Thursday, August 30, 2012

Exercise: Bone Density

There is a lot of emphasis on the importance of exercise for bone health. Doctors tell us to exercise because it will build up our bone density, there are instructive videos on YouTube about how to build bone density, and it is fairly easy to find exercise classes designed for people with osteoporosis; but does exercise really do anything positive for our bones? Can you really stimulate bone formation through exercise?

Considerable research has been devoted to this subject. The general consensus being that exercise, most importantly weight-bearing exercise, is what is best for bone health. Weight-bearing exercise not only increases muscle strength and coordination but it also sends messages, via mechanical strain, to bone cells. When bone cells receive activating signals they take action and fortify bone with new matrix and mineral deposits making them stronger. But there are limits to this process.

Every week patients tell me they are exercising and that this will help them build up their bone density. Trying not to sound negative, I explain that they shouldn't be discouraged if their next bone density scan (DXA) fails to show improvement as a result of their exercise program. I further explain that this does not mean their exercises are not therapeutic.

The time in your life to build bone density through exercise is when you are young. As you age, the ability of your bone cells to react to mechanical strain is less robust. What is important, I explain to my patients, is that you exercise for increased strength, coordination, improved cardiovascular health, reduced systemic inflammation and (for me at least) happiness. These are the important benefits of exercise and should be your intended goals. There are important reasons to exercise as you age but improving bone density should only be seen as a "possible additional benefit." To believe that exercise will improve your bone density, may lead to unnecessary disappointment.

recent study reported in the Journal of Bone and Mineral Research (Deere et al., 2012) was designed to test the response in bone density accrual in the hips of adolescents to various levels of mechanical strain (physical activity). The authors concluded that physical activity "associated with impacts [greater than] 4.2g, such as jumping and running (which further studies suggested requires speeds [greater than] 10 km/h) is positively related to hip BMD [bone mineral density]." On the other hand, "moderate impact activity (e.g., jogging) is of little benefit." "Hence, [physical activity] may only strengthen lower limb bones in adolescents, and possibly adults, if this comprises high-impact activity."

So I encourage you to exercise.* It is extremely important for your health. It will make you stronger, more supple, and less prone to falling which is the number one cause of hip fractures. Exercise, if done properly, will reduce your risk of breaking a bone. But do it for the right reasons. Do it because you know what the real benefits of physical activity are: joy, happiness, strength, coordination, flexibility, cardiovascular health, reduced inflammation, etc...etc... Do it for these reasons and you won't be disappointed. 

* Consult with your doctor first before beginning any new exercise program. And, I do NOT recommend jumping over cows! This would put anyone with osteoporosis (or for that matter anyone without osteoporosis) at great risk for fracture. At least this isn't a bull!


Deere K et al., 2012. Habitual levels of high, but not moderate or low, impact activity are positively related to hip BMD and geometry: results from a population-based study of adolescents. J Bone Min Res 27(9):1887-1895.

Wednesday, August 29, 2012

Homoarginine Improves BMD

Protein, and the amino acids from which they are built, are important for maintaining muscle mass. Just look at all the buff athletes chugging down whey protein shakes at your local gym. But what about protein for bone health? A debate rages over just how much dietary protein is enough and how much is so much that it becomes detrimental to bones? This is a common question my patients often ask.

Research shows that diets high in protein from red meat and dairy, contributes to a heavy acid load, a condition ripe for excessive bone resorption. Reducing protein intake, especially from these sources, is wise. But a problem arises when people become fearful of protein. A diet low in quality protein is devoid of important amino acid building blocks necessary for muscle and bone formation.

Of the most common 20 amino acids found in dietary protein, 10 of them are termed "essential." These essential amino acids must be obtained from food because your body is unable to manufacture them.  L-lysine is an essential amino acid and important for bone health. It is also commonly deficient, especially in the vegetarian diet.

Lysine aids in the absorption of calcium and it is a necessary component of bone collagen cross-linkage formation. Lysine is also necessary for the formation of another amino acid, homoarginine.

The amino acid homoarginine (an analog [similar] to L-arginine) is synthesized mainly in the kidneys. For years, scientists have known that homoarginine is important for nitric oxide production and energy metabolism making it extremely important for vascular health and heart function (low levels of homoarginine are associated with a high incidence of sudden cardiac death) but new research shows that homoarginine is also important for skeletal health.

