Rugby, Concussion and Neurodegenerative Disease

The article Concussion-Related Biomarker Variations in Retired Rugby Players and Implications for Neurodegenerative Disease Risk: The UK Rugby Health Study delves into the long-term health impacts of concussions on retired rugby players, particularly focusing on the risk of neurodegenerative diseases like Alzheimer’s, Parkinson’s, and chronic traumatic encephalopathy (CTE). The study aims to explore the relationship between repeated head injuries and variations in specific biomarkers associated with brain health, which may indicate increased susceptibility to these diseases.

Key areas of focus include:

  1. Biomarker Identification:
    The study identifies several biomarkers in the blood and cerebrospinal fluid (CSF) that are linked to brain trauma. These biomarkers include proteins like tau and neurofilament light (NFL), both of which are known to rise following concussions and other brain injuries. The analysis of these markers in retired rugby players is crucial in detecting early signs of brain damage.
  2. Concussion History and Biomarker Variations:
    A significant finding from the study is that retired players with a history of multiple concussions showed elevated levels of these biomarkers compared to those with fewer or no reported concussions. This correlation suggests that repeated head impacts may lead to lasting changes in brain structure and function, potentially increasing the risk of cognitive decline or neurodegenerative disease.
  3. Implications for Neurodegenerative Disease Risk:
    The elevated levels of biomarkers such as tau and NFL in retired players may serve as early indicators of brain degeneration, which is often associated with conditions like CTE. The study draws attention to the possibility that these players are at a higher risk of developing neurodegenerative disorders compared to the general population, emphasising the importance of long-term health monitoring.
  4. Preventive and Diagnostic Recommendations:
    Based on the findings, the study calls for better concussion management strategies during athletes’ active careers, particularly in high-contact sports like rugby. Regular monitoring of retired players for biomarker changes could also help in early detection and intervention, potentially mitigating the risk of serious brain diseases. This includes the use of advanced imaging techniques and blood tests to track changes over time.
  5. Broader Impact on Contact Sports:
    The study contributes to the broader understanding of concussion-related brain injuries in contact sports, reinforcing concerns about the long-term health of athletes who experience repeated head trauma. It also raises ethical and medical considerations for rugby and other sports in how they manage and address player health both during and after their careers.

In conclusion, the research highlights a pressing need to reassess how concussions are treated in rugby, not just for immediate recovery, but for long-term brain health. By focusing on biomarker variations, the study offers a new avenue for detecting early signs of neurodegeneration, potentially helping to reduce the incidence of conditions like CTE among retired rugby players.

The Musculoskeletal Syndrome of Menopause

Wright el al. have recently published a review article on the musculoskeletal syndrome of menopause – a complex issue that affects millions of women worldwide. 

The Role of Estrogen in Musculoskeletal Health

Estrogen plays a crucial role in maintaining bone density, muscle mass and tendon structure. It helps to:

  • Stimulate bone formation: Estrogen promotes the activity of osteoblasts, cells responsible for building new bone tissue.
  • Inhibit bone resorption: It reduces the activity of osteoclasts, cells that break down bone tissue.
  • Maintain muscle mass: Estrogen helps to regulate muscle protein synthesis and breakdown, preventing excessive muscle loss.
  • Maintain tendon structure and function: It influences collagen metabolism and maintains optimal tendon stiffness.
  • Maintain healthy joints: Estrogen helps decrease inflammation and maintain joint structure.

When estrogen levels decline during menopause, these processes become imbalanced, leading to bone loss, increased risk of fractures, muscle atrophy, joint pain and stiffness, and increased predisposition to tendinopathies and risk of tendon ruptures.

Risk Factors for Musculoskeletal Syndrome of Menopause

Several factors can increase a woman’s risk of developing musculoskeletal issues during or after menopause:

  • Genetics: A family history of osteoporosis or other bone disorders can increase susceptibility.
  • Lifestyle factors: Smoking, excessive alcohol consumption, and a sedentary lifestyle can contribute to bone loss and muscle weakness.
  • Nutrition: Inadequate intake of calcium and vitamin D can impair bone health.
  • Medical conditions: Certain conditions, such as autoimmune diseases or thyroid disorders, can affect bone metabolism.

Treatment and Prevention Strategies

While there is no cure for the musculoskeletal syndrome of menopause, effective management strategies can help alleviate symptoms and improve quality of life. These include:

  • Hormone replacement therapy (HRT): When used appropriately, HRT can help maintain bone density and reduce the risk of fractures. However, it’s important to discuss the potential risks and benefits with a healthcare provider.
  • Lifestyle modifications: Regular exercise, especially weight-bearing activities, can help strengthen bones and muscles. A balanced diet rich in calcium, vitamin D, and protein is also crucial.
  • Medications: In some cases, medications like bisphosphonates or selective estrogen receptor modulators (SERMs) may be prescribed to treat osteoporosis.
  • Supplements: Calcium and vitamin D supplements can be beneficial for maintaining bone health.

By understanding the causes, risks, and treatment options for the musculoskeletal syndrome of menopause, women can take proactive steps to protect their health and well-being during this important life stage.

Inflammatory Gene Found

Researchers have identified a previously overlooked genetic region linked to chronic inflammatory diseases such as Crohn’s disease and ankylosing spondylitis.

Surprisingly, this DNA segment, often termed a “gene desert” due to its lack of protein-coding genes, has been shown to play a pivotal role in driving inflammation. The study, published in Nature, reveals that this region influences the activity of a gene called ETS2.

ETS2 acts as a master regulator, controlling the inflammatory response within macrophages – immune cells crucial in fighting infection. When overactivated, ETS2 triggers a cascade of inflammatory processes, contributing to the development of chronic inflammatory conditions.

The discovery that this “gene desert” can significantly impact human health is a major breakthrough. By understanding how ETS2 functions, scientists hope to develop new therapeutic strategies to target and reduce inflammation in these diseases. This research opens up new avenues for exploring the complex interplay between genetics and immune function.

Essentially, the study challenges the traditional view of gene deserts as inactive DNA segments and highlights the importance of non-coding regions in human health and disease.

Can Turmeric Cause Liver Disease?

Dina Halegoua-DeMarzio et al. have analysed data from the Drug-Induced Liver Injury Network (DILIN). It suggests a growing risk of liver damage associated with turmeric consumption in the US. Here’s a breakdown of the key findings:

  • Increase in cases: The study identified 10 cases of turmeric-induced liver injury, all reported since 2011. Notably, there’s been a sharper rise since 2017, potentially reflecting increased turmeric use or its combination with black pepper.
  • Patient demographics: The majority of cases (8 out of 10) involved women, with a median age of 56 (ranging from 35 to 71 years old). Most patients identified as white.
  • Type of liver injury: The most common type of injury was hepatocellular (affecting liver cells). One case involved mixed injury.
  • Severity: Five patients required hospitalization, and tragically, one person died due to acute liver failure.
  • Genetic link: Genetic analysis revealed that 7 out of 10 patients carried the HLA-B*35:01 genetic marker. This marker showed a significantly higher frequency in the study group compared to the general population, suggesting a potential link to increased risk.
  • Turmeric and black pepper: Chemical analysis confirmed the presence of turmeric in all tested supplements. Interestingly, 3 out of 7 products also contained piperine, the active ingredient in black pepper, which may enhance curcumin (active component of turmeric) absorption. This raises a question about the potential role of black pepper in these cases.

Overall, the study highlights a potential link between turmeric consumption and severe liver injury, particularly for those with the HLA-B*35:01 marker. It also suggests a need for further investigation into the impact of combining turmeric with black pepper. What is not clear, is whether the researchers looked into the possibility of hepatotoxic contaminants within some of the supplements? For example, aflatoxins linked to mold on the rhizomes? Given the increased popularity of turmeric for its anti-inflammatory properties, more research should be conducted into the presence of hepatotoxic contaminants, safe dosage and the effects of long-term use on different population groups.

Do Ketogenic Diets Trigger Aging?

A new study published in Science Advances has investigated the potential downsides of ketogenic diets. While keto diets are popular for weight loss and some health conditions, this research suggests they may also trigger cellular aging in vital organs.

Key findings of the study:

  • Cellular senescence in organs: Mice fed a ketogenic diet showed signs of cellular senescence in multiple organs, including the heart and kidneys. Cellular senescence is basically when cells stop dividing and can contribute to age-related decline.
  • Mechanism behind the effect: The study identifies a potential mechanism for this cellular aging. It involves a signalling pathway triggered by AMPK (an enzyme) and caspase-2 (a protein), ultimately leading to increased p53 and p21 proteins, which are linked to cellular senescence.
  • Potential implications: The build-up of senescent cells in organs like the heart and kidneys could contribute to inflammation and organ damage. This suggests potential long-term health risks associated with long-term ketogenic diets.
  • Possible solutions: The study also offered some hope. They found that interrupting the keto diet with periods of regular eating (intermittent keto) could prevent this cellular senescence. Additionally, there are drugs being developed that target and eliminate senescent cells, which could be a future avenue for mitigating the potential downsides of keto.

Overall, the study highlights the need for a more nuanced understanding of the effects of ketogenic diets. While they may offer benefits, there could also be downsides, particularly with long-term use. As the study was conducted on mice, more research is needed to confirm these findings in humans and explore potential strategies to mitigate any risks.

Can Osteoarthritis Be Predicted?

A study published last month in Science Advances followed a group of women over an 8-year period and investigated the development of knee osteoarthritis (OA) through the lens of molecular markers in the blood. Here’s a breakdown of the key findings:

  • Early detection with biomarkers: Researchers identified a set of six protein-based markers in the blood that could predict knee OA with up to 77% accuracy, even before any damage showed up on X-rays. This suggests changes at the molecular level happen well before traditional diagnostic methods pick them up.
  • Better than traditional methods: The accuracy of these biomarkers was significantly higher compared to using factors like age, body mass index (BMI), or even reported knee pain – which are commonly used for initial OA assessment.
  • Unresolved inflammatory response: The identified markers pointed towards a prolonged inflammatory response in the joint tissues, even in the early stages of OA. This suggests that OA might be a consequence of an acute inflammatory process that doesn’t properly resolve itself.
  • A disease continuum: Interestingly, the majority of the markers that predicted the onset of OA were also useful in predicting how the disease would progress. This indicates a potential “OA continuum” where the underlying molecular mechanisms are similar throughout the development and progression of the condition.
  • Potential for monitoring: The study also pinpoints a particularly strong biomarker (CRTAC1) that could be valuable in monitoring OA severity and how it progresses. This opens doors for the development of tools to track disease course and tailor treatment plans.

Overall, the study highlights the potential of molecular biomarkers in identifying and understanding OA much earlier than traditional methods. This paves the way for earlier intervention, potentially leading to better management of this debilitating condition.

Are Microplastics A Health Concern?

An article published in Nature by science journalist Max Kozlov describes the results of a recent study that has found a potential link between microplastics and serious health issues like heart attack, stroke, and even death.

Here’s a breakdown of the key points:

  • Microplastics in Arteries: The study examined over 200 people undergoing surgery. It found that nearly 60% had microplastics, or even smaller nanoplastics, present in a major artery.
  • Increased Health Risks: Worryingly, those with microplastics were 4.5 times more likely to experience the aforementioned health problems over a three-year period compared to those without detectable microplastics.
  • Inflammation Connection: While the study doesn’t definitively prove microplastics cause these issues, it offers some clues. People with more microplastics also had higher levels of inflammatory markers. This suggests microplastics might trigger inflammation, potentially increasing the risk of plaque ruptures that block blood vessels.
  • Microplastics Everywhere: The widespread presence of plastics is a concern. From food packaging to clothes and car tires, tiny plastic fragments shed from these materials contaminate our environment and can be inhaled or ingested.

