Crossroads Nutrition Blog

OSTEOPOROSIS
By Paul Caragine MD, FACS, FAAOS

Part 1 –
What it is, Its Incidence,
Normal Bone Anatomy & Physiology,
and People at High Risk
January 2009

Part 2 -
Diagnosing Osteoporosis
X-Ray and Laboratory Tests,
Treatment Advice –
including Dietary
and CROSSROADS NUTRITION’S
Skel-guard (Osteoporosis) Formula
February 2009

Part 3 -
Summaries of The Latest Research
and Future Treatment Possibilities
March 2009

OSTEOPOROSIS – Part I

Part 1 –
What it is, Its Incidence,
Normal Bone Anatomy & Physiology,
and People at High Risk
January 2009

WHAT OSTEOPOROSIS REALLY IS…

OSTEOPOROSIS is one of the top medical problems in the United States and in the world in 2009. It affects 55% of Americans over age 50. It is a condition that is not really a disease in most people because it is really a “normal” stage of the aging process. The problem is that people are living longer and longer and the condition is causing more and more broken bones that are expensive to care for and that are associated with a high mortality rate.
What Osteoporosis really is – is a decrease in the thickness and density of otherwise normal bone, that results in weakness, and this leads to broken bones. Again, osteoporotic bone is normal bone – it’s just that there is not as much of it as there was a when any person was younger – it is not as thick, not as dense, and not as strong. The outer dense shell of long bones – called the cortex – becomes thinner. This results in weakness. The inner or medullary portion that also houses the marrow fat and cells, is normally cris-crossed with thousands of bony strands, much like the center of a skyscraper has a maze of steelwork to give strength and firmness to the structure. (The marrow, where blood cells are made, lies between the threads of medullary bone.) In Osteoporosis, there is a reduction in the number of these crossing struts and those that are there become thinner. This results in further weakness, and weakness makes people prone to developing fractures often with little or no trauma.

One in three women will suffer an Osteoporosis-related fracture in her lifetime. In particular, it is responsible for many if not most cases of fractures of the wrist, the upper arm (humerus), the ankle, and especially the hip (femoral neck) and the spine (compression fractures of the vertebrae) – in those over age 40. More than 2 million people in the United States will suffer a bone fracture every year due to osteoporosis. Women are at far greater risk than men – 80 percent of patients with osteoporosis related fractures are women.
In the case of the spine, fractures of the vertebral bodies occur from bending and twisting motions when 30-40% of the bone has disappeared because of Osteoporosis. The fractures are nearly spontaneous and result in compression of the front (or anterior) portions of the bones because that is where the weight is concentrated with bending and lifting. Gradually this happens to a number of vertebrae and little by little, the patient develops a bending of the spine so that the neck shifts forward and downward over a curved upper back. This condition in women results in a deformity called a Dowager’s Hump; it can happen in men as well; it explains why many elderly people are seen to be bent way over when they walk about. At the same time, as much as 5-8 inches of height can be lost.  Besides looking bad, this condition results in abnormal and constricted breathing and the patients don’t get optimal oxygen. Increased rates of heart failure and other chronic diseases also result. The best treatment is prevention.
It does not seem to matter whether the degree of trauma causing a break (or fracture) was severe or moderate or minimal; People with Osteoporosis have increased fracture rates in all groups by as much as 31%.

The Incidence of Osteoporosis

In the United States, Osteoporosis-related fractures number around 1.4 million each year and are responsible for an estimated 800,000 emergency room visits, 500,000 hospitalizations (300,000 osteoporotic fractured hips in women, with 20-25% dead within 1 year), 180,000 nursing home placements, and 2.6 million physician visits in the US each year. This costs the US healthcare system approximately $15.2-18.9 billion annually. The number of Osteoporosis hip fractures has quadrupled in the past decade and this number will continue to rise as our older Baby Boomer-laden population doubles in numbers by 2040.
The State of New Jersey alone in 2006 had 1.3 million people with Osteoporosis and Osteopenia, nearly 20% of the state’s population. According to the International Osteoporosis Foundation, the incidence of Osteoporosis-related hip fractures is estimated to rise 240% in women and 310% in men by the year 2050.
80% of Osteoporosis patients are women, only 20% are men. Men tend to have less for several reasons: 1) They don’t live as long as women – life expectancy in men is about 74 years, in women about 7 years longer – 81 years; 2) Men are larger and exercise more than women in most of their life so that their cortical and medullary bone is thicker, and so it takes longer to thin out; and 3) Although Testosterone slowly falls with age, men make Testosterone until they die; women makes sharply less Estrogen after menopause. Both Estrogen and Testosterone combat Osteoporosis.
Men account for about a third of all hip fractures, but they are much more likely to die after an injury of this nature than women – because they average being more than 10 years older – so it is important to identify possible risks of Osteoporosis at an early stage in men as well as women.
Total fractures in the US are actually higher each year in men than in women even allowing for the effects of Osteoporosis. 2.9% of Men have fractures while 2.3% of women do, for an overall total US fracture rate of 2.6%. 25% of the elderly men with fractures don’t even know they have had one. The total number of osteoporotic fractures in women is now about 1.4 million/year in a US population 304 million, with about 700,000 in the spine (44%) (with the average American woman losing 1½” in height each decade after menopause), 350,000 in the hip (in 2000, at a cost of $9.8 billion with 14% dying directly from them and 33% dying within 1 year), 200,000 in the wrist, and the rest – 400,000 or about 25% – in all other places like the upper arm, ankes, knees, ribs, and pelvis.
With each year of aging, however, women catch up more and more. By age 45, more women have fractures than men, and by age 65, women have 3 times as many fractures as men. By age 75, all women have the same high rates of Osteoporotic fractures whether they have taken Estrogen hormonal replacement or not. If a women has normal bone density at age 50, her remaining lifetime chance of a hip fracture is 17%; if she has full-blown Osteoporosis at age 50, that percentage rises to nearly 50%. It is estimated that half of all females in the US will suffer an Osteoporosis-related fracture in their lifetime (according to the National Osteoporosis Foundation); another survey says that 1/3rd of women age 50 or over will suffer from such a fracture. Since most hip fractures occur after age 70, the time interval between ages 50 and 70 represents a “Window of Opportunity” to correct or prevent Osteoporosis from developing.
One man in 4 over age 50 will suffer the same fate. In the US, The prevalence of Osteoporosis in men is estimated to be 7% in white men, 5% in black men, and about 3% in Hispanic men (Forbes magazine 5/15/08). Men account for about 1/3rd of all hip fractures in the US, but generally at a later age, and they are also more than twice as likely to die of this injury then women are. Men have about a 13% lifetime risk of getting an osteoporosis-related fracture, women a 40% chance. There was a definite relationship between low Calcium intake and low Bone Mineral density (BMD). Men with Prostate Cancer should be advised to take more than 1000 mg of calcium each day to reduce osteoporosis and fractures.
Keep in mind, however, that more than 90% of hip fractures in women are caused by falls, and 80% of total fractures in women occur in those who apparently don’t have significant Osteoporosis. Poor balance is as important or more so in this elderly group, than is Osteoporosis. It has been estimated that fall prevention efforts can reduce the incidence of falls by up to 50% in the elderly. Many of the falls are associated with conditions of aging: vision loss; deterioration of the inner ear and other changes that affect balance; and loss of strength that prevents seniors from recovering from a stumble. Many fall when they first stand up. Some incontinent patients slip on their own urine. Taken together, such things as balance training, certain exercises, decreasing hazards around the home (like loose rugs, stairs without banisters, and slippery floors), and taking substantial daily Vitamin D3 to improve balance – can do as much or more to prevent fractures as correcting Osteoporosis. Further, the death rate from falling has risen dramatically for elderly people since the 1990s say US health officials in November of 2006, probably because they are being kept alive longer from such chronic conditions like cancer and heart disease; that was the bad news. CDC researchers looked at death certificate data from 1993-2003 and counted cases in which falls were listed as a primary or underlying cause of death. They found more than 13,700 older adults died from falls in 2003. That translated to a rate of about 37 deaths per 100,000 people who were 65 and older. The rate in 1993 was about 24 per 100,000 – meaning such deaths increased by 55 percent in the 10-year span. The rate for men rose by about 45 percent in that time, from about 32 to 46 per 100,000. The rate for women rose 60 percent, from 19.5 to 31 per 100,000. It comes back to the issue of longevity. Women are living longer. There are even more frail women living to older ages than frail men,” Stevens said. The report also looked at nonfatal injuries during a smaller time frame, from 2001-05. Those too have been increasing, though at a rate of just 3 percent. And in a separate measurement, the hospitalization rate for hip fractures fell from nearly 918 per 100,000 in 1993 to 776 per 100,000 in 2003. The decline was driven by a 21 percent reduction in hip fractures in women, researchers found.
The good news was that for the first time, there was a decrease in women’s hip fracture rates, beginning after 1996. This was attributed to osteoporosis screenings and bone-building treatments, boosted by Medicare reimbursements to doctors for doing bone density screenings on men and women beginning in 1996. Between 1993 and 2003, the rate of hip fractures in women fell by 21%.
Only about 25% of women who suffer an osteoporosis-related hip fracture make a full recovery; 20% of them are dead within 3 months and 25% of those fracturing at age 50 or above are dead within 1 year. African-American women are twice as likely to die in the first year after an Osteoporosis-related hip fracture than White women are, and more than 1.5 times as likely to die while in the hospital.
The causes of death attributable to OSTEOPOROSIS are a variety of things including:
1 Bed sores;
2 Urinary Tract infections;
3 Pneumonia;
4 Wound Infections;
5 Psychiatric problems, like confusion, related to being confined and lying flat for long periods of
time;
6 Depression-related deaths;
7 Additional falls and bone fractures;
8 Phlebitis and embolisms from confinement to bed; and
9 All other causes.
Few Americans realize that more women die from complications of osteoporosis than from breast cancer, ovarian cancer and uterine cancer combined, and more men die from complications of osteoporosis than from prostate cancer. 25-per-cent of women and 34 per cent of men will die within a year of breaking their hip from osteoporosis. To put that into perspective, after open-heart surgery or a coronary bypass, the expected mortality is 1%, compared with the 20 per cent or 34-per-cent risk of mortality in one year after breaking a hip. So, it is incorrect to assume that if you have a broken bone, it’s no big deal, and to assume that it is not like cancer or a heart attack and that you can just put a cast on it and off you go. It’s not that simple; it doesn’t kill people the day of the (bone) fracture but it’s a huge risk later.
Osteoporosis is already a huge problem in the United States and with people living longer and an aging population demographic, the situation and the medical costs are only getting worse each year.
Peak bone mass is at age 25; thereafter, a loss of about 3%/year in both sexes is average. Currently, over 75 million people in the US, Britain, and Japan have osteoporosis or its milder forerunner Osteopenia; of them 44 million are Americans, and of these 10 million people (80% women) have the full-blown disease; another 34 million have the milder Osteopenia; Osteopenia is in every way the same as Osteoporosis, but is just less severe. 44 million people represents 55% of people over age 50 in the US. Osteoporosis is the most prevalent degenerative disease in developed countries. The number of patients with Osteoporosis in the US and Europe is expected to increase to 50 million in 2015. One in three women and 1 in 5 men over 50 will experience osteoporotic fractures. In fact, the combined lifetime risk for the common osteoporotic fractures is approximately 40%, equivalent to the risk for cardiovascular disease. Osteoporosis takes a huge personal and economic toll. In Europe, the disability due to osteoporosis is greater than that caused by most cancers. The global market for drugs for the prevention and treatment of osteoporosis is approaching $10 billion and is growing rapidly.

