Food Science & Technology · Foundations · also Principles of Nutrition, Food and Nutrition, Nutritional Biochemistry, Human Nutrition and Dietetics
What the body needs from food, how needs change across the life cycle, and how processing raises or lowers the nutritional value of a food. The second half — nutrient losses in processing, bioavailability and fortification — is what makes this a food technologist's nutrition course rather than a dietitian's.
In the exams: GATE XE-G and XL-U Section 1 (nutrition: balanced diet, EAAs, PER, vitamins, minerals, anti-nutrients, deficiency diseases); ICAR AIEEA-PG Code 18 Unit I; ICAR AICE 47 Food and Nutrition
Human nutrition is the science of what the body needs from food, what it does with each nutrient, and what happens when the supply is too low, too high or out of balance. For a food technologist it has a second half that a dietitian's course treats lightly: how milling, heating, drying, fermentation, storage and fortification change the nutrients a food delivers, and how much of what is on the label the body can actually absorb.
The subject matters in every plant and every regulator's office. A nutrition label is a calculation from Atwater factors and nutrient analyses. A claim of "high protein" or "source of iron" rests on reference values and on protein-quality scores. A fortified flour or rice programme succeeds or fails on the choice of fortificant, the overage added to cover losses and the bioavailability of the form chosen. Anti-nutritional factors in pulses, cereals and roots decide whether soaking, germination or fermentation is a quality step or a safety step.
The subject is examined in food technology and food science degrees worldwide and in the nutrition sections of national postgraduate entrance papers, research fellowship examinations, home-science and community-nutrition examinations, food technologist licensure in several countries and food safety officer recruitment. Examiners return to a short list: Atwater factors and energy calculations, essential amino acids and limiting amino acids, BV, NPU, PER, PDCAAS and DIAAS, the vitamins with their deficiency diseases and processing stability, minerals and their inhibitors, anti-nutritional factors and their removal, and fortification. Numerical items on energy, protein scores and nutrient retention are common.
This manual follows the curriculum units in order: energy, the macronutrients, vitamins, minerals, reference values and the life cycle, malnutrition and public-health nutrition, and then the technologist's half: anti-nutrients, processing losses and gains, bioavailability and fortification.
The body spends energy in three ways. Basal metabolic rate (BMR) is the energy used by a person lying at rest, awake, in a thermoneutral room, twelve or more hours after the last meal; it keeps the heart beating, the lungs moving, ion pumps working and the body warm. In most sedentary adults BMR is the largest part of daily expenditure, roughly 60 to 70 per cent. The thermic effect of food, also called diet-induced thermogenesis, is the energy spent digesting, absorbing and storing a meal; it is commonly taken as about 10 per cent of energy intake and is highest for protein. Physical activity is the most variable part, from small in a bedridden patient to more than half of expenditure in a heavy manual worker or endurance athlete. During growth, pregnancy and lactation there are extra costs for new tissue and milk. BMR rises with fat-free mass, so men, who on average carry more lean tissue, have a higher BMR than women of the same weight. It falls with age as lean mass falls, rises in fever (by roughly 10 to 13 per cent per degree Celsius is the figure most textbooks give), and rises with thyroid hormone. It falls in prolonged starvation, which is one reason weight loss slows on a long diet.
Total energy expenditure (TEE) is usually estimated as BMR multiplied by a physical activity level (PAL). The FAO/WHO/UNU expert consultation of 2001 (published 2004) classed lifestyles as sedentary or light (PAL 1.40 to 1.69), active or moderately active (1.70 to 1.99) and vigorous or vigorously active (2.00 to 2.40). BMR itself is predicted from equations based on weight, and sometimes height, age and sex. The FAO/WHO/UNU equations derived from Schofield's data use weight for each age band and sex. The Harris–Benedict equations (1919) and the Mifflin–St Jeor equations (1990) use weight, height and age; Mifflin–St Jeor is widely used in clinics: for men BMR (kcal/day) = 10 × weight (kg) + 6.25 × height (cm) − 5 × age (years) + 5, and for women the final constant is −161 instead of +5. Predictions for an individual can be off by 10 per cent or more; the reference method for free-living expenditure is doubly labelled water, and indirect calorimetry measures oxygen use and carbon dioxide output at rest. The energy requirement of an adult is the intake that balances expenditure at a healthy body weight and a desirable level of activity. Unlike nutrients such as vitamin C, there is no safety margin added to energy requirements: an "RDA" set two standard deviations above the average would make most people gain weight. Reference energy values are therefore average requirements for groups.
A bomb calorimeter burns food completely in oxygen and measures its gross energy. Average gross energies are about 4.1 kcal/g for carbohydrate, 9.4 kcal/g for fat and 5.65 kcal/g for protein. The body does not get all of this. Some of each nutrient is not absorbed, and protein is not burned completely: its nitrogen leaves in urea, which still carries about 1.25 kcal per gram of protein. Atwater corrected gross energy for digestibility and for this urinary loss and arrived at the general factors still used on labels: 4 kcal/g for protein, 4 kcal/g for carbohydrate, 9 kcal/g for fat and 7 kcal/g for ethanol (17, 17, 37 and 29 kJ/g). One kilocalorie equals 4.184 kilojoules. Many labelling rules add factors for other components. Dietary fibre is commonly given 2 kcal/g (8 kJ/g) because colonic fermentation yields short-chain fatty acids that are absorbed; organic acids are commonly given 3 kcal/g and polyols 2.4 kcal/g, though the factors and which components must be counted differ between jurisdictions. Specific Atwater factors, which vary by food (for example a lower factor for the protein of whole-grain cereals than for egg protein), are more accurate for single foods but are rarely used on labels. Whether carbohydrate is declared "by difference" (100 minus water, protein, fat, ash and sometimes fibre) or as the sum of analysed sugars and starch also changes the energy figure a little, which is why the same food can carry slightly different energy values in different countries.
