Early Detection and Intervention are Crucial to Stop the Progression of Bone Loss - How Biomarkers Can be Used to Improve Treatment of Osteoporosis

As you know from my book The Whole-Body Approach to Osteoporosis,(1) I am a strong advocate for working closely with your health care provider and using specific laboratory tests to gather critical information about your bone health.

Both men and women begin to lose a small amount of bone mineral density in their mid-thirties. A “healthy” person may lose 0.7% to 1.0% per year after they reach their 40s but this loss is slow and typically has a minimal detrimental effect on their over-all health longevity, especially if they had normal bone accrual as a young adult. But for women, the sharp loss of estrogen at menopause can precipitate a dramatic loss of bone density, up to 3 or 4% per year. A rapid decline in bone mineral density leads to unwanted changes within the microarchictecture of bone, such as cortical thinning and a loss of trabeculae – the microscopic support beams within bone. These changes cause a loss in bone quality. Together, when both bone quantity and quality are lost, there is a sharp decline in bone strength and an increased risk for fractures. Identifying women at greater risk for developing osteoporosis, and especially those who are loosing bone rapidly during transmenopause,* is of key importance. The earlier the detection the better!

When bone densitometry (a DXA exam) is used to determine bone loss, the doctor must compare two consecutive exams over a two-year period to assess the speed in which a person is loosing bone. The larger the loss in bone density, the more rapid is the bone loss and the greater is their risk of breaking a bone. Having to wait two years before identifying those at greater risk can, and often does, result in catastrophic results such as sustaining a hip fracture or spinal compression fracture. Once bone is lost it is very difficult to regain, placing these women at a much higher risk for fracture. With earlier

identification of those at high risk for rapid-bone loss…by eliminating this 2-year period of time…we can intervene with appropriate therapy and reduce the incidence of subsequent fractures.

The GOOD NEWS: Natural therapeutic methods to improve skeletal health works! Changing a person’s diet, taking quality supplements such as the OsteoNaturals line and engaging in bone-healthy exercise work to improve skeletal health by “gently nudging” bone cells into a new and healthier course of being. When working with nutrition, we aren’t just sprinkling more calcium into bones, we are changing the "habits" of cell metabolism. While we can't alter our genetic code - our DNA, we can improve the way a person's genes "express" themselves - the epigenetics of cells. It is through changes in a person's epigenetics that we can put a stop to rapid bone loss and move out of the "high risk for rapid-bone loss" osteoporosis category.

The “NOT SO GOOD NEWS”: Natural therapeutic methods to change skeletal health can take time to “engage”. If a person has had a poor diet for the past 20 years, is in a nutritionally sub-optimal state, and has low-level chronic systemic inflammation, simply improving his or her diet will NOT result in instant success. The sooner we can identify the heightened level of bone cell activity, the quicker we can start “encouraging” bone destroying cells to calm down and reduce their excessive level of bone resorption. Think of osteoclasts (the cells that break down bone) as a gang of wild maniacs on the loose. If you just tell them to stop their wild behavior they probably won’t just “normalize”….on the other hand, put them into a quality therapeutic counseling program, change their eating habits and destructive lifestyle habits and, over a period of years, they may be able to re-enter society as constructive members. The earlier a person is tapped into therapy, the better the results. Changing the way cells “behave” can take several years, several generations of cellular division, even after being immersed into a new, healthier environment.

Back to the GOOD NEWS: With the science of current biomarkers constantly improving and new, even more sophisticated biomarkers being developed, we have come a long way in our understanding of osteoporosis and ways to treat it effectively. Most recently, in a study published in the Journal of Bone and Mineral Research,(2) Shieh, et al. assessed the clinical utility of measuring N-telopeptide (a bone resorption laboratory marker) during the menopause transition as a way of identifying women at high risk for developing osteoporosis. The study included 604 women. The authors concluded that higher levels of N-telopeptide during the early postmenopausal period were most strongly associated with a higher rate of bone loss during transmenopause. This correlation, elevations in N-telopeptide to the rate of bone loss, was most pronounced in the lumbar spine but also in the hip. More studies like this are needed to ensure individuals at highest risk for rapid bone loss are identified as quickly as possible.

