Introduction to Nutrition

(PHS 103)
D. D. SEMELE
Office 235 Academic block
Ext. no. 5816

Introd. to Nutrition basics or

concepts

Definition of terms:

Nutrition = the science of study of processes involving food &

nutrient intakes, assimilation and use of nutrients in the body; to
maintain & repair body tissues, provide energy & protection from
diseases.

i.e. the study of nutrients and their contribution to health

Two fundamental areas in the science of Nutrition include the Physical Sciences
e.g. Bio-chemistry & Physiology.

Nutrients = substances in food or supplements that are essential

for energy-provision, growth, normal functioning of the body & for
maintenance of life.
Food =
Diet = a meal-composition; it involves the kind/type of food
consumed, quantity of portions/servings taken including the
description of how the food has been processed or cooked
i.e. a combination of foods aimed at performing a specific physiological
function in the body

Nutritional status = an indivs status with respect to nutrition.

Importance of Nutrition to
health

It is the foundation for health & life.

Eating = characteristic of living; Everybody has to eat to live.
In past few yrs around 2000s, a campaign was conducted in the UK;
emphasizing the importance of food in the human body & raising
awareness on healthy eating. Hence, the theme for the campaign
was: You are what you eat.
It provides the 1st line of defense against disease prevention (or in
protection).
Can be used to help people (gen public) or patients make nutritionally
informed decisions about their health status.
e.g. H/professionals taught Nutrition can advice patients well on matters relating to dietrelated-diseases, food/nutrient-drug-interactions, and so on, since they most likely have 1 st
hand contact with the patients (when consulting/treating them).

Nutrition knowledge can be used by people of different occupations/

professions to help them maintain or improve the working capacity or
output.
Nutrition knowledge helps to differentiate btwn the truth and myths
which could be used in promoting some nutrition-products for
commercial purposes rather than for the claimed health benefits labelled
on them.

Nutritional requirements
Are adequate amounts of nutrients
an individual or group should
consume to prevent deficiency
diseases or toxic effects
Each nutrient has its own nutritional
requirements
Types of nutritional requirements
that can be used include:
RDI, RDA, DRVs and SI levels

Nutritional requirements (cont.)

1) RDI = Recommended Daily Intakes

Previously used nutritional requirements for a particular nutrient

Too prescriptive- suggesting that amounts given referred to
what indiv.s must consume per day.

2) RDA = Rec. Daily Allowances (amounts)

intakes which fell below RDA were deemed to be deficient.
Hence;

3) DRVs = Dietary Reference Values

DRV s= were formulated, taking into account that indiv.s
differ in their requirements for each nutrient e.g. in a
community/population some people have low requirements,
some moderate/average while others have high reqnts for
the same nutrient; thus
DRVs have a range of figures (i.e. subdivided and tabulated
into 3 parts/tables) providing more flexibility in assessing
dietary adequacy.
3 distinct DRV figures for majority of nutrients are:

LRNI = Lower Reference Nutrient Intakes

EAR = Estimated Average Requirements
RNI = Reference Nutrient Intakes

Comparison of DRVs
LRNI

EAR

RNI

= a point towards
lower-end of the
distribution curve of
the nutritional reqnts
@ (Mean - 2SD)
- Meets requirements
(or is adequate only)
for ~2.5% of the
population

= mean intakes for

the reference group
thus, meets reqnts for
~50% of the
population

= a point towards
upper-end of the
distribution curve of
the nutritional reqnts
@ (Mean + 2SD) and
- Meets reqnts for
~97.5% of the
population

=used as reference
In practice, RNI is used
value for Energy
for majority of nutrients
intake; because it is not (EXCEPT Energy)
advisable to encourage
people to consume
level of Energy > their
needs.
LRNI = Mean 2SD

Reference values are

actually used for
GROUPS (not indiv.s)

RNI = Mean + 2SD

Distribution curve showing

DRVs
50
EAR
%

= average requirement

%
o
f
i
n
d
i
v
.
s

2.5%

97.5%

of

popn

popn

LRN
I

(low)

of

RN
I 2.5%

Level of requirement for a

nutrient

(high
)
NB: As intakes drifts far to the left of RNI (i.e. below RNI), the RISK OF

Importance of DRVs
DRVs are used for:
planning diets for groups of indiv.s
o e.g. in institutions to avoid preparing diets that are deficient or in
excess of the reqd amounts of nutrients for a group of people.

planning amounts of nutrients to be added in new food

products
o In such cases, the RNI should be taken as target (but for Energy,
EAR = target)

planning a dietary prescription for an indiv./patient whose

actual nutritional needs are not known
still RNI = target

verifying or cross-checking food label claims on food packs

o

e.g. if food label claims that a food product (in a typical serving) provides
100% RNI (or RDA) for a certain nutrient e.g. Vit C, then the actual amount per
its serving can be calculated using DRV figure. In this case; for Vit C, the food
product should have 40mg since RNI for Vit C = 40mg (while LRNI = 10 & EAR
= 25mg); otherwise, that claim will be misleading to consumers, and
therefore, illegal.

 determining if the population/nation is at risk of

some nutritional deficiencies or not
by analysing the results from
population/national food consumption surveys
(see the following slides)

For example;
As intake approaches RNI for a nutrient, the
RISK OF DEFICIENCY of that nutrient
decreases,
BUT
As intakes drifts far to the left of RNI (i.e.
below RNI), the RISK OF DEFICIENCY
increases.
AND
As the intake approaches LRNI, the risk of
defcy increases sharply!
The risk = 100% at LRNI (thus, such population/nation is
suffering from the concerned nutrient deficiency disease)

Sample cont. (explanation)

A

Position of indiv.s
intake wrt DRVs

Intakes <LRNI for

the reference
group

Intakes below EAR Intakes above

for the nutrient ,
EAR, but lower
but btwn LRNI &
than RNI
EAR

Interpretation

Indiv. not meeting

own nutritional
reqnts for the
nutrient

This does not

necessarily mean
indiv. has inadeq
intake
.eg. may be B=
child, hence has
low reqnt for that
nutrient

Indiv. meets the

mean intakes for
the reference
group

Hwever, if the
child- not growing
normally or is
showing signs of

But the indiv.

may not be
meeting his/her
reqnts (which

Caution:

Indiv. may show

signs of clinical
deficiency

At a glance,
intake seems
quite adeq.
(since it is close
to RNI for the
group)

Sample (for individuals)

A

50
%
C
EAR
= average requirement

o
f
i
n
d
i
v
.
s

2.5%

97.5%

of

popn

popn

LR
NI

(low)

of

RNI
2.5%

Level of requirement for a

nutrient

(high
)
NB: As intakes drifts far to the left of RNI (i.e. below RNI), the RISK OF

DRV Interpretation For

Groups
Group-mean-intakes eliminate intra-indiv.variability/difference
Hence allow more confident (or solid)
interpretation of the results;
e.g. The lower the group mean intake wrt
RNI, the GREATER the chance that some of
the group members have in-adeq intakes.
If group mean intake > RNI; there is a little likelihood
that most of the group members have intakes
substantially lower than RNI, i.e. intakes for v. few
members <RNI and most of the group members are
likely to have intakes around or >RNI
If group mean intake = < RNI; then intakes of most of
the group members may be in-adeq.

4) Safe Intakes /Safe levels of

Intake (SI)
Safe intake = a level or range of intake at which
there is no risk of deficiency, and below
which undesirable effects may occur

These are nutrient levels considered safe for some

nutrients whose DRVs could not be set, due to insufficient reliable data about their reqnts (amounts
required) for human consumption.
SI should not be taken as toxic levels, although
intakes need not exceed them. NB: There is no
evidence that exceeding SI would result in undesirable
effects and equally the same that exceeding them would
bring any benefits.

particularly set for infants & children

Factors influencing/affecting
Food Intake
SOCIAL
INFLUENCE
CULTURAL
FACTORS

PHYSIOLOGIC
AL FACTORS

DEMOGRAPHIC
/ENV. FACTORS

ECONOMIC
FACTORS

Food
intake

PSYCHOLOGICA
L FACTORS

SENSORY APPEAL
POLITICAL
INFLUENCE

Factors influencing Food Intake = DETERMINANTS OF what, when & how much people eat.

Ex.s of factors
influencing/affe
cting Food
Intake:

ECONOMIC FACTORS
household income
budget priorities
cost of foods
transport
SOCIAL INFLUENCE
distance from
Habits ; traditional
shops/market to home
practices e.g. social norms,
storage resources
timing, availability, peer
human resources
pressure/influence
people to buy, prepare &
Hospitality & eating for
social reasons
cook foods
Resources
Obligation
CULTURAL FACTORS
cultural practices affecting
food processing,
preservation and
preparation
taboos certain foods
forbidden (e.g. Totem,
during certain periods of the
year, during certain time in
life-cycle of humanity)
culturally-esteemed foods
which may not necessarily
be healthily-prepared

PHYSIOLOGICAL
FACTORS /NEEDS

hunger
satiety
metabolism hence
people on Special-diet or
Diet-Mgnt.
PSYCHOLOGICAL
INFLUENCE
e.g. positive influenceeating should be
pleasurable (pleasurable
activity)

SENSORY APPEAL
appearance
taste
texture
smell
pleasure
DEMOGRAPHIC/ENV.
FACTORS
soil quality
weather/climate
land availability
shops/market where
to buy foods
POLITICAL
INFLUENCE (on:)
Food policies &
regulations, food
availability, etc.

COMPONENTS OF AN
INDIV.S FOOD HABITS
No. of meals per day
People with whom the
food is eaten

How the food is

eaten

Timing of meals

Food
Habits

Food choices
Method of food
preparation

Size of meals

Duration of food
preparation

Factors influencing Food

choices (from nutritional
perspective)
Food availability

Food
acceptability

Physical/env.
factors
Psycho-social factors

Food handling
Food Legislatives

Economic factors

Physiological factors

Cultural
& religious
factors

Ex.s of factors influencing Food Choices

Food availability
Physical/environmental Factors
e.g. locality (soil/climate,
seasonality of foods),
transport/marketing of food,
distribution costs, perishability of
the foods, etc

Food handling
e.g. access to shops, cooking
skills, knowledge on nutrition (e.g.
meal planning & healthy-eating),
cooking facilities, time available, etc
Food Legislatives
e.g. national or international foodlaws, health or nutritional
guidelines or recommendations, tax
on foods, etc
Economic factors
e.g. HH finances, cost of foods,
budget priorities, significance of
foods, etc

Food acceptability
Psycho-socio-cultural
factors
e.g. status (of self/ the
food), emotional support,
means of communication,
form of reward or
punishment, group identity
(e.g. staple food for national
identity or any food for
cultural identity), ritual or
religious reasons,
taboos/food-prohibitions, etc
Physiological factors
e.g. physio-needs,
hunger/satiety,
appetite/food-aversion,
sensory appeal, personal
food-preference, therapetic
diet, etc

ENERGY
is the ability to do work;

E is reqd to maintain internal env. (at metabolic and cellular levels) of

the body & to fuel activities of organism (to do work on external env. e.g.
walk, talk, eat, sit-up, write, HH-chores, etc)
Thus, Energy (E) needed for all basic physiological functions of body
esp.
@ cellular-level e.g. in active transport pumps, cell-differentiation, etc
& also
@ metabolic level e.g. breathing, heart beat, digestion, excretion, etc
FACTORS INCREASING E-REQUIREMENT include; growth during early years of
life (infancy, childhood & adolescence), pregnancy & lactation, increased
physical activity, etc.
Energy can be measured in calories or joules, whereby; 1 calorie = 4.18
joules
Energy is produced from the macro-nutrients (CHOs, Fats and Proteins) found in
foods; Hence these are called ENERGY YIELDING NUTRIENTS. These
macronutrients are broken down (in digestion process) to their constituent parts
(glucose, fatty acids and amino acids, resp.) that are then metabolised in
tissues.
Some E is used immediately in the form of glucose, while some is stored in the
form of glycogen or fat.

ENERGY BALANCE
If E is consumed > than needed,
Net increase in
bodys content & size of the stores (esp. fat) often
leading to wt-gain i.e. POSITIVE ENERGY BALANCE
Conversely,
If E-intakes < than needed,
Some E is provided
from E-stores esp. fat (if prolonged leads to wt-loss) i.e.
NEGATIVE ENERGY BALANCE
When E-Intake = E-Expenditure (energy needed),
ENERGY BALANCE . Hence, body-wt often
remains constant.

Components of ENERGY
BALANCE
food

Fat
ProCHOs

TEF/heat
PA
BMR
Energy OUTPUT

Energy INTAKE

For body wt to be constant, E-taken-in (E-intake) in form of food (in CHO, Pr- & Fat)
should be = E-used for Basal Metabolic Rate (BMR), Physical Activity (PA) & Thermic

Energy Intake
E-Intake = 1st part/component of E-balance
equation
Includes a study of; Quantity of foods eaten by an indiv. &
the energy contents of those foods
Energy content of a food = the amount of E for a given
weight of the food.
Diff foods provide diff amounts of E and their E-contents are
determined/calculated by their contents of macro-nutrients
(CHO, Fats, Proteins & alcohol*).
NB: Micro-nutrients (vitamins, minerals & water*) do not
contribute to E-content of foods.
E-content of foods can be measured by using;
Bomb calorimeter
Diet Survey data e.g. % of E-supply from different macro-nutrients,
and % of overall E-intake contributed by different food groups
E-conversion-factors/Proximate principles/Fuel factors

ENERGY OUTPUT
E-Output = 2nd component of the E-balance
equation
It relates to the usage of energy by the body
in performing its normal functions & activities
Components of E-Output/Expenditure include;
Basal Metabolic Rate (BMR)
Physical Activity (PA)
Thermic Effect of Food (TEF)/Diet-Induced-Thermo-genesis or
heat related to food-intake
Growth (@ certain stages of life)

E-Output can be measured using;

Direct methods e.g. Direct Calorimeter
In-direct methods e.g. Respiratory gas analysis, Isotope
method (the most sig. isotope method = Doubly-labelled H2O
Technique using stable isotopes of hydrogen ( 2H) and oxygen (18O) where
the subject drinks a small volume of labelled water)

E-Output (cont.)
Other techniques used to measure
E-expenditure (or E-output):

Activity diaries
Heart rate monitoring
Skeletal muscle recorders (electro-myography)
Pedometers (to record movement)
Energy intake studies for subjects in energybalance

Importance of E-balance:

Is to ensure constant body wt & composition

When indiv has E-balance, the body wt & composition remain
constant.
But, a growing child or athlete in training aiming to increase
muscle bulk/mass, needs to be in positive E-balance to attain
that muscle mass.
On other hand, an indiv aiming at losing wt needs to be in
negative E-balance.
Hence, measuring body mass & body composition is
important, and can be done by using Body Mass Index
(BMI)*
BMI is mainly
BMIfocused on fat mass
GRADE
of the body rather
than muscle<mass.
20
Under-weight
BMI = Weight/Height2 (weight in kg, height in m)
20 - 25
Normal
Current BMI categories used:
26 - 30

Overweight

> 30

Obese

Body wt & composition

cont.

Degree of malnutrition in adults can be

classified according to BMI:
BMI

Grade of
malnutrition

< 16

3 (severe)

16 16.9

2 (moderate)

17 18.4

1 (mild)

- Also, the degree of over-weight may be

checked by using Weight-to-height
assessment charts for adults*.

Positive Energy Balance

Occurs if more E is consumed > than needed

Increasing concern about the growing prevalence of o/wt & obesity in pops
globally.
Causes for (+)E-balance incl:

1) Dietary intake e.g.

diet records over last 50yrs indicate that % of fat intake has increased @ expense of
the CHO-content of food consumed during the emergence of the typical Western diet
(of high fat content).
Studies on dietary intakes and wt (in both genders; F&M) show that the average BMI* &
the prop of those o/wt & obese decrease as total CHO intake increases (i.e. an inverse
relationship) mainly due to diffs in sugar intakes. BUT BMI INCREASES AS THE PROP
OF FAT IN THE DIET INCREASES irrespective of the total E-intake levels. Hence, FATS
= MAJOR CULPRIT *(leading to this +ve E-balance) COUPLED WITH SEDENTARY
LIFESTYLE (i.e. low P/A or reduced fat-burn-outs). Thus, high fat intake is more likely to
result in o/wt; which specifically then implies that o/wt = a result of a positive-fat-balance
(rather than generalising it as being caused by a positive-E-balance)
Studies on metabolic fate of dietary components confirm that there is well-matched
metabolism of CHO, proteins & alcohol (except for fat) e.g.
Alcohol must be broken down & eliminated quickly from the body due to its
toxic nature & absence of its storage sites (otherwise it dominates the metabolic
pathways & suppress metabolism of other substrates);
Aa oxidation matches protein intake effectively; while
Glycogen levels hv to be maintained in the body to maintain blood glucose levels
(esp. of the brain & NS). Hence, if CHO decreases, also glucose oxidation is reduced
to maintain circulating levels & satisfy the obligatory use of glucose (by brain & NS).
Conversely, a high CHO intake triggers storage of glycogen and inhibit fat oxidation.
NB: this v. precise AUTO-REGULATION OF CHO METABOLISM is caused by
changes in levels of circulating hormones e.g. Insulin wrt CHO.

Positive Energy Balance

*BUT in the case of cont.
fat;
(1) there is NO AUTO- REGULATION for FAT metabolism probably due to the v.
large storage capacity for fat; thus, an increase in fat-intake does not trigger
an increase in fat oxidation! Any fat consumed in excess of immediate
needs is STORED. Then the gap btwn amount of E-available from other
macro-nutrients & the total E reqd to meet E-o/p-needs (E-needed by
body), is filled by FAT METABOLISM. NB: This is not a problem if total-E-intake
from other macro-nutrients = the o/p. BUT,
(2) WHEN INTAKES ARE IN EXCESS OF NEEDS, FAT IS STORED IN PREFERENCE TO
THE OTHER METABLIC PRODUCTS.
(3) ADDITIONALLY, FAT IS STORED V. EFFICIENTLY i.e. with less E-usage (e.g.
only 4% of its E-content wasted/used during its storage process compared to
25% of the potential E wasted during the process of CHO storage which
involves E used to convert CHO to fat; thus a much less E-efficient process). THUS,
STORING FAT WASTES < E THAN STORING CHOs AS FATS.
(4) SATIETING EFFECT OF CHOs > THAT OF FATS Hence, it is easier for indiv to
over-eat fat-containing diet without reaching satiety, while with CHOs the indiv will
quickly feel full. After consuming excess fat, subsequent food-intake is not reduced.
Hence, continued over-consumption can occur (may without the subject being
aware of it).
(5) A FAT-RICH DIET HAS A HIGH-E-CONTENT PER GRAM, AND CONSEQ. IS OF A SMALL
BULK; making it quite posbl for indiv to eat more fat with a small bulk, but the same
E was to be obtained from CHOs a greater bulk would be reqd. i.e. the size of the
bulk of the food components can be deceiving if used to visually weigh the Econtent of foods (without considering the E-conversion factors for both CHO & fats).
Thus, these mechanisms indicate how FAT = MAJOR CULPRIT in +ve E-balance & how
it is effectively more fattening than CHO or intake of other substrates.

2)

Causes for (+)E-balance

cont.

Genetic pre-disposition wrt to genetic component in wt;

- there is relationship btwn parents wt & childs wt (some of which has bn inherited).
- there is also contribution of env. Factors (ie how the child is nurtured)
- an indiv from family with history of o/wt = more likely to hv difficulty in maintaining a
normal wt for his/her height; but it can be done.

3)

Age

wt-gain tends to increase with age (with particular fat increases occuring btwn ages of
25 & 45.

4) Gender - in women increases in body-wt may follow preg. (after which wt gained may not be
lost). In men peak-prevalence of increase in body-wt = up to 50 yrs, while in women this tend to
continue until mid-60s. But, both genders experience wt-loss in older ages.
NB: The trend in wt-gain thro-out the middle yrs of life = may b simply a reflection of reduced
PA levels.

5)

Socio-economic status -

in some Western countries there is an increases prevalence of

o/wt & obesity among people of low socio-economic status* (which used to b mainly among
pple of high socio-economic status); This can be attributed to factors e.g. food availability &
food selection, budget priorities wrt food choices, lifestyle factors (esp. sedentary lifestyle),
culturally-acceptable body-size (determine how much an indiv may want to change their wt),
etc.

6) Psychological factors these involve emotional eating, perceptions about body size and
other main reasons steering an indivs food-intake.
7)

Obesity is also associated with Birth-weight, Weight (contributed predominantly by

abdominal fat deposits rather than peripheral fat deposits), PA and dietary factors;
infants with lower birth-wt & those who are lighter for their age @ 1yr of age hv >risk of a no.
of diseases (e.g. obesity, HTN, high levels of clotting factors & diabetes) later in life.

Negative Energy Balance

Occurs when there is wt-loss or may be evidenced by failure to
grow/thrive; which may be caused by various reasons; e.g.
a deliberate wt-loss to maintain the right wt-for-ht as a target for health/medical
purposes, appropriating wt to a certain category for a particular
sport/activity/competition, etc.
A deliberate but out of control e.g. in anorexia & bulimia nervosa
In association with addiction- e.g. to alcohol or drugs which replace/reduce
normal food-intake
A conseq. of ill-health - e.g. subject unable to eat or absorb adeq amounts of
food, hence becoming mal-nourished or muscle-wasting occurs.
In cancer e.g. where substances produced by tumor may cause changes in
metabolism of nutrients (esp. macro-nutrients/EYNs), hence resulting in wt-loss.
NB: Some indivs simply genetically have low body-wt, despite an apparent high Eintake. For this indiv., if wt is maintained at this level then no intervention is reqd.
BUT wt-loss due to ill-health has to be fought against/rectified, e.g. by;
- Adding E-suppl to the indivs foods (if posbl)
- Reducing low-E & low-fat foods in the diet, replacing them with high-E snacks &
meals containing some fat (preferably veg oils/fats)
- Avoiding drinking with meals since fluids may induce an earlier satiety
- Reducing the amount of DF (or NSP) in the diet since it has a satiating effect;
hence will reduce total E-intake
- Reducing PA (if approp.), while may be including some muscle/body-building
activity e.g. work with weights
NB: Changes in nutrition cause changes in body composition (esp. lean-body-mass
i.e. FFM & fat-mass)

ENERGY-YIELDINGNUTRIENTS
Carbohydrates
Proteins
Fats
Basic immediate
energy source for the
body

Compensatory energysource

Basic alternative
energy source

Primary source of E &

heat (esp. starches &
sugars)

Thus, when fuel from

CHO & Fats is insufficient, the body
draws from Dietary
proteins or Tissue
proteins to obtain the
reqd E

Provides the bodys

alternative storage
form/source of E & heat

Maintain back-up source

of quick-E (or glycogen)
i.e. CHO stored in form
of glycogen
*Balanced diet of
healthy indiv. should
supply ~50 60% of
the total E from CHO

Concentrated
fuel/source of E

Quality proteins
should provide ~15 29% of the total E in a
healthy indivs wellbalanced diet.

