Monday, October 28, 2013

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.

Monday, October 21, 2013

Calcium Supplements and Cardiovascular Risk

As many of you know, I attended this year's Annual Meeting of the American Society for Bone and Mineral Research in Baltimore (October 4 - 7). While there, I sat in on some fascinating presentations on bone and muscle research--two of them, I thought may be of particularly interesting to you. 

In 2008, a study by Bolland et al. reported a possible association between calcium supplementation and cardiovascular risk. According to Bolland et al. in a 2010 follow-up study, "Calcium supplements (without coadministered vitamin D) are associated with an increased risk of myocardial infarction" The authors further concluded "A reassessment of the role of calcium supplements in the management of osteoporosis is warranted."

Since Bolland's two studies hit the press in 2008 and 2010, there has been considerable controversy over the safety of calcium supplementation as it relates to cardiovascular health. As a result, many people with osteoporosis have, unfortunately, reduced their calcium intake to sub-optimal levels. The two research presentations in Baltimore helped explain our current understanding of this important subject.

The first presentation was by Dr. Douglas Bauer, MD, from the University of California, San Francisco. Dr. Bauer's study assessed calcium intake and the incidence of death in 5967 men over the age of 65 years. The participant's dietary intake of calcium was 1142 ± 590 mg/day, and 65% used calcium supplements. The participants were followed over a 10-year period and 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 rate of death from heart 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." 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."

In the second presentation, Dr. Joshua Lewis, MD, PhD, from the University of Western Australia, Perth, reported on his analysis of 19 randomized controlled trials that studied women over the age of 50 who took calcium supplements. The study 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."  

I hope that the results of these new studies help reduce fears over calcium supplementation. Although these studies conclude that calcium supplementation, even without vitamin D, is not harmful, I still encourage you to maintain optimal vitamin D levels as well as an adequate intake of vitamin K, magnesium, and trace minerals. Vitamins and minerals work synergistically, and to flood the body with calcium without important utilizing factors has the potential to cause metabolic imbalance. So please, I hope you will all continue to take your calcium!

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 Feb 2;336(7638):262-6.

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.

Bauer D., S. Harrison, P. Cawthon, et al. 2013. Dietary and supplemental calcium intake and the risk of mortality in older men: the MrOS Study. 35th Annual Meeting of the ASBMR. Abstracts, 1001, pS1.

Lewis J., L. Rejnmark, K. Ivey, et al. 2013. The cardiovascular safety of calcium supplements with or without vitamin D in elderly women: A collaborative meta-analysis of published and unpublished trial level evidence from randomized controlled trials. 35th Annual Meeting of the ASBMR. Abstracts, 1002, p S1. 

Wednesday, October 16, 2013

Radio Show: Osteoporosis: Silent, Searing and Bone Breaking

Aches and Gains with Dr. Paul Christo will feature the following shows this Saturday on Sirius XM Radio- Family Talk 131 ( from 8-9 am Eastern time. Podcasts accessible after the shows air on

Follow Dr. Christo on Twitter or Facebook  for more information on cutting edge pain treatments, and success stories from those who have found relief.

Osteoporosis: Silent, Searing and Bone Breaking
Air Date October 19, 2013,
8:00 am EST

Osteoporosis occurs when the creation of new bone isn’t able to keep up with the removal of old bone.  Bones then become weak, brittle, and painful — so brittle that a fall or even mild stresses like bending over or coughing can cause what is known as a “fragility fracture.”  Our guest is Dr. Keith McCormick. He’s the author of The Whole-Body Approach to Osteoporosis and shares his experience as both a patient who overcame 12 fragility fractures, and an osteoporosis expert who’s developed a nutrition based prevention and treatment program.  

Tuesday, October 8, 2013

ASBMR Annual Meeting

I just returned from the Annual Meeting of the American Society for Bone and Mineral Research (ASBMR) held in Baltimore, MD. While there, I had the opportunity to meet lots of great researchers and doctors who specialize in osteoporosis plus sit in on lectures--all of which were absolutely packed with the latest discoveries in osteoporosis research and therapy.

On my first day in Baltimore I attended a course on densitometry and the diagnosis and management of osteoporosis that was sponsored by the International Society for Clinical Densitometry. I had attended one of their courses about 10 years ago but decided to take it again as a refresher. Although helpful, it also sadly reminded me that bone density testing is not as accurate as one might think.

