Ever wonder why some people seem to have naturally strong bones while others struggle with fragile bones and fractures?
The answer lies partly in our genetics.
Our genes play a crucial role in determining various factors related to bone health, including bone size, density, and resilience as we age.
This genetic blueprint can influence not only how strong our bones are but also how quickly they may break down over time.
For example, if osteoporosis runs in your family, especially across multiple generations, you may have a genetic predisposition to developing it.
This predisposition does not guarantee you will develop osteoporosis, but it can increase your risk, particularly when combined with environmental factors such as diet, exercise, and lifestyle choices.
But what exactly are the genetic factors that influence bone health, and how do they accelerate bone loss, putting some of us at greater risk than others?
Genetic Factors Behind Bone Loss
Osteoporosis is a chronic condition often referred to as a "silent disease" because it leads to a gradual loss of bone density, making bones weaker and more prone to fractures.
Studies suggest that genetics can account for approximately 50 to 85% of the risk for developing osteoporosis, although this may vary depending on individual circumstances and populations. (1)
It affects not only your bone density but also the size, quality, and how fast your bone matter turns over as you age, leading to increased fragility. (2)
Moreover, if your parents — especially your mom’s side — have a history of osteoporosis or hip fractures, you’re at much higher risk. (3)
In fact, a study published in The New England Journal of Medicine found that daughters of women with osteoporosis tend to have lower bone mass in areas like the lumbar spine and femoral neck. (4)
Researchers compared the bone mineral content (BMC) of 25 postmenopausal women with osteoporosis and their 32 premenopausal daughters to that of a control group of women without osteoporosis.
As expected, the postmenopausal women with osteoporosis had lower BMC in areas like the spine and hip.
Their daughters also showed lower BMC, albeit to a lesser extent, potentially increasing their susceptibility to porous bones and fractures in the future.
Another study in the Journal of Bone and Mineral Research found that bone mineral density (BMD) inheritance patterns vary by skeletal site and gender, which is crucial for targeted prevention strategies. (5)
The study involved 816 participants from 147 families with low BMD, revealing that both gender and bone location significantly influence BMD.
For instance, men often have a stronger genetic predisposition to low BMD in the lumbar spine, whereas women are more likely to experience it in the femoral neck.
Heritability estimates were notably high, with spine BMD ranging from 61% to 67% and hip BMD from 44% to 67%.
Siblings aren’t immune either. If one has low BMD, the other is about six times more likely to have low BMD in the spine and hip compared to the average individual.
Australian researchers also studied bone loss in peri- and postmenopausal women twins. (6)
They followed 724 twins over time and found that identical twins (monozygotic), who share nearly all their genes, exhibited more similar patterns of bone loss than fraternal twins, supporting the role of genetics in bone health.
Bone mineral density (BMD) measurements were assessed at the spine, hip, forearm, and whole body, with follow-up tests conducted approximately 4.9 years later.
The results revealed that genetic factors accounted for about 40% of the variation in bone loss across the spine, forearm, and whole body.
On average, BMD declined by 0.37% per year at the spine, 0.77% at the forearm, and 0.16% for the whole body.
These findings suggest that your genetic makeup may increase your risk of osteoporosis and fractures, particularly as you age.
This vulnerability often stems from common inherited genetic variants that can contribute to weak, porous bones and increased bone loss. (7)
In fact, genome-wide association studies have identified specific genes that may indicate your likelihood of developing osteoporosis, many of which affect bone mineral density (BMD) and bone remodeling pathways. (8)
So what are these genes and how might they impact your bone health?
Genes That Put Your Bone Health at Risk
Your genetics are essential for your bone health, and certain variations can raise your risk for conditions like osteoporosis. Here are some genes linked to increased bone fragility.
COL1A1 and COL1A2
Collagen constitutes about 90% of the organic component of your bones, providing structure, strength, resilience, and flexibility to your bones. (9)
Think of it as the glue that holds everything together, not just in your bones but throughout your body, including muscles, tendons, and ligaments.
Type I collagen, in particular, is the most abundant protein in bone tissue, comprising approximately 95% of the collagen in your bones and around 80% of the total bone proteins, which are crucial for maintaining bone structure and integrity. (10)
The COL1A1 and COL1A2 genes are responsible for encoding the protein chains (alpha-1 and alpha-2) that combine to form type I collagen. (11)
When these genes function properly, they ensure your bones are strong and capable of binding minerals like calcium and phosphorus, which helps keep your bones hard and durable.
