Major Minerals Flashcards
(43 cards)
What are the differences between major and minor minerals?
If needed at >100mg/day = major
If needed at <100mg/day = minor (trace)
Major minerals are found in the body structure in larger amounts than minor minerals (e.g. calcium vs copper)
Both major and minor (trace) minerals are elements, essential to humans because they are not produced endogenously
Same definition of “essentiality of nutrients” used for vitamins applies to minerals (=> symptoms of deficiency disappearing with re-introduction/supplementation)
What causes variation in minerals concentration in plant and animal food sources?
Genetic variation in animals in absorption pathways of nutrients from soils and feed => results in variation in concentration in animal sources of food
Variation in mineral content in soil => influences the concentration of minerals in produce/grains => variation in animal feeds and food supply for humans
Processing of grain for production of food products: milling reduces iron, selenium, zinc, copper etc.
What are some factors which impair the bioavailability of dietary minerals?
Excess fibre (above 38g/day) may lead to lower mineral status
- Phytic acid found in fibre (phytate in legumes and whole grains): binds to minerals and results in mineral excretion - Phytic acid not absorbed - Leavened breads with baker's yeast may break the bonds between phytates and the minerals: increased bioavailability of minerals
Oxalic acid in dark green leafy vegetables (not associated with fibre) binds minerals and makes them less available for absorption
- E.g. calcium in spinach: 5% vs 32% absorbed for calcium from dairy (Vegan diet?)
Polyphenols and tannins can reduce bioavailability of iron and calcium in particular
- E.g. black tea, dark chocolate, red wine contain high amounts of tannins that interfere with iron absorption
Consumption of several minerals of the same valence at once can decrease absorption of each (e.g. in multi-minerals supplements)
- E.g. Zinc (2+); iron (2+); calcium (2+); and other 2+ valences compete for absorption when taken together
What are some factors which enhance the bioavailability of dietary minerals?
Vitamin C: improves non-haem iron absorption within the same meal
- Vitamin C = non-specific reducing agent
Stomach acidity: assists in converting minerals form 3+ to 2+: helps their absorption (because 2+ is the absorption form of minerals)
- Therefore, antacids may impair bioavailability of minerals, because of reduced stomach acidity
Good vitamin D status facilitates dietary calcium absorption (because calcitriol upregulates expression of calcium channel proteins, calbindin and calcium ATPase-pumps)
In general, human absorption of minerals increases when needs are greater
Note: mineral content listed on labels doesn’t reflect actual absorption, but the content in the tablet. Before using supplements, a full nutrient status analysis should be performed
What is the general transport, storage, excretion and toxicity of minerals?
Minerals travel free in the blood of bound to proteins
Minerals that carry a charge are ions: cations and anions
Storage amount and sites vary greatly depending on minerals, and can be associated to function
Most are excreted via urine, but some are also secreted into the bile for excretion in faeces (e.g. copper)
Supplements are more likely to cause toxicity than minerals consumed through the diet
Minor minerals travelling free are often highly reactive => toxic if not bound
What are the overall functions of minerals?
Cell metabolism:
Calcium, Phosphorus, Magnesium, Zinc, Chromium, Iodide
Bone health:
Calcium, Phosphorus, Iron, Zinc, Copper, Fluoride, Manganese
Growth and development:
Calcium, Phosphorus, Zinc
Bone formation and clotting:
Iron, Copper, Calcium
Nerve impulses:
Sodium, Potassium, Chloride, Calcium
Antioxidant defences:
Selenium, Zinc, Copper, Manganese
Ion balance in cells:
Sodium, Potassium, Chloride, Phosphorus
What are the major minerals
Sodium
Potassium
Chloride
Calcium
Phosphorus
Magnesium
Sulphur
Describe the absorption, transport, storage and excretion of sodium
Absorption: small and large intestines. 98% efficient
Active transport: sodium potassium pump
“Storage”: 95% of body sodium is found in the ECF (blood and lymph). Kept outside cell by Na/K-ATPase pumps
Excretion
- Majority is excreted in urine as sodium concentration is tightly regulated - Some losses via faeces and sweat - Amount excreted varies by ethnicity - Conservation by reducing urine output (e.g. role of aldosterone)
Describe the sources of sodium in the diet and the associations between dietary salt intake and primary hypertension. Describe the DASH, and the reasoning behind the nutritional characteristics of this dietary prescription
77% from processed and restaurant foods, 12% naturally occurring, 5% added in home cooking, 6% added to the plate
In salt sensitive people (25-50%), there is a link between high sodium intake and hypertension
What are the major intra and extracellular anions and cations?