I have been using biomarkers such as N-telopeptide (and the other bone resorption markers C-TX and DPD) for over fifteen years to assess and monitor patients with bone loss. I have seen the benefits of early detection of those at great risk of developing osteoporosis and those who have rapid bone loss and thus even a higher risk for fracture. Please help pass the word to everyone you know – especially women approaching transmenopause – about the importance of specific laboratory tests to gather critical information about their bone health. Armed with this information, they can work with their health care provider to customize a plan to address the underlying causes of their bone loss, ultimately enabling them to improve bone health, reduce the risk of fracture, and enjoy a more active lifestyle.

* Transmenopause or menopause transition refers to the period of greatest estrogen loss. Rapid bone loss often begins 1 year prior to a woman's final menstrual period and lasts for 2 to 3 (or more) years after their last period. After this 3 to 5 year (up to 10 years in some cases) period, the rapidity of bone loss normalizes to prior menopause levels. 


(1) McCormick, R.K. 2009. The Whole-Body Approach to Osteoporosis, How to Improve Bone Strength and Reduce Fracture Risk. New Harbinger Publications.

(2) Shieh, A., Ishii, S., Greendale, G.A., Cauley, J.A., Lo, J.A., and Karlamangla, A.S. 2015. Urinary N-Telopeptide and Rate of Bone Loss Over the Menopause Transition and Early Postmenopause. Journal of Bone and Mineral Research DOI: 10.1002/jbmr.2889.

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C-Reactive Protein: Its Relationship to Fracture Risk and Bone Density

We have known for years that low-grade chronic systemic inflammation is associated with higher fracture risk. In my book, The Whole Body Approach to Osteoporosis, I explain this relationship in full. But what we do not fully understand is how this inflammation relates to bone mineral density (BMD).

This is exactly the question researchers from Norway set out to explore. In a study of 1902 women and 1648 men between the ages of 55 and 74, researchers tested the relationship of inflammation, as indicated by a biomarker called C-reactive protein (hs-CRP), to bone density and non-vertebral fractures.

The study showed an inverse relationship between hs-CRP and bone density in men (but not women). The higher the hs-CRP in men, the lower was their bone density. They also determined that elevated hs-CRP predicted increased fracture risk for both men and women. The authors concluded that inflammation influences fracture risk in both men and women.

So what can you do to lower chronic inflammation and reduce your fracture risk? A low-inflammatory diet rich in vegetables is a great way to start. Then try OsteoStim. This OsteoNaturals product is a potent blend of antioxidants, vitamins and medicinal herbs designed to limit the adverse effects of chronic inflammation on bone and encourage normal bone metabolism (as seen through the reduction in NTX, CTX, and/or DPD -- biomarkers that reflect the activity level of bone-resorbing osteoteoclasts).

One of the ingredients in OsteoStim is alpha-lipoic acid (ALA). This powerful antioxidant is an essential co-factor for cellular energy production. ALA also helps reduce the damaging effects of pro-inflammatory cytokines (Il-1, Il-6, TNF alpha, and NF-KB) and their tendency to spur on aggressive osteoclastic bone-resorbing activity.

In a recent article published in the European Journal of Pharmacology, researchers evaluated the protective effect of ALA on rat bone metabolism. They monitored pro-inflammatory cytokines (Il-1, IL-6, and TNF) to observe the inflammation process and how it was affected by ALA. The researchers concluded that "ALA had a protective effect on both senile and postmenopausal osteoporosis." "...ALA may be a candidate for radical osteoporosis treatment both in senile and postmenopausal types..."

Dahl, K., et al. 2014. High-sensitivity c-reactive protein is an independent risk factor for non-vertebral fractures in women and men: the Tromso Study. Bone Nov. 20. 

Polat, B., et al. 2013. The effect of alpha-lipoic acid in ovariectomy and inflammation-mediated osteoporosis on the skeletal status of rat bone. European Journal of Pharmacology 718(1-3):469-74.

