Tag: Bone

  • Scientists Made a Gum Disease Gel from Jackfruit Latex, Pomegranate Peel, and Simvastatin — Fights Infection, Reduces Inflammation, and Regrows Bone

    Scientists Made a Gum Disease Gel from Jackfruit Latex, Pomegranate Peel, and Simvastatin — Fights Infection, Reduces Inflammation, and Regrows Bone

    The treatment of severe gum disease has long faced a fundamental limitation: existing therapies can control infection and inflammation, but they cannot rebuild the bone and tissue that periodontitis destroys. A new biomaterial developed by researchers in Brazil — made from three ingredients that would look more at home in a kitchen than a pharmacy — may be closing that gap simultaneously.

    ScienceDaily reported on June 19, 2026 on research published in Polymer Bulletin by scientists at the Pontifical Catholic University of São Paulo (PUC-SP) in Sorocaba, Brazil, led by Professor Eliana Aparecida de Rezende Duek. The team developed a biomaterial combining jackfruit latex, pomegranate peel extract, and simvastatin — a cholesterol-lowering drug — into a mucoadhesive gel that, in early laboratory testing, demonstrated infection control, anti-inflammatory activity, and the ability to promote bone-forming tissue growth within 14 to 21 days.

    “We began to view latex extracted from jackfruit as an interesting alternative, as it has adhesive properties,” explained Professor Duek in the FAPESP Agency press release. “This led us to believe that it could remain longer at the site affected by periodontitis, promoting a more targeted release of therapeutic compounds and potentially reducing the need for systemic antibiotic use.”

    How the Three-Ingredient Combination Works — and Why Each Component Matters

    The biomaterial works through the combined action of three components that address different aspects of the disease process simultaneously — a design principle called multi-modal therapy that is increasingly recognized as essential for treating complex chronic inflammatory conditions.

    Jackfruit latex — the structural vehicle. Jackfruit (Artocarpus heterophyllus) is the world’s largest tree fruit, widely cultivated across South and Southeast Asia and increasingly in Brazil. When freshly harvested, it produces a natural latex — a sticky, adhesive substance that the PUC-SP team recognized as potentially valuable in periodontal treatment. As Phys.org reported: jackfruit latex has mucoadhesive properties — it can stick to mucous membrane surfaces like gum tissue. This adhesiveness is the delivery mechanism: the gel stays at the treatment site rather than washing away with saliva, allowing a “more targeted release of therapeutic compounds” over time.

    Pomegranate peel extract — the antimicrobial. Pomegranate peel extract has documented antimicrobial properties, specifically for topical application against the bacterial pathogens involved in periodontal disease. As Indian Defence Review reported: “Pomegranate extract contributes antimicrobial effects” in the biomaterial. This addresses the infection component of periodontitis — the bacterial accumulation around the gum line that initiates and perpetuates the disease.

    Simvastatin — the bone-forming driver. This is the component that most directly addresses the gap in current periodontal treatment. Simvastatin is widely known as a cholesterol-lowering drug, but it has been studied for an additional and less well-known property: it stimulates bone formation. As The Microbiologist reported: “simvastatin, an anti-inflammatory drug that has been studied for its ability to stimulate bone formation.”

    When administered orally as a cholesterol drug, simvastatin is predominantly captured by the liver, with only a small fraction reaching the systemic circulation, requiring high doses that carry significant side effects, including acute muscle degeneration (rhabdomyolysis). By delivering simvastatin directly into the periodontal pocket via the jackfruit latex gel, the researchers bypass the liver entirely. The drug acts locally, at the site of bone loss, at the concentrations needed for bone regeneration, without the systemic dose and risk profile of oral administration.

    Jackfruit-Pomegranate Biomaterial — Key Data Detail
    Published in Polymer Bulletin, March 9, 2026
    DOI 10.1007/s00289-026-06358-w
    ScienceDaily coverage June 19, 2026
    Institution PUC-SP (Pontifical Catholic University of São Paulo), Sorocaba, Brazil
    Lead researcher Professor Eliana Aparecida de Rezende Duek (FCMS)
    Components Jackfruit latex + pomegranate peel extract + simvastatin
    Jackfruit latex role Mucoadhesive vehicle — stays at treatment site, enables targeted drug release
    Pomegranate peel role Antimicrobial activity against periodontal pathogens
    Simvastatin role Anti-inflammatory + bone formation stimulation
    Simvastatin concentrations tested 0.3%, 0.6%, 1.2% (all safe; none altered gel structure)
    Osteoinduction (bone-forming activity) All three concentrations promoted it within 14 days
    Effect at 21 days Even stronger osteoinductive effect
    In vitro model Human adipose-derived stem cells
    Advantage of topical simvastatin Bypasses liver; acts at site of bone loss without systemic side effects
    Current periodontitis treatment limitation Controls infection and inflammation but does NOT regenerate bone/tissue
    Periodontitis global prevalence ~47% of U.S. adults over 30; hundreds of millions worldwide

