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If you’ve been diagnosed with osteoporosis or even osteopenia, there’s a good chance your doctor has brought up bisphosphonates. These are drugs like Fosamax, Boniva, and Reclast. They have a place. I also think they are often overprescribed. And I also think the fear around them is real. Sometimes that fear is justified.
So in this post, I want to do three things:
And I want you to leave this with a plan, not just more confusion.
I want to be very clear. I’m not anti-drug. We do use drugs in our practice, but rarely. When someone goes through our full framework, most people do not need drug therapy by the end. But there are situations where drug therapy is the right move.
Where I tend to push back is this: bisphosphonates are often offered as the first and only plan. That is not a long-term strategy. That is a short-term tool.
Bisphosphonates are in a class of drugs called anti-resorptives. That means they slow down bone resorption, or bone breakdown. The common names you’ll hear:
These can be taken by mouth or by IV. The basic idea is simple. Your bone is always turning over. Osteoclasts break down old bone. Osteoblasts build new bone.
Bisphosphonates bind to parts of the bone. When osteoclasts “chomp” on that bone during turnover, they also take in the drug. The drug then damages or shuts down the osteoclast.
That can be helpful if you are losing bone fast. It can also be helpful if breakdown is high compared to building. In many studies, bisphosphonates increase bone mineral density by about 5% to 10% over time.
That sounds good. But bone density is not the final goal. The final goal is fewer fractures.
This is where things get messy, because drug marketing often leans on the biggest sounding number.
There are two ways to talk about fracture risk reduction:
They are both real. They are also very different.
Let’s say 100 people take the drug and 100 people take placebo.
Relative risk reduction: going from 2 to 1 is a 50% reduction.
Absolute risk reduction: going from 2% to 1% is a 1% reduction.
Same data. Two totally different feelings.
That’s why you’ll hear big claims like 70% fracture reduction, and then you look deeper and see the absolute reduction is much smaller for the fractures that matter most.
Another key point is the type of fracture being counted.
Many drug trials include morphometric vertebral fractures. That means a vertebra looks a little more compressed on imaging. It does not always mean the person felt it or even knew it happened.
Hip fractures are different. They are obvious. They are life-changing. They are easy to confirm.
In the Reclast data, you can see big relative reductions for vertebral fractures, but when you look at hip fracture reduction, the absolute change can be close to about 1%.
That does not mean the drug is useless. It means you deserve the full picture.
Every intervention has risk. Drugs. Supplements. Surgery. Even doing nothing has risk.
Oral bisphosphonates can cause:
That’s why people are told to stay upright after taking them.
Both oral and IV forms can also cause:
Now let’s talk about the two scary ones.
A typical osteoporosis fracture in the femur is up near the hip. An atypical femur fracture happens lower, in a region that usually breaks only from high trauma.
Over time, bisphosphonates can make bone more dense but also more brittle by suppressing bone turnover too much. That is part of how atypical fractures can happen.
The other issue is healing. If bone turnover is suppressed, healing can be slower and harder.
This is rare, but real. The jaw bone turns over faster than many other bones because of chewing forces and dental stress.
If bone turnover is suppressed, healing after dental work can be impaired. Infection risk can rise. In severe cases, parts of the jaw bone can die.
Both atypical femur fractures and osteonecrosis of the jaw are rare. But rare does not mean “never.”
Bisphosphonates are not designed to be taken forever.
To reduce rare risks like atypical femur fractures, guidelines often recommend stopping after 3 to 5 years (depending on the drug and risk profile) and taking a “drug holiday.”
Then what?
This is my biggest issue. Especially if you are 50, 55, or 60. I’m less interested in a 10-year number and more interested in your 30-year plan.
Bone is not static tissue. It is metabolically active. If you shut it down for years, you may get short-term density gains. But you may also suppress both breakdown and building.
And clinically, that’s what we often see in lab markers.
When someone has been on a bisphosphonate, CTX (a breakdown marker) often drops hard. That is expected.
But what many people do not realize is that P1NP (a building marker) can drop too. That means the drug can suppress bone metabolism globally.
This matters because osteoporosis is not always a “too much breakdown” problem. Sometimes it is a “not enough building” problem. If the person is not losing fast, an anti-resorptive may not address the root issue.
This is the part I want you to really pay attention to, because it explains why online advice can go off the rails.
Let’s say a 52-year-old woman gets a DEXA. Hip T-score is -2.7. She has a family history of fracture. She drinks alcohol daily. Her FRAX risk crosses the guideline threshold, so her doctor recommends an oral bisphosphonate, calcium, vitamin D, and a repeat scan later.
Here is how I think about this scenario.
She is not wrong for being scared. Her doctor is not wrong for following guidelines.
But she likely has time to build a real plan.
What I would do first is run a full framework:
In my experience, most people in this scenario can improve direction without needing a bisphosphonate right away.
The key is not refusing. The key is having a real plan and retesting to prove it is working.
Now take another 52-year-old woman. But she is postmenopausal because of breast cancer treatment. She is on estrogen suppression therapy. Her bone loss is rapid. Markers suggest high turnover. DEXA confirms decline.
In this scenario, it is much harder to stop bone loss with lifestyle alone. We still do everything we can, but the medication driving bone loss is powerful.
This is the type of case where a bisphosphonate, or an IV drug like Reclast, may be a reasonable tool to protect bone while she gets through a defined high-risk window.
And this is where I hate what happens online.
A person like Case 2 goes into a forum and sees Case 1 saying, “I reversed osteoporosis without drugs.” That may be true for Case 1. It may be terrible advice for Case 2.
If you decide not to take a bisphosphonate, that is your choice.
But you cannot put your head in the sand. You need to:
Because the goal is not winning an argument. The goal is preventing fractures.
If you’re reading this and thinking, “Okay, but what’s my plan?” that’s exactly the right question.
If you want the framework we use to build a real bone health strategy, join our free Bone Health Masterclass. Bring your questions. And if you want ongoing support, weekly Q&A, and a community that is doing this together, consider joining us inside The OsteoCollective.
You do not need to guess your way through this.
This content is for educational purposes only and is not medical advice. It does not diagnose, treat, cure, or prevent any disease. Always consult your physician or qualified healthcare provider before making medical decisions, changing medications, or starting new supplements, exercise programs, or treatments.
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