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This paper synthesises what is known about that factors that affect development during the first 1000 days (the period from conception to the end of the second year), how these factors have their impact, and what are the long-term effects of early exposures and experiences. Further details can be found on the Centre for Community Child Health website: http://www.rch.org.au/ccch/first-thousand-days/
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Centre for Community Child Health
The First
Thousand Days
AN EVIDENCE PAPER
September 2017
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Centre for Community Child Health
The First Thousand Days:
An Evidence Paper
Prepared by:
Dr Tim Moore
Ms Noushin Arefadib
Dr Alana Deery
Ms Sue West
Prepared for the Strong Foundations: Getting it Right in the First 1000 Days initiative.
Strong Foundations is an initiative of the Australian Research Alliance for Children & Youth,
Bupa Australia, the Bupa Health Foundation, the Murdoch Children’s Research Institute, and
PwC Australia.
Strong Foundations has been generously supported by the Bupa Health Foundation.
Suggested citation: Moore, T.G., Arefadib, N., Deery, A., & West, S. (2017). The First
Thousand Days: An Evidence Paper. Parkville, Victoria; Centre for Community Child Health,
Murdoch Children’s Research Institute.
The writing team acknowledges the valuable commentaries by the following
expertreviewers:
Associate Professor Jill Sewell, Associate Professor Stephanie Brown, Associate Professor
Jerey Craig, and Dr Michael Little. Feedback on the section on Aboriginal children and
families was provided by Ms Claire Stacey and Mr John Burton from SNAICC – National Voice
for ourChildren.
This work is copyright. To request permission to reproduce any part of this material or
communication of, please contact the Centre for Community Child Health.
The Centre for Community Child Health is a research group of the Murdoch Children’s
Research Institute and a department of The Royal Children’s Hospital, Melbourne.
Centre for Community Child Health
The Royal Children’s Hospital Melbourne
50 Flemington Road, Parkville
Victoria 3052 Australia
Telephone +61 9345 6150
Email enquiries.ccch@rch.org.au
www.rch.org.au/ccch
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Centre for Community Child Health
Contents
Glossary iii
1. Introduction 1
1.1 The first 1000 days 1
1.2 Evolving ideas regarding the early years 1
1.3 Scope of paper 2
2. Biological processes shaping
health and development 4
2.1 The relationship between mind, brain and body 4
2.2 Developmental plasticity and the
developmental origins of health and disease 5
2.2.1 Developmental plasticity 5
2.2.2 Biological embedding 6
2.2.3 Epigenetic eects 6
2.2.4 Telomere eects 8
2.2.5 Synaptic pruning 10
2.2.6 Developmental origins of health and disease 10
2.3 Summary 12
3. Global factors influencing health
and development 14
3.1 Social climate change and its impact
on families 14
3.2 The mismatch hypothesis 14
3.2.1 The role of the microbiome 16
3.2.2 Allergies 17
3.2.3 Obesity 18
3.3 Summary 19
4. Social determinants of health 20
4.1 Social gradient eects in health and wellbeing 21
4.2 Poverty 21
4.2.1 Poverty in pregnancy 22
4.2.2 Poverty in infancy 22
4.3 Social determinants and Aboriginal health 24
4.4 Summary 27
5. Child, family, community and
environmental factors shaping health
and development 29
5.1 Child characteristics 29
5.1.1 Temperament 29
5.1.2 Dierential susceptibility 30
5.2 Parental and family characteristics 31
5.2.1 Neurobiology of interpersonal relationships 31
5.2.2 Parent-child attachment and parenting style 31
5.2.3 Contribution of fathers/male caregivers 32
5.3 Adverse interpersonal relationships
and sustained trauma 33
5.3.1 Child abuse and neglect: an Australian snapshot 33
5.3.2 Adverse early life experiences and poor lifelong
outcomes: the linking mechanisms 34
5.4 Impact of family and domestic violence 35
5.4.1 Domestic violence in pregnancy 36
5.4.2 Domestic violence during infancy and early childhood 36
5.5 Community environments 37
5.5.1 Social supports 37
5.6 Physical environment 38
5.6.1 Housing 38
5.6.2 Built environments 41
5.6.3 Natural environments 41
5.6.4 Environmental toxins and their eects 42
5.7 Summary 46
6. Individual level factors influencing
child health and development 48
6.1 Nutrition 48
6.1.1 Nutrition in preconception and pregnancy 48
6.1.2 Nutrition in infancy 49
6.2 Substance use 50