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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.

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High Iron Levels Associated With Accelerated Bone Loss and Fracture Risk

Iron is an essential nutrient and one that is vital for the oxygen-carrying capacity of red blood cells. It is not only important for blood formation, but it is also necessary for optimal bone health. Iron helps convert vitamin D into its active form and therefore is involved in calcium absorption. Iron is also important for normal osteoblastic activity and the formation of strong collagen fibers, the foundation of bone.

Low hemoglobin and iron-deficiency anemia can result from inadequate iron intake; poor absorption due to celiac disease and other GI disorders; or chronic bleeding from excessive menses, ulcers, bleeding hemorrhoids, or cancer. Without iron, or even in low iron anemic states, bone mineral density suffers and fracture risk increases.

On the other end of the spectrum, iron overload can be just as detrimental to a person's health. The two most common causes of iron overload are excessive iron intake (usually from over-supplementing) and hemochromotosis (a hereditary condition where the body absorbs too much iron). Excess iron can deposit within the tissues and organs of the body leading to liver disease, diabetes, heart disease, arthritis, and other maladies. It is also toxic to bone health.

We have known for years that excessive iron loads can have damaging effects to the bone metabolism of animals. But there were no clinical studies to show this effect in humans. Now, for the first time, we have clinical evidence that excessive iron levels can reduce bone density and bone strength in women. In a study by Kim et al. (2013) published in Osteoporosis International, women over the age of 45 with elevated serum ferritin (a blood test for iron levels) were associated with lower bone mineral density and greater risk for fracture. While iron is important for osteoblast function, excessive amounts can be toxic to osteoblasts, reducing their ability to form bone.

It is not unusual for me to see patients with osteoporosis who are consuming excessive amounts of iron. Red meat, liver, fortified cereals, and molasses are all sources high in iron. Take this into consideration if your supplements include iron. Also, while menstruating women may need to supplement with iron to avoid becoming anemic, most postmenopausal women should avoid iron-containing vitamin/mineral supplements.

To avoid inadvertently ingesting too little or too much iron, make sure you are reading labels.      

Kim B.J., S.H. Lee, J.M. Koh, G.S. Kim. 2013. The association between higher serum ferritin level and lower bone mineral density is prominent in women ≥45 years of age (KNHANES 2008-2010). Osteoporosis International 24(10):2627-37.

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Reducing Osteoporosis Fracture Risk

If you have been diagnosed with osteoporosis, or are at risk for this disease, you will need to strengthen your bones and reduce your risk for fracture. Options available to help reduce fracture risk include taking supplements, using prescribed medications, and/or making diet, exercise and lifestyle modifications. My philosophy is: “It doesn’t really matter how you get there…just so you get there….and, just so you don’t hurt yourself in the process.”  But I do admit to a bias for a whole-body approach. (1)

Supplements 
There is no one “best list” of supplements to take for reducing fracture risk. Sure, there are some basics that apply to pretty much everyone—calcium, magnesium, vitamins D and K—but to really be effective, we need to be a lot more specific. Everyone is unique; to gain optimal effect, each person will need to address his or her particular physiological strengths or shortcomings. Although I think OsteoNaturals products are great and they offer superior benefit to skeletal health, I still think people should continue to evaluate their progress. Loyalty to brand is fine but we still need to make sure that a product is providing benefit. If you require “X” and your supplement provides “Y,” then all the “Y” in the world, even if it is the best quality possible, won’t be of benefit. We should only care about one thing…results.

Medications
Many doctors recommend osteoporosis drugs as the primary mode of therapy to reduce fracture risk. This medical model is based on improving bone mineral density as opposed to bone quality. The bisphosphonate medications (currently the most commonly used osteoporosis drugs) significantly slow bone remodeling by essentially killing off bone resorbing osteoclast cells. Long-term use of these medications puts individuals at risk for serious adverse effects. In addition to a medication, the doctor may suggest 400 IU or so of vitamin D and some form of calcium carbonate, such as Tums. But in general, little or no focus, is placed on improving the overall health of the patient.

