Bone Health FAQ’s

Bone FAQ

Dr. Wimalawansa, M.D., Ph.D., M.B.A., FRCPath., CCD, CRCP, MACDS, MRCS, FACP, FACE, FCCP, FRCP, DSc

Vitamin D insufficiency: Measured serum 25(OH) vitamin D levels  less than 30 ng/mL. Vitamin D deficiency: Measured serum 25(OH) vitamin D levels  less than 20 ng/mL

This estimate was based on each counties and/or regions that reported the incidence of vitamin D insufficiency (<30ng/mL) and deficiency (<20 ng/mL), multiplied by the given number of population in the country or the region.  My estimates for vitamin D deficiency is approximately 2.3 billion and deficiency + insufficiency (the total) estimated is about 3.5 billion in the world.  This comes to about 50% of the world’s population.

The prevalence of vitamin D deficiency is rising worldwide and approaching epidemic proportions, and most common among the vulnerable groups and elderly.  Yet vast majorities of individuals have an undiagnosed and untreated vitamin D deficiency.

This is a real issues, which is getting worse; it has n been neglected for a while.  This is consequently to a combination of several factors, but predominantly due to inadequate sun-exposure.  Most patients who need vitamin D supplements are either not given or provide inadequate doses.  Moreover, long-term adherence to oral supplementation is poor.  Measurement of serum 25(OH)D is the most reliable way to evaluate vitamin D status.

Vitamin D deficiency is the most under-diagnosed and perhaps the most common medical condition in the world.  Many estimate that more than 2 billion people worldwide across all ethnic and age groups have vitamin D deficiency.  Many individuals in industrialized countries, especially in the northern hemisphere, have low serum vitamin D levels.  Recent literature on vitamin D is full of controversies on its measurements, diagnosis, benefits, and the management of deficiency.

Severe vitamin D deficiency leads to rickets in childhood and osteomalacia in adults.  Low vitamin D levels may aggravate a variety of non-skeletal disorders including cancer, diabetes, metabolic syndrome, infectious diseases, and autoimmune disorders.  In addition to enhancing calcium absorption from the intestine and mineralization of the osteoid tissue, vitamin D is important in many other physiological effects, including neuro-modulation, muscle strength and coordination, release of insulin, immune health.  For example, cardiovascular morbidity and mortality are increased in patients with all levels of renal dysfunction, especially in those with low serum vitamin D levels.

Inadequate serum 25(OH)D concentrations are associated with decreased performance and an increased propensity to falls and fractures secondary to muscle weakness and poor neuromuscular coordination.

Ultraviolet rays provide more than 80% of our vitamin D requirement; diet and supplements can augment it.  The two major causes of vitamin D deficiency are the lack of exposure to sunlight and less than adequate dietary intakes.

Widespread vitamin D deficiency may be related to the increasing incidences of cancer, type 2 diabetes, obesity, and heart disease remains to be determined.  However, the relationship of vitamin D to the skeletal and non-skeletal systems and the significance of non-classic functions and targets of vitamin D need further studies.

These definitions based on the World Health Organization (WHO) classifications.  Bone Mineral Density (BMD) is measures by Dual Energy Absorptiometry (DXA) testing.  Results are expressed as T-scores (variation of standard deviations from the mean/normal (T-score 0 is considered as normal.  Between -1.5 and <2.5 are considered as osteopenia; and ≤2.5 and/or anyone with a fragility fractures are considered of having osteoporosis.

A considerable number of patients with osteopenia and osteoporosis would also have vitamin D deficiency which most of the time undiagnosed by physicians.  This is because “low bone density” is commonly equvated with osteoporosis and, thereby ignores the possibility of having osteomalacia and vitamin D deficiency.  In the absence of correcting  of vitamin D deficiency first, A). None of the osteoporosis medications would work effectively, and B). Patients in fact, may be harmed by treating with these drugs.  Therefore, diagnosis and treatment of vitamin D deficiency, before a physician prescribe an anti-osteoporosis medication in all patients is paramount.

