In this Bulletin, we’re covering research racing to develop new drug treatments for osteoporosis. The discoveries surrounding these endeavors are nonetheless fascinating and contain new insights about how complex and multifaceted our bone-building systems are.
Read on to learn what Big Pharma has waiting in the wings since its current crop of osteoporosis drugs are now widely recognized as ineffective and risky.
Oxytocin May Help Prevent Osteoporosis
Scientists at Sao Paulo State University in Brazil have found that administering oxytocin to female rats at the end of their fertile period reversed precursors of osteoporosis.
The neuropeptide oxytocin is a hormone produced by a region of the brain called the hypothalamus and secreted by the pituitary gland. The hypothalamus links the nervous system to the endocrine system, which monitors and regulates hormone levels via the pituitary gland.
Oxytocin is sometimes called the “love hormone” for its role in pair bonding. However, research has found that oxytocin is also secreted by bone cells, and that postmenopausal women tend to have reduced oxytocin levels.1
The study included 10 female rats who were 18 months old and near the end of their fertile period, which is comparable to perimenopause in humans. Researchers gave the rats two doses of oxytocin 12 hours apart.
Thirty-five days later, the researchers analyzed the rats' blood and tissue samples from the femoral neck, and compared the results with 10 untreated rats of the same age. Below are the scientists’ observations.
“There was no evidence of osteopenia (loss of bone density) in the animals treated with oxytocin, in contrast with the control group. “Our results demonstrated that oxytocin helps to modulate the bone remodeling cycle in senescent rats,” Dornelles said. “The animals that received the hormone displayed an increase in biochemical markers associated with bone renewal and in the expression of proteins that support bone formation and mineralization.”
Analysis of the blood samples showed increased activity of key bone formation markers, such as alkaline phosphatase. “This substance is produced by osteogenic cells and associated with mineralization. We also observed reduced activity of tartrate-resistant acid phosphatase, a marker of bone resorption,” Dornelles said.
The rats treated with oxytocin had denser bones. “We found the femoral neck region to be stronger and less porous. Its biomechanical compression response was better, and it had physico-chemical properties that guaranteed higher density,” she said.”1
This research will most likely be used to create an oxytocin-based osteoporosis drug that will inevitably have unwanted side-effects. This information would be better applied to research to discover how to naturally increase oxytocin production, provided it doesn’t cause detrimental side-effects.
A study of rats found that the hormone oxytocin is linked to bone density. Rats who were treated with the hormone had denser bones. Unfortunately, this research will most likely be used to produce new osteoporosis drugs.
Blocking Estrogen In The Hypothalamus Increases Bone Density
A set of studies on brain cells in mice has found that blocking certain receptors in the brain causes them to grow unusually strong bones.
The studies, carried out at the University of California, San Francisco and UCLA were analyzing the effects of estrogen in the brain. Interestingly, like the previous study, this one also involves the hypothalamus.
“Stephanie Correa, PhD, then an Ingraham Lab researcher, discovered that deleting the estrogen receptor protein in hypothalamic neurons caused the mice to gain some weight and become less active. To find out why the mice gained weight, she used a laboratory technique that also examined any changes in bone density. Correa found that the mice weren’t just heavier, they had gained bone mass; in some cases, as much as 800%.
Fellow scientists at UCSF found the bones were extremely strong and ran experiments to understand the mechanism behind the bone strength. They believe that estrogen-sensitive brain cells in the arcuate nucleus, a region of the hypothalamus, typically signal the neurons to stop bone growth, but deleting the receptors had reversed this process.
The authors note that because most studies limit models to male mice, this effect had never been discovered in previous studies. Nothing like the bone growth pattern has been discovered previously, which could mean Correa’s discovery could lead to a whole new pathway to treat bone density in postmenopausal women without the effects of estrogen therapy.”2
While this discovery is a fascinating new insight into the many ways that our body regulates bone growth, it also offers a nightmare vision of drug treatment. Sudden weight gain and persistent fatigue are side-effects that would radically degrade anyone's quality of life.
Additionally, the health ramifications of increasing bone mass more than eight-fold are unknown. The red flags warning about the future of this discovery are already waving in the breeze. It may well result in another ineffective drug with shockingly detrimental side effects.
Researchers at two universities in California found that blocking an estrogen receptor protein in the neurons of the hypothalamus region of the brain caused an 800% increase in the bone mass of mice. This shocking result is being heralded as the discovery of a new way to treat osteoporosis, but likely it will simply lead to another ineffective and dangerous drug.
Another New Osteoporosis Treatment Looms
Today's final drug research news comes from a collaboration between scientists in Germany and Singapore. The scientists ran genetic analysis on a small laboratory fish model to identify a protein called CXCL9 that interfaces with the precursor cells for bone resorption, that interacts with those bone resorption precursor cells through a receptor called CXCR3.
The protein CXCL9 activates the precursor cells using the receptor CXCrR3, spurring them to become bone-resorbing cells set on a mission of dismantling bone.3
“Both CXCL9 and its receptor CXCR3 have long been known to modulate the migration of immune cells to inflammation sites, for example in psoriasis and rheumatoid arthritis. There are several chemical inhibitors blocking CXCR3 activity that have had little success in clinical tests for the treatment of psoriasis. The research team showed that these inhibitors are highly effective in blocking bone resorbing cells' recruitment and protecting bone from osteoporotic insult.
This has major advantages as excessive bone resorption can be prevented in a targeted manner but normal bone turn-over will still continue. This offers potential to avoid increased fracture risks in osteoporosis patients and to maintain healthy bone for improved quality of life.”3
This research is clearly aimed at finding a new use for the CXCR3-blocking drugs that pharmaceutical companies developed to treat psoriasis. Trying to apply a failed drug to a different problem is a recipe for disaster.
A drug based on this research wouldn't be the first one to suppress osteoclasts, the cells in charge of bone resorption. That's the same mechanism of bisphosphonates, a class of osteoporosis drugs now infamous for their awful side-effects and ineffectual results.
Researchers have identified a protein that is responsible for activating osteoclasts, the cells in charge of resorbing old bone. They intend to develop a drug that will apply this knowledge to artificially alter bone-resorption rates. Bisphosphonates also suppress osteoclasts, and have been shown to cause many dangerous side-effects.
What This Means To You
The new studies you learned about today will be most likely used to pursue new drugs for treating osteoporosis. The irony of these pursuits is, of course, that there is no need for drugs to reverse and prevent osteoporosis. That's the core of the Osteoporosis Reversal Program.
There is more than enough scientific research confirming that proper diet, exercise, and lifestyle changes can improve the quality and strength of your bones to reduce fracture risk. The only side effect of making those healthy choices is a healthier and happier life!
Comments on this article are closed.
My sister who is 64 years old is a quadriplegic with severe osteoporosis. She took Prolia for a year and a half with no positive results. Her doctor is now recommending Reclast and she’s not sure what to do. She works out and is physically fit, but because she has been in a wheelchair for 14 years, she feels she has no choice but to try another osteoporosis drug. Do you have any recommendations?
I fell a week ago and fractured my pelvis in two areas and my sacrum in another. I’m still in the hospital 5 days later.
The doctor says it is because of my osteoporosis and that I need to be on drugs. I’ve tried without but this has been terrible!
Thank you, Ita.
I love the idea of oxytocin boosting bone density. Who needs drugs to do that when you can get it from hugs and intimacy?? So, ladies, go for your lives and tell your partners that you need to do it for your bones’ sake! LOL
Which supplement do you recommend. I am 79 and have had osteoporosis for years.