Fats should supply no

more than 25 - 30% of
the total E in the diet of
a healthy indiv.

Energy conversion factors

Energy Yielding kcalories per g
Nutrient
(Calories/g)
CHO

kJ per g
(kJ/g)

3.75

16

Proteins

17

Fat

37

*Alcohol

29

Conversion formula:
kcal to kJ

(4n + 1)

Thus, 1g of CHO consumed from food yields/produces 3.75 kcal (or 16 kJ) of
Energy.
NB: - Energy can be measured in calories and joules.
- 1 kcalorie = 4.18 kjoules

Energy production
Central Metabolic pathways = how the body produces
E from EYN using the Krebs cycle/Tri-Carboxylic Acid (TCA)
cycle.
At rest, almost all the bodys E is supplied from fat oxidation
Fat = most efficient/concentrated E-source, providing 80-100 units of ATP per
molecule of fat, but
It is a slow E-producer & it uses more O 2 than CHO metabolism does. i.e. E obtained
from fat likened to a steam engine which can use up fuel for long periods of time &
maintain a steady pace.

At low rates of exercise, the body has to use a small amount of

CHO to complete the oxidation of fats. This shows that CHO stores (in
the form of glycogen) are important.
As exercise intensity increases, ATP must be produced more
quickly to maintain E-supplies (mainly to muscles cells). Hence,
increasingly more CHOs have to be used, which can provide 38 units of
ATP per molecule of glucose as long as O 2 supply is adeq. i.e. under Aerobic
conditions.

If the intensity of the exercise becomes so great that the

demand for E out-strips the O2 supply, glucose can still be broken
down but v. in-efficiently (such that only 2 units of ATP per glucose molecule will
be produced, & no other substrate can be broken down in this way); i.e.
by An-aerobic metabolism & such a burst of E can be harnessed for a short &
intense exercise e.g. a 100m race or power lift.

Energy production cont.

NB: Since Anaerobic metabolism = an incomplete metabolic process, hence
lactic acid will be produced; which conseqtly results in fatigue because a
build-up of lactic acid reduces pH in the muscle to the point where the
muscle can no longer contract. Therefore, that will terminate the exercise
Therefore, anaerobic exercise is of (necessity of) short duration of 90s.
The bodys tolerance to lactic acid increases with training, thereby
increasing the duration the exercise can continue. Once the demand for
rapid-E-supply stops, O2 can once again meet the needs of the metabolic
pathways and the in-complete oxidations can be
completed/ended /brought to a conclusion by (further) oxidation of
lactic acid into Pyruvic acid, thence via the Krebs cycle/TCA cycle. This
is called re-paying the O2 -debt.
Proteins make v small contribution to E-supply during exercise & are
hardly used up at all;
NB: An exercising muscle increases in mass or size (i.e. muscle mass
increases) over a period of time, so that when a person 1 st starts taking
regular exercise more proteins will initially be retained/stored by the body. But,
additional food eaten to meet E-needs should also provide more than enough
proteins in order to meet the needs for muscle-repair. Training increases
muscle mass/size, strength & exercise-capacity, but Increasing protein intake
does not!!!

SUMMARY for E-Prod :

n

Whatever the intensity of the exercise, both fat & CHO

are gen. used.
At low levels of exercise, the balance is mostly in
favour of fats, with little CHO used.
At high intensity, the exercise is fuelled mostly by
CHO, unless it is at maximal intensity & proceeds
anaerobically where CHO = sole fuel.
The longer the duration of the exercise, the > the
prop. of Fat:CHO used. Eventually, CHO supply is
exhausted, & exercise stops!
Proteins make v small contribution to E-supply during
exercise & are hardly used up at all; but exercising
leads to increased muscle-mass over time & a diet has
to meet E needs & supply more than enough proteins
to repair muscles.

Pathways for metabolism(s) involved in

E-Prodn
Under normal circumstances, glucose levels are maintained by

hormones (e.g. insulin, adrenaline & cortisol), which ensure that

sufficient glucose is present to fuel the essential tissues (e.g. of the
brain, nervous system (NS) & red blood cells (RBCs).
But, if there is no supply of glucose entering the body (via food
intake), then organs e.g. the LIVER capable of making glucose from
protein residues and glycerol from fat break-down.
Fat breakdown occurs by successful splitting of Acetic acid
molecules from the end of Long-chain FAs,
Then, those Acetic acids molecules enter the same common
pathway that serves CHO metabolism

On fasting, the body rapidly metabolizes body fat.

Initially, there is also a rapid breakdown of lean tissue (muscle
tissues), as the body uses protein residues to maintain blood
glucose supplies.
After a no. of days during the fasting, the brain & NS adapt to the
use of ketone bodies* for E-production and for survival to become
posbl fat stores have to be used.
Inevitably, a fatter person will be able to survive longer than a person with
limited fat stores at the out-set.

Metabolic pathways cont.

For complete fat oxidation, some CHO (glucose or glycogen) must be
present
Otherwise, the Acetic acid molecules (themselves) combine in pairs --to form KETONE BODIES*.
Once formed, the ketone bodies are sent to the peripheral tissues
where they can be converted back to Acetyl coenzyme A & be used in
the normal Krebs cycle (also called tri-carboxylic acid cycle (TCA
cycle) or citric acid cycle).
* Whenever fat mobilization (oxidation) occurs (e.g. during moderate
exercise, over-night fast, conditions associated with low food-intake
such as gastro-enteritis, or the nausea & vomiting in early preg.),
there will be a mild rise in ketone body production i.e. mild ketosis.
Symptoms assoc. with mild ketosis = lethargy, headache & loss of appetite;
however, these are v. gen and may be caused by many other factors

* A more severe type of ketosis may occur;

in severe states of the conditions above
during physio changes (e.g. muscle weakness & over-breathing), or
in diabetes mellitus (whereby insulin lack prevents normal entry of
glucose into cells, hence preventing normal glucose oxidation).

Descriptions of Eproduction pathways

Gluco-neo-genesis = synthesis of
glucose from other substances e.g. Aa &
FAs or glycerol (i.e. from proteins & fats)
Glyco-genesis = synthesis of glycogen
from blood glucose
Glycogen-olysis = production of blood
glucose from liver-glycogen
Glyco-lysis = cell oxidation of glucose
for energy production
Lipo-genesis = synthesis of fat from
blood glucose

Diagram of CENTRAL PATHWAYS OF

METABOLISM
PROTEIN
S

FATS

CHOs

glycogen
glucose
Pyruvic
acid

glycerol

Fatty
acids

Amino
acids

Acetyl coenzyme A

CO2 + H2O

Krebs/T
CA
cycle
ENER
GY

ATP

CHO
CHOs = a group of substances (found in plants &
animals) composed of C, H and O in the ratio of
1:2:1; whose empirical
formula
is Cn(H2O)n.
Simplest forms of CHO = sugars which are gen.
present as single units called Mono-saccharides,
or double units called Di-saccharides.
Chains of simple sugars with 3-10 units = Oligosaccharides.
The longer & more complex chains of the sugars
combined together, with 11 units = Polysaccharides

CHO Classification
CHOs in
food

Simple
CHOs

Complex
CHOs

i.e. poly-sacs

I.e. Sugars; e.g.

mono-sacs, disacs & oligo-sacs

Starch
= glucose units
arranged in straight &
branched chains (i.e.
amylose & amylopectin,
resp.)

Digestibl
e Starch

Resistant/
Indigestible
Starch

Cellulose
= glucose units
linked with (1-4)
bonds

NonStarch
Polysac
s

i.e. NSP/
Dietary Fibre

NonCellulos
ic
polysac
s
e.g. hemi-cellulose,
gums, pectins,
mucilages, etc

CHO classification cont.

CHOs in
food

Simple
CHOs

Intrinsic
Sugars
found with-in cellstructure of unprocessed foods e.g.
fruit & vegs

Complex
CHOs
i.e. sugars

Extrinsic
Sugars

Milk
Extrinsic
Sugars
(MES)

e.g. lactose & galactose (found in milk & dairy

products e.g. yogurt, cheese, cream, dairy
f/juices, etc)
= less likely to cause dental caries

e.g. table sugar (i.e. sucrose), sugar in

s/drinks, confectionery, f/juices, honey &
milk

Non-Milk
Extrinsic
Sugars
(NMES)
e.g. sucrose, glucose, maltose & fructose (found in sugar,
s/drinks & confectionery)
= Cariogenic sugars i.e. more likely to cause dental caries (tooth
decay) *1
= bcos of their rapid rate of digestn & absorptn, NMES can result
in rapid increase in b/glucose & high insulin levels; can b replaced
by f/v & starch esp. NSP*2

CHO classfn. cont.

NB:
Mono-saccharides (single-unit sugars) include; glucose, galactose &
fructose
Other mono-sacs occassionaly found in foods = xylose & arabinose (found in
white wine & beer), mannose (in fruits), fucose (in human milk &bran) and sugar
alcohols (e.g. sorbitol, mannitol & xylitol;
Sugar alcohols = absorbed and metabolised to glucose more slowly than the
simple sugars, hence cause a slower rise in blood glucose levels- and ie why
sometimes sorbitol is used to sweeten diabetic foods.
Although absorption rate of sugar alcohols is slower, amount of E they
ultimately produce = E from simple sugars (of same Qty) hence they hv no
benefit where E-reduction is reqd. But, sugar alcohols = useful in reducing
dental caries bcos they are not fermented by bacteria in the mouth, there4
do not contribute to acid production. e.g. xylitol has cario-static (cariespreventing) effect when added in chewing gums or candies.

Di-saccharides formed from mono-sacs combined in pairs in a

condensation reaction (i.e. where H2O is lost) e.g. maltose =glucose +
glucose; sucrose = glucose + fructose, & lactose = glucose +
galactose.
Maltose = malt sugar; mainly found in germinating grains (as their starch store is
broken down) or sprouted grains e.g. barley, wheat & momela (used in beer
manufacturing), mogetlo and malted drinks.
Sucrose is made from sugar cane/sweet beet; juice is extracted from these plants,
purified & concentrated, then finally sucrose id crystallised out & removed. By products
of this process = molasses, golden syrup & brown sugar. Also sucrose is contained in
honey & maple-syrup. It is naturally occuring in fruits, veg & some cereal grains.
Lactose = milk sugar; found in milk (from mammals incl human-milk) and in foods
containing milk-powder or whey e.g. milk chocolate, muesli, biscuits & creamed soups.

CHO classfn. cont.

Oligo-saccharides = sugars of minor nutnal sig. e.g.
galacto-syl-sucroses (found in legume seeds) & fructosyl-sucroses (found in leek, onion, garlic, lentils and
artichokes). of the same foods.
NB: Oligo-sacs = resistant to digestion in gastro-intestinal tract,
hence pass un-changed into colon where they are fermented then
produce volatile FAs + gases that cause flatulence; this can be uncomfortable & prevent further consumption.

Poly-saccharides = contain many mono-sac units

arranged in straight or branched and coiled chains;
may be made up of hexoses, pentoses or mixture of these and
sometimes with other constituents e.g. uronic acid
Both classes of poly-sacs (Starch & NSPs) = of plant origin,
comprising the store of E in the plant
A comparable CHO store in animals is in the form of Glycogen (but
its content in the diet is neg.)
For the body to use complex CHOs for E, they must be split into
mono-sacs (in a process called HYDROLYSIS) and absorbed.

Physiological functions of CHOs

CHOs = important source of E for the body; providing

glucose for immediate use*1 & glycogen for reserve.
CHOs also used in the synthesis of various
metabolically active complexes e.g.
glyco-proteins = important components of cellular
membranes esp. extra-cellular membranes or can be
found as circulating proteins in the blood or plasma
glyco-lipids (e.g. sphingo-lipids & gangliosides)
= which hv roles at receptor-sites on cells & in synaptic
transmission

muco-poly-sacs = hv important water-holding or binding

properties in many sites in the body and are found in
basement membranes & in inter-cellular cement and form
integral part of cartilage, tendon, skin, etc.

Health aspects/Nutritional advantages

of
CHO
Starchy foods (e.g. cereal products, potatoes, nuts, pulses & seeds) have many

nutnal advs:
Not only provide complex CHO(in form of starch), but also provide NSP &
other nutrients e.g. proteins, Fe, Vitamins B and E.
Starchy foods have a lower E-density and a higher satiety-value than most
foods which have a signt fat-content. Hence, increasing the consumption of
starchy foods in the diet can reduce the proportion of fat in the diet.
E.g. A plate of rice/maize meal/sorghum meal/potatoes contains same amount of E as 4 average
biscuits (a
10gbiscuit). Hwever, there is a great diff. in the filling effect (satiety or feeling of
fullness) produced by these
two foods; the starchy meal will produce more satiety than biscuits,
while biscuits also have hidden
fats.
Note the mis-conception about Starchy foods: For long it has bn believed that starchy foods are
fattening;
hence,
they were the 1st items to be cut out of diets intended for weightreduction/loss. While they actually hv lower E-density.

Starchy foods usually have an economic adv. because they are usually inexpensive compared to other foods (e.g. wrt cost per gram mass). There4,
they can be very valuable nutrient-rich foods for people on low-income.
During their passage in the digestive tract the products of starch digestion
(e.g. glucose) are released slowly. Therefore, they conseqtly have small
effects on blood sugar levels; thus, they tend to hv a lower glyceamic index.
For this reason starchy foods are particularly useful in the mgnt of diabetes.
Resistant starch (present in starchy foods) has similar properties as NSPs, hence
provide/share the same health benefits as this group of CHO.

Health benefits of NSPs

NSPs promote dental health; resulting from increased chewing & flow of
saliva in the mouth*1.
NB: Saliva rinses or washes away the sugar remnants from the mouth
around the teeth & buffer the acid.
NSPs contribute to satiety & posbly help in wt-mngt;
foods high in fibre often require more chewing, therefore an indiv is
unable to consume a lot of E within a short time. Hence, this helps in wtmgnt.
Fibre has no calories, yet it provides a filling effect. Also the increased
viscosity resulting from soluble NSPs slows emptying of the stomach.
The fibre bulks the food - leading to poorer access to enzymes of
digestion; leading to..

..Longer digestion process i.e. slower digestion & absorptn/liberation of

nutrients (CHO, proteins, Fe, Vitamins B and E) in the small intestine. Hence,

In the colon (large intestine); H 2O-retention, gas production & bacterial

growth cause faster transit & increased bulk.
H2O-retention (water-holding) helps in dilution of colon-contents & it
stimulates peristalsis, which reduce intra-colonic pressures leading to
easier expulsion of faeces
Ingested dietary fibre (DF) moves along the colon partially/completely
fermented by gut-bacteria producing by-products (e.g. short-chain FAs &
gases), which contribute to the following main physiological & ..

Health benefits of NSPs

cont.

..beneficial effects of dietary fibre in health:

BOWEL FUNCTION DF esp. Insoluble DF helps to prevent constipation by increasing
stool wt & decreasing gut-transit-time esp. if DF intake is paralleled/accompanied by
increased H2O intake;
also s/chain FAs (produced during fermentation of fibre by gut-bacteria) = important
E-source for colon cells* & might inhibit growth & proliferation of gut-tumor-cells (i.e.
colon cancer); By improving bowel function, DF can reduce risk of disorders e.g.
diverticular or haemorrhoids of the colon)

LOWERING BLOOD CHOLESTEROL LEVELS via the binding & elimination of waste
products Isolated viscous fibres (e.g. rice bran, oat bran, pectin, etc) lower total serum
cholesterol & LDL (bad cholesterol) levels, therefore improving blood lipid levels/profile;
thus preventing CHD:
MECHANISM (How?): The body eliminates cholesterol thro excretion of bile
acids; for example H2O-soluble-fibre binds bile acids; then thro excretion of the bile
acids, cholesterol is eliminated as well. This suggests that a high fibre diet may result in
increased cholesterol excretion
NB: - Insoluble fibre increases the rate at which wastes are removed from the body,
hence the body has less exposure to toxic substances produced during digestion. In this
way also, insoluble dietary reduces the risk of cancer esp. colon cancer
- Fibre in rolled oats > effective than fibre in wheat in lowering cholesterol levels.

LOWERING BLOOD GLUCOSE LEVEL - Soluble fibre may slow digestion & absorption of
CHOs, causing lower rise in the blood glucose (that follows a meal [post-prandial]) and
insulin response. Hence, this can help diabetes patients to improve their control over
glucose levels.

CHOs & DENTAL CARIES

NB: Teeth are generally covered in a layer of PLAQUE; made up

of BACTERIA (prevailing species = Streptococcus mutans) & STICKY
POLYSACS.
Dietary sugars provide the substrate for multiplication of oral
bacteria & production of acid (as fermentation product). Then the
acid formed causes a fall in pH (such that as the pH reaches 5.5 the
tooth enamel begins to de-mineralise.
However, BUFFERS in saliva RESTORE the pH to normal level
(generally with-in 30mins after consumption of sugar).
But, if sugar consumption occurs at frequent intervals, therefore
the teeth are exposed to the low pH for prolonged periods of
time resulting in the damaging de-mineralisation & dev. of d/caries.

Contributing factors to dental caries include:

amount of saliva produced to wash away sugar remnants &
buffer the acids
conc. of the sugar
period of contact &
freq. of consumption of the sugar; e.g. low conctd sugar that passes
thru the mouth will hv less effect than a concentrated source of sugar present in a
sticky form that remains in the mouth for a long time.

CHO & DENTAL CARIES

cont.
Advice on reducing D/C from sugar consumption:
Consumptn of NMES should be decreased & replaced with fruit, vegs
& starchy foods
Reduce the frequency of snacks provided with food for the families or
community (esp. sugary snack; or may be replaced by fruit as a
snack)
Simple sugars should not be added to bottle feeds for infants &
young children;
- sugared drinks should not be given in feeders where they can
have prolonged contact with
their teeth
- also dummies should not be dipped in sugars or sugary drinks

Schools may promote healthy eating by incl. dental health promotion

Elderly people should restrict amount & freq of consumptn of NMES
since their teeth more likely to decay due to exposure of their toothroots & the declining salivary flow
As much as posbl, when medicines are needed (esp. on long-term
basis), sugar-free formulations may be selected by medical
practitioners (or parents)
For people prone to D/C, the dietary advice given should incl.
reduction of NMES consumptn.

Role of CHO in health

(cont.)
CHOs & HYPO-GLYCERMIA:
Sug
ar
intak
e
Initially
causes
Hyperglyce
mia

Administering Diabetesdiet-therapy: Diet high in

Complex CHO, high in D/fibre
(NSPs) & low in simple sugars,
LEADS TO:
Increased blood glucose level
to normal levels in Diabetic
patients
BUT: In some
sensitive people,
blood glucose levels
drop below normal
levels i.e.

Triggers
release of
insulin
Insulin o/p
(which may b >
Reqd)

HYPOGLYCERMIA

Drop in blood
glucose level

Dietary mgnt/strategy for both types of

diabetes
Dietary strategy

IDDM (usually non-

NIDDM (usually

obese)

obese)

Reduce E-intake (kcalories)

no

yes

Increase freq of
feedings/meals

yes

usually no

Have regular intake of E, CHO,

proteins & fat

very important

Not important; if av. Eintake remains in the

low-range

Plan consistent daily ratio of

proteins, CHO & fat for each
feeding/meal

desirable

not necessary

Use extra or planned-ahead

food to treat or prevent hypoglycaemia

very important

not necessary

Plan regular times for

meals/snacks

very important

not important

Use extra food for un-usual

exercise

yes

usually necessary

During illness, use small, freq

feedings/meals of CHO to
prevent starvation ketosis

important

Usually not necessary

because of resistance
to ketosis

CHOs & Obesity

Nutrition-Truths:
NIDDM (which commonly develops in older people) is linked with overweight (o/wt); excessive intakes of any E-source leads to increased
risk of developing NIDDM.
Obesity in a popn increases as sugar intakes increase but;
Fat intakes are much better correlated with occurrences of obesity than are
sugar intakes; because
some epidemiological surveys of diff pops observed an inverse relationship btwn
reported sugar intake & degree of o/wt, and
some intervention studies show that removing sugar from diets of volunteers causes
wt-loss &
when sugar was unknowingly substituted by artificial sweeteners (leaving sweet taste),
E-intake is reduced & not compensated by an increase in other foods. HENCE;
INCLUDING SUGAR IN THE DIET IN-FLATES THE E-INTAKE.

Digested CHOs influence a no. of physio. mechs (e.g. serotonin hormone)

involved in satiety e.g. sensory characteristics of sweet CHOs encourage
consumptn at the out-set, later CHO acts as an effective appetitesuppressant, hence reducing hunger ratings & the subsequent foodintake.
On balance, there4, sugars a major culprit in dev of o/wt; (considering the Econversion factors for CHO(3.75 Cal) compared with fat (9Cal) & proteins(7Cal per g protein).

CHO & CROHNS DISEASE

People who suffer from Crohns disease have
consistently been reported to have history of a HIGH
SUCROSE INTAKE.
Mechanism (though not yet fully proven): Sugars in high
conc.'s may affect intestinal permeability & damage
mucosal cells ---leading to gastro-intestinal disease.
..
NB: Also, there is a suggested relationship btwn
SUGARS & HYPER-ACTIVECRIMINAL/DELINQUENT BEHAVIOUR!

