76-81% in Inuvialuit, Kitikmeot, and Kivalliq, to a high of 90% in Labrador. Among market food items, carrots, vegetables, butter, margarine, milk, and eggs were the leading sources of vitamin A intake.
The distribution of usual vitamin A intake derived from the 24- hour dietary recalls and repeat recalls, indicates that the predominant challenge is one of improving low vitamin A intake among the younger generations of Inuit. The large differences between the older and younger Inuit in vitamin A intake may be attributed to differences in traditional food consumption, given that older Inuit reported a greater percent of energy from traditional food than younger Inuit.14 Under-reporting of energy intake is unlikely to account for the large age differences observed in vitamin A intake.
For all women and for men 15-40, none exceeded the UL for preformed vitamin A. For men over 40 years of age, 7% were found to have preformed vitamin A intake above 3,000 g/day. The UL is based upon teratogenicity for women of childbearing age, and on liver abnormalities for all other adults and applies to preformed vitamin A only.17 For liver abnormalities, the lowest observed adverse effect level of 14,000 g/day from vitamin A supplements is divided by an uncertainty factor of 5 to provide a UL of 3,000 g of preformed vitamin A. As the high end of vitamin A exposure among those exceeding the UL was 5,090 g/day, these exposures are not excessive in terms of risk for liver toxlcity. High vitamin A exposures do lead to bone mineral loss in rats26 and may decrease bone mineral density in humans, however epidemiologic research findings are inconsistent27-29 and require further evaluation.
For the younger generations of Inuit, the data suggest the need for public health education and interventions aimed at improving low vitamin A intake. Also, low vitamin A intake may be more deleterious in northern communities where there is a high prevalence of binge drinking.30,31 There is evidence that the adverse effects of inadequate (and excessive) vitamin A exposures on the developing fetus is likely to be more pronounced among women who drink excessively and have had a history of alcohol abuse. Ethanol ingestion alters vitamin A metabolism and depletes vitamin A liver stores and alcohol intake has also been shown to increase the adverse effects of too little or too much vitamin A.32-35 The metabolic interactions between ethanol and vitamin A have been postulated to play a role in the pathogenesis of fetal alcohol syndrome (FAS) as there is remarkable similarity between the dysmorphic and teratogenic effects of ethanol and vitamin A.36-38 In addition to the metabolic interactions of ethanol and vitamin A, poor nutritional habits coincide with alcohol abuse and alcohol interferes with intestinal absorption of folate.39 A combination of low vitamin A intake and a high prevalence of excessive alcohol consumption, and reduced absorption of key nutrients, may contribute to the high rates of congenital heart defects and FAS observed in northern populations.40-42
Education programs regarding market food sources of vitamin A rich food and the importance of vitamin A are needed. Liver can provide a good source of vitamin A and help improve hepatic stores to compensate for nutritional inadequacies. Also, given the high prevalence of iron deficiency anemia in many communities,43,44 and the evidence that vitamin A and iron can reduce iron deficiency anemia to a greater degree than iron alone,45 liver may be particularly helpful in reducing iron deficiency anemia for women and children. Given the variability in retinol in traditional food liver and in serving sizes, advocating liver consumption raises theoretical concerns regarding excessive exposures during pregnancy. Advocating small servings (50 g) during early pregnancy or when there is a risk of early pregnancy is prudent. The U.S. Centers for Disease Control advises that liver can be consumed in moderation during pregnancy.46
Contexte : L’alimentation traditionnelle des Inuits est trs riche en vitamine A prforme, mais on craint que l’abandon progressif des aliments traditionnels entrane des carences alimentaires. La vitamine A est un lment nutritif essentiel dont le dficit ou l’excdent peut avoir des effets indsirables.
Objectif : valuer l’apport total en vitamine A provenant des sources de nourriture commerciales et traditionnelles dans l’alimentation des Inuits du Canada et valuer les concentrations en rtinol dans le foie et le petit lard.
Mthode : Nous avons administr des questionnaires sur l’alimentation dans 18 collectivits reprsentant 5 rgions inuites et valu le contenu d’aliments traditionnels en lments nutritifs.
Rsultats : Chez les Inuits de 15 40 ans, 68 % des hommes et 60 % des femmes avaient un apport alimentaire en vitamine A infrieur au besoin moyen estimatif (BME) quotidien en quivalents rtinol (ER). Chez les plus de 40 ans, par contre, seulement 11 % des hommes et 15 % des femmes avaient un apport alimentaire en vitamine A infrieur au BME. Les jeunes hommes prsentaient un risque relatif de carence alimentaire de 6,2 (IC de 95 %=4,5-8,4), et les jeunes femmes, un risque relatif de 4,0 (IC de 95 %= 3,1-5,0), respectivement, par rapport aux hommes et aux femmes plus gs. Nous avons compar la teneur mdiane en rtinol dans des foies de phoque annel, de caribou et de poisson et dans des foies vendus dans le commerce. Les Inuits de 15 40 ans consommaient moins souvent du foie que leurs ans.