Carbohydrates supply about half of dietary energy in most of the world and more than two-thirds where diets are built on rice, maize, cassava, sorghum or wheat. Nutritionists divide them by what the small intestine can do with them. Available (glycaemic) carbohydrates are digested and absorbed as monosaccharides: free sugars, lactose, sucrose, maltodextrins and digestible starch. Starch is broken by salivary and pancreatic amylase to maltose and limit dextrins, then by brush-border enzymes (maltase, isomaltase, sucrase and lactase) to glucose, fructose and galactose. Glucose and galactose are taken up by an active sodium-linked transporter; fructose by facilitated diffusion. Lactase activity falls after weaning in most of the world's adults; lactase persistence is common in populations of northern European, and some East African, Middle Eastern and South Asian pastoralist, descent. People with lactase non-persistence ferment undigested lactose in the colon and may get bloating and diarrhoea after large doses; fermented milks, hard cheese and lactase-treated milk are better tolerated. The glycaemic index (GI) ranks a food by the area under the blood-glucose curve after a portion containing 50 g of available carbohydrate, relative to glucose (or white bread) eaten by the same people, with glucose taken as 100. Glycaemic load (GL) adds portion size: GL = GI × grams of available carbohydrate in the portion ÷ 100. Processing changes GI: fine milling, puffing, extrusion and full gelatinisation raise it; intact grains, parboiled rice, pasta, viscous fibre, fat, protein and acidity lower it. WHO recommends that free sugars, those added by manufacturers or cooks plus the sugars naturally present in honey, syrups and fruit juices, be kept below 10 per cent of energy, with a further conditional recommendation of below 5 per cent.
Dietary fibre is the part of plant food that resists digestion in the small intestine. The Codex Alimentarius definition (2009) covers carbohydrate polymers with ten or more monomeric units that are not hydrolysed by the endogenous enzymes of the human small intestine, whether naturally present in food, extracted from raw material, or synthetic, provided the isolated and synthetic forms have a demonstrated physiological benefit; national authorities may decide to include polymers of three to nine units. Soluble, viscous fibres such as pectin, oat and barley β-glucan, guar gum and psyllium slow gastric emptying and glucose absorption and lower LDL cholesterol by binding bile acids. Insoluble fibres such as cellulose, many hemicelluloses and lignin hold water in the colon, increase stool bulk and shorten transit time. Most fibre is fermented by colonic bacteria to short-chain fatty acids (acetate, propionate and butyrate) and gases; butyrate is the main fuel of colonocytes. Resistant starch (RS) is starch that escapes small-intestinal digestion. RS1 is physically enclosed, as in coarse or whole grains and seeds; RS2 is native granular starch of the B-type, as in raw potato and green banana; RS3 is retrograded starch formed when cooked starch cools, as in cold cooked potato, rice or bread; RS4 is chemically modified starch; amylose–lipid complexes are sometimes called RS5. Processing therefore moves starch between digestible and resistant forms. WHO's 2023 guideline recommends that adults eat at least 25 g a day of naturally occurring dietary fibre, and many national guidelines set similar or slightly higher targets.
Dietary protein supplies nitrogen and the amino acids the body cannot make. Nine are indispensable (essential) for adults: histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan and valine. Others are conditionally indispensable: cysteine and tyrosine can be made from methionine and phenylalanine but spare them in the diet, and arginine, glutamine and glycine may be needed from food in stress, prematurity or rapid growth. In phenylketonuria, a genetic defect of phenylalanine hydroxylase, tyrosine becomes essential and phenylalanine must be restricted. Most proteins contain about 16 per cent nitrogen, so crude protein is estimated as nitrogen × 6.25; specific factors (5.7 for wheat, 6.38 for milk) are used for some foods. The WHO/FAO/UNU 2007 report set the average requirement for healthy adults at 0.66 g of good-quality protein per kg body weight per day and the safe level (meeting the needs of nearly all) at 0.83 g/kg/day. Needs per kg are higher in infancy and childhood, in pregnancy and lactation, and in recovery from illness or injury. Protein quality depends on two things: whether the indispensable amino acids are present in the proportions the body needs, and how much of the protein is digested and absorbed. The indispensable amino acid present in the smallest amount relative to need is the limiting amino acid. In most cereals it is lysine (maize is also low in tryptophan); in most pulses it is the sulphur amino acids, methionine plus cysteine. Eating cereals and pulses together, as in rice and lentils, maize and beans, or wheat bread with chickpeas, lets each supply what the other lacks; this is protein complementation.
Biological value (BV) is the proportion of absorbed nitrogen that is retained in the body: BV = N retained ÷ N absorbed × 100, where N absorbed = intake − faecal N and N retained = absorbed − urinary N. True BV subtracts endogenous faecal and urinary nitrogen measured on a protein-free diet; apparent BV does not. Whole egg protein has a BV near 94 to 100 and was long used as a reference; milk and meat are high; most cereals are lower. Net protein utilisation (NPU) is the proportion of intake retained: NPU = N retained ÷ N intake × 100, which equals BV × digestibility. Digestibility here is N absorbed ÷ N intake. A protein with high BV but low digestibility can have a modest NPU. Protein efficiency ratio (PER) is the oldest growth assay: weanling rats are fed a diet with about 10 per cent protein from the test source for 28 days, and PER = weight gain (g) ÷ protein consumed (g). Casein is run alongside, and results are often adjusted so that casein reads 2.5. PER is cheap and was written into labelling rules in several countries, but it measures what a growing rat needs, which overstates the importance of sulphur amino acids for humans, and it is not proportional: a PER of 2 does not mean half the value of a PER of 4. Net protein ratio (NPR) adds back the weight lost by a protein-free control group.