6.2.1 Alcohol 50
6.2.2 Illicit drugs and other psychoactive substances 51
6.2.3 Tobacco 53
6.3 Stress 54
6.3.1 Stress in pregnancy 54
6.4 Summary 55
7. Beyond the first 1000 days 57
7.1 Pathways to later outcomes 57
7.1.1 Biological embedding 57
7.1.2 Accumulation eects 58
7.1.3 Escalation of risks over time 59
7.1.4 Triple hit eects 59
7.1.5 Measuring the cumulative eects of experiences and
exposures 60
7.1.6 Summary 60
7.2 The long-term outcomes of early
experiences and development 60
7.2.1 Summary 62
8. Implications and key messages 63
8.1 Implications for action 63
8.2.1 Conclusions 67
8.2 Key messages 68
9. Final comment 71
References 72
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Glossary
Aboriginal: Aboriginal and Torres Strait Islander Australians
Aboriginal Health: Refers to physical, social, emotional and cultural
well-being of the whole Community in which each individual is able to
achieve their full potential as a human being, thereby bringing about
the total well-being of their Community.Connection to land, spirituality
and ancestry, kinship networks, and cultural continuity are commonly
identified by Aboriginal people as important health-protecting factors.
Adverse childhood experiences (ACEs): Adverse childhood
experiences (ACEs) are potentially traumatic events that can have
negative, lasting eects on health and well-being. These experiences
range from physical, emotional, or sexual abuse to parental divorce or
the incarceration of a parent or guardian.
Allergy: Occurs when a person’s immune system reacts to substances
in the environment that are harmless for most people. These
substances are known as allergens and are found in dust mites, pets,
pollen, insects, ticks, moulds, foods and some medicines.
Antenatal (also known as prenatal): Period before childbirth
Biological embedding: The process whereby environmental and
social experiences influence human biological and developmental
processes and influence health, well-being, learning, or behaviour over
the life course.
Central nervous system: The brain, brainstem, and spinal cord.
Child abuse: Refers to the four dierent types of child abuse: physical,
sexual, and emotional abuse, and neglect.
Colonisation: The forming of a settlement or colony by a group of
people who seek to take control of territories or countries. In Australia,
the British authorities maintained that the land was terra nullius (‘no
one’s land’) and believed they were legally entitled to occupy the land.
Complex childhood trauma: Exposure to multiple or prolonged
traumatic events and the impact of this exposure on development.
Co-morbidity: When two disorders or illnesses occur in the same
person, simultaneously or sequentially, they are described as comorbid.
Comorbidity also implies interactions between the illnesses that aect
the course and prognosis of both.
Council of Australian Governments (COAG): The peak
intergovernmental forum in Australia. Chaired by the Prime Minister,
COAG’s role is to promote policy reforms that are of national
significance, or which need co-ordinated action by all Australian
governments.
Developmental domains: Refers to the five key developmental
domains which are identified by the Australian Early Development
Census: physical health and wellbeing; social competence; emotional
maturity; language and cognitive skills; and communication skills and
general knowledge.
Developmental plasticity: The capacity to express specific adaptive
responses to environmental conditions. These can be immediate,
short-term or long-term changes in physiology and behaviour.
Dierential susceptibility: The association between certain genetic
profiles and increased susceptibility to environmental conditions. This
means that some children are more influenced by their environmental
conditions than others as a function of the presence or absence of
specific genetic characteristics.
Dysbiosis: Disturbances in the composition of the microbial
communities either in or on the body, usually associated with adverse
health conditions.
Early childhood trauma: The traumatic experiences that occur to
children aged 0-6. These traumas can be the result of intentional
violence—such as child physical or sexual abuse, or domestic violence—
or the result of natural disaster, accidents, or war. Young children also
may experience traumatic stress in response to painful medical
procedures or the sudden loss of a parent/caregiver. (See also Adverse
childhood experiences).
