Tuesday, December 11, 2018

Homocysteine and its Negative Impact on Bone

Elevated levels of homocysteine (Hcy) in the blood, a condition called hyperhomocysteinemia, is a common finding in patients with osteoporosis. Unfortunately, this not only increases a person's risk for fracture (by Hcy's adverse effects on bone quality), but for each 5 micromole/liter rise in Hcy, there is a 33.6% increase in all-cause mortality risk (Fan et al., 2017). 
Homocysteine is a byproduct from the metabolism of methionine, an amino acid found in meat (and nuts, soy, eggs, dairy). But even vegetarians can have elevated Hcy levels. This is because B12, a vitamin found in meat, is important for the conversion of Hcy into methionine and other metabolites. In addition to vitamin B12, several enzymes and the cofactors B2, B6, folate, betaine and magnesium are necessary to metabolize Hcy and lower its level in the blood. In cases of nutrient deficiency, and/or having the genetic polymorphism of the methylenetetrahydrofolate reductase (MTHFR) enzyme, Hcy levels rise and create breeding grounds for chronic disease.   
Homocysteine levels above 15 micromoles/liter can damage nerve cells and blood vessels leading to cognitive decline and cardiovascular insufficiency (Ostrakhovitch, 2018). In addition, hyperhomocysteinemia reduces bone strength by slowing osteoblastic bone-building activity, stimulating osteoclastic bone resorption, and disrupting bone collagen cross-linking molecules making collagen stiff and bones extremely fragile. Hcy creates oxidative stress in the body and increases the production of advanced glycation end products (AGEs) which reduces both bone quantity and quality and, therefore, bone strength.  
One of my goals, when helping patients reduce fracture risk, is to stop rapid bone loss and falling bone density T-scores. Through serial assessment of bone resorption biomarkers (CTX, NTX, and/or DPD) we are able to identify rogue osteoclastic activity and provide safe, appropriate, and effective therapy. Hyperhomocysteinemia can be effectively treated through exercise, diet, and nutritional supplementation. By lowering Hcy levels, we are able to see improvements in bone health through the lowering of bone resorption biomarkers.            
Fan, R. et al. 2017. Association between homocysteine levels and all-cause mortality: a dose-response meta-analysis of prospective studies. Scientific Reports 7, 4769.  
Ostrakhovitch E.A. and S. Tabibzadeh. 2018. Homocysteine and age-associated disorders. Ageing Research Reviews, https://doi.org/10.1016/j.arr.2018.10.010.  

Sunday, November 11, 2018

Lactoferrin and Alpha Lipoic Acid for Osteoporosis

One of my goals as president of OsteoNaturals is to provide our customers with up to date information about osteoporosis and therapeutic options. To do this I typically peruse hundreds of medical research articles each month while sitting in the basement of the University of Massachusetts library. Scouring PubMed for exciting (yes, I love it!) research is rewarding...and fun (yes, I'm a nerd). The more I learn about the pathophysiology of osteoporosis and possible therapeutic options--both pharmacological and nutritional--the better I can help others combat their bone loss. In the last blog, I wrote about the beneficial epigenetic effects of three biocompounds in OsteoStim. In this Newsletter I want to briefly mention two articles I came across this week, one about the bone building effects of lactoferrin and the other about alpha lipoic acid-- both of which are ingredients in our
Lactoferrin is a natural protein supplied by Bioferrin 1000 in our OsteoStim product. Lactoferrin boosts bone health in two ways: 1) it stimulates osteoblast bone formation activity, and, 2) it curtails bone loss by calming aggressive osteoclastic bone resorption. The overall effect of lactoferrin is that of improving bone quality and quantity for better strength and reduced fracture risk.  
In an article from the International Journal of Biological Macromolecules, researchers explore the molecular mechanisms of lactoferrin on bone building activity. Using cell cultures, Liu, et al. (2018)  investigated the enzymatic effects of various mitogen-activated protein kinase (MAPK) pathways on osteoblast cell function. They concluded that lactoferrin induced osteoblast cell proliferation and that it is "an osteogenic growth factor" and has the potential as a "therapeutic agent to treat low bone mass in patients with diseases such as osteoporosis." Yes, we have certainly found that to be true as we are hearing of great results from those who take OsteoStim!  
The second article is by Roberts and Moreau from the University of Nebraska. This article (2015, Nutrition Reviews) gives a fairly good explanation of the mechanisms alpha lipoic acid (ALA) has on improving bone health. This bioactive compound scavenges reactive oxygen species (ROS), disposes of heavy metals, regenerates vitamins C and E, and increases CoQ10 levels (for cell energy). ALA's antioxidant properties and ability to reduce oxidative stress and inflammation are the reasons it has been used successfully for years to treat chronic diseases such as diabetic neuropathy and liver disease...but it also works wonders for bone. 
Oxidative stress and chronic systemic inflammation are the prime destructive forces behind the accelerated bone loss of osteoporosis. ALA reduces bone loss by lowering ROS and inflammation which creates a calming effect on hyperaggressive osteoclastic bone-resorbing activity.  
What I have found over the years is that the unique combination of ingredients in OsteoStim produces a beneficial composite effect on bone, and that "the whole is far greater than the sum of its parts".  

