Letters to the Editor
Level of physical activity and adiposity in
children: relevance of sedentary behaviors
Dear Sir:
The main finding of the study by Ekelund et al (1) was that the
amount of time devoted to physical activity explained 1% of the
variation in fat mass in 10-y-old children. This conclusion appar-
ently reduces the relevance of the intensity of physical activity in the
maintenance of childhood obesity and seems to frustrate the reason-
able expectancy for the role potentially played by exercise and phys-
ical activity both in the prevention and treatment of overweight.
The energy cost of weight-bearing activities is higher in obese
than in nonobese children (2, 3). This finding promotes, by impli-
cation, the spontaneous reduction of time devoted to moderate-to-
vigorous physical activity (MVPA) by the obese, as previously re-
ported by others (3, 4). However, the higher cost of MVPA
compensated the lower time spent in MVPA so that no difference in
the cumulative energy expenditure for MVPA could be found be-
tween obese and nonobese children. However, obese children spend
more energy and, interestingly, oxidize much more fat during light-
intensity exercise than do nonobese children (5). Therefore, the time
spent in sedentary or light-intensity physical activities as well as the
ratio between sedentary and light-intensity physical activities could
be more crucial than their absolute values or MVPA for both the
development and the maintenance of obesity. Interestingly, the
results of a recent study conducted in young children, which
showed a clear relation between sedentary as well as light-
intensity physical activity and overweight, seems to support this
hypothesis (6). At present, a change from sedentary behavior to a
more active lifestyle remains the cornerstone of strategies to
prevent and treat childhood obesity.
No conflicts of interest were declared by the author.
Claudio Maffeis
Department of Mother and Child, Biology-Genetics, Pediatrics
Unit
University of Verona
Piazzale LA Scuro, 10
37134 Verona
Italy
E-mail: claudio.maffeis@univr.it
REFERENCES
1. Ekelund U, Sardinha LB, Anderssen SA, et al. Associations between
objectively assessed physical activity and indicators of body fatness in 9-
to 10-y-old European children: a population-based study from 4 distinct
regions in Europe (the European Youth Heart Study). Am J Clin Nutr
2004;80:584 90.
2. Maffeis C, Schutz Y, Schena F, et al. Energy expenditure during walking
Am J Clin Nutr 20054;81:1449 54. Printed in USA. 20054 American Society for Clinical Nutrition
and running in obese and nonobese prepubertal children. J Pediatr 1993;
123(2):1939.
3. Lazzer S, Boirie Y, Bitar A, et al. Assessment of energy expenditure
associated with physical activities in free-living obese and nonobese
adolescents. Am J Clin Nutr 2003;78(3):4719.
4. Maffeis C, Zaffanello M, Pinelli L, Schutz Y. Total energy expenditure
and patterns of activity in 8 10-year-old obese and nonobese children.
J Pediatr Gastroenterol Nutr 1996;23(3):256 61.
5. Maffeis C, Zaffanello M, Pellegrino M, et al. Nutrient oxidation during
moderately intense exercise in obese prepubertal boys. J Clin Endocrinol
Metab 2005;90(1):231 6.
6. Montgomery C, Reilly JJ, Jackson DM, et al. Relation between physical
activity and energy expenditure in a representative sample of young
children. Am J Clin Nutr 2004;80:591 6.
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Reply to C Maffeis
Dear Sir:
We thank Maffeis for his comments on our recently published
article (1). The main findings of our cross-sectional study are that
total activity is not significantly associated with body fat, and that the
time devoted to moderate-to-vigorous physical activity (MVPA)
explains 1% of the variation in body fat in the children studied. Our
results also suggest that the amount of time spent in sedentary ac-
tivities and in light-intensity physical activities does not contribute to
the explained variance in body fat in these children. These results
imply that the intensity of activity may be more relevant than the total
amount of PA, but our results should be interpreted while bearing in
mind the methodologic limitations we discussed in our article. These
limitations include the limited number of days of measurement and
the uncertainty in defining cutoffs for different intensity levels with
the use of an accelerometer (1).