In a recent paper published in Osteoporosis International, researchers (Pilz et al., 2012) found homoarginine deficiency to be associated with high bone turnover and low bone mineral density (BMD). A key enzyme (L-arginine:glycine amidinotransferace or AGAT) is necessary for the conversion of lysine to homoarginine in the kidneys and if any of these players are missing (i.e. lysine, enzyme, or kidney function), blood levels of homoarginine will drop.

Lysine rich foods are red meat, pork, poultry, fish, eggs, and cheeses. All common in the American diet but, unfortunately, acid forming. Because of this, vegetarians as well as those individuals wishing to avoid excess acid forming proteins, often become deficient in lysine and therefore unable to manufacture adequate amounts of homoarginine. Strict vegetarians can obtain their lysine from legumes such as soy, beans, peas, lentils, and peanuts. Quinoa is also fairly high in lysine. For individuals not on a vegetarian diet, but trying to maintain a more neutral body pH conducive for healthy bone remodeling activity, you need to remember that not all acidic foods are bad. Protein is important for the construction of bone. Wild-caught sea food, naturally raised poultry, and grass-fed beef are good sources of quality animal protein as well as lysine. In addition, supplementing with Osteo-pHBalance (an alkalinizing formula with potassium), is packed with spirulina and chlorella, which are both good sources of lysine.

Pilz S., A. Meinitzer, A. Tomaschitz, et al. 2012 Associations of homoarginine with bone metabolism and density, muscle strength and mortality: cross-sectional and prospective data from 506 female nursing home patients. Osteoporosis Int 10.1007/s00198-012-1950-9.




Saturday, August 25, 2012

Dried Plums: Osteoporosis

In my book, The Whole-Body Approach to Osteoporosis, I tout the benefits of dried plums for bone health. I was first introduced to the benefits of dried plums 11 years ago at the Twenty-Third Annual Meeting of the American Society for Bone and Mineral Research held in Phoenix. This 5 day seminar (held in different places around the globe each year) is where doctors and researchers go to "bone-up" on all the latest research about osteoporosis. Being especially interested in any research about bone health and nutrition, I was constantly on the look out for posters (small displays at conferences that presenters use to show their current research) and lectures about nutrition. If you have ever been to a major medical conference, you know what I'm talking about when I say you can always tell which research topics are "hot" and which ones are...well....not. If a poster doesn't have that much to offer in the way of new information/new research, it can get pretty lonely for the presenter. Just about everyone walks right by. It's pretty easy to rate the  "hotness factor" of a poster. If no one stops to even take a peek...well, it's pretty dull. One day, as I was walking around the poster hall looking at the hundreds of posters being presented, I saw this man standing, very lonely, by his poster. I had walked by him a few times earlier that morning but I was either engaged in talking with another researcher or heading off to a fascinating lecture on RANKL, OPG, JAK/STAT5 or some other bone-related subject (most everything at these seminars is about something so complex that it has a really long name so they have to use abbreviations). I remember noticing, as I would pass by, that no one...absolutely no one...was ever talking to him...or even, for that matter, looking at his poster.

Back then, in 2001, dried plums were more commonly referred to as prunes. My mom loved prunes...and that is what I connected prunes with, getting older and having internal plumbing problems. In those days, prunes were only of interest when, and only when, gastrointestinal purging was needed. In recent years however, the plum growers of America have gone to great lengths to distance their shriveled product from this association and re-brand them as promoters of health and as ultra-combatants of disease. It wasn't until the third time walking by the poster with the lonely man, that I glanced over at his poster. It read: PLUMB. Hmmm, with all the acronyms for complex bone signaling molecules and the like being thrown around at this seminar, my first thought was of a newly discovered molecule. What fancy bone-signaling molecule might the acronym, PLUMB, stand for?

The smile on his face as I approached was more like that of a lost puppy being found than that of a medical researcher. Poster M425," Dried Plums Improve Indices of Bone Formation in Postmenopausal Women." REALLY I asked?! And for the next half hour (Un-interupted....No, no one else was interested. Mind you now, there were about 2,000 attendees at this seminar.), I had the pleasure of talking with this brilliant professor from Oklahoma State University about "dried plums" and their amazing effect on the bones of postmenopausal women. Wow! I was totally blown away by his research. This was pretty hot stuff and no one seemed interested! For sure, nutrition for bone health was just not a hot topic.