The next day was all about the interconnectedness of muscle and bone. The ASBMR sponsored a full day symposium entitled Cutting Edge Discoveries in Muscle Biology, Disease and Therapeutics. I was absolutely riveted by some of the lectures. We saw video footage of muscle stem cells (called satellite cells), heard about new discoveries in mitochondrial bioenergetics and why this is so important to bone health, learned about myokines (muscle signaling molecules) that "talk" to bone, and honed in on the connection between sarcopenia (muscle wasting) and bone loss.

The next three days were spent at the ASBMR Annual Meeting proper. Not only did I get to listen, 8 to 5, to fascinating lectures but also viewed hundreds of posters and spoke with many of the lead researchers in these projects. I was absolutely blown away to hear things like:

- Vitamin D is not only important for ensuring gut absorption of calcium, enhancing immunological function, and promoting muscle strength through its direct action on bone--but vitamin D also improves neuromusclular function through its effects on the brain's central nervous system.

- There is a huge problem in our current ability to assess patient's vitamin D levels. Not only are assays commonly off by 15 to 20% (or more), but there is no industry standardization in the assessment or reporting of vitamin D levels. Also, for anyone taking vitamin D2, there is a huge variability of ingested vitamin D2 recovery. This means that any immunoassay testing (rather than HPLC/Tandem MS testing) of these patient's vitamin D levels will yield totally innacurate, and therefore useless, results.

- Bone mineral density examinations (DXAs) are absolutely fraught with potential errors not only by the technician performing the scan but also by the radiologist doing the reading and evaluation. It can be very helpful to know a scanning facility's "precision error" and also the date that it was last measured. The only way to determine "least significant change" (LSC) (the amount of change in bone density that is necessary to know that the change in density from one scan to the next is real) is by knowing a facility's precision error assessment. The bottom line is that you can't take DXA T scores at face value. You need to have the report evaluated by someone familiar with all the possible pitfalls in bone density measuring and reporting.

It was a very fruitful five days!

Wednesday, September 18, 2013

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)

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.

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.

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, 6th 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.

(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
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)
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
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.

Sunday, September 1, 2013

The Future: Targeting Bone-Cracks With Drug-Carrying Nanoparticles

Take a look at the future for osteoporosis drug therapy.

Research into drug delivery systems is hot, especially in the arena of nanotechnology. In a series of studies based at Penn State University and Boston University, researchers used self-powered nanoparticles to deliver medication (alendronate) right to the doorsteps of bone cracks themselves.

Molecules moving inside a nanotube
Interestingly, when microfractures occur in bone there forms a very small electric field. This small change in ionic gradient is all it takes for introduced negatively charged nanoparticles to migrate to the crack. When medication is attached to these particles, it can be delivered to the site where it can make the most the microfractures. When it comes to osteoporosis medications, this may help improve effectiveness and reduce adverse effects (by requiring less medication).

According to Yadav et al. in a paper published in Angewandte Chemie, "Bone cracks are detected by utilizing the damaged matrix itself as both the trigger and the fuel. A crack in a material with a high mineral content like bone generates ion gradients, which can be utilized for active targeting and treatment."

Yadav, V. et al. 2013. Bone-crack detection, targeting, and repair using ion gradients. Angewandte Chemie doi:10.1002/anle.201305759.

Thursday, August 29, 2013

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.

Wednesday, August 28, 2013

Mass Appeal Segment on Osteoporosis With Ashley Kohl

I had a great time today as a guest on Channel 22's (WWLP) Mass Appeal TV show in Springfield, MA. Ashley Kohl was the host and we talked about the importance of recognizing patient biochemical individuality when assessing the causes of osteoporosis and determining treatment protocol. Ashley was a phenomenal kind and gracious and professional. Actually, the whole staff at Mass Appeal was great. I was a bit nervous but everyone was so supportive that it made it a lot easier being in front of the cameras. Here's the link if you want to watch.  

Friday, August 23, 2013

Strontium: Does It Actually Build Bone Mass Or Just Look Like It?

There has been considerable debate over the benefits of strontium for treating osteoporosis. Prior research indicates strontium ranelate both increases bone mineral density and reduces fractures of the spine (but not the hip) by up to 40%. Although the benefits of strontium look promising, it has been difficult to determine how much of strontium's effect on bone density is from a real increase in bone mass and how much of it is simply artifact. The strontium atom is almost twice as heavy as calcium (38 vs 20 on the atomic chart) and when strontium enters bone tissue it creates more impedance to x-rays. On subsequent bone density (DXA) examinations, this creates the illusion of a higher than actual improvement in bone density.

