Good morning! (by the time I finish this, it is almost evening)
I’m here with another From the Nutrition Classroom post. My last one was all about calcium, but today’s will be about all of the nutrients that affect bone health, as well as having other major functions in the body.
**I’m writing this post because I have a test on this information tomorrow and writing on here helps me learn the material. If you’re not interested, feel free to exit and stop by later for a [really fun] weekend recap.
- Important for: blood clotting (blood clotting protein, fibrin, requires calcium to form), muscle movement (with myosin and actin), nerve transmission (facilitates neurotransmitter release from cells), regulation of enzymes and systems, and mediator of cellular messages.
- Food/ other sources: Leafy green vegetables, dairy, fortified soy milk, supplements in the form of calcium-carbonate or calcium-citrate.
- Absorption: Calcium is found as a salt and must be freed from the salt by the pH of the stomach. Active absorption depends on Vitamin D!
- Transport in the body: Can travel freely or bound to protein (eg Calmodulin), citrate, phosphate or sulfur. Calmodulin is inactive without calcium. Once calcium activates it, it becomes a regulatory protein. Calcium is absorbed into cellular organelles until it is needed in the body.
- Use in the body: Bone is 37-40% calcium. Soft, spongy bone is most susceptible to calcium deficiency. Blood calcium level is highly regulated in the body. 1% of the body’s calcium is ALWAYS in the blood, lymph and body fluids and it is critical that it stay at 1%.
- Bioavailability: Oxalates, phytates, age, and supplements can lower calcium retention in the body. A high fiber diet can also lower retention because fiber binds calcium and is then excreted. Reducing dietary salt intake by 5.75 g will reduce calcium excretion by 40 mg. That means the more salt you consume, the more calcium you excrete!
- Disease: 1. Osteoporosis- too littler bone (in matrix and mineral), 2. Osteopenia- less than normal bone mass. 3. Osteomalacia (rickets)- softening of the bone. Seen in children. 4. Hormonal dysfunction, liver and kidney disease.
- Supplements: Calcium carbonate- small and inexpensive. Calcium citrate- more easily absorbed and more expensive. People that may need calcium supplements include lactose intolerant people, the elderly, people on high protein diets.
- Deficiency: Symptoms of deficiency include muscle spasm and cramping, numbness or tingling of hands and feet.
- Toxicity: The Upper limit for calcium is 2500 mg/day. Symptoms of toxicity include nausea, vomiting, decreased appetite, calcification in kidneys, irregular heart rhythm.
- Calcium Assessment: There is NO good test for calcium because calcium levels are so strictly regulated in the body. Bone density tests will assess risk for fracture, but not Calcium levels.
- Regulation: When blood calcium levels are low, the parathyroid gland release parathyroid hormone, which causes bone breakdown by osteoclasts. Osteoclasts contain lysosomes that can dissolve the bone matrix. They are sensitive to vitamin D, calcitronin and PTH. If osteoclasts are not replaced, osteoporosis can occur. Bone breakdown releases calcium into the blood to raise calcium levels. If calcium levels get too high, the thyroid gland releases calcetonin to decrease calcium absorption.
- Other interesting information: Factors that decrease absorption in the intestine: fiber, oxalate, phytate, unabsorbed fatty acids. Factors that increase calcium losses from the kidney (the calcium has already been absorbed)- excessive sodium, protein, high caffeine intake. The name for the protein that binds calcium in the cell and controls cell activity is calmodulin–> it has 4 binding sites for calcium.
- How vitamin D increases calcium absorption: Vitamin D facilitates the intestinal absorption of calcium. In the absence of vitamin D, dietary calcium is not absorbed efficiently. Vitamin D stimulates the expression of a number of proteins involved in transporting calcium from the lumen of the intestine across the epithelial cells and into the blood. Calcium absorption is enhanced by the protein Calbindin and it’s synthesis is dependent on vitamin D. Calbinidin shuttles calcium from the brush border across to the basolateral side of the mucosal cell.
- Important for: cell membranes, bone mineralization, structural roles, energy storage and transfer (ATP), intracellular second messenger.
- Food/ other sources: meat, poultry, fish, eggs, dairy, whole grains (although the phytate must be hydrolyzed to release the phosphorus and we do not have the enzyme, but yeast do, so eat bread with yeast to get the phosphorus) Also, sprouting breaks down phytic acid and frees bound minerals.