Chemical (amino acid) scoring compares the content of each indispensable amino acid in the test protein with a reference pattern, and the lowest ratio is the amino acid score. The Protein Digestibility-Corrected Amino Acid Score (PDCAAS), adopted by FAO/WHO in 1991, multiplies that score by true faecal protein digestibility and truncates any result above 1.0 (100 per cent). So PDCAAS = (mg of limiting amino acid in 1 g test protein ÷ mg of the same amino acid in 1 g reference protein) × true faecal digestibility. Casein, egg and soy isolate all reach 1.0 after truncation, which hides real differences between high-quality proteins. An FAO expert consultation in 2011 (report 2013) recommended the Digestible Indispensable Amino Acid Score (DIAAS) as the replacement. DIAAS uses the true ileal digestibility of each indispensable amino acid separately, measured at the end of the small intestine, because nitrogen that reaches the colon is fermented by bacteria and is of no use for protein synthesis even though it disappears from faeces. For each amino acid, digestible content (mg per g protein × its ileal digestibility) is divided by the reference pattern for the age group, and the lowest ratio, times 100, is the DIAAS. Values above 100 are reported untruncated, though truncation is still suggested when protein sources are combined for a mixed diet or a claim. FAO suggested that a DIAAS of 75 or more supports a "good quality" claim and 100 or more an "excellent" claim. Heat damage, especially Maillard reaction with lysine, lowers both scores, a direct link between processing and protein quality.
Dietary fat supplies energy at 9 kcal/g, carries the fat-soluble vitamins and carotenoids, and supplies two fatty acids the body cannot make because humans lack the desaturases that insert double bonds beyond carbon 9 from the carboxyl end. These essential fatty acids are linoleic acid (C18:2 n-6) and α-linolenic acid (C18:3 n-3). From them the body makes, slowly and with limited efficiency, the longer-chain arachidonic acid (C20:4 n-6), eicosapentaenoic acid (EPA, C20:5 n-3) and docosahexaenoic acid (DHA, C22:6 n-3). Conversion of α-linolenic acid to DHA in particular is low, so oily fish, fish oil and algal oil are the practical sources of DHA, which is concentrated in retina and brain. The n-6 and n-3 families compete for the same enzymes, so a very high ratio of linoleic to α-linolenic acid can reduce n-3 conversion. Classical essential fatty acid deficiency, with scaly dermatitis, poor growth and poor wound healing, is rare and seen mainly in long-term fat-free parenteral feeding or severe fat malabsorption. Linoleic acid is plentiful in sunflower, safflower, maize, soybean and cottonseed oils; α-linolenic acid in linseed, rapeseed (canola), soybean and walnut oils and in green leaves. Long-chain n-3 fatty acids are associated with lower triglycerides and a lower risk of fatal coronary events.
Saturated fatty acids, especially lauric, myristic and palmitic acids, raise LDL cholesterol. Stearic acid has little effect on LDL. Replacing saturated fat with polyunsaturated fat lowers LDL and coronary risk; replacing it with refined starch and sugar does not help. WHO recommends that saturated fat provide less than 10 per cent of energy and that total fat be kept within a range appropriate to the population. Trans fatty acids have at least one double bond in the trans configuration. Industrially produced trans fat comes mainly from partial hydrogenation of vegetable oils, used to make shortenings, vanaspati and margarines with a solid texture and long frying life, and in smaller amounts from deodorisation of oils at high temperature. Ruminant trans fat, chiefly vaccenic acid, together with conjugated linoleic acid, is formed by bacteria in the rumen and occurs in milk fat and meat at a few per cent of fat. Industrial trans fat raises LDL and lowers HDL cholesterol, a worse combination than saturated fat gram for gram, and is consistently linked to coronary heart disease. WHO recommends that total trans fat be below 1 per cent of energy and in 2018 called for the elimination of industrially produced trans fat from the food supply. Many countries have set limits of 2 g of industrial trans fat per 100 g of total fat or have banned partially hydrogenated oils; the food technologist's response has been interesterification, fractionation and blending with tropical fats to get the same functional properties. Dietary cholesterol has a smaller and more variable effect on blood cholesterol than saturated and trans fat.
Vitamin A covers retinol, retinal, retinoic acid and the provitamin A carotenoids, chiefly β-carotene. Retinal combines with opsin to form rhodopsin in the rods of the retina; retinoic acid controls gene expression for epithelial differentiation and immunity. Deficiency first causes night blindness, then xerophthalmia: conjunctival xerosis, Bitot's spots (foamy patches on the conjunctiva), corneal xerosis and keratomalacia, which can blind. Deficiency also raises child deaths from measles and diarrhoea, which is why vitamin A supplementation and fortification programmes run in parts of sub-Saharan Africa and South and Southeast Asia. Preformed retinol comes from liver, dairy fat, egg yolk and fortified foods; provitamin A carotenoids from orange and dark-green vegetables, mango, papaya, orange-fleshed sweet potato and red palm oil. Activity is expressed as retinol activity equivalents (RAE): 1 µg RAE = 1 µg retinol = 12 µg dietary β-carotene = 24 µg of other provitamin A carotenoids; 2 µg of β-carotene dissolved in oil as a supplement also equals 1 µg RAE. Older tables used retinol equivalents with a 6:1 ratio for food β-carotene. One international unit (IU) of vitamin A equals 0.3 µg retinol. High intakes of preformed retinol are teratogenic and hepatotoxic; β-carotene from food is not toxic, because its conversion is regulated. Vitamin D is made in skin when ultraviolet-B light converts 7-dehydrocholesterol to cholecalciferol (D3); ergocalciferol (D2) comes from UV-exposed fungi and yeast. Both are hydroxylated in the liver to 25-hydroxyvitamin D, the circulating form used to judge status, and in the kidney to the active 1,25-dihydroxyvitamin D, which raises calcium and phosphate absorption. Deficiency causes rickets in children (bowed legs, widened wrists, the "rickety rosary" at the costochondral junctions) and osteomalacia in adults. One µg equals 40 IU. Few foods are rich in vitamin D apart from oily fish, cod liver oil, egg yolk and fortified milk, margarine or cereals, so status depends on sunlight, latitude, season, skin pigmentation, covering clothing and age.
