Magnesium Flashcards
RDA=
400mg (M)
310mg(F)
do canadians meet the RDA for Mg
No
What was the EAR set for
maintain Mg balance
T or F: Mg found in only 3 food groups
FALSE: Mg is found in all 4 food groups (F&V, grains, dairy and alt, meat and alt)
good food sources of Mg
green leafy veg, nuts, legumes, whole grains
why are dark green leafy veg especially good sources of Mg
lots of chloroplasts which produce energy by photosynthesis (Mg is used in over 300 mitochondrial reactions/ energy pathways in chloro)
what does refining whole grains do to Mg
refining whole grains reduces Mg by over 75%
3 steps of Mg digestion and absorption
- Mg crosses BBM of enterocyte through Mg channel TRPM6 *Ca is TRYPV6, different
- Mg may be absorbed between cells/ paracellular diffusion, influenced by electron chemical gradient and solvent drag
- Mg pumped out of cell across BLM by Na-dependent ATPase
inhibitors of Mg absorption
phytic acid
fibers
unabsorbed fatty acids
divalent cations compete
two systems of absorption:
- ACTIVE CARRIER-MEDIATED: (saturable) operates when Mg intake is LOW
- PASSIVE DIFFUSION: (conc dependent) Mg intake is HIGH
percent of dietary Mg typically absorbed?
30-60%
Mg Transport %’s in blood
50-55% free Mg+2 ion
20-30% bound to protein (albumin or globulin)
5-15% complexed with anions
how do kidneys control Mg losses
in response to plasma concentrations. increase Mg = increase excretion rate of Mg
how do bones control Mg
bones provide a reservoir of Mg, plasma conc can be maintained at the expense of bone mineral breakdown
how much of body’s Mg is in bones
50-60%
what hormones influence Mg balance
PTH (parathyroid hormone)
increase PTH = low Mg levels = decrease excretion of Mg = PTH stimulates Mg reabsorption = more Mg released from bones
high Mg levels = inhibit PTH
2 Mg Functions (function 1)
- Bone mineralization (several forms of Mg)
- on bone surface so that Mg is readily available for blood exchange
- a part of crystal lattice that contributes to structural strength and integrity of bones
2 Mg Functions (function 2)
- Enzymatic reactions
- Mg required for over 300 enzyme reactions
- structural cofactor (energy, DNA and protein synthesis) needed for proper functioning
- allosteric activator (change in enzyme conformation/structure) increase affinity and rate
clinical signs of hypomagnesemia & causes
- low Mg
- insomnia, muscle tremors, leg cramps
- excessive alcohol, malabsorptive disorders (Crohn’s), poorly managed diabetes, metabolic diseases
clinical signs of hypermagnesemia & causes
- high Mg, less common
- lethargy, muscle weakness, respiratory distress
- impaired renal function
nutritional signs of chronic Mg deficiency
many conditions:
hypertension, cardiac arhythmias, CVD, T2D, migraines
supplementation trials inconsistent - eat whole foods and variety
Mg and Ca absorption
- compete for channels
- high Mg inhibits Ca absorption
BOTH increased absorption by 1,25D
Mg and Ca plasma levels
- when plasma levels are low both signal increase PTH = increase reabsorption in kidneys and bone stores release minerals into blood
Mg and Ca intracellular interactions
- compete
- Mg acts to decrease intracellular Ca and competes for binding sites
-intracellularly Mg and Ca are tightly controlled (muscle contractions, nerves, enzymes)
Mg and Ca in cardiac and smooth muscle
- compete
- Mg inhibit contraction/antagonist, relax muscle
- Ca causes contraction
Mg and Ca in intestine
- compete for cation channel
too much Ca might decrease Mg absorption
Mg and Ca in kidneys
separate processes- no interactions BUT both effected by PTH
Mg interactions with other nutrients
inhibit phosphorus absorption
influence ICF and ECF potassium balance
excretion:
urine, depends on plasma conc
feces, mostly unabsorbed
skin, sweat
RDA specifics: 19-30 years
Men: 400mg
women and lactation: 310mg
pregnancy: 350mg
RDA specifics: 31 years and older
Men: 420mg
Women and lactation: 320mg
Pregnancy: 360mg
Mg deficiency common in …
hospitalized pts bc lack of appetite/food unappealing
Mg deficiency in general population
plasma conc may appear normal at expense of tissue conc/health
hypomagnesemia metabolic effects
decreased conc of: PTH, Ca, K, Vit D
symptoms: muscular, CV
factors that contribute to deficiency
inadequate intake
excess alcohol use
malabsorptive disorders
medications
uncontrolled diabetes or metabolic syndrome
CV disease develops more quickly if Mg deficiency
Why is UL for Mg an exception?
based on acute intake, not chronic
UL of Mg
350mg from NON FOOD sources (medications, supplements)
example of acute Mg intake
drug such as milk of magnesia (500mg/tbsp Mg(OH)2 ) or antacids
which forms of Mg are cathartic? Symptoms?
Mg(OH)2 and MgSO4
increased GI transit
over 350mg Mg causes diarrhea, nausea, dehydration
hypermagnesemia conc and effects
over 4.9mg/dL
impaired renal function, produce neuromuscular/cardiopulmonary effects
very high blood levels can result in muscular paralysis, cardiac/respiratory failure
Mg assessment of nutriture
serum concentrations:
low specificity and sensitivity (NOT ACCURATE bc body can maintain serum conc by using tissues or bones)
Measure renal excretion:
alone or as part of Mg retention (load) test
-dose Mg
- measure excretion of Mg = what’s absorbed
why is Mg deficiency a problem for Canadians
enzyme functions and bone health
symptoms: CV, metabolic, neurological, general well-being