    What Periodontitis Is — and Why Current Treatments Fail Regeneration

    Periodontitis is not simply “gum disease.” It is a chronic inflammatory disease of infectious origin that progressively destroys the supporting structures of the teeth: the periodontal ligament, the alveolar bone, and the cementum that anchors teeth roots. As the disease advances, patients lose the bone that holds their teeth in place — leading to tooth mobility and, eventually, tooth loss.

    Periodontitis affects approximately 47% of American adults over 30, with severe disease affecting approximately 9%. According to GB News’ coverage of the research: “Periodontitis affects hundreds of millions of people worldwide and remains a leading cause of tooth loss in adults.”

    Current standard treatments — scaling and root planing (deep cleaning to remove bacterial deposits) combined with antimicrobial therapy — are effective at controlling infection and halting further destruction. But they cannot regenerate lost bone. “Current treatments are designed to control infection and inflammation, but they generally do little to regenerate damaged periodontal tissue,” the ScienceDaily summary noted. More advanced techniques, including guided tissue regeneration (using barrier membranes to encourage natural tissue growth) and bone grafting, are available but have “inconsistent and sometimes unpredictable” clinical effects.

    A material that simultaneously controls infection, reduces inflammation, AND promotes bone regeneration within 14 days in laboratory conditions — using components that are naturally derived or already clinically approved — represents a meaningful advance over each of these existing approaches, if the results translate to clinical trials.

    Limitations and the Path to Clinical Translation

    The current research is in vitro — laboratory-based testing using human stem cells and physicochemical analysis. It has not been tested in animal models of periodontitis or in human clinical trials. Clinical translation requires multiple additional steps: animal model efficacy studies, safety profiling, formulation optimization for clinical application, and ultimately clinical trials comparing the biomaterial to existing treatments.

    Professor Duek and her team have expressed confidence in the material’s potential: “We observed that the developed biomaterial has great potential for future applications in treating periodontitis and in other areas as well.” The fact that simvastatin is already an FDA-approved drug with a well-established safety profile in humans is an advantage — not for its oral use, but because basic pharmacological safety data already exists, which may reduce some regulatory pathway complexity for the topical application.

    Frequently Asked Questions

    What is the jackfruit/pomegranate gum disease biomaterial?

    A mucoadhesive gel combining jackfruit latex, pomegranate peel extract, and simvastatin developed by PUC-SP researchers in Brazil and published in Polymer Bulletin(March 2026; ScienceDaily June 19, 2026). It sticks to gum tissue at the treatment site, fights infection with pomegranate’s antimicrobial properties, and uses locally delivered simvastatin to stimulate bone formation.

    What makes this different from current gum disease treatments?

    Current treatments (scaling, root planing, antimicrobials) can control infection and halt disease progression, but cannot rebuild lost bone. The jackfruit biomaterial is designed to do all three simultaneously: fight infection, reduce inflammation, and promote bone-forming tissue growth within 14 days in laboratory tests.

    Has this been tested in humans?

    Not yet. The current research is in vitro, using human adipose-derived stem cells in laboratory conditions. Animal model studies and clinical trials would be needed before clinical application. The study is a promising proof-of-concept finding, not a clinical treatment.

    Why use simvastatin in a gum disease treatment?

    Simvastatin is a cholesterol drug with the additional property of stimulating bone formation. When administered directly to the periodontitis site in the biomaterial gel, it bypasses the liver and acts locally at concentrations that promote bone growth — without the systemic side effects (including muscle damage) that can occur with high oral doses.

    Why jackfruit latex specifically?

    Jackfruit latex is naturally adhesive (mucoadhesive) — it sticks to gum tissue rather than washing away with saliva. This keeps the therapeutic compounds at the treatment site for prolonged local release, potentially reducing the need for systemic antibiotic use.