The main concern that Maffeis has with our findings seems to
relate to the fact that our results reduce the relevance of the inten-
sity of PA in the maintenance of childhood obesity and seems to
frustrate the reasonable expectancy for the role potentially played by
exercise and PA in both the prevention and treatment of overweight.
We agree with Maffeis that it is disappointing that our results for
PA do not explain a larger proportion of the variance in body fatness.
However, the association between PA or sedentary behavior and
obesity in young people has not been consistently shown, and we
believe that our interpretation of the results from the present study is
accurate. Nonetheless, we completely agree that sedentary behavior
should be prevented for many reasons, which is reflected by the
following quotes from our article: The relations that we observed
between PA and body fatness were small. Nonetheless, these find-
ings may have important public health implications because seden-
tary behavior is common in most industrialized societies. and
Thus, effective preventive strategies need to address the underlying
social, cultural, physical, and economical determinants of childhood
1449
1450 LETTERS TO THE EDITOR

obesity and are likely to include interventions designed to decrease Sigmund A Anderssen
sedentary behavior in children. (1). Lars Bo Andersen
Maffeis also put forward the hypothesis that time spent sedentary and
in light-intensity PA may be more closely related to body fat in children. Department of Sports Medicine
We are well aware that energy expenditure during weight-bearing PA is The Norwegian University of Sport and Physical Education
higher in obese than in normal-weight children when expressed in ab-
solute values (2). We also recently showed that time spent in MVPA, Norway
measured by accelerometry, is significantly lower in obese children than
in a matched normal-weight control group, whereas time spent in sed-
entary and in light-intensity PA and absolute PA energy expenditure Marike Harro
(simultaneously measured by the doubly labeled water method did not
differ significantly between groups (2). Maffeis argues that the higher Department of Public Health
energy cost of weight-bearing PA promotes, by implication, the spon-
taneous reduction of time devoted to moderate-to-vigorous physical University of Tartu
activity (MVPA) by the obese. However, this is questionable and needs Estonia
to be demonstrated. Indeed, it may actually be the high body weight per
se in obese children that contributes to their reduced activity levels.
Maffeis also suggests that obese children spend more energy Paul W Franks
(which is an effect of higher body mass) and oxidize much more fat
during light-intensity exercise (3). Walking at 4 km/h, the lowest Diabetes and Arthritis Epidemiology Section
activity intensity examined in the study by Maffeis et al (3), repre- NIDDK, National Institute of Health
sents an intensity similar to the lower cutoff we used for MVPA (1). Phoenix, AZ
We defined moderate-intensity PA as 2000 counts/min, which is
broadly equal to a walking speed of 3 4 km/h in 9 10-y-old children
(4, 5). Thus, MVPAas defined in our articleincludes intensity Ashley R Cooper

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levels that Maffeis argues are favorable for increased fat oxidation.
Finally, Maffeis cites a study by Montgomery et al (6) that he sug-
gests shows a clear relation between time spent in sedentary and light-
intensity PA and overweight in young children and, thus, supports his
hypothesis. However, we disagree with Maffeiss interpretation of
these data. The only associations reported by Montgomery et al (6) are
those between the percentage of daytime spent sedentary, in light PA,
and in MVPA (measured by accelerometry) and PAL (ie, the ratio of
total energy expenditure and resting metabolic rate). These authors
observed that time spent sedentary explained most of the variance in
PAL. However, we do not believe PAL can be used as a surrogate for
overweight.
It is possible that time spent in sedentary and in light-intensity PA is
more important than is the accumulated time spent in MVPA, or the total
amount of PA, in preventing overweight and obesity in children. How-
ever, in our large population-based cross-sectional study, which in-
cluded almost 1300 children from 4 different countries in Europe (1),
and in our matched case-control study (2), we observed associations
between MVPA and body fatness but not between body fat and the time
spent being sedentary. Although one needs to be cautious when infer-
ring causality from cross-sectional data, these findings support the view
that MVPA and body fatness are related, whereas our objective measure
of low intensities of PA and body fatness do not.
None of the authors had a conflict of interest.