Nutrition/Lifestyle/Exercise
A growing contingent of health care providers, including me, recommend using nutrition/lifestyle/exercise as the primary therapeutic platform for reducing fracture risk – and prescribing medications short-term, and only when necessary. This alternative model completely avoids the possibility of serious adverse effects from long-term osteoporosis medication use; is more effective than simply taking a lot of supplements and hoping for the best; and has the added benefit of improving the patient’s overall health and reducing his or her risk of developing chronic disease co-morbidity.

Monitoring Options Scientifically
I also advocate using laboratory tests to determine efficacy of the chosen therapeutic protocol for reducing fracture risk.

Currently, a bone mineral density (BMD) test is the best way we have for determining the health of your bones. This test can identify osteoporosis, determine your risk for fractures (broken bones), and measure your response to osteoporosis treatment. The most widely recognized BMD test is called a dual-energy x-ray absorptiometry, or DXA test. Unfortunately, bone mineral density scores from DXA exams change extremely slowly (typically you usually have to wait two years between DXA exams) and there MUST be fairly large numerical improvement to confirm significant change that correlates with lower fracture risk. Also, what most people do not realize is that bone density is NOT a measure of bone strength and “there is only a weak relationship between the change in bone mineral density and fracture risk reduction.” (Primer on Metabolic Bone Disease, 6^th ed. 2006, p. 274)

To make certain we are lowering fracture risk, I encourage changing lifestyle factors and improving certain laboratory biomarkers that have been correlated with bone health (2). When destructive lifestyle habits are improved and/or laboratory biomarkers are normalized, then the patient’s health benefits. Lab tests can be re-evaluated every 3 to 4 months and, by using multiple biomarkers, we can easily see “trends” in improvement that we can rely upon.

Let’s look at a comparison in order to understand this process
Note:  The result of the BMD test is given as a T-score. It stands for "standard deviation" and indicates how much ones bone density is above or below normal.
A T-score between +1 and -1 is normal bone density.
A T-score between -1 and -2.5 indicates low bone density or osteopenia.
A T-score of -2.5 or lower is a diagnosis of osteoporosis.

Mary Ann is a 60 year-old woman. The result of her first BMD test: Lumbar/Spine T-score of -3.4.  She was obviously deeply concerned. She did not want to take medications because she had heard about the possibility of severe adverse side effects. She decided to try and improve her bone density by taking vitamins D and K and 1,000 mg calcium/day. Then she waited…for two years…until her next DXA scan.

Joan is a 60 year-old woman. The result of her first BMD test: Lumbar/Spine T-score of -3.4 (exactly the same as Mary Ann’s T-score).   Joan, like Mary Ann, was deeply concerned. She also did not want to take medications for the same reasons as Mary Ann. Joan’s health care provider ordered several laboratory tests that have correlation to fracture risk. The results from two of these tests indicated that Joan was at increased risk for fracture. In addition, Joan’s doctor took note of her complaints of constipation, abdominal bloating, and white spots on her fingernails; all signs and symptoms of a digestive and nutrient malabsorption issue. Joan and her doctor worked out a treatment regime that included the same supplements as Mary Ann but with different dosages, as well as several other products, diet changes, and an exercise program. Retesting every several months indicated improvement in the abnormal tests, plus Joan began feeling better. Two years after her first DXA Joan went for her second scan.

Here are the results from Mary Ann and Joan’s second DXA exams:

Mary Ann:  L/S T-score:  -3.5

Joan:          L/S T-score:  -3.5

Neither of these scores indicate a statistically significant change from the -3.4 reading that each woman measured two years ago. For an observable change in bone density we would have to see a “least significant change” for this spine reading of at least a 5.4 % increase or decrease in Mary Ann and Joan’s T-scores (or at least a 0.05 g/cm2 for the “smallest detectible difference”). We would have needed to see an improvement to at least 

a  -3.0 to be sure of improved bone density and reduced fracture risk, or a loss to -3.8 to be sure of a reduction in bone mineral density and an increased risk of fracture. The T-score of -3.5 only tells us that if there was a change in fracture risk due to a density change; it is too small to make a determination one way or the other.

