Monday, December 31, 2012

New Year's Resolution--Make it a Great One!

I was never much for New Year's resolutions. I always thought that if you really wanted to do something...any day, not just the first day of a new year, would be perfect. If you want to start eating better, exercising more, thinking brighter thoughts, giving more hugs, smiling more often...what ever...any day is just fine to start doing something positive for yourself and others. "Just do it"... as the saying goes. Don't hesitate! But seeing as tomorrow is the first day of a brand new year, well, all the more reason to go for it! The world is yours. Make the most of it. Go out on a limb and make a New Year's resolution that will really make your life better. It is, after all, only one year...and, anyone can do something for a year. Who knows, maybe you will be healthier and happier for it in the long run! And, after a year, if it is just so easy to keep doing it.... well, what the heck... you get the idea...  Happy New Year!

Wednesday, December 26, 2012

Gluten Sensitivity and Osteoporosis

Gluten sensitivity is a reaction to the ingestion of gluten, a protein found in wheat, barley and rye grains. It is estimated that 6 to 10% of the U.S. population have adverse reactions to gluten. Symptoms may be gastrointestinal in nature (diarrhea, constipation, gas, bloating, abdominal pain) or manifest as other health related issues: anemia, weight loss, fatigue, general weakness, muscle cramps, achy legs, tingling sensations in the face or extremities, rash, mouth sores and tooth discoloration. But often, gluten sensitivity goes undiagnosed--silently lurking beneath the surface, causing system inflammation and the development of disease entities such as osteoporosis.

It is estimated that almost 1 out of every 100 people suffer from celiac disease--the more severe autoimmune form of gluten sensitivity, where the mucosa villi in the small intestines are flattened, limiting the body's ability to absorb nutrients--even if they are plentiful in the diet. But gluten sensitivity does not always manifest with gastrointestinal involvement. In fact, the disorders that have been linked to gluten sensitivity are extremely diverse. The following is just a sampling of those disorders: ADHD (attention deficit hyperactivity disorder), depression, migraines, cancer, heart disease, psoriasis, ulcerative colitis, rheumatoid arthritis, lupus, Hashimoto's thyroiditis, Sjogren's syndrome, recurrent pancreatitis, and osteoporosis. Because it has the potential to cause so many symptoms and has been linked to so many disorders, gluten sensitivity is frequently mistaken for other conditions or is overlooked entirely. However, awareness of gluten sensitivity is improving dramatically as more people speculate that gluten could be at the root of their health problems.

Doctors don't often look for gluten sensitivity in the assessment of their patients with osteoporosis. Unfortunately, this is a problem because gluten sensitivity can lead to bone loss not just from malabsorption but also through a systemic release of pro-inflammatory cytokines throughout the body. When mucosal cells become irritated (this can be from ANY food sensitivity, not just gluten) it causes gaps to appear at the junctions between the cells of the intestines. These gaping holes are large enough for undigested food molecules such as gluten to permeate the gut wall and set off an inflammatory response. Of all the food molecules that can potentially penetrate this "leaky gut," gluten seems particularly prone to producing a large inflammatory response.

If you have osteoporosis--even if you do not have the gastrointestinal signs and symptoms of celiac disease--you should still be tested for gluten sensitivity. It may be a contributing factor in your bone loss. The following tests can determine if you are sensitive to gluten: anti-tissue transglutaminase (tTG) IgA, total IgA, antigliadin antibodies (AGA) IgA and IgG.

The treatment for celiac disease and gluten sensitivity is to go on a gluten-free diet, to control signs and symptoms and prevent complications. Initially, following a gluten-free diet may be frustrating. But with time, patience and creativity, you'll find there are many foods that you already eat that are gluten-free and you will find substitutes for gluten-containing foods that you can enjoy.

If you are just starting a gluten-free diet, it's a good idea to consult a dietitian who can answer your questions and offer advice about how to avoid gluten while still eating a healthy, balanced diet. For gluten-free recipes and even hands-on classes in how to cook gluten-free, Leslie Cerier, "The Organic Gourmet" is a great resource. Leslie wrote Gluten-Free Recipes for the Conscious Cook which I highly recommend.

