NUTRITION SUMMARIES - EXAM PREP
Macronutrients: energy containing nutrients required in large amounts = protein, carbs, fats, water
Carbohydrates (fibre) → 45-65% DI
Protein → 15-25% DI
Lipids → 20-35% DI
Micronutrients: nutrients required in small amounts = vitamins, minerals, trace elements
Digestion:
CARBOHYDRATES - CHO
1g = 17kJ = 4kcal
45-65% of kilojoules from CHO (stick to lower end) = AMDR
Function: immediate source of fuel for metabolism/energy production
Sources: fruit, root veggies, legumes, grains, dairy, processed foods
Photosynthesis: synthesised in plants → stored as starch → eaten by humans
Digestion:
Mouth: salivary amylase enzyme → breaks down starch into shorter polysaccharides
Stomach: salivary amylase is inactivated - no further digestion
Small intestine: pancreatic amylase breaks down starch into monosaccharides, disaccharides and
oligosaccharides
Brush border: enzyme attached to brush border of small intestinal villi completes breakdown into
monosaccharides
Large intestine: fibre and other indigestible carbohydrates partially broken down/ fermented by colonic
bacteria → form short chain fatty acids, gas & energy → remaining fibre excreted in faeces
Monosaccharides absorbed into blood and travel to liver via hepatic portal vein
Classification:
Simple: sugars
Monosaccharides - single sugar unit
Glucose: blood sugar, stored as glycogen, no digestion,
Fructose: fruit sugar, slower absorption, metabolised in liver to triglycerides, not insulin
release
Galactose: milk, converted to glucose in liver
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Disaccharide - two sugar units
Maltose: glucose + glucose = malt sugar
Sucrose: fructose + glucose = table sugar
Lactose: galactose + glucose = milk sugar
Complex: starch and fibres - chains of monosaccharides
Oligosaccharides - 3-10 monosaccharides linked - 90% fermented in SI, prebiotics
Glycoprotein: sugar (oligosaccharide) + protein (amino acid)
Fructans: glucose + fructose
Raffinose, stachyose, verbascose: sucrose + fructose + galactose
Polysaccharides - long chains of monosaccharides
Glycogen: branched chains or glucose stored in liver and muscles - broken down when
glucose required
Starch: glucose storage in plants - a-glycosidic bonds (broken by human enzymes) amylopectin (branched-fast), amylose (unbranched-slow)
Fibre (NSP non starch polysaccharide): structural component of plants (cellulose) b-glycosidic bones (can't be broken down = no energy contribution) - soluble, insolbe,
resistant
Whole grain - bran/endosperm/germ contain nutrients/b vitamins/fibre = removed when refined
Glycaemic index/load
Glycemic response: how quickly glucose absorbed & how quickly blood sugar rises and returns to normal
Slow absorption = moderate rise & appropriate return
Fast absorption = fast rise & drastic drop to correct spike
Glycemic index (GI): effect of specific carbohydrate on blood glucose levels → influenced by fat, fibre,
protein, processing
Glycemic load (GL): considers GI and how much carbohydrates in food = more accurate info on impact on
blood sugar and insulin
CHO gm x GI / 100 = GL eg ½ cup white rich = 36g x 0.72 = GL of 26
Excess
Weight gain: if not used immediately for energy → stored as glucose in liver and muscles → full stores →
excess carbohydrates converted to triglycerides and stored in adipose tissue as fat
Insulin resistance from high GI, GL, glucose levels
Health effects: tooth decay, obesity, nutrient deficiencies (displaces), chronic high blood glucose levels
(forms advanced glycation end products AGEs = glycotoxins = inflammation, oxidation, insulin resistance,
kidney problems, atherosclerosis, blindness, dyslipidemia (HDL/LDL), diabetes vellits, gallbladder disease,
PCOS
Deficiency: fasting, staring, high intensity exercise or ketogenic (low carb) = gluconeogenesis (making glucose from
non carb sources in liver)
Measurements: Fasting blood glucose, oral glucose tolerance test
FIBRE (dietary fibre = non-starch polysaccharides NSP) eg cellulose, hemicellulose, pectins, gums, mucilages
NRV: 25 (F) 30 (M) g/day
Resists digestion and absorbs water and waste = fullness + bulk to stools
Complete or partial fermentation in large intestines
Sources: veggies, fruit, whole grains, legumes → psyllium, chia, cereal, beans, quinoa, oats, bread, apple
Deficiency: constipation, pain, bloating, diarrhoea, conditions
Therapeutic benefits: eliminates toxins/cholesterol/bile acids, slows insulin response/absorption of glucose
and lipids, feeds good bacteria, reduces inflammation, prevents constipation, cancer, diabetes, cvd
Soluble fibre:
Fermented and nearly completely degraded by gut microbiome in large intestine → produces SCFA
Dissolves in water forming gel
Slows digestion = fullness
Binds to cholesterol and bile acids = lowers bad cholesterol and glucose levels
Eg fruit (citrus, apples), oats, barely, legumes,seeds → gums/mucilages, pectins, psyllium
Insoluble fibre:
Less fermented
Not water soluble
Adds bulk, helps w/ constipation + laxative benefit - holds water
Eg whole grains and vegetables → cellulose , lignin, hemicellulose
Resistant starch:
Starch that acts as a fibre - escaping digestion and absorption in small intestine
Bacteria in large intestine ferment it → forming short chain fatty acids SCFA → energy source for intestines
Butyrate (SCFA) - secreted by bacteria fermenting fibre → absorbed by large intestine → boosts
blood flow = healthy tissue
eg whole legumes, cereals, beans, lentils, green bananas, oats, potatoes, brown rice + cook then cool
starch
Fermentation: colonic bacteria ferment fibre = energy and substrate for bacteria (prebiotic)
WATER → essential micronutrient
Sources: drinking water, solid food (20% of total intake), endogenous production
Losses: 2.2L daily eg lungs, skin, kidneys (urine), GI tract (faeces) = obligatory loss 1.6L = min intake
Balance: hormonal control of kidneys (retain/release) → impacts volume/concentration of urine, blood
volume, blood pressure - electrolytes attract water + regulate osmosis
Intake: Men = 2.6L fluid (3.4L total intake) - Women = 2.1L fluid (2.8L total intake)
Body weight x 0.03 = L/day eg 70kg x 0.03 = 2.1L day
Factors increasing demand: drugs/megs, alcohol, coffee, fever, burns, exercise, climate, diarrhoea, urine,
air travel, hormone imbalances, diabetes, kidney failure, thirst defects, osmorector/antidiuretic mechanism
defect etc
Deficiency: (urine colour) thirst, weakness, vague discomfort, loss of appetite, reduced urine, flushed skin,
headache, impaired temp regulation, increase respiratory rate, dizziness, spastic mucosa, delium, collapse,
death
LIPIDS (triglycerides)
1 gram = 37.8 kilojoules = 9 Kcal
AMDR = 20-35% (more for children)
ADGs: less than 1% trans fats, less than 10% saturated fats, essential fats 1-10%, improve cofactors for fat
metabolism eg B6, C, mag, zinc
Functions: energy, store energy, insulation, protecton, cell membranes, cell signalling, hormones, vitamin D
conversion
Digestion
Mouth: melt at body temp, sublingual salivary glands secrete lingual lipase
Stomach: lingual lipase hydrolyses TGA bonds forming triglycerides and fatty acids. Stomach churning
mixes fat w/ water and acid. + some hydrolysis by gastric lipase
Small intestine:
Bile flows from gallbladder (via common bile duct) = emulsifies fat
Pancreatic lipase flows from pancreas (via pancreatic duct) (an intestinal lipase) = hydrolase/digest
lipids into monoglycerides, glycerol, fatty acids (absorbed)
Absorbed via diffusion (SCFA/MCFA) or as michelle/chylomicrons (LCFA) → into bloodstream
Large intestine: fat and cholesterol trapped in fibre exit via faces
Types of lipids
1. Triglycerides: 1 glycerol group + 3 fatty acids
Saturated (no double bonds)
Unsaturated
Monounsaturated (1 double bond) eg omega 9
Polyunsaturated (>1 double bond) eg omega 3 and 6
2. Phospholipids: 1 glycerol + 2 fatty acids + organic molecule (eg choline in lecithin) → amphipathic
3. Sterols: multiple carbon ring structure eg cholesterol or steroid hormones
SATURATED FATS
Only single bonds between carbon atoms (H attached to each carbon)
Non essential (produced endogenously)
Sources: plant oils and animal fats eg butyric acid, stearic acid → animal fats, butter, cream, full fat dairy
pastries, coconut, plm oils
Characteristics: straight, stable and solid at room temp (<10 carbons long) - methyl and carboxylic acid
ends
Types
Short chain fatty acids (SCFAs)
2-5 carbons long
Digested and absorbed in small intestine
Dietary or endogenously (via colonic bacteria fermentation of soluble fibre)
Provide energy from colonic cells = health benefits for humans
Make up 10% of total fatty acids in butter and milk fat
Medium chain fatty acids (MCFAs)
6-10 carbons long
Sources: diary products, coconut and palm oils
Easy to digest and absorb = small, dont require micelles to enter enterocytes → absorbed
directly into bloodstream and metabolised as SCFAs are to produce energy
Saturated long chain fatty acids (LCFAs)
11- 40 carbons long
Source: meat
Insoluble in water
Hydrogenated and trans fatty acids
Hydrogenation = saturates unsaturated fatty acids with hydrogens → changes from cis to trans
Prevent rancidity and prolongs shelf life = alters textures, liquids become more solid
Sources: margarine, fried foods, take away, processed meats, pastry/sweets, taco shells, chips, lollies,
frozen dinners
High hydrogenation decreases bodies ability to reduce LDL cholesterol and triglyceride levels
Alter LDL:HDL ratio = high inflammation - CVD, thrombosis
Conjugated linoleic acid → Naturally occurring trans fats in meat and milk dont have same negative effect
UNSATURATED FATTY ACIDS
One or more double bond in chain (2 missing H)
Monounsaturated fatty acids (MUFAs)
1 double bond
Characteristics: bent (cis), less stable (can withstand some heat and light) , liquid at room temp,
used for energy storage
Sources: plant based oils eg olive, canola, sesame, nuts A, C, H, M, avocados and olives
Functions: memory, cognitive function, structural integrity of cell membranes, improve lipoprotein
profile, reduce blood clotting, reduce cellular oxidative stress, reduce atheroma plaque formation
and reduce gallstone formation
Polyunsaturated fatty acids (PUFAs)
Lack 4+ hydrogen atoms = 2+ double bonds present
Characteristics: bent, kinks (cis), unstable (sensitibe to heat, light and oxygen), liquid at room
temp
Functions: cell membrane integrity and fluidity, raising HDL (more than mono), provides essential
omega 3 and 6
Sources: nuts, seeds, seed oils, fish - vegetable oils
Essential fatty acids = cannot be synthesised by body
Omega 3 = double bond located in third position eg linolenic acid
Omega 6 = double bond located in sixth position eg linoleic acid
Essential fatty acids (EFAs)
Fats that cannot be produced endogenously = must be consumed in diet
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X carbon from methyl end
Function = Homeostasis
Cell membrane components, growth, development and maintenance if body and systems
(brain, reproduction, skin, hair, bones, metabolism), production of biologically active
compounds (eicosanoids → active shorted lived hormones eg prostaglandins, thromboxanes,
leukotrienes and lipoxins)
Omega 3: Humans cant produce ALA (alpha linolenic acid) (and minimal conversion of EPA and DHA in
body from ALA) = essential →
SDA
ETA
EPA (eicosapentaenoic acid)
DHA (docosahexaenoic acid)
Functions: Long-chain n-3 PUFAs, cell membranes, intracellular signalling, gene expression, DHA
abundant in: cerebral cortex, retina, testes, semen
Anti-inflammatory: prostaglandins, thromboxanes, leukotrienes
Sources of ALA: flax, rice bran, soybean, dandelion, walnuts, pumpkin seeds → 1.3g/day (M),
0.8g/day (F)
Sources of EPA/DHA: fatty fish (herring, mackerel, prawns, salmon, sardines), anchovies,
trevally, brown/red algae, flaxseed oil, walnuts
250/550mg/day
Therapeutic uses
Therapeutic 1-3g/day EPA+DHA or 3-10g fish oil
Chronic inflammation, asthma, psoriasis, RA, inflammatory bowel disease, allery,
atherosclerosis, CVD, cancer, foetal development
DHA: nervous system - eyes and memory
Omega 6: humans cant produce LA (linoleic acid), can produce AA from LA = conditionally essential
Sources: pine nuts, walnuts, safflower, soybean oil, pumpkin + sunflower seeds, chia and flax
seeds, canola and vegetable oil, dairy
Pro-inflammatory: prostaglandins, leukotrienes, throxanes
LA: safflower, sunflower, hemp, soybean, sesame → 14g/day (M), 8g/day (F)
GLA: borage, blackcurrant, evening primrose (individually anti-inflammatory)
DGLA: breast milk
AA (arachidonic acid): animal products + made from GLA
Must be consumed with correct ration to DHA for proper brain function
Functions: - Contraction of smooth muscle fibres, cell membranes, brain function,
testosterone production and constituent of sperm, pro-thrombotic
Therapeutic application
GLA or evening primrose oil
Diabetic neuropathy, RA, asthma, eczema, atipic dermatitis, schizophrenia, ADHA
N3:N6 ratio → approx 1:5
Imbalance leads to proinflammatory state = cvd and autoimmunity
Hard to get omega 3, easy to get omega 6
Functions
Eicosanoid = signalling molecules - synthesised from (long chain polyunsaturated fatty acids) the
conversion of omega 3 or omega 6
Eicosanoids made from w:3 EFA
Anti-inflammatory, vasodilating, and anti-thrombotic
Protect against and resolve inflammation
Eicosanoids made from w:6 EFA, AA very potent
Generally proinflammatory
Over production associated with heart disease, cancer, diabetes, osteoporosis, immune
and inflammatory disorders
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An excess of the omega 6 fatty acid LA can suppress the conversion of the omega 3 fatty
acid ALA to the omega 3 fatty acids EPA ​and DHA, and increase the production of AA
Factors increasing demand
Deficiency of cofactor nutrients for desaturase enzymes (B6, Vit C, Mg, Zn),
High intake of land animal foods and dairy/ imbalance diets
Certain drugs, smoking
Diabetes, CVD and autoimmune diseases with inflammatory disorders (rheumatoid arthritis, lupus,
hashimotos),
Ageing: less able to convert dietary EFA’s to GLA, EPA and DHA
Vegetarians
ALA endogenously converted to EPA and DHA, process slow and inefficient, and affected
by genetics, sex, age, dietary composition
Optimise conversion of ALA to EPA and DHA via reducing intake of linoleic acid ω:6
Fat malabsorption issues: - Liver disease, Crohn’s and IBD, coeliac disease, cystic fibrosis,
↓lipas
Physiological stress: - Injury, chronic illness or surgery (accelerated cell turnover)
Rapid growth: - Pregnancy, childhood, adolescence
Primary nutritional deficiencies (vegetarians etc)
Deficiency of essential fatty acids: impacts growth and mental retardation, reproductive failure, skin, liver
and kidney disorders and visual issues
Symptoms: dry flaky skin, brittle nails, lumps on eyelids, sparse hair growth, depressed immunity,
reproductive failure, fatty liver deposits, impaired wound healing, impaired brain/eye development,
eczema, leg pain, learning deficits, hypertension
Excess: hypercholesterolaemia (high blood cholesterol) → heart attack and stoke
PHOSPHOLIPIDS
Cell membranes, lipoproteins, bile (emulsify fats), lung surfactant, nerves
Water and fat soluble → allows for vitamins, minerals, hormones to enter and exit
Amphiphilic = polar hydrophilic head, non polar hydrophobic tail
Sources: eggs, liver, soybeans, wheat germ, peanuts + some endogenous production
Eg lecithin → emulsifier in food industry
Functions:
Cell membranes, bile: emulsify fats, anchor some proteins to membranes, signal mediators, lung
surfactant, lipoproteins, temporary storage of fatty acids, fatty acids are substrates for eicosanoid
synthesis (anti-inflammation), widely distributed in CNS: significant component of myelin
STEROLS
Structure differs → contain no fatty acids, no glycerol backbone multiple ring structure no hydrogen chain
Animal sterols: cholesterol (meats, offal, patem seafood diary, eggs)
Plant sterols and stanols: phytosterols → inhibit absorption of omega 3 fatty acids
Biological function: component of bile acids, sex hormones, adrenal hormones, vitamin D & cell
membranes
Cholesterol: essential component of cell membranes - maintains fluidity so substances can diffuse in all
temperatures - also a precursor for vitamin D and bile
Blood cholesterol : transported in blood with other lipids in lipoprotein molecules (excess
cholesterol here)
Endogenous cholesterol: biosynthesis regulated by amount in diet but not equivalent → less
cholesterol produced with small frequent meals opposed to few larger meals = fasting reduces
cholesterol production
Sources:
Organ meat, shellfish, eggs, dairy, friend foods
Animal origin - Offal (brain, liver) and to a degree, muscle tissues - Pate, kidney, prawns
Plants - Squalene: cholesterol precursor (olives) - Other phytosterols poorly absorbed and
reduce cholesterol absorption
LIPOPROTEINS
Carry cholesterol and triglycerides through circulation
Types →
Chylomicron: almost entirely triglycerides = made in small intestine
Transport dietary lipids via lymphatic system to cells → muscles and adipose for storage
Become remnants in liver used to build VLDL or form bile salts/free cholesterol
VLDL (very low density lipoprotein): composed primarily of triglycerides = made in liver
Contain remnants of chylomicrons
Transport triglycerides from liver → cells
Increased by high saturated and trans fat diets
LDL (low density lipoprotein): composed primarily of cholesterol = made in blood by VLDL
Circulate and deliver their contents to tissue/cells
Elevated LDL is risk factor for CVD = build up of atherosclertoic plaques on blood vessels
Receptors (especially of hepatocytes / liver cells) help control the amount of LDL cholesterol in circulation (no. receptors lowered by saturated, trans, oxidised fats and
increased by soluble fibre (binds to fats and removes from circulation))
HDL (high density lipoprotein): composed primarily of protein = produced in liver (+ small
intestine)
Originate in liver → Reverse cholesterol transport → collect excess cholesterol from cells
and return it to the liver for recycling, conversion or excretion via bile
High HDL → protective from heart disease, anti inflammatory, prevents plaque, reduces
LDL oxidation
Low HDL increase risk of arteriosclerosis
Density refers to amount of protein component
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Improving cholesterol metabolism
Reduce saturated fats, trans fats, foods w high cholesterol
Increase fibre: reduce enterohepatic reabsorption of cholesterol
Increase specific cholesterol regulatory foods: plant sterols, nuts, soy protein
Support liver and gallbladder function (if gb removed: increase lecithin to emulsify fat)
Increase MUFAs and EPA/DHA: both associated with reduced CVD risk
Lifestyle change: weight loss, stress, alcohol, smoking, refined sugar, increased physical activity
Insoluble fibres trap bile cursing body to use more cholesterol for bile replacement
PROTEINS
1 gram = 17KJ = 4 calories
AMDR: (NRV) 15-25%
RDI - 46g/day → 0.75g/kg/day females —---- 64g/day → 0.84g/kg/day males
Slightly larger for infants, children, in pregnancy and elderly + athletes 1.2-1.7g/kg/day athletes
Amino acids linked via peptide bonds
Contain nitrogen (unlike CHO lipids and carbs)
Amino acid → components
Amino group (nitrogen NH2)
Acid group (COOH)
Central carbon
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Hydrogen atom
Side group (makes each amino acid unique)
20 amino acids coded for in DNA (9 are essential/not made in the body)
Protein → longer than 50 amino acids
Structure → denatured by heat + acidity
Primary: order of amino acids (covalent peptide bonds)
Secondary: alpha helix, bete sheets (hydrogen bonds)
Tertiary: covalent bonds between cysteine (disulphide bridges) + hydrophobic cluster inwards =
determine shape
Quaternary: 2+ polypeptide chains eg haemoglobin
Protein turnover: continuous synthesis and breakdown of proteins ensuring optimally functioning proteins
→ 3.4g/kg of body weight is tuned over in the body every day
Amino acid pool - A mix of essential and non-essential amino acids derived from protein
breakdown and dietary protein intake
Nitrogen balance = Protein (nitrogen) intake - protein (nitrogen) loss (B=I-(U+F+S)
Positive nitrogen balance: intake greater than loss = bodybuilding protein = growth (infancy,
childhood, adolescent, pregnancy, recovery from protein deficiency or illness)
Negative nitrogen balance: nitrogen loss exceeds nitrogen intake = body loosing protein =
starvation, fever, infection, injury, sever burns.
