Spine Osteoporosis

[2cool4U]

1. Get your bone density checked at your index level and at least one non-spine site (hip or wrist) preoperatively. The non-spine measurement is important because you can have significant osteoporosis but have normal spine values due to increased density from degenerative disease (end plate sclerosis and osteophytes most commonly cause falsely higher density measurements.)

2. Have Vitamin D and serum calcium levels checked and treated if abnormal. Parathyroid testing is probably not needed routinely unless other labs point to a parathyroid problem, although you are unfortunately the rare exception to that.

I'm glad replacement therapy helped. It has made an amazing difference in my recovery as well.

-tc-

[Harrison]

I really wish that fixing our skeletal health problems was as easy as popping a pill, a supplement, or some other magic potion. But it’s not. We are hopelessly complex human beings. We in this community seem to have an assortment of different health conditions which affect our skeletal health. That’s why I started this topic a while back. Thank you TC, Fuzzy, Toebin for your comments.

The supplementation to correct a bone problem is fraught with both risks and questions. I covered some of this ground in my video interview with Dr. Tom Webster, when he addressed the “data” question with bone growth drugs. Speaking as an educated patient, I am not convinced that any supplement can “correct” a bone density problem in a localized area of the spine – especially if the disease process is localized to the spine vertebra(e) that may require surgery!

Think about the wild number of variables that should be accounted for when considering a supplement to remedy a localized bone-growth problem. Here are some of the tricky, variable issues I've heard from patients (reading about here; talking on the phone, in person, etc.):

• Race, genetic profile, gender, weight of patient
• Number of prescription drugs a patient may be taking;
• Number of supplements a patient may be taking;
• The dietary habits of the patient (beware highly processed foods and chelator diuretics like sodas and coffee);
• The mechanical condition of their spine (stresses, compensations of both hard & soft tissues);
• Pre-existing comorbidities: tumors, infections, systemic metabolic conditions:
  • Poor health of gastrointestinal tract ecosystem; known to be critical for bone growth and turnover;
  • Imbalances in the endocrine system, which may or may not be related to any and all of the above;
  • Any and all other immune system disorders or challenges that affect bone growth.

Now overlay these all-too-common conditions with new information on "D", some of which is confusing and conflicting:

• Quality and dosing of “D” supplements:
  • D2 vs. D3: which is better? Why? You will hear different arguments!
  • What about quality and formulations? See Jaime’s post on this from early March.
• Supplements vs. sunshine: can too much supplementation be immunosuppressive? Is sunshine better than supplements;
• Explanations of “D” as a prohormone, secosteroid and vitamin vary – these are seemingly three different things to patients in terms of understanding how they affect the human body;
• The Vitamin D receptor (VDR) agonist is recently said to inhibit certain kinds of cancer growth. So which is it: supplemental D is good or bad;
• In other German studies, specifically, D3 is thought to be absolutely beneficial as a critical “modulator” of the immune system, and accordingly, in disease states (in this study, the liver);
• In other studies, evidence shows that some autoimmune diseases can be reversed by gradually restoring vitamin D receptor function with a VDR agonist;
• Perhaps relating to all these things above, some patients do better with D supplementation than others. But even this observation bears more clarification.

Taking into consideration all these factors, some people may choose to supplement with various minerals and vitamins. For the sake of simplicity, let’s just look at “D,” the prohormone. When supplementing with it:

• Some people feel better in the first week, and may stay that way indefinitely;
• Some people feel better in the first week, then slide backward in terms of their desired state: energy, pain symptoms, etc.;
• Some people feel worse immediately and stop supplementing;
• Some people may or may not feel any difference taking D for months, but they cannot get their D metabolites (blood test results) and bone density to go up, no matter how much they take,
• Some people take loads of D for months, their bone growth accelerates, but their D metabolites stay low;
• Some people avoid all D for months, their D metabolites stay low, but their bone densities improve.

So, while I just scratched the surface here on this complicates issue, I hope you see my point: be careful when supplementing with anything for bone growth. There’s a lot to think about. I fear we are many years away from making hard conclusions about supplementation of any kind.

In the mean time, eat healthy, get your rest.

[Harrison]

Wake Forest University Baptist Medical Center
Vitamin D levels have different effects on atherosclerosis in blacks and whites

WINSTON-SALEM, N.C. – Vitamin D is quickly becoming the "go-to" remedy for treating a wide range of illnesses, from osteoporosis to atherosclerosis.