- Absorption: in grains, 80% of the phosphorus is phytic acid, but we don’t have the phytase enzyme. The presence of magnesium lowers phosphorus absorption. Aluminum containing gels and antacids also lowers phosphorus absorption.
- Transport: High dietary phosphorus can lead to high serum phosphorus. It is transported in the blood as phospholipids. Smaller amounts are bound to protein, calcium or magnesium (as inorganic phosphorus).
- Bioavailability: Presence of magnesium lowers absorption. You must consume foods with phytase to release phosphorus from phytic acid.
- Deficiency: Deficiency is rare because it is so abundant in foods.
- Toxicity: The upper limit for age 9-70 is 4000 mg (4 g), and 70+ is 3000 mg (3 g). Excess phosphorus may impair bone status, especially is calcium intakes are low. Calcium: Phosphorus levels of 1:4 are shown to raise PTH levels, which can increase bone loss (by osteoclasts). Renal problems or failure will cause people to have trouble clearing the phosphorus (phosphotemia), which signals the release of PTH and cause bone loss.
- Assessment: Serum concentrations or urinary excretions.
- Other Interesting Info: Excretion occurs through the kidneys,
- Important for: increase the absorption and retention of calcium, bone mineralization (calcitriol works with PTH to regulate blood calcium), regulation of cell growth, differentiation and proliferation, influences cell membrane and gene transcription.
- Food/ other sources: made in the skin when exposed to UV light. Fatty fish, cod liver pol, eggs, fortified foods, milk, fortified soy milk, juice, cereal and irradiated mushrooms. In order from lowest to highest amount of vitamin D: 1 oz cheese, 1 tsp butter, 1 egg, 1 cup of fortified milk, 3 oz of salmon.
- Absorption: Dietary vitamin D is absorbed in the ilium of the small intestine in a micelle, meaning it MUST be consumed with fat. 95% is excreted in bile.
- Transport: vitamin D is incorporated into the chylomicron for transport.
- Use in the body: most cholecalciferol travels in the blood bound to vitamin D binding protein (DBP). Calcitriol and calcium absorption–> receptors on enterocyte for calcitriol–> take it to the cell nucleus–> calcitriol interacts with specific genes encoding for calcium transport (calbindin). The net effect is increased calcium. Effects the kidneys/ intestines, heart, brain and blood and immune system.
- Disease: 1. Osteoporosis risk goes up. 2. Rickets in kids- seizures, growth retardation, bones don’t mineralize properly. 3. Osteomalacia in adults- bones don’t mineralize.
- Supplements: light skinned people: 5-10 minutes in the midday sun on arms and legs/face 3x/ week. Dark-skinned people need twice as much exposure.
- Deficiency: There is a deficiency risk for breast-fed infants, elderly, renal patients, people on certain medication because it interferes with absorption and processing, people with fat malabsorption or PTH, liver or kidney problems.
- Toxicity: RDA for 0-12 mo: 10 micrograms or 400 IU. 1-70 yrs: 15 micrograms or 600 IU, 70+ 20 micrograms or 800 IU. Upper limit: 100 micrograms or 4000 IU.
- Assessment: Plasma concentration of 25-OH D or plasma alkaline phosphatase, which is release from osteoclasts. Higher levels are indicative of rickets.
- Other interesting info: Dysfunction of the kidneys could cause vitamin D deficiency because vitamin D activation occurs in the kidneys. The starting material in the body is cholesterol, which is for the precursor 7-dehydrocholesterol. In the presence of sunlight, cholecalciferol (also known as D3) is produced by isomerization.
- Process of dietary vitamin D from food to liver: Cholecalciferol is converted to 25-hydroxyvitamin D in the liver. Then, 25-OH D3 is circulated in the blood to the kidneys where it is converted to 1, 25- dihydroxyvitamin D (1,25-(OH3) D3, which is called calcitriol and is the active form. Conversion of 25-OH D3 to calcitriol increases when calcium concentration in the blood is low. The increase is stimulated by PTH. Chlymicrons carry vitamin D through the lymph, then to the blood. Vitamin D receptors are located on all cells!
- Important for: blood clotting and bone health
- Foods/ other sources: green, leafy vegetables, legumes, cucumbers, tuna, blueberries and bacterial synthesis.