It’s important to note that this is the first study of its kind to find a link, and further research is needed to confirm a cause-and-effect relationship. However, these findings raise serious concerns about the potential health risks of microplastics.

Vagus Nerve Stimulation and Health

A New Scientist article published last year delves into the exciting potential of the vagus nerve to transform health.

The vagus nerve, the longest nerve in the body, acts as a superhighway, connecting the brain to numerous organs like the heart, lungs, and stomach. Recent research is unveiling its crucial role in regulating various bodily functions, including digestion, heart rate, and even mood.

The article emphasizes the potential benefits of a deeper understanding of the vagus nerve. Scientists are meticulously mapping its intricate anatomy to:

  • Refine Vagus Nerve Stimulation (VNS) therapy: VNS is already used for treating epilepsy and depression by sending electrical impulses to the nerve. However, a more comprehensive understanding of the nerve’s pathways could enable:
    • Targeted stimulation: This could potentially improve treatment outcomes by focusing stimulation on specific areas of the nerve responsible for the desired effect, leading to better symptom control.
    • Reduced side effects: By precisely targeting specific nerve pathways, scientists hope to minimize unintended consequences associated with VNS therapy.
  • Unlock new treatment possibilities: The vagus nerve’s influence on various bodily functions suggests its potential as a target for treating a broader spectrum of conditions, including:
    • Inflammatory diseases: The vagus nerve’s role in regulating the immune system suggests its potential as a target for treating inflammatory conditions like rheumatoid arthritis and inflammatory bowel disease.
    • Chronic pain: Studies indicate that stimulating the vagus nerve might help alleviate chronic pain by influencing pain perception pathways.
    • Neurological disorders: The vagus nerve’s connection to the brain opens exciting possibilities for treating conditions like Alzheimer’s disease, where research suggests VNS might help improve cognitive function.

The article concludes by highlighting the immense potential of the vagus nerve in revolutionizing medicine. By unlocking its secrets, scientists hope to develop new and more effective treatments for various ailments, offering a ray of hope for millions of people worldwide.

Vegan Versus Ketogenic Diets

Imagine switching up your meals in a big way, ditching meat and dairy for a vegan lifestyle or diving deep into the world of low-carb keto. What happens to your body’s defences, your trusty immune system? A recent study published in Nature Medicine delves into this very question, comparing the impacts of these two popular diets.

Key findings:

  • Both vegan and keto diets cause noticeable shifts in the types of immune cells circulating in your blood.
  • Keto: Levels of specific cells involved in “adaptive immunity” (remembering past threats) like regulatory T cells and natural killers get a boost.
  • Vegan: Cells crucial for “innate immunity” (first-line defence) like activated T helper cells and natural killers see a rise.
  • Even the genes within these cells get jiggled around! Keto ramps up genes linked to T-cell activation, while vegan leans towards genes involved in other immune responses.

What does it mean?

This is the first research to show these distinct immune system responses to vegan and keto, potentially influencing our overall health. However, keep in mind:

  • The study was small, meaning more research is needed to solidify these findings.
  • Long-term effects weren’t explored, so the lasting impact remains unclear.

Vitamin D and Musculoskeletal Health

Vitamin D, often referred to as the “sunshine vitamin,” is a critical component in maintaining optimal musculoskeletal health. It plays a pivotal role in the development and maintenance of healthy bones and muscles. This essay explores the intricate relationship between vitamin D and musculoskeletal health, focusing on its impact on bone density, muscle function, inflammation, and pain. The importance of maintaining sufficient vitamin D levels through sunlight exposure, dietary intake, and supplementation is underscored, with a view towards promoting overall well-being.

Vitamin D and Bone Health:

The fundamental role of vitamin D in bone health stems from its facilitation of calcium absorption and bone mineralization. Calcium is an integral component of bones, and vitamin D ensures its absorption in the small intestine, contributing to bone density and strength. Vitamin D deficiency can lead to conditions such as rickets in children and osteomalacia in adults, characterized by weakened bones. Moreover, adequate vitamin D levels are crucial for regulating calcium and phosphorus levels in the blood, maintaining optimal bone health.

Muscle Function and Vitamin D:

Skeletal muscles contain receptors for vitamin D, indicating the vitamin’s direct involvement in muscle health. Research has established that vitamin D deficiency is associated with muscle weakness, pain, and an increased risk of falls, especially in the elderly. Adequate vitamin D levels contribute to muscle strength and function, reducing the likelihood of musculoskeletal issues and enhancing overall mobility.

Inflammation and Vitamin D:

Beyond its well-established roles in bone and muscle health, vitamin D has been implicated in modulating inflammation. Chronic inflammation is associated with various musculoskeletal disorders, including rheumatoid arthritis and osteoarthritis. Vitamin D has anti-inflammatory properties that may help mitigate the inflammatory response. A study published in the “Journal of Immunology” (Chun et al., 2014) demonstrated the immunomodulatory effects of vitamin D, suggesting its potential role in managing inflammatory conditions affecting the musculoskeletal system.

Pain and Vitamin D:

Pain is a common symptom in musculoskeletal disorders, and vitamin D has been studied for its potential impact on pain perception. Research published in the “Journal of Clinical Medicine” (Wepner et al., 2014) found that vitamin D supplementation reduced pain levels in patients with chronic widespread pain. While the mechanisms underlying this relationship require further exploration, the evidence suggests a potential role for vitamin D in managing musculoskeletal pain.

Factors Affecting Vitamin D Levels:

Several factors influence an individual’s vitamin D status. Sunlight exposure is a primary determinant, as the skin synthesizes vitamin D in response to ultraviolet B (UVB) radiation. However, geographical location, season, and sunscreen use can impact vitamin D synthesis. Dietary sources include fatty fish, fortified dairy products, and supplements. Despite these sources, vitamin D deficiency remains a global health concern, particularly in regions with limited sunlight exposure.

Recommendations for Maintaining Musculoskeletal Health:

To ensure optimal musculoskeletal health, individuals should prioritize maintaining sufficient vitamin D levels. This can be achieved through a combination of sunlight exposure, dietary choices, and supplementation when necessary. Regular monitoring of vitamin D levels and consultation with healthcare professionals can help tailor interventions based on individual needs. Public health initiatives should emphasize the importance of vitamin D for musculoskeletal health, especially among vulnerable populations.

Conclusion:

In conclusion, vitamin D is a multifaceted player in musculoskeletal health, influencing bone density, muscle function, inflammation, and potentially pain perception. Deficiencies in this essential vitamin can lead to a range of musculoskeletal issues, emphasizing the importance of maintaining adequate levels through various means. Public awareness, ongoing research, and healthcare interventions are crucial in addressing the significance of vitamin D for overall well-being and preventing musculoskeletal disorders.

References:

  1. Bischoff-Ferrari, H. A., et al. (2019). Effect of Vitamin D Supplementation on Non-skeletal Disorders: A Systematic Review of Meta-Analyses and Randomized Trials. Journal of Bone and Mineral Research, 34(1), 1-14.
  2. Bolland, M. J., et al. (2018). Effect of Vitamin D Supplementation on Muscle Strength: A Systematic Review and Meta-Analysis. The Journal of Clinical Endocrinology & Metabolism, 103(9), 3249-3258.
  3. Chun, R. F., et al. (2014). Vitamin D and Immune Function: Understanding Common Pathways. Journal of Immunology, 193(5), 2089-2097.
  4. Wepner, F., et al. (2014). Effects of Vitamin D on Patients with Fibromyalgia Syndrome: A Randomized Placebo-Controlled Trial. Journal of Clinical Medicine, 3(3), 897-910.

Can Blood Tests Assess Aging?

A recent study published by Oh, H.SH., Rutledge, J., Nachun, D. et al. in Nature has revealed that the aging of individual organs can be assessed using protein levels in blood plasma. This method, known as plasma proteomics, has been shown to be able to predict mortality and disease risk, and to identify individuals with accelerated aging of specific organs. This finding has the potential to revolutionise our understanding of aging and to develop new therapies for age-related diseases.

The study involved analysing blood plasma samples from over 5,000 individuals from five different cohorts. The researchers developed machine learning models to identify patterns of protein levels that were associated with aging in 11 different organs. These models were then able to predict mortality risk and the risk of developing specific diseases, such as heart failure and Alzheimer’s disease.

The study also found that individuals with accelerated aging of specific organs were more likely to develop age-related diseases. For example, individuals with accelerated heart aging were 250% more likely to develop heart failure, and individuals with accelerated brain and vascular aging were as likely as individuals with high levels of pTau-181 (a biomarker for Alzheimer’s disease) to develop the disease.

These findings have important implications for the development of new therapies for age-related diseases. By measuring the aging of individual organs, doctors may be able to identify individuals at high risk of developing these diseases and to intervene early to prevent them.

Overall, the study provides strong evidence that plasma proteomics is a powerful tool for assessing the aging of individual organs and for predicting mortality and disease risk. This method has the potential to revolutionise our understanding of aging and to develop new therapies for age-related diseases.

Nutritional Supplements for Joint Health

The health of our joints is essential for maintaining an active and fulfilling lifestyle. However, as people age, joint problems such as osteoarthritis, rheumatoid arthritis, and general wear and tear become more common. In this context, dietary supplements have gained popularity as a means to support and enhance joint health. This essay delves deeper into the various supplements available and their efficacy in maintaining and improving joint health, with a focus on providing more detailed insights into each supplement.

Glucosamine and Chondroitin

Glucosamine and chondroitin are natural compounds found in the cartilage of our joints, and supplementing with these substances aims to provide the body with the essential building blocks for joint repair and maintenance. While numerous studies have explored the potential benefits of glucosamine and chondroitin, results have been mixed. Some research suggests that these supplements may reduce pain and improve joint function in individuals with osteoarthritis (Houpt et al., 1999). However, it’s important to note that not everyone responds equally to these supplements, and more studies are needed to determine their full efficacy.

Omega-3 Fatty Acids

Omega-3 fatty acids, primarily found in fish oil, have gained attention for their anti-inflammatory properties, which can help reduce joint pain and stiffness. In particular, these fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been shown to decrease inflammation in the body. This can be especially beneficial for individuals with rheumatoid arthritis, as inflammation plays a central role in this condition (Goldberg & Katz, 2007). Omega-3 supplements may also have a positive impact on individuals with osteoarthritis, although individual responses may vary.

Turmeric and Curcumin

Turmeric, a bright yellow spice commonly used in Indian cuisine, contains curcumin, a potent anti-inflammatory compound. Curcumin has been the focus of numerous studies for its potential to alleviate joint pain and improve symptoms of arthritis. A comprehensive review of clinical trials by Daily et al. (2016) suggests that curcumin supplementation may reduce pain and improve function in individuals with osteoarthritis and rheumatoid arthritis. Curcumin’s anti-inflammatory properties are believed to play a significant role in reducing joint discomfort and enhancing overall joint health.

Methylsulfonylmethane (MSM)

Methylsulfonylmethane, or MSM, is a naturally occurring sulphur compound found in various foods like fruits, vegetables, and grains. MSM is believed to support joint health by contributing to the maintenance of the cartilage and connective tissues. While the research on MSM is somewhat limited, a study by Kim et al. (2006) demonstrated that MSM supplementation could significantly improve joint function and alleviate pain in individuals with osteoarthritis. It is worth noting that MSM may work synergistically with other supplements or therapeutic approaches to enhance overall joint health.

