Estrogen is the only clearly effective treatment.  Low estrogen levels cause a gradual loss of bone calcium.  Youthful estrogen levels not only stop this loss but cause a modest increase in bone density.   Avoid bisphosphonates because they increase bone density by going to the bone but done strengthen them.  There is no reduction in fractures and an association with at least 2 issues, femur fracture and deterioration of the mandible.

Osteoporosis

Merck:  Osteoblastic (cells that make the organic matrix of bone and then mineralized bone) and osteoclasts (cells that reabsorb bone) are regulated by parathyroid hormone (PTH), calcitonin, estrogen, vitamin D, cytokines (e.g. interleukin-1, tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor, interleukin-6) and other local factors such as prostaglandins.  After the age of 30 bone loss occurs at the rate of 0.3 to 0.5% per year.  Beginning with menopause bone loss accelerates in women to about 3 to 5% /year for about 5 to 7 years.  Because stress is necessary for bone growth, immobilization or extended sedentary periods results in bone loss.[i]  Cigarette smoking (inhibits the activity of osteoblasts) and excessive caffeine or alcohol use adversely affect bone mass.  Bisphosphonates are the first line drug therapy.  Diagnosis is by dual energy X ray absorptiometry (DXA or DEXA).  Exercise reduces risk.[ii]   

Conns Therapy 2002: 

Alendronate & glucocorticoid induced osteoporosis

Nearly all postmenopausal women will lose bone mass if not receiving specific ERT therapy despite receiving adequate calcium and vitamin D.  (Prostesterone is needed to protect against uterine estrogen effects.)  Early preventive postmenopausal bone loose will help prevent fragility fractures later in life.  A bone density of -2.5 S.D. at the age of 70 has a 10-year hip-fracture risk of 24% (both men and women).  The osteoporosis field is being damaged by calcium marketers who claim that calcium alone is adequate.  For elderly women who were previously estrogen users, but had discontinued estrogen for over 5 years, both their BMD and fratyur4e rates may differ little from those women how had not previously taken estrogen.  90% of hip fractures occur after a fall; therefore treatment which reduce the risk (exercise, improving eyesight, and reducing use of nervous system altering drugs reduce the tendency to fall).  Heritability ranges from 25-80%.  There are at least 30 genes associated with the development of osteoporosis.  Those who have a fracture are at least twice as likely to have another fracture compared to someone of the same age and sex.    

Goodman & Gilman (2007)

Osteoporosis is a condition of low bone mass and microarchitectural disruption that results in fractures with minimal trauma.  Between 30% and 50% of women and between 15% and 40% of men suffer a fracture related to osteoporosis. It is defined in women as a bone mineral density of 2.5 standard deviations below peak bone mass (20-year-old healthy female average).  Type I osteoporosis is characterized by loss of trabecular bone owing to estrogen lack at menopause, and type II osteoporosis is characterized by loss of cortical and tabular bone in men and women owing to long-term remodeling inefficiency, dietary inadequacy, and activation of the parathyroid axis with age.  The disease is a result of multiple physical, hormonal, and nutritional factors acting alone or in concert.  Secondary osteoporosis (accounts for <5% cases) is due to systemic illness or medications such as glucocorticoids or phenytoin[iii].  {Glucocorticoid any of a group of steroid hormones, such as cortisone, that are produced by the adrenal cortex, are involved in carbohydrate, protein, and fat metabolism, and have anti-inflammatory properties.  Phenytoin: An anticonvulsant drug, C₁₅H₁₂N₂O₂, used most commonly in the treatment of epilepsy--also called diphenylhydantoin.    

Treatment is of two types, those that reduce bone resorption, (anti-resorptive therapy) and by promoting bone formation (anabolic therapy).  Since bone remodeling is a coupled process, anti-resorptive drugs ultimately decrease the rate of bone formation.  Until recently, anti-resorptives were the only drugs approved in the US for treating osteoporosis.  The increase in bone density is general under 10% after 3 years.  .  The situation changed in 2002 when the FDA approved the biologically active PTH fragment for use in treating postmenopausal women with osteoporosis and to increase bone mass in men with primary or hypogonadal osteoporosis.