Ulf Ekelund
Sren Brage
MRC Epidemiology Unit
Elsie Widdowson Laboratory
Fulbourn Road
Cambridge CB1 9NL
United Kingdom
E-mail: ulf.ekelund@mrc-epid.cam.ac.uk
Luis B Sardhina
Faculty of Human Movement
Technical University of Lisbon
Portugal
Department of Exercise and Health Sciences
University of Bristol
Bristol
United Kingdom
Chris Riddoch
London Sport Institute
Middlesex University
United Kingdom
Karsten Froberg
Institute of Sport Science & Clinical Biomechanics
University of Southern Denmark
Odense
Denmark
REFERENCES
1. Ekelund U, Sardinha L, Anderssen SA, et al. Associations between
objectively assessed physical activity and indicators of body fatness in 9-
to 10-year old European children: a population based study from four
distinct regions in Europe (The European Youth Heart Study). Am J Clin
Nutr 2004;80:584 90.
2. Ekelund U, man J, Yngve A, Renman C, Westerterp K, Sjstrm M.
Physical activity but not energy expenditure is reduced in obese adoles-
cents: a case-control study. Am J Clin Nutr 2002;76:935 41.
3. Maffeis C, Zaffanello M, Pellegrino M, et al. Nutrient oxidation during
moderately intense exercise in obese prepubertal boys. J Clin Endocrinol
Metab 2005;90:231 6.
4. Brage S, Wedderkopp N, Andersen LA, Froberg K. Influence of step fre-
quency on movement intensity predictions with the CSA accelerometer: a
field validation study in children. Pediatr Exerc Sci 2003;15:277 87.
5. Eston RG, Rowland A, Ingledew DK. Validity of heart rate, pedometry,
accelerometry for predicting the energy cost of childrens activities.
J Appl Physiol 1998;84:326 71.
6. Montgomery C, Reilly JJ, Jackson DM, et al. Relation between physical
activity and energy expenditure in a representative sample of young
children. Am J Clin Nutr 2004;80:591 6.
 LETTERS TO THE EDITOR
Measuring calcium absorption
Dear Sir:
In their article on calcium absorption in Nigerian children with
rickets, Graff et al (1) report no difference in absorptive efficiency
between children with and without rickets, despite a substantial differ-
ence in serum 25-hydroxyvitamin D concentrations [25(OH)D]. Both
groups had fractional absorption values that the authors judged to be
higher than would have been predicted for their age or for the calcium
loads used to test absorption. They also noted that the measured
absorption fraction did not correlate with dietary calcium, serum
25(OH)D, or serum 1,25-dihydroxyvitamin D concentrations. These
latter inconsistencies are not surprising in themselves, because other
studies have produced similar failures. However, the finding of no
difference in absorptive efficiency leaves the authors with no other
explanation for the rickets than the low absolute calcium content of
the diets of these children. This does not, however, explain why one
group with low calcium intakes had rickets and the other, with
equally low calcium intakes, did not.
There is another, more likely, methodologic explanation for their
finding of equivalent absorption in the 2 groups. Although the au-
thors used the gold standard double-tracer method to measure the
absorption fraction, their description of the labeling of the breakfast
meal suggests that the food calcium was not well labeled with the
extrinsically added tracer. Several studies have shown that extrinsic
labeling of food calcium sources is usually incomplete (25), which
leads to absorption values that are always spuriously high and often
nutritionally misleading or uninterpretable. The reason is that the
tracer is added in microgram amounts in a solubilized form, and as
such would likely be readily absorbed, even in persons with limited
absorptive capacity. In all such applications of the tracer methods, it
is essential to show that the oral tracer is uniformly distributed
through all of the moieties of the calcium source used to test absorp-
tion. I suggest that this did not occur in the study by Graff et al, and
that as a result we actually know very little about absorptive effi-
ciency in these Nigerian children (healthy or rachitic).
There was no conflict of interest.
Robert P Heaney
Creighton University
601 North 30th Street
Suite 4841
Omaha, NE 68131
E-mail: rheaney@creighton.edu
REFERENCES
1. Graff M, Thacher TD, Fischer PR, et al. Calcium absorption in Nigerian
children with rickets. Am J Clin Nutr 2004;80:141521.