In a recently accepted article for publication in the Journal of Bone and Mineral Research,
Chavassieux et al. compared the effects of strontium ranelate and alendronate (a bisphosphonate) on bone. Strontium is often considered to have both an antiresorptive effect by reducing osteoclast cell activity plus an anabolic effect by stimulating osteoblasts to form bone. Alendronate, on the other hand, is only antiresorptive in its therapeutic effect.

The study included 387 postmenopausal women with osteoporosis. Bone biopsies (transiliac) were performed at baseline and then again after 6 or 12 months to determine the effects of these two medications. The results indicated that although bone formation remained higher and there was overall less of a decrease in bone remodeling with strontium compared with alendronate, the strontium did not show significant anabolic (bone building) action.

Chavassieux, P., et al. 2013. Bone histomorphometry of transiliac paired bone biopsies after 6 or 12 months of treatment with oral strontium ranelate in 387 osteoporotic women. Randomized comparison to alendronate. Journal of Bone and Mineral Research doi: 10.1002/jbmr.2074.

Thursday, August 22, 2013

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]

Sunday, August 18, 2013

Alpha-Lipoic Acid Increases Bone Mineral Density--Protects Against Bone Loss

Alpha-lipoic acid (thioctic acid) is a powerful antioxidant and free-radical scavenger. It is also an essential cofactor for mitochondrial enzymes that stimulate energy production. Unlike other antioxidants that act only in water (such as vitamin C) or fat (vitamin E), alpha-lipoic acid can access all areas of the body...even the fatty contents of your bone marrow. This is important because it is within your marrow that cellular "coupled" activity determines the health and density of your bones. Alpha-lipoic acid can help maintain balance between the osteoclasts that tear down bone and the osteoblasts that form bone.

The following are some of the powerful benefits related to bone health that we have seen with alpha-lipoic acid:     

-  Protects against oxidative stress which is part of the inflammatory process that
    drives bone loss.
-  Reduces the proinflammatory cytokines (Il-1, Il-6, TNF-alpha) that stimulate
    osteoclast activity.
-  Lowers NF-kB, the protein that commands a cell's nucleus to turn on
    inflammatory-inducing genes.
-  Reduces RANKL, the signaling molecule that activates osteoclasts.
-  Activates the enzyme AMPK (a negative regulator of RANKL) in osteoclasts.
-  Inhibits the production of advanced glycation end-products (AGEs) seen with
    elevated glucose levels. AGEs make bone stiff and vulnerable to breaking.
-  Chelator of heavy metals that can cause bone loss.
-  Suppresses osteoclast formation.
-  Inhibits excess bone resorption.

recent study conducted by Beyzagul, et al. out of Turkey used rats to assess the effect of alpha-
lipoic acid on bone metabolism. The researchers concluded that alpha-lipoic acid "had a protective effect on both senile [inflammation induced] and postmenopausal osteoporosis" and that it "may be a candidate for radical osteoporosis treatment." This is one more study that we can add to the volumes of research before it showing the benefits of alpha-lipoic acid for bone health.

Dietary sources of alpha-lipoic acid are minimal and endogenous (within the body) production, especially during times of stress or disease, is insufficient for controlling oxidative stress and promoting optimal energy production. This is why supplemental alpha-lipoic acid can be so beneficial and it is why we at OsteoNaturals include alpha-lipoic acid as a primary ingredient (300 mg) in our OsteoStim. Yes, as the authors of this study write, alpha-lipoic acid can be a "radical osteoporosis treatment"...but then, we've always known that OsteoNaturals formulas are way ahead of the curve.

Beyzagul P. et al. 2013. The effect of alpha-lipoc acid in ovariectomy and inflammation-mediated osteoporosis on the skeletal status of rat bone. Eur J Pharmacol doi: 10.1016/j.ejphar.2013.07.033. [Epub ahead of print]

Wednesday, August 14, 2013

Wakefield Marathon

As many of you may know by now, my race to qualify for the Boston Marathon went fairly well...considering I wasn't in the best of shape. The marathon was in Wakefield, MA--the Around the Lake Marathon. I finished in 3:37, just under the 3:40 Boston qualifying time for my age (59). It was a fun race...(if you consider running 26.2 miles fun)...but I sure was stiff and sore for a few days afterwards.

I just thought I would show everyone the absolutely GORGEOUS rainbow that came out to add brilliance to the course. This may be the brightest rainbow I've ever seen...and a double one at that!

Sunday, August 11, 2013

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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