We do not know.  No information or reliable research data are available on vitamin D status or response rates in women and children with Turners syndrome.  We do need research in this area.  All we know is that due to hormonal deficiencies, patients with Turners syndrome have lower bone mass with age-matched population.

Yes, very much so.  However, the use of Growth Hormone to treat osteoporosis is not a good option.  Too expensive and has too much adverse effects; hence unjustifiable therapy for osteoporosis.

Absolutely.  For example, girls with delayed puberty and women who had premature menopause will have low BMD, and have a tendency to have fractures early than others.  Hormone replacement therapy (HRT) had been a main stray of therapy for osteoporosis for decades,  for women age between 55 and 65 years,  However, as a results of poorly designed and interpreted Women’s Health Institute study, many physicians now do not use HRT as a main line therapy.

BMD is best assessed by using DXA technology, which is widely available in North America.  However, as a result of decreasing its reimbursement by the CMS to about ~28% of what was used to be three years ago, many of the DXA facilities are now being closed,; thus preventing access to care for our elderly  population.  This is in spite on only 20% of the eligible Medical postmenopausal women actually have had DXA testing done. Consequently, fracture rates are likely to increase in the years to come that would significantly increase the costs to the CMS (rather than decreasing the costs by cutting reimbursements).

Postmenopausal women above 55 years and men over 65 years should have a screening DXA done.   Medicare/CMS recommend conducting BMD testing every other year.

Most certainly with, A). Identification of those who are at risk, including carrying out BMD testing, B). Identification and eliminating secondary cause of bone losses, C). Correcting calcium and vitamin D deficiency, D). Teaching and engaging in a weight-bearing (not weight–lifting) exercise program, and E) In selected patients, treatment with specific anti-osteoporosis therapy.

One third of the risks of osteoporoses and associated fractures are genetically driven.  Especially, mother or grandmother having osteoporosis or a hip fracture would increase the risks of having a osteoporotic fracture in the sibling.

Refer to item #12; Overall healthy life style with a balanced diet, avoiding smoking, alcohol and excess salt intake, and engaging in adequate exercises would decrease osteoporosis risks.

What you eat is what you are.  Diet provides al the ingredients that is necessary for healthy bones; and b the body will provide necessary hormones, and the person is responsible for the weight-bearing exercises.

High protein consumption does not necessarily mean that it causes an internal acid production in the body.  Internal body acidity (pH) is very tightly controlled by several mechanisms; in fact evolutionary, designed to protect us.  The statements made such as, “drinking milk can cause osteoporosis” are erroneous.  In fact, there are a large number of studies in children and in adults demonstrating the beneficial effects of milk consumption on bone and in general health.

There seems to be a misconception that measurable acidity of the foods (e.g. oranges or tomato) that we consume causes “internal” acid environment.  In contrast, generation of internal acidity depends on the “type” of protein consumed, especially those containing disproportionate amounts of sulphur-containing, hence “acid-generating” amino acids.  This cannot be simply compartmentalized into vegetarian diets vs. animal protein, or milk diet.  Attached article explains and clarifies these myths.  I encourage reading several original articles from Dr. Susan New, in this regard.

The typical North American diet consists of high intake of animal protein together with a low intake of vegetables.  Such is generally associates with chronic, low-grade metabolic acidosis.  The sulfur-containing amino acids, cysteine and methionine are non-polar and hydrophobic, and predominantly present in meat protein.  These sulfur-containing amino acids when oxidized, generate high acid-loads, relative to base products obtained from the consumption of fruits and vegetables.  This sub-clinical metabolic acidosis promotes calcium mobilization from the bone and increase urinary calcium losses; acid-load effect.  Ingestion of high meat proteins (not milk  or vegetable proteins) increase urinary calcium excretion, raise parathyroid hormone levels and markers of bone turnover.  Markers of bone formation however, remain steady, suggesting that high protein/predominant meat diets increase bone resorption without increasing bone formation (i.e., overall negative).  Excess consumption of such in the long-term may lead to increase bone loss and fractures.
Milk contains calcium, vitamin D as well as protein; all these are essential ingredients for bone formation and maintenance of skeletal health.  Globally, calcium and vitamin D intakes are far less than optimal, including in the majority of North American population.  Worldwide, more than half the population is not getting these three elements that are essential for skeletal health.  For these people, milk is the backbone of their health that provides essential dietary ingredients for survival.  In most western countries, milk is fortified with small amounts of vitamin D (~100 IU per glass of milk); which in fact can be safely, double.  For various reasons, a significant proportion of population, especially African-Americans do not consume adequate amounts of milk.  Therefore to help them, it is important to consider fortifying other foods such as bread and cereal with vitamin D.

