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KENYATTA UNIVERSITY

DEPARTMENT OF FOODS, NUTRITION AND DIETETICS

HFN 453: Nutrition and Behavior

COURSE OUTLINE

Course description

Introduction to nutrition behavior and psychology; Concepts in Nutrition and Behaviour; Brain-
Behaviour Connections; Short-term Effects of Nutrition on behavior; Effects of the following on
brain functioning, the central nervous system and behavior, Chronic and Acute Forms of Under
nutrition; B vitamins, Minerals, Dietary Supplements; Dietary Sugar;Caffeine; Alcohol; Eating
Disorders Syndromes: Anorexia and Bulimia Nervosa; Behavioral Aspects of Overweight and
Obesity; Alcoholism, Nutrition and Behaviour; Methods of Measuring Health Behaviour

Course Objectives

By the end of the course the students should be able to


Explain various concepts in Nutrition and Behaviour
Describe the effects of nutritional practices including alcoholism on the brain and
behavior
Describe the effects of different forms of malnutrition of brain functioning , the central
nervous system and behavior
Describe different forms of eating disorder syndromes
Highlight the Behavioral aspects of Overweight and Obesity
Describe the Methods of Measuring Health Behaviour

Course content
-Introduction to Nutrition behavior and Psychology

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-Concepts of Nutrition and Behaviour
-Brain –Behaviour Connections
-Short term Effects of Nutrition and Behaviour
-Effects of the Following on brain functioning, the Central Nervous System and
Behaviour:
 Chronic and Acute Forms of Undernutrition
 B Vitamins
 Minerals
 Dietary Supplements
 Dietary Sugar
 Caffeine
Alcoholism, Nutrition and Behaviour
-Eating Disorders Syndromes: Anorexia and Bulimia Nervosa
-Behavioral Aspects of Overweight and Obesity
-Methods of Measuring Health Behaviour

Course Evaluation
Two CATs- 30%
Exam- 70%
Total 100%

References
FAO, (2011). Nutrition Education Book of Quotations from a Case Study Survey in Africa.
http://www.fao.org/humannutrition/nutritioneducation/69725/en/
Andreasen, A. R. (2002). Marketing social marketing in the social change marketplace. Journal
of Public Policy and Marketing, 21(1): 3-13..
Sokolik C.A, Bauer K.D. (2001). Basic nutrition counseling Skills Development Cengage
Learning: 1st Edition..
Gochman D (1988). Health Behaviour; Emerging Research perspectives , Plenum Press, New
York

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Kasl K V.(2002). Health Behaviour, illness behavior and sick role behavior. Archives of
Environmental Health, 23.
Bandura A. (1986). Social Fundamentals of thought and Action. A social cognitive theory NJ
Prentice-Hall
Manson, J& Powell K. (1985). Physical Activity, behavioral epidemiology and public health.
Public Health.

LECTURE 1

INTRODUCTION

DEFINITION OF CONCEPTS

Nutritional status- this is the condition of well being of a person and not necessarily the
absence of illness as is influenced by the intake and utilization of nutrients. It can also be
defined as the physiological state of an individual as it is influenced by the relationship
between nutrient intake and requirements and from the body's ability to digest, absorb
and use these nutrients.

Malnutrition- is a condition that results either from imbalanced intake of nutrients or


faulty utilization of nutrients

Under nutrition- is the condition of health of a person that results due to the lack of one
or more nutrients

Over nutrition- a condition that results from excess intake of nutrients both macro and
micro nutrients

Nutrition Assessment Process-The assessment process is the systematic way of


collecting objective information about the client, his/her environment and the support
system

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– healthy habits. Adopting for example behavioral changes, such as quitting smoking,
adopting a healthy diet, and increasing physical activity

– Obesity- This is a body condition that is associated with affluent lifestyle. When, over
prolonged period, more energy is ingested in food than is expended by physical exercise,
work and basal metabolism, weight will be gained and obesity will result

– Nutrition knowledge - knowledge of nutrients and nutrition.



– Protein-Energy Malnutrition (PEM) is a common macronutrient deficiency that occurs
when children consume insufficient amounts of protein and energy (carbohydrates and
fat) to meet the body’s needs.
– A good nutrition status is when the body receives all the nutrients in the right amounts
so as to meet the needs of the body.

– Toxic- The capacity to produce injury at some level of intake.

– Risk factor - A characteristic or circumstance that is associated with the occurrence of a


particular disease.

– Cognition`- a term referring to the mental processes involved in gaining knowledge and
comprehension. These processes include thinking, knowing, remembering, judging and
problem-solving. These are higher-level functions of the brain and encompass language,
imagination, perception, and planning.

– Nutrition- “The act or process of nourishing or of being nourished.”


– “The study or science of the dietary requirements of humans and animals for
proper health and development.”
– “The process by which organisms take in and utilize food material”
Nutrition is usually taken to be important for physical health, but also mental health – brain
health in its widest sense
A diet lacking essential nutrients or containing too many ingredients that are detrimental in

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excess is likely to have adverse consequences for brain function and thus mental health and
behaviour. It is widely agreed that a balanced diet is required to support physical health. It is
likely that a balanced diet is beneficial for the healthy functioning of the brain.

The Importance of Good Nutrition

Humans need food because it provides them with energy and the chemicals they need to keep the
body working and in good repair. The body requires different substances in varying amounts.
The nutrients that people need in their diet are:

* Carbohydrates are sugars and these can be simple or complex. This nutrient is required
because it provides energy.
* Protein is made up of different amino acids. All the tissue in the body is made up using amino
acids, and it is also required for repairing damaged structures.
* Fats is another source of energy in the body. It can act as stored energy. Fat in the body can
also offer a protective cushion for organs and help keep people warm.
* Minerals are inorganic compounds that are needed by the body to assist with certain functions
such as blood cell formation.
* Vitamins are required because they play a role in different chemical processes.
* Water is the most abundant substance in the human body. The body will not be able to survive
for long without regular fluid intake.

If the body does not get the food it needs, it can lead to a situation called malnutrition. Even if
the individual is consuming plenty of calories, they can still suffer from malnutrition if they are
missing any of the vital components in their diet. If this situation is allowed to continue, it can
lead to permanent damage to their health. For example for the young, Multiple nutrition factors
have been taken into consideration, such as:
– the motivation of young people for a healthy diet;
– the information they possess about right nutrition and their attitudes for a healthy
lifestyle.

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It is known that parents can influence the development of their children’s behavioural skills. The
success of achieving a correct nutrition depends on parents’ attitude towards food, because it is
necessary to make smart decisions about what children should eat, and to apply them in real life.

Children’s education on healthy food is something that in our culture does not get enough
attention. It is very important to educate young people’s behaviour to consume natural foods like
vegetables, fruits and to change their preference for fast food or sweets.
The health of population can be maintained only if our young generation increases the
consumption of fresh fruits and vegetables, rather than canned food, to which sweeteners,
coloring agents and preservatives have been added. This is possible by introducing courses on
healthy eating; such courses, to be taught only by professional nutritionists, should be attended
by both children and parents. In this way we could cultivate the taste of the young generation for
fruits and vegetables, because it is known that natural products are healthier than industrially
processed products.

Food behaviours
What do we mean by food behaviours? The term can cover a multiplicity of distinct behaviours
from ‘simple’ chewing of food to food shopping, food preparation, etiquette, and food policy
decision-making. It can be general (e.g. doing the weekly grocery shopping) or quite specific
(e.g. choosing brand A over brand B according to their saturated fat contents). Much knowledge
is required for these behaviours-only a little of which is related to nutrition. For example,
imagine the steps required in making a Soup, including knowing where to buy the best
ingredients, how to combine and cook them. Where exactly in this chain of events does nutrition
knowledge play a part? Behaviours are dynamic processes most of which involve ‘decision
points’ (e.g. knowing when it is safe to swallow that bolus of tough meat). Simple linear
measures of association between knowledge indices and the final behavioural outcomes (as in
correlation-based statistics) are unlikely to reflect the key influence of nutrition knowledge on
decision-making.

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Influences on food behaviours

There are many models of human behaviours in relation to ‘dietary’ behaviours, several of which
have been reviewed . Researchers found that most of these models yielded similar predictiveness
(about 30% of variance) but having any model was better than having no explicit model. Some
of the key components of these models are described briefly to demonstrate that nutrition
knowledge is only one among many likely influential factors:
1. The perceived consequences of the behaviour. These can be favourable or unfavourable, likely
or less likely. Expectancy value models like the health belief model, theory of planned behaviour
stress this aspect.
2. Attitudes and beliefs about the behaviour and the object of the behaviour (e.g. perceptions
about ‘value for money’) are important.
3. Skills like knowing how to shop and how to cook are important.
4. Confidence in being able to perform the behaviour is stressed as self efficacy in models like
Social Learning Theory.
5. The social and physical, internal and external environment. The situations in which foods are
purchased . Nutrition knowledge and food consumption are extremely important as they often
include both social constraints (e.g. ‘It is not “cool” to eat pizzas daily.’) and highly attractive or
aversive physical stimuli (e.g. the sight of a chocolate bar, the smell of freshly baked bread).
6. Motivators are extremely important. These include social influences (e.g. doing as your peer
group does), environmental rewards (reinforcers), biological needs (e.g. hunger) psychogenic
needs (e.g. need for ego recognition) and personal and cultural values – which define what are
‘good’ and ‘bad’ consequences of behaviours. Motivators are often subtle, for example, food
may signify desired states (e.g. eating habits may signify one’s wealth and influence) hence the
importance of hermeneutics. People make and use knowledge to meet their own goals and
purposes – do consumers and nutritionists share the same goals?

The transtheoretical theory, assumes that people go through a series of stages when changing
their behaviours. It has been successfully applied to fruit and vegetable consumption by Ling and
Horwath. This is an important model because it emphasizes that individuals may be affected by
almost unique combinations of factors. This has led to tailoring methods of nutrition promotion;

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which are about twice as effective in bringing about dietary behaviour change as other
approaches.

WHO definition of health_“…health is a state of complete physical, mental and social well-being
and not merely the absence of disease or infirmity”(

Playing together, choosing healthy food, participating in social and cultural activities,are all
signs and causes of health and well-being. Feeling a part of the life of the community is
important in maintaining self-esteem, happiness, and a sense of wellbeing. Conversely,
alienation and isolation from the community and its life and customs can lead to physical, mental
and social ill health. This wider concept of health has many consequences for the principles and
practice of nutrition education, and it is important that those involved in education agree on its
validity. It means, for example, that we will never think of nutrition only from a scientific and
biological point of view – as a matter of calories and vitamins – but rather as a social and
personal concept, too. The relationship between nutrition and behaviour is bi-directional in
nature, with nutritional factors able to affect activity and disposition, and behavior impacting diet
and food intake and which can be positive or negative.

Fundamental conditions for health


Of course, health is not always within our control: it depends on many factors. Some of these are
fundamental – peace, shelter, education, income, gender equity, a stable ecosystem and
sustainable resources (WHO). To these we can add a stable economy, good sanitation and health
facilities, an absence of endemic disease and, of course, food variety and safe food.

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Optimum Health and wellness

Heartiness

• Health promotion – combined educational, organizational, policy, financial, and


environmental supports to reduce risk factors and promote healthy lifestyles
• Objective of Healthy People
• Assist individuals in their pursuit of specific behavior changes
• Identify healthy people who are engaged in risk behaviors
• Motivate people to change their actions
• Provide support that increases chance of success

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• Educational support: provides info. about risk behaviors and consequences, helps
facilitate learning
• Organizational support: provide programs and services that encourage participation and
set up systems of social support
• Environmental supports: provide rules that govern behaviors and support behavior
change
• Financial support: provide monetary incentives to motivate change toward healthy
behaviors
• Health promotion increases likelihood of long term success on the road to health
and wellness

Disease prevention:
• Primary prevention – reduce risk and avoid health problems before they start
• Secondary prevention – interventions that take action to stop risk behaviors before
an actual illness
• Tertiary prevention – treatment/rehabilitation after an illness
• 2 out of 3 deaths in the U.S. and 1 out of 3 hospitalizations are linked to
preventable lifestyle behaviors
• i.e. tobacco use, sedentary lifestyles, alcohol consumption and
overeating
• Chronic diseases from these behaviors leads to financial & societal burden
• 70% of deaths and 75 % of the nations annual healthcare cost
• Primary and secondary prevention best chance to reduce incidence and prevalence
of disease and disability
• Incidence: # of new cases of an illness in a given time period
• Prevalence: # of existing cases of an illness in a given time period
• Certified Health Education Specialists (CHESs): trained health
workers with special credentials and competencies to help plan,
implement, and evaluate prevention programs

Changinging Health Behaviors

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• Change depends on the individual:

• Identify what is most important to you or what poses the most immediate threat to
health; for example:

• Diet

Factors That Influence Behavior Change

• Predisposing factors:

• Knowledge, beliefs, and attitudes based on life experiences as well as gender, age,
race, socioeconomic background

• Enabling factors:

• Skills and abilities, resources available; can be positive or negative

• Reinforcing factors:

• Presence or absence of support, encouragement or discouragement from those


around you

• Motivation

• Wanting to change is important to begin the change process

• Must be combined with common sense, commitment and realistic


understanding of the process

• Rewards or incentives can be good tools for motivation to change

• Beliefs and attitudes

• Belief : appraisal of the relationship between some object, action, or idea and
some attribute of that object, action or idea

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• May develop from direct experience (you experience health changes from
behavior), or indirect experience (someone you know experienced
changes)

• Attitude: relatively stable set of beliefs, feelings, and behavioral tendencies in


relation to someone or something

Choosing a Behavior Change Strategy

• Select a technique or combination of techniques that is best suited to you:

• Shaping – start slowly, keep steps small and achievable, be able to change the
plan if it is not working, be committed

• Visualization – mental practice of the planned action to become better prepared


for the actual event

• Modeling – learning behaviors through observation of others performing that


behavior

• Controlling the situation – putting yourself in a situation that will positively


influence your behaviors

• Reinforcement – promotes behavior by providing a reward upon completion of


the behavior

• Consumable, Activity, Manipulative, Possessional, and Social Reinforcers

• Changing self-talk – improving one’s self-image to encourage the behavior


change

• Rationale-Emotive Therapy, Meichenbaum’s Self Instructional Methods, and


Blocking/Thought Stopping

Changing your Behaviour

• Self-assessment:

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• Antecedents and consequences – identify situations that cause a behavior and
acting to modify them

• Analyzing personal behavior – determine the specific behavior you want to change

• Frequency, duration, seriousness, basis for problem behavior, antecedents

• Decision making – be prepared to make decisions for positive change

• Setting realistic goals – keeps goals challenging but also attainable

Taking Charge

• Make assessment – identify the specific behavior change you would like to make

• Make change – follow these steps to make that change:

• Evaluate behavior and identify patterns

• Select one pattern of behavior to change

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• Use the Behavior Change Contract to formulate a plan

• Chart your progress

• Revise your plan as needed

Summary of Influencers on food behavior

The lifestyles practices that influence food and drink are:

 Family training
 Culture including religion, festivals
 Personal beliefs attitudes and ideas
 Appearance of food
 Medical conditions e.g allergies
 Peer group pressure, fashion
 Personal likes and dislikes
 Availability and cost
 Knowledge understanding,, ideas of health
 Local practices and social expectations

LECTURE 2

PSYCHOLOGICAL DETERMINANTS OF HEALTH BEHAVIOUR

While there is a variety of potential psychological determinants of health behavior,


– personality and
– emotion has been paid attention to.
Cognitions are defined as mediating internal mental processes such as knowledge, attitudes and
beliefs that allow individuals to ‘. . . enact their self-conceptions, revise their behaviour, or alter

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the environment so as to bring about outcomes in it in line with their self-perceptions and
personal goals’.

What is particularly appealing about focusing on cognitions is that they are considered to be
relatively open to manipulation and therefore represent an important channel through which
health behaviour can be modified.

Research in this area has sought to define the different types of cognitions (also referred to as
constructs) that act as behavioural determinants and has attempted to combine them into
structured explanatory models (also referred to as social cognition models or social cognition
theories. Popular examples of these models include the:
 health belief model,
 the theory of planned behaviour (TPB).
 the transtheoretical or stage of change model.

Social cognition models tend to focus on the cognitions that are thought to be important in
decision making and motivation to adopt health behaviours. This process is conceptualised in the
TPB, probably the most dominant model in current health behaviour research.

The theory of planned behaviour (TPB).

The TPB suggests that the likelihood of an individual behaving in a certain way is best predicted
from their intention to perform that behaviour. Intention is an indication of an individual’s
readiness to perform a given behaviour and is considered to be the immediate antecedent of the
behaviour. Intentions are a product of the individual’s:

1. attitude towards the behaviour, which is composed of behavioural beliefs about the
consequences of engaging in the behaviour and outcome evaluations about the extent to which
these consequences are positive or negative;
2. subjective norm, which is composed of normative beliefs about the way in which significant
others would wish them to behave and motivation to comply with these social pressures;

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3. perceived behavioural control, which is composed of control beliefs about the factors that
would facilitate or impede performance of the behaviour and beliefs about the power of control
factors to facilitate or impede performance.

It follows that the more positive an individual’s attitude and subjective norm towards a certain
behaviour, and the greater the extent of control they perceive they have over this behaviour, the
stronger should be the individual’s intention and the greater the likelihood of them performing
the behaviour. An application of the TPB to eating a low fat diet therefore suggests that a strong
intention to eat a low-fat diet (e.g. strongly agreeing with the statement ‘I intend to eat a low-fat
diet over the next month’) would be predicted by a positive attitude to eating a low-fat diet (e.g.
‘My eating a low-fat diet in the next month is beneficial’), strong social pressure to eat a low-fat
diet (e.g. strongly agreeing that ‘People who are important to me want me to eat a low-fat diet’),
and the perception of having a great deal of control over eating a low-fat diet (e.g. strongly
agreeing that ‘Whether or not I eat a low-fat diet in the next month is entirely up to me’).

