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View Full Version : Would you say Calcium is underrated?



jpetitclerc
09-27-2008, 08:37 PM
We all know on how important is the Calcium but yet, we don't see a lot of post or product with it.

Discuss?

Neopragmatist
09-27-2008, 08:42 PM
I blame milk.

jpetitclerc
09-27-2008, 09:03 PM
Wow, died fast...

Guess no one like calcium x)

Motley_Muscle
09-28-2008, 02:45 AM
We all know on how important is the Calcium but yet, we don't see a lot of post or product with it.

Discuss?

I think there can be a great discussion on Calcium. Maybe if this was posted in the Supplement Science section instead....

I used to hit very stubborn plateaus in my dieting before I put more focus on Calcium and Vitamin D (my oils and macros have always been in check) and now it seems like the results keep coming until I hit my goal. Refeeding is one of the best ways to overcome plateaus, and Calcium has significant benefits when doing so.

I'm sure if PubMed posted a newly studied herb or mineral that "results in a coordinated stimulation of lipogenesis and inhibition of lipolysis" and that it "increases fat oxidation, potentially via regulation of serum parathyroid hormone (PTH) concentrations." ... it would be in all the new overhyped fatloss supps. :)


1: FASEB J. 2000 Jun;14(9):1132-8.Click here to read Links
Regulation of adiposity by dietary calcium.
Zemel MB, Shi H, Greer B, Dirienzo D, Zemel PC.

Department of Nutrition, The University of Tennessee, Knoxville, Tennessee 37996-1900, USA. mzemel@utk.edu

Recent data from this laboratory demonstrate that increasing adipocyte intracellular Ca(2+) results in a coordinated stimulation of lipogenesis and inhibition of lipolysis. We have also noted that increasing dietary calcium of obese patients for 1 year resulted in a 4.9 kg loss of body fat (P<0.01). Accordingly, we tested the possibility that calcitrophic hormones may act on adipocytes to increase Ca(2+) and lipid metabolism by measuring the effects of 1, 25-(OH)(2)-D in primary cultures of human adipocytes, and found significant, sustained increases in intracellular Ca(2+) and a corresponding marked inhibition of lipolysis (EC(50) approximately 50 pM; P<0.001), suggesting that dietary calcium could reduce adipocyte mass by suppressing 1,25-(OH)(2)-D. To test this hypothesis, we placed transgenic mice expressing the agouti gene specifically in adipocytes on a low (0.4%) Ca/high fat/high sucrose diet either unsupplemented or with 25 or 50% of the protein replaced by non-fat dry milk or supplemented to 1.2% Ca with CaCO(3) for 6 wk. Weight gain and fat pad mass were reduced by 26-39% by the three high calcium diets (P<0.001). The high calcium diets exerted a corresponding 51% inhibition of adipocyte fatty acid synthase expression and activity (P<0.002) and stimulation of lipolysis by 3. 4- to 5.2-fold (P<0.015). This concept of calcium modulation of adiposity was further evaluated epidemiologically in the NHANES III data set. After controlling for energy intake, relative risk of being in the highest quartile of body fat was set to 1.00 for the lowest quartile of Ca intake and was reduced to 0.75, 0.40, and 0.16 for the second, third, and fourth quartiles, respectively, of calcium intake for women (n=380;P<0.0009); a similar inverse relationship was also noted in men (n=7114; P<0.0006). Thus, increasing dietary calcium suppresses adipocyte intracellular Ca(2+) and thereby modulates energy metabolism and attenuates obesity risk.


Interestingly, adding a little dairy to your diet will enhance the benefits you get from Calcium.. It doesn't seem to be the Calcium form itself, but the bioactive compounds, so it seems logical to supplement with Calcium and also include good 'ol milk. If I remember correctly, a cup of milk has around 300mg of Calcium. I get 1 to 2 cups a day, and take 500 mg of Calcium 3 times daily. I'm still not sure if this is optimal, but it has definitely made a difference.


1: J Am Coll Nutr. 2002 Apr;21(2):146S-151S.Click here to read Links
Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications.
Zemel MB.