However, new evidence from a Wake Forest University School of Medicine study suggests that supplementing vitamin D in those with low levels may have different effects based on patient race and, in black individuals, the supplement could actually do harm.

The study is the first to show a positive relationship between calcified plaque in large arteries, a measure of atherosclerosis or "hardening of the arteries," and circulating vitamin D levels in black patients.

It appears in the March issue of the Journal of Clinical Endocrinology and Metabolism.

"In black patients, lower levels of vitamin D may not signify deficiency to the same extent as in whites," said the study's lead investigator, Barry I. Freedman, M.D., John H. Felts III Professor and chief of the section on nephrology at the School of Medicine

"We should use caution when supplementing vitamin D in black patients while we investigate if we are actually worsening calcium deposition in the arteries with treatment."

Vitamin D is widely used to treat patients with osteoporosis and/or low vitamin D levels based on a medically accepted normal range.

This "normal" range is typically applied to all race groups, although it was established predominantly in whites.

It is thought that as low vitamin D levels rise to the normal range with supplementation, protection from bone and heart disease (atherosclerosis) may increase, as well.

Blacks generally have lower vitamin D levels than whites, partly because their darker skin pigmentation limits the amount of the vitamin produced by sunlight.

Blacks also consume fewer dairy products and ingest less dietary calcium than whites, said Freedman, an affiliate of the Maya Angelou Center for Health Equity, part of the School of Medicine.

Despite these lower vitamin D levels and dietary calcium ingestion, blacks naturally experience lower rates of osteoporosis and have far less calcium in their arteries.

Studies further reveal that black patients with diabetes have half the rate of heart attack as whites, when provided equal access to health care.

This shows that lower levels of calcified atherosclerotic plaque in blacks are associated with a lower risk of heart disease.

However, blacks in the general community have higher rates of heart attack than whites, potentially due to unequal access to medical care, Freedman said.

The research team determined the relationship between circulating vitamin D levels and arterial calcium in 340 black men and women with type 2 diabetes.

Calcium can deposit in blood vessel walls forming a bone-like material called "calcified atherosclerotic plaque" and this plaque can be detected by computed tomography (CT) scans.

Calcified atherosclerotic plaque is a reliable predictor of risk for heart attack and stroke. The investigators measured vitamin D levels in all study participants and then performed a CT scan to detect calcium in the heart and major arteries.

"We found that higher circulating levels of vitamin D in blacks were associated with more calcium in the artery walls," Freedman said.

"This is the opposite effect of what is felt to occur in white patients and shows that the accepted "normal" range of vitamin D may be different between blacks and whites.

"Many of these study patients would be placed on supplemental vitamin D by their physicians simply because their levels were felt to be in the low range."

Freedman added that physicians should use caution in supplementing vitamin D levels in blacks – especially if they do not have weak bones or other reasons to take this vitamin – until the effects of supplementing vitamin D on blood vessels and heart disease are better understood.

"Doctors frequently prescribe supplemental vitamin D," Freedman said. "However, we do not know all of its effects and how they may differ between the races.

The bottom line is that racial differences in calcium handling are seen and black and white patients have differing risk for bone and heart disease.

We should more clearly determine the effects of supplementing vitamin D in black patients with low levels based on existing criteria and should not assume that the effects of supplementation will be the same between the races."

###

Co-authors of the study, which was funded by the National Institutes of Health, were Lynne E. Wagenknecht, Dr.P.H., Kristen G. Hairston, M.D., Donald W. Bowden, Ph.D., J. Jeffrey Carr, M.D., R. Caresse Hightower, Ethel J. Gordon, Jianzhao Xu, Carl D. Langefeld, Ph.D., and Jasmin Divers, Ph.D., all of the School of Medicine.
____________________________

Below abstract from the March issue of the Journal of Clinical Endocrinology and Metabolism

Vitamin D, Adiposity, and Calcified Atherosclerotic Plaque in African-Americans

Barry I. Freedman, Lynne E. Wagenknecht, Kristen G. Hairston, Donald W. Bowden, J. Jeffrey Carr, R. Caresse Hightower, Ethel J. Gordon, Jianzhao Xu, Carl D. Langefeld and Jasmin Divers

Departments of Internal Medicine-Nephrology (B.I.F.), Public Health Sciences (L.E.W., J.J.C., C.D.L., J.D.), Endocrinology (K.G.H., D.W.B.), and Biochemistry (D.W.B., J.X.), Centers for Diabetes Research and Human Genomics (D.W.B.), and Radiologic Sciences (J.J.C., R.C.H.), Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1053; and Department of Biology, North Carolina A & T University (E.J.G.), Greensboro, North Carolina 27411

Address all correspondence and requests for reprints to: Barry I. Freedman, M.D., Section on Nephrology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157-1053.