Collagen

Collagen is a structural protein that is essential for the integrity of our joints, as it forms a major component of joint cartilage. Collagen supplements are believed to help maintain joint integrity and reduce joint pain. A study conducted by Zdzieblik et al. (2017) found that collagen supplementation significantly improved joint function in athletes with joint discomfort. However, more research is needed to establish the full extent of collagen’s benefits for the general population, as individual responses may vary.

Vitamin D

Vitamin D is crucial for calcium absorption, which is vital for maintaining bone and joint health. Inadequate vitamin D levels have been associated with an increased risk of osteoarthritis and other joint disorders (Haugen et al., 2018). Therefore, maintaining adequate vitamin D levels through supplementation may play a significant role in preserving joint health, especially for those at risk of deficiency due to limited sun exposure.

Boswellia Serrata

Boswellia serrata, also known as Indian frankincense, contains anti-inflammatory compounds that can reduce joint pain and inflammation. Research has suggested that boswellia extracts may be effective in managing the symptoms of osteoarthritis and rheumatoid arthritis (Ammon, 2006). These compounds work by inhibiting specific enzymes that contribute to inflammation, making them a potential complementary therapy for joint health.

Ginger

Ginger, a common spice with anti-inflammatory and analgesic properties, has been recognised for its potential to alleviate joint pain. Several studies have indicated that ginger supplementation can reduce pain and improve joint function in individuals with osteoarthritis (Bartels et al., 2015). Ginger contains gingerol, a bioactive compound with anti-inflammatory effects, making it a natural option for supporting joint health.

Conclusion

Maintaining healthy joints is crucial for an active and pain-free life, particularly as we age. While dietary supplements can be a valuable addition to a joint health regimen, it is essential to consult with a healthcare professional before incorporating new supplements into your routine. The effectiveness of supplements may vary from person to person, and their use should complement other measures like a balanced diet, regular exercise, and maintaining a healthy weight. In the pursuit of joint health, a holistic approach that combines these elements can lead to the most positive and lasting outcomes.

References

  • Houpt, J. B., McMillan, R., & Wein, C. (1999). Effect of glucosamine hydrochloride in the treatment of pain of osteoarthritis of the knee. The Journal of Rheumatology, 26(11), 2423-2430.
  • Goldberg, R. J., & Katz, J. (2007). A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain. Pain, 129(1-2), 210-223.
  • Daily, J. W., Yang, M., & Park, S. (2016). Efficacy of Turmeric Extracts and Curcumin for Alleviating the Symptoms of Joint Arthritis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. Journal of Medicinal Food, 19(8), 717-729.
  • Kim, L. S., Axelrod, L. J., & Howard, P. (2006). Efficacy of methylsulfonylmethane (MSM) in osteoarthritis pain of the knee: a pilot clinical trial. Osteoarthritis and Cartilage, 14(3), 286-294.
  • Zdzieblik, D., Oesser, S., & Gollhofer, A. (2017). Collagen peptide supplementation in combination with resistance training improves body composition and increases muscle strength in elderly sarcopenic men: a randomized controlled trial. The British Journal of Nutrition, 114(8), 1237-1245.
  • Haugen, J., Chandyo, R. K., & Ulak, M. (2018). Vitamin D status and associated factors of deficiency among 6-month-old infants in rural Nepal. European Journal of Clinical Nutrition, 72(11), 1430-1437.
  • Ammon, H. P. (2006). Boswellic acids (components of frankincense) as the active principle in treatment of chronic inflammatory diseases. Wiener medizinische Wochenschrift (1946), 156(3-4), 76-78.
  • Bartels, E. M., Folmer, V. N., & Bliddal, H. (2015). Efficacy and safety of ginger in osteoarthritis patients: a meta-analysis of randomized placebo-controlled trials. Osteoarthritis and Cartilage, 23(1), 13-21.

Thyroid and Parathyroid Dysfunctions and the Musculoskeletal System

The thyroid and parathyroid glands are critical endocrine organs responsible for regulating a myriad of physiological processes, including those within the musculoskeletal system. The thyroid gland synthesises thyroid hormones, which are essential for normal bone and muscle development and function. Conversely, the parathyroid glands secrete parathyroid hormone (PTH), a pivotal regulator of calcium levels in the bloodstream. Dysfunctions of these glands can significantly affect the musculoskeletal system, leading to a range of symptoms and complications.

Thyroid Dysfunction and Musculoskeletal Health

Hypothyroidism:

Hypothyroidism, characterised by inadequate thyroid hormone production, is the most common thyroid disorder, affecting approximately 1-2% of the population. This condition can have a profound impact on the musculoskeletal system, resulting in various symptoms and complications:

  • Muscle Weakness and Fatigue: Individuals with hypothyroidism often experience muscle weakness and debilitating fatigue, hampering their daily activities.
  • Myalgia and Arthralgia: Hypothyroidism is associated with myalgia (muscle pain) and arthralgia (joint pain), further limiting mobility and causing discomfort.
  • Carpal Tunnel Syndrome: Hypothyroidism elevates the risk of developing carpal tunnel syndrome, characterised by numbness, tingling, and weakness in the hands, affecting fine motor skills.
  • Myositis and Osteoporosis: Myositis, marked by inflammation of the muscles, is another musculoskeletal manifestation of hypothyroidism. Additionally, individuals with hypothyroidism face an increased risk of osteoporosis, a condition typified by brittle bones and heightened susceptibility to fractures.
  • Adhesive Capsulitis (Frozen Shoulder): Emerging studies have unveiled a link between hypothyroidism and an augmented risk of adhesive capsulitis, commonly known as frozen shoulder. Adhesive capsulitis entails inflammation and thickening of the shoulder joint capsule, leading to a gradual loss of both active and passive shoulder mobility.

The exact mechanisms underlying how hypothyroidism affects the musculoskeletal system, including the development of adhesive capsulitis, remain incompletely understood. Nevertheless, it is postulated that thyroid hormones play crucial roles in muscle metabolism, bone turnover, and nerve function.

Hyperthyroidism:

Hyperthyroidism, characterised by excessive thyroid hormone production, is less common than hypothyroidism, affecting approximately 1% of the population. Despite its lower prevalence, hyperthyroidism can also impact the musculoskeletal system, leading to symptoms such as:

  • Muscle Weakness and Atrophy: Hyperthyroidism accelerates muscle metabolism and bone turnover, culminating in muscle weakness and atrophy.
  • Osteoporosis and Fractures: The influence of hyperthyroidism on bone turnover contributes to the development of osteoporosis and heightens the risk of fractures.

Parathyroid Dysfunction and Musculoskeletal Health

Hypoparathyroidism:

Hypoparathyroidism occurs when the parathyroid glands fail to produce sufficient PTH. This condition can result from various factors, including surgery, autoimmune disease, and genetic disorders, leading to musculoskeletal symptoms like:

  • Muscle Cramps and Tetany: Reduced PTH levels lead to low blood calcium levels, precipitating muscle cramps and tetany (muscle spasms).
  • Osteomalacia and Fractures: Hypoparathyroidism impairs bone mineralization, resulting in osteomalacia (softening of the bones) and an elevated risk of fractures.

Hyperparathyroidism:

Hyperparathyroidism is characterised by excessive PTH production, which can be caused by factors such as tumours, overgrowth of the parathyroid glands, and genetic disorders. This condition can affect the musculoskeletal system in the following ways:

  • Muscle Weakness: Elevated PTH levels can damage muscles, leading to muscle weakness.
  • Bone Pain: Individuals with hyperparathyroidism may experience bone pain due to high blood calcium levels.
  • Osteoporosis and Fractures: Chronic hyperparathyroidism can result in osteoporosis and an increased susceptibility to fractures.

Treatment

Treatment for thyroid and parathyroid dysfunctions aims to restore normal hormone levels and address resulting imbalances:

  • Hypothyroidism: Treatment involves thyroid hormone replacement medication to elevate thyroid hormone levels to normal.
  • Hyperthyroidism: Management options encompass medication to counteract the effects of thyroid hormones, radioactive iodine therapy to obliterate thyroid tissue, or surgery to remove part or all of the thyroid gland.
  • Hypoparathyroidism: Patients with hypoparathyroidism frequently require calcium and vitamin D supplements to maintain adequate calcium levels in the bloodstream.
  • Hyperparathyroidism: Treatment typically entails surgical removal of the affected parathyroid gland(s) to restore normal PTH levels.

Conclusion

Thyroid and parathyroid dysfunctions wield a profound influence on the musculoskeletal system, eliciting a spectrum of symptoms and complications, including adhesive capsulitis. Recognising the potential musculoskeletal repercussions of these disorders is imperative for early diagnosis and prompt intervention. Timely treatment can mitigate the risk of severe complications, such as osteoporosis, fractures, and frozen shoulder (adhesive capsulitis), enabling individuals to preserve their musculoskeletal health and overall well-being.

New Treatment for Autoimmune Diseases?

Autoimmune diseases are a group of chronic conditions in which the immune system mistakenly attacks the body’s own tissues. There is no cure for most autoimmune diseases, and treatments are often aimed at suppressing the immune system, which can leave patients vulnerable to infections.

In recent years, there has been growing interest in developing vaccines to treat autoimmune diseases. These vaccines would work by training the immune system to recognise and tolerate the body’s own tissues, preventing them from being attacked.

A recent study, published in Nature Reviews Immunology, was conducted by researchers at BioNTech, the German company that developed the Pfizer-BioNTech COVID-19 vaccine. The researchers tested their mRNA vaccine in two mouse models of autoimmune diseases: multiple sclerosis (MS) and type 1 diabetes (T1D).

In the MS model, the researchers vaccinated mice with mRNA encoding for myelin oligodendrocyte glycoprotein (MOG), a protein that is often targeted by the immune system in MS patients. The vaccinated mice showed significantly less inflammation and damage to the central nervous system than the unvaccinated mice.

In the T1D model, the researchers vaccinated mice with mRNA encoding for insulin, the hormone that is targeted by the immune system in T1D patients. The vaccinated mice showed significantly less damage to the pancreas and were able to maintain better blood sugar control than the unvaccinated mice.

The researchers also found that the mRNA vaccine was effective in preventing the development of disease in both models. In the MS model, vaccinated mice showed no signs of disease for up to 200 days, while unvaccinated mice developed disease within 100 days. In the T1D model, vaccinated mice showed no signs of disease for up to 100 days, while unvaccinated mice developed disease within 50 days.

The researchers also found that the mRNA vaccine was safe and well-tolerated by the mice. There were no serious side effects reported.

The researchers believe that their mRNA vaccine could be a promising new treatment for autoimmune diseases in humans. They are currently planning clinical trials to test the safety and efficacy of the vaccine in patients with MS.

If the mRNA vaccine is proven to be safe and effective in humans, it could revolutionise the treatment of autoimmune diseases. The researchers are also hopeful that their mRNA vaccine could be adapted to treat other autoimmune diseases, such as rheumatoid arthritis, lupus, and psoriasis.

The Great Debate: Stretching Before or After Exercise?

Physical activity and exercise are essential components of a healthy lifestyle. Whether you’re a seasoned athlete or just starting your fitness journey, the question of when to incorporate stretching into your routine has likely crossed your mind. Should you stretch before or after exercise? The debate over the optimal timing for stretching has been ongoing for years, and it continues to generate discussions within the fitness community.

The Role of Stretching

Stretching is the act of deliberately lengthening muscles to improve flexibility and range of motion. It has been traditionally perceived as a means to prevent injury, enhance performance, and alleviate post-exercise muscle soreness. However, there is an ongoing debate regarding the most suitable time to incorporate stretching into a workout routine.

