BCH419:

Food and Nutritional Biochemistry

You are what you eat!

 Overview of Food & Nutritional Biochemistry

•The composition, structure & functions of nutrients & other dietary constituents;

•Food sources of nutrients & factors affecting nutrient content & bioavailability;

•Physiological & biochemical basis for nutrient requirements;

•Integration, coordination, & regulation of nutrients digestion, absorption,

metabolism & transport;

•Interaction of nutrients with the genome; nutrient control of gene expression;

•Dietary bioactive components (functional foods/nutraceuticals) – non-

traditional roles of nutrients;

•Nutritional toxicology - upper limits of intake; nutrient–nutrient & drug–nutrient

interactions;

•Nutrition & disease

 FOOD ANALYSIS
•Food analysis comprises the different chemical & physical methods used in determining
the chemical composition & physical characteristics of the food.

•The chemical composition & physical characteristics of foods are indicators of the
nutritive value, functional attributes, & acceptability of the food product.

•The choice of analytical methods depends on the nature of the sample & the specific
reason for the analysis.

Proximate Composition Analysis

•The proximate composition of foods includes moisture, ash, lipid, protein &
carbohydrate contents.

•These food components are usually of interest in the food industry for product
development, quality control or regulatory purposes.
Sample preparation for proximate composition analysis

•Sampling is a process of obtaining a representative portion (sample) of the whole

population.

•It is done randomly to avoid bias.

•If sampling is not properly done, the reliability of analytical data is compromised.

•There are different sampling techniques (Check up).

•For proximate composition analysis, a good sample preparation technique will ensure
that the sample is homogenous.

•Homogeneity can be achieved by grinding the sample (e.g., grains) into flour.
Procedures of Proximate Composition Analysis

Moisture content analysis:

i.Clean drying can/dish & dry it in a hot-air oven at 103 ± 2oC for 20 minutes.
ii.Transfer the can from the oven with tongs into a desiccator, & allow it cool to room
temperature.
iii.Weigh the empty can on a weighing balance & record the mass as W1.
iv.Tare the balance & weigh 2-3 g of the sample into the can, recording the mass as W2.
v.Place the can containing the sample in the oven maintained at 103 ± 2oC for 18-24 h.
vi.After 18-24 h, transfer the can with the sample into a desiccator to cool at room
temperature.
vii.Weigh the can with the sample, recording the mass as W3.

Calculation of moisture content:

% Moisture content = ((W1 + W2) – W3) x 100

W2
Where W1= Mass in (g) of empty can; W2 = Mass of sample; W3 = Mass of can &
sample after drying.
Ash content analysis:

i.Clean a porcelain crucible & pre-ignite it in a muffle furnace maintained at 600 °C for 20
minutes.
ii.Transfer the crucible from the furnace with tongs into a desiccator, & allow it cool to
room temperature.
iii.Weigh the empty crucible on a weighing balance & record the mass as W1.
iv.Tare the balance & weigh 2-3 g of the sample into the crucible, recording the mass as
W2.
v.Place the crucible containing the sample in the furnace maintained at 600 °C for 6 h.
vi.After 6 h, transfer the crucible with the ash into a desiccator to cool at room
temperature.
vii.Weigh the crucible with the ash, recording the mass as W3.

Calculation of ash content:

% Ash content = (W3 - W1) X 100
W2
Where: W1 = Mass of empty crucible; W2 = Mass of sample; W3 = Mass of crucible and
ash after ashing
Lipids (crude fats) analysis:

i. Clean a fat extract cup by rinsing with hexane & oven-drying at 103 oC for 20
minutes.
ii. Transfer the cup with tongs into a desiccator, & allow it cool to room temperature.
iii. Weigh the empty cup, recording the mass as W1.
iv. Weigh 3 g of the sample into a clean & dry thimble, recording the mass as W2.
v. Plug the thimble with cotton wool & insert into a Soxtec HT extraction unit.
vi. Dispense 50 mL of hexane into the dried & pre-weighed extraction cup, & load in the
extraction unit.
vii. Extract the sample for 15 minutes in boiling mode, & for 30-45 minutes in rinsing
mode; after which the hexane is evaporated.
viii.Remove the cup containing the fat & oven-dry at 100 oC for 30 minutes.
ix. Cool the cup in a desiccator to room temperature.
x. Measure the final weight, recording the mass as W3.

Calculation of % crude fat content:

% Fat = (W3 – W1) X 100
W2
Where: W3 is weight of the cup with the extracted fat; W2 is weight of the sample; W1 is
weight of empty cup.
Crude protein analysis:

i.Weigh 0.20 – 0.25 g of the sample into clean digestion tube.

ii.Add one tablet of Kjeldahl catalyst (Cu or Se salt tablet) to the sample.
iii.Add 4 mL of concentrated H2SO4 to the sample.
iv.Add 4 mL of H2O2 to the sample.
v.Digest the sample on the digestion block maintained at 420 °C for 1 hour.
vi.Allow the digestate to cool to room temperature.
vii.Dilute the digestate with 10 mL of distilled water.
viii.Add 20 mL of 40% NaOH to the digestate.
ix.Heat the digestate to distil out the NH3 in it into a boric acid receiver solution (1% boric
acid containing bromocresol green/methyl red indicator).
x.Titrate the NH3 against 0.1 M HCl.