Endocrine system: Collection of glands in the body that produce
hormones and release them into the bloodstream. The endocrine
system works with the nervous system and the immune system to
help the body cope with dierent events and stresses.
Epigenetic changes: DNA modifications that do not change the DNA
sequence, but can modify gene activity by helping determine whether
genes are turned on or o. Epigenetic change is a regular and natural
occurrence but can also be influenced by several factors including age,
the environment/lifestyle, and disease state.
Family and domestic violence: The intentional use of violence,
threats, force or intimidation to control or manipulate a family member,
partner or former partner.
Foetus: An unborn ospring, from the embryo stage (the end of the
eighth week after conception, when the major structures have formed)
until birth.
Foetal alcohol spectrum disorder (FASD): The eects of alcohol on
the embryo or foetus produce a spectrum of disorders that impact
physical, learning and behavioural outcomes. The range of eects is
collectively termed ‘foetal alcohol spectrum disorder’.
Genome: An organism’s complete set of DNA, including all of its genes.
Genotype: The genetic makeup of an organism.
Global climate change: A change in the typical or average weather of
a region or city (e.g. change in a region’s average annual rainfall, or a
city’s average temperature for a given season). It also refers to a
change in earth’s overall climate (e.g. the earth’s average temperature,
or typical precipitation patterns).
Gut-brain-immune axis. Bidirectional connections between gut
microbiota, brain and immune system which act as an interconnected
network.
Harm: Any detrimental eect of a significant nature on the child’s
physical, psychological or emotional wellbeing and development.
Health: A state of complete physical, mental, and social well-being and
not merely the absence of disease or infirmity. (Health is defined
dierently by Western and Aboriginal people – see Aboriginal health).
Homelessness: There is no one definition of homelessness. However,
in this report, homelessness refers to when a family does not have a
sense of security, stability, privacy, safety, and the ability to control
living space. It also refers to persons or families with no place of usual
residence who move frequently between various types of
accommodations (including dwellings, shelters and institutions for the
homeless or other living quarters).
Homeostatic: The body’s tendency to maintain a condition of balance
within its internal environment, even when faced with external
changes. These relate to steady levels of internal balance with things
such as temperature and other vital conditions such as the water and
contents of the blood.
Human Rights: Human rights are rights inherent to all human beings,
whatever our nationality, place of residence, sex, gender, national or
ethnic origin, colour, religion, language, or any other status. These
rights are all interrelated, interdependent and indivisible.
Illicit drug: A drug that is prohibited from manufacture, sale or
possession in Australia.
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Immune system: Made up of a network of cells, tissues and organs in
the body, designed to protect from, or get rid of, infection. (See also
Gut-brain-immune axis.)
Intergenerational trauma: Trauma that is passed down through
generations of families as a result of traumatic experiences such as
loss and grief.
Low-grade inflammation: The body’s immune system response which
serves to initiate the elimination of toxic agents and the repair of
damaged tissue. A chronic inflammatory response is likely to be
involved in the early stages of a range of chronic conditions.
Matthew eects: Refers to the pattern of increasing advantage or
disadvantage following early advantage or disadvantage where the
gap between the advantaged and disadvantaged expands with time.
Mental health: A state of well-being in which every individual realizes
his or her own potential, can cope with the normal stresses of life, can
work productively and fruitfully, and is able to make a contribution to
her or his community.
Mental illness: A health problem that significantly aects how a
person feels, thinks, behaves, and interacts with other people. It is
diagnosed according to standardised criteria. The term ‘mental disorder’
is also used to refer to these health problems.
Microbiome: The communities of bacteria, viruses, fungi and other
symbiotic organisms that live in and on the human body.
Neglect: Neglect is the most common form of abuse and occurs when
a parent or caregiver does not give a child the care he or she needs
according to its age. Neglect can mean not giving food, clothing, and
shelter, medical attention, exposing a child to dangerous environments,
not responding to the child’s emotional needs, poor supervision of a
child, and abandoning the child.
Neuron: A nerve cell that processes and transmits information.
Neuroplasticity: The biological capacity of the central nervous system
to change structurally and functionally in response to experience, and
adapt to the environment
Non-communicable diseases: Also known as chronic diseases, they
tend to be of long duration and are the result of a combination of
genetic, physiological, environmental and behavioural factors.