But what happens if there’s a mutation (or a change in the DNA sequence) in one of these genes?
Mutations in the COL1A1 and COL1A2 genes account for roughly 90% of osteogenesis imperfecta cases, a genetic disorder characterized by fragile bones that break easily, often due to minor impacts or sometimes without any obvious cause. (12)
Variations in the COL1A1 gene can also influence your risk of developing osteoporosis, increasing your susceptibility to fractures due to decreased bone density and quality. (13)
In a study published in Osteoporosis International, researchers found that specific variations in the COL1A1 gene were associated with lower bone mass and increased bone loss during menopause, particularly among postmenopausal women. (14)
The study, which included 1,717 women, showed that those carrying a particular variation of COL1A1 had lower bone mineral density (BMD) in the lumbar spine and hip, as well as increased bone turnover, so their bones were breaking down faster than they were being replaced.
Thus, if you have COL1A1 polymorphisms, you are at higher risk of bone loss, particularly during perimenopause and postmenopause.
TNFRSF11B
Bone health relies on a delicate balance between two critical processes: breaking down old bone (bone resorption) and forming new bone (bone formation). (15)
This ongoing cycle, known as bone remodeling, is essential for keeping your bones strong and healthy throughout life.
A key player in maintaining this balance is osteoprotegerin (OPG), a protein encoded by the TNFRSF11B gene. (16)
You see, the process of bone remodeling involves three main components: (17)
- RANKL: A protein that activates osteoclasts, promoting bone breakdown. It helps regulate osteoclast formation, activation, and survival during normal bone modeling and remodeling, and in various conditions characterized by increased bone turnover.
- RANK: A receptor located on osteoclast precursors. When RANKL binds to RANK, it matures these precursors into active osteoclasts, triggering the process of bone resorption.
- OPG: A decoy receptor that competes with RANK for RANKL. By binding to RANKL, OPG prevents it from interacting with RANK, thereby inhibiting osteoclast activation and protecting bone from excessive resorption.
However, when the TNFRSF11B gene, which encodes OPG, isn’t functioning properly, it can disrupt this balance, leading to weakened bones. (18)
Polymorphisms in this gene can impair OPG production, resulting in overactive osteoclasts that break down bone too quickly.
This can lead to bone issues such as juvenile Paget’s disease, a rare disorder characterized by uncontrolled bone breakdown due to a lack of functional OPG.
As a result, bones become large, misshapen, and fragile, making them more prone to fractures. (19)
Even more commonly, an imbalance in the RANKL-RANK-OPG axis has been linked to osteoporosis, where insufficient OPG allows for excessive bone loss and reduced bone density, increasing fracture risk.
In fact, research published in the Journal of Maturitas revealed that genetic polymorphisms in the TNFRSF11B gene are associated with reduced bone mineral density (BMD) in the femoral neck and lumbar spine. (20)
In this study, 478 postmenopausal women were assessed for two specific TNFRSF11B gene polymorphisms: 245T > G (rs3134069) and 1181G > C (rs2073618).
Alongside this, their bone mineral density (BMD) and serum OPG levels were measured.
The findings revealed that the common gene combinations GT and CT were present in 41.2% and 52.4% of participants, respectively.
Among women with osteoporosis, lumbar spine BMD was associated with both gene variations as well as the CT combination, while femoral neck BMD was linked to the 245T > G variation.
Therefore, if you carry genetic polymorphisms in TNFRSF11B, your decoy receptor OPG may struggle to prevent excessive bone resorption, increasing your risk of bone-related diseases, such as osteoporosis.
SOST
Another important gene involved in bone formation and resorption is the SOST gene, which encodes the protein sclerostin. (21)
Sclerostin acts as a negative regulator of bone formation by inhibiting the Wnt signaling pathway, crucial for activating osteoblasts. (22)
When sclerostin levels are normal, there is a healthy balance between bone resorption and formation.
However, certain mutations in the SOST gene can lead to increased bone formation due to reduced sclerostin activity. While this might initially seem beneficial, it disrupts the normal remodeling process, leading to abnormal bone turnover.
With low sclerostin, osteoblasts may become overly active, causing excessive bone formation without sufficient resorption to match, resulting in structural issues over time.
