- Exoprin Supplement Facts
- Strontium Bone Maker Side Effects
- Nutritional Supplements for Osteoporosis
- Exoprin Interactions
- Prolia Osteoporosis Treatment
- Learn More About Products for Osteoporosis
- Exoprin: Frequently Asked Questions
- The Role of Zinc in Osteoporosis.
- Fennel, Butter, and Other Foods For Osteoporosis
- The Vitamin Combo That May Prevent Osteoporosis
Fosamax Side Effects - Is it Safe?
Fosamax is one of the leading prescription osteoporosis drugs. It contains alendronate, a compound that inhibits the breakdown of bones. However, Fosamax does nothing to build new bones. These effects on bone homeostasis can temporarily increase bone mineral density but eventually produce old, weak bones. Over the last 10 years, reports of adverse effects with Fosamax use have grown. One such side effect of Fosamax is the paradoxical increase in the risk of osteoporotic bone fractures in the thigh, hip and femur. But is bone fracture really a paradoxical side effect of Fosamax? Read on to find out why Fosamax is not only bad for your bones but also for your health.
by Brad Chase
Fosamax is a Merck drug used for preventing and treating osteoporosis in men and postmenopausal women as well as also for treating Paget’s disease (another bone disease).
It is available in 5 mg, 10 mg, 35 mg, 40 mg and 70 mg tablets as a 70 mg/75 ml solution. The active ingredient in Fosamax is a sodium salt of alendronic acid also known as alendronate sodium.
The manufacturer recommends users to take Fosamax first in thing in the morning before eating. The drug should also be taken with a full glass of plain water. Mineral water and beverages may affect its absorption. Lastly, users are advised to stay upright for at least 30 minutes after taking Fosamax.
Milk and drugs that contain calcium, aluminum and magnesium should also not be taken along with Fosamax.
The risk of gastric ulcers is increased when Fosamax is combined with NSAIDs (non-steroidal anti-inflammatory drugs) such as aspirin, diclofenac and ibuprofen. In fact, Fosamax should be avoided by people with any form of gastrointestinal inflammation.
The drug should also be avoided by people with low blood calcium levels, osteomalacia, renal impairment as well as by pregnant and breastfeeding women.
Alendronate belongs to a class of drugs known as bisphosphonates. Therefore, alendronate is made up of two phosphonate groups and each of them is negatively charged. This creates a strong negative charge that ensures the absorption of alendronate is very low (0.6 – 0.7%) after oral dosing.
The strong negative charge of the alendronate molecule also ensures that the drug preferentially binds to bones rather than other tissues. It is estimated that about half of the alendronate absorbed into the body binds to bone surface while the other half is eliminated unchanged from the kidneys.
However, once bound to the bone, alendronate is not easily displaced. It takes 10 years to halve the concentration of the drug bound to the bone.
Once bound to the bone, alendronate inhibits the activity of osteoclasts. Osteoclasts are the cells responsible for bone resorption.
By inhibiting osteoclasts, alendronate prevents the breakdown of bones. Because it does not affect the formation of new bone, the inhibition of osteoclasts should produce an overall increase in bone mineral density with time.
This means that alendronate does not increase bone mineral density on its own. Rather, optimal levels of calcium and vitamin D are required to drive normal bone mineralization.
Alendronate only tilts the balance of bone homeostasis in favor of bone formation rather than bone resorption.
A special formulation of alendronate with vitamin D added is known as Fosamax + D. This may produce faster results because its vitamin D content will increase bone mineralization while alendronate reduces bone breakdown.
Since its introduction in 1995, Merck has ruthlessly marketed and defended the effectiveness and safety of Fosamax. The company even went to court to prevent the FDA (Food and Drug Administration) from approving generic alendronate sodium after the patent of Fosamax expired. It lost.
When Merck opened its “non-profit” Bone Research Institute, it fought to expand the market for Fosamax.
Soon, doctors were not only prescribing Fosamax for preventing osteoporosis in postmenopausal women but also for men. By broadening the perceived risks of bone fracture, Merck and the medical community expanded the definition of poor bone health to ensure that Fosamax can be prescribed for osteopenia too.
However, the FDA has not always agreed with Merck’s sleazy marketing of Fosamax. The regulatory body has rebuked Merck for falsely presenting the benefits of its drug on several occasions.
The years of needless prescription of Fosamax is now catching up with the drug. As the number of people who were blindly exposed to a drug they did not need grew, severe adverse effects not reported in clinical trials have appeared with increasing frequency.
In 2008, a letter published in the New England Journal of Medicine made public the FDA record of 23 cases of esophageal cancer linked to Fosamax use.
Soon after, a study published in the Journal of the American Dental Association revealed the shocking discovery that Fosamax can weaken the bones of the jaw.
However, users of Fosamax are not waiting for the FDA to take action. Since 2004, some users have taken class action suits against Merck for not warning them about the adverse effects of Fosamax.
In 2009, ABC News carried the story of 59-year old Sandy Potter from Queens, New York who was jumping rope with the neighborhood kids. While working on this low impact exercise, she felt her thigh bone snap.
Sandy Potter was diagnosed with osteoporosis when she was 48 years and had been using Fosamax for the last 8 years prior to the accident.