FATS
Fats = substances soluble in organic solvents (e.g. acetone) but insoluble
in H2O
Greasy in texture & non-volatile
Solid @ r/temp = fats, liq. = oils; But both hv same chemical structure &
both = lipids
Lipid molecules contain C, O & H atoms linked together in a specific way.
Major factors attributing to diffs in solubility = size of molecule &
types of bonds present in the lipid.
In nutrition, most important lipids = triglycerides/triglycerols (found
in ~95% of fat we consume)
Hwever, other examples of fats/lipids in the diet = phospholipids, sterols,
glyco-lipids & cholesterol (often contributing ~5% of the fat we consume)
Fats are made up of smaller units = FATTY ACIDS (FAs)
There are 3 types of FAs;
Saturated FAs
Mono-unsaturated FAs
Poly-unsaturated FAs.

Classification of Fats
FA classification by:

i.e. according to
no. of C-atoms in
the chain

Shor
t
chai
=FAs withn 6Cs

Degree
of
saturati
on

Chain
length

Mediu
m
chain
=FAs with 8-12Cs

Lon
g
chai
n 14Cs
=FAs with

Satura
ted

Family
i.e. according to
position/location of
the 1st d/bond from
the methyl-end

Unsaturat
ed

n3
i.e. omega-3
FAs

FA classification by: No.

of double bond present in
the FA

FA classification by:
ORIENTATION* e.g. cis- or
trans- configurations

n6
i.e. omega-6
FAs

FAs classification according to chainlength

The human diet predominately would contain = Long-chain

FAs (~95% of the fats); hence these occur as liqs (or oils) at
room temp., while the remaining ~5% of the fats commonly
consumed = Medium or Short chain FAs (occuring as solids
(i.e. hard-fat).
NB: The longer the chain, the more likely that the fat
occurs/becomes liquid (@r/temp), because long-chains have lower
melting point. Conversely, medium/short chains (12Cs) hv higher
melting points.

Among the predominating class of long-chain FAs, the most

commonly occuring = chain lengths of 14 & 16 Cs.
Most naturally-occuring FAs contain an even no. of Cs in the
chain (normally ranging btwn 4 & 24 Cs); hence,
Basic formula for FAs =
no. btw 2 & 22 (inclusive)*

CH3.(CH2)n.COOH

where n= any even

Classification of Fats (by saturation, family &

isomerism)
FAT

(in food)

Saturat
ed FAs

Unsaturat
ed FAs

= Hv no double bonds, (but only

single bonds, thus; Cs hold as many
Hs as chemically can/posbl)
Ex.= palmitic acid*1
= High intakes leads to adverse
effects

CisMUFA
s

Mono
Unsaturat
ed FAs

Poly
Unsaturat
ed FAs

i.e. MUFA
= hv 1 double bond
Ex. = oleic acid found
in olive oil, etc.

Trans
MUFA
s
Hv > adverse effect
than high intake of
saturated FAs

n-9
MUFAs
e.g. *3 18:1 (n-9), 20:1 (n-9)
& 22:1(n-9)

Cisn3
PUFAs
*1CH3

Hv 1 double bond

COOH

i.e. PUFA
= hv 2 double
bonds*2 (i.e.
ethylenic bonds)

n-3
PUFAs
= e.g. EPA & DHA
= mainly from marine foods

Tran
s- n3
PUFA
s

n-6
PUFAs
mainly from plant foods

Cisn6
PUFA
s

Tran
s- n6
PUFA
s

FA classification by saturation & family

cont.

Besides chain-length, the hardness of a fat is also affected by the prop. of

saturated & un-saturated FAs in it.
Location of double bonds random, hence
If the location of the 1st d/bond (counting from the methyl-end [-CH3]) is identified,
the remainder of the chemical formula for the FA can be predicted using the
system of nomenclature, as follows:
Multiple d/bonds are separated by 3Cs btwn the next d/bond in this manner;

- CH = CH-CH-CH=CH-

These locations of the 1st d/bonds are mainly used in naming FAs classified
according to families (e.g. the n-3, n-6 & n-9 FAs).
Example 1: Oleic acid = 18:1 (n-9),

where 18 = no. of C-atoms (thus, long-chain FA,

hence = oil)

1 = no. of d/bonds (thus, mono-unsaturated),

n- = omega

family &
9 = position of the 1st d/bond from the methyl end.

This implies that oleic acid = an omega-9, long-chain MUFA (oil)

Example 2: *Linoleic acid = 18:2 (n-6), thus = an omega-6, long-chain
PUFA (oil)
Example 3: *Alpha-linolenic acid = 18:3 (n-3), = an omega-3, longchain PUFA (oil)

FA classification by
Orientation/Configuration/Isomerism
Trans FAs Trans vs Cis
Cis FAs
FAs
= produced by chemical alteration of
molecules occuring during transformations
by anaerobic bacteria in the stomach
(rumen) of ruminants (hence, trans-FAs
sources = meat & meat products e.g. milk, dairy
products, eggs, etc), or mainly during food
processing or hydrogenation in the
manufacture of fat spreads (hence, other
trans-FAs are found in products containing
hardened fats e.g. hard margarine, pastries,
biscuits, etc)
(NB: trans-orientation = where the H-atoms

The naturally occuring unsaturated FAs

hv a cis-orientation (where the H-atoms

are on the same side of the

d/bond)

are arranged on opposite sides of the

d/bond)
In trans-configuration, the molecule remain
elongated & similar to a saturated acid; hence
making the trans-FA molecule to pack more
tightly together thereby increasing the melting
point of the fat. Therefore, the fat = HARD fat
(solid)
Most trans-FAs = MUFA.
The most predominant trans-MUFA = trans-oleic
acid
Large amounts of consumptn of trans-FAs lead to

In cis-configuration, the molecule is folded

back or bent into a U-shape; hence FAs
pack less tightly, thus increasing the fluidity
of the membranes. This reduces melting
point of the fat, therefore, the fat = OIL
(liquid)

Health aspects of the n-3, n-6 &

n-9 FAs

n-3 PUFAs

n-6 PUFAs

n-9
MUFAs

Found only in some PUFAs

Found only in some PUFAs

Only found
among MUFAs

Health benefits: n-3 series/family

causes less vaso-constricting
effects on blood vessels, hence
overall effects of n-3 incl these; n-3
are less likely to produce
inflammation, thrombosis or
increases in BP; hence reducing risk
of heart attack. Also, higher intake of
n-3 acids stabilizes the rhythm of the
heart & allows it to continue beating
normally during a heart attack, hence
ensuring a higher chance of survival.
(this = main reason for n-3 series to
b believed be beneficial in the
prevention of heart disease)

- Hv an LDL-cholesterol
lowering effect
(independent of any change
in saturated fat intake); by
enhancing the activity of the
LDL receptor sites in
opposition to the effect of
saturated FAs on the same
receptors, hence, increasing
the removal of LDL from the
blood circulation (i.e. n-6
FAs & saturated FAs
compete for the
receptors sites on which to
bind and enter the
circulation).

MUFAs hv
beneficial role in
heart disease
prevention by
reducing LDL
levels. (via
increasing LDL
clearance
/removal from
the blood).
But, the LDLlowering effect of
MUFAs does not
affect HDL levels.

n-3 acids appear to reduce the VLDL

levels, hence may cause reduction in
LDL.

Hwever, n-6 PUFAs in the

membrane lipids are
vulnerable to f/radical attack

n-3 PUFAs

n-6 PUFAs

n-3 series of prostaglandins &

eicosanoids has less
aggregating potency than
those made from n-6 family.
(NB: Ingestion of sig. amounts
of n-3 PUFAs displace n-6
series from enzyme sites, so
that n-3 series eicosanoids are
produced.)

Also, caution to be
taken about
excessively high
intakes of PUFAs

Also, n-3 FAs e.g. EPA & DHA

particularly important in
the dev. of NS and retina in
young infants & dietary source
is needed in v. early stages of
life. Also, breast milk supply
enough amounts while formula
milk may hv in-adeq. amounts.
Summary: n-3 FAs
beneficial effects = n-3 hv

n-9 MUFAs

FA classification by essentiality (or source)

2 classes = Essential FAs & Non-essential FAs
Essential FAs = FAs that cannot be synthesised by the body
because vertebrates (incl. humans) lack enzymes that
introduce d/bonds @ n-3 and n-6 positions; hence should be
supplied only by the DIET.
e.g. n-3 sources = dark g/leafy veg, flax-seed oils, some veg. oils (e.g.
olive oil, sunflower oil), cold-water fish (e.g. tuna, salmon, mackerel)
and fish oils (contain v. long n-3 FAs e.g. EPA & DHA) *1

n-6 sources =
If they are excluded, def syndrome develops e.g. retarded
growth, skin lesions (e.g. dermatitis)
Exs of EFAs = 18:2 (n-6) i.e. Linoleic acid &
18:3 (n-3) i.e. Alpha-linolenic acid
From these 2 EFAs, other members of the same family are
produced by a series of de-saturation (removal of d/bonds) &
elongation (addition of C-atoms to the chain*2) reactions.
Ex. 1)

acid

Ex. 2)

DIET -------provides 18:2 (n6)

DIET -------provides 18:3 (n3)

22:6 (n3) or DHA

18:3 (n-6)

18:4 (n3)

20:4 (n-6) or Arachidonic

x-x-x-x-x

20:5 (n-3) or EPA

FA classification by essentiality (or

source) (cont.)

There is competition for enzymes & enzyme/receptor sites btwn

the n-3 & n-6 families of FAs, hence predominance of one
family can limit the qty of the other family
*3e.g. n-6 = predominant over n-3, so it can limit the amount of
synthesis of the larger members of n-3 family (e.g. EPA & DHA) which are
not made in large amount in the body

But, Ingestion of sig. amounts of n-3 PUFAs may displace n6 series from enzyme sites, so that n-3 series eicosanoids
are produced.

Therefore, both n-6 and n-3 FAs should be supplied in

sufficient amounts in the diet, where
the n-6 : n-3 ratio is v. important in nutrition
with the
recommended dietary ratio = 1:3

Common types of fats

Recall:
In nutrition, most important lipids = triglycerides/tri-glycerols (found in ~95% of fat we
consume)
However, other examples of fats/lipids in the diet = phospholipids, sterols, glyco-lipids &
cholesterol (often contributing ~5% of the fat we consume).
***********************************

In nutrition the COMMON TYPES OF FATS consumed include:

a) TRIGLYCERIDES made up of glycerol + 3 FAs
- can be readily broken down & re-synthesised; a FA can be removed from the glycerol by

de-esterification (which occurs during fat digestion), hence resulting in di-glycerides & monoglycerides (containing 2 or 1 FAs resp.).
- NB: The reverse process = re-esterification (i.e. re-synthesis process) is important for formation of
tri-glycerides (to meet bodily reqnts).

b) PHOSPHOLIPIDS - made up of glycerol + 2FAs + phosphate group + base * (NB: 1 FA is replaced by a PO

group & base);

3-

FA-end of the phospholipid = fat soluble tails (hydro-phobic) while the phosphate-end = watersoluble
heads (hydro-philic), hence this allows phospholipids to mix well in both water
& fats. Therefore;
-

they can be used to transport other lipids within water-soluble blood stream. In the cellmembranes, phospholipids form a bi-layer allowing aqueous env. both inside & outside the cell
while lipid env. is sandwiched in-btwn;
they are found in high conc.'s in the brain & NS, and a phospholipid e.g. sphingo-myelin
(found in myelin sheath) covers nerve fibres.
All phospholipids serve essential function in the body - as emulsifiers
e.g. lecithin = a major constituent of the cell membrane reqd for optimal function of the cell
membrane & is reqd
for synthesis of neurotransmitter called acetyl-choline; vital in the
memory centers of the brain
(Lecithin supplements marketed to improve memory & maintain proper cell function).

COMMON TYPES OF FATS

cont.

NB : All phospholipids are synthesised in the body,

hence = non-essential in the diet. For lecithin, although

ample amounts are made in the body, some dietary sources = eggs &
soya-beans as natural sources. Also, lecithin can be used in food
industry as an additive to margarine, salad dressings, chocolate (e.g.
milk chocolate), frozen desserts & baked foods, to keep/prevent oil from
separating from other (aqueous) ingredients in the same food product.
c)

GLYCOLIPIDS - e.g. sphingo-lipids & gangliosides

= which hv roles at receptor-sites on cells & in synaptic

transmission
d)

STEROLS e.g. CHOLE-STEROL (from animal sources) & Phyto-sterol

(from plant sources), bile acids and hormones; Cholesterol = waxy
substance that can be synthesised by the body from Acetyl-coenzyme
A, and main production site for cholesterol = LIVER, while minor
synthesis site = all cells of the body & >90% of cholesterol in the body
is found in cell membranes. Hence, non-essential in the diet.

Functions of Cholesterol

Cholesterol = part of myelin (a coating for nerve fibres/cells)

Needed for synthesis of;
a) vit D (in the skin),
b) cholic acid = a component necessary for fat digestion
c) steroid hormones*1 e.g. testosterone & estrogen (which
promote growth & dev. of sex characteristics), and
d) cortisol which promote glucose synthesis in the liver.

Cholesterol has a role in the maintenance of cell structure &

permeability of cells
In the blood, cholesterol has important role of transporting other
lipids to body tissues via chylomicrons
- i.e. cholesterol grouped together with triglycerides,
phospholipids & small amounts of proteins = a type of lipoprotein (combination of lipids & protein)
- NB: Other lipo-proteins = HDL, LDL & VLDL (see proceeding slides)

Cholesterol cont.
NB:
From the diet, cholesterol is only found in foods from animals e.g.
meat, fish, milk & dairy products, eggs, etc.
While Ex. of phyto-sterols = beta-sito-sterol found from plant sources
e.g. in nuts, cereals, veg. fats & oils.
Vegetarian diets = low in cholesterol unless they contain/include animal
products (e.g. milk & eggs).

Large intakes of phyto-sterols may inhibit chole-sterol absorption! And,

Reduced dietary intake of cholesterol leads to increased cholesterol
synthesis*2 (in the liver) in order to maintain optimal cholesterol levels
in the body.
Balancing of cholesterol levels done by the body itself e.g.
When dietary intake of cholesterol is low, then cholesterol
synthesis in liver
increases (and vise versa) partly genetically
controlled.
- However, in some ppl, plasma cholesterol levels respond
minimally/ maximally to changes in dietary cholesterol intake (i.e. ppl
genetically less/ more-sensitive, resp. to dietary cholesterol)
RAISED BLOOD CHOLESTEROL LEVELS = MAJOR RISK OF
DEVELOPING CVD.

Lipo-proteins
Lipo-protein = a compound containing a core of triglyceride
surrounded by a shell of protein, phospholipids & cholesterol.
protein
phospholipid
cholesterol
triglyceride

Exs of lipoproteins = chylomicrons, HDL, LDL & VLDL

Lipo-proteins are classed according to their density (& they
can be separated by ultra-centrifugation of blood sample).

Typical compositions of lipo-protein

particles (as %)

CHYLOMICRONS

VLDL

LDL

HDL

Lipo-proteins

Lipo-protein CHYLOMICRONS
= a compound containing VLDL
a core of triglyceride
by
LDL surrounded
HDL
SIZE a shell of protein,
largest phospholipids & cholesterol
smallest
Exs = chylomicrons,
HDL, LDL & VLDL
DENSITY
lightest
Heaviest
(densest)
Lipo-proteins are classed according to their density (& they can
be
LARGEST
Triglycerides
(~
Cholestero Proteins
separated byTriglycerides
ultra-centrifugation of blood
sample).
COMPONENT

twice the size of 2

cholesterols in
chylomicrons)

TRANSPORTS
OTHER LIPIDS
FROM:

Blood to body tissues

COMMON LIPID
CARRIED

Blood cholesterol

COMMENTS

to body tissues

- Starts to appear in blood

within 30mins after fatcontaining meal; with peak
after 3 hrs. NB: Chylomicrons

Blood to
body
tissues

Body tissues
(via blood) to
liver for
disposal

*Transformatio
ns occuring:
VLDL minus
triglycerides =
LDL and,
Lipopro Apo-CII
= Apo-B100

Blood
cholestero
l to body

HDLs function
= clearance
of
spare/surplus
cholesterol
& apo-lipoprs
from body
cells and
other lipoprs

As VLDLs travel
thro the body,
lipoprotein
lipase removes

LDLs
function =
major
carrier of

tissues

i.e. reverse
cholesterol
transport
Cholesterol is

COMMENT
S cont.

CHYLOMICRONS

VLDL

LDL

HDL

As chylomicrons
circulate in blood, FATS
are removed from
them by specific lipoprlipase in blood vessel
walls esp. of liver,
skeletal muscles &
adipose tissue

ANOTHER
TRANSFORMATIO
N = loss of some
of Apo-CII ;
hence remainder
= Apoliprotein
B100 (Apo-B100) =
an identity tag
for LDLs needed
for metabolic
function of LDLs.

Specific receptors
for apo-B100 (on
cell-surfaces) allow
LDLs to attach to
cells to form LDLreceptor
complexes which
then are taken into
the cells

This esterification
of cholesterol
allows it to be
taken into the
hydro-phobic core
of HDL.
Hence, the outer
layer of HDL
maintains a
diffusion gradient
for more
cholesterol to be
picked up & be
eliminated form
the body

Free FAs & Glycerol

are released and
may be used for
fueling muscle
contraction or
stored in adipose
tissue for later use,
while

Once inside the

cells, LDL is broken
down by enzymes
to Cholesterol &
other components
to be used in the
cell. High levels of

Some of the
cholesterol in HDL
is removed from
body tissues to
the LIVER for
disposal
(elimination);
hence, HDLs
protect the
body against
CVD.

Chylomicron-remnants
are broken down in
liver & and used to

Remainder from
broken LDL = HDL.

LDLs are associated

with increased risk
of Cardiovascular
disease (CVD)

Some of the
cholesterol is
transferred to

Summary of the Lipid-transport cycle

Dietar
y fat
intake
LIVER
Chylomicr
ons

Some cholesterol
returned to liver for
disposal (in HDL)

HDL

Fat removed

VLDL

Triglycerides (& apo-CII) removed

Some cholesterol
transferred to VLDL

Cholesterol (& other

components) used
by body cells

LDL

-Both chylomicrons & VLDL hv apo-CII, which activate lipoprotein lipase.

- Lipoprotein lipase removes fats (mainly phospholipids) from the Chylomycrons and the resultant is VLDL. Then, triglycerides
(another type of fat) is removed from VLDL by lipoprotein lipase forming LDL. LDL carries cholesterol from blood circulation to body
tissues for synthesis of metabolites e.g. Vit D on skin, cholic acid, cortisol, steroid hormones, etc; for maintaining integrity & stability

Physiological functions of Fats

Fats serve diverse function in the body, which can be classified as:

1.Metabolic roles e.g.

a) E-production/supply from fats*(note disadv.s attached; next slide)
b) Stability & Integrity of membranes of the cells, hence, signs of
deficiency of EFAs incl changes in properties of cell membranes esp. increases in
membrane permeability. These changes are accompanied by reduced efficiency in Eprodn, and there4, poorer growth.

c)

EFAs = Precursor of a family of compounds called EICOSANOIDS which acts

as metabolic regulators* e.g. prostaglandins, prostacyclins, leukotrienes &
thromoxanes (more details on proceeding slides)

d)

Prodn of cholesterol derivatives

e.g.

Cholesterol = precursor for synthesis of steroid hormones & sex hormones.

= pre-requisite for formation of vitamin D in the skin
= used in the manufacture of bile salts (vital for normal fat digestion) in
the
liver, and some bile salts can b re-absorbed from lower gut & reused by
the liver. Some bile salts can be trapped in faeces & removed from
the body;
in this case then, more bile salts hv to b synthesised from
cholesterol.

2.Storage roles fat stores offer additional benefit (besides being an Ereserve) of thermal insulation & protection;

adipose tissue covers some more delicate

organs (e.g. kidneys, spleen, lungs, spinal cord, brain, etc), protecting them from injury. Also,..

Physiological functions of Fats

cont.
Also, this protective fat is less readily used as fuel in a fasting indiv.
-

Most of the fuel-storing adipose tissue is found under the skin as

subcutaneous fat; where it provides insulation to facilitate
maintenance of body temp. (i.e. thermal insulation).
E.g. in hot climate, o/wt indiv will sweat readily to lose heat, while anorexia
nervosa sufferers (who hv little subcutaneous fat) will feel cold even on a warm
day & may put on several layers of clothing to provide extra warmth or
insulation.

3. Structural roles lipid molecules (incl. cholesterol) often

associated with other residues e.g. phosphate groups, CHO &
proteins = Constituents of membrane structure.
- The exact nature of the cell membranes depends mainly on; types
of FAs present,
their chain-length, degree of saturation & spatial
arrangement/geometric
isomerism (e.g. trans- or cis)
- various fats (e.g. fats containing chains with odd no. of C-atoms,
branched chains & d/bonds in un-usual locations/positions) occur on our
skin, hence contribute to the
skins water-proof properties.
- Free FAs may also be present on the skin = providing some bacterial
properties

Spectrum of fats from food

Dietary
Linoleic
acid (18:2
n-6)

= an EFA
= helps prolong b/clotting time
= increases fibrinolytic activity
= combines with cholesterol to form
cholesterol esters for transporting
cholesterol in blood
= major precursor of eicosanoids
= helps lower cholesterol serum levels
and plays a role in cholesterol transport &
metabolism
= strengthen cell membranes, hence
helping to prevent harmful increase in
skin & membrane permeability

Arachidonic
acid (20:4 n6)

Phospholipi
ds (in the
tissue pool)

= a FA

Leuko-trienes
(found in
macrophages,
neutrophils &
monocytes)

= for leukocyte chemo-taxis &

= cell adhesion

Thromboxa
nes

Prostacyclins

(in platelets)

= cause pro-aggregation of cells,

= vasoconstriction &
= increased blood pressure

(in
= for endothelium)
anti-aggregation of cells,
= vasodilation &
= lowered blood pressure

Prosta-glandins
(found in widespread
tissue)

= for contraction of s/muscles,

= lowered BP
= regulation of - gastric acid secretion
- body temp. &
- platelet aggregation
= control of inflammation & vascular permeability

Effects of poor intake of EFA

Increased permeability of cells

(since
EFAs are reqd for membrane stability & permeability)

Decreased efficiency of E-utilisation

leading to poorer growth.