Nitrogen equilibrium: intake sufficient to maintain and repair tissue = normal healthy
Protein functions
Growth and repair
Structural constituent providing strength and support → contractile (actin and myosin), fibrous
(collagen and elastin), globular (myoglobin and calmodulin), proteoglycans (extracellular matrix)
Transport → carry and store materials via transport proteins such as lipoproteins, transferrin (iron)
Enzymes → proteins increase rate of chemical reactions as enzymes
Fluid and salt regulation → albumin and globulin (fluid volume in capillaries), protein in plasma
maintains blood volume, cell membrane channels and pumps (sodium/potassium gates), buffer of
acid/alkaline balance (accept/donate hydrogen ions)
Quality → high level of digestibility and contains all essential amino acids
Digestibility → animal sources (90-99% digested), plant sources (70-90% digested)
Amino acid composition (complete or incomplete)
Complete - containing all 9 essential amino acids in the approximate amounts needed by
humans. eg soy, animal protein sources (red and white meat), dairy products (milk,
cheese, yoghurt) and egg + teff, lupin, hemp seeds, buckwheat
Incomplete - missing one or more of the essential amino acids eg most vegetable
sources, grains, nuts, seeds, and legumes = soybeans, buckwheat, quinoa, teff,
amaranth, chickpeas, and lupin
Essential amino acids
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Protein combining → Incomplete paired to ensure essential acids are proteided
Factors increasing demand
Growth periods and breast feeding, Injury and wound healing (including burns), Illness: diabetes, cancer,
infection, Prescription drug use, Drug use: alcohol and cigarettes, Low birth weight infants, Stress, Age:
increases with age
Sources
Oats, chickpea flour, red kidney beans, peanuts, lentils, beef mince, pumpkin seeds, cheese, lipin, egg, soy
Protein digestion
Mouth → mastication (chewing) begins breaking down protein
Stomach → gastric cells release gastrin into blood → stimulates gastric juices, gastric juices and
hydrochloric acids denature proteins and convert stomach pepsinogen to pepsin → pepsin hydrolyses
peptide bonds → partially digested protein enter small intestine and stimulate release of secretin and
cholecystokinin hormones
Pancreas → secretin and cholecystokinin stimulate pancreas to release bicarbonate (which neutralises
chyme), as well as proenzymes into intestine
Small intestine (complete digestion) → pancreatic enzymes activated and digested polypeptides, enzymes
in intestinal mucosal cells and lumen complete digestion
Amino acids are absorbed into bloodstream and travel to the liver → transaminated (make non
essential AA, deaminated (make glucose/fat storage), deaminated for energy
Deficiency
Lack of intake or digestion and metabolism → results in progressive loss of body composition due to
inadequate food intake
Protein energy malnutrition (PEM) = deficiency
Acute PEM: may lead to impairment of function of skeletal muscles and immune system, morbidity
and mortality
Chronic PEM: may lead to progressive loss of body composition but may show increase risk when
faced with infection or traumatic change
Protein deficiency - mild to moderate (symptoms) - if causes by low intake, address why (nausea, low
appetite problems chewing or swallowing, anxiety or pain, frequent infections, bloating, poor muscle tone,
low bp, brittle nails and hair, anaemia, poor kidney function )
Causes
Maldigestion: impaired breakdown in intestinal lumen → intact molecules cross intestinal mucosal
barrier: immune sensitivity, allergic response
Malabsorption: impaired absorption of digested food due to altered intestinal mucosa
Anti Nutritive foods → adversely affect bodies ability to digest and absorb protein → Substances
and alcohol → Liver congestion: less able to rebuild and supply proteins
Nutrient deficiency: nutrients biochemical processes required for digestion and absorption
Diseases
Kwashiorkor: severe deficiency in child (18months - 2 years) - high carb - rapid onset = growth
reduced 60-80% of weight for age = bulging abdomen, bloating and oedema, swollen, inability to
grow/gain weight, fatty liver, apathy, sadness, loss of a peptide, hair and skin
Marasmus: malnutrition in infants deprivation/impair absorption- developes slow = body weight
reduced to less than 60% normal + muscle wasting → anxiety, apathy, weight loss, diarrhoea,
dehydration, shrinking stomach, hair/skin, good appetite
Cachexia: muscle wasting - chronic illness eg cancer = physical weakness, immobility, lost
peptide, asthenia, anaemia, fatigue, weight loss
Protein toxicity = excess
Due to: supplementation
Maple syrup urine disease ?? - small of urine, treat with B1, B2, biotin, dietary control of BCAA
Kidney disease: increase work on kidneys
Osteoporosis: increase calcium secretion
Heart disease: sources of protein commonly high in saturated fat
Cancer: excess red meat = colon cancer
Protein status and assessment
Dietary analysis: calculating protein intake through diary or recall - doesn't account for digestion and
absorption
Physical assessment: presence of oedema, unintentional weight loss, muscle wasting and subcutaneous
fat loss → subjective global assessment SGA and mini global assessment, mid-upper arm circumference
MUAC, hand grip strength (dynamometer)(average of 3 attempts
Biochemical lab testing: albumin and prealbumin, nitrogen balance (urine), BRP, transferrin, total
cholesterol, CRP, TLC
Protein synthesis
Transcription - mRNA made from DNA template in nucleus (RNA polymerase unzips DNA and puts RNA
nucleotides in the right places (complementary)
Translation - mRNA strand read - start codon, specific amino acids - bond bia peptide bonds - stop codon
Types of mRNA
Messenger RNA - carry sequence code of AAs required to make specific protein
Ribosomal RNA - directs protein synthesis as it reads mRNA
Transfer RNA - anticodon matches codon on mRNA, determines the amino acid added
Nucleic bases
Adenine - thymine → RNA uses uracil instead of thymine
Guanine - cytosine
Purines and pyrimidines
Purines: adenine and guanine
Pyrimidines: cytosine, thymidine, uracil (CUT)
Purine and pyridine metabolism
Purines (a, g)
Mostly in liver: purines → xanthine → uric acid
Uric acid: secreted via urine (sometimes digestive tract) - can crystallise in small vessel eg joints
→ gout
Foods rich in purines: meat and seafood = increase uric acid levels = increase risk of gout
(arthritis) and renal disease
Small fish, meat, alcohol (beer), coffee, surgery drinks, exacerbate gout
Legumes are high purines but NOT associated with gout
Diary and sour cherry are protective/therapeutic
Uric Acid excreted by kidneys, disorders of kidneys can lead to excess uric acid in blood
Health Benefits of Purines
Mental function (stimulating CNS) - dementia patients
Preventing lung cancer
Deactivate free radicals (ie an ‘antioxidant’)
Pyrimidine (c, u,t)
Degradation → ammonia → enters urea cycle → secreted
Deamination and transamination
Fate of amino acids
Adequate → haemoglobin, hormones, enzymes, antibodies.
Excess → burnt off or stored as fat
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Amino acid pool = excess amino acids used for
Production of glucose
Energy generation
Synthesis of fat
Non essential amino acids or other nitrogen containing compounds
Deamination - nitrogen amino group NH2 removed from amino acid producing a keto acid
Catabolism of AA yields nitrogen (NH2-) which becomes toxic ammonia (NH3) → ammonia travels to liver
and combines with CO2 forming urea and water → excreted by kidneys (nitrogen exists via urea cycle or
skin)
Remaining amino acid carbon skeleton enters TCA cycle (citric acid/krebs)
Transamination - transfer of nitrogen group NH2 from amino acid to keto acid = makes non essential amino acid
Frees up carbon backbone (as alpha-keto acid) for metabolic processes
Requires vitamin B6
New keto acid formed from orginical AA enters TCA cycle (CAC)
Ketone synthesis preserves degradation of protein in muscles
TCA/CAC/Krebs cycle - series of chemical reactions that produce energy
Amino acid metabolism - 10-15% total energy production
1. Breakdown in small intestines
2. Protein synthesis in liver
3. Excretion of ammonia through urea cycle
Transamination occurs first → nitrogen removed (as toxic ammonia → travels to liver with CO2 →
enters urea cycle and is converted to urea (less toxic) for excretion via urine, carbon backbone
remains)
Fed (insulin increase)→ proteins → amino acids → intestine → bloodstream → liver → protein synthesis OR
conversion to glucose or fatty acids
Glucogenic amino acid - converted to glucose precursors = pyruvate, oxaloacetate or
intermediates = glucose = glycogen stored in liver (gluconeogenesis)
Ketogenic amino acid - Converted to fatty acids precursors = acetyl coA or acetolactic = fatty
acids = TAGs storage stored in adipose tissue
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Leucine and lysine = exclusively ketogenic (converted to fatty acids if consumed in
excess)
Fasted → fatty acids released from adipose tissue to liver for synthesis of glucose + amino acids released
by muscles (tissue) → blood → liver → gluconeogenesis ?
Ketones produce in prolonged fasting or low carbohydrate intake
Acid-Alkaline Theory (chales bernard) → Based on pH of ash (inorganic material) taken from bomb calorimeter
Fruits and vegetables left alkaline ash
Grains and meats left acidic ash
Net endogenous acid production (NEAP)/ potential renal acid load (PRAL) = acid or alkaline forming
potential of foods after metabolism
Homeostasis = blood pH maintained neutral = 7.35-7.45
Classification
Foods classified based on effect on blood pH and kidney (renal) acid load - not taste or raw
composition eg lemon tastes acidic but is alkaline
Acid forming foods - contain anions which bind H+ ions from pancreatic bicarbonate HCO3- in the
gut and reduce bicarbonate availability as blood buffer
Alkaline forming foods - contain cations as salts (eg magnesium citrate) which metabolise to form
HCO3- (bicarbonate) in the liver (key acid buffer), releasing it into the blood = removes hydrogen
ions
Balance = 20% acid, 80% alkaline
High acid → affects blood and tissue = gout, inflammation, osteoporosis (due to damage on
calcium to buffer excess acidity)
Neutral foods (buffer) → correct acid/alkaline balance when eaten together eg fruit and yogurt
Proteins (main source of acidic minerals) important to maintain balance = ammonia NH3 is
key H+ acceptor in kidney tubules for excretion as ammonium ion NH4 = acid-alkaline theory
debated
Acid foods
Most flours, grains, legumes, nuts and seeds
Most animal proteins (meat, fish, some cheese)
Dairy is neutral (milk and yoghourt) to very acidic (parmesan cheese)
Alkaline foods
Millet, adzuki, almonds, quinoa
Fruits and vegetables (except cherries due to hippuric acid)
Sugar and honey are slightly alkaline
FINAL EXAM CONTENT (SESSIONS 8-26)
NUTRITION ASSESSMENT - nutritional status and nutrition-related disease risk of an individual or population with
the purpose of initiating appropriate treatment or intervention
Malnutrition - both under and over nutrition
Primary nutritional deficiency: inadequate intake in diet (assessment through diet record)
Secondary nutritional deficiency: other factors affecting absorption, metabolism, storage and excretion
Nutritional imbalances, deficiency or excess progress in stages and are assessed in different methods
(subject + objective methods)
1. Initial stages are convert or sub-clinical and cannot be observed
2. Overt stage is the unaddressed progression of subclinical and can be observed / obvious
Methods of nutritional assessment (A, B, C, D, E) → holistic combination of methods
A - Anthropometric: measurement of the body (objective) - calibrated instruments
BMI: weight/height - inaccurate
Waist circumference - distribution
Waist-hip ratio
Growth charts
Skin fold thickness - body fat percentage
Bioelectrical impedance analysis - electrical current - body water free from fat
Dual energy Xray absorptiometry DEXA - body composition - bone density
Air displacement plethysmography - body volume and density of fat
B - Biochemical: laboratory and functional pathology tests (objective) - measure nutrients and biomarkers
for nutrient status and disease progression
Used to identify 2nd and 3rd stage nutrient imbalance (covert) and assess secondary nutrient
imbalance
1. Static biochemical tests - biological tissue and fluids (blood urine, saliva, hair, stool)
2. Functional pathology tests - indirect measures of nutrient status via intermediate
metabolites and enzymes dependent on nutrient cofactors
Blood: (whole, serum or plasma)
Assess nutrient absorption reflecting recent intake (24-48 hours) - not reflect nutrient
storage and function
Erythrocytes reflect 120 day storage of some nutrients (FAs, B6, Zn, Cu, Se, folate)
Urine → iodine, magnesium, toxic metals
Saliva → (functional) → Hormonal, inflammatory and metabolic markers such as cortisol,
melatonin, leptin, oestrogen, testosterone, eicosanoid
Hair mineral analysis → assessing toxic metal exposure eg cadmium toxicity
Stool testing → assesses gastrointestinal function, gastrointestinal tract inflammation, liver and
pancreatic function + microbial infections (yeasts, bacteria, viruses, parasites)
Functional pathology tests
Complete digestive stool analysis
Functional liver detoxification profile
Intestinal permeability - urinary lacutolse ectreation after test does
Hydrogen breath testing - CHO malabsorption, lactose intolerance, SIBO and IBS
Finger prick test (dried blood) - measures Vit D, FA, AA, soluble transferrin and retinol binding
protein (no need to see GP)
Urinary metabolic phenotyping - objective assessment of dietary intake = quality of diet and
metabolic health
Questions to ask → validated, will it change treatment invasive/expensive, less
invasive/expensive option, needed?