Note that the distillation & titration stages can be done using automated Kjeldahl
analyzer.

Calculation of % nitrogen (N):

%N= (sample titre – blank titre) x N x 14.007 x100

Sample weight (mg)

Where N = Normality of the acid.

% Crude protein = % Nitrogen x Conversion factor (6.25).
Determination of total carbohydrate

•The total carbohydrate (%) of a given food sample is simply calculated by difference as
follows.

% Total carbohydrate = 100 – (% MC + % AC + % CFC + % CPC)

Where MC = moisture content; AC = ash content; CFC = crude fat content; CPC = crude
protein content
 ENERGY VALUES OF FOODS AND ENERGY EXPENDITURE BY
MAMMALS

•Energy is the capacity to do work.

•The energy needed by mammals to perform work is derived from the

carbohydrate, fat & protein in the diet.

•The body’s storage energy (potential energy) is continuously available in the

body from the glycogen in muscle & liver.
•This stored energy is transformed to other forms in which the body uses it to
do its work.
E.g.:
I. Osmotic energy: Maintains transport of nutrients.
II. Electrical energy: Transmits nerve impulse.
III. Chemical energy : Synthesizes new compounds.
IV. Thermal energy: Regulates heat.

•Hence, body energy obeys the 1st law of thermodynamics.

Unit of energy:
1Kcal = 4.184 KJ (Kilo Joules)
1 KJ = 0.239 Kcal.
Energy Value (Heat of Combustion) of Foods

•The maximum amount of energy that food sample is capable of yielding when
it is completely burnt or oxidized.

•Measured by calorimetry, which is the measurement of heat loss.

•The energy measured in nutrients using a Bomb Calorimeter is as follows:

1g of Carbohydrate yields 4.1 kcal;

1g of fat yields 9.45 kcal;

1g of protein yields 5.65 kcal.

Table 1. Physiological fuel value of Carbohydrate, Fat & Protein

Nutrient Heat of Coefficient of Digestibility Physiological fuel

Combustion digestibility percent value (Atwater
(Kcal) Bryant factors cal)

Carbohydrate 4.1 0.98 98 4.0

Fat 9.45 0.95 95 9.0

Protein 5.65 0.92 92 4.0

ENERGY EXPENDITURE BY MAMMALS

•The total energy expenditure (TEE) constitutes ~ ⅔ of the energy expended by

the body to maintain basic physiological functions plus the thermic effect of a
meal & energy expended during physical movement.

•The basic physiological functions include heart beat, muscle function, &
respiration (resting or basal metabolic rate).
Estimation of Total Energy Requirement

•The energy requirement of an individual is the level of energy intake from food
that will balance energy expenditure when the individual has a body size &
composition, & level of physical activity, consistent with long-term good health;
& that will allow for the maintenance of economically necessary & socially
desirable physical activity.

•In children & pregnant or lactating women the energy requirement includes the
energy needs associated with the deposition of tissues or the secretion of milk
at rates consistent with good health.

•Energy requirements are best determined by measurements of energy

expenditure.
Components of Energy Expenditure (EE)

•EE from a physiological point of view is made up of 3 major components:

1.Basal metabolic rate (BMR);

2.Physical activity.

3.Dietary thermogenesis (thermic effect of food)

Basal Metabolism Rate (BMR)

•Basal metabolism (BM) is the minimum amount of energy needed by the body
to maintain life when the person is at post-absorptive state, physical &
emotional rest.

•BMR is a measure of the energy required by the activities of resting tissue.

•It can be measured directly from the heat produced (using a respiration
calorimeter & metabolic chamber) or indirectly from O 2 intake & CO2

expenditure when the subject is at rest.

Table 2. Factors affecting BMR

Factor Effect on BMR

Body composition The more the lean body mass, the
higher the BMR; this is due to greater
metabolic activity in these tissues when
compared to bones & fat.

Fever Fever raises the BMR. There is a 7%

increase in BMR for each degree rise in
temperature in Fahrenheit.

Stress Stress raises BMR.

Tobacco smoking & caffeine Increases the BMR

Hyperthyroidism (over-secretion of BMR is elevated as much as 50-70%.
thyroxin)

Hypothyroidism (under-secretion of The basal metabolic rate is decreased

thyroxin) by 30%

Growth In growing children, BMR is higher.

Pregnancy During the last trimester of pregnancy,
BMR is increased by 15-25% as there
is an increase in muscle mass of
uterus, size of mammary gland, foetal
mass & placenta, cardiac work &
respiratory rate.

Fasting/starvation Lowers BMR

Age & height Lean body mass diminishes with age,
slowing the BMR.

In tall people the BMR is higher.

Under-nutrition Prolonged under-nutrition lowers the

BMR.
Energy Cost of Physical Activities

•Physical activity accounts for the largest EE of the body, next to BM.

•It varies from individual to individual .

•Type of occupation, which can be sedentary, moderate or heavy occupation,

determines the energy requirement .

•A Sedentary occupation, e.g. an executive manager, requires about 80-180

Kcal/hr;

•A moderate occupation e.g. fisherman, needs about 170-240 Kcal/hr;

•A heavy occupation, e.g. mason, requires about 250-350 Kcal/hr.