Discussion : Un apport sous-optimal en vitamine A proccupe davantage les ditticiens qu’un apport excessif. Il faudrait mener des campagnes de sensibilisation du public afin d’amliorer l’apport en vitamine A chez les jeunes gnrations d’Inuits.
1. Semba RD. The role of vitamin A and related rctinoids in immune function. Nutr Rev 1998;56(Suppl):38-48.
2. Azais-Braesco V, Pascal G. Vitamin A in pregnancy: Requirements and safety limits. Am J Clin Nutr 2000;71 (Suppl): 1325- 33.
3. Zile MH. Vitamin A and embryonic development: An overview. J Nutr 1998;128(Suppl):455-58.
4. Ross SA, McCaffery PJ, Drager UC, Luca LM. Rctinoids in embryonal development. Physiol Rev 2000;80(3):1021-54.
5. Sommer A. Vitamin A: Its effect on childhood sight and life. Nutr Rev 1994;52(2)Suppl:60-66.
6. Institute of Medicine (US). Vitamin A. In: Dietary Reference Intakes. Washington: National Academy Press, 2000;82-161.
7. Kuhnlein HV, Receveur O, Chan HM. Traditional food systems research with Canadian indigenous peoples. Int J Circumpolar Health 2001;60:112-22.
8. Kuhnlein HV. Nutrition of the Inuit: A brief overview. Arctic Med Res l991;Suppl:728-30.
9. Lawn J, Langner N, Brule D, Thompson N, Lawn P, Hill F. Food consumption patterns of Innit women. Int J Circumsolar Health 1998;57(SuPPl 1):198-204.
10. Godel JC, Basu TK, Pabst HF, Hodges RS, Hodges PE, Ng ML. Perinatal vitamin A (retinol) status of northern Canadian mothers and their infants. BiolNeonate 1996;65:133-39.
11. Jenkins AL, Gyorkos TW, Culman KN, Ward BJ, Pekeles GS, Mills EL. An over-view of factors influencing the health of Canadian Inuit infants. Int J Circumpolar Health 2003;62(l):17-39.
12. Kuhnlein HV, Receveur O, Chan HM, Loring E. Assessment of Inuit Dietary Benefit/Risk in Inuit Communities. Project Report to DIAND, 2000.
13. Kuhnlein HV, Bardlet V, Lcggee D, Farren A. Vitamins A, E and D in traditional arctic food (submitted).
14. Kuhnlein HV, Receveur O, Soueida R, Egeland GM. Arctic indigenous peoples experience: The nutrition transition with changing dietary patterns and obesity. J Nutr 2004; 124:1447-53.
15. Receveur O, Botilay M, Kuhnlein HV. Decreasing traditional food use affects diet quality for adult Dene/Metis in 16 communities of the Canadian Northwest Territories./Nutr 1997:127:2179-86.
16. Institute Of Medicine. Applications in dietary assessment. In: Dietary Reference Intakes. Washington: National Academy Press, 2000.
17. Barr SI, Murphy SP, Poos MI. Interpreting and using the Dictaty Reference Intakes in dietary assessment of individuals and groups. J Am Diet Awf2002;102(6):780-88.
18. Murphy SP. Changes in dietary guidance: Implications for food and nutrient databases. J Food Composition Analysis 2001; 14:269- 78.
19. Holden JM, Eldridge AL, Beecher GR, Buzzard IM, Bhagwat S, Davis CS, et al. Carotenoid content of U.S. foods: An update of the database./Food Composition Analysis 1999; 12:169-96.
20. Murphy SP, Gross KR. The UCB Mini-list Diet Analysis System. MS_DOS Version Users Guide.The Regents of the University of California; Revised I 987JiUi.
21. Dubuc MB, Lahaic I.C. Nutritive Value of Foods. Socit Brault- Lahaie, 1994.
22. Morrison N, Kuhnlein HV. Retinol content of wild foods consumed by the Sahtu (Hareskin) Dene/Metis./Food Composition Analysis 1993:6:10-23.
23. Iowa State University Statistical Laboratory. Software for Intake Distribution Estimation (SIDE). A User’s Guide to SIDE. Version 1. Technical Report 96-TR 30. Department of Statistics and Center for Agricultural and Rural Development, Iowa State University, 1996.
24. U.S. Department of Agriculture, Agricultural Research Service. 2002. USDA National Nutrient Database for Standard Reference, Release 15. Nutrient Data Laboratory Home Page, http:// www.nal.usda.gov/fnic/foodcomp.
25- Helms P. Kostvurderingstabeller. Kopenhagen: Akademisk Forlag, 1980.
26. Rohde CM, Manatt M, Clagett-Dame M, DeLuca HF. Vitamin A antagonizes the action of vitamin D in rats. JNutr 1999:129:2246- 50.
27. Fretidcnheim JL, Johnson NE, Smith EL. Relationship between usual nutrient intake and bone-mineral content of women 35-65 years of age: Longitudinal and cross-sectional analysis. AmJ Clin Nutr 1986;44:863-76.