Furthermore, it is predicted that strength of intention to eat a low-fat diet would be positively
correlated with actual behaviour (e.g.dietary intake assessed using an FFQ).

Limitations of social cognition models


Although social cognition models such as the TPB are widely used to predict a range of health
behaviours, they have received harsh criticism.
One of the main issues is that many of these theories are based on very similar theoretical
constructs that they label differently, creating confusion. The claim is that this situation has led
to fragmentation rather than synthesis of the body of knowledge about the determinants of
human health behaviour.

Another major criticism of social cognition models is that even the best of them have been found
to account for a relatively small amount of variation in observed behaviour. It has been estimated
that social cognition models explain at worst 1% of variation in behaviour and at best 65%. A
meta-analysis of results from 185 applications of the TPB has concluded that this model explains

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on average only 31% of self-reported behaviour and only 20% of objectively-measured
behaviour.
In addition, social cognition models have had more success in accounting for some types of
health behaviour than others. For example, meta-analyses indicate that the TPB has accounted
for an average of 39% of the variance in drug use, alcohol use and smoking, but only an average
of 16% of the variance in dietary behaviours.
One explanation for the relatively-poor predictive power seen by many applications of social
cognition theory is the inadequate assessment of theoretical constructs). In order to investigate
individual differences in cognitions it is necessary to quantify the constructs of interest.

Cognitions are by their very nature unobservable and so measurement most often relies on self-
report, whereby participants respond in a verbal or written manner to statements about the object
in question, most often in the form of a self completed questionnaire. There are a range of
guidelines about the construction of questionnaires for many social cognition models and, as
with any quantitative measure, it is essential that the questionnaire is both reliable and valid. The
construction of psychometrically-sound, salient and user-friendly questionnaires, however,
requires both expertise and adequate resources, not always available to practitioners trying to
apply theory to the design of behaviour-change interventions. Other explanations are less easily
remedied. Social cognition theories predict deliberate behaviour (behavior that is conscious and
planned) and it is now known that much of eating behaviour is not deliberate in the way of other
health behaviours.

Recent research has shown how very susceptible human eating behaviour is to environmental
cues; for example, although they are completely unconscious of these effects, individuals eat
more at a meal eaten with other individuals and they eat less if served in a smaller bowl or on a
smaller plate.

According to the latter analysis, individuals make on average 200 daily food decisions of which
they are unaware, in addition to those of which they are aware. The fact that individuals are

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largely unaware of much of their eating behaviour may explain why models based on the
premise that the decisions are deliberate and conscious fail to predict what individuals choose to
eat.
All social cognition theories focus on an individual’s own beliefs in determining their behaviour.
As such, they tend to down play the role of structural factors that shape and constrain individual
choices.

In the case of nutrition behaviour, factors such as socio-economic status, age, gender and place
of residence all have marked effects on diet. Social cognition theories assume that such factors
have ultimately to play out through the beliefs and actions of the individual, which might mean
that an individual’s attitudes to healthy eating might be given more weight in these models than,
for example, the relative cost or difficulty of accessing healthy food. These latter factors would
be treated as incidental rather than central to social cognition theories.

Other researchers argue that contextual factors completely outweigh an individual’s beliefs in
determining their health behaviour. The emphasis in the TPB and other social cognition models
on the amount of variance in behaviour that can be explained by particular cognitions in a given
population has been rejected. It is dismissed as fundamentally reductionist, and it is claimed that
individual behaviours can only have meaning if they are considered in context. The implication
is that cognitions relating to behaviour such as healthy eating in one situation will not generalise
to healthy eating in another, and therefore trying to accurately predict behaviour from
measurements of underlying attitudes and beliefs is futile.

Finally, social cognition models as a whole have been criticised for giving little consideration to
how cognitions can be most effectively modified to create behavior change. For example, it is
suggested that ‘The theory of planned behavior can provide general guidelines . . . but it does not
tell us what kind of intervention will be most effective. We could consider persuasive
communications, perhaps in the form of newspaper advertisements, flyers’. Indeed, a systematic
review of health interventions based on the TPB has revealed that the majority of the reported
studies have used some form of information provision or persuasive communication, although
they have also employed a range of behavioural techniques.

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Readiness to seek preventative health care is shaped by 4 core beliefs…
– Perception of SUSCEPTIBILITY to disease
(perceived personal vulnerability)
– Perceived SEVERITY of disease
– Perceived BENEFITS of action
– Perceived COSTS of action
– Readiness to Take Action = Perceived Threat
– Readiness to Change Behavior = Perceived Benefit of Taking Action (Threat Reduction)
– Cost-Benefit Analysis

+ =
Perceived Threat Perceived Likelihood of Acting
Benefit

Changing nutrition behaviour

So where does this position leave researchers and practitioners wishing to design and run
interventions to change individuals’ cognitions? Clearly, psychological theory is not only needed
to explain individual propensity to engage in health behaviour but is essential for the design and
evaluation of interventions. Without theory it may be possible to determine the extent to which
an intervention affects the target behaviour, but not how or why it has such an effect. Without an
organising governing theory of health behaviour there would be no way of understanding why,
for example, delivering nutrition information in person is so much more successful in changing
eating behavior than simply handing out a leaflet that describes the benefits of a healthy diet.

If an intervention of this type were to be based on a theory of human behaviour, it would help
explain the relationship between the provision of information and the behavioural outcome.
Answers to ‘how?’ and ‘why?’ can be provided by theory and tested by mediation analyses and
are essential if researchers and practitioners are to go on and create new and innovative
interventions. The relationship between theory and practice is not only one-way. As has been

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pointed out ‘Theory is not theology. Theory needs questioners more than loyal followers . . . The
advancement of . . . theories . . . will come from those who are willing to use the theories, test
them, and subject them to rigorous evaluation’.
Although theory-based interventions to change health behaviour are encouraged and recognised
as likely to be more effective, unfortunately very few are explicitly theory based. This approach
may seem woefully shortsighted, but it is perhaps unsurprising when the limitations of social
cognition models, the most widely used psychological theory, are considered.
Bridging the gap between theory and practice : There appears to be an unhelpful disconnection
between academics working to develop psychological behavior change theory and practitioners
working to develop interventions to change health behaviour.

Nutrition knowledge and food consumption: can nutrition knowledge change food behaviour?

Nutrition knowledge may play a small but pivotal role in the adoption of healthier food habits.
Indeed, most of us implicitly accept the simple knowledge–attitude–practice model. If people
know what is good for them then they are likely to behave in their best interests.

The implications of this overview for public health nutrition are:

(i) we need to pay greater attention to the development of children’s and adults’ knowledge
frameworks (schema building);
(ii) there is a need for a renewed proactive role for the education sector;
(iii) we need to take account of consumers’ personal food goals and their acquisition of
procedural knowledge which will enable them to attain their goals;
(iv) Much more research into the ways people learn and use food-related
Knowledge is required in the form of experimental interventions and longitudinal studies.

What kinds of knowledge are there?

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Psychologists have distinguished two key types of knowledge:
1. Declarative knowledge, knowledge of ‘what is’, awareness of things and processes. For
example, that lemons are a good source of Vitamin C, that high intakes of fruit and vegetables
can prevent hypertension, that milk contains psychotropic peptides, that skin wrinkling is linked
to the type of fats you consume.
Declarative knowledge is very important for individuals’ survival, (e.g. it can be important to
know that railway lines are not a good place to sleep, or, high fat diet will cause obesity).
Obviously declarative knowledge can be divided into many domains, some of which include
various types of nutritional knowledge.

2. Procedural knowledge, this is knowledge about how to do things. For example, how to choose
a low salt packet of soup, how to lay out the cutlery for a dinner party, or how to make a forest
cake. We require a lot of procedural knowledge even to perform the most basic tasks, such, as
how to follow table etiquettes.

LECTURE 3

INTRODUCTION

Diet and behaviour

Diet can affect cognitive ability and behaviour in children and adolescents. Nutrient composition
and meal pattern can exert immediate or long-term, beneficial or adverse effects. Beneficial
effects mainly result from the correction of poor nutritional status. For example, thiamin
treatment reverses aggressiveness in thiamin-deficient adolescents. sucrose and additives were
once suspected to induce hyperactivity, but these effects have not been confirmed by rigorous
investigations. In spite of potent biological mechanisms that protect brain activity from

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disruption, some cognitive functions appear sensitive to short-term variations of fuel (glucose)
availability in certain brain areas. Eg

– A glucose load acutely facilitates mental performance, particularly on demanding, long-


duration tasks. The mechanism of this often described effect is not entirely clear.
– Breakfast omission deteriorates mental performance in malnourished children.
– Intelligence scores can be improved by micronutrient supplementation in children and
adolescents with very poor dietary status.

Good regular dietary habits are the best way to ensure optimal mental and behavioural
performance at all times. Children and adolescents with poor nutritional status are exposed to
alterations of mental and/or behavioural functions that can be corrected, to a certain extent, by
dietary measures.

It is now established that certain essential fatty acids (EFAs) especially Arachidonic Acid (AA)
and Docosahexaenoic Acid (DHA) form an important part of the cellular structure of the brain
and in maintaining its normal functions. No nutrient works in isolation; a deficiency in one leads
to sub optimal functioning of others. The lack of certain nutrients, however, may be associated
with a range of mental and behavioural disorders. A deficiency of omega-3 EFAs is associated
with certain mental and behavioural disorders, such as ADHD, depression, dementia, dyspraxia,
greater impulsivity and aggressive behaviour, but the association is still only partly understood.

BRAIN BEHAVIOUR CONNECTIONS

An intimate relationship exists between nutritional imbalances and psychological or behavioral


symptoms and conditions.  This is sometimes called the body-mind connection.  Hair tissue mineral
analysis (A hair mineral analysis test reveals your mineral deficiencies and heavy metal
toxicity.), when performed and interpreted correctly, illustrates this close connection.  It can also
indicate causes and corrective action needed in most cases of mental and emotional illness.
           

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Human Brain
100 billion neurons ( 1000 potential connections for a single neuron)
100 trillion total possible neuron connections
The brain- Behaviour Connections: Have 3 major and intertwined components
 Genetics/epigenetics ( what you inherit from both parents)
 Intra-uterine environment( during pregnancy)
 Extra-uterine environment(after pregnancy)

The specialist functions of different cells requires nutrients to play particular roles, which implies
specific needs for certain nutrients; the neurones and other brain cells do not escape this rule. In
consequence, some dietary deficiencies can alter cerebral function. Human physiology, and thus
the brain, requires substances of dietary origin called nutrients: vitamins, macroelements such as
carbon, oxygen, hydrogen, calcium, and magnesium; trace elements such as iron, magnesium,
selenium, iodine; as well as copper, zinc, manganese, 8 essential amino acids; and 2 essential
fatty acids, without which life would be impossible, they have been termed vitamin F: linoleic
acid (LA) and alpha-linolenic acid (ALA); DHA (Docosahexaenoic Acid) being conditionally
essential. The brain thus needs nutrients to build and maintain its structure, both to function
harmoniously and to avoid premature ageing. Certainly the brain has priority in supplies, and it is
served before the other organs. If needs be, it can even draw on their reserves and weaken them.
The brain is extremely well protected by a “wall”, the blood-brain barrier. But that does not alter
the fact that it still needs food and nutrition, and that it is best not to ingest toxic substances.

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The brain is always “on.” It takes care of your thoughts and movements, your breathing and
heartbeat, your senses — it works hard 24/7, even while you’re asleep. This means your brain
requires a constant supply of fuel. That “fuel” comes from the foods you eat — and what’s in
that fuel makes all the difference.

What you eat directly affects the structure and function of your brain and, ultimately, your mood.

Your brain functions best when it gets a balanced diet. Eating high-quality foods that contain lots
of vitamins, minerals, and antioxidants nourishes the brain and protects it from oxidative stress
— the “waste” (free radicals) produced when the body uses oxygen, which can damage cells.

The brain can be damaged if you ingest anything other than these nutrients. If you eat too much
of processed or refined foods, the brain has little ability to get rid of them. Diets high in refined
sugars, for example, are harmful to the brain. In addition to worsening your body’s regulation of
insulin, they also promote inflammation and oxidative stress. Multiple studies have found a
correlation between a diet high in refined sugars and impaired brain function — and even a
worsening of symptoms of mood disorders, such as depression.

If your brain is deprived of good-quality nutrition, or if free radicals or damaging inflammatory


cells are circulating within the brain’s enclosed space, further contributing to brain tissue injury,
consequences are to be expected. What’s interesting is that for many years, the medical field did
not fully acknowledge the connection between mood and food.

There are many consequences and correlations between not only what you eat, how you feel, and
how you ultimately behave, but also the kinds of bacteria that live in your gut.

How the foods you eat affect how you feel

Serotonin is a neurotransmitter that helps regulate sleep and appetite, mediate moods, and inhibit
pain. Since about 95% of your serotonin is produced in your gastrointestinal tract, and your
gastrointestinal tract is lined with a hundred million nerve cells, or neurons, it makes sense that
the inner workings of your digestive system don’t just help you digest food, but also guide your
emotions.

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What’s more, the function of these neurons — and the production of neurotransmitters like
serotonin — is highly influenced by the billions of “good” bacteria that make up your intestinal
microbiome. These bacteria play an essential role in your health. They protect the lining of your
intestines and ensure they provide a strong barrier against toxins and “bad” bacteria; they limit
inflammation; they improve how well you absorb nutrients from your food; and they activate
neural pathways that travel directly between the gut and the brain.

Studies have shown that when people take probiotics (supplements containing the good bacteria),
their anxiety levels, perception of stress, and mental outlook improve, compared with people
who did not take probiotics. Other studies have compared “traditional” diets, like the
Mediterranean diet and the traditional Japanese diet, to a typical “Western” diet and have shown
that the risk of depression is 25% to 35% lower in those who eat a traditional diet. Scientists
account for this difference because these traditional diets tend to be high in vegetables, fruits,
unprocessed grains, and fish and seafood, and to contain only modest amounts of lean meats and
dairy. They are also void of processed and refined foods and sugars, which are staples of the
“Western” dietary pattern. In addition, many of these unprocessed foods are fermented, and
therefore act as natural probiotics. Fermentation uses bacteria and yeast to convert sugar in food
to carbon dioxide, alcohol, and lactic acid. It is used to protect food from spoiling and can add a
pleasant taste and texture.

This may sound unbelievable to you, but the notion that good bacteria not only influence what
your gut digests and absorbs, but that they also affect the degree of inflammation throughout
your body, as well as your mood and energy level, is gaining traction among researchers. The
results so far have been quite amazing.

Examples are of some conditions:

a) Autism

( a mental condition , present from early childhood characterized by difficulty in


communicating and forming relationships with other people and using language and
abstract concepts).

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 More and more research indicates that autism is a biochemical disorder of the brain.   The role of
mercury, other vaccine-related toxins, toxic metals, toxic chemicals found in mother’s milk,
pharmaceutical drugs, vaccines and other sources, can all contribute to it.

 Intestinal dysbiosis and food allergies also play a significant role in many cases.  These children
can do extremely well on a nutritional balancing program. 

b) Calcium, Magnesium, and Zinc - The biochemical sedatives for hyperkinesis and
many learning disabilities

 Joey, age three, was diagnosed as learning disabled and hyperkinetic.  It was difficult for him to sit
still for more than a few minutes.  Based on his hair tissue mineral analysis, he began taking a food
supplement containing calcium, magnesium, and zinc - three elements that help calm the nervous
system.  Within two days his mother reported he was more relaxed and easier to manage.  He
began to sleep better, and was able to sit still and play like a normal child.

Calcium raises the threshold at which nerves cells fire, thus reducing the irritability or sensitivity of
the nervous system.  A person whose tissue calcium level is low is prone to nervous
irritability.  Zinc is another anti- stress nutrient.  Zinc deficiency is associated with emotional
instability.  Magnesium is another powerful sedative.  Magnesium sulfate is routinely given to
patients during heart attacks as a sedative medication

c) Biochemical depression – many types exist

Case history. Norma complained of fatigue and depression.  A tissue mineral test revealed very
elevated calcium and magnesium levels, and low levels of sodium and potassium.

 This pattern is associated with great fatigue and a very sluggish thyroid and adrenal glandular
activity.  We call this tendency an exhaustion stage of stress or a slow metabolic or oxidation
rate.  It is the most common pattern associated with feelings of depression.
With corrective diet and the several nutritional supplements, Norma's moods became normal within
three months.  She has since remained well for over 10 years.

Norma also had a second indicator for depression.  Her hair tissue calcium level was above about
175-200 mg%.  This is called a calcium shell pattern.
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 This pattern is associated with psychological withdrawal.  Often it occurs in persons who are very
emotionally sensitive who are under a lot of stress, or who do not handle stress that well.  They
withdraw and depression is one of their common symptoms.

  Correction is similar to the first situation, namely to support and enhance the activity of the adrenal
glands and the thyroid gland to allow the person to make more energy within the body cells.

This approach, using only a natural diet high enough in protein and vegetables, low in sugars and
fats, plus a few nutritional supplements of thyroid, adrenal, B-complex vitamins, a digestive aid and
some calcium and magnesium to allay anxiety and help the person relax, usually resolves this type
of depression as well.  It might take a little longer than the first situation above, but not
necessarily.   

 Norma does not have this situation, which is more serious than the other two.  It is a ratio of
sodium to potassium in the hair tissue that is less than about 2.5:1.  This is called an inversion of the
Na/K ratio. A low Na/K ratio of this type is a further indicator of fatigue, blood sugar imbalance,
resentment, frustration, hostility and other metabolic problems as well.
            In these instances, the supplement program must include a little copper (up to 3 mg/day),
some extra manganese (up to 15 mg/day) and some zinc as well.  A product called Limcomin by
Endomet Labs is used to supply all these and more in one tablet.