African-American women have higher rates of Osteoporosis-related fractures than White women do supposedly because the increased melanin in their skin cells prevent the sun’s Ultra-Violet-B radiation from promoting production of Vitamin D in the skin. This relative lack of Vitamin D results in relatively less absorption of Calcium from the GI tract. A study done in 2005 and reported in the Archives of Internal Medicine reported that giving black women Vitamin D supplements did not seem to decrease the number of Osteoporosis-related fractures. The authors thought the reason was that 75% of black women are lactose intolerant, and so did not consume many calcium rich dairy products to begin with. Another possible reason was that they were not given enough Vitamin D3 – it is now thought that 2000-5000 IU of Vitamin D3 each day is probably optimal. In all regions of the world, more than half of postmenopausal women with Osteoporosis are Vitamin D deficient, regardless of age, latitude, or season, according to researchers from US, the Netherlands and the UK (reported at the 11th World Congress on the Menopause).

Osteoporosis Around the World
The costs in the UK with more than 230,000 osteoporosis-related fractures per year were 1.7 billion pounds, or over 5 million pounds per day.
In Canada, where 1.4 million women have Osteoporosis or Osteopenia, Osteoporosis is often called “the silent thief”. Over 80% of fractures in women over age 50 have been found to be Osteoporosis-related and an astonishing 80% of the female patients had never been diagnosed nor treated for the problem.
In Australia, a report dated 1/11/09 stated that 1/6th of the population suffers from either Arthritis (3.3 million) or Osteoporosis (1.3 million, 6% of the population), or both.
In Ireland, over 300,000 of their total population of 4 million have Osteoporosis, most over age 50; only 15% have been diagnosed. Ireland has limited sunlight compared to the US.
In Germany, with over 4 million cases of Osteoporosis and Osteopenia, 1/3rd of all women over age 60 are affected, half of those over age 70.
In Sweden, over 15,000 vertebral fractures occur each year, most due to Osteoporosis; most are treated by analgesicas and exercise.
In South Korea, 2 million people have Osteoporosis, and the number has grown by 10 fold between 1995 and 2003.
In Saudi Arabia, 40% of adult women suffer from Osteoporosis, according to the King Faisal Specialty Hospital and Research Center; 80% of women between ages 60 and 70. Much of this is thought to be caused by the Islamic codes of dress (covering the body of women and thereby blocking the formation of Vitamin D) and the use of sun-screen lotions (same effect).
In the nearby United Arab Emirates, the same social mores prevail and it has been noted that exercise, which also helps to build robust bones, is considered unfeminine; this combined with frequent child-bearing, more sedentary lifestyles, and a changing diet has created an epidemic of osteoporosis where one in three women over age 50 have Osteoporosis. It was reported on 1/03/08 that the New Zealand’s Fontera Dairy Company is promoting low-fat milks (called Anlene) and yogurts there to supposedly combat the problem; for reasons discussed under “How about Milk” below in the section “Foods for Osteoporosis”  neither of these initiatives may help. The same article describes portable Ultrasound machines made by General Electric and bone scans too in shopping malls in the UAEs.  Fontera claims that Anlene has been a great success there in reducing Osteoporosis; if so, it is the only milk product proven to benefit Osteoporosis.
A study reported in 10/2005 found that 52% of European women had Vitamin D inadequacy in their blood, and 81% in the Middle East, despite efforts there to get women to take Vitamin D supplements.
Finally in mainland China, the 5th National Census done in 2000 reported that a staggering 88,260,000 Chinese suffer from Osteoporosis, by far the highest number in the world, and the Chinese population continues to age!

Medications can help to lower these numbers but they have to be taken for life and many people stop taking them along the way. Additionally, all of the synthetic pharmaceuticals have side effects, even those given monthly (like Fosomax) or even yearly (like Zoledronic Acid (Reclast)). Seemingly the best way to go is to try to take daily nutritional supplements instead; they have far fewer, almost nil side effects, and are a lot less expensive. Consuming Calcium products – such as the dairy products milk, cheese, and yogurt – taking Vitamin D3, and eating a high protein low-salt diet, are excellent examples of how to get such nutrients and have diet that works against Osteoporosis, at least early on. There are many nutrients that contribute to lower Osteoporosis rates and they will be described later.
Other ways to keep the incidence down are by doing regular weight bearing exercise like brisk walking, jogging, step aerobics, etc.

There is an uncommon, self-limiting condition called Transient Osteoporosis of the Knee. It was first described in 1959. since then it was realized that the problem could affect only a part of a joint, such as the medial femoral condyle of the knee. In 1969, a patient was found to have a similar disease affecting several joints later coined Regional Migratory Osteoporosis, and soon after a series of 10 cases was reported of the problem affecting only the hip joint. Over time, a number of other descriptive names were used to describe the condition including Bone Marrow Edema, Transient Bone Demineralization, Hip Algodystrophy, Regional Migratory Osteoporosis, and even some cases of Reflex Sympathetic Dystrophy
The problem presents in the legs as a painful joint condition worsened by bearing weight on the limb, not caused by memorable trauma, and not related to any medication such as steroids. 2/3rds of the patients are men, the typical age is over 30, and the problem affects the hip joint most often. Inflammatory markers like C-Reactive Protein and Sedimentation Rate are typically normal. Bone scans show increased uptake, and MRIs show tissue edema. The condition may spontaneously slowly clear up in 8-12 weeks.
The etiology (cause) is unknown but is suspected to be temporary blockage of the nearby venous system, causing edema, or a temporary blockage of the arterial supply to an area causing fat cell necrosis before bone cell death; this could be described as an early reversible stage of the longer lasting and permanent Avascular  Necrosis of bone.
Other possible causes include small fractures between the bone and its cartilaginous coverings from minor forgotten trauma. Some have suggested Vitamin C deficiency might be the cause.
Recommended treatment is conservative wait and see with symptomatic treatment. Some have added agents that decrease inflammation like cortisone, but steroids worsen Osteoporosis. Others have used anti-Osteoporosis drugs like biphosphonates, calcitonin, PTH, etc. Another treatment has been surgical core bone decompression (drilling a hole into the bone) which relieves all pressure and generally results in immediate pain relief, but others consider this too radical when done early on. More needs to be learned.

More on Normal Bone Anatomy & Physiology

Bone is a living thing, that is, it is chock-full of living cells. These cells live in small little caves within and on the surfaces of the hard outer shell of bones called the cortex. The carved out little caves barely large enough to enclose one cell. The different caves are connected with each other by a network of thin tubules that carry blood with oxygen and nutrients to the cells and blood plus waste materials away from the cells.
There are two kinds of normal bone cells: OsteoBlasts, which make new bone, and OsteoClasts which dissolve away old bone. Normally both kinds of cells are working at the same time to yield a net zero production of bone in adults. OsteoBlasts and OsteoClasts are both in the family of connective tissue cells called Mesenchymal cells. They derive from what have been identified in recent years as Mesenchymal Stem Cells. The OsteoBlasts are small and have single nuclei and are very active metabolically. They have rapid rates of DNA, RNA and Protein production, because they produce a fibrous, protein material called OSTEOID. Materials and minerals like calcium deposit upon Osteoid to form bone. Think of the Osteoid as fibrous scaffolding upon which bone forms. The Osteoid links to Calcium with the help of a glue-like material, also a protein, called Osteocalcin. Osteocalcin  is made with the necessary help of Vitamin K. Once calcium links to it, other minerals such as Magnesium, Boron, Silica, and others join as well in specific patterns to form bony crystals that we call HydroxyApetite. This is the way bone is formed in growing bones and knitted together in broken or “fractured” bones.
The hard outer portion of a bone, the cortical  bone, is made in a layer upon layer fashion. Inside the outer shell of Cortical Bone lies the softer (but still bone) tissue called Medullary (or Cancellous) Bone. Medullary bone is NOT formed by layer upon layer deposition, but rather forms in a strand-like way to create an inner lattice of bone fibers, again similar to the steelwork inside modern sky-scrapers office buildings.