Monday, October 29, 2018

Bio-Active Compounds and the Epigenetics of Osteoporosis

To better understand how bio-active compounds in food and certain supplements (such as the berberine, milk thistle, and taurine found in OsteoStim) work to improve health, we first need to understand the epigenetics of nutrigenomics (a fancy word for how nutrition affects our genetics).
Epigenetics: We know what genetics is about: a biological map of how we are put together and what makes us who we are...what makes us unique...but what about epigenetics? Epigenetics refers to external modifications to DNA (not actual changes to DNA sequencing) that turn genes "on" or "of". A good example of this is methylation. Methyl groups are molecules consisting of one carbon and 3
hydrogen atoms. When a methyl group is added to other molecules it is called methylation, and when a methyl group is taken away it is called demethylation. When adding or detaching methyl groups to molecules, it has the effect of 'turning on" or "turning off" a biochemical reaction. It's kind of like turning a light on or off with a switch. This is epigenetics at work. In epigenetics, the DNA sequence has not changed, only how that DNA is being read. The modifications caused by methylation (and other histone modifications) only affect how that genetic information is going to be used: for example how the DNA will or won't produce proteins.
When it comes to nutrigenomics and bone health, DNA methylation is extremely important. (Too much is not good and too little is not good...both can lead to osteoporosis and other chronic diseases.) "Methyl switches" (and other switch forms) work to control just about everything in the body, including how bone forms and how it is broken
down; how it is remodeled. We usually hear of methylation as it relates to cardiovascular and neurological disease, but methylation is also important for skeletal health.  
We know that when bone remodeling gets out of balance, it leads to osteoporosis. Bone cells (the osteoclasts and osteoblasts) must stay in harmony, balanced in their activity for bone to stay healthy. It is through cytokine-orchestrated genetic expression that this activity remains in sync. A person may have genes for strong bones, but the regulators of how those genes manifest are, for some reason or other, not turned on or off correctly and the bone strength is not realized. Epigenetics--how genes are expressed--becomes important when we talk about nutrition beyond the basic bone-building blocks of protein and minerals. Good nutrition encourages a person's genetic makeup to be expressed fully. It allows the epigenetics to engage and bring that person's genetic potential to its optimal expression. But poor nutrition may lead to an under-expression of the genetic code and result in physiological dysfunction and disease.   
DNA methylation also plays a major part in the immune system's response. It therefore is a major regulator of inflammation and that of the chronic systemic inflammation we see in accelerated bone loss.  
One of the reasons it is so important to eat lots of vegetables is because they are a great source of bio-active compounds that are methyl switches and have anti-inflammatory properties. This is also why we put several bone-specific bioactive compounds in our OsteoStim formula. Berberine, milk thistle (silymarin), and taurine are all active bio-compounds involved in either the promotion or reduction of methylation and the regulation of skeletal epigentics.    

Saturday, October 13, 2018

Berberine, a key ingredient in OsteoStim

Berberine is one of the key ingredients in OsteoStim. OsteoStim is our unique (there is nothing even close to it on the market) bone-health supplement that
promotes normal bone remodeling activity through bio-active compounds such as berberine. A strategic blend of antioxidants, vitamins, and medicinal herbs, OsteoStim aids skeletal health by calming osteoclastic bone resorption and boosting osteoblastic bone formation.  
Berberine is a traditional Chinese medicinal herb that is recognized around the world for its health-promoting benefits and treatment of disease. Not only does berberine lower blood sugar and cholesterol levels, but it is extremely effective for dampening chronic systemic inflammation and reducing oxidative stress...two major reasons for osteoporosis and accelerated bone loss as we get older. In addition, berberine activates an enzyme, AMP activated protein kinase (AMPk), within cells. AMPk acts as a chemical sensor to help maintain energy mechanisms including the formation of mitochondria, the power generators within cells. It is through the stimulation of AMPk that berberine is able to reduce osteoclastic bone resorption when RANKL (a cell signaling molecule) is excessively elevated.
Some of you may be familiar with the medication, Prolia (denosumab), for osteoporosis. This drug is an antibody against RANKL (you can read more about RANKL in my book, The Whole-Body Approach to Osteoporosis). By blocking RANKL, Prolia dramatically lowers osteoclast cell activity and thus bone resorption. The end result is higher bone mineral density and less fracture risk, at least initially.  
One of the actions of berberine is similar to Prolia in that it reduces RANKL activity. But, unlike Prolia, berberine does not carry the high risk for serious allergic reactions or adverse side effects. The reasons:
1) Prolia can excessively reduce RANKL levels: RANKL is important not only for activating bone resorbing osteoclasts (some resorption of bone is necessary to keep the skeleton youthful and devoid of excessive microfracture accumuation) but also for a healthy immune response. Excessive lowering of RANKL can cause bone to become "old" and brittle from overly limiting osteoclastic activity. Excessive lowering of RANKL also compromises the immune response, and creates increased risk for infection and serious allergic reactions. Long term use of Prolia (over 3 years) can increase the risk for atypical femur fractures and osteonecrosis of the jaw.  
2)  The Prolia rebound effect: There is an increased risk of broken bones if Prolia therapy is discontinued. When the anti-resorptive effects of Prolia wear off, the body senses the absence of the RANKL antibodies and reacts by hyper-producing RANKL. This leads to accelerated osteoclastic activity and rapid bone loss.  
Berberine, on the other hand, does not excessively reduce RANKL levels. Berberine works to NATURALLY lower inflammation and oxidative stress which are promoters of excess RANKL production. By lowering RANKL to normal levels, berberine does not cause bone to get "old" or brittle.  And, with berberine, there is no accelerated bone loss if for any reason it is discontinued.  
Bio-active berberine is just one of the reasons that makes OsteoStim your number one choice for supplemental bone health. In addition to berberine, OsteoStim also contains therapeutic amounts of vitamins D3 and K2 (MK4 and MK7), biotin, alpha-lipoic acid, N-acetyl cysteine, taurine, Bioferrin 1000, MBP (milk basic protein), and silymarin (milk thistle).
Many of you have been asking, "What can I do in the short term until OsteoStim is available?" My suggestions are:
1) It is not harmful to take intermittent supplement "holidays". Going for a week or two without taking OsteoStim is perfectly fine as long as you are continuing to eat a healthy diet rich in vegetables and devoid in bone robbing food stuffs.
2) If, after two weeks or so, you want to supplement your diet with alpha-lipoic acid (200 mg/day) and berberine (250 mg/day) this will hold you over until OsteoStim is back on our shelves.   