Since those early days of research on dried plums, there have been plenty of supporting papers to substantiate their health benefits, especially for osteoporosis. Dried plums ARE good for bone health. In fact, dried plums are great for bone health. I think I have actually become the dried plum industry's most fervent purchaser over the years. Try them! Just put a dozen or so (organic only) into a bowl, pour some water over them, and by the next morning they will be delicate, tasty, morsels of healthy goodness. And make sure to drink the juice when you finish eating the prunes. There has been so much interest lately on the benefits of prunes that there are now supplement companies selling products with dried plum extract. This is good...and bad...  Let me explain.

My concern about using dried plum extract for bone health is that its use may cause the consumer to substitute extract for the whole dried fruit. They are not the same. Dried plum extract consists mostly of polyphenolic compounds. Polyphenols are phytochemicals with antioxidant activity that are found not only in dried plums but also in other fruits and in vegetables. Blackberries, blueberries, grapes, melons, pears, broccoli, kale, etc...etc...(all the things you should be eating for bone health) have high levels of polyphenols.

But dried plums, like other fruits and vegetables, are way more than just polyphenols, and their positive effects go beyond improving bone health. Dried plums are linked to the improvement in vascular health, to reduced blood lipids and lowering of blood pressure. They help with anxiety and depression, and even have anti-cancer activity. But it is the WHOLE dried fruit that needs to be consumed for all these benefits...not just the extract.  In addition to the polyphenols, dried plums are rich in vitamins (A, B, and K), minerals (potassium, calcium, magnesium, zinc, copper, manganese, selenium, boron...), and fiber. They also contain antioxidant compounds other than polyphenols, and in fact, only 23% of the total antioxidant activity of dried plums is attributed to their polyphenols (Madaru et al. 2010). The benefits of dried plums, therefore, should be received from the WHOLE package...the whole dried plum. This is where you will receive the most benefit from the spectacular bone-mega-helper-signaling molecule, PLUMB.  

If you are interested in reading more about the benefits of dried plums, check out the review article by Qaiser Jabeen and Naveed Asiam in the Journal of Medicinal Plants Research (2011).

Thursday, August 23, 2012

DJD and BMD

Degenerative joint disease (DJD) of the lumber spine (in addition to compression fractures, scoliosis, and aortic calcification) often leads to misinterpretation of bone density (DXA) scans and the under-diagnosis of osteoporosis. In a study published in Osteoporosis International (Tenne et al., 2012), researchers reported: "Clinical use of spinal BMD [bone mineral density] measurements become increasingly problematic with age, and in fact difficulties in accurately assessing spinal BMD may already be apparent soon after menopause. Consequently, recommendations suggest that the hip is a more reliable site for BMD measurement particularly because while rate of bone loss in the spine and distal radius appears to cease in the elderly, this does not apply to the hip where continuous bone loss is seen with advancing age."

"In the most recent recommendations from the International Society for Clinical Densitometry (ISCD), it is recommended that all vertebrae (L1-L4) are included in the average values used for diagnosis compared to the previously most used L-2-4. Furthermore, it is also suggested that a vertebra that is not possible to evaluate because of local structural changes or a more than 1.0 T-score difference compared to adjacent vertebrae, should be excluded." But even with these recommendations "falsely elevated spinal BMD with advancing age is an important reason for underdiagnosis and insufficient initiation of osteoporosis medication, and it also allows for misinterpretation of drug effects during monitoring of therapy."

Results from this study indicate that "by choosing the more superior vertebrae for BMD measurements, a large proportion of degenerative changes potentially distorting the diagnostic score would be excluded." By measuring the density of  L1-L2 instead of L1-L4, the study found 20% more cases of osteoporosis (29% more at 10-year follow-up) and 37% more when subjects without degenerative changes were measured. The authors argue that these findings are clinically important especially in patients "around the age of 75 since it has been suggested that in the elderly, the hip should be used to diagnose osteoporosis by BMD measurement." According to the researchers, because the rate of bone loss in the hip is less than that in the spine, using the hip as the focus for diagnosing osteoporosis in the elderly does not compensate for those missed (osteoporosis) diagnoses using the standard spine BMD (L2-L4). The authors argue that it is of more value to use the L1-L2 measurement (in conjunction with an estimation of degenerative manifestations) for identifying patients in need of therapy. "Since fractures seconday to osteoporosis are an extensive source of human suffering and cost to society, early diagnosis is essential for preventive treatment and relief on an increasingly burdened health care due to an ageing population."

