Osteoporosis - Not Just a Woman’s Disease

Osteoporosis or "porous bone" is a disease of the skeletal system characterized by low bone mass and deterioration of bone tissue. Osteoporosis leads to an increased risk of bone fractures typically in the wrist, hip, and spine. Because so much of the focus surrounding osteoporosis tends to focus on women, it’s easy to forget that men get this condition too. Osteoporosis is more common in women—affecting an estimated 30 percent of postmenopausal women. But one in five men over the age of 50 will at some point suffer a bone fracture as a result of osteoporosis. After the age of 75, men become even more vulnerable to bone loss and breaks than their younger peers. And, by some estimates, the number of hip fractures in men worldwide will double by 2025.

What’s to Blame?

As with women, osteoporosis in men is caused, in part, by declining estrogen levels. (Just as women have small amounts of testosterone in their bodies, men have small amounts estrogen.) Estrogen has various roles—it reduces the amount of calcium drawn from the bones, and it boosts the levels of bone-enhancing hormones like calcitonin, which stimulates bone growth.

While very little can be done to stop this natural decline in estrogen, new research has found that it is possible for older men to lessen the risk of developing osteoporosis by making a few lifestyle adjustments.

In this study, researchers followed 1,122 men aged 70 to 97 for two years who were part of the Concord Health and Ageing in Men Project (CHAMP). They collected data on these men’s mobility, muscle strength, balance, medication use, cognition, medical history, lifestyle factors and serum vitamin D levels. They each also had baseline and follow-up measurements of total hip bone mineral density.

At the conclusion of the study, researchers found that annual loss of bone mineral density accelerated with increasing age - 0.4 percent in men 70 to 75 years of age, to 1.2 percent in men older than 85. They also learned that these men lost bone density faster with increasing age; with the use of thiazolidinedione or loop-diuretic medications; if they had kidney disease, poor balance or larger hip bone area; or if they had lower serum vitamin D levels.

On the other hand, older men who used walking as a form of exercise and who worked on achieving better balance were able to slow the progression of osteoporosis. Interestingly, the use of beta-blocker medication (used to treat hypertension and heart problems) also appeared to reduce bone loss. Previous studies have found a link between the use of this particular medication and reduced fracture risk, as well as higher bone mineral density.

The jury is still out on how exactly beta-blockers prevent osteoporosis, but some research indicates that it has to do with the hunger-regulating hormone leptin, which also has been shown to control bone formation and resorption (destruction). The resorption characteristic associated with leptin is controlled by the sympathetic nervous system via a specific receptor present on bone cells. Without this receptor, people would make more bone and destroy less bone, leading to fewer osteoporotic fractures.

Beta-blockers come into play because they inhibit the sympathetic nervous system, thereby reducing the bone-destructive characteristics of leptin.

Recommendations for Preventing Osteoporosis

Despite the results of this study, don’t be too quick to resort to beta-blockers to prevent your risk of osteoporosis. Like all drugs, beta-blockers have some unpleasant side effects and should only be used for their intended purpose and under the supervision of a doctor. Side effects include fatigue, cold hands, digestive troubles, dizziness and headache.

In addition, beta-blockers deplete levels of the hormone melatonin, which is important for many aspects of health, including sleep, immunity and heart health. Ironically, researchers also have linked low melatonin levels to high blood pressure.

Realistically, the two best ways to build strong bones and reduce the risk of osteoporosis are to take bone-supportive supplements and to exercise regularly. Walking is good, but strength training or weight-bearing exercise is even better.

As for supplements, be sure you’re taking a combination of calcium, vitamin D, magnesium, vitamin K, zinc, copper, silicon, vitamin C and phosphorus every day to protect your bones.

by

Dr.Akshaya Srikanth

Pharm.D India

Suicidal Risk of Antiepileptic drugs for Pain

Antiepileptic drugs (AEDs, also known as anticonvulsant medications) have a prominent role in the treatment of several types of chronic pain, particularly relating to neuropathy and fibromyalgia. Yet, there have been strong concerns about suicide risks associated with these medications and a new review article examines the relatively weak evidence behind this apprehension.

The recent research on suicidality and AEDs and discuss implications for the treatment of neuropathic pain and fibromyalgia. According to background information in their article, gabapentin and pregabalin are recommended as first-line treatments for various neuropathic conditions, while carbamazepine and oxcarbazepine are commonly used in trigeminal neuralgia, and other AEDs are considered second- or third-line treatments for neuropathic pain. Additionally, pregabalin is recommended for fibromyalgia, and topiramate and valproic acid are considered first-line treatments for migraine prophylaxis.

Given the major role of AEDs in pain management, it is important to consider findings regarding these medications and suicidality, which includes both suicidal ideation and actual suicidal behavior. Furthermore, the researchers note that chronic pain it is also associated with suicidality, and as many as 50% of patients with chronic pain have comorbid depression, which is a well-established risk factor for suicide.

Three articles were discovered as demonstrating increased suicidality risks of AEDs:

• The first article was a large meta-analysis conducted by the FDA that focused on 199 placebo-controlled trials of 11 AEDs and included a total of nearly 44,000 patients. Approximately half of the patients had epilepsy or psychiatric disorders (52%), and the remainder were classified as having “other” conditions, including obesity, insomnia, migraine, and various pain disorders.  Based on adjusted risk estimates, 0.43% of patients in the AED groups had suicidal ideation or behavior vs. 0.24% in the placebo groups. The FDA concluded that AEDs appeared to increase the risk of suicidality regardless of treatment indication, specific AED, or mechanism of action, and that increased risk was observed as early as one week after treatment initiation and continued for at least 24 weeks.  The odds ratio for increased suicidality risk in the “other” group in the FDA meta-analysis, which included patients with various pain conditions, was a moderate 1.87 (95% Confidence Interval, 0.81-4.76), but this was not statistically significant. Patients in this group were taking divalproex, gabapentin, lamotrigine, levetiracetam, oxcarbazepine, pregabalin, topiramate, or zonisamide. 
• A Danish study assessed 6,780 suicides compared with a cohort of 169,725 treatments-naïve patients. The cohort population consisted of patients with epilepsy, psychiatric disorders, and those taking opioids, presumably for chronic pain. The authors concluded that valproate, lamotrigine, clonazepam, and phenobarbital may increase the risk of suicide shortly after treatment initiation.
• A third investigation, using a medical claims database, was an observational study of 297,620 patients treated for various neurologic and psychiatric conditions. Suicidal acts and violent death were compared in patients beginning AEDs and those taking topiramate, the reference AED. Various statistical analyses demonstrated that several AEDs, including gabapentin, increased the risk of suicidal acts. Of particular interest, nearly 17% of the gabapentin group were being treated for neuropathic pain; whereas, less than 1% were treated for epilepsy. 

Several other studies evaluated the association between AEDs and suicidality but did not examine pain patients. Based on their findings, and despite limitations in the data, Pereira et al. conclude that that “the risk of suicidality ─ although small in absolute terms ─ should be considered carefully in the treatment of patients with neuropathic pain, fibromyalgia, and other chronic pain conditions for which treatment with an AED is being considered.”

The risk of suicidality can be evaluated in patients initiating AED therapy for pain and periodically thereafter, the authors suggest. This would be especially appropriate in those with evidence of past or current suicidality, past or present mood disorders, and other risk factors for suicidality, including treatment with antidepressant medications in individuals under the age of 25.

Article: Suicides associated with Antiepileptic Drugs

by

Dr.Akshaya Srikanth, 

Pharm.D India