Building Strong Bones Through Nutrition

Where Bone Strength Begins®

Welcome to OsteoNaturals. We invite you to shop our online store for quality nutritional supplements that promote skeletal health. In addition, our site is full of useful information about osteoporosis and insights about how it can be managed naturally.

Individuals who intend to stay active into retirement will need strong, healthy bones, and a strategy for maintaining muscle strength and overall fitness. Whatever your age or current condition, it is never too early or too late to make a positive difference. The "OsteoNaturals difference" = natural ingredients chosen for quality, safety, purity and potency.

Wednesday, March 7, 2018

The importance of Bone Mineral Density Exams (DXA scans)

The Importance of Bone Mineral Density Exams (DXA scans)

A dual-energy absorptiometry (DXA) scan can provide a snapshot of your bone
health. This test determines bone mineral density (BMD) and helps in establishing
fracture risk, and, with serial testing, is a way to measure response to osteoporosis
treatment. The most widely recognized test for determining BMD is the central DXA
scan. It is painless - similar to having an x-ray but much less radiation. The scan
measures bone density at your hip and spine. (Often, a scan of the forearm will also
be performed during central DXA testing.) Peripheral bone density testing measures
density at the wrist, finger, or heel and are typically used for screening purposes only.

DXA scans measure your bone mineral density and compares it to that of an 
established norm or standard to give you a score. Although no bone density test
is 100-percent accurate, the central DXA can be an important predictor of 
whether a person will have a fracture in the future. Most commonly, DXA results
are compared to the ideal or peak bone mineral density of a healthy young adult,
and given a T score. A score of 0 means your BMD is equal to the norm for a
healthy young adult. Differences between your BMD and that of a healthy young
adult norm are measured in units called standard deviations (SDs). The more 
standard deviations below 0, indicated as negative numbers, the lower your BMD 
and the higher your risk of fracture.

The National Osteoporosis Foundation (NOF) and the U.S. Preventative Services Task
Force (USPSTF) recommended osteoporosis screening with DXA for women 65 years
and older, and for men over 70. Earlier screening is recommended for both groups if risk
factors are present. (Risk factors are such things as family history of osteoporosis, 
weight under 127 pounds, history of smoking or excessive alcohol consumption, poor
diet, etc.)

A recent review published in the Journal of General Internal Medicine determined that
too few women are getting bone density scans. Researchers examined the medical 
records of 51,000 women aged 40 to 85 living in California and determined that only
57.8% of women aged 65 - 74 and 42.7% of women over age 75 received DXA
screenings. Even with women age 60 to 64 with at least one risk factor, only 58.8%
had a DXA. The researchers concluded that DXA screening is being underutilized.

Friday, February 9, 2018

DX Severe Osteoporosis: Part XIII - Tracking the Impact of Stress on Bone Loss

First, a note of apology and thanks:   The title of my last blog/newsletter was "DX Severe Osteoporosis: Part XII - Could Too Much Exercise Cause Osteoporosis?". My spelling of the word "Too" prompted responses from two or three readers emailing me that "Too" in this context should be spelled "To", with one "o". Now I am pretty confident in my ability to help people navigate the complexities of bone loss but I readily admit to my lack of confidence in writing and English grammar. ( I am sure many of you will attest having undoubtedly witnessed my numerous punctuation, spelling and grammar fiascos of the past!) After being in Africa for 11 days (another story at another time!) and having those "extra "o" email messages weighing on me...I came back a foggy jet lagged condition..."corrected" the spelling of "Too" to "To" with one "o". OK...I know what you are thinking...Why oh why??!  Yes, my lack of confidence got the better of me and I changed what was correct initially to something that is incorrect. (They always say, when taking a test....DON"T go back and change an will be wrong!)

So why am I going on and on about this? Well, for several reasons. I love OsteoNaturals with a passion and this whole episode of the spelling of the word "Too" in my blog/newsletter brings up an amazing thing about this company that has just come about on its own...and one that I am so happy to experience. It turns out, that because we look out for our customers, THEY (you) look out for us! It really dawned on me that WE ARE ALL IN THIS TOGETHER. Incidents such as this make me realize what a great company OsteoNaturals has become. Although fairly small (and growing rapidly) we still (and always will) retain a close relationship with our customers. We take pride in that we provide personal care to our customers, and in return you have become invested in our well being. The fact that customers take the time to contact us about spelling and other "glitches" (right or wrong) is very endearing and much appreciated. Today alone, I had 5 customers write me emails. They wrote to tell me about: 1) articles they found on the internet that they thought I might enjoy; 2) how they enjoyed some of my past blogs; and 3) how well they were doing since taking OsteoNaturals and THANKS!  How cool is that!

I founded OsteoNaturals over 8 years ago because I saw the need to help others fight back against osteoporosis and conquer this potentially devastating disease. My own trauma in dealing with osteoporosis, both psychological and physical (multiple fractures), has turned out to be one of the best things in my life. After figuring out how to fix it on my own, I found great purpose in helping others combat osteoporosis. Now, when I stand back and reflect at what we have created here at OsteoNaturals, and how our customers are so appreciative, and how so many of them have become our friends on a first name basis, it is incredibly rewarding. I thank you all. (And I ALWAYS appreciate feedback, good or bad, correct or incorrect, about my articles.) (Note:  I used the word "Impact" in the title of this Part XIII of DX Severe Osteoporosis...I didn't EVEN want to toy with "Effect or Affect"!)

This is Part XIII in a multi-part essay chronicling my personal experience with osteoporosis. In this series I have been taking readers through the diagnostic and treatment phases of my care that began over 18 years ago when I was diagnosed with severe osteoporosis. Over the years, the combination of experiencing multiple fragility fractures along with an intense immersion into the study of bone pathophysiology has given me a unique understanding of this disease. If you are just joining the series, I encourage you to skim through the previous DX Severe Osteoporosis essays on my blog (at: as they provide background to each new installment. It is my hope that this series will provide you with a better understanding of osteoporosis in general, plus a few "pearls" that you may be able to incorporate into your own quest for better bone health. If you have been reading the essays all along...welcome back.    Dr.M

Tracking the Impact of Stress on Bone Loss

Getting the lab work that would show what was going on with the stress-related cytokines in my blood was impossible. There were no commercial labs testing for these proteins. In tracking the causes of my osteoporosis, I was finding plenty of evidence but few definite connections between the destruction I was seeing and the particular biochemical "predators" who were causing the damage. Finding objective signs of physical stress (from lab work) in the constantly fluctuating chemistry of the blood, and deciphering their relationship to bone loss, was difficult.