28. Houtkooper LB, Ritenbaugh C, Aicken M, Lohman TG, Going SB, Weber JL, et al. Nutrients, body composition and exercise are related to change in bone mineral density in premenopausal women. J Nutr 1995; 125:1229-37.
29. Melhus H, Michaelsson K, Kindmark A, Bergstrom R, Holmberg L, Mallmin H, et al. Excessive dietary intake of vitamin A is associated with reduced bone mineral density and increased risk for bip fractures. Ann Intern Med 1998;129:770-78.
30. CDC. Prevalence and characteristics of alcohol consumption and fetal alcohol syndrome awareness – Alaska, 1991 and 1993. MMWR 1994;43(1):3-6.
31. Sant Quebec. Use of tobacco, alcohol and illicit drugs. In: A health profile of the lnuit: report of the Sant Qubec Health Survey among the lnuit of Nunavik, 1992;121.
32. Leo MA, Lieber CS. Hepatic vitamin A depiction in alcoholic liver injury. N Engl J Med 1982;307:597-601.
33. Leo MA, Lieber CS. Alcohol, vitamin A, and beta-carotene: Adverse interactions, including hepatotoxicity and carcinogenicity. Am J Clin Nutr 1999;69:10710 -85.
34. Sato M, Lieber CS. Hepatic vitamin A depletion after chronic ethano! consumption in baboons and rats. J Nutr 1981; 111:2015-23.
35. Whitby KE, Collins TFX, Welsh JJ, Black TN, Flynn T, Shackelford M, et al. Developmental effects of combined exposure to ethanol and vitamin A. Food Chem Toxicol 1994;32:305-20.
36. Duester G. A hypothetical mechanism for fetal alcohol syndrome involving ethanol inhibition of retinoic acid synthesis at the alcohol dehydrogenase step. Alcohol Clin Exp Res 1991;15(3):568- 72.
37. Pullarkat RK, Azar B. Retinoic acid, embryonic development, and alcohol-induced birth defects. Embryonic Deve lopment 1992;16(4):317-23.
38. Zachman RD, Grummer MA. The interaction of ethanol and vitamin A as a potential mechanism for the pathogencsis of fetal alcohol syndrome. Alcohol Clin Exp Res 1998;22(7):1544-56.
39. Halsted CH, Villanueva JA, Devlin AM, Chandler CJ. Metabolic interactions of alcohol and folate. J Nutr 2002; 132 (Suppl):2367- 72.
40. Arbour L, Gilpin C, Millor-Roy V, Pekeles G, Egeland GM, Hodgms S, Eydoux P. Congenital heart defects and other malformations in the Inuit of Baffin Island and Arctic Quebec between 1989 and 1994 (In press).
41. Egeland GM, Perham-Hester KA, Hook EB. Use of capture- recapture analyses in fetal alcohol syndrome surveillance in Alaska. Am J Epidemiol 1995;141:335-41.
42. Egeland GM, Perham-Hester KA, Gessner BD, Ingle D, Berner JE, Middaugh JP. Fetal alcohol syndrome in Alaska, 1977 through 1992: An administrative prevalence derived from multiple data sources. Am J Public Health 1998;88:78186.
43. Willows ND, Dewailly E, Gray-Donald K. Anemia and iron status in Inuit infants from northern Quebec. Can J Public Health 2000;91:407-10.
44. Hodgins S, Dewailly K, Chatwood S, Bruneau S, Bernier F. Iron- deficiency anemia in Nunavit pregnancy and infancy. Int J Circumpolar Health 1998;57(Suppl 1):135-40.
45. Suharno D, West CLi, Muhilal Karyacli D, Hautvast JGAJ. Supplementation with vitamin A and iron for nutritional anaemia in pregnant women in West Java, Indonesia. Lancet 1993;342:1325-28.
46. Oakley GP, Erickson JD. Vitamin A and birth defects: Continuing caution is needed. N Engl J Med 1995;333(21):1414-15.
Received: August 22, 2003
Accepted: May 28, 2004
Grace M. Egeland, PhD1
Peter Berti, PhD2
RuIa Soueida, MSc1
Laura T. Arbour, MD4
Olivier Receveur, PhD3
Harriet V. Kuhnlein, PhD1
Correspondence: Dr. G.M. Egeland, Centre for Indigenous Peoples’ Nutrition and Environment (CINE) and School of Dietetics and Human Nutrition, McCiII University, Macdonald Campus, Ste-Anne- deBellevue, QC H9X 2T6, Tel: 514-398-8642, Fax: 514-398-1020, E- mail: email@example.com
Acknowledgements: We thank the Inuit participants and the Inuit Tapiriit Kanatami for their assistance throughout all stages of the work, and the Canadian Institutes of Health Research, Institute of Aboriginal Peoples’ Health and the Institute of Nutrition, Metabolism and Diabetes for their financial support.
Copyright Canadian Public Health Association Nov/Dec 2004