•The energy cost of rest & physical activity is expressed as multiples of BMR,
which is called the physical activity ratio (PAR).

•The PAR expresses the energy cost of an individual activity per minute as ratio
of the cost of BMR per minute.

Thermic Effect of Food (Specific Dynamic Action, SDA)

•The overall stimulating effect of food ingestion on metabolism to provide the

energy required to meet the multiple activities of digestion, absorption &
transport of nutrients.

•The increase in energy cost because of thermogenesis is 10%.

Energy Balance

•The body is said to be in a state of energy balance if the energy intake is

equivalent to energy expenditure.

•To achieve this, there will be equal periods of fed-state metabolism (during
which nutrient reserves are accumulated as liver & muscle glycogen, adipose
tissue triacylglycerols & labile protein stores) & fasting-state metabolism, during
which these reserves are utilized.

•Human physiology complies with the 1st law of thermodynamics.

•For the body energy balance, this law is usually stated as follows:

(ES = EI – EO); all of these terms are expressed as energy per unit of time.

EI, energy intake, is the chemical energy from the food & fluids ingested;

EO, energy output, includes the radiant, conductive, & convective heat lost; any
work performed; & the latent heat of evaporation.
•Any imbalance btw the intake & utilization of the macronutrients that provide
energy to the body will lead to an alteration in body composition.

•Thus, obesity represents a positive energy balance resulting from an excess of

energy intake over energy expenditure.

•On the other hand, extreme weight loss is a state of negative energy balance,
resulting from a deficit energy intake over energy expenditure.
 ASSESSMENT OF NUTRITIONAL STATUS

•Nutritional status is the condition of health of the individual as influenced by

the utilization of the nutrients.

•Nutritional health is maintained by a state of equilibrium in which nutrient

intake is balanced by nutritional requirements.

•Malnutrition occurs when the net nutrient intake is less than the requirements
(under-nutrition) or exceeds the requirements (over-nutrition).

•Nutritional status can be determined by correlation of information obtained

through medical & dietary history, thorough physical examination & lab
investigation.
Significance of Nutritional Status Assessment

It helps in identifying the following:

•Under-nutrition;

•Over-nutrition;

•Nutritional deficiencies;

•Individuals at the risk of developing malnutrition;

•Individuals at the risk of developing nutrition-related diseases & the resources

available to assist them to overcome nutritional problems.
Methods of assessing nutritional status

•Methods could be direct or indirect.

I. Direct methods:
a) Nutritional anthropometry
b) Clinical examination
c) Biochemical & haematological tests
d) Biophysical methods.

II. Indirect methods:

a) Vital statistics of the community
b) Assessment of socio–economic status
c) Diet surveys
Nutritional Anthropometry

•Is concerned with the measurements of the variations of physical dimensions

& body composition at stages of life cycle & different plans of nutrition.

•It is a field-oriented method, which can be easily adopted & interpreted.

•The basic measurements are weight in kg, length/height & arm circumference
in cm.
Anthropometric indices

Weight:

•Weight gain is an indicator of growth in children.

Weight for age:

Nutritional status can be interpreted using Gomez classification as follows:

• Weight > 90% weight for age = Normal;

•Weight 76 - 90% weight for age = Grade I malnutrition;

•Weight 61 - 75% weight for age = Grade II malnutrition;

•Weight < 60% weight for age = Grade III malnutrition.

Linear Measurements

2 types of linear measurements are commonly used:

•Height or length of the whole body; &

•Circumference of the head & the chest.

Height:

•The height of the individual is the sum of 4 components: leg, pelvis, spine &
skull.

•It is measured using a stadiometer.

Head & chest circumference:

•The measurement of head circumference is a standard procedure to detect

pathological condition in children.

•The chest/head circumference ratio is of value in detecting under-nutrition in

early childhood.
Mid Upper Arm Circumference (MUAC)

•The WHO has recommended 14 cm as a desirable value for MUAC for pre-
school children.

•MUAC < 12 cm among 1–5 year old children = malnourished.

Body mass index (BMI)

•BMI for age is used to classify the nutritional status of a child.

•BMI = weight (kg) / height (m²), per age.

Clinical Examination

•Is based on examination for changes, believed to be related to inadequate

nutrition that can be seen or felt in the superficial epithelial tissues especially
the skin, eyes, hair & buccal mucosa or in organs near the surface of the body
e.g. the parotid & thyroid glands.
 Guide for interpretation of deficiencies & identifying the clinical signs.
Condition
Protein-Energy Malnutrition (PEM)
Vitamin A deficiency
Riboflavin deficiency
Thiamine deficiency
Niacin deficiency
Clinical signs
Odema; depigmentation; sparseness &
easy pluckability of hair; moon face;
enlarged liver; muscle wasting.
Night blindness; Bitot’s spots in the
eye; Xerosis of skin.
Angular stomatitis; cheilosis
Oedema; sensory loss; calf muscle
tenderness.
Rough tongue; pigmentation of the
skin.
Condition Clinical signs
Vitamin C deficiency Spongy & bleeding gum
Vitamin D deficiency Rickets; beading of ribs; Knock –
knees; bowed legs
Iron deficiency Pale conjunctiva; spoon-shaped nails
Iodine deficiency Enlargement of thyroid gland
Biochemical & haematological tests

•Used to detect deficiencies by analyzing blood, urine, stools & phlem.

