Thank you for the reply. Do you have a place online that is good for ordering dark chocolate? I cant find any locally that doent have additives like soy lecithin and such.

Ok one more. On average, how much in the way of antioxidants should one eat with a meal? I know it will change depending on what and how much is eaten. Say we are using blueberries, how many should be eaten? 10? 20? 4.4 oz container they come in?

Hans, why do you recommend to drink coffee either cold or with no milk? 

 

 

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

I wouldn't say that it is misleading per se, just that it is only part of the overall picture. There is no one factor involved in any bodily process. And there are several destructive metabolites in inflammatory conditions, simply referred to as inflammatory mediators. The problem I see the most is that people, including scientists attach the wrong conclusion to these mediators and typically view them as "bad". This view is erroneous in the fact that they are all normal by products of metabolism. The problem is the imbalances of them which occur due to faulty diet.

 

Longstanding dietary habits cause longstanding deficiencies and excesses of nutrients and metabolites such as these, which in turn causes chronic inflammatory states to exsist over a lifetime. Another problem I see is the illogical approach taken to combat these chronic conditions. Aside from labeling a metabolite as "bad", the most common method of mainstream dedicine in dealing with that excessive destructive element is to produce a drug to combat it's ill effects, rather than to look at the big picture and see what is going wrong and treat it with proper diet.

 

Then on the other side of the fence we have the supplement industry who determine what natural substance blocks the effects of the questionable substance, and push for supplementation of it to ward off disease. While natural food substances may be safer and less toxic than a drug, to overuse them in large amounts is also not safe. Every molecule in the body has an effect, and excesses of one can cause deficiencies of another. But all the "health gurus" out there would interpret the above study as proof that more omega 3 is needed in the diet to prevent excessive AA production. While it is shown that omega 3 does also inhibit PGE 2 and therefore bone resorption, taking huge amounts of it is not without ill effects. IMO, the added burden of free radicals caused by such supplementation can only add fuel to the fire.

 

No logical treatment is found on either side of the fence. How can that be? How is it that the supplement industry is as bad as the pharmaceutical companies in distorting information and leading us down a primrose path of more destruction. Even the AHA is recommending "heart healthy" omega 3 supplementation. The reason is simple, and that is that big pharma is also profitting from the supplement industry, because they are the ones producing all the vitamins and other supplements. So if they can't get you to take a drug, they get you to take highly processed, fractionated nutraceuticals instead. Some of these supplements cost more than drugs, so they are not losing profits in any way, they are simply covering all the bases.

 

There are plenty of studies which compare saturated fats vs polyunsaturated fats, and both show cancerous effects as well as other maladies. The problem is the sources of fats used in these studies. Using oxidized saturated fats in comparison to omega 3 fats would have the same outcomes, as both produce free radicals. To get the beneficial effects of CLA noted above without any deleterious effects would require consuming fresh cream from raw milk, rather than the highly pasteurized stuff we are forced to consume.