Saturday, March 29, 2014

Magnesium Intake Affects Vitamin D Status

If you feel like you're ingesting bucket loads of vitamin D capsules yet your blood levels remain lower than you would like...make sure you're getting enough magnesium. Research conducted by Deng et al. and published in BMC Medicine concludes that magnesium intake can affect vitamin D status.

Magnesium is vital for a whole host of biochemical reactions in the body--at least two of which are critical for bone health. Magnesium is necessary for the parathyroid glands to produce
parathormone (PTH), a hormone that regulates blood calcium levels. If blood calcium levels are too low, the release of PTH activates osteoclastic degradation of bone to help raise blood calcium levels back to normal. Normal levels of PTH are important for bone remodeling activity and the maintenance of healthy bones.

Magnesium is also involved in vitamin D production. As it turns out, magnesium is necessary for the production of three enzymes that are key to the production of 25(OH)D (vitamin D) and its active form, 1,25(OH)2D. Without optimal blood levels of vitamin D (40 to 80 ng/ml) we are unable to absorb calcium from the gut (among other things) which is critical for optimal bone health.

By analyzing data from the National Health and Nutrition Examination Survey (NHANES: 2001 to 2006), Deng et al. concluded that "magnesium was independently associated with significantly reduced risks of vitamin D deficiency and insufficiency respectively. Intake of magnesium significantly interacted with intake of vitamin D in relation to risk of both vitamin D deficiency and insufficiency." They concluded that "it is possible that magnesium intake alone or its interaction with vitamin D intake may contribute to vitamin D status."

Although magnesium is derived from foods such as legumes, whole grains, broccoli, green leafy vegetables, seeds, and nuts, deficiency is common. Ever wonder why you get muscle cramps, twitching of the skin below your eye, constipation, fatigue, rapid heart rate...these could be signs of low magnesium. The best lab test for assessing magnesium status is to have your doctor order a red blood cell magnesium. The standard serum magnesium test is not ideal.

To ensure adequate magnesium intake, make sure you are getting a total of 500 to 700 mg between food and supplements. When supplementing with magnesium, I prefer the forms of magnesium bisglycinate chelate, dimagnesium malate, and magnesium citrate (all of which can be found in our OsteoNaturals products OsteoSustain and OsteoMineralBoost) over what may be less bioavailable forms such as magnesium oxide and magnesium carbonate.  

Deng, X, et al. 2013. Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III. BMC Medicine 11:187.


Friday, March 21, 2014

Diabetes and Fracture Risk


Your skeletal health is only as deep as its microarchitecture. With almost 50% of women and 20% of men predicted to sustain an osteoporosis-related fracture in their lifetime, the possibility of fragile bones is always something everyone should be aware of. With the diabetic individual, he or she will need to take extra vigilance as they have greater fracture risk.

Diabetes has reached epidemic proportions in the United States. Over 25% of adults have diabetes and this population—especially that developing type 2 diabetes (T2D)—is growing. With medical advances, people with type 1 diabetes (T1D) are living longer and into an age where osteoporosis becomes of greater concern.

How much greater is the fracture risk for diabetic individuals?
Compared to non-diabetic individuals, the bone mineral density (BMD) of type 1 diabetic patients is only slightly lower on average than non-diabetic individuals, so one might expect only a slightly higher fracture risk. But the risk level is much greater: individuals with T1D are 12 times more likely to fracture a hip according to data from the Iowa Women’s Study.1

In contrast to T1D, individuals with T2D are often overweight and have higher than average BMD. With higher weight and increased bone density one would expect lower fracture risk. But T2D also carries an increase in fracture risk: 40% to 70% increase in risk for hip fracture and over 20% increased risk for all fractures.

It is clear that both T1D and T2D carry increased risk for spinal and hip fractures, yet BMD T scores and FRAX analysis underestimate their fracture risk. The bottom line: middle-aged and elderly diabetics are suffering a decrease in bone strength that is not measurable by current methods. Diabetes-related fracture risk is linked to reduced microarchitectural bone quality. Of course, an increase in falls due to hypoglycemic episodes, poor balance from diabetic neuropathy, and retinopathy-induced visual impairment may also be factors.