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  • Why This Silent Bone Disease Is Often Missed

    Why This Silent Bone Disease Is Often Missed

    Osteoporosis is often called a silent disease because bone damage happens quietly, without early pain or obvious warning signs. Many people feel healthy for years while their bones gradually lose strength, making them fragile and prone to fractures. By the time osteoporosis symptoms appear, bone density loss may already be severe enough to affect daily life and mobility.

    This condition affects millions worldwide, especially women after menopause and older adults. As bone tissue breaks down faster than it rebuilds, the skeletal structure becomes weaker and less resilient. Understanding how osteoporosis develops, what signs to watch for, and how it can be detected early is essential for protecting long-term bone health and independence.

    Osteoporosis Symptoms and Early Warning Signs

    Osteoporosis symptoms tend to appear only after significant bone weakening has occurred. Common signs include a gradual loss of height, a stooped posture caused by spinal compression fractures, and persistent back pain that develops without a clear injury. Fractures of the hip, wrist, or spine from minor falls or simple movements often signal advanced bone density loss.

    According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), many people with osteoporosis do not experience symptoms until a fracture occurs, which is why routine screening is strongly recommended for high-risk individuals. The agency explains that spinal fractures can happen silently, contributing to posture changes and reduced mobility over time.

    Because symptoms are subtle, osteoporosis is frequently overlooked. Paying attention to physical changes and risk factors helps prompt earlier testing before serious fractures develop.

    Causes and Risk Factors Behind Bone Density Loss

    Bone density loss occurs when the body breaks down bone tissue faster than it can rebuild it. Hormonal changes play a major role, particularly the drop in estrogen after menopause, which accelerates bone resorption. In men, lower testosterone levels with age also contribute to gradual bone thinning.

    Based on information from the U.S. Office of the Surgeon General, lifestyle factors such as low calcium intake, vitamin D deficiency, smoking, and excessive alcohol use significantly increase osteoporosis risk. Long-term use of corticosteroids and certain medical conditions, including thyroid disorders and autoimmune diseases, further disrupt bone remodeling.

    Genetics also influence peak bone mass and long-term bone strength. When multiple risk factors combine, bone density loss can accelerate rapidly, increasing fracture risk even in relatively active individuals.

    How Osteoporosis Is Diagnosed Early

    Diagnosing osteoporosis before fractures occur relies on imaging and risk assessment rather than physical symptoms alone. The primary diagnostic tool is a DXA scan, which measures bone mineral density at the hip and spine. A T-score of −2.5 or lower confirms osteoporosis, while scores between −1.0 and −2.5 indicate low bone mass.

    According to the International Osteoporosis Foundation, DXA scanning is the most reliable method for identifying fracture risk and monitoring bone changes over time. The organization also highlights fracture risk calculators, such as FRAX, which estimate a person’s likelihood of sustaining a fracture within ten years.

    Early diagnosis allows treatment to begin before irreversible bone damage occurs, reducing the likelihood of life-altering fractures.

    Prevention and Treatment Options That Protect Bone Health

    Preventing osteoporosis focuses on slowing bone density loss and strengthening existing bone. Weight-bearing activities such as walking, stair climbing, and resistance training stimulate bone formation and improve balance. Adequate intake of calcium and vitamin D supports mineralization and helps maintain bone structure.

    Treatment options include medications that slow bone breakdown or stimulate new bone growth. Bisphosphonates reduce fracture risk by limiting osteoclast activity, while newer therapies encourage bone formation in severe cases. Lifestyle changes, fall prevention strategies, and regular monitoring work together to preserve mobility and independence as people age.

    Building Stronger Bones for a More Secure Future

    Protecting bone health requires awareness long before osteoporosis symptoms appear. When bone density loss is identified early, targeted lifestyle changes and medical care can dramatically reduce fracture risk. Strong bones support mobility, confidence, and quality of life well into older age.

    By understanding risk factors, prioritizing screening, and committing to consistent prevention habits, individuals can stay active and resilient. Bone health is not just about avoiding fractures—it is about maintaining freedom of movement and long-term independence for years to come.

    Frequently Asked Questions

    1. What are the earliest osteoporosis symptoms to watch for?

    Early osteoporosis symptoms are often subtle or completely absent. Some people notice gradual height loss or mild back discomfort over time. Because pain is uncommon early on, fractures may be the first noticeable sign. This is why screening is important even without symptoms.