C - Clinical: assessment
Physical signs (objective) = overt eg tissue with fast turn over - nails
Symptoms (subjective) = how client feels
Medical and family history (subjective and objective)
D - Dietary: nutrient intake (subjective) (susceptible to under, over or misreporting)
Identifies → primary nutrient deficiencies, excesses, first stage nutrient imbalances + adhearances
of dietary guidelines, nutrient reference values and dietary interventions
The 3 conventional methods of dietary assessment = food frequency questionnaire, food
records, 24 hour dietary recalls
Retrospective: recalling past intake
Memory eg 24h recall (actual intake)
FFQ food frequency questionnaire
Prospective: recording intake as it occurs
Food daily/3 day weighed food fiety (actual intake)
Less memory but higher burne - under reporting
Actual intake: what was consumed over given time
Usual intake: what is typically consumed
Qualitative: variety and quality of diet
Quantitative: how much of each nutrient is consumed
E - Ecological: socio-cultural, economic, environmental factors (subjective)
Nutrition monitoring in populations - every 10 years = surveys, surveillance, screening, intervention
ENERGY BALANCE (sum of energy in and energy out)
Energy in + energy out = energy balance
Positive energy balance: intake exceeds expenditure = excess stored = weight gain
Negative energy balance: expenditure exceeds intake = energy lost = weight lost
Estimated energy requirement (EER) = BMR + PAL + TEF
Basal metabolic rate (BMR): increased by body size, lean tissue, sec, growth, illness, caffeine decreased by fasting
Physical activity level (PAL)
Thermic effect of food/energy expended on digestion (TEF)
When PAL or appetite decreases (age/illness/disability) consuming nutrient dense foods is
essential
Measured in kilojoules kJ or megajoules (1MJ = 1000kJ), 4.18kJ = 1 kilocalories (calorie)
Energy in food
AMINO ACIDS - Know = sources, biochemical structures, physiological functions, deficiency indications and toxicity
Nitrogenous compounds
Number, kind and order = protein
No RDI as adequate protein = AA
Don't need digestion
Essential (need to be consumed)
Non essential (can be produced endogenously)
Glucogenic → may be catabolized to form pyruvate - essential intermediate in many biochemical pathways
eg gluconeogenesis
Ketogenic → catabolized into acetyl-CoA - for ketone body production
Side chains: characteristics determine shape and function of AA
Hydrocarbons (CH): leucine, isoleucine, valine, glycine, alanine
Hydroxyl groups (OH): serine, threonine
Acidic groups (COOH): glutamate, aspartate, glutamine, asparagine
Basic groups (NH): lysine, arginine, histidine
Aromatic groups (ring structure): tryptophan, phenylalanine, tyrosine
Sulphur groups (S): methionine, cysteine
Imino group (NC): proline
Non protein amino acids → function on their own, don't make peptide bonds eg taurine, carnitine,
carnosine, ornithine, creatine
Amino acid Isomers (forms) Not interchangeable
L-amino acid → amino group positioned on left (main body type)
D-amino acid → amino group positioned on right
AA’s w/ HYDROCARBONS (CH) → leucine, isoleucine, valine, glycine, alanine
Branched chain amino acids BCAA → energy and protein synthesis (used to develop muscle and promote
recovery) = essential AAs
Isoluthine
Leucine
Valine
Food sources → meat (beef, chicken, snapper), eggs, dairy (milk, cheddar cheese), legumes, brown rice,
tofu , sunflower seeds, oats
Functions → energy and protein synthesis
Make up 20-30% of all amino acids consumed
Preferred nitrogen source for glutamate synthesis
Detoxify ammonia in skeletal muscles
Useful for organ damage/tissue repair
Essential substrate for synthesis of body proteins
Used by athletes → enhance performative, prevent fatigue, improve concentration, reduce protein
and muscle breakdown (little evidence)
Maple syrup urine disease MSUD → genetic disease inhibits ability to breakdown BCAAs = urine smells
sweet due to ketones
Presents in neonates with feeding difficulties, vomiting irregular respiration and neurological
degeneration = dietary intake control
Therapeutic uses
Hypermetabolic states eg burns, sepsis or Liver disease and cirrhosis
VALINE → essential → glucogenic amino acid
Interchangeable with isoleucine
Main pathway of metabolism →metabolised into succinyl-CoA for CAC
Functions/role - Energy production, protein synthesis, muscle growth and tissue repair, muscle
coordination, lowers elevated blood sugar levels, increase growth hormone prediction, role in
mental and emotional health
Disease: hypercalcemia → presents at birth and causes deficiency of enzyme valine transaminase
(irritability, hallucinations, headache)
LEUCINE → essential → ketogenic amino acid
Interchangeable with isoleucine
Main pathway of metabolism → metabolised into acetyl-CoA for citric acid cycle
Food sources → higher in most grains than other BCAAs; infacts have high needs - improves
insulin release (increase vit B3 excreaton as B3 is insulin binding)
Functions/roles → Synthesis of protein, contributes to regulation of blood sugar levels, growth and
repair of muscle and bone tissues, growth hormone production, wound healing, prevents
breakdown of muscle proteins after trauma or sever stress, beneficial for phenylketonuria
Toxicity → high doses (through supplements) may stimulate vitamin B3 excretion and lead to
deficiency + intolerance may result in hypoglycemia
ISOLEUCINE → essential → glucogenic and ketogenic amino acid
Interchangeable with leucine and occasionally valine
-
Main metabolism pathway → metabolised into acetyl CoA and succinyl-CoA for CAC
Food sources → high in legumes, meat, dairy - low in grains
Functions/role → synthesis of proteins, energy regulation and feul for skeletal muscle, muscle
development and repair, wound healing, detoxification of nitrogenous wastes, stimulating immune
function, promoting secretion of several hormones, regulating blood sugar
GLYCINE - Non essential AA with simplest AA structure
Can be converted to serine in reversible reaction
Glycine metabolism location → liver and kidneys → metabolised into carbon dioxide and ammonium in
glycine cleavage system
Sources: peanuts, tuna, snapper, sunflower seeds, almonds, chicken, turkey, cashews, oats
Therapeutic dose → 4g/d pr 200-800mg/kg/d used in divided doses
Functions and therapeutic application
Antioxidant → utilised in production of glutathione
Inhibitory neurotransmitter inhibiting norepinephrine = used for anxiety, panic disorders, addiction,
insomnia
Antispasmodic → used for muscle tension, spasm, cramping and twitching
Toxicity
No known toxicity (well tolerated orally and topically)
Side effects → nausea, vomiting, upper gastrointestinal discomfort, soft stool, mild sedation
ALANINE → Non essential, glucogenic AA - second most common circulating AA (after glutamine)
Side group - methyl CH3
Absorbed in small intestine & synthesised endogenously from pyruvate in the liver or breakdown of DNA and
dipeptides carnosine and anserin
Sources: tune, snapper yeast/vegemite, chicken, salmon, sunflower seeds, peanuts, almonds, wheat bran,
flour, kidney beans
Dosage - Therapeutic range of DL-alanine = up to 40g/day and beta-alanine = 2.4-6.4g/day daily in divided
doses
Functions/therapeutic action
Organ specific AA found in liver and muscles (glucose-alanine cycle)
Glucose alanine cycle = glucose → pyruvate → alanine = deamination process
Recycles glucose from muscle to liver → reused when glycogen stores are full
Pyruvate gains NH3 in muscle from AA (often GLU) → alanine
Alanine carries NH3 to liver
ALA deaminates to pyruvate (NH3 is excreted)
Gluconeogenesis occurs in liver and glucose released into blood
Muscles take up glucose again for energy
https://www.youtube.com/watch?v=dCzu9KE7a9c&t=79s
Assists with energy and carnosine production
Immune system - activating T-cells (play a role in adaptive immunity)
Protein synthesis
Athletes → performance and reduced fatigue (main energy source) and muscle damage (free
radical scavenger reducing oxidative stress), removes ammonia and recycles glucose
Older people → preserve protein and muscle status
Hypoglycemia
Forms
Alpha-alanine , DL alanine, L-alanine - supplements
Beta-alanine - animal sources, supplemental form and activated from the body
Free alanine - from the brain
Factors increasing demand → ageing, pregnancy, inadequate dietary intake (vegan, vegetarian),
athletes/excursion
Deficiency symptoms → blood glucose dysregulation, immunity, plasma alanine is decreased when BCAA
are deficient, symptoms associated with B6 deficiency as alanine metabolism is dependent on enzymes
containing B6
Toxicity → orally beta-alanine is tolerated well
AA w/ AROMATIC SIDE CHAINS → phenylalanine, tyrosine, tryptophan
TRYPTOPHAN (Trp) → essential AA - aromatic side chain (ring) = B3 link
Mainly metabolised in liver
Biochemical application/functions: tryptophan → 5-HTP → serotonin and melatonin
Serotonin/melatonin synthesis 5-HTP pathway (parasympathetic nervous system (rest and digest)
indolamines)
Niacin (B3) synthesis
Energy production: ketogenic and glucogenic role in krebs cycle
Protein synthesis
Therapeutic application
Mood and sleep regulation - anxiety, depression, insomnia
Minimisation of tension, irritability, depression
Gut -brain connection → guts role in metabolism of trp; supports intestinal motility and regulation
of gut brain axis also improves immune function
Recommended daily intake dietary proteins
Suggested daily requirement → 290-350 mg/d (4-5 mg/kg/d)
Requirements relate to intake of niacin (B3)
Therapeutic range: 1-6 g daily
Dietary sources: soy flour, pepitas, seaweed, chicken, chia, tuny, cheese, turkey, cashews, cacao, oats
Factors increasing demand: Increase requirement for protein, Inadequate protein, Impaired
gastrointestinal function (poor gastric acid secretions), Low intake of niacin B3, Pharmaceutical drugs eg
oral contraceptive pill
Deficiency signs and symptoms (associated with niacin deficiency) - Irritability, depression, anxiety,
insomnia, muscle wasting, delayed growth and development in children
Toxicity
Low toxicity levels of trp linked to → anorexia and inability to gain weight = discontinue use
Too much 5-HTP linked with → serotonin syndrome = mild (shivering, diarrhoea), sever (muscle
rigidity, fever, seizures) pain, fatal
PHENYLALANINE (Phe) → essential AA - aromatic side chain (ring)
Mainly metabolised in liver and kidneys
Biochemical pathway + Functions
Precursor of → tyrosine, dopamine, noradrenaline (norepinephrine) and adrenaline (epinephrine) =
SNS (fight/flight) catecholamines
Phe → L-tyrosine → L-dopa → dopamine → norepinephrine → epinephrine
Energy production → ketogenic and glucogenic role in krebs cycle
Protein synthesis
Therapeutic application → for vitiligo (oral and topical use), insufficient evidence for use in alcoholism,
depression and parkinsons, memory and addiction
-
-
Intake/therapeutic range
DL-Phe 1-4 g/d
L-Phe 1-14 g/d
Early pregnancy recommendations → 15 mg/kg/d - Late pregnancy recommendations → 21
mg/kg/d
Supplemental form → D-phenylalanine, L-phenylalanine (essential amino acid form),
DL-phenylalanine (synthetic, found in 50% supplements)
Food sources: gelatin, lentils, peanuts, almonds, snapper, chicken, vegemite, turkey, cashews, egg,
broccoli
Toxicity/adverse effects
Toxicity due to PKU - rare autosomal, metabolic disorder enzyme that breaks phe into tyrosine
absent = phe toxicity → irreversible damage to CNS = mental retardation, microcephaly, seizures,
spasticity = manage though strict low protein → diagnosis routine newborn screen (heel prick) tests
for PKU
Schizophrenia, parkinson's disease, oralling (anxiety, contripation, fatigue, headache, heartburn,
hypomania, insomnia, nausea, sedation, vertigo), topically (erythema, itching, burning
TYROSINE (Tyr) → conditionally essential AA (produced for phenylalanine - except PKU) aromatic side chain
(ring)
Mainly metabolised in the liver
Biochemical pathway
L-tyrosine → L-dopa → dopamine → norepinephrine → epinephrine
Thyroxine (T4) and triiodothyronine (T3) (thyroid hormones)
Melanin (skin, eyes, hair)
Functions
Energy production → ketogenic and glucogenic role in krebs cycle
Protein synthesis
Required for thyroid function
Precursor to dopamine, norepinephrine and epinephrine
Therapeutic application
Supplementation required in PKU
Cognitive performance, Memory, Sleep deprivation, Depression, ADHD, stress, PMS, Alzhimers
and other dementia etc, Alcoholism, heroin and cocaine withdrawal, Cardiovascular disease and
hypertension, impotence, loss libisio and schizophrenia, Suntan agent, appetite suppressant,
exercise performance, Topically for signs of ageing
Intake
Therapeutic range → 100-150 mg/kg/d (up to 3 months)
Available as L-tyrosine, N-acetyl-L-tyrosine (NALT) which is more soluble
Food sources: cheese, tuna, chicken, lentils, vegemite, sunflower seeds, egg, turkey, almonds, oats, brown
rice
Factors increasing demand
Increase protein requirements
Those with PKU (due to inability to convert Phe to Try
Adverse effects
Exacerbate hyperthyroidism and graves disease
Caution with prescription medications including levodopa and thyroid hormones
AA’s w/ ACIDIC (COOH) SIDE CHAINS → aspartic acid, glutamic acid, asparagine, glutamine
GLUTAMINE AND GLUTAMATE
Glutamine → conditionally essential AA
Found in all protein foods (most abundant AA)
Synthesised from → ammonia and glutamate = in muscle, adipose tissue and organs
Can cross blood brain barrier → metabolise to glutamate an excitatory neurotransmitter metabolism to
GABA in inhibitory neurotransmitter
(glutamine → glutamate → GABA) - requires B6
Supplemental form → L-glutamine
Therapeutic dose → 7-21g/day for gut repair, 2-4g/x2 daily for cancer therapy
In children 0.7g/kg/d
Infants 300mg/kg/day
Functions + Therapeutic application
Gastrointestinal protection and repair - fuel enterocytes, regulation of proliferation and
differentiation (deficiency - atrophy, ulceration and necrosis of intestinal epithelium)
Immunomodulation - fuel for lymphocytes, production of igA antibodies
Antioxidant
Cardio protective
Synthesis of proteins
Energy source for hepatocytes
Precursor to nucleotides (purines and pyrimidines) → make DNA and RNA
Functions of glutamate
Excitatory neurotransmitter (active NMDA receptors)
Precursor for GABA (inhibitory NT) synthesis (eth vit B6)
Antioxidant (precursor for glutathione production) ‘
Deaminates to oxaloacetate
Deficiency signs and symptoms → Increased gut permeability and impaired wound healing
Toxicity → nausea, non cardiac chest pain, fatigue, musculoskeletal pain
ASPARTIC ACID (Asp) Aspartate → non essential AA
Required in urea cycle
Asparates amine → asparagine
Functions
Energy production: aspartic acid plays a glucogenic role in CAC cycle and deaminates to
oxaloacetate
Protein synthesis and nucleic acid synthesis (purines and pyrimidines)
Amino acid synthesis: asparagine, arginine, lysine, methionine, isoleucine
Therapeutic application → salts used to increase mineral supplements, enhance athletic performance,
reduce fatigue, opiate withdrawal and increase muscle strength
Toxicity → none
Therapeutic range → D-aspartic aicd: 3-6g/day (1-3 months)
-
Food sources: gelatin, mung beans, peanuts, tuna, chicken, sunflower seeds, almonds, fish, cheese,
apricot, walnuts, eggs
Forms
L-aspartic acid (L-Asp) metabolised in resting muscles
D-aspartic acid (D-Asp) functions in nervous and reproductive systems
Don't confuse with aspartame
AA’s w/ SULPHUR SIDE CHAINS→ methionine, cysteine (+homocysteine & taurine)
METHIONINE → essential AA → sulphur side chain - glucogenic (generates succinyl CoA for CAC)
Metabolised by liver to A-adenosyl methionine - begins with activation of SAM (S-adenosylmethionine methyl donor)
SAM-e → dependent of folate and b12 - useful for depression
SAM – AA synthesis (creatine + carnitine), hormone synthesis (epi, melatonin), myeline sheath,
gene expression, cell membrane fluidity
Methylation involved in synthesis of → creatine and carnitine, epinephrine and melatonin, myelin sheath
maintenance, gene expression, cell membrane phospholipid bilayer fluidity, polyamine synthesis,
metabolism of homocysteine (sulphur containing) and other amino acids
Functions
Methylation = (transfer of one carbon group (CH3) methyl group addition or substitution,
necessary for many metabolic pathways
eg methionine → homocysteine → cysteine → glutathione. Necessary cofactor nutrients
include B vitamins, especially B12. via remethylation and trasulfuration
Transsulfuration = synthesis of cysteine from homocysteine (requires B6 and serine →
cystathionine → cysteine)
CARNITINE → Synthesised in liver and kidneys, stored in muscle tissue, synthesised
from lysine + CH3 (methyl)
Support folate metabolism
Protein synthesis (start codon for translation of mRNA)
Energy production (glucogenic - deaminated carbon skeleton plays a role in CAC + precursor for
gluconeogenesis)
Homocysteine metabolism - synthesis of SAMe and cystine
Hyperhomocysteinemia = indicates low folate and B12, too much homocysteine in blood
and compromised cysteine synthesis
Therapeutic range → 1.5-2.5g/d ( or 400-3200mg/d of SAMe divided dose = strong side effects )
Therapeutic application → detoxification pathways (heavy metals, alcohol, pollutants, drugs) + help with
depression (synthesis of epi, nor epi, serotonin, dopamine)
Supplementation → L-methionine, D0methionine, DL_methionine, S-adenosyl-L-Methionine (SAMe)
Factors increasing demand → low homocysteine (methionine used for its production) - depends on protein
intake + growth state and ageing state
Signs of deficiency → none
Toxicity → dosage over 100mg/kg lead to severe cerebral effects, hypermethioninemia (genetic disorder),
gastrointestinal upset, dizziness, leukocytosis, increase urinary calcium secretion, headaches, hepatic
encephalopathy, increase homocysteine levels, hypotension ,irritability, drowsiness
Food sources → beef, fish (tuna, snapper, salmon) and dairy products (cheese), sunflower seeds, chicken,
eggs, oats, Tofu, Brown rice,
CYSTEINE → conditionally essential - sulphur containing
-
-
-
2 oxidised cysteine molecules joined via disulphide bonds
Metabolised to protein
Functions
Protein synthesis and structural maintenance (stabilised tridimensional protein structure via
disulfide bonds)
Precursor of - cystine, taurine and glutamate production
Energy production - glucogenic
Synthesis of taurine (sulphur containing)
Synthesis of glutathione GSH (antioxidant)
Detoxification via liver conjugation with sulfhydryl groups (SH)
Mucolytic
Therapeutic application → NAC used to increase metabolite of glutathione and L-cysteine levels in body +
treating mucolytic conditions
