VITAMIN D: Its importance for Bone and Systemic Health by A/Prof Terry Diamond Vitamin D is an essential regulator of calcium homeostasis, cellular division and immune function. It is therefore not withstanding that vitamin D deficiency can result in an array of medical disorders such as abnormal bone metabolism and osteoporosis, cellular dedifferentiation and cancer and immune derangement and auto-immune disorders. The active vitamin D metabolite, 1,25 dihydroxyvitamin D, is central to the regulation of vitamin D physiology. Vitamin D deficiency and bone: Vitamin D is very important for maintaining normal bone integrity and calcium balance. It is predominantly responsible for most of the calcium absorption from the gut. A mild deficiency in vitamin D is referred to as vitamin D insufficiency. This may lead to a transient decrease in circulating blood calcium levels leading to a compensatory increase in parathyroid hormone production that activates bone resorbing cells to replenish the calcium deficiency from skeletal stores causing high bone turnover. If untreated and chronic, age- related bone loss is accelerated, predominantly from areas such as the hip. This may result in increased risk of osteoporosis and hip fractures. Serum 25 hydroxyvitamin D concentrations are usually reduced to levels between 30-50 nmol/L. True or severe vitamin D deficiency is also termed osteomalacia or in children called Rickets. Serum 25 hydroxyvitamin D concentrations levels are usually less than 12.5 nmol/L. Patients often present with bone and muscle pains, weakness and multiple stress or fragility fractures. Many patients are frequently misdiagnosed with conditions such as fibromyalgia or rheumatism. Bone fragility may occur at any site, but fractures are more commonly found to involve the pelvis, sacro-iliac bones and the proximal regions of long bones. Due to the chronicity of this disorder, progressive bone loss is often evident and osteoporosis co-exists. Many patients presenting today with fragility fractures have a combination of both osteoporosis and vitamin D deficiency. Figure 1: Example of fragility fractures occurring with vitamin D deficiency X-RAY: Osteoporotic hip fracture, treated by surgical stabilizion. X-RAY: Stress fracture of femoral shaft (crack or called “loosers” zone). Bone Biopsy: Classical osteomalacia - decreased bone volume (blue) and increased osteoid or unmineralised bone (orange).
Transcript
VITAMIN D: Its importance for Bone and Systemic Healthby A/Prof Terry Diamond
Vitamin D is an essential regulator of calcium homeostasis, cellular division and immune function. It is therefore not withstanding that vitamin D deficiency can result in an array of medical disorders such as abnormal bone metabolism and osteoporosis, cellular dedifferentiation and cancer and immune derangement and auto-immune disorders. The active vitamin D metabolite, 1,25 dihydroxyvitamin D, is central to the regulation of vitamin D physiology.
Vitamin D deficiency and bone:Vitamin D is very important for maintaining normal bone integrity and calcium balance. It is predominantly responsible for most of the calcium absorption from the gut. A mild deficiency in vitamin D is referred to as vitamin D insufficiency. This may lead to a transient decrease in circulating blood calcium levels leading to a compensatory increase in parathyroid hormone production that activates bone resorbing cells to replenish the calcium
deficiency from skeletal stores causing high bone turnover. If untreated and chronic, age-related bone loss is accelerated, predominantly from areas such as the hip. This may result in increased risk of osteoporosis and hip fractures. Serum 25 hydroxyvitamin D concentrations are usually reduced to levels between 30-50 nmol/L.
True or severe vitamin D deficiency is also termed osteomalacia or in children called Rickets. Serum 25 hydroxyvitamin D concentrations levels are usually less than 12.5 nmol/L. Patients often present with bone and muscle pains, weakness and multiple stress or fragility fractures. Many patients are frequently misdiagnosed with conditions such as fibromyalgia or rheumatism. Bone fragility may occur at any site, but fractures are more commonly found to involve the pelvis, sacro-iliac bones and the proximal regions of long bones. Due to the chronicity of this disorder, progressive bone loss is often evident and osteoporosis co-exists. Many patients presenting today with fragility fractures have a combination of both osteoporosis and vitamin D deficiency.
Figure 1: Example of fragility fractures occurring with vitamin D deficiency
X-RAY: Osteoporotic hip fracture, treated by surgical stabilizion.
X-RAY: Stress fracture of femoral shaft (crack or called “loosers” zone).
Bone Biopsy: Classical osteomalacia - decreased bone volume (blue) and increased osteoid or unmineralised bone (orange).
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Vitamin D deficiency, muscle function and falls:Falls remain a crucial part to the pathogenesis of osteoporotic fractures. Vitamin D deficiency has been demonstrated to be an independent predictor of falls in the elderly. The findings that 1,25 dihydroxyvitamin D may effect skeletal muscle function have gained much attention in recent years. Vitamin D has been shown to be responsible for the active transportation of calcium into the muscle cells and regulation of muscle function.
In osteomalacia (severe vitamin D deficiency), a metabolic myopathy has been noted, consisting histologically of atrophied type 2 muscle fibres with fat infiltration, fibrosis and glycogen granules. Patients present typically with gait (walking) disturbances and difficulties in climbing from a chair. More recently, an increased in body sway and quadriceps (thigh) muscle weakness have been reported with serum 25OHD levels below 20-30 nmol/L. These findings suggest a link between vitamin D deficiency, falls and osteofragility fractures.
Who is at risk of Vitamin D deficiency?Vitamin D metabolites decrease by approximately 40-50% after age 65 resulting in approximately a 40% reduction in calcium absorption. This may occur as a result of age-related factors (such as reduced intake, diminished sunlight exposure, low previtamin D3 synthesis and decline in renal function) and secondary causes (Table 1).