OsteoBlastic cells are formed from Mesenchymal Stem Cells in the marrow, while OsteoClasts form from Macrophage cells (a kind of white blood immune cell) when acted upon by a series of 3 proteins (cytokines) secreted by of all people – OsteoBlasts! The first two of these promote OsteoClast formation and the 3rd suppresses it. The 1st  protein is called Macrophage Colony Stimulating Factor (MCSF) that binds to a receptor on the macrophage and causes the macrophages to multiply; the 2nd is a protein called RANKL (“Receptor Activator of Nuclear Factor – Kappa B Ligand” or abbreviated as NF-kB) binds to a different receptor on the now many macrophages surfaces causing them to differentiate from Macrophages into OsteoClasts. OsteoClasts are multi-nucleated so multiple Macrophages must either fuse or the Macrophage nucleus must replicate to create the multi nuclei; in recent years it has been learned that they fuse together to form OsteoClasts. OsteoClasts are very large cells, a form of what we call giant cells. The 3rd OsteoBlast protein is called OsteoProtegerin and it blocks or holds back OsteoClast formation by getting onto the RANKL receptor and there serving as a blocking decoy – a check and balance relationship with the first two proteins. This prevents too many Osteoclasts from forming and help maintain a balance between OsteoBlasts and OsteoClasts. Other hormonal chemicals such as Estrogen, Parathormone (PTH) and the cytokine Insulin Growth Factor-1 (IGF-1) influence things here by binding to OsteoBlasts and induces them to either increase or decrease their output of OsteoProtegerin to suppress or promote OsteoClast formation triggered by RANKL.
Bone remodeling or the healing of a fracture always occurs in the same 2-part sequence – first, a rapid 2-3 week bone resorption phase takes place followed by a slower 2-3 month bone formation phase. The first phase begins when OsteoClasts attach to bone surfaces and release substances that degrade the structural part of bone, working primarily on the calcium, the other minerals, and the osteoid template; then they are released back into the blood. This degradation forms an indentation called a resorption pit or Howship’s Lacunae. Then the OsteoClast disappears, presumably by programmed cell death (aptosis).
New research at the Weizmann Institute of Science, has revealed in unprecedented detail how the roving OsteoClast cells, whose job is to digest bone seal off their work area, get down to business. The OsteoClasts, have some unique features not seen in any other cell type. OsteoClasts move around the bone until they reach a site where they sense that their services are required, at which point they undergo a transformation called polarization. The polarized OsteoClast sticks itself tightly to the bone, while an impermeable ring forms around the cell perimeter. This ring functions to keep the OsteoClasts’ bone-eating acids and enzymes only between the cell and the bone confined to the demolition site. How does this ring form? To solve the mystery, researchers used electron microscope imaging that allowed them to see fine details of the ring structure, and also a light microscope method in which specific features glow. Because each method captures different information at a different scale, combining them was tricky, but the two together gave a much more extensive picture than either alone. The researchers found that the ring is composed of dot-like structures called podosomes, which are anchored to the cell membrane. When the OsteoClast is on the move, these little dots amble randomly around the cell, but when the cells prepare to dissolve the bone, they make a beeline for the edge. Scientists had been unsure how podosomes were involved in ring formation or, if they did form the ring, whether they somehow fused together or kept their individual shapes. The research team’s findings showed clearly that the ring is made of individual podosomes held together by interconnecting protein filaments they throw out to each other. The podosomes are like folk dancers. As soon as the music starts up, they join hands and form a tight circle. From afar, a circle of dancers looks like a blur, but now we have managed to make out the individual dancers. From above, isolated podosomes look like a tent with rope-like lines radiating from a central pole. In effect, the podosomes may be more than just seals. They appear to act as highly connected nodes of communication between the inside and outside of the cell, enabling the cell to adjust its activity according to the condition of the bone underneath.

Next, bone-forming OsteoBlasts are drawn to the resorption pit by growth factor cytokines released during the resorption phase. The OstoeBlasts fill in the resorption pit with new bone by first laying down osteoid, and then with the help of Vitamin K and Osteocalcin, bring in calcium and other minerals to form the Hydroxyapetite bone crystals. This mineralized part of the bone makes up about 90+% of its weight. If calcium levels in the blood are low, OsteoClasts are activated by the parathyroid hormone and pull calcium from the bones. Calcitonin, made in the thyroid glands, is the hormone that does the opposite – it stimulates OsteoBlasts to deposit more calcium into the bones. Milk has about 10 times more calcium than Magnesium, and we need about the same amount of Magnesium as Calcium for normal bone mineral balance. When we relatively lack magnesium from drinking milk, the balance between PTH and Calcitonin tilts too far toward PTH. This results in excessive stimulation of OsteoClasts, which, over a long period of time, causes net bone loss. Increasing magnesium is the only natural way to correct this. Rates of osteoporosis are lowest in cultures where the ratio of calcium to magnesium is between 2 parts calcium to 3 parts magnesium, down to as much as 3 parts calcium to 2 parts magnesium. Again, the ratio of calcium to magnesium in dairy products is 10:1, way too high. In nations with high rates of osteoporosis, the ratio of total calcium to magnesium intake is at least 2:1, usually over 3:1. South Africa, with a ratio of 2 parts calcium to 3 parts magnesium in the average diet, has an osteoporosis rate of 7. In the USA the ratio is 4 parts calcium to 1 part magnesium and the osteoporosis rate is 144. In dairy loving Switzerland with a ratio of 5.5 calcium to 1 magnesium, the rate is 188. So Magnesium suppresses the hormone (PTH) that tells your body to pull calcium from the bones, and stimulates the hormone (Calcitonin or ThyroCalcitonin) that tells the body to put calcium in your bones. Lack of magnesium causes calcium to be pulled from the bones. This calcium is all too often deposited in soft tissue, where it can cause arthritis and arteriosclerosis. If you have been accumulating calcium in your body for a length of time you may need to take an absorbable magnesium supplement to balance the excess calcium with the magnesium deficiency. It will pull out the unwanted calcium from arteries and joints and help to put it back in the bones. On the average, a vegan diet (no meat or milk) provides about 500 mg. per day of both calcium and magnesium. Studies show that vegans have stronger bones than meat and milk product eaters, especially after the age of 50. Studies also show that magnesium supplements, even when used without calcium, increase bone density. In two such studies, bone density was increased, within nine months, by 7% and 8%. Another study, by renowned gynecologist Guy Abraham, provided a supplement that included 500 mg. per day of calcium, and 600 mg. of magnesium. Women using this supplement increased bone mass by over 11% within nine months.
Vitamin D Prevents Osteoporosis by producing c-Fos which Blocks Osteoclast Development – Oral Vitamin D treatment play inhibits the production of the protein c-Fos, which in turn plays a key role in the development of bone absorbing OsteoClasts. Chemical modifications of Vitamin D such as DD281 act even more powerfully (2/06 J of Clinical Investigations, from Japan)

It has recently been found that OsteoBlasts and regular bone cells (OsteoCytes) also contribute to the control of this process. Attention is also shifting from the OsteoClast as a target for new therapies to the OsteoBlast and the OsteoCyte, with its complex network within the depths of bone. A form of signaling called Wnt signaling on OsteoBlasts, through the frizzled receptor and its coreceptor, the low-density lipoprotein receptor related protein-5, appears to be a pivotal pathway for modulating OsteoBlastic activity, bone formation, and bone strength. The recently identified product of the SOST gene or sclerostin has also been shown to block Wnt signaling. Sclerostin is produced by the OsteoCytes buried in the bone and is a new target to treat bone loss.

In past times, researchers tried to break down cases of osteoporosis into type I – Overactive OsteoClasts, (or Estrogen Depletion type with large deep Howship’s Lacunae cavities around OsteoClasts) and Type II – Underactive OsteoBlasts (or Osteoporosis of Aging and Hormonal Problems). It now appears that most cases are really combinations of both and this classification has not proved valuable

APPARENTLY NORMAL PEOPLE WHO ARE AT HIGH RISK for OSTEOPOROSIS

The following groups of people are at high risk for developing Osteopenia and subsequent Osteoporosis:

1  Older men and women – beginning at age 50, and over age 65 is a definite risk
factor; women are 4-times as likely to develop Osteoporosis.

2  Northern European Caucasians and women with fair skin and blond
hair – and more fair Ashkenazi Jews have more Osteoporosis than their darker-skinned
Sephardic Jewish brethren. Then come Asian; then Native American women; then Latinos; and
least African-Americans.

3   Small, frail, and thin women, especially those who are underweight –
and especially those under 125 pounds with little buttock padding to protect bones in a fall.

4a    Women with abdominal obesity – these women have low levels of the beneficial
protein Apo-AI. Low levels of Apo A1 are correlated with decreased bone mineral density at
the hip, as well as with lower levels of beneficial HDL-Cholesterol and of Atherosclerosis.

4b   Women who are very tall or very lean

5    Women with Scoliosis – or sideways curvatures of the spine with one shoulder higher
than the other, and/or Kyphosis – a bending forward curve of the spine.