Fat Malabsorption

Fat digestion = normally v. efficient (e.g. ~ 96% of fat-ingested is absorbed) except in

some disease condition e.g. steatorrhea
Steatorrhea = defective fat digestion &/or absorption; leading to fat appearing in
faeces, hence
producing a characteristic appearance of waxy stools
with a foul smell & being light in
density therefore float and diff. to
flush.
= un-absorbed fat will remove with it other fat-soluble components from the
body esp.
fat-soluble vitamins (Vit A, D, E & K). Hence, Chronic
Steatorrhea is associated with
some specific vitamin deficiencies.
Causes of Steatorrhoea (fat mal-absorption) incl.:
Failure to produce lipase* (esp. pancreatic lipase) due to pancreatic insufficiency or problems with production or secretion of bile
Gallstones; which block secretion of bile into the gut
In-efficient fat absorption due to defects in the surface of s/intestine; which may
be flattened or inflamed e.g. in the following disease conditions;
Coeliac disease = due to defects on surface of the s/intestine (e.g. surface
either inflamed or flattened); hence, leading to fat mal-absorption
Liver disease
Pancreatic or biliary diseases
leading to fat mal-absorption
Cystic fibrosis

Proteins

Proteins = Energy Yeilding Nutrient (EYN)

= distinguished from CHO & fats by the fact that proteins contain N,
in
addition to C, H and O.
= essential components of the muscles, but i.e. only one of the
many
functions in the body e.g. proteins are used to
repair body tissues
= made up from the same twenty (20) amino acids (Aas), but there is a
far greater variety of proteins than that of CHO & fats.
Each protein has its own particular sequence & no. of Aas contained in it
which determine its nature (i.e. its properties & functions).
NB: Even if only 1 Aa is missing or mis-placed in the chain, the properties of that protein will
change.

This sequence of Aas = controlled genetically within our body cells, and
that genetic mech. is encoded in the DNA & RNA chains.
NB: This critical relationship btwn No. of units contained & Function, does not apply in the case
of CHO; For instance, there may be fewer or more monosacs contained in a CHO without
causing any sig. change in the properties of that CHO.

Majority of Aas originate from plants, which are able to combine N (from
the soil & air) + C + other substances to produce .. Aas. Then,
these Aas are built into proteins by plants. Hence, humans obtain those proteins directly by
eating plants or in-directly by eating animals or animal products, which themselves hv
consumed the plants.

Proteins cont.

Then, the proteins we consume from food (animal or plant sources)

are broken down into their constituents Aas & the proteins are rebuilt into diff. ones
OR
some new Aas may be 1st made, before the new proteins are
made in the body.
- Hence, the human body does not contain exactly the same
proteins as those
in plants or animals.
Some Aas can be made from other Aas by the human body,
But
Certain Aas cannot be synthesised by the body; called Essential
or In-dispensable Aas. Hence, they must be supplied by the
diet.

If an indiv fails to obtain adeq. proteins from food, the structural proteins (tissue
proteins) are broken down to meet metabolic needs for repair, and other protein
reqnts not met; there4, resulting in muscle-wasting, illness or possibly death.

Classification of proteins according to

essentiality/source
Essential Aas

Non-essential Aas

Semi-essential or
Conditionally essential Aas

Histidine

Alanine

Cysteine

Isoleucine

Arginine

Cystine

Semiessential

Leucine

Aspartic acid

Tyrosine

=
Conditionally
essential Aa

Lysine

Asparagine

Methionine

Glutamic acid

Phenylalanine

Glutamine

Threonine

Glycine

Tryptophan

Serine

Valine

Proline

NB:
- They are formed in the body from
metabolism of Essential Aas;
Methionine & Phenylalanine, resp.
-If the essential Aa from which they are
formed is in short supply, then they
too become essential (thus, must be
supplied from diet!).
- Ex 1: If the diet is low in cysteine, then

= essential Aa
profile
NB: Must be

NB: They can b made by the body

thro process called transamination; where amino group
from 1 Aa (donor Aa)* is

cysteine can be made from methionine; but

on other hand, if the diet is low in methionine,
adeq. cysteine must be consumed because
there is in-sufficient methionine to make it.
- Ex 2: Cysteine & tyrosine can also become
in-dispensable (essential) in the Neonate,
while Arginine bcomes essential in

Sources of proteins

Proteins in the diet come from both animal & plant sources
Rich pr- sources = mainly animal sources e.g. meat, fish, eggs,
milk
= plant sources e.g. legumes i.e. lentils, beans (esp.
kidney, black, red- beans)
& peas (esp. black-eye & chick- peas)
Other pr- sources = nuts & seeds (though high in fat), and cereal grains (e.g.
wheat, oats & rye)

NB: Some dietary protein sources may also contain small

amounts of CHO or fat.

Proteins cont.

All Aas hv the same basic structure:

a Carbon (known = -carbon) attached to 4 groups of atoms, namely;
-

an Amino group (-NH2)

an Acid group (-COOH)

a Hydrogen atom (-H)

a Side-chain (identified = -R or an R-group); which varies btwn diff Aas and

characterizes each Aa.
NH2
Therefore, the generic formula of an Aa =

COOH

H
The SIMPLEST Aa = Glycine, with R = H atom.
For another Aa called Alanine, its R = CH3, hence its structure is .
Aas can be classified according to the nature of their Side-chains or Rgroups (see next slide)

Classification of Aas according to the

nature of their Side-chains (or Rgroups)
Aromatic
Aas

Aliphatic Aas

Basic Aas

Aas)

Acidic Aas &

their amides

Phenylalanine

Glycine

Aspartic acid

Lysine

Tyrosine

Alanine

Asparagine

Arginine

Tryptophan

Valine

Glutamic acid

Histidine

(=Neutral

(=Neutral Aas;
i.e. pH 7)

Leucine
Isoleucine

= branchedchain Aas

Serine
Threonine

R = - OH
(alcohol group)

Cysteine
Cystine
Methionine
Proline

S groups
in the
R- group or
side chain

Glutamine

Structure of a protein
Process of protein synthesis
Aas are linked by unique chemical bonds
called peptide bonds
A peptide bond is formed btwn the acidgroup C of one Aa & the N on the amino
group of the next Aa.
H
H

H2
N

C
R
I

G
R
O
U
P

O
C

N
I
H

O
C

R
I
G
R
O
U
P

peptide bonds

N
I
H

C
R
I
G
R
O
U
P

COO
H

Structure of a protein
cont.
Formation of poly-peptides

When 2 Aas are linked with a peptide bond = di-peptide

When 3 Aas are linked together = tri-peptide
When many Aas are linked together = a poly-peptide
A polypeptide chain is folded into a complex threedimensional shape, and the shape the protein folds into is
determined by the order of Aas in the peptide chain.

NB: It is the 3-dimensional shape of a protein that determines its function; hence,
if the shape changes the function is altered too. e.g. in sickle cell anaemia a change
in only 1 of the Aas in Hb causes characteristic change in that Hb-molecule.

- A Protein chain = polypeptide backbone + Side-chains

(R-groups)
- Changes in the shape/structure of a protein may be due to; genetic
error (e.g. in sickle cell anaemia) or physical stress e.g. heat, acid, etc.
- NB: This changes in the shape/structure of a protein = DENATURATION (i.e. change from nature).

Physiological functions
of Proteins
Proteins serve several functions in the body e.g. some pr-s are;
key components of structures of the body
- all cells contain proteins as part of their cell membranes & within their cytoplasm.
- muscles, bones, connective tissues, blood cells, glands and other organs in the body are composed of
proteins
- the proteins are synthesised during growth, repaired, maintained & replaced during life.
- proteins form a source of Aas (i.e. Amino acid pool)*; which can be drawn on during emergencies/
trauma (e.g. tear/fractures, burns/inflammation, after bleeding, surgery, fasting, etc) although this will be
the expense of tissues it comes from.

at

enzymes, hormones or buffers

- almost all enzymes are proteins; thus serve in catalysing/facilitating chemical reactions occuring in the
body e.g. enzymes involved in digestion process, reg. of E-production in cells, synthesis of all chemical
substances found in the body, etc.
- many hormones contain Aas e.g. thyroid hormone (regulating metabolic rate); insulin & glucagon (reg.
b/glucose levels); parathyroid hormone (PTH) & calcitonin (reg. calcium levels); cholecystokinin (CCK)*1 &
secretin (reg. in digestion process); adrenaline (in response to stress), etc.
- proteins act s buffers (in the circulation) by accepting or donating H+; hence maintaining fairly constant pH
in
the blood & body fluids. Thus; they contribute to the acid-base balance of the blood & b/fluids.

play a role in immunity, transport of substances around the body, blood

clotting, etc
- proteins are needed for normal cell-differentiation to produce cellular components
- anti-bodies are composed of Aas
Hence; a protein def ----will result in defective/suppressed immune function; clearly evidenced in children
suffering from Protein-Energy Malnutrition (PEM), who hv increased susceptibility to infection due to
poor immune function.

Functions of Proteins
cont.
- many substances which need to b carried around the body are usually insoluble or
harmful, but when attached to carrier-proteins (e.g. albumin or globulin) their transport
is facilitated (without harm to the body); hence, the level of the carrier-protein may
determine or limit the utilization, availability or transport of that substance to the body
tissues.
e.g. Haemoglobin (Hb) = transporting or carrier protein for O2
= reduced availability of Hb either due to iron or protein deficiency ---- affects
provision of O2 to tissues.
- transport proteins also carry substance across cell membranes e.g. during absorption in
the digestive system
- proteins may bind with some constituents of the body providing safe mode of storage
for that constituent e.g. Fe is stored (in association with or ) bound to ferritin.
- some proteins (e.g. prothrombin & fibrinogen) found in plasma hv essential role in
blood clotting; hence, failure to synthesise them (such as due to Vitamin K deficiency) ----- will

cause prolonged bleeding times.

Some Aas produce non-protein nitrogenous compounds

Proteins also = major components of hair, nails & structural

framework of bones.
Proteins can serve as E-source when there is in-adeq. CHO & fats to
meet the bodys needs.

e.g. Glycine is
used in synthesis of haem, nucleic acid & bile acids; while Tryptophan is used for making nicotinic
acid; Tyrosine in catecholamine synthesis.

Balance btwn Amino acid pool & Protein

compartments
urea

NH3

de
am

in
at
io
n

Dietary
proteins

Amino
acid
pool
Tissue
protein
breakdo
wn

ca

N- containing
compounds e.g.
purines
uric acid

- keto

Glycogenic
(CHO)

residues

Ketogenic
(ketones-----fats)

an
ab
oli
sm

l i sm
o
t ab

Plasma
protein
s

Tissue
protein
synthesis

NB: For Aa use to b optimal, E-needs must also be satisfied pref. from CHO & fat sources; hence, described as
Protein-sparing. .

Protein balance
In periods of growth;
anabolism rate > catabolism rate,
so that new tissues can be formed.
In starvation, wasting disease &
aging;
catabolism > anabolism,
so the body gradually deteriorates.

Nitrogen balance

The overall indicator of protein metabolism in the body = Nitrogen balance

Nitrogen balance = Nitrogen intake Nitrogen output (or

losses)

N-balance = +ve; occurs when dietary pr- intake > loss of body pri.e. when pr-s are being retained in the body--- indicating tissue synthesis
N-balance = -ve; occurs when loss of body pr- > dietary pr- intake
i.e. when there is net loss of pr- from the body --- (because or) indicating that
there is catabolism or that protein/energy intakes are in-adeq to meet daily needs
When N-intake & N-output are in equilibrium (i.e. are equal), then that indicates that
proteins are neither being gained or reduced.

But note; Sources of N = pr-N & non-pr- N . Thus, there is some metabolism of non-protein N and
some retention of N may represent/lead to increases in this non-pr-N instead of protein content. However,
it is gen assumed that N in most diets consumed is of protein origin. Hence,

Conversion factor used to convert btwn N-content & Protein content = N x

6.25

This implies that, all proteins contain 16% N

Loss of N from the body can occur thro many ways; e.g.

faecal loss (representing un-absorbed dietary N),

residual N from digestive juices & mucosal cells shed into d/tract,
urinary loss (N lost in urine is in form of urea (mainly), uric acid, ammonia & creatinine. NB: Urea content reflects dietary
intake; hence, urea decreases as protein intake increases. Creatinine levels are relatively constant since they are related to
muscle mass (& represents its daily turn-over).

Skin cells, hair, nails, sweat & saliva

g/kg body weight.

NB: An obligatory daily protein loss for adults = 0.34

Protein Quality
Protein quality = nutritive value of a protein; which depends on
its content of
Essential Aas.
NB:
For a protein to be useful to the body, it must provide all of the
Essential Aas in approp amounts, because the body is unable
to synthesise incomplete proteins.
Otherwise, any reqd pr- synthesis can take place only thro
breaking down some already existing proteins or
alternatively a limited pr-synthesis may occur until when all Aas
present in least amounts get used-up. Then the process of prsynthesis would stop because there will be shortage of those Aas (which
initially were in small amounts); even though Aas which were present in
large amounts may still be remaining. Thus, pr-synthesis would be limited
by those Aas. Hence, such Aas are called limiting Aas, and the
protein from which those limiting Aas is derived would then be
described as a low-quality protein.
When consuming foods with low-quality proteins, it is posbl to
achieve an overall protein balance/quality; by adding to the diet
different plant foods termed complementary foods which contain
the limiting Aas concerned.

The use of complementary foods

to make-up for limiting Aas in
some plant foods
PLANT FOOD

LIMITING Aa

COMPLEMENTA
RY FOOD

Ex. OF A MEAL

Grains (or
cereals)

Lysine,
Threonine

Legumes/pulses

Beans on toast, dikgobe

(samp + beans),
Sorghum grains +
beans, Rice & beans,
Rice & nuts, etc

Nuts & Seeds

Lysine

Legumes/pulses

Chick-peas with
sesame seeds

Soya beans &

other
legumes/pulses

Methionine

Grains; nuts &

seeds

Lentil curry & rice,

Sorghum meal
with lentils,

Maize

Tryptophan,
Lysine

Legumes

Tortillas & beans,

Maize meal &
beans, Maize rice
& beans, dikgobe
(samp + beans),
etc

Vegetables

Methionine

Grains; nuts &

Vegetable & nut-

Measurement of protein quality

Protein quality can be measured using:
a) Chemical score based on Aa-composition of a protein by comparing;
Amount of each EAas in a Test-proteins vs Amount of the same EAas in
a Reference-protein
i.e.

Chemical Score = EAa in test-pr / EAa in ref-pr x 100

Traditionally; Reference proteins = Milk or Egg proteins (bcos their Aas patterns
conform most
nearly to that of total body protein)
Recently; Standard protein = Human milk-protein (against which all other proteins
can be judged/measured for their efficiency in meeting human body needs)
Ref scoring pattern for the most freq. limiting Aas:

Amino acid
Leucine

19

Lysine

16

Threonine
Valine

Ref. Score (mg Aa/g

protein)

9
13

Methionine
Cystine
17vs Ref (or Std) proteins
CS = value
of ratio+for
the limiting Aa in both the Test
CS = v. theoretical bcos calculations do not account for the digestibility/availability of
the proteins

Measurement of protein quality

cont.

b) Biological value based on the Nitrogen balance; whereby

- Test protein is fed to the experimental animal as only source of pr- , then
- nitrogen retention & nitrogen loss(urinary + faecal N) are measured
- if N-retention > N-loss, (i.e. +ve N-balance); this indicates that more protein hs bn used in the body
- BV = measure of how efficiently a protein can meet the bodys needs,
hence

BV = Nitrogen retained/ Nitrogen absorbed x 100

more precisely;

BV =

Dietary N (Urinary & Faecal N)/[ Dietary N Faecal N] x 100

NB: - For Egg protein BV = 100; for fish & beef protein BV = 75
- BV 70 - can support growth, as long as E-intakes are adeq.
- Protein reqnts are calculated on basis of N-balance studies; which estimate
Amount of high quality protein (milk or egg pr-) needed to meet equilibrium
c) Net Protein Utilization (NPU) based on BV & degree of digestibility of the
protein
d) Protein Efficiency Ratio (PER) based on wt-gained by a growing testanimal/its
dietary protein intake

DRVs for proteins (for

adults)
GENDER/AGE

EAR (g/day)

RNI (g/day)

Males: 19 -50 yrs

> 50 yrs

44.4
42.6

55.5
53.3

Females: 19 -50
yrs
> 50
yrs

36.0
37.2

45.0
46.5

NB: DRVs are calculated on the basis of 0.75g pr- / kg body-wt per day

Health aspects of proteins

1) Protein Energy Malnutrition (PEM)
Protein deficiency disease which mostly occur in children
2 classic forms of PEM = Marasmus & Kwashiorkor
Signs: growth failure of the child esp. a slowing of linear growth resulting in stunting, child
looks miserable & irritable, likely to be liver-enlargement (why????), posbly oedema, changes
in hair & skin, there may be sunken eyes & signs of Vit A def. on eyes, increased susceptibility
to infections, co-existence of infection & malnutrition leading to death.
Main cause of these signs = low protein intake (which results in many of those signs)
= low albumin levels responsible for the oedema
= im-balance of Aas (since this PEM syndrome does not occur in areas with
high consumption of
wheat, but common in areas where staple foods =
maize, plantain, cassava & yams)*
= suppression of immune responses & reduced T-lymphocytes levels.leading to
increased
risk of opp. Infections & poor recovery.

Dietary management; restoring nutritional status by ensuring adeq. Protein & Energy intakes, treating
electrolytes im-balances (while also treating infections & hypothermia, educating the whole family about
nutrition & health for long-term improvements & prevention of the condition from recurring).
Other vulnerable groups (besides children)
= Hospitalised patients (e.g. co-existence of pre-existing illness, poor appetite, surgical or medical
treatment &
prolonged hospitalisation may result in in-adeq nutrient intake
and occurrence of
protein catabolism.leading to protein def.)
= Traumatised indivs (catabolic responses to trauma increases pr- breakdown, hence contributing to ve
N-bal)
= O/wt patients (adiposity may mask muscle wasting, so, the ve N-bal. may persist for some time being
recognised & action being taken); hence

Health aspects of
proteins
cont.
..Other measures to taken incl:
Weighing in-patients (hospitalised patients) regularly;
Assessment of their Nutritional status (esp. Mid-Arm Muscle Circumference
(MAMC), grip strength or plasma albumin levels which relate to body protein);
Careful monitoring of at-risk in-patients (with medical team aware of
potential problems)

2) Chronic Renal Failure (CRF)

- high protein intake (esp. consuming 2 x RDA proteins)*, puts extra
work on kidneys (and liver)
because N in excess of need (from excess printake) should be excreted and that reqs
increased production of urea
which contributes to de-hydration &
.conseq leads to kidney failure [NB: N protein intake]

3) Increased fluid needs

High protein intake causes increased fluid needs because
protein metabolism reqs ~7 times more water than CHO or fat metabolism
Increased urea (produced during protein breakdown) would req. large
amounts of water for its excretion in urine.
Also to prevent the dehydration emanating from the increased urea
production, there would then be need for increased fluid intake.

Health aspects of
proteins cont.
4)

Phenylketonuria (PKU)
= genetic disorder* in which enzymes (made of pr-) needed to convert
phenylalanine
(essential Aa) to tyrosine (semi-essential Aa) are not functional.
Instead, phenylalanine is converted to phenylketones, which then
accumulate in the
blood & may cause brain damage when they reach high levels.
infants should be tested at birth for PKU, &
those at risk should be restricted from high dietary phenylalanine from
birth to
prevent severe brain damage which can be caused by PK.
- indivs with PKU must consume a diet with just enough phenylalanine to
meet body needs for protein synthesis, but not more than reqd by the body
- the diet must also provide extra tyrosine since the disease prevents
conversion of phenylalanine to tyrosine
- special low-phenylalanine or phenylalanine-free formulas are available for
use by
infants with PKU
- pregnant women with PKU should consume low-phenylalanine diets to
protect the
fetus from exposure to high phenylketone levels and the conseq. mental
retardation & other birth defects.

Vitamins

Vitamins = group of organic compounds needed in the diet in small amounts (e.g.
in mg
or micro-grams) to promote & regulate chemical reactions in the
body; thus;
vitamins are essential organic nutrients
= provide no E (but may help in reactions that produce E from CHO, fats &
proteins, e.g. B1, B2 & B3, hence their amounts reqd in the body directly related to E-reqnt )
In brief; Vitamins = essential organic and non-energy- yeilding nutrients
(NEYN) reqd
chemical reactions.

in the body in only v. small quantities to promote & regulate

General overview of vitamins:

1) Specific characteristic features
Vitamins are:

organic and can be readily destroyed (unlike minerals)

essential i.e. needed from diet (cannot be made by the body, & but their absence/def
can lead to failure of some body functions)
gen. work individually; but some vitamins work in co-operation with others & can
replace or spare each other to some extent due to having similar effects.
present in food in small amounts & needed in those small amounts
grouped/classed according to their solubility in water or fat; this feature
determines how they are absorbed, transported, excreted & stored in the body
e.g. Fat soluble vitamins = Vitamin A, D, E & K while,
Water soluble vitamins = Vitamin B1, B2 ,B3 ,B6, B12, C, Folate, Biotin &
Pantothenic acid

General overview of vitamins cont.

2) Factors affecting bio-availability of vitamins
NB: Bioavailability = how well a nutrient can be absorbed & utilised by the body

Mode of absorption - some vitamins are easily absorbed by simple diffusion* (e.g. water-soluble
vits),
some by facilitated diffusion and yet some by active transport
Specific conditions in the gastro-intestinal tract
e.g. - presence of bacteria (reqd for absorption of vit K, biotin & pantothenic acid)
- bile (for fat soluble vitamins absorption),
- digestion enzymes, etc

The need for binding medium

e.g. - Vit B12 absorption reqs a protein to bind to (which is produced by the stomach)
- Fat soluble vitamins (FSVs) are absorbed along with dietary fat.
(whereas; Vit C on the other hand is easily absorbed without the need for any medium)
- Once in the body, FSVs are transported in the blood bound to carrier proteins; hence, the
amount of these vitamins delivered to body tissues (where they will be used) depends on the
availability, efficiency & amount of those carrier proteins.
- Most of the water soluble vitamins (WSVs) - should also bind to proteins in the blood for transport

The need for conversion from pro-vitamin or precursor forms to active form after
entry into cells
e.g. from ~ 50 provitamins for vitamin A; the quantity of the active vitamin A available for use by the
body is
dependant on the quantity of the provitamin to be converted & the rate of conversion of
the provitamin.