Why is the bone quality of diabetic individuals so poor?
Diabetes may affect bone in a number of ways:

1.     Chronic elevations in blood glucose weakens skeletal microarchitecture through the formation of advanced glycation end-products (AGEs) (such as carboxy-methyl-lysine and pentosidine) in both the bone-matrix collagen and the non-collagenous protein, osteocalcin2.  This non-enzymatic glycation is a spontaneous reaction that lowers bone biomechanical competence. AGE induced collagen cross-links between reducing sugars and proteins stiffen collagen, making bone less pliable and less resistant to fracture.
2.     Hyperglycemia affects bone cells leading to low bone turnover osteoporosis.
3.     Reduced osteocyte function and higher sclerostin levels may inhibit bone formation by osteoblasts.3
4.     Reduced osteoblast bone formation and increased cortical porosity may explain accelerated bone loss at the hip in T2D.
5.     A reduction in trabecular microarchitectural quality as assessed through trabecular bone score (TBS) has been implicated as contributing to the increased fracture risk in T2D despite a higher than average BMD.4
6.     Altered bone marrow fat composition (higher saturated fat) is linked to fragility fractures and diabetes.5 Excessive marrow fat leads to reduced hematopoetic stem cells and increased adipocytokine production. This lowers bone turnover rate and allows for the development of “old bone” weakened by the accumulation of microfractures.
7.     Diabetes leads to lower “insulin-like growth factor 1” production. IGF-1 is a powerful natural anabolic peptide that stimulates both muscle and bone growth.
8.     The pharmacological treatment of T2D with thiazolidinediones (PPAR gamma agonists) promotes marrow stem cell differentiation into adipocytes rather than osteoblasts.

The typical medical approach to the treatment of T2D often includes medications. Although not all diabetes medications increase fracture risk, the thiazolidinediones (rosiglitazone and pioglitazone) can double the fracture risk of women (not men) with osteoporosis. These PPAR (peroxisome proliferator activator receptor) agonist medications stimulate adipogenisis in bone marrow and reduce bone formation.

Bisphosphonates are the current medications of choice for treating osteoporosis; they work by subduing osteoclast bone resorption and slowing overall bone remodeling (including bone formation) activity. The medical community has expressed concern about using bisphosphonate drugs to treat osteoporotic T2D’s patients because a further reduction in bone formation (bisphosphonates reduce both resorption and formation activity) through the use of bisphosphonate medications in the already bone-formation suppressed microenvironment of the type 2 diabetic, could increase bone fragility even further. This seems highly likely especially with atypical femur fractures already linked to long-term bisphosphonate use in non-diabetic individuals.

If you are diabetic, talk with your doctor about things you can do to improve your blood glucose levels naturally: 

·       Diet – You will benefit from a lower carbohydrate intake and increased quality protein, healthy fats, and vegetable intake.
·       Exercise – Try to exercise 45 minutes to an hour, five days a week, and reduce stress.
·       Supplementation – Talk to your doctor or nutritionist about what specific nutrients and therapeutic compounds you can take that work synergistically to decrease insulin resistance, lower inflammation, balance blood lipids, and improve liver function, while controlling their glucose levels and preventing glycation-induced damage. The following are some of the key components to consider using if you are diabetic: activated B-complex vitamins; vitamin D3; essential minerals (especially magnesium, zinc, chromium, and vanadium) and trace minerals; antiglycating agents such as alpha lipoic acid, L-Taurine, L-Carnosine and benfotiamine; herbal support including green tea extract (EGCG) and Gymnema sylvestre leaf extract.
·       Tracking – Make sure your blood glucose and hemoglobin A1C levels are monitored. Hb A1C levels above 7% are correlated with increased fracture risk. The American Diabetic Association (ADA) recommends that people with diabetes have the Hb A1C tested every 3 to 6 months depending upon glycemic control.