Context: Inverse associations are reported between circulating 25-hydroxyvitamin D and visceral adiposity. The effects of vitamin D levels on atherosclerosis are unknown.

Objective: The objective of this study was to test for relationships between vitamin D, adiposity, bone density, and atherosclerosis in African-Americans.

Design: Circulating 25-hydroxyvitamin D, 1,25 dihydroxyvitamin D, intact PTH, C-reactive protein and computed tomography-derived calcified atherosclerotic plaque (CP), bone density, and fat volumes were measured.

Setting: Examinations were performed at a single outpatient general clinical research center visit.

Subjects: Three hundred forty African-Americans with type 2 diabetes were evaluated. Mean ± SD age was 55.6 ± 9.6 yr, diabetes duration 10.6 ± 8.3 yr, glomerular filtration rate 1.6 ± 0.5 ml/sec, body mass index 35.6 ± 8.7 kg/m2, and 25-hydroxyvitamin D concentration 50.4 ± 30.5 nmol/liter.

Main Outcome Measure: Biomarkers were tested for association with pericardial, visceral, im, and sc adipose tissues; thoracic and lumbar vertebral bone density; and aorta, coronary, and carotid artery CP.

Results: Adjusting for age, gender, body mass index, glycosylated hemoglobin, and glomerular filtration rate, 25-hydroxyvitamin D was negatively associated with visceral adiposity (P = 0.009) and positively associated with carotid artery CP and aorta CP (P = 0.013 and 0.014, respectively) but not with coronary artery CP or bone density.

Conclusions: We confirmed an inverse association between vitamin D and visceral adiposity in African-Americans with diabetes. In addition, positive associations exist between 25-hydroxyvitamin D and aorta and carotid artery CP in African-Americans. The effects of supplementing vitamin D to raise the serum 25-hydroxyvitamin D level on atherosclerosis in African-Americans are unknown. Prospective trials are needed to determine the cardiovascular effects of supplemental vitamin D in this ethnic group.

[Harrison]

I continue to “bone up” on the osteoporosis issue. My gosh, there’s a lot to learn! The more I read, the less I know…

One of the points I was making (or trying to make) in the previous topic is the criticality of recognizing that our immune profiles are complicated and unique; what remedy works for one may not work for another. Time published an interesting article illustrating the differences in how statins present different risks for women than men, see: Do Statins Work Equally for Men and Women? The notion of gender-based medicine is interesting…

I’ve been hunting for a comprehensive overview of osteoporosis written for the layman. I found a few web references, as did others, and they are noted earlier in this topic. I found what I think is a comprehensive overview of the condition in Phyliss A. Balch’s “Prescription for Nutritional Healing.” I bought it at GNC last year for $25, but you can find it at the library or on Amazon for $19. I think it’s an amazing resource and took the trouble to copy & scan the section on osteoporosis, which is absolutely packed with useful information. I’ll bet you ten bucks you’ll learn a lot if you read it carefully…especially the parts about “risk” categories and calcium absorption. Note the information therein frequently refers to scientific journals or papers.

Please talk to your doctor about any questions you may have about the nutrients or products described on page 607. As mentioned earlier, bone turnover and growth problems are very complex. The normal and “natural” processes in the body all work in concert to keep your skeletal system healthy, so be careful about what you put down the old pie hole!

I’ll start another topic soon, picking up on the DEXA scan issue. A patient kindly offered us his sample scans, so you can look at all the information in those reports.

[Harrison]

A thoughtful member provided copies of his DEXA scan report and I’ve attached the images with his permission. Please note: I’ve removed personal identifier information and the first page (attached thumbnail) offers a basic interpretation of the scan results.

Since people that are thought NOT to be in high risk categories can in fact have osteoporosis (also mentioned in the above PDF), please talk to your doctor about getting a DEXA scan – it may save you a lot of trouble. I hope and predict it will become a recommended diagnostic procedure for ADR patients; many doctors in the U.S. do it routinely in their preoperative screening of patients.