Vitamin E is a family of tocopherols and tocotrienols; α-tocopherol has the highest biological activity and is the form the body retains. It is the main lipid-soluble chain-breaking antioxidant in membranes, protecting polyunsaturated fatty acids from peroxidation, so requirement rises with intake of polyunsaturated fat. Deficiency is rare and occurs in fat malabsorption, in rare genetic defects of the α-tocopherol transfer protein and in premature infants, where it causes haemolytic anaemia; long-standing deficiency causes a spinocerebellar neuropathy. Vegetable oils, especially wheat germ, sunflower and safflower oil, nuts and seeds are rich sources. Refining and deodorisation remove part of the tocopherol in crude oil, and tocopherols are added back as antioxidants. Vitamin K exists as phylloquinone (K1) in green leafy vegetables and some oils, and as menaquinones (K2) made by bacteria, found in fermented foods such as natto and some cheeses. It is the cofactor for γ-carboxylation of glutamate residues in clotting factors II, VII, IX and X and in bone proteins such as osteocalcin. Deficiency causes bleeding. Newborns are at risk because little vitamin K crosses the placenta, breast milk is low in it and the gut is not yet colonised; vitamin K deficiency bleeding is prevented by an injection or oral doses at birth, practised in most countries. Warfarin-type anticoagulants act by blocking vitamin K recycling, so patients taking them are advised to keep their vitamin K intake steady.
Thiamin (B1), as thiamin pyrophosphate, is the coenzyme of pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase, so need rises with carbohydrate intake. Deficiency causes beriberi: dry beriberi with peripheral neuropathy, wet beriberi with heart failure and oedema, and infantile beriberi in breastfed infants of deficient mothers. In alcohol misuse it causes Wernicke–Korsakoff syndrome. Beriberi spread across East and Southeast Asia with machine-polished rice, because the thiamin of rice is concentrated in the bran and germ. Thiamin is destroyed by heat, especially at neutral or alkaline pH, and by sulphite, and is cleaved by thiaminases in raw fish and some ferns. Riboflavin (B2) forms FMN and FAD, the flavin coenzymes of oxidation–reduction. Deficiency (ariboflavinosis) causes angular stomatitis, cheilosis, glossitis and seborrhoeic dermatitis. Milk, eggs, meat and leafy vegetables are sources. Riboflavin is fairly heat-stable but destroyed by light, which is why milk in clear glass or plastic in sunlight loses riboflavin and develops a light-induced off-flavour. Niacin (nicotinic acid and nicotinamide) forms NAD and NADP. Deficiency causes pellagra, the disease of the "three Ds": dermatitis on sun-exposed skin, diarrhoea and dementia, ending in death. Pellagra was common where maize was the staple, from southern Europe to the southern United States to parts of Africa, because the niacin in maize is largely bound (niacytin) and maize protein is low in tryptophan. The body makes niacin from tryptophan, about 1 mg from 60 mg, so requirements are given as niacin equivalents (NE): 1 NE = 1 mg niacin = 60 mg tryptophan. Traditional Mesoamerican nixtamalisation, cooking maize with lime (calcium hydroxide), releases the bound niacin, which is why pellagra was rare where it was practised. Vitamin B6 (pyridoxine, pyridoxal, pyridoxamine), as pyridoxal phosphate, is the coenzyme of transamination and decarboxylation of amino acids. Deficiency causes dermatitis, glossitis, convulsions in infants and a microcytic anaemia; the drug isoniazid increases need.
Folate (as tetrahydrofolate) carries one-carbon units for DNA synthesis and methylation. Deficiency causes megaloblastic anaemia, and low folate around conception raises the risk of neural tube defects such as spina bifida and anencephaly. Women who may become pregnant are advised to take 400 µg of folic acid daily, and mandatory fortification of wheat flour or maize flour with folic acid, in place in many countries across the Americas, Africa, the Middle East and Oceania, has cut neural tube defects. Because synthetic folic acid is better absorbed than food folate, intakes are given as dietary folate equivalents (DFE): 1 µg DFE = 1 µg food folate = 0.6 µg folic acid taken with food = 0.5 µg folic acid on an empty stomach; so 1 µg of folic acid with food counts as 1.7 µg DFE. Folate is lost by leaching and by oxidation during cooking. Vitamin B12 (cobalamin) is made only by microorganisms and is found in animal foods; plant foods contain it only through bacterial contamination or fortification, so vegans need fortified foods or supplements. Absorption needs intrinsic factor from the stomach; lack of intrinsic factor causes pernicious anaemia. Deficiency causes megaloblastic anaemia and a neuropathy (subacute combined degeneration of the cord); high folate intake can correct the anaemia but not the nerve damage, a reason for care in folate fortification. Older people with atrophic gastritis absorb food-bound B12 poorly. Biotin is the coenzyme of carboxylases; deficiency is rare but follows a diet heavy in raw egg white, whose avidin binds biotin; cooking denatures avidin. Pantothenic acid forms coenzyme A; deficiency is almost unknown in ordinary diets. Vitamin C (ascorbic acid) is a reducing agent needed for hydroxylation of proline and lysine in collagen, for iron absorption and as an antioxidant. Deficiency causes scurvy: bleeding gums, perifollicular haemorrhages, poor wound healing and joint pain. Humans, other primates and guinea pigs cannot make it. It is the most labile vitamin in processing, destroyed by heat, oxygen, alkali, copper and iron ions and ascorbate oxidase released when plant tissue is cut, and is lost by leaching. Because it is the most sensitive, its retention is often used as an index of how gentle a process has been.