Nevertheless, overall, the results of epidemiologic studies of association between dietary protein intake and BMD, rates of change in BMD and risk for hip fracture have been inconclusive.  Protein under-nutrition is a common feature in older people and an important additional risk factor for increased propensity to falls leading to osteoporotic fracture.  Data suggest that in the elderly and in malnourished populations, any protein supplementation would reduce this risk.  In this regard, vegetable and milk proteins are friendlier to the skeleton than meat proteins.

More detail information on calcium, vitamin D and general nutrition/protein are illustrated in the book entitled, “Vitamin D: All you need to know”, (publisher, Karu & Sons)

http://www.vitamindwiki.com/tiki-index.php?page=Vitamin+D%3A+Everything+You+Need+to+Know+-+book+Spring+2012

http://www.vitamindwiki.com/tiki-index.php?page_id=2382  

There is compelling scientific and epidemiologic data suggesting that the humans requires a minimum blood level of 25(OH)D above 30 ng/mL (75 nmol/L) for health.  Although controversy exists of the definition of low normal vitamin D status, there is increasing agreement that the lower limit of the circulating 25(OH)D level is to be approximately 30 to 32 ng/mL.  .  Due to the high safety margin and the variability in measurements of serum 25(OH)D levels, to assure adequate serum vitamin D levels, a value around 40 ng/ml would be useful for maintenance.  The optimum level is between 30 and 40 ng/mL.  Levels up to 60 ng/mL (150 nmol/L) are safe and in fact may be necessary to sustain the non-skeletal beneficial effects of vitamin D.

Obtaining vitamin D via diet is not easy.  Only fatty fish like salmon have higher amounts of vitamin D.  Among the vegetable, irradiated mushrooms have a high contents of vitamin D.

An additional 1,000 IU of vitamin D/day is generally sufficient for lighter-skinned individuals, whereas older people and dark-skinned individuals may need an extra 2,000 IU/day to maintain normal serum 25-hydroxyvitamin D [25(OH)D] levels, of over 30 ng/nL (50 nmol/L).

Better compliance seems to occur with supplementation with 50,000 or 100,000 IU doses administered once a month.  Such a maintenance dose can be commenced following a therapeutic loading dose of 50,000 IU of vitamin D given once or twice a week for few weeks.  Such a regimen is efficacious and safe in replenishment of vitamin D storage in the body and maintaining optimal serum 25(OH)D levels.  American endocrine society guidelines indicate the upper safety limit of intake of vitamin D as 10,000 IU/day

Although no consensus exists, many endocrinologists and bone specialists prefer to keep their patients’ serum vitamin D levels between 30 and 40 ng/mL (75 to 100 nmol/L) or more.  People with intestinal diseases, obese people, and those who have had bariatric surgery have difficulty in maintaining serum vitamin D levels; they may need very high intakes of vitamin D on daily basis.

Vitamin D deficiency during pregnancy has serious consequences for woman and the fetus.  Changes in vitamin D metabolism also occur during pregnancy including increases in the maternal plasma 1,25(OH)2D levels thought to due to placental synthesis of this hormone Placental transfer of vitamin D from mother to fetus is essential for establishing the newborn’s growth; the goal of ensuring adequate vitamin D status with prenatal vitamin D supplements should be encouraged.  Pregnant woman with low 25(OH)D levels have an increased risk of preeclampsia.  Supplementation is important during pregnancy, but not essential during lactation period.