2. Heaney RP, Dowell MS, Rafferty K, Bierman J. Bioavailability of the
calcium in fortified soy imitation milk, with some observations on
method. Am J Clin Nutr 2000;71:1166 9.
3. Heaney RP, Rafferty K, Bierman J. Not all calcium-fortified beverages
are equal. Nutr Today 2005;40:39 44.
4. Weaver CM, Heaney RP. Isotopic exchange of ingested calcium be-
tween labeled sources. Does dietary calcium form a common absorptive
pool? Calcif Tissue Int 1991;49:244 7.
5. Weaver CM, Heaney RP, Martin BR, Fitzsimmons ML. Extrinsic vs.
intrinsic labeling of the calcium in whole wheat flour. Am J Clin Nutr
1992;55:452 4.
1451
Reply to RP Heaney
Dear Sir:
The letter from Heaney raises one of the major issues concerning
the methodology for measuring intestinal calcium absorption. We
recognize that there are no perfect methods for evaluating usual
dietary absorption of calcium or any isolated nutrient within the
context of whole diets as typically consumed. Balance methods often
involve the use of nonrepresentative diets and do not isolate nutrient
sources. Furthermore, tracer methods can only trace, as Heaney
notes, certain aspects of the diet. Therefore, such studies must eval-
uate either the bioavailability of calcium from a particular food,
which requires either intrinsic labeling or assurance of full distribu-
tion of the extrinsic label, or a component of absorptive capacity by
providing the label as part of a meal, which may not completely
mix with all of the components. The former method does not
necessarily assess whole dietary absorption and is most suitable
for supplement and fortification studies, such as those referenced
by Heaney. The second method, although it may overestimate
food-based absorption, provides substantial information regard-
ing absorptive capacity.
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In our study, a large amount of phytates in the diet, which are
known inhibitors of calcium absorption, might have been expected
to inhibit the absorption of calcium from the test meal. In fact, this did
not occur in children with or without rickets, undoubtedly because of
the very low calcium content of the test meals. At low calcium
intakes, vitamin D dependent active transport is most critical for
calcium absorption (1). It is reasonable to conclude from our data that
there is no evidence that Nigerian children with rickets have a fun-
damental inability to absorb calcium; thus, vitamin D deficiency is
excluded as a factor in the causation of the disease. Our results are
also consistent with those of early calcium balance studies conducted
in South African children with dietary calcium deficiency rickets
(2). After nutritional rehabilitation, calcium absorption increased to
a very high level in children who previously had rickets. This finding
is inconsistent with Heaneys hypothesis that the tracer was absorbed
independent of nutritional status and suggests that children with
rickets may appropriately respond to overall nutritional rehabilita-
tion with bone growth and remineralization.
It should be noted that we recently found fractional calcium ab-
sorption to be similar in rachitic children and in pubertal children
with low calcium intakes (3), in whom calcium was traced from milk
(in which there has been shown to be appropriate interchange be-
tween the tracer and natural calcium). Although the children in that
study and in another study involving pregnancy (4) and very high
absorption levels were in physiologic states of high absorption, these
data indicate that a direct comparison of our values with those of
adults may be erroneous and that the absorption values we found are
probably not spuriously elevated.
None of the authors had a conflict of interest.
Steven A Abrams
USDA/ARS Childrens Nutrition Research Center
Department of Pediatrics
Baylor College of Medicine and Texas Childrens Hospital
Houston, TX 77030
1452 LETTERS TO THE EDITOR

Tom D Thacher Effects of a gluten-free diet on gastrointestinal

symptoms in celiac disease
Department of Family Medicine
Jos University Teaching Hospital Dear Sir:
PMB 2076
Jos In their recent article in the Journal, Murray et al (1) presented the
Nigeria results of a follow-up study of the effects of a gluten-free diet on both
typical and atypical gastrointestinal symptoms related to celiac dis-
Philip R Fischer ease. The effects are presented as if they had occurred within 6 mo
of the intervention, which would have been very rapid. However, I
Department of Pediatric and Adolescent Medicine have several concerns about the presentation of some of the results.