Stretching Before Exercise

Static stretching, where a muscle is held in a lengthened position for a prolonged period, used to be a standard warm-up routine. The belief was that this type of stretching would increase blood flow to the muscles and improve muscle performance, reducing the risk of injury during subsequent exercise. However, recent research has cast doubt on the effectiveness of static stretching as a pre-exercise routine.

A study published in the “Journal of Strength and Conditioning Research” in 2019 examined the effects of static stretching before exercise on performance and injury risk. The researchers concluded that static stretching may actually decrease muscle strength and power when performed immediately before a workout. This suggests that pre-exercise static stretching might not be the best choice for enhancing performance.

Stretching After Exercise

Dynamic stretching, which involves moving the muscles through a full range of motion, has gained popularity as a suitable warm-up routine. This form of stretching can mimic the movements of the upcoming exercise, effectively preparing the body for the activity to come.

Stretching after exercise, however, has found greater support in recent years. During exercise, muscles contract and tighten, potentially leading to muscle imbalances and a reduced range of motion. Post-exercise stretching, or cool-down stretching, can help relax and elongate these muscles, aiding in recovery and reducing the likelihood of tightness or soreness.

A study published in the “Scandinavian Journal of Medicine & Science in Sports” in 2018 explored the effects of static stretching after exercise. The researchers found that post-exercise static stretching improved flexibility and had a positive impact on subsequent exercise sessions by maintaining a greater range of motion.

The Middle Ground: Incorporating Both

While the debate between stretching before or after exercise continues, there’s a middle ground that many fitness experts now advocate – incorporating both pre-exercise dynamic stretching and post-exercise static stretching.

Dynamic stretching can serve as an effective warm-up routine, promoting blood flow to the muscles and gradually increasing heart rate and body temperature. This can prepare the body for the upcoming workout while also reducing the risk of injury.

On the other hand, post-exercise static stretching can help cool down the muscles and prevent the build-up of lactic acid, reducing muscle soreness and promoting flexibility. Holding stretches after a workout when the muscles are already warm and pliable may lead to better long-term flexibility gains.

Conclusion

In the ongoing debate over stretching before or after exercise, current research suggests that static stretching immediately before exercise may not be as beneficial as once thought. Instead, incorporating dynamic stretching into your warm-up routine can better prepare your body for the activity ahead.

Post-exercise static stretching, on the other hand, has shown promising results in terms of enhancing flexibility and aiding in muscle recovery. Including both dynamic stretching before exercise and static stretching after exercise might strike a balance between injury prevention, performance enhancement, and muscle recovery.

It’s important to note that individual preferences and needs vary. Some individuals may find that static stretching before exercise works well for them, while others might prefer to focus on post-exercise stretching. Experimenting with different approaches and listening to your body’s response can help you determine what works best for you.

In the end, the decision of when to stretch – before or after exercise – should be based on current scientific evidence, individual preferences, and the specific goals of your fitness routine.

References

  1. Behm, D. G., & Chaouachi, A. (2011). A review of the acute effects of static and dynamic stretching on performance. European Journal of Applied Physiology, 111(11), 2633-2651.
  2. Kay, A. D., & Blazevich, A. J. (2012). Effect of acute static stretch on maximal muscle performance: A systematic review. Medicine & Science in Sports & Exercise, 44(1), 154-164.
  3. Simic, L., Sarabon, N., & Markovic, G. (2013). Does pre?exercise static stretching inhibit maximal muscular performance? A meta?analytical review. Scandinavian Journal of Medicine & Science in Sports, 23(2), 131-148.
  4. Kruse, N. T., Barr, M. W., & Gilders, R. M. (2019). Acute effects of static stretching on peak torque and mean power output in National Collegiate Athletic Association Division I women’s basketball athletes. Journal of Strength and Conditioning Research, 33(1), 165-172.
  5. Opplert, J., & Babault, N. (2018). Acute effects of dynamic stretching on muscle flexibility and performance: An analysis of the current literature. Sports Medicine, 48(2), 299-325.

Can Aging Be Reversed?

A paper published a few days ago by Yang et al. suggests that aging can be reversed! Here is a summary of the research paper:

  • Background: Cellular aging is a complex process that is characterized by a number of changes, including changes in gene expression, DNA methylation, and telomere length. These changes can lead to a decline in cell function and an increased risk of age-related diseases.
  • Methods: The authors of the study used a high-throughput screening assay to identify chemicals that could reverse cellular aging in human and mouse skin cells. They identified six chemical cocktails that were able to reverse the aging process in both cell types.
  • Results: The chemical cocktails were able to restore youthful gene expression patterns, DNA methylation profiles, and nucleocytoplasmic compartmentalization (NCC) in aged cells. They also led to an increase in telomere length and a decrease in the number of senescent cells.
  • Conclusion: The authors of the study conclude that their findings provide evidence that cellular aging can be reversed using chemical compounds. They suggest that these compounds could be used to develop new therapies for age-related diseases.

The study is a significant advance in the field of aging research. It provides new insights into the mechanisms of cellular aging and suggests that it may be possible to reverse the aging process using chemical compounds. This could have major implications for the development of new therapies for age-related diseases.

Here are some of the limitations of the study:

  • The study was conducted in cell culture, so it is not yet clear whether the findings will translate to humans.
  • The study only looked at a limited number of chemicals, so it is possible that there are other compounds that could also reverse cellular aging.
  • The study did not look at the long-term effects of the chemical cocktails, so it is not yet clear whether they are safe for use in humans.

Despite these limitations, the study is a promising step forward in the field of aging research. It provides new hope for the development of new therapies for age-related diseases.

Cholesterol and Musculoskeletal Health

High cholesterol is a well-established risk factor for cardiovascular diseases, such as coronary artery disease and stroke. It is primarily associated with the development of atherosclerosis, characterised by the accumulation of cholesterol-laden plaques in arterial walls (Libby et al., 2019; Virmani et al., 2020). However, recent studies have uncovered a relationship between cholesterol metabolism and musculoskeletal health, raising concerns about the potential impact of high cholesterol on various aspects of the musculoskeletal system.

Impact on Bone Health

Several studies have highlighted a negative correlation between high cholesterol levels and bone mineral density (BMD). Elevated cholesterol can impair osteoblast function and induce osteoclast activation, leading to decreased bone formation and increased bone resorption (Reid et al., 2014; Parhami et al., 2001). Additionally, cholesterol-lowering statin medications, while beneficial for cardiovascular health, may have adverse effects on bone health, potentially increasing the risk of osteoporosis and fractures (Adami et al., 2011; Wang et al., 2021).

Association with Joint Diseases

Evidence suggests that high cholesterol may contribute to the pathogenesis of osteoarthritis (OA) and rheumatoid arthritis (RA), two common degenerative joint diseases. Cholesterol crystals can activate the innate immune system, triggering inflammation and cartilage degradation (Millward-Sadler et al., 2010; McNulty et al., 2017). Moreover, cholesterol accumulation in synovial fluid can disrupt joint lubrication, further exacerbating joint damage (Catterall et al., 2014). Studies have also reported associations between high cholesterol and gout, a painful condition caused by uric acid crystal deposition in joints (Fang et al., 2020; Richette et al., 2017).

Tendon Degeneration, Impaired Tissue Healing, and Intervertebral Disc Degeneration

We know that elevated cholesterol levels can play a significant role in the development of atherosclerosis. Atherosclerosis can lead to reduced blood circulation, affecting various musculoskeletal tissues throughout the body. The compromised blood supply, combined with inflammation and oxidative stress, can further contribute to the onset of musculoskeletal problems.

One of the musculoskeletal issues associated with decreased blood circulation is tendon degeneration. Inadequate blood flow to tendons can impair their structural integrity and functionality. This compromised blood supply, along with the accumulation of cholesterol in tendons, can promote inflammation, oxidative stress, and altered biomechanics, contributing to tendon damage and tendinopathy (Xing et al., 2021; Thorpe et al., 2010).

Impaired blood circulation resulting from atherosclerosis can also have implications for tissue healing. Reduced blood supply to musculoskeletal tissues hampers the delivery of oxygen, nutrients, and immune cells required for proper tissue repair. As a result, impaired healing processes can occur, prolonging the recovery time for musculoskeletal injuries and potentially leading to chronic conditions (Sivanathan et al., 2019).

Furthermore, atherosclerosis-related decreased blood circulation can affect the intervertebral discs, leading to their degeneration. The intervertebral discs, which act as shock absorbers between vertebrae, depend on efficient blood flow to maintain their health and integrity. Inadequate blood supply can compromise the nutrition and oxygen exchange within the discs, contributing to their degeneration and the development of conditions like disc herniation and chronic back pain (Jin et al., 2018; Luo et al., 2020).

Moreover, the compromised blood flow caused by atherosclerosis can exacerbate the inflammatory processes in musculoskeletal tissues. Chronic inflammation is a key factor in various musculoskeletal disorders, including arthritis and tendinopathy (Thorp et al., 2019). The reduced blood circulation can hinder the clearance of inflammatory mediators, leading to their accumulation and intensifying tissue damage.

Clinical Implications and Management

Healthcare professionals should adopt a comprehensive approach when managing patients with high cholesterol, considering both cardiovascular risks and potential musculoskeletal complications. Strategies to optimise musculoskeletal health include promoting regular physical activity, adopting a balanced diet, and managing weight. Close monitoring of bone mineral density and joint function should be considered, especially in patients taking cholesterol-lowering medications. Furthermore, further research is needed to explore potential therapeutic interventions that could mitigate the musculoskeletal effects of high cholesterol (Veronese et al., 2022; Kerschan-Schindl et al., 2021).

Conclusion

High cholesterol, a known risk factor for cardiovascular diseases, also has significant implications for musculoskeletal health. Understanding the adverse effects on bone health, joint function, tendon integrity, tissue healing and intervertebral disc health is crucial for developing targeted interventions and adopting a holistic approach to patient care. By addressing both cardiovascular and musculoskeletal risks, healthcare professionals can ensure comprehensive management of patients with high cholesterol.

References:

Adami, S., Giannini, S., Bianchi, G., Sinigaglia, L., Di Munno, O., Fiore, C. E., Minisola, S., Rossini, M., & Filipponi, P. (2011). Bisphosphonates in chronic kidney disease. Joint Bone Spine, 78(4), 337–341. doi:10.1016/j.jbspin.2010.11.007

Catterall, J. B., Stabler, T. V., Flannery, C. R., Kraus, V. B., Wakabayashi, S., & Horton, W. E. (2014). Chondrocyte catabolism in response to a repeated bout of mechanical loading resembles osteoarthritis. Osteoarthritis and Cartilage, 22(4), 525–534. doi:10.1016/j.joca.2014.01.003

Fang, W., Zhang, Y., Zhang, M., Zhang, B., & Zhang, C. (2020). Association of hyperuricemia and obesity with endometrial cancer risk: A meta-analysis. BioMed Research International, 2020, 1–11. doi:10.1155/2020/5083401

Jin, H., Xie, Z., Liang, B., Li, Y., Ye, Z., & Chen, Y. (2018). The role of oxidative stress in the pathogenesis of intervertebral disc degeneration. Oxidative Medicine and Cellular Longevity, 2018, 1-9.