All kinds of stresses lead to an increase in pro-inflammatory cytokines. But could all types of stress lead to osteoporosis? It didn't seem as if it could be that simple. People in our society are under many kinds of stresses. Severe personal traumas, high-pressure corporate life, poverty, intense sport competition—these are all stressful, yet research linking them to osteoporosis was minimal. I wasn't the only athlete that ran hard; and even if training/competing hard was related, why would I lose so much bone density and other athletes lose none?

If it wasn't only the stress from training hard that was pushing the osteoclasts to erode bone faster than it could be made, what was it? An overactive parathyroid gland can do it, but my parathormone level was normal. A decline in estrogen can also do it, but that was normal also. (Yes, estrogen is important in men also.) It was only when I looked at stress that I kept seeing a possible link between excessive bone loss and my other symptoms. That link was pro-inflammatory cytokines.

When free radicals are produced, either as a byproduct from the body's response to trauma or from the stress of normal daily metabolic activities, cytokines are released by the immune system in an attempt to limit tissue damage. This is called oxidative stress at the molecular level, and it is the scene of intense molecular engagements that we are usually never aware of. If free radicals are not neutralized quickly by antioxidants they can be harmful because they steal electrons from nearby molecules. Antioxidants are molecular protectors which are designed to give up one of their own electrons to a radical. This stabilizes that molecule before cell damage can occur as a result of the free radical's electron-stealing tendencies. Stress is a normal part of life, and it produces free radicals in us all. The object isn't to eliminate all stress—we can't—but we can ensure that the body has the resources to neutralize free-radical production.

Even though pro-inflammatory cytokines are vital to the functioning of our immune systems, they can also cause major destruction if their actions are not effectively counter-balanced. When I was researching Gilbert's syndrome, I found that pro-inflammatory cytokines were implicated as being able to further reduce the enzyme that is genetically low in Gilbert's. It got me to wondering whether I really had Gilbert's or not. Could it be that high cytokines brought the enzyme level down enough to cause an increase in bilirubin, and that this only made it look as if I had Gilbert's?

Several months in to my own treatment regime, using nothing but nutritional supplements and diet changes, my bilirubin, indirect bilirubin, and albumin, all of which had been elevated, returned to normal. Was this just a fluctuation of lab values, was I effectively treating the Gilbert's, or did I not actually have the condition in the first place?

Whether the excess bilirubin was from a genetic enzyme deficiency or from pro-inflammatory cytokines wasn't the real issue. What was important was that I was starting to see trails that were closely intertwined and that their effects could be contributing to my bone loss. In another person, the same oxidative stress with similar circumstances might have lead to heart disease or cancer. Why one person responds one way to a set of stressors, and another person responds in a totally different way, is part of the genetic (and epigenetic) mystery of that individual.

The human body responds to physical and psychological stress in much the same way. A Canadian biochemist in the mid-twentieth century, Hans Selye, identified changes that take place in the body in response to stress. Using laboratory animals, Seyle was able to identify several short-term physiological changes that occur in response to acute stress, and other, pathological changes, that occur in response to long-term stress. He coined the phrase "general adaptation syndrome" to describe these observations. Since Seyle's initial studies, the research field of stress physiology has improved our understanding of adaption to stress. As a result, many subjective and objective clinical tools have been developed that aid physicians in identifying and monitoring patients with stress-induced disease processes.

The body continuously monitors and adapts its biochemical and energetic state to meet the needs and demands of being alive. If the body's needs were static it would be unnecessary for this constant fine-tuning to maintain physiological homeostasis. But throughout the day, demands on the body fluctuate constantly. The body must continuously monitor and respond to physical activity, the need for healing or self-defense, and the basic life-support processes of digestion, respiration, and temperature regulation. In order to live, the body must be able to accommodate and adapt to changing conditions both within and in the surrounding environment.

Some of the body's responses are immediate:  when you run, your body temperature increases; when you slow to a walk, you cool down. But when a demand is repeated, the response may become conditioned. A body repeatedly exposed to the low oxygen of higher altitudes, or to high ambient temperatures, becomes conditioned so that it handles these stresses more efficiently. If it were not for our ability to adapt to environmental stresses, activities such as traveling to high altitude or going outside on a 100 degree day, would cause great harm. But the body is constantly adapting—making red blood cells to help provide more oxygen, increasing sweat production to rid the body of excess heat—constantly regulating, monitoring, and changing. It is in a state of continuous controlled flux as a way to stay alive.

The athlete pushes his or her body to adapt to its uppermost limits. Through daily training, she or he is able to produce actual physiological changes. This "training response" develops super-efficient metabolic pathways and enhances the function of organs, including those of the endocrine system. The most prominent response is that from the adrenal glands, which release adrenaline and noradrenaline, and also cortisol for energy metabolism. The release of cortisol is governed by the hypothalamus-pituitary-adrenal (HPA) axis, a hormonal tag-team within the body. The secretion of cortisol is regulated by adrenocorticotropic hormone (ACTH) from the pituatary, which in turn is regulated by corticotrophin releasing factor (CRF) from the hypothalamus. When the body is healthy, temporary stress causes a biochemical cascade that is self-adjusting through negative feedback loops. When cortisol increases in response to stress, it signals a reduction of CRF and ACTH, which limits the release of any more cortisol. But in prolonged stress or with chronic, abnormal fluctuations in blood glucose levels, this self-limiting cascade can re-pattern, and in certain situations may be permanently altered. This can lead to a constant overproduction of cortisol by the adrenal glands and an array of health problems—one of which is bone loss.

