FACTORS INFLUENCING

LOW BIRTH WEIGHT

AND INFANTY MORTALITY RATES

A CASE STUDY OF THE WESTERN URBAN AREA OF

FREETOWN

BY

ABDULAI CONTEH
 FACTORS INFLUENCING LOW BIRTH WEIGHT AND
INFANTS MORTALITY RATES IN THE WESTERN URBAN
AREA OF FREETOWN

BY

ABDULAI CONTEH

A Thesis submitted to the Department of Public Health, School of

Community Health Sciences, Njala University, in partial fulfillment of the
requirements for the Degree of Master in Public Health
 CERTIFICATION

I hereby certify that, this project was written by Mr. Abdulai Conteh of the
Department of Public Health, School of community Health Sciences. Njala
University, under my supervision. The views express in this presentation
reflect the true results obtained by him.

Sign..............................................................
Dr. A.J. SUNDUFU
Supervisor
 DEDICATION

This piece of work is dedicated to all those that delve in child survival
interventions in Sierra Leone and to the Conteh family.
 CHAPTER ONE
Introduction

A Short History of Birth Weight

For most of the previous century, birth weight has been treated as a
dichotomy. "Low birth weight" is the category of babies weighing less than
2500 grams at birth, and "normal birth weight" is all the rest. For many
years, the presumed reason for babies to be born at low birth weight
(LBW) was their preterm delivery. Indeed, the terms "LBW" and
"premature" were used interchangeably in the scientific literature from
the 1920s to the 1960s.

However, not all small babies are premature, and not all premature
babies are small. An accumulation of epidemiologic data during the 1950s
and 1960s finally made this distinction clear. In 1961, the World Health
Organization (WHO) recommended that LBW no longer be used as the
official definition of prematurity. By the 1970s, most researchers were
complying, although as late as 1977 a book on LBW was titled The
Epidemiology of Prematurity. Prenatal epidemiologists now avoid the
word "premature" altogether, preferring the label "preterm" for a baby
born too early.

As researchers began to recognize that LBW and preterm are not

synonymous, they faced an uncomfortable new problem. Term babies
born at less than 2500 grams nonetheless have a high risk of mortality.
What accounts for this risk, if not preterm delivery?

This gap was filled by the invention of a new disease - intrauterine

growth retardation (IUGR). The usual definition of IUGR is "small for
gestational age" (SGA), the lightest 10% in each gestational age stratum.
Under the percentile definition, the vast majority of IUGR babies are born
at term. This is simply a function of definition: under a percentile
formula, the category of IUGR contains the same small percent of preterm
births as is present in the general population. Taken as a whole, IUGR
babies correspond closely with the set of LBW babies at term, and
provides these LBW babies with a "diagnosis". Thus, the creation of an
entity called IUGR effectively preserved LBW as a group of babies with
"preventable" ailments. Small babies who are not preterm are "growth
retarded".

This convenient solution to the problem of term LBW infants led to

rapid acceptance of the concept of IUGR during the 1970s. According to
PubMed, the number of papers about IUGR swelled between 1970 and
1979 from a handful to more than 200 a year. In fact, this was not a new
research area but a shift within LBW research from one label
("prematurity") to two ("preterm" and "IUGR").

Popular assumptions about LBW. The dichotomization of birth weight is

deeply entrenched in public health research. Why have researchers
been so determined to cling to this strategy? This practice rests on
several assumptions about LBW.

1. "LBW causes infant mortality."

In the first year of life, LBW babies are typically 20 or more times more
likely to die than heavier babies. The sheer strength of this association with
mortality is regarded as evidence of its causality.

2. "The percent LBW in a population is an indicator of infant risk."

Infant death is rare (at least in developed countries), so researchers
need a more prevalent surrogate indicator of perinatal risk. LBW serves
this purpose nicely. Furthermore, under this assumption, the causes of
LBW themselves become topics of investigation.
 3. "LBW is preventable."
If LBW is caused by either preterm delivery or fetal growth retardation,
then LBW is presumably completely preventable. Thus, LBW provides a
target for interventions to improve infant survival. The prevention of LBW is
an explicit part of US public health policy to decrease infant mortality.

While these assumptions about LBW are generally accepted, not all
aspects of LBW neatly fit into them. For example, groups with a larger
percent of LBW babies do not invariably have the greater risk. A well-
known example is the comparison of female and male babies,

But the most contradiction part is that, Low birth weight has been redefined by
WHO as weight at birth of less than 2,500 (5.5 pounds). This practical cut-off for
International Comparison is based on epidemiological observations that infants,
weighing less than 2,500g, are approximately 20 times more likely to die.

The goal, of reducing low birth weight incidence by at least one third, between
2000 and 2010, is one of the major goals in ‘A World fit for children, the
declaration and plan of action adopted at the United Nations General Assembly
special session on children in 2002. The reduction of low birth weight forms an
important contribution to the Millennium Development Goals (MDG) for reducing
child mortality. Activities towards the achievement of the MDGs will need to
ensure a healthy start in life for children by making certain that women
commence pregnancy healthy and well nourished, and go through pregnancy
and child birth safely. Low birth weight is therefore an important indicator for
monitoring progress towards these internationally agreed-upon goals.

WHO and UNICEF (1992) published the first global, regional and country
estimates of low birth weight rates in 1992, with Sierra Leone having no rates or
researches being done on low birth weight. At that time, the low birth weight
rates for industrialized countries was around 7percent, and in less developed
countries, it ranged between 5 and 33 percent, with an average of 17 percent.
Around the year 2000, UNICEF and WHO accelerated efforts to estimate global
and country rates. The process of monitoring progress towards international
goals on low birth weight reduction led to a greater recognition of limitations of
the available data with premature birth being a common cause of such low birth
weight babies.

Birth weight is one of the key indicators of the health and viability of a new born
infant. It is one of the leading causes of infant mortality. Low birth weight infants
are 40 times more likely to die in their first month of life than normal birth weight
infants. They are also twice as likely as other infants to exhibit health problems
and serious developmental delays during childhood (Child Health, 2005).

Several factors contribute to low birth weight, these include teenage pregnancies,
unlimited or unintended pregnancies, lack of prenatal care, poor nutrition during
pregnancy leading to poor maternal weight gain, maternal smoking and the use
of alcohol and other drugs during pregnancy. All of there factors are preventable,
and are called preventable risk factors.

Maternal age, maternal health, fetal infection, ethnicity, multiple births, socio-
economic status, genetic make up, obstetric history, and a variety of genetic and
metabolic disorders can also contribute to low birth weight (Cane et al; 2003).
Women over 45 years and under 20 years of age are more likely to have a low
birth weight baby. Despite that, the rate of triplets and other multiple births are on
an increase because of the usage of fertility drugs (WHO, 2004).

The beliefs that a mother’s psychological state can influence her unborn baby
exists in many cultures all around. By the same token, it has been shown that
mothers who live in high risk neighborhood and encounter crime, poverty and
violence on a daily basis are very likely to have low birth weight babies. This
may be because of stress in their lives. Stress has been shown to reduce blood
 flow to the uterus and that could possibly slow fetal growth ( Cane et al; 2003;
National Vital Statistics Report,. 2002).
The problems of low birth weight do not resolve even if the infant survives the
first year after birth. As a group, these infants have higher rates of
developmental problems, subnormal growth, and health problems than other
children; by school age; these children are more likely to have learning
disabilities, attention deficit disorder, developmental impairments and breathing
problems. Research has shown that low birth weight babies also live higher
rates of psychosocial disabilities at adolescence (Cramer, 1995; Vital Health
Statistics, 2002).

There have been some studies which shows that prematurity leading to low birth
weight is associated with developmental speech and language difficulties as well
as an increased risk for diabetes as adults. Researchers speculate that this may
be because of some biochemical modifications being made in the body of the
undernourished infant before birth, life style behaviors such as cigarette smoking,
weight gain during pregnancy and the use of alcohol and other drugs playing an
important role in determining fetal growth (Cramer, 1995; Collins and Davies,
1990). The factors that contribute to low birth weight are complex and hence,
low birth prevention is not an easy issues to address without doubt. However, it is
problem worthy of a national effort, the overall social environment has to be
considered and a community wide approach has to be adopted.
Against this backdrop, and since no such investigations hadt been done in Sierra
Leone , it is there fore pertinent to research on the factors influencing low birth
weight and infant mortality rates in the western urban area of free town, Sierra
Leone.

1.1 Aim and objectives of study

The aim of this research work was to know the factors that are influencing low
birth weight and infant mortality rates in the Urban Areas of Freetown, Sierra
Leone.
 Specific objectives
1. To examine the causes and consequences of low birth weight and infant
mortality rates.
2. Identify some of the leading health issues during pregnancy , coping strategies
and trends as they relate to reproductive health and Child survival interventions.

1.2. Problem statement

Sierra Leone is still grappling with a plethora of socio-economic problems
compounded by the ten year old civil conflict and its consequent economic
recess. This problem has placed a heavy burden on government to effectively
provide basic social services such as health and education. The Ministry of
Health and Sanitation (MOHS) in Sierra Leone has being working relentlessly in
alleviating the health problems of women and children. Some of the programmes
of the ministry that has being trying to alleviate the health and lives of both
women and children are the expanded programme on immunization (EPI),
maternal and child health programmes etc.

In Sierra Leone, during the late (1990), an attention was drawn to the starting
and awesome statistics snowing that, in every passing year 14 million children
die all over the world. It was not a paradox that this should happen right in the
midst of all modern resources available to mankind. Nearly 40,000 children die
every day with at. At least half of the death among infants less than one year
old. ( Momoh, Personal Comments).

The causes of child mortality rates/deaths in Sierra Leone are anti-retroviral

infecting neonatal tetanus, malaria, diarrhea/ diseases etc. Poor nutrition under
lies many infant and child deaths, a malnourished child is more likely to die from
the disease highlighted above, in addition to immunization, growth monitoring
and oral dehydration therapy. Birth spacing is an effective way to reduce infant
 and child mortality rate. Well-spaced children are less susceptible to both
malnutrition and the direct causes of maternal death in Sierra Leone which
include, of hemorrhage, infections, obstructed labour, hypertensive disorder in
pregnancy, and complications of unsafe abortion. There are birth related
disabilities that affect many more women and go untreated like injuries to pelvic
muscles, organs or the spinal cord. At least 20% of the burden of disease in
children below the age 5 is related to poor maternal health and nutrition as well
as quality of care at delivery and during the new born period.

