Lecture By: Dr.EHAB ABUSINNA Orthopedic specialists Meeqat General Hospital ,Medina Munawara ,KSA

2. BY
EHAB ABUSINNA
VITAMIN D
DEFICIENCY

3. VITAMIN D
Fat-soluble vitamin
Sources
 Foods
 Naturally found in very few foods
 Added to many foods on the market
 Supplements
 Sunlight

4. A QUICKREVIEWOF VITAMIN D
METABOLISM
Vitamin D3 (cholecalciferol) is made in sun-exposed skin,
or can be absorbed in the diet or as a supplement.
liver Vitamin D3 is converted into 25-OH vitamin D (calcidiol) in the liver. I
It can also be taken as an oral supplement.
This is the form of the hormone we test for in the blood.
kidney 25-OH-vitamin D is converted to 1,25-OH vitamin D (calcitriol)
in the kidney.
This is the active form of the hormone.

5. METABOLISMOF VITAMIN D

6. ACTION OF VITAMIN D
 Vitamin D is a steroid hormone that
primarily acts to increase transcription of
vitamin D responsive genes primarily in the
small intestine
 These genes mediate increased absorption of
calcium and phosphorous in the gut
 However, there is evidence that other cell
types express the vitamin D receptor
 Vitamin D plays a role in maintaining normal
neuromuscular function and immunity
 There is some evidence that vitamin D
regulates apoptosis, cell proliferation and
inflammation as well

7. Involved in cellular growth, differentiation and
apoptosis
 Simulates insulin secretion
Modulates the immune system.
Reduces inflammation
Muscle development

8. VITAMIN DDEFICIENCY
Vitamin D deficiency causes osteomalacia in which
bone mineralization is defective
 In children this causes rickets. A common presenting
syndrome is bowing of the legs
 In adults this causes fragility of the bones which can lead
to fractures
Other symptoms of vitamin D deficiency include
diffuse body aches and muscle weakness

9. VITAMIN DDEFICIENCY
oSubclinical deficiency
oSilent epidemic.
oPresent in approximately 30% to 50% of the general
population.
oMore prevalent in elderly, women of child bearing age and
infants.
oOften unrecognized by clinicians.
oMay contribute to development of osteoporosis &
increased risk of fractures related to falls in the elderly.

10. CAUSES
Inadequate sun exposure
 Sunscreen
 Pigmented skin
 Aging (older than 65 years)
 Winter season
Decreased absorption
 Bowel bypass surgery
 Crohn’s disease
 Celiac disease
 Fat and cholesterol absorption inhibitors

11. OTHERCAUSES
Breastfeeding
Liver failure
Chronic renal disease
Medications; Steroids decrease half life of vitamin
D. Dilantin, Phenobarbital, and Rifampin can induce
hepatic p450 enzymes to accelerate the catabolism
of vitamin D.

12. RISKFACTORS FORVITAMIN
DDEFICIENCY
Female gender
Age > 50
Minimal sun exposure
Dark skin
Fat malabsorption
Obesity

13. RISKFACTORS
 Individuals older than 50 years
 Nursing home residents
 Individuals with non-vertebral or hip
fractures
 Individuals with kidney disease
 Individuals with low bone mass or
osteoporosis
 Individuals with a history of falls
 Breastfed infants

14. ASSOCIATEDCLINICAL
CONDITIONS
Muscle Weakness and Falls
 Proximal muscle weakness
 Chronic muscle aches
 Myopathy
 Increase in falls

15. Risk of osteoporosis may be reduced with adequate
intake of vitamin D and calcium.
Studies support the concept that vitamin D at doses
between 700 and 800 IU/d with calcium
supplementation effectively increase hip bone density
and reduced fracture risk, whereas lower vitamin D
doses may have less effect.
BONEDENSITYANDFRACTURES

16. MODERN DAY INTEREST
Vitamin D & metabolites
 Significant role in calcium homeostasis & bone
metabolism
Deficiency
 Rickets in children
 Osteomalacia in adults
Rickets ? rare in most developed populations

18.  Vitamin D supplementation is associated with a lower
risk of autoimmune diseases.
 In a Finnish birth cohort study of 10,821 children,
supplementation with vitamin D at 2000 IU/d reduced the
risk of type 1 diabetes by approximately 78%, whereas
children who were at risk for rickets had a 3-fold higher
risk for type 1 diabetes.
 In a case-control study of 7 million US military personnel,
high circulating levels of vitamin D were associated with
a lower risk of multiple sclerosis.
 Similar associations have also been described for
vitamin D levels and rheumatoid arthritis.
AUTOIMMUNE DISEASE

19.  Low intake of vitamin D and calcium has been
associated with an increased risk of non-Hodgkin
lymphomas, colon, ovarian, breast, prostate, and other
cancers.