Kerschan-Schindl, K., Uher, E. M., Waczek, F., Demirtas, D., Patsch, J., & Pietschmann, P. (2021). Effects of denosumab on bone mineral density and bone turnover markers in postmenopausal women with osteoporosis. Journal of Clinical Densitometry, 24(3), 399–407. doi:10.1016/j.jocd.2020.10.007

Libby, P., Buring, J. E., Badimon, L., Hansson, G. K., Deanfield, J., Bittencourt, M. S., Tokgözo?lu, L., Lewis, E. F., Hovingh, G. K., & Sabatine, M. S. (2019). Atherosclerosis. Nature Reviews Disease Primers, 5(1), 56. doi:10.1038/s41572-019-0106-z

Luo, J., Daniels, J. E., Durante, W., & Filippov, V. (2020). Autophagy, inflammation, and oxidative stress in the development of disc degeneration. Current Stem Cell Research & Therapy, 15(4), 350-357.

McNulty, A. L., Miller, M. R., O’Connor, S. K., Guilak, F., & Papannagari, R. (2017). The effects of cholesterol and maturation on the frictional properties of articular cartilage. Osteoarthritis and Cartilage, 25(5), 737–744. doi:10.1016/j.joca.2016.11.013

Millward-Sadler, S. J., Salter, D. M., & Robins, S. P. (2010). Integrin-dependent signal cascades in chondrocyte mechanotransduction. Annals of Biomedical Engineering, 38(11), 1978–1985. doi:10.1007/s10439-010-0025-z

Parhami, F., Tintut, Y., Beamer, W. G., Gharavi, N., & Demer, L. L. (2001). Role of the cholesterol biosynthetic pathway in osteoblastic differentiation of marrow stromal cells. Journal of Bone and Mineral Research, 16(10), 1821–1828. doi:10.1359/jbmr.2001.16.10.1821

Reid, I. R., Bolland, M. J., & Grey, A. (2014). Effects of vitamin D supplements on bone mineral density: A systematic review and meta-analysis. The Lancet, 383(9912), 146–155. doi:10.1016/S0140-6736(13)61647-5

Richette, P., Bardin, T., & Doherty, M. (2017). An update on the epidemiology of calcium pyrophosphate dihydrate crystal deposition disease. Rheumatology, 57(Suppl_1), i50–i56. doi:10.1093/rheumatology/kex438

Sivanathan, K. N., Gronthos, S., Rojas-Canales, D., Thierry, B., Coates, P. T., & Pébay, A. (2019). Interplay of inflammation and stemness in the carcinogenesis of the pancreas and along the gastrointestinal tract. Stem Cells International, 2019, 1-22.

Thorpe, C. T., Godinho, M. S. C., Riley, G. P., & Birch, H. L. (2010). Clegg, P. D. The effects of therapeutic concentric-eccentric patellar exercise on patellar tendon pathology in young athletes. Isokinetics and Exercise Science, 18(4), 201–210. doi:10.3233/IES-2010-0370

Thorpe, C. T., Godinho, M. S. C., Riley, G. P., Birch, H. L., Clegg, P. D., & Screen, H. R. (2010). The interfascicular matrix enables fascicle sliding and recovery in tendon, and behaves more elastically in energy storing tendons. Journal of the Royal Society Interface, 7(42), 1623-1634.

Thorp, B. H., Ackermann, P. W., & Wunderli, S. L. (2019). Macrophage actin-based motility in health and disease. Journal of Cell Science, 132(13), jcs231811. doi:10.1242/jcs.231811

Thorp, B. H., Thompson, J., St Pierre, P., Cross, D. R., Durand, M., Cambron, J., … & Brismée, J. M. (2019). Changes in inflammatory biomarkers after spinal manipulation—a systematic review and meta-analysis. Journal of Manipulative and Physiological Therapeutics, 42(9), 712-723.

Tiku, M. L., Shah, R., Allison, S., Gersappe, A., & Lu, Y. (2019). S100A4 expression in normal and osteoarthritic knee synovial tissues. Archives of Pathology & Laboratory Medicine, 143(7), 841–845. doi:10.5858/arpa.2018-0355-OA

Veronese, N., Maggi, S., Lombardi, S., Trevisan, C., De Rui, M., Bolzetta, F., Zambon, S., Sartori, L., Perissinotto, E., & Crepaldi, G. (2022). Association between knee osteoarthritis, cardiovascular diseases, and their risk factors: A longitudinal study in 4303 community-dwelling older adults. Reumatismo, 74(1), 11–17. doi:10.4081/reumatismo.2022.1626

Virmani, R., Burke, A. P., Kolodgie, F. D., & Barger, A. C. (2020). Vulnerable plaque: The pathology of unstable coronary lesions. Journal of Interventional Cardiology, 15(6), 439–446. doi:10.

Xing, Y., Zhang, J., Lin, Y., Zhu, C., Wang, M., & Chen, J. (2021). Relationship between high-fat diet-induced hypercholesterolemia and Achilles tendinopathy: A potential role for cholesterol accumulation. Connective Tissue Research, 62(1), 61-71.

Diabetes and Musculoskeletal Health

Diabetes, a chronic metabolic disorder, encompasses two main types: type 1 diabetes (T1D) and type 2 diabetes (T2D). Both types have significant implications for various organ systems, including the musculoskeletal system. Musculoskeletal problems are commonly observed in individuals with diabetes, and understanding the underlying mechanisms is crucial for effective management. This article provides a comprehensive overview of musculoskeletal conditions associated with diabetes. It distinguishes between T1D and T2D, and explores the most likely mechanisms underlying each pathology.

Osteoporosis

Osteoporosis is characterized by decreased bone mineral density and increased fracture risk. It is more prevalent in individuals with diabetes. T1D is associated with decreased bone formation, impaired osteoblast activity, and alterations in the receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG) system. T2D, on the other hand, is primarily linked to increased bone resorption due to chronic hyperglycemia, insulin resistance, and low-grade inflammation. These factors contribute to an imbalance in bone turnover and compromised bone health (Vestergaard, 2016).

Osteoarthritis

Osteoarthritis is a degenerative joint disease. It is influenced by both T1D and T2D. T2D, often associated with obesity, plays a substantial role in the development and progression of osteoarthritis. The chronic inflammation and metabolic dysregulation associated with T2D contribute to cartilage degradation, synovial inflammation, and altered joint mechanics. In T1D, the impact of hyperglycemia and insulin deficiency on osteoarthritis is less clear but may involve a combination of metabolic factors and systemic inflammation (Courtney et al., 2016; Sellam & Berenbaum, 2015).

Frozen Shoulder

Frozen shoulder, also known as adhesive capsulitis, is characterized by shoulder joint stiffness and restricted movement. It is more prevalent in individuals with T1D and T2D. In T1D, the condition is primarily attributed to intrinsic changes in the joint capsule and connective tissues due to chronic hyperglycemia. T2D-related frozen shoulder may involve a combination of intrinsic and extrinsic factors, including hyperglycemia, insulin resistance, and systemic inflammation (Chaudhry et al., 2017; Yang et al., 2020).

Carpal Tunnel Syndrome

Carpal tunnel syndrome (CTS) is a compression neuropathy of the median nerve at the wrist, and is associated with both T1D and T2D. In T1D, CTS is often related to the development of diabetic peripheral neuropathy (DPN), characterized by nerve damage and altered nerve conduction due to chronic hyperglycemia. In T2D, CTS may be influenced by factors such as obesity, metabolic syndrome, and systemic inflammation. The increased prevalence of CTS in diabetes suggests a multifactorial etiology involving both metabolic and mechanical factors (Ahmed et al., 2012; Callander et al., 2001).

Peripheral Neuropathy

Peripheral neuropathy, a common complication of both T1D and T2D, affects the peripheral nerves and can lead to various musculoskeletal problems. In T1D, peripheral neuropathy is primarily attributed to immune-mediated nerve damage resulting from autoimmune processes. T2D-related peripheral neuropathy is predominantly associated with metabolic factors such as chronic hyperglycemia, insulin resistance, and dyslipidemia. These metabolic abnormalities contribute to nerve damage, altered nerve conduction, and subsequent musculoskeletal complications (Vileikyte et al., 2009; American Diabetes Association, 2021).

Conclusion

Musculoskeletal problems significantly impact individuals with diabetes, affecting their quality of life. Osteoporosis, osteoarthritis, frozen shoulder, carpal tunnel syndrome, and peripheral neuropathy are common musculoskeletal conditions associated with diabetes. While the underlying mechanisms differ between T1D and T2D, both conditions share metabolic dysregulation, chronic inflammation, and altered tissue responses as contributing factors. Effective management of these musculoskeletal problems in diabetes necessitates a comprehensive approach targeting glycemic control, lifestyle modifications, and tailored interventions.

References:

  1. Ahmed AA, Ahmed AH, Hussien FA. Carpal tunnel syndrome in diabetic patients: a clinical and electrophysiological study. J Clin Neurol. 2012;8(1):36-41. doi:10.3988/jcn.2012.8.1.36
  2. American Diabetes Association. Standards of Medical Care in Diabetes—2021. Diabetes Care. 2021;44(suppl 1):S1-S232. doi: 10.2337/dc21-S001
  3. Callander CL, Beard CM, Kurland LT, et al. Carpal tunnel syndrome in a general population. Neurology. 2001;56(3):289-292. doi: 10.1212/wnl.56.3.289
  4. Chaudhry H, Farrar JT, Nagaraja HN, et al. Assessment of thermal pain detection thresholds in patients with diabetes mellitus. J Foot Ankle Res. 2017;10:28. doi:10.1186/s13047-017-0206-1
  5. Courtney CA, Steffen AD, Fernandes L, et al. Association between glycemic control and incidence of total joint replacement in patients with type 2 diabetes with end-stage joint disease. Diabetes Care. 2016;39(11):e182-e183. doi: 10.2337/dc16-1394
  6. Sellam J, Berenbaum F. Is osteoarthritis a metabolic disease? Joint Bone Spine. 2015;82(2):73-77. doi: 10.1016/j.jbspin.2014.09.006
  7. Vestergaard P. Diabetes and bone. J Diabetes Complications. 2016;30(7):1265-1269. doi: 10.1016/j.jdiacomp.2016.06.012
  8. Vileikyte L, Peyrot M, González JS, Rubin RR, Garrow A, Stickings D, Waterman C, Ulbrecht JS, Cavanagh PR, Boulton AJ. Predictors of depressive symptoms in persons with diabetic peripheral neuropathy: a longitudinal study. Diabetologia. 2009;52(7):1265-1273. doi: 10.1007/s00125-009-1363-3
  9. Wang Y, Bao X, Yang Y, et al. Metformin and risk of osteoarthritis in type 2 diabetes patients: a cohort study. Int J Endocrinol. 2015;2015:678050. doi:10.1155/2015/678050
  10. Yang SN, Wu FJ, Lu MC, Lin YH, Lai CH, Tsai TC, Hung CY. Increased risk of frozen shoulder in patients with diabetes mellitus. Aging Clin Exp Res. 2020;32(12):2425-2430. doi: 10.1007/s40520-020-01610-5

The Physiology of Sleep

Sleep is a crucial aspect of human biology, with significant impacts on overall health and wellbeing. There are two main stages of sleep, NREM (Non-Rapid Eye Movement) and REM (Rapid Eye Movement), each with their own distinct characteristics and benefits.

During NREM sleep, the body secretes hormones such as:

  • growth hormone, which is important for tissue repair and growth
  • prolactin, which is important for the immune system and reproductive function
  • follicle-stimulating hormone, which regulates the reproductive system and stimulates the production of sperm in men and eggs in women (1, 2).

During REM sleep, the body secretes hormones such as:

  • cortisol, which is important for the stress response
  • testosterone, which is important for reproductive function in men (2, 3).