Wednesday, August 29, 2018

RBC Level Can Be An Important Therapeutic Target

If you have read my book, The Whole-Body Approach to Osteoporosis, you know that I focus on therapeutic targets (especially lab test results) to design bone-strengthening therapy and monitor progress.

One of the tests I look at when evaluating patients with bone loss is the CBC (complete blood count) and specifically the index, RBC (red blood cell) count. People with osteoporosis often have lower RBC counts than individuals with normal bone density. The reason for this seems to be two fold: 1) lower sex hormones, estradiol and testosterone (a risk factor for osteoporosis), in both women and men is correlated to higher bone marrow fat, and 2) chronic systemic inflammation and higher oxidative stress (also risk factors for osteoporosis) lead to a build-up of bone marrow fat and PPAR-
More than 50% bone marrow fat (round white objects) in severely osteoporotic bone
gamma (nuclear) receptors. High levels of bone marrow fat (over 50%) crowds out the hematopoetic stem cells that form RBCs. The PPAR-gamma receptors, when activated, pull a "molecular switch" that converts mesenchymal stem cells into fat cells instead of bone-forming osteoblasts.  
In plain English...this means that low RBCs in people with osteoporosis can mean higher rates of bone loss, lower rates of bone formation, deficient levels of sex hormones, and higher chronic systemic inflammation. Proper therapy not only increases RBC levels over time, but also improves skeletal health and reduces fracture risk.   
OsteoNaturals OsteoStim is a unique complex designed to repress PPAR-gamma activity, lower free radicals and oxidative stress (thus, chronic systemic inflammation), reduce osteoclastic bone resorption, stimulate osteoblastic bone formation...and yes, increase RBCs.    

Saturday, May 12, 2018

Long-Term Effects of Bisphosphonate Therapy

In a March 6, 2017 Scientific Report article, Dr. Ma (Dept. of Mechanical Engineering, Imperial College, London), et al. presented findings from a study that investigated the effects of bisphosphonate therapy on the microstructure and strength of bone. Dr. Ma looked at three cohorts of individuals from a total of 21 bone samples: 1) eight were from bisphosphonate-treated patients who
had sustained bone fractures, 2) eight were from patients who had sustained bone fractures but who had not received bisphosphonate therapy, and 3) five samples from cadavers of healthy, ageing, non-fracture individuals.

By using X-ray micro-CT and image segmentation technology, the researchers could assess both trabecular microdamage and mechanical strength of the bone samples. What they found was that bisphosphonate therapy is capable of reducing trabecular perforations (A phenomenon that weakens bones when excessive and one which I describe as "disconnected trabeculae" in my book - pages 14 and 15 - The Whole-Body Approach to Osteoporosis.) but causes an accumulation of microcracks. This abundance of microcracks (compared to the cohort that did not receive bisphosphonate therapy) lead to a loss of microstructural integrity and bone strength.

This study explains why short-term bisphosphonate use (2 years or less) can be beneficial (especially in a person with elevated osteoclastic bone resorption that is not being controlled through diet, lifestyle changes, and nutritional supplementation), but that long-term use of these drugs can be detrimental to skeletal health and strength.

The bottom line is that bisphosphonate medications can be of help in reducing immediate fracture risk in the short term but should not be used as the primary long-term treatment for osteoporosis. What SHOULD be used as primary long-term therapy for bone loss is bone-healthy nutrition and exercise, ensuring optimal GI health, and making changes in life style to promote overall health. 