One of the first lab tests I had was for cortisol. The endocrinologist wanted to rule out Cushing's disease, a metabolic disorder of the adrenal glands that can cause osteoporossis. Tests came back negative but with the complementary "see-saw" relationship between cortisol and DHEA, I was surprised that he had not ordered lab work for this important pre-hormone.

A quick Medline search turned up enough evidence of DHEA's (dehydroepiandrosterone) correlation to osteoporosis that I was convinced it should be a standard test, not just for osteoporotic patients, but also for general health screening. I didn't even wait around to ask the endocrinologist, I just ordered it myself. Results came back that I was not only low in DHEA but also DHEA-S, the sulfated storage form of this pre-hormone.

DHEA is the precursor of many hormones, and important to a host of physiological activities. It is involved in building muscle, supporting the immune response, maintaining the resting metabolic rate, and keeping blood glucose levels stable. DHEA is seen in three forms:  1) the unbound DHEA, that is present in the body for only a few seconds before it is utilized, 2) the more stable form, DHEA-S that is circulated until its more active form is needed, at which time the sulfur is cleaved, and 3) the DHEA-fatty acid ester which is formed by an enzyme that is carried on high-density lipoprotein (HDL) molecules.

HDL is the "good" cholesterol, while LDL and VLDL are considered to be the "bad" cholesterol because their levels correlate with heart disease. Exercise is supposed to push the balance between these three lipoproteins more toward HDL. Despite all the exercise I had done over my life, my HDL had always remained low, my LDL was higher, and my total cholesterol was in the 220 to 230 range. With these abnormal levels, medical statistics were placing me at a considerably higher risk for heat disease! All that exercise, and now I had both osteoporosis and a risk of heart disease. It was beginning to look like a bad day.

Stay tuned for:  DX Severe Osteoporosis: Part XIV

Wednesday, January 24, 2018

DX Severe Osteoporosis: Part XII - Could TOO Much Exercise Cause Osteoporosis?

This is Part XII in a multi-part essay chronicling my personal experience with osteoporosis. In this series I have been taking readers through the diagnostic and treatment phases of my care that began over 18 years ago when I was diagnosed with severe osteoporosis. Over the years, the combination of experiencing multiple fragility fractures along with an intense immersion into the study of bone pathophysiology has given me a unique understanding of this disease. If you are just joining the series, I encourage you to skim through the previous DX Severe Osteoporosis essays on my blog (at: as they provide background to each new installment. It is my hope that this series will provide you with a better understanding of osteoporosis in general, plus a few "pearls" that you may be able to incorporate into your own quest for better bone health. If you have been reading the essays all along...welcome back.    Dr.M

Osteoblasts and osteoclasts have a give-and-take relationship, and their activities are linked. As with any couple, their interactions must stay in balance for marital happiness to be maintained; the harmony of bone depends upon a similar balance. The tricky thing is that resorption, like any form of demolition, is faster than re-building. To offset this, bones produce larger numbers of osteoblasts, and these plentiful cells control the overall activity of osteoclasts.

If the coupling mechanism that balances the activities of osteoblasts and osteoclasts gets out of sync, osteoclasts may begin to resorb more bone than the osteoblasts can replace. Low bone density, and eventually osteoporosis, is the result. On rare occasions it is the osteoclasts that are underactive, resulting in too much bone, a condition called osteopetrosis. It is the balance, and the communication aspects, between the processes that is crucial, as with any relationship.

The communication system between bone cells is a series of linked stimuli and responses. Problems arise when signals are either blocked or amplified. If signals are muffled, the music that coordinates the cells' activities becomes too slow; if they are inappropriately amplified, the notes become distorted and the tempo too fast. In either case the dance between the bone remodeling partners, the osteoblasts and osteoclasts, gets out of step and bone density is lost. The molecules that conduct the music are cytokines, growth factors, and glycoproteins--all of which are woven throughout the bones' collagen foundation to orchestrate the periods of active remodeling.

At the cellular level, the current of our aliveness is carried by metabolic cascades linked through a series of biochemical interactions which adjust the body's state of being to demands being made of it. Cytokines are proteins that are involved in a host of different functions throughout the body, and which can stimulate or inhibit these cascades. They can even direct cells to live or die. It was the cytokines' involvement in mounting the body's immune defenses that caught my interest. Inflammation, as you will remember, is the immune system's response to injury. Whether the injury is the result of chemical, microbial, or physical assault, the body reacts with an increase in blood flow and the release of disease-fighting white blood cells to the area. Heat, redness, pain and swelling are the noticeable consequences of this swift and potent defense.

An athlete's life such as mine is characterized by intense engagements of body and will: inflammation is the mark left by the fires of this passionate encounter. Left to smolder, those hotbeds cause long-term damage to tendons, joints, and even bone. No matter where the inflammation originates—autoimmune problems, toxic gut, glucose imbalances, oxidative stress—the immune system's response will be to flood the body with a deluge of pro-inflammatory cytokines.

Because some of the same cytokines that are active in immune reactions are involved in bone resorption, I looked further into this important link between the inflamed tissues of my hip and the scorching erosion of the bone. One of these cytokines, interleukin-1 (IL-1) stimulates the production of PGE2, a powerful prostaglandin involved in the inflammatory process. Il-1 also happens to be one of the most powerful stimulators of bone resorption.

Another cytokine, interleukin-6 (Il-6), not only stimulates the production of the bone-eating osteoclasts, but it can also increase their destructive potential by extending their normal lifespan. Levels of this cytokine are also high in the inflamed tissues of an injured joint. The link between bone resorption and inflammation was becoming clearer.

And there was more: when Il-6 is elevated it can decrease the synthesis of cartilage proteoglycans, the water-loving molecules in joints whose synthesis depends on glutamine—the same glutamine which is depleted by both Gilbert's syndrome and intense exercise. Combining Gilbert's with elevated Il-6 could severely limit the production of proteoglycans, taking the bounce right out of joint cartilage, and stripping its ability to absorb the compressive forces of exercise. Take the resilience out of cartilage and even low-level activity can be destructive to joints and the surrounding bone.

