Vitamin D Flashcards
Calcium and vitamin D
increased intake during rapid bone growth increases peak bone mass -> more complicated than this
Higher calcium intakes
increased incidence of hip fractures
Low calcium intake and less from milk
less osteoporosis and fewer fractures
Adaptation hypothesis
dietary calcium intake above a minimum low level is unimportant as a regulator of bone health -> since plasma free calcium is regulated so finely, adaptive mechanisms exist to maintain calcium balance over a wide range -> because societies with low calcium intakes have low levels of osteoporosis -> OTHER dietary factors and physical activity are more important
Plasma Ca concentration
highly regulated by Vitamin D and PTH -> calcitriol (active vitamin D) and PTH act to maintain plasma Ca at a supersaturating level with respect to bone mineral and to prevent hypocalcemic neuromuscular tetany
Adaptive responses to low calcium intakes
reduction in plasma Ca -> increased PTH secretion -> increased active vitamin D, increased Ca absorption (both add to increased Ca absorption), decreased urinary calcium and increased conservation of dietary calcium (both lead to reduced calcium loss) -> all lead to the restoration of normal plasma calcium
Low intakes of dietary calcium
Very low intakes can cause rickets without vitamin D deficiency
Rickets (with normal vitamin D)
low dietary calcium intake, high phytate and oxalate, genetics -> inadequate calcium for absorption to meet needs for skeletal growth -> decreased plasma calcium, increased serum PTH -> increased mineralization defect (hyperosteoidosis) -> rickets and osteomalacia
Calcium
Adequate amounts are needed for peak bone mass (PMB) development, diets low in this are also low in other respects
Extra calcium
reduces bone mass loss -> proven to aid with bone mineral density -> beneficial in post-menopausal women (milk is better than supplements)
Fruit and vegetables
important for bone health -> provide alkali to neutralize dietary acid -> as people age the ability to excrete acid declines and they become more acidic
Bone mineral balance
extremely sensitive to acid base balance with demineralization occurring as pH drops below a critical point -> dietary acid and PO4+3 can be buffered by fruits and vegetables (K+ salts of bicarbonate and weak organic acids) -> cheese and meat are high in renal acid loads, fruits and vegetables are negative
Osteoclast resorption
increases with increasing acidity
K+ and HCO3-
markedly reduced in present day diet -> now Na and Cl -> used to have high diet in this -> supplementation improves calcium and PO4 balance (as does carbonated mineral water)
DASH (dietary approaches to stop hypertension)
high in fruits and vegetables and low-fat dairy products, reported improved calcium balance
Ca citrate/malate
supplements supplies alkali and this may be a part of their effectiveness for bone health (might have nothing to do with the minerals and more with alkaline pH)
Vitamin D how does it regulate Ca and PO4
regulates calcium and PO4 homeostasis -> from sun UVB to skin or from diet -> 25 hydroxylase takes D2 and D3 to 25-OH vitamin D (measure of status -> tissue supply) in the liver -> 1alpha hydroxylase in the kidney hydrolyzes it to 1,25 (OH)2D4 (active hormone)
Vitamin D how does it influence Ca PO4
influences calcium-phosphate homeostasis -> in the intestine it increases Ca absorption, in bone it causes Ca release, in kidney it causes Ca retention -> increase free Ca
25-OH vitamin D
tissue supply of vitamin D -> can become active form in tissues other than the kidneys -> immune system, CV system, muscle/cartilage, adipose, liver, pancreas, brain, lung, skein, breast, ovary, uterus, placenta, prostate, testes -> 5 % of all human genes have a response element for this
Where do you get vitamin D
exogenous hormone -> main source is sunlight (don’t get much in the diet -> high in oily fish, fish oils and some added in dairy and fortified cereals)
Vitamin D deficiency
at risk infants, pregnant women, elderly, ethnic minorities in temperate countries, those with limited sun exposure -> rickets in children and osteomalacia in adults
Cut off for rickets <25nmol/L
25% deficient for several age groups -> infants, children, pregnant women and elderly
Cut off for deficiency in most clinical labs
50% deficient for several age groups (people of all ages)
Causes of vitamin D deficiency
reduced skin synthesis (sunscreen use, skin pigment decreased, aging, season, latitude, time of day), decreased bioavailability (fat malabsorption, obesity), increased catabolism (anticonvulsants, glucocorticoids, HAART AIDs treatment, anti-rejection medicines), decreased synthesis (liver failure/dysfunction, nephrotic syndrome, chronic kidney disease)
Rickets
increased melanin pigmentation and decreased exposure to sunlight + vegetarian diet (low in Ca, and vitamin D, high phytate and oxalate) + vitamin D deficiency (low 25-OHD is diagnostic) + inadequate calcium absorption to meet requirements =
Consequences of vitamin D deficiency
multifactorial chronic disease -> osteoporosis and fracture, reduced muscle strength and increased falls, CVD, cancer (colon, breast and prostate), autoimmune diseases (osteoarthritis, diabetes, psoriasis, wheezing illnesses, lung function), tuberculosis, schizophrenia and depression
Vitamin D
inhibits angiogenesis in growing tumors, getting some sunlight can be protective against melanoma!
Sun exposure
Significant benefit in elderly people in regards to their vitamin D levels
Subclinical deficiency
may contribute to poor bone health, other chronic diseases -> increased food fortification and increased supplements
Bone health
reflects diet (especially fruits and veggies), lifestyle (moderate sun exposure and resistance exercise) and genes -> alkali sources, vitamin D sources and calcium all contribute
