Anybody out there have medication induced Osteoporosis?
I do. 45 years on antiseizure meds. 60 years old and feeling it. I feel like I lost time. New diagnosis and know prevention AND sustaining bone density is of utmost importance. My question - if you take a med that actively reduces the body’s ability to absorb calcium - what then? Do the OP meds help with absorption or just bone turnover and building? My concern is I will always be fighting the lack of absorption. Vit D facilitates this “normally” but I am not normal (😊) Nothing I have read talks about how to help with Calcium absorption of a med is blocking it. Any help is appreciated. Insee my doc again in March.
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I am not sure which antiseizure drug is blocking your calcium. Not sure what your dexa levels are or if you have fractured. Nor am I sure if your doctor is monitoring your vit d levels, test to monitor calcium levels, or markers of bone formation. If all of this is being done then the best question is why was the problem not caught and what else needs to be done to monitor and keep me safe.
Just some background on the condition:
It is my understanding that these medicines accelerate the liver's metabolism of Vitamin D, reducing its active levels. Since active Vitamin D is essential for calcium absorption in the intestines, this leads to lower calcium levels, triggering bone resorption (calcium withdrawal from bones) to compensate.
A higher amount of vitamin D is usually prescribed to offset this problem.
Plus, Key Tests to Monitor Levels:
Serum 25-hydroxyvitamin D [25(OH)D]: The standard test for measuring Vitamin D deficiency.
Serum Calcium & PTH: To monitor calcium balance.
Bone-specific alkaline phosphatase (bALP): A marker of bone formation.
Vitamin D, whether from food, sun, or drops, must undergo 25-hydroxylation in the liver to become 25(OH)D, and then activation in the kidneys. The issue with Antiseizure medications is that they speed up this liver metabolism too much, breaking down 25(OH)D faster than it can be used. Therefore, higher doses of oral vitamin D are required to compensate for this accelerated metabolism.
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7 Reactions@kathleen1314 Wow. I am so grateful for this information. I have been on various meds over the decades. My Dexas are low. But not frightening so. My PCP wants me to start Prolia. I have reg D and Calcium tests. Both say normal so I am suspect of the tests’ ability to detect metabolism and absorption. I need to decide about the meds and this information is soooo helpful going forward. Thank you! 🙂
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1 Reaction@kathleen1314 2/2 replies.
Also. I fractured my leg and foot in a fall this past summer. Took more time to heal (4.5 months) than normal (2 months). Orthopedists were confounded.
My lowest Dexa score is femoral neck at -2.6. I consider myself lucky to have found out now.
Thanks again for the wealth of information. I am hopeful.
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1 ReactionI was on low-dose prednisone (5 mg daily) for psoriatic arthritis for about 5 years. When I had spinal surgery I bent over too early in recovery and developed a compression fracture at T10. That’s when they discovered I had osteoporosis.
I see a bone health professional who prescribed more calcium and vitamin D supplements, as well as Tymlos, a daily injection you take for two years. I just finished my first year and blood markers indicated I’m building bone. Evidently there is a way to reverse osteoporosis. So grateful!
I’ll have another DEXA scan at the end of this year. Needless to say, I’m no longer on prednisone.
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2 Reactions@osteocurious
What are your dexa number and did you have a TBS interpretation of your bone quality?That would be very valuable.
@calofmichigan Thank you for sharing your journey. Can you share what kind of bone health professional you see? Understood if not.
I have lots of questions for my endo before I start anything. Yours is a success story and I will keep this info in mind. Thank you.
@kathleen1314 My femoral neck is -2.6. My others are all -2.5.
No TBS but that is on my list of requests. Thank you for the support.
@osteocurious
Well, the time for the fracture to heal is concerning, but it healed and that is what is most important.
That dexa is not bad compared to many of us. Yes TBS will give you some good information and peace of mind too, I hope.
Now even more interesting, I am seeing where strontium citrate is not bound by the 25-hydroxylation in the liver to become 25(OH)D, and then activation in the kidneys. In other words, this earth mineral, strontium, that acts like calcium in our body bypasses the problem which your use of antiseizure drug is causing by blocking or slowing your calcium uptake.
Strontium’s anabolic effect is not strictly dependent on the Vitamin D pathway.
Strontium accelerates the filling of bone defects and improves cortical/trabecular microarchitecture.
Long-term (up to 10 years) strontium use has shown sustained increases in BMD at the femoral neck.
To say it another way: Strontium functions differently than calcium because it primarily exerts its effects by acting directly on bone cells. While calcium's metabolism is heavily dependent on vitamin D levels—which are frequently depleted by the liver enzymes induced by certain antiseizure medications (ASMs)—strontium does not appear to rely on those same pathways.
I am a strontium citrate user and am now in normal bone density and normal bone quality.
I have research on strontium if you are interested.
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1 ReactionI took Effexor for over 20 years. Only after that did I learn it could cause osteoporosis. Even my internist was surprised, but he also thought you could get off of Effexor in two weeks. (It took two YEARS to get off of it!). I am off now and hoping I will re-gain some bone density. I don’t and won’t take osteoporosis drugs. There is some indication that I may regain SOME. I did start resistance training. We will see.
@llynch17056
I am so sorry, but glad that you are doing so well.
For those who are unaware with what you are dealing: "Effexor (venlafaxine), a serotonin-norepinephrine reuptake inhibitor (SNRI), is linked to accelerated bone loss and increased osteoporosis risk primarily by increasing osteoclast activity (bone-breaking cells) and decreasing osteoblast activity (bone-forming cells). By inhibiting serotonin reuptake, the medication may disrupt bone remodeling, leading to lower bone mineral density (BMD)"
It does this by increasing CTX (a marker for bone resorption/loss) and decreasing P1NP (a marker for bone formation), accelerating the rate at which bone is broken down.
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