Ma, et al. 2017. Long-term effects of bisphosphonate therapy: perforations, microcracks and mechanical properties.
Scientific Reports DOI: 10.1038/srep43399

Thursday, April 5, 2018

DX Severe Osteoporosis: Part XIV - The Final Chapter, Time to Move On

This is Part XIV (the final part) 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 www.osteonaturals.com as they provide background to this final installment. It is my hope that this series has provided 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 and I apologize for the long delay in writing this final chapter. 

First: a short disclosure: 

The reason for my delay in writing this episode of DX Severe Osteoporosis was that it evoked a bit of emotion within me. It was definitely time to bring this series to a close as there are so many other important topics concerning bone loss to write about. But my journey, from the time I was first diagnosed, through the intense tracking down of the possible causes of my severe bone loss, to finally implementing treatment (and all those sleepless nights of the "fear of the unknown" in between) was difficult to rehash and share in a public way. I tried hard not to belabor things and I left out most of the emotional toll. Being side-lined by a chronic disease is difficult for anyone who has to go through it and it often becomes a huge part of her or his life. It did in mine. In retrospect, I am glad I embarked on this series but I am also happy to bring it to a close.

As I was writing this fourteenth and final part of DX Severe Osteoporosis, I realized that I left a lot of what happened out. For example, one patient ask me last week if I ever went chasing leads down dead-end rabbit holes? OH YES!...For the better part of a year I chased osteopontine, a glycoprotein that is capable of activating integrins for a cell's attachment to bone. Osteopontine can form intermittent laminated plaques in bone and give what could be the appearance of zebra striping (remember the Zebra Striping from Part IV?!)...just like what was seen in my bone biopsy. Osteopontine also can cross-link with transglutaminase (think gut damage from gluten sensitivity...yes, I had that too) creating havoc at the area of bone mineralization where osteoclasts and osteoblasts come to repair microfractures. Many trails such as this one ended in frustration and limited understanding due to a lack of available commercial lab and/or procedure testing. 

In addition, I also failed to describe all the supplements I used over the years, the results from using them, and a list of all the labs (over 250 of them!) I performed to track the results (well over $20,000—in addition to what my insurance paid) over a five year period. Explaining all of this would have taken another fourteen chapters and I just didn't think anyone would want to sit through all of that. 

The bottom line from my five-plus years of intensive research into osteoporosis was that compounds such as alpha lipoic acid, NAC, and berberine (to name a few) are the most effective for balancing bone remodeling and improving skeletal health. By working with these compounds (plus diet changes and improved GI health) to enhance bone health, I was able to raise bone density scores, substantially reduce bone resorption markers (NTX, CTX, and DPD), reduce fracturing, and return myself and others back to "normal" life activities. For me, this included being able to return to Ironman triathlon competitions. (I always referred to it as going from being a "Fragileman" to an "Ironman.") Best of all, as I worked with patients to improve their skeletal health I happily saw them reap the benefits also. By using a combination of diet, exercise, and specific supplements, I was able to turn around my patients' declining skeletal health and substantially reduce their fracture risk. Out of this consistent success came the founding of OsteoNaturals.

And finally, people often ask "Dr. McCormick, have you reversed your osteoporosis and what is your bone density?" Eighteen years ago I was diagnosed with severe osteoporosis (-4.3 of the spine). I fought tooth and nail to climb out of that deep dark hole and I certainly don't want to go back there. Back then I would break a rib just leaning up against a wall. Now I have returned to competing in road races and triathlons and the only walls that sometimes slow me down are the ones at the end of a marathon or an Ironman (when I sometimes "hit the wall"!). As to how my skeleton is doing?...Well, you will just have to keep reading this final chapter...

My personal education into the inner workings of osteoporosis and success in treatment gave me the valuable skills I needed to help others with their bone loss. OsteoNaturals, and the formulation of products designed specifically to target bone health, was the obvious next step. I wanted to make a huge dent in the sides of osteoporosis...yes, kick it in the !#*@ and help others regain structural strength and improve their quality of life. At times, my education was a bit painful...as many of you know who have sustained fractures...but I would do it again in a heartbeat for all the thanks I have received from patients taking OsteoNaturals products. Thank you for tuning in and trusting OsteoNaturals.     Dr.M

The Final Chapter, Time to Move On

I will never forget the day my friend Greg died. We had been through a lot together over the years. From the first day I met Greg when he reached out his huge warm hand to shake mine, we became best of friends. For the next eight years we trained hard together at the Modern Pentathlon Olympic Training Center. We encouraging each other, supported each other, and fought hard against each other in competitions as we often vied for one of the few slots on World Championship and Olympic Teams. Sometimes he won...sometimes I did...sometimes we made teams together...but no matter what, we always encouraged each other, cheered each other on, and always...reached out to each other with a supporting hand.

I had just left his bedside five days before; massaged his back and feet to help him still feel some of the pleasures of life. His translucent skin—his skeleton—were all that was left to sense it. I wanted so much to whisper into his ear, "just let go." Let go so he could be finished with all this suffering. But he didn't want to give up, it wasn't in his genes to stop short. It was the fight that was worth the living, no matter how much this cancer ravaged his body or how much pain came along with it. The words just wouldn't form in my mouth, only the thought. They were so close to coming out, but they stayed twisted around my tongue. Those words would have betrayed all that we had stood for throughout our lives; to take that away, in his last moments of breath, would have been like taking down the finish line in a marathon when he was only ten feet away.

