Hi again Drew,

 

I have an interesting study on the issue of bone formation and lipids for you. It's quite lengthy and abit technical to absorb, so I will just copy the conclusion here, along with the link to the full article. Hans' statement about it being an inflammatory problem is right on the mark. The study basically says that AA from excess omega 6 causes too high a production of the inflammatory eicosanoid, PGE 2 in bone, which causes resorption of bone. CLA (congugated linoleic acid) from milkfat reduces omega 6 levels and therefore AA and it's inflammatory metabolite, PGE2. This in turn reduces bone resorption.

 

Essentials in Osteodynamics"

- Discussion:
    - bone remodeling functions reshaping or replacement of of bone during
            growth and following injury;
            - in the first year of life, almost 100% of the skeleton is replaced;
            - in adults, remodeling procedes at about 10% per year;
    - bone responds to functional demands and muscle attachments;
    - w/ remodeling, bone will be added where needed and removed where it
          is not required;
    - bone remodeling begins w/ bone resorption, followed by subsequent
            by bone formation;
            - remodeling process occurs w/ a specific sequence of events termed the
                  Bone multicellular unit (BMU);
    - sequence of events;
            - remodeling may begin w/ parathyroid hormone induced resorption;
            - osteoclastics resorb bone removing both organic and inorganic
                  components are removed;
            - subsequently, new bone by osteoblasts, replacing bone that was resorbed;

- Wolfe's Law:              
    - described by Julius Wolff in 1868.
    - law holds that every change in the form or function of a bone is followed by
          adaptive changes in its internal architecture and its external shape;

 

Also, bone remodeling occurs wherever bone is damaged. In the case of the spine it's due to worn cartilage allowing the vertebrae to rub together, wearing it down. Bone formation then takes place at the worn area to heal the bone. This is how spurs form as abnormal protrusions on bones. The worn cartilage is also caused by PUFA's, due to lipid peroxidation occuring in the cartilage. Here are two studies on that:

 

 

 

And below is the CLA study and link regarding bone and inflammation:

 

Dietary Conjugated Linoleic Acids Alter Serum IGF-I and IGF Binding Protein Concentrations and Reduce Bone Formation in Rats Fed (n-6) or (n-3) Fatty Acids^*

DISCUSSION

IGF-I, the most abundant growth factor in bone, is believed to function as both a systemic and local growth factor for bone tissue.³⁶ The anabolic effects of IGF-I in bone include the stimulation of longitudinal growth and increase of bone mass.^36,37 Production of IGF-I is also regarded as a key factor for mediating the effects of a number of independent signaling molecules in bone cells.³⁸ Thus, understanding the regulation of the production and activity of IGF-I is critical for elucidating the potential impact of dietary factors on bone metabolism. This is the first study to show that CLA, a dietary anticarcinogen present in dairy products and red meat, influenced the serum IGF/IGFBP system and was associated with reduced bone formation.

In the present investigation, CLA was shown to down-regulate the circulating levels of IGF-I in the growing rat. Based on these data, CLA could have exerted its effect by modulating eicosanoid metabolism, which is consistent with previous work showing that CLA reduced ex vivo bone organ culture PGE₂ production.¹⁰ Serum IGFBP was also affected by dietary CLA supplementation although it was dependent on the dietary PUFA type. CLA increased the serum IGFBP level in rats given the high (n-6) PUFA diet, but decreased it in rats fed the high (n-3) PUFA diet. Since IGF-I and its binding proteins were affected differently by CLA depending on the (n-6) and (n-3) PUFA type, dietary PUFA may potentially impact bone metabolism via IGF mechanisms depending on the ratio of (n-6) and (n-3) PUFA in the diet.

CLA supplementation reduced MAR and BFR in rats regardless of the dietary source of PUFA in this study. Furthermore, CLA lowered serum IGF-I level. The dietary (n-6) and (n-3) PUFA treatments did not significantly affect IGF-I concentration and bone histomorphometric measurements. Serum intact osteocalcin was not affected by dietary PUFA type or CLA supplementation. PUFA treatments, however, did affect bone mineral density. Rats fed (n-6) PUFA had a lower ash weight per millimeter of bone length in humeri compared with those fed (n-3) PUFA. These findings suggest that excessive consumption of (n-6) PUFA could have a negative effect on bone metabolism by increasing bone resorptive activity through increased endogenous production of PGE₂. This is consistent with the results of a previous study wherein chicks fed SBO for 21 days showed decreased total bone and cortical bone areas in cross-sections of tibiae compared with chicks given menhaden oil.³²

Dietary PUFA treatment and CLA supplementation both had a significant effect on ex vivo PGE₂ production in tibia and femur organ cultures. Rats supplemented with CLA had lowered ex vivo PGE₂ production in bone. PGE₂ is an important factor in regulating local bone metabolism²³ including bone modeling and remodeling.³⁹ Sugano et al.⁷ reported that the concentration of PGE₂ in serum and spleen tended to be reduced by CLA. Raisz and Koolemans-Beynen showed that PGE₂ inhibited bone matrix formation at a high concentration in bone organ culture⁴⁰ ; however, at lower concentrations, PGE₂ stimulated bone formation in vitro and in vivo.^40-43 Therefore, excessive production of PGE₂ may adversely affect bone modeling, whereas a lower level of PGE₂ is believed to stimulate bone formation in animals fed diets containing moderate levels of (n-6) PUFA. For example, reduced PGE₂ production in chicks fed a higher (n-3) diet was associated with increased rate of bone formation.^32,44 Although CLA and (n-3) PUFA may follow different pathways in modulating tissue PGE₂ production, the fact that they both lowered ex vivo bone PGE₂ level suggests dietary moderation of bone prostanoid production.

In the current study, rats fed CLA had decreased values for MAR and BFR which likely reflect some impact on osteoblastic function. While these CLA effects may be mediated through the regulation of PGE₂ synthesis (via the inducible enzyme cyclooxygenase-2 or isomeric analogs of CLA), which in turn influence IGF-I concentrations, they may also be mediated by other potent cytokines, such as interleukins (IL-1 and IL-6), tumor necrosis factor (TNF) or the lipoxygenase product, leukotriene B₄ (Fig. 3). Dietary CLA was recently shown to lower basal, and lipopolysaccharide stimulated IL-6 production and basal TNF production by resident peritoneal macrophages in rats.⁴⁵ Furthermore, CLA reduced the release of leukotriene B₄, a lipoxygenase product of AA, one of the most potent chemotaxins for polymorphonuclear leukocytes and monocytes⁴⁶ and a strong bone resorption factor,⁴⁷ from peritoneal exudate cells.⁸ Assuming CLA has similar effects on these cytokines in bone, together with the fact that CLA reduced the production of PGE₂ in bone tissue, one could hypothesize that at a proper dietary level, CLA anti-inflammatory effects could be beneficial for the treatment of inflammatory bone disease. Further study, however, is needed to unequivocally establish how CLA mediates its effect on bone cell metabolism.

This research is the first to show that CLA isomers affect bone metabolism in laboratory animals. The level of CLA used in this study (1% dietary CLA), though higher than that found in conventional diets without supplementation, compares favorably to the range used (0.5�?.5%) in other studies that examined anti-inflammatory and anticarcinogenic properties of CLA.^8,27-30 Further work is needed to evaluate more typical dietary levels of CLA on bone metabolism.

http://www.jbmronline.org/doi/full/10.1359/jbmr.1999.14.7.1153?cookieSet=1

You didn't really think I wouldn't make you work for the answer now did ya? LOL