Reply to HA Weiler and MC Kruger

Osteoporosis Research Unit
Victoria Pavilion
Woolmanhill Hospital
Aberdeen AB25 1LD
United Kingdom
E-mail: h.macdonald{at}abdn.ac.uk
Department of Medicine and Therapeutics
University of Aberdeen
Aberdeen
United Kingdom
Centre for Nutrition and Food Safety
School of Biomedical and Life Sciences
University of Surrey
Guildford
United Kingdom

Dear Sir:

We thank Weiler and Kruger for their interest in our study. We agree that it would be interesting to investigate the relation between polyunsaturated fatty acids (PUFAs) and bone health further because more research is required in this area. However, although databases for analyzing individual fatty acids are available, there has been concern about their accuracy (1). In addition, our food-frequency questionnaire may prove too blunt a tool for estimating the effect of individual n–3 and n–6 fatty acids on markers of bone health.

Although specific fatty acids may have potential benefits for bone health, minimum recommendations in the United Kingdom are just 0.2% of total energy intake for n–3 PUFAs and 1% for n–6 PUFAs (2). In our research, we found that high PUFA intakes were associated with poor bone health in early postmenopausal women and reported an interaction with calcium intake such that PUFAs were detrimental when calcium intake was low (3). Intakes of fatty acids at baseline and at follow-up, which were not included in our original article, are shown in Table 1.

View this table:
TABLE 1. Fatty acid intakes at baseline and at follow-up¹

 
Weiler and Kruger highlight the results of several other studies, which they claim support the view that n–3 fatty acids are beneficial to bone health. We do not dispute the findings of the animal studies or disagree that particular n–3 fatty acids could play a role at the cellular level in bone metabolism. However, we do not think that the evidence in human studies is sufficient to recommend that the population increase n–3 fatty acid intake to protect against osteoporosis as Weiler and Kruger suggest.

Our reasons for not thinking so are as follows. First, Blanaru et al (4), who reviewed the evidence on PUFAs in the introduction to their article, state that the amount or type of PUFAs required to enhance bone health during growth is unclear. This particular study found that 0.75% arachidonic acid with 0.1% docosahexaenoic acid was associated with increased bone mineral content in piglets, but too much fish oil appears to be detrimental to the skeleton in growing rabbits (5). Second, the study in children and adolescents (6) examined only forearm bone mineral density, a limitation pointed out by the authors; the study also apparently made no adjustment for pubertal age. In addition, the authors acknowledge that whether an increased intake of PUFAs, above the recommended allowance, influences peak bone mass needs to be verified. Third, although the olive oil that provided the monounsaturated fatty acids in the study of Greek men and women aged 25–69 y (7) also contained PUFAs, it cannot be assumed that n–3 or n–6 fatty acids are the explanation for the association between monounsaturated fatty acids and increased bone mineral density. Fourth, the results of the pilot study in 80-y-old women who were supplemented with evening primrose oil and fish oil (8) have not been replicated in British premenopausal and postmenopausal women, although the amount of supplemental calcium was greater in the latter study (1000 mg compared with 600 mg). The lack of effect is not incompatible with our own findings because calcium intake is high. Unfortunately, because the details of the Japanese research mentioned in the review by Terano (9) are not available to us, we cannot comment on Terano's findings.

In our article, we examined the diet as a whole and hence were restricted in our discussion of each nutrient. However, we did cover several other possible explanations in addition to the one involving calcium absorption; these included indication of a dietary pattern low in important nutrients, hyperinsulinemia, confounding by retinol, and possible interaction with leptin. We also mentioned, in the section on retinol, that the presence of n–3 fatty acids in cod liver oil could be a confounder. Although we welcome more research in the area of PUFAs and bone health, we firmly believe that the recommendation of n–3 PUFAs as a component in the primary prevention of osteoporosis is premature.

REFERENCES

1. McNeill G, Peace H, Masson L. Beware the fatty acid–free sausage! J Hum Nutr Diet 2004;17:71–2.
2. Department of Health. Dietary reference values for food energy and nutrients for the United Kingdom. London: HMSO, 1991.
3. Macdonald HM, New SA, Golden MH, Campbell MK, Reid DM. Nutritional associations with bone loss during the menopausal transition: evidence of a beneficial effect of calcium, alcohol, and fruit and vegetable nutrients and of a detrimental effect of fatty acids. Am J Clin Nutr 2004;79:155–65.
4. Blanaru JL, Kohut JR, Fitzpatrick-Wong SC, Weiler HA. Dose response of bone mass to dietary arachidonic acid in piglets fed cow milk–based formula. Am J Clin Nutr 2004;79:139–47.
5. Judex S, Wohl GR, Wolff RB, Leng W, Gillis AM, Zernicke RF. Dietary fish oil supplementation adversely affects cortical bone morphology and biomechanics in growing rabbits. Calcif Tissue Int 2000;66:443–8.
6. Gunnes M. Bone mineral density in the cortical and trabecular distal forearm in healthy children and adolescents. Acta Paediatr 1994;83:463–7.
7. Trichopoulou A, Georgiou E, Bassiakos Y, et al. Energy intake and monounsaturated fat in relation to bone mineral density among women and men in Greece. Prev Med 1997;26:395–400.
8. Kruger MC, Coetzer H, de Winter R, Gericke G, van Papendorp DH. Calcium, gamma-linolenic acid and eicosapentaenoic acid supplementation in senile osteoporosis. Aging (Milano) 1998;10:385–94.
9. Terano T. Effect of omega 3 polyunsaturated fatty acid ingestion on bone metabolism and osteoporosis. World Rev Nutr Diet 2001;88:141–7.