1. Vitamin D Deficiency and Prevention
Dr. Asif Rehman

2. Vitamins Fat soluble: (Vitamin A, D, E, K)
Water soluble: (Vitamin B & C)
Each vitamin has specific function to perform and deficiency of any particular vitamin may lead to specific deficiency disease.

3. Vitamin D Deficiency
Vitamin D deficiency prevails in epidemic proportions all over subcontinent, with a prevalence of 70%–100% in the general population
Vitamin D deficiency is highly prevalent in both urban and rural settings and across all socioeconomic and geographic strata.
A study done by (Riaz H et al, 201d) on Vit D deficiency on 4830 randomly selected people in Pakistan found 53.5% deficient (less then 20ng/ml) 31.2% insufficient (20-29ng/ml) and 15.3% sufficient (above 30ng/ml).
Another study done by (Ritu et al, 2014) on Vit D deficiency in 18 cities in India found 79% deficient (less then 20ng/ml) 15% insufficient (20-29ng/ml) and 6% sufficient (above 30ng/ml).

4. Vitamin D
The two major physiologically relevant forms of vitamin D are
D2 (Ergocalciferol)
D3 (Cholecalciferol).
Vitamin D3 is photosynthesized in the skin of vertebrates by the action of solar ultraviolet (UV)B radiation on 7 dehydrocholesterol
Vitamin D2 is produced by UV irradiation on Ergosterol, which occurs in molds, yeast, and higher-order plants.
Under conditions of regular sun exposure, dietary vitamin D intake is of minor importance.

5. Sources Vitamin D is found in: Animal fats, Liver.
Fish-liver oils, fatty fish,
Mushrooms, egg yolks
Butter & Milk
Most of the dietary intake of vitamin D comes from fortified milk products and other fortified foods such as breakfast cereals and orange juice

6. 25-hydroxy vitamin D
Vitamin D from the skin or diet is only short-lived in circulation (with a half-life of (1–2 days), as it is either stored in fat cells or metabolized in the liver (Mawer 1972).
In circulation, vitamin D is bound to vitamin D-binding protein and transported to the liver, where it is converted to 25-hydroxyvitamin D [25(OH)D] (DeLuca 1984). This major circulating form of vitamin D is a good refection of cumulative effects of exposure to sunlight and dietary intake of vitamin D (Haddad 1973; Holick 1995)
25(OH)D is converted in the kidneys to 1,25-dihydroxyvitamin D [1,25(OH)2D], which is thought to be responsible for most, if not all, of the biologic functions of vitamin D
25-hydroxyvitamin D is used by clinicians to determine vitamin D status.

7. Function of Vit D
Active vitamin D functions as a hormone, and its main biologic function in people is to maintain serum calcium and phosphorus concentrations within the normal range by enhancing the efficiency of the small intestine to absorb these minerals from the diet (DeLuca 1988; Reichel 1989).
When dietary calcium intake is inadequate to satisfy the body’s calcium requirement, 1,25(OH)2D, along with PTH, mobilizes calcium stores from the bone. In the kidney, 1,25(OH)2D increases calcium reabsorption by the distal renal tubules.

8. Causes
Rickets:
Usually observed in young children between 6 month to 2 yrs.
Reduce calcification of growing bone
Characterized by growth failure, bone deformity, muscular hypotonia, dental hypoplasia and convulsion due to hypocalcaemia.
The bone deformities includes curved legs, deformed pelvis, Pigeon chest, Harrison Sulcus and frontal bossing.
Osteomalacia:
Occurs mainly in women specially during pregnancy & lactation when requirement in increased.

9. Rickets

10. Who is at risk
Worldwide, naturally occurring dietary sources of vit D are limited, and food fortification is optional, inconsistent, inadequate, or nonexistent.
Vitamin D is primarily obtained by cutaneous production from sun exposure. However, many variables influence the amount of UVB from sunlight that reaches the skin and its effectiveness. These include time of day, season, latitude, altitude, clothing, sunscreen use, pigmentation, and age.
Even those who normally reside in sunny climates are commonly found to be deficient in vit D, probably due to cultural habits and/or dress. Even if regularly exposed to sunlight, elderly people produce 75% less cutaneous D than young adults.
Further barriers to cutaneous vitamin D production are ongoing public health campaigns promoting sunscreen use.

11. Who should be tested for Vit D Defeciency
Although vitamin D deficiency is prevalent, measurement of serum 25(OH)D levels is expensive, and universal screening is not supported.
However, vitamin D testing may benefit those at risk for severe deficiency or those with laboratory or radiographic findings commonly associated with vitamin D deficiency. E.g (Low 24-hour urine calcium excretion, Elevated parathyroid hormone level, Elevated total or bone alkaline phosphatase level, Low serum calcium or serum phosphorus level, Decreased bone mineral density (osteopenia or osteoporosis) Non traumatic (fragility) fracture.
Vit D supplementation without testing can be justified for patients who have no overt risk factors or evidence of deficiency but are thought to have inadequate sun exposure or dietary intake.

12. Who should be tested for Vit D Defeciency
It has been suggested that clinicians should routinely test for hypovitaminosis D in patients with musculoskeletal symptoms, such as bone pain, myalgias, and generalized weakness.
Some studies and numerous anecdotal observations report vitamin D deficiency in 80% to 90% of children and adults with pain, myalgias, and weakness.

13. Risk factor for Vit D Deficiency
Decreased intake: Inadequate oral intake, Malnutrition (poor oral intake) Limited sun exposure.
Gastrointestinal: Malabsorption (short bowel syndrome, pancreatitis, inflammatory bowel disease, amyloidosis, celiac sprue, and mal- absorptive bariatric surgery procedures)
Hepatic : Some antiepileptic medications (increased 24-hydroxylase activity), Severe liver disease or failure (decreased 25-hydroxylase activity)
Renal: Aging (decreased 1-α hydroxylase activity), Renal insufficiency, glomerular filtration rate <60% (decreased 1-α hydroxylase activity), Nephrotic syndrome (decreased levels of vitamin D–binding protein)

14. Reference range of [25 (OH)D] (to convert to nmol/L, multiply by 2
Severity
Range
Severe deficiency
<10 ng/mL
Mild to moderate deficiency
10-24 ng/mL
Optimal
25-80 ng/mL
Possible Toxicity
>80 ng/mL

15. Prevention
Educating parents to expose their children regularly to sunshine.
Vitamin D fortification food, specially Milk.
Periodic dosing of young children with Vitamin D.

16. Prevention
What constitutes the optimal intake of vitamin D remains a matter of some disagreement. Current daily recommendations from the Institute of Medicine US (1997) call for :
200 IU from birth through age 50
400 IU for those aged 51–70 years
600 IU for those older than 70 years.
According to the Dietary Guidelines (U.S. Department of Health and Human Services and U.S. Department of Agriculture 2005) older adults, people with dark skin, and people exposed to insufficient UV B radiation should consume extra vitamin D from vitamin D-fortified foods or supplements.

17. THANK YOU