Mayo Clinic First, in the Methods section, it is stated that questions were asked
299 First Street, SW about the situation 6 mo after the start of a gluten-free diet. In the
Rochester, MN 55905 Results section, the is dropped, and the wording is 6 mo after
E-mail: fischer.phil@mayo.edu starting a gluten-free diet. Were the interviews retrospectiveie,
asking about the situation 6 mo after the start of the gluten-free
diet or cross-sectionalie, asking about the situation at the time of
Mariaelisa Graff follow-up (which for subjects with a new diagnosis would be 6 mo
after the start of a gluten-free diet and for those diagnosed at the
Division of Foods and Nutrition earliest time would be 14 y after the start of a gluten-free diet)?
Emory University Second, also in Results, the authors state, Ninety-one patients
771-2 Houston Mill Road gained weight between the time of diagnosis and 6 mo after starting a
Atlanta, GA 30329

Downloaded from www.ajcn.org by on March 2, 2010

gluten-free diet, and the weight gain ranged from 0.5 to 46 kg (average
of 7.5 kg). In the same period, 25 patients lost an average of 12.5 kg
Diane D Stadler (range: 1 63 kg). Both gaining 46 kg and losing 63 kg within a space
of 6 mo seems unrealistic. There appeared to be no consideration of the
Division of Endocrinology, Diabetes, and Clinical Nutrition age of the subjects (range: 190 y at diagnosis) or of the fact that, at the
Department of Medicine time of the study, 1314 y had passed since diagnosis (and most likely
Oregon Health Sciences University School of Medicine also since the start of a gluten-free diet) for some of the subjects. Gain-
Portland, OR 97201 ing 46 kg between the ages of 1 and 14 y is not remarkable and might
not be wholly attributable to the effect of the diet.
Third, body mass index (BMI; in kg/m2) is given as median
Sunday D Pam (SEM) in the text (p 670) and as mean (SD) in Table 1, which is
very confusing. In addition, SEM should not be used together with
Department of Paediatrics median values.
University of Jos Fourth, it is not clear whether the patients were diagnosed from
PMB 2084
1990 through 1997 (as stated in the abstract), between 1984 and 1998
Jos
(as stated in the Methods section, p 669), or between 1984 and 1997
Nigeria
(as stated in the Methods section, p 670).
I believe that these faults should have been spotted by the referees,
John M Pettifor and the authors should have been given a chance to rewrite their
manuscript, but unfortunately this was not done.
MRC Mineral Metabolism Research Unit The article has already been cited in the Minerva section of the
Department of Paediatrics journal BMJ (2), where it is written, As many people present atyp-
University of the Witwatersrand and Chris Hani Baragwanath ically with coeliac disease as present with the more classical triad of
Hospital steatorrhoea, diarrhoea, and weight loss. A long follow up of a cohort
PO Bertsham 2013 of patients already diagnosed as having coeliac disease and put on a
South Africa gluten-free diet shows that the diet substantially and rapidly im-
proved all the gastrointestinal symptoms previously reported, not
just the typical ones. The authors point out, however, that their cohort
REFERENCES was a highly motivated group, which included few teenagers.
1. Bronner F, Pansu D. Nutritional aspects of calcium absorption. J Nutr
1999;129:9 12. The author had no conflicts of interest.
2. Pettifor JM, Ross P, Wang J, Moodley G, Couper-Smith J. Rickets in
children of rural origin in South Africa: is low dietary calcium a factor?
J Pediatr 1978;92:320 4. Agneta Hrnell
3. Abrams SA, Griffin IJ, Hicks PD, Gunn SK. Pubertal girls only
partially adapt to low dietary calcium intakes. J Bone Miner Res Department of Food and Nutrition
2004;19:759 63. Ume University
4. Vargas Zapata CL, Donangelo CM, Woodhouse LH, Abrams SA, Spen-
cer M, King JC. Calcium homeostasis during pregnancy and lactation in Ume
Brazilian women with low calcium intakes: a longitudinal study. Am J Sweden
Clin Nutr 2004;80:41722. E-mail: agneta.hornell@kost.umu.se
 LETTERS TO THE EDITOR
REFERENCES
1. Murray JA, Watson T, Clearman B, Mitros F. Effect of a gluten-free diet
on gastrointestinal symptoms in celiac disease. Am J Clin Nutr 2004;
79:669 73.
