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LETTERS TO THE EDITOR |
Human Nutritional Sciences
University of Manitoba
Winnipeg, MB R3T 2N2
Canada
E-mail: hweiler{at}ms.umanitoba.ca
Institute of Food, Nutrition and Human Health
Massey University
Private Bag 11222
Palmerston North
New Zealand
E-mail: m.c.kruger{at}massey.ac.nz
Dear Sir:
The recent article by Macdonald et al that was published in the Journal (1) represents one of the largest studies of the relation between dietary polyunsaturated fatty acids (PUFAs) and bone mass in humans. The authors are to be commended for this, but several important points must be shared with the readership of the Journal. In the study by Macdonald et al, 891 women were studied at 2 time points 5–7 y apart for bone mass, anthropometric variables, diet, and lifestyle. At each assessment, usual dietary intake was assessed by using a food-frequency questionnaire. The questionnaire included questions only on total PUFAs but not on specific n–6 or n–3 series or on essential compared with long-chain PUFAs. The authors observed negative associations through both correlation and regression analyses and concluded that at low intakes of dietary calcium, dietary PUFAs have a negative effect on bone mass in this cohort of menopausal women. In the discussion, only intestinal absorption is discussed as a potential explanation, and the focus is on the controversy in the area of PUFAs and the formation of calcium soaps. The authors failed to acknowledge that expressing dietary intake of PUFAs as a total does not account for potential benefits of specific fatty acids or that PUFAs may affect bone differently during other life stages. On the basis of animal studies, we know that when diets high in n–6 PUFAs are modified to have a lower ratio of n–6 to n–3 dietary fatty acids, bone mass is enhanced (for review see reference 2). Thus, it is important to communicate to the readership of the Journal that total dietary PUFAs may in fact be linked to poorer bone health but that this does not negate the research indicating that lower n–6:n–3 fatty acid ratios and the addition of long-chain PUFAs to the diet enhance bone health.
To date, there is no comprehensive review of all studies related to dietary PUFAs and long-chain PUFAs in both humans and animals with respect to outcomes in bone. However, we can summarize the results of a few other epidemiologic studies. In growing females residing in Norway, a country whose population has a lower dietary n–6:n–3 PUFA ratio than does the US population because of frequent consumption of fish, dietary total PUFAs are positively associated with the change in bone mineral density of the ultradistal radius (3). In both men and women (25–69 y of age) in Greece, monounsaturated fatty acids are positively associated with bone mass (4). The source of most of the monounsaturated fatty acids is olive oil, which also contains n–6 and n–3 PUFAs in a ratio of 
10:1. Other evidence comes from a review by Terano (5), in which higher n–3 status is linked to higher bone mineral density in Japan. Experimental studies in humans are more controversial. In elderly women, 
-linolenic acid (GLA) from evening primrose oil plus eicosapentaenoic and docosahexaenoic acids from fish oil and 600 mg Ca increased femoral bone mass by 1.3% over 18 mo, whereas placebo decreased femoral bone mass by 2.1% (6). However, no benefit or harm to bone mass is observed in premenopausal women consuming a similar PUFA supplement plus 1 g Ca daily (7). Evidence from animal studies suggests that excess precursor of prostaglandin E2 (arachidonic acid in particular) leads to bone loss (for review see reference 2). In the study by Macdonald et al, the negative association with bone loss at the lumbar spine and femoral neck might be explained by excess PUFAs or an imbalance between the n–6 and n–3 fatty acids and not by PUFAs in general. The amount of PUFAs consumed was unfortunately not provided in the table of nutrient intakes. In fact, in growing chicks, rodents, and pigs (for review see reference 2), the addition of long-chain PUFAs to the diet within acceptable limits has been shown to positively affect bone mass. The only negative report is in rabbits fed very high amounts of fish oil, which resulted in reduced long bone growth (8). In ovariectomized rats and mice, moderate supplementation with dietary fish oil or purified long-chain PUFAs prevents bone loss (9).
On the basis of the studies reviewed above, the article by Macdonald et al would have been enhanced by examination of the relations between dietary amounts of n–6 and n–3 PUFAs, the quality of PUFAs (ie, GLA or long-chain n–3 PUFAs), and changes in bone mass. Additional information regarding fatty acid status would have been helpful also. The authors should have discussed the findings of other studies in both humans and animals, especially because this is a very new area of nutritional science but also because of the message in the article's title. The title unfortunately sends a very strong message to the readership that all PUFAs are detrimental to bone. The discussion was incomplete in addressing this finding, which was deemed important enough to be included in the title. The discussion did not differentiate the findings of Macdonald et al from other reported benefits of specific PUFAs such as GLA, longer-chain PUFAs such as eicosapentaenoic or docosahexaenoic acid, or the n–6:n–3 ratio. At the very least, the epidemiologic studies by Terano (5), Gunnes and Lehmann (3), and Trichopoulou et al (4) should have been discussed.
Lastly, regarding Ott's commentary (10) on the article by Macdonald et al, diets with eicosapentaenoic and docosahexaenoic acids will likely be shown to have benefits for both heart and bone health. GLA aside, however, diets high in n–6 PUFAs are not beneficial to bone health. Perhaps diets higher in n–3 PUFAs and n–3 long-chain PUFAs should be recommended as components of primary prevention or treatment regimens for diseases of both heart and bone.
REFERENCES
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