7   Men and Women with gray hair before age 40.

8   People with Freckles

9   People with Hypermobile joints

10    People with very sedentary lifestyles or limited by immobility and
little exercise.

11   Women who have had past fractures, especially after age 50, and/or with
relatives (parents or siblings) who have either had fractures or been diagnosed as having
Osteoporosis.

12  People who smoke – Tobacco use decreases both estrogen and calcium absorption, contains the Heavy
Metal poison Cadmium, and also causes bone resorption. It has been found that a woman smoking 1 pack of cigarettes per day throughout adulthood will end up with 5-10% less dense bone by the time she reaches menopause, which will result in a much higher rate of fractures of all kinds from falls. The 3 most important important lifestyle changes a woman can make to protect herself from Osteoporosis are to 1) not smoke; 2) exercise every day; and 3) take Calcium and Vitamin D each day, especially beginning from a young age (age 10-12).
It has recently been found that besides causing various forms of lung cancer, cigarette smoke gets absorbed in men’s and women’s  blood, travels to the cervix in women, and there interferes with the cervical cells ability to fight off Human Papilloma Virus (HPV), which the main cause of cervical cancer. So cigarette smoking increases cervical cancer.

15)  People who drink too much alcohol (over 3 drinks per day) – Against this are associations between higher BMD and beer drinkers, who were mostly men, and wine drinkers, who were mostly women, compared to plain liquor drinkers.  More studies might tell us if antioxidants in wine offer benefits for preventing loss of bone mineral density and osteoporosis. In another study, men and women with an average age of 74 who drank at least 1.5 drinks a day had a 20-50 percent less chance to develop heart failure as compared to non-drinkers, those in the group
In 2001, Dr. Kenneth Mukamal found that the light to moderate consumption of alcohol is associated with fewer brain lesions and so-called silent strokes. Alcohol is a blood thinner; therefore it improves circulation in the brain.
For beer to be healthy for you, you need to do it in moderation. Moderation is defined as 12 ounces a day for women and 24 ounces a day for men. Alcohol is a blood thinner; therefore it improves circulation in the brain. Beer is also a great energizer and very refreshing, but only in moderation. Non-drinkers have the most strokes and white matter disease; Light (1-6 drinks/week) to moderate (7-14 drinks/week) drinkers have fewer strokes and the least amount of white matter disease, but somewhat greater atrophy. Moderately heavy drinkers (15-21drinks/week) had the fewest strokes but more white matter disease and the most atrophy.” Interestingly, beer is high in Silica content (which increases the deposition of Calcium onto the osteod protein matrix, so that beer actually combats Osteoporosis – but not other forms of Alcohol. Further, Beer has been shown to decrease the incidences of heart attacks and strokes as well as Osteoporosis. In beer production, the grain Barley is malted (which means it is brought to its highest point of starch content by allowing it to germinate), added to hops (from flowering hops vines) a preservative that also contributes aromas, oils, and flavors, and then yeast turns the sugars and starches into alcohol. Apparently it is the grains in beer that prevent Osteoporosis. Beer also contains high amounts of the vitamins B, which may lower the levels of certain amino acids in the blood that increase heart attacks. Drinking a pint of beer can be substituted for drinking a glass of milk – good news for those with lactose intolerance who want to strengthen their bones.

18)      Women who drink caffeinated beverages like Coffee or Colas – Green and Black Teas
also contain caffeine, but they also contain other chemicals that fight Osteoporosis, so that their net effect is
beneficial in fighting Osteoporosis. A prospective study from Australia dated 1/26/08 looked at 1,500
women aged 70-85 and showed that non-tea drinkers lost an average of 4.0% of their Bone Mineral density
(BMD), while tea drinkers lost only 1.6% per year. Note that tea is a major source of flavanoid anti-oxidants
and lignans, some of which have estrogen-like activities; the study was irrespective of other variables such
as whether participants added milk to their tea or not. Caffeine has been shown to worsen Osteoporosis by
increasing Calcium loss in the urine. A 6 oz cup of regular coffee contains about 100 mg of caffeine.
Current US govt. recommendations are that adults not consume more than 400mg of caffeine daily.

19)  People who drink a lot of Phosphoric Acid-containing Sodas – the equivalent of
eating an acid diet.

20)  People who consume high-carb diets – especially those high in sugar, because sugar consumption
increases urinary loses of Calcium and Zinc, and raises Cortisol and Cortisone levels (Cortisol
and cortisone are known causes of Osteoporosis).

21)  People who eat an acid diet – the body does not function very well biochemically when the blood is too acid, so the body responds by dissolving bone in order to release calcium that can be part of a chemical buffer system to make the blood more alkaline. This dissolving of bone creates Osteoporosis. Thus diet is very important regarding acidity vs. alkalinity. Cancers also thrive in acidic environments. Most grains are acid-forming, except millet and buckwheat, which are slightly alkaline. Sprouted seeds and grains become more alkaline in the process of sprouting. Nuts, legumes, vegetable and fruit are highly alkaline. – essentially the Mediterranean Diet.   The most alkaline foods are: figs, juices of all green vegetables, tops of carrots and beets, celery, pineapple and citrus juices.

22)   People on Fluoride Therapy in any form – At one time, fluoride therapy was recommended for building denser bones and preventing fractures associated with osteoporosis. Now several articles in peer-reviewed journals suggest that fluoride actually causes more harm than good, as it is associated with bone breakage, in spite of the fact that it makes bone look denser on x-rays. Three studies reported in The Journal of the American Medical Association have shown links between hip fractures and fluoride. Findings here were, for instance, that there is “a small but significant increase in the risk of hip fractures in both men and women exposed to artificial fluoridation at 1 ppm.” In addition, the New England Journal of Medicine reports that people given fluoride to cure their osteoporosis actually wound up with an increased non-vertebral fracture rate. Austrian researchers have also found that fluoride tablets make bones more susceptible to fractures. The U.S. National Research Council states that the U.S. hip fracture rate is now the highest in the world.
A 2000 article in the journal Fluoride describes the bone effects of fluoride in detail. Fluoride may increase bone quantity (osteofluorosis, osteosclerosis) but also decrease bone quality and bone strength. It is well known that pharmacological doses of fluoride increase the risk of torsion-type fractures (such as hip fractures) despite the appearance of greater bone density.
Conventional medicine interprets the observed fluoride-induced increase of serum alkaline phosphatase concentration as a sign of osteoblast activity. Actually, it is a reflection of increased mortality of osteocytes within bone. Osteocytes are rich in alkaline phosphatase, which is released when the cells are killed by fluoride. It is unlikely, therefore, that a window of fluoride-induced bone benefit exists.
Dr. Paul Connett cites two epidemiological studies suggesting a possible association with osteosarcoma, (a bone cancer) in young men living in fluoridated areas. One is the report of the U.S. National Toxicology Program mentioned earlier, which first uncovered the epidemiological evidence of increased osteosarcoma in boys and young men living in fluoridated areas. The second is a study conducted by the New Jersey Department of Health. Dr. Perry Cohn studied the incidence of the rare bone cancer in seven New Jersey counties relative to water fluoridation. In fluoridated areas incidence of osteosarcoma in boys under the age of ten was 4.6 times higher than in unfluoridated areas, 3.5 times higher in the 10 to 19 age group, and over twice as high in the 20 to 49 age group.
Scientists at Yale University discovered that doses as low as 1 ppm of fluoride decrease bone strength and elasticity, making fracture more likely. Another group of researchers found that fluoride accelerated the development of osteoporosis. A 1992 study of elderly patients found ‘a small but significant increase in the risk of hip fracture in both men and women exposed to artificial fluoridation at 1 part per million’. As with the bone cancer, the adverse effects of fluoride accumulation on bone strength were greater with men.
Fluoride has the potential to increase skeletal mass to a greater extent than any other pharmacologic agent, yet it has proven difficult to translate this into therapeutic benefit for patients with low bone mass in diseases such as osteoporosis, according to a 1996 study by Michigan’s Center for Osteoporosis Research. This apparent paradox can be explained in part by toxic actions of the ion on skeletal mineralization, impairment of the normal processes of bone resorption, and fluoride-induced decreases in strength per unit of bone (mass or volume). Belgian arthritis researchers reviewed thirty years clinical research on fluoride in the treatment of osteoporosis. They point out that fluoride has a dual effect on osteoblasts (the cells from which bones are made). On the one hand, it increases the birthrate of osteoblasts, while on the other hand it has a toxic effect on the individual cell with mineralization impairment and reduced apposition rate resembling osteomalacia. Fluoride has a positive effect on medulary  bone density, they say, but the this bone gain is not matched by similar changes in cortical bone. (The cortical bone is the hard outer part of bone where a bone’s main strength lies.). Among the studies cited, two show an increased rate of hip fracture among patients treated with high doses of fluoride (50-75 mg per day).

23)  People who consume Excessive Chocolate – although a great source of anti-oxidants, Chocolate
decreases Calcium absorption

24)  People who consume Excessive Salt – this decreases Calcium absorption and increases  urinary loss
of calcium.

25)  People consuming Excessive Phytic Acid (also called Inositol HexaPhosphoric Acid) found in fruits, cereal grains, and in soy. Consuming too much Phytic Acid, as in eating too much cereal fiber in the form of rye, will result in the chelation of calcium and the formation of insoluble calcium and magnesium salts in the GI tract – resulting in a relative deficiency of calcium and magnesium.  We now also know that Phytic Acid itself strengthen bones, is a powerful anti-oxidant, and fights cancer.