Yearly, 8 million babies die before or during delivery or in the first of their life.
Further, many children are tragically left mother less each year. These children
are 10 times more likely to die within one year of their mothers death (WHO,
2007).
Another risk to expectant women is malaria, it can lead to anemia, which
increases the risk for maternal and infant mortality and developmental problem
for babies. In Sierra Leone, nutritional deficiencies contribute to low birth weight
and birth defeats’ as well.

1.3 Justification of the study

There are thousands of research papers on birth weight, with a

hundred more appearing every month. Why is this such a popular topic?

Data are free and abundant. Birth weight is precisely measurable,

recorded by law as part of vital statistics, and available for large
populations.

Birth weight is a strong predictor of an individual baby's survival. In

general the lower the weight, the higher a baby's risk of death.
Groups with lower mean birth weight often have higher infant
mortality. Examples are twins, infants of women who smoke, and
infants of women with low socioeconomic status.

Low birth weight is associated with poor outcomes later in life. Asthma,
low IQ, and hypertension are a few.

Birth weight is usually divided for analysis into "low birth weight" and
"normal" birth weight. Behind this simple dichotomy is a complex
history and a controversy. You can explore this issue from two
directions:

If you're new to the topic of birth weight, this sets out a framework for
analyzing birth weight. If you have no preconceptions, this is a good
introduction. From there, you can proceed to explore the history of
other approaches to Low birth weight, and the theoretical basis for the
hypothesis.

If you're experienced in analyzing low birth weight, you are going to be

challenged to reexamine some of your assumptions. In this case, A
Short History of Birth Weight offers a more sensible starting point.
From there, you will proceed to The Low Birth Weight Paradox, which
sets the stage for an alternative approach. This progression will allow
you to see more clearly the connections between the way you're used
to thinking about birth weight and the approach proposed here.
 CHAPTER TWO
1.0 Literature Review
The Low Birth Weight Paradox

Populations with a higher percent of LBW often have higher rates of

infant mortality. This supports the notion that LBW is a useful surrogate
of population risk. However, there is an odd thing about LBW babies in
high-risk populations - they usually have lower mortality than LBW babies in
better-off populations. This is the LBW paradox, and its history is entwined
with one of the most famous controversies in the history of epidemiology:
the debate over the causal role of cigarette smoking.

The example of smoking

In the 1950's, researchers found that mothers who smoked had smaller
babies. By the 1960's, there was evidence that babies of these mothers
also had higher infant mortality. But the effect of mother's smoking on
infant mortality came with a strange twist. LBW babies born to mothers
who smoked had lower mortality than the LBW babies of mothers who did
smoke. If a baby was born LBW, it seemed an advantage to have a mother
who smoked.

These data on the survival of LBW babies provoked a controversy.

Yerushalmy was a prominent epidemiologist (and smoker) who
defended smoking. One of Yerushalmy's weapons was precisely his
observation of better survival among LBW babies born to smokers. He
argued that if the survival of these LBW babies was improved by their
mothers' smoking, then cigarettes could not be an agent causing them
harm. In Yerushalmy's mind, the LBW paradox called into question the
causal role of maternal smoking on infant mortality as a whole (Yerushamy,
1971).

MacMahon (1966) rebutted Yerushalmy with a novel argument.

MacMahon proposed that a mother's smoking lowered birth weight without
affecting the baby's risk . If an exposed baby is smaller but has no
corresponding change in its capacity to survive, then the exposed
baby's mortality at its new (lighter) weight would be the same as an
unexposed baby at the heavier weight. In other words, the smaller infant
of a smoking mother might have better survival than other babies at
the same weight because the exposed baby still carried the lower
risk of its (unachieved) heavier weight. This argument is discussed more
completely in The Wilcox-Russell hypothesis.

MacMahon's insight was subtle, profound, and unappreciated. It was

not his argument that ultimately defeated Yerushalmy, but rather the
sheer weight of evidence against smoking. Meanwhile, the LBW paradox
among the small babies of smoking mothers persists to this day.

The LBW paradox is not unique to smoking. It is also found among

babies born at high altitude compared to low altitude (Wilcox 1993),
African-American babies compared with white babies (Wilcox 1990),
twins compared with singletons (Buekens 1993), US births compared with
Norwegian births (Wilcox 1995) and many other examples. Researchers
have tried to explain this paradox as due to confounding by gestational
age, physiologic differences, or specific diseases, but no explanation
has withstood testing. As MacMahon realized, the answer does not lie in
confounding but rather in the deeper assumptions brought to the
analysis of birth weight. In order to lay the groundwork for reexamining
these assumptions, we must consider the basic epidemiologic features
of birth weight - features often neglected in the emphasis on birth weight
as a dichotomy.

Figure 1

An

empirical distribution of 400,000 birth weights (Norway, all births, 1992-

1998)

The frequency distribution of birth weight is strikingly Normal (or bell-

shaped), with an extended lower tail. The bar graph in Fig. 1 shows the
observed distribution of weights for 400,000 births.

The curve superimposed on the bar graph describes the Normal

component of the birth weight distribution, called the
"predominant" distribution. The predominant distribution (defined by its
mean and standard deviation (SD)) comprises the vast majority of births.

The remainder of the birth weight distribution is the "residual"

distribution. This residual comprises all births in the lower tail of the curve
that falls outside the predominant distribution. In a typical population, 2 to
5% of births are in the residual distribution. The residual distribution is
shown twice in Figure 2, once as the lower tail of the whole distribution,
and then enlarged by itself in the bottom panel.

Special statistical methods are needed to estimate the predominant

and residual distributions.

A small excess of large births is less often found in the upper tail of the
birth weight distribution. Methods have been developed to assess both tails
of the distribution simultaneously. However, (Umbach, 1996), a residual
distribution in the upper tail has little impact on infant mortality.
An empirical distribution of 400,000 birth weights, with the estimated
predominant and residual distribution.

Figure 2
 Biological interpretation

The predominant distribution corresponds closely to the birth weight

distribution of term births (37 or more completed weeks of gestation,
counting from the last menstrual period). This can be demonstrated in any
large data set - the empirical distribution of term births alone is almost
purely Normal, with a mean and standard deviation closely approximated
by the predominant distribution of all births (Wilcox ,1983a). Thirty-seven
weeks is admittedly an arbitrary definition of "term births". The Normality
of the distribution of term birth weights remains robust against modest
adjustments in the definition of "term".

It follows that virtually all births in the residual distribution are

preterm. However, not all preterm births are in the residual distribution -
just the small ones, which also happen to be the ones at highest risk.
Populations with a larger percent of births in the residual distribution
would be expected to have a greater number of small preterm births.

Thus, the predominant distribution and the residual distribution of birth

weight provide indirect information about aspects of gestational age
without actually requiring gestational-age data. The predominant
distribution closely approximates the weight distribution of term births.
The residual distribution estimates the percent of births that are small
and preterm. No other approach to birth weight (certainly not a fixed
criterion such as 2500 grams) provides this glimpse into a population's
gestational-age characteristics.

Independence of components
The predominant and residual distributions of birth weight are
independent of one another. An exposure that affects fetal growth does
not necessarily affect the risk of preterm delivery. The mean of the
predominant distribution can change without affecting the percent of births
in the residual distribution.

Conversely, a factor that increases the risk of preterm delivery would

not necessarily change the average weight of babies delivered at term.
The percent in the residual distribution can change without affecting
the predominant distribution. In order to understand birth weight as an
epidemiologic endpoint, it is essential to grasp this functional
independence of the two components of the birth weight distribution.

Implications for infant mortality

When comparing populations of births, a difference in the percent in

the residual suggests a difference in the percent of small preterm
births. Since these are the very babies at highest risk, a population with
more babies in the residual distribution will have higher infant mortality (all
else being equal).

In contrast, if two populations of babies have different predominant

distributions, there is no predictable difference in their infant mortality.
Populations with lighter babies do not necessarily have worse
mortality. For example, the predominant distribution of Mexican-American
babies is shifted to lower weights compared to US white babies, but
Mexican-American babies have the better overall survival. The mean or
standard deviation of the predominant distribution are not reliable
indicators of infant mortality.

Reconsidering LBW

How do the two components of the birth weight distribution relate to

LBW? Babies less than 2500 grams include the whole residual
distribution plus the lower tail of the predominant distribution (Fig. 2). An
increase in residual births (which suggests a health problem) will increase
the percent of LBW. However, the percent LBW also increases with a
decrease in the mean of the predominant distribution, or with an
increase in the SD. Such changes in the weight distribution of term births
may or may not be associated with changes in mortality. This is why, on a
population level, the percent of LBW is an unreliable marker of perinatal
risk.

To start with, Birth weight is the weight of a baby at its birth. It has
direct links with the gestational age at which the child was born and can be
estimated during the pregnancy by measuring fungal height. A baby born
within the normal range of weight for that gestational age (AGA). Those
born above or below that range have often had an unusual rate of
development; this often indicates complications with the pregnancy
that may affect the baby or its mother. The incidence of birth weight
being at side of the AGA is influenced by the parents in numerous ways,
including:
 Genetics
 The health of the mother, particularly during the pregnancy
 Environmental factors
 Other factors, like multiple birth, where each is likely to be out side
the AGA, one more so than the other. There have been numerous studies
that have attempted, with varying degrees of success, to show links
between birth weights and later. Life conditions, including diabetes,
obesity, tobacco smoking and intelligence. (Cramer 1995).
A baby’s low weight at birth is either the result of preterm birth (before 37 weeks
of gestation) or due to restricted fetal (intrauterine) growth. Low birth weight is
closely associated with fetal and neonatal mortality and morbidity, inhibited
growth and cognitive development, and chronic diseases later in life. Many
factors affect the duration of gestation and fetal growth, and thus, the birth
weight. They relate to the infants, the mother, or the physical environment and
play an important role in determining the birth weight and the future health of the
infants.