Sunday, December 23, 2012

COPD and Osteoporosis

Chronic obstructive pulmonary disease (COPD) is a disease of the lungs primarily caused by cigarette smoking. Years of exposure to free-radical-producing tobacco smoke initiates a chronic inflammatory response in the lungs that leads to a breakdown of cellular tissue and increased mucus secretion. This makes it difficult to breath and can shorten an individual's life by 7 to 10 years.

Unfortunately, the damage from smoking cigarettes does not stop there. Smoking, and the inflammation of COPD, also causes systemic problems such as muscle weakness and atrophy, arterial stiffness and cardiovascular disease, and bone loss. In fact, more than 50% of patients with COPD have osteoporosis and a high risk for fracture. Graat-Verboom et al. (2012) suggest that "screening for osteoporosis should be performed even in moderate COPD patients."

There are three major reasons for this close relationship:

   1.  Vitamin D insufficiency is common in patients with COPD.
   2.  Compromised lung capacity reduces the ability to exercise which is important for
        stimulating bone growth and for maintaining muscle strength to prevent falling.
   3.  The inflammatory response within the lungs of patients with COPD does not remain
         local but instead leads to oxidative stress and a constant outpouring of
         proinflammatory cytokines into the rest of the body, which in turn causes chronic
         systemic inflammation.

        Chronic systemic inflammation, the primary driving force behind the development of
        osteoporosis, leads to reduced hormone function such as estrogen and calcitonin
        (important for blood calcium regulation), lower calcium absorption, increased cortisol
        levels, poor blood supply to bone, and death to the bone-building osteoblast cells.

Both COPD and osteoporosis are catabolic processes in that they are the result of a whole-body destructive process. Both of these chronic diseases are fueled by the destructive effects of oxidative stress and chronic systemic inflammation. Common signs of a catabolic physiology are: low body mass index (BMI), low IGF-1 (the most powerful bone and muscle building growth factor in the body*), and muscle wasting (sarcopenia)...all of which are often seen in individuals with COPD and those with osteoporosis.

Although more than half of patients with COPD have osteoporosis, neither a DXA exam, which measures bone mineral density, or FRAX scores** are useful for predicting fractures in patients with COPD (Ogura-Tomomatsu et al., 2012). So no matter what your bone density reading is, if you have COPD, you are likely at greater risk for fracture.

Considering the fact that every thoracic vertebral compression fracture reduces the amount of air a person can take in and breath out by up to 9%, improving bone health in patients with COPD is truly a matter of life or death. So, what can be done for people with COPD and osteoporosis besides smoking cessation and osteoporosis-specific medications? Lots!