Moreover, even if bone density appears stable, these mutations in the SOST gene can still negatively impact bone quality and microarchitecture, making them more susceptible to fractures.
Bones may appear normal or slightly denser, yet they can be structurally compromised, making them more vulnerable to fractures.
In osteoporosis, this structural integrity diminishes, resulting in porous and brittle bones that are at risk of breaking from even minor trauma.
In a study published in the European Journal of Trauma and Emergency Surgery, researchers investigated the relationship between sclerostin levels and osteoporosis in 179 patients, primarily women over 50. (23)
They worked with people aged 50 and older who experienced extremity fractures due to low-energy trauma from 2012 to 2018.
After measuring serum sclerostin levels and bone density through dual-energy X-ray absorptiometry, researchers found significant differences in sclerostin levels between those with and without osteoporosis.
Specifically, osteoporotic patients had an average sclerostin level of 41.9 pmol/L, while non-osteoporotic patients had levels of 48.1 pmol/L.
This suggests that lower sclerostin levels may contribute to weakened bones, increasing the risk of fractures.
CYP2R1
Vitamin D is a secosteroid hormone important for maintaining bone strength, particularly as we get older.
It helps with calcium absorption and supports mineralization, assisting in the maintenance of optimal bone mineral density (BMD). (24)
However, its benefits extend beyond bone health — vitamin D also supports muscle strength, which can improve balance and reduce the risk of falls and fractures. (25)
Without adequate vitamin D, the body struggles to absorb calcium properly, leading to weakened bones and a higher risk of fractures.
To support bone health, it's important to get enough vitamin D, either through sunlight, supplementation, or diet.
This is where the CYP2R1 gene comes in.
When vitamin D enters your bloodstream, it binds to a carrier protein called vitamin D-binding protein (DBP) and is transported to the liver. (26)
In the liver, the enzyme produced by the CYP2R1 gene converts vitamin D into 25-hydroxyvitamin D (25[OH]D3), the primary form circulating in your body.
From there, 25-hydroxyvitamin D heads to the kidneys, where it’s further hydroxylated into calcitriol, the form of vitamin D that your body can use to regulate calcium and maintain strong bones.
CYP2R1 is crucial because it triggers the initial conversion of vitamin D into 25-hydroxyvitamin D, which is later activated in the kidneys. (27)
However, when the CYP2R1 enzyme doesn’t function effectively, or if there are polymorphisms in the gene, vitamin D may not efficiently convert into 25-hydroxyvitamin D, impairing its further conversion to calcitriol, which affects calcium and phosphate absorption.
This deficiency can result in vitamin D-dependent rickets type 1B (VDDR1B) in children, marked by low calcium (hypocalcemia) and phosphate (hypophosphatemia) levels. (28)
Over time, this can cause bones to become soft and weak, increasing the risk of fractures and deformities.
In adults, polymorphisms in the CYP2R1 gene can lead to a persistent deficiency in calcium and phosphate, causing a gradual decrease in bone mineral density and, ultimately, osteoporosis.
This makes bones porous and fragile, increasing the likelihood of fractures and slowing recovery.
A study published in PLoS One found that variations in six out of eight specific genetic markers related to the CYP2R1 gene are linked to levels of 25-hydroxyvitamin D. (29)
The researchers analyzed data from 2,868 older men participating in the MrOS Sweden study, focusing on eight genetic markers.
They discovered that certain variations in the CYP2R1 affected how vitamin D is processed in the body, resulting in lower levels of 25-hydroxyvitamin D and lower bone density, increasing the risk of osteoporosis.
Therefore, even if you get vitamin D from food or supplements, if your CYP2R1 gene has significant genetic variations, your body may struggle to efficiently process that vitamin D — leading to a higher risk of weak, porous bones.
VDR
Another gene that regulates vitamin D’s role in supporting bone health as you age is the vitamin D receptor or VDR. (30)
The VDR gene codes for the vitamin D receptor, a protein that helps regulate calcium and phosphate levels by controlling how genes respond to calcitriol, the active form of vitamin D.
It consists of several important domains, including the: (31)
- N-terminal domain (NTD), which plays a role in receptor function.
- DNA-binding domain (DBD), which binds to vitamin D response elements (VDREs) on DNA.
- Ligand-binding domain (LBD), which recognizes and binds to calcitriol, the active form of vitamin D, and pairs with another receptor called retinoid X receptor (RXR).
