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. (…as 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 and…in 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 answer…it 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

(Start from Part I)

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.

Continue to Part XIV