Osteoporosis, or porous bone is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures, especially of the hip, spine and wrist, although any bone can be affected.
Several studies revealed that 44 million Americans are known to have low bone mass. That amounts to 55% of everyone over age 50. One in 2 women and one in 4 men over age 50 will have an osteoporosis-related fracture in his or her lifetime.
Osteoporosis is responsible for more than 1.5 million fractures annually, including roughly:
- 300000 hip fractures
- 700000 vertebral fractures
- 250000 wrist fractures
- 300000 fractures at other sites of the body
In 2001, more than 315000 people were admitted to American hospitals with hip fractures, most of them due to osteoporosis. In the year 2000, it was estimated that osteoporosis caused 37500 deaths in the United States alone. Men over 50 are more likely to suffer from a hip fracture than prostate cancer. A woman’s risk of hip fracture is equal to the combined risk of breast, uterine and ovarian cancer.
32% of women will fracture a hip before reaching the age of 80. After reaching 50, the mortality rate in the first year following a hip fracture is 25%. 20% of those who could walk before a hip fracture were relegated to long-term care afterward.
In fact, osteoporosis is a global problem, excluding no ethnic group or gender. More than 200 million people worldwide are faced with the progressive weakening of already thinned bones and the prospect of often-fatal, always painful and disabling fractures.
Is Osteoporosis Dangerous?
Osteoporosis is simply a condition that breaks bones. Generally, spine and hip fractures grimly result in painful nights awake, invalidism and demise.
A staggering percentage of the 10 million Americans whose bones have thinned below a critical level will have spinal fractures, the most common and possibly the most painful type. As a matter of fact, 34 million people have low bone strength, not quite low enough to warrant the label “osteoporosis”, but significant enough to have a name of its own, which is “osteopenia”.
Although each individual in this group has lower risk, people with osteopenia will actually have more spinal fractures than people with osteoporosis. Vertebral fractures may occur as a result of a fall. However, the mechanism is usually different, simple forward slumping, kyphosis or “dowager’s hump”, often seen in the later years, puts so much pressure on the forward parts of the spinal column that osteoporotic bones spontaneously collapse. This type of break is referred to as a wedge fracture.
Thoracic kyphosis places more weight on the forward part of the vertebrae. When one vertebrae fractures, the angle of the spine is even more acute, and the weight of the head, shoulder, chest, arms and vertebrae above the level of the fracture is further concentrated on the front of the spinal column.
The previous angle of the un-injured spine was sufficient to cause one vertebra to collapse. The more acute angle that results from the fracture is even more likely to disrupt another vertebra. Subsequently, more angling will made the third fracture more probable.
Hip fractures are strong and sinister the second most common fracture overall. Wrist, ankle, elbow, shoulder and knee fractures are also common, usually occurring when a person uses an arm or a leg to break a fall.
It is the unbroken fall that fractures the hip. A new osteoporotic fracture of any kind raises the risk of mortality by 32%, regardless of a person’s age. A hip fracture subjects people to time in bed and wheelchairs, weakening muscles and bones still further, and de-conditioning the balance mechanisms in the body that were already inconstant enough to produce the fracture.
The fracture itself is not the killer. Mortality derives from the life changes that result weeks of bedrest with the increased chance of pneumonia and other opportunistic infections, decubitus ulcers (bedsores), weaker muscles, digestive ills and isolation from society, even family.
Fighting osteoporosis is a lifelong battle. As such, rather than waiting for osteoporosis to knock on our doors, it is recommended to understand the factors that affects bone strength and exercise precaution measures.
4 Main Factors That Affect Bone Strength
- Age Factor
This is an obvious, reliable factor that determines one’s risk for fracture. In a study of 200,160 women, researchers at Columbia University came up with results showing that between the age of 50 years old to 64 years old, the risk of fracture stands at 31%. As for those who are above 65 years old, the risk is almost double at 62%.
Though no one can entirely halt the aging process, we can still control our lifestyle that can affect bone density or risk of fractures in little as 2 years. In fact, the most important thing about age is how to take advantage of it. Basically, most of our bones are build up by the age of 30. Next, the bones tend to thin and weaken at an accelerating rate.
Therefore, the very best thing we can do is to generate a high peak bone mass before age 30 since it is easier to combat osteoporosis when we are younger. Osteoporosis is best countered through prevention.
- Genetics Factor
Some studies have reported that ethnic groups have different boney characteristics. An American study of 197,848 people recorded BMD and fracture in women from 5 ethnic groups consisting African Americans, Asians, Latin Americans, Native Americans and White.