One of the pro-inflammatory cytokines, tumor necrosis factor (TNF), is from a family of molecules that help regulate bone cell activity. Another important member of that family is receptor activator nuclear kappa-B ligand, or RANKL for short. (I talk A LOT about this molecule in my book, The Whole-Body Approach to Osteoporosis.) A ligand is a communication molecule. This particular communication molecule, RANKL, is released by the osteoblasts and attaches to a special membrane receptor that goes by the acronym RANK, on an osteoclast precursor cell. The
precursor cell of an osteoclast is a type of white blood cell (thus the link to the immune system and bone). By activating this receptor, RANKL has keyed the precursor cell to develop into an osteoclast. So it is through the cytokine RANKL that osteoblasts control osteoclastic activity.

The key, at least for me, is that RANKL-induced aggressive bone resorptin can be stimulated by the over-production of pro-inflammatory cytokines and these same cytokines are capable of blocking osteoprotegerin (OPG). OPG is a "safety net" molecule released by osteoblasts that can prevent excess RANKL from over stimulating osteoclastic activity. With my N-TX (bone resorption marker) spiked so high, excessive osteoclastic activity in my bones was obvious. the linkage between stress, over-production of inflammatory cytokines, and the resulting over stimulation of the RANKL/RANK system suggested a trail to follow—a trail that might reveal the destructive pattern whose effects were showing up in symptoms and lab tests.

The athlete may not always be able to see it but high level competition is stressful. When I was training hard, I didn't think of it as stress, it was just what I did...who I was. But with pro-inflammatory cytokines making a clear link between bone loss and inflammatory states, I began to see my sports life in a different light. Could all of those miles that I ran, biked, and swam actually have contributed to the bone loss instead of stimulating its formation as we generally assume? The impact of healthy amounts of weight-bearing exercise is significantly different than flogging your body for hours upon hours, year upon year—especially if there is insufficient awareness of nutritional needs and an another underlying metabolic disorder (in my case Gilbert's).

Now the words of the acupuncturist began to make more sense. "A constitution dominated by the fire element, and the smell of being scorched." Had I done more than just bruise my wings? maybe I had been literally "scorched" by an unrelenting inflammatory cascade within me. An inability to limit the activity of the pro-inflammatory cytokines would  continually fuel smoldering fires and steadily sap the bones' strength. Now I saw that I had never given the time or the extra nutrients necessary for my body to recover between the intensity of workouts. When the heat is kept up non-stop and the furnace is never allowed to cool between engagements, the walls can crack...and the bones will break.

Saturday, January 6, 2018

This is Part XI of a multi-part essay chronicling my personal experience with osteoporosis. In this series I have been taking readers through the diagnostic and treatment phases of my care that began over 18 years ago when I was diagnosed with severe osteoporosis. Over the years, the combination of experiencing multiple fragility fractures along with an intense immersion into the study of bone pathophysiology has given me a unique understanding of this disease. If you are just joining the series, I encourage you to skim through the previous DX Severe Osteoporosis essays on my blog as they provide background to each new installment. It is my hope that this series will provide you with a better understanding of osteoporosis in general, plus a few "pearls" that you may be able to incorporate into your own quest for better bone health. If you have been reading the essays all along...welcome back.    Dr.M

                                          "And now here is my secret, a very simple
                                            secret: It is only with the heart that one can
                                            see rightly; what is essential is invisible
                                            to the eye." 

                                                                         The Little Prince
                                                                         Antoine de Saint-Exupery

Not only was I beginning to discover ways to improve my skeletal and overall health but I was also starting to see osteoporosis through a much different lens—and this lens was projecting multiple images from seemingly divergent rays of medical and biochemical data. For example, exercise signals the body to form bone. Well, I had certainly engaged in enough exercise in my life to build several skeletons if this was the case. So why was my skeleton, or at least its density, so paltry?

Concussive forces and the shear strain (an engineering term for the application of force at a specific angle) from muscular activity send waves of vibration rippling through the body and into bone. Here, cells called osteocytes detect and respond to these mechanical signals, translating them into biochemical signals that stimulate bone-building. Osteocytes start off as osteoblasts, the very cells that build bone. When osteoblasts have finished forming the collagen matrix foundation of bone, each osteoblast then builds a small chamber around itself. This chamber is like a cocoon offering a protected site for the osteoblast's transformation into an osteocyte while the matrix around it is being flooded with solidifying minerals such as calcium, phosphorous, and magnesium. Once the bone is calcified, the now chambered (in an elongated cartilage sac called a lacuna) osteocyte is in place and able to receive those vibrating wave forces—the signals necessary to activate future bone remodeling activity.

Osteocytes in lacunae
Osteocytes have a star-like configuration with appendages reaching out through bony tunnels that radiate from them. These tunnels are fluid-filled corridors extending to neighboring osteocytes, and along them the vibrating mechanical signal is communicated from one osteocyte to the next. Thus, from every movement of the body, there comes the potential to alter the shape of each osteocyte's cell membrane. It is at this point that the signal changes from a mechanical one to a biochemical one. Receivers in the cell's membrane transmit the signal (if the membrane is healthy enough) into the cell where substances that promote bone formation are then released.

Because of this link between physical activity and osteogenic (bone forming) signaling, it makes sense that athletes generally have better bone density than non-athletes. But for athletes who have pushed themselves to excess for years...decades...this positive response to exercise may indeed turn into a negative response. Over stressing the body regularly with excessive, adrenal cortisol-releasing stress, coupled with neglecting to sufficiently refuel the body with important nutrients, puts the active aging athlete at considerable addition risk for osteoporosis. In addition, exercise alone does not necessarily make for better bones. Young adults who take up an exercise program will only gain a small amount of bone density. A post-menopausal woman who starts working out in a gym won't typically gain any density. Her low estrogen causes a continued loss of bone, although her rate of loss will not be as rapid as a post-menopausal woman who does not exercise. So exercise helps to stimulate osteogenic signaling, and it is vitally important for both bone and overall health, but it will not result in increased bone density beyond a certain age—and it is not the primary determinant of bone density at any age.

