The skeletal system comprises bones, cartilage, ligaments, and other  connective tissues that provide structure, support, and protection for  the body. Its primary functions include facilitating movement,  protecting vital organs, producing blood cells, storing minerals like  calcium and phosphorus, and providing structural support for the body.  Bones are dynamic structures that undergo continual remodeling through  processes such as bone formation (ossification) and resorption.  Additionally, the skeletal system plays a crucial role in maintaining  mineral homeostasis and acid-base balance in the body. Through its  interactions with muscles and joints, the skeletal system enables  mobility and locomotion, allowing humans and other vertebrates to  perform a wide range of activities, from basic movements to complex  tasks. Overall, the skeletal system serves as the framework of the body,  contributing to its shape, stability, and overall function. 

The skeletal system can be affected by various disorders, including:

1. Osteoporosis: A      condition characterized by decreased bone density and strength, leading to      an increased risk of fractures, particularly in postmenopausal women and      older adults.
2. Osteoarthritis: The      most common form of arthritis, osteoarthritis involves the breakdown of      cartilage in the joints, leading to pain, stiffness, and loss of mobility,      especially in weight-bearing joints such as the knees and hips.
3. Rheumatoid Arthritis: An      autoimmune disease that causes chronic inflammation of the joints, leading      to pain, swelling, and eventual joint deformity and destruction.
4. Fractures: Breaks or cracks in the bone resulting      from trauma, overuse, or underlying bone conditions.
5. Scoliosis: A sideways curvature of the spine,      which can range from mild to severe and may require bracing or surgical      intervention, especially in adolescents.
6. Osteomyelitis: An      infection of the bone, often caused by bacteria, which can lead to bone      pain, swelling, and fever.
7. Paget's Disease: A      chronic disorder characterized by abnormal bone remodeling, leading to      enlarged and weakened bones, fractures, and deformities.
8. Bone Cancer:      Including primary bone tumors (arising in the bone) and secondary bone      tumors (metastases from other cancers), which can lead to bone pain,      fractures, and other complications.

These disorders can significantly impact quality of life and may require various treatments, including medications, physical therapy, lifestyle modifications, and sometimes surgical interventions, depending on the severity and underlying causes.

1. Osteoporosis:      Insulin resistance and hyperinsulinemia may disrupt bone metabolism by      affecting osteoblast and osteoclast function, leading to decreased bone      formation and increased bone resorption, thereby contributing to reduced      bone density and increased fracture risk.
2. Osteoarthritis:      Insulin resistance and metabolic syndrome components such as obesity can      exacerbate inflammation in the joints, leading to cartilage degradation      and accelerated joint degeneration.
3. Fractures: Insulin resistance and metabolic      syndrome are associated with increased risk factors for falls, such as      obesity, impaired balance, and neuropathy, which can contribute to a      higher incidence of fractures.
4. Paget's Disease: Some      studies suggest a potential association between insulin resistance and      Paget's disease, although the exact mechanisms are not fully understood.
5. Bone Cancer:      Insulin resistance and hyperinsulinemia may promote cancer cell      proliferation and metastasis, potentially increasing the risk of bone      cancer development or progression.

Overall, the dysregulation of insulin and metabolic processes seen in hyperinsulinemia, insulin resistance, and metabolic syndrome can adversely affect bone health and contribute to the development or exacerbation of skeletal disorders.

xcess body weight places increased mechanical stress  on bones, leading to accelerated wear and tear, especially in  weight-bearing joints like the knees and hips. This strain can  exacerbate conditions such as osteoarthritis and contribute to postural  changes, increasing the risk of spinal issues. 

Diabetes can lead to decreased bone mineral density (BMD), increasing  the risk of osteoporosis and fractures. Additionally, diabetes-related  complications like neuropathy and vascular issues can impair bone  healing and increase the risk of fractures, particularly in the feet and  lower extremities. 

 Amputations, the surgical removal of a limb or part of a limb, may be influenced by insulin resistance, hyperinsulinemia, or metabolic syndrome in several ways:

1. Peripheral arterial disease (PAD): Insulin resistance, hyperinsulinemia, and metabolic syndrome are significant risk factors for PAD, a condition characterized by narrowed or blocked arteries in the legs. PAD reduces blood flow to the extremities, leading to tissue ischemia and an increased risk of non-healing wounds and infections. In severe cases, PAD can necessitate amputation due to tissue necrosis and gangrene.
2. Diabetic neuropathy: Individuals with diabetes, often associated with insulin resistance and metabolic syndrome, are at increased risk of developing diabetic neuropathy, a type of nerve damage that affects sensation and function in the extremities. Peripheral neuropathy can lead to the loss of protective sensation in the feet, making individuals vulnerable to foot injuries, ulcers, and infections that may progress to the point of requiring amputation.
3. Non-healing wounds: Insulin resistance, hyperinsulinemia, and metabolic syndrome can impair wound healing processes, prolonging the time it takes for wounds, ulcers, or injuries to heal. Chronic wounds, particularly in the lower extremities of individuals with diabetes, may become infected and progress to the point of requiring amputation.
4. Infections: Insulin resistance, hyperinsulinemia, and metabolic syndrome can compromise immune function, increasing the risk of infections, particularly in individuals with diabetes. Foot infections, such as diabetic foot ulcers, can become severe and difficult to treat, necessitating amputation to prevent the spread of infection.
5. Obesity-related factors: Obesity, a common feature of metabolic syndrome, is associated with an increased risk of lower extremity complications, including chronic wounds, infections, and poor circulation. The excess weight can also place additional stress on the feet and legs, increasing the risk of injuries and complications that may lead to amputation.