  • Have your doctor check your vitamin D level. Strive for blood levels of 50 to 60 ng/ml. Many providers suggest taking 2,000 to 4,000 IU/day of vitamin D3.
  • Have your doctor check your hsCRP. This is a protein released by your liver in response to inflammation. It will probably be high if you have COPD.
  • Eat healthy to promote an anabolic state and help tissues obtain energy for growth and cell maintenance.      
       -  Drink whey protein shakes (15 to 20 grams/day)
       -  Eat lean protein such as chicken, turkey and fish
       -  Cook with healthy oils like olive and virgin coconut
       -  Eliminate caffeinated and carbonated beverages
       -  Reduce refined carbohydrates
  • Reduce or eliminate red meat, hard cheeses, sugar, and coffee -- choices that lead to an acidic body and more inflammation.
  • Get more alkaline:
       -  Enjoy green drinks
       -  Eat LOTS of fruits and vegetables (preferably organic). I favor broccoli, kale,
          squash, prunes, apricots.....and lots more!
       -  Take advantage of OsteoMineralWhey -- a great source of alkalinizing minerals.
       -  Use OsteoSustain...a perfect calcium/magnesium/mineral complex with vitamins D
          and K.
       -  Snack on plump juicy alkaline and antioxidant rich fruit with a cup of warm
          OsteoMineralWhey. (Soak dried organic apricots and prunes in water over night.)
  • Reduce inflammation and oxidative stress.
       -  Again, eat LOTS of fruits and vegetables. In addition to being rich in alkaline
           minerals, they are high in antioxidants.
       -  Include fish oil and flax seed in your diet for their inflammation-reducing
          omega 3s.
       -  Supplement with selenium, beta-carotine, and vitamins C and E (preferably
          mixed tocopherols and tocotrienols).
       -  Coenzyme Q10 can be a great energy booster.
       -  Curcumin is very important for reducing inflammation. You can also try resveratrol,
           quercetin and boswellia serrata.
       -  There are two powerful antioxidants that can be extremely helpful for slowing the
           progression of COPD: N-acetyl cysteine (NAC) and alpha lipoic acid. These two
           anti-aging compounds help dissolve mucus, reduce inflammaiton, and aid in the
           production of glutiathion, the body's own powerful anti-oxidant.
       -  Our OsteoStim is not only great for its bone building properties but because it
           contains vitamin D, alpha lipoic acid and NAC it is a perfect fit for those with
           COPD.
       -  Take advantage of probiotics...they not only reduce inflammation and boost your
           immune system but can help prevent candida yeast infections which can be a
           problem when taking inhaled corticosteroids.
       -  Creatine monohydrate (preferably buffered) is great for building muscle and
           slowing the progression of muscle wasting that is often seen with COPD. Speaking
           of which, you can't keep your muscle tone without exercise. Of course you need to
           check with your doctor before engaging in any new exercise regime but lifting light
           weights can be extremely beneficial. As COPD progresses, so does muscle
           wasting and the risk of falling. Supplemental creatine, whey protein shakes,
           and engaging in light-weight exercises can offer significant help.
  • Now, after you have done at least some of the above for 2 to 3 months (you don't have to do it all to gain benefit but, of course, the more you do the better)...get your hsCRP tested again. It will probably be lower (indicating that you have less inflammation) and you should feel better too!

*  For more on the importance of IGF-1 for bone health and how to strive for an anabolic body. Check out pages 140 - 141 and 171 - 177 in my book, The Whole-Body Approach to Osteoporosis.

** FRAX is a diagnostic tool developed by the World Health Organization to evaluate the 10-year probability of fracture risk. This scoring system integrates various risk factors for osteoporosis (such as smoking) plus bone mineral density scores to calculate the risk of fracturing a bone in the next 10 years.

Graat-Verboom L. et al., 2012. Risk factors for osteoporosis in Caucasian patients with moderate chronic obstructive pulmonary disease: a case control study. Bone 50(60):1234-9.

Ogura-Tomomatsu H. et al., 2012. Predictors of osteoporosis and vertebral fractures in patients presenting with moderate-to-severe chronic obstructive lung disease. COPD 9(4):332-7.

Saturday, December 22, 2012

Is There a Need for Supplemental Antioxidants?

I was talking with a group of people a week or so ago on the topic of...yes, of course, osteoporosis. While on the topic of oxidative stress and how free radicals* can tax the body's antioxidant status leading to oxidative cell damage and chronic disease such as osteoporosis, a person asked "Why do I have to take supplemental antioxidants if I eat a really healthy diet?" Good question.

My response was that it may be completely reasonable to assume that a healthy person could get all of his or her nutrients for antioxidant activity from diet alone. The body, after all, has evolved mechanisms to deal with the naturally occurring free radicals/oxidants produced during everyday physiological processes. When these innate mechanisms (endogenous antioxidants) are bolstered by dietary antioxidants derived from organic fruits and vegetables, there is no doubt, this should suffice...in a healthy individual. But the reality is that if a person's system is struggling, if it is catabolic**...as it often is with osteoporosis...then, even if that person is taking in lots of nutritious food loaded with antioxidants, it still might not be enough to pull them back to health.

Several factors can increase the number of free radicals produced in the body, overwhelming the ability of natural antioxidants to cope. Examples include exposure to chemicals, drugs, tobacco (even second-hand smoke), radiation, sunlight, electronic pollution, and known and unsuspected toxins and pollution in our food, water and air.

Excessive exercise, dysfunctional internal metabolic processes, physical strains and emotional stresses of all kinds can also cause a healthy body to get overwhelmed and spike free radical production. Add to that a drop in estrogen levels at menopause or low blood levels of vitamin D on a cold winter day, or an abnormal microbial overgrowth in the gut from either past antibiotic use or current low-grade food sensitivity...now you have an overwhelming accumulation of free radicals in the body.