Most (if not all) patients have not had trouble getting their insurance to cover DEXA scans. Worse case scaenario, one may be able to pay out-of-pocket for it and it costs appr. $300.

Hope this helps. I feel a resident bone expert may be in this topic’s future….

[ans]

My DEXA scan had readings of -2.75 and -2.50.

A lumbar QCT-5000 Bone Densitometry gave me a T-score of -1.0 (=osteoporosis). This test checked T12, L1, and L2. I am told that this is the definitive "word".

Makes me think that the DEXA scan is less ideal.

(I guess I should be on bisphosphates).

[2cool4U]

With some caveats, of course.

The Vitamin D Newsletter

March 20, 2010

Quest Diagnostics and Cardiovascular Disease

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you want to unsubscribe, go to the end of this newsletter. If you are not subscribed, you can do so on the Vitamin D Council’s website.

The Annals of Internal Medicine published two important reviews this month. In the first review, Dr. Anastassios Pittas and colleagues from Tufts University reviewed 106 articles and combined the 32 quality studies, a meta-analysis, looking at “cardiometabolic” outcomes such as diabetes, hypertension and cardiovascular disease. Their conclusion: “Lower vitamin D status seems to be associated with increased risk for hypertension and cardiovascular disease, but we do not yet know whether vitamin D supplements will affect clinical outcomes.” Read on.

Pittas AG, et al. Systematic review: Vitamin D and cardiometabolic outcomes. Ann Intern Med. 2010 Mar 2;152(5):307-14.

The second Annals of Internal Medicine review, by Dr. Lu Wang and colleagues at Harvard, looked at studies of vitamin D supplementation and found two randomized placebo controlled trials to combine. Dozens of different types of studies have looked at vitamin D and cardiovascular outcomes. The latitude studies are clear, the closer you live to the equator, the less cardiovascular disease. The dietary studies are mixed, because vitamin D is not contained in the diet, at least in significant amounts. The epidemiological studies are clear.

Wang L, et al. Systematic review: Vitamin D and calcium supplementation in prevention of cardiovascular events. Ann Intern Med. 2010 Mar 2;152(5):315-23.

Dr. Wang concluded, “To date, evidence from prospective observational studies and randomized controlled trials suggests that vitamin D supplementation at moderate to high doses may have beneficial effects on reducing the risk for cardiovascular disease.”

About the same time that the two above meta-analyses were published, Dr. Brent Muhlestein, director of cardiovascular research at the Intermountain Medical Center Heart Institute in Murray, Utah, presented a paper at this year’s American College of Cardiology’s annual scientific session in Atlanta.

The Utah group studied 31,000 patients over one year and found those with the lowest vitamin D levels had a 170-per-cent greater risk of heart attacks than those with the highest levels. Those with the lowest vitamin D levels also had an 80-per-cent greater risk of death, a 54-per-cent higher risk of diabetes, a 40-per-cent higher risk of coronary artery disease, a 72-per-cent higher risk of kidney failure and a 26-per-cent higher risk of depression.

Mittelstaedt, M., Vitamin D may slash risk of heart-disease risk. Globe and Mail, 3/15/2010

In order to prove that it was the vitamin D, and not a confounder (confusing fact), Dr. Muhlestein took 9,400 patients and gave them vitamin D, finding a 30% reduced risk of death. He did not think it was ethical to withhold vitamin D in a placebo control group, in order to do a randomized controlled trial.

This Utah study is unique in that these remarkable results were obtained in only one year – not the usual ten years - so the initial 25(OH)D blood test probably represented an accurate picture of vitamin D health. Dr. Muhlestein is not waiting for further studies, saying, “My recommendation to all my patients, and certainly I did it for myself, is to get your vitamin D checked and if you’re very low or even a little bit low, start taking supplementation and then get it rechecked.”

My recommendation is if you have cardiovascular disease – and even if you don’t – take at least 5,000 IU of vitamin D3 (cholecalciferol) per day and be sure to have your blood tested periodically for 25-hydroxy-vitamin D. (You may not need any vitamin D in the summer.) Since you already have a fatal disease, and cardiovascular disease is a fatal disease, maintain your 25(OH)D levels in the high normal range, 70-100 ng/ml, not the mid-normal range, 50-70 ng/ml, you want if you are healthy.