Minerals needed at more than about 100 mg a day are called major or macrominerals: calcium, phosphorus, magnesium, sodium, potassium, chloride and sulphur. Calcium makes up most of the mineral of bone and teeth, as hydroxyapatite, and in small amounts controls muscle contraction, nerve transmission and clotting. Absorption is helped by 1,25-dihydroxyvitamin D and lactose and reduced by oxalate (spinach, amaranth leaves) and phytate. Milk and dairy foods, small fish eaten with bones, calcium-set tofu, some leafy greens and fortified foods are sources. Low calcium and vitamin D over life contribute to osteoporosis. Phosphorus is in bone, nucleic acids, ATP and phospholipids, and deficiency is rare because it is in nearly all foods. Magnesium is a cofactor for hundreds of enzymes, especially those using ATP. Sodium, potassium and chloride control fluid balance and membrane potentials. Most people eat far more sodium than they need, much of it from processed foods, bread and sauces, and high intake raises blood pressure. WHO recommends adults eat less than 2 g sodium a day, equal to less than 5 g of salt (salt = sodium × 2.5), and more potassium, at least 3.5 g a day, from fruit, vegetables and pulses. Salt reduction in bread, processed meat and snacks, done gradually so consumers do not notice, is one of the most cost-effective public-health measures, and food technologists do it with salt replacers, flavour enhancement and changed crystal size.
Iron carries oxygen in haemoglobin and myoglobin and is part of cytochromes. Iron deficiency is the most common nutritional deficiency in the world and the main cause of anaemia in young children and women of reproductive age; it impairs work capacity and child development. Haem iron from meat, fish and poultry is absorbed far better than non-haem iron from plants, eggs and fortificants, and its absorption is little affected by other foods. Non-haem iron absorption is raised by ascorbic acid and by meat, fish and poultry tissue, and lowered by phytate, polyphenols such as tannins in tea and coffee, and calcium. The body controls iron by absorption (through hepcidin), not excretion, so absorption rises when stores are low. Iodine is part of the thyroid hormones. Deficiency causes goitre, hypothyroidism and, during pregnancy, cretinism and lower intelligence in the child; it is most common where soils are leached of iodine, as in mountain regions and flood plains. Universal salt iodisation, endorsed by WHO and UNICEF, is the main control measure. Zinc is a cofactor for many enzymes and for immunity and growth; deficiency causes growth failure, delayed sexual maturation, poor immunity and dermatitis, and is common where diets are high in phytate and low in animal foods. A phytate-to-zinc molar ratio above about 15 indicates poor zinc bioavailability. Selenium is part of glutathione peroxidases and deiodinases; deficiency is linked to Keshan disease, a cardiomyopathy in selenium-poor regions of China, and excess causes selenosis. Copper is in cytochrome oxidase and ceruloplasmin, and copper deficiency causes anaemia. Fluoride at suitable levels protects against dental caries, while excess from naturally high-fluoride groundwater causes dental and skeletal fluorosis in parts of East Africa, South Asia and China.
Dietary reference values are estimates of nutrient needs for groups of healthy people, set by national or regional expert bodies and by FAO/WHO. The names differ but the concepts are the same. The average requirement (EAR in North America, AR in the European Union) is the intake that meets the need of half the healthy people in an age and sex group. The recommended intake (RDA in North America, PRI in the European Union, RNI in the United Kingdom and in FAO/WHO reports) is set at the average requirement plus two standard deviations, so it covers about 97.5 per cent of the group; if the coefficient of variation of requirement is 10 per cent, the RDA is 1.2 × EAR. The UK also sets a lower reference nutrient intake (LRNI), two standard deviations below the average, which only a few people's needs fall under. When there are too few data for an average requirement, an adequate intake (AI) is set from observed intakes of healthy people. The tolerable upper intake level (UL) is the highest daily intake unlikely to cause harm to almost anyone in the group. These values are used differently for groups and individuals. For assessing a group's intake, the proportion below the EAR estimates the proportion with inadequate intake; the RDA is a target for an individual. For labels, a single nutrient reference value (NRV) per nutrient is used to express a serving as a percentage; Codex has adopted NRVs for labelling, and countries also set their own. Acceptable macronutrient distribution ranges (AMDR) in North America are 45 to 65 per cent of energy from carbohydrate, 20 to 35 per cent from fat and 10 to 35 per cent from protein for adults.
A balanced diet supplies energy and every nutrient in adequate amounts, without excess, from foods that are available, affordable and culturally acceptable. Food-based dietary guidelines translate nutrient targets into food groups and are drawn as plates, pyramids, pagodas or circles: the plate in North America and the UK, the pagoda in China, the spinning top in Japan, a "food circle" in several countries of Latin America and Africa. Most share the same core: plenty of vegetables, fruits and whole grains, pulses and nuts, moderate dairy and animal foods, and limited salt, free sugars, saturated and trans fats and highly processed foods. Guidelines also give practical portion advice, such as filling half the plate with vegetables and fruit, and they are revised as evidence on sugar, fats, processing and sustainability changes, so the version in force should always be checked. A diet chart for a group, such as a hostel or a school meal, is planned by setting energy and protein targets, choosing amounts of each food group, and checking micronutrients against reference values.
Needs change with age and physiological state. In pregnancy the extra energy need is small in the first trimester and larger later; protein, iron, folate, iodine and calcium needs rise. Folic acid before conception and in early pregnancy prevents neural tube defects, iron and folic acid supplements are widely given, and iodine deficiency in pregnancy harms the brain of the foetus. In lactation energy and protein needs are higher than in pregnancy. WHO recommends exclusive breastfeeding for the first six months, then nutritionally adequate and safe complementary foods while breastfeeding continues to two years or beyond. Breast milk changes from colostrum, rich in immunoglobulins, to mature milk. Infant formula is regulated to a Codex standard so that its composition approaches that of breast milk. Complementary foods must be energy- and nutrient-dense; thin cereal gruels are bulky and low in energy, which is why germinated (malted) flour, whose amylase thins the gruel, and fortified blended foods are used. School-age children and adolescents have high needs for energy, protein, calcium and iron, the last especially in girls after menarche. Adults need to keep a healthy weight and limit salt, sugar and saturated fat to lower the risk of non-communicable disease. Older people need less energy but the same or more protein, vitamin D, calcium and vitamin B12; they are at risk of sarcopenia (loss of muscle), poor appetite, dental problems and reduced B12 absorption from atrophic gastritis. Foods designed for them are energy- and protein-dense, soft and easy to swallow.