NAC - Vascular health, muscle strength, bone density, cell mediated immunity, preservation of
cognitive function, systemic inflammation
L-cysteine - antioxidant, mucolytic function, immune system, protection/detoxification of liver, heart
disease, diabetes, ageing, digestive system
Supplement form → N-Acetyl cysteine (NAC) , L-cysteine
Therapeutic dose NAC → 1.2-2g/d, 900/2700mg/d children (8-12 weeks), only when necessary in
pregnancy
Toxicity → (not cysteine - only IV NAC) → digestion disturbance, nausea diarrhoea, headache, dizziness,
tiredness, disorientation, poor concentration, rash, dysuria, joint pain, pain in legs, respiratory effect
Food sources: sunflower seeds, cashews, peanuts, oats, eggs, almonds, whiting, snapper, chicken wheat
NOT AA AS CANT FORM PEPTIDE BONDS
TAURINE → non essential amino acid = not one of 20 amino acids as cant form peptide bond
B-amino sulfonic acid
Widely distributed in animal tissue - not plants
Made from cysteine in liver → concentrated in muscle and central nervous system + found in heart, liver
and kidneys
Functions
Conjugates cholesterol in bile formation (makes bile salts)
Antioxidant action
Inhibitory neurotransmitter activity
Eye function and health, particularly in retina
Cytoprotective action (improves heart contractility)
Improves insulin sensitiviy
Factor in brain development, optic and immune system, osmotic regulation, reproduction,
stabilisation of membranes, cardiac muscle regulation and inflammation
Cytoprotective to integumentary, cardiovascular, respiratory, muscular, skeletal, circulatory and
endocrine systems
Neurological disorders
Therapeutic application → ** + congestive heart failure and hepatitis
Therapeutic range → 1500mg/d divided x3 doses), 250-1000mgd for children OR 1000-6000mg/d and
40-50mgkg for athletes
Signs of deficiency → retina (photoreceptor loss), negatively alters energy metabolism, altered gene and
protein expression, accelerate ageing, development abnormalities, inadequate protein intake (vegan/vego)
Toxicity → none, safe dose is 3g/d
GLUTATHIONE (GSH) → not an AA, a tripeptide made of 3 AA → Sulphur based compound, tripeptide and
antioxidant
Synthesised from → glycine, cysteine and glutamate = endogenous production relies on intake and
digestion of proteins
Oxidised by GSHPx enzyme, reduced by GSH reductase enzyme (requireds B2 FAD)
-
-
Functions
Antioxidant in cells and blood
Cellular homeostasis
Role in DNA synthesis and repair
Prostaglandin synthesis
Therapeutic application → supports detoxification (liver), aids chemotherapy, chronic degenerative
diseases, infertility, cofactor for antioxidant enzymes, regenerates vitamin C and vitamin A
Factors increasing requirements - declines with age - neurodegenerative diseases, cvs, diabetes, liver
and autoimmune diseases, cancer, HIV/Aids, cataracts, muscular degenerative disease, glaucoma
Deficiency symptoms (protein deficiency) → fatigue, pale skin, shortness of breath, lightheadedness,
haemolytic anaemia
Toxicity → none
Food sources → garlic, plant and animal tissue
AA’s w/ HYDROXYL (OH) SIDE CHAINS → serine, threonine
THREONINE → Essential → ketogenic and glucogenic AA
Functions
Liver function (fat metabolism and prevention of build up)
Immune function (epithelial integrity (cell junctions tight) protecting intestinal mucosa and
supporting igA levels
Enhances phosphorylation (intracellular communication) in nerve cells
Metabolism pathways
Succinyl-CoA
Pyruvate (via glycine and serine)
Acetyl CoA
Threonine cleavage complex = Threonine → glycine + acetaldehyde (acetyl-CoA) → serine (reversible
reaction requiring folate)
Glycine receptors in CNS mediate inhibitory neurotransmission in spinal cord
Therapeutic application → 2.5g/day reduces spasticity in inactive/progressive multiple sclerosis + fatty
liver disease, digestion, immune health, hepatitis
Therapeutic range → L-threonine - 15mg/kg/day, 0,51gram from diet per day
Food source → found in animal and plant sources and activated form in body → milk, snapper, sunflower
seeds, spreads, chicken, cheese, almonds, oats, wholemeal flour, lentils, baked beans, bread, broccoli
Factors increasing demand → poor dietary intake, pregnancy, digestive malabsorption, non alcoholic fatty
liver disease
Deficiency → reduced motor function, fatty liver, fatigue, digestive disorders
Toxicity → tolerated up to 4d/day - stomach upset, headache, nausea, skin rash
SERINE → Conditionally essential → gluconeogenic AA (metabolised to pyruvate and choline)
Derived from → dietary intake, glycine, protein and phospholipid degradation and biosynthesis from
glycolytic intermediate 3--phosphoglycerate (glycerate)
Can form glycine in reversible reaction
Liver and kidneys
-
-
-
Functions → cell membrane fluidity/integrity, potentiates excitatory effect of glutamate, energy production
and metabolism of fatty acids, muscle growth, cellular proliferation, immune function and antibody
production, biosynthesis of purines and pyrimidines for DNA and RNA, tryptophan production with d-serine,
nerve protection and brain health
Therapeutic application → schizophrenia, amyotrophic lateral sclerosis, alzhimers, insomnia, depression,
PTSD, hereditary motor sensory neuropathy, muscle fatigue, tourette syndrome
Therapeutic range - 500-2000mg/day
L-serine - plant and animal sources, activated form in body and supplements
D-serine - form used in brain
Food sources: milk, peanut, egg, sunflower, snpper, cashew, almond, oats, lentils, brown rice, spinach,
sweet potato
Factors increasing demand → protein deficit, pregnancy, growth
Deficiency → congenital microcephaly (lack enzymes to biosynthesize L-serine) = seizures, epilepsy,
psychomotor retardation
Toxicity → safe, some digestive discomfort and reduced appetite
AA w/ BASIC SIDE CHAINS → lysine, arginine, histidine
ARGININE → conditionally essential, basic side chain - glucogenic AA
Absorption via small intensive via active and passive transport
Primarily metabolised in liver → forming urea, ornithine, proline and (ARG + GLY + CH3 = creatine)
creatine (providing P for quick ATP in muscles) → further metabolism (kidneys synthesis arginine from
citrulline to assist with liver synthesis of creatine), + in intestines, lunks and leukocytes
Functions → energy production (gluconeogenesis precursor), disposing ammonia through urea cycle,
substrate for enzymes, vital replication, production of biochemically diverse products, changes arginine
concentration (regulation of cellular metabolism and function via arginine senors)
Therapeutic application → CVD (high bp, heart disease), pregnancy (preeclampsia and bp), wound
healing infection (t helper cells), chronic kidney disease, erectile dysfunction, migraine, blood sugar in
diabetes → Avoid use with cold sores and stress
Therapeutic dosage → < 6g/day single dose (higher if divided) - more bioavailable is smaller doses
(L-arginine)
Food sources → plant and animal proteins, supplements, activated form used in body → peanuts,
sunflower seeds, walnuts, almonds, cashews, snapper, tuna, milk, egg, oats, lentils, beans, spinach
Factors increasing demand → childhood pregnancy, diet deficiency (staration), catabolic states due into
increased arginase levels (sepsis, infection, cancer, CVD, etc)
Deficiency → hypertension, preeclampsia
Toxicity → well tolerated but mild gastrointestinal symptoms at high dose - contraindicated for herpes (as it
assists with viral replication - competes with lysine)
LYSINE → Essential AA, basic side chain - ketogenic
Catabolized for acetyl-CoA
Metabolism occurs in → skeletal muscles, heart, kidneys, diaphragm and adipose tissue
Metabolised to hydroxylysine by hydroxylase enzyme (fe + vit c) = (pre collagen)
Methylated → by SAM to synthesised Carnitine AA
-
-
Competes for cellular uptake with arginine
Functions → immune, protein/peptide synthesis (collagen, hormones, elastin), creatine synthesis (B3, B6,
B9, vit C, SAMe and Fe), polyamine synthesis for cell growth and proliferation (B6), carnitine synthesis
Therapeutic application → herpes (inhibits viral replication and reduces revaluation of outbreak), competes
with arginine (low arginine diet enhances lysine function), schizophrenia (blocks nitric oxide through
competition with arginine), bone health (reduces calcium loss and aids absorption)
Therapeutic dose (300-3000mg/day) → adults 12mg/kg/day, infants 97mgkg/day (3-6m), children
44mg/kg/day (11-12)
Food sources - L-lysine (food and supplement form) → tuna, milk, chicken, vegemite, peanut butter,
almonds, lentils, oats, beans, peas, coconut, brown rice
Factors increasing demand → genetic conditions (errors in lysine metabolism), high intakes of arginine,
inadequate dietary intake of protein, growth, development, ageing
Deficiency → poor concentration, fatigue, irritability, nausea, red eye, anaemia, reproductive issues
Toxicity → well tolerated
HISTIDINE → essential AA → basic side chain – glucogenic
Absorbed in small intestine via active transport
Synthesis of carnosine (with beta-alanine) and histamine (mast cell release)
Urinary secretion of histidine → measure of muscle breakdown
Functions → energy production, protein synthsis, growth and tissue repair, myeline sheaths, precursor for
histamine and carnosine biosyntheisis, histamine role in immunity, hydrocholeroic acid secertion (HCL,
decreases appetite), sexual functions, arousal (sleep/wake), brain neurotransmitter, blood cell
meanufacture, antioxidant, anti-inflammatory and anti secretory properties, folate metabolism, improves
absorption of minerals Zn, Cu, Fe, Mn, Mo
Therapeutic applications → metabolic syndrome, rheumatoid arthritis, allergic disease, ulcers, anaemia +
potentially high intensity exercise, age related disorders (cognitae, neurological cataracts), metabolic
syndrome, folate metabolism rheumatoid arthritis, inflammatory bowel disease, cardiac surgery, and organ
reservation, malignancy atopic dermatitis anaemia
Therapeutic dosage (range >4gday) → 11-14mg/kg/day for adults, 33/gkf infants (4-6m)
Food sources → found as L-histidine → tuna, milk, cheese, sunflower seeds, shark, peanuts, vegemite,
almonds, egg, lentil, banana, broccoli, pumpkin
Factors increasing demand → childhood, chronic kidney disease, digestive disorders, growth and
development, ageing, inadequate dietary intake, neurodegenerative disorders
Deficiency → anaemia, altered nitrogen balance, (genetic condition histidinemia benign - no symptoms)
Toxicity → histadelia - cognitive, psychological or behavioural outcomes such as obsessive compulsive
disorder and depression
IMINO ACID
PROLINE → proteinogenic amino acid (functions primary in protein synthesis especially collagen)
Imino side group bound to amine group with C-S forming ring (amine gives up H to bind to side group C)
Hydroxylated (OH) to make hydroxyproline (procollagen matrix)= stability to connective tissue along with
glycines and lysine
Abundant in gelatine and collagen
Made from glutamate (reversible) and arginine (via ornithine in urea cycle)
Therapeutic application → wound healing, immune support and antioxidant & collagen proteins
Supplementation → hydrolysed form of collagen
-
Therapeutic dosage range → 2.5-10g/day (skin and ageing), 2-10g/day (osteoarthritis), 5-10g (joint pains
for athletes)
SUMMARY OF AMINO ACID METABOLISM
No individual reference values for AA due to being contained in proteins
Sufficient protein = sufficient AA
VITAMINS
Micronutrients (don't yield energy, act as cofactors)
WATER SOLUBLE VITAMINS
Vitamin C - antioxidant, collagen synthesis, iron absorption +
B complex vitamins - energy metabolism and nerve health
Absorption: absorbed into circulation (blood) via small intestine
Transport: travel freely in water filled parts of body eg blood plasma (not B12 which needs blood transporter
and can circulate in bile)
Excretion: kidneys detect and remove excess/unused vitamins via the urine = not stored = unlikely toxic
LIPID SOLUBLE VITAMINS
Vitamin A - eye, skin, nerve, bone, immune function
Vitamin D - mineral metabolism, cell differentiation
Vitamin E - antioxidant
Vitamin K - blood clotting and bone mineralisation
Absorption: with fats into lymphatic circulation (bile in stomach/intestine breaks up fat preparing it for
absorption through intestinal wall) - chylomicrons: carriers of fat soluble vitamins
Transport: protein carriers
Storage: stored in liver and fat cells = more susceptible to toxicity from supplements
Excretion: less readily excreted - accumulate in fat storage sites
VITAMIN C → ascorbic acid
Sources: lime, kakadu plum, kiwi, parsley, watercress, orange, broccoli, capscium, seaweed
RDI: 46mg/day
Therapeutic dose: 250-10000mg/day
Functions: antioxidant (2H donation), enzyme cofactor, collagen synthesis, energy production, iron
absorption, stress and immunity (adrenal gland and leukocytes), hormone and neurotransmitter production
Factors increase demand: stress and disease, oxidative stress, chemical substance use (eg smoking),
elerdy, pregnancy, growth, athletes
Deficiency: fatigue, bleeding gums, naemia, bone fragility, altherloscorsis, infections, muscle degeneration,
low mood, rough skin and bruising + scurvy (impired wound healing, bruising, bone breaking etc - pool less
than 300-400mg 0 takes 1-2 months)
Toxicity: nausea, diarrhoea, fatigue, insomnia, hot flashes, kidney stones, vental enamel erosion, heartburn
B VITAMINS (water soluble nutrients) = synergistic action
Function: energy metabolism = coenzymes aiding to extract energy from carbohydrates, hematopoietic, lipids and
proteins & nerve health
Sources: vegemite
Factors increasing demand: intake of coffee, alcohol, medications, pregnancy and lactation, GIT disorders,
B1 (THIAMIN) → TPP (TDP), TMP, TTP
Sources: yeasts, cereals, grains, breads, nuts, meat (pork), liver, sunflower seeds, vegemite
RDI: approx 1.1mg.day
Therapeutic dose: 300-4000mg per day
Functions: Energy metabolism, acetyl coA formation, nerve and brain function, TPP removes 1 carbon,
growth
Factors increasing demand: alcoholism, excessive carbohydrate intake, dysbiosis, pregnancy
Deficiency: loss of appetite, nausea, weakness, fatigue, irritation, sleep disturbances, anorexia, abdominal
discomfort → Beri beri (nerve damage, wasting/weakness, cvd, resp), wernicke-korsakoff syndrome (brain
damage, eye rolling, consion, loss memory)
Toxicity: none
Assessment: bloods
B2 (RIBOFLAVIN) → FAD, FMN
Sources: lamb/liver, eggs, mushrooms, weet-bix, almond meal, fortified breads/cereals, dairy
RDI: approx 1.2mg/day
Therapeutic dose: 300-400mg/day severe
Functions: energy metabolism, growth, health of skin, eyes, liver, antioxidant pathway, nutrient metabolism
Factors increasing demand: alcoholism, pregnancy, chronic conditions, psychological distress
Deficiency: (common) redness/cracked corners of mouth (cheilosis), purple/sore tongue (glossitis),
stomatitis, numbness/pins needles, anaemia, fatigue, depression, weakness, vision issues
Toxicity: none
Assessment: bloods
B3 (NIACIN) → NAD, NADP, NADH, NADPH (manufactured by tryptophan=semi essential)
Sources: peanuts, chicken, sunflower seeds, mushrooms, salmon, tryptophan containing foods
RDI: 16mg men, 14mg women
Therapeutic dose: 500-2000mg/day for pellagra + used for cholesterol management
Functions: energy metabolism as coenzyme NAD. (!!), cell replication, antioxidant/anti inflammatory
Factors increasing demand: corn intake, refined grain intake, low protein, low B2, B6 or iron intake,
Deficiency: pellagra (4Ds-diarrhoea, dermatitis (dry/cracking skin), dementia, death), git malabsorption,
sore tongue, fatigue, muscle weakness/dysfunction
Toxicity: 50-100g vasodilation of upper body, nausea, diarrhoea, liver toxicity, increase blood glucose
levels, niacinamide (3000mg od)
Assessment: urinary metabolites
B5 (PANTOTHENIC ACID) → Coenzyme A
Sources: vegetables, wholegrains (milling removes), animal proteins, lamb, liver, legumes, broccoli,
peanuts, cheese, salmon, cashews, egg, chicken, bread, mushrooms, sunflower seeds, avocado
Stability: ok to o2 and uv, destroyed by heat, acid, alkali
RDI: 4mg female, 6mg male
Therapeutic dose: 10-3000mg/day
Functions: energy metabolism (CoA), stress adaptation, steroid hormone production, immunity, health of
hair and skin, glucose regulation, nerves (neurotransmitter acetylcholine)
Factors increasing demand: high refined carb, low protein, undernutrition, diabetes, GIT disorders
Deficiency: rare, gastrointestinal and neurological issues eg burning/pins needles in hands/feet, fatigue, GI
issues, postural hypertension, tachycardia, weakness, insomnia, nausea hyperactive deep tendon reflex
Toxicity: 15-20g - intestinal distress
B6 (PYRIDOXINE) → PLP, PMP, PNP
Sources: widely available, animal sources, chickpeas, tomato, eggplant, cucumber, veal, sunflower seeds,
silverbeet, cabbage, chia seeds, banana
Stability: heat stable, destroyed with processing
RDI: 1.3mg/day
Therapeutic dose: 200mg/day reduction of nausea in pregnancy
Absorption: dephosphorylated for absorption, concentrated in muscles
-
Functions: Energy metabolism, DNA and RNA synthesis, amino acid metabolism, red and white blood cell
formation, synthesis of antibodies and neurotransmitters (eg dopamine, epi), steroid hormone metabolism,
immunity, thyroid hormone metabolism ,homocysteine metabolism (protects cardiovascular system from
build up of hcy), methylation cycle
Factors increasing demand: growth, the pill, inflammation, age
Deficiency: depression, neurological consequences (convulsions), numbness/tingling, fatigue, dermatitis,
inflamed/cracked skin around mouth eyes (cheilitis), swollen tongue, rashes, conjunctivitis hypochromic
microcytic anaemia, poor immunity
Toxicity: nerve damage, fatigue, headaches, skin lesions (resembles deficiency) - UL 50mg
Assessments: bloods
BIOTIN (B7) → Carcoxylaseses
Sources: + bacteria in gut, peanuts, almonds, oats, sweet potato, carrot, avo, bananas, cauliflower,
raspberries, hazelnuts, tomato, sunflower seeds, cacao powder, eggs, chicken, mushrooms, broccoli, wheat
flour
Stability: heat ok, destroyed by light, acid, alkali, 02
RDI: (AI) - 25um women, 30ug men
Therapeutic dose: 25ug-20mg day
Absorption: small intestine (pancreatic enzyme biotinidase)
Functions: energy metabolism (eg gluconeogenesis and CAC and c transfer, carboxylase enzyme),
building fat, nervous system, health of skin and hair, gene expression, blood glucose regulation
Factors increasing demand: magnesium deficiency, reduced biotinidase available (genetic disease)
Deficiency:(rare) avidin in raw egg white prevents biotin absorption - symptoms: neurological (lethady,
nerve pain, weakness, depression), scaly dermatitis, brittle nails, hair loss, anorexia, nause, loss of taste,
hyperglycemia.