Full-size image (28 K)Healthy diets can be compromised by processed foods which are hard to avoid. Increasingly, our food supply is being degraded through harmful growing practices and soil depletion, and can no longer be relied upon to protect us from oxidative stress.

If an individual is suffering from a chronic disease, such as osteoporosis, his or her biological systems are already stressed. There is no doubt, excess free radicals will damage cells and incite inflammation.

But does supplementing with antioxidants help? 

Research on this topic often says "yes" but there are some inconsistent findings. Da Costa et al., (2012) in Progress in Molecular Biology and Translational Science tell us that these inconsistent findings may be, in part, due to genetics.

"Polymorphisms [discrete genetic variations] in genes coding for endogenous antioxidant enzymes or proteins responsible for the absorption, transport, distribution, or metabolism of dietary antioxidants have been shown to affect antioxidant status and response to supplementation. These genetic variants may also interact with environmental factors, such as diet, to determine an individual's overall antioxidant status." When free radical production "exceeds the ability of the antioxidant networks to manage them, oxidative stress results. Macromolecule damage and abnormal cellular signaling and gene expression associated with oxidative stress may then lead to chronic disease development."

Supplemental antioxidants, especially key ones such as alpha lipoic acid, N-acetyl cysteine, berberine, green tea, taurine, and milk thistle can help to pull the body, especially one that is struggling to improve bone health, out of oxidative stress and onto the road of recovery. That's exactly why we put all these antioxidants into OsteoStim, our special formulation designed to help relieve oxidative stress, the prime culprit in the uncoupling of bone remodeling that leads to bone loss.

Da Costa et al., 2012, Genetic determinants of dietary antioxidant status. Prog Mol Biol Transl Sci, 108:179-200.

*   By way of a refresher about free radicals, antioxidants, and oxidative stress:

When oxygen interacts with carbohydrates and fats in our cells during the creation of energy, it is termed oxidation. The formation of free radicals or oxidants is a normal byproduct of regular energy metabolism. Free radicals are unstable, highly reactive molecules that lose an electron as a result of this activity. These molecules then "steal" electrons from other molecules and can lead to cell damage.

Exogenous (derived from outside of the body) antioxidants are certain vitamins, herbs and other substances that supply missing electrons for unstable molecules, thus neutralizing the free radicals and allowing the body to undergo metabolic processes without harm.

Oxidative stress occurs when free radicals, which are not neutralized by antioxidants, go on to create more volatile free radicals and damage cell walls, vessel walls, proteins, fats and even the DNA in the nucleus of our cells. Oxidative stress has the potential to overpower all of our protective systems and cause chronic degenerative diseases.


**  Catabolic:

A catabolic physiology is when there is a destructive breakdown of complex molecules in the body--a classic description of someone with osteoporosis. The opposite of catabolic is anabolic, which refers to the constructive synthesis and a building up or repair process of the body.

Monday, December 17, 2012

Therapeutic Targets for Managing Osteoporosis


I wrote an article several years ago in the Alternative Medicine Review outlining how common laboratory biomarkers (tests) have been found to be correlated in some manner or another with excessive bone loss and/or a heightened risk for breaking a bone. These tests can therefore be used, not as direct indicators of bone density or strength, but as indirect "indicators" or surrogates, of bone health and fracture risk. The use of therapeutic targets for reducing fracture risk is one of the most important things you and your doctor can do in managing your treatment of osteoporosis.
 