Remember to obtain a copy of your 25-hydroxy-vitamin D [25(OH)D] blood test report to guarantee your doctor ordered the correct test. Too many doctors are still ordering the wrong test, a1,25-dihydroxy-vitamin D, thinking they are checking for vitamin D deficiency, when they are doing nothing but falsely reassuring you and wasting your money. Get an actual copy of your lab report and be sure it says 25-hydroxy-vitamin D or 25(OH)D.

Also, remember that vitamin D needs numerous co-factors to work in the body. The ones you have to worry about are magnesium, zinc, boron and vitamin K because many people are deficient in these four nutrients. You can get these by simply eating a handful of seeds and nuts every day, while being careful to eat green leafy vegetables once a day.

At least one professor is having none of this. Dr. Lenore Buckley of Virginia Commonwealth University thinks vitamin D may do cardiovascular harm, even at low doses. She also thinks vitamin D supplementation should be racial, with Whites getting more than Blacks, Whites enough to obtain blood levels of 20-30 ng/ml, and Blacks enough to only obtain levels of only 15 ng/ml.

Jancin B. Skepticism Mounts on Need for Vitamin D Supplementation. Family Practice News Volume 40, Issue 3, Pages 1-2 (15 February 2010)

Dr. Buckley quotes two papers only. One – on calcium supplementation alone – was a randomized controlled trial while the second paper on vitamin D levels was cross-sectional, meaning it was a picture in time. In the first paper, Dr. Mark Bolland and colleagues of the University of Auckland gave 1,000 mg of calcium citrate over five years to 700 women in the treatment group who were already getting 800 mg/day of calcium in their diet and compared the treatment group to placebo controls who were getting 800 mg/day of calcium from their diet alone. So the study compared 1800 mg/day to 800 mg/day.

Bolland MJ, et al. Vascular events in healthy older women receiving calcium supplementation: randomised controlled trial. BMJ. 2008 Feb 2;336(7638):262-6.

They found 1800 mg/day of calcium may well do harm, with apparent increased rates of cardiovascular disease. However, they excluded anyone with frank vitamin D deficiency, exactly the patients who may benefit the most from extra calcium. (The extra calcium may decrease renal metabolic clearance of the little vitamin D such patients have.) The real problem came when they tried to verify the reported cardiovascular events with the national database in New Zealand; their findings were then of marginal significance (P=.05).

The authors noted that previous studies of total calcium intake (both diet and supplements), such as the Boston Nurses Study or the Iowa Women’s Health Study have both found that women with the highest total calcium intake had either the lowest death rates or the lowest cardiovascular disease. That said, it seems it is better to get your calcium from your diet and not from a pill, always a good rule.

This is a good time to say that vitamin D sufficient adults need about 1,000 mg of calcium a day from all sources, including diet and supplements and even that recommendation is based largely on studying vitamin D deficient people. In my opinion, no vitamin D sufficient person should be taking 1,000 mg of calcium/day in supplements, unless they get zero from their diet, pretty difficult to do.

NIH: Dietary Supplement Fact Sheet: Calcium

No one knows how much calcium supplements vitamin D sufficient older people need to take, but it is undoubtedly less than 1200 mg/day the NIH recommends, as someone with a 25(OH)D level of 32 ng/ml absorbs a lot more calcium than does someone with a level of 10 ng/ml. If you want an answer to the question of vitamin D/calcium interactions, the person to ask is Professor Robert Heaney and I know where you can ask him. Dr. Heaney is speaking to an all-day Grassroots Health seminar on vitamin D in San Diego on Friday, April 9, 2010. His talk is “Interactions: vitamin D, calcium and safety.” Please tell me what he says.

Diagnosis & Treatment of Vitamin D Deficiency Seminar

Getting back to Dr. Lenore Buckley of Virginia Commonwealth University, she based her racial recommendations (Blacks should be given less, not more, than Whites) entirely on a single cross-sectional study by Dr. Barry Freedman and colleagues at Wake Forest University (In the spirit of full disclosure, Wake Forest University is my old nemesis as I am a UNC grad).

Freedman BI, et al. Vitamin d, adiposity, and calcified atherosclerotic plaque in african-americans. J Clin Endocrinol Metab. 2010 Mar;95(3):1076-83.

Dr. Freedman and his Wake forest colleagues measured vitamin D levels and plaque (the build-up in your arteries) on 340 diabetic obese (BMI 35) African Americans and found higher vitamin D levels were associated with more plaque build up in the arteries.

