I'm talking about selective serotonin reuptake inhibitors or SSRIs. These are the most widely used antidepressants, and are one of the most commonly prescribed of all medications. Researchers have known about the increased risk of osteoporosis in people taking SSRIs for years. They have also known that SSRIs concentrate in bones even more than they do in the brain. What they didn't know until recently is how they cause osteoporosis. Now they do. It has to do with osteoclasts and osteoblasts.
Bone strength is controlled by special cells called osteoclasts and osteoblasts. Osteoclasts are the cells that tear down bone. Osteoblasts are the cells that rebuild and strengthen bone. Both are important for bone strength, because it's through this remodeling process of tearing down and rebuilding bone that it maintains its strength. So, what does this have to do with SSRIs?
It's because SSRIs work by interfering with the actions of the neurotransmitter (brain chemical) called serotonin. Recently, researchers discovered that both osteoclasts and osteoblasts have receptors for serotonin. That means that because the SSRIs are interfering with serotonin function, they are also interfering with bone metabolism.
So, not surprisingly, when they grew osteoclasts and osteoblasts with SSRIs, they found out that the cells were inhibited by the drugs. They inhibited both the formation of and the resorption of osteoclasts. And they inhibited the bone mineralization of the osteoblasts. Basically, they decreased the function of both cells. And if that's not enough to give you the creeps, here's what else they discovered.
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The drug induced apoptosis in both osteoclasts and osteoblasts "in an identical pattern to inhibitory effects." Apoptosis is controlled cell death. And what this means is that not only did the drugs shut down the bone-maintaining activity of the cells, they also caused them to die! And they did it in a dose-dependent manner. Which means that the higher the dose of the drugs, the greater were the bone-killing effects. The authors concluded, "These data demonstrate that SSRIs differentially inhibit bone cell function via apoptosis. This may explain the mechanisms of bone loss with chronic use."
The authors of one recent meta-study review on SSRIs not so humorously entitled, "SSRIs: Bad to the Bone?" had this to say about their findings: "Despite an overall favorable side-effect profile, our examination of 19 studies, one review, and one meta-analysis indicates that these unique antidepressants [SSRIs] appear to have negative effects on bone, particularly with regard to bone mineral density and fracture risk."
SSRI drugs are dangerous to your health in all kinds of ways. Typical side effects include: drowsiness, flat emotional tone, suicidal tendencies, aggressive behavior, sexual dysfunction, dry mouth, headaches, and others. And now we can list one more - weak bones.
It's pretty clear. If you want to live a long and healthy life, SSRIs are something you'll want to avoid. And here's the good news. There are all kinds of natural ways to treat depression that have nothing to do with drugs. In fact, depending on which study you look at, the natural treatments come out either equal in effect to the drugs, or in some cases, more effective than the drugs. Just look up "depression" on my website. I've written quite a lot about this. You can also go to my clinic website (www.antiagingmedicine.com) and watch my video entitled, "Treating Brain Chemistry and Other Brain Disorders." In it, I discuss some of the most effective natural therapies for depression. But there is one caution.
SSRIs are addictive, and it can be dangerous to stop them without working with a doctor well versed in the natural treatment of depression. Here is a good site to find a doctor like that: www.acam.org.
Yours for better health,
Frank Shallenberger, MD
Hodge JM, Wang Y, et al. Selective serotonin reuptake inhibitors inhibit human osteoclast and osteoblast formation and function. Biol Psychiatry. 2013 Jul 1;74(1):32-9.
Sansone RA, Sansone LA. SSRIs: Bad to the Bone? Innov Clin Neurosci
. 2012 Jul-Aug; 9(7-8): 42-47.