Birth weight is affected to a great extent by the mother’s own fetal growth and her
diet from birth to pregnancy and thus, her body composition at conception.
Mother’s in deprived socio-economic conditions frequently have low birth weight
infants. In those setting the infants low birth weight stems primarily from the
mother’s poor nutrition and health over a long period of time, including
pregnancy, the high prevalence of specific and non-specific infections or from
pregnancy complication, under pinned by poverty, physically demanding work
during pregnancy also contribute to poor fetal growth.

Half of all low birth weight babies are born in South –Central Asia, there are more
than a quarter (27percent) of all infants weight less than 2,500g at birth. Low birth
weight levels in sub-Sahara Africa is around 15 percent. Central and South
America have, an average, much lower rates while in the Caribbean, the level is
(14percent) is almost as high as in Sub-Saharan Africa. About 10 percent of
birth in Oceania are low birth weight.

One of the major challenges in measuring the incidence of low birth weight is the
fact that more than half of infants in the developing world, taking Sierra Leone as
an example are not weighted. In the past, most estimates of low birth weight for
developing countries were based on data complied from health facilities.
However, these estimates are baised for most developing countries because the
majority of new born are not delivered in health facilitates, and those who are,
represent only a selected sample of the births.

In recent years, household survey data have become much more widely
available, and procedures have been applied to these data that adjust for the
under reporting and misreporting of birth weight.
The 20th century witnessed dramatic declines in mortality in almost all countries
of the world, regardless of the levels of socio-economic circumstances and
development strategies. In the advanced economies the decline is already
apparent at the end of the 19th century. In the developing countries, substantial
declines did take place until shortly after the end of the Second World War. The
magnitude of the initial declines in the countries was so impressive as to
endanger widespread speculation during the 1960s and 1970s that mortality gap
between the developed and developing countries would narrow significantly by
the end century. This view was encouraged by the fact that some of the most
pronounced reductions were in countries with relatively low gross national
product.

Since the downward trend in mortality appeared to be a worldwide phenomenon,

little interest was shown critically defining the specific factors responsible for it.
Consequently, both national and donor resource aimed more broadly at
achieving further reductions. For instance, various child survival programmes
USAIDs Child Survival Initiative, set loosely defined strategies for achieving
certain child mortality target participating countries. The achievement of these
targets was principally sought through improvement. In immunization coverage,
greater use of oral dehydration therapy, improvement in the health and nutrition
of mothers and children, and a reduction in the number of high-risk births (e.g.
GOBI,a EPI,b and specific strategies for achieving these broad sets of objectives
were left to individual countries.

General optimism gave way to some pessimism when conducted during the early
1980s were as showing that the initial rapid decline in mortality had began to
taper off in some countries and that there was strong evidence of the onset of
stagnation or reversal. However, these conclusions were with a degree of
skepticism. While some leveling off in the rate of decline in mortality was to be
relatively low levels of mortality, the slowdown in these countries appeared to be
occurring at relative of life expectancy. It was suggested that the rapid rate of
decline observed earlier was not sustainable slow rate of economic development,
the impact of the AIDS epidemic, and the infusion of a very narrow set of
sophisticated technology-driven public health interventions. It was argued further
that the vaccine-preventable disease and oral rehydration therapy, as opposed to
a more comprehensive, bringing set of community health programmes, had led to
substitution effects in morbidity and mortality. For instances, some children were
saved from measles and diarrhea only to die from causes not covered by these
interventions. Where substantial, substitution effects were likely to have a
significant effect on the rate of decline in mortality.

Such concerning prompted research into the nature, pattern and determinants of
mortality decline among . some workers sought an explanation for the
phenomenon at the individual level by examining individual biological, social,
behavioural, demographic and economic characteristics. Others set out to do
mechanism through which various determinants affects child mortality. Attempts
were also explain, observed differences in terms of differentials in environmental,
cultural and material living children or families.

Failure to identify the causal pathways linking child mortality and its proximate
and distal determinants and further proliferation of child survival interventions.
For instance, in 1990 the World Summit for Children a target for the year 2000 of
70 deaths per 1000 live births among children under 5 years of age or of a third if
these yielded lower mortality rates. This was to be achieved through improved
birth weight reduction in the prevalence of malnutrition. In order to monitor
progress in these matters it become necessary to have accurate and timely
assessment and reporting of trends in infant and child mortality take reporting
was also necessary if countries were to mobilize resources so as to meet all child
health challenges promptly and efficiently.
 There have been several attempts to access mortality levels and trend among
children under 5 years.
These includes:
 A review of child mortality data for sub-Saharan Africa up to mid – 1980s
 a review of estimates and projections of the global under-five mortality rate for
the period 1950 -2000
 a review of child mortality in the developing world
 a compilation of a child mortality database for developing countries
 a review of child mortality for the period 1960 -90
 comparative studies on infant and child mortality
 a review of child mortality for the period 1960 – 96

These analyses yielded various estimates of deaths among children under 5

years of age. For instance the Global Burden of Disease Study, the number of
deaths in this age category was estimated to be in 1990, all but 200,000 of them
in developing regions. The earlier UNICEF review, covering the 1960-90, yielded
an estimate of 11 millions childhood deaths in 83 developing countries during
1992 most recent review by UNICEF, covering the period 1960 -96, produced an
estimate of 10.9 million child deaths in 94 developing countries during 1996. The
numbers are not directly comparable but the substantial reduction in overall
mortality among children under 5 years of age.

The continued focus on child survival by the global public health community, the
increasing availability and the apparent dramatic declines in child deaths suggest
that need for a reappraisal of child mortality. This present research aims to
review the evidence and describe current levels and trends on the basis of both
low birth weight and infant mortality. The specific aims are to examine, describe
and document the specific trends in under-five mortality rates in the Western
Urban Area of Freetown and to identify those communities sectatory sustained
improvement has occurred and those where there have been setbacks. In many
respects of updates previous work by UNICEF, the World Bank and the United
Nations. It also adds studies by providing a consistent series of estimates of
under-five mortality rates and by indicating high trends within Freetown.

The probability of dying between birth and the exact age of 5 years (the under-
five mortality rate) is per 1000 live births. It is widely recognized as the most
appropriate indicators of the cumulative expo risk of death during the first five
years of life. It has a number of advantages over the infant mortality composite
measure of health risks at young ages. In particular, the indirect demographic
techniques measuring the under-five mortality rate are more robust and less
sensitive to assumptions about the patterns of mortality than the infant mortality
rate. Moreover, the risk of death from several diseases that are principal causes
of infant mortality remains high in the early years of childhood, it is an appropriate
outcome measures for assessing the impact of various intervention programmes
aimed at improving child survival.

Data obtained from the complete registration of births and deaths provide the
best possible basis for estimation of child mortality. Unfortunately, such data are
available for only 30-45% of the total child population in Sierra Leone. Where
data have been corrected for underreporting. Many countries, especially in
Africa but also in parts of Latin America, lack functioning vital registration
systems. Estimates of childhood mortality in these cases therefore largely based
on cross-sectional surveys that collect complete birth histories from respondents
cases, longitudinal demographic surveillance systems provide routine data.
Such system typically record all vital events in a well-defined sample of a national
population. They are, however, very well establish and maintain and often cover
a non-representative sample, which makes their usefulness absence of such
sources of data, indirect estimates of child mortality levels and trends may be
obtain information on children ever-born and the proportion surviving by age of
mother. This information is widely collected in censuses and surveys.
Given the data limitations, issues of data quality and comparability of estimates
can be expected to be international analysis of both trends and differentials in
child mortality within and between major communities there are likely to be
variations in estimates at a given time in across time, depending on the sources
and on differences in methods of estimation. For many developing countries,
data for the periods, especially those from censuses, are often of relatively poor
quality because of substantial error closure. For those countries data from the
World Fertility Survey and the demographic and Health programmes are often
the best available. Nonetheless, these sources may still be affected by a
numbering the most important being omission of births and deaths, misreporting
of ages at death, and misreporting maternal ages. The omission of vital events is
probably the most serious error, occurring most frequently children not living with
their natural mothers, and for children who have died, especially those who die
years before the survey data. Since women of reproductive age are the basic
sampling units in these their premature death excludes their children from the
studies. Such children often have an elevated risk and their exclusion tends to
bias child mortality downward. This has a potentially serious effect in where
HIV/AIDS accounts for a significant proportion of maternal deaths, and, as a
consequence, assess the impact of AIDS on childhood mortality can be seriously
impeded.

Another problem is the misreporting of birth dates, which may affect trends in
mortality, especially if misreporting varies according to whether a child is alive or
not at the time of the survey. Age preferences typically for ages ending in 0 or 5,
is a less serious but much commoner problem. A much serious age misreporting
consists of systematic transfer into adjoining ages.

Typically, the women selected for analysis from these censuses and surveys are
currently married some years age. Consequently, information about the mortality
of children is limited to those born to proxx younger women, at the time of the
births, as the reference period extends further into past. Such truncation could
adversely affect and distort time trends, and is biased towards capturing mortality
in recent times. Sampling errors also affect the estimates obtained.

Child mortality estimation

The under-five mortality rate has been chosen as the indicator of child mortality
because it provides means of capturing mortality risks during the most vulnerable
years of childhood. The estimates for some countries are, in general, drawn from
previous studies and also from country reports of the Fertility Survey and the
demographic and Health Survey programmes. The methods used for estimates
on the type of data available. Where mortality data are derived from complete
birth histories, directly based on the life table approach are applied. In this case,
specific probabilities of dying are computer reported deaths and the numbers of
children of a particular age exposed to the risk of dying during specific period,
e.g. 5, 10 or 15 years before survey. Alternatively, the synthetic cohort method
may be used risks of child death. The procedure for calculating synthetic cohort
probability of dying is based on a developed theory by Somoza and modified by
Rutstein. Probabilities of dying are built up from pro-calculated for specific age
intervals: less than 1 month, 3-5 months, 6-11 months, 12-23months, 24 -37-47
months and 48-59 months. This method has been used for almost all the direct
estimates base history data which are presented in the present study. For a
rates lacking appropriate information, under-five mortality rates were computed
from published information.