26)  People consuming too much Vitamin A (over 25,000 IU/day) or too much Vitamin D
(over 10,000 IU/day) – In the case of Vitamin A, excessive consumption triggers an increase in the numbers of OsteoClasts that re-absorb bone, and also interference with the function of the Vitamins D. Constantly taking in over 10,000 IU/day of Vitamin A results in a 10-15% increase in fracture rates. The Retinol form of Vitamin A is the problem; better to supplement with Beta Carotene.

27)  People consuming inadequate Vitamin C – which will cause scurvy-like interference with bone
matrix formation.

28)  People consuming inadequate Vitamin D (which will cause rickets-like inadequate absorption of Calcium) – Taking Vitamin D with Calcium dramatically slows bone turnover of calcium, maintaining calcium levels and keeping bone density constant for a 5-year period; taking just Calcium led to only temporary reduction in bone loss. It is thought that these results were not only because Vitamin D improves calcium absorption from the GI tract, but also because it seems to slow bone reabsorption from bone into the circulation and also suppress parathyroid hormone secretion which controls blood calcium levels by also slowing bone reabsorption from bone into the circulation (See J Clin. Endo & Metab, 3/08). Another study against the use of calcium alone is one from the University of Auckland, New Zealand that links pure calcium supplements to an increased risk of heart attacks in post-menopausal women! Several other studies have confirmed this; note that it is a well established problem associated with calcium use in dialysis patients. Prof Moynihan of the U of Newcastle, Australia cautions that doctors and drug companies have t be disentangled to get meaningful conclusions.

29)  People consuming too much or too little Protein – Too much Protein pulls calcium out of bones
to be lost in the urine and feces, because protein is acidic and  calcium is a buffer system that tries to keep blood
pH constant. Some scientists have likened this acidification to pouring acid rain on your bones. This is a small
effect, but over time, it is significant so don’t over eat protein such as red meats; have several vegetarian days per week. Calcium is carried out of the body (with protein). This results in increased fractures. Eskimos eat large amounts of protein in their dietary staple – fish; their diet also has high levels of Calcium, but they still suffer a high rate of Osteoporosis. Vegetarians consume far less protein and so require far less protein to stay in calcium balance, and, in fact, have lower rate of Osteoporosis than do Eskimos. Taking in adequate amounts of folic acid, B6, and B12 decrease the amount of calcium needed to stay in balance regardless of how much protein you eat, because they help convert homocysteine into a form more easily excreted by the kidneys.
Too little protein prevents formation of the protein osteoid matrix, upon which the hydroxyapetite mineral crystals are deposited

MEDICATIONS Can Also Cause OSTEOPOROSIS, Including:

1)    Antacids and Anti-depressants (SSRI’s), which decrease stomach absorption of Calcium
2)    Tetracycline-family antibiotics;
3)    The Anti-Cancer drug Methotrexate;
4)    Certain Anti-Tuberculosis drugs like Isoniazid;
5)    Anti-Convulsive drugs like Dilantin, Phenobarbital, and Carbamazepine;
6)    So-called “Loop Diuretics” like Lasix, Ethacrynic Acid, Torsemide and Bumetanide – work by pulling water out of the body, but pull a lot of calcium along with it. HydrochlorThiazide (HydroDiuril) is NOT one of them. A study showed that women aged 50-79 taking these drugs for more than 3 years had a 16% higher fracture rate, according to the U of Tennessee in the Arch. Int. Med.. Loop diuretics are often used in the treatment of congestive heart failure and high blood pressure.
7)    Anti-Coagulants like Heparin.
8)    The Type II Diabetes drug Rosiglitazone. It is in the Glitazone drug family. It apparently inhibit OsteoBlast (bone forming) function.
9)    Aluminum in any form, including in AntAcid medications (it inhibits OsteoBlast activity);
10)    Non-Aluminum Anti-Acids such as Cimetidine – decrease absorption of Calcium;
11)    Mercury in any form, including leaching from the amalgam of dental fillings;
12)    Certain Anti-Transplant-Rejection drugs like Cyclosporin and Tacrolimus;
13)    Any drug with Steroid activity, such as Cortisone, Cortisol, Prenisone, and Prednisolone.
although patients on steroid inhalers for Asthma and Chronic Lung disease do not seem
to have increased Osteoporosis.
14)   Avandia – which is a drug for Type II Diabetes made by Glaxo-Smith-Kline (GSK) has been found to decrease bone formation and result in higher risks of hip and other fractures, according to data published in February 2007. Those taking it for 14 weeks or more had a decrease of 1.4% in hip Bone Density, and also a significant decrease in bone density in the lumbar spine. This followed another study published in December 2006 that showed increased fractures in the wrists and ankles of patients on Avandia in a study called ADOPT.

Drugs that increase the speed of Osteoporosis development include corticosteroids, cigarette
smoking, anti-convulsants, and (in Pakistan) sheesha and hookah.

MEDICAL CONDITIONS ASSOCIATED with OSTEOPOROSIS Including:

1)  Diseases featuring Hypo- (or low levels of) Estrogen or Progesterone,
or low levels of Testosterone (as in aged or castrated men); Low testosterone problems can happen in WOMEN too, as they make some Testosterone and need it for healthy bones, and for libido. Testosterone can reverse Osteoporosis in men. Together, all these conditions are called Hypo-Gonadism. Related Syndromes include Kleinfelter’s and Turner’s Syndromes. Difficulty in maintaining an erection is an osteoporosis risk factor indicator in men.
Estrogen deficiency is the primary post-menopausal cause of osteoporosis in women.
However, Progesterone, not Estrogen, is gaining acceptance as the primary female hormone needed to repair that osteoporosis. This is still somewhat controversial. The bottom line is that post-menopausal women should use natural progesterone tablets, patches or skin creams for optimal hormonal protection against Osteoporosis.
We now know more details of just how Estrogen helps preserve bone. If you care to know, and this is very technical, estrogen acts within the nucleus of bone cells on the DNA receptors of two genes – genes called ER-Alpha ( or “Estrogen Receptor-Alpha”) and ER-Beta. These genes are members of the nuclear receptor super-family of what are called ligand-activated transcription factors, and the transcription factors suppress the formation of OsteoClasts. If you decrease the amount of estrogen and you increase the number of OsteoClasts, the result is less bone, or Osteoporosis and Osteopenia.]

2)  Anovulatory, but menstruating, athletic thin young women; we know they
produce Estrogen or they would not build up endometrial tissue to menstruate; the latest hypothesis is that Progesterone deficiency is an important factor in the pathogenesis of Osteoporosis, and anovulatory women don’t produce sufficient Progesterone. Natural Progesterone can be provided by skin patches (to avoid its removal in its first Liver pass if consumed orally); it is inexpensive, has few side effects, and is found in many plant foods.

3)    Depressed Women – Pre- and Post- Menopausal depressed women both have
higher rates of  Osteoporosis than non-depressed women because depression resulted in over-
activity of certain aspects of the immune system, with the production of too many chemicals that
promote inflammation and bone loss. (Arch Int Med 12/07).A US study found that 17% of
depressed women had Osteoporosis compared to only 2% of non-depressed women, all aged
21-45.
The level of bone loss was at least as high in depressed women as in those who smoked, ate
poor diets, and didn’t exercise. significance of Depression was found to be as high. The immune
system in the depressed patients excessively produced the cytokine protein Interleukin -6  (or
IL-6). Anti-Depressant use did not appear to play a role in the lower bone density seen among the
depressed women.
People with depression were also somewhere between two and four times as likely to get heart
disease, depressed people were more likely to get Type 2 Diabetes, so a lot of chronic diseases
can be actually caused by depression.

4)  In men with abnormally low levels of Testosterone. Treatment with Testosterone not only helps treat flagging libido in men (and in women!) with low levels of Testosterone, but it has clearly been shown to treat or prevent Osteoporosis in men with low Testosterone levels.
In women, both Testosterone and natural Estrogen help combat Osteoporosis.
Recall that both these hormones decline as we age in both men and women, that men produce small amounts of Estradiol, the active form of Estrogen, that women produce small amounts of Testosterone. Also note that most men produce significant amounts of Testosterone throughout life, but that after menopause, women’s ovaries produce virtually no Estrogen and that only small amounts of Estradiol are made by fat cells, more so in obese women. All of this puts women at a comparative disadvantage to men regarding Osteoporosis. Yet, falling levels of both Testosterone and the less abundant Estrogen in aging men do contributes to increasing Osteoporosis in aging men as well. It was shown in a study by Wascher MD et al and published in the Archives of Internal Medicine in January of 2008, that men with the lowest Testosterone levels had an almost 50% greater incidence of Osteoporosis and double the number of hip fractures as the men with the highest levels of Testosterone. Interestingly, the group of men with the lowest levels of Estradiol had a 21% relative increase in the hip fracture incidence as well when compared to the group with the highest levels.
Other studies reported in May 2007 have shown the same effects in young men with hypogonadism accompanied by  infertility and sexual dysfunction. 38% had low BMD, 21% met criteria for Osteoporosis, and most had high FSH and low Estradiol. It was advised that all hypogonadal men have base line bone density studies.