Overall, insulin resistance, hyperinsulinemia, and metabolic syndrome can contribute to the development of conditions such as PAD, diabetic neuropathy, non-healing wounds, infections, and obesity-related complications, all of which increase the risk

of amputations. Managing these metabolic abnormalities through lifestyle modifications, medication, or other interventions is crucial for preventing or minimizing the risk of complications and improving outcomes in individuals at risk for amputations. This includes maintaining optimal blood glucose levels, controlling blood pressure and cholesterol levels, promoting healthy lifestyle habits such as regular exercise and a balanced diet, and seeking prompt medical attention for any foot or leg problems to prevent their progression to the point of requiring amputation. Additionally, comprehensive foot care, including regular foot exams, proper footwear, and early treatment of foot ulcers or injuries, is essential for individuals with diabetes or other conditions that increase the risk of amputations.

 "Mortality rate within 4 years following amputation was 19.3 % and was higher in females and individuals with multiple comorbidities."

Arthritis primarily affects the musculoskeletal system. Specifically, it involves inflammation and damage to the joints, which are the structures that connect bones and allow for movement. Arthritis can affect various components of the joints, including the cartilage, synovium (the lining of the joint), and surrounding tissues such as ligaments and tendons.

There are many different types of arthritis, but the most common ones include:

1. Osteoarthritis: This is the most common type of arthritis and occurs due to wear and tear on the joints over time. It typically affects older individuals and commonly involves weight-bearing joints such as the knees, hips, and spine.
2. Rheumatoid arthritis: This is an autoimmune disease where the immune system mistakenly attacks the synovium, causing inflammation and damage to the joints. Rheumatoid arthritis can affect people of any age and often involves multiple joints, including the hands, wrists, and feet.
3. Juvenile idiopathic arthritis: This is a type of arthritis that occurs in children and adolescents, and it encompasses several subtypes of arthritis with onset before the age of 16. The specific cause of juvenile idiopathic arthritis is not well understood, but it involves chronic inflammation of the joints.

Other types of arthritis include psoriatic arthritis, ankylosing spondylitis, and gout, among others. These conditions can affect different joints and have various underlying causes and mechanisms of inflammation.

While arthritis primarily affects the musculoskeletal system, it can also have systemic effects, impacting other parts of the body. For example, rheumatoid arthritis can affect organs such as the lungs and heart, and certain types of arthritis are associated with increased risk of cardiovascular disease.