•E.g. estimation of haemoglobin in blood can be used to detect iron deficiency.

Biophysical methods

•Used to assess the alterations in functions associated with inadequate

nutrition.

•E.g. dark adaptation test is used to evaluate the ability to see in the dim light.
Indirect methods

Vital Statistics
•Infant mortality rate, maternal mortality rate & morbidity rate are the vital
statistics that can be used to assess the nutritional status of the community.

Assessment of socio-economic status

•Low food availability, increased family size, unsanitary living conditions,
inadequate knowledge of nutritional needs, inappropriate weaning practices

Diet surveys
•Diet surveys are helpful in studying the quality & quantity of food consumed by
the family & the community.
Techniques of collecting information on family food consumption:

Food inventory method:

•Applicable where homogenous group of people take their meals in a common

kitchen e.g. hostels, orphanages.

•The amount of food stuff issued to the kitchen as per the issue register is
taken into consideration.

Food expenditure pattern method:

•The amount spent on food & non-food items during the previous month or
week is collected using a questionnaire.

24-hour recall:

•Standard cups help the respondent to recall the quantities of the food prepared
& fed to individual members on the previous day. This is usually done for 3
consecutive days.
Diet History:

•The procedure includes assessment of the frequency of consumption, different

foods, daily or number of times in a week or fortnight (2 wks) or occasionally.

Weight method:

•The food either raw or cooked is actually weighed using an accurate balance.

• It is ideal to conduct the survey for 7 consecutive days.

•Nutrient intake is then calculated using the food composition tables.

 NUTRITIONAL REQUIREMENTS

Carbohydrate (CHO) Requirement & Glycaemic Index

•CHOs are the main source of energy in most human diets.

•The absolute dietary requirement of carbohydrates is not precisely known, but

will depend on the amount of fat & protein ingested.

•Intake of 50 to100 g per day will prevent ketosis.

•Intake of 130 g per day for both children (>1 year) & adults is sufficient to
cover the needs of glucose for the brain.
•Glycaemic CHOs (also called digestible or available CHOs): glucose &
fructose (monosaccharides); sucrose & lactose (disaccharides); malto-
oligosaccharides; & starch (polysaccharide).

•Non-digestible (“unavailable”) CHOs = dietary fibre

Glycaemic Index (GI)

•Defined as the incremental area under the blood glucose response curve
during 1.5 – 3 hours after intake of a 50 g CHO portion of a test food, &
expressed as a percentage of the response to the same amount of CHO from a
standard food taken by the same subject.

•Glucose or white bread is used as standard.

•Foods with a lower glycaemic index (~ < 60) cause a slower release of
glucose into the bloodstream & thus a decreased insulin response.

•They also help to achieve & maintain satiety & have been shown to be helpful
as a treatment for obesity & useful for blood glucose control for people with
diabetes.

•E.g.: legumes, vegetables, & whole grains like whole wheat, & barley.
•Most foods with low GI are high in fiber; so fiber content can be used as a
marker of general GI effect of foods.

•Factors such as sugar level, starch composition (amylose/amylopectin ratio),

physical/chemical state (gelatinization) & presence of organic acids (acetic,
propionic & lactic acid), can affect the GI of food.

Glycaemic Load

•GL is defined as the amount of glycaemic CHO in a food multiplied by the GI of

the food divided by 100.

•In practice, the blood glucose response after a meal is influenced by both the
GI & the amount of CHO in a portion of a food.

•The sum of individual GL values for foods & meals can be used to estimate the
glycaemic load of the whole diet.
•The glycaemic response can be influenced by:

•the protein & fat content of the food; &

•the type & amount of beverage taken with the food.

Regulation of blood glucose concentration

•In healthy people, blood glucose conc. (glycaemia) is homeostatically

controlled within a fairly narrow range (~ 5 mM);

•As the glucose conc. in blood rises above 5 mM after a meal, the β-cells of the
endocrine pancreas respond by secreting insulin.

•Insulin has several effects on metabolism, including facilitating the transport of

glucose into adipocytes & myocytes (muscle cells) by GLUT4.

•In the post-absorptive state, ~ 8 g glucose/hr is provided for those tissues with
an obligatory demand for glucose – the brain, red blood cells, mammary gland,
& testis – by breakdown of stores of glycogen in the liver & muscle via
glycogenolysis.
•During long periods of fasting & starvation, glucose is formed from non-CHO
sources (pyruvate, lactate, glycerol, & amino acids) by gluconeogenesis which
occurs in the liver & kidney.

•Glucogenic amino acids (all amino acids, except lysine & leucine) are derived
by catabolism of the body’s proteins; triacylglycerols (from adipose tissue) are
catabolized to release glycerol.

•Gluconeogenesis is triggered by a fall in blood glucose conc. below ~ 5 mM, &

is signaled to the tissues by the secretion of glucagon & the glucocorticoid
hormones.
Protein Requirement & Protein Nutritional Quality

•Dietary protein requirement is described as the minimum level of protein

necessary to maintain short-term nitrogen balance under conditions of
controlled energy intake & is quantified as the Recommended Daily Allowance
(RDA).