5)   Men and women (especially after menopause) with any sex hormone deficiencies for whatever reason. Taking SYNTHETIC female hormones – according Dr. Jerilynn Prior and a   University of British Columbia study in the J of Clin Endo & Metab (93,#1,208-211 2008, did help Osteoporosis according to this study, but they increased the rates breast of cancer by 26%, heart attacks by 29%, strokes by 41%, and of blood clots by 21% (by stimulating the liver to make clotting proteins).
Several years ago, the US Food & Drug Administration ordered a “Black Box” label warning on Depo-Provera warning of irreversible bone loss in women taking it. Recently a study done in Canada by Health Canada and the manufacturer of Depo-Provera (a synthetic progesterone from horse urine) confirmed the US finding that Depo-Provera caused Osteoporosis to worsen. Interestingly, it was shown in mice studies that taking the Pituitary hormone FSH, the hormone that stimulates Estrogen release by the ovary (and adrenals) actually itself CAUSES Osteoporosis in mice and may do so in post-menopausal women. In 2006, the Journal of Clin. Endocrinology and Metabolism reported on testosterone deficiency in older men. They defined it as a testosterone of <200ng/dl; Estradiol deficiency in older men was defined as <10ng/dl. Rapid bone less was defined as 3% loss or more each year. The prevalence of Osteoporosis in men with deficient and normal total testosterone was 12.3% and 6.0%; for estradiol the numbers were 15.4% and 2.8%. Among osteoporotic men and those with normal BMD, prevalence of total testosterone deficiency was 6.9 and 3.2% (P = 0.01), and prevalence of total estradiol deficiency was 9.2 and 2.4% (P = 0.0001). Incidence of rapid hip bone loss in men with deficient and normal total testosterone was 22.5 and 8.6% (P = 0.007) and in those with deficient and normal total estradiol was 14.3 and 6.3% (P = 0.08). Conclusions were: Older men with total testosterone or estradiol deficiency were more likely to be osteoporotic. Those with osteoporosis were more likely to be total testosterone or estradiol deficient. Rapid hip bone loss was more likely in men with total testosterone deficiency. BMD testing of older men with sex steroid deficiency may be clinically warranted. A study done at the Washington University school of Medicine concluded that low amounts of estrogen increases Osteoporosis in both men and women. Most people don’t think about the need for estrogen in men and don’t realize that adult men have on-average higher estrogen levels than do post-menopausal women. A significant amount of research done many other groups has suggested that Estrogen may be more important than Testosterone for maintaining bone health in men. This was studied, and it was found that men with higher levels of Estrogen and of bio-active Estrogen metabolites (formed during passages through the liver) have higher bone density than those with lower levels of estrogen and its active metabolites. Estrogen may also give some protection to men against Prostate Cancer. Testosterone did not effect bone density very much in this study. It seems to matter more in the formation of men’s bones, resulting in their larger size and thicker (initial) cortex. About 35 per cent of a mature adult’s peak bone mass is built-up during puberty, with its surge of hormones, both male and female.

6)  Women with Elevated Levels of the Pituitary Hormone FSH (Follicular
Stimulating Hormone). It has been found that FSH itself may CAUSE Osteoporosis in Postmenopausal women. FSH has long been known to trigger the formation of Estrogen, which is known to RETARD Osteoporosis through its suppression of OsteoClastic function. A study has shown that FSH leads to bone loss in mice; mice who lack FSH or its bone Receptor are resistant to bone loss even if lacking in estrogen. The findings open up the possibility that therapies other than estrogen to treat or prevent bone loss may one day be possible. Estrogen-replacement therapy is not an ideal solution because it has been linked to a heightened risk of breast cancer, especially when administered in combination with the hormone progestin. “In essence, we’re revisiting the pathophysiology of bone loss, attributing it not simply to loss of estrogen but to the accompanying elevation of FSH which occurs during menopause,” said study author Dr. Mone Zaidi, a professor of medicine and physiology and director of the Mount Sinai Bone Program, at Mount Sinai School of Medicine in New York City. “The importance is that you could actually prevent bone loss without using a load of estrogen.” “It has really become virtually gospel that estrogen loss in women after menopause leads to bone loss,” Zaidi said. However, there were some holes in that theory. In some animal studies, taking away estrogen did not always result in bone loss, Zaidi said. About two years ago, Zaidi’s group discovered that thyroid-stimulating hormone, a sister hormone to FSH, affected bone remodeling. “The next step would be to have a small molecule or antibody to mop up FSH in circulation and see if bone loss can be prevented,” Zaidi said. “If that is the case, we have a new target” for prevention and treatment strategies.

7)  People with any disorder elevating Cortisone or Cortisol – or who are on
medications containing them – because they are known causes of Osteoporosis
This includes diseases that feature Hyper-Cortisonism (or high levels of Cortisone) – like Cushing’s Disease and other Adrenal Gland conditions, and some Pituitary Tumors or diseases; or taking large amounts of cortisone-equivalent medications for such conditions as Rheumatoid Arthritis, Psoriasis, Lupus Erythematosis, etc.  As little as 10mg per day can have major effects on decreasing GI Calcium absorption, increasing Renal calcium loss, increasing OsteoClastic (bone destroying cells) activity, decreasing OsteoBlastic (bone forming cell) activity, and decreasing the activity of the bone forming protein OsteoCalcin. Calcium and Vitamin are crucial to preventing Vetrebral and Hip bone loss in these patients. The effects on OsteoBlasts and OsteoClasts are being restudied in the laboratories of St. Louis’ Washington University School of Medicine where recent results suggest that Cortisone slows OsteoClastic activity, and this soon results in a backward chain reaction that slows OsteoBlastic bone formation as well. It has been found that OsteoClasts have cortisone receptors on them and it is because of these that Cortisone slows OssteoClastic (as well as Osteoblastic) activity.

8)    Hyper -and Hypo- Prolactinemia – a hormone made in the Pituitary Gland. Hypo is a
problem especially affecting Men, because Prolactin (the Milk-forming Hormone in women) is
needed for LH to work properly and form Testosterone in men. Taking Testosterone bypasses the
need to replace Prolactin.
Hyper- is a problem in women because it prevents Ovulation, which in turn causes premature
bone loss. This problem is treated with bromocriptine or parlodel.
Women suffering from schizophrenia may be at increased risk of osteoporosis as a result of the medication they are taking, according to a new study by Irish researchers. Schizophrenia is associated with high rates of osteoporosis (brittle bones) which it is believed may be caused by the prolactin-raising properties of some antipsychotic medication being taken by women with schizophrenia.The study of premenopausal women with schizophrenia compared those who had received prolactin-raising or non-prolactin-raising antipsychotic medication and found that those taking the prolactin-raising medication had higher rates of bone problems. It was found that the group of patients taking drugs that raised prolactin had higher levels of prolactin, lower levels of sex hormones and lower bone mineral density than the group taking the other medication.The authors say their findings suggest that the high rates of osteoporosis associated with schizophrenia may result from anti-psychotic drug induced hyperprolactinaemia (raised prolactin levels in the blood) and the prolactin-raising profile of some antipsychotic drugs should be considered when choosing such drugs for women with schizophrenia, they advised.

9)  Parkinson’s Disease – The study of 166 Parkinson disease patients found that 51% of the female patients had osteoporosis; the rate of osteoporosis among women of the same age without Parkinson’s is about 25%. Among the males with Parkinson disease, 29% had osteoporosis, compared with about 7% of men without Parkinson’s. Large percentages of the Parkinson patients also had osteopenia, which is low bone mass that puts them at risk of developing osteoporosis. Osteopenia rates in Parkinson patients are 45% for women and 48% for men. Current guidelines do not list Parkinson’s disease as a risk factor for osteoporosis, but this study suggests that it should be included. The increased risk for osteoporosis could result from the decreased mobility and ambulation that people with Parkinson’s experience as the disease progresses, and even early on before the diagnosis is made. Exercise can help prevent osteoporosis. People with Parkinson disease also become more susceptible to falls, which can result in a higher risk of fractures. All Parkinson patients benefit from vigorous exercise programs including boxing for the elderly.

10)  Down’s Syndrome – Patients have a number of orthopedic and rheumatologic disorders. Adults with Down Syndrome may have long bone fracture from poor bone quality; hip dislocation and dysplasia; scoliosis; patello-femoral instability; metatarsus primus varus, with hallux valgus or varus and pes planus; compression fracture of the vertebral body with osteoporosis; osteoarthritis; atlanto-occipital instability; paraplegia caused by compression fracture; or quadriplegia to atlantooccipital instability. Considering that a recent life-table study of live-born individuals with Down syndrome reported a survival rate of >50% to age 50, 40% to age 60, and 13% to age 68, musculoskeletal disorders such as functional disabilities caused by Osteoporotic complications must be given more consideration in these patients. Angelopoulo et al found adults with Down syndrome (average age, 26.22±4.45 in men and 23.65±3.23 in women), particularly men, have a lower bone mineral density, even those without accompanying disorders that may cause osteoporosis (eg, hypogonadism, insulin-dependent diabetes mellitus, hypothyroidism, and epilepsy treated with anticonvulsant medication). The pathogenesis of this disease in bone tissue is multi-factorial and includes a sedentary lifestyle and poor mobility, endocrine abnormalities, and epilepsy treated with anticonvulsant medications. Because of the increased life expectancy of patients with Down syndrome, long-term treatment with anticonvulsant drugs has a much greater impact on bone metabolism.

11)  Hyper- and Hypo- Thyroidism –excessive thyroid hormone causes osteoporosis by increasing bone resorption more than bone formation.

12)  People with Congenital Defects in Calcium Absorption (so-called “Vitamin D-Resistant Rickets”).

13)  HyperParaThyroidism – for which we check for HyperCalcUria and Kidney stones; the
bone condition is called Osteitis Fibrosa and includes areas of O.F. Cystica.