2. Minerva. BMJ 2004;328:904.
Reply to A Hrnell
Dear Sir:
We are glad to have the opportunity to respond to the letter of Dr
Hrnell and to the concerns she raised about our recent article (1).
First, the questionnaire was administered after 6 mo of a gluten-
free diet, and the results reflect the patients perceptions and reports
of the effects of that diet on their gastrointestinal symptoms at a point
6 mo after beginning the diet.
Second, the correspondent is surprised at the wide range of vari-
ation in weight change reported by subjects in the period after the
start of a gluten-free diet. In most but not all cases, it was possible to
verify the patient-reported weight during his or her clinic visit.
Whereas most patients had weight changes that were well within a
range that could result from changes in absorption or modification of
food intake, wide ranges of weight change were reported. The ex-
tremes of the ranges of change were quite dramatic. A small but
significant proportion of these patients were morbidly obese at the
time of diagnosis of celiac disease, and large changes in weight are
certainly possible in this cohort, a finding that has been reported
anecdotally and recently in another cohort (2).
We agree that it would be naive to believe that these morbidly obese
patients who lost so much weight did so only because of treatment of
celiac disease. Patients of this size would certainly have been advised to
lose weight. We did not control for confounding events such as inter-
vening bariatric surgery, which is quite common in the Midwest United
States. It is certainly possible that patients with morbid obesity may
have received substantial additional therapy to address their morbid
obesity, although this was not provided or advised by the physicians
treating the celiac disease (3). Such dramatic weight loss could be
explained if patients, for example, underwent a bariatric procedure (4).
With regard to weight gain, whereas this degree of weight gain is
unusual, several patients were extremely malnourished at the time of
their diagnosis and often were substantially dehydrated. The patient
who had the largest weight regain had reported losing 40 kg over a
9-mo period with frank steatorrhea before treatment. His baseline
weight before weight loss was 115 kg.
However, these are the extremes of the range, and most patients
weight gain or weight loss was well within what would normally be
expected in response either to substantial dietary intervention or
fairly rapid correction of malabsorption (or both). These extreme
cases were adults at the time of diagnosis of celiac disease, as were
the vast majority of our patients, and that reflects the usual circum-
stance in the United States (2).
Clinicians must be prepared to deal with nutrition-related issues in
addition to the institution of a gluten-free diet, because most patients
currently being diagnosed with celiac disease do not present with
severe malabsorption.
Third, Hrnell quite correctly points out our incorrect use of the
SEM with the median, as written in the Results. The SD is provided
in the table. Nonetheless, the data are correct as published.
Fourth, with regard to the time period of the study, the abstract is
correct. We included only patients who were evaluated during the
period of 1990 through 1997, when the primary author was engaged
1453
in seeing these patients. Patients who were seen before 1990 were no
longer available for follow-up and were not included, and patients
seen for the first time after 1997 were not included. The correct
period for initial diagnosis was 1984 1997. The follow-up period
for some of the patients diagnosed toward the end of 1997 stretched
into 1998, and that is the source of our error.
We thank Dr Hrnell for her interest in our publication and for the
opportunity to correct these errors and provide clarification.
Neither of the authors had any personal or financial conflicts of interest
with respect to the subject under discussion or to the author of the letter, Dr
Hrnell.
Joseph A Murray
Beverlee Clearman
Mayo Clinic
200 First Street, SW
Room 301, Guggenheim Bldg
Rochester, MN 55905
E-mail: murray.joseph@mayo.edu
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REFERENCES
1. Murray JA, Watson T, Clearman B, Mitros FA. Effect of a gluten- free
diet on gastrointestinal symptoms in celiac disease. Am J Clin Nutr
2004;79:669 73.
2. Murray JA, Van Dyke C, Plevak MF, Dierkhising RA, Zinsmeister AR,
Melton LJ. Trends in the identification and clinical features of celiac
disease in a North American community. Clin Gastroenterol Hepatol
2003;1:19 27.
3. Owen DA, Thorlakson TK, Walli JE. Celiac disease in a patient with
morbid obesity. Arch Intern Med 1980;140:1380 1.