I feel sorry for Dr. Freedman at Wake Forest but not for Dr. Buckley, the physician who decided that one Wake Forest study was enough to keep her black patients vitamin D deficient. Dr. Buckley, in considering only one vitamin D study, has decided to treat her African American patients different then her white patients. She apparently gave no consideration to the thousands of vitamin D studies in other diseases, and no consideration to the other calcification and plaque study, this one a much larger and better controlled (prospective cohort controlled study), published 8 months ago.

de Boer IH, et al. 25-hydroxyvitamin D levels inversely associate with risk for developing coronary artery calcification. J Am Soc Nephrol. 2009 Aug;20(8):1805-12.

Dr. Ian de Boer and colleagues at the University of Washington studied 1370 patients for three years finding coronary calcifications are indeed associated with vitamin D deficiency, concluding that “each 10-ng/ml lower 25(OH)D concentrations was associated with a 23% increased risk” for developing calcification. And, in direct contradiction to the Wake forest study, Dr. de Boer found the 201 vitamin D deficient black patients were more likely, not less likely, to develop such plaque then the Whites were.

Getting back to the Wake Forest study, why did their group get such different results than the researchers at the University of Washington? When I looked at Figure 1 in the Wake Forest study, the 25(OH)D measurements were all over the place, including about 30 Black patients with 25(OH)D levels greater than 40 ng/ml and one with a level of 90 ng/ml. The way the Wake Forest study was designed, a few bogusly elevated 25(OH)D levels will invalidate all their results.

One only has to look at the Wake Forest group’s methods section. Unlike the Washington study, which used the gold standard to measure vitamin D (DiaSorin RIA), Wake Forest decided to send their samples out to, you guessed it, Quest Diagnostics.

For new readers, this newsletter was the first to report Quest’s 25(OH)D results were suspicious, in a July 2008 newsletter.

The Vitamin D Newsletter, Supplementing with Vitamin D, July 2008

The New York Times picked up on the story six months later.

Pollack A. Quest Acknowledges Errors in Vitamin D Tests January 7, 2009 The New York Times

Since the New York Times story, Robert Michel, editor of the Dark Report had 24 Aliquot samples (small amounts of the same blood drawn at the same time) sent to labs all over the country for a vitamin D test. Quest’s results varied from 36 ng/ml to 66 ng/ml, on the same blood sample. The good news was the methods used by LabCorp all clustered around 44 ng/ml.

After the New York Times story, Quest assured me they have fixed their test. But I don’t know how Quest can run a million 25(OH)D tests every year on complicated mass spec machines that require meticulous sample preparation and highly trained operators, while requests for additional tests mount next to the operators. (In the spirit of full disclosure, I used to be a paid consultant for DiaSorin but have decided not to exercise my contract.)

Quest Diagnostics says they have fixed their diagnostic vitamin D testing. If they haven’t, look at the consequences. Researchers at Wake Forest relied on Quest and Dr. Buckley relied on Wake Forest and is now treating her black patients different than her white patients, keeping her black patients vitamin D deficient. Some of Dr. Buckley’s black patients will die from vitamin D deficiency.

The first thing Wake Forest needs to do is take the same frozen samples they sent to Quest Diagnostics and send them to LabCorp, which uses a reliable and idiot proof DiaSorin testing method. I predict many of Wake forest’s high 25(OH)D levels are, in reality, much lower, invalidating their findings.

You can help. Email Dr. Freedman and ask him to retest his samples using a DiaSorin method (bfreedma@wfubmc.edu.)

Second, call around and find out which lab in your area uses Quest. At the same time, find out which lab in your area uses LabCorp or call Life Extension Foundation at 1-800-544-4440 (Life Extension uses LabCorp). Then have your 25(OH)D drawn on the same day. This will cost you, in total, several hundred dollars. (If you can’t afford it, the Vitamin D Council will pay $100.000 of your total costs, once you send me copies of both Quest’s and LabCorp’s reports and your receipts.)

We need about 30 duplicate blood samples. We need copies of both Quest’s and LabCorp’s actual 25(OH)D lab reports, drawn on the same day. I will publish the findings in this newsletter, no matter what they show. The lives of thousands of African Americans may be at stake.

And yes I have thought about what vitamin D could do for health care, and yes I have thought about what it could do for health care costs, and yes I have thought about what it could do to lower the accelerated death rate among Blacks, and yes I have written newsletters about it, and yes I have contacted the Obama administration and no, no one has answered my pleas.