Once calcitriol binds to VDR, the latter changes its shape, making it easier to interact with coactivator proteins. (32)
There, it binds to DNA to turn on certain genes, which support bone health and the immune system by controlling calcium and phosphate levels.
When VDR is activated, it helps turn stem cells into osteoblasts and boosts the production of key markers, such as runt-related transcription factor 2 (Runx2), osterix (Osx), and alkaline phosphatase (ALP), important for building healthy bone structure.
It contributes to maintaining a balance between bone formation and breakdown, partly by influencing the expression of RANKL (which helps form osteoclasts) and OPG (which prevents bone breakdown) (33)
VDR decreases osteoclast activity by lowering the production of factors that promote their growth and activity.
This balance between building and breaking down bone is essential for bone health, preventing conditions like osteoporosis.
The problem is that when the VDR gene isn't functioning properly, or if there are variations in the gene, our bodies struggle to absorb calcium and phosphate, which can weaken bones and increase the risk of disorders like osteoporosis, particularly as we age.
This is especially concerning for postmenopausal women, who experience a natural decline in estrogen levels — a hormone that independently supports bone health.
In a study published in the Journal of Current Issues in Molecular Biology, researchers worked with Saudi postmenopausal women to discover the relationship between vitamin D receptor (VDR) gene variants and osteoporosis. (34)
A total of 600 women were tested, with 300 diagnosed with osteoporosis and 300 as controls.
The researchers analyzed three specific VDR gene variants and found that certain heterozygous combinations were more frequent in women with osteoporosis.
These gene variants were also linked to a higher risk of osteoporosis, regardless of age or BMI.
This goes to show that variations or changes in the VDR gene can result in reduced bone mineral density and increased susceptibility to osteoporosis, especially in postmenopausal women.
LRP5
LRP5 (Low-Density Lipoprotein Receptor-Related Protein 5) is a protein that helps regulate bone health by maintaining bone mineral density (BMD). (35)
BMD contributes to the strength of bones and their resistance to fractures, which is crucial for their integrity.
LRP5 is expressed in osteoblasts, where it plays a critical role in the Wnt signaling pathway, which regulates bone formation, remodeling, and repair over time. (36) (37)
Acting as a co-receptor, LRP5 works alongside Frizzled receptors to transmit signals essential for the growth and maintenance of bone tissue. This is to ensure that old bone tissue is replaced with new, stronger material, particularly during periods of growth, such as childhood and adolescence.
When functioning correctly, LRP5 promotes healthy bone formation, keeping bones dense and less susceptible to fractures.
However, mutations in the LRP5 gene can disrupt this process, leading to serious bone health conditions like osteoporosis-pseudoglioma syndrome. (38)
These mutations may prevent the production of the LRP5 protein or cause it to malfunction, impairing the Wnt signaling pathway and ultimately affecting bone density. Gain-of-function mutations, on the other hand, can lead to high bone mass syndrome.
For people with LRP5 mutations, osteoporosis can manifest as early as childhood, leading to a heightened risk of fractures throughout their lives.
These fractures frequently affect critical areas such as the spine, hip, and wrist, with vertebral fractures potentially causing loss of height, development of kyphosis (a hunched posture) if multiple vertebral fractures occur, and persistent back pain. (39)
This was supported by a study published in the Journal of Bone and Mineral Research. (40)
In a study of 372 patients with early-onset osteoporosis (EOOP), genetic variations in the LRP5 and LRP6 genes were linked to lower BMD and a higher risk of fractures, particularly in the spine.
Out of the 50 patients analyzed, 37 had vertebral or peripheral fractures.
Therefore, if you want to maintain healthy and strong bones as you age, your LRP5 genes must function properly.
This is to maintain balance in the minerals in your bones and support the bone remodeling process, both of which are crucial for preventing osteoporosis.
ESR1
Sex hormones are essential for skeletal growth and the preservation of bone mass and strength.
Specifically, estrogen influences the activity of both osteoclasts, which break down bone, and osteoblasts, which build it.
It inhibits osteoclast activity, reducing bone resorption, and supports osteoblast survival and function, ultimately preserving bone mass. (41)
As estrogen levels decline, especially during menopause, the resulting estrogen deficiency leads to increased osteoclast activity, accelerating bone resorption, which increases the rate of bone loss and puts you at risk of osteoporosis.