    2. Can bone density loss be reversed?

    Severe bone density loss is difficult to fully reverse, but it can often be slowed or partially improved. Medications, proper nutrition, and weight-bearing exercise help strengthen bones. Early intervention produces the best results. Ongoing monitoring helps guide treatment adjustments.

    3. Who should get tested for osteoporosis?

    Women over age 65 and men over age 70 are commonly advised to get tested. Younger individuals with risk factors such as early menopause, steroid use, or family history may need earlier screening. Doctors may recommend testing after fractures from minor falls. Personalized risk assessment guides timing.

    4. Is osteoporosis only a concern for women?

    While osteoporosis is more common in women, men are also affected. Men tend to develop it later in life but face higher mortality after hip fractures. Hormonal changes, lifestyle factors, and medical conditions contribute to risk in both sexes. Awareness and prevention matter for everyone.



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  • Bone Fractures, Lung Cancer, and Vitamin B12 Supplements? 

    Bone Fractures, Lung Cancer, and Vitamin B12 Supplements? 

    What do randomized controlled trials of high-dose daily vitamin B12 supplementation show about its effects on cancer risk, death, and longevity? 

    In 2019, “Association of High Intakes of Vitamins B6 and B12 from Food and Supplements with Risk of Hip Fracture Among Postmenopausal Women in the [Harvard] Nurses’ Health Study” was published. Note, though, that only the combined high intake of vitamins B6 (≥35 mg/day) and B12 (≥20 mcg/day) was associated with an increased hip fracture risk. We know that treatment with high doses of vitamin B6 may increase hip fracture risk on its own. After a decade or so, those who had been taking high-dose (40 mg) B6 supplements had about a 40 percent higher hip fracture risk, but not those taking B12, as you can see below and at 0:35 in my video Do Vitamin B12 Supplements Cause Bone Fractures and Lung Cancer?.  

    That’s what the Harvard study found, too. High intake of vitamin B12 alone was not associated with increased risk. In fact, some observational studies suggest a slightly lower fracture risk at high B12 blood levels. What we care about most, though, are interventional studies, where people are randomized to B12 so we can see what happens, and when we look at those, we find there is no increased fracture risk among those given B12. In conclusion, based on randomized controlled trials, high doses of vitamin B12 have not been shown to be associated with the risk of fractures.

    Okay, but what about this? In 2017, a study found that men taking vitamin B12 supplements appeared to have increased lung cancer risk. Now, the researchers didn’t find any such association in women, and the increased risk was mostly among men who smoked. Could it be that B12 was feeding budding tumors? It’s hard enough imagining a vitamin being carcinogenic on its own, especially if it somehow only affects men and not also women. “Replication of these findings in additional prospective studies with careful measurement of B vitamin supplement use is warranted.” And, indeed, when you put together all the observational studies, there is no significant correlation between lung cancer and levels of B12 in the blood, whether you’ve smoked or not. If anything, most studies seemed to trend towards higher B12 levels being protective, as you can see below and at 2:03 in my video

    Then, in 2018, a new study found an association between overall lung cancer risk and higher circulating levels of B12, again appearing to be more of a concern with smokers, as seen here and at 2:16 in my video

    Now, this was another observational study. Those with higher B12 levels were just observed to have higher cancer levels. Those of you who have been following my work know the drill: There are two potential issues that arise in observational studies that prevent us from ascribing cause-and-effect: confounding factors, also known as “lurker variables,” and reverse causation.

    What might be a lurker variable in this case? What might be a third factor associated with both higher B12 levels and cancer that may be the true cause? Well, who has higher levels of B12 circulating in their blood? Those who eat a lot of meat and dairy, which are, in fact, “the most important contributors to serum vitamin B-12,” that is, B12 in our blood. And those who eat more meat do tend to have more lung cancer: “Dose-response analysis showed that consumption of red meat for 120 g per day might increase the risk of lung cancer by 35%, and consumption of processed meat for 50 g per day might increase the risk of lung cancer by 20%.” So, we’re generally talking about 35 percent more risk for every quarter-pound burger eaten each day and about 20 percent increased risk for every breakfast sausage link. It’s no wonder those with higher B12 levels in their blood could have more lung cancer. The B12 could just be a marker for meat intake.