John Cannell, MD

Executive Director

Vitamin D Council

This newsletter may be reproduced as long as you properly and prominently attribute it source. Please reproduce it, post it on Internet sites, and forward it to your friends.

[Harrison]

Allan, sorry about the latest news. What are your next steps? Tim, the info you provided is interesting, but some of it conflicts with recent studies – maybe those are the caveats you are referring to? Whatever the case, as you know, the D issue is definitely worth tracking, as D (and the D receptor) is critical to almost every aspect of health – not just healthy bones.

That said, I wonder if D is overemphasized. For example, in the PDF I posted above, Balch references the three types of osteoporosis conditions (see page 606) which are new classifications based on newer studies; the interpretation report posted with the DEXA results references a 1999 guideline. A newer report from the National Osteoporosis Foundation is available here and is more comprehensive. My concern is that the report describes many pharmaceutical medications and offers no nutritional approaches (though there’s a helpful dietary calculator on page 17).

In hoping to understand more about osteoporosis, I read Balch’s three classifications of causes, then cross referenced it to a Medscape article (it’s free with registration). If one reads about the risk factors, primary and secondary causes and the statistics from this article, it’s clear that “D” is sometimes a good remedy and diagnostic data point for part of the osteoporotic populations, but only that. Supplements or meds may help alleviate the symptoms of a condition and their positive effects may even help solve the puzzle. Perhaps this is obvious, but that’s the point I annoyingly keep repeating.


__________________________________________________ ________________

(Excerpted from a different article - Medscape) – Osteoporosis

Primary causes: Estrogen deficiency, changes associated with aging.

Risk factors for secondary osteoporosis

Secondary causes - Up to one third of postmenopausal women, as well as many men and premenopausal women, have a coexisting cause of bone loss.21,22

• Endocrine disorders -Hyperparathyroidism, hypogonadism, hyperthyroidism, diabetes mellitus, Cushing disease, prolactinoma, acromegaly, adrenal insufficiency
• Gastrointestinal/nutritional conditions -Inflammatory bowel disease, celiac disease, malnutrition, history of gastric bypass surgery, chronic liver disease, anorexia nervosa, vitamin D or calcium deficiency
• Renal disease - Chronic kidney disease, idiopathic hypercalciuria
• Rheumatologic diseases -Rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus
• Hematologic disease -Multiple myeloma, thalassemia, leukemia, lymphoma, hemophilia, sickle cell disease, systemic mastocytosis
• Genetic disorders -Cystic fibrosis, osteogenesis imperfecta, homocystinuria, Ehlers-Danlos syndrome,Marfan syndrome, hemochromatosis, hypophosphatasia
• Other - Porphyria, sarcoid, immobilization, pregnancy/lactation, chronic obstructive pulmonary disease(COPD), parenteral nutrition, HIV/AIDS

Medications known to cause or accelerate bone loss

• Corticosteroids - Prednisone (³ 5 mg/d for ³ 3 mo)23
• Anticonvulsants - Phenytoin, barbiturates, carbamazepine (These agents are associated with treatment-induced vitamin D deficiency.)
• Heparin (long-term)
• Chemotherapeutic/transplant drugs - Cyclosporine, tacrolimus, platinum compounds, cyclophosphamide, ifosfamide, methotrexate
• Hormonal/endocrine therapies - Gonadotropin-releasing hormone (GnRH) agonists, luteinizing hormone-releasing hormone (LHRH) analogs, depomedroxyprogesterone, excessive thyroid supplementation
• Lithium
• Aromatase inhibitors - Exemestane, anastrozole

[hey_look_its_dave]

I note that the "lumbar" DEXA scans only look at L1 to L4. By looking at the images, I understand that to be the case because below L4 the pelvic bone gets into the image and overstates the density, while above L1 the ribs get into the image and again, overstate the density.

My disc trouble level is L5-S1, so I can't get a measurement of that exact level.

Does this jive with everyone's understanding?

Dave

[Harrison]

Dave, that's my understanding. Last month, that was my question to a CEO of a software company that does imaging "reprocessing" for orthopedic applications. I still hope to learn more about this and will in the next few months.

In the meantime, thanks for helping us find some more DEXA reports to review! I attached three of the five you sent me. Elsewhere, you raised a really interesting point -- your question about epidurals for your left-side disc herniation and peri-vertebral cortisone injections at L4-S1. You were wondering if cortisone or prednisone are aggravating agents for osteoporosis, right? I've heard this is a possibility and will spend some looking for answers as this is really important!