•Not all proteins have the same capacity to meet the physiological requirements
for total nitrogen & the essential amino acids.

•The conc. & availability of the individual essential amino acids are major
factors responsible for the differences in the nutritive values of food proteins.
•A complete protein contains all essential amino acids in relatively the same
amounts as human beings require to promote & maintain normal growth; an
e.g. of complete protein is egg albumin.

•A partially complete protein contains sufficient amounts of amino acids to

maintain life but fail to promote growth; an e.g. is gliadin in wheat.

•Incomplete proteins are incapable of replacing or building new tissue & cannot
support life or growth; an e.g. is wheat germ protein, being deficient in
tryptophan.
Nitrogen Balance

•The technique most generally accepted for the evaluation of human amino
acid & nitrogen requirement.

NB = I – (U + F +S)

•Where NB is nitrogen balance; I is nitrogen intake; U is urinary nitrogen; F is

fecal nitrogen; S is loss of nitrogen through the skin.

•The body is in a state of nitrogen (or protein) equilibrium when the intake &
usage of protein are equal.

•Positive nitrogen balance exists when the intake of protein is greater than that
expended by the body.

•Negative nitrogen balance exists when the intake of protein is less than that
expended by the body.
•A negative nitrogen balance represents a state of protein deficiency, in which
the body is breaking down tissues faster than they are being replaced.

Factors that affect nitrogen balance of the body:

•physiological state of the body;

•body protein reserves;

•essential amino acid intake; &

•total nitrogen intake.

Methods of Assessing Protein Quality:

1. Biological assays
2. Chemical assays
3. Mixed assays (chemical + biological)

Biological assays

The biological assays include Biological Value (BV), Protein Efficiency ratio
(PER), & Net Protein Utilisation (NPU).

Biological Value (BV) of Protein

•The percentage of a protein nitrogen that is absorbed & is available for use by
the body for growth & maintenance.

BV = Nitrogen retained = (I – (FN – EFN) – (UN – EUN))

Nitrogen absorbed (I – (FN – EFN))

Where: I is nitrogen intake; FN is faecal nitrogen; EFN is endogenous faecal

nitrogen; UN is urinary nitrogen; EUN is endogenous urinary nitrogen.
•Complete proteins, i.e., proteins that contain all essential amino acids in
proportions capable of promoting growth are described as good quality protein,
or proteins of high BV.

•Egg protein is a complete protein & is considered as a reference protein with

the highest BV.

•The amino acid, which is not present in sufficient amount in food protein, is
called the limiting amino acid of that food. E.g. lysine in cereal protein, &
tryptophan in wheat germ.

Protein Efficiency Ratio (PER)

•Compares the amount of weight (in grams) gained by a growing rat after 10
days or more of eating a standard amount of protein (9.09% of its energy
intake) from a single protein source to the grams of protein consumed.

PER = Weight gain of the test animal

Protein consumed by test animal
Net Protein Utilization (NPU)

•NPU is the proportion of protein nitrogen intake retained by the body.

•It is similar to NPR, except that body nitrogen rather than body weight is used.

NPU = Retained Nitrogen = I – (FN – EFN) – (UN – EUN)

Nitrogen intake I
Chemical assays:

Chemical score (CS);

Amino Acid Score (AAS).

Amino Acid Score (AAS):

•The amount of each essential amino acid provided by a gram of the food’s
protein is divided by an “ideal” amount for that amino acid per gram of food
protein.

•The lowest amino acid ratio calculated for any essential amino acid is the
chemical score.

•Scores vary from 0 to 1.0.

Mixed assays:

Protein Digestibility Corrected Amino Acid Score ((PDCAAS);

Digestible indispensible amino acid score (DIAAS)

PDCAAS:

•The most widely used measure of protein.

•To calculate the PDCAAS of a protein, its chemical score is multiplied by the
digestibility of the protein (generally, 0.9 to 1.0).

•The maximum PDCAAS value is 1.0, which is the value of milk, eggs, & soy
protein.

•A protein totally lacking any of the 9 essential amino acids has a PDCAAS of
0, since its chemical score is 0.
 NUTRITION & DISEASE
•Nutritional quality & quantity of foods eaten, & nutritional status are major
modifiable factors in promoting health & well-being, in preventing disease, & in
treating some diseases.

•Nutritional status influences health & risk of both infectious & NCDs.

•Based on nutritional status, individuals can be broadly categorized as:

•having optimum nutrition (well-nourished);

or

•malnourished.

•Optimum nutrition ensures health, well-being, normal development & high

quality of life.

•Malnutrition is a gateway to under-development, compromised health (higher

incidence of infections & diseases) & low quality of life.
 MALNUTRITION
•A pathological state resulting from a relative or absolute deficiency or excess
of one or more essential nutrients; this state being clinically manifested or
detected only by biochemical, anthropometric or physiological tests.

•Also defined as a state of nutrition in which a deficiency or excess (or

imbalance) of energy, protein & other nutrients causes measurable adverse
effects on tissue/body forms (body shape, size & composition) & function, &
clinical outcome.