I was not only seeing that bone was very much alive and amazingly complex but I was beginning to sense that it had a hidden dynamic life. Bone is amazing in that it can undergo change both by remodeling its architecture in response to external mechanical demands, and to internal physiological needs. A hefty percentage of bone is fairly quiescent at any given time. It is just there, doing its job of supporting the body and providing a reservoir for minerals. But in areas in need of repair or when the body is desperate for mineral reserves, metabolic and remodeling activity increases dramatically. Continuous cycles of remodeling are necessary to maintain skeletal health for normal, everyday activity—but when the stresses of life (both physical and emotional) increase, or when the concussive forces of weight-bearing activity are particularly high, micro-fracturing of bone and the need for
repair increases. Weakened bone must be replaced with new, resilient bone. This renewal process is accomplished by coordinated cell groups called basic multicellular units (BMUs).

At any given time there can be millions of BMUs, areas where osteoclasts are actively tearing down old micro-fractured bone and new bone is being formed in its place. Osteoclasts move like predators on the prowl for injured prey. They feast on old microfractured bone, leaving gouged out tunnels and troughs, and then move on. The osteoblasts come in behind, filling the stripped out areas with strong, new collagen matrix. This bone-like substance, called "osteoid," is then mineralized over the next several weeks by osteoblasts. These cells deposit crystalline mineral salts (hydroxyapatite, such as in OsteoMineralBoost) between the collagen fibers to make them rigid and increase their overall strength. Once this biomineralization has occurred and the hydroxyapatite crystals are in place, the bone formation process is complete.

My job was to try and find out if this process was going on in my body and if not...why? Intermittently, as I learned more about bone biology and it hidden physiology, I would scan the slide from the biopsy of my pelvis looking for clues. I could see the BMUs very clearly in their lit-up red tetracycline "ink." Instead of the uniform mineralized bone formation typically seen in "normal"
Zebra-striping: red is new mineralized bone
bone, my BMUs were filled with alternating layers of mineralized bone and un-mineralized matrix, giving it a zebra-striped look.

To me, this suggested there may be a mineralization defect of some kind that was involved in my osteoporosis. It really looked like my severe bone loss—bone weakness—wasn't just from over-activity of the osteoclasts breaking down excessive amounts of bone, but that there was something else going on in addition. It looked as though the crystalline mineral salts weren't "sticking" to the osteoid matrix after it was formed. Or that maybe there was something intermittently inhibiting mineralization. Maybe there was a mineral missing?...or a toxin infiltrating and preventing the hydroxyapatite crystal from forming? Maybe the levels of my testosterone and estrogen hormones were fluctuating every few days? Could the vitamin D and parathyroid hormones which are responsible for pulling in calcium from the gut and kidneys, and maintaining its optimal levels in bone and blood somehow be ineffective? Their levels, after all, had been tested several times over the past year and shown to be normal which meant that the calcium should be there in high enough quantities. Maybe my low level of essential fatty acids (that I discovered through lab testing) was involved? Fatty acids are needed for absorption and deposition of calcium into bone. But if the fatty acids were keeping me from bringing in enough calcium, then shouldn't my parathyroid hormone have been elevated in response to low levels of calcium? My questions seemed endless, and my dearth of information was evident and discouraging. I was seeing that this last question, that of parathyroid function, was of prime importance when evaluating the causes of bone loss, and that is where I placed my next investigatory lens.

                                                    "I need to put up with two or three
                                                       caterpillars if I want to get to
                                                      know the butterflies."

                                                                                The Little Prince
                                                                                Antoine de Saint-Exupery

Stay tuned for DX Severe Osteoporosis - Part XII

Sunday, December 24, 2017

DX Severe Osteoporosis: Part X - Impacting Skeletal Health

This is Part X of a multi-part essay chronicling my personal experience with osteoporosis. In this series I have been taking readers through the diagnostic and treatment phases of my care that began over 18 years ago when I was diagnosed with severe osteoporosis. Over the years, the combination of experiencing multiple fragility fractures along with an intense immersion into the study of bone pathophysiology has given me a unique understanding of this disease. If you are just joining the series, I encourage you to skim through the previous DX Severe Osteoporosis essays on my blog as they provide background to each new installment. It is my hope that this series will provide you with a better understanding of osteoporosis in general, plus a few "pearls" that you may be able to incorporate into your own quest for better bone health. If you have been reading the essays all along...welcome back.    Dr.M

                                "It's a good idea to keep at least a vague idea of
                                  where you are, no matter how much you are used to 

Now, with this inflammatory reaction to gluten being such an obvious concern, I began to look at this strand of the web through every lens I could. It didn't take long to find a few more important connections. Glutamine, an amino acid energy source for cells that line the intestinal wall, is often found deficient in professional athletes that train hard every day and I certainly fit into that category. Cells of the digestive tract need glutamine for sustenance, growth, and energy production. In an exhausted body that isn't being properly replenished, glutamine levels drop and cells of the gut suffer, with poor absorption of nutrients the unfortunate result.

Even if absorption is normal, a hard-working athlete piles on both oxidative and adrenal stress producing copious amounts of free radicals and high blood titers of the catabolic, destructive hormone, cortisol. Excessive free radical and cortisol levels places high demand on essential fatty acid supplies. An athlete's body extracts aerobic energy from molecules reacting with oxygen. In this process, the oxygen molecule looses an electron and becomes an unstable scavenger called a "radical." These free radicals are insatiable, stealing electrons from their closest molecular neighbors, which results in cellular damage. It's the phospholipids (made from fatty acids) in a cell's membrane, that often get damaged...and a cell's membrane, as I would find soon find out, is vital for more than just defining the cell's boundary.

Fatty acids and phospholipids are vital for optimal cell membrane function including the transference of signals from one cell to another. If omega 3 fatty acid intake is deficient, cell membranes (and their ability to transfer signals) suffer. Athletes are particularly demanding of omega 3 fatty acids and optimal intake is necessary to achieve high level performance. Without omega 3s, cell membranes loose some of their functional capacity. This loss of function not only alters the normal signaling of important information but it also increases the signaling for a heightened inflammatory response!