Vitamin D is present in some foods including mushrooms, cod-liver oil, and fatty fish such as herring, mackerel, sardines, and tuna.  Most other food has little vitamin D.  To make vitamin D more widely available, in several countries the vitamin is added to dairy products, juices, and breakfast cereals.  A healthy diet should contain a variety of fruits and vegetables (five servings a day), whole grains, and fat-free or low-fat milk and milk products.

In dietary supplements and fortified foods, vitamin D is provided as either D2 or D3.  The two forms are considered as equivalent based on their ability to cure rickets.  Many supplements have been reformulated to contain vitamin D3 instead of vitamin D2.  In the absence of rigorous comparative studies, both forms (as well as vitamin D in foods) are considered equally effective in increasing serum 25(OH)D levels.

Excessive sun exposure will not cause vitamin D toxicity.  Hypervitaminosis D is very rare, but can be a potentially serious problem.  It can cause kidney damage, growth retardation, calcification of soft tissues, and even death.  Vitamin D toxicity may (indirectly) manifest as a variety of non-specific symptoms, including nausea, vomiting, and constipation, loss of appetite, dry mouth, metallic taste, fatigue, sleepiness, headaches, weakness, irritability, and weight loss.  Daily doses over 15,000 IU regularly may lead to vitamin D toxicity.

We need more controlled clinical studies on dose-responses of vitamin D (and correlation with the achieve serum 25(OH) D levels) with non-skeletal outcomes such as cancer, heart disease, all-cause deaths, etc.

Low vitamin D levels may aggravate a variety of non-skeletal disorders including cancer, diabetes, metabolic syndrome, infectious diseases, and autoimmune disorders.  While we wait for such studies that may take 10 years or more, it is rational to advice physicians to keep their patients serum vitamin D levels above 30 ng/mL (75 nmol/L).

I have no conflicts of interest, except to state that I have published a book for primary care physicians on vitamin D; title “Vitamin D: Everything you need to know”.

Sunil Wimalawansa is a University Professor, Professor of Medicine, Endocrinology, Metabolism, and Nutrition, and former Chief of Endocrinology at the University of Medicine and Dentistry, Robert Wood Johnson Medical School, New Jersey, USA.1  He is also a Professor of Physiology and Integrative Biology at the University of Medicine and Dentistry, Graduate School Biomedical Sciences.  He holds an Executive Master’s of Business Administration Degree from the Rutgers University School of Business and a Diploma in Medical Administration from Johns Hopkins School of Business.

He had his education at Ananda College, Colombo and postgraduate studies at the University of Peradeniya in Sri Lanka, Royal Postgraduate Medical School in United Kingdom, Rutgers and Johns Hopkins Universities in the United States.  He is a member or a board director of several committees of national and international scientific societies.  He is the founder-president of few charitable organizations, including the International Foundation for Revitalization, Empowerment, Education, and Development; Hela Empowerment Foundation–International; International Foundation for Chronic Disabilities; and the chairperson of the Education Trust Fund for Needy Children, and the Wimalawansa Charitable Foundation.

His original contributions to science and medicine include current worldwide practiced standard of care in some medical methods.  He holds 6 medical patents, and has given more than 170 invited presentations at national and international scientific and medical meetings.  He has published over 130 peer-reviewed scientific articles, 4 books, and 45 scientific book chapters; and has made 260 scientific presentations worldwide.

Dr. Wimalawansa is the recipient of many awards including Dr. Oscar Gluck International Humanitarian award in 2007 and the prestigious Lifetime Achievement Award in 2005 from the Sri Lankan Foundation for his worldwide contributions to science, philanthropic work, and humanity.  Other awards he received include an International Award for Clinical Excellence in Metabolic Bone Diseases in 1991, multiple young-investigator scientific awards, and American Endocrine Society Glen Foundation Awards.  He is also the recipient of The Doctor of Science (D.Sc.) degree in 2001.

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