Osteoporosis: Calcium Deficiency or Excess?

Osteoporosis is the most widely recognized disease connected with calcium and affects over 15 million people in the USA alone. But did you know that both too little and too much calcium can make your bones fragile? A recent study by the Mayo clinic showed that extra calcium supplementation tripled the risk of non-spinal fractures in women already suffering from osteoporosis.¹ This confirms findings of previous studies that calcium supplementation can increase the risk of hip fractures.⁸ How can this be?

Osteoporosis can be classified into two categories: type I and type II.

Type I Osteoporosis

Type I osteoporosis is the classical type associated with calcium deficiency. It occurs in people with a fast metabolism. An overactive thyroid gland causes the body to partially lose its ability to retain calcium and magnesium. At the same time, activity of the parathyroid gland slows down because thyroid and parathyroid glands are each other’s antagonists². With decreased parathyroid function, cells that normally produce hard bone (osteoblasts) become inactive. Less calcium and magnesium are absorbed into the bone while more is excreted through the kidneys. As a result, bones become deficient in calcium and magnesium, grow brittle and easily break.^1,2 People who suffer from this type of osteoporosis benefit from extra calcium supplementation.

Type II Osteoporosis

People with a slow metabolism, on the other hand, do not benefit from calcium supplementation at all. In fact, the opposite: it makes the problem worse. In their case, a sluggish thyroid triggers increases activity of the parathyroid gland^2,3. This leads to more absorption and retention of calcium, while at the same time increasing the number of cells that break down bones (osteoblasts).^5,6 This allows calcium to be drawn from the bone, weakening the bones. Since the calcium can’t be reabsorbed into the bone due to increased osteoblast activity, the body deposits it in soft tissue. This can result in gall stones, kidney stones, stiffness in joints due to calcium deposits, increased arterial plaque formation^1,8 and dry skin. In those cases calcium supplementation will not solve the problem. In fact, it will make it worse.^1,2,8

Osteoporosis due to insulin resistance

Calcium bone loss can also be the result of an underlying metabolic problem. For instance, people with adult onset diabetes or insulin resistance have an increased insulin production. The pancreas can only release insulin when there is enough calcium available.^4,7 To make sure enough calcium is available, the body starts to retain calcium by reabsorbing it in the kidneys, while at the same time the parathyroid also steps up its activity to withdraw calcium stored in the bones. In summary, calcium is stopped from being excreted through the kidneys, and is withdrawn from its storage in bones, to meet the increased demand by the pancreas to produce insulin. Any calcium that is not used for insulin production will not be reabsorbed into the bones due to osteoblast acivity but stored elsewhere, once again not only leading to gall stones, kidney stones etc but also to osteoporosis.¹

How to test?

So how do you know if you should or shouldn’t be taking extra calcium to prevent osteoporosis? A blood test is not useful, because the body will do its utmost to keep levels in the blood the same – either by storing excessive levels in the tissue if levels in blood become too high or withdrawing it from the bones if levels in the blood become too low (homeostasis). It is only when stores in bones are depleted or when the body runs out of tissue to deposit it, that blood levels will start to fluctuate, but by then it is far too late.

Hair Mineral Analysis is more effective way to asses storage levels of calcium. Hair is the second most metabolically active tissue and it provides a reliable record of metabolic activity during its period of growth. The first 4 cm closest to the scalp can provide a good indication of nutrient exposure over the previous 8 – 16 weeks. Mineral deficiencies or excesses can indicate a possible deficiency, excess or bio-unavailability of one or more minerals within the body.

If you are interested in getting a hair mineral analysis done, please contact our clinic on 1300 133 536 or visit our website at:

https://www.massattack.com.au/contactUs.html

References:

1.     Dr D.L Watts, “Trace elements and other essential nutrients” – 6^th Writer’s B-L-O-C-K, USA 2010, p 52-58

2.     Tortora & Grabrowski, “Principles of anatomy and physiology” 9^th edition, p 581-587 – Biological Sciences Text Books, 2000

3.     Tarrage Lopez PJ et all, “Osteoporosis in patients with subclinical hypothyroidism” – Clin Cases Mineral Bone Metabolism, 2011 Sep;8(3):44-8

4.     Curry DL, Bennett LL, Grodsky GM: Requirement for calcium ion in insulin secretion by the perfused rat pancreas. Am J Physiol214 :174–178,1968

5.     Nagata Mutsuko et all, “Subclinical hypothyroidism is related to lower heel QUS in postmenopausal women” – Endocrine Journal, 2007, vol. 54, n^o4, pp. 625-630

6.     Bertoli A, Fusco A, Andreoli A, Magnani A, Tulli A, Lauro D, de Lorenzo A, “Effect of Subclinical Hypothyroidism and Obesity on Whole-Body and Regional Bone Mineral Content” - Horm Res 2002;57:79–84

7.     L. Bent-Hansen, K. Capito, C.J. Hedeskov, “The effect of calcium on somatostatin inhibition of insulin release and cyclic AMP production in mouse pancreatic islets” - Biochimica et Biophysica Acta (BBA) - General Subjects Volume 585, Issue 2, 12 June 1979, Pages 240–249

8.     Reid IR, Bolland MJ, Grey A, “Effect of calcium supplementation on hip fractures” – Osteoporosis Int (2008) 19:1119-1123          

Exciting New Research - Tummy Troubles Cause Hormonal Havoc

Healthy digestion is high up on the list of health priorities for many women.   However, did you know, tummy troubles are considered the top triggers of hormone imbalances in women?  