Mary Ann was distraught. Even though she understood scientifically that the -0.1 change was not significant, she still felt it as a defeat emotionally. To her, a 0.1 loss in her T-score was just that, a LOSS. 

Joan, on the other hand, saw that during the two years between her DXA exams the following things had changed:

·       NTX (a marker for osteoclast bone resorption ): dropped from 78 nmol to 51

·       hsCRP (a marker for inflammation): dropped from 2.1 to 1.4.

·       Vitamin D: increased from 28 to 42 (ensuring that she would absorb more calcium and have greater muscle strength)

·       Urine pH (measure of the acidity of urine): increased from 5.5 to 6.6 (this would help reduce urinary losses of calcium and lower osteoclast bone resorption)

·       Plus Joan felt better, her bowel movements improved, she no longer experienced abdominal bloating, the white spots on her fingernails disappeared (indicating improved absorption of minerals), and she felt stronger and more stable.

In short, Joan felt encouraged (as she should be) that she was going in the right direction and that her risk for fracture was less…even though her bone density T-score did not show an improvement.

Monitoring change is important and relying completely on DXA scans and bone mineral density to determine fracture risk is frustrating and inadequate. Bone mineral density changes VERY slowly AND we must not forget that it is NATURAL to lose bone density as we age (we just don’t want to loose it too rapidly). When laboratory biomarkers are used with this natural method to scientifically guide the patient and health care provider, then this approach can be highly effective.

Improving bone quality, gaining over-all health, and becoming stronger with more coordination and agility do amazing things for helping reduce fracture risk…even if bone mineral density does not change. My suggestion is to meet with your doctor and talk about how you can reduce your fracture risk by monitoring change.

Whatever your level of bone loss and whatever your age or current condition, the great thing is that there is something that can be done to help strengthen your bones. Research has come a long way in the past 10 years; today we know so much more about osteoporosis prevention and treatment. There are supplements, prescription drugs, dietary recommendations, exercise regiments and lifestyle modifications that can be evaluated. There are also a number of factors and tests that can be used as baseline measures for monitoring progress toward reducing your fracture risks. Thankfully, it is never too late to make a positive impact on your skeletal health. All it takes is a game plan and a good dose of tenacity.

(1)    In my book, The Whole-Body Approach to Osteoporosis, I provide a scientific rationale for this unique functions-based methodology to treat osteoporosis.   http://shop.osteonaturals.com/product/the-whole-body-approach-to-osteoporosis

(2)    Below is a partial list of factors and tests that are related to bone health and fracture risk.