The ability to store & excrete the vitamin also regulates the amount allowed to be present in
the body
e.g. B-complex vits & vit C not stored in the body to any great extent & are easily excreted via urine;
hence their supplies are rapidly depleted & must regularly be included in the diet; yet their def.
symptoms do not develop immediately when these vits are not included in the diet. Conversely, ..

General overview of vitamins cont.

Conversely,

FSVs are retained in the body for longer duration & it gen takes
longer to develop
their def, but their risk of toxicity is
greater.

Fat soluble vitamins

Vitamin A

There are many compounds related to vitamin A, since they posses vitamin A activity; thus
3 forms of Vitamin A = RETINOL, RETINOIC ACID & RETINAL collectively called
RETINOIDS.
NB: - RETINOL = pre-formed vitamin A
= primary alcohol with high molecular wt (C 20H29OH) & derives its name from
its nature of being an alcohol & its specific function in the retina of the eye.
- There is inter-conversion btwn Retinol & Retinal
i.e. RETINOL
RETINAL
- Once RETINOIC ACID has been formed, it cannot be re-converted (to RETINAL).
There are pro-vitamin A compounds called CAROTENOIDS e.g. beta-carotene (-carotene)
Carotenoids can be converted to RETINOL (varying degree of efficiency)
i.e. CAROTENOIDS
RETINOL
Carotenoids are found in plant foods & they account for the red, green or yellow
pigments in many f/vegs e.g. carrots, dark green leafy vegs, broccoli, red peppers,
tomatoes, apricots, peaches, mangoes, etc.
-carotene = most important carotenoid bcos it provides ~ (67%) of Vitamin A needed in human
nutrition & is original substance (i.e. pro-vitamin A) from which the animal sources of vitamin A are derived
thus

the

= Animals consume plants containing the -carotene pigment, then in the bodies of those
animals -carotene is converted to Vitamin A. Then we consume that Vitamin A from those animals
= The remaining -carotene not converted to Vitamin A, is absorbed & transported dissolved in
fat - part of the lipo-proteins (e.g. VLDL, LDL & HDL).

Inter-conversion btwn
Vit A & its related
compounds
VITAMIN A

RETINOIDS
e.g. Retinol, Retinal & Retinoic acid

CAROTENOIDS
e.g. -carotene, -carotene & -carotene

Physiological functions of Vit A

1) Vision Eyes ability to adapt to changes in light depends on the light-sensitive pigment in the rods
of the retina called
RHODPSIN (or visual purple).
NB: RHODPSIN = RETINAL + OPSIN (where retinal = form of Vit A, & Opsin = protein)
- In daylight; when light strikes Rhodopsin, 11-cis RETINAL (in rhodopsin )
ALL trans RETINAL; hence,
triggering series of complex changes which initiate & propagate a
nerve impulsewhich is then
detected by VISUAL CORTEX.
NB: This happens continuously in daylight, so that Rhodopsin is constantly broken down.
Most of our daylight vision comes from changes occuring in pigments in the CONES.
- In darkness (or when blinking); ALL trans RETINAL
11-cis RETINAL; hence
causing Rhodopsin synthesis
& a series of complex changes and detection by VISUAL SIGNALS
NB: On entering a dark-room, rhodopsin is re-synthesised v. quickly (provided there is adeq supply
of RETINOL/ RETINAL available). Then, one becomes accustomed to the dark, hence can see
again*.
BUT, if there is in-adeq RETINOL/ RETINAL to restore rhodopsin dim-light vision fails
(i.e. Night blindness)
- GEN; When Vit A is def in the body, rhodopsin cannot be made.RODS & CONES of the
retina become
increasingly sensitive to light changes .causing Night blindness.
- TREATMENT: Vitamin A rich foods or injection of retinol (Vit A precursor)
. RETINOL
RETINAL
Rhodopsin Good night-sight.

2) Cellular differentiation - RETINOIC ACID = major form of Vit A involved in GENE EXPRESSION
& control of CELL DIFF.
- GENE EXPRESSION; RA binds to specific binding site on cellular nuclei & interacts with DNA, then
RA controls
synthesis of proteins in the body & gene expression.
- CELL DIFF (esp. diff. of epithelial cells e.g. which line the conjuctiva of the eye, trachea & lungs,
digestive tract , urethra & bladder); RA ensures the mucus-secreting properties of the epithelial cells
to maintain
their integrity & functions.

Physiological functions of Vit A

cont.

Hence, RA deficiency ..Dry & flat epithelial cells, which in the case of the;
body part

Disease condition caused*

eye

Dry eye = XEROPHTHALMIA (i.e. dried & hardened cornea due to no tears
produced, no lysozyme to keep cornea cleanhence susceptible to infections
resulting in CONJUCTIVITISthen to BITOT SPOTS (i.e. damaged patches);
if not treated .KERATO-MALACIA (with involvement of entire cornea & full
breakdown of eyeball; often linked to more acute def.) & Blindness (loss of
sight) occur.

skin

Keratinisation i.e. hardened epithelial cells form keratin(=pr- that forms dry
scale-like tissues) or follicular hyperkeratosis (roughened skin)

respiratory
tract

-ciliated epithelium in the nasal passages driescilia is lost; hence, No barrier

to entry of infections
- salivary glands dry up (due to no saliva & lysozyme)
-mouth becomes dry & cracked; hence vulnerable to invading infections

gastrointestin
al tract

- mucosal membrane secretion decreases.hence, tissues dry & slough

off adversely affecting digestion & absorption

genito-urinary
tract

- epithelial tissues breakdown.increasing urinary tract infections, vaginal

infections

tooth
formation

- specific epithelial cells surrounding tooth-buds in fetal gum-tissues fail

to dev; hence, Amelo-blasts [i.e. specialised cup-shaped organs which form
enamel of the developing tooth] do not form properly (they become flat &
dry)therefore, No enamel will form (for the tooth that is supposed to dev
after the baby is born)

Physiological functions of Vit

A cont.
3) Growth vitamin A is reqd for normal linear growth by regulating bone re-modeling
(bone
resorption & deposition); hence, in VAD.bones thicken
(instead of linear or bone growth) &
in the case of the skull, the thickening
bones can cause pressure on the brain & cranial nerves.
- Also, Vitamin A participates in tunneling out the old bonemaking way for the
new bone;
thus, growth & maintenance of the bone which req. constant remodeling of bone tissues.
4) Anti-oxidant role CAROTENIODS [e.g. -carotene & lycopene (found mainly in
tomatoes)] have antioxidant role i.e. the quenching of free radicals
reactions (esp. oxygen singlets).
Thus, they prevent chain
rxns which could lead to lipid-peroxidation (=precursor
of the disease process)
.CHD or to damage of DNA..resulting in CANCER.
5) Reproduction RETINOIDS (esp. retinol & retinal; but not retinoic acid)

support normal
sexual maturation during adolescence & are necessary
for normal function of the adult reproductive system. Therefore, VAD can
cause glandular
degeneration & sterility.
6) Immunity Vit A has important role in immunity esp. T-lymphocytes
function & Antibody
response to infections.
NB: Children with VAD are vulnerable to MEASLES & INFECTIONS of
the Respiratory & Gastrointestinal tracts. These = severe infections that
further depletes Vit A make the child more likely to die.

Summary on Vit A
functions
Role in visual adaptation to light &
darkness;
hence Vit A has
function that influence; - - vision
Role that influence or promote;
the health of body coverings & linings
(epithelial linings)
process of growth
anti-oxidant capacity
reproductive functions
immunity

Factors that can alter Vit

A reqnts in the body
Amount of Vit A stored in the liver

Large amounts of Vit A can be stored in the liver. For instance;

LIVER RESERVES = 90% of the total body Vit A; hence, mean daily intake is reqd to maintain a liver conc. of
20g/g

Form in which it is taken

(e.g. as Vit A, Retinoids or

Carotenoids)

Illness or infections
Gastrointestinal or hepatic defects

Causes of VAD
In-adeq. intake
In-adeq. conversion of carotenes due to
liver disease or intestinal disease
Poor absorption due to lack of bile or
defective absorbing surfaces

TOXIC EFFECTS OF
EXCESS VIT A

- Since large amounts of Vit A can be stored in the

liver, it is posbl to consume potentially toxic quantity
of Vit A (esp. via taking mega-dose vitamin supplements!!!)
- Some of the toxic effects of Vitamin A include:
HYPER-VITAMINOSIS A
.whose symptoms incl; joint pains, thickening of
long bones, loss of hair, double vision, vomiting,
headaches & jaundice
LIVER INJURY/DAMAGE
.leading to portal hypertension & ascites.
BIRTH DEFECTS
Concern: In early preg, high doses of Vit A (i.e. > 3000g/day)* can harm the
embryo causing
birth defects (TERATO-GENESIS).

- Acute poisoning can also occur when consuming polar-bear

liver (which has excessively high amount of Vit A compared to livers of other animals e.g.
calf, sheep, pig, etc = good sources of Vit A).

VITAMIN D

Wrongly classed as vitamin because it can be synthesised in the body (on human skin); however,
under certain circumstances it cannot be made in the body e.g. when there is in-adeq exposure to
UV light of = 290 320 nm.
Vit D = pro-hormone of sterol made in the skin when there is adeq exposure of UV light of =
290 320 nm
Its precursor base in human skin = 7-dehydro-cholesterol
2 forms of Vit D = ERGO-CALCIFEROL (Vitamin D2) found in yeast, ergot (fungus growth on rye & other grain
cereals)

&

= CHOLE-CALFEROL (Vitamin D3) found in skin, fish-liver oil, animal fats;

Vit D3 is made from

cholesterol

Active form of Vitamin D = 1,25 di-hydroxy-cholecalciferol i.e. 1,25 (OH)2D3

= Calci-tri-ol
= active hormonal form

Vitamin D Formation: Stage 1:

Stage 2:

Vitamin
D3

i.e. 7-dehydrocholesterol

-OH added to D3 @ position

25 on the side chain (in the liver)
forming

25-OH D3

-OH added to 25-OH D3 @

position 1(in the kidney,
catalysed by renal enzyme; 1--hydroxylase )

forming

1, 25
(OH)2 D3
i.e. Active Vitamin D

Chemical structure of Vit

D..
indicating formation of active Vit D:

OH

25

OH
1

HO

2nd activation (occurs

in kidney)

1st activation
(occurs in liver)

Vitamin D formation cont.

Some of Vit D from the diet (i.e. ~50% of dietary Vit D) leaves the digestive
system in the lymph to the LIVER (in the chylomicrons with chylomicron
remnants); while also
Some of the in-active Vitamin D 3 (7-dehydrocholesterol) is synthesized in the SKIN
& diffuses into the BLOOD. Then, it is picked up by some Vit D Binding Proteins
(DBP), which transports that Vit D3 to the LIVER.
In the LIVER; Stage 1 of Vit D formation occurs, then from the liver still DBP
transports the product to the KIDNEY for Stage 2 of the formation process of active
Vit D to be done by a renal enzyme called 1--hydroxylase (which catalyses the
reaction).
NB: Some in-active Vitamin D 3 are not bound to the DBP, but remain FREE and are
deposited in the fat & muscles.
The process of active-Vit D formation is tightly controlled in such a way that it
maintains/ensures Calcium homeostasis..Thus,

When Ca levels are low, that increases activity of PTH which in turn activates 1-hydroxylase; which then catalyses the addition of OH @ position 1 of 25-OH D3 to form
active Vit D. Then the active Vit D.leads to more Ca absorption (by stimulating synthesis
of Ca-binding-proteins), which increases Ca plasma levels. When plasma Ca levels reach
normal levels, PTH stops being released.
On the other hand, when Ca levels are high, PTH (in the kidney) stimulates rmal Ca
withdrawal from the bone & stimulates excretion of Phosphorus in urine. Then, high levels
of P inhibit Vit D formation (in the liver & kidney); by rather performing an alternative
hydroxylation @ position 24 on the 25-OH D3 (instead of position 1). Therefore, 24, 25
(OH)2 D3 is formed, not active Vit D; hence, switching off production of active Vit D.

Summary: How Vit D formation is controlled

to ensure Ca homeostasis
Ca levels

More Caabsorption

+
1--hydroxylase
(enzyme)

PTH activity

which causes

Active Vit D
1,25 (OH)2 D3

Normal
Ca levels
PTH stop being
released.

forming

Catalyses the addn

of OH @ position 1
of 25-OH D3

Summary: Vit D formation controlled in

such a way to ensure Ca homeostasis
Ca levels

PTH

Ca withdrawal

+
P excretion via urine

Reduced Caabsorption

Normal
Ca levels

which stops Vit D

formation process

24,25 (OH)2 D3
(instead of active Vit D)

forming

High P levels causes

the addn of OH @
position 24 of 25-OH
D3 (instead of @ position 1)

Vit D cont.
If there is in-adeq 25-OH D3 brought to the
kidney from the liver OR the kidneys are
diseased (e.g. chronic renal failure), then more
Parathyroid hormone (PTH) will continue to be
secreted & accumulate in the kidney.leading
to HYPER-PARATHYROIDISM (= sign of Vit
D deficiency).
SOURCES OF DIETARY VITAMIN D

= liver, oily
fish, eggs, milk, fortified margarine & low-fat spreads, butter,
breakfast cereals, evaporated milk, yogurt & infant foods
Other source = fish oil supplements taken as prophylactic
treatment of rheumatism & joint pains

Physio Functions of Vit D

NB: The most notable target tissues for Vit D function = INTESTINE, BONE & KIDNEY.
1) Vit D can cause increase in Ca plasma levels in the;
a) Intestine - Vit D stimulates synthesis of Ca-binding-proteins which are needed for Ca absorption. Also, Vit D
stimulates P absorption in the intestine.
b) Bone - *The presence of both Ca & P then stimulates their deposit in the bone tissue. Thus, allowing approp
amount of those minerals to be available in the bone for bone synthesis while simultaneously
facilitating
their release to maintain plasma levels (i.e. the Ca-P balance in the blood)
c) Kidney Vit D in the kidney promotes Ca re-absorption into the blood to maintain Ca levels.
NOTE: Before the role of kidneys on Vit D & bone metabolism was fully established or known, patients with
kidney
diseases developed un-explained bone diseases. But currently: To prevent these problems (bone
& kidney diseases), treatment with Vit D is administered. E.g. Osteo-dystrophy characterised by defective bone
formation = 2ndary

disease to kidney failure.

2) New role of Vit D have been found in the;

a) Brain e.g. Cellular differentiation & growth: Vit D is involved in basic cell-processes on tissues of these
organs
brain , kidney, liver, skin, reproductive tissues, hormones,
etc.
- Immuno-regulation: Vit D is also involved in cell-processes such as in secreting glands & some
cells
of the immune system
b) Nervous system Vit D receptors hv recently been discovered.

3) Vit D contributes to prevention & treatment of the following Vit D def. diseases;
a) Osteoporosis characterised by loss of bone & bone fracture; =abnormal thinning of bone leading to
porous, fragile, lattice-like bone tissue with enlarged space; hence prone to bone fracture or bone deformity.
b) Osteodystrophy = disease secondary to kidney failure, characterised by defective bone-formation.
c) Osteomalacia - characterised by soft & de-mineralised bone (i.e. poorly calcified bone); But = normal
amount of bone, bowing of spine + diff. in walking, muscular weakness & bone pain, with un-mineralised
areas & loss of bone detail, low plasma Ca & P levels and raised plasma alkaline phosphatase. (Common
among adults)
d) Rickets - characterised by bent limb-bones under body wt; spine curved, pelvis & thorax may b deformed (common among
children).

Vulnerable groups to Vit

D Def.

People staying in the farthest poles of the earth* where sun rays (of UV light =
290 320 nm)
hardly reach the earth surface there.
People who cover their entire body most of the times.
Elderly people house-bound or institutionalised (e.g. in nursing homes)
Bed-confined patients
Pre-mature infants
Indivs with malabsorption diseases (e.g. of fat, Vit D, Ca, etc)
NB: Malabsorption of Vit D & Ca commonly occur in Coeliac disease, or as conseq. of
gastrectomy & intestinal by-pass surgery.

People with diseases involving the parathyroid glands, liver or kidney.

Those treated with anti-convulsants (why?) they decrease bioavailability of nutrients
(vit D incl) hence increase the reqnt for Vit D. There4, less Vit D available to do its physio functions e.g.
Ca absorption.

Indivs with high incidence of

strict vegetarianism; since diet with large amounts of NSPs &
phytates consumed (often to compensate for meat & its products) may reduce
Ca absorption
culturally predominant use of few dairy productswhich results in
low dietary Ca intake.

Vit D Toxicity
Excess cholecalciferol can be TOXIC!
Effects of excess vit Ds* include:
Loss of appetite
Thirst
Increased urine output
Increased Ca levels.hence, Ca deposits laid down
on soft tissues (i.e. calcification s/tissues)
NB:
- Vit D toxicity may be caused by: regular intake of
50g Vit D/day
(often from supplements)
- This toxicity is common in children due to accidental
ingestion of Vit D supplements.

DRVs for Vit D

= 10 g Vit D per day
= Only for people
- not receiving enough sunlight exposure
or
- people with special needs e.g. preg.
women, lactating mothers, people of
Asian origin (esp. women & childrenwho cover most of the body)

Vitamin E

Vitamin E consists of a group of substances belonging to 2 closely related families;

= Toco-pherols & Toco-trienols

Each of these 2 families exists in a no. of isomeric forms; -, -, - and - forms, totaling to 8 different members of the Vit E group.

The most important member of which = - tocopherol (with the greatest potency & contributing 90% Vit E activity in the body tissues; hence, - tocopherol = representative of Vit E) Chemical structures of Tocopherol &
Tocotrienol:

The OH group on ring structures of both tocopherol & tocotrienol makes them v. effective H+ donors; When Vit E donates H+, it becomes oxidised* while preventing the oxidation of other more metabolically important
substances found in the cell membrane (e.g. PUFAs) from forming lipid-peroxides that serve as free radicals (which may cause oxidative damage to the membranes). Thus, Vit E has an anti-oxidant role (see next slide)

 The H+ reacts with free radicals (e.g. lipid peroxides),

hence rendering them in-active & unable to cause
oxidative damage to lipids or proteins in the body.
Thus; the free hydroxyl group on the aromatic ring is
responsible for the antioxidant properties. The
hydrogen from this group is donated to the free
radical, resulting in a relatively stable free radical
form of the vitamin.

Characteristic features &

Sources of Vit E
Characteristic features
Vit E =
a pale yellow oil
stable to acids
insoluble in water, but soluble in fats
oxidises v. slowly; hence hv anti-oxidant role & wide clinical applications
Absorption rate decreases as dosage (intake) increases; hence, large dosage of
supplements will provides only 10% Vit E absorbed.
In plasma, Vit E is transported in LDL* & is concentrated in cell membranes.
Therefore, highest conc. of Vit E = in adipose tissue, & level of Vit E in adipose
tissue increasing Vit E intake.

Sources of Vit E
- tocopherol = found in Only Animal fats in v. small amounts e.g. poultry, fish, eggs. Hence,
animal products are gen. not good sources of Vit E.
Other isomeric forms of tocopherol & the tocotrienols = found in plant sources e.g. whole
grain cereals (rich source of tocotrienols), breakfast cereals fortified with Vit E (check food
labels), green leafy vegs, some fruits & nuts, margarine made from veg/seed oils* (although
amounts of Vit E in them differ).
NB: Veg Oils = richest source of Vit E, BUT also, Veg oils = richest sources of PUFAs
(which are antagonist to Vit E; since Vit E functions to prevent oxidation of PUFAs into lipidperoxides that serve as free radicals).
Therefore, the ratio of Vit E: PUFAs is v. important in nutrition & should be 0.4 mg
Tocopherol per 1g dietary PUFAs.
But, DRV for Vit E = 4mg for men & 3mg for women.

Physio functions of Vit E

1. Anti-oxidant role; NB: in the a/o role of Vit E, there is interaction
btwn Vit E & other nutrients e.g.
a) Selenium Se-containing enzymes provide an added defense
because even when Vit E intake is adeq., some cell-damaging
peroxides can still be formed, hence a 2 nd line of defense is reqd
to quench them. Therefore, Se is often used for that defense.
Thus, Se spares Vit E by reducing Vit E reqnts and vice versa.
b)Vitamin C is involved in the re-generation of Vit E
NB: Vitamin E = v. important (much needed) where there are large
amounts of oxygento prevent singlet oxygen atoms (free
radicals) from forming e.g. in the lungs & RBCs. Also, these are
parts exposed to env. pollutants which may contain f/radicals;
therefore, Vit Es protection is essential.
2. Vit E = essential in maintaining the cell membranes by
contributing to the INTEGRITY, STABILITY & FUNCTION of the cell
membranes esp. of liver, heart, skeletal muscles, adrenal glands,
lungs & adipose tissue (organs or tissues that usually contain Vit E).

Vit E Deficiency (VED)

People vulnerable to Vit E def

People with FAT MALABSORPTION* e.g. due to

Liver disease
Pancreatic or biliary disease
Cystic fibrosis
Coeliac disease
People with increased needs or un-met needs e.g.
pre-mature infants (since they would hv had received little Vit E via
placenta & have increased
needs because of growth or
exposure to high oxygen levels in incubators)

adults exposed to high f/radical load e.g. smokers & those

working in polluted env. such as mines or chemical factories.
people consuming high levels of PUFAs in their diet; hence need
for protection by a/o e.g. Vit E

Signs of VED
NB:
- sometimes called the neurological syndrome of VED
- The syndrome is associated with functions of the NS, & main nerves involved = Spinal
cord fibres (that affects PA e.g. walking) & Retina of the eye (which affects vision).
- These signs are also rare.