Assessment: urine, 3-HIA measurements
FOLATE (B9) → THF (masks symptoms of B12 deficiency)
Sources: liver, fortified breads, cereals, vegetables/legumes, fruits, leafy greens yeast, chicken liver,
seaweed, mung bean, cabbage, red kidney beans (high in uncooked foods)
Stability: destroyed by heat, O2, UV
RDI: 400ug/day (+ in women) (pregnancy 600ug)
Therapeutic dose: 400-5000mcg/day
Form/absorption: in monoglutamate form. Absorbed in duodenum, Folic acid (already monoglutamate = no
digestion needed)
Functions: pregnancy, foetal development (neural tube), DNA, nucleic acid and protein AA synthesis,
methylation, cell growth, reproduction, neurotransmitter synthesis (domaine, epi), hematopoiesis,
homocysteine metabolism (protects cardiovascular system from build up of hcy)
Factors increasing demand: growth and development, hyperhomocysteinemia, genetic disorders
Deficiency: (common in alcoholics, eldery, pregnact) megaloblastic anaemia, impair immunity, cracked sore
mouth and tongue, depression, fatigue, headaches, high homocysteine levels, lactic acidosis
hyperpigmentation, digestive functions (affects fast developing cells - red, white, digestive) → pregnancy
neural tube defects (spine and brain)
Toxicity: B9 supplementation marks B12 deficiency (maintains red blood cells), skin rashes, digestive upset,
insomnia, irritability, increase cancer risk
Assessment: bloods
B12 (COBALAMIN) → methylcobalamin, deoxyadenosylcobalamin (works with folic acid)
Only water soluble vitamin that can be stored (in liver)
Requires intrinsic factor for absorption (binds)
Sources: lamb liver, octopus, chicken, oyster, yeast, sardines, egg, soba noodle, dairy, seaweed, shiitake,
button mushrooms
Stability: stable, not microwave
RDI: 2.4ug day
Therapeutic dose: 500-2000mcg day (orgalm sublingual, nasal)
Digestion/absorption: bound to protein, R protein (haptocorrin) release from salivary glands, in stomach
hydrochloric acid and pepsin free B12 from protein, it binds to haptocorrin, parietal cells release intrinsic
-
-
-
factor. In small intestine pancreatic enzymes free B12, it binds to intrinsic factor and is absorbed + produced
by gut bacteria
Functions: energy production, red blood cell production, methylation, works with folic acid, dna synthesis,
neurological function, myelin sheath (nerve health), homocysteine metabolism (protects cardiovascular
system from build up of hcy)
Factors increasing demand: folate (B9) deficiency, vegan/vego, pregnancy, age, chronic illness,
institutionalisation, pernicious anaemia (autoimmune damage to gi so intrinsic factor not produced.
Deficiency (common in vegans) takes time: megaloblastic anaemia, severe and irreversible nerve damage ,
high hcy levels, neuroplastic symptoms (senses/memory), yellow pallor, greying, sore tongue, low grade
fever, hyperpigmentation
Toxicity: 100-4000mcg well tolerated. Allergic reaction, nausea, dysphagia, hypertension, gout, fata
hypokalemia
Assessment: blood 12–68-pmol/L
Choline - synthesised from methionine = conditionally essential
Sources: egg yolks, liver, flax seeds, cereals
RDI: AI - 423/550mg UL-3500mg
Therapeutic dose: 1000-6000mg/day
Functions: Used to make lecithin phospholipid (phospholipid bilayer) and sphingomyelin (nerve cells), part
of acetylcholine (neurotransmitter), methyl donor when B12 or folate low (methylation)
Factors increasing demand: pregnancy brain development), B12/folate deficit (methylation)
Deficiency: liver or muscle damage, neurodegeneration
Toxicity: +7.5g nausea, diarrhoea, hypotension, fishy odours sweatt
Inositol - water soluble sugar alcohol - synthesised by gut and B3 = non essential
Sources: gut, stone ground wheat bread, prunes, rockmelon, oranges, almonds, green beans, kiwi
RDI: none
Therapeutic dose: 1000-4000mg day
Functions: Used to make lecithin phospholipid (phospholipid bilayer) cell membranes, blood glucose
regulation, liver function, fat metabolism, reduces androgens (decreases egg health)
Factors increasing demand: low fibre, metabolic syndrome, high GI/GL (high blood glucose inhibits
absorption)
Carnitine → needed for fat metabolism
Lipoic acid → energy metabolism, antioxidant
VITAMIN A Food sources: lamb, beef liver, chicken liver, carrot, diary, sweet potato, seaweek, dill, spinach pumpkin,
sundried tomato, watercress, cheese, eggs, capsicum, fish, pumpkin
RDI → 900ug (M), 700 ug (F)
Therapeutic range: 5000-10,000 IU (less than 5000 IU in pregnancy)
Dosage: safe up to upper intake level UL 10,000 IU (3000mcg) per day
-
-
-
-
Forms
Animal food: retinoids/preformed vitamin A - sources are retinol (active), retinol and retinoic acid
Plant food: carotenoids provitamin A - eg beta carotene (oils, fruits, veggies) = dietary precursors
for retinol → converted to retinol → absorbed in michelles by small intestine
Lutein and zeaxanthin - carotenoids not converted to vitamin A - similar quality = eye
health → Lutein (peas, spinach, dark green leafy vegetables, corn, egg yolk, kiwi, grapes)
→ Zeaxanthin (corn, egg yolks, orange capsicum, kiwi)
Storage: in liver (transported on retinol binding protein)
Stability: unstable, lost when processing, cooking, storing food (except beta carotene - bioavailability
increase by processing and heating)
Functions
Vision and eye health,
Protein synthesis and cell differentiation
Reproduction and growth
Antioxidant
Immune function
Bone health - assists enzymes that degrade - allowing remodelling
Factors increasing demand: fat malabsorption, growth, meds, alcohol smoking, eye disorders, excessive
sun exposure, cancers
Deficiency: Affects retina, conjunctiva and cornea → nyctalopia/night blindness, xerophthalmia, bitot's
spots, keratomalacia, dry and scaly skin, bone overgrowth, xerosis, keratinisation
Toxicity: oral/consumption = acute or chronic, topical retinoids = irritation eg acute hypervitaminosis A
(nausea, vomiting, blurred vision, headache, vertigo, diarrhoea, incoordination) , chronic hypervitaminosis A
(decrease bone mineral density, increase bone fracture), birth defects, beta-carotene inefficiency conversion
Assessment methods: vitamin A testing (0.7-2.8 umol/L), prealbumin (assesses transport proteins - retinol
binding protein secreted by liver), fat soluble vitamin profile
VITAMIN E
Food sources: tahini, sunflower, almonds, olive oil, vegetable oils, egg, sundried tomato, wheat germ, olive,
capsicum, tomato pasta, hass avocado, spinach/leafy greens, kiwi
RDI → AI = 10mg (M), 7mg (F) UL 300mg/day (brain resistant to depletion)
Therapeutic range: 0.15-2.0 mg/kg a day
Forms → family of 8 molecules → either tocopherols or tocotrienols (alpha, beta, gamma, delta forms) = dietary is
predominantly alpha and gamma tocopherol
Only a-tocopherol maintained in body - NRV values
Supplement form → dl-a-tocopherol
Stability: destroyed during processing and storage
Functions
Antioxidant (prevents oxidation of LDL and carbs??)
Anti-inflammatory
Immune function
Regulation of gene activity
Factors increasing demand: low fat diets (less absorption), high polyunsaturated fat diets, digestive disorders,
laxatives, cholesterol lowering medication, orlistat (xenical) prevents fat absorption to promote weight loss
Deficiency: (rare) - malabsorption in cystic fibrosis → fragility of red blood cells, degeneration of neurons, peripheral
axons and posterior column neurons, milk haemolytic anaemia, neurological changes, children but
neurological/muscular weakness, long term damage to eyes, nerves, liver, brain
Toxicity: least toxic/rare → blood thinning (bleeding, haemorrhage, stoke), muscle weakness, fatigue, nausea,
diarrhoea, large a-tocopherol (1200iu) deplete plasma tissue levels of gamma-tocopherol
Assessment methods → bloods - not medicare - RBC levels better long term indicator = Children 7-35 umol/L Adults 11-46 umol/L
VITAMIN D
Non essential (produced endogenously from sunlight and cholesterol in skin)
Biologically inactive until activated in kidneys
Food sources:animal foods and supplements, sunlight, vegetable/plant sources, cholesterol = mushrooms,
barramundi, salmon, margarine, chicken, pork, egg, salmon, milk, breast milk
RDI → AI 5ug/day increase with age
Q IU = 0.025ug → 1ug = 40 IU
UL = 80 ug.day
Therapeutic dose: 1000-5000 IU
Forms - natural, supplemented, activated
Vitamin D3 or cholecalciferol - obtains through vivo synthesis, animal foods and supplements
Vitamin V2 or ergocalciferol - obtained through vegetable/plant sources
Calcitriol - active form in body - acts as hormone 1,25-dihydroxy vitamin D
Stability: stable - not lost by cooking or processing
Absorption: no digestion → absorbed from micelle with fat and aid of bile → passive diffusion into enterocyte small
intestine (duodenum rapid - jejunum largest)
Synthesis
1. Synthesised in sebaceous glands from cholesterol metabolite → exposure to UVB sunlight converts
7-dehydrocholesterol to previtamin D3
2. Converted to cholecalciferol (D3) over 2-3 days
3. Transported in blood on D-binding protein (DBP) to liver and body tissues
4. Hydroxylated to calcidiol in liver → Further hydroxylated in kidneys → active form calcitriol (endocrine
feedback)
Serum calcium falls below homeostasis → parathyroid glands release parathyroid hormone → stimulates
conversion of calcidiol to calcitriol in kidneys → increases calcium absorption from intestine and bone
resorption of calcium to replenish serum levels –. Calcitonin inhibits conversion of calcidiol to calcitriol in
kidneys stopping resorption once homeostasis is returned
Functions: Calcitriol (active form)
Bone development, metabolism, health, calcium/phosphorus homeostasis (intestines, kidneys, bone
receptors)
Cell differentiation, proliferation, growth
Immune function activity
Brain function
Functions as a hormone
Factors increasing demand: lack of sunshine (elderly), dark skin (less UV absorption), reduced skin exposure to
sunlight (religion), fat malabsorption, latitudes farthest from equator, autoimmune or inflammatory conditions
Deficiency: fatigue/generalised weakness, muscle/bone pain, myalgias, lowered immunity, frequent infections,
impaired wound healing
Diseases: rickets (failure of bone mineralisation in kids eg cowed legs), osteomalacia (adults, soft painful
bones), osteoporosis (inadequate synthesis of vit D = calcium loss from bones = lost bone density)
Toxicity: mainly just via supplementation - continuous intake over 10,000 IU = confusion, apathy, drowsiness,
recurrent vomiting, abdominal pain, anorexia, contripation.