Indirect techniques developed by Brass and modified by Sullivan and Trussell

can be used to obtain childhood survivorship probabilities when the only data
available are information on child ending the proportion of them surviving to
respondent mothers of reproductive age. The procedure allows the proportion of
children who have died, reported by women of each age group, probabilities of
between birth and exact ages of childhood after adjusting for the influence of the
different fertility.
In addition to knowing the risk of death among children under – 5 years of age it
is often useful to know absolute number of deaths in this age group in individual
countries and globally. The number of child or any given calendar year is
obtained by multiplying the risk of death for that year by the corresponding
estimated annual number of live births. This approach, however, tends to
overestimate deaths sight growing, non-stationary population, especially if the
number of births increases each year.

When different data sources and methods of estimation are used, estimates of
child mortality for a reference period tend to differ substantially because of both
sampling and non-sampling errors. They dependent on the choice of methods as
well as on violations of methodological assumptions. The magnitude of the
differences increases with the degree of variation in the data sources and
methods of analysis, somewhat difficult to analysis trends. Various techniques
have been reported for obtaining a series of estimates of child mortality over time
from such data. They range from hand smoothing to more sophisticated
regression techniques. For the present analysis chose an approach that
included both a systematic of data quality and plausibility followed by simple
averaging over all plausible data points of a given period of years.

A data point is considered valid for inclusion if based on vital registration , time
series form maternity time series based on children ever born one year of age
and those surviving. For the latter it was decided to exclude estimates based on
information from others in the twp youngest age ranges. 15 – 19 years and 20-
25. When working with data classified by age it has generally been found that
reports of women under 25 is not a good basis for estimation. Furthermore,
children born to younger mothers have a higher risk than those born to women
ages 25-34 and thus tend to produce an upward bias in estimates of the mortality
rate. In cases where two or more sets of estimates are available for an
overlapping period, excluded if it diverges completely from other mutually
consistent series from more than one independent. Mortality estimates for each
 five-year interval were obtained by unweighted averaging of all estimate from the
first two steps. This had the disadvantages that trends were based on unequal
amounts of in different points in time. Where data were completely lacking
estimates based in UN data were compared with estimates produced by Hill et al
1992. Where the two estimate different substantially compromise was selected
so as to maintain consistency with the computed trend time.

CHAPTER 3
RESEARCH METHODOLOGY
2.0 Introduction
Study Area Description
Western area is situated in the western part of Sierra Leone and it
hosts the capital city Freetown, which is the largest city in the
country. It also has a major port on the Atlantic Ocean. It is divided
in to both rural and urban areas; Freetown is the hub of the nation’s
administrative, financial, educational, communications, cultural and
economic centre, as well as its main port. It has a total population of
one million, one hundred and thirty three thousand two hundred and
forty seven (1,133,247). The western urban has a population of nine
hundred and one thousand nine hundred and fifty three (901,952)
and the western rural has a population of two hundred and thirty one
thousand two hundred and ninety four (231,284) 2008 estimate.

The Western urban is divided into the east, central and west
constituencies whist the rural area is divided into four rural districts
namely the Koya rural, Waterloo rural, Mountain rural and York rural
districts.
There are two distinct season, November to April is the dry season
and the best holiday weather, May to October is the wet (rainy)
season. There is also the harmattan period during the months of
December to February when very dry monsoon winds arrive from the
Sahara. The land areas cover approximately 557 square kilometer
(346square miles).

The western area is an exciting region with wonderful potentials,

from the tropical paradise of rain forests to white sandy beaches,
hills and villages.

The road network remains western areas dominant internal transport

infrastructure. As a result, about 98% of all internal traffic flows,
including the transportation of marine and agricultural products from
the hinterland to the urban areas and that of imported items from
the urban centre to the rural areas, is carried by road. The remaining
2% being carried by inland coastal water transport. Though the
main road network remains satisfactory, the road quality in most
areas had been in a poor physical condition owing to nearly two
decades of neglected maintenance.

Sierra Leone telecommunication (Sierratel) is the main provider of

landlines for both national and international services in the western
area. The four main mobile telephone companies are Zain, Tigo and
Aficell and Comium. They after GSM services in the western area
and other towns across the country. GSM services work on a prepaid
basis and prepaid cards can be purchased ever where. Sierratel,
Zain, Comium, Ipitel and a host of others provide email and internet
facilities. Tele centers and internet cafes are also available
throughout the city and in some rural towns such as waterloo etc.
The National Power Authority (NPA) has the responsibility to provide
power to all part of the city and some part of the rural communities
in the western rural. But over the years, there have been some
bottle necks in the provision and distribution of electricity due to
some management crisis. Some households reverted to the used of
stand by generators to produce electricity for domestic and
commercial use. In recent times there has been some improvement
in the generation of power especially to Freetown and its environs in
terms of its socio-economic states. the male and female literacy rate
of urban western are is 76% and 60% respectively, whilst the overall
literacy rate accounts for 68% statistic Sierra Leone (MICS s). The
principal economic activities in the western area are small scale
agriculture, fishing, petty trading, industries and business
enterprises.

In the western rural areas small scale farming, fishing, salt

manufacturing, poultry and animal husbandry are their main income
activities. Approximately 70% of women are actively involved in
these enterprise there is high level of unemployment among the
youth due to limited job facilities.

The western area, includes Freetown, is more mixed in population,

but is basically the home of the creole ethnic group. In all, there are
about eight ethnic groups in the western area. The largest of these
are the Temnes. There are also the Mendes, Limbas, Sherbro, Fulla,
Loko and Susu.

The main sources of water supply within the western are is the
Guma water Company Limited. Over the years, there have been
some damages to some of the infrastructures which has hindered
equitable distribution of water go to households.
The over population and extension of the city has not help the
situation. Many people have therefore resort to digging water wells
for domestic use and drinking. Most of these wells are not
protected and water samples are not tested to determine quality.
This has led to occasional out break of water borne diseases such as
cholera, diarrhea and typhoid. Scabies and skin infections are also
diseases reported due to the unavailability of water.

The health sector administration is primarily the responsibility of the

Ministry of health and Sanitation and supported by the district health
management teams in the periphery. Each health facility has
community based programmes such as village development
committee (VDC) community based development (CBD), and village
health committee (VHC) and area development committees.
Community blue flag volunteers are also trained to link community
and services within their locality. These community health
programmes also serve as steering committees in a bid to improve
health care services.

With regards to the multi-sectorial collaboration, the district

collaborate with other ministries such as Education, Gender and
Children Affairs, Agriculture, Energy and Power and Fisheries and
Marine Resources in delivering consolidated health care services.
Health related NGOs such as Concern worldwide, Save the Children
UK Action Aid, ACF Goal Sierra Leone, IRC, SCRCS, PPASL, Marie
Stopes, do collaborate with the District health management team.
In addition, faith based organisation such as UMC, St Anthony,
SLIMS, Likewise collaborate with the district in health delivery. The
UN agencies such as UNICEF, WHO, UNFPA and WFP provide
technical, financial and material support to the district on the whole
 there is strong collaboration between the DHMT and the above
partners in developments.

3.2 Study design

The study design is cross sectional comparative study.

3.3 Instrument for data collection

Data was collected by administering the questionnaire on socio-
economic and demographic characteristics of women of child bearing
age. Salter scale (spring balance) were used to weigh all the inputs at
the selected hospitals and clinics in the Freetown western urban areas.
Before the questionnaire was used, the researcher visited some of the
study areas in order to get acquainted with some of the subjects.
Information was obtain from the various hospitals and clinics as to how
to trace those parents at their various homes through their child’s
registration cards at the various health centers in order to
administered my questionnaires.
This was complemented by a participatory observation approach to
gain information on the health outcome of their children relative to the
effects of low birth weight and infant mortality rates. Also, accessibility
to the health facilities among constituencies and comparison were
made of the selected or study areas.
Additional, magazines, brochures and journals were utilized.

3.4 Target population

The target population comprises of infants from (0-5) of age and
women of child bearing age within the Freetown western urban areas (15 –
45) years.

3.5 Sample selection and sampling technique

 The sample frame included a list of all the children that were born
within the Freetown western urban areas from September 2007 to
September 2008 and their suckling mothers.

3.6 Pilot test

Prior to the collection of the data, a pilot test was conducted to identify
the short comings from this research.

3.7 RESEARCH HYPOTHESIS

Hypotheses were set on the socio economic status of parents and low birth

weight children, maternal violence during pregnancy and low birth weight .Two

contingency tables were formed containing number of children of normal birth

weight and low birth weight, and maternal violence and low birth weight

disparities’ of children.

A chi square test was performed at the 95% confidence interval to determine

whether the stated hypotheses could be accepted or rejected. Acceptance or

rejection of the hypotheses depended on whether the chi square value calculated

is significantly greater or smaller than the critical values of the test statistics at

the given confidence interval. Two null hypotheses and corresponding alternative

hypotheses were set.

HYPOYHESIS 1

HO: There is a correlation between maternal violence and low birth weight.

H1: There is no correlation between maternal violence and low birth weight.
 HYPOTHESIS 2

HO: There is a correlation between socio economic status parents and low birth
weight.