- Absorption: phylloquinone (the plant form) is absorbed in the small intestine in micelles. Menaquinone (the bacterial form) is absorbed by passive diffusion from the ilium/ colon. It bypasses the blood and goes to lymph via chylomicron.
- Transport: Transported in chylomicrons by LDL cholesterol. Stored in the liver and other tissues.
- Use in body: Blood clotting proteins need vitamin K to bind calcium. Vitamin K is needed for the carboxylation of glutamate. Thrombin enables fibrinogen to break down to form a blood clot. Thrombin is inactive as prothrombin until it is needed, but it needs calcium and vitamin K to activate it. GLA residues bind calcium, then that binds to the phospholipid membrane surface to initiate a blood clot.
- Disease: Deficiency can lead to osteoporosis risk increased. In animals, vitamin K deficiency causes bone crystallization problems and cessation of longitudinal bone growth.
- Deficiency: People at risk for deficiency are people that don’t eat fat, people with a gall bladder or liver problem, celiac’s disease, which leads to absorption issues. Newborns don’t have bacteria to synthesize vitamin K, so they are given an injection at birth. Also, vitamin K does not easily pass from mother to fetus, there is low vitamin K in milk, and colonic bacteria are not yet established. People on antibiotics because antibiotics may kill the bacteria that make vitamin K. Bacteria are responsible for up to 50% of vitamin K production. Deficiency is unlikely in healthy adults, but more likely in trauma patients, renal patients, people with liver disease, people on antibiotics.
- Toxicity: Adequate Intake: Men- 120 micrograms, women- 90 micrograms. There is only an AI because everyone is different, meaning they have different bacteria that synthesize different amounts of vitamin K. Synthetic menadione can lead to a toxicity.
- Assessment: Test plasma phylloquinone, blood clotting or prothrombin time (more than 25 seconds can lead to major bleeding).
- Other interesting information: Vitamin K’s role in blood clotting and bone mineralization occurs by carboxylating glutamate–> important coenzyme. VKDB stands for vitamin K deficiency bleeding and can occur in newborns because of their low vitamin K. To prevent, newborns are given an oral dose of 2 mg of phyloquinone (the plant form of vitamin K), or .5-1 mg injection of phyloquinone.
- Important for: intracellular ion in bones and muscles. Central role in intermediary metabolism-required for enzyme metabolism (like glycolysis). It helps to stabilize the phosphate group on ATP. Magnesium is part of the bone lattice and surface. It is required for PTH secretion and effects and is required for the liver’s hydroxylation of vitamin D. About 60% of magnesium in the body is associated with bones.
- Food/ other sources: widely found in unprocessed plant foods. Green plants have chlorophyll and chlorophyll has a Mg ion in the center, so they are high in Mg. Grains, beans, vegetables, coffee, tea, cocoa and seafood. Processed foods have very low Mg.
- Absorption: active and passive absorption. There is high absorption when magnesium status is low and low absorption when there is a high level of phytates, fiber, calcium (because calcium and magnesium compete for absorption), and unabsorbed fatty acids. We absorb magnesium fairly well, but only about 30-40%. Decreased retention is caused by high protein, high calcium, high sodium and high caffeine.
- Transport: Mg travels in the blood freely (55%) or bound to protein.
- Use in the body: Stabilizes enzymes, neutralizes negatively charged ions, used in energy metabolism, used as a cofactor for over 300 enzymes, nerve and muscle function an stabilizes ATP.
- Bioavailability: Influenced by the presence of calcium and phosphorus. Three factors that decrease magnesium retention are caffeine, high sodium and high protein.
- Disease: Neuromuscular symptoms, vomiting and cardiac arrest.
- Supplements: There is only an upper limit set for supplemental Mg. The upper limit is 350 mg/day.
- Deficiency: Alcoholics, people with abnormal nerve and muscle function. Symptoms: muscle spasms, anorexia, nausea, psychological changes, cardiac arythmia. Many people are deficient in magnesium because of the high processed foods diets. Processing food strips it of the magnesium and it is not enriched back in.
- Toxicity: RDA: men- 420 mg/day, women- 320 mg/day, 30 years old or less: Men- 400 mg/day, women- 300 mg/day. Toxicity is unlikely because it is cleared from the kidneys.
- Assessment: Test RBC, which is much better than serum. Only 1% is in the blood and serum levels are controlled. You can also do an oral magnesium load test to see how much is excreted. If you excrete a lot, it means you had sufficient magnesium to begin with.