By the time they reach the age of 80, more than 20% of the women in each ethnic group had bone mineral density T-scores below -2.5. and have osteoporosis. African American women had the highest BMD and Asian women had the lowest. One year after the study, 2414 new fractures of the spine, hip, forearm, wrist or rib appeared.
White and Latin American women had the highest risk for fracture, Native Americans were next, follow by African Americans and lastly, Asian Americans. There is a correlation between BMD and likelihood of fracture, the lower the T-scores, the greater the risk of fracture within each group.
But obviously there are other factors at work here, since overall Asian Americans had the lowest BMD, but also the lowest risk of fracture. Heredity probably plays a role in bone development but not necessary the primary factor.
In one study, hereditary factors were estimated for 3300 people in southern China. Researchers studied environmental differences such as calcium intake, smoking status, phyto-estrogen intake, exercise and alcohol consumption.
The environmental factors altered the heritable BMD, but did so differently in males and females. Females were found to be more sensitive to environmental changes than men, and therefore were better able to alter their BMD through diet and exercise.
This factor present a situation in which we definitely have some control, but it is limited. Most hormones can be created synthetically, and over-active glands can be removed surgically. There are homeostatic and feedback loops that provide for a good deal of self-adjustment.
Nevertheless, the balance, the equilibrium points, the greater harmonies of the entire orchestra do not always come naturally. If they did, there would be no need for the medications or the surgeries. Bone tissue is quite sensitive to hormonal changes. Estrogen, testosterone, growth hormone, parathyroid hormone, calcitonin and thyroid hormone all have positive and negative effects on the processes that maintain strong and healthy bones.
Naturally, there are genetic factors that influence hormonal timing and balance. But contemporary medicine can monitor all the hormones and therefore their balance. Furthermore, the surgical, chemical, radioactive and nutritionally supplementary alterations can be monitored too.
Estrogen And Testosterone
Estrogen generally seems to affect the dual processes of laying down and re-absorbing the cancellous/ trabecular bone. In a well-controlled German study on rats, estrogen and testosterone seemed to play a part in improving the trabecular region’s density. Estrogen improved mechanical stability, testosterone did not.
Testosterone seems to have even more of an effect. An Estonian study of 60 boys between ages 10 and 18 found that testosterone levels were the best predictor of hip, lower spine and pelvic bone mineral density.
We can conclude that the effect of exercise will be amplified or minimized depending upon the amount of estrogen or estrogen-like substances in the blood. Testosterone exerts perhaps an even stronger influence in building healthy bone mass. It can be hypothesized that bones build up before age 30 because estrogen and testosterone production is highest at that time.
The Estonian study also found that relative amounts of free insulin-like growth factor (IGF) are strongly correlated with bone mineral density. IGF, a hormone-like protein, comes in 2 forms. IGF-1 is active in almost every adult cell and is secreted by the liver. IGF-2 is critical for early development of the brain and bones of the fetus, and is secreted by the brain, kidneys, muscles and pancreas. Exercise seems to stimulate their secretion.
It will not come as a surprise that growth hormone influences bone growth in children. It is also well-known that excessive growth hormone in later years produces acromegaly, a condition in which the long bones get thicker, but neither longer nor stronger. It is unclear whether this condition artificially elevates the T- and Z-scores of a DEXA scan.
Parathyroid Hormone (PTH) has very complex and important effects on bone. It is a leading cause of osteopenia, and yet paradoxically it also helps build new bone. One European study suggests that within reasonable limits, the full parathyroid hormone molecule stimulates bone resorption, while one of the naturally occurring fragments of the molecule increases bone production.
The study goes on to report that the ratio of these 2 molecular pieces in the bloodstream is influenced by heritable characteristics, underlying kidney ailments, vitamin D levels, cortico-steroids and phosphate-related factors.
One of these molecular fragments might lurk behind the dual mechanism whereby the parathyroid hormone acts directly on osteocytes, causing them to start producing bone, and simultaneously stimulates them to begin secreting a factor that activates osteoclasts, promoting bone loss.
To complicate things further, estrogen deficiency seems to increase the bones’ receptivity to PTH, which induces them to give up more calcium to the bloodstream. The higher blood calcium serves to decrease the parathyroid glands’ PTH secretion, decrease vitamin D production and slow calcium absorption from the intestines.
Poor absorption especially weakens trabecular bone, opening the door to vertebral and wrist fractures. Independent research has shown that parathyroid abnormalities are also associated with osteoporosis in the forearm bones.