2 major forms of malnutrition:

•Under-nutrition

•Over-nutrition
Under-nutrition:

•Inadequate quantity of food over an extended period of time

•The major form of malnutrition in developing countries due to poverty

Causes:

•Poverty

•Psychological disorders e.g. anorexia nervosa;

•Severe, prolonged diarrhea, renal failure, infection, or diseases that cause

malabsorption of nutrients;

•Rapid growth & development in children;

•Addiction to alcohol or drugs ;

Categories:
•Macro-nutrient deficiency: PEM
•Micro-nutrient deficiency: IDD; IDA; VAD.
Over-nutrition

•Results when energy intake >> energy expenditure

•Leads to overweight & obesity

•More prevalent in developed countries due to the excessive intake of food

products, thereby leading to higher incidence of complications of over-nutrition
including:

•Cardiovascular disease;

•Diabetes mellitus;

•Hypertension;

•Respiratory problems;

•Gallbladder disease;

•Cancer.
PROTEIN-ENERGY MALNUTRITION (PEM)

•A spectrum of pathological conditions arising from a deficiency of protein &

energy, having marasmus at one end, & kwashiorkor at the other end, with
marasmic-kwashiorkor in between.

•Almost always accompanied by micronutrient (minerals & vitamins) deficits.

•A syndrome characterized by its progressive onset & a series of symptoms &

signs that encompass a continuum, ranging from clinically undetected
manifestations to the full-blown clinical picture of marasmus or kwashiorkor

•May be present at any time during the life cycle, but it is more common in the
extreme ages – infants & the elderly.
•Present in adolescents & adults, mostly lactating women, during periods of
famine or other emergencies

•More prevalent in the developing world

•An unintentional loss of >10% of usual body weight is often thought to be the
threshold beyond which significant declines in clinical outcome are observed.
Classification

Primary PEM

•Insufficient dietary intake leading to inability to meet the protein & energy
metabolic demands

Secondary PEM

•Illness or other factors that impair the uptake or utilization of nutrients,

increase protein or energy requirements, or increase metabolic losses beyond
nutrient availability

•Acute illness usually creates PEM through a combination of primary &

secondary mechanisms.
Etiology of PEM

Primary:

•Lack of food to meet the protein & energy need of the body

Secondary:

•Includes several conditions that impair food intake, absorption, or utilization, or

that increase energy &/or protein requirements or losses.

•Secondary causes of PEM may be biological or social conditions.

Marasmic Child Kwashiorkor Child
Clinical picture/features of Kwashiorkor

•Characterized by a limitation in protein intake, with a lesser involvement of

energy deficit, affecting slightly older children (1 to 3 yrs of age).

•Presence of edema, body weight loss & anaemia.

•Skin lesions that range from a flaky paint dermatosis with skin dryness &
depigmentation to deep ulcerations.

•Apathetic to external stimuli.

•Presence of petechiae & ecchymoses.

• Hair discoloration with bands of dark & light hair (the “flag sign”).

•An enlarged, fatty liver.

•Concurrent micronutrient deficiencies are common.

•Gives the impression of misery.

Clinical pictures/features of Marasmus

•Characterized by a chronic & severe restriction of both energy & protein to the
body.

•More frequent at a younger age than kwashiorkor, usually in children under

one year of age.

•Severe wasting, with a very low weight-for-age & reduced length-for-age, often
-3 below standard deviation of the reference population values

•Striking loss of subcutaneous fat & muscle wasting, observed as markedly thin
limbs, an evident rib cage, sunken cheeks & eyes that give the child a
“monkeylike” or gaunt appearance
Clinical pictures/features of Marasmus cont’d

•Prominent abdomen & a relatively big head, but absence of skin rashes or
dermatosis.

•Thin & dry hair that comes off easily.

•Co-occurrence of micronutrient deficiencies e.g. vitamins A & D, zinc, & iron

•Presence of anemia, but less common than in kwashiorkor.

The clinical history of a marasmic child may reveal:

•Poverty or famine affecting the family

•Inadequate childrearing practices, e.g. starvation wrongly prescribed as part of

the management of diarrhea;
Clinical pictures/features of Marasmus cont’d

•An early stopping of breast-feeding; over-dilution of formula; a history of

repeated &/or chronic infections, e.g. diarrhea or tuberculosis;

•Some physical condition that affected the child’s growth & development, e.g.
prematurity, mental defects, or a malabsorption syndrome.

•On a first appreciation, the child may be interested in the environment, with an
active cry & reaching for food if offered; else he/she may be depressed to the
point of coma.
Functional consequences of PEM:

Growth impairment;

Reduced immune response;

Disruption in cognitive ability.

Growth impairment:

•Manifests very early in life, with stunting growth starting about 3 to 4 months of
age & is complete before 18 months.
Reduced Immune response:

•PEM is the most common cause of immunodeficiency worldwide.

•Malnutrition & infection interact in a vicious cycle with the presence of one
leading more easily to the development of the other.

Mechanisms:

•Impairment of cell-mediated immunity, phagocytic function, & the complement

system.

•Diminishing of immunoglobulin (IgA, IgM, & IgG) concentrations

•Decreased cytokine production

•Conversely, infectious diseases lead to malnutrition by several mechanisms

that often interact with each other.
Disrupted cognition:

•PEM may affect brain growth & development, which will be reflected in
cognitive disabilities, motor impairment, or lower intelligent quotient (IQ).