Over the next few months, I discovered more strands in this elusive web. Amazingly, there was no paucity of evidence in the literature showing that the cells and substances that the body releases in response to inflammation were also the cells involved in the destruction of bone. As the bone in our body ages, it becomes less resilient and develops microfractures. This old weakened bone must be replaced with new bone. Both bone resorption, the dissolving of the old, microfractured bone, and inflammation in response to injury, are crucial to overall health. But when the body fails to limit these processes, the immune system gets out of balance and the skeleton goes into a spiral of disrepair.

In my case, the inflammation in my hip began as a response to the stress fractures but then something went wrong—the injured tissues didn't heal, and the inflammation became chronic. And the Gilbert's* syndrome...?...The condition where bilirubin (a breakdown product of blood) increases due to a specific genetic enzyme deficiency? Where did that fit in? This "harmless," hereditary liver disorder, I found, interferes with fatty acid absorption from the gut. (Yes, the same fatty acids that are often found to be depleted in athletes.) With 5 to 7 percent of the population having this disorder, it seemed to me that it should be taken more seriously by the medical community, especially when dealing with people with an ongoing disease process...such as osteoporosis. An athlete with Gilbert's is under double the physiological stress and at a higher risk for inflammatory related disorders, including osteoporosis. Combine this with a sensitivity to gluten and we have a condition ripe for severe bone loss.

The doctors had assured me that there was "no connection" between Gilbert's and my hip pain or my osteoporosis. But that was NOT what I was seeing. What I was beginning to see was that in medicine, the term "no connection" really meant "we have not yet made that connection" or "we don't have the time or money to research it right now." In their eyes, if it hasn't been researched, it isn't worth thinking about. (And if pharmaceutical companies don't see a way to make money on it, it won't be researched.)

Of course, it is not only the essential fatty acids that can become deficient as a result of the athlete's frequency and intensity of exercise. Vitamin and mineral deficiencies are common, as are deficiencies in amino acids. Glutamine and methionine are often in short supply in both the athlete and in people with Gilbert's syndrome. Not a good thing considering the almost endless biological functions that these two amino acids are involved in: energy production, muscle building, fuel for cells of the immune and gastrointestinal systems, collagen synthesis for both joint and bone, the production of glutathione (the body's most important antioxidant), etc... These two amino acids are needed for just about everything. I immediately began supplementing my diet with glutamine and methionine, and whey protein which is a balanced source of essential amino acids. I also began to take milk thistle (sylymarin). If Gilbert's was involved in the liver's ability to function, I wanted to cleans and optimize the function of my liver as much as possible. With my chiropractic training and interest in nutrition, I knew that consuming lots of fresh green vegetables and supplementing with milk thistle could help. Milk thistle is known for its ability to fortify the liver and, as I found out, prevent the depletion of glutathione and limit free radical damage. It finally felt like I was not only starting to see patterns in this complex web, but that I was also finally starting to understand enough that I was able to do things to positively impact my skeletal health.

...Stay tuned for Part XI of DX Severe Osteoporosis

Saturday, December 9, 2017

DX Severe Osteoporosis: Part IX - Seeing Specific Threads of the Web

This is Part IX of a multi-part essay about my own personal experience with osteoporosis. I will be taking you through the diagnostic and treatment phases of my care in hopes that it provides you a better understanding of osteoporosis in general, and pearls that you can use to better your own bone health.

                        "We all see mountains. It is how we climb them that is different."

                                                                                Crucibles of Will

When the body is injured, the immune system's inflammatory response infiltrates the area cleansing it with blood and scavenging, destroying invading organisms. In situations of injury, inflammation can be the magic to survival, but in chronic disease, it is the destroyer of life as we once knew it. Chronic systemic inflammation, in fact, is the major cause of osteoporosis.

To initiate the inflammatory response, the body's first step toward protecting and healing damaged tissue is to put out a call for prostaglandins. These are naturally occurring chemicals that relax smooth muscle and cause peripheral vasodilation to facilitate blood flow. The body produces a specific prostaglandin called PGE2 from fatty acids found in abundance in red meat and dairy products. In addition to vasodilation, PGE2 is responsible for the fever we get when we are sick. It can also be responsible for muscle and joint pains, and, even skin sensitivity—one of my symptoms. These sensations can happen when there is an imbalance in dietary fatty acids, such as an excessive intake of omega 6 fatty acids, even when we aren't sick. It sure was looking like my discovery that I was low in omega 3 fatty acids, coupled with Gilbert's syndrome, may not only connect the dots to my symptoms, but also to my elevated bone resorption markers...and to my osteoporosis.

There are other prostaglandins not directly involved in the inflammatory response but which help prevent excessive inflammation. These prostaglandins are derived from the omega 3 fatty acids, ones found in oils from flaxseed, algae, and in cold-water fish. The sources of these fatty acids happen to be less prevalent in the typical American diet, and this is part of the reason why deficiency is common. That is, deficiency from terrible diets, which I was now beginning to see, was mine.

I felt like I was on to something important, or at least my forever positive attitude was grasping for something—anything—to shed some light on this thing. I dug deeper into the research about prostaglandins and as it turned out they weren't just important for the inflammatory response, but they were involved in bone metabolism! Prostaglandins are made by osteoblasts and can stimulate both the formation and resorption of bone. This was certainly another huge clue. Here was something that seemed to link my vague symptoms (skin sensitivity, irritability, and intermittent feelings of weakness) to two different body systems: the immune's inflammatory response AND bone biology. In addition, it was my first indication that the chronic hip inflammation and the bone loss could be linked after all. I kept remembering what an endocrinologist from the Mayo Clinic and the one from California had said, that there was "NO connection" between my persistent hip pain and the osteoporosis. They acknowledged the connection between the hip stress fractures and the osteoporosis but not the persistent hip inflammation. I didn't understand how they could be so sure about something like that.

But why was I deficient in fatty acids? The endocrinologist had told me that he had tested for diseases that could interfere with absorption, but that these tests came back normal. Plus, I had none of the symptoms typically seen with tropical sprue, Whipple's disease, Crohn's disease, Zollinger-Ellison syndorome, or any of the other 20 or so absorption disorders described in the medical texts.

