The Many Risks Of Osteoporosis

“Osteo” means bone, and “porosis” means porous. Osteoporotic bones become more porous with less solid and less dense bone masses. Bone is an active tissue where new bone is being made continuously by osteoblasts, the bone forming cells, and old bone is removed by osteoclasts, the bone resorbing cells, via a process known as remodeling. In childhood, more bone is built than removed, and so the bones grow in both mass and size. In older age, osteoporosis results from increased bone resorption and decreased bone formation. The cells that build new bone do not keep up with those that remove bone. The total amount of bone mass then decreases, and osteoporosis may develop as a result. This condition finally makes bone thinner, weaker and more fragile, ultimately leading to loss of their structural and functional protein framework.

Osteoporosis is a chronic disease affecting one in three women and one in five men over the age of 50 years. Overall, risk factors for osteoporosis include disease activity, age, gender, and menopausal status. Unfortunately, in the daily practice, osteoporosis treatment too often consists of drug prescription, without any other preventive or therapeutic measure. Besides drug prescription, non-pharmacological osteoporosis management is important. Diets deficient in calcium, proteins or vitamin D impair skeletal integrity. Most experts think that the role of diet, including alcohol, caffeine, and phytic acid, on bone quality is complex and the optimal health of the skeleton requires a good equilibrium between all nutrients. As already mentioned above, it is probable that mononutrient supplementation, as frequently recommended in several diets will not necessarily lead to an adequate bone quality.

Bone quantity, quality, and turnover contribute to whole bone strength. Although bone mineral density, or bone quantity, is associated with increased fracture risk, less is known about bone quality. Bone mineral density (BMD) is a strong predictor of fracture, yet most fractures occur in women without osteoporosis by BMD criteria. Various conditions, including disorders of mineral homeostasis, disorders in bone remodeling, collagen disorders, and drugs, affect bone quality. Bbehavioral factors such as cigarette smoking or physical inactivity also play an important role. Additionally, the role of diet, including alcohol, caffeine, and phytic acid, on bone quality is complex; therefore, further review in this particular issue is warranted.



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Calcium is a macromineral that plays an important role in bone health, muscle contraction, blood clotting, nerve conduction, enzyme regulation, and possibly weight loss (Guéguen and Pointillart, 2000; Tremblay and Gilbert, 2011). In humans, intestinal calcium absorption is controlled by complex homeostatic mechanisms involving calcitriol and the parathyroid hormone (PTH). Calcitriol (1,25(OH2) vitamin D3) increases the synthesis of a cytosolic calcium-binding protein (calbindin) resulting in increased calcium transport in intestinal cells.

Excesses in sodium intake have a negative impact on calcium balance by increasing the urinary calcium excretion. For every 100 mmol of sodium excreted, approximately 1 mmol loss of urinary calcium is observed. It has been suggested, however, that enough calcium in the diet could overcome the salt deleterious effect. There could be 2-fold differences in sodium-induced calciuria with low and high calcium intakes.

The role of protein intake remains controversial in the development of osteoporosis. Excessive protein intake can be responsible for a metabolic increase of acid production and acid renal excretion, with increased calciuria potentially favouring bone loss and hip fracture. Research has shown that higher-protein diets do promote increased excretion of Ca in the urine, which is taken to suggest adverse effects on bone or to support the impact of bone loss. The underlying premise is that an HP (especially animal protein) diet creates a higher acid load due to the high S amino acid content, which cannot be neutralised by the kidneys. To compensate, the body pulls Ca from the skeleton to balance the pH at the expense of the bone structure, and Ca is excreted in the urine. However, few studies have supported this theory. gative effects of the acid load of protein on bone health. On the basis of recent findings, consuming protein (including that from meat) higher than current RDA for protein is beneficial to Ca utilisation and bone health, especially in the elderly. A HP diet with adequate Ca and fruits and vegetables is important for bone health and osteoporosis prevention.3

Potassium content, high in fruits and vegetables has a protective effect against urinary calcium loss. However, this positive effect can be completely offset by a low calcium intake or a reduction in intestinal absorption. The best way to preserve the body calcium economy is to encourage the consumption of foods such as dairy products, which are rich in calcium, proteins, phosphorus, and potassium.