Pathogen: A bacterium, virus, or other microorganism that can invade
the body and produce disease.
Peripheral nervous system: This is our second nervous system and
contains all the nerves in the body that lie outside of the spinal cord
and brain (the nerves that go from the skin, muscle, and organs to the
spinal cord and eventually the brain). It conducts information to and
from the central nervous system.
Phenotype: The outcome of the interaction between the genotype
and the environment, and is the organism’s actual physical form and
behaviour
Placenta: An endocrine organ that develops in the uterus during
pregnancy and provides oxygen and nutrients to the foetus, while
removing waste products from its blood.
Postnatal: Period after childbirth
Poverty: When a family’s income fails to meet basic necessities such
as adequate food, shelter and clothing, and impacts a family’s lifestyle.
Poverty often has a federally established threshold that diers across
countries. Australia does not have an established poverty threshold.
Typically poverty is measured with respect to families and not the
individual, and is adjusted for the number of persons in a family.
Poverty is associated with the undermining of a range of key human
attributes, including health and wellbeing.
Psychoactive substance: Substances that, when taken in or
administered into one’s system, aect mental processes, e.g. cognition
or aect. Refers to the whole class of substances, licit and illicit.
Racism: The avoidable and unfair phenomena that lead to inequalities
in power, resources and opportunities across racial or ethnic groups. It
can be expressed through beliefs and stereotypes, prejudices and
discrimination, and occurs at many social levels, including
interpersonally and systemically, and as internalised racism.
Social determinants of health: The social, economic and
environmental conditions into which we are conceived, born, grow, live,
and age.
Social gradient of health: The phenomenon where the higher a
person’s socioeconomic position, the healthier they are likely to be.
That is, at any given point along the socioeconomic continuum, one is
likely to experience inferior health outcomes to those above them.
Social supports: In this report, the terms ‘social supports’, ‘social
connections’ and ‘social relationships’ are used interchangeably and
refer to three categories of family support: practical; emotional; and
advice and information.
Socioeconomic status: The social standing or class of an individual or
group. It is often measured as a combination of education, income and
occupation.
Synapse: Junction between two neurons which allows for information
to be carried from one neuron to another
Telomeres: The caps at the end of chromosomes which stop DNA from
unravelling during cell division, and shorten as we age.
Temperament: Distinct patterns of feelings and behaviours which
shape aective, attentional and motor responses in various situations.
Individual dierences in the regulation of experience emerge early in
life and remain moderately stable across development.
Temperamental bias: A bias towards certain temperamental
characteristics which is often (but not always) genetic.
Trauma: An emotional response to a terrible event like an accident,
violence against an individual, or natural disaster.
Triple hit eects: The theory that there are three conditions or
events that are required to disturb development: an existing
predisposition or vulnerability, a critical period of brain development,
and exposure to environmental stressors.
United Nations: An international organisation founded in 1945. It is
currently made up of 193 Member States. The mission and work of the
United Nations are guided by the purposes and principles contained in
its founding Charter.
United Nations Convention on the Rights of the Child: The
Committee on the Rights of the Child is the body of 18 Independent
experts that monitors implementation of the Convention on the Rights
of the Child by its State parties. It also monitors implementation of two
Optional Protocols to the Convention, on involvement of children in
armed conflict and on sale of children, child prostitution and child
pornography.
World Health Organisation: A specialised agency of the United
Nations which directs and coordinates international health in six
primary areas: Health systems; promoting health through the life-
course; non-communicable diseases; communicable diseases; corporate
services; preparedness, surveillance and response.
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1. Introduction
1.1 The first 1000 days
The focus of this paper is on the earliest stages of child development, the period from conception to the end of
the child’s second year. This period has become known as the first 1000 days, a catchphrase that has become
the rallying point for a number of Australian and international initiatives. While some of these have a general
focus, such as the work of a cross-parliamentary group in the UK Parliament (Leadsom, Field, Burstow & Lucas,
2013; WAVE Trust, 2013, 2015), others are more narrowly focused on issues such as nutrition (Save the
Children, 2012; Thousand Days, 2016) or on specific populations such as Aboriginal children (Arabena, Howell-
Muers, Ritte, & Munro-Harrison, 2015; Arabena, Ritte & Panozzo, 2016).