Malnutrition includes undernutrition, micronutrient deficiencies, and overweight and obesity with their diet-related diseases. Many countries now carry all of them at once, a "double burden" that can exist within one household: a stunted child and an overweight mother. In children, anthropometry against the WHO Child Growth Standards (2006) is the main tool. Stunting is height- or length-for-age more than two standard deviations (z-score below −2) below the median and reflects chronic undernutrition, repeated infection and poor diet from conception to two years. Wasting is weight-for-height below −2 z and reflects acute weight loss. Underweight is weight-for-age below −2 z and combines both. Severe acute malnutrition (SAM) in children aged 6 to 59 months is diagnosed by weight-for-height below −3 z, a mid-upper arm circumference below 115 mm, or bilateral pitting oedema. Marasmus is severe wasting with loss of fat and muscle; kwashiorkor is oedematous malnutrition with skin and hair changes, a fatty liver and apathy; marasmic kwashiorkor combines them. Uncomplicated SAM is now mostly treated at home with ready-to-use therapeutic food (RUTF), an energy-dense, low-moisture paste of peanut, milk powder, oil, sugar and a vitamin–mineral premix that needs no cooking or water, an example of food technology in public health. Complicated cases are stabilised in hospital with therapeutic milks. In adults, body mass index (BMI = weight in kg ÷ height in m²) classifies underweight (below 18.5), normal (18.5 to 24.9), overweight (25 to 29.9) and obesity (30 or more); some Asian populations have higher disease risk at a given BMI, and lower cut-offs are used in several countries.
Deficiencies of iron, iodine, vitamin A, zinc and folate are called "hidden hunger" because they can exist without a shortage of energy. Their burden is greatest in low- and middle-income countries of sub-Saharan Africa and South Asia, but iron and iodine deficiency also occur in high-income countries, and vitamin D deficiency is common at high latitudes. Their consequences are anaemia, impaired cognitive development, blindness, higher child mortality and birth defects. Public-health nutrition uses four broad approaches. Dietary diversification changes what people eat, through home gardens, nutrition education and better access to animal foods, fruits and vegetables. Supplementation gives nutrients as capsules or tablets to groups at risk, such as vitamin A capsules for young children and iron–folic acid for pregnant women. Fortification adds nutrients to commonly eaten foods. Biofortification breeds staple crops with more micronutrients. These are supported by measures against infection, such as clean water, sanitation, deworming and vaccination, because infection both raises needs and lowers absorption. Surveys, national nutrition monitoring, and global targets such as the World Health Assembly targets for stunting, wasting, anaemia and low birth weight measure progress. For non-communicable diseases the main tools are taxes on sugar-sweetened beverages, front-of-pack labels, limits on trans fat, reformulation of salt and sugar in processed foods, and restrictions on marketing to children.
Anti-nutritional factors are natural compounds in foods that reduce nutrient use or, at higher doses, are toxic. Protease inhibitors, such as the Kunitz and Bowman–Birk trypsin inhibitors of soybean, inhibit pancreatic trypsin and chymotrypsin, reduce protein digestibility and cause pancreatic enlargement in animals fed raw soy. They are proteins and are largely destroyed by moist heat, which is why soy meal is toasted and soy milk is heated. Lectins (haemagglutinins) bind to the gut wall; raw or undercooked red kidney beans contain phytohaemagglutinin that causes vomiting and diarrhoea within hours, prevented by soaking and boiling vigorously for at least ten minutes; slow cookers at low temperature have caused outbreaks. Phytic acid (myo-inositol hexakisphosphate) is the storage form of phosphorus in cereal bran and legume seeds. It chelates iron, zinc and calcium and is the most important single inhibitor of mineral absorption in plant-based diets. Tannins and other polyphenols in sorghum, millet, tea, coffee and some beans bind iron and proteins. Oxalates in spinach, amaranth, rhubarb and taro bind calcium and contribute to kidney stones. Some are frankly toxic. Cyanogenic glycosides, such as linamarin in cassava and amygdalin in bitter almonds and apricot kernels, release hydrogen cyanide when the tissue is crushed and the plant's own β-glucosidase acts; poorly processed bitter cassava is linked to konzo, a paralytic disease, in parts of Africa. Glucosinolates in brassicas and their breakdown products, and thiocyanate from cassava, are goitrogens that worsen iodine deficiency. Gossypol in cottonseed is toxic to pigs and poultry and limits use of cottonseed meal. β-N-oxalyl-L-α,β-diaminopropionic acid (ODAP) in grass pea (Lathyrus sativus), eaten in droughts in parts of South Asia and the Horn of Africa, causes lathyrism, an irreversible spastic paralysis of the legs. Vicine and convicine in faba beans cause favism, haemolytic anaemia in people with glucose-6-phosphate dehydrogenase deficiency. Avidin in raw egg white binds biotin, thiaminase in raw fish destroys thiamin, saponins taste bitter, and raffinose-family oligosaccharides cause flatulence.
Traditional and industrial processes reduce anti-nutrients, often by several mechanisms at once. Soaking leaches water-soluble factors such as oligosaccharides, some tannins and cyanogens, and activates endogenous phytase; discarding the soak water removes them. Germination (sprouting) activates phytase and α-galactosidase, cutting phytate and flatulence sugars, and raises some vitamins. Fermentation by lactic acid bacteria and yeasts lowers pH, which favours cereal phytase, and microbial enzymes break down phytate, tannins and cyanogenic glycosides; this is part of why fermented foods such as injera, idli, ogi, tempeh and fermented cassava products have better mineral availability than the raw ingredients. Cooking and moist heat destroy heat-labile protein inhibitors and lectins; dry heat is less effective. Dehulling and milling remove tannins and phytate concentrated in the seed coat and bran, though at the cost of fibre and minerals. For cassava, grating, soaking, fermenting, sun-drying and roasting together bring cyanide to safe levels; Codex sets limits for hydrocyanic acid in cassava products. Plant breeding has produced low-glucosinolate, low-erucic rapeseed (canola), glandless low-gossypol cotton and low-ODAP grass pea varieties. Added enzymes, such as microbial phytase in animal feed and in some cereal processing, break down phytate directly. Not every "anti-nutrient" is only harmful. Phytate, polyphenols, saponins and some protease inhibitors have antioxidant or other effects that may be beneficial at the levels in a mixed diet, so the goal is to reduce them where they matter, as in complementary foods for infants in high-phytate diets, rather than to remove them everywhere.