1. Strath  LJ, Jones CD, Philip George A, et al. The Effect of Low-Carbohydrate  and Low-Fat Diets on Pain in Individuals with Knee Osteoarthritis. Pain  Med. March 2019. doi:10.1093/pm/pnz022 ABSTRACT 
2. Schönenberger, K.A. et al. (2021) ‘Effect of Anti-Inflammatory Diets on Pain in Rheumatoid Arthritis: A Systematic Review and Meta-Analysis’, Nutrients, 13(12). doi:10.3390/nu13124221.
3. Lyman, K.S. et al. (2022) ‘Continuous care intervention with carbohydrate restriction  improves physical function of the knees among patients with type 2  diabetes: a non-randomized study’, BMC Musculoskeletal Disorders, 23(1), p. 297. doi:10.1186/s12891-022-05258-0.
4. Liu  S-Y, Zhu W-T, Chen B-W, Chen Y-H, Ni G-X. Bidirectional association  between metabolic syndrome and osteoarthritis: a meta-analysis of  observational studies. Diabetol Metab Syndr. 2020;12(1):38. doi:10.1186/s13098-020-00547-x
5. Lawford, B. et al. (2023) ‘“The fact that I know I can do it is quite a motivator now”: a  qualitative study exploring experiences maintaining weight loss 6 months  after completing a weight loss programme for knee osteoarthritis’, BMJ Open, 13(5), p. e068157. Available at: https://doi.org/10.1136/bmjopen-2022-068157.
6. Lawford  BJ, Bennell KL, Jones SE, Keating C, Brown C, Hinman RS. “It’s the  single best thing I’ve done in the last 10 years”: a qualitative study  exploring patient and dietitian experiences with, and perceptions of, a  multi-component dietary weight loss program for knee osteoarthritis. Osteoarthritis Cartilage. Published online January 9, 2021. doi:10.1016/j.joca.2021.01.001
7. Cooper, I. et al. (2022) ‘An anti-inflammatory diet intervention for knee osteoarthritis: a feasibility study’, BMC Musculoskeletal Disorders, 23. doi:10.1186/s12891-022-05003-7.
8. Hagström, N. et al. (2023) ‘A qualitative evaluation of the specific carbohydrate diet for  juvenile idiopathic arthritis based on children’s and parents’  experiences’, Pediatric Rheumatology, 21(1), p. 127. Available at: https://doi.org/10.1186/s12969-023-00914-8.
9. Rondanelli, M. et al. (2023) ‘Very low calorie ketogenic diet and common rheumatic disorders: A case report’, World Journal of Clinical Cases, 11(9), pp. 1985–1991. Available at: https://doi.org/10.12998/wjcc.v11.i9.1985.
10. Tchetina  EV, Markova GA, Sharapova EP. Insulin Resistance in Osteoarthritis:  Similar Mechanisms to Type 2 Diabetes Mellitus. Journal of Nutrition and  Metabolism. doi:https://doi.org/10.1155/2020/4143802
11. Dickson  BM, Roelofs AJ, Rochford JJ, Wilson HM, De Bari C. The burden of  metabolic syndrome on osteoarthritic joints. Arthritis Res Ther.  2019;21(1):289. doi:10.1186/s13075-019-2081-x
12. Wang  X, Hunter D, Xu J, Ding C. Metabolic triggered inflammation in  osteoarthritis. Osteoarthritis and Cartilage. 2015;23(1):22-30. doi:10.1016/j.joca.2014.10.002
13. Tan Q, Jiang A, Li W, Song C, Leng H. Metabolic syndrome and osteoarthritis: possible mechanisms and management strategies. Medicine in Novel Technology and Devices. Published online December 17, 2020:100052. doi:10.1016/j.medntd.2020.100052
14. Meng  T, Antony B, Venn A, et al. Association of glucose homeostasis and  metabolic syndrome with knee cartilage defects and cartilage volume in  young adults. Seminars in Arthritis and Rheumatism. October 2019. doi:10.1016/j.semarthrit.2019.10.001 ABSTRACT
15. Athanassiou P, Athanassiou L, Kostoglou-Athanassiou I. Nutritional Pearls: Diet and Rheumatoid Arthritis. Mediterr J Rheumatol. 2020;31(3):319-324. doi:10.31138/mjr.31.3.319
16. Gallagher  L, Cregan S, Biniecka M, et al. Insulin Resistant Pathways are  associated with Disease Activity in Rheumatoid Arthritis and are Subject  to Disease Modification through Metabolic Reprogramming; A Potential  Novel Therapeutic Approach. Arthritis & Rheumatology (Hoboken, NJ). Published online December 16, 2019. doi:10.1002/art.41190 ABSTRACT
17. Babu S, Vaish A, Vaishya R, Agarwal A. Can intermittent fasting be helpful for knee osteoarthritis? Journal of Clinical Orthopaedics & Trauma. 2021;16:70-74. doi:10.1016/j.jcot.2020.12.020 ABSTRACT
18. Jiang  Y, Jarr K, Layton C, et al. Therapeutic Implications of Diet in  Inflammatory Bowel Disease and Related Immune-Mediated Inflammatory  Diseases. Nutrients. 2021;13(3). doi:10.3390/nu13030890
19. Ciaffi, J. et al. (2021) ‘The Effect of Ketogenic Diet on Inflammatory Arthritis and  Cardiovascular Health in Rheumatic Conditions: A Mini Review’, Frontiers in Medicine, 8. doi: 10.3389/fmed.2021.792846 

https://nutrition-network.org/research/other-conditions-3/

Bones are rigid, mineralized structures that form the skeleton of vertebrates, providing support, protection, and structure to the body. They serve several important functions, including:

1. Support: Bones provide a framework that supports the body and maintains its shape. They give structure to soft tissues and organs and help maintain posture and alignment.
2. Protection: Bones protect vital organs and tissues from injury and damage. For example, the skull protects the brain, the rib cage protects the heart and lungs, and the vertebral column protects the spinal cord.
3. Movement: Bones, along with muscles, joints, and ligaments, form the musculoskeletal system, which allows for movement and locomotion. Muscles attach to bones via tendons, and when muscles contract, they pull on bones, causing movement at the joints.
4. Hematopoiesis: Bone marrow, found within the central cavities of certain bones, is responsible for the production of blood cells, including red blood cells (erythrocytes), white blood cells (leukocytes), and platelets (thrombocytes), in a process called hematopoiesis.
5. Mineral Storage: Bones serve as a reservoir for minerals, particularly calcium and phosphorus, which are essential for various physiological processes, including muscle contraction, nerve function, and blood clotting. When blood levels of calcium are low, bones release calcium into the bloodstream to maintain homeostasis.
6. Acid-Base Balance: Bones act as buffers to help regulate the body's acid-base balance by absorbing or releasing alkaline salts, such as calcium carbonate and calcium phosphate, depending on the body's needs.

Bones are composed of a dense outer layer called cortical bone (compact bone) and a spongy inner layer called cancellous bone (trabecular bone). The outer surface of bones is covered by a fibrous membrane called the periosteum, which contains blood vessels and nerves that nourish the bone. The inner cavity of certain bones contains bone marrow, which is responsible for hematopoiesis and fat storage.

Bones are made up of various types of cells, including osteoblasts (which build bone), osteoclasts (which break down bone), and osteocytes (mature bone cells). The extracellular matrix of bone consists mainly of collagen fibers and mineralized calcium salts, such as hydroxyapatite, which give bone its strength and hardness.