In addition to lowering your fracture risk, these strategies will also help lower your risk of diabetic-related comorbidity. Hypertension, coronary and peripheral artery disease, stroke, and even spinal degeneration are all common comorbidities of diabetes.

Current medical therapy for the diabetic osteoporotic patient is problematic and a more natural, conservative, approach using diet, supplements, and exercise can substantially improve the long-term outcome. If you are diabetic, you can reduce your risk of fractures and improve your over-all health by following the simple suggestions outlined above.

 
1  Nicodemus, K.K. and A.R. Folsom. 2001. Iowa Women’s Health Study. Type 1 and type 2 diabetes and incident hip fractures in postmenopausal women. Diabetes Care 24:1192-1197.

2  Sroga, G. and Vashishth, D. 2013. Glycated osteocalcin. ASBMR Symposium: Cutting Edge Discoveries in Muscle Biology, Disease and Therapeutics. ASBMR Annual Meeting: Oct 4-7. P024

3  Kim, J.Y., et al. 2013. Extendin-4 increases bone mineral density in type 2 diabetes OLETF rats potentially through the down-regulation of SOST/sclerostin in osteocytes. Life Sciences Mar 21;92(10):533-40.

4  Dhaliwal, R., J. Spadaro, C. Ghosh, J. Kelly, and A. Moses. 2013. ASBMR Symposium: Cutting Edge Discoveries in Muscle Biology, Disease and Therapeutics. ASBMR Annual Meeting: Oct 4-7. SA0304

5  Patsch, J.M., et al. 2013. Bone marrow fat composition as a novel imaging biomarker in postmenopausal women with prevalent fragility fractures. J Bone Miner Res Aug;28(8):1721-8.

Thursday, March 13, 2014

Calcium: Is it a Cardiovascular Risk?

As a chiropractic physician specializing in osteopenia and osteoporosis, being questioned by my patients about the safety of calcium was something I never would have foreseen. For years, in addition to recommending various dietary, supplemental and life-style changes to improve bone health and reduce fracture risk, I have recommended that patients take in a total of 1,000 to 1,200 mg/day of calcium from dietary and supplemental sources. Then, in 2008, a study by Bolland et al. (2008) reported the possible association between calcium supplementation and cardiovascular risk1 and my job got a little more difficult. This study (and two subsequent studies: Bolland et al. (2010) and Li, et al. (2012) that supported Bolland’s initial findings2,3) hit the newsstands and literally struck fear in hearts of many osteoporosis patients. According to Bolland, et al. (2010) “Calcium supplements (without coadministered vitamin D) are associated with an increased risk of myocardial infarction.” “A reassessment of the role of calcium supplements in the management of osteoporosis is warranted.”
 
Comments from some of my patients such as “Doc, what are you trying to do, kill me?...I’m not taking that calcium!” soon followed the media blitz. (That’s a slight exaggeration, but you get the gist.) As a chiropractor working to improve his patients’ skeletal health mainly through natural means, and one who understands the importance of calcium and vitamin D for bone health, this type of response could impede optimal care. It is true, calcium isn’t everything when it comes to bone health…but it is important.

Thankfully, there has now been time to evaluate these studies and new research has countered their conclusions. For example, Abrahamsen, et al. (2011) and Nordin, et al. (2011) have criticized Bolland’s research pointing out design flaws in the study and questioning how the cardiovascular events themselves were determined.4,5 Research by Samelson, et al. (2012) found no support to conclude that high calcium intake increases coronary artery calcification and that there is not sufficient evidence regarding vascular calcification risk to modify current recommendations for calcium intake to protect skeletal health.6 Heaney, et al. (2012) from Creighton University Medical Center reviewed data from 2 epidemiological studies, a meta-analysis of controlled clinical trails and other cohort studies and found that “little evidence exists for plausible biological mechanisms to link calcium supplement use with adverse cardiovascular outcomes.”7 And, in an effort to determine the exact physiological mechanism, if any, that could explain the connection between acute rises in blood calcium (as seen with supplemental calcium intake) and heart attacks, Burt et al. (2013) studied the effects of giving 25 subjects 1,000 mg oral calcium citrate. They then evaluated changes in blood markers and specific cardiovascular function parameters linked to cardiovascular risk. The authors concluded that further research was needed but that “the rise in serum calcium following supplement administration does not acutely exert an adverse effect on these parameters of cardiovascular function.”8