Calcium has to be soluble in the gastrointestinal tract before it can be absorbed. Certain dietary factors can impact calcium solubility, thereby affecting calcium bioavailability at the absorptive surface of intestinal cells. Components in plant foods like phytate can form insoluble complexes with calcium, thereby reducing its bioavailability. Phytate's inhibitory role on calcium absorption is significant only when the phytate to calcium molar ratio is above a certain value; below that value, the inhibitory effect is trivial. Alginic acid, guar gum, and locust bean gum are used as thickeners reduce calcium availability.4 Overall, high-fibre diets (≥30 g/day) could provoke a 20–30% decrease in intestinal calcium absorption.

Osteoporosis is generally considered to be a disease of the elderly, yet it may present in a bowel disease patient of any age. Osteoporosis may also be the initial sign of bowel disease in otherwise asymptomatic patients, who then may be referred to a gastroenterologist for further evaluation and management. Osteoporosis is common in gastrointestinal diseases, particularly those associated with malabsorption and maldigestion (celiac disease, postgastrectomy, short gut, pancreatic insufficiency); inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis); chronic liver disease (cholestatic and hepatocellular diseases); or may be secondary to therapy for GI disease (liver and small bowel transplant, total parenteral nutrition, gastric bypass, or medications such as proton pump inhibitors [PPIs] in gastroesophageal reflux disease [GERD] patients).

Celiac patients are prone to vitamin D and calcium malabsorption, reduced calcium intake, secondary hyperparathyroidism, and neutralizing antibodies to osteoprotegerin, all leading to an increased fracture risk. Low BMI, insulin-like growth factor (IGF-10), and leptin levels also contribute to a reduced BMD, which improves with therapy. Asymptomatic celiac patients may present only with low bone density.

There are also links between the immune system and bone at the anatomical, vascular, cellular, and molecular levels. In both rheumatoid arthritis (RA) and ankylosing spondylitis (AS), bone is a target of inflammation. Activated immune cells at sites of inflammation produce a wide spectrum of cytokines in favor of increased bone resorption in RA and AS, resulting in bone erosions, osteitis, and peri-inflammatory and systemic bone loss. Peri-inflammatory bone formation is impaired in RA, resulting in non-healing of erosions, and this allows a local vicious circle of inflammation between synovitis, osteitis, and local bone loss.

Can depression cause osteoporosis? Yes, chronic stress can cause breakdown of energy stores and body tissues. Major depression and anorexia nervosa are associated with elevation of serum cortisol levels and with increased bone loss. Increased sympathetic nervous system activity stimulates resorption of bone by osteoclasts and inhibits bone formation by osteoblasts.

How much vitamin A is harmful for bones? Vitamin A (retinol) intake of more than 3000 mcg/day, both from food ad supplements, is associated with a significantly increased risk of hip fracture. Consumers should use supplements that contain less than 2000 mcg of retinol, or preferably products that contain only beta-carotene or mixed carotenoids.

Is caffeine harmful for bones? Moderate caffeine intake, about 2 cups a day, is considered safe, while excessive caffeine intake, which amounts to 300 mg caffeine a day, or 4 cups of coffee or caffeinated soft drinks, is associated with a modest increase in the risk of fracture in women who also have low calcium intake.

Can hot dogs cause osteoporosis Hot dogs and processed cheese contain additives such as phosphorus. Although phosphorus is required to form a key component of bone, hydroxyapatite, excessive intake of phosphorus may be harmful to bone health. The Recommended Daily Allowance (RDA) is 700 mg, while processed foods can add additional 1000 mg per day.

I have inflammatory bowel disease (IBD). Will I have osteoporosis? Osteoporosis is common in gastrointestinal diseases, particularly those associated with poor absorption and digestion, such as celiac disease, short gut and pancreatic insufficiency. Inflammatory bowel disease, such as IBD, Crohn's disease and ulcerative colitis also increase osteoporosis risks. Proton pump inhibitor type medications used in the treatment of gastroesophageal reflux disease (GERD) also may affect calcium absorption by your body and cause osteoporosis.

Can eating meat increase the risk for osteoporosis? The role of protein intake remains controversial in the development of osteoporosis. On the one hand, excessive protein intake can be responsible for an increase of acid production with increased excretion of calcium in the urine potentially resulting in bone loss and hip fracture. On the other hand, in postmenopausal women, but also in men, increased protein intake favorably affects bone mineral density and decreases the risk of hip fracture.