            When done properly, all three types of depression can be resolved, often in a matter of
months or less, without the need for drugs.  Of course, if there is a lifestyle or emotional issue that
must be addressed, this should be done as well or one is simply treating a symptom, nothing
more.  This will not be as effective as a complete improvement in the lifestyle of the
person.  However, the nutrition programs we offer will assist with psychological treatments of all
kinds by strengthening the body and assisting the brain to function more clearly.   

Copper imbalance.  This is another common cause of depression.  Still others involve other toxic


metals and other tissue mineral imbalances such as a fast oxidation rate with a low
sodium/potassium ratio.  This is more common in men, while the copper imbalance is more
common in women. 

d) Obsessive-Compulsive Disorder OR OCD     

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  This is commonly associated with copper imbalance, manganese toxicity and perhaps other
biochemical imbalances.  As these improve, often the symptoms of OCD also improve a lot.

 
e) Bipolar Disorder
Individuals with bipolar or manic-depressive disorder often have an underlying
imbalance of slow oxidation and often copper imbalance.  In addition, they often have a
four highs pattern on a hair test or others indicating extreme stress.  The combination of
these two traits leads to the common pattern of days of high energy followed by a period
of very low energy and depression.  This can be corrected in most cases with nutritional
balancing science in a relatively short time of months, usually, and with relatively little
difficulty if one is willing to follow the program carefully.
 
f) Schizophrenia ( a chronic and severe mental disorder that affects how a
person thinks, feels and behaves)
 
    Copper imbalance, mercury toxicity, manganese toxicity, cadmium toxicity and
other imbalances are associated with schizophrenias.  Most respond beautifully to
balancing the body chemistry.  Results can be fast, but may take longer if a person is
far out of balance. 
   Copper and Schizophrenia.  Joan, age 18, was a patient in Scottsdale Camelback
Hospital with a diagnosis of schizophrenia.  She responded poorly to medication and
psychotherapy.  Tissue mineral testing revealed a copper level of 40 mg%, about 15
times normal.  Joan was placed on a diet and nutritional supplements to reduce
tissue copper.
 Her condition improved so radically she was released from all psychiatric care
within six months, and returned to high school the following September.  Excess
tissue copper stimulates the biogenic amines, neurotransmitters associated with
depression, anxiety, mood swings and schizophrenia.  Copper imbalance is quite
common but goes undiagnosed because the tissue mineral test is not often done.
 
g) Seizures or Epilepsy
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 Nutritional balancing programs have helped many people with epilepsy and
seizures even when medical tests have failed to detect an obvious cause for the
seizures, and even when drug therapy has not worked at all. 

 h) Other toxic metals and mental health

   More on Copper.  
Copper is involved in numerous emotional and psychological disorders and random
symptoms such as anxiety, mind racing, mood swings, irritability and others.  This is
because copper is a very bioactive mineral, especially in relation to the nervous
system.  It is associated with stimulation of the biogenic amines, epinephrine,
norepinephrine and dopamine. It is also involved in serotonin, monoamine oxidase
(MAO) and other extremely powerful neurotransmitter substances and chemicals
that influence nervous activity.
  Lead.  Thousands of children in the United States are affected by lead
poisoning.  Lead can cause mental retardation and hyperactivity in children, and
violent behavior in adults.
  Mercury.  The mad hatters in Alice in Wonderland were mercury-toxic.  They
rubbed mercury on felt to make hats.  Mercury accumulates in the brain, where it
can cause severe behavior changes.  Silver amalgam fillings, fungicides and paints
are sources of mercury.
 Aluminum.  Hair levels of aluminum are increasing rapidly in the American
population.  Research links excess aluminum with Alzheimer's disease and other
dementias.  Aluminum is acquired by drinking soda and beer from aluminum cans,
and from anti-perspirants, anti-acids, table salt, cosmetics, salted foods, tap water,
aluminum cookware and perhaps occupational exposure.  It can be removed from
the body if detected early enough.

 Cadmium.  The Journal of Learning Disabilities, Vol. 18, #10, 1985, pp. 609-612
reported that among 980 male U.S. Navy recruits entering basic training, a

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significant correlation was found between hair cadmium levels and behavior
problems.  "The three subjects with the highest cadmium level all displayed serious
behavior difficulties in recruit training". 

i) Other nutrient deficiencies and behavior

  B-complex vitamins are essential for proper nervous system functioning.  Many


people report more energy and less depression when they take thiamine (B1),
riboflavin (B2), niacin (B3) and pyridoxine (B6).  Pantothenic acid (B5) also helps
in energy production.  Two other members of the B-complex family, choline and
inositol, act as natural tranquilizers. 
Many other nutrients can affect behavior. L-Taurine and l-tryptophan have a
calming effect.  L-phenylalanine and l-tyrosine can enhance thyroid activity and
improve energy and mood.  There are others as well.

Hyperglycemia and behavior disorders            


 Carbohydrate intolerance is a common nutritional disorder that produces severe
behavior changes.  Diets high in carbohydrates, and deficiencies of manganese,
chromium and other minerals are often involved.  Among the most common
symptoms of hyperglycemia are confusion, irritability, anxiety and at times
violence.  It is quite simple to identify carbohydrate intolerance and correct it with
diet and food supplements, yet this common malady is often overlooked.  

Food intolerance and behavior

 Any food can cause reactions that affect the nervous system.  One possible reason
for these reactions is that histamine, the chemical that is released in allergic
phenomena, can be released in the brain causing alterations in brain chemistry.
     Brain allergies are often overlooked in the search for reasons for anti-social
behavior.  One cause of Attention Deficit Hyperactivity Disorder (ADHD) is a
reaction to allergic foods or chemical additives found in children’s foods.  

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Depression can also be the result of food allergies, or allergies to chemicals in food
or drinking water. 

Anxiety and panic attacks


 This is one of the easiest conditions to correct using nutritional balancing
science.  Common imbalances include low or high and bio unavailable calcium and
magnesium in the body, low zinc, high copper, high levels of toxic metals, and
rarely other imbalances

Alcoholism and drug abuse


  Nutritional imbalances play a role to some degree with these conditions.  Balancing
body chemistry can particularly help some people to avoid a relapse by reducing
cravings for alcohol, sweets and drugs.  .
 

Short term effects of nutrition on behaviour

As any other organ, the brain is elaborated from substances present in the diet (sometimes
exclusively, for vitamins, minerals, essential amino-acids and essential fatty acids, including
omega- 3 polyunsaturated fatty acids). However, for long it was not fully accepted that food can
have an influence on brain structure, and thus on its function, including cognitive and
intellectuals. In fact, most micronutrients (vitamins and trace-elements) have been directly
evaluated in the setting of cerebral functioning. For instance,

1) to produce energy, the use of glucose by nervous tissue implies the presence of vitamin
B1; this vitamin modulates cognitive performance, especially in the elderly.
2) Vitamin B9 preserves brain during its development and memory during ageing.
3) Vitamin B6 is likely to be of benefit in treating premenstrual depression.
4) Vitamins B6 and B12, among others, are directly involved in the synthesis of some
neurotransmitters.

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5) Vitamin B12 delays the onset of signs of dementia (and blood abnormalities), provided it
is administered in a precise clinical timing window, before the onset of the first
symptoms.
6) Supplementation with cobalamin (B12) improves cerebral and cognitive functions in the
elderly; it frequently improves the functioning of factors related to the frontal lobe, as
well as the language function of those with cognitive disorders.
7) Adolescents who have a borderline level of vitamin B12 develop signs of cognitive
changes. In the brain,
8) the nerve endings contain the highest concentrations of vitamin C in the human body
(after the suprarenal glands).
9) Vitamin D (or certain of its analogues) could be of interest in the prevention of various
aspects of neurodegenerative or neuroimmune diseases.
10) Among the various vitamin E components (tocopherols and tocotrienols), only alpha-
tocopherol is actively uptaken by the brain and is directly involved in nervous
membranes protection.
11) Even vitamin K has been involved in nervous tissue biochemistry.
12) Iron is necessary to ensure oxygenation and to produce energy in the cerebral
parenchyma (via cytochrome oxidase), and for the synthesis of neurotransmitters and
myelin; iron deficiency is found in children with attention-deficit/hyperactivity disorder.
Iron concentrations in the umbilical artery are critical during the development of the
foetus, and in relation with the IQ in the child; infantile anaemia with its associated iron
deficiency is linked to perturbation of the development of cognitive functions. Iron
deficiency anaemia is common, particularly in women, and is associated, for instance,
with apathy, depression and rapid fatigue when exercising.

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13) Lithium (works with other elements, drugs, enzymes, hormones, vitamins, and growth
factors in the body in many different ways. People use it for medicine) importance, at least
in psychiatry, is known for a long time. Lithium is used for mental illnesses,
including bipolar disorder, depression, and schizophrenia; for eating disorders,
including anorexia and bulimia; and for blood disorders, including anemia and low white-cell
count (neutropenia). Lithium is also used for
headache, alcoholism, epilepsy, diabetes, liver disease, kidney disorders, arthritis,
a skin condition called seborrhea, and overactive thyroid. Other uses include treatment of
asthma, Huntington’s disease, Graves' disease, herpes simplex, a movement disorder
called tardive dyskinesia, Tourette’s syndrome, cyclical vomiting, Meniere's disease, a
tingling or “crawling” sensation in the skin (paresthesias), and aggressive behavior in people
with attention deficit-hyperactivity disorder (ADHD).
How does it work?
Exactly how lithium works is unknown, but it might help mental disorders by increasing the
activity of chemical messengers in the brain.

14) Magnesium plays important roles in all the major metabolisms: in oxidation-reduction
and in ionic regulation, among others.
15) Zinc participates among others in the perception of taste.
16) An unbalanced copper metabolism homeostasis (due to dietary deficiency) could be
linked to Alzheimer disease.
17) The iodine provided by the thyroid hormone ensures the energy metabolism of the
cerebral cells; the dietary reduction of iodine during pregnancy induces severe cerebral
dysfunction, actually leading to cretinism.
18) Among many mechanisms, manganese, copper, and zinc participate in enzymatic
mechanisms that protect against free radicals, toxic derivatives of oxygen.

More specifically, the full genetic potential of the child for physical growth and mental
development may be compromised due to deficiency (even subclinical) of micronutrients.
Children and adolescents with poor nutritional status are exposed to alterations of mental and
behavioural functions that can be corrected by dietary measures, but only to certain extend.
Indeed, nutrient composition and meal pattern can exert either immediate or long-term effects,
beneficial or adverse. Brain diseases during aging can also be due to failure for protective

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mechanism, due to dietary deficiencies, for instance in anti-oxidants and nutrients (trace
elements, vitamins, non essential micronutrients such as polyphenols) related with protection
against free radicals

Short-term effects of skipping breakfast

Fourteen percent of UK school children skip breakfast, with this being more likely in the case of
secondary school children and in areas of deprivation. The studies looking at what happens to
children’s performance in school when they miss breakfast show that performance is most
clearly affected when tasks are more mentally demanding, when they involve working memory
(storing and manipulating information in the short term), and in the case of children who are
poorly nourished in general.

1.These studies primarily assume that breakfast is first and foremost a way of increasing levels of
blood glucose, meaning that more energy is available to the energy-hungry brain throughout the
morning. However, the short-term effects of eating on cognition could operate in at least two
other ways:
 consuming carbohydrates and
 consuming protein lead indirectly to the release of neurotransmitters in the brain, which
control communication between neurons and regulate mood, arousal and motivation,
which in turn are likely to influence academic performance. At the moment there isn’t
much work considering the type of breakfast that children consume and therefore the
short-term influence of protein and carbohydrates on learning in school.

2. Another indirect effect of diet on cognition is via the negative impact of hyperactive
behaviour. This has been a controversial issue for many years, but a recent comprehensive
review found that artificial food colours have a small but measurable negative impact on
children’s behaviour. Both school aged and pre-school children were found to be more
hyperactive (over-active, inattentive and impulsive) after consuming artificial food colours,
including but not limited to those with diagnosable ADHD. The authors suggest that there may
be an impact on the classroom learning environment if the majority of children are experiencing

34
these small behavioural changes; they also note that the magnitude of reported effect is
reminiscent of the subclinical lead poisoning that resulted in the banning of leaded petrol. There
is evidence that some children may be genetically at risk for being sensitive to artificial food
colours.

Long-term effects

The most extreme long-term effect of diet on cognition is from malnutrition ( overnutrition or
under nutrition and behaviours associated with the conditions).

Why isn't nutrition incorporated more into mental health care?         
    Most likely, it is a combination of several factors:
1. Ignorance.  Most health professionals of all kinds are unaware of the strong
links between nutritional and biochemical imbalances and mental or
emotional disorders.
2. Reticence on the part of medical and psychological professionals to change
their mode of practice.  Nutrition is not among the disciplines stressed in
medical school or counseling and psychology programs.
3. The drug companies and others who do not want the people healthy control a
lot of medical care everywhere in the developed world.  They influence
professional education, journal advertising, government policies, television
and media coverage, and more.
4. There is little money to be made giving people dietary advice and nutritional
supplements.   Hence, there is no incentive to conduct large-scale studies and
to promote the ideas discussed in this article.
5. The best remedy for this would be to allow free competition among all the
healing arts.  However, the drug companies and other special interest groups
know this, and they deliberately restrict competition through licensing laws,
mainly, and through concentration of power in the hands of governments
around the world. 
            

35
What does this mean for you?

Start paying attention to how eating different foods makes you feel — not just in the moment,
but the next day. Try eating a “clean” diet for two to three weeks — that means cutting out all
processed foods and sugar. Add fermented foods like porridge, sauerkraut, or pickles. You also
might want to try going dairy-free — and some people even feel that they feel better when their
diets are grain-free. See how you feel. Then slowly introduce foods back into your diet, one by
one, and see how you feel.

When patients “go clean,” they cannot believe how much better they feel both physically and
emotionally, and how much worse they then feel when they reintroduce the foods that are known
to enhance inflammation.

References
1. Abramson, E.M. and Pezet, A.W.,  Body, Mind and Sugar, Holt, Reinhart and
Winston, New York, 1951.
2. Chatsworth, L., and Chatsworth, C., Energy, Healthview Publishing,
Charlottsville, Virginia, 1985.
3. Dufty, W.,  Sugar Blues, Warner Books, New York, 1975.
4. Feingold, B., Is Your Child Hyperactive, Random House, New York, 1975.
5. Larson, J.M., Seven Weeks to Sobriety - The Proven Program To Fight
Alcoholism Through Nutrition, Ballantine/Wellspring, New York, 1997.
6. Pfeiffer, C., Mental and Elemental Nutrients, Keats Publishing, New Canaan,
Connecticut, 1975.

LECTURE 4

EFFECTS OF VITAMINS ON BRAIN FUNCTIONING , NERVOUS SYSTEM AND


BEHAVIOUR

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All the vitamins are indispensable for normal functioning of the brain. However, some of them
are very closely involved in the functioning of neurones and other brain cells. In fact, it is even
possible to assign a specific efficacy to each vitamin for certain activities in the cognitive
domain. Thus,
 thiamine (B1), riboflavin (B2), niacin (B3), and the folates improve the level of abstract
thought and lead to a more favourable biochemical status;
 vitamin C improves visuo-spatial performance;
 vitamins B12, B6, A, and E ensure a better visuo-spatial memory and improve abstraction
test results.
It has even been calculated that during ageing, intellectual levels are best protected with daily
vitamin intakes equal to or higher than 150 mg for vitamin C (French Recommended dietary
allowances, RDA, 110), 3 mg for vitamin B6 (RDA, 5), and 3 mg for riboflavin (RDA, 1.6).

As far as pregnant women and infants are concerned, the major purveyors of mental deficiency
in the world are protein-energy malnutrition and deficiencies of iron and iodine. However,
deficiencies of vitamin A and zinc have also been incriminated.
During ageing the antioxidants protect against peroxidation (and other damage) and are thus
involved in the prevention of progressive deterioration of memory . Consumption of fruit,
vegetables, and vitamin E do not totally explain all the favourable effects on cognitive
performance; that is why other antioxidants are being considered, among them the polyphenols.
Numerous other vegetables substances could be advantageous .

Vitamin A
Introduction
Vitamin A is a genetic descriptor for retinoid exhibiting the qualitative biological activity of
retinal (form of vitamin A ). The main molecule structure contains a cyclic part and non cyclic
chain with 5 double bonds in the all transposition. A functional group is found at the end of the
non-cyclic part which can be an alcohol, an aldehyde and a palmitite. The term provitamin, a
carotenoid should be used as the generic descriptor for all the carotenoids exhibiting qualitatively
the biological activitied of beta carotene.

37
1 mcg(microgram) retinal requirement =1mcg retinal
(– Vit A IU is the biological equivalent of 0.3 mcg retinol or 0.6 mcg betacarotene)
=6 mcg beta carotene
=12 mcg Carotenoids
Vitamin A is absorbed in the gut, the chylomicron fraction and then transported to the target
organs bound to the protein, the retinal binding protein (RBP). Zinc and an adequate intake of
protein are required for normal production of RBP.
Function of vitamin A
 Function as the rhodopsin for night vision.

 Helps in the differentiation of the epithelial tissues.

 Necessary for the normal ciliary( about the eye) function.

 Role in the synthesis of glycogen.

 Stabilizer of the lysosomal membranes.

 Function in the cell mediated immunity

 Reproduction

As a result the deficit of vitamin A deficiency will have a diversified effect; that is, causing
blindness, xerophthalmia, increased overall mortality, increased morbidity, increased frequency
of diarrhea, acute respiratory infections, it is also a contributing factor in the causality of
stunting.

In the nervous system, vitamin A is primordial at many levels: for example


 in the synthesis of visual pigments (the eye is part of the nervous system),
 the control of differentiation and proliferation of cells during foetal life.
 It has an important role in the neutralisation of the toxicity of certain substances by the
liver, i.e. hepatic detoxification, thus indirectly protecting the brain.
 Retinol, and especially its active form, “all trans” retinoic acid, carry on their molecular
actions in the different target cells by binding with certain receptors of cell nuclei.