4. Logan RF, Ferguson A. Jejunal villous atrophy with morbid obesity:
death after jejunoileal bypass. Gut 1982;23:999 1004.
Nutrigenomic explanation for the beneficial
effects of fish oil on cognitive function
Dear Sir:
Whalley et al (1) analyzed subjects erythrocyte fatty acid profiles
and compared these with measures of cognitive function. Various
correlations indicated that n3 fatty acids in the diet are associated
with better cognitive performance in old age. The authors discussed
possible reasons for this. They addressed confounding variables
such as the likely overall healthier diet of those who consume more
n3 fatty acids. They also examined 2 mechanisms by which n3
fatty acids might maintain cognitive function in adults as they age.
n3 Fatty acids are beneficial to vascular health and may forestall
cerebrovascular disease and thus dementia. Also, a lower ratio of
n6 to n3 fatty acids may promote a healthier balance of eico-
sanoids, which would protect membrane function.
A third, nutrigenomic mechanism might work in conjunction with
the first 2. Diets rich in n3 fatty acids alter gene expression in the
brain (2 4). Genes whose expression is altered include those in-
volved in controlling synaptic plasticity, cytoskeleton and mem-
brane association, ion channel formation, signal transduction, and
energy metabolism and in counteracting the appearance of amyloid
aggregates (2, 3). Fish oil induces the transcription of the gene for
prealbumin (3). Prealbumin sequesters amyloid -polypeptide, keep-
ing it from forming the aggregates that are a characteristic of Alzheimer
1454 LETTERS TO THE EDITOR

disease (3, 4). Thus, fish oil consumption might encourage gene expres-
sion conducive to brain maintenance during aging. This might be one
reason Whalley et al found that their subjects erythrocyte fatty acid
profiles were related to cognitive function at the age of 64 y.
The author had no conflicts of interest to report.
Celia M Ross
36 Ridgewood Circle
Wilmington, DE 19809
E-mail: celiamaryross@aol.com
REFERENCES
1. Whalley LJ, Fox HC, Wahle KW, et al. Cognitive aging, childhood
intelligence, and the use of food supplements: possible involvement of
n3 fatty acids. Am J Clin Nutr 2004;80:1650 7.
2. Kitajka K, Puskas LG, Zvara A, et al. The role of n3 polyunsaturated
fatty acids in brain: modulation of rat brain gene expression by dietary
n3 fatty acids. Proc Natl Acad Sci U S A 2002;99:2619 24.
3. Puskas LG, Kitajka K, Nyakas C, et al. Short-term administration of
omega 3 fatty acids from fish oil results in increased transthyretin tran-
scription in old rat hippocampus. Proc Natl Acad Sci U S A 2003;100:
1580 5.
4. Kitajka K, Sinclair AJ, Weisinger RS, et al. Effects of dietary omega-3
polyunsaturated fatty acids on brain gene expression. Proc Natl Acad Sci
U S A 2004;101:10931 6.

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Erratum

Houston DK, Stevens J, Cai J, Haines PS. Dairy, fruit, and vegetable intakes and functional limitations and
disability in a biracial cohort: the Atherosclerosis Risk in Communities Study. Am J Clin Nutr 2005;81:51522.

Two errors appeared in this article. First, the second sentence in the Results section of the Abstract should read,
For example, in African American women, baseline dairy intakes were inversely associated with impaired
ADLs and IADLs [odds ratio (95% CI): 0.60 (0.40, 0.90) and 0.69 (0.48, 0.98), respectively, in the 3rd versus
the 1st tertile of intake (P for trend 0.05)]. Second, the sentence beginning in the third line of the lefthand
column on page 517 [We excluded from our analyses participants who used a wheelchair, crutches, or walker
or walked with a cane (n 61); those with prevalent coronary artery disease, stroke, cancer, or chronic lung
disease (n 1481); and those with poor self-rated health at baseline (n 105).], which repeated information
from the previous sentence, should have been deleted.

Both of the errors were the fault of the Journal office in Bethesda and not of the authors of the manuscript. The
Journal office regrets the errors.