Other factors, including genetics and lifestyle, can also contribute to accelerated bone loss during this period.
This condition leads to weaker bones by creating an imbalance between bone resorption and formation, making you more prone to fractures, especially in the spine, hips, and wrists.
The ESR1 gene is critical in this process, as it encodes the estrogen receptor α, which is the primary receptor that allows estrogen to bind to bone cells and regulate bone metabolism. (42)
However, polymorphisms in the ESR1 gene can modulate how efficiently estrogen works in bone cells, thereby influencing bone strength.
For instance, certain genetic variants may accelerate bone loss and increase the risk of osteoporosis.
Growing studies have even found that specific ESR1 polymorphisms are associated with lower BMD and a greater risk of fractures. (43)
In a study published in Genetics and Molecular Research, researchers worked to identify the link between ESR1 gene polymorphisms and postmenopausal osteoporosis in Chinese women. (44)
They recruited 198 postmenopausal women with osteoporosis and 276 healthy women.
They measured the bone mineral density (BMD) of the lumbar vertebrae using dual-energy x-ray absorptiometry and analyzed ESR1 genotypes with PCR-restriction fragment length polymorphism.
The results showed that the osteoporosis group had lower BMD compared to the healthy group.
These findings suggest that ESR1 gene polymorphisms are linked to a higher risk of postmenopausal osteoporosis and could help identify women at risk.
BMP-2
Bone Morphogenetic Protein 2 (BMP-2) is a protein known for its ability to promote bone formation, helping with bone healing and fracture repair. (45)
Part of the Transforming Growth Factor-β (TGF-β) superfamily, BMP-2 helps regulate the differentiation and activity of osteoblasts, the cells responsible for forming new bone tissue. (46)
During bone repair, BMP-2 helps in the maturation and mineralization of osteoblasts, supporting the regeneration of strong and healthy bone.
This protein’s osteoinductive properties also mean it is highly effective in stimulating bone growth, particularly in cases of bone fractures or deficiencies.
BMP-2 signals mesenchymal stem cells (MSCs), cells that promote tissue repair and regeneration, to develop into osteoblasts, promoting the production of bone matrix and the healing process. (47)
This is not only important in natural bone formation but also in clinical applications, such as enhancing bone grafts and supporting bone regeneration in orthopedic surgeries.
Given its importance, BMP-2 is studied for its therapeutic benefits in treating bone-related conditions, including osteoporosis, helping to accelerate the repair process and lower the risks of fractures or bone defects.
However, if BMP-2 signaling is disrupted, not only can bone density be compromised, but your body will also struggle to regenerate damaged bone, which can lead to longer healing times or, in severe cases, incomplete healing. (48)
This dysfunction can result in non-union fractures, where the bone fails to heal properly, often requiring surgical intervention to encourage recovery. (49)
BMP-2 is also involved in the health of intervertebral discs, the cushioning structures between vertebrae that support and protect the spine.
By influencing the integrity of these discs, BMP-2 helps maintain flexibility and stability in the spinal column. (50)
However, overexpression of BMP-2 in degenerative disc disease is linked to abnormal matrix remodeling, which reduces disc height and impairs overall function. (51)
A study published in The Spine Journal investigated the expression levels of genes, including BMP-2, in intervertebral disc (IVD) specimens from patients undergoing surgery for disc degeneration. (52)
The findings showed that BMP-2 expression levels were higher in degenerative discs compared to those from healthy controls.
Furthermore, there was a strong connection between BMP-2 expression and the severity of disc degeneration, as evaluated by the Pfirrmann MRI grading system.
Specifically, higher BMP-2 levels were linked to more severe degeneration, particularly in grades III and IV.
BMP-2 also promotes osteoblast differentiation and mineralization, which are essential for bone and disc health.
In healthy discs, BMP-2 helps maintain the integrity of the extracellular matrix, crucial for disc hydration and functionality.
However, in degenerative conditions, overexpression of BMP-2 can lead to abnormal disc matrix remodeling, reducing disc height and impairing function.
Therefore, if you’re carrying variations in the BMP-2 gene, you may be at an increased risk of developing intervertebral disc degeneration, experiencing fractures, and suffering from bone loss.
WNT16
Wnts are proteins that support joint development and maintain healthy bones.