The second of the thyroid gland’s hormone trio that helps regulate mineral metabolism, calcitonin, responds to high calcium and phosphorus levels. Its primary effects are to reduce osteoclastic resorption of calcium and increase its urinary excretion, thereby lowering the blood calcium, a critical task in humans and most mammals. It does not have a very strong effect, and although it might seem like a paradox, this is highly desirable.
Our normal calcium levels have a very narrow range of safe fluctuation. Just a little too high and calcium will be deposited in our organs and other tissues, with disastrous results. But if the level falls very much, muscles go into deep and possibly fatal spasm.
Nevertheless, calcitonin, a 32 amino-acid protein that is found throughout blackbone-supported members of the animal kingdom, can be used as a medicine for people with too much calcium in their blood, and is effective against certain types of osteoporosis in pharmacological does that are significantly greater than what the body produces on its own.
Thyroxin encourages metabolism of just about every kind. Hyperthyroidism means accelerated heart rate, raised body temperature, and big appetite but thin body, all due to the increased rate of energy production and use. Hypothyroidism implies just the reverse. The person with the normal thyroid appears to have the best bones.
Bone growth and health are strongly influenced by hormones. The physiology and inter-relationships of hormones require individual medical consultation. Being alert to the effects of hormones helps one to know when medical advice should be sought.
When we talk about nutrition for strong bones, it is always Do’s and Don’ts as below:
- Opt for diet high in protein and calcium, up to 5 servings of vegetables daily and adequate sunshine or vitamin D supplementation during early growth and the teen years.
- If you are over age 75 or have problems with circulation involving heart or your brain, then restrict yourself to 500mg of calcium each day. Otherwise, 1000 to 1500 mg per day appears to be fine. In fact, in the healthy person under age 75, a daily dose of 1200 to 1500 mg of calcium is optimal. Sources of calcium include a glass of milk, cup of yogurt, serving of cheese or a dish that includes dairy such as an enchilada, lasagna or quiche.
- Vitamin D is a MUST match with calcium. The hormone-like derivatives of vitamin D are organically converted from vitamin D in sun-exposed skin. Once activated, they promote calcium and phosphorus absorption and hold the parathyroid ratios in line. The proper dose of vitamin D is 400-800 international units daily.
- Magnesium is a necessary part of the body’s cycle for activating vitamin D. The body’s ability to absorb magnesium drops as it ages, and this critical component of hydroxyapatite is excreted even more if you drink alcohol or take diuretics. Recommended dose is 600 mg from sources like licorice, coriander, almonds, brown rice and green vegetables.
- Copper competes with calcium for absorption, so supplements for one might necessitate a supplement for the other, taken at separate times. Recommended dosage is 3 to 10 mg.
- Strontium is important as it migrates to boney sites. Dosage is 0.5 to 3 mg.
- Zinc is critical for osteoblasts and osteoclasts which are the basic elements in making and resorbing bone. Dosage is 20mg.
Beside the above metallic substances and vitamins, some other essential minerals include:
- Boron (3 mg): Important for the effects of estrogen, calcium and magnesium retention, and a large number of other reactions. Fruits, vegetables and nuts contain all you will probably need. Overdoses occur at 30 times the recommended amount.
- Silicon (1-2 mg): Essential for all connective tissue, including bone. Silicon makes up most of the dirt vegetables are grown in, and it is abundant in the four B’s which are beer, beets, bell peppers and brown rice as well as leafy vegetables.
- Manganese (5-10 mg): Manganese is part of the boney matrix and thus necessary for bone health. Whole grains, spinach and pineapple are particularly rich in manganese.
- Vitamins: Vitamins important to bone health include vitamins B6, B9, B12, C and K. Bell peppers give you B6, B12 and C, green leafy vegetables gives you K and B9, but the most reliable source of B12 are meat, dairy products, eggs and vitamin pills.
- If you have kidney disease, ask your doctor before taking supplements, especially calcium, magnesium or silicon.
- Salt uses up calcium when it is excreted, limit daily salt intake to 2000 mg.
- Avoid smoking and more than 2 alcoholic drinks per day, one carbonated beverage, one cup of coffee and more than 5 to 6 ounces of protein a day. Protein metabolism requires calcium and the body loses 30-40 mg of calcium for each ounce of protein it digests.
It is important to have some understanding of the factors that contribute to bone formation, regardless of whether one has any conscious control over them. Age, genetics, hormones and nutrition all influence bone formation, as well as the disintegration that leads to osteopenia and osteoporosis. As such, prevention measures can be adopted to avoid bones loss or strength that may lead to complicated problems later on.