   Studies 

1. Hu  T, Yao L, Bazzano L. Effects of a 12-month Low-Carbohydrate Diet vs. a  Low-Fat Diet on Bone Mineral Density: A Randomized Controlled Trial. The FASEB Journal. 2016;30(S1):678.12-678.12. doi:https://doi.org/10.1096/fasebj.30.1_supplement.678.12 ABSTRACT
2. Athinarayanan  SJ, Adams RN, Hallberg SJ, et al. Long-Term Effects of a Novel  Continuous Remote Care Intervention Including Nutritional Ketosis for  the Management of Type 2 Diabetes: A 2-year Non-randomized Clinical  Trial. Front Endocrinol. 2019;10. doi:10.3389/fendo.2019.00348
3. Papageorgiou, M. et al. (2023) ‘The effects of time‐restricted eating and weight loss on bone  metabolism and health: a 6‐month randomized controlled trial’, Obesity (Silver Spring, Md.), 31(Suppl 1), p. 85. Available at: https://doi.org/10.1002/oby.23577. ABSTRACT
4. Vargas-Molina, S. et al. (2021) ‘Effects of a low-carbohydrate ketogenic diet on health parameters in resistance-trained women’, European Journal of Applied Physiology. Available at: https://doi.org/10.1007/s00421-021-04707-3.
5. Partial  Replacement of Animal Proteins with Plant Proteins for 12 Weeks  Accelerates Bone Turnover Among Healthy Adults: A Randomized Clinical  Trial | The Journal of Nutrition | Oxford Academic. doi:10.1093/jn/nxaa264  ABSTRACT
6. Tonks  KT, White CP, Center JR, Samocha-Bonet D, Greenfield JR. Bone Turnover  Is Suppressed in Insulin Resistance, Independent of Adiposity. J Clin  Endocrinol Metab. 2017;102(4):1112-1121. doi:10.1210/jc.2016-3282 
7. Almsaid  H, Muhsin H. The effect of Ketogenic diet on vitamin D3 and  testosterone hormone in patients with diabetes mellitus type 2. Current Issues in Pharmacy and Medical Sciences. 2021;33:202-205. doi:10.2478/cipms-2020-0033
8. Islamoglu  AH, Garipagaoglu M, Bicer HS, Kurtulus D, Ozturk M, Gunes FE. The  effects of dietary changes on bone markers in postmenopausal vertebral  osteopenia. Clinical Nutrition. 2020;0(0). doi:10.1016/j.clnu.2020.04.001 ABSTRACT
9. Campillo-Sánchez  F, Usategui-Martín R, Ruiz -de Temiño Á, et al. Relationship between  Insulin Resistance (HOMA-IR), Trabecular Bone Score (TBS), and  Three-Dimensional Dual-Energy X-ray Absorptiometry (3D-DXA) in  Non-Diabetic Postmenopausal Women. Journal of Clinical Medicine.  2020;9(6):1732. doi:10.3390/jcm9061732 
10. Lobene  AJ, Panda S, Mashek DG, Manoogian ENC, Hill Gallant KM, Chow LS.  Time-Restricted Eating for 12 Weeks Does Not Adversely Alter Bone  Turnover in Overweight Adults. Nutrients. 2021;13(4):1155. doi:10.3390/nu13041155
11. Hunt  HB, Miller NA, Hemmerling KJ, et al. Bone tissue composition in  post-menopausal women varies with glycemic control from normal glucose  tolerance to type 2 diabetes mellitus. Journal of Bone and Mineral  Research. n/a(n/a). doi:10.1002/jbmr.4186 ABSTRACT
12. Karadeniz  B, Gur C, Cakir D, et al. The relationship between glycemic control and  osteocalcin, type 1 collagen C-terminal telopeptide, bone-specific  alkaline phosphatase and the effects of anti-diabetic regimens on  circulating markers of bone turnover in newly diagnosed diabetic  patients: Bone health in diabetics. Clin Nephrol. Published online May 27, 2021. doi:10.5414/CN110394 ABSTRACT
13. Silva VN da, Goldberg TBL, Silva CC, et al. Impact of metabolic syndrome and its components on bone remodeling in adolescents. PLOS ONE. 2021;16(7):e0253892. doi:10.1371/journal.pone.0253892
14. Heikura IA, Burke LM, Hawley JA, et al. A Short-Term Ketogenic Diet Impairs Markers of Bone Health in Response to Exercise. Front Endocrinol (Lausanne). 2020;10. doi:10.3389/fendo.2019.00880
15. Chiu  H, Lee M-Y, Wu P-Y, Huang J-C, Chen S-C. Development of Metabolic  Syndrome Decreases Bone Mineral Density T-Score of Calcaneus in Foot in a  Large Taiwanese Population Follow-Up Study. Journal of Personalized Medicine. 2021;11(5):439. doi:10.3390/jpm11050439
16. Rendina  D, D’Elia L, Evangelista M, et al. Metabolic syndrome is associated to  an increased risk of low bone mineral density in free-living women with  suspected osteoporosis. J Endocrinol Invest. Published online September  22, 2020. doi:10.1007/s40618-020-01428-w ABSTRACT
17. Onkarappa  RS, Chauhan DK, Saikia B, Karim A, Kanojia RK. Metabolic Syndrome and  Its Effects on Cartilage Degeneration vs Regeneration: A Pilot Study  Using Osteoarthritis Biomarkers. JOIO. Published online July 24, 2020.  doi:10.1007/s43465-020-00145-z ABSTRACT
18. Saleem  U, Mosley TH, Kullo IJ. Serum Osteocalcin Is Associated With Measures  of Insulin Resistance, Adipokine Levels, and the Presence of Metabolic  Syndrome. Arterioscler Thromb Vasc Biol. 2010;30(7):1474-1478. doi:10.1161/ATVBAHA.110.204859
19. Bilinski  WJ, Szternel L, Siodmiak J, et al. Effect of fasting hyperglycemia and  insulin resistance on bone turnover markers in children aged 9–11 years.  Journal of Diabetes and its Complications. Published online July 30, 2021:108000. doi:10.1016/j.jdiacomp.2021.108000 ABSTRACT
20. Crivelli  M, Chain A, da Silva ITF, Waked AM, Bezerra FF. Association of Visceral  and Subcutaneous Fat Mass With Bone Density and Vertebral Fractures in  Women With Severe Obesity. Journal of Clinical Densitometry. Published online October 16, 2020. doi:10.1016/j.jocd.2020.10.005
21. Bredella MA, Fazeli PK, Bourassa J, et al. The Effect of Short-Term High-Caloric Feeding and Fasting on Bone Microarchitecture. Bone. Published online September 24, 2021:116214. doi:10.1016/j.bone.2021.116214