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 Vitamin A and the retinoids are even implicated in synaptic plasticity in a brain region,
the hippocampus, suggesting they have a role in the establishment and maintenance of
cognitive functions.
 Vitamin A can act as a “gene regulator” and as a nuclear receptor modulator; as shown,
For instance in the striatum, a region highly sensitive to vitamin A bioavailability; in
relation with neurobiological alterations and spatial learning impairments observed in
vitamin A-deprived animals .

Vitamin A, and more particularly its precursor, betacarotene,


 contribute to the stabilisation of biological membranes.
 Vitamin A and the carotenoids (among them betacarotene, provitamin A) participate with
other micronutrients (notably vitamins E, C, and selenium) in the protection of tissues, in
particular nervous tissues, from aggression by free radicals or active forms of oxygen.

Food of animal origin supplies ready-to-use vitamin A, whereas that of vegetable origin contains
a precursor that has to be transformed in the body. Vitamin A of animal origin is thus six times
more efficacious than vegetable provitamin A. Due to this, vegetarians can be deficient in
vitamin A if they do not eat sufficient fruit and coloured vegetables.
Retinol-rich products are liver, milk, butter, eggs, some cheeses, and fish; while
green vegetables, carrots, coloured tubers, yellow fruit, and oranges are rich sources of
carotenoids. The addition of vegetable oil increases by at least six fold the bioavailability of beta-
carotene in the intestine.
Causes of vitamin A deficiency
 Insufficient intake: from the animal protein, the vegetables, fruits and oils.

 Infections of the gut, malabsorption, and worm infestation decrease vitamin A absorption.

 Increased need due to infections.

 Protein Energy Malnutrition.

Vitamin A toxicity

39
 Acute Vitaminosis

Ingestion of large doses of Vitamin A can lead to acute hypervitaminosis. This manifests itself as
headache, bulging fontanel in young children, nausea and vomiting, dizziness in adults.
Desquamation of the skin, bone pains and hair loss can be seen in the following days.

 Chronic hypervitaminosis

This is felt due to large daily doses; this can lead to hepatitis, cirrhosis, hair loss, dry scaling
skin, hyper pigmentation and anemia. It is therefore recommended not to exceed 3000mcg for
adults and 7500 in children

 Teratogenicity

This is the relationship between congenital malformation and large doses of vitamin A. However
it is recommended during pregnancy not to give large doses of vitamin A and not exceed 10,000
IU per day as treatment dose.

Vitamin B1, (thiamine)


Introduction
Thiamine is required for the generation of energy from macronutrients and the synthesis of the
neurotransmitter acetylcholine.
Researchers continued to work on isolating the cause of the different effects of diets of polished
and whole-grain rice, but despite many attempts it was not until 1926 that vitamin B1 was finally
isolated in crystalline form. It was synthesized ten years later, and now the term thiamine is used,
rather than vitamin B1.

Properties
Thiamine is one of the most unstable vitamins. It has a rather loosely bound structure and
decomposes readily in an alkaline medium. Thiamine is highly soluble in water. It resists

40
temperatures of up to 100°C, but it tends to be destroyed if heated further (e.g. if fried in a hot
pan or cooked under pressure).
Much research has been carried out on the physiological effects and biochemical properties of
thiamine. It has been shown that thiamine has a very important role in carbohydrate metabolism
in humans. It is utilized in the complicated mechanism of the breakdown, or oxidation, of
carbohydrate and the metabolism of pyruvic acid.

Dietary sources
Thiamine is widely distributed in foods of both vegetable and animal origin.
The richest sources are cereal grains and pulses. Green vegetables, fish, meat, fruit and milk all
contain useful quantities. In seeds such as cereals, the thiamine is present mainly in the germ and
in the outer coats; thus much can be lost during milling .
Bran of rice, wheat and other cereals tends to be naturally rich in thiamine. Yeasts are also rich
sources.
Root crops are poor sources. Cassava, for example, contains only about the same low quantity as
polished, highly milled rice. It is surprising that beriberi is not common among the many people
in Africa, Asia and Latin America whose staple food is cassava.
Because it is very soluble in water, thiamine is liable to be lost from food that is washed too
thoroughly or cooked in excess water that is afterwards discarded.
For people on a rice diet, it is especially important to prepare rice with just the amount of water
that will be absorbed in cooking, or to use water that is left over in soups or stews, for this water
will contain thiamine and other nutrients.
Cereals and pulses maintain their thiamine for a year or more if they are stored well, but if they
are attacked by bacteria, insects or moulds the content of thiamine gradually diminishes.
Absorption and storage in the body
Thiamine is easily absorbed from the intestinal tract, but little is stored in the body. Experimental
evidence indicates that humans can store only enough for about six weeks. The liver, heart and
brain have a higher concentration than the muscles and other organs. A person with a high intake
of thiamine soon begins to excrete increased quantities in the urine. The total amount in the body
is about 25 mg.

41
Human requirements
A daily intake of 1 mg of thiamine is sufficient for a moderately active man and 0.8 mg for a
moderately active woman. Pregnant and lactating women may need more. FAO and WHO
recommend an intake of 0.4 mg per 1 000 kcal for most persons.
Deficiency
Deficiency of thiamine leads to the disease beriberi, which in advanced forms produces paralysis
of the limbs. In alcoholics thiamine deficiency leads to a condition termed Wernicke-Korsakoff
syndrome.

The energy used by the nervous system is derived entirely from carbohydrate, and a deficiency
of thiamine blocks the final utilization of carbohydrate, leading to a shortage of energy and
lesions of the nervous tissues and brain.
Because thiamine is involved in carbohydrate metabolism, a person whose main supply of
energy comes from carbohydrates is more likely to develop signs of thiamine deficiency if his or
her food intake is decreased. For this reason, thiamine requirements are sometimes expressed in
relation to intake of carbohydrate.

This vitamin is extremely important for the brain, because it facilitates the use of glucose, thus
ensuring the production of energy. Deficiency results in a very severe disease, beri-beri. After six
days of research vitamin B1 deficiency in young volunteer men, are observed signs of lassitude,
lower intelligence, irritability, and cramps, and electrocardiographic abnormalities. If the
deficiency continues, the patient complains of pain, particularly of the extremities that is often
painful. All these signs disappear when the vitamin is readministered.

Indeed, thiamine deficiency is found in alcohols abusers. A borderline thiamine status in women
is associated with mood swings; in any case, it is certain that this vitamin modulates cognitive
performance , especially in the elderly. Reduced thiamin (as well as reduced vitamin C,
cobalamin, homocystein and alpha-tocopherol) can contribute to the development of Alzheimer
disease .
In rat, thiamine deficiency results in selective neuronal cell death in thalamic structures; this
may be related with increased brain endothelial nitric oxide synthase expression .

42
Prevention of beriberi
People should be encouraged to consume a varied diet containing adequate quantities of vitamin
B. If highly milled white rice is the staple diet, part of the rice should be replaced by a lightly
milled cereal such as millet, and the diet should be supplemented with foods rich in thiamine
such as nuts, groundnuts, beans, peas and other pulses, whole-grain cereals or cereal brans and
yeast-based products.

The sale of thiamine-deficient rice and other cereals should be prevented by:
· Encouraging the consumption of lightly milled rice and other cereals;
· Legislation or other inducement to ensure that all rice put up for sale is lightly milled,
parboiled or enriched;
· Legislation to ensure vitamin enrichment of cereals made deficient by milling.
Instruction should be given in the most satisfactory ways of preparing and cooking foods to
minimize thiamine loss.
Thiamine should be administered in natural food, yeast products, rice polishings or as tablets to
certain vulnerable groups in the community.
Nutrition education should be implemented to stress the cause of the disease and to indicate the
foods that should be consumed and the ways of minimizing vitamin loss during food preparation.
It is important to strive for early diagnosis of cases of thiamine deficiency and appropriate
measures of treatment and prevention.

Vitamin B3 (PP or niacin) and B6 (pyridoxin)


Introduction
Niacin coenzymes are important in the breakdown of carbohydrates, proteins and fat and in the
synthesis of fatty acids and steroids. Supplements of the nicotinic acid form of niacin can lower
elevated blood cholesterol, but their use is limited by toxicity symptoms such as flushing,
tingling sensations and a red skin rash.
The history of niacin is closely linked with the disease pellagra.
Beriberi is associated with the East and a rice diet, and pellagra with the West and a maize diet.
Pellagra was first attributed to a poor diet over 200 years ago by the Spanish physician Gaspar

43
Casal. At first, it was believed that pellagra might be caused by a protein deficiency, because the
disease could be cured by some diets rich in protein. Later it was shown that a liver extract
almost devoid of protein could cure pellagra.

Pelagra is associated to alcoholism. Between depression due to vitamin B1 deficiency and the
excitation induced by deficiency of B3, the appropriate balance can be found . Vitamin B2
(riboflavin) ensures the harmonious use of the other two vitamins.
The greatest alimentary catastrophes the world has ever known affected two continents and were
due to vitamin deficiency: beri-beri in Asia caused by the consumption of polished rice and
pellagra in North America due to incorrectly cooked maize.

Pyridoxine (B6)
The Pyridoxal phosphate, the coenzyme form of vitamin B6 is needed for the activity of more
than 50 enzymes involved in the metabolism of protein, carbohydrates, and fat.

Functions
 Vitamin B6 is essential for amino acid and fatty acid metabolism, so its requirement is
affected by protein intake.
 It’s involved in making non-essential amino acids and neurotransmitters.
 It also helps to make the blood cells.

Concentration of vitamin B6 (pyridoxin) in the brain is one hundred times greater than in
blood. In general, by ensuring synthesis of chemical mediators, vitamin B6 combats asthenia,
irritability, and depression; vitamin B6 is likely to benefit in treating premenstrual symptoms and
premenstrual depression. The highest levels of B6 in the blood are associated with the best
performance in memorisation tests . Pyridoxin could play a role in tryptophan metabolism,
increasing the production of 5- hydroxytryptophan .

Niacin
Properties
Niacin, a derivative of pyridine, is a white crystalline substance, soluble in water and extremely
stable. It has been synthesized. The main role of niacin in the body is in tissue oxidation. The

44
vitamin occurs in two forms, nicotinic acid and nicotinamide (niacinamide). Niacin is measured
in milligrams.

Dietary sources
Niacin is widely distributed in foods of both animal and vegetable origin.
Particularly good sources are meat (especially liver), groundnuts and cereal bran or germ. As for
other B vitamins, the main source of supply tends to be the staple food. Whole-grain or lightly
milled cereals, although not rich in niacin, contain much more than highly milled cereal grains.
Starchy roots, plantains and milk are poor sources. Beans, peas and other pulses contain amounts
similar to those in most cereals.
Although the niacin in maize does not seem to be fully utilizable, treatment of maize with alkalis
such as lime water, which is a traditional method of processing in Mexico and elsewhere, makes
the niacin much more available.
Cooking, preservation and storage of food cause little loss of niacin.

Human requirements
An adequate quantity for any person is 20 mg per day. Niacin requirements are affected by the
amount of tryptophan containing protein consumed and also by the staple diet (i.e. whether it is
maize-based or not). The FAO/WHO requirement is 6.6 mg per 1000 kcal in the diet.

Deficiency
A deficiency of niacin leads to pellagra, the "disease of the three Ds": dermatitis, diarrhoea and
dementia. Initially manifested as skin trouble, pellagra, if untreated, can continue for many years,
growing steadily worse.

Causes and epidemiology


Pellagra, caused mainly by a deficiency of dietary niacin, is generally associated with a maize
diet in the Americas, just as beriberi is associated with a rice diet in East Asia.
As mentioned in the discussion of niacin, a number of factors have at different times been
suggested as the cause of pellagra. Each theory seemed, when first expounded, to oppose
another. Three of the principal theories appear to have an element of truth. Pellagra was first

45
thought to be caused by a toxin in maize, then by a protein deficiency and finally by a lack of
niacin in the diet.

Vitamin B9 (folic acid)


Folate is necessary for DNA synthesis; it plays a major role in cell differentiation and division so
it is particularly important for rapidly dividing cells such as those in the bone marrow where
blood cells are formed. The requirements are increased during pregnancy and folate supplement
before and during pregnancy have been shown to prevent neural tube defects,this can be reduced
by 85% with systematic folate supplementation .
In the elderly, deficiency decreases intellectual capacity and impairs memory.
Food sources: Foods rich in folate are liver, eggs, many green vegetables (cress, spinach, leeks,
lentils, asparagus, broccoli, cauliflower), and maize, chickpeas, almonds, chestnuts.

Vitamin B12 (cobalamin)


Vitamin B12 is needed to maintain metabolism of folate and fatty acids and to maintain the
insulation – myelin, surrounding nerves. The absorption of B12 requires intrinsic factor, which is
a protein secreted in the stomach. Deficiency is a problem in vegetarians and individuals who do
not produce intrinsic factor.
Deficiency in vitamin B12 in humans and in animal models induces neurological disorders,
psychic disturbances, and haematological alterations.

In fact, the neurological signs can largely precede the haematological signs. Malaise is extremely
frequent. Early diagnosis is essential to avoid irreversible damage to the nervous system. The
main symptoms are memory loss, pain, and abnormal sensations at limb extremities. Vitamin
B12 deficiency during childhood not only retards myelinisation (growth)but causes damage, in
particular neurological, that persists. It can also cause nerve injury leading to blindness. It is
obvious that vegans (excluding all food form animal origin) and even ovo-lacto-vegetarian
(eating only eggs milk and milk-derived products) are at risk.

An important finding is that:

46
 adolescents who have a borderline level of vitamin B12 develop signs of cognitive
changes).
 B9 and B12 vitamins are efficient when used simultaneously in aged people. Vitamin B6
and B12 intakes are positively related to memory performance of middle-aged men and
intakes at around RDI are associated with better memory functioning for women. For
instance, in community dwelling older women, significant vitamin B12 deficiency is
associated with a twofold risk of severe depression. Supplementation with cobalamin
improves cerebral and cognitive functions in the elderly. In fact, vitamin B12 levels
should be measured in all elderly patients with behavioural disorders, because
supplementation frequently improves the functioning of factors related to the frontal lobe,
as well as the language function of those with cognitive disorders. However,
supplementation is unfortunately not successful in the insane. In human, vitamin B12
must be given at the very beginning of the clinical signs, afterward it is non or poorly
efficient. In human, pernicious anaemia is a sign of dementia and is associated with
vitamin B12 deficiency. In fact, measurement of plasma homocysteine is a good marker
of cobalamin and folate deficiency in patients with severely altered cognitive
performance . In rats, vitamin B12 deficiency may play a role in neuronal degeneration
through disturbance of polyamine concentrations in brain .

Practically no animal or higher plant possesses genetic material able to synthesise vitamin B12.
In fact the cobalamins are exclusively synthesised by micro-organisms, bacteria, and yeasts.

Food sources: In human alimentation, vitamin B12 is exclusively present in food of animal
origin: meat, eggs, shellfish, fish; and, to a lesser extend, cheese (notably compressed cooked
cheese), milk and its derivatives. Cobalamine is nonetheless elaborated by a few vegetables but
is poorly bioavailable , some algae seem to be the exception.

Vitamin C (ascorbic acid)

Introduction

47
The discovery of vitamin C is associated with scurvy, which was first recorded by seafarers who
made prolonged journeys. In 1497 Vasco da Gama described scurvy among the crew of his
historical voyage from Europe around the southern tip of Africa to India; more than half the crew
died of the disease. It gradually became apparent that scurvy occurred only in persons who ate no
fresh food. It was not until 1747, however, that James Lind of Scotland demonstrated that scurvy
could be prevented or cured by the consumption of citrus fruit. This finding led to the
introduction of fresh food, especially citrus products, to the rations of seafarers. Subsequently
scurvy became much less common. In the nineteenth century, however, scurvy began to occur
among infants receiving the newly introduced preserved milk instead of breastmilk or fresh
cows' milk. The preserved milk contained adequate carbohydrate, fat, protein and minerals, but
the heat used in its processing destroyed the vitamin C, so the infants got scurvy. Later vitamin C
was found to be ascorbic acid, which had already been identified.
Vitamin C is necessary for the maintenance of connective tissue in the body. In some settings,
vitamin C helps specific enzyme perform its job such as synthesis of essential molecules such as
collagen, neurotransmitters, and hormones, but in others, it acts as an antioxidant. It also
strengthens resistance to infection and in absorption of iron. High doses cause diarrhea and
abdominal pain.

Properties
Ascorbic acid is a white crystalline substance that is highly soluble in water. It tends to be easily
oxidized. It is not affected by light, but it is destroyed by excessive heat, especially when in an
alkaline solution. It is a powerful reducing agent and antioxidant and can therefore reduce the
harmful action of free radicals. It is also important in enhancing the absorption of the non-haem
iron in foods of vegetable origin.
Ascorbic acid is necessary for the proper formation and maintenance of intercellular material,
particularly collagen. In simple terms, it is essential for producing part of the substance that
binds cells together, as cement binds bricks together. In a person suffering from ascorbic acid
deficiency, the endothelial cells of the capillaries lack normal solidification. They are therefore
fragile, and haemorrhages take place. Similarly, the dentine of the teeth and the osteoid tissue of
the bone are improperly formed. This cell-binding property also explains the poor scar formation
and slow healing of wounds manifest in persons deficient in ascorbic acid.

48
It is a common belief, claimed also by some scientists, that very large doses of vitamin C both
prevent and reduce symptoms of the common cold (coryza). This claim has not been verified.
One large study did suggest a modest reduction in the severity of cold symptoms in those taking
vitamin C medicinally, but the vitamin did not prevent colds from occurring. It is not advisable
to take very large doses of medicinal vitamin C for long periods of time.