Processing can lose nutrients by four routes. Physical removal happens in peeling, trimming and milling: highly milled white rice and white flour lose much of the thiamin, niacin, vitamin E, iron, zinc and fibre in the bran and germ, which is why enrichment of flour and parboiling of rice were introduced. Leaching moves water-soluble vitamins and minerals into blanching water, cooking water, brine and thaw drip; the loss rises with the cut surface area, water volume and contact time, so steaming and microwave cooking usually retain more than boiling in excess water. Chemical destruction by heat, oxygen, light, pH and metal ions is the main loss for vitamin C, thiamin, folate, vitamin A and carotenoids; riboflavin is sensitive to light, thiamin to alkali and sulphite, vitamin C to oxygen and copper. Reaction with other components includes the Maillard reaction, in which reducing sugars react with the ε-amino group of lysine during baking, roasting, drying and storage, leaving lysine present by analysis but nutritionally unavailable; this matters most in milk powders and infant foods. Lipid oxidation destroys vitamins A and E and essential fatty acids. Vitamin destruction during heating usually follows first-order kinetics: C/C0 = e^(−kt), with the rate constant rising with temperature. The z-values for vitamins and colour are much larger, typically 20 to 40 °C, than the z-value of about 10 °C for bacterial spores. So raising the temperature speeds spore death far more than vitamin loss, and a high-temperature short-time (HTST) or UHT process of equal lethality retains more vitamins than a lower-temperature longer process. This principle underlies aseptic processing, HTST pasteurisation and rotary retorts.
Blanching inactivates enzymes such as peroxidase and lipoxygenase that would destroy vitamins during frozen storage, but loses some water-soluble vitamins; steam blanching loses less than water blanching. Canning loses heat-labile and water-soluble vitamins, part of which ends in the liquid of the can; after canning, losses during storage are slow. Freezing itself causes small losses; most loss comes from blanching before and slow storage reactions after. Drying and dehydration lose vitamin C and carotenoids to oxidation, and sulphite used to protect colour destroys thiamin. Ultra-high-temperature milk keeps most vitamins, though some vitamin C, B12 and folate are lost; pasteurised milk loses little. Extrusion cooking, being high-temperature short-time, retains many vitamins, but losses of lysine and heat-sensitive vitamins rise with temperature and lower moisture. Frying loses heat-labile vitamins and adds fat; oils used repeatedly lose tocopherols. Processing also brings gains. Cooking gelatinises starch and denatures protein, making them more digestible, and destroys protease inhibitors and lectins. Heating tomato and cooking carrots in oil release lycopene and β-carotene from the cell matrix and raise their bioavailability. Parboiling rice, soaking and steaming paddy before milling, drives thiamin and other water-soluble nutrients from the bran into the endosperm, so parboiled milled rice carries more thiamin than raw milled rice; this is why beriberi was rarer in parboiled-rice regions of South Asia and West Africa. Fermentation can raise B vitamins and lower anti-nutrients; germination raises vitamin C and folate. Nixtamalisation releases niacin in maize and adds calcium. Nutrient retention is expressed in two ways. Apparent retention compares nutrient concentration per gram of cooked and raw food (often on a dry basis); true retention, which accounts for the change in weight, is: true retention (%) = (nutrient per g cooked × g cooked) ÷ (nutrient per g raw × g raw before cooking) × 100.
Bioavailability is the proportion of an ingested nutrient that is absorbed and becomes available for normal body functions or storage. It differs from bioaccessibility, the fraction released from the food matrix in the gut and so available for absorption, which is what in vitro digestion models such as the INFOGEST static protocol measure. A food can contain plenty of a nutrient and still be a poor source if the nutrient is bound, in an unabsorbable chemical form, or opposed by inhibitors in the same meal. Factors that affect bioavailability are grouped as dietary and host factors. Dietary factors include the chemical form (haem versus non-haem iron, folic acid versus food folate polyglutamates, retinol versus β-carotene), the food matrix (whole cells versus ruptured cells, fat present or absent), enhancers and inhibitors in the same meal, and processing. Host factors include nutrient status (iron absorption rises when stores are low), age, pregnancy, gut health, infection, genetic variants and medication. Because of host factors the same meal yields different absorption in different people.
The food matrix is the physical and chemical structure in which nutrients are held: cell walls, starch granules, protein networks, emulsions and crystals. It explains several observations. Carotenoids in raw carrot are trapped in chromoplasts inside intact cells; chopping, cooking and adding fat raise their absorption several-fold. Lycopene from cooked tomato paste is better absorbed than from raw tomato. The same amount of sugar in a whole apple and in apple juice gives different glucose responses because the cell walls slow its release. Almond cell walls hold part of the fat away from digestion, so the energy absorbed from whole almonds is lower than Atwater factors predict. Dairy calcium, protected from phytate and oxalate, is well absorbed, whereas spinach calcium, bound as oxalate, is poorly absorbed. For minerals, enhancers and inhibitors in the same meal dominate. Ascorbic acid reduces ferric to ferrous iron and forms a soluble chelate, counteracting phytate and polyphenols; a glass of citrus juice with a cereal meal can increase non-haem iron absorption markedly, while tea or coffee with the meal reduces it. Phytate is reduced by fermentation, germination or added phytase. Calcium inhibits both haem and non-haem iron absorption in single meals. For fat-soluble vitamins and carotenoids, a few grams of fat in the meal is needed for micelle formation. Nutrient bioavailability is measured by balance studies, by the rise in blood or tissue levels, by stable isotope methods (for example, erythrocyte incorporation of an iron isotope), and for protein by ileal digestibility in pigs or humans.