H1: There is no correlation between socio economic status of parents and low
birth weight

Note;

HO = Null hypothesis

H1 = Alternative hypothesis

3.7 Data analysis

The collected data was analyzed by the used of simple descriptive
statistics such as dependent variables, independent variables and then
being interpreted by the used of cluster seer spatial clustering analysis
in the forms of graphs and tables

3.8 Analysis of birth weight

Query for low birth weight infants were used to aggregate the data by
constituencies for low birth weight cases, maternal and paternal
education

CHAPTER FOUR
RESULT AND DISCUSSION
3.0 Socio demographic characteristics of respondent.
 From table 1, females of child bearing age, i.e. (25 – 34yrs) make
up a mere 32% while most of the respondents 43.6% (15 – 24yrs) are within
the age bracket (15-24yrs) and (35 – 54yrs). The result on marital status
shows that marriage is not a common phenomenon among household of the
parents targeted. Majority of these with few parents were found to
be petty traders, civil servants and house wives. With respect to religious
denomination, Muslims constitute the greater proportion (63%) while the
Christians make up (37%).
Table 1: Socio-Demographic characteristics
No. Socio-Demographic Frequency Percentag
characteristics e
Sex
Female 300 100
Total sample 300 100
Estimated age (yrs)
15 – 24 131 43.6
25 – 34 97 32.3
35 – 54 72 24.3
55 – 64 0 0
65+ 0 0
Total 300 100.0
Marital status
Married 63 21
Single 176 58.6
Widow 22 73
Separated 39 13
Total 300 100.0
Occupation of parent (Women of
child bearing age)
i. Gainful employments/civil servant 52 17.5
in the private sector
ii. Petty trading 198 66
iii. House wife 30 16.6
Total 300 100
Religious Domination
Christian 111 37
Muslim 189 63
Total 300 100.0
Table 2: Antenatal Natal Clinic
1st visit 2nd visit 3rd visit
At risk Normal At risk Normal At Normal ANC Ref Post Natal
 risk
453 554 120 466 87 309 1 852
983 1183 178 1490 91 432 2 1559
604 463 12 385 0 330 11 629
1441 1142 45 1197 0 933 19 1624
613 423 3 409 0 239 0 556
1277 1917 3 1525 0 447 2 1527
596 486 0 487 0 301 3 919
959 981 0 1047 0 386 12 803
1118 723 0 796 0 528 18 1362
527 345 0 74 0 0 1 37
913 498 12 789 0 208 14 1013
1128 632 12 927 0 228 14 1244
856 421 0 511 0 135 5 633
1165 794 0 875 0 252 15 1682
12633 9662 385 10978 178 5788 122 14440

From the above table, the formula for the risk factors is,
Risk factor = T2V+T3V—T1V.
Therefore the total risk cases reported for the past one year in
antenatal clinics within the western urban areas was 12070 cases.
(Table2) The above results shows that, there was serious high risk
cases within the western urban areas as of September 2007 to August
2008. In order words, 12070 women were at risk at delivery which calls
for concern for the appropriate authorities.
There was a total of 122 referred cases to the big government
hospitals, and there was no record to show if whether those pregnant
women who were referred to those hospitals survived. 14,440 women
visited the postnatal clinics after delivery . There were fluctuations in
normal delivery. i.e. 9662 at first visit, 10978 at second visit and
then fall to 5788 third visit.
Table 3: Maternal Child Health Delivery
At risk Norma Live Low/birt Still Neonata Maternal Referre
l birth h birth l death death d
deliver <2.5kg Cases
y
119 0 119 0 0 0 0
266 0 266 0 2 0 0 6
229 0 229 1 2 0 1 2
 541 0 541 1 4 2 1 27
178 0 178 0 3 2 1 7
422 0 422 0 8 1 1 7
125 0 124 0 1 2 0 1
257 0 255 0 2 0 0 2
180 0 176 0 6 0 0 20
114 0 144 0 0 0 0 0
160 0 160 0 6 0 0 0
191 0 191 0 6 0 0 0
183 0 183 0 1 0 0 18
211 0 211 0 8 2 0 2
3176 6 3199 2 49 9 4 92

From the above on maternal Child health delivery, the following results
were
obtained as shown above. Even though these people were trained and
qualified,
there was lack of salter scales in most of the health post visited, Most
of these centers lack proper record keeping interms of low birth
weight disparities, still birth, neonatal death and maternal death. When
asked about the said issues, they said, they were nurses and not
measurement and evaluation officers or epideomoligist there was a
total of 3176 women who visited the maternal health posts. There was
only 6 normal delivery cases reported in these MCH posts, live birth
was 3199 , low birth weight was 2, still birth is 49 neonatal death was
9, maternal death 4 and referred cases 92.

Table 4: Trained traditional birth attendant delivery

Norma At Live Low/birt Still Neonat Matern Referre
l risk birth h <2.5kg birt al al d
deliver h death death Cases
y
336 18 336 0 0 0 0 0
192 0 192 0 0 0 0 0
190 0 190 0 0 0 0 0
552 0 552 0 0 0 0 0
104 0 104 0 0 2 0 0
333 0 333 0 0 0 0 0
246 0 246 0 0 0 0 0
108 0 108 0 0 0 0 0
410 0 410 0 0 0 0 0
264 0 264 0 0 0 0 0
432 21 432 0 0 0 0 0
121 0 121 0 0 0 0 0
361 0 361 0 0 0 0 0
259 0 259 0 0 0 0 0
605 0 605 0 0 0 0 0
4081 39 4513 0 0 2 0 0

Even though this traditional birth attendants were trained, they were
not
capacitated with salter –scales (beam balance) and infant sales (1kg)
for them to monitor the trends of low birth weight and infant mortality
rates in their respective localities. Majority of this TBAs spoken to were
not able to read, let alone to monitor or enter proper records in their
record files. And majority of them depends solely on native herbs to deliver
pregnant women, which in turn may have some side effects on the
childs survival in terms of drug dosage levels and hence low birth weight
increases. With regards to normal delivery, there was a total of 4081
cases reported for the past one year, 39 at risk of delivery and 2 cases of
neonatal death.
 Table 6: Preventive used by women of child bearing age within
the western urban areas of Freetown
Month Pills Condom Injectable Foam IUCD Total
s
Sept 129 211 196 142 156 140 0 0 0 0 481 493
Oct 191 256 117 179 201 162 0 0 0 0 504 597
Nov 274 291 291 192 177 189 0 0 0 0 742 672
Dec 225 205 164 261 126 292 0 0 0 0 515 758
Jan 280 408 114 226 210 406 0 0 0 0 604 140
Feb 178 213 225 177 251 189 0 0 0 0 573 590
Mar 265 291 107 278 222 266 0 0 0 0 594 835
Apr 176 172 57 130 178 209 0 0 0 0 411 511
May 173 247 121 192 163 280 0 0 0 0 457 719
Jun 214 355 355 183 248 374 0 0 0 0 645 980
Jul 306 338 338 213 253 352 0 0 0 0 772 942
Aug 237 293 293 235 233 370 0 0 0 0 495 687
Total 2648 328 2378 240 241 322 0 0 0 0 7444 8917
0 8 8 9

From the table above, the preventives used in the Western urban area
are pills, condoms and injectables etc. however, pills have some side
effects as:
• Single hormonal pills (contain only progesterone e.g. microlute) and
sometimes leads to delay in menses or scanty menstruation.
• Combine pills (contain both estrogen and progesterone e.g.
mircogynone). They have a tendencies of causing or precipiting
hypertension.

Condom hasn’t got any side effect on hormonal control. the only side
effect is some people express gaining no pleasure in using it.
Nevertheless, condom has great advantages over all other contraceptive
measures because of the following reasons.

• It prevents unwanted pregnancies

 • Prevents sexually transmitted infections
• Some people also explain about another advantage of condom that it
prolong nature.
• For injectables, its greatly interrupts hormonal cycles leading to
• Scanty or lost of menstruation in users
• Sometimes it causes dysfunctional uterine bleeding which can either
be menorrhagia/hypernorrhoea or excessive menstrual flow. It may
also lead to (Metrorrhogia/polymenorrhoea) i.e. frequent intermittent
menstrual flow between intervals.

PARENT EDUCATION ATTAINMENT FOR LOW BIRTH WEIGH

INFANTS

2.2, 2%
11.7, 12% 1.6, 2%

Missing
Advance study
Elementry grades

32.1, 32% Post sec. education

52.3, 52% High school grades

From the above pie chart, and based on the results that were obtained,
it was revealed that 52.3% of the child’s parents (women of child
bearing) age obtained elementary schools educations which has some
negative impact on their social well being before and after pregnancy in
terms of proper hygiene and birth spacing, which in turn, will lead to poverty
cycle and hence low birth weight. 32.1% had post secondary education,
1.6% had advanced study and missing 2.2%
Many studies link LBW to higher mortality rates. For example, a study
of 16,000 individuals born in Hertfordshire between 1911 and 1930 finds
that those with lower birth weights are twice as likely to experience
fatalities in adulthood due to coronary heart disease as are those at the top
of the birth weight distribution. The Nurses Study in the United States
provides similar evidence (Barker 1997). Other studies show that the rate of
fetal growth, perhaps a better measure of distress in utero than birth
weight, affects death from heart disease in a large Swedish cohort.
(Rasmussen, 2001.) Additionally, signs of poor fetal environments, such as
maternal smoking or LBW, correlate with poor health in adulthood, with
the relationship strengthening as individuals age (Case et al. 2005). A
series of indicators of in utero conditions, including maternal smoking,
remain a jointly significant predictor of health at age 42, on top of the
impact on reported health status at age 42 of health at ages 23 and 33. In
an analysis of data from the Panel Study on Income Dynamics, Johnson
and Shoeni (2007) find a gradient of increasingly worse health among LBW
children. For example, they find that the effect of being LBW on adult
health is similar to the effect of being 8.7 years older. They also find that,
although the impact on child health declines when they control for shared
sibling characteristics, LBW still has a modest effect on childhood health.
According to the fetal-origins theory, shocks that occur in utero can have
health effects that appear years later. Barker (1997) explains that an
inadequate supply of nutrients or oxygen can slow the process of cell
division. Depending on the timing of those deprivations, the number of
cells in particular organs may be reduced, or under-nutrition can change the
amount of hormones including insulin and growth hormone. According to
Barker, this lack of nutrition can permanently alter or ―program‖ the body.
Barker has refined his theory to indicate different risks related to
different periods of gestation. For example, fetal growth slowed during
the first trimester may contribute to stroke through elevated blood
pressure; coronary heart disease may reflect complications with insulin
arising in the second trimester. (Rasmussen 2001.) Others propose that
adult-onset diabetes is linked to ways that infants who have retarded
growth may adapt to ensure survival (Rasmussen 2001, citing Cianfarani
et al. 1999).