Lifestyle Factors / Laboratory Tests	Impact on Bone Health and Fracture Risk
Weight	Under 127 pounds increases fracture risk
Body Mass Index (BMI)	A BMI of less than 18.5 increases fracture risk
Blood Pressure (BP)	High blood pressure is correlated to increased fracture risk
Pulse (resting heart is generally 60 to 80 beats per minute)	High pulse rate is indicative of inflammation and elevated sympathetic nervous system tone; both of which increase fracture risk.
Bone resorption markers (NTX, CTX, DPD)	A measure of collagen breakdown products from the resorption of bone by osteoclasts. These markers can indicate the rate of bone loss through blood and urine samples.
hsCRP  (High-sensitivity C-reactive Protein)	Measure of the level of inflammation which correlates to bone loss.  (Best if below 1.3mg/L)
Homocysteine (amino acid found in the blood)	Elevated homocysteine levels in the blood are correlated to inflammation and increased risk of heart disease and osteoporosis. It also causes collegen fibers to harden which makes bone more prone to breaking. (Best if kept below 8 micromoles per liter of blood)
Lipid peroxides  (index of oxidative stress)	Indirect measure of free radicals that promote bone loss.
8OH2dG   (index of oxidative stress)	Indirect measure of free radicals that promote bone loss.
Anti-tissue transglutaminase (tTG) and other gluten biomarkers such as AGA IgA and IgG	People sensitive to gluten in wheat, barley and rye often have increased bone loss.
AA to EPA ratio  [arachidonic acid (omega-6) (“bad” fats) to eicosapentaenoic acid (omega-3) (“good” fats) ratio]	Ideal ratio is less than 3 but not less than 1.5. If over 10, it is considered inflammatory.
Blood glucose  (blood sugar concentration)	Blood glucose that remains high over time can reduce bone quality and increase fracture risk.
A1C  (average level of blood sugar over 2-3 months)	Measure of glycemic control; the higher the level, the greater the development of advanced glycation end-products (AGES) which cause inflammation and make collagen fibers brittle, both of which increase fracture risk.
MPV   (Mean platelet volume) http://www.ncbi.nlm.nih.gov/pubmed/22684618	The higher the MPV the larger the platelet size and the greater the risk for inflammatory states. Elevated MPV is an early marker of platelet activation and heart disease.
TSH  (Thyroid stimulating hormone)	An underactive or overactive thyroid correlates to less than optimal bone health
Triglycerides  (type of fat found in the blood)	Elevated levels increase inflammation and is correlated with increased fat in the bone marrow which crowds out bone-building osteoblasts and promotes bone-resorbing osteoclast activity.
Mitochondrial function   (mitochondria are cell organelles that produce energy)	Functional tests that correlate to the body’s ability to produce energy; the more energy you have the healthier you will be.
DHEA  (hormone produced primarily in the adrenal glands – precursor to sex hormones)	Low DHEA concentration has been associated with low bone density in women.
Testosterone  (hormone primarily secreted in the testes of males and the ovaries of females)	Testosterone is known to decrease bone resorption and stimulate bone mineralization, so low levels could be cause for concern in both men and women.
Estrogen  (primary female sex hormone)	Estradiol, the primary estrogen in humans, aids in maintaining bone density. Postmenopausal levels below 10 to 12 pg/ml is cause for concern.
SHBG  (Sex hormone-binding globulin)	There is an inverse correlation between serum SHBG levels and bone mineral density in both males and females
Hypercalciuria (excessive urinary calcium excretion)	Loss of too much calcium is cause for concern.  Levels should be below 275 mg/day for women and 300 mg/day for men.
Vitamin D     (needed for calcium absorption and metabolism)	Ideally blood levels should be kept between 40 to 60 ng/ml. Levels below 32 ng/ml increase fracture risk.
Under-carboxylated osteocalcin	Measure of vitamin K functional capacity; elevated levels increase fracture risk.
Serum calcium (should be between 8.5 and 10.0 mg/dL)	Too much calcium in the blood (over 10 mg/dL) can indicate parathyroid disease. In most cases, this is from a benign tumor called an adenoma.
PTH  (parathyroid hormone) (should be below 50 pg/mL)	When the parathyroid glands release too much parathormone (most often, from an adenoma) osteoclast bone resorption is stimulated.
Red blood cell magnesium	Measure of magnesium levels; magnesium acts as an anti-inflammatory and is needed for bone formation by osteoblasts
Urine Ph  (measure of the acidity of urine)	An acidic body increases osteoclastic activity and causes more loss of calcium in the urine. Ideal value range of first morning urine pH is 6.6 – 7.2.
Eating Disorders www.nationaleatingdisorders.org/learn	An adequate supply of nutrients is required if you are to have healthy bones.
Thiazolidinediones  (common drugs for glucose control for type 2 diabetics)	These drugs promote bone loss.  An alternative to these medications is to control blood glucose through diet, lifestyle, exercise and supplementation.
PPIs  (Proton pump inhibitors - medications used for Gastroesophageal reflux disease (GERD) / heartburn.)	These drugs promote bone loss.  An alternative to these medications is to eliminate the need through better digestion and improved gastrointestinal health.
SSRIs  (serotonin-specific reuptake inhibitors - class of compounds typically used as antidepressants)	These drugs used for treating anxiety and depression have been linked to bone loss.
Cigarette smoking	Smoking reduces bone mass and increases fracture risk.
Inadequate exercise	Exercising regularly builds and strengthens bones. Weight-bearing exercises—where bones and muscles work against gravity—are best. These include aerobics, dancing, jogging, stair climbing, tennis, walking, and lifting weights. People who have osteoporosis may want to attempt gentle exercise, such as walking, rather than jogging or fast-paced aerobics, which increase the chance of falling. Exercising three to four times per week for 20-30 minutes each time helps.
Poor diet	A balanced diet rich in calcium, magnesium, vitamins D and K, and antioxidants reduces fracture risk.
Excess alcohol intake	Heavy drinking reduces bone mass. Limiting alcoholic drinks to no more than two per day reduces risks. An alcoholic drink is one-and-a-half ounces of hard liquor, 12 ounces of beer, or five ounces of wine.