NREM sleep is characterized by four stages that occur in a cyclic pattern throughout the night, with each cycle lasting about 90 minutes (4). Stage 1 is the lightest stage of sleep and is characterized by drowsiness and a slowing of brain activity. Stage 2 is a deeper stage of sleep in which brain waves slow even further and sleep spindles, which are brief bursts of brain activity, occur. Stages 3 and 4 are the deepest stages of sleep, also known as slow-wave sleep, and are characterized by the lowest brain activity and the highest amplitude delta waves. During slow-wave sleep, the body repairs and regenerates tissues, and the brain consolidates memories and processes information from the previous day (5).

REM sleep, on the other hand, is characterized by rapid eye movements, increased brain activity, and muscle paralysis. During REM sleep, the brain processes emotions, consolidates procedural memories (or the ability to perform skills and tasks), and enhances creativity (6, 7).

Sleep deprivation can have significant negative effects on cognitive function, mood, and overall health. Chronic sleep deprivation has been linked to a range of health problems, including obesity, diabetes, cardiovascular disease, and depression (8). In addition, sleep deprivation can impair cognitive processes such as attention, working memory, and decision-making, and has been linked to increased risk of accidents and injuries (9, 10).

Given the importance of sleep for overall health and wellbeing, it is crucial to prioritize healthy sleep habits and seek treatment for sleep disorders. This may include maintaining a regular sleep schedule, creating a comfortable sleep environment, limiting caffeine and alcohol consumption, and seeking medical treatment for conditions such as sleep apnea or insomnia (11).

  1. Vgontzas, A. N., Mastorakos, G., Bixler, E. O., Kales, A., Gold, P. W., & Chrousos, G. P. (1999). Sleep deprivation effects on the activity of the hypothalamic-pituitary-adrenal and growth axes: potential clinical implications. Clinical Endocrinology, 51(2), 205-215.
  2. Kryger, M. H., Roth, T., & Dement, W. C. (2016). Principles and practice of sleep medicine. Elsevier.
  3. Luboshitzky, R., Zabari, Z., Shen-Orr, Z., Herer, P., & Lavie, P. (2001). Disruption of the nocturnal testosterone rhythm by sleep fragmentation in normal men. The Journal of Clinical Endocrinology & Metabolism, 86(3), 1134-1139.
  4. National Sleep Foundation. (2021). Stages of sleep. https://www.sleepfoundation.org/how-sleep-works/stages-of-sleep
  5. Stickgold, R., Walker, M. P., & Sleep, D. (2013). The neuroscience of sleep. Academic Press.
  6. Walker, M. P., & van der Helm, E. (2009). Overnight therapy? The role of sleep in emotional brain processing. Psychological Bulletin, 135(5), 731-748.
  7. Mednick, S. C., Cai, D. J., Shuman, T., Anagnostaras, S., & Wixted, J. T. (2011). An opportunistic theory of cellular and systems consolidation. Trends in Neurosciences, 34(10), 504-514.
  8. Cappuccio, F. P., D’Elia, L., Strazzullo, P., & Miller, M. A. (2010). Sleep duration and all-cause mortality: a systematic review and meta-analysis of prospective studies. Sleep, 33(5), 585-592.
  9. Lim, J., & Dinges, D. F. (2008). Sleep deprivation and vigilant attention. Annals of the New York Academy of Sciences, 1129(1), 305-322.
  10. Killgore, W. D. S. (2010). Effects of sleep deprivation on cognition. Progress in Brain Research, 185, 105-129.
  11. National Institute of Neurological Disorders and Stroke. (2019). Brain basics: Understanding sleep. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Understanding-Sleep

The Physiology of Acupuncture

Acupuncture is a traditional Chinese medicine technique that involves the insertion of thin needles into specific points on the body to stimulate natural healing processes. The practice has gained popularity as a complementary therapy for a variety of conditions, including chronic pain, digestive disorders, and depression. The mechanisms behind acupuncture’s therapeutic effects are not fully understood, but research suggests that it has a number of physiological effects.

One of the most well-known effects of acupuncture is its ability to produce analgesia, or pain relief. Research has found that acupuncture can activate various mechanisms in the body, including the release of endogenous opioids, which are natural painkillers produced by the body (Lin et al., 2016). Acupuncture has also been shown to reduce inflammation, which can contribute to pain, and improve blood flow to the affected area, which can promote healing (Chen et al., 2019).

Acupuncture has also been found to have a significant impact on brain function. Studies using functional magnetic resonance imaging (fMRI) have found that acupuncture can activate various regions of the brain, including the prefrontal cortex, limbic system, and hypothalamus, which are involved in pain perception, emotion regulation, and homeostasis (Huang et al., 2012). Acupuncture can also modulate the activity of the default mode network, a network of brain regions involved in self-referential thinking and mind-wandering (Chen et al., 2019). These effects on brain activity may contribute to the pain relief and other therapeutic effects of acupuncture.

Acupuncture’s effects on the autonomic nervous system are also well-documented. The autonomic nervous system is responsible for regulating many of the body’s involuntary functions, such as heart rate, blood pressure, and digestion. Studies have shown that acupuncture can modulate the activity of the autonomic nervous system, shifting the balance from sympathetic (fight-or-flight) to parasympathetic (rest-and-digest) activity (Cheng et al., 2014). This shift can have numerous beneficial effects, such as reducing stress and anxiety, improving digestion, and promoting relaxation.

Acupuncture may also regulate the release of neurotransmitters and hormones in the body. Studies have found that acupuncture can increase the levels of endorphins, serotonin, and other neurotransmitters that play a role in pain perception and mood regulation (Huang et al., 2012). Acupuncture has also been shown to increase the release of oxytocin, a hormone involved in social bonding and stress reduction (Uvnäs-Moberg, 2014).

The practice of acupuncture has also been found to have immunomodulatory effects, meaning that it can modulate the activity of the immune system. Research has found that acupuncture can increase the production of natural killer cells, which are important for fighting off infections and cancer cells (Chen et al., 2019). Acupuncture can also modulate the activity of inflammatory cells, such as T cells and B cells, which can reduce inflammation in the body. These effects have been observed both locally, at the site of needle insertion, and systemically throughout the body.

In addition to its effects on the immune system, acupuncture has been found to improve blood circulation by increasing the production of nitric oxide, a molecule that helps to dilate blood vessels (Chen et al., 2019). This increases blood flow to various tissues, including the skin and muscles, which can promote healing and reduce inflammation (Huang et al., 2012).

SystemEffectsApplications
AnalgesiaAcupuncture can help to reduce pain by stimulating the release of endogenous opioids and activating descending pain-inhibitory pathways.Used for chronic pain, such as back pain, neck pain, and osteoarthritis.
Brain ActivityAcupuncture has been found to modulate brain activity in areas associated with pain perception, emotion, and autonomic regulation.Used for depression, anxiety, and addiction.
Autonomic Nervous SystemAcupuncture can affect the autonomic nervous system, increasing parasympathetic activity and reducing sympathetic activity.Used for hypertension, digestive disorders, and menstrual cramps.
Neurotransmitter RegulationAcupuncture can regulate the release of neurotransmitters such as dopamine, serotonin, and norepinephrine.Used for depression, anxiety, and addiction.
Hormone ReleaseAcupuncture can stimulate the release of hormones such as endorphins, cortisol, and oxytocin.Used for infertility, menopausal symptoms, and stress.
Immune SystemAcupuncture can modulate immune function, with research suggesting an increase in anti-inflammatory markers and a decrease in pro-inflammatory markers.Used for allergies, asthma, and autoimmune diseases.
Blood CirculationAcupuncture has been found to increase blood flow in both local and distant regions of the body, which may contribute to its analgesic effects.Used for peripheral vascular disease, diabetic neuropathy, and erectile dysfunction.

In summary, acupuncture has a wide range of physiological effects on the body, including the regulation of neurotransmitters, hormones, and immune system function. It can also affect brain activity, the autonomic nervous system, and blood circulation, and has been shown to have analgesic effects. While the exact mechanisms underlying these effects are still being explored, the growing body of research suggests that acupuncture can be a valuable tool in promoting health and treating a variety of conditions.

References:

  1. Langevin HM, Schnyer RN. Acupuncture research: where are we and where are we going? J Altern Complement Med. 2002;8(6):635-639.
  2. Stener-Victorin E, Waldenstrom U, Andersson SA, Wikland M. Reduction of blood flow impedance in the uterine arteries of infertile women with electro-acupuncture. Hum Reprod. 1996;11(6):1314-1317.
  3. Xu J, Yang Y. Traditional Chinese medicine in the treatment of opioid addiction: from detoxification to long-term management. J Tradit Chin Med. 2012;32(2):151-157.
  4. Choi S-M, Park J-E, Li S-S, et al. Acupuncture for acute low back pain: a systematic review. Clin J Pain. 2013;29(2):172-185.
  5. Linde K, Allais G, Brinkhaus B, et al. Acupuncture for migraine prophylaxis. Cochrane Database Syst Rev. 2016;6:CD001218.
  6. Wang Y, Liu Z, Zhang J, et al. Effects of electro-acupuncture on brain-derived neurotrophic factor and cyclic AMP response element binding protein in the spinal cord and dorsal root ganglion of rats with chronic constriction injury. Acupunct Med. 2017;35(3):178-183.
  7. Kavoussi B, Ross BE. The neuroimmune basis of anti-inflammatory acupuncture. Integr Cancer Ther. 2007;6(3):251-257.
  8. Zhao Z-Q. Neural mechanism underlying acupuncture analgesia. Prog Neurobiol. 2008;85(4):355-375.
  9. Napadow V, Kaptchuk TJ. Patient characteristics for outpatient acupuncture in Beijing, China. J Altern Complement Med. 2004;10(3):565-572.
  10. Wang C, de Pablo P, Chen X, et al. Acupuncture for the treatment of hypertension: a systematic review. F1000Res. 2015;4:40.
  11. Smith CA, Armour M, Lee MS, Wang LQ, Hay PJ. Acupuncture for depression. Cochrane Database Syst Rev. 2018;3:CD004046.
  12. Yang CP, Chang MH, Liu PE, Li TC, Hsieh CL, Hwang KL. Ac

Sweeteners Increase Cardiovascular Risk

Earlier this year I wrote about the results of a large study evidencing the association between artificial sweeteners and cancer risk. Debras et al. used the same cohort (Nutrient-Sante) of over 100,000 participants. But this time, they looked at the association between artificial sweeteners and cardiovascular disease risk. The study was published in The British Medical Journal last month.

The results show that “artificial sweeteners (especially aspartame, acesulfame potassium, and sucralose) were associated with increased risk of cardiovascular, cerebrovascular, and coronary heart diseases“.

This reinforces previous evidence suggesting that artificial sweeteners are not just benign additives. They may actually have a detrimental impact on health.

Vitamin D Decreases Inflammation

Chronic inflammation is a well-known disease risk factor affecting both physical and mental health. One of the most common ways of measuring inflammation is by measuring levels of C-reactive protein (CRP) in the blood. Zhou and Hypponen, from the Australian Center for Precision Health, recently conducted a study on the link between Vitamin D and inflammation. The authors analysed a database of almost 300,000 people of White-British ancestry.

The analysis revealed the presence of an inverse relationship between vitamin D levels and CRP – as vitamin D levels increased, CRP levels decreased. The relationship was only present at low levels of vitamin D. The authors confirmed that the association was most likely due to an effect of vitamin D on CRP. Vitamin D may lead to the production of anti-inflammatory cytokines and inhibit the release of pro-inflammatory cytokines.

The results suggest that supplementing with vitamin D, in order to prevent low Vitamin D levels, may reduce chronic inflammation and reduce the severity of cardiovascular disease, diabetes, autoimmune disease, neurodegenerative disease and other diseases with an inflammatory component.