This vitamin also plays many roles. Ascorbic acid also has a subtle influence on the elaboration
and functioning of nervous tissue, among others.
 Its presence is required for the transformation of dopamine into noradrenaline. Moreover,
the biosynthesis of catecholamines occurs in tissues rich in ascorbic acid like the brain
and the adrenal gland. At very high doses, at least in the rat, vitamin C even has an anti-
stress effect.
 In the elderly, ingestion of vitamin C is associated with a lower incidence of major
alterations in cognitive performance.
 Others have reported a relationship between the serum level of vitamin C and the
intelligence quotient: this increase by four points when the plasma concentration of
vitamin C could increase by half. Indeed, some of the elements used in tests to determine
IQ (non-verbal) are altered as a function of the serum concentration of vitamin C.
 Vitamin C and degenerative pathologies have been reviewed. A regular intake of vitamin
C reduces the risk of cataract.
 In fact, the vitamin plays an important role in protection against different harmful
oxidation reactions that involve molecular oxygen. Its properties as a reducing agent and
its reaction with oxygen-derived free radicals seem to be its most important biological
functions.
Dietary sources
 The main sources of vitamin C in most diets are fruits, vegetables and various leaves. In
pastoral tribes milk is often the main source. Plantains and bananas are the only common
staple foods containing fair quantities of vitamin C. Dark green leaves such as amaranth and
spinach contain far more than pale leaves such as cabbage and lettuce. Root vegetables and
potatoes contain small but useful quantities. Young maize provides some ascorbic acid, as do
sprouted cereals and pulses. Animal products such as meat, fish, milk and eggs contain small
quantities.
49
 As vitamin C is easily destroyed by heat, prolonged cooking of any food may destroy much
of the vitamin C present.
 Ascorbic acid is measured in milligrams of the pure vitamin.

Scurvy
 Scurvy is not now a prevalent disease. Outbreaks have occurred in famine areas and recently
in several refugee camps in Africa.

Causes and epidemiology


 Dietary surveys in many countries in Asia, Africa and Latin America indicate that large
segments of their populations consume much lower amounts of vitamin C than is considered
essential or desirable. Nevertheless scurvy, the classical and serious disease that results from
severe deficiency of vitamin C, now appears to be relatively uncommon. No country reports
scurvy as a major health problem, but outbreaks are seen in refugee camps, during famines
and occasionally in prisons.
 Scurvy was first recognized in the fifteenth and sixteenth centuries as a serious disease of
sailors on long sea voyages who had no access to fresh foods including fruits and vegetables.
Before the era of vitamin research it became practice in the British navy to provide limes and
other citrus fruit to prevent scurvy.
 Some oral contraceptives lead to lowered plasma vitamin C levels.

Clinical manifestations

The following symptoms and signs may occur: ·


 Tiredness and weakness;
 · Swollen gums which bleed easily at the base of the teeth;
 · Haemorrhages in the skin;
 · Other haemorrhages, e.g. nosebleeds, blood in the urine or faeces, splinter haemorrhages
below the fingernails or subperiosteal haemorrhages;
 · delayed healing of wounds;
 · Anaemia.

50
 A patient who has scurvy and exhibits some of the above symptoms, though not appearing
very seriously ill, may suddenly die of cardiac failure.
 Although scurvy is a relatively rare disease, swelling and bleeding of the gums occur fairly
frequently in certain regions and may be due to vitamin C deficiency. Subclinical vitamin C
deficiency may also result in the slow healing of wounds or ulcers. Patients who are to
undergo surgery should be given vitamin C if they may be deficient.
 Vitamin C deficiency may also contribute to anaemia in pregnancy.

Infantile scurvy (Barlow's disease)


Scurvy sometimes occurs in infants, usually aged two to 12 months, who are bottle-fed with
inferior brands of processed milk. During the processing of the milk, the vitamin C is frequently
destroyed by heat. Good brands of processed milk are fortified with vitamin C to prevent scurvy.
Prevention
 Vitamin C deficiency can most easily be prevented in all societies by consumption of
adequate amounts of fresh foods, particularly generous intakes of fruits and vegetables,
including green leaves. Guavas and various other tropical fruits, for example, are high in
vitamin
 Recommended preventive measures are as follows:
 · increased production and consumption of vitamin C-rich foods, such as fruit and vegetables;
 · provision of vegetables, fruit and fruit juice to all members of the community, including
children, beginning in the sixth month of life;
 · provision of vitamin C concentrates if for any reason the previous two measures are not
possible;
 · improved horticulture, including the provision of village and household gardens, orchards
and vegetable allotments in towns and school gardens;
 · encouragement of the wide use of edible wild fruits and vegetables known to be rich in
vitamin C (e.g. amaranth, baobab fruit);
 · action to avoid and discourage the replacement of fresh vegetables, fruit and other foods by
canned and pre-served foodstuffs, and encouragement of the greater use of fresh fruit and
juices in place of bottled products;
 · nutrition education, which should cover the reasons and need for eating fresh foods, and
instruction in means of minimizing vitamin C loss in cooking and food preparation.

51
Vitamine D
Introduction
Vitamin D is different from other nutrients in that the body can synthesize it with the help of
sunlight; it is therefore not an essential nutrient but the dietary requirement varies depending on
the amount synthesized. Vitamin D is essential for calcium absorption from the intestine,
calcium deposition and release from the bone and the kidney.

Physiology
The unique feature of vitamin D is that it is mostly produced in the human body by
transformation of cholesterol metabolites to vitamin D3 in the skin under the influence of
ultraviolet light. The 7 dehydrocholesteral (also called provitamin D) is transformed to pre-
vitamin D3 by UV waves. Once formed, this previtamin D3 is further metabolized in two
metabolites that can revert to previtamin D3. It is thought that this process is a away to both
protect against toxicity(high doses of vitamin D are toxic) and that these metabolites constitute in
fact a reservoir of precursors which can revert to previtamin D3 by UV light.
Vitamin D3 is bound to a vitamin D binding protein to be metabolized in the liver to 25 hydroxy
D3 (25 OH cholecalciferol). The half life of RBP-25OHD3 complex is 15-45 days and
constitutes a factual reservoir of the vitamin. The final conversion happens in the kidney where
the 25.OH cholecalciferal is transformed to 1, 25 dihydroxy cholecalciferol. It is this last
metabolite that is metabolically active.

Regulation and biological actions of 1,25(OH)2D


When the calcium concentration drops, the parathyroid glands secrete the parathyroid hormone
(PTH). This stimulates the production of 1,25(OH)2D. As a result of this, the active absorption
of calcium in the intestine is stimulated, the loss of calcium through the kidneys is decreased
(resorption is stimulated) with increase in phosphate excretion and bone cells (osteoclasts) are
stimulated to resorp bone minerals and release calcium in the extracellular compartments. As a
result of this the calcium concentration will rise and the secretion of PTH decrease.

Vitamin D production

52
The main source of vitamin D is the production in the skin through the conversion of precursors
under the influence of ultraviolet light. It is estimated that a one erythema producing dose of UV
is equivalent to a dose of 10,000 IU of vitamin D. The angle of incidence of the sun determines
how much of the UV range needed for the transformation is present in sunlight. The lower the
inclination of the sun the lesser the amount. Glass and particles in the air often reflects UV lights.
In countries where rickets is still reported, their calcium intake from milk is low. The diet, which
is largely cereal based, contain large amounts of phytates which decrease considerably the
bioavailability of calcium. This in turn stimulates the PTH secretion and the production of 1,
25(OH)2D.

It has been demonstrated that the high doses of 1,25(OH)2D enhance the biological inactivation
of 25 OHD. Overtime this will lead to a decrease in vitamin D and produce rickets. Thus an
adequate supply of calcium may be as important for maintaining vitamin D status as it for
calcium homeostasis.

Food sources of vitamin D


Although vitamin D is present in a number of foods such as eggs York, oily fish, and some
extend milk, the natural diet can only be considered a trivial source of vitamin D

Vit D Deficiency

Symptoms of vitamin D deficiency include:

Rickets in children

Osteomalacia in adults

Prevention:
Rickets :
 Exposure to sunlight is the best prevention.
 In high altitude countries, however supplements may be needed. Breast fed children
should receive 400 IU per day. Large doses of 200,000 IU can also be given every three
months.

53
 Food fortifications can also be used to prevent rickets.
 The elderly are particularly at risk, those who stay indoors most of the time and get very
little exposure to sunlight. This can develop to demineralization of the bone with bone
pains and fractures, daily supplements can be necessary.

Toxicity

Toxicity can increase calcium absorption and bone mineralization. High blood calcium causes
deposition of calcium in the kidneys, heart, lungs and arteries.

Vitamin D and Brain/CNS.


This vitamin is currently undergoing investigation in connection with the structure and function
of the brain, since vitamin D or certain of its analogues are of interest in the prevention of
various aspects of neurodegenerative or neuroimmune diseases.
 Vitamin D protects the neurones of the hippocampus, and modulates the transport of
glucose to the brain.
 Its role in models of multiple sclerosis is under study as a result of recent positive
findings, in particular concerning the duration and intensity of crises.

Self test
 List three main food sources of Vitamin D.

 . Explain the interaction between calcium and Vitamin D in causing rickets.

 Describe the hormonal activities which proceed low levels of calcium in the body.

 Outline three steps in place to prevent rickets.

Vitamin E (tocopherol)
Introduction

Functions:

54
 Vitamin E functions as a fat soluble antioxidant Primary defender of the body against
oxidation, protecting the lipids and other vulnerable components of the cells and their
membranes from destruction. Since polyunsaturated fats are particularly susceptible to
oxidative damage, its requirement increases as the polyunsaturated fat content of the diet
increases.
 Vitamins E are very active in the lungs and red blood cells where there is high exposure
to oxygen; it also helps to protect the lungs against air pollutants especially when a
person is breathing hard during exercising.
 Vitamin E plays a role in the immune system by protecting the white blood cells.

 This vitamin protect especially against ageing, in particular the brain, notably in
association with selenium. However,
 alpha-tocopherol also plays a role at the level of cognitive functions. In fact, what is
known as vitamin E is in reality a mixture of numerous substances: tocotrienols and
tocopherols (alpha, bêta, gamma, delta); moreover, alpha tocopherol has 3 asymmetric
carbons, hence 3 different molecules. Each of these molecules is classically ascribed a
coefficient of vitamin activity determined by various methods, either in vivo or in vitro.
In terms of nutrition, only alpha-d-tocopherol - and not gamma-tocopherol - is
bioavailable and integrated in biological membranes, including those in the brain. The
eventual specific roles of gamma-tocopherol are currently investigated.

Deficiency:
Nutritional vitamin E deficiency alters brain fatty acid profile. Experimental vitamin E
deficiency induces retinal abnormalities.
Early vitamin E supplementation reduces Abeta levels and amiloid deposition in a transgenic
model of Alzheimer disease. High doses of vitamin E are proposed in the treatment of disorders
of the central nervous system in the aged and using antioxidant vitamin supplements (including
vitamin E) reduces risk of Alzheimer disease .
The risk of dementia is significantly reduced by neutralization of the active and toxic forms of
oxygen and scavenge free radicals.

55
That is to say, they protect unsaturated fatty acids against peroxidation, and thus contribute to
maintaining the integrity and stability of cellular structures in the brain. They act in lipid phase at
a very low concentration (about one molecule per two thousand fatty acid molecules) and take
part in a vast complex and interactive protective system, in cooperation with beta-carotene,
vitamin A, vitamin C, and various enzymes that function with selenium, copper, zinc, and
manganese. A distinct clinical syndrome (with paralysis) of combined vitamin E and vitamin C
deficiency have been described in guinea pigs.

Summary of deficiency

 Hemolysis of red blood cells


 Loss of muscle co-ordination and reflex.
 Impaired vision and speech
 Deterioration of respiratory muscles
 Associated with some types of cancers.

Toxicity

High doses of vitamin E can interfere with functions of vitamin K.


A lot of people take vitamin E supplements for various reasons e.g. improved physical
performance, enhances sexual performance, slows process of aging, slow progression of some
diseases. These claims have no scientific basis.

Food Sources

Oil seeds, meats and tripes, eggs, nuts, soybean oil, wheat germ, and green vegetables.

Vitamin K

Vitamin K is found in plants and synthesized by bacteria in the gastrointestinal tract. Vitamin K
is essential for blood clotting. It also participates in the synthesis of bone protein. A deficiency
of vitamin K results in a failure of blood to clot. Since this is a problem in new born, an anti
vitamin K factor, dicumarol is used medically as an anticoagulant.

56
Recently, it was demonstrated a correlation between vitamin K and sphingolipids concentrations
in rat brain; moreover this vitamin present a protective effect on aging retina, the sparing effect
being most evident in the inner plexiform layer and in the photoreceptor inner and outer
segments Assays with vitamin K remain to be made on human.

Food sources
Liver, leafy vegetables and cabbage.

LECTURE 5

EFFECTS OF MINERALS ON BRAIN FUNCTIONING, NERVOUS SYSTEM AND


BEHAVIOUR

Minerals
The trace elements are present only in low but variable amounts. However, their physiological
importance cannot be deduced by simple deduction from their concentration, even if it is low.
Some, like iodine and cobalt, have only one main role. From among many we will only examine
iron, zinc, iodine, magnesium, and selenium.

Iron
The common cause of anaemia is a deficiency of iron, although not necessary a dietary
deficiency of total iron intake. In anaemia the blood has less haemoglobin than normal.
Haemoglobin is the pigment in red cells that give blood its red colour. It carries oxygen in the
blood to all parts of the body.
In anaemia either the amount of haemoglobin in each red blood cell is low- hypochronic
anaemia; or there is a reduction in total number of red blood cells in the body. The life of each
red blood cell is about 4months and the red bone marrow is constantly manufacturing new cells
for replacement. This process require adequate amount of nutrients especially iron.

57
Some anaemias do not have causes related to nutrition but are caused by, for example, congenital
abnormalities or inherited characteristics such as sickle cell diseases, aplastic thelassaeminas
and circle haemmorrhage.

When a person progresses from adequate iron balance to overt iron deficiency anemia, the
deficiency may be considered to develop in a sequence of three stages. First is the depletion of
the iron stores from the liver, spleen and the bone marrow, secondly is the decrease in the
transport iron transferring saturation, these two are the two stages of iron deficiency. Third stage
develops when the supply of transport iron decreases sufficiently to restrict hemoglobin
production. This is characterized by an elevation of erythrocyte protoporphyrin and the gradual
development of detectable anemia and microcytosis.

Iron therapy is usually directed at the correction or prevention of the anemia that characterizes
the third stage of iron deficiency.
Iron deficiency can be determined by hemoglobin levels which are different from one population
to the other. The mean corpuscular volume of microcytic hypochromic anemia (MCV). The
serum Iron and iron binding capacity and the serum ferritin can also be determined which is
roughly proportional to the abundance of storage iron at all stages a serum ferritin value of less
than 12 mg/L indicates a depletion of iron stores. Erythrocyte protoporphyrin in the red blood
cells when insufficient iron is available to combine to form haem.
Causes of iron deficiency
This can be due to monthly menses, delivery losses, lactation, and poor intake of iron rich diets,
infection by malaria and infestation by worms.
Symptoms
Many symptoms have been reported to be clinical signs of iron deficiency, even in the absence
of anaemia:
for example apathy, somnolence, irritability, decreased attention, inability to concentrate, and
memory loss. But these symptoms are difficult to interpret because of their subjective nature.
However, it is evident that iron modulates cerebral development, and the relationship between
iron status and cognitive performance is currently attracting interest.

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– The deficit in iron acts globally at two different levels: on one hand by less efficient
supply of oxygen to the brain; and on the other by decreasing brain energy production, as
iron deficiency decreases the activity of the enzyme cytochrome oxidase in certain
cerebral regions. This results in less production of energy because of the decreased
activity of the enzyme, and consequently a decrease in metabolic activity of the cerebral
cells.
– Iron deficiency during embryogenesis impairs myelination via the metabolism of
oligodendrocytes . But all nervous cell types are affected, and as a result iron deficiency
during early development affects cognitive functions in the long term, and this persists
even after iron supplementation. It is unfortunately common to observe that severe iron
deficiency during early childhood induces cognitive deficits that can persist after 10 years
of treatment with iron. In fact, iron concentrations (and those of magnesium, copper, zinc,
and selenium) are higher in the umbilical artery than in the vein, which makes them
critical during the development of the foetus. The transfer of dietary iron to the foetus
depends on its level in the mother’s digestive tube.
– Infantile anaemia with its associated iron deficiency is linked to perturbation of the
development of cognitive functions, and exists in school children and adolescents even in
Western countries. It is important that iron deficiency be sought even in the absence of
anaemia .
– In the domain of public health, the distribution of biscuits enriched in iron improves the
intellectual performance of children in the underprivileged sector of the population. It
should be noted that in some countries iron deficiency can be due to loss of blood (and
thus iron) caused by infection, particularly parasitic, leading to the same cognitive
problems as nutritional deficiency of iron.

– Iron deficiency also causes perturbations in the electroencephalogram. The dopaminergic


system may be especially involved, and this observation could be related to iron
deficiency in children with attention deficit/ hyperactivity disorder. During aging, trace
elements protect cognitive function.