Reviews 

1. Cooper  ID, Brookler KH, Crofts CAP. Rethinking Fragility Fractures in Type 2  Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas. Biomedicines. 2021;9(9):1165. doi:10.3390/biomedicines9091165
2. Lecka-Czernik B. Diabetes, bone and glucose-lowering agents: basic biology. Diabetologia. 2017;60(7):1163-1169. doi:10.1007/s00125-017-4269-4 
3. Fernandes  TAP, Gonçalves LML, Brito JAA. Relationships between Bone Turnover and  Energy Metabolism. Journal of Diabetes Research. 2017. doi:10.1155/2017/9021314 
4. Gravenstein  KS, Napora JK, Short RG, et al. Cross-Sectional Evidence of a Signaling  Pathway from Bone Homeostasis to Glucose Metabolism. J Clin Endocrinol  Metab. 2011;96(6):E884-E890. doi:10.1210/jc.2010-2589 
5. Kawai  M, de Paula FJA, Rosen CJ. New Insights into Osteoporosis: The Bone-Fat  Connection. J Intern Med. 2012;272(4):317-329. doi:10.1111/j.1365-2796.2012.02564.x 
6. Merlotti  D, Cosso R, Eller-Vainicher C, et al. Energy Metabolism and Ketogenic  Diets: What about the Skeletal Health? A Narrative Review and a  Prospective Vision for Planning Clinical Trials on this Issue. Int J Mol Sci. 2021;22(1). doi:10.3390/ijms22010435

Fractures are breaks or cracks in bones that can occur due to trauma, overuse, or underlying medical conditions. They can range from minor hairline fractures to severe breaks that require surgical intervention. Fractures are typically classified based on various factors including their location, severity, and whether the bone has broken completely or partially.

Hyperinsulinemia, insulin resistance, and metabolic syndrome are all conditions related to abnormal insulin function and metabolism. Here's how they can contribute to fractures and influence recovery:

1. Hyperinsulinemia: This refers to high levels of insulin circulating in the bloodstream. Insulin is a hormone produced by the pancreas that helps regulate blood sugar levels. Elevated insulin levels can lead to increased bone resorption, where bone tissue is broken down faster than it is replaced. This imbalance in bone remodeling can weaken bones and increase the risk of fractures.
2. Insulin Resistance: Insulin resistance occurs when cells in the body become less responsive to the effects of insulin. As a result, the pancreas produces more insulin to compensate for this resistance. Insulin resistance has been associated with decreased bone mineral density (BMD), which is a measure of bone strength. Lower BMD is a risk factor for fractures as bones become more fragile and prone to breaking.
3. Metabolic Syndrome: Metabolic syndrome is a cluster of conditions that includes abdominal obesity, high blood pressure, high blood sugar levels, and abnormal lipid levels. Individuals with metabolic syndrome often have insulin resistance as a central feature. Metabolic syndrome is associated with several factors that can increase the risk of fractures, including obesity (which can increase stress on bones), inflammation, and altered hormone levels.

Recovery from fractures in individuals with hyperinsulinemia, insulin resistance, or metabolic syndrome can be influenced by several factors:

• Delayed Healing: High insulin levels and insulin resistance may impair the body's ability to heal fractures efficiently. Insulin is involved in the regulation of bone metabolism and plays a role in the formation of new bone tissue. Disrupted insulin signaling can delay the healing process, leading to prolonged recovery times.
• Complications: Individuals with metabolic syndrome may have other health conditions such as cardiovascular disease and diabetes, which can complicate fracture healing. Poorly controlled blood sugar levels can impair wound healing and increase the risk of infection at the fracture site.
• Nutritional Considerations: Proper nutrition is essential for bone health and fracture healing. Individuals with metabolic syndrome may have dietary patterns that are high in processed foods, sugars, and unhealthy fats, which can negatively impact bone health. Ensuring adequate intake of nutrients such as calcium, vitamin D, and protein is important for supporting bone repair and recovery.