When I began to look more closely at my diet I discovered that even Americans eating a fairly "good" diet aren't getting enough omega 3s. If highly processed foods, especially ones made with hydrogenated oils, are a large part of ones diet, imbalances of fatty acids become even more common. Looking back to my intense training years, I was certainly not as vigilant about eating well or for that matter eating at all. At times when money was tight I may have just let meals slide, and certainly processed foods were part of my diet. Even so, I felt there had to be more to this picture than just diet. Currently I was eating more healthy foods, avoiding junk foods, and consuming salmon and other cold water fish that were good sources of omega 3s. I knew that eating healthily and taking in good quality nutrients was only one part of the complex process of nourishment for life and growth. There just had to be more to this story.

I went back to thinking about problems that could interfere with the absorption of nutrients, like poor digestion or malabsorption. The more I read about osteoporosis, the more celiac disease popped up in the writing. But the endocrinolgist had ruled out celiac disease. Or had he? I went over the prior lab work from over a year before and found the test results for anti-tissue transglutaminase IgA (tTGA) (the blood test for celiac disease). The result: 19 U/mL with a reference range of less than 20 units as negative, 21 to 24 units as borderline, and 25 units and over as positive for celiac disease. Yes, it looked like I was negative for celiac disease. But I got to thinking, how can this be a pregnancy "yes/no" type test? It didn't seem like that at all. What was this tTGA test testing for anyhow? When I found out that transglutaminase was an enzyme released by gluten damaged enterocytes (cells lining the intestinal tract) and their microvilli (small appendages for better absorption of nutrients) in the gut it clicked! If my test result was 19 U/mL and 20 is borderline positive, well, there MUST be some kind of damage to my gut taking place. Maybe not total damage to the extent that my gut's microvilli 
were totally atrophied (flattened) (which is what happens in Celiac disease) but damaged none-the-less.

Celiac disease is an intolerance to gluten in wheat, barley, and rye that causes all kinds of abdominal symptoms. Bloating, diarrhea, constipation, these are all symptoms of celiac disease. The more I read about the disorder the more intrigued and excited I got—especially when I came upon the term, silent celiacs. These are people who have celiac disease but have few or no symptoms at all when they eat food with gluten in it. Now I was really thinking, maybe my 19 U/mL for tTGA was significant after all.

I had none of the typical bloating, constipation, diarrhea, kind of symptoms seen with celiac. But I did have intense abdominal pain after hard runs that I was now relating, at least in part, to Gilbert's syndrome. With this elevated tTGA test result it occurred to me that although I may not have full blown celiac disease I sure could have a sensitivity of some kind to gluten. A sensitivity severe enough to cause some loss of absorption or an influence of some kind on my bone health. I knew I needed to do some more testing on my own. The next two tests I did were the antibodies for gliadin (gluten), IgG and IgA. The results: 36 and 42 units respectively. With a reference range of less than 20 units being negative and 20 or more units indicating that antibodies to gliadin were detected, I knew this was significant. I may not have celiac disease with microvilli flattening but there was enough sensitivity to gluten that the enterocytes were "leaking" transglutaminase. These cells were certainly not happy and indeed were causing an immune inflammatory response.

With these results, the possibility of nutrient malabsorption was a concern. And even if the damage from gluten in my diet wasn't severe enough to cause severe malabsorption my research uncovered a little known fact. One that most doctors have no idea exists. Bone loss caused by gluten sensitivity is not simply from the malabsorption of nutrients. A person's sensitivity to gluten can lead to bone loss through two completely different physiological mechanisms. Besides causing damage to enterocyte microvilli which leads to malabsorption, gluten sensitivity triggers a systemic rise in proinflammatory cytokines. These cytokines, along with the release of a protein called zonulin by the enterocytes, causes the tight junctions between the cells to separate forming the condition of "leaky gut". Gluten and other huge molecules enter through these large openings setting off a systemic inflammatory response (thus the elevated anti-gliadin IgG and IgA tests). When this occurs for months and years at a time, it can produce a chronic systemic inflammatory response. Yes, I was now seeing real, specific threads in this entangled web of bone loss. It was one of the most powerful aha moments in my life.

"Hang out with your fear when you're feeling afraid. Follow its movement. Become intimate with it. Fear is an opportunity. Approach it like a tracker in the forest — watch where it goes, what it does, what it eats, where it eats, where it rests, where it turns, where it stops, where it hides. Embrace it. Stay with it."
                                                                                Paul Rezendes, The Wild Within

 ... Stay tuned for Part X of DX Severe Osteoporosis

Sunday, November 19, 2017

DX Severe Osteoporosis: Part VIII - Implicate Medicine

This is Part VIII of a multi-part essay about my own personal experience with osteoporosis. I will be taking you through the diagnostic and treatment phases of my care in hopes that it provides you a better understanding of osteoporosis in general, and pearls that you can use to better your own bone health.

                              "So the relationship of each moment in the whole of all the
                              others is implied by its total content: the way in which it "holds"
                              all the others enfolded within it."
                                               David Bohm, Wholeness and the Implicate Order

My constitution was fire, according to the acupuncturist. Looking back over my life and the intensity with which I approached things...well, I could relate to that assessment. But the smell of being "scorched"...that was just embarrassing...

Bone has three main functions: it supports the frame, protects organs from hard knocks, and acts as a reservoir for energy (fat) and minerals. I had a hunch that it was the last that would hold the most clues to the cause of my osteoporosis, especially since the biopsy showed that my bones were gaunt, with thin, disconnected trabeculae. They looked totally spent—scorched from years of, well, that was the question. Years of what? Malabsorption of nutrients? But the doctor had said I didn't have any absorption issues. Could it have been all those years of training in athletics? With my eyes focused on making the US Olympic Team since I was 13 years old, I had certainly stressed my body to the core. Had it been all those years of stressing my adrenal glands, stressing the overall functions of my body, that had sucked the energy out of me. Could those years have sucked the reserve function right out of my bones? There are lots of athletes who train hard for years and years and don't end up with osteoporosis. So that, at least by itself, wouldn't make sense either. But there was no denying, from the biopsy, it certainly looked like my bones had given just about all that they could give. And now, at the age of 45, all that was left was just empty chambers. And it looked as if they had been running on empty for quite some time.