Treatment of Iron deficiency

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The treatments of iron deficiency can be
 oral, this is done to correct the Hb deficit and to restore the liver stores.
 Secondly it can be administered parenteraly as intramuscular or intravenous.
There are two approaches for the control and prevention of iron deficiency that is through

 improvement in the habitual diets to enhance iron availability by using nutrition education
and agricultural extension programmes aiming at changing food productions and food habits.
 The second approach is through direct interventions where iron is given in the form of
fortification by the use of a food vehicle or a supplement.
Food sources
Dietary iron exists in two main classes: heme iron and nonheme iron.
An heme iron molecule was found in the brain, which is to be expected related to the oxygen
requirements of that organ. Physiology enables human to absorb 25 to 30% of heme iron, but
only 2 to 4% of that present in vegetables (mineral). Consequently, the human organism can take
up one hundred times more iron (6 mg) in one hundred grams of the food richest in heme iron
(cooked blood sausage) than in the vegetable food that is richest in heme iron (cooked lentils,
0.06 mg).
The bioavailability of iron in a vegetable food depends on what is served with it. Thus, for
example, a cup of tea drunk during a meal (and, to a lesser extent, coffee) decreases fourfold the
amount of iron taken up by the organism, whereas a glass of orange juice doubles it. Animal
proteins (of whatever source, terrestrial, maritime, aerial) increase the uptake of mineral iron,
independently of whether they contain heme iron; on the other hand, soybean proteins decrease
uptake slightly(anti-nutrients in them inhibit this).

Copper
In brain aging and in nerodegenerative disorders, abnormal interactions of iron or copper with
metal-binding protein, such as neuromelanin or amyloid-beta peptide (Abeta), leading to
oxidative stress, are important mechanisms. An unbalanced copper metabolism homeostasis (due
to dietary deficiency) could be linked to Alzheimer disease. In mouse, APP-induced alteration
linked to copper homeostasis can be reversed by addition of dietary copper. Moreover,

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permanent impairment to motor function persists in rat after long-term recovery from perinatal
copper deficiency.

Function
 Necessary for the absorption and use of iron in the formation of hemoglobin
 Part of many enzymes

Food sources: Beef liver, Sunflower seeds, Lentils, molasses, asparagus, almonds, chocolate.

Zinc
Introduction
Zinc is one of the most important trace elements needed by your cells.
Functions:
 It helps your immune systems,
 aids in protein synthesis, cell reproduction and wound healing,
 and plays a major role in fertility and conception, among others.

The importance of zinc can not be over-emphasized.

This element plays a role in cognitive development , and it also participates in the mechanisms
for perception of taste and smell: a deficit induces anosmia. The sensory receptors and brain
regions that perceive and interpret the pleasures of eating are themselves very rich in zinc, and
levels in the taste buds are very high, zinc is necessary for their function. Zinc acts by its
presence in the gustin , which participate in the perception of taste. However, there is a danger
that a vicious circle can be established which, unfortunately, is often met in elderly people: the
low zinc level (due mainly to a decrease in the consumption of meat, finfish and seafood) leads
to reduced appreciation of taste. Food seems insipid, and less is eaten due to the loss of pleasure
– which increases zinc deficiency, thus the circle becomes even more vicious.
Food Sources:
Zinc is naturally present in various foods and it food sources such as meat, poultry, dairy
products, beans, whole grains and nuts are rich in zinc. However, the body can only absorb about
30% of the zinc that we take in. Because of this nature of zinc absorption, zinc deficiencies

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happen to many of us. Oysters are the food that is richest in zinc, they contain ten times more
than the next richest foodstuffs, some cheeses, as well as steak and poultry livers. On the other
hand, green vegetables, fruit, sugar, fats, and drinks are low in zinc.

Zinc deficiency:
This metal plays a role in a multitude of physiological mechanisms. Interestingly, zinc deficiency
impairs whole-body accumulation of polyunsaturated fatty acids, thus brain supplying could be
affected. Part of cerebral zinc (10 to 15 %) is present in synaptic vesicles for some glutaminergic
neurons. Consequently, zinc deficit induces behavioural changes.

It has been suggested that some psychiatric problems can stem from the reduction in dietary zinc;
animal experiments have shown clearly that deficiency (in particular during pregnancy) results in
loss of neurones and a reduction in brain volume.
In contrast, giving pregnant women zinc supplements has not been proved effective for
improving the cognitive performance of their children.
Perinatal omega-3 polyunsaturted fatty acid supply modifies brain zinc homeostasis during
adulthood, this being important in relation with the fact that neuronal zinc is involved in
formation of amiloid plaques, a major characteristic of Alzheimer’s disease ; in fact, perinatal
omega-3 deficiency induces over expression of ZnT3 (transporter identified in synaptic vesicles
and found in some régions such as cortex and hippocampus) and cause abnormal zinc
metabolism in the brain.

Causes of Zinc Deficiency


 Inadequate intake of zinc in the daily diet

 Increase in the losses of zinc from the body, such as when copper exposure is high

 When requirement for zinc increases for one reason or another (such as when lactating or
pregnant). These conditions tend to occur more in the elderly, in mothers, and in young children.

 Gastrointestinal mal-absorption can also lead to zinc deficiency symptoms.

Symptoms of Zinc Deficiency

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The symptoms of zinc deficiency vary greatly from one person to another.
• behavioral and sleep disturbances
• dandruff
• different kinds of skin lesions such as eczema, psoriasis and acne
• growth retardation
• hair loss
• hang nails• inflammation of your nail cuticles
• hyperactivity
• increased allergic sensitivity
• inflammatory bowel disease
• loss of appetite
• loss of senses of taste or smell •
• mild anaemia
• pre-eclampsia (toxaemia) in pregnancy and post-natal depression • pre-menstrual syndrome,
disturbance in your menstrual cycle
 Weight loss

 Intercurrent infections

 Hypogonadism in males

 Lack of sexual development in females, loss of sex drive

 Delayed puberty in adolescents

 Mental lethargy

 Delayed wound healing

 Diarrhea

 Pneumonia

 Stretch marks (striae)

 Poor Immune system

Abnormal levels of zinc have been found in the eyes of people with:

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 cataracts

 cataracts or glaucoma

 macular degeneration, myopia or retinal detachment

Zinc has been found useful in treating myopia (nearsightedness).


Zinc Deficiency Treatment
 Increasing intake of foods rich in zinc content : oysters, nuts, peas, meat products, eggs, whole
wheat grains, oats and pumpkin seeds
Also intake of vitamins such as vitamin A, E and B6, as well as minerals such as magnesium,
phosphorus and calcium, can help in the absorption of zinc

 Severe zinc deficiency can be managed through intake of zinc supplements in two forms: zinc
sulfate and zinc gluconate, the doses of which range from about 15 to 300 milligrams. The
chelated zinc form is most recommended. However, when taking these supplements, make sure
that you are aware of the risks and interactions of high amounts of zinc.

Iodine
Introduction
Iodine is an oligo-element that is present in the human body in a very small quality (15-20 mg
for adults). It is only known function is an essential element in the production/composition of the
thyroid hormones. These hormones have a role in the metabolism of cells in the brain in a
situation of iron deficiency, thyroid hormones synthesis and availability is reduced, with
numerous health consequences.

Iodine Deficiency disorder in the life cycle


In the past the deficiency was called endemic goiter, it is now called iodine deficiency anaemia.
The spectrum of deficiency is as shown in the table below
The spectrum of iodine deficiency disorders(IDD)
Fetus abortions Still birth
Congenital anomalies

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Increased perinatal mortality
Endemic cretinism
Neonate neonatal goiter Adolescent(sub clinical)hypothyroidism
Impaired mental retardation
Increased susceptibility of the thyroid glands to nuclear
radiation
Adult goiter with its complications Hypothyroidism
Impaired mental function
Spontaneous hyperthyroidism in the elderly
Iodine induced hyperthyroidism
Increased susceptibility of the thyroid glands to nuclear
radiation
Table: Adapted from Hetzel(1) Aurberg et. al (52,171) and Stanbury et. al(158)

The effects of iodine deficiency I growth and development can be considered at the various
stages of life as follows.

Iodine deficiency in the fetus


This can be as a result of the maternal deficiency resulting into impaired synthesis of the thyroid
hormones by the mother and the fetus. An insufficient supply of thyroid hormones by the
developing brain may result in mental retardation. Brain development in the human fetus and
neonate occurs in 2 main stages. In the first phase that is in the first and the second trimester, this
phase the supply of thyroid hormones solely depends on the maternal stores of iodine. The
second phase occurs between the third trimester and year two postnatally, the supply of thyroid
hormone depends on the fetal origin.

Iodine deficiency in the neonate


And increased perinatal mortality due to iodine deficiency often results to perinatal mortality.
Low birth weight of any cause is generally associated with a higher rate of congenital
abnormality and higher risks through childhood. The state of thyroid function in the neonate
relates to the fact that the brain of the human infant at birth has only reached about one third ofits

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full size and continues to grow rapidly until the end of the second year. The thyroid hormone,
depends on an adequate supply of iodine, is essential for normal brain development.

Iodine deficiency in the adults


A high degree of apathy has been noted in populations living in severely iodine deficient areas. It
is apparent that reduced mental function due to cerebral hypothyroidism is widely prevalent in
iodine deficient communities. Which affects their capacity for initiative and decision making?
The impact to the brain and neorointellectual development, iodine deficiency at any period in
life, including during childhood, can induce the development of goiter with mechanical
complications. It is also now accepted that hyperthyroidism is one of the disorders induced by
iodine deficiency.

Causes of iodine deficiency


The immediate cause of IDD is a deficiency of iodine in the diet. The underlying cause is a
deficiency of iodine in the local soil on which the vegetation grows, animals graze and crops are
cultivated, which results in a shortage of iodine in local foodstuffs. The effects of iodine
deficiency are mostly seriously manifest during pregnancy and parturition. Iodine deficiency also
has economic and social consequences for development.
The severity of IDD is classified on the basis of prevalence of goiter and the mean level of
urinary iodine in the test population.

The existence of an inverse relation between the prevalence of goiter and the urinary excretion of
iodine over 24 hours is used as an indicator of iodine intakes. The correction of the iodine
deficiency decreases the prevalence of endemic goiter, of cretinism and hypothyroidism.
Factors explaining the iodine intake
 The level of iodine in the soil and water determines the rates of deficiency, secondly is the
phenomenon of isolation that is due to poor food diversity and fortification programmes.

 Goitrogenous factors-additional factors play a role in the iodine deficiency especially in


regions where its intake is very adequate. Thiocyanates are derived from intestinal breakdown of
cyanogenic glycoside, lamarin from cassava and its conversion to thiocyanate by the liver. In
regions with high incidence of endemic cretinism an iodine deficiency, local foods may

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contribute to this. Thiocyanate may cross the human placenta and affect the thyroid of the fetus.
Cabbages may also have goitrogenic substances.

 The thioureas affect the level of the oxidation and metabolism of iodine in the thyroid glands.

Iodine needs in man


The physiologic needs are equal to the hormonal quantity of iodine that is produced everyday,
which is 50-100ug/daythe quantity starts increasing in puberty, certainly among the women.
Among the girls of 11-12 years a slight increase in the volume of the thyroid body is not rare.
The prevention of iodine deficiency =a regular and stable iodine administration
Vulnerability of the problem
Several factors can be taken into account when determining and quantifying the enemicity of the
problem related to iodine deficiency:
 The prevalence of endemic goiter

 The dose of urinary iodine

 The dose of Thyroid stimulating hormone

 The prevalence of cretinism.

The revised classification of goiter is as


shown below
CLASSIFICATION DESCRIPTION
Grade 0 No palpable or visible goiter
Grade 1 A goiter that is palpable but not visible when the
neck is in the normal position (i.e. the thyroid is
not visibly enlarged). The thyroid nodules in a
thyroid which is otherwise not enlarged fall into
this category.
Grade 2 A swelling in the neck that is visible when the
neck is in normal position and is consistent with
an enlarged thyroid when the neck is palpated

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Intervention strategies
 Iodized salt-this is one of the most simple, least expensive and most efficient measures in
nutrition and public health

 Iodization of water-water has been used as a good means of transport with a large distribution
by the use of a slow release capsule put in water distributing systems

 Iodized oil has been used as supplementation programmes when other methods have proven
not effective, it can be given orally or by injection. This should be avoided over the age of 45
because of the possibility of precipitating hyperthyroidism in subjects with long standing goiter.

The side effects of iodine supplementation


 Iodine induced hyperthyroidism

 Thyroid cancer.

This trace element is directly involved in cerebral functioning and intelligence. In fact “cretin”
was originally strictly a medical term, a consequence of the mental retardation in children due to
iodine deficiency during pregnancy. Iodine is one of the trace elements present in the human
body in extremely small amounts: 15-20 mg in the adult or 0.0285.10-3% of body weight.

In humans, the only known role of iodine is to participate in the composition of hormones
secreted by the thyroid gland. In humans, cerebral development takes place mainly during the
foetal period, but it continues up until the end of the third year of life. Consequently, a deficiency
of either iodine or thyroid hormones during this critical period
– induces not only a slowing of the metabolic activity of all the cells but also
– permanent alterations in the development of the brain, of which the most evident sign is
irreversible mental retardation.
The WHO stresses that iodine deficiency is the first cerebral disease in the world that it would be
possible to prevent. In fact, with goitre it affects 740 million human beings on earth. At the
general population level, iodine deficiency lowers IQ on average by 10 to 15. Iodine deficiency
perturbs the intellectual and neuromotor functions even in apparently normal people. It is

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therefore recommended that iodine levels in pregnant women should be monitored to avoid
possible intellectual problems in their children. In many countries, an insufficient intake is made
worse by the consumption of vegetables rich in goitrogenic substances such as thioglucosides
(like brassica) or the cyanoglucosides (manioc, sorgum, maize, sweet potatoes, etc.).

In addition, salt used by the food-processing industry should be iodinated. Meanwhile, iodine
can be found in useful amounts in mussels, oysters, seafish and eggs .

Magnesium
Magnesium is a mineral that affects the metabolism of calcium, sodium and potassium. About
40% of body magnesium is in muscle and other soft tissues, about 1% is in the extracellular fluid
and the remainder is in bone.

Functions
 Involved in bone mineralisation
 The building of protein
 Enzymes action
 Normal muscular contractions
 Nerve impulse transmission
 Maintenance of teeth
 Immune system

Deficiency
 Weakness, confusion, convulsion
 Bizarre muscle movement e.g eye and face
 Hallucinations
 Difficult in swallowing
 Growth failure in children

Toxicity RDA

Rare 350mg/day men,

280mg/day women

Its deficiency is usually linked to spasmophilia, a state characterised by tetany without calcium
being quantitatively low in the organism. The magnesium reserves (twenty-two grams in adults)
are stored mainly in bone (more than half) and in skeletal muscle (one quarter). The rest is

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distributed throughout the organism, especially in the nervous system. It has two roles, structural
and metabolic. It is a stabiliser of the different compartments of the cell (organelles, such as the
nucleus, or the mitochondria that produce energy, etc). Magnesium plays a role in all the major
metabolisms: oxidation-reduction, ionic regulation, etc. It activates about three hundred
enzymes. In animals, brain from magnesium deficient rats is more susceptible to permanent focal
ischemia . Magnesium participates in the formation and use of chemical links rich in energy that
are the basis of all biological activity in the cell. Magnesium is indispensable both for the
synthesis and action of ATP, and most enzymatic reactions depending on ATP require
magnesium, whether for carbohydrate, lipid, nuclear, or protein metabolism. Magnesium
deficiency concerns up to one fifth of the french population: 18% of men and 23% of women
have intakes lower than 2/3 of the RDA; 77% of women and 72% of men have intakes lower
than the RDA .

Food sources
Magnesium intake is generally directly correlated with calorie intake. This is because most foods
rich in magnesium also have high calorie content, among the various possible sources, the
magnesium in water and milk occupies a privileged position. It should be noted that milk is
richer in magnesium than the high-magnesium mineral waters, in addition its bioavailability is
excellent. Other foods sources are, spinach, beetroot, Nuts, legumes, whole grains, dark green,
seafood, chocolate and cocoa

Selenium

Selenium deficiency may have profound effects on the thyroid hormonal metabolism and
possibly also on the thyroid glands itself. The function of selenium is deionization in the
peripheral tissues. It has been shown that in an area of combined iodine and selenium deficiency,
only selenium is supplemented. Selenium synthesis remains impaired because of continued
iodine deficiency. Selenium deficiency also leads to a reduction of the selenium containing
(GP).GP helps in detoxification in the thyroid. Selenium deficiency also plays a role in the
endemic cretinism in central Africa

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In the brain, only about 15% of this important trace element is expended in its association with
glutathione peroxidase, a crucial enzyme for protection against peroxidation. The role of the
remaining 85% still remains to be explained.
Food sources:
Selenium is found in few mushrooms (cepes), finfish and animal seafood, some tripe products,
mussels, oysters, eggs, and fish.

Other trace elements


Chromium - modulates carbohydrate metabolism, but its effect have on nervous tissue has not
been studied.
Cobalt is illustrated by the role of vitamin B12 nervous tissue (a cobalamin) in the nervous
tissue.
Lithium important in neurotansmitters and phospholipids metabolism.
Molybdenum deficiency has been associated to neurological alterations.

Conclusions
Non essential micronutrients are also involved in the brain functions. They consist principally of
substances whose main quality is their antioxidant activity. Increased levels of oxidative stress
and/or antioxidant deficiencies may pose risk factors for cognitive decline. Like vitamin C, the
carotenoids may reduce cognitive loss during ageing.
In general, the role of antioxidant micronutrients is probably important during the course of
Alzheimer’s disease . For example, apple juice prevents oxidative stress and impaired cognitive
performance caused by genetic and dietary deficiencies ,vegetables as well as in egg yolk, can
reduce the risk of cataract (by 20%) and macular degeneration due to age associated with visual
loss (by 40%), because the retina is particularly rich in these substances.

Nutrition is an important determinant of human mental performance. Especially during aging,


dietary compounds prevent or delay age-related cognitive impairment, which is known to result
from changes in the diet, whether they are short term (breakfast in the morning), middle term
(iron to ensure oxygenation) or long term (fatty acids changing brain structure and functions .