14)  Both Diabetes Type I (Insulin-Dependant ) and Diabetes Type II (Maturity Onset) – because Diabetes decreases blood flow to distal skin and muscle while increasing it to bones, which activate bone-destroying OsteoClasts. Researchers have found that children and adolescents with Type I diabetes in Pakistan seem to lag in their bone development. They have lower bone mineral content by an average of 8.5%, but greater muscle mass. The loss of bone mineral density correlated with high blood sugar.  It was also found that diabetics eating fish-proteins have decreased circulation, which in turn decrease blood flow to bones activating OsteoClasts. It is also known that lower levels of Insulin-like Growth Factor-1 (IGF-1), an anabolic hormone that maintains bone formation, are seen in patients with type-1 diabetes. People with Type II Diabetes are also thought to be in a chronic inflammatory state.

15)  HemoChromotosis – or the tendency to Iron Overloads, which also increase the incidence of
Diabetes, Heart Attacks, and Cirrhosis of the Liver, all supposedly on the basis of chronic
Inflammation.

16)  People who don’t absorb enough calcium -  from their food or from supplements. The main dietary form of Calcium is Calcium Carbonate. It is also the form of Calcium in TUMS. This requires an acidic environment (in the stomach) to optimally absorb Calcium after the compound has been broken up into Calcium++ and Carbonic Acid (H2CO3). Vitamin B-12, Folic acid, and Copper also require acidic environments for absorption. After age 50, as many as 40% of women secrete less than optimal amounts of stomach acid and therefore absorb less than optimal amounts of Calcium. The Parathyroid glands respond by secreting Parathormone to increase Calcium levels, but it does so by pulling Calcium out of the bones, and thereby worsening Osteoporosis.
If a person is achlorhydric (secreting no stomach acid) or hypo-chlorhydric (secreting below-normal  amounts stomach acid), or if you are on AntiAcids from your doctor (which decrease the amount of stomach acid) then you should take supplemental calcium in forms other than Calcium Carbonate, preferably Calcium Citrate; some othe well-absorbed  but more expensive calcium preparations include Calcium/Magnesium Aspartate, Calcium Glycinate, and Calcium Lactose Gluconate.
Non-Aluminum Antacids, like Cimetidine (Tagamet ) cause Osteoporosis the same way.
Pernicious Anemia (Vitamin B-12 deficiency in part caused by a lack of stomach acid) causes
Osteoporosis by failing to lower Homocystiene.

17)  People, and especially women, with Inflammatory Bowel Diseases – such
as Cystic Fibrosis, Crohn’s Disease, Ulcerative Colitis, and Celiac Disease (Non-Tropical Sprue)
- they interfere with the absorption of Nutrients needed for bone formation, including Calcium,
Magnesium, Boron, and Manganese.

18)  High Homocysteine levels – are associated with increased risk of fractures and
Osteoporosis according to the 4/09 issue of the J. Clinical Endocrinology & Metabolism reporting combined work from 12 leading US medical centers. It is known that Folate, Vitamin B-6, and vitamin B-12 all lower Homocysteine by catylizinig methylation reactions that convert it from harmful homocysteine to the harmless essential amino-acid Methionine. It is also known that chemical methyl group donors like DMG (Di-Methyl Glycine), TMG (Tri-Methyl Glycine) and Choline (or Tetra-Methyl Glycine) all do the same thing, but generally less dramatically.
Homocysteinemia also causes Heart Disease (increased rates of Myocardial Infarction), Marfan-like Syndrome; Neurological deformities in fetuses and infants including Spina Bifida and the horrible crippling MyeloMeningocele; Alzheimer’s Disease in older people; and also facial deformities in fetuses and children including Cleft Lip and Cleft Palate.
The exact mechanism causing osteoporosis unknown, but is suspected that elevated homocysteine disturbs the cross-linking of collagen in bone and disturbs also osteoblast formation.
It has bee reported that men and women with Schizophrenia often have abnormally high
Homocysteine levels and osteoporosis, and for this reason the two findings may be linked.
HomoCystinemia and HomoCystinuria – are caused by a deficiency of the enzyme
Cystathione B-Synthase.
Note that those with poor renal (kidney) function for any reason also have high Homocysteine levels. Higher levels of Cystatin-C diminished this effect, but higher levels of Folate, B6, and B12 did not. Cystatin-C, formerly called Cystatin-3 is a protein encoded by the CST3 gene (on the short arm of Chromosome 20) and is a biomarker of kidney function, and is being studied as a possible biomarker of cardiovascular disease as well. It also seems to play a role in brain disorders involving amyloid protein, such as Alzheimer’s Disease. It inhibits proteinase enzymes both within and without all cells of the body. It is removed by normal glomerular filtration by the kidney; if kidney function declines, Cystatin-C rises. Cystatin-C has been found to be a more reliable indicator of kidney function than Creatinine, which can vary more with age, race, and muscle mass.

19) People with  Blood Diseases that infiltrate the Bone Marrow – and thereby
erode the bone – such as Leukemia, Lymphoma, Multiple Myeloma, Thallessemia Major and
Minor (Cooley’s Anemia), Sickle Cell Disease, Hemoglobin C Disease, Gaucher’s Disease, and
(congenital) Osteogenesis Imperfecta. Anemia and elevated ESR suggest Multiple Myeloma, and
the need for an Immune Electrophoresis Test.

20)  People with Pancreatitis – independent of its connection to alcoholism

21)  Paget’s Disease of Bone – with its abnormally rapid bone turnover rates.

22)  Renal (or Kidney) Failure – for any reason – whether on dialysis or not; Amyloid is often
involved in this condition and speed the dissolving of bone

23)  People with Diseases featuring Amyloid Deposition – which are a number of
chronic inflammatory diseases – because Amyloid dissolves bone.

24)  Lactose Intolerance – which is linked to poor intestinal Calcium absorption.

25)  Certain Cancers – including especially those of Breast, Kidney, Thyroid, Prostate, and
Lung; look for them when the complaint is night pain. Further, some women with the diagnosis of Breast Cancer cut out fats to decrease the number of fat cells that estrogen dissolves in. They do this by cutting out dairy products (milk fat), which decreases their daily intake of calcium, which further worsens Osteoporosis.

26)  People with any inflammatory disease or condition within their body that involves the Skeletal System – This happens because inflammation stimulates the OsteoBlasts to increase their production of natural glucocorticoid substances including cortisone. In patients with skeletal inflammation, treatment with more externally supplied cortisone results in rapid bone loss. In those without inflammation, treatment with more (externally supplied) cortisone does NOT result in decreases in bone density.
Other fewer types of  Cancers cause deposition of bone , the opposite of ossteoporosis. Look for these Cancers or for Paget’s Disease (of bone) if the patient had a low-energy fracture but was found to have normal bone density.
Night pain is also a clue to the presence of almost all malignancies.
Researchers  reported on April 30, 2009 that Androgen-Deprivation Therapy (ADT), a common treatment for men with prostate cancer, puts men at an increased risk for skeletal fracture, higher incidences of diabetes, and cardiovascular-related mortality. According to an analysis of 14 studies published online April 27,2009 in the Journal of Cancer, patients who received ADT had a 23% increase in the risk for overall fracture and a 17% increase in cardiovascular-related mortality, compared with men who did not undergo treatment with ADT. Data from 2 large studies also indicated significant elevations in the risk for diabetes. ADT is currently the most common form of treatment for advanced prostate cancer, and is being increasingly used as adjuvant therapy with radiotherapy for localized disease and as salvage therapy for increasing prostate-specific antigen levels after localized treatment. The authors note that although ADT has been successful in improving overall quality of life in patients with advanced prostate cancer, it can cause potential adverse events.
However, another study found that combining a Biphosphonate (Fosamax family) drug,
such as Pamidronate with the Anti-Prostate Cancer drug Leuprolide (lowers male Androgens like
Testosterone) allowed for effective cancer treatment WITHOUT the usual accompanying
Osteoporosis.

27)  Fat and Carbohydrate Storage diseases – like Gaucher’s Disease, in which fatty
substance (GlucoCerebroside) accumulates in the bone marrow, increasing pressure there and
expanding and thinning the cortical bone shell. Thus, the appearance of Ossteoporosis

28)  People with HyperCalcuia – diseases featuring increased urinary excretion of Calcium for
any  reason

29)  Inflammatory, Rheumatologic, and Infectious Diseases of the Bowel –
decrease absorption of Calcium; disorders of this type include Cystic Fibrosis, Ulcerative Colitis,
Regional Enteritis (or Crohn’s Disease), and Malabsorption Syndromes like Celiac Disease.
The risk of osteoporosis is greater in patients with inflammatory bowel disease (IBD) because of several related risk factors such as the prolonged use of corticosteroids, the malabsorption of calcium, vitamin D, and other nutrients used in the formation of bone following small-bowel disease or small-bowel resections, and the inflammatory process resulting from the illness. A reduction in bone mineral density (BMD) has been reported in 30-75% of patients with IBD (Crohn’s disease or ulcerative colitis). An evaluation of the risk factors of osteoporosis should be performed to identify those in need of antiresorptive drug therapies (ART) and/or calcium and vitamin D supplements.

30)  Reflex Sympathetic Dystrophy (Causalgia Major) – through the malfunctioning
of sympathetic nerves in the arms or legs; the Sympathetic nervous system sends nerve fibers to
bones  giving bone “trophic” or vitalizing stimuli. Without such stimuli, bone crumbles and
Charcot Joints are produced.

31)  People with Rheumatoid Arthritis – presumably on the basis of its chronic
inflammation and the release of the pro-inflammatory cytokines related to it.