Causes of Vitamin D deficiency (Table 1):1. Reduced intake or conversion of vitamin D
pigmentation, ageing, veiling, sunscreens, avoidance of sun due to chronic skin disorders or cancers)
2. Reduced absorption of vitamin D from the gut. - pancreatic and bile duct disorders - Small bowel disorders – celiac disease,
inflammatory bowel disorders, and small bowel resection.
3. Reduced synthesis of 25 vitamin D - chronic liver diseases – hepatitis, cirrhosis - chronic anti-convulsant therapies (epilepsy)
4. Reduced synthesis of 1,25 dihydroxyvitamin D - chronic renal disease
Therapeutic effects of Vitamin D on bone: Vitamin D and its analogues correct vitamin D deficiency by normalizing parathyroid function, establishing normal bone turnover, increasing bone mass, reducing falls and fracture risk.
Adequate sunlight exposure remains the simplest effective therapy to treat vitamin D deficiency, but this has to be balanced by the maximal erythematous dose of ultraviolet radiation hat may cause skin damage. Oral preparations such as ergocalciferol, cholecalciferol and calcitriol (1,25 dihydroxyvitamin D ) are available in Australia to treat vitamin D deficiency.
While the daily requirements for vitamin D is probably between 1-2000 IU per day, a much larger dose is required to treat vitamin D deficient patients. Vitamin D is stored in fat and slowly released. Ideally, and in order to facilitate compliance in elderly patients, vitamin D can be administered either orally or by intramuscular injection as a monthly (50,000 IU), 4 monthly (100,000 IU), 6 monthly (300,000 IU) or even 12 monthly (600,00 IU) dose. These dosage regimens are considered safe provided patients do not have underlying conditions associated with hypercalcemia. Calcitriol, is not considered ideal for treating patients with simple vitamin D deficiency.
The greatest therapeutic effect of vitamin D supplementation is seen in high risk individuals who demonstrate increases in bone densities, ranging from 0-4% in vitamin D insufficient patients and from 10-40% in vitamin D deficient patients (with osteomalacia). Vitamin D supplements have been shown to reduce vertebral fracture risk by 37% and non-vertebral fracture (hip and wrist) risk by 23% in patients with vitamin D insufficiency. Optimal vitamin D supplementation is therefore essential for all patients presenting with osteoporosis or fragility fractures.
VITAMIN D: Its importance for Bone and Systemic Health (cont’)by A/Prof Terry Diamond
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VITAMIN D: Its importance for Bone and Systemic Health (cont’)by A/Prof Terry Diamond
10 important facts relating to vitamin D:1. Vitamin D is important for all cellular function.
2. Vitamin D deficiency results in calcium malabsorption from the gut.
3. Chronic vitamin D deficiency results in increased parathyroid hormone activity, liberation of calcium from skeletal bone stores, osteoporosis and increased risk of fragility fractures.
4. Patients with serum 25 hydroxyvitamin D levels of less than 50 nmol/L are at risk.
5. High risk individuals include: the elderly, those who avoid sunlight due to medical reasons or are institutionalised, those who are modestly clothed (veiled) for religious reasons, overzealous use of block-out sunscreens, individuals from the Horn of Africa, Middle-East and Asia, those with secondary medical disorders such as chronic hepato-biliary and renal disease and obese individuals undergoing bariatric surgery for their metabolic disorder.
6. Correcting the Vitamin D deficiency with optimal therapy reduces fracture risk by increasing bone strength and reducing falls risk.
7. Serum 25 hydroxyvitamin D level of greater than 70-80 nmol/L is considered optimal for restoring good “bone health”.
8. The principle source of vitamin D is from sunlight.
9. Vitamin D supplements should always be administered with adequate calcium supplements (because of the combined deficiency) to be most effective.
10. The recommended daily vitamin requirement is controversial, but dosage of 1-2000 IU per day is considered optimal for all body functions. Larger dosages of greater than 5000 IU per day may be required to correct vitamin D deficiency.
Food Fact: Carrots Nutrition InfoCarrots are also a very good source of dietary fiber, vitamin C, vitamin K, folate and manganese, and a good source of vitamin B6, pantothenic acid, iron, potassium and copper. The orange-colored taproot of the carrot contains a high concentration of beta-carotene. Beta-carotene is a substance that is converted to vitamin A in the human body. A 1/2 cup serving of cooked carrots contains four times the recommended daily intake of vitamin A in the form of protective beta-carotene.
Health BenefitsBeta-carotene is also a powerful antioxidant effective in fighting against some forms of cancer, especially lung cancer. Current research suggests that it may also protect against stroke, and heart disease. Research also shows that the beta-carotene in vegetables supplies this protection, not vitamin supplements. Carrots can be eaten raw or cooked, but to obtain maximum benefit it is best to eat them raw.
Did You Know?Alcohol increases your risk for fractures!Alcohol causes a dysfunction of the cells that form bone and decrease in the quality of the bone that is formed. In a study of 84,484 American women aged 34-59, alcohol intake was independently associated with increased risk of both hip and forearm fractures. Compared to non drinkers, women consuming more than 25g alcohol/day had an increased risk for both hip and forearm fractures. In a study by Professor Diamond, forearm bone mineral densities, spinal bone mineral densities and iliac crest cancellous bone areas were significantly lower in the patients drinking alcohol compared to patients that do not drink alcohol.