This is how it works: A lab test is performed and the results come back as abnormal. The physician attempts to normalize the result (through diet, changes to life-style, supplementation, exercise and/or medication) and then, through subsequent serial testing, determines success or failure. The doctor’s ability to design and fine tune therapeutic protocol is enhanced. Using lab tests in this manner as a way to determine success or failure of therapy is far superior to waiting the recommended two years between bone density evaluations. In addition, when measuring bone density, only one aspect (quantity) of bone is assessed. The assessment of changes in bone quality, as can be inferred through lab testing, provides intermediate indicators of bone health to help guide therapy.
Cortisol can be one such marker. Cortisol is a hormone produced by the adrenal glands in response to stress. Measuring cortisol through saliva is simple, non-invasive, and accurately reflects the amount of unbound cortisol levels in blood. This is important because elevated cortisol levels, while often asymptomatic*, increase a person’s risk for fracture by silently eroding away bone density and strength – reducing bone quantity and quality. It is estimated that approximately 1 to 10% of people with osteoporosis have elevated levels of cortisol. 
In one study, Morelli et al. (2011) found that in patients who have an excess production of cortisol (a condition called subclinical hypercortisolism or SH) who had normal or osteopenic (not osteoporotic) bone density, 48% sustained fractures compared to 13% in the non-SH group. In a second study conducted by researchers at the University of Milan, Italy, 102 patients with adrenal incidentalomas** (with and without subclinical hypercortisolism) were assessed for bone quality and fracture risk. The authors concluded "that in patients with subtle cortisol excess, TBS (trabecular bone score) [a method of determining bone quality and strength] is reduced and correlates with the number and severity of vertebral fractures and with the degree of cortisol excess."
In the cortisol example, a simple saliva lab test may provide important clues to the causes of your bone loss. Any abnormal test results provide you and your doctor with therapeutic targets for improvement. On subsequent testing, positive changes will indicate that the therapy you and your doctor have initiated are making an impact—and that your health, and that of your bones, are improving. 

*       Symptoms when displayed include central weight gain, excess sweating, thinning of skin and bruising, high blood pressure, elevated blood glucose, muscle weakness, irritability, etc.
**    Incidentalomas are adrenal gland tumors that have been found incidentally while performing another,
       unrelated, diagnostic procedure. Approximately 30% of patients with subclinical hypercortisolism are found
       to have adrenal masses.
Morelli et al. 2011. Risk of new vertebral fractures in patients with adrenal incidenaloma with and without subclinical hypercortisolism: a multicenter longitudinal study. Journal of Bone and Mineral Research. 26:1816-1821.
 
Eller-Vainicher et al. 2012. Bone quality, as measured by Trabecular Bone Score (TBS), in patients with adrenal incidentalomas with and without subclinical hypercortisolism. Journal of Bone and Mineral Research. doi 10.1002/jbmr.1648.

Sunday, December 16, 2012

Using Lab Tests for Oxidative Stress to Monitor Bone Health


Waning estrogen in post-menopausal women is a major cause of oxidative stress, a powerfully destructive force that causes cell damage and bone loss. Identifying the presence of oxidative stress in an individual with osteoporosis would therefore be extremely important. 

In my book, The Whole-Body Approach to Osteoporosis, I explain how biomarkers (lab tests) can be used as therapeutic targets to indirectly monitor changes in bone health and use them to direct therapy. When specific lab tests related (directly or indirectly) to bone health are found to be abnormal, changes in diet and supplemental nutrition can be directed to cause a positive change. Labs can then be retested after 3 to 4 months to determine therapeutic effectiveness. If there is improvement, the patient and health care provider are reassured that they are on the correct therapeutic path. If not, a change in therapy can be applied.
In the case of waning estrogen, serum lipid peroxides and urine 8-hydroxy-2-deoxyguanosine (8OH2dG) can be used to determine oxidative stress levels in individuals with osteoporosis. In my book, I cite several examples were patients’ bone health improved and fracture risk was reduced by using these labs to help direct therapy. In research published in Clinical Chemistry and Laboratory Medicine, Cervellati et al. demonstrate this same negative correlation between bone density and lipid hydroperoxides in post-menopausal women.
This is another example of how the assessment of changes in bone quality, as can be inferred through lab testing, provides intermediate indicators of bone health to help guide therapy.
Cervellati et al., 2012, Bone mass density selectively correlates with serum markers of oxidative damage in post-menopausal women, Clin Chem Lab Med, doi:10.1515/cclm-2012-0095.

Sunday, December 9, 2012

Teriparatide (Forteo®) Safety: What are the Risks for Osteosarcoma??