32)  People with Cirrhosis of the Liver secondary to Hepatitis – an inflammatory state – and who have NOT consumed excessive alcohol – have been shown to also have high numbers of Tumor Necrosis Factor (TNF) Receptors p55 (also called sTNFR-55) which also causes osteoporosis bone loss via increased bone resorption.

33)  Dizziness (Vertigo) -  has been linked to Osteoporosis, says a study in the Journal of Neurology published in 3/09. Dizzy spells are sometimes harmless, but if they occur regularly, they might be a symptom of osteoporosis. That’s because people who suffer from osteoporosis are more likely to suffer from vertigo, according to a study printed in last month’s journal of the American Academy of Neurology. Vertigo is an inner ear disorder that leads to the sensation of spinning and motion even when standing still. It’s associated with loose calcium carbonate crystals in the inner ear. The study included more than 200 people suffering from benign positional vertigo without any known cause. Those people were compared to another 200 people without any history of dizziness. Osteoporosis sufferers proved three times more likely to have vertigo compared to people with normal bone density. Participants who suffer from osteopenia, a precursor to osteoporosis, were twice as likely to have the condition. The link between vertigo and bone disease was even stronger for women than for men. Women far outweigh men as osteoporosis sufferers, and they usually start experiencing vertigo symptoms around the time that menopause sets in and estrogen production ends. But researchers haven’t determined if estrogen plays a direct role in the onset of vertigo and noted that men with osteoporosis are also at increased risk for the condition.

34)  Elevated Cholesterol – levels are correlated with thinner bones – we don’t know why

35)  Emotional Depression and those under Chronic Stress – has been shown to
Make Osteoporosis in 41-year old depressed women look like that in 70–year old women who are not depressed. This results from alterations in behavior and in the neuroendocrine system; for example, depression may trigger stress which, in turn, triggers increased cortisone production, and cortisol triggers osteoporosis. It can happen in Anorexia Nervosa for the same reasons – anorexics are depressed and stressed physically and mentally.  Depressed women average 6.5% less bone density in the Spine, and 10-14% less bone density in the hips, which doubles the  probability of this group fracturing their hips compared to women who are not depressed. Interestingly, some Psychotropic drugs used to treat depression and chronic stress also increase Osteoporosis.
In November of 2006, an Israeli research team under the leadership of Dr. Raz Yirmiya, Professor of Psycho-Biology at Hebrew University, clinically proved that depression actually weakens bones, that is, directly causes Osteoporosis. They induced an animal mode of depression called chronic mild stress (CMS). Biochemically, the depression triggered the Brain to send signals via the Sympathetic Nervous System to most of the body’s organs, including the skeleton, which then released nor-epinephrine into the bones, a drug known to have a negative effect upon OsteoBlastic function. The result was under activity of OsteoBlasts, and hence Osteoporosis. They found further that the anti-depressant drug Imipramine (Tofranil) blocked the depression-like behavior and also the malfunctioning of the OsteoBlasts, so that the mice did not lose bone and did not become Osteoporotic. Imipramine is a tri-cyclic anti-depressant that is known to act on both the norepinephrine and the serotonin reuptake systems. The beta blocker drug Propanolol is known to be a nor-epinephrine inhibitor; when it was given, the bone loss from depression was stopped, and it did so without affecting the animal’s behavior. So perhaps it will stop bone loss in depressed people without affecting their behavior.
It was further and later found at Harvard University (see Harvard Women’s Health Review 6/07) that people ages 50 and over who regularly took antidepressants called selective serotonin reuptake inhibitors (SSRIs) had double the rate of fractures as people not using such medications. Researchers working with an animal model found further that depression triggers the release of noradrenaline (nor-epinephrine), which interferes with bone-building cells. They found that imipramine – a member of an older class of drugs called tricyclic antidepressants – reversed both depression and depression-induced bone loss, but NOT SSRI’s. Research continues.
It has recently been shown that Vitamin D not only fights Osteoporosis in its own rite,
but also fights depression. One must get sunlight in the winter (ideally 15-30 minutes per
day) and be sure to consume enough Vitamin D (600-800 IU/day) in the diet or by
supplements.

36)   Rare Genetic Disorders of Collagen such as Osteogenesis Imperfecta,
Ehlers-Danlos Syndrome, and Marfan’s Syndrome.

37)   Radiation Therapy – kills OsteoBlasts in the radiation field

38)   Abuse of legal Life-style Drugs, including:
a)  Alcoholism – which stimulates bone-destroying OsteoClasts and impedes bone
-building OsteoBlasts
b)  Tobacco use – Cigarette smokers heal from fractures much slower; Nicotine decreases
Estrogen production, accelerates degradation of Estrogen, decreases GI Calcium
absorption, and lowers the age of Menopause. Tobacco products also contain the
toxic heavy metal Cadmium that causes further resorption of bone.
c)  Excessive Caffeine consumption – over 2 cups of Coffee, or over 12 oz of
Cola sodas  increases urinary calcium excretion.
d)    Excessive consumption of Sodas (especially Colas) with
Phosphoric Acid – that pull calcium out of the skeleton and replace calcium
rich milk  in the diet.

39)  Those with Arterial Calcifications of Arteries in the Thorax and Breasts -
according to a paper published in the January 2008 issue of the J Clin Endo Metab, researchers at the Harvard Medical School have shown a strong independent correlation between Osteoporosis and the Arterial Calcifications of Atherosclerosis in arteries about the Breasts. They conclude that Osteoporosis may identify women at risk of vascular disease. They don’t state the biochemical connection of the two disorders but excessive acidity of the blood from eating food such as too much red meat, could account for both.

40)  Those with Obstructive Coronary Artery Disease – is more frequent in those with Osteoporosis or Osteopenia than in those with normal Bone Mineral Density (measured by DEXA). 146 women and 52 men and all averaged 66 years of age. In the study, roughly 1/3rd had Osteoporosis, 1/3rd had Osteopenia, and 1/3rd had normal Bone Density. The incidences of Coronary Artery Disease were 76%, 68%, and 47% in the 3 groups. The researchers aren’t sure why except to say that those with normal BMD had a higher percentage taking statins.

41)  Chocolate – Even though Chocolate (especially dark chocolate, is loaded with healthful anti-Oxidants, its regular consumption seems to weaken bone density and strength, which in turn increases the risk of osteoporosis. According to a new study, women who eat chocolate daily have an overall bone density 3.1 percent lower than those who consume it less than once a week. More than 1,000 women aged 70-85 were asked to keep a diary of how often they consumed chocolate or cocoa-based drinks. The researchers did not distinguish between types of chocolate consumed. Even though chocolate contains flavonols and calcium, both of which are linked to a positive effect on bone density, it also contains oxalate, an inhibitor of calcium absorption, and sugar, which is linked to calcium excretion.This study comes less than a month after British medical journal the Lancet warned consumers that manufacturers usually remove the healthy element — the flavonols. The standard manufacturing process of milk chocolate destroys about one-quarter to one-half of its flavonoid content, which, as you’ll find out below, is where the health benefits are. Dark, unprocessed chocolate, on the other hand, has been exonerated in several studies as actually having some positive impact on your health. The flavonols it contains have antioxidant properties that can help protect your body from damaging oxidative stress. It also contains far less sugar than its processed milk chocolate counterpart.

42)  Chronic Kidney Disease – moderate or severe – is found in 76% of Osteoporosis case says a report from Ireland in May 2007. The rest had mild kidney disease. Patients with moderate or severe glomerular disease averaged 80 years of age, and had double the normal risk of vertebral fractures. Generally doctors think about this connection the other way, recognizing Osteoporosis as a complication of Glomerular Kidney Disease (Glomerular Filtration Rate falling below 60nl/min.

43)   Rare Familial Genetic Mutations – have occurred in an Iranian family that kills most of its members (23 of 28 relatives at an average age of 52). This same gene also leads to heart failure, diabetes, high blood pressure, high cholesterol, and osteoporosis. A Yale professor, Dr. Richard Lifton, has further established that heart disease and osteoporosis occur more often than would be predicted by chance.

… and also if have a very advanced and academic doctor who has told you that lab tests show that …
44)   You have below average levels of Insulin Growth Factor (IFG-1) which
leads to less OsteoBlastic (bone –forming) activity, and therefore a dominance of OsteoClastic
bone resorption.
45)    You carry a defective gene for Vitamin D Receptors; the “BB type” – is
related to increased Osteoporosis.
46)   You carry a certain form of a gene (a haplotype) that programs for
production of the enzyme Aromatase, that apparently increases its efficiency in converting Estrogen into Testosterone and vice-versa, effectively lowering the level of estrogen, and thereby increasing the incidence of osteoporotic vertebral fractures in post-menopausal women. These data support the hypothesis that aromatase plays an important role in bone homeostasis in post-menopausal women.

STATISTICAL SCALES FOR PICKING OUT THOSE WITH HIGHEST RISK OF OSTEOPOROSIS

5 criterion scales have been developed to evaluate and pick-out people at greatest risk for Osteoporosis. They were developed to qualify women for referral for DEXA (X-Ray) evaluation. They include scales called National Osteoporosis Foundation Guidelines. They are called:
1) SCORE
2) ORAI
3) ABONE, and
4) Weight Criteria

SCORE was the most sensitive strategy for detecting decreased Bone Mineral Density (BMD), selecting 86.6% of women with mild osteopenia, 96.2% with moderate osteopenia, and virtually all (99.6%) of those with osteoporosis. It selected 69.2% of those with normal BMD results.