1. Red cell haemolysis

When Vit E is deficient, lipid membranes of RBCs are

exposed to oxidation of their structural PUFAs. Then, membranes are broken, contents
of RBCs split out/lost (e.g. Hb), and the cells (RBCs) are destroyed. Continued loss of
RBCs .leads to ANAEMIA esp. Haemolytic anaemia*

2. Oedema

due to increased permeability of the membranes.

3. Neurological symptoms e.g.

loss of muscle coordination VED disrupts synthesis of myelin (protective fat
covering) for
along to the
Vit E reqnt**]

long axons of nerve cells that help pass messages

muscles they serve. [NB: Older people hv increased

impaired vision & speech VED causes pigment degeneration of the rods &
cones in the
critical for

retina because they are rich in PUFAs, hence Vit E is

preventing oxidative stress/damage.

High Vit E intake

Currently, no evidence of harm
(Vit E = only fat soluble vitamin with no toxic effect known in humans)

NO
T

RE
CO
M

ME
ND
ED

Other claims recommended

Improved sports performance

Slowed aging processes
Cure for muscular dystrophy
Improved sexual potency
Prolonged cardiac function

e.g.

Vitamin K
A no. of compounds have been identified as having Vitamin K activity & are
classed as members of the naphtho-quinone family. Thus,
Most important forms of Vit K =
1) Phyllo-quinone (K1)
=
=
=
=

found in plants
most important naturally-occuring members &
major form of Vit K
C3H46O2

Sources = g/leafy vegs (e.g. broccoli, cabbage, spinach, Brussel sprouts, peas, margarine
based
on soy-oil, tea, etc)

2) Mena-quinone (K2)
= synthesised in the body by intestinal flora (in the colon & some in GI tract).
= contributes ~ 1/2 of our daily supply/intake of Vit K.
Sources = found in the colon & GI tract*; hence, dietary source reqd e.g. animal foods
esp. liver; other meat & dairy products - hv smaller amounts

3) Mena-di-one (K3)
= synthetic compound (or copy) widely used in animal feeds,

but no longer used in clinical

medicine

= water-soluble analog** that does not reqs bile for absorption since it goes directly into
the hepatic portal veininto the blood system, then carried to the liver to be activated &
released with other forms. Then all Vit K forms are carried in LDL to target sites (where they
perform the redq functn)

Physiological functions of Vit K

1) Catalyses the synthesis of the 4 blood-clotting factors (in the liver) namely;

Vit2 K
Prothrombin (i.e. factor II); e.g. Glutamic acid + CO

Prothrombin* (-

carboxy-glutamate)

Factor VII
Factor IX
Factor X
2) Helps to prevent haemorrhagic disease in new-born babies; hence, new-born
babies are usually given Vit K injection soon after birth, because the sterile intestinal
tract of new born cannot supply Vit K during the 1st few days of life until normal
bacterial flora develop in the intestinal tract. Therefore, during this immediate post-natal
period haemorrhagic disease can occur in the new born with spontaneous bleeding that
can happen in the brainleading to brain damagethen death.
3) Vit K is used in Vit K supplementation to increase bone density in osteoporosis.
NB: Osteo-calcin = (found in the bone), = another gla-protein i.e. Vit K dependent,
reqd for normal binding of Ca in the bone matrixincreasing bone density in the
prevention of osteoporosis.
Besides the bone, other Vit K-dependent gamma-proteins are found in other organs thro
out the body (whose roles are not yet clear).
4) Vit K is usually given before/after surgery related to fat malabsorption e.g.
Before surgery, patients with bile-duct obstruction are given Vit K to prevent prolonged
blood-clotting time caused by failure in Vit K absorption (due to any defect in fatabsorption). Also, After chole-cystomy, Vit K is not readily absorbed because
cholecystomy hinders normal bile-release. However, Vit K needs bile & fat for its
absorption, therefore Vit K is given to the concerned patients.

Physiological functions of Vit K

cont.
5) Vit K may be used as a balancing anti-dote
a) to anti-clotting drug (e.g. bis-hydroxycoumarin or di-cumarol) used in the
mngt of b/clotting time (such as when treating conditions e.g. blood clots in
the lungs or blood vessels); because this anti-clotting drug = an antimetabolite* to Vit K (i.e. it mimics Vit K but inhibits the action of Vit K in
blood clotting).
b) During extended/prolonged use of antibiotics** because prolonged use
of mineral oil laxatives or antibiotics causes a reduction in intestinal bacteria
(which are the bodys main source of Vit K esp. mena-quinone, K2). Hence
reduction in intestinal bac .leads to reduced Vit K in the body. Therefore,
Vit K should be used as a balancing anti-dote.
NB: - Persons who are taking anti-biotics (who are fed by tube or Total
Parentereral Nutrition
TPN) for long periods OR
- Persons with biliary obstructions OR
- Persons with chronic malabsorption disease (e.g. fat malabsorption due to
liver, biliary or

pancreatic diseases)

need monitoring & therapeutic supplementation

of Vit K

Vit K deficiency
Almost never occurred due to dietary
lack in adults.
But, may occur due to fat
malabsorption, chronic use of mineral
oil laxatives or antibiotics, poor intake
esp. in anorexia nervosa, etc.
May occur in new-born infants* due to sterile
intestinal tract at birth or low Vit k levels in breast milk; hence infants @ risk
of haemorrhagic disease of the new-born with spontaneous bleeding
which can occur in the brainleading to brain damagethen death
(mortality).

DRV for Vit K

Diff. to set bcos of in-determinate (or
varying) amounts of bacterial synthesis in
the colon/intestine; hence,
Conc.'s of Normal b/clotting factor =
indicator for adeq status of Vit K; which is
Usually achieved thro daily intake of 1g
Vit K/kg body wt per day (in adults) &
Prophylactic Vit K rec. in all infants.

Vit K toxicity
Not been observed even when
large amounts of Vit K were taken
over extended periods but caution
need be taken!

Water soluble vitamins

Vit B1, B2, B3, B6, B12 & C, Folic acid, Pantothenic
acid and Biotin

include

Characteristics of WSVs:
Soluble in water; hence,
Absorbed into portal blood (i.e. via hepatic portal vein)
Excreted in urine when present in excess
Have limited storage capacity in the body (EXCEPT Vit B 12) & most reserves in the
body are found in association with enzymes; where the Vit = plays a co-factor role.
More readily lost during food preparation e.g. on heating esp. in water or on
exposure to light & air
WSVs (except Vit C) = belong to B-complex group because they;
- share similar functions e.g. they facilitate in E-release (e.g. B1, B2 & B3), and
are involved in inter- conversion btwn diff groups of metabolites
- often work together (i.e. they co-work), hence broadly described as co-factors
in metabolism e.g.
folate & Vit B12 involved in cell-division
B6, B12 & folate (with Aas e.g. methionine & cysteine) ---- in prevention of the
build-up of
homo-cysteine in the blood that can lead to risk of
atherosclerosis (CVD)

Summary of WSVs
vitamin

Major functions

Def disease

Toxicity

B1
(thiamin)

- Coenzyme* (TPP) in
glyco-lysis & in TCA
cycle;
- nerve function

- BERIBERI; nerve
tingling, poor
coordination,
weakness, heart
effects

Weakness,
headache,
irritability

B2
(riboflavin
)

- Coenzyme (FAD,
FADH2, FMN) in TCA
cycle
- e- transp. chain
- Fat metab

Inflammation of
mouth & tongue

None (reported)

B3
(niacin)

-Coenzyme (NAD, NADP,

NADH, NADPH) in glycolysis;
- e- transp. chain
- Fat metab

- PELLAGRA:
dermatistis,
diarrhea,
dermentia

Flushing, nausea,
heartburn

vitamin

Major functions

Def. disease

B6
(pyridoxin
e)

- Coenzyme (PLP) in
protein metabolism
- neurotransmitter
synthesis (e.g. histamine,

Headache, sore tongue, - Nerve

nausea, vomiting, nerve destruction
changes e.g. irritability or

dopamine & serotonin; from

tryptophan) &

-Anaemia

- Hb synthesis

Toxicity

depression, confusion & convulsions

(esp. in infants)

(due to reduced
haem synthesis caused by B6
def)
- B6 def often co-exists with
defs of other WSVs (e.g. B1,
B2 & B3) SEE NXT SLIDE

B12
(cobalami
n)

- Coenzyme
(Adenosyl-Co &
Methyl- Co) in folate
metabolism

- Pernicious anaemia
- Macro-cytic
anaemia
- poor nerve function

None

Folic acid

- Coenzyme (THF, 5-M

THF, 10-M THF) in
RNA & DNA
synthesis
- nerve function

- Neural tube defect

(NTD)
- Macro-cytic
anaemia
- inflammation of
tongue
- Diarrhoea
- Poor growth

Masks B12
deficiency

- Dermatitis

Un-known

Biotin

- Co-factor for

CO-EXISTENCE OF DEFs OF VIT BCOMPLEXES

Vit B6 def plus B12 and/or folic acid defs
can lead to accumulation of homocysteine
.leading to risk of atherosclerosis (CVD) i.e.
Protei
ns

Build-up of Homocysteine

Methionin
e
B12
Homocystei
ne
folate

B6
Cysteine

*Risk of
atherosclerosis (CVD)

Richest sources
groups
Sources
& VulnerableVulnerable
groups
(to def.)
B1 (thiamin) pork & liver (but
- Alcoholics
not beef)
(WSVs)
- The poor
vitamin

Other good sources = beans, seeds & nuts (esp. vital for
vegetarian popn), whole grain cereals e.g. unrefined
products such as brown rice, brown bread, B1 fortified
cereals e.g. fort. b/fast cereals, fort. maize meal, etc.

B2
(riboflavin)

milk & dairy products, meat esp.

liver & eggs i.e. animal sources bcos B2 absorption

- No specific group

is better from animal sources that plants sources

Tea provides small amounts of B2.

Cereals & f/vegs good sources EXCLUDING B2 enriched- cereals
& d/green leafy vegs eaten regularly

B3 (niacin)

liver, fish, peanuts & fort. cereals,

coffee & cocoa

- ppl consuming diet

limited to high maize
products
- Alcoholics

B6
(pyridoxine)

Liver, whole cereals, meat (incl. poultry),

fish (esp. salmon), peanuts, banana*1,
etc.
moderate sources = Vegs e.g. spinach,
broccoli, potatoes
RNI = 15 g B6/ g protein (for both
men/women)

- Women (preg. &

women taking
contraceptive pills)
- Infants ( increased needs due to

Liver

- Vegans, elderly, those

with stomach/intestinal
diseases

B12
(cobalamin)

Other sources = meat, eggs & dairy (all sources = of

animal origin) *5

growth; esp. those born with low B6

levels)

- Alcoholics

Vit B1 (Thiamin)

has un-usual structure; since it contains S in the thia-zole* ring

fairly stable, but destroyed by alkalis (more unstable esp. in
alkaline condns @ temp >100C) &
readily absorbed in acid medium e.g.
in the 1st section of s/intestine = duodenum and
@ high levels of intake, most of the absorption = passive.
Conversely, as food continues down the duodenum, @ lower part of duodenum
the acidity of the food is buffered by alkaline intestinal secretion (e.g. of bile);
hence, decreases Vit B1 absorption.

not stored in large quantities in the tissues & its tissue stores
depend on adequacy of the diet & diet composition e.g. CHOs
increase need for B1, while Fat & Pr- spare B1
Any un-used B1 constantly excreted in urine.

Vit B1 sources
Richest sources = pork & liver (but not beef)
Other good sources = beans, seeds & nuts (esp.
important
in vegetarian popn)
= whole grain cereals e.g. unrefined
products such as brown rice, brown bread, etc
= B1 fortified cereals e.g. fort. b/fast cereals, fort. maize meal

Foods naturally containing low B1 conc.s =

e.g. milk, beef, potatoes, w/b flour, polished

rice (refined foods)

= when eaten freq. they can make useful

overall daily intake of Vit B1.

contribution to

PHYSIO FUNCTIONS OF VIT B1

1. Basic co-enzyme role in E-metabolism

i.e. it serves as a metabolic control agent in E-

metab.

NB: - On absorption, thiamin (vit B1) is phosphorylated (actively combined

with
phosphorus)to form a co-enzyme called Thiamin Pyrophosphate (TPP)
(esp. in the liver)
major function of TPP = co-factor in some important
reactions e.g.
a)Prodn of Acetyl-coenzyme A from Pyruvate thro which 90% of E is
released from glucose as ATP in the Krebs cycle.
b)Acetyl coA needed for synthesis of lipids & acetyl-choline (an
neurotransmitterhence B1 is linked with proper function of NS)
2. TPP reqd to complete branched-chain Aa metab. E.g. large doses of B1
may help in maple-syrup urine disease . caused by genetic defect in this
pathway
3. TPP reqd in inter-conversions btwn sugars of diff C chain lengths e.g.
4 .
TPP reqd in R BCs of enzyme called trans-ketolase whose activity
is used to measure Thiamin status in the body

Thiamin def.
= BERI-BERI*1
- a paralysis disease
- characterised by extreme weakness*2, paralysis, anaemia & wasting.
Clinical effects of B1 def involve the following systems:
a) GI system B1 def. causes various GI symptoms e.g. loss of appetite, in-digestion,
constipation, gastric atony & deficient HCl secretion
NB: When cells of the smooth muscles (e.g. on GI tract) & secretory glands do
not receive adeq. E from glucose (due to B1 def), they cannot do their work
in digestion process hence, no more glucose is produced. Then, a vicious
cycle re-occurs as B1 def continues.

b) Nervous system in the case of B1 def, there is no constant fuel (glucose) reqd
for CNS (esp. the
obligatory E users or high E- demanding organs) to carry out
their functions. Hence,
Neurological activity is impaired
Reduced alertness & reflex responses.both leading to gen. apathy &
fatigue.
If B1 def continues, then Lipo-genesis is hindered therefore, damage
or degeneration of myelin sheath*3 follows. This causes nerve irritation,
pain & prickly/deadening sensation. If B1 def remains un-treated (unchecked), paralysis (= classic B1 def symptom) occurs.

Clinical effects of B1 def

cont.
c) Cardiovascular system continuing B1 def;

weakens heart muscles

negatively affects smooth muscle of vascular system, hence, dilation of peripheral
b/vessels
.both leading to Cardiac failure then Oedema in the lower limbs occurs.
NB: 2 clinical forms of BERIBERI

Dry beriberi

Wet beriberi

= excessive fatigue
= excessive fluid collecting in the legs indicating cardiac involvement
= heaviness & stiffness in leg-muscles
= respiration compromised (probable) due to oedema in
lungs
= in-ability to walk far &
= serious damage to brain which can cause neurological
= abnormal breathlessness during exercise
changes affecting cerebellumeventuallyConfusional
state
= complaints of;
leading to Psychosis (or Wernickle-Korsakoff syndrome)
- mental & mood changes later followed by
- sensory loss (numbness) &
- abnormal sensations from the skin
- severe paralysis where patient is unable to stand & walk (but bed-ridden)
- anaemia (probable) &
- abnormally fast H/rate during exercise
= common in older adults who may hv had low B1 intakes for long (many yrs).

Characterised by:

Clinical effects of B1 def

cont.
d) Musculo-skeletal system in-adeq
amounts of TPP in muscle tissues causes a
chronic painful musculo-skeletal condition
called Primary Fibrio-myalgia (a wide spread
muscle pain that responds to TPP therapy*)

Contributing factors to B1 def

risk

Poor dietary intakes esp. in rice-eating communities* e.g. where common

foods incl polished rice, refined w. bread flour, or refined foods; since preparing &
processing e.g. polishing or refining foods remove B1 from w/grain foods on their
outer layers where B1 is conc.
Alcoholism in some areas e.g. in the West, B1 def is esp. assoc with alcoholism
due to poor dietary intake & interference of alcohol to B1 absorption & metab.

Diseases that involve;

Clinical manifestation in alcoholics often presents as psychosis/Wernickle-Korsakoff

syndrome (confusional state of mind)
Both primary malnutrition (due to lack of adeq diet) & conditioned malnutrition (due
to alc. condition itself) may develop into serious neurological disorders e.g. psychosis
Therefore, Thiamin = most important in nutritional therapy for persons with
alcoholism!
Vomiting since low B1 intake may be exacerbated by vomiting
Malabsorption e.g. biliary or inflammatory bowel disorders (IBD) i.e. inflamed or
alkaline condition from bilehence leading to reduced B1 absorption; in-adeq secretion of
HCl reqd to create acidic medium for readily absorption of B1reduced B1 uptake.
Increased cellular E reqnts e.g. fevers & infections

Increased needs e.g. during preg, lactation, strenuous exercise, cancer, etc
Infancy, childhood & adolescence due to continuing growthrequiring
increased E and/or B1
Consumption of diet high in CHO increases demand for B1, which may not b
met if foods consumed are highly refined.

DRV for Vit B1

B1 reqnts related to E-metab, there4 Eintake
B1 reqnts E-intake
B1 def occurs when intakes of B1: E falls
< 0.2mg B1 per 1000 Cal. of E
hence, to cater for variance in pple &
provide safety margin;
RNI for B1 = 0.4mg B1 per 1000 Cal. of E
Excess intakes > 3mg per day = toxic (2b
avoided)

Vit B2 (Riboflavin)

Adopted its name as follows:

it was 1st observed in milk whey as a pigment with a perculiar yellow-green fluorescence. Hence the vit
was given chemical-group name = FLAVIN meaning yellow
Later it was found to contain a sugar named = RIBOSE

Hence, its full name = RIB0-FLAVIN

Features

More stable to heat & less soluble in water than other B-vits
Destroyed by exposure to sunlight (i.e. light & radiation) e.g. leaving milk exposed to sunlight in glass
bottle leads to loss of ~10% B2 per hr. There4, opaque paper/plastic cartons = better for protecting
Vit B2 milk-content
Readily absorbed in duodenum (upper section of s/intestine) esp. when combined with phosphorus
from/in the intestinal mucosa
Absorption hindered by long term use of laxatives (of some bulk fibre-supplnts e.g. psyllium); esp.
when taken with milk or when taken near meals (with B2 in them)
Drugs e.g. tetracycline & di-uretics increase B2 excretion; while sulfon-amides depress bac synthesis
of B2.
Storage = limited (small qties stored in liver & kidney)

Sources

Rich sources = milk & dairy products, meat esp. liver & eggs i.e. animal sources bcos B2
absorption is better from animal sources that plants sources.
Tea provides small amounts of B2.
Cereals & f/vegs good sources EXCLUDING B2 enriched- cereals & d/green leafy vegs eaten regularly

Physio functions of Vit

B2

Crucial roles =
1) Macro-nutrient (CHO, fat & pr-) metabolism & E-release
2) Inter-relationships with other nutrients in the body e.g.

B2 is carried in plasma in assoc with Albumin; which carries both

free vitamin B2
coenzyme forms e.g.
- FADH2 i.e. Hydrogenated FAD

- FAD = flavin adenine di-nucleotide

- FMN = flavin mono-nucleotide
In tissues, riboflavin is converted into FMN & FAD which = active groups in a no. of flavoproteins
Both FMN & FAD act as e- & H+ donors & acceptors allowing them to play important role in
many REDOX*1 reactions of metabolic pathways, passing e- to the electron transport chain for
ATP production in the Krebs cycle e.g.
- FAD used in = Krebs cycle
= purine catabolism working in conj with many oxidase & dehydrogenase enzymes* 2
= (needed in) metabolism of pyridoxine (Vit B6) & Vit A ; working with aldehyde oxidase
= to quench f/radicals; in conj with glutathione reductase* 3 (a Se-requiring enzyme)
= for neurotransmitter metab; in conj with mono-amine oxidase
= drug metab; in conj with mixed function oxidases
= -oxidation of FAs to form FADH2
- FADH2 is needed in folate metabolism.

Vit B2 def
Rarely occur alone & if it occurs = usually mild
Mild B2 def - occurs as Multiple Vit B-complex
deficits
i.e. in conj with defs of other B-complexes e.g. pyridoxine, niacin & folate

Due to: = Poor dietary intake assoc with increased needs for growth (most often in
the...)
- alcoholics
- economically challenged
- elderly
- preg, lactation, childhood and, adolescents (often not consuming milk/dairy prod.)
= Severe GI disease & hyper-motility of GI tract (that causes vomiting)
= Poly-uria (increased urine excretion) resulting from uncontrolled diabetes
= Pathological states which incl negative N balance (i.e. reduced pr-status)
e.g. cancers, trauma, burns, etc that increases B2 reqnt.

Intakes of 0.55mg B2/day over 4 months..results in B2

def.

Signs of B2 def

Gen non-specific
But involve the following:

Area
diagnosed

Clinical diagnosis

Mouth

- Angular stomatitis = mouth with cracks &

inflammation @ corners
- Cheilosis = sore, burning lips which may become
ulcerated
- Glossitis = inflammation of tongue (purple to red
tongue with flattened papillae & a pebbled appearance

Eyes

-Capillaries may envade the cornea creating corneal

vascularization
- There may be sticky secretion which makes eye-lids
stick together dithoko, with
- burning & itching sensation & tears
- sensitivity to light
- loss of visual acuity (VA)

Skin

- Oily dermatitis = dermatitis characterised by a

Treatment of B2 def
1st consideration = good diet with; liver, (meat), eggs & enriched
cereals & special emphasis on milk (daily)*

2nd consideration = therapeutic multi-vit capsule (containing 5mg B2; taken 2

or 3 times a day)

DRV for B2
RNI for Vit B2 = 1.3mg/day (men) & 1.1mg/day
(women)
- Based on tissue saturation of B2
- Upper range of glutathione reductase activity

(as = more sensitive indicator of B2

saturation)

NO EVIDENCE OF TOXICITY

bcos excess intakes of B2 = poorly absorbed!

