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R.B. · 07-03-2006, 02:47 AM

Another reason and a familiar cast of players.

RB
http://www.ajcn.org/cgi/content/abstract/81/4/934

ABSTRACT

There are a plethora of biologically plausible pathways whereby PUFAs may regulate the factors involved in bone metabolism, such as prostaglandins, cytokines, insulin-like growth factor I, and calcium. Reviewers have suggested that one or a combination of these factors may have an effect on bone (5, 6, 13, 23). For example, PGE2, the major prostaglandin involved in bone metabolism, is synthesized from n–6 fatty acids, whereas n–3 fatty acids inhibit its production (1, 13). Normal or moderate concentrations of PGE2 support bone formation, whereas greater quantities promote bone resorption (5). Fatty acids are also involved in calcium metabolism. Higher n–3 fatty acid intake enhances calcium absorption, decreases calcium loss, and increases bone calcium (13, 20,23). In addition, the inhibition of cytokine production has been implicated as a potential mechanism of the favorable effects of fatty acids on bone, with higher intakes of n–3 fatty acids inhibiting the synthesis of proinflammatory cytokines, such as interleukin 6, interleukin 1, and tumor necrosis factor {alpha} (24, 25). Kettler (6) suggested that bone loss is mediated by cytokines, and n–3 fatty acid supplementation in animals and humans reduces cytokine synthesis and increases calcium absorption.

In the present study, there was a significant interaction between hormone use and the ratio of dietary n–6 to n–3 fatty acids on BMD at the hip and spine. Fatty acids could potentiate the effect of HT on bone through increasing calcium absorption (26). A study in ovariectomized rats showed that estrogen plus a combination of n–6 and n–3 fatty acids increases bone formation and decreases bone resorption, whereas estrogen alone only increases bone formation (27).

To our knowledge, this is the first large epidemiologic investigation of the association between PUFAs and BMD in older, community-dwelling white men and women who had a wide range of dietary n–6 and n–3 fatty acid intake. The latest longitudinal study by Macdonald et al (11) investigated the association between total PUFAs and bone in women only and did not differentiate between various types of PUFAs (eg, n–3 versus n–6). Previous experimental studies had limited ability to assess a range of fatty acid intakes because of study design and small sample sizes.

http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract

1: Altern Med Rev. 2001 Feb;6(1):61-77. Related Articles, Links
Click here to read
Can manipulation of the ratios of essential fatty acids slow the rapid rate of postmenopausal bone loss?

Kettler DB.

Sky Park Wellness Center, Irvine, CA 92614, USA dr.debra@home.com

The rapid rate of postmenopausal bone loss is mediated by the inflammatory cytokines interleukin-1, interleukin-6, and tumor necrosis factor alpha. Dietary supplementation with fish oil, flaxseeds, and flaxseed oil in animals and healthy humans significantly reduces cytokine production while concomitantly increasing calcium absorption, bone calcium, and bone density. Possibilities may exist for the therapeutic use of the omega-3 fatty acids, as supplements or in the diet, to blunt the increase of the inflammatory bone resorbing cytokines produced in the early postmenopausal years, in order to slow the rapid rate of postmenopausal bone loss. Evidence also points to the possible benefit of gamma-linolenic acid in preserving bone density.

Publication Types:

* Review

PMID: 11207457 [PubMed - indexed for MEDLINE]

07-03-2006, 02:47 AM	#25
R.B. Senior Member Join Date: Mar 2006 Posts: 1,843	Another reason and a familiar cast of players. RB http://www.ajcn.org/cgi/content/abstract/81/4/934 ABSTRACT There are a plethora of biologically plausible pathways whereby PUFAs may regulate the factors involved in bone metabolism, such as prostaglandins, cytokines, insulin-like growth factor I, and calcium. Reviewers have suggested that one or a combination of these factors may have an effect on bone (5, 6, 13, 23). For example, PGE2, the major prostaglandin involved in bone metabolism, is synthesized from n–6 fatty acids, whereas n–3 fatty acids inhibit its production (1, 13). Normal or moderate concentrations of PGE2 support bone formation, whereas greater quantities promote bone resorption (5). Fatty acids are also involved in calcium metabolism. Higher n–3 fatty acid intake enhances calcium absorption, decreases calcium loss, and increases bone calcium (13, 20,23). In addition, the inhibition of cytokine production has been implicated as a potential mechanism of the favorable effects of fatty acids on bone, with higher intakes of n–3 fatty acids inhibiting the synthesis of proinflammatory cytokines, such as interleukin 6, interleukin 1, and tumor necrosis factor {alpha} (24, 25). Kettler (6) suggested that bone loss is mediated by cytokines, and n–3 fatty acid supplementation in animals and humans reduces cytokine synthesis and increases calcium absorption. In the present study, there was a significant interaction between hormone use and the ratio of dietary n–6 to n–3 fatty acids on BMD at the hip and spine. Fatty acids could potentiate the effect of HT on bone through increasing calcium absorption (26). A study in ovariectomized rats showed that estrogen plus a combination of n–6 and n–3 fatty acids increases bone formation and decreases bone resorption, whereas estrogen alone only increases bone formation (27). To our knowledge, this is the first large epidemiologic investigation of the association between PUFAs and BMD in older, community-dwelling white men and women who had a wide range of dietary n–6 and n–3 fatty acid intake. The latest longitudinal study by Macdonald et al (11) investigated the association between total PUFAs and bone in women only and did not differentiate between various types of PUFAs (eg, n–3 versus n–6). Previous experimental studies had limited ability to assess a range of fatty acid intakes because of study design and small sample sizes. http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract 1: Altern Med Rev. 2001 Feb;6(1):61-77. Related Articles, Links Click here to read Can manipulation of the ratios of essential fatty acids slow the rapid rate of postmenopausal bone loss? Kettler DB. Sky Park Wellness Center, Irvine, CA 92614, USA dr.debra@home.com The rapid rate of postmenopausal bone loss is mediated by the inflammatory cytokines interleukin-1, interleukin-6, and tumor necrosis factor alpha. Dietary supplementation with fish oil, flaxseeds, and flaxseed oil in animals and healthy humans significantly reduces cytokine production while concomitantly increasing calcium absorption, bone calcium, and bone density. Possibilities may exist for the therapeutic use of the omega-3 fatty acids, as supplements or in the diet, to blunt the increase of the inflammatory bone resorbing cytokines produced in the early postmenopausal years, in order to slow the rapid rate of postmenopausal bone loss. Evidence also points to the possible benefit of gamma-linolenic acid in preserving bone density. Publication Types: * Review PMID: 11207457 [PubMed - indexed for MEDLINE]