Just six hours after Greg's heart finally let him rest, I lay on the exam table. He was gone and my day of reckoning was here. The room was familiar, even the technician remembered me from 1 1/2  years before—I was "that guy," the one that made her normally sensitive heart come out with such an insensitive statement:  "Wow, your bone density is worse than a 100 year-old-woman!" she had blurted out. Now she positioned me once again on the table. I was thinking of Greg. They had probably taken his body away by now. His hands would be cold and his home would forever be different; his kind and supportive wife would struggle to make sense of his way-too-early departure from this earth. Change is relentless; we can't get away from it. If we could, there would be no precious jewels to treasure.

A bone density machine sounds like a computer matrix printer as the scanner goes back and forth across the body, searching for the pixels that spell out your substance. I couldn't hope for too great of a change...after all, I had ONLY been working on improving my bone density a little more than a year. But I HAD crammed TONS of calcium down my throat during that time so there should be SOME change, I remember hoping. I thought, "I had to at least hold steady on my bone density, but maybe, just maybe, I had gained a tenth or two."..."Wouldn't that be nice!"..."Three-tenths of a point improvement would be great...four-tenths would be incredible!" I had so many grand visions in my head.

Gaining bone mineral density is a slow process, it usually takes years for improvement even when powerful drugs such as bisphosphonates are prescribed. At that point I hadn't taken any of those osteoporosis-specific drugs...as a chiropractor and as one who wanted desperately to "fix" this problem "naturally"...I didn't want to have anything to do with drugs.

The DXA scanner hummed back and forth. It reminded me of the old television set I used to watch back in 1980 after a long day of training. Every time I turned it on there was a long droning hum, like it was thinking of what to do next. I was living in California at the time, training for the U.S. Olympic
My 1976 Olympic Coke Commercial...(not really)
Trials. It had been almost four years since my first Olympic debut; four years to get stronger, four years for the hunger to burn deeper. It had been a beautiful spring day, much like all the days seem to be on the West Coast—but a dark cloud soon moved in overhead.

I had already put in hard run and swim workouts that day, and just finished a long fencing session. There was some talk among the athletes at the salle about the President of the United States giving some kind of statement on television about the upcoming Olympics in Moscow. He was going to be talking about Afghanistan and its invasion by the Soviets. One of the athletes whispered that something bad was coming down, but he didn't know what.

The black and white screen flickered up and down with snow from an antique antenna. I could barely
make out Carter's face standing at the podium with its presidential shield. But his words came out loud and clear: "We will not go...," "We will not go..." Our USA Olympic Team would not be allowed to go to Moscow to compete in the 1980 Olympic Games. It was his way of swatting flies on Brezhnev, his way of telling the Russians they shouldn't have invaded Afghanistan—that they needed to get out.

My brain flickered worse than the TV screen. I couldn't believe it—I just stared at the light that came from it, a screen that had already gone on to other things in life; an ad for a fancy car, another for cheap hamburgers at McDonald's. But there wasn't anything else for me. How could my Olympic dream just stop because the five minute press conference was over? Just because the TV station had to get back to its "regular viewing" didn't mean that I could just switch my life to another channel. It was as if the Olympics were there one second, in all their glory and as the symbol for world unification in Olympism...a global celebration of the human body and its amazing potential...and then, in the next second, they were gone, yanked away by the words of the President.

The political situation took the Olympics away...not just from me and the thousands of other hopeful, dream-filled athletes, but from the world and all those people who held the Olympic Games as a sacred celebration of spirit and hope for world peace. The modern Olympic Games were supposed to be sacred. A gathering every four years of ALL nations, where they would come together as one, in peace and understanding and respect for each other under the setting of fair athletic competition. It is where nations can put away their political differences and maybe, just maybe, come out at the end of those two weeks with more respect for each other than when they went in. The Olympic Games are NOT to be touched or used for political gain. (Yes, I am an idealist to the bitter end.) But now, there would be no Moscow Olympics—at least for U.S. athletes—no complete international celebration of sport and peace and human athleticism...not for another four years.

There was never another "four years" for me. My life moved on to other places, to other goals that needed saddling. Greg stayed, and made the 1984 Olympic Team and almost again, four years after that. And even though our lives went separate ways, we always stayed in touch and we were always there to lend each other a supporting hand. Now, standing in this small hospital room, 1973 and my
first foray into international sports competition seemed so long ago; so long since Greg and I had first met and embarked on the Olympic journey together. It was hard to believe that Greg wouldn't be around any more, and that our unshakeable friendship was gone. The fire from his heart, extinguished, even though I could still feel his incredibly strong and always supportive grip in my hand.