Specifically, Wnt16, a member of the Wnt family, was discovered to support bone mineral density, bone thickness, and bone strength, protect against the risk of fractures related to osteoporosis, and promote new bone growth. (53)
This gene helps maintain bone mass by primarily influencing cortical (outer) bone, with a lesser effect on trabecular (inner) bone.
It also supports the balance in the natural remodeling process where old bone is replaced by new bone tissue, ensuring our bones stay strong and healthy.
The problem is that disruptions in WNT16 signaling can lead to an imbalance in bone remodeling.
Bone resorption increases and bone formation decreases, resulting in a loss of bone mass and greater fragility. (54)
In particular, a deficiency in Wnt16 significantly affects cortical bone, making it thin and porous, which can increase your risk of spontaneous fractures. (55)
This can increase your risk of osteoporotic fractures, especially in the vertebrae and hips, and can result in:
- Frequent fractures even from minor falls
- Decreased bone strength
- Chronic back pain
- Height loss
- Stooped posture
- Limited mobility
In a study published in the Journal of Bone, researchers aim to determine how the WNT16 gene can affect bone mineral density (BMD) in healthy Caucasian men from the Odense Androgen Study (OAS).
This study involved two groups: 783 young men aged 20 to 29 and 600 older men aged 60 to 74.
To investigate the genetic factors related to bone health, researchers selected five specific genetic markers (tagSNPs) to study common variations in and around the WNT16 gene.
They confirmed that two markers (s3801387 and rs2707466) were associated with BMD at different bone sites.
They also discovered that another marker (rs2908007) was strongly linked to BMD in both younger and older participants, suggesting that carrying the minor allele leads to higher BMD.
The researchers also sequenced WNT16 in test subjects with very high or very low BMD and identified a marker (rs55710688) that enhanced the production of the WNT16a protein.
This protein was found in higher amounts in people with greater BMD.
Additionally, a test revealed that WNT16 did not activate a pathway usually associated with bone formation (the β-catenin pathway) but instead modulated bone mass through non-canonical signaling pathways in a dose-dependent manner.
This goes to show that variations in the WNT16 gene are associated with bone mineral density (BMD), bone strength, and cortical bone thickness.
These findings are consistent with earlier studies that revealed similar links in human genetics and research on Wnt16 knockout mice, showing reduced bone mineral density (BMD) and weaker bones. (56)
Should You Be Concerned About Genes Associated With Osteoporosis?
Many people believe that bone loss is an inevitable part of aging, especially if they have a family history of osteoporosis.
However, while genetics can play a role in your bone health, it doesn’t mean that osteoporosis is inevitable.
At OsteoIQ™, we are committed to empowering individuals with the knowledge and tools they need to take control of their bone health.
We believe that your genes don’t have to define your future.
Fractures don’t have to be your fate.
By actively supporting strong bones through personalized lifestyle habits, appropriate supplementation, and effective exercise, you can lower your osteoporosis and fracture risk, regardless of your genetic predisposition.
But to do this, you have to understand whether you carry any genetic variations that could impact your bone health.
So, do you have issues with any of these genes?
The only way to know for sure is through genetic testing, and that's where OsteoIQ™ Optimal Genomics can help.
OsteoIQ™ Optimal Genomics is a comprehensive DNA test to help uncover your unique osteoporosis risks, personalize your bone health plan, and take control of your bone strength.
This first-of-its-kind bone health intelligence test can help…
- Identify specific genetic markers within your DNA that influence bone density and health.
- Assess your genetic predisposition to osteoporosis and other bone-related conditions.
- Provide personalized guidance based on your individual genetic profile to support near- and long-term bone health.
- Establish a genetic baseline for monitoring and maintaining optimal bone health throughout your life.
With this powerful combination of osteoporosis genetics and DNA analysis, you’ll gain invaluable insights into how your genetic makeup affects your bone health today and into the future.
These insights empower you to take proactive steps to strengthen your bones, maintain bone health, and reduce your risk of fractures as you age.
If you're worried about osteoporosis, have a family history of bone-related conditions, or just want to stay ahead…
The OsteoIQ™ Optimal Genomics test offers critical, science-backed information to understand your genetic risks so you can make informed decisions about how to protect and enhance your bone health for the future.
Don’t wait until it’s too late to support your bone health.
OsteoIQ™ Optimal Genomics can help you, your loved ones, family and friends understand their bone health picture and take preventative steps for an active future.