Hypercalcaemia: excess vit D intake = calcification of soft tissue eg kidneys, heart, lungs, blood vessels =
hypertension, headache, renal dysfunction, polyuria, polydipsia, azotemia, nephrolithiasis, heart damage,
death
Assessment methods: blood tests for 25-hydroxy-vitamin D - medicare sometimes = >50 nmol/L sufficient,
<30nmol/L deficiency
VITAMIN K
Storage: minimal = stores depleted with low dietary intake
Food sources: cooked greens (spinach, kale), pesto, broccoli, brussel spouts, cabbage, lettuce, prunes, asparagus,
green beans, kiwi fruit,
Forms
K1 (phylloquinone) - plant food supplements
K2 (menaquinones or MKs) - animal and bacterial: bacterial synthesis in colon provides 80% requirements
Vitamina K3: menadione (synthetic form)
Hydroquinone: reduced form
RDI → AI - 70ug/day (M), 60ug/day (F) = UL 300ug
Therapeutic range 1000ug-45mg menatetrenone (synthetic form)
Functions
Blood clotting
Bone metabolism and health
Brain and nerve function
Integrity of blood vessel walls
Hormone like activity (osteocalcin bone protein) secreted into blood, insulin sensitivity
Kidney function
Retinal function
Sulphur and prostaglandin metabolism
Blood clotting/coagulation: vit K dependent carboxylation reactions
Vit K activates proteins (eg prothrombin made my liver as precursor of thrombin)
1. Blood exposed to air, foreign substances and secretions from injured tissues
2. Platelets release phospholipid thromboplastin
3. Thromboplastin catalyses conversion of inactive protein prothrombin to active enzyme
thrombin
4. Thromin catalyses conversion of precursor of fibrinogen to fibrin to form clot
Factors increasing demand: Liver disease, alcohol, drugs eg antibiotics synthesis by intestinal bacteria,
anticoagulants → Diet: fat malabsorption, low fat diets, newborns, vitamin A (absorption) and E supplementation
(interferes enzymes)
Deficiency: excessive bleeding, easy bruising, hypoprothrombinemia, haemorrhaging, calcification of artery walls,
atherosclerosis, bone weakness age related cognitive decline → infants bruising, bleeding from nose/mouth, blood in
urine
Vitamin K hemorrhagic disease: high risk in newborns due to sterile intestinal tract and low vit k in breast
milk → prevented by single dose of vit K in naturally occurring form at birth (orally or intramuscular induction)
Toxicity
Natural vit K (phylloquinone) - no adverse effects (can decreases effectiveness of anti clotting medication
Synthetic vitamin K (menadione) - damage liver, haemolysis, haemolytic anaemia, jaundice in new borns
Assessment methods: primary test re bleeding is prothrombin time (PT) time taken for clot to form + fat soluble
vitamin profile via vloods
MACROMINERALS
Required in large quantities → 100mg/day +
-
-
Types
Calcium (Ca), magnesium (Mg), phosphorus (P) - required for structural function
Sodium (Na), potassium (K), chloride (Cl) - required for electrolyte balance
Sulphur - requirements met via protein intake
Inorganic - come from the earth = mineral content of plant depends on mineral content of earth they grow in
→ transferred to plants and animals (through plants) and water
No endogenous production
Dont breakdown within body (vitamins do) = more stable, less destroyed in processing (lost in water)
Some substances bind to minerals affecting absorption and utilisation eg phytates in legumes and grains
and oxalates in spinach and kiwi + minerals compete with each other when taken in large doses
Excessive intake = accumulation in body organs
MICROMINERALS
Required in quantities less than 100mg/day
Iron (Fe), zinc (Zn), copper (Cu), manganese (Mn), iodine (I), selenium (Se) and chromium (Cr)
Also fluoride, molybdenum, silica, boron and vanadium
CALCIUM
2 % of total body weight → 99% stored in bones and teeth (1% in blood and fluid)
Dietary sources
Poppy seed, milk powder, cheese, sardines, wattle seed, licorice, almonds, flaxseed, bread, kale, bok choy,
tofu
Nutrient references values
RDI 1000mg day
1300mg during adolescence and menopause
Digestion and absorption
In small intestine
Lactose, vitamin D and stomach acid increase absorption
High fibre and oxalates (spinach/kiwi) may reduce absorption
Regulation and homeostasis → vitamin D, calcitonin and parathyroid hormones = bones reservoir when high
(osteoblast), source when low (osteoclast)
Absorption: vitamin D activated parathyroid hormone in kidneys = UPREGULATES
Storage:
Low serum calcium levels stimulate PTH secretion = promotes osteoclast activity = calcium
released from bones
High serum calcium levels stimulate thyroid to release calcitonin = diminished osteoclast activity
-
Excretion: parathyroid hormone acts on kidneys increase tubule reabsorption of calcium
Functions - cation Ca2+
Bone mineralisation and formation - growth
Blood clotting
Nerve transmission - allows neurotransmitters to be released from nerve terminals
Cell signalling and function - secondary messenger
Muscle contraction - skeletal, cardiac and smooth
Factors increasing demand
Digestive disorders, tannins, sodium (bone loss and urine), competition for absorbtion (iron), life stages
(menopause, adolecvnce elderly), alcohol and drugs, dietary patterns (vegan, lactose intelorant)
Deficiency signs and symptoms
Bone disorders in adults (osteoporosis, osteopenia, osteomalacia), bone disorders in children (rickets,
stunted growth, irritability, low energy), muscle soreness, camps, spasms, altered BP, irregular heart rhythm,
paresthesia (mouth, throat, limbs), mental disorders (depression, anxiety, confusion)
Toxicity signs and symptoms
Supplements : constipation, bloating, flatulence, kidney stones, kidney dysfunction
Hypercalcaemia → headache, constipation, pain in abdomen polyuria, no appetite, weakness, fatigue,
elevated CSF protein, heart dysfunction, mental dysfunction/confusion, muscular weakness
Assessment methods
Blood test (2.10-2.60mmol/L) - not good as calcium depleted from bones
Urine test (150-300mg)
DEXA scan - x ray - measures bone mineral density and bone loss
MAGNESIUM
Intracellular mineral - 0.05% body weight → 60% in bones
Functions - enzymatic reactions and muscle relaxation
Food sources
Food processing/refining greatly affects it - flour and rice poor sources
Mineral and tap water
Pumpkin seeds, wheat bran, flaxseed, sunflower seeds, brazil nuts, chia seeds, oats, spinach, wholemeal
bread, avocado, banana, dark chocolate, tuna
NRVs
RDI = 310mg/day(F), 400(M) - increase by 10-20 after age 30
UL 350 mg/day
Optimal dose 500 mg divided into 100 mg doses
Therapeutic dose 600-1500mg
Absorption
Passive transport in distal small intestine (jejunum and ileum) + active transport when low + sometimes
colon
Required bile, gastric and pancreatic secretions
30-50% of ingested magnesium is absorbed in healthy adults
Enhanced with - vitamin D, lactose and fructose
Reduced by phytate, non fermentable fibre and divian minerals
Functions
Energy metabolism - cofactor for macronutrient oxidation and production of creatine phosphate (muscle) needed for ATP function
Bone mineralisation
Glucose metabolism - insulin/pancreas
Enzyme cofactor - all enzymes involving nucleotides
Cardiovascular function - smooth and cardiac muscle regulation of casual tone and stabilisation of heart
rhythm + production of vasodilators to low BP
Platelet activity
Hormone receptor binding and signal transmission
Membrane ion transfer
Factors increasing demand
Digestive disorders, medications, alcohol, chronic diarrhoea, ageing, inadequate protein, hospitalisation,
poorly manages disease (heart related or cancer)
Deficiency signs and symptoms
Early = fatigue, lethargy, weakness, anorexia, nausea, vomiting, insomnia, cramps, migraines
Late = hypomagnesemia - hypocalcemia and hypokalemia = confusion, cramps, PMS, heart
rhythm/palpitations, diarrhoea, convulsions, bizarre muscle movements (face/eye), hallucinations, difficulty
swallowing, growth failure in children
Toxicity (from supplements - food usually excreted)
Diarrhoea GI upsets, thirst, muscle weakness, drowsiness, back/pelvic pain, hypotension, dizziness,
confusion, difficulty breathing, deterioration of kidney function
Hypomagnesemia (death)
Overdose - unconsciousness, respiratory arrest and cardiac arrhythmias
Assessment methods
Blood 0.70-1.10 mmol/L (usually normal as its depleted from the body not the blood)
Urine after 24 hours loading
PHOSPHORUS
Second most abundant mineral - 85% combined with calcium in hydroxyapatite crystals of bones and teeth
= 85% found in bones and teeth, 14% in soft tissue/muscle, 1% in blood
Forms
Organic - found to proteins sugars and lipids
Inorganic - phosphate
Supplements - phosphate salts or phospholipids
Absorption
Passive transport through small intestine - mainly inorganic/unbound
50-70% of dietary phosphate absorbed
Phytate containing foods impair absorption
Food sources
Pumpkin seeds, tuna, lean pork, tofu, chicken, lentils, wheat bran, milk, yeast, wholemeal flour, poppy
seeds, sunflower seeds, cheese, brazil nuts, almonds, veal
Therapeutic dosage rams - <1500mg of elemental phosphate, <1800mg tricalcium phosphate
Functions
Bone mineralisation
Carbohydrate metabolism and energy storage and transfer - ATP, GTP and creatine phosphate. B1 and B6
actuated when phosphate group attaches
Transport of lipids through lymph and blood systems
Cell structure and function - component of phospholipids, cell membranes, myelin sheaths, chylomicrons,
bile salts, RNA and DNA
Phosphorylation - activates protein by adding phosphate group (usually supplied by ATP)
Factors increasing demand
Alcoholism, high dose calcium supplementation (binds) , drugs increasing bone resorption and decreasing
bone formation eg contraceptives, lack of vitamin D , malnutrition
Deficiency signs and symptoms
Rare, asymptomatic
Rickets in children
Reduced cardiac output, arrhythmias, myopathy, decreased diaphragmatic contractility, respiratory failure,
neurological problems, death
Chronic - osteomalacia, low BMD, soft bones, bone pain
Toxicity
Calcification of non skeletal tissue - kidneys = kidney failure
Risk of CVD
Hyperphosphatemia
Atherosclerosis and left ventricular hypertrophy
Assessment methods
Blood 0.75-1.50 mmol/L (also text Ca, Mg, PTH, vit D, FGF23)
ELECTROLYTES
Mineral salts that dissolve in water and dissociate into charged particles called ions
Mineral salt = one mineral attached to another = cation (+) & anion (-)
Rely on transport channels/pumps to move between ICF and ECF
Distribution → electrolytes move across cell membrane attracting water = electrolytes distributed
throughout all body fluids
Extracellular - sodium and chloride
Intracellular - potassium
Fluid regulation (kidneys, hypothalamus and adrenal glands) - maintain homeostasis (ECF) via feedback
systems responding to BP, blood volume and body fluid concentrations
DASH - diet plan prevents hypertension - low sodium high calcium
SODIUM Na+
6th most abundant element on earth
Sources
1 teaspoon salt = 2,300mg sodium
High in packaged foods - a preservative
Iodised table salt, bicarb soda, baking powder, curry pasta, vegemite, bacon, olives, cheese, bread
Intake
AI - 460-920mg/day
Older people with high BP and weight = SDT 2000mg/day
Forms
Sodium chloride - table salt, kosher salt, sea salt, himalayan salt
Processed foods - sodium phosphate, sodium bicarbonate, sodium aluminosilicate, sodium benzoate and
monosodium glutamate
Digestion and absorption
98% absorbed
-
60-70% found in extracellular fluid, 30-40% on bone surfaces, 10% intracellular components such as nerve
and muscle tissue
Stomach → released from chloride
Small intestine and proximal colon → absorbed via 3 mechanisms
SI active transport via sodium/chloride transport
SI active transport via sodium/glucose transporter
Colon passive transport via sodium channels
Travels freely in blood to kidneys = filter sodium and reabsorb only what's needed
Key functions
Water and electrolyte balance: water volume, osmotic pressure, regulates electrolytes (potassium and
chloride)
Cell function: maintains blood pressure, homeostasis of cellular hydration via sodium/potassium pump
Nerve and muscle: with potassium and calcium sodium assists with nerve impulse generation and
stimulation of muscle contraction
Bone and minerals: constituent of bone
Therapeutic application
Abnormally low blood sodium levels = hyponatremia - due to intense physical activity, severe vomiting,
diarrhoea
Reduce intake by - less pickled, fast foods, smoked, condiments cheese, processed foods, read levels,
increase potassium rich foods, substitute fresh herbs and spices
Factors increasing demand
Over consumption of water (dilutes extracellular fluid), physical activity (excreted in sweat), excess
potassium intake (promotes excretion), reduced kidney function in elderly, diarrhoea/vomiting/fever (loss of
electrolytes, medications
Diabetes Mellitus (high glucose causes sodium excretion)
Cystic fibrosis - excretion via sweat and faulty membrane transport of electrons out of cell
Endocrine /kidney disorders: disrupt absorption/secretion
High progesterone: promotes urinary loss of sodium
Factors decreasing demand
Reduced kidney function in elderly
High cortisol (fluid/sodium retention)
Medications: enhance retention of sodium
High processed/refined foods
High fructose intake ( decrease absorption)
Hypertension - high sodium = kidneys retain fluid to dilate RAAS = increase BP
Deficiency signs and symptoms
Dry mucous membranes, poor skin turgor, tachycardia, postural hypotension, poor thinking ability, nausea,
constipation, dark urine
Sodium deficiency disorder = hyponatremia (infants and elderly) = sodium below 135mmol/L
Anorexia, lethargy, headaches, nausea, vomiting, dehydration → personality change, depression,
hallucination, muscle cramps, weakness → server <120mmol/L ICU care brain oedema (swelling)
fixed, dilated pupil, drowsiness, seizures, coma, brain damage, death
Toxicity
Nausea, vomiting, diarrhoea, abdominal brams, Excessive ECF, Increase BP
Hypernatremia - due to excessive water loss & impaired thirst mechanism (unlikely due to high sodium
intake)
Assessment methods
Blood concentrations
-
-
Urinary analysis - recent intake
POTASSIUM (K)
8th most abundant element on earth
Sources
Cacao powder, sun dried tomatoes, nori, vegemite, black licorice, tomato pasta, pumpkin seeds, spinach,
pistachio, garlic, red kidney beans, banana, green beans, wholemeal bread, green capsicum, milk, soy,
beef, salmon, avocado
Intake
AI 3800mg/day (males), 2800mg/day (females)
Therapeutic range 3000-8000mg/day
Forms
Food - potassium citrate, potassium malate
Supplements - potassium bicarbonate, potassium salts
Digestion and absorption
98% found within cell, potassium is considered a major intracellular cation
85-90% is absorbed through small intestine via active/passive transport
Plasma concentrations regulated by kidney uptake and excretion
Insulin and aldosterone regulate K+ uptake by muscle and liver cells
Sodium potassium pumps maintain intracellular K+ levels
Excretion
Via kidneys + some in sweat and faeces
Healthy/high K+ may reduce urinary excretion and bone resorption induced by high sodium levels
Regulation
Kidney functions - between meals muscles release potassium - communicated with kidneys to increase
reuptake and reduce excretion as needed
Hormones - control sodium/potassium pumps, insulin promotes uptake via muscle and liver, aldosterone
regulates urinary excretion of potassium
Key functions
Maintenance of normal fluid and electrolyte balance (with sodium and chloride)
Activation of sodium/potassium pump
Supports cell integrity
Synthesising protein and metabolising carbohydrates
Regulates heartbeat
Nerve impulse transmission and muscle contraction, especially of smooth, skeletal and cardiac muscles
Cofactor for several metabolic enzymes - carbohydrate metabolism into ATP
Component of gastric acid secretions
Bone mineral homeostasis - stabilised pH = protects bone density
Therapeutic application
Regulates BP and reduce stroke risk 3510mg-4680mg/day
Improve bone mineral density BMD in eldery 6480mg/day
Improve BMD - increase fruit and veg servings
Prevention of recurrent kidney calcium oxalate stones 3240mg=6480mg/day
Factors increasing demand
Food processing in water, vomiting, sweating, endocrine disorders, caffeine (increase excretion), chronic
illness, magnesium deficiency (increases urine loss), altered pH levels acidosis/alkalosis, medications
Potassium deficiency signs and symptoms
Salt sensitivity - high BP, stoke, Kidney stones, osteoporosis/osteopenia
Hypokalaemia - asymptomatic or serve nerve muscle dysfunction, cramping, heart rhythm, low bp, digestive
symptoms, GI, depression, confusion
Toxicity
Over-supplementation + kidney failure, Arrhythmia, Muscle weakness/twitching/cramping, Paralysis, Death
Current research/controversies
Diabetes management → low potassium = less insulin release = higher blood glucose = type 2 diabetes
Assessment methods
Serum potassium / bloods
-
24 hour faecal and urinary analysis
CHLORIDE
Major anion of extracellular fluid
Usually found in foods rich in sodium
Electrolyte → 88% found extracellular, 12% intracellular
Neutralises positive charge of sodium
Food sources
Widely available (bound to Na+ as sodium chloride table salt) = added salt = added chloride
Iodised table salt, curry paste, olives, mayonnaise, rice bubbles, salted potato chips, cheese, smoked cod,
wholemeal bread, coffee, black licorice, pink salmon (canned), chickpeas (canned)
Intake
Due to high/easy intake no NRV or RDI
AI 2300mg/day
Therapeutic dose - in synergy with electrolytes, important in foetal development
Forms
Nature - chlorine (poisonous gas → combined with sodium or hydrogen forming mineral salt sodium
chloride)
Food - sodium chloride, hydrochloric acid (digestive secretion)
Digestion and absorption
Stomach: chloride and sodium separated (ionised)
Small intestine: absorbed via passive transport (same mechanism as sodium)
Kidneys: filter and reabsorb 99% of chloride, reabsorbed from digestive secretion content
Excretion - sweating
Regulation
Balanced with bicarbonate (inverse relationship)
Same mechanism as sodium
Channels in tissue allow chloride movement in/out cells
Key functions
Maintenance of fluid, pH and electrolyte balance
Low pH - chloride excreted and bicarbonate retained