And now, I was looking at the piece of paper that the DXA technician handed me. The typed print was so small but the numbers seemed so huge—so heavy that they could have ripped the paper in half and crashed to the floor. She was looking at me, the technician, quiet this time...quiet like the walls of the room...and my breath. It seemed like the last grains of slickrock just let loose from the grip of my fingers. This time there was no one there, no one to reach out a hand; no one to break the fall. It seemed like such a long way down, no hand holds, just a piece of paper that read...-4.4...-4.5...-4.3.

It was worse. My bone density T scores were worse. They had dropped by a "statistically significant" amount...not enough bone to hold anything together. I felt like a total fool, a loser that had fallen prey to his own warnings about seeing, about categorizing, and about truth. I had felt so smug, sure that I had found the answers to osteoporosis. I remembered now the warnings from another close friend of mine. Paul had said that just when you think you have found truth, that's when you lose the ability to be aware and open to the truth. That's when your mind tricks you and you start following the wrong trail. I had wanted so desperately to find the answers to curing my osteoporosis, maybe I had just been grabbing onto any morsel that I could and turning them into something that wasn't real. "Always let the tracks come to you...don't expect to see the tracks.", Paul said. "If you are arrogant about your conclusions, they will become definite and you will close your mind to further awareness of the truth."

It was as if I were holding my breath so none of the words telling of these dismal numbers would settle within me. For weeks after this 3rd bone density test in 1 1/2 years, it seemed as though my lungs were empty and my skin rigid to block out the realness of uncertainty. I wanted control, not the eroding laps of this invisible phantom called osteoporosis.

That same burning rawness that had stripped through my lungs in hard runs came racing back from the past and latched deep in my gut and wouldn't let go. I was afraid that if I breathed, I would be choked by thoughts of failure, but if I didn't, I would never even see who won the race.

I had no choice but to step back out and run again. The thoughts of failure and my need to not give up pulled me into the forest of osteoporosis research for the first time since Greg had died. My legs felt heavy and it was hard to get going again. But even with the world looking so dark, I could still taste the scent of the white pines and spring's shad-bush blossoms in the air as I headed out for a run. The pines were so tall that I had to look up to see their tops, and the shad blossoms so white they were like tiny scent-clouds trapped against the earth. But in all of their beauty, I noticed that even they were not "perfect." There were crooks where there should be straightness, voids where there should be branches; the trees were all different—individuals—uniquely special and genetically encoded with particular capabilities, tendencies, and vulnerabilities.

I was seeing life in its purest form. Right in front of me was the answer to my confusion. Some of the tree's differences, like more branches toward the side of a clearing, or more blossoms on the ones that grew in direct sunlight, were clearly from their interactions with the environment around them. Their actual individual presence was revealing the interaction of their genetically encoded patterns with the conditions in which they were growing. I could see that their particularity was an integral part of the particularity of their surroundings. And their woody bodies carried a record of their experiences with light and wind and rain, with the pulsing of ground water, and with the alternating warmth and cold of the seasons.

The trees were not perfect; there were vulnerabilities encoded in their patterns of structure and functioning. They had limits in their ability to respond to the stresses of wind, disease, drought, and cold. But it wasn't just the interaction of their encoded physical genome and the environment that formed their presence. There was something more. There was a certain counteracting of these vulnerabilities and limitations that they all seemed to posses: a persistence, an ability to fight for life. I saw trees growing up through boulders, cracking them in half and forcing them apart. There were small oak saplings that spread out huge leaves for capturing what little light shown through to the forest floor. And there were massive roots extending across rocky slabs, grabbing for any foothold possible, clinging to life. These were all evidence to me of their drive to live; a force that speaks in the innate voice common to us all. It was this drive and their genetic script that was unfolding together—life and form revealing the individual to the world.

I was seeing that the mystery of the trees' individuality was the result of an entwined interaction between their internal genetic script being read, being enunciated or dampened, by the world all around them. People too are affected by their surroundings, and their genetics are a huge part of the whole equation. Yes, my bone density had dropped over the past 18 months—a failure of treatment in anybody's eyes—but what I had forgotten to take into account was that it takes time to figure things out, time to put out the destructive fires, and more time to then build back healthy, living, new bone. This, getting healthy again with new stronger bone, had been a physiological process that I had read in medical texts to be impossible...but I wouldn't believe.

Gorging my body with mega-nutrients and expecting an immediate change in my bone density was unrealistic. Nutrients are found only in small amounts in nature and our body's ability to absorb and utilize substances such as calcium and magnesium takes time. Taking the attitude of "packing them in" was the fire in me that wouldn't succeed without the balancing energy of water's wet blanket to slow the process of excess bone resorption down, and allow for the flowing spirals of osteons and the graceful fluid curves of trabeculae to form. It was now clear, I needed to balance my constitution of fire that the acupuncturist had spoken of. This would be the most important step in my recovery, not the voracious gluttony of calcium.

Of those one and a half years, the first six months were used to gain insight into the tracks of this illusive animal and how it walked through the forest. It took another six months to quite the fires and bring the lab tests and what they indicated back to normal. All the while my bone density had still been dropping. How could I expect that in just a small part of a year the effects of this decades-old pattern of bone destruction would be erased, and the bones pixeled improvement?