A surprising finding from this study was that "in women without apparent degenerative changes, spinal bone mass appears to remain stable from age 75 to 85 years" and "the absence of bone loss is not explained by pharmacotherapy." I thought this particulary encouraging.

Tenne, M., F. McGuigan, J. Besjakov, et al. 2012. Degenerative changes at the lumbar spine--implications for bone mineral density measurement in elderly women. Osteoporosis Int 10.1007/s00198-012-2048-0.

Monday, August 20, 2012

Olive Oil and Bone Health

For the past several days my patients have been asking about a recent study (published in the Journal of Clinical Endocrinology & Metabolism) that explored the effects of olive oil on bone health. Dr. Fernandez-Real, MD of the Hospital of Girona in Spain, and colleagues, compared the bone-promoting effects of a low-fat (i.e. low-inflammatory) Mediterranean diet enriched with olive oil to that of two similar low fat diets, one which included nuts and the other with fat obtained from animal and vegetable sources. The study looked at the effects of these three diets on the blood levels of osteocalcin and P1NP (two laboratory biomarkers indicative of bone-building activity) in elderly men at high cardiovascular risk.

The authors concluded that "consumption of a Mediterranean diet enriched with virgin olive oil for 2 years is associated with increased serum osteocalcin and P1NP concentrations, suggesting protective effects on bone." (The other two diets did not have the same positive results.) The message to take from this study is that the anti-inflammatory effects of olive oil can have a profound impact on bone health. Olive oil is rich in the phytonutrient oleocanthal which helps to reduce inflammation. It is also a good source of the powerful antioxidant, vitamin E. Finally, because olive oil is high in monounsaturated fat, which does not readily oxidize (oxidation is one cause of inflammation) it is considered to have anti-inflammatory effects. The less oxidation of fats, the less inflammation in the body. The less inflammation, the healthier the bones.

So yes, include olive oil in your diet.

Fernandez-Real J.M., et al. 2012. A Mediterranean diet enriched with olive oil is associated with higher serum total osteocalcin levels in elderly men at high cardiovascular risk. Journal of Clinical Endocrinolgy & Metabolism. doi:10.1210/jc.2012-2221.


Saturday, August 18, 2012

Homocysteine: Fracture Risk

In my book, I write about the use of therapeutic targets to help guide health care providers in their design and optimization of nutritional support for individuals with bone loss. By identifying "targets" such as abnormal lab results, or persistent abnormal physical signs or symptoms to improve upon (instead of just recommending a nutritional regimen and hoping for the best), providers can more effectively apply therapy for improving bone health and reducing fracture risk. Two laboratory tests for inflammation that I commonly use for this purpose are C-reactive protein and homocysteine. In this month's issue of Bone, (Yang et al., 2012) report on their meta-analysis and systematic review that was designed to help clarify the association between blood plasma levels of homocysteine (a sulfur amino acid) and fractures.

When homocysteine increases to abnormal levels in the blood, this is a sign of chronic systemic inflammation and nutrient deficiency. These elevated homocysteine levels can result in an accumulation of the amino acid in bone which adversely affects normal collagen formation and bone strength. Normally, homocysteine is converted to methionine and cysteine in processes that require folic acid, B12, and pyridoxal-5'-phosphate (active B6). But if these nutrients are deficient (or if an individual has a genetic-related difficulty in converting vitamin B6 into its active form, pyridoxal-5'-phosphate), blood levels rise and homocysteine deposits into the bone.

The authors of this study concluded that their findings "provided strong evidence that homocysteine was associated with an increased future risk of incident fracture" and that the "risk appeared more pronounced in men."

Yang, J., et al. (2012) Homocysteine level and risk of fracture: A meta-analysis and systemic review. Bone 51(3):376-382.