In summary, hyperinsulinemia, insulin resistance, and metabolic syndrome can contribute to an increased risk of fractures and may also affect the recovery process by influencing bone metabolism, healing mechanisms, and overall health status. Managing these conditions through lifestyle modifications, medication, and appropriate medical care can help reduce the risk of fractures and support optimal healing.

NOVEMBER 23, 2022 - In a study published in Arthritis  & Rheumatology that included nearly 1.3 million men aged 20–39 years  who participated in three serial health check-ups at two-year  intervals, men with metabolic syndrome (MetS) and those who developed  MetS—especially those with the MetS components of elevated triglycerides  and abdominal obesity—had higher risks of developing gout.

Among  participants, 18,473 developed gout, and those with MetS at all checkups  had a nearly four-fold higher risk than participants who were  MetS-free. Development of MetS more than doubled the risk of incident  gout, whereas recovery from MetS reduced incident gout risk by nearly  half.

“This is the first large-scale study to explore the  association between dynamic changes in MetS and risk of gout,” said  co–corresponding author Jaejoon Lee, MD, PhD of the Sungkyunkwan  University School of Medicine, in South Korea. “Prevention and recovery  from MetS can significantly lower the risk of gout in young adults.”

Conclusion:   Changes in the status and clinical characteristics of metabolic  syndrome were associated with altered risk of incident gout. These  results suggest that metabolic syndrome is a modifiable risk factor for  gout.  

Gout, a type of inflammatory arthritis caused by the buildup of uric acid crystals in the joints, may be influenced by insulin resistance, hyperinsulinemia, or metabolic syndrome in several ways:

1. Increased uric acid levels: Insulin resistance and metabolic syndrome are associated with elevated levels of insulin and glucose, which can lead to increased production of uric acid in the body. Hyperinsulinemia may also reduce urinary excretion of uric acid, further contributing to elevated levels. High uric acid levels increase the risk of gout attacks by promoting the formation of uric acid crystals in the joints.
2. Chronic inflammation: Insulin resistance and metabolic syndrome are characterized by chronic low-grade inflammation, which can exacerbate the inflammatory response in the joints during gout attacks. Chronic inflammation may also contribute to the development of comorbidities commonly associated with gout, such as obesity and cardiovascular disease.
3. Impaired kidney function: Insulin resistance, hyperinsulinemia, and metabolic syndrome can impair kidney function, leading to decreased excretion of uric acid and further elevating uric acid levels in the blood. Impaired kidney function is a risk factor for gout and may worsen the severity of gout attacks.
4. Obesity-related factors: Obesity, a common feature of metabolic syndrome, is a risk factor for gout and is associated with insulin resistance and hyperinsulinemia. Adipose tissue produces cytokines and hormones that promote inflammation and may contribute to the development or exacerbation of gout.
5. Dietary factors: Insulin resistance, hyperinsulinemia, and metabolic syndrome are associated with dietary habits that increase the risk of gout, such as consumption of high-purine foods, sugary beverages, and alcohol. These dietary factors can contribute to elevated uric acid levels and gout attacks.

Overall, insulin resistance, hyperinsulinemia, and metabolic syndrome can increase the risk of gout by promoting elevated uric acid levels, chronic inflammation, impaired kidney function, obesity, and dietary habits that exacerbate the condition. Managing these metabolic abnormalities through lifestyle modifications, medication, or other interventions may help reduce the risk of gout and improve outcomes in affected individuals.

NOVEMBER 23, 2022 - In a study published in Arthritis  & Rheumatology that included nearly 1.3 million men aged 20–39 years  who participated in three serial health check-ups at two-year  intervals, men with metabolic syndrome (MetS) and those who developed  MetS—especially those with the MetS components of elevated triglycerides  and abdominal obesity—had higher risks of developing gout.

Among  participants, 18,473 developed gout, and those with MetS at all checkups  had a nearly four-fold higher risk than participants who were  MetS-free. Development of MetS more than doubled the risk of incident  gout, whereas recovery from MetS reduced incident gout risk by nearly  half.

“This is the first large-scale study to explore the  association between dynamic changes in MetS and risk of gout,” said  co–corresponding author Jaejoon Lee, MD, PhD of the Sungkyunkwan  University School of Medicine, in South Korea. “Prevention and recovery  from MetS can significantly lower the risk of gout in young adults.”

Conclusion:   Changes in the status and clinical characteristics of metabolic  syndrome were associated with altered risk of incident gout. These  results suggest that metabolic syndrome is a modifiable risk factor for  gout.  