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Food safety -must not limit itself to weeding out poisons and contaminants. True food safety
consists in finding foods that contain nutritive substances (nutrients) and at the same time give
pleasure. This principle is true for all populations, whether they belong to the over privileged or
underprivileged world, because both are threatened. True food security consists in having access
to the whole diversity of nutrients, as dietary habits impacts on the human brain and feelings: “

LECTURE 6

EFFECTS OF DIETARY SUPPLEMENTS ON BRAIN FUNCTIONING , NERVOUS


SYSTEM AND BEHAVIOUR

Intelligence scores can be improved by micronutrient supplementation in children and


adolescents with very poor dietary status. Good regular dietary habits are the best way to ensure
optimal mental and behavioural performance at all times. Children and adolescents with poor
nutritional status are exposed to alterations of mental and/or behavioural functions that can be
corrected, to a certain extent, by dietary measures.

 Dietary supplements are defined as products that are not used exclusively as food, but are
intended to be consumed in addition to an individual’s diet.
 Dietary supplements are defined as any product (other than tobacco) that is intended to
supplement the diet and contains one or more of the following: a vitamin, mineral, herb
or other botanical; an amino acid or metabolite; an extract; or any combination of the
previously mentioned items.
 The law states that dietary supplements are taken by mouth and contain one or more
dietary ingredients. Examples of dietary ingredients include vitamins, minerals, herbs or
other biological material, amino acids, and enzymes.
 Dietary supplements are sold in the form of tablets, capsules, powders, liquids, extracts,
or teas. Products sold as dietary supplements are required to be clearly labeled as such.
 Dietary supplements comprise a variety of products ranging from familiar multivitamins
found in every supermarket to exotic botanicals like the famous alovera drink.

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According to Food and Drug Administration (FDA) regulations, a dietary supplement may be
marketed in food form if it is not "represented" as a conventional food and is clearly labeled as a
dietary supplement. Specific health or structure/function claims are allowed on dietary
supplements provided the FDA deems adequate scientific substantiation exists for the claim.Due
to the large number of different supplements and their range of uses, testing and regulation of
these products is difficult and often ineffective.

Lecture Objectives

By the end of this lecture the learner should be able to

1. Define the term dietary supplements and their role in nutrition

2. Explain why certain precautions are necessary in the consumption of supplements.


3. Discuss the relationship between supplements and conventional medicine.

Regulation of dietary supplements

Manufacturers of supplements are required to follow federal Good Manufacturing Practices


(GMPs) that regulate sanitary and other conditions under which these products are prepared,
packaged, and stored. These GMPs are much less stringent than those that regulate the
manufacture of conventional drugs. They do not, for example, assure that the amount of active
ingredient in each pill or capsule of a dietary supplement is the same. Some supplement
manufacturers try to assure consistency of their product by making sure each batch contains the
same amounts of active ingredients. This type of standardization is not required by law, and the
word “standardized” on the label is not an indication that the product meets any legal
requirements as to quality or consistency of contents.

Dietary supplements are required to be clearly labeled with the word “supplement.” The label
must also show the volume or weight of the contents, the serving size, a list of dietary
ingredients and non-dietary ingredients (e.g., artificial color, binders, fillers, and flavorings), the
name of the manufacturer, packer, or distributor, and directions for use. If the supplement is an
herb, the label must contain its scientific name.
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 Health claims—Statements indicating a relationship between an ingredient in the
supplement and the reduction in the risk of developing a disease or condition. (e.g.,
increased intake of folic acid by pregnant women helps reduce the risk of neural tube
defects in their offspring.)
 Nutrient content claims—Statements describing the amount of supplement in the product
and may contain words such as “high in,” “good source of,” “fortified,” “enriched,” or
“high potency.”
 Structure or function claims—Description of how the supplement may affect organs or
systems in the body without mentioning a specific disease or condition. (e.g., Calcium
builds strong bones.) Labels with structure or function claims must also contain the words
“This statement has not been evaluated by the FDA. This product is not intended to
diagnose, treat, cure, or prevent any disease.”

Dietary supplements in conventional medicine

Conventional medicine, also called Western or mainstream medicine, is practiced by licensed


medical doctors (MD) and doctors of osteopathy (DO), dentists (DDS or DMD), registered
nurses (RN), licensed practical nurses (LPN), pharmacists, and similar health care professionals.
Some dietary supplements are routinely used as an accepted part of conventional medicine. The
most common of these are vitamin and mineral supplements taken in accordance with
established dietary reference intakes (DRIs). DRIs are a set of values for different nutrients that
indicate the daily amount of that nutrient necessary to meet the needs of most individuals, as well
as the largest amount of the nutrient that can be consumed daily without harmful effects. Other
supplements, such as folic acid, are prescribed for pregnant women in order to decrease the risk
of neural tube defects in their offspring.

Still other supplements, such as enzymes, may be given when the body fails to produce adequate
amounts of the enzyme as the result of a genetic disorder such as cystic fibrosis. When taken
under supervision of a conventional health care professional, dietary supplements tend to be
extremely safe.

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Dietary supplements in complementary and alternative medicine

Most dietary supplements are used within a system of complementary and alternative medicine
(CAM). Complementary medicine uses treatments that are not part of conventional medicine to
supplement conventional medicine. Alternative medicine uses treatments that are not part of
conventional medicine as a complete replacement for conventional medicine. Alternative
medicine includes well-established treatment systems such as homeopathy, traditional Chinese
medicine, and Ayurve-dic, or traditional Indian medicine, as well as newer fad-driven treatments.
Many CAM treatments have their roots in tradition and folklore.

Herbs are some of the most common dietary supplements used in CAM. Many have been used
for hundreds of years and show evidence of effectiveness. Others are ineffective or may harm the
individual either directly or when used as a replacement for conventional drugs and treatments
whose effectiveness has been proven. Vitamin and mineral supplements used as part of
conventional medicine become part of the CAM system when they are used in mega-doses that
far exceed DRI values or when they are used to prevent or treat a specific condition (e.g., vitamin
C to prevent colds). Likewise, enzymes and amino acids that have specific uses within
conventional medicine become part of the CAM system of dietary supplements when they are
used in non-conventional ways or in non-standard doses. Some dietary supplements, such as bee
pollen, are used exclusively in CAM.

Precautions

Individuals interested in using dietary supplements should consult their health care provider and
other reputable sources of information before taking any new supplements. Pregnant or
breastfeeding women should be especially careful to discuss the supplements they may want to
take with their health care provider. Many herbs and other dietary supplements cross the placenta
or are secreted into breast milk and may affect the fetus or nursing baby. In addition, care should
be taken in giving children dietary supplements. Few studies have been done specifically on
children and the recommended dosage for adults may be harmful to children. As with any
medication, more is not necessarily better. Overdose is a common cause of adverse side effects in

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dietary supplements. In the event of side effects, the supplement should be stopped immediately
and the side effects reported to a health care professional.

Interactions

Dietary supplements may interact with both conventional drugs and other herbs or dietary
supplements. Individuals should seek information about specific interactions from their health
care provider. Many dietary supplements should be stopped several days before surgery to
reduce the risk of excess bleeding.

Complications

There is strong evidence that some dietary supplements can cause serious harm or death. For
example, the weight-loss supplement ephedra was found to have contributed to the death of the
Baltimore Oriole’s pitching prospect Steve Belcher in 2003. The FDA later banned ephedra-
containing supplements. According to the American Association of Poison Control Centers, there
have been over 62,000 reports of vitamin poisonings, over 23,000 cases linked to minerals, and
over 23,000 reports linked to herbs. Twenty-seven deaths were attributed to dietary supplements
in 2005, of which 13 were attributed to herbs. It should be remembered that “natural” does not
mean safe; for example, many wild mushrooms are completely natural and cause death when
eaten. Complications may arise from dietary supplements themselves or their misuse or poor
regulation of the manufacturing process.

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Summary

In this lecture we have learnt that dietary supplements are any product that is intended to
supplement the diet and contains one or more of the following: a vitamin, mineral, herb or other
botanical; an amino acid or metabolite; an extract; or any combination of the previously
mentioned items. We have also learnt that Most dietary supplements are used within a system of
complementary and alternative medicine (CAM) and that dietary supplements may interact with
both conventional drugs and other herbs or dietary supplements hence it is recommended that
Individuals should seek information about specific interactions from their health care provider.

Questions

1. Define the term dietary supplements and their role in nutrition

2. Explain why certain precautions are necessary in the consumption of supplements.


3. Discuss the relationship between supplements and conventional medicine.

Further Reading
1. Sue Rodwell Williams, 1989 Nutrition and Diet Therapy., C.V. Mosby Company.

2. Sue Rodwell Williams, 1990 Essentials of Nutrition and Diet Therapy. 5th ed.,
C.V. Mosby Company.

3. Robinson, C.H; Lawler, M.N.; Chenoweth, L.W. and Garwick, E.A 1986. Normal
and Therapeutic Nutrition. 17th ed. Macmillan Publishing Company.

LECTURE 7

EFFECTS OF DIETARY SUGAR ON BRAIN FUNCTIONING , NERVOUS SYSTEM


AND BEHAVIOUR

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The World Health Organization recommends no more than 10 per cent of a person's daily energy
should come from added sugars, or those found naturally in juices and honey.

That equates to around 50g or 12 teaspoons a day.

While the links between a high-sugar diet and obesity are well documented, in light of the
mounting evidence, experts are turning their attention to the other ways sugar can affect the
body. In a recent study, a team at the University of New South Wales in Australia, found sugar is
as damaging to the brain as extreme stress or abuse.

Glucose, a form of sugar, is the primary source of energy for every cell in the body. Because the
brain is so rich in nerve cells, or neurons, it is the most energy-demanding organ, using one-half of
all the sugar energy in the body. Brains need lots of energy.  At rest a quarter of the body’s total
energy consumption is by the brain.  Most of this is normally provided by glucose derived from
starch or sugar (which is rare in the wild). 

Brain functions such as thinking, memory, and learning are closely linked to glucose levels and
how efficiently the brain uses this fuel source. If there isn’t enough glucose in the brain, for
example, neurotransmitters, the brain’s chemical messengers, are not produced and communication
between neurons breaks down. In addition, hypoglycemia, a common complication of diabetes
caused by low glucose levels in the blood, can lead to loss of energy for brain function and is
linked to poor attention and cognitive function.

“The brain is dependent on sugar as its main fuel,”

Although the brain needs glucose, too much of this energy source can be a bad thing. A 2012 study
in animals by researchers at the University of California at Los Angeles indicated a positive
relationship between the consumption of fructose, another form of sugar, and the aging of cells,
while a 2009 study, also using an animal model, conducted by a team of scientists at the University
of Montreal and Boston College, linked excess glucose consumption to memory and cognitive
deficiencies.

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The effects of glucose and other forms of sugar on the brain may be the most profound in diabetes,
a group of diseases in which high blood glucose levels persist over a prolonged period of time.
Type 1 diabetes is a disease in which the immune system destroys the cells in the pancreas that
produce insulin, a hormone used by the body to keep blood glucose levels in check. Type 2
diabetes, caused by dietary and other environmental factors, is a condition in which cells become
overwhelmed by insulin and fail to properly respond; they become resistant to insulin.

Long-term diabetes—either type 1 or type 2—has many consequences for the brain and for
neurons in the brain. High blood glucose levels can affect the brain’s functional connectivity,
which links brain regions that share functional properties, and brain matter. It can cause the brain
to atrophy or shrink. And it can lead to small-vessel disease, which restricts blood flow in the
brain, causing cognitive difficulties and, if severe enough, spurring the development of vascular
dementia.

In her laboratory, Novak is studying ways to prevent these effects in people with type 2 diabetes.
One of these ways involves a nasal spray called intranasal insulin (INI). When used, INI enters the
brain and binds to receptors in its memory networks, including the hippocampus, hypothalamus,
and insular cortex. As signaling within these memory networks become more efficient, the
cognitive functions associated with these areas, such as learning and visual perceptions of spatial
relationships, improve.

“Type 2 diabetes accelerates brain aging,”, “which, in turn accelerates the progression of functional
decline. With intranasal insulin, we’re hoping to find a new avenue for treatment to slow down
these effects or prevent them altogether.”

A single dose of INI has a positive effect on memory, verbal learning, and spatial orientation

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Sugar and the Brain

Blood levels of glucose are controlled by two hormones released by the pancreas: insulin which
lowers them, and glucagon which raises them. They are also controlled by glucose-sensitive
nerve cells in the hypothalamus that control your feelings of hunger or satiety associated with the
release of key hormones into the bloodstream by the pituitary gland, e.g. growth hormone, stress
and sex steroids; these modulate blood glucose and fat levels.  Blood levels of fats are also
affected by insulin which reduces blood fat levels by increasing fat storage.  So excessive sugar
intake is converted into body-fat.

Sugar (sucrose) is actually made of two molecules, glucose and fructose. The body has far less
control over blood fructose levels. Excess glucose is diverted into glycogen stored in liver and
muscle or converted into stored fat, but fructose bypasses the main glucose control point and,
particularly in the liver, may be converted into fat that stays there and can damage it.
Worse, long-term over-consumption of sugar weakens all the regulatory mechanisms, often
leading to insulin resistance, hyperglycaemia and greater risk of diabetes, fatty liver, heart
disease and neurodegeneration. Hyperglycaemia can also damage the platelets which help blood
to clot, worsening the damage after haemorrhagic strokes (brain bleeding).

LECTURE 8

EFFECTS OF CAFFEINE ON BRAIN FUNCTIONING , NERVOUS SYSTEM AND


BEHAVIOUR

The caffeine-brain connection

Caffeine is a naturally occurring substance in some plants. It can also be


manufactured and artificially added to most foods and beverages. Once
caffeine enters your body it is absorbed quickly and sent to your brain.
Caffeine has a stimulating effect on your nervous system, which directly
affects your metabolism. This is the primary reason you experience a burst of
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energy when you drink your favorite caffeinated beverage. It may also
increase your mental alertness, along with your physical stamina and
endurance. Caffeine is used to temporarily treat fatigue and migraines in
some people.
Up to 400 milligrams (mg) of caffeine a day appears to be safe for most healthy adults. That's
roughly the amount of caffeine in four cups of brewed coffee, 10 cans of cola or two "energy
shot" drinks. Although caffeine use may be safe for adults, it's not a good idea for children

Caffeine as an energy source is not all bad: In fact, 250 milligrams of caffeine per day—that’s
two to three cups of it—wakes up the brain, improves concentration, relieves stress, and may
also help you live longer. But if intake is turning into addiction, you may notice side effects ,
including dehydration, trouble sleeping, anxiety, an upset stomach, and even problems during
prenancy.

The reason you get a quick wakeup call after drinking a mug of coffee has to do with the way
caffeine tricks your brain. Not only is caffeine a brain stimulant, but it also blocks receptors for a
chemical called adenosine, which normally prevents the release of excitatory brain chemicals.
With adenosine out of the way, these brain-sparking chemicals can flow more freely—giving
you a surge of energy and potentially improving mental performance and slowing age-related
mental decline. If you like drinking caffeinated beverages, enjoy them.

NB/

Caffeine has the ability to affect the brain because it has a chemical structure similar to
adenosine, a natural brain chemical. Normally, the body produces adenosine to help you unwind
-- the adenosine binds to cells in your brain and you start to feel drowsy. Because caffeine has a
similar molecular structure, it can bind to the same brain cells and prevents adenosine from
doing its job, blocking the brain's natural "drowsy" signals. As a result, you feel more alert for a

few hours after consuming caffeine, until adenosine starts working again.

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People who consume caffeine do better on tests for memory, cognition and attention than those
who don't. Caffeine's effect on the brain also helps you during workouts by increasing the
amount of dopamine in your brain. This helps improve endurance during exercise.

But keep in mind that adding lots of sugar or cream, or getting caffeine via sugar-sweetened
soda, may counter any benefits

SIDE EFFECTS

Water loss

Your body cannot store caffeine. Up to six hours after intake, caffeine is excreted from the body
through increased urine output. Therefore, caffeine actually helps alleviate water loss because it
acts as a diuretic. Caffeine also speeds up thermogenesis, which is a way your body generates
heat, so you may perspire more when using caffeine. As with any diuretic, you should consume
water during use to avoid dehydration. Caffeine may lead to short-term water-weight loss, but it
is not a weight loss solution.

Do not take caffeine if you have high blood pressure, an overactive thyroid, or suffer from
anxiety.

Caffeine can cause insomnia, nervousness and restlessness, stomach


irritation,,nausea and vomiting,  increased heart rate and respiration, and other side effects
like:

 Adrenal fatigue
 Irregular heartbeat
 Hallucinations
 Accelerates bone loss. 
 Tremors

Caffeine is a drug and can affect people differently just like any other substance. It’s important
that consumers understand how caffeine interacts with their bodies in regards to their personal
health histories.

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Food sources
Caffeine is an alkaloid occurring naturally in some 60 plant species, of which cocoa beans, kola
nuts, tea leaves and coffee beans are the most well-known. Others include soft drinks like pepsi,
cola

EFFECTS OF ALCOHOL ON BRAIN FUNCTIONING , NERVOUS SYSTEM AND


BEHAVIOUR

The Relationship between Alcohol and Nutrition

The body needs certain nutrients in order to function properly. Poor nutrition leads to ill-health.
A balanced diet is made up of all the key components needed by the body to do its job properly.
Those who abuse alcohol often fail to get sufficient nutrition. Many of the diseases associated
with substance abuse will have malnutrition as at least a contributing factor. It is important for
anyone who consumes alcohol to have an understanding of the relationship between alcohol and
nutrition.

Alcohol Metabolism

The body does not require alcohol. Instead, it is treated like a toxin that needs to be removed
before it can cause damage to cells. When an individual drinks alcohol, the body gives priority to
metabolizing alcohol. This means that other digestive processes are stopped while the alcohol is
dealt with. Most of the detoxification of alcohol occurs in the liver. This organ works hard to
make alcohol safe.

The extent of intoxication from alcohol depends on blood alcohol levels. The higher the blood
alcohol level, the more intoxicated people will feel. Alcohol absorption is affected by body
weight, sex, race, age, and, of course, the amount of alcohol that has been consumed, and over
what period of time. Individuals who are on certain medications may become intoxicated faster.