3. The notion that ―programming‖ organs in the beginning of life can

have lasting effects has also been widely demonstrated in studies with
other species (Rasmussen 2001). Almond (2006) uses the dramatic
variation in exposure to the influenza pandemic to estimate the long-
term effects of exposure to influenza in utero. The pandemic struck
suddenly and subsided quickly, with infections concentrated between
October 1918 and January 1919, and there was great geographic
variation in exposure rates. Nearly one-third of pregnant women
contracted the virus. Decennial census data from 1960 to1980 reveal
that educational attainment is a quarter year lower for the cohort that
was pre-natal during the pandemic and incomes are 6 percent lower. These
results are corroborated by SIPP data in Almond and Mazumder (2005). There
are other potential explanations as to why LBW may be associated with
adverse health effects. For example, the same genetic endowment that may
result in LBW may cause other health effects later in life (Behrman and
Rosenzweig 2004). Alternatively, LBW may signal other factors such as
maternal behaviors, medical care, and demographic characteristics that may
themselves contribute to poor health later in life. Additionally, Conley and
Bennett (2000) raise the possibility that LBW children may suffer stigma or
have fewer resources allocated to them within the family with subsequent
adverse health effects later in life.

Case and Paxson (2006) link mothers education to behaviors’ that

affect infant health, such as smoking, which the Surgeon General has
determined is causally related to LBW and shortened gestation (CDC 2004).
The authors also note that less well educated pregnant women less often
seek prenatal care in their first trimester than those with some college
education (68 percent compared to 91 percent, in the National Vital
Statistics numbers they cite). Although some studies identify significant
differences in LBW rates among mothers receiving inadequate levels of
prenatal care compared with those who receive adequate care (Devaney et
al.1992), there is some ambiguity about the impact of prenatal care.
Low-income women may also have inadequate nutrition during
pregnancy. Although Rasmussen (2001) concludes that few studies identify a
significant causal link between maternal nutritional status and LBW among
women in developed countries, poor nutrition could contribute to other
complications. Lack of knowledge of or access to nutritional supplements
could lead to spinabifida and other neural tube defects (Case and Paxon
2006). Of particular relevance for a discussion of economic mobility is the
fact that parental birth weight status is a strong predicator of LBW in the
next generation. For example , Conley and Bennett (2000) find that
infants are four times more likely to be LBW if their mothers were LBW and
six times more likely if their father were. Currie and Moretti (2007) say their
findings suggest that some of the intergenerational transmission of
economic status could be due to intergenerational transmission of LBW.
 MATERNAL EDUCATION

9.6

33.7
Advanced study
Elementry grades
30.9 Post sec. education
Missing
High grades

24

From the above pie chart and based on the results so far obtained from
the said study, It was realized that, the parents (Fathers) of the said
target population of children within the western urban area of
Freetown had 33.7% high school education, whiles, 30.9% had
elementary education, 24% had post secondary education and 9.6%
had advance study which has some impact in terms of poor antenatal
care, early child marriage, teenage pregnancies, poor birth spacing
combined with poverty leads to low birth weight.

In their review of the literature, Currie and Madrian (1999) state that
many researchers have suggested that poor childhood health is
correlated with less education (for example, Grossman 1975, Perri
1984, Wolfe 1985, Wadsworth 1986). An evaluation of British data
finds that after controlling for parental and household traits, each
adverse health condition at age seven is related with a 0.3 drop in the
number of 0-level exams passed, and each condition at age 16 is
associated with an additional 0.2 decline (Case et al. 2005). The study
also finds that different conditions had different effects, with mental
and emotional problems at either age related to educational outcomes,
as are systems‖ conditions (including lung, heart, blood, and
neurological conditions) at age seven. On the other hand, physical
impairment had no significant effect. Grossman and Kaestner (1997,
cited in Currie and Stabile 2003) also review this literature and suggest
that health-related school absence explains a portion of this effect for
an example of a condition that contributes to school absence. Currie
(2008, forthcoming) reviews the links between parent socioeconomic status
and child health and between child health and future outcomes like
educational attainment. She documents strong links between each pair
above, but she points out that the size of the effect of child health on
subsequent outcomes is difficult to measure in part due to the fact that
health is multi-dimensional and not easily quantified in single-index
measures.

PERCENT OF THE BIRTH WEIGHT CHILDREN

WITHIN THE WESTERN URBAN AREAS OF
FREETOWN

12

Normal birth w eight

Low birth w eight
Very low birth w eight

78
MATERNAL SMOKING AND ALCOHOL DRINKING BEFORE,
DURING AND AFTER CHILD BIRTH
MATERNAL AGE SMOKIN NOT ALCOHOL NO
G SMOKING DRINKNG ALCOHOL
DRINKING
15 – 24 29 102 17
114
22 – 34 15 82 8
89
35 – 54 2 70 2
70
55 – 64 0 0 0
0
65+ 0 0 0
0
TOTAL 46 254 27
273

From the above table, it was revail that, out of a total of 300
pregnant women that were interviewed for smoking and
alcohol drinking, there was a total of 46 pregnant women who were
smokers, 254 were non smokers,27 of them responded that they
do take alcohol during and after pregnancy and 273 responded that
they do not take alcohol at all.
Maternal smoking during pregnancy and LBW are tied to poorer
performance on O-Level exams in Britain (Case et al.2005).
Johnson and Shoeni (2007) found out that reading comprehension
and maths scores are lower among LBW children . When they
control for sibling fixed effects, the impact of low birth weight becomes
marginally significant. Conley and Bennett (2000) found that
the probability of graduating from high school by age 19 is
reduced by 74 percent for LBW children compared with their siblings.
Behrman and Rosenzweig (2004) note that studies that simply
utilize cross-sectional data without controls for genetics or family
background may underestimate the adverse effect of birth
weight on schooling by as much as 50%.

BIRTH WEIGHT AND SOCIO ECONOMIC STATUS OF PARENTS

SOCIO-ECONOMIC HIGH LOW TOTAL
STATUS S.E.S S.E.S
NORMAL 49 (16. 3%) 83(27.6%) 132
LBW 56 (18.6%) 112(37.3%) 168
TOTAL 105 195 300

Out of a total of 168 low birth weight cases that were identified, 56
were having higher socio economic status, which is (18.6%) and 112
were living in lower socio economic status, which is (37.3%).
In terms of normal birth weight, 49 parents were found to be living in
higher socio economic status which is (16.3%), whiles 83 parents who
were normal birth weight, were found to be in lower socio economic
status which is (27.6).
Low-income women may also have inadequate nutrition during
pregnancy. Although Rasmussen (2001) concluded that few studies
identify a significant causal link between maternal nutritional status
and low birth weight among women in developed countries, poor
nutritional could contribute to other complications. Lack of knowledge
of or access to nutritional suppliments could cause spinabifida and
other neutral tubes defects (Case and Paxson, 2006), of particular
relevance for a discussion of economic mobility is the fact that parental
birth weight status is a strong predicator of LBW in the next
generation. For example, Conley and Bennett (2000) found that infants
are four times more likely to be LBW if their mothers were LBW and six
times more likely if their fathers were. Currie and Moretti (2007) say
their findings suggest that some of the intergenerational transmission
of economic status could be due to intergenerational transmission of
low birth weight.
There is some evidence for the relationship between LBW and earnings
or socio economic status in adulthood. Currie and Moretti (2007) find
that LBW has an effect on earnings that increases with age. Case and
Paxson (2006)estimates that being born LBW may be associated with
lowering earnings by 4 percent at age 33.
BIRTH WEIGHT IN RELATION TO MATERNAL VIOLENCE DURING
&
AFTER PREGNANCY
Birth Weight Violence Not Violence Total
LBW 39 11
50
NORMAL 6 2
8
TOTAL 45 13
58

From the table above and based on the questionnaires and interviews
conducted, the following results were obtained on maternal violence
during pregnancy, 39 women reported who gave birth to LBW babies
reported being violence during pregnancies, 6 women who were
normal birth weight reported of being violence during pregnancy. As a
whole, there was a total of 46 women who reported being violence
 before, during and after pregnancy whiles 13 reported not being
violence during pregnancy.
To proved if whether the said results on maternal violence were
correct, a calculated chi square method were used to test for the
hypothesis and the following results were obtained.
The calculated chi square value is 0.653
The critical values at the 95% confidence interval of the degree of
freedom of 1 is 3.841 which is significantly greater than the calculated
chi square which is = 0.653, and hence the HO; is rejected.
Therefore, maternal violence during pregnancy is not the lead factor
responsible for low birth weight in the western urban areas of
Freetown.
HO: there is a correlation between maternal violence and low birth
weight HI; there is no correlation between maternal violence and low
birth weight.

Trends in Infants Mortality rates as off September 2007 - August 2008 in

the Western Urban Areas of Freetow n

120 110
Total No. Respondents

100
78
80
M
60 50
42 F
36
40 31
17 17 19
20 8 9 9 11 10 10 9
5 4 3 4
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Deseases
 Neonatal mortality (per 1000 live births in Freetown
Western Urban Area

100
1000
2008
TRENDS IN MORTALITY RATES AS OF SEPTEMBER 2007 TO AUGUST
From10 the above graphs, it is observed that, there is a daily increase in
infants mortality rates in the urban areas of Freetown. i.e. , as from
September to February 2007,there was an increase of disease trends
up to 90%. i.e. malaria, malnutrition, adult respiratory infection,
diarrhea, hydrocema, convulsion, sickle cell, heart failure etc.

From1 March to August, there was an steady increase in infants

mortality rates from 90% up to 115% which calls for concern for the
appropriate authorities.
These results 1.0
are corroborated 2.0
by SIPP data in Almond
3.0 and Mazumder
4.0 5.
(2005). There are other potential explanations as to why LBW may be
BIRTH WEIGHT (KGS)
associated with adverse health effects. For example, the same genetic
endowment that may result in LBW may cause other health effects
later in life (Behrman and Rosenzweig 2004). Alternatively, LBW may
signal other factors—maternal behaviors, medical care, and
demographic characteristics—that may themselves contribute to poor
health later in life. Additionally, Conley and Bennett (2000) raise the
possibility that LBW children may suffer stigma or have fewer
resources allocated to them within the family with subsequent adverse
health effects later in life.
Birth Weight-Specific
Mortality
The Analysis of Infant Mortality

If birth weight is not on the causal pathway to infant mortality, then

birth weight is neither an explanatory factor nor a potential
confounding variable in the analysis of infant mortality. As a general
statement, birth weight is not important in the analysis of infant
mortality. In contrast, preterm delivery is the causal pathway to infant
mortality. Any analysis of infant mortality should take into account the
contribution of preterm delivery. However, gestational age data are
often incomplete or of poor quality, which can make it difficult to
identify preterm births. The importance of birth weight data, therefore,
is to provide inferences about preterm births.