High pH - bicarbonate excreted, chloride retained
Maintenance of cellular osmotic pressure
Component of hydrochloric acid (HCl) released by parietal cells in stomach
Membrane transport of CO2 between cells, blood and lungs via chloride shift
Production of normal body fluid mucous, sweat, calica and tears - assists movement across cell membrane
via CFTR channels
Immune function: chloride release from white blood cells as hypochlorous acid during phagocytosis
Therapeutic applications Defective chloride transport = Cystic fibrosis, bartter syndrome, congenital adrenal hyperplasia, Epilepsy,
myotonia, deafness, kidney stones, osteoporosis metabolic alkalosis
Factors increasing demand
Low salt diet, Loss of body fluid eg vomiting, burns, excessive sweating, urine (adrenal/hormone or kidney),
Medical conditions eg cystic fibrosis, Medications that affect sodium or GI symptoms or kidney functions
Deficiency
Rare due to sodium
Weakness lethargy, confusion, muscle twitches, spasms, low BP, slowed breathing, tachycardia, digestive
discomfort, anorexia, irritability, confusion, aggression
Toxicity - rare - due to dehydration
Assessment methods (related to pH)
Serum chloride - 95-110mmol/L (not effective)
24 h urinary analysis
Sweat
MICROMINERALS
Essential: Chromium, copper, iodine, iron, manganese, molybdenum, selenium, zinc and fluoride
Non essential: arsenic, boron, cobalt, nickel, silicon, vanadium
Trace: (between 1mg-100mg/day): iron, copper, zinc, fluoride and manganese
Ultra trace: <1mg/day
IRON
Sources
High protein foods eg liver, red meats, beans/legumes, seeds, wholegrains, some vegetables, dried apricots,
quinoa, mushrooms, spinach
Intake
RDI 8mg/day (18 for menstruating women) - UL 45 mg/day
Therapeutic dose 50-100mg divided doses (for deficiency anaemia or during pregnancy) - 4-6mg/kg/d
children
Forms
Ferrous iron (Fe2+) = haem iron
Ferric iron (Fe3+) = plant foods
Found in haemoglobin (RBC), myoglobin (muscle cells), in enzymes, storage/circulation
Stored as ferritin
Heme iron - animal foods - redness of meat - 25% absorption rate
Nonheme - plant foods - less absorbable (17%) - enhanced by MFP factor, vit C, citric acid/lactic acid, HCl,
sugars
Digestion
Stomach: hydrochloric acid and pepsin release haem from globin (protein). Non haem iron is reduced from
ferric (Fe3+) to ferrous (Fe2+)
Small intestine: absorbed at brush border
Absorption
Heme ferrous absorption: directly across brush border via specific carrier protein = efficient
Non haem/ferric absorption: any Fe3+ not reduced to Fe2+ in stomach must undergo a reduction via
reductase enzymes in intestinal brush border - remaining ferrous iron is absorbed via shared mineral
transporter
Inhibitors: polyphenols (tannins in tea/coffee), oxalates (spinach), phytates (legumes) + competitive minerals
Ca, Zn, Mn
Storage
To prevent oxidative damage - quickly taken up by transporters, cells or stored as ferritin (in liver + circulates
in blood)
Regulation
Absorption depends on needs - hepcidin hormone (liver derived)
Needed = mucosal ferritin (store and release to) → mucosal transferrin (hands iron to) → serum transferrin
Not needed = excreted with intestinal cells as they shed every 4-5 days
Functions
Accept, carry, release oxygen
Enzymes component or cofactor - neurotransmitters, hormones, skin pigments, connective tissue
Energy production - ATP production via CAC cycle and ETC
Free radical metabolism
Immune function - T lymphocyte proliferation and bactericidal activity of macrophages
Amino acid metabolism - production and conversion of many amino acids - hydroxylation
Factors increasing demand
Menstrual bleeding, pregnancy, Growth, athletes (due to increase RBC), vegetarian/vegan, excess coffee
etc (tannins/polyphenols), nutrient deficiencies (A, B6, B12, copper required to mobilise iron from storage),
disease and ageing (hypochlorhydria (low HCl acid), heavy/chronic bleeding, chronic inflammatory diseases
(celiac disease)
Iron deficiency = iron deficiency anaemia (IDA) = microcytic (small) or hypochromic (pale) blood cells
Deficiency signs - microcytic anaemia
Fatigue, impaired cognitive function, behavioural disturbances, pallor, breathlessness. thin/brittle/spoon
nails, cold intolerance, pica/pagophagia (eg eating dirt or ice)
Iron stores decline → iron transport diminishes → haemoglobin synthesis falls
Microcytic hypochromic anaemia
Toxicity
Rare due to absorption regulation
Haemochromatosis
Symptoms: fatigue, headaches, increase respiration, arthritis, anorexia, increase oxidative stress, cancer,
heart disease, liver damage
Assessment methods
Serum iron, transferrin (iron transporter) or total iron binding capacity, transferrin saturation % or ferritin
(stored)
Serum ferritin = best indicator for storage
COPPER
Trace mineral found in all body tissues and secretions (salica, gastric and pancreatic juices and bile)
Essential component of enzymes - including for iron metabolism and antioxidant pathways
Competes with zinc
Sources
Nuts, shellfish, liver and grains - oysters, shitake mushrooms, tofu, sweet potato, cashews, chickpeas,
salmon, dark choc, avo
Rusty colour eg prawns, snapper, liver
Intake
RDI 1.2mg/day F, 1.7mg/day M
Therapeutic dose: 0.1g/kg/day or 2-5 g/day
Digestion - bound to protein foods
Stomach: gastric secretions HCL and pepsin digest copper - reduced for Cu2+ to Cu+ by reductase
enzymes (require vit C) before absorption
Absorption
Small intestines: SI duodenum - via active transport, carrier mediated in low concentrations or passive
transport, diffusion in higher concentrations
50% absorbed, 20% when intake is >5mg, 50% when intake is <1 mg/day
Inhibitors: iron, zinc, calcium, phytates, molybdenum, vit C, antacid use
Enhancers: histidine, methionine, cystine, organic acids
Storage: mainly in skeleton and muscles = 75-150mg
Excretion: via bile or urine:
Functions = essential enzyme cofactor
Energy production - ATP
Iron utilisation/metabolism
Cofactor for formation of haemoglobin
Antioxidant
Connective tissue formation - bones, ligaments, blood vessels, skins etc = bone density
Blood clotting
Neurotransmitter and neuropeptide activation - domain → noradrenalin
Also angiogenesis, immune, nerve myelination, endorphin action, gene expression
Factors increasing demand
Pregnancy.lactation (infant growth), ageing (bone density), chronic conditions (diabetes, CVD), high intake
or exposure to zinc, iron, molybdenum lead, cadmium, gastric surgery, medications
Deficiency
Hypochromic, microcytic anaemia (no response to iron), leukopenia (neutropenia low neutrophils)
Hypopigmentation, poor immunity, blood vessel, connective tissue or bone abnormalities, altered cholesterol
metabolism, cardiovascular and pulmonary dysfunction
During pregnancy: spontaneous abortion, prolonged pregnancy, premature rupture of membranes,
compromised connective tissue of baby
Mankes - genetic condition - no transporter
Toxicity
Supplementation, water contamination
Epigastric pain, nausea, vomiting, diarrhoea, weakness, lethargy, anorexia, hematuria, liver damage
(jaundice), kidney damage, Wilson's disease (genetic disease where copper accumulates in liver and brain
causing toxicity, menkes disease
Assessment methods
Serum or plasma copper - 13-22umol.L
Urinary copper - < 1.2 uol/24 hours
Hair analysis - indicated copper toxicity
ZINC
Required in enzymatic reactions and transcription factors - very important
Sources
Protein rich foods, the ocean, oysters, lamb, tomato, cacao powder, pumpkin seeds
Plant foods have lower content and absorption
Endogenous zinc from pancreatic and biliary secretions can be absorbed
Absorption depends on requirements
Pancreatic enzymes are rich in zinc
Intake
Higher in childhood and pregnancy
RDI 14mg M, 8 mg F
Therapeutic dose - 25-50mg/day to prevent negative effects due to competition
Digestion and absorption - hydrolysed from amino and nucleic acids to be absorbed → requires proteins for
transport (metallothionein )
Stomach: HCl required to release zinc from amino acids/proteins
Absorption: via carrier mediated process in jejunum, high intake (passive diffusion)
Enterocytes: zinc involved in cell metabolism of stored within protein metallothionein (regulates)
Dietary phytates reduce absorption of plant sources
Albumin = chief transport substance of zinc
Functions → brain and nerve function, antioxidant, anti inflammatory, HCl and pancreatic enzyme
production, metalloenzyme component
Growth and development - cell division and differentiation
-
Embryogenesis - conception and pregnancy
Immune function
Carbohydrate, protein and alcohol metabolism
Synthesis of superoxide dismutase SOD
DNA metabolism and repair - zinc fingers
Reproduction, vision, taste and cognition/behaviour
Neurogenesis, synaptogenesis nerve growth, neuronal growth and neurotransmission = brain and nerve
function
Component of metalloenzymes
Digestion - maintains intestinal barrier and cells that secrete digestive enzymes, also HCl production,
pancreatic enzyme synthesis, folic acid absorption, vitaminA conversion
Antioxidant, anti inflammatory and detoxifying activity
Therapeutic applications: wilson's disease (copper), age related macular degeneration, anorexia nervosa
(improves appetite), wound healing, loss of taste, male infertility, skin conditions, acute infections (colds),
diarrhoea, depression, ADHD, dementia/alzheimer's disease
Factors increasing demand
Dietary components in plant foods (phytates, oxalates, polyphenols, fibres and nutrients that inhibit
absorption, Vitamin A, folate, iron, calcium, copper - compete for bind and transporters, Interaction with folic
acid and divalent minerals inhibiting uptake, vegetarian/vegan diet, Chronic alcohol consumption,
Inadequate protein intake, Inadequate HCl, digestive disorders, bowel disorders, gastric surgery, Diabetes,
liver disease, surgery burns, trauma, Growth, Medications
Deficiency
In children - Growth retardation, skeletal abnormalities, poor wound healing, diaarhoea, skin issues, delayed
sexual matruation
In adults - anorexia, diarrhoea, lethargy, depression, dermatitis, hypogeusia (taste), alopecia (hair loss),
vision problems, poor immunity, protein synthesis and wound healing
Toxicity
Chronic intakes over 40mg can cause copper deficiency + numbness, weakness, ataxia, spastic gait 57mg metallic taste, headache nausea, vomiting, epigastric pain, abdominal cramps, bloody diarrhoea, reduced
immune function and altered copper/iron status
Assessment methods
Plasma zinc 12-20 mmol/L in adults is not reliable
Urinary reference range 8-11 mmol/24h
IODINE
Essential trace mineral - iodine or iodate → converted to iodide in body
15-25mg in body, 70% in thyroid gland
Food sources
Seaweed, muscles, oysters, fortified breads, eggs, snapper, milk, yoghourt, tuna
RDI
150ug/day more if pregnant/lactating
Therapeutic dose 150-1100ugday
Absorption and pathway
Found to AAs or free as iodate
Absorbs in stomach (+ SI) → blood → tissues eg thyroid
Goitrogens (eg cauliflower and soy) - inhibit iodine metabolism and thyroid hormone production
Iron and selenium aid use
-
Tyrosine AA needed to synthesise thyroid hormones
Functions
Thyroid hormones = thyroxine T4 and triiodothyronine T3 → nuclear receptors and gene expression =
metabolic rate
Foetal development
Factors increasing demand
Growth and development (child, teen), diarrhoea, goitre, thyroid deficiency, high goitrogen exposure,
pregnancy, breast disorders, inadequate diets, vegetarian/vegans
Deficiency
Hypothyroidism → lethargy, sleepiness, reduced mental capacity, sluggish physical movement, constipation,
cold intolerance
Reporductive issues → gastointal hyptesion, increase miscarriage, birthdepects, infant mortaility
Neurological deficits → brain damage in infants, cretinism (mental retardation, hearing, speech loss,
shortness, spasticity
Goiture
Toxicity
Hyperthyroidism, reduced TSH, brassy taste, burning sensation in mouth/throat, gut irritation, diarrhoea,
hypersensitivity
Assessment methods
Urine - 100-190 mg/L or TSH
SELENIUM
Essential trace mineral similar to sulphur (sulphur containing amino acids)
Non metal - organic (selenomethionine - plant, selenocysteine - animal) inorganic (selenite, selenate)
Sources
Brazil nuts, mullet, mussels, snapper, sardines, chickpeas, chia seeds, cashews, mushrooms, egg
RDI
F 60ug/day F, 70ug/day M → UL 400ug.day
Therapeutic dose 25-250ug/day
Digestion and absorption 80%
Small intestine via AA transport system
Functions - similar to vitamin E
Converts T4 to T3
Antioxidant
Immune function - WBC production, prevents viral mutation
Hormone synthesis - thyroid hormone production, insulin metabolism
Cell replication - enzymes that suppress tumour and induce apoptosis, DNA methylation
Part of enzyme glutathione peroxidase
Male reproductive - structure of sperm mitochondria
Therapeutic applications: kash-beck disease, hypothyroidism, hashimotos disease, graves disease,
congestive heart failure, heart surgery, preeclampsia, autoimmune thyroiditis, psoriasis, cancer
Factors increasing demand
Agriculture (soil), impiared nutrition or digestion, oxidative stress, pregnancy and lactation
Deficiency - Rare
Hair loss/depigmentation, muscle pain/tenderness, increase risk of cancer, haemolytic anaemia, worsening
autoimmune conditions, reproductive failure, depression, mood, memory
Kashan-beck syndrome - childhood osteoarthritis - dwarfism, joint deformation, CVD
Toxicity
Selenosis - miners or supplements
Nausea, vomiting, fatigue, diarrhoea, garlic breath, brittle hair/nails, skin rash, irritability, muscle cramps,
paresthesia, interference with sulphur metabolism, inhibition of protein synthesis, acute poisoning
Assessment methods
Blood, urine, hair, thyroid function test (high T4, low T3)
MANGANESE
In bones, liver, kidneys and pancreas, hair
Food sources (easy)
Lobster, wheat germ, pine nuts, pecans, trout, brown rice, silverbeet, flour, choc, chickpeas, muscles, tofu,
sweet potato
Intake
RDI 5-5.5mg/dy
Therapeutic dose 2-11mg/day
UL 11 mg/day
Digestion and absorption
Bound to food components requiring digestion
Absorption via SI (less than 5%) → transport in blood bound to carrier protein or free as Mn to the liver
Competes with iron and copper
Absorption regulated based on need and intake
Functions = enzyme cofactor, bone formation, macronutrient metabolism
Enzymes
Bone formation - cartilage and connective tissue manufacturing
Energy metabolism - AAs, cholesterol, carbohydrates,
Antioxidant and free radical control
Chemical messenger - second messenger pathways cAMP - regulate calcium metabolism
Therapeutic actions - osteoporosis, arthritis, metabolic disorders, allergies, wouldn healing and chronic
obstructive pulmonary disease, preeclampsia
Factors increasing demand
Poor absorption (tannins, males, oxalates, high intake of phosphorus, magnesium, copper and non-heme
iron)
Deficiency (rare)
Skin rashes, bone/joint abnormalities, decrease clotting proteins, impiared carbohydrate and lipid
metabolism, low serum cholesterol, decrease growth of hair and nails, loss of pigmentation of hair
Toxicity (environmental contamination) - motor and nervous system sydnfunction
Muscle fatigue impotence, anorexia, coughs/lung illnesses, insonia, headache, mood, memory, axiciety,
parkinson's disease
FLUORIDE (F)
Non essential naturally occurring mineral
Safe range
0.3-2mg/day (anything less than 5mg) = over 8-10 is toxic
2.6g found in human body in bones and teeth - in calcified tissue as fluorapatite
Sources
Fluoridated water and unfluoridated water
Fluoridated toothpaste
Food: dairy, turkey, fish, tea, grain, avocado, green leafy vegetables, legumes, root vegetables, tap water
Digestion and absorption
Bound to proteins → hydrolysed by pepsin → absorbed in stomach and SI (passive diffusion)
High fluoride uptake = increase urinary excretion, skeletal growth influences absorption
Insoluble complexes w/ calcium or magnesium decrease absorption
Function
-
Teeth: fluorapatite in tooth enamel - alters crystalline structure protecting from acid forming bacteria and
demineralisation
Bone and joints - stimulates osteoblast proliferation and mineral deposition
Deficiency
Tooth decay (caries)
Toxicity
High fluoride intake: delta fluorosis - excess can cause discoloured enamel of teeth
Chronic toxicity: skeletal fluorosis (bone deformities, restricted joint movement, abnormal bone formation,
increase risk of fracture + impaired muscle, nerve and kidney function
Acute toxicity: nausea, vomiting, diarrhoea, acidosis, cardiac arrhythmia
Death: high dose
CHROMIUM (Cr)
Essential
Food sources
Liver, eggs, legumes = zinc foods
Abalone, black pepper, ocean throat, bread, muesli, potato, spinach, salmon, almonds, broccoli
Stability: available in unrefined foods, solubilized from stainless steel and cans
RDI
F 25ug/day, M 35ug/day
Therapeutic dose: 100-300mcg/day
No UL
Absorption and digestion
Absorbed in SI via diffusion or carrier mediated transport
Stored with ferric iron in kidneys, liver, muscles, spleen, pancreas and bone
Concentrations decline with age
Functions
Enhances insulin activity: blood sugar regulation diabetes, pcos, antioxidant and antiinflammatory role impacts neurotransmitters (increase tryptophan and norepinephrine release, lowers cortisol) - bipolar,
depression
Metabolism: glucose and lipid metabolism (also cholesterol, protein, muscle, bone metabolism) → TA
hyperlipidemia, hypertension,
Nucleic acid metabolism: DNA structure and gene expression
Component of glucose tolerance factor (cytosolic complex that enhances insulin binding)
Factors increasing demand
Medications, high phytate and carb intake, ageing, disease and infections, diabetes, excess minerals
(compete), pregnancy/lactation, prolonged stress, non steroidal antiinflammatory drugs, stress/decrease
glucose utilisation/metabolism of chromium
Deficiency symptoms
Glucose intolerance (insulin resistance), peripheral neuropathy (numb), cvd, decrease male fertility
Toxicity
Rare, can interfere with iron uptake
MOLYBDENUM (Mo)
Essential
Concentrated in liver and kidneys → found in cells mostly bound to protein
Sources
Lamb liver, legumes, peanut butter, rick crackers, spelt flour, muesli, vegemite, almonds
Found in plants → content reflects soil content
RDI
45ug/day
Therapeutic dose 100-500ug/day
Wilson's disease 120mg/day (to reduce copper)