 The anti-cancer activity of vitamin D is thought to
result from its role as a nuclear transcription factor
that regulates cell growth, differentiation, apoptosis
and a wide range of cellular mechanisms central to
the development of cancer. These effects may be
mediated through vitamin D receptors expressed in
cancer cells.
 Vitamin D is not currently recommended forreducing
cancerrisk
ROLE IN CANCERPREVENTION

20. VITAMIN DANDCANCER
Roles in prevention of
 Colon cancer
 Breast cancer

21. Role in Reproductive Health
 Vitamin D deficiency early in pregnancy is associated with
a five-fold increased risk of preeclampsia.
Role in All Cause Mortality
 Researchers concluded that having low levels of vitamin
D (<17.8 ng/mL) was independently associated with an
increase in all-cause mortality in the general population.

22. Vitamin D deficiencyactivates the renin-
angiotensin-aldosterone system and can
predisposeto hypertension and left ventricular
hypertrophy.
Additionally,vitamin D deficiency causes an
increase in parathyroid hormone,which increases
insulin resistance secondary to down regulation of
insulin receptors and is associated with diabetes,
hypertension, inflammation, and increased
cardiovascularrisk.
ROLE IN CARDIOVASCULARDISEASES

23. TYPE 2 DIABETES
Altered vitamin D and calcium homeostasis may
play a role in development of type 2 diabetes
Low serum levels of 25(OH)D are associated with
impaired pancreatic β cell function and insulin
resistance
High calcium intake is inversely associated with
body weight

24. SOURCES OF VITAMIN D
Sunlight (UV)
Intestinal absorption (only ~20%)
 Oily fish
 Fortified milk / bread / cereal
 Supplements

26. DIETARY SOURCES
 Natural sources of vitamin D include:
 Fish liver oils, such as cod liver oil, 1 Tbs (15 mL) provides 1,360 IU
 Fatty fish species, such as:
 Herring, 85 g (3 ounces) provides 1383 IU
 Catfish, 85 g (3 oz) provides 425 IU
 Salmon, cooked, 100 g (3.5 oz]) provides 360 IU
 Mackerel, cooked, 100 g (3.5 oz]), 345 IU
 Sardines, canned in oil, drained, 50 g (1.75 oz), 250 IU
 Tuna, canned in oil, 85 g (3 oz), 200 IU
 Eel, cooked, 100 g (3.5 oz), 200 IU
 A whole egg, provides 20 IU
 Beef liver, cooked, 100 g (3.5 oz), provides 15 IU

27. FOODSOURCES OF VITAMIN D
3 oz smoked salmon = 583 IU
3 oz light tuna, canned in oil = 229 IU
1 large, whole egg = 29 IU

29. FORTIFIEDSOURCES
Some of the dietary sources:
 Fortified milk (100 IU/8 oz)
 Cheeses and yogurt
 Fortified cereals

30. DIETARY SUPPLEMENTS
 Calcium
Carbonate or citrate
Dose dependent absorption
Two doses per day
 Vitamin D
 D2 or D3
 D3 is best

31. TAKE HOME MESSAGE
 There is considerable evidence to support vitamin D
deficiency screening and supplementation in elderly
individuals at risk for osteoporosis, falls and fractures.
 Do all age, racial, geographic groups require the same
vitamin D levels for general health?
 Is widespread supplementation of vitamin D safe in all
populations?
 Would supplementation benefit younger people?
 Is it possible that some people have low calcidiol
levels, but adequate calcitriol levels and thus no
adverse consequence to “low” vitamin D?

32. CONSEQUENCES OF VITAMIN D
DEFICIENCY
o Reduced intestinal absorption of calcium &
phosphorus
o Hypophosphataemia precedes hypocalciaemia
o Secondary hyperparathyroidism
o Bone demineralisation
o Osteomalacia / rickets

33. True or False.
Vitamin D is not necessary
for Calcium to be absorbed
in the body.

34. True or False
Vitamin D is not necessary
for Calcium to be absorbed
by the body.

36. WHERE DO WE GO FROMHERE?
o Routine screening
o Rectify deficiency / insufficiency
o Maintain levels through a patient-specific
combination of diet, supplementation, and sun
exposure

37. RECOMMENDATIONS
o Annual testing of 25(OH)D
o Consider time of year in testing
o Lowest levels generally towards end of winter, early
spring

38. GOALS IN MAINTAINING
VITAMIN DLEVELS
o Prevent disease of deficiency – rickets, osteomalacia
o Prevent complications of insufficiency – impaired calcium
absorption and increased bone resorption
o Minimize risks of future disease – cancer,
cardiopulmonary diseases, diabetes, other immune-
related diseases

39. VITAMIN DOVERVIEW
o It is a fat soluble vitamin.
o Not just a vitamin it is a prehormone
o Found in some food and made in the body after
exposure to UV rays
o Major biological function is to maintain normal
blood levels of Ca and Po4
o Other tissues like macrophages, prostrate tissue
also have vit D receptor

40. CONCLUSION
o Commoner than we think!
o Can be prevented:
o Promote awareness, especially in high-risk groups
o Sun-exposure
o Safe, 10-15 minutes per day (longer with darker skin)
o Adequate intake of fortified products in diet

42. THANKYOU