•Infections due to PEM lead to physical damage to the brain, particularly during
sensitive periods of development (first 2 yrs of life) when about 80% of the
brain’s growth is achieved.

•This decreased intellectual performance found at early ages in children

affected by PEM carries on to later stages in life.
 OBESITY

•Defined as a condition in which excess body fat has accumulated to the extent
that it may have an adverse effect on health, leading to reduced life expectancy
&/or increased health problems.

•A disease of positive energy balance, resulting from dysregulation in the

energy balance system.

Indices of Obesity:

•The body mass index (BMI);

•Waist-to-hip ratio
The body mass index (BMI):

•The most accepted & most widely used crude index of obesity.

BMI = weight (kg) / height (m2)

•Normal adult BMI range is 18.5–24.9 kg/m2.

•Obesity in adults is defined as a BMI > 30.0 kg/m2

•BMI in the range of 25–30 kg/m2 is considered overweight.

•In children, it is more difficult to classify obesity by BMI because height varies
with age during growth; thus, age-adjusted BMI percentiles must be used.
Limitation:

•BMI does not distinguish btw excess muscle weight & excess fat weight.

•E.g. the BMI of a heavy football player or body-builder with a large muscle
mass that may have a BMI > 30 kg/m2 but is not obese; rather, this man has a
high body weight for his height resulting from increased fat-free mass (FFM).

Waist-to-hip ratio:

•A marker of upper versus lower body-fat distribution.

•Waist circumference alone provides the best index of central body-fat pattern
& increased risk of obesity-related conditions.

•The recommended location for the measurement of waist circumference is at

the midpoint btw the lowest point of the rib cage & the iliac crest.

•The risk of obesity-related diseases is increased above a waist circumference

of 94 cm in men & > 80 cm in women.
Classes/Types of Obesity:

Classified based on BMI & type of body fat distribution.

Based on BMI:

•Class I is BMI of 30.0 to 34.9 kg/m2;

•Class II is BMI of 35.0 to 39.9 kg/m2;

•Class III is BMI greater than 40 kg/m2.

•As the class increases, the likelihood of risk factors increases.

Based on body fat distribution:

1. Android obesity (apple shape):

•Central distribution of body fat in & around the abdomen;

•Associated with an increased risk for a number of co-morbidities including

diabetes, hyperlipidemia, hypertension, & cardiovascular disease.

2. Gynoid obesity (pear shape):

•Fat distribution over the hips & buttocks;

•Associated with less disease risk.

Fig. Android & Gynoid Obesity
Etiology of obesity:

•Diet;

•Lifestyle;

•Genetic
Diet & lifestyle:

•It is often stated that obesity is simply the result of over-eating or lack of
physical activity.

•An increased reliance on high-fat & energy-dense fast foods, with larger
portion sizes, coupled with an ever-increasing sedentary lifestyle could cause
obesity.

Other dietary factors:

•increased daily caloric intake;

•increased portion sizes of foods;

•a high sugar/refined carbohydrate intake;

•a low fiber intake

•sedentary lifestyle due to an increased reliance on technology & labor-saving

devices (e.g. computers & automated transport system – lift).
Genetic factors:

•Influence the various components of body-weight regulation

•Play a major role in the differing individual susceptibilities to obesity.

Factors underlying the genetic contribution obesity:

•Resting energy expenditure (REE);

•Hormonal response to overfeeding;

•DNA polymorphisms or mutations in beta-adrenergic receptors & mitochondrial

uncoupling proteins;

•Regulation of adipocyte differentiation;

•Patterns of energy expenditure, compulsive behavior, dietary intake, & taste

preference.
Health Risks associated with obesity

•Increased the risk for type 2 diabetes.

•Increased risk for elevated blood pressure (hypertension).

•Higher risk for several cardiovascular diseases including coronary heart

disease.

•Increased risk for gallstones, although the relationship has been more
consistently found in women than men.

•Increased risk of certain cancers (e.g. endometrial, breast - post-menopause,

colon & kidney cancers)

•Others include: Obstructive sleep apnea; Osteoarthritis; Obesity

hypoventilation syndrome; Immune dysfunction.
 NUTRITION & DISEASE: DIABETES MELLITUS (DM)

•DM is a metabolic disorder of multiple etiology characterized by chronic

hyperglycaemia , with disturbances of carbohydrate, fat & protein metabolism
resulting from defects in insulin secretion, insulin action, or both.

•The kidney removes the extra sugar from the blood & excretes it in the urine,
to maintain the normal level of blood glucose.

•This results in the elevated glucosuria that characterizes diabetes mellitus.

•The body is under constant impression of hunger; a reason for increased

appetite (polyphagia) in diabetics than non-diabetic individuals.
Fig 1. Regulation of glucose uptake into the myocyte by insulin
Symptoms of diabetes mellitus:

•Frequent urination;

•Excessive thirst;

•Unexplained weight loss;

•Extreme hunger;

•Sudden vision changes;

•Tingling or numbness in hands or feet;

•Feeling very tired most of the time;

•Very dry skin;

•Sores that are slow to heal;

Fig. 2. Metabolic disorders of DM
Diagnostic Criteria of DM

•Fasting plasma glucose ≥ 7.0 mmol/L (126 mg/dL);

NB: Fasting is defined as abstinence from caloric intake for at least 8 hours, & it
is usually overnight.