The University of Tennessee, Knoxville 37996, USA. mzemel@utk.edu

Dietary calcium plays a pivotal role in the regulation of energy metabolism; high calcium diets attenuate adipocyte lipid accretion and weight gain during periods of overconsumption of an energy-dense diet and increase lipolysis and preserve thermogenesis during caloric restriction, thereby markedly accelerating weight loss. Intracellular Ca2+ has a key role in regulating adipocyte lipid metabolism and triglyceride storage, with increased intracellular Ca2+ resulting in stimulation of lipogenic gene expression and lipogenesis, suppression of lipolysis, and increased lipid filling and adiposity. Moreover, we have recently demonstrated that the increased calcitriol released in response to low calcium diets stimulates Ca2+ influx in human adipocytes and thereby promotes adiposity. Accordingly, suppressing calcitriol levels by increasing dietary calcium is an attractive target for the prevention and management of obesity. In support of this concept, transgenic mice expressing the agouti gene specifically in adipocytes (a human-like pattern) respond to low calcium diets with accelerated weight gain and fat accretion, while high calcium diets markedly inhibit lipogenesis, accelerate lipolysis, increase thermogenesis and suppress fat accretion and weight gain in animals maintained at identical caloric intakes. Further, low calcium diets impede body fat loss, while high calcium diets markedly accelerate fat loss in transgenic mice subjected to caloric restriction. These findings are further supported by clinical and epidemiological data demonstrating a profound reduction in the odds of being obese associated with increasing dietary calcium intake. Notably, dairy sources of calcium exert a significantly greater anti-obesity effect than supplemental sources in each of these studies, possibly due to the effects of other bioactive compounds, such as the angiotensin converting enzyme inhibitor found in milk, on adipocyte metabolism, indicating an important role for dairy products in the control of obesity.



1: J Nutr. 2004 Nov;134(11):3054-60.Click here to read Links
Calcium and dairy products inhibit weight and fat regain during ad libitum consumption following energy restriction in Ap2-agouti transgenic mice.
Sun X, Zemel MB.

Department of Nutrition, University of Tennessee, Knoxville, TN 37996, USA.

We demonstrated previously that dietary calcium suppression of calcitriol reduces adipocyte Ca(2+), suppresses lipogenesis, and increases lipid utilization during energy restriction. Notably, dairy calcium sources exert markedly greater effects. To determine the effects of dietary calcium and dairy products on energy partitioning during subsequent refeeding, we induced obesity in aP2-agouti transgenic mice with a high-fat/high-sucrose diet, then restricted energy intake from a high-calcium (1.3%) diet for 6 wk to induce fat loss, and then provided free access to a low-calcium (0.4%) diet or to high-calcium (1.3%) diets that utilized either calcium-fortified foods or dairy products (milk or yogurt) for 6 wk. Refeeding the low-calcium diet caused the regain of all weight and fat, whereas all high-calcium diets reduced fat gain by 55% (P < 0.01). All high-calcium diets stimulated adipose tissue uncoupling protein (UCP)2 and skeletal muscle UCP3 expression (P < 0.001) and slightly increased core temperature (P = 0.136), but only the dairy-based diets elicited a marked (>10-fold, P < 0.001) increase in skeletal muscle peroxisome proliferator-activated receptor-alpha expression. All 3 high-calcium diets produced significant increases in lipolysis, decreases in fatty acid synthase expression and activity, and reduced fat regain (P < 0.03), but the 2 dairy-containing high-calcium diets exerted significantly greater effects on regain (P < 0.01). Thus, high-Ca diets elicit a shift in energy partitioning and reduction of weight gain during refeeding, with dairy Ca sources exerting markedly greater effects.

...some of the additional benefits could just be the Leucine in dairy.


1: Lipids. 2007 Apr;42(4):297-305. Epub 2007 Feb 20.Links
Leucine and calcium regulate fat metabolism and energy partitioning in murine adipocytes and muscle cells.
Sun X, Zemel MB.

Department of Nutrition, University of Tennessee, 1215 W. Cumberland Avenue, Knoxville, TN 37996-1920, USA.

Dietary calcium modulation of adiposity is mediated, in part, by suppression of calcitriol, while the additional effect of dairy products is mediated by additional components; these include the high concentration of leucine, a key factor in the regulation of muscle protein turnover. We investigated the effect of leucine, calcitriol and calcium on energy metabolism in murine adipocytes and muscle cells and on energy partitioning between adipocytes and skeletal muscle. Leucine induced a marked increase in fatty acid oxidation in C2C12 muscle cells (P<0.001) and decreased FAS expression by 66% (P<0.001) in 3T3-L1 adipocytes. Calcitriol decreased muscle cell fatty acid oxidation by 37% (P<0.001) and increased adipocyte FAS gene expression by threefold (P<0.05); these effects were partially reversed by either leucine or calcium channel antagonism with nifedipine. Co-culture of muscle cells with adipocytes or incubation with 48-h adipocyte conditioned medium decreased muscle fatty acid oxidation by 62% (P<0.001), but treating adipocytes with leucine and/or nifedipine attenuated this effect. Leucine, nifedipine and calcitriol also modulated adiponectin production and thereby exerted additional indirect effects on fatty acid oxidation in C2C12 myotubes. Adiponectin increased IL-15 and IL-6 release by myotubes and partially reversed the inhibitory effects of calcitriol. Comparable effects of leucine, calcitriol and adiponectin were found in myotubes treated with conditioned medium derived from adipocytes or co-cultured with adipocytes. These data suggest that leucine and nifedipine promote energy partitioning from adipocytes to muscle cells, resulting in decreased energy storage in adipocytes and increasing fatty acid utilization in muscle.