The reason for focusing on this specific period is the growing body of evidence which shows that experiences
during this period can have life-long consequences for health and wellbeing. Thus, as noted in the report of the
World Health Organisation’s Commission on Social Determinants of Health (2008),
Many challenges in adult society have their roots in the early years of life,
including major public health problems such as obesity, heart disease, and
mental health problems. Experiences in early childhood are also related to
criminality, problems in literacy and numeracy, and economic participation. This
paper seeks to summarise what is known about the biological processes and
environmental characteristics that shape development during the first 1000
days, and what impact these have over the life span.
While there have already been many reviews of the literature on early development, all concluding that this
period of life is critical in shaping health and wellbeing over the life course, there are several reasons why a
new review of the evidence is needed, and why this paper diers from previous reviews.
First, research in this area is rapidly advancing, and our understanding of the specific mechanisms that impact
upon development is becoming more and more detailed and nuanced. Keeping up with the exponential growth
in research is an ongoing challenge, and regular updates such as this one are needed.
Second, the new research has revealed whole aspects of biological functioning that were not previously
recognised as playing a role in development, such as telomere eects and the role of the microbiome. This
review is the most comprehensive attempt yet to incorporate all known sources of influence on development,
and even those well read in this area will learn from the paper.
Third, the focus of the paper is on the first 1000 days, rather than the early years in general as in most previous
reviews. This is on the grounds that the first 1000 days is the period of maximum developmental plasticity, and
therefore the period with the greatest potential to aect health and wellbeing over the life course.
1.2 Evolving ideas regarding the early years
Although the notion of critical / sensitive periods in development has been around for many years (e.g. Bailey,
Bruer, Symons & Lichtman, 2001), the full extent of early developmental plasticity has not become evident
until recently. Moreover, in Australia at least, the general public’s perception of how young children develop and
learn is often based on the perception that children are passive absorbers of knowledge who do not show
signs of genuine learning until they are older (Bales & Kendall-Taylor, 2014; Kendall-Taylor & Lindland, 2013).
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The recent interest in the early years (Allen, 2011; Field, 2010; Shonko & Phillips, 2000; Social Research Unit at
Dartington, 2013) has been prompted by growing awareness that what happens during this period of
development has lifelong consequences for children’s health and wellbeing (Center on the Developing Child at
Harvard University, 2010; Fox, Levitt & Nelson, 2010; Moore, 2014a, National Scientific Council on the
Developing Child, 2007; Shonko, Garner, Committee on Early Childhood, Adoption, and Dependent Care, &
Section on Developmental and Behavioral Pediatrics, 2012). It has also been prompted by a growing
understanding of how early disparities in children’s functioning can develop and the problems that this can create
for future education, employment and opportunities (Brinkman et al., 2012, 2013; Centre for Community Child
Health, 2008; Woolfenden et al., 2013).
This heightened awareness of the importance of the early years has led to many government initiatives,
nationally and internationally. In Australia, this includes the National Early Childhood Development Strategy.
However, many of these initiatives have primarily focused on the 3-5 year period and ensuring school ‘readiness’
(e.g. the Council of Australian Governments National Partnership Agreement on Early Childhood Education).
New evidence is now leading to a focus on the earliest stages of development, including the prenatal period
(Barouki et al., 2012; Paul, 2010; Prescott, 2015; Shonko, Richter, van der Gaag & Bhutta, 2012). There are
currently three key concepts that are supported by this growing body of evidence:
Developmental plasticity and the developmental origins of health and disease (DOHaD) hypothesis
Social climate change and the ‘mismatch’ hypothesis
Ecological impacts on development and the social determinants of health and disease.
Collectively, evidence relating to these key concepts transforms our understanding of how children develop and
highlights the critical role of the very earliest stages of development – the first 1000 days.
1.3 Scope of paper
This paper examines the impact of early experiences on all aspects of development and functioning, including
physical health and wellbeing, mental health, social functioning and cognitive development. This is in keeping
with the broader definition of health adopted by the World Health Organization (WHO) which defines health as
‘a dynamic state of complete physical, mental, spiritual and social wellbeing and not merely the absence of
disease or infirmity’ (WHO, 1998). In Australia, Aboriginal and Torres Strait Islander people take this position
even further, viewing health as ‘not just the physical wellbeing of the individual but the social, emotional and
cultural wellbeing of the whole community’ (National Aboriginal Health Strategy Working Party, 1989).