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C-Reactive Protein: A Measure Of Oxidative Stress

Your body constantly reacts with oxygen as you breathe and your cells produce energy. As a consequence of this activity, highly reactive molecules are produced within our cells known as free radicals. If your body is unable to stop the spiraling free radical chain reaction (a molecule stealing an electron from another molecule, causing that molecule to steal an electron from another molecule, causing that molecule to steal an electron, etc...) this can cause oxidative damage to proteins, membranes and genes.

Bombardment of cells by free radicals.

When oxidation is excessive and the body is unable to neutralize high levels of free radicals with enough antioxidants, we refer to this as oxidative stress. The deeper the body goes into oxidative stress the more extensive will be the cellular damage that will then trigger an inflammatory response. Free radical damage, oxidative stress and systemic inflammation are all implicated in a number of chronic degenerative disease states and premature aging.

If oxidative stress continues for days, weeks or months, the body can go into a condition called chronic systemic low-grade inflammation. This type of inflammation can stimulate aggressive osteoclastic bone resorption and lead to osteoporosis.

Unfortunately, there is no one test that will tell us if a person has this type of inflammation. But there are tests for general inflammation and others for oxidative stress which, when reviewed in conjunction with the person's signs and symptoms, can give us a good indication of whether that individual has chronic systemic inflammation.

A recent paper by Park et al. in Clinical Endocrinolgy shows that C-reactive protein (CRP), a protein in the blood that rises in response to inflammation, is also a measurement of oxidative stress. The study involved 1821 nondiabetic postmenopausal women with elevated CRP (≤ 10 mg/l) levels. The researchers used an oxidized low-density lipoprotein, a known marker of oxidative stress, to compare with CRP. The authors concluded that CRP is strongly associated with oxidative stress.

Oxidative stress and its impacts can be alleviated with early detection. Having lab markers such as C-reactive protein to provide important clues to the causes of bone loss is of great benefit to a clinician designing a diet/nutrition therapeutic protocol for chronic disease conditions such as osteoporosis. 

Park, S. et al. 2013. Oxidative stress is associated with C-reactive protein in nondiabetic postmenopausal women, independent of obesity and insulin resistance. Clinical Endocrinology 79, 65-70.

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Jumping Power: A Better Test For Sarcopenia Than Muscle Strength

In a study from the Department of Health and Exercise Science at the University of Oklahoma, Singh et al. examined the relationship between jumping power, muscle strength and sarcopenia (the loss of muscle mass seen with aging and illness). Sarcopenia is often seen with osteoporosis and leads to weakness with an increased risk for falls and fractures.

This study is fascinating because it showed that individuals with

sarcopenia had significantly lower jumping power but not necessarily lower muscle strength when compared to individuals without sarcopenia. "Based on our findings, JPow [jumping power] may be useful for sarcopenia screening in the middle-aged and older adults; however, more research is needed to determine the utility of this method in clinical populations." [No...their method did not include having men and women 55 to 75 years of age jump over cows.]