Should I eat more whole grains to prevent osteoporosis? High-fibre diets ( more than 30 g/day) could provoke a 20–30 percent decrease in intestinal calcium absorption, but the effect on the bone health has not been clearly settled. High-fiber fruits and vegetables include artichoke, green peas, split peas, lentils, black beans, lima beans, baked beans, broccoli, whole-wheat pasta and baked goods, raspberries, pears, and oat bran. Components in plant foods like phytates in whole grain baked goods, seeds and tree nuts can form insoluble complexes with calcium, thereby reducing its absorption. Certain thickeners such as alginic acid, guar gum, and locust bean gum can also reduce calcium absorption.

What diseases are associated with osteoporosis? Osteoporosis is generally considered to be a disease of the elderly, yet it is seen in persons with bowel disease of any age. Osteoporosis is common in gastrointestinal diseases, particularly those associated with poor absorption and digestion (celiac disease, postgastrectomy, short gut, pancreatic insufficiency); inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis) and chronic liver disease (cholestatic and hepatocellular diseases). Osteoporosis can also result from therapy for liver and small bowel transplant, total parenteral nutrition, gastric bypass, or medications such as proton pump inhibitors [PPIs] in gastroesophageal reflux disease [GERD] patients). In recent years, it was demonstrated that bone metabolism is influenced by some atherosclerosis-inducing disorders such as diabetes mellitus, dyslipidemia, hypertension, and chronic kidney disease. In particular, osteoporosis caused by diabetes mellitus or chronic kidney disease is established as "osteoporosis secondary to lifestyle-related diseases."

What are the signs of osteoporosis besides fractures Osteoporosis affects all bones, including facial skeleton. Hearing loss and poor dentition are sometimes seen in patients with osteoporosis. If you have a gastrointestinal disease, particularly one associated with poor absorption and digestion (celiac disease, postgastrectomy, short gut, pancreatic insufficiency), inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis) or chronic liver disease (cholestatic and hepatocellular diseases), you should ask your doctor for osteoporosis evaluation.

Can chronic inflammation cause osteoporosis? In both rheumatoid arthritis (RA) and ankylosing spondylitis (AS), bone is a target of inflammation. Activated immune cells at sites of inflammation produce a wide range of chemicals that promote increased bone resorption, resulting in bone erosions and bone loss. Bone formation at sites of inflammation is impaired in RA, resulting in non-healing of erosions, and this allows a local vicious circle of inflammation between inflammatory bone diseases and local bone loss.

What other mineral deficiencies besides calcium may cause osteoporosis? Copper deficiency can cause osteoporosis, which is thought to occur because of defective cross-linking of collagen fibers. Nutrients needed to build bones include calcium, magnesium and manganese; they should be consumed regularly during childhood and adolescence. Foods rich in boron, a trace element that can conserve calcium stores in bone, should also be consumed in adequate amounts. Boron-rich foods include cabbage, dates, peas, almonds, beans, hazelnuts, apples, and raisins.

References

  1. Diseases Affecting Bone Quality: Beyond Osteoporosis. Aasis Unnanuntana, MD, Brian J. Rebolledo, BA, M. Michael Khair, MD, Edward F. DiCarlo, MD, and Joseph M. Lane, MD
  2. Non-pharmacological management of osteoporosis: a consensus of the Belgian Bone Club. J.-J. Body, P. Bergmann, S. Boonen, Y. Boutsen, Bruyere, J.-P. Devogelaer, S. Goemaere,6 N. Hollevoet, J.-M. Kaufman, K. Milisen, S. Rozenberg, and J.-Y. Reginster
  3. Safety and efficacy of high-protein diets for weight loss. Alexandra M. Johnstone, Rowett Institute of Nutrition and Health, University of Aberdeen
  4. Application of in vitro bioaccessibility and bioavailability methods for calcium, carotenoids, folate, iron, magnesium, polyphenols, zinc, and vitamins B6, B12, D, and E. Paz Etcheverry, Michael A. Grusak, and Lisa E. Fleige
  5. Japanese 2011 guidelines for prevention and treatment of osteoporosis—executive summary. Hajime Orimo et al.
  6. Osteoporotic fracture and parathyroid hormone. Nabanita S Datta
  7. Osteoporosis and Gastrointestinal Disease. Seymour Katz, MD, FACP, MACG and Stuart Weinerman, MD, FACP
  8. Integrative Medicine. Elsevier Health Sciences 2012



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