Connection to land, spirituality and ancestry, kinship networks, and cultural continuity are commonly identified
by Aboriginal people as important health-protecting factors (Zubrick et al., 2014).
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This paper also recognises that, as enshrined in the United Nations Convention on the Rights of the Child
(1990), children have the fundamental human right to a high standard of health and wellbeing. The Committee
on the Rights of the Child, charged by the United Nations with promoting and monitoring progress towards
world-wide implementation of the Convention, has adopted a number of General Comments to guide
governments in fulfilling their obligations under the Convention (Committee on the Rights of the Child, 2005,
2006, 2013). General Comment No. 7 (2005) – on implementing child rights in early childhood – stresses that
young children have rights from the beginning of their lives. It acknowledges the special vulnerability of the
very young to poverty, discrimination and other adversities that can compromise their rights and undermine
their capacities and well-being. General Comment 13 (2013) – on the right of the child to the enjoyment of the
highest attainable standard of health – interprets children’s right to health as
an inclusive right, extending not only to timely and appropriate prevention,
health promotion, curative, rehabilitative and palliative services, but also to a
right to grow and develop to their full potential and live in conditions that enable
them to attain the highest standard of health through the implementation of
programmes that address the underlying determinants ofhealth.
This paper seeks to identify these underlying determinants of health, understood in the broad terms noted
earlier, so that children’s rights to high standards of health and wellbeing may be better observed.
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2. Biological processes shaping
health and development
This section provides a synthesis of the evidence regarding the three key concepts that have led to the current
focus on the earliest stages of development. Before considering this evidence, we need to understand the
relationship between mind, brain and body.
2.1 The relationship between mind, brain and body
In seeking to understand early development, there has been a tendency to focus on neurological development
at the expense of other aspects of development. Thus, eorts to disseminate new research knowledge have
used the metaphor of ‘brain architecture’ to convey the sense of the importance of early neurological
development (National Scientific Council on the Developing Child, 2007), and discussed how positive early
experiences build neuronal connections and adverse experiences disrupt them (National Scientific Council on
the Developing Child, 2004, 2005). This way of framing early development reflects an underlying belief in the
importance of the brain as the seat of personhood and learning.
However, as Moore (2014a) has noted, ‘framing brain development in terms of building neuronal connections
and brain architecture fails to capture the fact that brain functioning is not purely cognitive, that ‘learning’ is
not purely conscious, that the brain is not purely skull-based, and that the brain is closely linked with other key
bodily systems.
First, the brain is not purely cognitive, but is also profoundly emotional (Davidson & Begley, 2012). Thus, our
emotions directly influence the functions of the entire brain and body, from physiological regulation to abstract
reasoning. In fact, emotion serves as a central organising process within the brain, and our ability to organise our
emotions directly shapes the ability of the mind to integrate experience and adapt to future stress (Siegel, 2012).
Second, learning is not a purely conscious process. Much of our most important emotional and interpersonal
learning during the first few years occurs before we have developed the neurological capacities for conscious
awareness and memory (Cozolino, 2016; Siegel, 2012). Thus, many of the most important aspects of our lives
are controlled by reflexes, behaviours, and emotions learned and organised outside our awareness.
Third, the brain is not just skull-based, but ‘embodied’, being shaped by messages from all over the body via the
central and peripheral nervous systems. 1 This embodied brain shapes and is shaped by both its external and
internal environments (Barrett, 2011; Beilock, 2015; Claxton, 2015; Craig, 2015; Edelman, 2006; Johnson,
2006; Varela, Thompson & Rosch, 1991).
Finally, the brain is not a stand-alone bodily system, but is intricately connected to other major bodily systems,
including the immune, endocrinal, metabolic, gastrointestinal, cardiovascular, enteric and musculoskeletal
systems (Barrett, 2011; Beilock, 2015; Claxton, 2015; Damasio & Damasio, 2006; McFarlane, 2017; Mayer,
2016). These systems shape and are shaped by each other, and function as an integrated mind-brain-body
system. This means that what is ‘learned’ in the prenatal and first two to three years of life aects not only the
neurological system but also the other bodily systems to which the brain is connected, with potentially
profound consequences over the life course (Moore, 2014a).