Antiresorptive agents, bisphosphonates have emerged as the most effective drugs.  Alendronate and risedronate have sufficient potency to suppress bone resorption at doses that do not inhibit  mineralization.  The results of 10-year daily treatment with 10 mg of alendronate (supplemented with 500 mg of calcium)reported a 14% increase of lumbar spine BMD, and a smaller increments at the trochanter, total hip, and femoral neck.  On reduction and discontinuation of treatment BMD at the lumbar spine was maintained, but not at the hip and neck.  Risedronate for women with low bone density but no previous vertebral fracture displayed increased of lumbosacral and femoral neck BMD with a significant reduced risk of first vertebral compression fracture.

Calcium:  Although little effect of calcium on trabecular bone has been reported, reduction in cortical bone loss has been observed, and in elderly subjects calcium supplements suppress bone turnover, improves BMD, and decreases the incidence of fractures.  Traditional dosing of calcium is about 1000 mg/day, nearly the amount in a quart of milk. 

Vitamin D and its analogs.  Modest supplementation may improve intestinal Ca⁺² absorption, suppress bone remodeling, and improve BMD in individuals with marginal deficient vitamin D status.  A prospective study found that neither dietary calcium nor vitamin D intake was of major importance for the primary prevention of osteoporotic fractures in women (1672).

Estrogen.   There is an unambiguous relationship between estrogen deficiency and osteoporosis.  Likewise, overwhelming evidence supports the positive impact of estrogen replacement on the conservation of bone and protection against osteoporotic fractures after menopause.  Raloxifene (EVISTA) acts as an estrogen agonist on bone and liver, is inactive on the uterus, and acts as an antiestrogen in the breast {which would accelerate the sagging of the breasts with age}.  

{The assorted other benefits of estrogen entail that this would be the drug of choice--contrary to the press generated by Big PhARMA} 

Calcitonin: inhibits osteoclastic bone resorption and modestly increases bone mass in patients with osteoporosis; the largest increase occurred in patients with high intrinsic rates of bone turnover.   

Combination Therapies:  Teriparatide stimulates bone formation, bisphosphonates reduce bone resorption, thus it is presumed that the combination would enhance the effect on BMD.  However, addition of alendronate to PHT treatment provided no additional benefit for BMD. 

From http://www.worstpills.org/member/ealert.cfm?ea_id=67 WORST PILL

Kidney Damage Due to Osteoporosis Treatment

March 11, 2011

If you or someone you care about is using the osteoporosis drug Reclast, please read the alert below. This medication has been linked to serious kidney damage.

On October 12, 2010, presumably at the behest of the Canadian govenment, Novartis, the maker of the osteoporosis-infusion drug zoledronic acid (known as Reclast in the U.S. and Aclasta in Canada) sent Canadian health professionals and patients letters warning them of the possibility of kidney toxicity with use of the drug.

Since Novartis did not send similar letters to U.S. health professionals and patients, we are providing our readers with the information sent to Canadian doctors and consumers. We also urged the FDA to require Novartis to issue these warnings to U.S. doctors and patients.

As of April 2010, Novartis had received 265 reports of kidney damage after consumers used Reclast. The true number of patients whose kidneys have been harmed is likely far greater, as only a small percentage of adverse events are ever reported.

Renal failure requiring dialysis or with a fatal outcome has occured. The elderly, those taking drugs that had the potential to damage kidneys, and those on diuretics or who experienced dehydration after Reclast administration were found to be most at risk.

What You Should Do
Novartis provided the following guidance for consumers:

• “Before you take [Reclast], talk to your doctor or pharmacist if you have, or used to have, a kidney problem.”
• “Tell your doctor or pharmacist if you are taking or have recently taken any other medicines, including any you have bought without a prescription. It is especially important for your doctor to know if you are taking any medicines known to be potentially harmful to the kidneys (such as nonsteroidal anti-inflammatory drugs (NSAIDs)).”
• “Make sure that you drink a sufficient amount of water (at least two glasses or 500 mL) before and after your treatment with [Reclast].”
• “[Reclast's] infusion should take a minimum of 15 minutes.”

Read the full letter for health professionals and the full letter for consumers.

View all of WorstPills.org’s resources on Reclast.

If you are currently being treated with Reclast, you should consider discussing alternative treatments with your physician. Possible alternatives include lifestyle changes and the medications alendronate (FOSAMAX) and risedronate (ACTONEL).