Thursday, August 16, 2012

Odanacatib

It appears there may soon be a new medication available for the treatment of osteoporosis. In the most recent issue of the Journal of Bone and Mineral Research, two articles (Masarachia, P.J., et al. 2012 and Cusick T., et al. 2012) from researchers at Merck Research Laboratories report on the new antiresorptive compound odanacatib. The studies confirmed that this inhibitor of cathepsin K (an enzyme released by osteoclasts that breaks down bone) not only inhibits bone resorption but increases bone mass. What is truly interesting about these reports is that odanacatib increased bone mass in the outer cortex of bone because, unlike bisphosphonates, it does not harm the bone resorbing osteoclasts.

By simply inhibiting production of the bone resorbing enzyme cathepsin K by osteoclasts (instead of destroying these cells like the bisphosphonates), odanacatib may indeed be a step in the right direction for a safer and more effective medication for osteoporosis. The jury is, of course, still out but odanacatib does show promise. Unfortunately, it wasn't until many years after bisphosphonates came to market that the severity of their adverse effects were realized. Now with osteonecrosis of the jaw, atrial fibrilation, and increased brittleness of bones from long-term use of bisphosphonates becoming Merck's nightmare, who is to say what odanacatib might bring? But for the time being, I'm being positive and hopeful that this new medication will be of benefit to severely osteoporotic individuals.

The major simulators of cathepsin K release by the osteoclasts are proinflammatory cytokines. When the body is in a chronically inflamed state (a major contributor to osteoporosis), these cytokines cause all sorts of symptoms. (I explain this whole cytokine connection to disease and dysfunction in my book.) The great thing about antioxidants such as lipoic acid, N-acetyl cysteine, milk thistle, etc. that are found in OsteoNaturals' OsteoStim is that these help neutralize proinflammatory cytokine production all through-out the body, not just in the bone marrow. This is a much more sensible approach for reducing excessive cathepsin K production, and for improving bone health in the long run.

Odanacatib is currently in pre-marketing or phase 3 trials. Time will only tell if it is successful in improving the lives of osteoporosis sufferers or, over time, only lead to more problems.

Masarachia P.J., et al. 2012. Odanacatib reduces bone turnover and increases bone mass in the lumbar spine of skeletally mature ovariectomized rhesus monkeys. Journal of Bone and Mineral Research 27(3):509-523.

Cusick T., et al. 2012. Odanacatib treatment increases hip bone mass and cortical thickness by preserving endocortical bone formation and stimulating periosteal bone formation in the ovariectomized adult rhesus monkey. Journal of Bone and Mineral Research 27(3):524-537.

Wednesday, August 15, 2012

Mean Platelet Volume

Chronic systemic inflammation sets the stage for disease. It is also the common unifying link between osteoporosis and cardiovascular disease. In my book The Whole-Body Approach to Osteoporosis, I explain how biomarkers of inflammation such as homocysteine, hsCRP, 8OH2DG, and lipid peroxides can be used as therapeutic targets in the nutritional management of bone loss.

Now there may be another inflammatory marker linked to osteoporosis and it's called mean platelet volume or MPV. Platelets are small cell fragments that circulate in your blood and are involved in the formation of blood clots. It's important to know how many platelets you have, and also their size. When your doctor orders a CBC to evaluate your blood, one of the indices is the MPV. Your doctor is always interested in MPV because it's an early inflammatory marker for platelet activation and seen a contributor to coronary heart disease.

In addition to contributing to the formation of blood clots, platelets also contain growth factors. We know, for example, that platelets produce growth factors that stimulate the development and activation of bone cells. Platelets are therefore very important for bone remodeling and for maintaining a healthy skeleton. But there is more. In a recent study from China (Yue-song, L., 2012), researchers found that platelets may have even more importance to bone health. The study evaluated 410 subjects and found a negative correlation between MPV and bone mineral density (BMD). In other words, the higher your MPV the lower your BMD. This makes sense since MPV is a marker of inflammation. The results of this study not only provide additional evidence that chronic inflammation is a common mechanism in the development of osteoporosis and heart disease, but it may also point to another marker to target in the therapeutic management of bone loss.

Yue-song Li, et al. 2012. Mean platelet volume is negatively associated with bone mineral density in postmenopausal women. Journal of Bone and Mineral Metabolism DOI:10.107/s00774-012-0362-4.