Vit B3 (Niacin)
Tryptophan = precursor of niacin &
Conversion of tryptophan to Nicotinic acid = v. in-efficient bcos
60mg Tryptophan is converted to 1mg B3 i.e. 60:1 conversion ratio*
For this conversion to occur, adeq amounts of Vit B6 & B2.
2 forms of Niacin exists = NICOTINIC ACID &
NICOTINAMIDE
Niacin can b easily converted to its amide (Nicotin-amide)
i.e. N.A + Nicotinamide = collectively called NIACIN
Most of Vit B3 in the diet is in the form of its 2 co-enzymes =
NAD & NADP.
NAD = Nicotinamide Adenine Di-nucleotide
NADP = Nicotinamide Adenine Di-nucleotide Phosphate
NAD & NADP = collectively called Pyridine nucleotides

Sources of B3
Rich sources = meat esp. liver, fish,
peanuts & fort. cereals* e.g. fort. rice,
maize-meal, bread, etc
Other sources = coffee & cocoa
NB: Since Niacin in the NAD &NADP
coenzymes is relatively stable to light,
air & heat, losses during cooking can
occur only by leaching into water.

B3 (note:)
Although, Niacin may b found in cereals esp. maize; it may
be present in un-absorbable form bound to complex CHOs
or peptides (unless it is hydrolysed). This = particular
problem with maize & to lesser extent in other cereals.
Therefore, communities/indivs with poor diet or diet
mainly composed of maize = increased risk of B3 def
(pellagra); maize = low in tryptophan & Nicotinic acid in
maize is bound/unabsorbable
But some popns with diet low in niacin may never develop
pellagra
bcos - they may be consuming adeq amounts of
Tryptophan (e.g.
from milk = high in tryptophan) which can
b converted to niacin
- soaking maize in lime-water releases bound niacin
making it
available/absorbable (traditional practice in Mexico,
where maize = staple, but pellagra

health concern there)

Physio functions of B3
1) NAD used in E-releasing rxns e.g. glycolysis,
Krebs cycle & Oxidation of alcohol
2) NAD & NADP act as H acceptors in oxidative
rxns forming NADH & NADPH which then act
as H donors.
NB: - the H that NAD & NADP donate is
eventually
passed thro e- transport chain
to yield H2O.
- NADPH- mostly used in E-requiring, biosynthesis rxns e.g. mostly for FA synthesis.
3) NAD & NADP - important in metab of Vit C
and folate[to regenerate Vit C after acting as a/o by restoring ascorbate from
dehydro-ascorbate]

B3 functions (cont.)
4) NAD & NADP also reqd for
activation of glutathione reductase*1
(used for assessing B2 status)

5) Niacin = component of the glucose

tolerance factor*2 that facilitates
action of insulin
6) Niacin = vital in maintaining
integrity of skin & mucus
membranes

B3 def.
B3 def = PELLAGRA
3 main features/characteristic symptoms =
Dermatitis;

mainly affects body parts exposed to sunlight

hence may appear as sun-burns. When chronic, it worsens in sunny
weather & improves in winterforming patches of thickened rough
skin. Skin may become cracked & infected in more acute cases.
NB: Dermatitis is almost always symmetrical.

Diarrhoea;

entire GI tract lining affected by mucosal

inflammation, resulting in heart burn, in-digestion, abdominal pain,
diarrhoea & soreness of rectum.

Dementia;

occurs only in advanced pellagra, mainly range from

headache, deep sleep, loss of memory; thenanxiety/emotional instability*, depression to hallucinations, confusion, severe
dementia with convulsions, if un-treated.

i.e. 3Ds ultimately leading to Death (4th D).

Risk factors of B3 def.

Poor & maize/millet-based diet
millet = high in lysine (limiting Aa), which inhibits the use of
tryptophan for niacin formation.leading to pellagra

Alcoholism due to low food intake

Increased needs e.g. in cancer
Altered metab caused by some drugs
or conditions e.g.
isoniazid (anti-TB drug) or
Hart-nup disease (an in-ability to absorb tryptophan)
NB: If problem not anticipated, these may result in pellagra.

DRVs for B3
Level reqd to prevent/cure def = 5.5mg
B3 per 1000Cal. Hence,
RNI (set higher @) = 6.6 mg B3 per 1000Cal
(for adults; both men & women)

B3 toxicity
High doses can b toxic (esp. from
supplements)
Foods not contain adeq NA (to cause a toxic
rxn)
High doses of NA (>200mg B3/day) may cause;
Vasodilation
Flushing of skin & tingling sensation in hands & feet + red
skin rash
GI discomfort (stomach pain), nausea, diarrhoea
High blood uric acid levels.liver toxicity/damage*
High b/sugar
Changes in heart beat .a fall in BP

Notes on other WSVs

B6
3 forms of B6 = collectively called PYRIDINES
= Pyridoxine or pyridoxol, Pyridoxal & Pridoxamine*
= phosphorylated to pyridoxal phosphate (PLP)
PLP serves as co-enzyme for many enzyme systems
related to Pr- metab esp. Aa metab i.e. the brkdwn of
Aas & Aa synthesis e.g. in;
a) De-carboxylation for prodn of HISTAMINE (from histadine),
DOPAMINE & SEROTONIN (from tryptophan). NB: these are
neurotransmitters

b) Trans-amination for synthesis of Non-essential Aas

c) Synthesis of porphyrin (for haem), nicotinic acid (from
tryptophan) & cysteine (from methionine)*2
d) Other minor roles of B6 = fat metab (e.g. conversion of Linoleic acid
to Archidonic acid & synthesis of sphingolipids); glycogen metab
(esp. in muscles) & modulation of action of steroid hormones (e.g.
those used in contraceptive pills) & other hormones. NB: Hence, women
using oral contraceptive pills req add nal Vit B6.

Folic acid
= pteroyl-mono-glutamic acid (PGA)
= made up of 3 acids; Pteroic acid, Para-amino-benzoic acid
(PABA)
& Glutamic acid (an Aa)
= a salt form of folic acid = folate (conversion of folic acid to folate occurs w-in
b/tissues) &

= folate group of substances with folic acid activity

e.g. tetra-hydro-folate (THF), folic acid, poly-glutamate, mono-glutamate, 5-methyl-THF and

10-methy-THF
NB: 5-MTHF & 10-MTHF = co-enzyme forms of folic acid
Most folic acid in diet is in bound form mainly as poly-glutamate (~75%) or mono-glutamate
(~25%);
Hence, for optimal absorption glutamates are removed from poly-glutamates by Zincdependent conjugase enzymes forming mono-glutamates.
There may b Conjugase inhibitors in some foods e.g. in beans, alcohol, etc; that prevent
folate from being freed.
Therefore, only 50% of dietary folate is absorbed; most of which will be stored in the liver
while,
Some of the folate is taken up by target cells to form poly-glutamate, which then are
trapped within cells & used as THF co-enzymes.

THF acts as coenzyme for 1) Aa metab; synthesis of body proteins (from

serine & glycine), homocysteine (from methionine B12 requiring) & cysteine (from
homocysteine - B6 requiring), purines & pyrimidines for forming thymidylatebase for DNA & RNA.

 Also, THF acts as coenzyme for

2) Conversion of histidine to Glutamic acid - an Aa present in brain vital for NS
3) purines & pyrimidines reqd for/in rapidly dividing cells* e.g.
- Blood cells (RBCs-haem synthesis & WBCs-for immune systemfor n/functioning of haematopoetic
system)

- Cells lining GI tract

- Cells in skin
- Cells of a developing fetus -for fetal growth to prevent NTD

Folic acid def. include;

Neural tube defect
Megalo-blastic/Macrocytic anaemia:
In folic acid def, bone marrow cannot make DNA, hence the developing RBCs
cannot divide, but they just grow bigger; thus, RBCs become immature yet
larger in size than normal (hence, termed megalo-blasts).
Then, those megaloblasts mature to become larger than normal matured
RBCs (the macrocytes).
Those macrocytes will be released into blood & resulting in macrocytic anaemia
[whereby few mature RBCs are produced hence reduced O2-carrying capacity
of the blood]

Increased risk of developing CVD

When folate is lacking, less homocysteine is converted back to methionine to
accomplish homeostasis. Therefore, homocysteine accumulates in bloodleading to
Atherosclerosis (CVD)
This also happens during B6 & B12 def.s.

B12 (Cobalamin)
Active coenzymes = Adenosyl-Cobalamin & Methyl- Cobalamin
Protein intake B12 reqnt; B12 reqnts increases with protein intake
increases i.e. a high protein diet leads to increased the need for B12
Because increased Aa metab e.g. Increased conversion of homocysteine to
methionine reqs the presence of B12 & folate. Otherwise, there will be a build-up of
homocysteine in the blood leading to atherosclerosis.

Functions: metabolic role of B12 is associated with 2 coenzyme systems;

e.g.
Coenzyme system involved in the availability of THF (for folate metab); where Vit
B12 = acts as co-factor for methyl-transferase enzyme needed for removing a methyl
group from (5/10-)M-THF making THF available.

Coenzyme system involved in metab of some FAs; where Vit B12 = needed in
metab of FAs with odd no. of Cs in their chains.
Other minor functions; Vit B12 linked with Aa metab, haem synthesis (RBCs formation),
maintenance of myelin for nerves (in NS), prevention/control of pernicious anaemiavia
THF (i.e. thro co-factoring with folate)

Vit B12 def = Pernicious anaemia, Macrocytic anaemia & poor nerve
function
Some causes of Vit B12 def =
failure of cell- division due to failure to synthesise sufficient purines & pyrimidines
for DNA & RNA formation; hence, Main sign of B12 def = megaloblastic/macrocytic
anaemia
neurological element which involv progressive damage of myelin sheaths of
nerve fibres leading to loss of conduction velocity or synaptic transmission &
gradual loss of sensory motor function in the periphery.. i.e. peripheral neuropathy

- failure to produce the intrinsic factor (i.e. Glyco-protein secreted by gastric mucosal
cells)

since the body is believed to destroy its own intrinsic factor possibly as part
of an auto-immune response*; hence, No factor to bind Vit B12 in the stomach
to form the vit-intrinsic factor complex reqd to aid Vit B12 absorption in the ileum
leading to in-ability to absorb Vit B12, causing Vit B12 def. Therefore, this Vit B12
def may result in a type of anaemia called . Pernicious anaemia*
i.e. Anaemia caused by vit B12 def occuring due to inability to absorb Vit B12 in the
ileum.
* Pernicious anaemia = an auto-degenerative disease.
NB: B12 def detected by presence of megaloblasts in bone marrow biopsy
specimens since when megaloblasts are present in b/marrow then RBCs in
peripheral circulation are usually macrocytic.

- Failure to absorb Vit B12

due to malabsorption or interference/interaction of drugs

e.g. alcohol, potassium suppl, etc.

- Repeated exposure to nitrous oxide anasthetics

which may in-activate Vit

B12 in the body .signs of B12 def.

- In- adeq dietary intake of Vit B12;

though common cause of B12 def

DRVs for vit B12: RNI = 1.5 g/day

No toxicity syndrome reported
RNI).

for adults (both men & women)

with vit B12 intakes 100 g/day (i.e. ~ 67 x

Pantothenic acid
Pantothenic = every where, name derived from the widespread
sources in nature of Pantothenic acid, hence its widespread bodily
functions.
Bio-chemically, Pa = part of co-enzyme A, hence
= involved in release of E from catabolism of CHO, pro- & fats
= initiates the Krebs cycle & release ATP
= the starting substance for bio-synthesis of long-chain FAs,
cholesterol, other sterols & porphyrin (a component of haem for Hb)
For Pa to be an active component of co-enzyme A after being
absorbed in the s/intestine it has to combine with phosphorus
i.e. Pa + Phosphorus
active Acetyl co-enzyme A.
Pa gen available as in the form of its Ca salt = Calcium
patothenoate
Since No natural def ..No reqnt (RNI) has been set for Pa. But
estimated safe & adeq range = 5.5 mg Pa/day for adults.
Biotin
Occasional Biotin def reported in subjects with; un-usual dietary
practices, un-balanced TPN, severe malabsorption (due to bowel
disease or alcoholism) or freq intake of r/egg whites.

Vitamin C
Discovery of Vit C emanated from search for a cause &
cure of the ancient haemorrhagic disease called scurvy
Characterised by; = haemorrhagic spots in the skin
= anaemia
= bleeding gums
= poor wound healing & re-opening of
healed wounds
= bone & joint pains/aches & bone fractures
= improperly formed teeth &
= capillary walls that rapture causing bleeding

previously

That led to discovery of an anti-scorbutic food factor

found in lemons (initially called limes), oranges & other
citrus fruit

 The anti-scorbutic food factor was later named

Acsorbic acid (bcos of its anti-scorbutic or anti-scurvy properties). Since it was
discovered after B-complexes hence Ascorbic acid was given letter C; thus, it was called
Vitamin C.

Popn groups at risk of scurvy (currently) =

refugees or ppl in relief camps - where diet does not provide adeq Vit
C

teenagers who gen consume highly refined diets

the homeless or institutionalised elderly ppl due to wasteful practices in
food handling (food processing, preparation & catering)

the alcoholics & smokers

gen. hv poorer vit C status; explanation not clear, but

may include lower intake, poorer absorption & increased turnover in combating f/radicals
generated by the smoke.

Structure of Vit C = similar to that of glucose

NB: Glucose = a metabolic pre-cursor of Vit C in most animals except in human beings bcos human
beings do not hv a specific enzyme that converts glucose.. to ascorbic acid.

2 forms of compounds with Vit C activity =

Ascorbic acid &
De-hydro-ascorbic acids
Ascorbi
NB: These 2 forms = inter-convertibleci.e.
acid

Dehydroascorbic

 Both forms readily absorbed by active & passive diffusion

BUT, De-hydro-ascorbic acid > (better) absorbed than Ascorbic acid
% of Vit C absorbed decreases as amount of Vit C consumed increases;
thus, high consumption of Vit C leads to reduced Vit C absorption.
i.e. Vit C intake 1/ Vit C absorption
Usual absorption rate (@ usual average intake) = 80 95%
Vit C in plasma occurs as free ascorbate & the plasma levels reflect size of
dietary intake
Normal body pool (i.e. total body content) of Vit C = 2 3g in an adult &
When body pool falls < 300mg = clinical signs of scurvy may appear.

PHYSIO FUNCTIONS OF VIT C

1. Vit C = an anti-oxidant;
i.e. It protects molecules found in the water-soluble compartments by neutralising (thro
donating H+
ions/working as a reducing agent*) reactive oxygen molecules (singlet
oxygen i.e. O ) before they
can damage cellular components & lead to chronic illnesses
e.g. atherosclerosis, cancer, etc OR
whose cumulative effects can play role in speeding up
aging process..
-

*Thus; since Vit C in plasma occurs as free ascorbate, then ASCORBATE ..is readily oxidised to DEHYDRO-ASCORBIC ACID. In this way, donating hydrogen ions to reverse oxidation which may try to
occur in the body
Once Vit C has acted as a/o, it must be re-generated by reductase enzymes e.g. reduced glutathione/
glutathione reductase (a B2-dependent enzyme), NADH or NADPH; in order to restore Ascorbate from
Dehydro-ascorbic acid, hence making Ascorbate to be available for further reactions..thus repeating the
cycle

Regeneration of Vit C
In plasma, Vit C is in form
of:

Ascorbate

readily oxidised to

Dehydro-ascorbic acid

H+ ions
donated
Vit C re-generated
by:
reductase enzymes, NADH, NADPH

PHYSIO FUNCTIONS OF VIT C

cont.

2. Vit C = co-factor (or serves in) for a no. of hydroxylation

reactions e.g. rxns essential for synthesis of;
hydroxy-proline & hydroxy-lysine (Aas precursors) reqd for

synthesis of collagen* (a protein which forms the bases for all connective
tissues in the body; such that without Vit C collagen cannot be formed &
maintained resulting in symptoms of scurvy.

carnitine reqd for release of E from FAs esp. in the muscles

nor-adrenaline
other vital cell compounds e.g. neurotransmitters, bile
acids, hormones such as adrenaline, thyroid hormone,
steroids, etc.
3. Vit C closely linked to Fe metabolism e.g. Vit C:
- enhances Fe absorptn from food by reducing Ferric iron

(Fe2+)

to Ferrous iron

(Fe3+)

NB: Ferrous iron >

(better )

absorbed than Ferric iron.

- helps to incorporate Fe into Ferritin

..which may be challenge for ppl already with excess Fe in the
body.

PHYSIO FUNCTIONS OF VIT C cont.

4. Vit C reqd for de-toxification of foreign substances in the liver
5. Vit C for promotion of immune function e.g. to prevent common
occurrence of
common colds.
6. Vit C is involved in the regeneration of Vit E.
7. From recent findings; Also, Vit C may protect blood-vessel integrity &
- help prevent cognitive impairment in the
elderly.

VIT C DEFICIENCY

Many signs of SCURVY can be linked to functions of Vit C e.g.

Failure to synthesise collagen

Lack of carnitine synthesis contributes to fatigue or progressive

a/c for bleeding from raptured

capillaries, failure/delayed wound healing & bone fracture
weakness (since cartinine is reqd for FAs metab to produce E from fats)

Poor neurotransmitter synthesis linked to suppressed immune

functions

Vulnerable groups to Vit C def.

Infants fed on diets consisting exclusively
of cows milk
Alcoholics

due to poor food intake & absorption

The elderly

due to poor intake & decreased

absorption

Smokers

may also hv poorer Vit C status due to

increased
exposure to f/radicals from
the smoke & poor absorption.

DRVs for Vit C

Vit C reqnts = defined based on amount reqd to
prevent scurvy i.e.
= 10mg Vit C intake per day
= Further increase in intake of Vit C beyond
10mg/day
does not increase plasma levels
until intakes
reach 40 mg Vit C/day when
measurable amount of Vit C begins to appear in
plasma; which is an indicator of adeq supply of
Vit C to distribute to body tissues for use. Hence,

RNI for Vit C = 40 mg/day.

But, plasma levels may continue to increase until they reach
plateau of 1.4mg/dl @ Vit C intake of 70 100mg/day.

 Vit C = an un-stable, easily oxidised acid

= can be destroyed by air/oxygen, alkalis, high temp
(heat) &
light.
Ways of preserving Vit C content of foods:
Cover cooking vegs with a lid to reduce exposure to air
Peel the fruits at the time they are consumed (To be remembered esp. when
packing lunch for child who cannot peel fruits e.g. oranges, naartjies, etc for themselves)

Keep juices tightly closed

Avoid keeping vegs hot after cooking; serve immediately

(Otherwise,

after 1hr almost no Vit C may b remaining in the vegs)

Cook Vit C rich foods with little water as posbl for short periods &
keep them covered.
Immerse vegs directly into already boiling or hot liq. e.g. water or
oil
Minimise bruising when cutting vegs/fruit e.g.
Avoid cutting vegs into small pieces and
Avoid cutting them in advance (e.g. over-night), until at the time of their use.

Avoid adding sodium bi-carbonate (sebediso) to vegs

(e.g. in delele to
reduce its sliminess or adding/spraying its solution over vegs to enhance their green colour)

bcos sodium bi-carbonate (= alkaline) destroys most of the Vit C in

the vegs.

Minerals/Trace elements
Major minerals = Ca, P, Mg, Na, K & Cl
Ca, P & Mg important in bone health
Na, K & Cl = electrolytes

Minor minerals = Fe, Zn, Cu, Se, Mn, F &

I
Fe, Zn & Cu = co-workers in metabolism
Se = a/o mineral & spares Vit E
Mn = constituent of enzymes in CHO & lipid metab.
F = important in dental health
I = vital in thyroid integrity & function

Mineral

Major functions

Def disease

Toxicity

Calcium
(Ca)

- bone & teeth

formation/structure
- nerve impulse transmission
- muscle contraction
- blood clotting

-Increased
risk of
Osteoporosis
- Rickets
- Tetany*
- Lower BP

-Kidney stones in
susceptibl ppl

Phosphoru - bone & teeth

s (P)
formation/structure
- buffers
- constituent in cell
membranes (e.g. in
phospholipids), ATP & DNA

- bone loss,
weakness,
lack of
appetite

- Ca reabsorption from
bone

Magnesiu
m (Mg)

- used in rxns involving ATP

prodn
- nerve & muscle function
- maintain bone structure

- nausea,
vomiting &
weakness

- Weakness
among ppl with
poor kidney
function

Sodium
(Na)

- major Extra-Cellular (EC) ion - muscle

- nerve impulse transmission
cramps
- regulates fluid balance

- Hypertension in
sensitive ppl

Potassium
(K)

- major Intra-Cellular (IC) ion

- nerve impulse transmission
- regulates fluid balance

- Abnormal heart
beat

- Irregular
heart beat
- Fatigue

Note: Major minerals

Ca
Many roles of Ca & P = un-separable
But, Ca = most abundant mineral present in the body,
accounts for
~40% of the total mineral mass (TMM)
= most of it is found in the bone together with P; in the
form
of hydroxy-apatite [Ca10(PO4)6 (OH)2] esp. in
mature bones,
where it plays a role in hardening or
strengthening the
skeleton and teeth
= young bones, mainly contain Ca in the form of
amorphous
tri-calcium phosphate*
= ~1% of the Ca in the body is found in:
- soft tissues bound in plasma proteins as part of
various
membrane structures
- ECF as free ionised Ca (Ca 2+); NB: The amount of circulating
Ca = not
dependent of dietary Ca intake; essential for nerve impulse
transmission, muscle
contraction*2, enzyme activatn, cell membr permeability,
normal homeostasis &b/clotting

 Ca levels regulated to remain within narrow limits of 2.2

2.6 mmol/L
by regulatory hormones* e.g. Calcitonin, PTH & active
Vitamin D (1, 25 (OH) D ) acting on the gut, bones &
kidneys; in
response to changes in the circulating
(ECF) Ca levels e.g.
- When Ca levels are low (or phosphate levels are high),
PTH is secreted, which in turn increases Ca levels
by;
= increasing synthesis of active Vit Dthat stimulates bio2

synthesis of CaCa.leading

binding proteins involved in cellular transp. of

to increased Ca

absorption from gut

(intestinal mucosa)

= decreasing Ca - excretion @ the kidneys

= stimulating Ca release from the bone
- High Ca levels cause release of Calcitonin from thyroid
gland which;
= promotes Ca- uptake into the bone &
= inhibits bone mobilisation
*2

Ca homeostasis as controlled by regulatory hormones

High Ca levels in
blood

Thyroid gland

Calciton
in
secretio
n

-Ca release from bone

Low Ca levels in
blood

Parathyroid gland

PTH
secretion
+
Ca release
from bone

More Ca
re-absorbed
by kidney

Normal Ca levels in blood

Vitamin
D

 Total amount of body Ca - maintained by Constant balance of

Dietary Ca &
Tissue Ca within the body
Besides this constant Ca balance, there are also a no. of
Dynamic Ca balance mechanisms;
1. Intake-absorption-output balance (ideal dietary Ca : P =
2:3)
NB: - Ppl with incr. reqnts e.g. children, preg & lactating
women req a 1:1 dietary balance*
- Gen, as Ca needs incr. .Efficiency of Ca absorptn incr. too
- As Ca intake incr. .% Absorptn (absorption rate) decr.
2. Bone-blood balance involves Ca-balance maintained @ 99%
in bone & teeth, and 1% in body fluids (blood, ECF, etc)
3. The Ca-P blood serum balance (Ca : P = 1:1 in the blood)
- based on the relative solubility (mg/dl) of Ca & P in the blood;
hence,
Ca P serum-balance = Solubility of Ca x Solubility of P

 Contributing factors to Ca absorptn:

Enhancing factors =

Vit D
Lactose (found in milk)
Other sugars & proteins
the acidic nature of d/tract (also facilitates solubility of Ca)

Inhibitory factors =
Phytic acid (present in w/g cereals).converted to Calcium
phytate (insoluble salt)
Oxalic acid (present in spinach, beetroots, chocolate, wheat bran,
peanuts, strawberries, etc) . converted to Calcium oxalate (insoluble
salt)

High NSP trap some of the Ca making it un-absorbable in the s/intestine

Un-absorbed fats combine with Ca forming Soaps ; hence
removing Ca from body common problem in Steatorrhoea

High dietary P intake (e.g. 1:3 Ca : P intake levels)may alter Ca

metabolism in the bodyleading to Hypo-Calcaemia & Hyperparathyroidism (over-excretion of PTH)

Summary of Ca metab.: relative distribution of Ca in the body

Dietary
Ca (~600-

Urinary
Ca lost

800mg/day)

~30% Ca
absorbed &
contributing to:

Faecal loss of
Ca

- decr. by high
intakes of P, Mg
& K and in old
age

Plasma
Ca

~70% Ca unabsorbed due to:

- high fats
- high phosphates
- oxalic acids Ca oxalates
- phytic acids Ca phytates
- low Vit D
- high pH (alkalinity, e.g. bile & FAs
excretion)

- incr. by high
intakes of Ca,
Pr- & Na, and @
menopause

Absorption increased by:

Ca depletion, growth, Vit D, low pH
(acidity), certain Aas, lactose, etc.