Singh, H, et al. 2013. Jump test performance and sarcopenia status in men and women, 55 to 75 years of age. J Geriatr Phys Ther August 16. [Epub ahead of print]

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Magnesium--A Key Mineral in Human Metabolism

Magnesium (Mg) is one of the most important nutrients in your body. It is involved in cell energy

Magnesium's central position in the chlorophyll molecule

metabolism, muscle tone (including heart contractions), nerve conduction, cell membrane formation and maintenance, electrolyte balance, enzyme function, and in biological mechanisms that protect you from the damaging effects of inflammation and free-radicals. Magnesium is also absolutely vital for good bone health. It is used by osteoblasts to build new bone and it is necessary for the production of bone-regulating calcitonin and parathyroid hormones. Magnesium is also important for preventing calcium from depositing into soft tissues.

Unfortunately, magnesium deficiency is common, and more so in older adults. In fact, it has been estimated that up to 80 percent of elderly individuals are deficient in magnesium. Magnesium can be difficult to absorb and as we age reduced digestive capacity lowers absorption further. Stress and disease also contribute to increased magnesium demands.

Signs of magnesium deficiency can include muscle spasms, skin twitching below the eye, constipation, hypertension, rapid heart rate, arrhythmias, depression, fatigue, asthma, muscle weakness, irritability, and hypersensitive skin.

How can you know for sure if you have magnesium deficiency? The gold standard lab test for determining magnesium levels is to evaluate the levels in red blood cells. (Blood serum testing is not a good indicator for magnesium because most (99%) of this mineral is stored within cells and not in the extracellular fluids.) In addition, because deficient magnesium can affect many systems throughout the body, other lab results may alert the physician (or you) that a red blood cell analysis of magnesium is indicated. The following labs are the most helpful:

-  Low serum calcium.
-  Low serum potassium
-  Low active vitamin D or calcitriol [1,25(OH)2D]
-  Elevated parathyroid hormone (PTH)
-  Low osteocalcin
-  Elevated C-reactive protein (hs-CRP)

It pays to ensure that you get adequate magnesium before signs of deficiency occur. Your best sources of dietary magnesium are found in whole grains, seeds, nuts, and especially in green vegetables (Notice the central position of the magnesium ion in the chlorophyll molecule in the picture...chlorophyll is what gives plants their green color and the ability to absorb energy from light.) But magnesium supplementation (300 to 600 mg/day), especially if you have bone loss, is usually a good idea. I've always touted the virtues of high-end magnesium sources such as what I use in our OsteoNaturals products. OsteoSustain is formulated with Albion's TRAACS magnesium glycinate chelate and our OsteoMineralBoost has dimagnesium malate. Both of these forms of magnesium are known for their superior absorbability and effectiveness.

I have always complained about vitamin-mineral products that used magnesium oxide and felt that they were inferior. Well...not so fast...I may have to eat my words. Research by Shechter et al. recently demonstrated that supplemental magnesium oxide was actually superior to magnesium citrate for increasing intracellular magnesium levels. Magnesium oxide also appeared to be more effective in reducing hs-CRP. This is pretty impressive so, even though there are some limitations* to this study, I will go a bit easier on magnesium oxide from now on. I'm not thoroughly convinced, but at least I will not object so vehemently.

     * My concerns about this study:  The author's choice to use x-ray dispersion analysis
      for measuring intracellular magnesium is not your standard testing method. In my
      opinion, it would have been better to have included the tried-and-true red blood cel
      l analysis in the study for comparison. Secondly, one of the authors of the study is
      the Research Director and President of IntraCellular Diagnostics, Inc., the company
      that uses this form of magnesium testing commercially. And finally, the researchers
      used two different dosages of magnesium products for their comparison: Diasporal
      (magnesium citrate) has 295.8 mg of elemental magnesium while Magnox
      (magnesium oxide) has 520 mg of elemental magnesium. This is a huge discrepancy
      and one that may indeed invalidate the study.

Shechter M. et al. 2012. Comparison of magnesium status using X-ray dispersion analysis following magnesium oxide and magnesium citrate treatment of healthy subjects. Magnesium Research 25(1):28-39.   

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