And what about the "crooks" and "voids" in my structure that told of my own uniqueness in this world...those differences in each of us that we can see in our reflections? My genetics—my genome—how did this biography of DNA patterning and sequencing of small nucleotides play into all of this?

Much of the DNA within humans is remarkably similar from one person to the next. We are really not that much different from one another. In fact, only a small percentage of the DNA patterns within individuals, is unique. Of course some genetic aberrations can create severe physical defects or even death to the human embryo. There are fundamental functions, such as cell division, that must remain genetically intact for the organism to survive. But other genetic changes, ones that do not threaten life-supporting functions, can be kept within the gene pool of species. Variations within the nucleotides of the DNA that can be tolerated and evolutionarily conserved because their importance is limited—that is, they are not life-threatening—are passed on from generation to generation. These differences are called polymorphisms and are what make us the individuals that we are. For example, having red or brown hair or blue or green eyes is the result of polymorphisms written into our genetics and are unaffected by our environment.

Other human genetic differences, like many that are linked to bone density, are expressed only in response to environmental factors. For example, our genetic inheritance includes a greater or lesser ability to meet the specific demands of the environment. As human beings, we have the ability to compensate, to an extraordinary degree, for limitations both in our genetic inheritance and for the stresses we experience in the course of living.

Polymorphisms can also cause changes within the structure and function of enzymes, structural proteins, and receptors in a cell's membrane. These changes can adversely affect metabolic pathways and reduce our functional efficiency or predispose us to disease. In my case, I had several interactions between polymorphisms and environmental influences that may have contributed to my bone loss. I was homozygous positive for a polymorphism of IL-1RA, the receptor antagonist of interleukin 1. Interleukin 1 (IL-1) is a pro-inflammatory cytokine that initiates an inflammatory cascade and is a powerful stimulator of osteoclastic bone resorption. IL-1RA acts as a guardian to help limit excessive inflammatory (and osteoclastic) activation.

By itself, a polymorphism of IL-1RA may not pose any immediate health risks. But if this polymorphism is sitting in an environment of substantial environmental stress, then it may be detrimental to the individual. Prolonged states of oxidative stress (read: excess physical activity such as over-training for the Olympics or Ironman triathlons) can alter the immune environment and lead to bone loss. Gastrointestinal problems are also a form of environmental stress that can compound the adverse effects of polymorphisms. For example, microbial overgrowth can produce a whole host of toxic byproducts that interfere with hormones, enzymatic function, tissue repair, detoxification, and methylation pathways (to name just a few). All of these situations increase pro-inflammatory cytokines and impair the immune system. This physiological cascade can compound the effects of polymorphisms such as that of IL-1RA and cause bone loss due to a rise in chronic systemic inflammation.

Normally there are other measures in the body to help decrease the effects of IL-1 should it get out of control. For example, essential fatty acids (EFA) help moderate the inflammatory response. DHEA and the stabilizing effects of estrone are vital to limiting the adverse effects of pro-inflammatory cytokines such as IL-1. And it looked like this link to IL-1 may have been a contributor to my bone loss as I was low in EFAs, DHEA, and estrone.

In addition to IL-1RA, I also tested homozygous positive for a vitamin D receptor polymorphism on the 12th chromosome. My vitamin D level had been normal but with a receptor polymorphism, vitamin D's effectiveness in its role in bone formation may be impaired. Vitamin D is not just involved in improving calcium absorption from the gut but it is also responsible for stimulating the production of specific glycoproteins involved in bone remodeling. Polymorphisms of the vitamin D receptor could detrimentally affect this part of the mineralization process. With my vitamin D levels normal, there was no way to know if there was a problem with the stimulation of its receptors. Supplementing with more vitamin D in this situation may not be as helpful as in someone without this polymorphism. Taking supplemental calcium, and insuring its absorption by optimizing other substances like essential fatty acids, may on the other hand, have a substantial therapeutic effect.

There are also known polymorphisms of the genes for collagen, calcitonin receptors, parathyroid hormone receptors, tumor necrosis factor, osteoporotegerin...and just about ALL the known major (and minor) players involved in osteoporosis. These, and others that are currently being identified, are all linked to low bone density. Put in combination with environmental influences, they can all increase a person's risk of fracture. Commercial testing for polymorphisms related to osteoporosis have recently come under scrutiny and availability of testing is limited. But in the not-so-distant future, this will change, and it will change the way we approach our health care.

Genetic testing in the future will no doubt change the way we approach the course of our life. I once read that "osteoporosis is a disease of the young that is manifested in the old." To start out early in life to try to prevent disorders such as osteoporosis, or perhaps even cancer, is obviously preferable to finding yourself in a hole and trying to claw your way out. Genetic testing that alerts us to our particular, individual vulnerabilities may soon make this possible.

Like the shad bushes and every other living being in the world, I was beginning see that my skeleton was greatly influenced by the genetics and epigenetics hidden deep within every cell of my body. In  my case, the answer was not necessarily to have run fewer miles in training, but with my genetic susceptibility including polymorphisms and Gilbert's syndrome, gluten sensitivity, deficiencies in nutrients, and reduced production of hormones, the answer would have been to take better care of myself—to put out the fires before they worked so deep down into the sub-soil of my being. The answer would have been to have not allowed my bones to suffer at the hands of my passion for intense long-distance running and incessant over-training. The answer would have been to achieve better nutrition and take more time for rest and recovery.