    And, if you remember, reverse causation is when X may not lead to Y, but, instead, Y may lead to X. So, instead of high B12 blood levels leading to cancer, maybe cancer leads to high blood levels of B12. And, indeed, nearly 75 percent of patients diagnosed with cancer exhibit elevated B12 levels. So, elevated B12 levels may simply be a marker for cancer. Besides taking extra B12, there are all sorts of reasons your levels can rise, such as liver problems, kidney problems, bone marrow problems, and cancer, as you can see below and at 3:50 in my video. So, high B12 levels may just be a marker of brewing, but not yet diagnosed, cancer. 

    What about observational studies specifically linking B12 supplement use to lung cancer, though? Those could also be reverse causation: “The consequence of being at risk for cancer is that patients will engage in healthier behaviors, including taking multivitamins (reverse causality). The well-established causes, such as smoking, chronic obstructive pulmonary disease, and previous cancers, are the real lung cancer risks.” So, we’re left with this “chicken or the egg causality dilemma,” which is why, ideally, we need randomized controlled trials to see if there’s any cause and effect.

    This became even more urgent with genetic evidence suggesting that those born with higher lifelong levels may be at increased risk. Thankfully, as you can see below and at 4:47 in my video, we do have randomized controlled trials—more than a dozen randomized controlled trials randomizing thousands of people up to 2,000 micrograms of B12 every single day for years, in fact. 

    The findings? “Vitamin B supplementation does not have an effect on cancer incidence, death due to cancer, or total mortality.” And this includes specifically looking at lung cancer, as seen below and at 5:02 in my video. In fact, if anything, vitamin B supplements may actually lower the risk of the most dangerous form of skin cancer. 

    If you missed my previous video, check out Do Vitamin B12 Supplements Cause Acne?.

    For my other B12 updates, see related posts below. All of these videos can be found in one digital download: Latest Vitamin B12 Recommendations.

    I’ve also explored vitamin B12’s role in stroke risk. See the related posts below. That series is available for digital download, too: Why Do Vegetarians Have Higher Stroke Risk?.



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  • Vitamin D During Pregnancy Linked To Better Bone Health In Children At Age 7: Study

    Vitamin D During Pregnancy Linked To Better Bone Health In Children At Age 7: Study

    Vitamin D is essential for maintaining healthy bones, and a recent study reveals that supplementing with this vitamin during pregnancy can have a lasting impact on children’s bone health, keeping them strong into mid-childhood.

    Researchers found that children have greater bone mineral density at age 7 when expectant mothers had taken vitamin D supplements during pregnancy.

    “Our findings show that the benefits of vitamin D supplementation during pregnancy persist into mid-childhood. This early intervention represents an important public health strategy. It strengthens children’s bones and reduces the risk of conditions like osteoporosis and fractures in later life,” said Dr. Rebecca Moon, lead investigator of the study in a news release.

    The researchers began the MAVIDOS study in 2009, enlisting over 1,000 pregnant women in England to explore the potential effects of vitamin D on child bone health. During the trial, the women were randomly divided into two groups: one received an additional 1,000 International Units of vitamin D daily, while the other took a placebo. The participants and healthcare providers who attended them did not know which group they belonged to.

    As part of the study’s first phase, researchers assessed the bone mass of the children at age four using detailed bone scans. The results showed that children born to mothers who received vitamin D supplements during pregnancy had greater bone mass compared to those whose mothers had taken a placebo.

    In the latest phase of the study, researchers examined whether the benefits of prenatal vitamin D would extend into mid-childhood. They conducted follow-up bone scans on 454 children between the ages of six and seven, finding that those whose mothers had received vitamin D supplements continued to show stronger bone density at age seven.

    “These findings suggest that pregnancy vitamin D supplementation may represent a population health strategy to improve bone health, although further work is needed to demonstrate the persistence of this effect into adulthood, together with, ideally replication in additional studies,” the researchers wrote in the study published in The American Journal of Clinical Nutrition.

    Although vitamin D deficiency during pregnancy remains a significant concern, the U.S. dietary recommendations for vitamin D intake in pregnant women remain conservative. It is primarily due to concerns over potential toxicity. However, current evidence suggests that a daily intake of 4,000 IU of vitamin D3 is both safe and necessary to meet the needs of all pregnant women, with no adverse effects reported.

    Since the effects and harms of vitamin D supplementation on maternal and infant health are not yet fully understood, WHO does not recommend vitamin D supplementation as part of standard prenatal care.

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