Those niggling symptoms of bloating and irregular bowel movements are important signs that things are not right.  They are your bodies way of crying out for help.  Ignoring these can lead to heightened imbalances in female reproductive hormones such as estrogen, progesterone and testosterone and those associated with metabolic performance such as insulin.  This combination creates the perfect blend for unexplained weight gain, especially around the middle.

New and Exciting Research  

While traditional research indicates rises in obesity and type 2 diabetes mellitus (T2DM) to be due to a combination of genetics, inflammation and environmental influences [i] [ii] [iii][iv] [v] [vi] [vii] [viii] [ix] [x], exciting new research suggests tummy troubles or ‘digestive dysbiosis’ also play a role and contribute to female reproductive disorders [xi] [xii] [xiii] [xiv] [xv] [xvi][xvii] [xviii]. This is one reason why getting on top of your health and maintaining a healthy body weight may prove so challenging! 

 

Break Free and Restore Health 

Getting on top of your tummy troubles and health is like peeling back the layers of an onion and takes expertise, experience and time. Establishing the cause of your bloating and digestive upsets is an involved process, requiring professional symptomatic screening techniques and targeted dysbiotic testing. But this is only the first stage.  Repairing the damage and restoring balance with medicinal herbs and targeted probiotics is fundamental to finally becoming symptom free.

Narelle Stegehuis, CEO of Mass Attack is a practicing naturopath with over 30,000 hrs of in-clinic experience and health editor for Empower magazine. Specializing in the natural treatment of women's hormonal imbalances, she has a trained eye for hormonal weight gain. She is both an accomplished writer and recipient of the Australian Naturopathic Excellence Award. To find out if your hormones are making you fat, visit http://www.massattack.com.au

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[i] Hossain P, Kawar B, El Nahas M (2007) Obesity and diabetes in the developing world–a growing challenge. N Engl J Med 356: 213–215.

[ii] Lazar M. A (2005) How obesity causes diabetes: not a tall tale. Science 307: 373–375

[iii] Doria A, Patti M. E, Kahn C. R (2008) The emerging genetic architecture of type 2 diabetes. Cell Metab 8: 186–200.

[iv] Rankinen T, Zuberi A, Chagnon Y. C, Weisnagel S. J, Argyropoulos G, et al. (2006) The human obesity gene map: the 2005 update. Obesity (Silver Spring) 14: 529–644. 

[v] Walley A. J, Asher J. E, Froguel P (2009) The genetic contribution to non-syndromic human obesity. Nat Rev Genet 10: 431–442.

[vi] Freedman A. S, Freeman G. J, Rhynhart K, Nadler L. M (1991) Selective induction of B7/BB-1 on interferon-gamma stimulated monocytes: a potential mechanism for amplification of T cell activation through the CD28 pathway. Cell Immunol 137: 429–437.

[vii] Wellen K. E, Hotamisligil G. S (2005) Inflammation, stress, and diabetes. J Clin Invest 115: 1111–1119. 

[viii] Weisberg S. P, McCann D, Desai M, Rosenbaum M, Leibel R. L, et al. (2003) Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest 112: 1796–1808. 

[ix] Xu H, Barnes G. T, Yang Q, Tan G, Yang D, et al. (2003) Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest 112: 1821–1830.

[x] Arkan M. C, Hevener A. L, Greten F. R, Maeda S, Li Z. W, et al. (2005) IKK-beta links inflammation to obesity-induced insulin resistance. Nat Med 11: 191–198. 

[xi] Meadows R (2011) Gut Bacteria May Override Genetic Protections against Diabetes. PLoS Biol 9(12): e1001215. doi:10.1371/journal.pbio.1001215

[xii] Cani P. D, Amar J, Iglesias M. A, Poggi M, Knauf C, et al. (2007) Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56: 1761–1772.

[xiii] Cani P. D, Bibiloni R, Knauf C, Waget A, Neyrinck A. M, et al. (2008) Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Diabetes 57: 1470–1481. 

[xiv] Creely S. J, McTernan P. G, Kusminski C. M, Fisher M, Da Silva N. F, et al. (2007) Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. Am J Physiol Endocrinol Metab 292: E740–E747.

[xv] Chung S, Lapoint K, Martinez K, Kennedy A, Boysen Sandberg M, et al. (2006) Preadipocytes mediate lipopolysaccharide-induced inflammation and insulin resistance in primary cultures of newly differentiated human adipocytes. Endocrinology 147: 5340–5351.

[xvi] Spor A, Koren O, Ley RUnravelling the effects of the environment and host genotype on the gut microbiome. Nat Rev Microbiol 9: 279–290.

[xvii] Khan, K.N., et al., Toll-Like Receptors in Innate Immunity: Role of Bacterial Endotoxin and Toll-Like Receptor 4 in Endometrium and Endometriosis. Gynecologic and Obstetric Investigation, 2009. 68(1): p. 40-52.