The normal fasting blood sugar is usually between 3.5-6.7 mmol/L.

•2-hour postprandial (after meal) plasma glucose ≥ 11.1 mmol/L (200 mg/dL);

•whole blood glucose > 6.1 mmol/L (110 mg/dL);

•Glycosylated haemoglobin (HbA1c) ≥ 6.5%.

Types of Diabetes mellitus

•2 main types of diabetes mellitus depending upon its etiology & treatment: type
1 & type 2 DM.

Type 1 Diabetes Mellitus (T1DM)

•Previously termed insulin-dependent diabetes mellitus (IDDM), or juvenile-

onset diabetes;

•Accounts for only 5–10% of the total number of those with DM;

•Results from a cellular-mediated autoimmune destruction of the beta-cells of

the pancreas, leading to absolute insulin deficiency;

•Patients absolutely depend on exogenous insulin for the regulation of their

blood glucose level;

•Risk factors are less well defined but autoimmune, genetic, & environmental
factors are involved.
Type 2 Diabetes mellitus (T2DM)

•Previously referred to as non–insulin-dependent diabetes (NIDDM), or adult-

onset diabetes;

•Accounts for about 90–95% of those with diabetes mellitus;

•Results from insulin resistance &/or relative insulin deficiency.

•Risk factors include older age, obesity, family history of diabetes, prior history
of gestational diabetes, impaired glucose tolerance & physical inactivity.

•Patients may not need exogenous insulin treatment to survive;

•Decreased stimulation of muscle glycogen synthesis;

•Defects in glucose uptake;

•Increased phosphatase activity

Figure 3. Etiology of T2DM
Gestational Diabetes Mellitus (GDM)

•Develops during pregnancy due to complex hormonal & metabolic changes

•Usually normalizes when pregnancy is over; thus, GDM is a normal

physiological state

•Obesity is risk factor

GDM increases risk for later development of T2DM

Management of DM

Management of strategy includes:

•Dietary control;

•Exercise;

•Oral medication &/or insulin

Dietary Control

•Use of low glycaemic, high fiber foods e.g. fruits & vegetables, whole grains,
pulses (cowpea);

•Use of plant foods rich in polyphenols & other antioxidant phytochemicals;

•Polyphenols are able to inhibit CHO-digesting enzymes e.g. α-amylase & α -

glucosidase, thereby lowering the amount of glucose absorbed into the blood
stream.

•Polyphenols also inhibit aldose reductase of the polyol pathway, thereby

reducing the complications of DM.

• Plant-derived inhibitors have less side effects.

Exercise:

•Increases utilization of glucose

•Increases the sensitivity of insulin

Oral medication:

•Oral antidiabetic drugs e.g. acarbose reduces hyperglycaemia through the

inhibition of α-amylase & α-glucosidase;

•Produce gastrointestinal side effects such as abdominal discomfort, flatulence

(gas), & diarrhea, due to excessive inhibition of pancreatic α-amylase.

•Insulin is administered on a regular interval for T1D.

Complications of DM:

•Acute Complications

•Chronic Complications

Acute Complications:

•Diabetic ketoacidosis;

•Diabetic hypoglycaemia.

Chronic Complications:

•Occur because of the chronic exposure of the body’s tissues to

hyperglycaemia, hypoinsulinaemia or their associated metabolic disturbances.

•Divided into microvascular & macrovascular complications.

Microvascular (microangiopathic) complications lead to damage of the
capillary wall & include:

•diabetic retinopathy;

•diabetic neuropathy;

•diabetic nephropathy;

•diabetic skin problems (the “diabetic foot”).

Macrovascular complications of DM include:

•atherosclerosis/atheroma;

•coronary heart disease;

•myocardial infarction;

•Hypertension;

•Increased susceptibility to bacterial infection, leading to

diabetic foot ulceration and amputation.
The Polyol Pathway

•Explains a possible biochemical mechanisms by which hyperglycemia could

impair the function & structure of the cells affected by diabetic complications.

The Polyol pathway

•Saturation of hexokinase of the glycolytic pathway in the presence of excess

glucose in the diabetic state favours the polyol pathway;

•In response to hyperglycemia, sorbitol accumulates in complication-prone

tissues that have a high capacity for polyol pathway enzymes e.g. the eye lens;

•Sorbitol does not easily diffuse across cell membranes;

•In the lens, the upsurge of sorbitol causes osmotic swelling due to absorption
of water into the lense fiber,

•The swelling increases the permeability to substances that are at a higher

concentration in the lens than in the surrounding intraocular fluids.

•Therefore, concentrations of potassium, amino acids, glutathione, inositol, &

ATP decrease, & Na+ & Cl- concentrations start to increase.

•This results in the lens membranes becoming permeable to all substances

except the larger proteins.

•The resulting redox imbalance & protein insolubilization leads to cataract

formation in diabetic patients.
Figure 5. The Polyol pathway hypothesis of diabetic complications
Microvascular & macrovascular complications that can lead to the following:

•visual impairment/blindness;

•kidney disease;

•nerve damage;

•amputations;

•heart disease;

•stroke.