Fortification is the addition of one or more essential nutrients to a food, whether or not they are normally present, to prevent or correct a deficiency in the population or a group. Enrichment, a term common in the Americas, is restoration to roughly the level present before processing, such as adding back thiamin, riboflavin, niacin and iron to white flour; restoration is the general term for replacing nutrients lost in processing. Standardisation adds nutrients to make up natural variation, as in vitamin A and D in milk. Codex General Principles for the Addition of Essential Nutrients to Foods guide all of these. WHO and FAO guidelines distinguish mass fortification of foods eaten by most of the population (salt, wheat and maize flour, rice, edible oil, sugar, milk), targeted fortification of foods for specific groups (complementary foods for infants, foods for school feeding, fortified blended foods in emergencies) and market-driven fortification by manufacturers within regulatory limits. Examples: iodised salt worldwide; wheat flour fortified with iron and folic acid in many countries of the Americas, Africa and the Middle East; vitamin A-fortified sugar in Central America; vitamin A-fortified edible oil in parts of West Africa and South Asia; vitamin D in milk and margarine in North America and parts of Europe; double-fortified salt with iodine and iron in some South Asian programmes. A good food vehicle is eaten regularly by the target group in fairly constant amounts, is centrally processed so fortification can be controlled, and does not change in colour, taste or shelf life with the fortificant. Fortification levels are set from the gap between usual intake and requirement, the amount of vehicle eaten, the upper level and the cost.
The chemical form decides both bioavailability and sensory problems. For iron, ferrous sulphate is highly bioavailable but can oxidise fats and change colour in some foods; ferrous fumarate is also well absorbed and is used in cereal-based complementary foods; electrolytic iron is cheap and inert but less well absorbed; ferric pyrophosphate, often micronised, is used in rice and salt because it is white and inert; sodium iron EDTA (NaFeEDTA) is protected from phytate and is recommended for high-extraction flours. Iodine is added to salt as potassium iodate, more stable in hot humid climates and impure salt, or potassium iodide. Vitamin A is added as retinyl palmitate or acetate, usually in stabilised beadlets; folic acid and B vitamins as their synthetic forms; vitamin D as D3 or D2. Rice is fortified mainly by making fortified kernels, by extrusion or coating, and blending them with ordinary rice, commonly at 1:50 to 1:200, because rice is eaten as whole grains and washed before cooking. Rinsing and cooking in excess water can remove coated nutrients, so extruded kernels are preferred where rice is washed. Because nutrients degrade during processing and storage, manufacturers add an overage so the label value is still present at the end of shelf life. If a fraction L is expected to be lost, the amount to add is the label value ÷ (1 − L); adding label value × (1 + L) under-doses. Quality control includes premix certificates, dosing equipment checks, qualitative spot tests (such as the iodate test kit for salt and iron spot tests for flour) at the mill, and quantitative laboratory analysis, with monitoring of household coverage. Biofortification raises nutrient content through plant breeding, agronomy or genetic modification. Examples are orange-fleshed sweet potato and provitamin A maize and cassava in sub-Saharan Africa, iron-rich beans and pearl millet, zinc-rich wheat and rice in South Asia, and Golden Rice, genetically engineered to make β-carotene and approved in a few countries. Selenium or zinc fertilisers raise grain content agronomically, as in Finland's selenium programme. Biofortification reaches rural people who eat their own crops and buy few processed foods, which mass fortification may miss.
A student uses this subject to answer the most predictable questions in food science papers: the energy of a food from its composition with Atwater factors, the limiting amino acid of a cereal or pulse, BV, NPU, PER, PDCAAS and DIAAS from given data, the deficiency disease of each vitamin and mineral, and which anti-nutrient is in which food and how it is removed. In the laboratory the same student runs Kjeldahl nitrogen and multiplies by 6.25, measures vitamin C before and after blanching to calculate retention, and tests phytate before and after germination. Knowing which nutrients are lost in milling, blanching, canning and drying links nutrition to every processing subject that follows.
Five years into a product development, regulatory or quality role, a technologist calculates nutrition panels and per-serving values, checks that protein, fibre or vitamin claims meet the reference values of each market, and sets fortification overages from stability trials so that the declared value is present at the end of shelf life. They choose fortificants that do not discolour or oxidise the product, reformulate for lower salt, sugar and saturated fat, and remove partially hydrogenated oils. In a flour mill or salt plant they run premix dosing checks and spot tests and keep the records an inspector will ask for.
With twenty-five years of experience, a senior technologist or programme manager designs or audits national fortification of flour, rice, oil or salt: choosing vehicle, fortificant and level from intake surveys and upper limits, writing the standard, setting up monitoring and judging cost. They lead reformulation across a company's portfolio to meet salt and sugar targets, advise regulators on labelling rules and nutrient reference values, and weigh trade-offs between shelf life, cost, nutrition and taste in products sold in many countries, including ready-to-use therapeutic and supplementary foods for humanitarian use.
A researcher with a doctorate and long experience works on the questions that remain open: in vitro digestion models that predict human bioavailability, ileal digestibility data for DIAAS of new protein sources, stable isotope studies of iron and zinc absorption from fortified and biofortified foods, kinetics of vitamin loss in new processes, and the food matrix effects that make energy and nutrient content on paper differ from what the body receives. They sit on expert panels that set reference values and evaluate fortification and biofortification evidence.
This manual gives no full tables of nutrient reference values, because they differ between countries and age groups and are revised; students should use their own jurisdiction's tables. It does not cover clinical and therapeutic dietetics, nutritional biochemistry pathways in depth, nutrigenomics, or detailed methods of dietary assessment. Figures such as fever effect on BMR, z-values for vitamins and biofortification approvals are stated as textbook ranges or examples and should be checked against current literature before professional use.
Original practice questions written to the syllabus and pattern of the exams named in each question's examTags. They are not past papers and do not reproduce any board's questions.
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