Vitamin D and Alzheimer’s Disease

Unfortunately there is currently an absence of curative and preventative interventions for Alzheimer’s Disease (AD). Last year, Panza et al. reviewed the research on the links between vitamin D and AD. Low vitamin D levels have been associated with an accelerated decline in cognitive functions. They have also been associated with the development of chronic brain conditions such as AD and other dementias. As such, vitamin D is often thought of as a neurosteroid due to its effect on brain conditions. The authors believe more research is required to determine the effect of vitamin D supplementation on the prevention and/or treatment of AD.

Eating For Health And Longevity

Valter Longo et al. recently published a paper that examined research on the relationships between nutrition, health and longevity. Here are some of the main components of a longevity diet:

  • mid to high carbohydrate intake (45-60%) – mostly non-refined
  • fat intake (25-35%) – mostly plant-based
  • low protein intake (10-15%) – mostly plant-based but includes regular consumption of peso-vegetarian-derived proteins. Low protein intake or normal protein intake (with high legume consumption) lowers the intake of amino acids such as methionine. This in turn lowers pro-aging substances such as GHR, IGF-1, insulin and TOR-S6K.
  • over 65s need to be careful to avoid malnourishment and prevent frailty and diseases resulting from reduced muscle mass, reduced bone mass or low blood cell count.
  • the largest gains in longevity come from diets rich in legumes, whole grains and nuts. With reduced amounts of red meat and processed meats
  • a 12-13hr daily fasting period is key to reducing the insulin resistance that may have developed from a high calorie diet. The fasting window also helps decrease levels of IGF-1, lowers blood pressure, lowers total cholesterol and decreases inflammation.
  • our daily food intake should be established by our body fat/lean body mass composition rather than generic pre-set calorie amounts.

Sweeteners Increase Cancer Risk

The use of artificial sweeteners by the food industry has become ubiquitous. They reduce the sugar content whilst still retaining the sweet pleasant taste. However, the safety of artificial sweeteners has been questioned, particularly regarding carcinogenicity.

Last month, Charlotte Debras et al. published the results of a study looking into the link between the consumption of sweeteners and cancer incidence. They followed a group of over 100,000 French adults for about 8 years.

The researchers found that “artificial sweeteners (especially aspartame and acesulfame-K) were associated with increased overall cancer risk (13%) for higher consumers compared to non-consumers. More specifically, aspartame was associated with increased breast (22%) and obesity-related (15%) cancer risks“.

We can conclude that reducing or eliminating our consumption of artificial sweeteners can play a significant role in cancer prevention.

Low Back Pain Could Affect How We Eat

A recent study by Lin et al. uncovered a relationship between longstanding low back pain and a preference for fat-rich foods. The authors found that the nucleus accumbens may be linked to the change in eating behaviour. The nucleus accumbens is a part of the brain that plays an important role in reward and pleasure processing. This could partly explain the high prevalence of obesity in people with longstanding pain.

Fat Injections For Plantar Fasciitis?

Beth Gusenoff et al. have just published the results of their study looking into the effects of fat cell injections for patients with plantar fasciitis. Plantar fasciitis is a common musculoskeletal condition that can lead to inflammation, degeneration and thickening of the plantar fascia. Patients usually present with heel pain during weight bearing activities. The symptoms are often worse in the morning and after periods of inactivity.

There are treatments such as arch-supporting insoles, night splints, soft tissue work, acupuncture, progressive stretching and strengthening, steroid injections, etc. But, the condition sometimes becomes chronic and lingers.

This was a very small study but it showed significant improvements in pain, function and structure of the plantar fascia after receiving perforating fat injections into the plantar fascia. It’s possible that the beneficial effects may be due to a healing response from the microtrauma caused by the needle. And/or the regenerative ability of stem cells and growth factors within fat.

The authors are planning large scale clinical trials to validate their results. It would be interesting for the authors to have a control group that is exposed to the needle microtrauma without the injection of fat cells. This would help determine whether it is the fat or the microtrauma that is responsible for the positive findings.

Covid-19 Research Update

Gu et al. (Nature) recently published a paper explaining the association between Covid-19 and inflammatory and blood coagulation disorders involving platelets and endothelial cells. This is probably why patients with cardiovascular risk factors such as diabetes, obesity and ageing have been particularly vulnerable to Covid-19.


Malas et al. have published a meta-analysis of 42 studies (8271 patients) looking into the association between thromboembolism (blood clots) and Covid-19. The overall venous thromboembolism rate was 21%, deep vein thrombosis (DVT) rate was 20% and pulmonary embolism rate was 13%. There was a positive correlation between disease severity and risk of blood clotting. The risk of thrombosis can affect any organ in the body. This has led to guidelines recommending the use of anticoagulants for Covid-19 patients, especially when hospitalised.


A Chinese cohort study published in The Lancet followed 1733 patients after they were discharged from hospital. They found that at 6 months after onset of Covid-19 symptoms most patients still had at least one symptom. The most common persisting problems were: fatigue or muscle weakness (63%), sleep difficulties (26%) and anxiety and/or depression (23%). Those that had been more severely ill had a high risk of pulmonary diffusion abnormalities and abnormal chest imaging. Persistent kidney dysfunction, diabetes and blood clotting disorders were also observed.

Vegans At Greater Risk of Fracture?

About a month ago a worrying study was published by researchers working on the EPIC-Oxford Study. They looked into the differences in fracture risk between meat eaters, vegetarians and vegans. It was done by following a group of around 55,000 men and women for an average of 17 years. It should be said that most fractures are generally due to poor bone health leading to decreased bone mineral density (BMD) and eventually osteoporosis.

The authors note that previous studies have shown that vegetarians (and vegans) have lower BMD than non-vegetarians but that the associated fracture risk is unclear. The combination of vitamin D and calcium has been found to be effective in decreasing fracture risk. Studies have also linked protein intake to bone health. High protein intake increases intestinal calcium absorption and stimulates the production of insulin-like growth factor (IGF-1) which is associated with better bone health. And finally, body mass index (BMI) could also play a part in fracture risk. The lower BMD found in US vegetarians may be explained by their lower BMI.

Tong et al. summarise their findings as follows:

 “The higher observed risks of fractures in non-meat eaters were usually stronger before BMI adjustment, which suggests that the risk differences were likely partially due to differences in BMI. Vegetarians and vegans generally have lower BMI than meat eaters, and previous studies have reported an inverse association between BMI and some fractures, particularly hip fractures, possibly due to reasons including the cushioning against impact force during a fall, enhanced oestrogen production with increased adiposity, or stronger bones from increased weight-bearing.”

Although a statistically significant higher risk of total and hip fractures was only observed in vegans in the lower BMI category (<?22.5?kg/m2), our interpretation is limited by the small numbers of cases in each stratum in these analyses, especially because of the strong correlation between diet group and BMI, which results in very few vegans in the higher BMI category, and vice versa comparatively small numbers of meat eaters with a low BMI.”

In this study and previous studies, vegans had substantially lower intakes of calcium than other diet groups since they do not consume dairy, a major source of dietary calcium, while both vegetarians and vegans had lower protein intakes on average. In the human body, 99% of calcium is present in bones and teeth in the form of hydroxyapatite, which in cases of calcium deficiency gets resorbed to maintain the metabolic calcium balance, and thus, osteoporosis could occur if the calcium was not restored.”

Overall, vegans in this study had higher risks of total and some site-specific fractures (hip, leg, vertebra) than meat eaters. The strongest associations were observed for hip fractures, for which fish eaters, vegetarians, and vegans all had higher risks. These risk differences might be partially explained by the lower average BMI, and lower average intakes of calcium and protein in the non-meat eaters. However, because the differences remained, especially in vegans, after accounting for these factors, other unaccounted for factors may be important.

We have known for some time that astronauts suffer from bone loss whilst in space. This is partly due to the effect of weightlessness and reduced physical activity leading to decreased bone compressive forces. Bone compressive forces help increase BMD and create stronger bones. As vegans usually have lower BMIs, their bones are subject to smaller compressive forces than meat-eaters. This can be overcome by resistance exercise and weight lifting. And of course, it is particularly important for those eating a plant-based diet to ensure they get an adequate intake of vitamin D, calcium and protein to maintain bone health.

Breathe Through Your Nose

This post is inspired by “Following Your Nose: Nasal Function and Energy” by Rudolph Ballentine (in Science of Breath, 1992).

The nose is the most restricted part of the respiratory tract and creates 150% more work than mouth breathing. So why should we breathe through our noses? Because the nose fulfils several crucial respiratory functions that our mouth is unable to fulfil. As air passes through the nose it’s filtered, humidified (98% humidity) and warmed (32-34 degrees C). This prepares it for passage to the lungs. When we breathe out through the nose, much of the moisture and heat is retained within the nose to be transferred to the next in-breath.

As we breathe deeply through our nose, mechanoreceptors on epithelial cells are activated and this results in the release of nitric oxide. Nitric oxide leads to bronchodilation and vasodilation which in turn increase circulation and the delivery of oxygen. Nitric oxide also has antimicrobial properties and promotes mucus production and ciliary movement which facilitate the evacuation of debris and microbes.

Apparently, the shape of our nose depends on the climate in which our ancestors evolved: a long big nose in cooler and dryer climates and a wide nose with open nostrils in warm, moist climates.

“Yesterday I was clever,

so I wanted to change the world.

Today I am wise,

so I am changing myself.”

Rumi

Nutrition, Immunity and COVID-19

Our immune system protects us from pathogens like viruses, bacteria, cancerous cells, etc. and it can be separated into 2 distinct branches: the innate immune system and the adaptive immune system. Our innate immune system uses cells such as macrophages, neutrophils and mast cells to mount a fast, generic response to pathogens. Inflammation is the hallmark of the innate immune system. On the other hand, the adaptive immune system uses T cells, B cells and natural killer cells to mount a slow, targeted response to pathogens. It’s the adaptive immune system that’s responsible for life-long immunity to certain diseases. In practice, the 2 branches interact to provide a comprehensive immune response.

In a recent article, Butler and Barrientos (2020) summarised the interactions between diet, immunity and COVID-19. They state that the typical western diet (high in saturated fats, refined carbohydrates and sugars, and low in fibre, unsaturated fats and antioxidants) “significantly impairs adaptive immunity while ramping up innate immunity, leading to chronic inflammation and severely impairing host defence against viral pathogens.

The authors note that “T and B cell counts were also significantly lower in patients with severe COVID-19; thus, there could be a potential interaction between western diet consumption and COVID-19 on adaptive immunity impairment.” They suggest the higher rates of obesity and diabetes among ethnic minority populations may partly account for the health disparities seen in response to COVID-19.

Butler and Barrientos conclude “that individuals refrain from eating foods high in saturated fats and sugar and instead consume high amounts of fibre, whole grains, unsaturated fats, and antioxidants to boost immune function.”

Early Feeding Improves Pre-Diabetes and Blood Pressure

About a year ago Sutton et al. published a study that showed that intermittent fasting has benefits that are independent of food intake and weight loss. Their trial tested the effects of 5 weeks of “early time-restricted feeding” (eTRF) on 8 men with pre-diabetes. The subjects were asked to start breakfast between 6:30-8:30 and to eat their 3 meals in a 6-hour window with dinner before 15:00. They were fed enough food to maintain weight. The control group had similar meals but within a 12-hour feeding window. Five weeks of eTRF significantly improved insulin levels, insulin sensitivity, blood pressure and oxidative stress levels. The blood pressure improvements were particularly dramatic – morning levels of both systolic and diastolic blood pressure were reduced by about 10 mm Hg each.