Monday, August 13, 2012

Formononetin, Red Clover

Red clover and soy are rich sources of isoflavones. They have been used extensively to treat symptoms of menopause and reduce bone loss in women with osteoporosis because of their estrogen-like effects. In a recent paper published in Menopause (Tyagi, A.M., et al., 2012) the isoflavone, formononetin, (found in high amounts in red clover and soy) was found to have "a substantial anabolic effect [on bone], thus raising the possibility of its use in postmenopausal osteoporosis." This study demonstrated that formononetin "significantly restored the lost trabecular microarchitecture in the femurs and tibia of osteopenic Ovx [ovariectomized] rats and promoted new bone formation."

Although the use of phytoestrogens to treat women with osteoporosis appears promising, caution should always be used when taking any supplement containing estrogen-like compounds. These compounds could potentially contribute to the formation of blood clots or worsen some forms of cancer. It's always good to check with your doctor before taking supplements containing phyto-estrogens.

Tyagi, A.M., et al. 2012. Formononetin reverses established osteopenia in adult ovariectomized rats. Menopause 19(8):856-863.

Saturday, August 11, 2012

Oxidative Stress = Bone Loss

As we age, chronic disease such as atherosclerosis, diabetes, Alzheimers, and others, are not uncommon and go along with our overall decline in functional capacity. Osteoporosis is no exception. In fact, we actually begin to loose bone in our 30s, long before sex hormone production in women begins its decline around the age of 45 or 50. (Estrogen production begins to wan about 5 years before menopause.) This should make us think twice about what really IS the cause of bone loss. There must be something else going on besides low estrogen that causes women to loose bone density. And, yes, there is! A decline in estrogen and testosterone levels clearly affect bone density but this occurs only when the body is under oxidative stress.

Oxidative stress, the production of reactive oxygen species (ROS) without neutralization though adequate antioxidant mechanisms, causes progressive cellular damage. Normal body metabolism actually generates radical forms of oxygen. This is normal and we have built in mechanisms to counteract any damage produced by these endogenous (produced within the body) free radicals. But when other ROS producing factors such as pollutants, physiologic stress, or gastrointestinal dysfunction overwhelm the body's antioxidant capacity the result is oxidative stress. When it comes to bone loss, oxidative stress leads to insufficient production of bone-forming osteoblasts, and a hyper-stimulation of osteoclasts, the cells that degrade bone. Not a good combination if bone density and integrity are to be maintained.

Oxidative stress is a critical contributor to the aging effects on bone and muscle, and it is the number one cause of osteoporosis. Way back in 2007 Grassi, et al., reported at the Proceedings of the National Academy of Sciences that the rise in ROS in bone marrow, as seen with low estrogen levels, increases white blood cell and T cell activity fivefold. These T cells then release copious amounts of RANKL, the potent signaling molecule that stimulates the formation and activation of the bone resorbing osteoclasts. This is the reason we see a dramatic rise in bone loss for at least five years after menopause. And this is where OsteoStim comes to the rescue. This powerful supplement is loaded with anti-oxidants, to help neutralize ROS and reduce the adverse effects of free radicals on bone. Not only that but OsteoStim has bone building compounds such as milk basic protein as well as vitamins D and K.  Check out OsteoStim!

Grassi, F., et al. 2007 Oxidative stress causes bone loss in estrogen-deficient mice through enhanced bone marrow dendritic cell activation. Proceedings of the National Academy of Sciences 104(38):15087-15092.

Thursday, August 9, 2012

Mt. Washington Road Race

I know this is old news (June) but it was such a great New England day to race up Mt. Washington that I just had to show it! I always thank my lucky stars that I can do things like this again...without breaking.
Make sure to include weight bearing exercise (maybe not like this though), at least 3 times a week, into your bone health program. As I say in my book (The Whole-Body Approach to Osteoporosis), exercise can be "like a heaping spoonful of good medicine!" Running up Mt. Washington was definitely good medicine.

Wednesday, August 8, 2012

Too Much Vitamin D?

By now, most people are getting the message loud and clear that--LOW LEVELS OF VITAMIN D ARE NOT HEALTHY. Blood levels need to be maintained above 32 ng/ml and the upper range of "healthy" is often considered to be 80 ng/ml. Low levels not only increase your risk for osteoporosis but also heart disease, cancer, depression, and even death. But how much vitamin D is too much? That is a good question. In my office I like my patient's vitamin D levels to be between 40 and 60 ng/ml, but I know other practitioners differ in their opinions on this subject.