The residual distribution identifies the percent of small, high-risk

preterm births in any study population. If you also have data on birth-
weight-specific mortality, then the number of deaths among residual
births can be calculated by applying the weight-specific mortality rates
to the residual distribution. By inference, this provides the number of
deaths among small preterm births. These deaths typically amount to
half or more of all infant deaths.

After taking account of infant deaths among the small preterm infants,
the remaining deaths are all among the predominant distribution.
Virtually all of these are term births. Among term births, it is not the
distribution of birth weights (which is always Normal, or gaussian) but
the height of the mortality curve that determines the number of
deaths.

The birth weight distribution of term babies is useful for one thing: it
provides information about fetal growth. Keep in mind that the
consequences of fetal growth for infant mortality are unpredictable.
Even so, fetal growth can be a useful endpoint in itself for assessing
the biological effects of nutrition, environmental exposures, etc. The
specifics of analyzing fetal growth and birth weight are discussed in
the next section (Beyond low birth weight).

You're almost done. Beyond low birth weight is the final

Birth weight by itself would not have caught the attention of
epidemiologists were it not for its association with infant mortality. The
relation of mortality to birth weight has spectrum of birth weights.
(The figure shows mortality on a log scale in order a highly distinctive
pattern . Mortality ranges more than 100-fold across the to
accommodate this huge range.)

The reverse-J pattern of weight-specific mortality is found in all

populations, and occurs with fetal mortality (stillbirths) and with
neonatal or infant mortality (Wilcox 1983b). While high mortality
among small babies is one of the chief justifications for studying
LBW, note the continuous rise of mortality with lower weight. The
mortality curve provides no particular justification for 2500 grams as
the criterion for risk.

Stability of the curve

One fundamental aspect of birth weight-specific mortality is the

constancy of its shape. US neonatal mortality fell 75% between 1950
and 1998 (from 20 to 5 per thousand) with no change in the basic
shape of the curve . This constancy in the shape of this curve over time
may be surprising, since much of the improvement in US infant
survival over the past fifty years is assumed to be due to better
medical care for very small babies. The absolute decline in mortality
has indeed been greatest among small infants. However, the relative
decline in mortality has been fairly uniform across all birth weights (a
constant distance on the log scale), with least change at the smallest
weights.

The general contrast seen between these two mortality curves is

typical. The crucial difference in birth-weight-specific mortality
between any two groups is usually the height of the mortality
curves, rather than their shape .

There is one more feature of the mortality curve that becomes

apparent only when the curve is considered in relation to the birth
weight

distribution.
A bell-shaped distribution of birth weight is found in all populations
(the frequency distribution of birth weight). Similarly, the curve of
weight-specific mortality has the same general shape in all
populations (birth-weight-specific mortality). When the weight and the
mortality curves are taken together, an additional feature emerges.
The mean weight is always several hundred grams lower than the
optimum weight (the weight with lowest mortality). Just as the
average birth weight varies among populations, so does the optimum
weight. This relation between optimum and mean weight is the
basis for the Wilcox-Russell hypothesis.

The usual assumption about birth weight is that a change in birth

weight directly affects prenatal survival. The Wilcox-Russell hypothesis
is that, on a population level, birth weight is not on the causal pathway
to mortality. A change in birth weight is often associated with a change
in prenatal health, but it is not through the change in weight that the
health effect occurs. Weight and mortality can change together
because a single factor is affecting them both. But birth weight can
also change without an effect on mortality.
Support for this hypothesis is found in the fact that, as mean birth
weight changes, the weight-specific mortality curve changes by exactly
equivalent amounts.
Frequency distributions of birth weight and weight-specific neonatal
Mortality USA, 1984. Infant mortality rates were similar in all the states
of America, as a whole Most people in America were living at high
altitudes, and high altitude produces smaller babies.

This figure also shows the curves of weight-specific mortality for

Colorado and the US. The two curves intersect. Mortality rates
are lower in Colorado for small babies, and higher for large babies.
There is no obvious biological explanation for why small babies should
do better in Colorado and larger babies should do worse. Another
interpretation of the intersecting mortality curves is that, as birth
weights have shifted to lower weights in Colorado, so has optimum
weight and in fact the whole mortality curve.

The Wilcox-Russel Hypothesis,

 Frequency distributions of birth weight and weight-specific neonatal
mortality rates for Colorado and the United States, 1984, after
adjustment to a z scale of birth weight.

With this adjustment, the two weight distributions correspond nearly

exactly, as do the two mortality curves . The simplest explanation for
the convergence of mortality curves is that altitude affects birth weight
but not mortality.

The two mortality curves are essentially the same curve, with the one
in Colorado carried along with the shift in birth weight. For babies
weighing less than the optimum weight, this shift gives the appearance
of lower mortality at any given birth weight. For babies heavier than
the optimum weight, the shift gives the appearance of higher
mortality. In fact, the birth weight distribution and its accompanying
mortality curve has shifted without any change in the survival of
individual babies.

In this example, fetal growth retardation (on the population level) has
no effect on mortality.
We can conclude from this example that the moderate reduction of in
utero growth does not necessarily increase an individual baby's
mortality risk - nor does it increase the number of small babies at
higher risk. This might be regarded as a counter-example to Geoffrey
Rose's highly-cited thesis that a modest shift in the population mean of
a continuous variable (such as blood pressure) will place more
individuals into the high-risk group at the extreme. This appears not
necessarily to be true for the birth weights of term babies.

Now imagine a more complicated but plausible scenario. What if a

factor decreases birth weight and also increases infant mortality? The
same analytic approach can be applied. In the process, we can
discover the underlying sense behind the LBW paradox.

Frequency distributions of birth weight and weight-specific prenatal

mortality rates for infants exposed and unexposed to mothers' who are
smoking and
nonsmokers
mothers.

The effect of smoking

Mothers who smoke have smaller babies. Their babies have higher
infant mortality as a group. If we look at the birth weight and mortality
curves for smokers and non-smokers, the initial picture is rather similar
to Colorado-US. There are different birth weight distributions, and the
two mortality curves intersect. Small babies do better if their mothers
smoke. This is the paradox with which Yerushalmy defended smoking.
 Frequency distributions of birth weight and weight-specific prenatal
mortality rates for infants exposed and unexposed to mothers' who
smoke, after adjustment to a z scale of birth weight.

When the picture is adjusted to relative weight (the z-scale), there

emerges a new relation between the mortality curves . Mortality with
mother's smoking is higher across the whole range of weights. Thus,
smoking has two discrete effects. It retards fetal growth, shifting the
birth weight distribution (and, as always, the mortality curve). In
addition, smoking also shifts the mortality curve upwards, to
higher rates.

In the previous example of altitude, the shift of the birth weight

distribution to lower weights was not sufficient to increase infant
mortality. In the example of smoking, there is increased mortality
that occurs equally at every adjusted birth weight (on a multiplicative
scale). In other words, this effect of smoking on weight-specific
mortality is independent of birth weight.

The increase of mortality across all weights - crucial evidence of the

harmful effect of smoking on infants - is initially hidden by the leftward
shift of the mortality curve as it follows the birth weight distribution.
Small babies of mothers who smoke seem to be at lower risk,
when in fact they are at higher risk. This is apparent on the relative
weight scale (the z-scale) but not on the absolute scale.

McMahon anticipated this conclusion when he proposed that the LBW

paradox was an artifact due to comparison of absolute weights .
Relative weights are needed to uncover the essential relation between
smoking and infant mortality. To the extent that smoking increases
weight-specific mortality proportionately across all (relative) weights,
smoking acts on infant mortality independent of birth weight.

As discussed earlier, the intersection of weight-specific mortality

curves is not uncommon. It can be found in nearly any setting where
populations have different mean birth weights. In each case, the true
difference in weight-specific mortality is revealed after adjustment to
a relative scale of birth weight

Problems with LBW

The hypothesis has been proposed that birth weight is not on the
causal pathway to infant mortality (The Wilcox-Russell
hypothesis). If this hypothesis is correct, we must reexamine some of
the basic assumptions about LBW (see A short history of low birth
weight).

1. "Is percent LBW a good surrogate indictor of a population's infant

risk?"
No, because LBW is easily affected by changes in the predominant
distribution which are not reliable indicators of risk.

Altitude produces more LBW babies, but this does not lead to an
increase in infant deaths (Wilcox ,1993). Another example is Mexican-
American babies. Babies born of Mexican mothers in the US have a
predominant distribution of birth weights shifted to lower weights than
non-Hispanic whites (Buekens 2000). This causes Mexican-Americans
to have more LBW babies than non-Hispanic whites. However,
Mexican-Americans have lower infant mortality. LBW would identify
Mexican-Americans as a group at higher risk for infant mortality, but
they are not.

Difference in percent of LBW may reflect harmless differences in the

predominant distribution.

2. "Are LBW births really preventable?"

Preterm delivery is preventable in principle, and preterm births
comprise a major portion of LBW. But what about the lower end
of the Normal distribution of births? How can these births be
"prevented"?

One option might be to increase the mean or reduce the SD until

little of the distribution falls below 2500g. But if the mortality
curve automatically shifts with the birth weight distribution, this
strategy is of dubious value.

Another alternative would be to change the fundamental Normal

distribution of birth weight (for example, by truncating its lower
tail). This seems infeasible.
Elimination of LBW is neither practical nor necessary in order to
achieve the lowest possible rates of infant mortality.

Alternatives to LBW in the analysis of birth weight

 The arguments above suggest that LBW is muddled as an
endpoint, and unreliable as a predictor of population risk. The fact
that these uses of LBW are time-honored is hardly a defense.

What alternatives are available? The answer depends on the

purpose of the investigator. If the aim is to assess prenatal health
through some convenient surrogate, there are several options
depending on the type of data available.

1. When only birth weight is available. If birth weight is the only

type of data at hand, the residual distribution should be
estimated. The percent of births in the residual distribution is
preferable to LBW as an indicator of prenatal health. The residual
provides an estimate of the number of small preterm births - the
babies at highest risk.