Teriparatide, the bone-building medication produced by Eli Lilli (Forteo®) and approved by the FDA in 2002, is now in its tenth year of use for the treatment of osteoporosis. Teriparatide has been shown in numerous studies to provide great benefit to patients with severe bone loss and high risk for fracture. It not only increases bone mineral density by increasing bone mass (not just density) but it also substantially reduces fracture risk. Common side effects of teriparatide are headaches, nausea and vomiting but the real concern has been that of bone cancer. During safety studies, rats given teriparatide for 2 years (which is most of their lifetime) at dosages 3 to 58-fold that of human doses, frequently developed oseteosarcomas, the most common primary malignant bone tumor seen in humans. Because of this, teriparatide carries a "black box warning" and is limited to 2 years of use.

When teriparatide was approved by the FDA, one of the stipulations was that there be a postmarketing evaluation of the potential association between teriparatide and osteosarcoma. Thus, the establishment of the Osteosarcoma Surveillance Study, an ongoing 15-year surveillance study. In this months issue of the Journal of Bone and Mineral Research, Andrews et al. (2012) report on the findings half-way through this study. "After 7 years of the study, there were no osteosarcoma patients who had a prior history of teriparatide treatment. Thus, approximately halfway through this 15-year study, the study has not detected a pattern indicative of a causal association between teriparatide treatment and osteosarcoma in humans."

In another article, Capriani, et al. (2012) tell us that there are differences in rat versus human bone metabolism that are important for understanding why teriparatide does not pose a substantial risk for osteosarcoma to humans. In their perspective article in the Journal of Bone and Mineral Research, they explain: "The rat is a species that models [* see below] its skeleton for virtually its entire life [about 2 to 3 years]. The modeling is associated with lifetime skeletal growth. When exposed to an osteoanabolic [bone building] agent like PTH [teriparatide], the rat responds exuberantly with a profound increase in endocortical and trabecular bone mass and a significant reduction in marrow space. Older studies from the 1930s showed that the entire marrow space can be obliterated by chronic exposure of rats to PTH [parathyroid hormone]. The ever-growing rat skeleton, therefore, is a developing organ harboring immature and potentially tumorigenic [cancerous] cells that might respond to PTH [teriparatide] with uncontrolled behavior, losing its capacity for ordered modeling or growth. In contrast to rat skeletal physiology, the mature adult human skeleton remodels itself on a continual basis. Modeling essentially ceases as a normal occurrence after skeletal maturity has been reached."

In other words, after humans reach the age of 21 or so, modeling of bone ceases and remodeling becomes the predominant form of bone activity. It is because of this important difference between rat and human bone physiology that teriparatide presents less risk of cancer to humans. In addition, studies with macaque monkeys exposed to dosages of up to 40 times that of the human dose did not show evidence of osteosarcoma formation.

* Bone modeling and remodeling are different. In bone modeling, which occurs predominantly when a child is growing, bone resorption and formation are not coupled in their actions and bone is undergoing a change in size and shape (i.e. children are growing). Bone remodeling is quite different and is a process where the old, worn-out bone seen in adults is replaced with new bone (i.e. adults are not growing but their bones are simply in need of constant repair). In remodeling, the resorption and formation phases are coupled and are taking place in the same bone surface area.

Andrews EB, et al., 2012. The US Postmarketing Surveillance Study of adult osteosarcoma and teriparatide: Study design and findings from the first 7 years, Journal of Bone and Mineral Research 27(12):2429-2437.

Capriani C, et al., 2012. Safety of osteoanabolic therapy: A decade of experience. Journal of Bone and Mineral Research 27(12):2419-2428.

Friday, December 7, 2012

Calcium Intake is Not Associated with Increased Coronary Artery Calcification

Recently, several studies have reported an increase in heart attacks with supplemental calcium. To examine this relationship further, Samelson et al. (The American Journal of Clinical Nutrition) reviewed food-frequency questionnaires and CT scans of over 1,200 men and women in the Framingham Offspring Study. The authors used coronary artery calcification (atherosclerosis) as their measure of predictive risk for heart disease.

Conclusions: "Our study does not support the hypothesis that high calcium intake increases coronary artery calcification, which is an important measure of atherosclerosis burden. The evidence is not sufficient to modify current recommendations for calcium intake to protect skeletal health with respect to vascular calcification risk."

Samelson, et al., 2012. Calcium intake is not associated with increased coronary artery calcification: the Framingham Study. The American Journal of Clinical Nutrition doi: 10.3945/ajcm/112/044230.

Wednesday, December 5, 2012

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