Major Minerals Flashcards
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
How is calcium absorption impacted by the type of food consumed?
Foods with high calcium content have poor absorption. Foods with low calcium content have good absorption. Dairy lies in the middle. Ratio of absorption to amount
Describe the mechanisms involved in calcium homeostasis
Blood calcium is critical = tight regulation
Elevated BC –> Thyroid releases calcitonin –> Decreases Ca release from bones and increases Ca excretion –> returns to normal range
Low BC –> Parathyroid releases PTH –> Calcium release from bone, increased Ca uptake in GIT, increased Ca retention in kidneys –> returns to normal range
Describe the primary functions of calcium
Bone development and maintenance = forms calcium-hydroxyapatite with phosphate (lattice-like = strength), binds to collagen (flexibility)
Blood clotting = involved in cascade
Muscle contraction = influx in myocytes triggers muscle protein contraction
Transmission of nerve impulses = influx of Ca ions when nerve impulse reaches cell = triggers vesicles recruitment to presynaptic membrane = vesicles release neurotransmitters which carry the impulse
Helps decrease BP via smooth muscle relaxation in BV
Describe the association between bone health and risk of fracture
Dietary calcium intake is not associated with risk of fracture, and there is no clinical evidence that increasing calcium intake from dietary sources prevents fractures
What are the requirements for calcium?
RDI, UL
Increased needs with age due to reduced absorption and increased excretion
Describe the signs and symptoms of calcium deficiency and/or toxicity if applicable
Deficiency = Hypocalcaemia (muscle cramps, paraesthesia, confusion, fatigue, anxiety); osteopenia and osteoporosis
Toxicity = Hypercalcaemia (kidney stones, high BP due to calcification of blood vessels, renal calcification and failure)
High risk of toxicity with supplements at above 1500mg/day
If using supplements: calcium carbonate and calcium citrate appear best; may be combines with vitamin D3 or calcitriol (prescription). Limit to 500mg dose and take with food
Risk of interference with absorption of other minerals: e.g. iron, zine, magnesium
Describe the absorption, transport, storage and excretion of phosphorus
Absorption
- In upper small intestine - 70% of dietary source absorbed - Active transport and diffusion - Calcitriol enhances absorption (like calcium) - But phosphorus from gains/legumes is poorly absorbed because present as phytate phosphorus. Humans lack adequate digestive enzymes to free it from phytate - In bread, the (traditional) yeast, and sour dough, breaks down phytate bonding for best absorption
Storage:
- 85% found in bones and teeth as hydroxyapatite - The rest is in all other cells and ECF
Excretion: via urine
Describe the primary functions of phosphorus
- Major component of bone and teeth as hydroxyapatite
- Main ICF anion as HPO42- or HPO4-
- Buffer of acid in acid-base balance
- Critical in energy production/storage: part of ATP and creatine phosphate
- All phosphorylation reactions, such as those required to activate hormones
- Part of DNA and RNA, phospholipids in cell membranes, enzymes and cellular signalling pathways
What are the requirements for phosphorus?
RDI, UL
Describe the signs and symptoms of phosphorus deficiency and/or toxicity if applicable
Deficiency = Hypophosphatemia
Presents as respiratory failure if severe, anorexia, anaemia, muscle weakness, bone pain, rickets, osteomalecia, confusion
Toxicity = Hyperphosphatemia Occurs in poor kidney function where excretion is reduced
Leads to vascular calcification and this progression of disease. Formation of calcium phosphates that lodge in cell wall
In non-kidney disease patients: hyperphosphatemia increases risks of CVD due to deposit of calcium phosphate in vasculature
What are the primary sources of phosphorus in the diet?
Protein and dairy sources mainly
Describe the absorption, transport, storage and excretion of Mg
Absorption:
- Small intestine by active and passive transport - Supplement form: generally poor absorption - High fibre intake lowers absorption: phytate binds magnesium - High intake of zinc reduces magnesium absorption
Storage:
- 50% found in bone as part of calcium hydroxyapatite - 35% in muscles and soft tissue
Excretion:
- Via urine; kidney monitors levels: reduce excretion if intake is low - High calcium (>2600mg/day) and high sodium intake enhance magnesium excretion
Describe the functions of Mg
- Second most abundant ICF cation
- Cofactor in >300 enzymes
- Binds to phosphate of ATP to stabilise the molecule
- Energy production, CHO and lipid metabolism
- DNA, RNA, and protein synthesis
- Nerve transmission
- Smooth muscle and heart contraction
- Vaso-relaxation: promotes healthy endothelium function and thus prevention of HTN (one of the “nutritional targets” of the DASH)
Describe the requirements of Mg
RDI, UL related to supplements
Describe the signs and symptoms of phosphorus deficiency and/or toxicity if applicable
Deficiency:
- Irregular heartbeat, weakness, muscle spasms due to imbalance in the Na/K pumping
- Associated with hypertension and type 2 diabetes
Toxicity:
- Excess from supplements results in diarrhoea, kidney failure
- High circulating Mg = weakness, nauseam coma, death
What are some good food sources of Mg?
Nuts, seeds, green leafy vegetables
Describe what we learnt about sulphur
Is part of vitamins and amino acids
Required in the synthesis of sulphur containing compounds (e.g. glutathione)
Involved in the stabilisation of protein structure (collagen, nails, hair, skin)
Participates in acid-base balance
No NRV set
Widely available in protein foods (animal and vegetarian sources)
No known deficiency of toxicity associated
What is primary hypertension?
Chronic elevation of BP = hypertension (HTN)
Consequences = increased pressure on heart; may lead to keart, kidney and eye disease as the arterial wall thickens, narrowing the lumen, making the blood vessels less elastic
Causes damage particularly in organs with small blood vessels
Systolic BP = as the heart contracts
Diastolic BP = as the heart relaxes
May be due to arteriosclerosis, increased blood volume due to fluid retention
Primary hypertension: not secondary to another disease/condition
Describe the mechanisms of action of the DASH in HTN
- High potassium to sodium ratio
- High K intake promotes sodium and water excretion, reducing blood volume and this HTN
- DASH is about the combination of both high K and low Na
- High magnesium and calcium intake
- Magnesium and calcium act as smooth muscle relaxants and vasorelaxants
- E.g. blood vessels elasticity is maintained, thus allowing for adaptation to blood volume and reducing HTN
- Low sodium (down to 1500-2300mg)
- For salt sensitive individuals, this will reduce water retention, e.g. blood volume and thus HTN
- In overweight subjects, high salt intake tends to promote more food intake because it is appetising, worsening the energy balance and struggles to lose weight. Excess weight is a risk factor for HTN. So if relevant for that person, weight loss can assist in reducing hypertension
- Moderate total fat, low saturated fat and low cholesterol intake
- Improvement of blood lipid profile, reducing the risk of LDL build-up and peroxidation, and thus risk of arteriosclerosis which hardens the arterial wall and narrows the lumen leading to HTN
- High fibre
- Can assist in appetite control to avoid over snacking where overweight is an issue, and the resulting weight loss can reduce HTN
- Fibre also contributes to reduced cholesterol “re-absorption” via bile reabsorption which results in reduced blood cholesterol when new bile is made by the liver. This improves the lipid profile and reduces arteriosclerosis risk, thus reducing the risk of HTN via the hardening of blood vessels
- Avoid added sugar
- Improves blood glucose management which reduces the risk of endothelium damage due to inflammation and thus the risk of arteriosclerosis development and the related effect on HTN
- High in vegetables and fruit
- Provides plant sterols