Alcohol and Nutrition

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The use of alcohol can interfere with the ability of the individual to meet their nutritional needs.
Drinking small amounts of alcohol may bring certain health benefits, but there can be dietary
problems related to even a modest intake. Over consumption of alcohol can negatively impact
nutrition in a number of ways such as:

* Malnutrition due to the calories in alcohol replacing calories from more wholesome food. The
individual replaces food with alcohol and this means that they miss out on important nutrients.
Chronic alcoholics may get at least half their calories each day from alcohol instead of food.
* Alcohol also_ impairs normal digestion of nutrients _. It does this by causing damage to cells
in the digestive tract and by interfering with the secretion of enzymes needed for digestion.
Alcohol can also impede the ability of the liver to store important vitamins. It has also been
shown that drinking too much can prevent the body from absorbing enough protein.
* Too much alcohol can lead to obesity. There are a lot of empty calories in alcohol. If the
individual is drinking a lot on top of their normal diet, it could lead to them becoming
overweight.

Malnutrition due to alcohol abuse can lead to a number of serious health complications such as:

* Pancreatitis
* Alcoholic liver disease
* Stomach ulcers
* Impotence
* Increased risk of cancer and heart disease
* Mental health problems

It is also reported that drinking too much alcohol can lead to other chronic conditions such as
diabetes.

How to Avoid Nutritional Problems Caused by Alcohol

It is possible to enjoy alcohol without developing nutritional problems. If the following


guidelines are respected, then it should never become an issue:

* Those who are unable to control their intake should avoid alcohol completely. If the individual
is alcohol dependent, they may need assistance to quit. Lifetime abstinence will be the only

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solution in a lot of cases.
* The recommended amount of alcohol is 2 units for men and 1 unit for women per day_. Those
who consume above the recommend level are at risk of nutritional and other problem. People
should not “save up” their daily units so that they can drink a lot in one session.
* People who are overweight should avoid alcohol as it contains too many empty calories. This
means that it can lead to weight increase without providing any nutritional value.
* It is important that people avoid drinking alcohol on an empty stomach. This is because the
presence of food in the digestive system will help reduce the rate of alcohol absorption.
* Young people and pregnant women should avoid alcohol completely. There is also evidence
that tolerance will decrease as people get older. Those who are taking certain medications will
be advised to refrain from drink.

ALCOHOL’S DAMAGING EFFECTS ON THE BRAIN

Difficulty walking, blurred vision, slurred speech, slowed reaction times, impaired memory:
Clearly, alcohol affects the brain. Some of these impairments are detectable after only one or two
drinks and quickly resolve when drinking stops. On the other hand, a person who drinks heavily
over a long period of time may have brain deficits that persist well after he or she achieves
sobriety. Exactly how alcohol affects the brain and the likelihood of reversing the impact of
heavy drinking on the brain remain hot topics in alcohol research today.
Heavy drinking may have extensive and far–reaching effects on the brain, ranging from simple
“slips” in memory to permanent and debilitating conditions that require lifetime custodial care.
And even moderate drinking leads to short–term impairment, as shown by extensive research on
the impact of drinking on driving.
A number of factors influence how and to what extent alcohol affects the brain, including

 how much and how often a person drinks;


 the age at which he or she first began drinking, and how long he or she has been drinking;
 the person’s age, level of education, gender, genetic background, and family history of
alcoholism;
 whether he or she is at risk as a result of prenatal alcohol exposure; and

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 his or her general health status.

Some common disorders associated with alcohol–related brain damage and the people at
greatest risk for impairment on the brain.

BLACKOUTS AND MEMORY LAPSES

Alcohol can produce detectable impairments in memory after only a few drinks and, as the
amount of alcohol increases, so does the degree of impairment. Large quantities of alcohol,
especially when consumed quickly and on an empty stomach, can produce a blackout, or an
interval of time for which the intoxicated person cannot recall key details of events, or even
entire events.
Blackouts are much more common among social drinkers than previously assumed and should
be viewed as a potential consequence of acute intoxication regardless of age or whether the
drinker is clinically dependent on alcohol. White and colleagues surveyed 772 college
undergraduates about their experiences with blackouts and asked, “Have you ever awoken after a
night of drinking not able to remember things that you did or places that you went?” Of the
students who had ever consumed alcohol, 51 percent reported blacking out at some point in their
lives, and 40 percent reported experiencing a blackout in the year before the survey. Of those
who reported drinking in the 2 weeks before the survey, 9.4 percent said they blacked out during
that time. The students reported learning later that they had participated in a wide range of
potentially dangerous events they could not remember, including vandalism, unprotected sex,
and driving.

Binge Drinking and Blackouts

• Drinkers who experience blackouts typically drink too much and too quickly, which causes
their blood alcohol levels to rise very rapidly. College students may be at particular risk for
experiencing a blackout, as an alarming number of college students engage in binge drinking.
Binge drinking, for a typical adult, is defined as consuming five or more drinks in about 2 hours
for men, or four or more drinks for women.

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Equal numbers of men and women reported experiencing blackouts, despite the fact that the men
drank significantly more often and more heavily than the women. This outcome suggests that
regardless of the amount of alcohol consumption, females—a group infrequently studied in the
literature on blackouts—are at greater risk than males for experiencing blackouts. A woman’s
tendency to black out more easily probably results from differences in how men and women
metabolize alcohol. Females also may be more susceptible than males to milder forms of
alcohol–induced memory impairments, even when men and women consume comparable
amounts of alcohol.

ARE WOMEN MORE VULNERABLE TO ALCOHOL’S EFFECTS ON THE BRAIN?

Women are more vulnerable than men to many of the medical consequences of alcohol use. For
example, alcoholic women develop cirrhosis, alcohol–induced damage of the heart muscle (i.e.,
cardiomyopathy), and nerve damage (i.e., peripheral neuropathy) after fewer years of heavy
drinking than do alcoholic men. Studies comparing men and women’s sensitivity to alcohol–
induced brain damage, however, have not been as conclusive.
Using imaging with computerized tomography, two studies compared brain shrinkage, a
common indicator of brain damage, in alcoholic men and women and reported that male and
female alcoholics both showed significantly greater brain shrinkage than control subjects.
Studies also showed that both men and women have similar learning and memory problems as a
result of heavy drinking. The difference is that alcoholic women reported that they had been
drinking excessively for only about half as long as the alcoholic men in these studies. This
indicates that women’s brains, like their other organs, are more vulnerable to alcohol–induced
damage than men’s.

BRAIN DAMAGE FROM OTHER CAUSES

People who have been drinking large amounts of alcohol for long periods of time run the risk of
developing serious and persistent changes in the brain. Damage may be a result of the direct
effects of alcohol on the brain or may result indirectly, from a poor general health status or
from severe liver disease.

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For example, thiamine deficiency is a common occurrence in people with alcoholism and results
from poor overall nutrition. Thiamine, also known as vitamin B1, is an essential nutrient required
by all tissues, including the brain. Thiamine is found in foods such as meat and poultry; whole
grain cereals; nuts; and dried beans, peas, and soybeans. Many foods in the United States
commonly are fortified with thiamine, including breads and cereals. As a result, most people
consume sufficient amounts of thiamine in their diets. The typical intake in mg/day; the
Recommended Daily Allowance is 1.2 mg/day for men and 1.1 mg/day for women

Wernicke–Korsakoff Syndrome

Up to 80 percent of alcoholics, however, have a deficiency in thiamine, and some of these


people will go on to develop serious brain disorders such as Wernicke–Korsakoff syndrome
(WKS) WKS is a disease that consists of two separate syndromes,

 a short–lived and severe condition called Wernicke’s encephalopathy and


 a long–lasting and debilitating condition known as Korsakoff’s psychosis.
The symptoms of Wernicke’s encephalopathy include mental confusion, paralysis of the nerves
that move the eyes (i.e., oculomotor disturbances), and difficulty with muscle coordination. For
example, patients with Wernicke’s encephalopathy may be too confused to find their way out of
a room or may not even be able to walk. Many Wernicke’s encephalopathy patients, however, do
not exhibit all three of these signs and symptoms, and clinicians working with alcoholics must be
aware that this disorder may be present even if the patient shows only one or two of them. In
fact, studies performed after death indicate that many cases of thiamine deficiency–related
encephalopathy may not be diagnosed in life because not all the “classic” signs and symptoms
were present or recognized.

Human Brain

88
Schematic drawing of the human brain,
showing regions vulnerable to alcoholism-
related abnormalities.

Approximately 80 to 90 percent of alcoholics with Wernicke’s encephalopathy also develop


Korsakoff’s psychosis, a chronic and debilitating syndrome characterized by persistent learning
and memory problems. Patients with Korsakoff’s psychosis are forgetful and quickly frustrated
and have difficulty with walking and coordination. Although these patients have problems
remembering old information (i.e., retrograde amnesia), it is their difficulty in “laying down”
new information (i.e., anterograde amnesia) that is the most striking. For example, these patients
can discuss in detail an event in their lives, but an hour later might not remember ever having the
conversation.

Treatment

The cerebellum, an area of the brain responsible for coordinating movement and perhaps even

89
some forms of learning, appears to be particularly sensitive to the effects of thiamine deficiency
and is the region most frequently damaged in association with chronic alcohol consumption.
Administering thiamine helps to improve brain function, especially in patients in the early
stages of WKS. When damage to the brain is more severe, the course of care shifts from
treatment to providing support to the patient and his or her family .Custodial care may be
necessary for the 25 percent of patients who have permanent brain damage and significant loss of
cognitive skills.
Scientists believe that a genetic variation could be one explanation for why only some alcoholics
with thiamine deficiency go on to develop severe conditions such as WKS, but additional studies
are necessary to clarify how genetic variants might cause some people to be more vulnerable to
WKS than others.

LIVER DISEASE

Most people realize that heavy, long–term drinking can damage the liver, the organ chiefly
responsible for breaking down alcohol into harmless byproducts and clearing it from the body.
But people may not be aware that prolonged liver dysfunction, such as liver cirrhosis resulting
from excessive alcohol consumption, can harm the brain, leading to a serious and potentially
fatal brain disorder known as hepatic encephalopathy.
Hepatic encephalopathy can cause changes in sleep patterns, mood, and personality; psychiatric
conditions such as anxiety and depression; severe cognitive effects such as shortened attention
span; and problems with coordination such as a flapping or shaking of the hands (called
asterixis). In the most serious cases, patients may slip into a coma (i.e., hepatic coma), which can
be fatal.
New imaging techniques have enabled researchers to study specific brain regions in patients with
alcoholic liver disease, giving them a better understanding of how hepatic encephalopathy
develops. These studies have confirmed that at least two toxic substances, ammonia and
manganese, have a role in the development of hepatic encephalopathy. Alcohol–damaged liver
cells allow excess amounts of these harmful byproducts to enter the brain, thus harming brain
cells.

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Treatment
Physicians typically use the following strategies to prevent or treat the development of hepatic
encephalopathy.
 Treatment that lowers blood ammonia concentrations, such as administering L–ornithine
L–aspartate.
 Techniques such as liver–assist devices, or “artificial livers,” that clear the patients’ blood
of harmful toxins. In initial studies, patients using these devices showed lower amounts
of ammonia circulating in their blood, and their encephalopathy became less severe .
 Liver transplantation, an approach that is widely used in alcoholic cirrhotic patients with
severe (i.e., end–stage) chronic liver failure. In general, implantation of a new liver
results in significant improvements in cognitive function in these patients and lowers
their levels of ammonia and manganese.

ALCOHOL AND THE DEVELOPING BRAIN

Drinking during pregnancy can lead to a range of physical, learning, and behavioral effects in the
developing brain, the most serious of which is a collection of symptoms known as fetal alcohol
syndrome (FAS). Children with FAS may have distinct facial features (see illustration). FAS
infants also are markedly smaller than average. Their brains may have less volume (i.e.,
microencephaly). And they may have fewer numbers of brain cells (i.e., neurons) or fewer
neurons that are able to function correctly, leading to long–term problems in learning and
behavior.

Fetal Alcohol Syndrome

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Children with fetal alcohol syndrome (FAS)
may have distinct facial features.

Treatment
Scientists are investigating the use of complex motor training and medications to prevent or
reverse the alcohol–related brain damage found in people prenatally exposed to alcohol).

– Complex rehabilitative motor training can improve motor performance of children, or


even adults, with FAS.
– Treatments using antioxidant therapy and vitamin E
– 1–octanol, which ironically is an alcohol itself. Two molecules associated with normal
development have been found to protect nerve cells against a variety of toxins in much
the same way that octanol does.
– And a compound (MK–801) that blocks a key brain chemical associated with alcohol
withdrawal (i.e., glutamate) also is being studied. MK–801 reversed a specific learning
impairment that resulted from early postnatal alcohol exposure.
– Not drinking during pregnancy is the best form of prevention; FAS remains the
leading preventable birth defect ..

GROWING NEW BRAIN CELLS

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For decades scientists believed that the number of nerve cells in the adult brain was fixed early in
life. If brain damage occurred, then, the best way to treat it was by strengthening the existing
neurons, as new ones could not be added.

In the 1960s, however, researchers found that new neurons are indeed generated in adulthood—a
process called neurogenesis. These new cells originate from stem cells, which are cells that can
divide indefinitely, renew themselves, and give rise to a variety of cell types. The discovery of
brain stem cells and adult neurogenesis provides a new way of approaching the problem of
alcohol–related changes in the brain and may lead to a clearer understanding of how best to treat
and cure alcoholism.
For example, studies with animals show that high doses of alcohol lead to a disruption in the
growth of new brain cells; scientists believe it may be this lack of new growth that results in the
long–term deficits found in key areas of the brain (such as hippocampal structure and function).
Understanding how alcohol interacts with brain stem cells and what happens to these cells in
alcoholics is the first step in establishing whether the use of stem cell therapies is an option for
treatment.

SUMMARY

Alcoholics are not all alike. They experience different degrees of impairment, and the disease has
different origins for different people. Consequently, researchers have not found conclusive
evidence that any one variable is solely responsible for the brain deficits found in alcoholics.
Characterizing what makes some alcoholics vulnerable to brain damage whereas others are not
remains the subject of active research.
The good news is that most alcoholics with cognitive impairment show at least some
improvement in brain structure and functioning within a year of abstinence, though some people
take much longer. Clinicians must consider a variety of treatment methods to help people stop
drinking and to recover from alcohol–related brain impairments, and tailor these treatments to
the individual patient.
Advanced technology will have an important role in developing these therapies. Clinicians can
use brain–imaging techniques to monitor the course and success of treatment, because imaging
can reveal structural, functional, and biochemical changes in living patients over time. Promising

93
new medications also are in the early stages of development, as researchers strive to design
therapies that can help prevent alcohol’s harmful effects and promote the growth of new brain
cells to take the place of those that have been damaged by alcohol.

Summary

Nutritional management of Alcoholics 


Alcohol is a major cause of nutritional deficiency in the the world. Alcohol provides calories but
little nutrition to the body. Many alcoholics are malnourished, either due to ingesting a
nutritionally inadequate diet or changes in the body's ability to use the nutrients it receives.

Alcoholism affects every area of the body. It can cause insomnia, anorexia, weight changes,
gastrointestinal cramping, decreased digestive enzymes, ulcers, muscle wasting, liver disease,
and abnormal glucose levels depending on the amount of alcohol ingested. Those who take in
more than 30% of their total calories in alcohol generally have a significant decrease in their
intake of all macronutrients and deficiencies in vitamin A, vitamin C, and thiamine.

Alcohol's impact on digestion and the absorption of essential nutrients is important to understand
when treating an alcoholic. Alcohol interferes with protein metabolism, leading to important
clinical consequences, including low albumin levels, increased fluid in the abdomen, reduced
blood clotting, and decreased urea production (resulting in excessive ammonia levels), which
may increase the likelihood of altered brain function (eg, hepatic encephalopathy).

Liver disease resulting from alcoholism alters the organ's ability to take up beta-carotene and/or
convert it to vitamin A, causing disorders such as night blindness. Dietitians should be cautious
when treating alcoholics with low vitamin A levels because blood levels may be inconsistent
with what's stored in tissues and because high doses are toxic. It's recommended that patients
with low vitamin A and night blindness be treated with 2 mg of vitamin A per day for several
weeks. Zinc treatment also may be useful, as it's needed for vitamin A metabolism.

The body moves through four stages of liver damage as alcoholism progresses: fatty liver,
alcoholic hepatitis, cirrhosis, and encephalopathy or coma. Protein-calorie malnutrition predicts

94
survival in patients with alcoholic liver disease. Forty-five percent to 70% of alcoholics with
liver disease also are glucose intolerant or diabetic.

Treatment goals for patients with alcoholism are to reverse malnutrition, prevent alcoholic liver
disease, and establish a healthful lifestyle and coping skills for avoiding alcohol use. If
malnourished, alcoholics benefit from a diet high in carbohydrates and moderate in protein.
Low-calorie diets and fasting should be avoided because of the nutritional risks and the
possibility that a patient has an existing eating disorder or may cross over to a new addiction
with food, dieting, or exercise.

The diet should include a mix of omega-3 and omega-6 fatty acids since the amount and type of
fats impact hepatic steatosis, fibrosis, and cirrhosis. If tube feeding or total parenteral nutrition is
required, dietitians should avoid glutamine-enriched formulas, as they increase ammonia levels.
The amino acid taurine, in addition to patients' prescribed diets, has been used to help maintain
recovery after detoxification, as it represses the rewarding effect in the brain associated with
alcohol.

Wernicke-Korsakoff's syndrome (wet brain), which occurs with heavy alcohol use due to a lack
of thiamine, may be prevented with thiamine supplementation during intervention. Thiamin
deficiency occurs because of decreased absorption as a result of the diuretic effect of alcohol and
the utilization of thiamin in detoxifying alcohol.

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