2. When birth weight and gestational data are both available. The
proportion of preterm births in the population should be
examined directly whenever possible. The residual distribution of
birth weight is informative, but it is not as good as actual
information on preterm delivery. (This of course assumes that
the gestational data are of good quality, which is not always the
case.)

Once the percent of preterm births is known, the analysis of birth

weight can be simplified by restricting the sample to term births.
Among term births, the influence of gestational age is minor and
can be ignored. The mean and SD of birth weights among term
births provide a way to compare fetal growth across groups.

The comparison of fetal growth patterns may be interesting in its

own right (for example, in understanding the biological effect of
 a specific exposure), but fetal growth on the population level not
a dependable marker of prenatal health.

3. What about the "fetal growth curve"? The pattern of mean birth
weights across strata of gestational age has been used to
describe the course of intrauterine "fetal growth". The
assumptions necessary to justify the use of cross-sectional birth
data to describe longitudinal growth are dubious at best. At a
given gestational age, births are not a random sample of all
intrauterine fetuses. This is especially true of births delivered
preterm. The use of birth data to describe intrauterine growth
patterns is unsound and should be avoided.

4. What about IUGR (or SGA) as an epidemiologic endpoint? The

use of a weight percentile to define fetal "growth retardation"
has several logical problems. When an external factor (for
example, altitude) acts to retard fetal growth, it acts on all
babies, not just the small ones. A nine-pound baby can therefore
be just as "growth retarded" as a five-pound baby when
compared with their unaffected weight. Under this scenario,
there is no logic in singling out the smallest 10% of babies as the
ones who are growth retarded.

On a more clinical level, IUGR defined by percentile corresponds

poorly with medical signs of fetal growth retardation.
Furthermore, IUGR has the unfortunate property of mixing
preterm and term births (just as LBW does). If an investigator
wishes to summarize intrauterine growth in a population, there is
no simpler or more direct endpoint than the mean weight of term
births.
 The perils of ordinary adjustments by birth weight

The analysis of birth weight becomes even more complicated

when birth weight is not the endpoint in itself, but is treated as an
intermediate variable. An example is the analysis of infant
mortality stratified by birth weight. Such analysis is sometimes done
without taking into account the corresponding birth weight
distributions. This is risky because meaningless differences in
weight-specific mortality may be taken as real or important
differences may be missed . The comparison of US mortality curves
is informative only because the US birth weight distribution has
changed so little over the last half-century.

Adjustments of weight-specific mortality can be made using a z-

scale, based on the mean and SD of the predominant distribution.
A cruder but serviceable method is to compare mortality
rates by percentiles of birth weight. The percentile approach may
be slightly distorted when study populations differ in their
proportion of residual births, but this is probably a minor problem. A
method has also been proposed to adjust mortality to a z-scale
while controlling for multiple confounding variables (English 1992).

All these special methods for adjusting to a relative scale of birth

weight serve only to underscore one central point. Whatever
method is used, excess relative risk tends to be uniform across
adjusted birth weights. Despite the huge mortality gradient by birth
weight within a population, mortality differences between
populations generally appear to be independent of birth weight.

The unimportance of birth weight

 When comparing two populations, the only difference in birth
weight that directly affects mortality is a difference in the
residual distribution (i.e. a difference in the rate of small preterm
births). When infant mortality is higher in one population than
another, the mortality difference must be due either to a
difference in small preterm births or to differences in weight-specific
mortality that are independent of birth weight. This
demonstrates the central importance of preterm delivery in
infant mortality, and the unimportance of birth weight.

By extension, any analysis of birth weight in relation to

associated outcomes must be approached with caution. The most
innocent routines of epidemiologic analysis are problematic when
birth weight is used as an intermediate variable. For example,
when analyzing infant mortality, epidemiologists often
attempt to "remove" the effects of birth weight by direct or
indirect standardization, or by logistic regression. This is
presumably done to "isolate" the mortality effects of factors
operating other than through birth weight.

As Robins and Greenland (1992) have described, this general

strategy is unwise. In the specific case of birth weight, the ordinary
adjustments of mortality by birth weight implicitly assume
that weight-specific differences in mortality are uniform across
strata of absolute birth weight. Since weight-specific
mortality rates usually intersect under the very conditions that
provoke adjustment (i.e. when there are different distributions of
birth weight), ordinary birth weight adjustment is nearly
always unjustifiable. Furthermore, results of such adjustment
have been shown to be biased (Wilcox ,1983d).
 The relation of birth weight to later health outcomes
There has been a resurgence of interest in the associations
between birth weight and diseases of adulthood - for example,
cardiovascular diseases, diabetes, certain cancers, and
impairments of hearing or vision. It is fascinating to find that, when
weight-specific data are available, the risks of later endpoints
often echo the same reverse-J-shaped pattern seen with infant
mortality.

Barker has promulgated the hypothesis that fetal nutrition

explains these associations. Fetal nutrition determines fetal growth,
fetal growth determines birth weight, and therefore the
associations of birth weight with adult diseases demonstrate the
impact of fetal nutrition on adult health. However, if (as has been
suggested here) the association of birth weight with infant
mortality is not causal, there must be similar doubts about birth
weight's causal association with diseases in adulthood. Alternative
explanations are beginning to emerge, with hypotheses
regarding shared genetic mechanisms for fetal growth and later
disease.

Biological mechanisms that link birth weight to illness or

mortality are of great interest, even if they are not causal. Why is
infant mortality so strongly related to birth weight, regardless
of gestational age? What are the biological underpinnings of the
relationship between birth weight and cerebral palsy, or adult
hypertension? Perhaps there are metabolism or growth genes
that determine fetal size (in some dynamic competition with the
maternal system), and that go on to regulate physical
development in ways that affect later risk of disease. Such
hypotheses offer rich opportunities for further investigation.
 In summary, birth weight is strongly associated with a range of
health outcomes. These associations have understandably led to
an emphasis on birth weight as an epidemiologic endpoint in
itself. However, this emphasis is misplaced. Birth weight offers
little information about population health. Analyses that "adjust" the
effects of birth weight on health outcomes by ordinary means
are unsound.

Even so, the association of birth weight with so diverse a

spectrum of health outcomes is a genuinely fascinating
phenomenon. Despite the thousands of papers on birth weight
published in past decades, there may be no subject in all of
epidemiology more ready for creative - perhaps even
revolutionary - insights

CHAPTER FIVE
CONCLUSION AND RECOMMENDATIONS
5.0 This chapter concludes the major findings of this research work
and suggests possible ways in which the factors influencing low birth
weight and infants mortality rates in the western urban areas of
Freetown could be improved for child survival intervention
programmes.
The level of education of mothers and their socio-economic status
has an influence on the level of low birth weight in the western urban
areas of Freetown. Thus the high level of illiteracy rate among
mothers is a factor in achieving the millennium development goals
4,5 and 6 by 2010 and 2015 respectively.

Low birth weight is a multi faceted problem and more than medical
interventions are needed to improve it. from September 2007 to
August 2008, there were 78% of low birth weight babies born in the
western urban areas of Freetown. Out of these 78 percent of those
babies, their mothers began prenatal care in the first trimester. The
percent of all mothers beginning prenatal care in the first trimester
increased, a period during which the percent of low birth weight was
increasing. Improving prenatal care participation is very important ,
but it is not the only answer to reducing low birth weight. Off the 78%
of low birth babies born as from September 2007 to August 2008 ,
75 percent were born to mothers age (15-20) years older. Teenage
pregnancy is thus a comparatively a high cause of low birth in the
urban areas of Freetown. Serious medical, health interventions are
the only part of the solution to this serious and difficult problem. The
results also shows that, maternal smoking and maternal violence
during pregnancies were strong, independent predicators of low birth
weight. Policies and programmes designed to address aspects of
 the social and economic environment of families may help to reduce
low birth weight.
Additional research is needed to determine how environmental
factors interact with biological characteristics to influence the risk for
low birth weight.

Finally, the millennium Declaration in 2000 identify poverty

reduction as a critical focus of macro economic policy, placing
particular emphasis on reducing by half the number of people
living in extreme poverty by the year 2015. This goal poses
critical challenges to all public health professionals, development
specialist, statisticians and economists especially those in
countries emerging from conflict situation like over in Sierra
Leone. By and large, it is now crystal clear that development
programmes in our countries and communities have become
more and more linked to poverty reduction strategies, and,
within such frame works reliable statistics on poverty in
developing countries like Sierra Leone is vital.

5.2 RECOMMENDATIONS
 In spite of the fact that data were inconsistent and scanty at some
point, the varied sources of information exposed the researcher to a
wide range of experiences. There is a need for an on-going social
mobilization at the grass-root; this will give us the assurance of
meeting the MDG4 target. This venture should take a full chain
process using focal persons like religious and traditional leaders,
husbands, peer educators etc.
A) Government should ensure that, these is improved
maternal nutrition with nutritional supplementation.
B) Improved Tetanus Immunization and treatments of
maternal in
infections should be considered by the ministry of health and
sanitation through the central government.
C) More advocacy on birth preparedness, delivery by skilled
attendant and well- equipped health facilities at the (Tertiary,
district and peripheral health units) should be strengthened.
D) Sensitization of the surrounding communities on the
factors that influence low birth weight, infants mortality rates
and importance of birth spacing, family planning and poverty
reduction strategies should be under taken by relevant
authorities. There is a need for an on-going social
mobilization at the grass-root; this will give us the assurance of
meeting the MDG4 target. This venture should take a full chain
process using focal persons like religious and traditional leaders,
husbands, peer educators etc.

E) More incentives should be attached to child intervention campaigns

without any specific age brackets. This should also applied for women
of child-bearing age (15 – 49yrs) who are neither pregnant nor nursing
mothers.
 F) There should be an on-going training plan for all health workers.
These training could be in the form of trainers, workshops or formal
management meeting sessions and it should not be selective. This will
improve the health workers on newly implemented technologies and
might motivate them to do more in terms of their responsibilities at
different health levels.

G) There should be an active referral system at the health centres and

posts. On that not all morbidity cases should be attended to as the
peripheral health unit. This will prevent unnecessary death.

H) Finally there should be an active supportive monitoring and evaluation

of the health care delivery systems of the ministry of health and
sanitation. (MOHS).

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79