As a member of the American Society for Bone and Mineral Research, I recently attended our 2013 Annual Meeting in Baltimore, MD (October 4 – 7) and was fortunate to attend talks by the lead authors of two important new studies that evaluated cardiovascular risk and calcium intake. The first presentation was by Dr. Douglas Bauer, MD, from the University of California, San Francisco. Dr. Bauer’s observational trial assessed calcium intake (both dietary and supplemental) and mortality in 5967 men over the age of 65 years in the Osteoporotic Fractures in Men (MrOS) study. The participants’ intake of calcium was 1142 ± 590 mg/day and 65% used calcium supplements. Over a 10-year follow-up period, those who took in more than 1565 mg/day of calcium had lower mortality than those who took in less than 621 mg/day. The highest mortality from cardiovascular disease was seen in those with the lowest calcium intake (less than 621 mg/day). The authors concluded there was “no evidence that supplements increased the risk of mortality among those with the highest dietary calcium intake (interaction p value = 0.84).” And, “total calcium intake, use of calcium supplements and the combination of high dietary calcium intake and supplement use were not associated with total or cardiovascular mortality.”9

In the second presentation, Dr. Joshua Lewis, MD, PhD, from the University of Western Australia, Perth, reported on his meta-analysis of 19 randomized controlled trials that studied women over the age of 50 who took calcium supplements. The analysis encompassed 59,844 participants. The authors concluded “data from this meta-analysis does not support the concept that calcium supplementation with or without vitamin D increase the risk of ischemic heart disease or total mortality in elderly women.”10

Hopefully the Bauer and Lewis studies will help reduce patient fears concerning supplemental calcium and heart disease. That said, I do believe that when supplementing a patient with calcium it is important to maintain optimal vitamin D levels and encourage adequate intake of vitamin K, magnesium, and trace minerals. Vitamins and minerals work synergistically, and to flood the body with calcium without the necessary utilizing factors has the potential to cause metabolic imbalance. 

1  Bolland M.J., P.A. Barber, R.N. Doughty, et al. 2008. Vascular events in healthy older women receiving calcium supplementation: randomized controlled trial. BMJ 336(7638):262-6.
2  Bolland M.J., A Avenell, J.A. Baron, et  al. 2010. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ 341:c3691.
3  Li K., R. Kaaks, J. Linseisen, and S. Rohrmann. 2011. Associations of dietary calcium intake and calcium supplementation with myocardial infarction and stroke risk and overall cardiovascular mortality in the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition study (EPIC-Heidelberg). Heart 98(12):920-5.
4  Abrahamsen B. 2011. Editorial: Do calcium plus vitamin D supplements increase cardiovascular risk? BMJ 343:d2080.
5  Nordin B.E., J.R. Lewis, R.M. Daly, et al. 2011. The calcium scare—What would Austin Bradford Hill have thought? Osteoporos Int 22(12):3073-7.
6  Samelson E.J., S.L. Booth, C.S. Fox, et al. 2012. Calcium intake is not associated with increased coronary artery calcification: the Framingham Study. Am J Clin Nutr 96(6):1274-80.
7  Heaney, R.P., S. Kopecky, K.C. Makl, et al. 2012. A review of calcium supplements and cardiovascular disease risk. Adv Nutr 3(6):763-71.
8  Burt M.G., B.L. Mangelsdorf, D. Srivastava, C.J. Petersons. 2013. Acute effect of calcium citrate on serum calcium and cardiovascular function. J Bone Miner Res 28(2):412-8.
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