Ca in
complex
forms e.g.
in bones,
teeth, etc

Diffusib
le or
Ca2+
Excess Vit D
PTH

Vit D, A & C
Proteins

Bone compartment

Ca2+ used
in body

Factors contributing to high Peak Bone

Mass (PBM)*1 in young adults (<20yrs)
Physical activity
wt-bearing exercise esp. promotes bone metab
exercise promotes food intake ensuring higher Ca
intakes & helps to maintain normal body wt
Body wt
Excessively thin females with BMI < 20 may be
amenorheic*2; absence of normal menstrual cycles &
lack estrogen.prevent normal bone accretion
Alcohol & smoking decr. bone accretion
Vit D & other dietary factors e.g. enhancers or inhibitors
of Ca absorption

DRVs for Ca: RNI = 700mg/day, EAR = 525 & LRNI

= 400mg/day

P
2nd most abundant mineral in the body (after Ca)
In blood, Ca & P hv reciprocal relationship & are controlled by
similar mechs [NB: P = metabolic twin to Ca]
~ 80% of total amount of P in the body found in bones (in the
form of Ca-salt responsible for rigidity of the skeleton/bones)
~ 20% of remaining P in the body found in soft tissues* in
form of:
in-organic phosphate &
as constituent of major classes of bio-chemical compounds e.g.
phosphorylated compounds (TPP, NADP, PLP, ATP& other high-E phosphate compounds)
phospholipids in cell membranes,
nucleotides (e.g. DNA & RNA), etc

Absorption rate of P = ~ 60% of dietary intake; But

Amount of P in the body is controlled mainly by urinary renal
excretion (under the influence of PTH) rather than absorption.
Physio functions of P;
Bone & teeth formation
Prodn & transp of high E phosphates e.g. for E-metab

- plays role in absorptn & transp. of other nutrients e.g.

glucose, glycerol, FAs
for instance; glucose & glycerol are each
phosphorylated to facilitate their absorption to glucose-6phosphate . then absorbed.
To use that glucose, P in glucose-6phosphate promotes renal tubular re-absorption of
glucose to return the glucose back into the blood.

Richest sources
Vulnerablegroups
groups (to def.)
Sources
& Vulnerable
Calcium (Ca) Milk & dairy products,
- post menopausal women,
girls, ppl with kidney
(WSVs)teenage
disease
Mineral

Phosphorus
(P)

Meat, fish, eggs, milk & dairy

products
Cereals, nuts & legumes
(s/amounts in tea & coffee)
Widely present in bakery foods, processed
meats & s/drinks as food additive

Magnesium
(Mg)

w/grain cereals, nuts, legumes,

sea foods, coffee, tea, cocoa &
chocolate

- premature infants,
vegetarians, alcoholics & the
elderly
- alcoholics & ppl with kidney
disease

NB: g/leafy vegs = poor source bcos

chlorophyll in them contains no Mg.

Sodium (Na)

Table salt (i.e. NaCl), preserved

meats, dairy products & vegs;
cheese, crisps, packet soups,
processed breads, etc.

- ppl consuming a severely Narestricted diet

Other sources = fresh veg/fruits =

low in salt

Potassium (K) Dried fruits & nuts, raw vegs

tend to decrease as intake of processed foods

increase; hence reversing the Na : K ratio.

-ppl consuming diet high in

processed foods
- ppl taking high blood
medication

Most dietary Cl derived from

- no one

Other sources = milk & dairy

products, cereals. NB: f/veg intakes

Chloride (Cl)

Mineral

Major functions

Def disease

Toxicity

Iron (Fe)

- part of Hb for O2 delivery to

cells
- part of Myoglobin which
stores Fe in muscles

Fe-def anaemia
Weakness,
lethargy

Siderosis i.e.
Liver damage
due to Fe
overload

Zinc (Zn)

- involved in metab. of all

macronutrients (EYN) & E
prodn
-regulates protein synthesis*1
- functions in growth & dev,
wound healing & immunity,
and a/o mechs*2

-Poor growth &

dev
- Poor wound
healing
- Suppressed
immune
function

Decreased Cu
& Fe
absorption

Copper
(Cu)

- involved in proteins*3 &

enzymes in Fe & lipid metab
- nerve & immune function
- collagen synthesis

- Anaemia
- Poor growth

Vomiting &
Wilsons
diseases* - for ppl

- anti-oxidant as part of
glutathione peroxidase (GPO)
- spares Vit E

- Keshan
disease*5

Selenium
(Se)

with its genetic

predisposition

(heart

disease)

- Kashin-Bek
disease*6
- Muscle pain &
weakness

Nausea,
vomiting,
fatigue & hair
loss

Iron (Fe)
Total quantity of Fe in the body consists of 2 major fractions;
~ 70% essential body Fe found in Haemo-globin*, Myo-globin* & intracellular enzymes e.g. cytochromes (essential in oxidation-reduction
(REDOX) reactions
~ 30% mobiliseable Fe stores/reserves contained in ferritin & hemosiderin

Ferritin = major protein involved in Fe storage

Hemosiderin = an insoluble iron-protein compound formed in the liver when Fe storage capacity of ferritin is
exceeded

Fe occurs in the diet*2 in 2 forms:

Haem iron (or organic iron); mainly from foods of animal origin e.g.
Richest sources of haem-Fe = liver, meat, fish & eggs. Other sources = milk
& dairy products (NB: Intakes of large amounts of milk is associated with poor iron status,
bcos milk = low in Fe, & Ca in milk binds to iron making it un-available for absorption).

Non-haem iron (or in-organic iron); predominantly from plant sources

e.g. Good sources of non haem Fe = legumes, green vegs & cereals.
(However, Fe present in cereals is usually bound to insoluble compounds
e.g. phytates. Fortification of cereals (e.g. bread flour) with Fe ensures
that Fe is restored & made available for absorption without competing
with phytates bcos in the milling process phytates are removed.
Other sources of non haem Fe = nuts & dried fruits
NB: Bio-availability of Fe is much less in plant sources than in animal
sources.

 The 2 forms of Fe are absorbed with diff. efficiencies e.g.

Haem-Fe must be hydrolysed from any protein, then absorbed relatively
easily although slowly; while, Non-haem Fe must 1 st be solubilised, then
hydrolysed by HCl in the stomach before being absorbed.
The hydrolysis involves the use of HCl in converting Fe3+ to Fe2+ (ferric to
ferrous iron i.e. in-absorbable to absorbable form of Fe)
This rxn also facilitated by ascorbic acid (Vit C); which dramatically incr. nonhaem Fe

Overall absorption of Fe from meat = ~20 25%, while that from plant
foods = ~2 5%.
NB: - Absorption of non haem inhibited by; phytic acid (in w/cereals),
poly-phenols (in tea, coffee & nuts), oxalic acid (in tea, chocolate &
spinach), phosphates ( in egg yolk), Ca & Zn as well as inorganic
elements e.g. Cu, Mn, Cd, Co, etc
Tea reduces Fe absorptn by ~ 60%. These inhibitors gen bind with
ferrous iron (Fe2+), making it un-available for absorptn (i.e. unabsorbable).
- Absorption of non haem enhanced/facilitated by; Vit C (ascorbic
acid), citric acid, lactic acid, malic acid & tartaric acid, fructose, sorbitol
& peptides derived from meat (Aas e.g. cysteine, lysine & histidine).
These enhancers form ligands with ferrous iron (Fe2+), hence,
maintaining its solubility & thus facilitating its absorptn.* 2

Absorption of Fe takes place most efficiently in the duodenum & is inversely related
to level of Fe stores in the body!!! e.g. If Fe stores = high, then less Fe is absorbed.

Control of Fe absorption:
Amount of Fe absorbed from the diet:
a) depends on the body needs e.g.
If Fe stores are high, then more Fe from the diet will be absorbed and vice versa.
During Fe deficiency, absorption of non-haem Fe increases ~10 times while haem Fe
absorptn doubles.

b) is regulated by several proteins e.g.

Caeruloplasmin (a Cu-containing enzyme) reqd to convert absorbed Fe into

a form that can be bound to Transferrin (Fe transport protein) and to Ferritin
(Fe storage protein)

Control of Fe absorptn depends on amount of excess Fe3+ deposited in Ferritin

temporarily stored in the mucosal cells (for ~2-5 days)
i.e. how much Fe will be absorbed from dietary intake is controlled by Qty of
excess Fe already temp. stored in ferritin in mucosal cells.
If that excess Fe3+ in the mucosal cells is not picked by Transferrin within 2
5 days, it will be lost when the mucosal cells are sloughed off & excreted in
faeces.
When Fe is in short supply in the body (common in women & children), No. of
transferrin receptors & Amount of transferrin increase to bind &
transport more Fe from mucosal cells to the rest of the body. The opposite is
true when Fe is plentiful, in order to reduce Fe-carrying capacity of transferrin
to b/tissues. Some Fe is stored bound to ferritin in the liver, spleen & b/marrow.
If Ferritin conc. in the liver becomes high (as Fe stores become v. large), then
Ferritin molecules clump together forming Hemosiderin (which allows safer &
3+

more Fe storage)*

 Once Fe has bn absorbed into the body, there is no means of eliminating

excess Fe; EXCEPT thro loss of blood since excess Fe in the body can
be toxic!
Therefore, in severe Fe-overload, the patient may be
Bled to remove excess Fe or
Prescribed/given chelating drug which binds to Fe allowing it (excess Fe) to
be excreted.

Hence, there is mech. that prevents the entry of excess Fe into

b/circulation (in 1st place) & the main control of the bodys Fe-balance =
intestinal absorption thro mech. called MUCOSAL BLOCK*.
The mucosal block regulates amount of Fe allowed/entering into
circulation &
- operates according to the level of Fe stores already present in
the body.
Mech.;*1 - As Fe2+ passes thro the mucosal cells (in s/intestine), it (Fe 2+ ) is
oxidised
back to Ferric iron (Fe3+ i.e. in-absorbable form of Fe) by
Caeruloplasmin.
- Then, Ferric iron (Fe3+) is attached to transferrin, then circulated in
blood
plasma around the body to sites of utilisation or of
storage as ferritin (also
known as apo-ferritin).
- NB: Excess Fe (Fe not reqd by body) trapped within the mucosal
cell &
lost in faeces when the lining cells of the gut are
shed/sloughed off @
the end of their life-cycle.

Summar
y:
Fe3
+

HCl
Vit C, or
other Fe
enhancers

Fe2
Fe2

..

Fe3
+

in the stomach

Excess Fe3+ stored in liver

bound to FERRITIN

in s/intestine; as Fe
passes via mucosal
cells

Fe3+ transported in TRANSFERRIN

to b/marrow, muscles & other cells
(for synthesis of RBCs, Myoglobin &
Fe-containing Pr-s)

Ways of preventing iron def.

Include more dietary Fe sources in the diet e.g.
liver, g/leafy vegs, etc (but not unbalancing the meals)
Include Fe enhancers e.g. citrus fruit & citrus fruit
juices incl. grapefruit juice, etc
Use more bio-available Fe sources (haem Fe) as
much as posbl
Reduce intake of foods that inhibit Fe absorption
(esp. avoid taking them with Fe-rich meals e.g. drinking
tea/coffee/chocolate after Fe rich meal will inhibit Fe absorption,; instead a
juice from citrus fruit or grape juice will enhance Fe absorptn.

Choose Fe-fortified foods if available

(To boost Fe esp. in

women, infants & children)

Take Fe supplements when Fe-losses are high

(e.g. in
women with heavy menstruation); but with doctors consultation!!!

Iron Toxicity
Not observed in gen popn from dietary sources, BUT,
Seen in some cases e.g.
Ingestion of home-brews made in iron-vessels
Aspirin poisoning, high doses of Fe suppl, vit & mineral suppl
containing Fe
Haemo-chromatosis = genetic disease characterised by
increased Fe absorptn which causes Fe overload i.e. an inherited
abnormality of Fe metabolism that contributes to Fe overload.

Conseqs of Fe overload;
Siderosis i.e. liver damage due to Fe overload
Damage to intestinal lining (esp. mucosal cells; where
Ferrous Fe is converted back to Ferric Fe by Caeruloplasmin after
absorptn and temporarily stored by Ferritin)
Abnormalities in body pH; due to over-secretion of HCl &
other gastric juices

Summary of Fe-def
Sign of Fe def = drop in amount of Ferritin in the blood
to

due

depleted iron stores

Daily physio reqnts for Fe will still be met with recycled Fe

Then, as the recycled Fe becomes depleted &
Saturation of transferrin decreases (to < 10 15 %), = Fedeficiency Anaemia occurs leading to:
in-adeq supply of Fe for synthesis of new RBCs,
hence,
RBCs produced contain less Hb, are smaller in
size & fewer in no.
= typical picture/clinical manifestation of Fe def
anaemia.
Hence, Fe def results in a hypo-chromic, micro-cytic anaemia.*

Zinc (Zn)

Zn = widely distributed thro out the body; but,

Major sites where Zn is found = Muscles (~60%), bone (~30%),
skin (4-6%), liver, kidney & plasma (r=~4-6%)
However, there is no identified storage organ for Zn.
Zn absorption is regulated by a cysteine-rich protein called
Metalothionein* in the intestinal mucosal cells.
e.g. When Zn intakes = high,
more Zn is absorbed into the mucosal cells of the intestinal walls,
then metalothionein is synthesised to bind with that Zn to form
metalothionein-Zn complexes.
Hence, limiting entry of the large amounts of Zn from diet into the
b/circulation!!!

NB: Metalothionein - binds both Zn & Cu in the intestinal

mucosa cells, but has high affinity for Cu than for Zn. Hence it
binds Cu more tightly than Zn; thereby reducing/inhibiting the
absorption of Cu. This commonly occurs during high intakes of Zn.
Thus, High intake of Zn inhibits Cu absorption!!!

Zinc (Zn) cont.

The Liver acts as a centre for the fine tuning/control of plasma Zn levels;
e.g.
Mech. of regulating body Zn
Zn levels are gen well controlled thro:
releasing Zn from metalothionein-Zn complexes (found in liver cells)
when needed by body for use e.g. when Zn plasma levels are low
loss of Zn from the body thro shedding off the mucosal cells
(containing Zn that had previously being taken into them & bound to
metalothionein).
For instance,
During infection, Zn is taken up by metalothionein in the liver & Zn levels
decr.
In catabolic states (e.g. PA, starvation/low food intake & fasting) , Zn is released
from muscles & made available to the plasma
Once Zn has bn absorbed, homeostasis can be maintained (to some
extent) by regulating excretion.
Zn excretion occurs mainly via faeces- thro secretion into d/tract
(from pancreatic juice & other intestinal secretions/juices e.g. bile)
Small amounts of Zn- lost in urine & skin cells.

Physio Functions of Zn
Zinc is involved in:
-

metab. Of all macronutrients & E-prodn

Nucleic acid synthesis (therefore, cell differentiation)
O2 & CO2 transport ( in Carbonic anhydrase)
a/o mechs (via SOD = super-oxide dismutase)
immune system

Zn def.
- Zn status = diff. to measure; bcos plasma Zn levels are affected by
many factors not related to status

- Concerns related to poor Zn status incl:

- Reduced Zn-content in commonly consumed foods esp. processed food
(= great concern in developed countries) NB: Processing reduces Zn
content of foods
- Inhibited or reduced absorptn by many factors found in foods (e.g.
phytic acid esp. in presence of Ca, oxalic acid, poly-phenols & folic
acid); (=Great concern in developing countries.)
- Average absorption rate of Zn =~30% (although there may be variations due to diff.
dietary combinations)

- Vulnerable groups to poor Zn status incl:

- Preg women (esp. in 1st trimester); preg in 1st trimester associated with intrauterine growth retardation (IUGR). Though evidence = conflicting.
- Alcoholics (due to reduced food intake & absorptn in alcoholism)
- Patients with malabsorptn
- Diabetics (why?)

- Signs of Zn def:
- Depressed appetite, poor taste acuity, delayed wound healing, immunosuppression, poor growth, skeletal abnormalities & delayed sexual maturation
( in children)

- Zn def
may occur in:
- PEM (why?)
- Prolonged intravenous nutrition

- Severe Zn def
= may be caused by; liver disease, chronic kidney disease, poor diet, excessive
alcohol
intake, cutaneous disease, severe GI disease & other genetic disorders.

= associated with acro-dermatitis entero-pathica i.e. an in-born error/genetic

disorder of
Zn metab. This condition is characterised by severe rash
(prone to secondary infections); growth failure & behavioural abnormalities.
= Severe Zn def - may be intensified by sickle-cell anaemia & recently hs bn
discovered that Zn def = component in anorexia nervosa & treatmt with Zn-sulphate helps
restore normal eating patterns

Copper (Cu)
Adult human body has ~75mg of Cu
Amount of body-Cu decrease with age
Out of total body Cu- ~40% is found in muscle & ~60% in the liver, brain,
blood (in RBCs & plasma as Caeruloplasmin)
Physio functions of Cu:
Cu functions in a no. of proteins (e.g. Caeruloplasmin) involved in Fe (&
lipid) metab
Caeruloplasmin = essential for Fe metab. (where it converts Ferrous Fe to Ferric
Fe for
Fe in the

transport of Fe in the blood as Transferrin or for temp. storage of excess

mucosal cells as Ferritin)

= involved in response to infections as one of the acute-phase proteins

= component of the f/radical- quenching or a/o enzyme called Super-oxide
dismutase (SOD); which is important in protecting body from damage by
products of the response to infection.

Cu occurs as component of several enzyme systems e.g.

- Cyto-chrome oxidase (CCO), SOD, glutathione per-oxidase (GPO),
various amine oxidases (e.g. Cu-containing amine oxidase enzyme reqd
for cross-linkage formation in the connective tissue pr-s such as collagen
& elastin), and Cu-containing enzymes involved in synthesis of myelin &
neurotransmitters (e.g. encephalins, catecholamines & dopamine).

Richest sources
Vulnerable
groups (to
Sources
& Vulnerable
groups
def.)
Iron (Fe)
See previous slides(WSVs)
on Haem & Non- haem Fe
Mineral

women of child-bearing age,

athletes, preschool children &
adolescents

Zinc (Zn)

Lean meat esp. offal; seafoods &

dairy products
Moderate sources = pulses, &
w/grains
NB: Animal sources = more useful dietary sources than
plant sources

Copper
(Cu)

Organ meats esp. liver & kidneys;

shellfish, nuts, seeds (incl cocoa),
legumes & outer parts of cereals (i.e.
whole-grain/ moroko

- vegetarians, children, women

& the elderly in low income
HHs, alcoholics, prolonged
intravenous feeding, patients
with malabsorptn & diabetes

- ppl who over-suppl Zn

Moderate sources = banana, potatoes, tomatoes &

mushroom

Selenium
(Se)

- popns in areas with low-

Manganese
(Mn)

- none

Fluoride
(F)

Se soil content

Seafoods e.g. fish & fish products,

- Popns in areas with untea & water
fluoridated water
Other sources = fluoride tooth-paste
(esp. for children who may swallow s/amounts

Dietary/Meal Planning
Dietary planning planning diet for one meal, the
whole day & for a life-time period
Meal planning planning for a one meal irrespective
of the previous or the proceeding one
Concept of Balanced diet & Balancing a meal
Meal planning tools = Food Guides e.g. Food
Pyramid, Plate Model, etc
Aim of Dietary/Meal planning To ensure healthy
eating

Objectives of D/M Planning

To achieve an overall intake of

foods containing approp. range of nutrients thro:
Grouping together foods which gen provide similar nutrients & that may be
inter-changeable in the diet (i.e. that may be inter-changeably consumed)
Making a quantitative statement about a no. of servings/portion sizes of
foods from each food group to be taken daily.

Healthy eating & its guidelines (plus PA)