Some of the benefits of eTRF are believed to originate from eating in alignment with our internal biological clocks which are primed for feeding early in the day. The authors state that “in humans, insulin sensitivity, beta cell responsiveness, and the thermic effect of food are all higher in the morning than in the afternoon or evening, suggesting that human metabolism is optimized for food intake in the morning”. Fortunately eTRF lowers the desire to eat in the evening!

Slow Breathing Regulates High Blood Pressure

Several years ago I wrote a few articles showing that exercise, yoga and other strategies were helpful at regulating high blood pressure (BP). Even small reductions in blood pressure can significantly reduce the risk of heart disease, stroke and kidney failure. The risks associated with hypertension are continuous – this means that with each 2mm Hg rise in systolic BP there is an associated 7% increase in mortality from heart disease and 10% increase in mortality from stroke.

I recently came across a few studies that have shown that paced, slow breathing can significantly decrease blood pressure in patients with hypertension. Joseph et al. (2005) demonstrated that paced breathing at 6 breaths/min for only a couple of minutes was able to decrease systolic BP by more than 8mm Hg and diastolic BP by about 5mm Hg. Similarly, Li et al. (2018) found that paced breathing at 8 breaths/min for 5min lowered systolic BP by about 4mm Hg and diastolic BP by over 8mm Hg. Because the slow breathing was only tested for a few minutes…the long-term effects of daily practice remain to be determined.

For those that are interested in giving it a go, I would recommend wearing loose-fitting clothing and either lying down or sitting back into a chair in a warm environment. Aim to progressively slow your breathing down to 5-7 breaths/min (there are several apps that can help pace your breathing). Breathe with an equal inhalation and exhalation. It may take several sessions to comfortably slow your breath to 5-7 breaths/min…take your time. Enjoy for 15-20min a day!

Ever since happiness heard your name,

it has been running through the streets trying to find you...

…let it catch up.”

Hafez (modified by Joseph Goldstein)

Meal Times Crucial For Weight Loss

A few months ago Lopez-Minguez et al. reviewed studies looking at the effect of meal times on obesity and metabolic risk. Their findings are summed up in the following points:

  • skipping breakfast is linked to obesity
  • eating a large breakfast (within 2hrs of waking) decreases the probability of being obese by 50%
  • a late lunch (after 3pm) hampers weight loss and has a negative effect on the diversity and composition of our microbiota
  • a late dinner (less than 2hrs before bedtime) decreases glucose tolerance
  • eating a large, late dinner (less than 2hrs before bedtime) leads to a 5-fold increase in the risk of becoming obese
  • the timing of breakfast seems to be hereditary whereas the timing of dinner is mainly cultural

There may be some truth in the following quote by Adelle Davis.

Eat breakfast like a king, lunch like a prince and dinner like a pauper

As well as getting the timing right obviously!

Could Sunlight Aid Weight Loss?

Nayak et al. have recently published the findings of their fascinating research into the effects of light on fat metabolism in mice.

Animals have adapted to use light in various ways. The most obvious is our sense of sight – it creates images in the brain through the detection of photons by light sensitive proteins (opsins) in the retina. But there are also non-visual ocular photoreceptors that help regulate our circadian rhythms (body clock), pupillary light reflex and eye development. Interestingly, light sensitive proteins are also found outside the eye. Opsins in our skin can regulate the circadian clock and others can influence blood vessel dilation. In birds, it’s photoreceptors deep within the brain that regulate seasonal breeding behaviour.

There have been suggestions that adipocyte (fat cell) function may be modulated by light. White fat (WAT) acts as a storage site whereas brown fat (BAT) generates heat through a process called non-shivering thermogenesis (NST). During lipolysis, white fat can be broken down into free fatty acids (FFAs) and glycerol. The brown fat can then use the FFAs to generate heat by oxidation. This process plays a crucial role in the regulation of body temperature during cold exposure.

In the current study, Nayak et al. found that lipolysis was brought about by the exposure of light receptors within white fat (encephalopsin, OPN3) to light. OPN3 was particularly sensitive to blue light. The mice lacking OPN3 or light exposure had diminished heat-generating responses when placed in cold environments. The authors conclude: “If the light-OPN3 adipocyte pathways exist in humans, there are potentially broad implications for human health. Our modern lifestyle subjects us to unnatural lighting spectra, exposure to light at night, shift work, and jet lag, all of which result in metabolic disruption. Based on the current findings, it is possible that insufficient stimulation of light-OPN3 adipocyte pathway is part of an explanation for the prevalence of metabolic deregulation in industrialized nations where unnatural lighting has become the norm.”

“Keep your eye fixed on the way to the top,

but don’t forget to look right in front of you.

The last step depends on the first.

Don’t think you’re there just because you see the summit.

Watch your footing,

be sure of the next step,

but don’t let that distract you from the highest goal.

The first step depends on the last.”

René Daumal

Soft Drinks May Cause Menopausal Hip Fractures

A study published this month in the journal Menopause looked into the relationships between carbonated soft drink consumption, osteoporosis (hip and lumbar spine) and incidental hip fractures. For almost 12 years Kremer et al. followed over 72,000 postmenopausal women from the Women’s Health Initiative Observational Study.

The results showed no associations between soft drink consumption and hip or lumbar spine bone mineral density – this finding was in contradiction with previous studies that had found an association. Consuming at least 14 carbonated soft drinks per week was associated with incident hip fractures. The relationship was statistically significant for caffeine-free soft drinks but not for caffeinated soft drinks. Interestingly, there was no significant risk if the intake was less than 14 servings per week, suggesting a ‘threshold effect’ rather than a ‘linear dose-response’ relationship. Drinking more than 14 carbonated soft drinks (non-caffeinated) per week led to a 32% increase in risk of hip fracture compared to women that didn’t drink any soft drinks.

The authors postulate that added sugars may have “a negative impact on mineral homeostasis and calcium balance“. Also, the carbonation of soft drinks “results in the formation of carbonic acid that might alter gastric acidity and, consequently, nutrient absorption“.

Excess Dietary Salt Leads To Cognitive Impairment

Faraco et al. recently discovered mechanisms by which salt-rich diets can lead to cognitive dysfunction in mice. An increase in dietary salt led to a deficiency of nitric oxide in cerebral blood vessels. As nitric oxide is a vasodilator, the reduced levels resulted in decreased cerebral blood flow. In addition, nitric oxide deficiency causes the distortion of a brain protein (tau) which affects the structure and function of nerve cells. The authors conclude that the “avoidance of excessive salt intake and maintenance of vascular health may help stave off the vascular and neurodegenerative pathologies that underlie dementia in the elderly.”

Loving-Kindness Meditation Slows Aging

A recent study by Le Nguyen et al. published in Psychoneuroendocrinology has looked at the effect of loving-kindness meditation on telomore length. Loving-Kindness is a Buddhist meditation that focuses on sending good wishes and kindness to ourselves and others by silently repeating a series of mantras. Telomeres sit at the end of chromosomes and protect the chromosomes from deterioration. Our telomeres gradually shorten over time and this is believed to contribute to aging.

The researchers randomised 142 middle-aged adults into 3 groups: a waiting list control group, a mindfulness meditation group and a loving-kindness meditation group. Telomere length was measured 2 weeks prior to the start and 3 weeks after the end of the 6-week meditation workshop. The results showed that there was significantly less telomere attrition in the loving-kindness meditation group than the control group. The mindfulness meditation group had results that were in between the other 2 groups without being statistically significantly different from either.

We can infer that loving-kindness meditation can slow aging by decreasing the rate at which our telomeres shorten.

Meditation and the Brain

Meditation can be defined as “a family of mental training practices aimed at monitoring and regulating attention, perception, emotion and physiology” (Fox and Cahn, 2019). As with other forms of learning, meditation has the potential to change the brain (neuroplasticity). Fox and Cahn (2019) reviewed decades of meditation research in a paper entitled “Meditation and the brain in health and disease”. Here are some of their findings. The table below summarises the areas of the brain that have been implicated in meditation.

Brain Region Function
Insula Awareness of internal environment (breathing, heartbeat, abdominal sensations, etc.)
Somatosensory Cortex Awareness of external environment (touch, pain, etc.)
Rostrolateral Prefrontal Cortex ‘Higher’ thinking ability
Anterior Cingulate Cortex Emotional awareness and regulation
Hippocampus Memory
Corpus Callosum Integration of information between the 2 hemispheres

Although “psychologically distinct meditation practices show correspondingly diverse neural correlates”, most practices modulate activity in the insula. Given that awareness of breathing or other body sensations is central to most forms of meditation, and the insula’s role in the awareness of the internal environment, it’s not surprising that meditation leads to a change in structure and function of the insula.

Some interesting discoveries have been made regarding pain. The experience of pain is the combination of the purely sensory aspect of pain with feelings of distress, thoughts relating the pain to the self and various negative emotional interpretations of the experience. “These cognitive-affective elaborations appear to be dissociable from, and temporarily subsequent to, the purely sensory aspects of pain – and what’s more, they may contribute significantly to the subjectively experienced unpleasantness of nociceptive experience (Rainville et al., 1997)”. Meditators were found to have lower pain sensitivity. This may be due to their decreased functional connectivity between primary sensory pain areas and secondary affective-elaborative areas. This supports the idea that seasoned meditators remain focussed on purely sensory aspects of pain whereas non-meditators dwell on emotional and cognitive associations of pain.

Other fascinating discoveries are the impact of meditation on aging. There is usually a decrease in function (glucose metabolism) and structure (amount and density of grey matter) of the brain with aging. However, studies show that meditation may help stave off the effects of aging. In fact, some studies have found no age-related decline in function and/or structure!

But, the limitations of current research must be acknowledged:

  • It’s a new field of inquiry
  • Agreement amongst researchers is the exception rather than the norm
  • Few studies control for factors that may exist between meditators and controls e.g. Diet, stress, sleep, personality, etc.
  • Publication bias (the preferential publication of only positive studies)

Paleo Diet May Be Bad For Cardiovascular Health

Research published earlier this month in the European Journal of Nutrition questions the health benefits of the Paleolithic diet. The Paleo diet claims to mimic the diet of our ancestors. It’s high in meat, fruits, vegetables, nuts and seeds but avoids dairy, legumes and grains.

Genoni et al. studied a group of about 100 people over a year. Half the group followed a Paleo diet and the rest followed a diet typical of national recommendations. The authors found that there was a significant difference in the gut bacteria between groups, with an increased presence of Hungatella in the paleo group. Hungatella produces trimethylamine-N-oxide (TMAO), a gut-derived metabolite associated with cardiovascular disease. Consequently the levels of TMAO were higher in the Paleo group and this was inversely associated with whole grain intake.

The authors conclude that “although the Paleo diet is promoted for improved gut health, results indicate long-term adherence is associated with different gut microbiota and increased TMAO. A variety of fiber components, including whole grain sources may be required to maintain gut and cardiovascular health.”

Vagus Nerve Stimulation Reduces Rheumatoid Arthritis Symptoms

Genovese et al. recently presented the results of their research at the Annual European Congress of Rheumatology. They implanted mini neurostimulators in 14 rheumatoid arthritis (RA) patients that had failed to respond to anti-rheumatic medication. In the treatment groups, the vagus nerve was stimulated daily for 12 weeks. The results showed that stimulation of the vagus nerve reduced signs and symptoms of RA as well as decreasing by 30% the levels of cytokines (inflammatory mediators).

The vagus nerve is known to have anti-inflammatory effects and can also be stimulated by less invasive methods such as meditation, breathing exercises, relaxation techniques and acupuncture.