The case of Sandy Potter is not really an isolated incident. Rather, increasing number of women are coming in to ERs with femur, hip and thigh bone fractures.
Dr. Kenneth Egol, a professor of orthopedic surgery in New York University, Langone Medical Center reported seeing more Fosamax patients come in with femur fractures sustained while doing low-energy exercises such as walking.
Because the femur is one of the strongest bones of the body, there is a valid concern about what Fosamax may be doing to other bones of the body.
Dr. Egol also reported that X-ray examinations of the fractures showed that the bones were shattered in a manner consistent with road traffic accident and not simple falls.
Besides the thighbone, femur and hip bone, Fosamax has also been linked to fracturing of the bones of the jaw.
The term for this bone condition is osteonecrosis of the jaw. It is also commonly known as bis-phossy jaw or Dead Jaw Syndrome.
Osteonecrosis of the jaw describes a condition in which the bones of the jaw fails to heal after sustaining a minor injury such as a routine dental work like the pulling of the tooth.
This condition involves the restriction of blood supply to the jawbone. The tissues around it then swell up and get infected causing the bone to die.
While Merck contends that these side effects are rare and are not conclusively linked to Fosamax, they are serious enough that the FDA has forced Merck to include increased risk of bone fractures on the label of Fosamax.
In compliance, the label of Fosamax states the drug can cause “low energy femoral shaft and subtrochanteric fractures”. Big words but clear admission of the dangers of Fosamax.
The alendronate in Fosamax inhibits bone resorption without improving bone mineralization. While this can increase bone mineral density and bone health in the short term, the truth is that this disrupts normal bone homeostasis.
Ideally, old bone is always being destroyed while new bones are formed. The balance of the two processes ensures a healthy bone turnover that produces strong bones.
However, by blocking one process and not the other, Fosamax soon encourages the “hypermineralization” of bones. Hypermineralization refers to the unhealthy addition of calcium (and other bone minerals) to old bones that should have been broken down and reabsorbed.
Therefore, in this case, higher bone mineral density does not translate to stronger bones.
In fact, the hypermineralization promoted by Fosamax can make bones more brittle and less resistant to strains. Therefore, Fosamax produces dense bones that have low tensile strength and are prone to fracturing.
Hypermineralization is most likely responsible for the cases of femur and thighbone fractures increasingly reported among postmenopausal women taking Fosamax.
Another way in which Fosamax is bad for bone health is through its inhibition of bone repairs.
While alendronate is deposited in bone matrix, it may displace calcium from those sites. Therefore, the drug may reduce the formation of new bones. However, this effect does not seem to affect bone mineral density but rather the bone’s ability to repair the microscopic cracks it inevitably sustains.
The daily wear and tear on the bone normally causes tiny, fine cracks to appear on the surface of the bone. These cracks are lines of fault that must be repaired to preventing them from widening and growing into fractures.
By impeding the repair of these fractures, Fosamax increases the risk of bone fractures that occur sooner than later.
Such bone fractures may be triggered by the smallest strain placed on the bone. Therefore, sudden unwarranted fractures may occur during light exercises but will appear severe from X-ray scans. This is actually consistent with the kind of femur and thighbone fractures that affect postmenopausal women placed on Fosamax.
Some doctors now recommend that Fosamax should not be taken until bone test results show clear risks of osteoporosis and that the drug should not be used for longer than 5 years in order to reduce the risk of bone fractures.
Even when Fosamax is stopped after 5 years, studies show that the drug persists for longer (it takes 10 years for the body to get rid of half of the alendronate stored in the bone matrix) in the bone even after it has been withdrawn.
This means that the harmful effects of Fosamax can still rage on for a long while after the drug has been stopped.
Therefore, it is difficult to even defend the use of Fosamax in the first place.
There are alternative ways of preventing osteoporosis in postmenopausal women. Rather than shift to another drug for osteoporosis, you should try dietary and lifestyle changes as well as exercise and natural supplements.
There are lifestyle changes to make to improve your bone health. First, you should stop smoking and make sure to exercise more.
For exercise, do more strength training and weight bearing exercises. These strengthen your bones by especially giving it tensile strength to withstanding daily wear and tear.
There are also dietary supplements that are safer alternatives to Fosamax. The most common of these is calcium.
Calcium is important for bone health but not as important as you have been made to believe. Instead of taking high dose calcium (above 1,000 mg/day) supplementation, try smaller doses especially from dietary sources such as vegetables.
Vegetables are better than milk as dietary sources of calcium. However, you should choose vegetables that do not contain oxalic acid (oxalate) which may bind calcium and reduce its absorption.
Other important minerals to take are magnesium, zinc, boron, silicon and manganese. These also increase bone mineral density but, more importantly, they improve bone strength.
Vitamins D and K are also essential to bone health. These can be taken as supplements even though they are also found in certain vegetables. These vitamins can increase the absorption of calcium from your diet and ensure that the mineral is moved from the blood to the bones where it is needed.
[+] Show All
|Next Article: Eating Fermented Vegetables May Increase Bone Health|
Nutritional Support For Osteopenia and Osteoporosis Sufferers.