To determine the effects of vitamin D on mortality risk, researchers from the University of Copenhagen studied the vitamin D blood levels of 247,574 subjects. They published their results in a recent paper in the Journal of Clinical Endocrinology and Metabolism (Durup D., et al. 2012). What they found was that both too little and too much vitamin D increase mortality risk. It was determined that blood levels below 10 nmol/liter (that's 4 ng/ml)* raised mortality risk 2.31 times while levels above 140 nmol (56 ng/ml) raised mortality risk 1.42 times. The researchers concluded, "all-cause mortality was observed, indicating not only a lower limit but also an upper limit."

This makes sense, too little of anything, just as too much, is not good. My concern though is with the analysis that levels above 140 nmol (56 ng.ml) raise mortality risk. Please read the response below by Dr. Armin Zitterman. His explanation is helpful and explains why most vitamin D proponents now suggest keeping blood levels between 32 and 80 ng/ml.


*[Note: Conversion for vitamin D: 1.0 nmol/L = 0.4 ng/ml]

Durup D., et al. 2012. A reverse J-shaped association of all-cause mortality with serum 25-hydroxyvitamin D in general practice, the CopD Study. J Clin Endo Metab, doi:10.1210/jc.2012-1176.


In response to the above study, Armin Zitterman from Ruhr University Bochum writes, "Very high 25-hydroxyvitamin D levels may sometimes reflect low availability of the active vitamin D hormone [1,25 dihydroxyvitamin D]. This assumption is in line with experimental data demonstrating that high circulating 25-hydroxyvitamin D levels can be the result of low renal 1 alpha-hydroxylase activity." [1 alpha-hydroxylase is an enzyme produced in the kidney that is often diminished in the elderly due to poor kidney function] Zitterman further explains, "older patients do not only have reduced 1,25 dihydroxyvitamin D levels but also have significantly higher circulating 25-hydroxyvitamin D levels."

Zitterman, A. 2012. Cautious interpretation of the reverse J-shaped association between circulating 25-hydroxyvitamin D and total mortality is necessary. JCEM

Sunday, August 5, 2012

Vitamin D3 or D2?

I often have new patients tell me that their doctor prescribed them vitamin D2 (50,000 IU) for eight weeks to improve their blood levels of vitamin D. I have even had patients placed on this prescription for years while repeat testing revealed their vitamin D blood levels to remain low or barely adequate (30 ng/ml). My response has been to encourage a switch to 5,000 to 10,000 units of vitamin D3 per day with repeat testing. In most cases, their vitamin D levels improve and the patient can then be placed on a maintenance dose of 2,000 to 5,000 IU/day.

In a study published in the Journal of Clinical Endocrinology and Metabolism, researchers (Heaney, R.P., et al. 2011) at Creighton University found "D3 is approximately 87% more potent in raising and maintaining serum 25(OH)D concentration and produces 2- to 3-fold greater storage of vitamin D than does equimolar D2."

They concluded, "Given its greater potency and lower cost, D3 should be the preferred treatment option when correcting vitamin D deficiency."

Heaney, R.P., et al. 2011. Vitamin D3 is more potent than vitamin D2 in humans. Journal of Clinical Endocrinology and Metabolism. doi:10.1210/jc.2010-2230.



Thursday, August 2, 2012

Low Vitamin D: Risk of Dying

In a study by Smit, E et al. (2012) published in the European Journal of Clinical Nutrition the correlation between vitamin D levels and the risk of dying in older adults was investigated. This study examined data from the Third National Health and Nutrition Examination Survey and included over 4,300 adults over the age of 60. The researchers found that older individuals with low vitamin D levels had a 30% higher chance of dying than those with higher vitamin D levels. The study also found a correlation between increased risk of dying and frailty. Frail adults had twice the risk of dying as those who were not frail and individuals who were both frail and had low vitamin D levels were three times more likely to die.

Smit, E., et al. 2012. The effect of vitamin D and frailty on mortality among non-institutionalized US older adults. European Journal of Clinical Nutrition. (June 13) doi:10.1038/ejcn.2012.67.
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