1 This is our second nervous system and contains all the nerves in the body that lie outside of the spinal cord and brain (the nerves that go from the skin,
muscle, and organs to the spinal cord and eventually the brain). It conducts information to and from the central nervous system.
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With this understanding in mind, we will now examine the evidence regarding the three key concepts
mentioned earlier:
Developmental plasticity and the developmental origins of health and disease (DOHaD) hypothesis
Social climate change and the ‘mismatch’ hypothesis
Ecological impacts on development and the social determinants of health and disease.
2.2 Developmental plasticity and the developmental origins
of health and disease
2.2.1 Developmental plasticity
One of the most significant features of human biology is our capacity to adapt to dierent social and physical
environments. This capacity is known as developmental plasticity (Bateson & Gluckman, 2012; Gluckman &
Hanson, 2006; Gluckman et al., 2009; Gluckman, Hanson & Buklijas, 2010; Gluckman, Hanson & Low, 2011;
Hanson et al., 2011; Low, Gluckman & Hanson, 2012; Padmanabhan, Cardoso & Puttabyatappa, 2016; West-
Eberhard, 2003, 2005). While we retain some capacity to adapt throughout our lives, developmental plasticity
is at its greatest in the first 1000 days or so of life (Barker, 2012; Gluckman et al., 2010), and it plays an
important role in development from the moment of conception (Lane, Robker & Robertson, 2014).
Adapting to the immediate environment is the major developmental goal or activity during the first 1000 days
and this developmental focus makes the influence of the environment particularly critical over this time. During
development, there are brief critical periods during which a system or organ has to mature (Barker, 2012).
These occur at dierent times for dierent systems, and they occur in utero for most systems. After birth, only
the brain, liver and immune system remain plastic. Thus, much of human biological development is completed
during the first 1000 days (Barker, 2012).
In the brain or central nervous system, it is more accurate to talk about sensitive periods, time windows during
which the eect of experiences on brain development is unusually profound and can strongly shape the neural
circuits (Ismail, Fatemi & Johnston, 2017). This is another instance of developmental plasticity, known as
neuroplasticity, and refers to the biological capacity of the central nervous system to change structurally and
functionally in response to experience, and adapt to the environment (Ismail, Fatemi, & Johnston, 2017).
Neuroplasticity is greatest during pre- and postnatal brain development: the young brain has a repertoire of
neuroplasticity responses that are not evident in adults, and which allow the young brain to develop
appropriately and adapt constantly to environmental experiences and exposures.
This capacity to adapt makes the human species both versatile and vulnerable at the same time: the changes
made might be adaptive for the immediate environment, but they can come with long-term costs, both
psychologically and physically (Blair & Raver, 2012; Gluckman et al., 2009; Thompson, 2014). For instance, in
the early development of the brain, neuroplasticity can lead to significant maladaptive outcomes depending on
factors such as the nature and extent of adverse exposures, and the stage of neurodevelopment during which
they occur. Patterns of abnormal neuroplasticity have been identified as core features of many paediatric
disorders of the central nervous system, including cerebral palsy, intellectual disabilities, autism spectrum
disorders, and neuropsychiatric disorders such as attention deficit hyperactivity disorder (Ismail, Fatemi, &
Johnston, 2017).
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2.2.2 Biological embedding
Adaptation involves a process variously known as biological embedding (Gluckman et al., 2010; Hertzman,
1999; Hertzman & Boyce, 2010; Nelson, 2013; Social Research Unit at Dartington, 2013), developmental
programming (Barker, 2012; Lucas, 1991, 1998; Social Research Unit at Dartington, 2013; Thornburg, 2015;
West-Eberhard, 2003) or conditioning (Hanson & Gluckman, 2014). It is through this process of biological
embedding that the foetus (and infant), in response to cues such as nutrition or hormones, adapt their
phenotype to their particular environment in ways that have life-long consequences.