1. Jamnik  J, Rehman S, Blanco Mejia S, et al. Fructose intake and risk of gout  and hyperuricemia: a systematic review and meta-analysis of prospective  cohort studies. BMJ Open. 2016;6(10):e013191. doi:10.1136/bmjopen-2016-013191
2. Goldberg  EL, Asher JL, Molony RD, et al. β-hydroxybutyrate deactivates  neutrophil NLRP3 inflammasome to relieve gout flares. Cell Rep.  2017;18(9):2077-2087. doi:10.1016/j.celrep.2017.02.004
3. Juraschek  SP, McAdams-Demarco M, Gelber AC, et al. Effects of Lowering Glycemic  Index of Dietary Carbohydrate on Plasma Uric Acid: The OmniCarb  Randomized Clinical Trial. Arthritis Rheumatol. 2016;68(5):1281-1289.  doi:10.1002/art.39527
4. Dessein  P, Shipton E, Stanwix A, Joffe B, Ramokgadi J. Beneficial effects of  weight loss associated with moderate calorie/carbohydrate restriction,  and increased proportional intake of protein and unsaturated fat on  serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum  Dis. 2000;59(7):539-543. doi:10.1136/ard.59.7.539

Osteoarthritis, a degenerative joint disease, can be influenced by insulin resistance, hyperinsulinemia, or metabolic syndrome in several ways:

1. Chronic inflammation: Insulin resistance and metabolic syndrome are associated with chronic low-grade inflammation, which may contribute to the progression of osteoarthritis by promoting cartilage degradation and joint inflammation. Elevated levels of pro-inflammatory cytokines in individuals with metabolic abnormalities can accelerate the breakdown of cartilage and exacerbate symptoms of osteoarthritis.
2. Obesity-related factors: Obesity, a common feature of metabolic syndrome, is a significant risk factor for osteoarthritis, particularly in weight-bearing joints such as the knees and hips. Excess body weight places increased stress on the joints, leading to accelerated wear and tear of cartilage and an increased risk of osteoarthritis development and progression.
3. Altered lipid metabolism: Dyslipidemia, a common feature of metabolic syndrome, may contribute to the pathogenesis of osteoarthritis through alterations in lipid metabolism. Elevated levels of circulating lipids and cholesterol may promote inflammation and oxidative stress in joint tissues, further exacerbating cartilage damage and contributing to the progression of osteoarthritis.
4. Insulin signaling pathways: Insulin resistance and hyperinsulinemia can dysregulate insulin signaling pathways in joint tissues, potentially affecting cartilage metabolism and repair processes. Impaired insulin signaling may compromise the ability of chondrocytes (cartilage cells) to maintain cartilage integrity and repair damaged tissue, thereby accelerating the progression of osteoarthritis.
5. Mechanical stress: Insulin resistance, hyperinsulinemia, and metabolic syndrome may indirectly contribute to mechanical stress on the joints through obesity-related factors such as excess body weight and altered gait mechanics. Increased mechanical stress on the joints can accelerate cartilage degeneration and worsen symptoms of osteoarthritis.

Overall, insulin resistance, hyperinsulinemia, and metabolic syndrome can exacerbate the progression of osteoarthritis through multiple mechanisms, including chronic inflammation, obesity-related factors, dyslipidemia, dysregulation of insulin signaling pathways, and increased mechanical stress on the joints. Managing these metabolic abnormalities through lifestyle modifications, weight management, exercise, and medical interventions may help mitigate the impact of metabolic syndrome on osteoarthritis and improve outcomes in affected individuals.

Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic inflammation of the joints. While the exact cause of RA is not fully understood, there is evidence to suggest that metabolic factors, including hyperinsulinemia, insulin resistance, and metabolic syndrome, may contribute to the development and progression of the disease.

Here's how these metabolic factors can be related to rheumatoid arthritis:

1. Hyperinsulinemia and Insulin Resistance: Elevated insulin levels and insulin resistance have been associated with chronic low-grade inflammation, which is a hallmark of rheumatoid arthritis. Insulin resistance can lead to dysregulation of inflammatory pathways, contributing to the development and exacerbation of RA symptoms.
2. Metabolic Syndrome: Metabolic syndrome is characterized by a cluster of metabolic abnormalities, including abdominal obesity, hypertension, dyslipidemia, and insulin resistance. Individuals with metabolic syndrome have an increased risk of developing inflammatory conditions like rheumatoid arthritis. Adipose tissue in obesity is known to release pro-inflammatory cytokines and adipokines, which can promote inflammation in joints and exacerbate RA symptoms.

In the context of rheumatoid arthritis, hyperinsulinemia, insulin resistance, and metabolic syndrome can influence the disease in several ways:

• Increased Inflammation: Insulin resistance and metabolic abnormalities can promote systemic inflammation, exacerbating joint inflammation in individuals with rheumatoid arthritis. This heightened inflammatory response can lead to more severe symptoms and joint damage.
• Joint Degeneration: Chronic inflammation associated with insulin resistance and metabolic syndrome can contribute to the progressive degradation of joint tissues, including cartilage and bone. In individuals with rheumatoid arthritis, this can accelerate joint damage and worsen functional impairment.
• Complications and Disease Progression: Metabolic abnormalities can complicate the management of rheumatoid arthritis and may contribute to the progression of the disease. For example, obesity and metabolic syndrome are associated with increased disease activity, decreased response to treatment, and higher rates of comorbidities such as cardiovascular disease.

Managing metabolic factors such as hyperinsulinemia, insulin resistance, and metabolic syndrome through lifestyle modifications (such as diet and exercise), weight management, and appropriate medical treatment may help mitigate inflammation and improve outcomes in individuals with rheumatoid arthritis. Additionally, addressing these metabolic abnormalities may enhance the effectiveness of RA therapies and reduce the risk of complications associated with the disease.