After a certain age, perhaps the best we can do for the severe osteoporotic patient is to support his or her whole system, put out as many fires as we can through diet, supplements, exercise, and health care modalities that strengthen the body's natural ability to heal, and, at the same time, be open to the benefits of medications (at least in the short run as I had to do) which can help protect against the immediate threat of high fracture risk. (I used Forteo for 18 months and backed it up with 6 months of a bisphosphonate to stop the run-a-way landslide of fracturing that was pummeling my body.) In cases of severe osteoporosis, our best for optimal health is a combination of natural healing and medical ingenuity—staying open to both ways of healing, not being closed to the benefits of either.

In Reflection:

Over the years I have learned to manage my osteoporosis well. After that first one and a half years of frustration, I finally found many of the keys for improving bone health and my density scores steadily improved and my fracture incidence went down to zero. That's a HUGE improvement from breaking 12 bones in the 5 year period immediately following my diagnosis. The fact that I don't break any more, is SO COOL...and I thank my lucky stars EVERYDAY. My last bone density was a -3.3 which is more than one whole standard deviation better than it was 18 years ago. And my NTX bone resorption marker score now hovers around 40, not 124 which it was when I first started monitoring it 18 years ago. This indicates that I not only have better bone density but also better bone quality, and this is actually more important when speaking of fracture risk. If that isn't success, I don't know what is. I have thankfully been able to "move on" from my own quest for skeletal health and now totally concentrate on that of others. My self-mission completed, it is extremely rewarding to help others and empower them in their own quest for regaining skeletal health and reducing fracture risk.

Healing comes in many forms. For me, the most important healing did not come in the way of improved bone density and bone quality (although that helped!), but in the way of acceptance, and of seeing how a flame can come close to being extinguished and still come back as fire. We ALL have that capacity even in the most difficult of times, even when severe injury, disease, or aging has opened up deep seams into our vulnerabilities. It is during these times that it becomes most difficult to continue listening to our inner burning form—to the way of being that makes us who we are. But take even the smallest of smoldering hot coals and cup it carefully within a nest of fine fibers of downy milkweed, thistle tops, and dried fine grasses. Hold it carefully, feel the hopefulness of its warmth within your hands. Then, gently, but relentlessly, blow it into a strong and healthy flame. Your breath and your will to commit to nurturing it into fire are all that you need.

When disease or dysfunction comes into our lives, we never expect it—it takes us by surprise, and often leaves us changed forever. But no matter how compromised we may become, continue listening to your passions, breathing in your basic form. What matters is your being—holding on to, and taking care of that flame.

Thank you.

Webinar Announcement: What Supplements Do You Need for Osteoporosis?

Please Tune In To Our Webinar!
What Supplements Do You Need for Osteoporosis /Ostepenia?
Date / Time:  Monday, April 16th at 7:30 p.m.
With:  Dr. R. Keith McCormick and Irma Jennings
This educational event is free but you must register to get call in details. The following is the registration link:  https://zoom.us/webinar/register/WN_nhTTRleJTrSIPtLsbow-JQ
Hope you can join us!

Wednesday, March 21, 2018

Irma Jennings - Great Resource for Dietary Guidance to Better Bone Health

I was first introduced to Ms Irma Jennings several months ago and quickly realized that she is one of those special people in the field of bone health. As the founder of Food For Healthy Bones Irma is a great resource for anyone in need of help in designing and sticking to a bone-healthy diet.
Irma is one of those bright (literally!) stars in our field. An x-Wall Street heavy, Irma had an epiphany one day and got out of Dodge (NY City) in search of healthier ways. Her story is both endearing and up-lifting...and one that I would like to share with you.

When Irma joined her son's 5th grade class for a week-long stay on an organic biodynamic farm, she was struck by the peace and harmony of the early morning farm routines. She says, "It was as though farmers and animals were in a timeless dance of joy." Many of us have important events that change the directions of our lives and this day certainly interjected an abrupt 90 degree turn in hers.

"It was an ah-ha moment for me," she says. "It gave me a deep belief in the power of Nature's rhythms and food to affect your body, mind, and spirit. Now I know that food is more than just fuel. What you put in your mouth becomes your bones, your blood, and your brain."

Shortly after "seeing the light" as the barn doors (metaphorically speaking) opened, Irma split Wall Street and began studies at the Institute For Integrative Nutrition. And when she was diagnosed with osteopenia she knew she wasn't interested in the script her doctor handed her but instead wanted to use food as her medicine. Her diagnosis prompted Irma to establish Food For Healthy Bones where she offers an "Optimal Bone Health Program" of 7 modules including the importance of good digestion, optimal foods, bone healthy recipes, and exercises for improved bone strength.

Ms Jennings blogs monthly to her community of 4,500 readers. You can visit her web site at
https://www.food4healthybones.com  to learn more.  

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. (...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: www.osteonaturals.com 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: www.osteonaturals.com 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.

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