ICF:
Cations = K+, Mg2+
Anions = Phosphate, Sulphate (SO4-)
ECF:
Cations = Na+, Ca2+
Anions = Cl-, biocarbonate (HCO2-)
Describe the requirements for sodium
No EAR or RDI
AI
UL undetermined, SDT 2000ug
Describe the signs and symptoms of sodium deficiency and/or toxicity if applicable
Deficiency = Hyponatremia: headache, nausea, vomiting, muscle craps, fatigue, disorientation, cerebral oedema, fainting and coma if left untreated rapidly
- Occurs when losses exceed intake: with excessive diarrhoea and vomiting, or excessive sweating (>2% of total body weight)
Toxicity = Hypernatremia due to excessive water losses => low BO, fainting, stupor, convulsions
Other effects in high intake
- > 2g/day can increase urinary calcium losses
- Salt-sensitive people: primary hypertension (25-50%) and thus increased risk of heart disease and stroke
Describe the signs and symptoms of sodium deficiency and/or toxicity if applicable
Deficiency = Hyponatremia: headache, nausea, vomiting, muscle craps, fatigue, disorientation, cerebral oedema, fainting and coma if left untreated rapidly
- Occurs when losses exceed intake: with excessive diarrhoea and vomiting, or excessive sweating (>2% of total body weight)
Toxicity = Hypernatremia due to excessive water losses => low BO, fainting, stupor, convulsions
Other effects in high intake
- > 2g/day can increase urinary calcium losses
- Salt-sensitive people: primary hypertension (25-50%) and thus increased risk of heart disease and stroke
What is the allure of using salt in processed foods
Salt preserves food = increased shelf life
Processing increases the sodium content of food
Describe the absorption, transport, storage and excretion of potassium
Absorption
- 90% absorbed in small and large intestine - Passive diffusion or Na-K-ATPase pump active absorption
Storage
- 95% stored inside cells (K+) - Uptake via active transport
Excretion
- Via urine - Some excreted in faeces and sweat - Aldosterone is responsible for excretion of potassium via the kidney
What are the primary functions of potassium?
- Major cation in ICF
- Contractility of smooth, skeletal and cardiac muscle, and excitability of nerve tissue: responsible for changing the electrical potential during depolarisation/repolarisation of nerve/muscle cells for conduction of impulse
- High (dietary) potassium intake reduces serum calcium excretion
- High potassium intake promotes sodium + H2O excretion: resulting in reduced blood volume and reduced blood pressure in hypertension = This is the main mechanism of action of the DASH
What are the requirements for potassium?
No EAR/RDI
AI, no UL (for dietary intake)
Describe the signs and symptoms of potassium deficiency and/or toxicity if applicable
Deficiency:
- Hypokalaemia leads to cardiac arrhythmia, muscle weakness, fatigue, hypercalciuria, glucose intolerance - Usually due to profound fluid loss rather than lack of intake: vomiting, diarrhoea, use of diuretics, eating disorders, alcoholism (poor diet), athletes with excessive sweating
Toxicity:
- Hyperkalaemia results in cardiac arrhythmia and cardiac arrest, muscle weakness and temporary paralysis, GI ulceration and perforation - Does not occur from dietary intake, but through supplements use, or use of salt substitute: potassium chloride (to replace salt in low-salt diets)
In chronic kidney disease: potassium is not well excreted; restriction of dietary potassium is required, which affects quality of life because many foods are limited or excluded. Use of potassium binders may also be prescribed
Describe the signs and symptoms of potassium deficiency and/or toxicity if applicable
Deficiency:
- Hypokalaemia leads to cardiac arrhythmia, muscle weakness, fatigue, hypercalciuria, glucose intolerance - Usually due to profound fluid loss rather than lack of intake: vomiting, diarrhoea, use of diuretics, eating disorders, alcoholism (poor diet), athletes with excessive sweating
Toxicity:
- Hyperkalaemia results in cardiac arrhythmia and cardiac arrest, muscle weakness and temporary paralysis, GI ulceration and perforation - Does not occur from dietary intake, but through supplements use, or use of salt substitute: potassium chloride (to replace salt in low-salt diets)
In chronic kidney disease: potassium is not well excreted; restriction of dietary potassium is required, which affects quality of life because many foods are limited or excluded. Use of potassium binders may also be prescribed
Describe the absorption, transport, storage and excretion of chloride
Absorption
- Follows sodium absorption => electrical neutrality - In small and large intestines; highly efficient
“Storage”: mainly found in the ECF associated to sodium
Excretion: mainly via kidneys
Describe the functions of chloride
Electrical neutrality: balancing sodium positive charge Main anion for ECF Fluid balance Acid/base balance Nerve impulse transmission Component of NaCl and HCl
Describe the signs and symptoms of chloride deficiency and/or toxicity if applicable
Deficiency:
- Loss of appetite - Failure to thrive in children - Muscle weakness, lethargy, convulsions - Severe metabolic alkalosis on blood test - Deficiency is usually rare as it is consumed as part of salt. Has occurred in infants fed chloride deficient formula. May occur in GIT disorders with excessive diarrhoea and vomiting
Transport into cells issues (cystic fibrosis):
- A genetic dysfunction in chloride transporters in epithelial cell membrane of organs (lung, liver, pancreas, GIT, reproductive tract, skin) results in chloride trapped inside the cell, and the production of thick mucus in cystic fibrosis; may lead to premature death due to respiratory failure
Describe the requirements for chloride
No specific NRVs in Australia, but intake matches sodium intake as NaCl
Describe the absorption, transport, storage and excretion of calcium
Absorption
- SI and LI: most efficient in upper duodenum where the pH is slightly acidic => keeps calcium in 2+ form - Usually only 25-30% absorption from foods; the food source largely impacts on absorption - Absorption increases to 75% in pregnancy and in childhood (because increased needs) - Calcitriol increases calcium absorption from GIT - Absorption declines with age => HCl decline? - Lactose and presence of protein in food enhances absorption due to increased production of HCl
Limiting factors to absorption:
- Phytic acid, oxalic acid, polyphenols and tannins (applies to most minerals absorption, but calcium appears particularly impacted) - Fat mal-absorption (calcium binds with unabsorbed fat in the intestine and gets excreted)
Transport: transported to cells as free ionised calcium or bound to proteins
“Storage”: Skeleton and teeth = 99%; All cells contain calcium as required for function
Excretion: via urine, sweat, faeces