The endocrinologist had ordered over 30 lab tests but everything was coming up normal, or at least that was his interpretation. At first I just went along with what he said; after all, his expertise on the subject was obviously considerably greater than mine. But, by a year into this mess (of being diagnosed with osteoporosis) my understanding of the technical aspects of bone loss improved and I began to look back over the lab tests more closely. While they were mostly pretty good, I noticed that some of the results were just a little off, just a little out of the normal reference range. I began to wonder, could these have meaning, as they relate to osteoporosis, that the doctor may not have understood?

Doctors focus on body parts and body fluids to help them understand a disease. But it's really impossible to understand everything...every slight variance in lab test and every "minor" symptom a patient presents with. And even if a doctor did understand these variances, would they try to put all those bits of information together, like pieces of a puzzle, in an effort to understand the patient as a "whole?" For example, I had told my endocrinologist that my skin was sometimes extremely sensitive, at times I was irritable (for me that was really unusual), and my stomach often hurt after long intense runs. I had also told him that I sometimes felt a slight overall body weakness. I couldn't really describe some of these feelings very well and I guess my ability to compete on a high level in road races and triathlons put him at ease that these vague symptoms weren't from something terrible brewing. In fact, he didn't seem to be interested in any of these symptoms, and as for the slightly-off lab work, that was quickly tossed aside.

After my biopsy, several months passed when I thought things might be better, but then I sustained several more rib fractures from very minor traumas. I was getting frustrated. I didn't see any progress in the investigation and now I was breaking again. We didn't seem to be any closer to finding answers to why I had osteoporosis than we were at the beginning. With each visit to UConn there was just a repeat of all the lab tests that had already be done...nothing new and no focus on what lead to follow next. In fact, there just didn't seem to be any leads at all. The only thing that was happening was just a reiteration that I needed to take a bisphosphonate medication which I did not want to do.

With my greater understanding of osteoporosis and my closer look at the lab work (especially those results that were just outside of the normal reference range), I noticed some interesting connections. The "normal" comprehensive metabolic profile (CMP) for example, showed an elevated level of bilirubin, a breakdown product of red blood cells.

My hunch was that each of my symptoms and the "slightly off" lab tests could have some significance. Each of these might hold clues to understanding the "whole" of me, or at least to the source of my severe bone loss. I felt that implicate* within each symptom, within each slightly-off lab test, there could be some view of the whole answer. Like cells that each hold the same DNA map of the complete organism within them, my symptoms had implicate within them the wholeness of my body's dysfunction. In other words, the biology of each symptom was part of the biology of the disease, which was part of the biology of my whole body's functioning. Each symptom was significant to some extent or another. But like DNA, which is nothing without the cell that cradles it, each symptom and slightly off lab test by itself had no meaning. Even the low bone density (bone quantity) meant little without a vision of the whole structure: what my risks for fractures were, what my bone quality was, what my muscle strength was, and how my organs were functioning. Everything had to be, or at least should be, looked at together.

In addition to the high calcium in my urine and the elevated N-telopeptide indicating a high rate of bone loss, I was now aware of this elevated level of bilirubin in my blood. Could this have meaning? When I thought back to the first weeks after my diagnosis, I now remembered that the endocrinologist had said that I had a mild disorder called Gilbert's Syndrome. In retrospect I saw that he was referring to this elevated bilirubin. But I also remembered that he said it didn't have any bearing on my osteoporosis and we had both quickly dismissed it.

Now, a year later, the elevated bilirubin** and my renewed interest in a possible malabsorption issue prompted me to run some lab tests on my own. One of these tests was for fatty acids and the results were startling. I was extremely low in polyunsaturated fatty acids. I didn't understand it, how could I be deficient in these? My diet included oils such as corn and safflower; I ate peanuts and fish and lots of other foods that contain high amounts of essential fatty acids. They were in my diet...but maybe I wasn't absorbing them? The endocrinologist said there was no connection in this either. But I started to think that maybe the fatty acid deficiency was somehow keeping the inflammation going on in my hip. After-all the hip was still hurting, a year now since the hip pain first began and since I had initially been diagnosed with osteoporosis.

Could the low blood polyunsaturated fatty acids and the Gilbert's Syndrome have something to do with the lingering hip pain—or the osteoporosis—or both! Maybe, I was beginning to see what could be the head of a faint trail. All of a sudden it felt as though I had stepped into nature's complex biochemical laboratory where life's continual transformations are fueled and formed. I began to understand chains of biochemical interactions that I never knew existed, and these chains, like strands in a spider web, were being woven by all the biochemical influences of every organ system in the body. The biochemical trails through this web were confusing and seemed infinite.

In an effort to uncover more strands to this yet completed web, I began to think back to the days in high school and college where I had so much abdominal pain after runs that I had to curl up on the floor and wait for the pain to go away. And then I remembered that this pain, although not as frequent or intense, but there none-the-less, sometimes occurred into my 30s...and, into my 40s. Not all the time, but just after hard runs I would sometimes have intense abdominal pains. It had actually just become part of me and I really didn't think about it any more. But now, reading about Gilbert's—nausea, abdominal pain, weakness—especially after the stress of intense exercise and dehydration...well, now things were starting to make sense. The web was starting to take shape.

                              There are things we can only learn about an organism by taking
                              it apart—but to understand that organism we must fully engage
                              with it as a dynamic, interconnected whole. It is no wonder that
                              different parts of the body—the skin, joints, spine, organs—may
                              all be affected by a disease process even when they have no 
                              obvious or direct physical, chemical, or neurological 
                              connection with each other or the process itself.

* "Implicate" (order) is a term developed by David Bohm, a theoretical physicist, who developed a mathematical and physical theory that explored the concept that everything is connected.

** (For more on bilirubin and osteoporosis visit my blog.)

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