Rheumatoid arthritis (RA) patients have an incidence of cardiovascular  (CV) diseases at least two times higher than the general population.  Atherosclerosis, the main determinant of CV morbidity and mortality, and  carotid intima-media thickness, an early preclinical marker of  atherosclerosis, also occur early on in RA. Traditional CV risk factors  seem to have the same prevalence in RA and non-RA patients, and thus do  not fully explain the increased CV burden, suggesting that RA  inflammation and therapies play a role in increasing CV risk in these  patients. The metabolic syndrome and fat tissue are likely to be the  major players in this complex network. The metabolic syndrome (MetS)  represents a cluster of cardiovascular risk factors that have in common  insulin resistance and increased visceral adiposity. This entity has  received great attention in the last few years due to its contribution  to the burden of cardiovascular morbidity and mortality. Moreover,  recently the adipose tissue has emerged as a dynamic organ that releases  several inflammatory and immune mediators (adipokines). The association  of MetS and atherosclerosis is thought to be partly mediated by altered  secretion of adipokines by the adipose tissue and, on the other hand,  there are evidence that adipokines may play some role in inflammatory  arthritides. Obesity is now regarded as a systemic, low-grade  inflammatory state, and inflammation as a link between obesity,  metabolic syndrome, and cardiovascular diseases. To obtain a full  control of the CV risk, data suggest that it is therefore mandatory a  "tight control" of both RA and MetS inflammations.      

"Fatty acids, such as medium-chain fatty acids (MCFAs) and short-chain  fatty acids (SCFAs), both important components of a normal diet, have  been reported to play a role in bone-related diseases such as rheumatoid  arthritis (RA). However, the role of medium-chain triglycerides (MCTs)  has not been investigated in RA to date. The aim of this study was to  investigate the effect of supplementation of regular diet with MCT with  and without fiber on disease activity as measured with the SDAI  (Simplified Disease Activity Index) in RA patients. A total of 61 RA  patients on stable drug treatment were randomly assigned to a  twice-daily control regimen or to a twice-daily regimen of a formulation  containing medium-chain triglycerides (MCTs) 30 g/day for 8 weeks  followed by a second twice-daily regimen of combining MCT (30 g/day)  plus fiber (30 g/day) for an additional 8 weeks. The control group  received a formulation containing long-chain triglycerides (LCTs)  instead of MCTs. The preliminary results showed a significant reduction  in SDAI from baseline to week 16 in the test group and a significant  increase in β-hydroxybutyrate (BHB) levels, while no improvement in SDAI  was observed in the control group.      

 Medium chain fatty  acids (MCFAs) has unique transport system and is rapidly metabolized in  the body. It mainly occurs in coconut oil, palm kernel oil and milk  products. Dietary supplementation with MCFAs can improve metabolic features as well as cognition in humans. 

(Available lipid emulsions made from soybean or safflower oil are classified as long-chain triglycerides (LCT). In contrast,  medium-chain triglyceride (MCT) emulsions have different physical  properties and are metabolized by other biochemical pathways). 

MetS frequency was higher in RA patients than in controls. Among RA patients, MetS was associated with disease activity. The higher prevalence of cardiovascular risk factors in RA suggests that inflammatory processes play a notable role in the development of cardiovascular disease (CVD), and indicates that tight control of systemic inflammatory activity and CVD modifiable risk factors should be recommended. 

" Various nutritional therapies have been proposed in rheumatoid  arthritis, particularly diets rich in ω-3 fatty acids, which may lead to  eicosanoid reduction. Our aim was to investigate the effect of  potentially anti-inflammatory diets (Mediterranean, vegetarian, vegan,  ketogenic) on pain 

 The main conclusion is that anti-inflammatory diets resulted in significantly lower pain than ordinary diets  "

Teeth are hard, mineralized structures found in the mouths of vertebrates, including humans. They are specialized organs that serve several important functions, including:

1. Mastication (Chewing): Teeth are essential for breaking down food into smaller particles during the process of chewing, which helps facilitate digestion and nutrient absorption.
2. Speech: Teeth play a role in articulating speech sounds by controlling the flow of air through the mouth.
3. Aesthetics: Teeth contribute to facial aesthetics and appearance, impacting smile and facial structure.

Teeth are composed of several layers of tissue, including:

1. Enamel: Enamel is the hardest and outermost layer of the tooth, consisting mainly of calcium hydroxyapatite crystals. It serves as a protective covering for the underlying tooth structures.
2. Dentin: Dentin is a hard, calcified tissue located beneath the enamel. It makes up the bulk of the tooth structure and provides support and strength.
3. Pulp: The pulp is the innermost part of the tooth, containing blood vessels, nerves, and connective tissue. It nourishes and maintains the vitality of the tooth.

Teeth are anchored within the jawbones by specialized connective tissues called periodontal ligaments, which attach the tooth roots to the surrounding bone. Teeth vary in shape and size depending on their location and function within the mouth. For example, incisors are sharp-edged teeth used for cutting, canines are pointed teeth used for tearing and piercing, and molars are flat-surfaced teeth used for grinding and crushing food.

Humans typically have two sets of teeth during their lifetime: primary (baby) teeth and permanent (adult) teeth. Primary teeth begin to erupt around 6 months of age and are gradually replaced by permanent teeth starting around age 6 and continuing into early adulthood. Permanent teeth include incisors, canines, premolars, and molars, and the full set typically consists of 32 teeth in adults.

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