Digestion and absorption
No digestion required - mostly absorbed passively in proximal small intestine
Sulphates compete for absorption
Functions - cofactor
Sulphite oxidase - sulphate metabolism, conversion and sulphur containing AAs methionine and cysteine
Aldehyde oxidase - converts Vit A to retinol, converts B6 to pyridoxal
Xanthine oxidoreductase - hydroxylation of purines, pyrimidines and pteridines + converts xanthine to uric
acid for excretion
Amidoxime reductase - drug metabolism
Removal of copper - treatment of wilson's disease
Antitumour and inhibits proinflammatory cytokines eg arthritis
Deficiency
No clear deficiency
Genetic defects inhibit functional role in enzymes = neurological deterioration
Toxicity
Rare - Gout, kidney damage, reproductive abnormalities
NUTRITION TOXICOLOGY - TOXIC METALS AND OTHER SUBSTANCES
Compete with essential minerals
Accumulate in body
Testing methods
Blood: acute exposure
Urinalysis: chronic exposure
Hair mineral analysis: chronic low grade exposure - less invasive, not affected by fluctuating
exposure but affected by shampoo etc
Detoxification → chelation and excretion
Chelation: agents which bind (covalently) to metal ion forming ring structure
Chelating agents: thiol groups eg methionine, cystine and SAMe, disulfide bonds in
metallothioneins OR dimercaprol and EDTA drugs
Nutrition methods of chelation, detoxification and excretion
Antioxidants and micronutrient cofactors - zinc (metallothionein synthesis), selenium,
vitamina C and E, quercetin
Chelation with glutathione (GSH), turine, N-acetylcysteine, NAC, a-lipoic acid and
methionine
Foods containing chelating compounds and phytonutrients in → garlic, gotu kola,
coriander, green tea and turmeric
Excretion: channels of elimination via bowels, kidneys, integumentary (skin) and lungs)
Acute and chronic exposure
Exposure = oxidative damage and decrease available chelators and antioxidants
-
LEAD
Binds to thiol (SH) and amide (NH2) in enzymes and competes with metallic cations (Ca2+ and Fe2+)
Stored in bones, directly targets calcium increase excretion = demineralisation
Substitutes zinc for iron in haemoglobin
Neurotoxicity (disrupts calcium needed for nerve firing)
Deplete antioxidant enzymes
Induces oxygen free radicals
Interferes with iron, zinc and calcium
Sources
Inhaled or swallowed → distributed around body, (can cross placental barrier), stored in bones and teeth
0.01mg/L allowable in drinking water
Environmental contamination eg contaminated soil and hair
Vulnerable populations
High traffic flow, miners, growth, children and pregnant women, risky hobbies eg mechanics, soldering,
glazing pottery
Toxicity
Children more susceptible
Low IQ scores
Treatments
Removal of exposure
Chelation therapy
Calcium prevents lead from mobilising (in pregnancy)
ARSENIC (has potential essential role in methylation)
Inorganic forms = toxic → reduced to GSH in lover and methylated to SAMe or chlorine then extreated via
urine OR bound to thiols such as metallothionein in connective tissue = found in water and food
Organic forms = non toxic - incorporated into phospholipids
Can bind to transferrin after absorption reducing availability
Biochemical reactions
Inhibits enzymes like pyruvate dehydrogenase and others involved in gluconeogenesis and beta oxidation
Substitutes phosphate reducing ATP production
Inhibits uptake & metabolism of selenium and iodine in thyroid
Facilitates methylation increase SAMe, polyamines and taurine production
Inhibits anti-tumour activity
Sources
Food grown in contaminated water and soil - imported foods - molluscs, fish, hijiki seaweed
Water - allowable limit is 0.01mg/L
Tobacco smoking and industrial processing
Toxicity
Blackfoot disease (blood vessels = gangrene)
Treatment
Acute = dimercaprol
-
Chronic - NAC and zinc to promote production of metallothionein MT, exerting protective effects for lungs,
kidneys and liver + vitamin C, garlic, quercetin, taurine and iron (chelating agents)
MERCURY (Hg)
Inorganic eg mercury hydroxide from environmental exposure
Elemental eg liquid metallic Hg from delta amalgams and industries
Organic eg methylmercury from bacterial conversion in food sources = most toxic
Biochemical reactions
Methylmercury from human bacteria
Binds to thiol and sulfhydryl groups = destroys 3+4 structure of protein = damages cell membranes and
inactivates enzymes
Metallothioneins in connective tissue and CNS binding
Sources
Inhalation, swallowing, skin contact → distributed in soft tissue
Mining exposure
(!!) Dental amalgams, batteries, light bulbs, cosmetics, thermometers, pharmaceuticals, vaccines
Fish consumption - limit to 2-3 times per week (less of shark, flake, swordfish, marlin) and less for
pregnant women and children
Toxicity signs and symptoms
Minamata disease - chemical dumping caused neurological and birth defects in japan
Treatments
Acute = dimercaprol or derivatives like DMSA + immediate removal of source
Chronic = selenium and NAC - chelate
Soluble fibre (binds and excretes from GIT)
Coriander
Zn to increase MT
Vitamin C and E
Avoidance of food sources
Selenium
Removal of metal amalgams
CADMIUM (Cd)
Inorganic metal (rare)
Biochemical reactions
Attaches to thiol groups in epithelial cells inhibiting metalloenzyme activity, methylation and DNA repair
Competes with calcium and zinc
Depletes antioxidants and induces oxygen and hydroxyl radicals
Toxicity lung and kidney damage, chronically bone loss, epigenetic changes and cancer
Sources
Ingestion or inhalation
Mining !, batteries, fertilisers, paint, pPVC, electronics
Tobacco smoke
Contaminated water and the foods that use it eg rice (asians)
Pregnant women and placental cross risk
Toxicity
Itai-itai (ouch ouch disease - working in contaminated rice paddies) - bone pain, fracture, osteomalacia
osteoporosis
Treatment
Acute - chelating agents (EDTA and GAS) - intravenously for 12 days also MAC
Chronic
N-actelcystine (NAC) and zinc to increase MT
Zinc to inhibit 5 a-reductase BPH
Vitamin C, E, Se, methionine
Zinc and magnesium to reverse Cd induced renal toxicity
Ca to remove bone losses
ALUMINIUM (Al)
Biochemical reactions
Al binds to transferrin affecting transit of iron
Distributed to bone for storage & excreted in urine
Interfere with calmodulin binding affecting absorption of calcium and other minerals
Depleted antioxidant enzymes eg glucose 6 phosphate dehydrogenase required for glycolysis and to
prevent RBC oxidative damage
Sources - Low absorption level
Tolerable weekly intake 1mg/kg
Packing, containers and cookware especially acidic foods
Paint pigments, insulation and building materials,vehicle bodies
Drugs, antacids, vaccines, cosmetics, antiperspirants
Foods - vegetables, root veggies, food additives (anticaking agents) and colours eg cereal, baked goods,
infant formula and beverages
Main source is processed foods
Risk - those with kidney failure/dialysis due to reduced clearance
Toxicity
Treatment
Acute = deferoxamine
Chronic = increase Ca, mg, Zn to inhibit absorption
Coriander chelates Al and enhances renal excretion
NICKEL (Ni)
Absorbed and binds to albumin or AAs → distributed to soft tissues and hair and bone → excreted in urine,
sweat and bile
Biochemical reactions
Enhance enzyme function when replacing magnesium and improve C3 convertase in complement system =
potential role in immunity
When substitutes for zinc, copper and iron = decrease activity of iron in bone, thyroid, RBC, aconitase =
competition for absorption with iron
Sources
Inhalation and swallowing
Stainless steel manufacturing eg rechargeable batteries, jewellery, coins
Foods processed, stored and cooked in stainless steel eg canned foods !
Allowable limit in Aus drinking water 0.02mg/L
Toxicity
Iron, copper, zinc and iodine deficiency can develop from nickel exposure
Treatment
Acute = EDTA, calcium carbonate chelation, removal of exposure source
-
Chronic = removal of exposure source, NAC and zinc to increase MT for chelation and restore
GSH(glutathione) , Vit C and E, iron therapy
OTHER NUTRIENTS AND NON NUTRIENT HEALTH PROMOTING COMPOUNDS
BORON - Useful but non essential
Food sources
Avocado, nuts, (peanuts and pecans), wine, grapes, raisins, pulses
Fruit and vegetables
RDI
Acceptable range 1-13mg/day
Tolerable UL 20ng/day
Therapeutic dose 3-9mg/day
Digestion and absorption
90% from boric acid by passive diffusion in GIT
3-20mg in body bones, nails, teeth, spleen, parathyroid
Functions
Metabolism of calcium and magnesium
Metabolism of triglycerides and glucose and nitrogen containing AAs and proteins
Metabolism of ROS, neurotransmitters and hormones
Bone growth and maintenance
Immune and anti inflammatory functions
Embryogenesis
Therapeutic application
Dysmenorrhea, vaginal candidiasis, age related cognitive decline, osteoarthritis, osteoporosis, hormones
Demand
Low soil levels, high fast food intake, menopausal women, osteoporosis, rhumatoid arthritis
Deficiency
Impaired calcium metabolism, brain function and energy metabolism
Bone composition
Toxicity
Rare as easily excreted in urine
Acute toxicity: nausea, vomiting, diarrhoea, dermatitis, lethargy
Chronic toxicity: nausea, poor appetite, anaemia, dermatitis, seizures
SILICA (silicon)
Non metal, highly abundant (silicon dioxide)
Non essential
Orthosilicic acid or colloidal silliate - human absorbed
Additives such as calcium silicate
Food sources
Whole grains (oat bran), lentils, soybeans, bananas, pineapple, mango, dried fruits, beans, spinach, root
veg, nuts, seafood
Water, tea, coffee, juices, beer
Food additives eg thickeners
Medications eg antacids
RDI
Estimates 10-25mg/day (therapeutic dose)
Digestion and absorption
More bioavailable in beverages than solid food
Orthosilicic acid readily absorbed in proximal small intestine - paracellular or via small pore transcellular
pathways
Plant foods - photolithic silica - requires digestion
Concentrates in body connective tissues, bone, blood vessels, cartilage tendons = 1-2g
Functions
Bone mineralisation, crystallisation, calcification and collagen synthesis
Metabolic and structural roles in connective tissue
Reduce aluminium toxicity
Therapeutic applications
Bone formation and density, alzhimers, immunodeficiency, skin,hair, nails, antitumour
Toxicity
Inhalations = fibrosis and scarring of lungs (silicosis) = occupational exposure
General toxicity = bruising, stomach irritations, skin rashes, irritations and diminished antioxidant enzyme
activity
Chronic use of antacids = kidney stones
VANADIUM - Non essential trace mineral
Mimics insulin activity by prolonging binding of insulin to insulin receptors (inhibiting phosphatase) = blood
sugar regulation
Vanadate in human body
Intake
UL 1.8mg/day
Absorbed via digestive and respiratory tract - food water air
Poorly absorbed (99% excreted)
Functions
Essential in chickens diet
Enhances response to insulin
Bone health
Intracellular interactions, metabolic transformations, modulation of signalling pathway
Therapeutic applications
Hypoglycemia, hyperlipidemia, cvd, oedema, diabetes, athlete performance, cancer, tuberculosis, syphilis,
anaemia
Toxicity
GI upset, kidney damage, malnutrition (diarrhoea)
Green discolouration of tongue, fatigue, lethargy focal neurological lesions
COBALT = essential in B12
Non essential trace element
Organic form = essential component of B12 <1.2mg in body = liver, heart, kidneys, spleen, brain, serum
Inorganic form present in ions = toxic
Functions
Same as B12
Stimulates synthesis of erythropoietin - erythrocytes and bone marrow
Assists in formation of AAs and proteins, myelin sheath in nerve cells and neurotransmitters
Substitute for metals such as zinc
Toxicity
Food, water, air, skin (inorganic through orthopaedic implants)
Skin issues, kidney and lung and heart damage - pulmonary fibrosis (scaring), heart failure
Possible carcinogen
Excessive intake inhibits selenium absorption = goitre and thyroid issues
Assessment methods
Hair mineral analysis (high cobalt = selenium deficiency, low cobalt = B12 deficiency), organic acid testing in
urine
PHYTONUTRIENTS / PHYTOCHEMICALS
Natural compounds produced by plants to protect against UV radiation, fungal and bacterial attach and injury by
insects
Non essential but beneficial
POLYPHENOLS
Prevent chronic degenerative disease - dementia, cardiovascular disease, cancer
Antioxidants, prebiotic
Fruits and vegetables = eat the rainbow
Phenolic acids
Ellagic acid, benzoic acid, gallic acid, caffeic acid, cinnamic acid, vanillic acid
Aromatic compounds with and phenol ring and carboxylic acid group
Antioxidant, antiulcer, antidiabetic, anticancer, cardioprotective, anti inflammatory, neuroprotective,
hepatoprotective, antimicrobial activity
Fruits, coffee, cinnamon, vanilla
Stilbenes
Resveratrol - red grape skins, red wine, peanuts, mulberries
Antioxidants - low toxicity - activity apoptosis and cancer cells
Lignins
Fibrous seeds and cereals = linseeds/flaxseeds, sesame seeds
Antioxidant, antitumour, anti inflammatory, phytoestrogenic effects - bind to oestrogen receptors
Flavonoids
Isoflavins = soy beans, tofu, miso, soy sauce, tamari, tempeh = soy isoflavones = phytoestrogenic effects
and antioxidants (menopausal, tumour growth)
Anthocyanins = blue = blueberries, purple carrots, balck rice, quinoa = antioxidants = cvd, brain health
Flavonols = tea, wine, cherries, grapes, apple, kale, broccoli, onions = antihistamine, anti inflammatory
effects → eg quercetin (onions - immunity, inhibits histamine release), kaempferol and myricetin
(antioxidant and antiinflammatory)
Flavanones = orange, lemon, grapefruit = hesperidin and naringenin (antidiabetic) and rutin (vascular
integrity ) = anti inflammatory
Flavonoids = green tea, apples, apricots, cocoa = catechin and epigallocatechin gallate ECGC (blood
glutathione and inhibit amyloid plaques/dementia)
Proanthocyanidins = apples, chocolate, grapes, purple colour in berries= antioxidant
Flavones = white cream pigments, parsley, celery, camomile, peppermint, tea = UV absorption and
protection = luteolin and apigenin (leaves of field grown herbs)
Others polyphenols
Curucumin (constituent of turmeric) - yellow = antioxidant, anti inflammatory, anti tumour, antimicrobial,
neuroprotective
Gingerol and shogaol (constituent of ginger) = anti inflammatory, antacid, antiemetic (nausea)
Oleuropein (green olives and extra virgin olive oil = bitter and green) = antioxidant = cvd, t2dm, cancer,
cognitive decline
Coumestans (coumestrol - isoflavones) = red clover, alfalfa = estrogenic activity
Capsaicin (capsaicinoids) = capsicums and chilli = antioxidant, anti inflammatory, analgesic
Glucosinolates = broccoli, broccoli sprouts, kale, brussel sprouts,cauliflower, cabbage, bok choy = brassica
vegetables containing sulfhydryl groups (SH - thiols) - fermented into anticarcinogenic compounds
(isothiocyanates) eg sulforaphane (cvd, cancer)
Carotenoids = orange red fruits and veg eg carrots, sweet potato, mangos, green leafy veg (consume with
fat to enhance absorption) = antioxidants = provitamin A (a-carotene and b-carotene) and non pro vitamin A
(lutein, lycopene zeaxanthin, xanthophylls) = decrease age related macular degeneration
Sterols and stanols (phytosterols) = olives, sunflower, corn, soybean, almonds, wheatgerm oils = found in
plant cell membranes similar role to cholesterol = intake decreases absorption of cholesterol = cvd
NUTRITIONAL SUPPLEMENTATION
Variable
Beneficial = compromised digestion
DIETARY STRATEGIES
Mediterranean diet = better cvd, obesity, diabetes, cancer, alzhimers
DASH diet study (dietary approaches to stop hypertension)
Protein, fibre, potassium, magnesium, calcium, fruits vegetables, beans, nuts, wholegrains, low fat diary →
limit saturated fat, sugar and salt
FODMAP diet
Fermentable oligosaccharides, disaccharides, monosaccharides and polyols
-
Links to IBS gas bloating pain diarrhoea constipation
LIFESTYLE DIETS
Coeliac
Immune mediated response altering surface of intestine inhibiting absorption of nutrients in individuals with
permanent gluten sensitivity
Gluten = protein found in wheat, spelt, rye, barely, triticale, oats
CSIRO therapeutics
CSIRO total wellbeing diet - Evidence based 12 week high protein low GI eating
Intermittent fasting diet
Impromy meal replacement diet
CSIRO low carb diet
CSIRO very low calories diets (VLCD) - 600 calories while still providing sufficient nutrients = meal
replacements and ketosis
Low amine, salicylate, glutamate diet
Intolerances are not allergies = not immune - chemicals that irritate nerve endings causing
reactions → Genetic predisposition or environmental triggers
Food causes = tastiest as they have highest level of natural chemicals
RPA diagnostic elimination diet (allergy testing) = very restrictive diet for 2 weeks = eliminate, then
reintroduce food groups eg diary, gluten, grains, eggs, seafood
LIFESTYLE DIETS = improve health and reduce risk of diet related disease
Vegetarian/vegan diet
-
Ethical
Nutrient concerns: low protein, iron, calcium, B12, EFAs - high sodium, fat, sugar
Bluezone diets
Places in the world with health and longevity - live beyond 100 (ceniterians)
Sardinia italy, ikaria greece, loma linda california, okinawa japan, nicoya costa rica
Rarely over eat, eat predominantly plant based, drink alcohol moderately and regularly → life natural,
purposeful, stressless, faithful, family orientated, social lifes
Palaeolithic diet (stoneage)
Lean meat, fish, shellfish, vegetables, roots, tubers, eggs and nuts → no grains, legumes, diary, salt or
refined fats and sugar
Ketogenic diet
Fat = 70% of energy
Seizure control, diabetes, weight loss, neurodegenerative conditions
Absence of circulating sugars = body breaks down stored fat into ketones to generate energy
Can be harmful to kidneys and cause nausea, bad breath, fatigue, gout etc etc
Detox and cleansing diets
Claims: rest organs, stimulate liver, promote toxin elimination etc
Concerns: lack of nutrients, impact potassium/calcium homeostasis
Intermittent fasting overview
Decreased energy intake over 1-2 days per week
Claims: kickstart metabolism, reduce calorie intake, lower insulin like growth factor, stabilise blood sugar,
inflammation, bp etc
Concerns: diabetics, eating disorders, active growth stages, increase risk of binge eating and food
obsession
SMART goals