Two central mechanisms underlie this adaptation process: epigenetics (whereby the ‘genes listen to the
environment’) and synaptic pruning (whereby the ‘brain listens to the environment’) (Keating, 2016). In both
cases, developmental experiences and the social context in which they occur have the capacity to become
biologically embedded with lifelong impacts on health and other outcomes (Keating, 2016).
2.2.3 Epigenetic eects
The first key mechanism underpinning biological embedding and developmental programming is epigenetic
change (Bilbo & Schwarz, 2012; Burris, Baccarelli, Wright, & Wright, 2016; Denburg & Daneman, 2010;
Hertzman & Boyce, 2010; Keating, 2016; Kundakovic & Champagne, 2015; Moore, 2015; Szyf, McGowan, &
Meaney, 2008; Szyf, Weaver, & Meaney, 2007). Contrary to common understanding, genes do not single-
handedly determine any of our characteristics (Moore, 2015). Instead, development is a dynamic process that
involves interplay between genes and the environment (Kundakovic & Champagne, 2014). Neither genes nor
the environment have a direct and independent impact on development or functioning. Thus, a child may have
a combination of genes that predisposes them to a particular condition or behaviour, but never develop the
condition or behaviour because they were never exposed to the particular environment needed to trigger this
condition – and the gene thus remains ‘dormant’.
Similarly, a child may be exposed to a particular triggering environment but lack the genes that would
predispose them to respond adversely to that environment. When genes and environment do interact, they
result in epigenetic changes. These involve changes in how the genes function but do not alter the genes’ DNA
sequence – in eect, epigenetic changes determine whether genes are expressed or otherwise (turned on or
o) (Carey, 2011; Duncan, Gluckman & Dearden, 2014; Francis, 2011; Lester, Conradt & Marsit, 2016; Moore,
2015).2 This means that, rather than being born with a fixed genome3, we are born with a developing genome
that changes in response to environmental context (Moore, 2015).
In humans, the epigenetic system is most sensitive to environmental influences during the period of
developmental plasticity (i.e. the first 1000 days) because this is the time when epigenetic marks undergo
critical modifications. Once a tissue or system is fully developed, while still somewhat plastic, it is less
sensitive to alterations by environmental stimuli (Barouki et al., 2012).
Epigenetic changes have been implicated in the development of a wide range of disorders, from cardiovascular
disease (Thornburg, 2015) to autism spectrum disorders (Loke, Hannan & Craig, 2015; Schanen, 2006) and
cognitive disorders (Gra & Mansuy, 2009), and may be triggered by a wide range of environmental exposures
and experiences (Coe & Lubach, 2008; Guyer et al., 2009; Gluckman & Hanson, 2005; Hertzman, 2010;
Hertzman & Wiens, 1996; Keating, 2016; Martin & Dombrowski, 2008; Meaney et al., 2007; Robinson, 2013;
Shonko, 2010).
2 Moore (2015) suggests that the analogy of a dimmer switch more accurately captures this eect: DNA can be turned on ‘a little bit, a moderate amount,
a lot, full blast, or any amount in between’.
3 The genome is an organism's complete set of DNA, including all of its genes. Each genomecontains all of the information needed to build and maintain
that organism. In humans, a copy of the entiregenome is contained in all cells that have a nucleus.
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The pre- and peri-conceptional periods (before and just after fertilization) are highly sensitive periods
(Chavatte-Palmer et al., 2016). Epigenetic changes can start to occur shortly after conception, and continue to
occur during both the prenatal and postnatal periods. At conception, the egg and sperm combine their genetic
material to form an embryo, whose set of genes reflects both the age and the environmental exposures of
both parents (Lane et al., 2014). During fertilisation and the first cell divisions, the embryo is highly sensitive
to signals from the mother’s reproductive tract: the fluid that surrounds the embryo during its passage to the
womb varies according to the mother’s nutritional, metabolic, and inflammatory states, reflecting the particular
world in which she lives (Leese et al., 2008). The embryo has a high degree of developmental plasticity, and
responds to these environmental cues by modulating its metabolism, gene expression, and rate of cell division.
In this way, the maternal tract and the embryo collaborate to generate a developmental trajectory adapted to
suit the anticipated external environment, to maximize survival and fitness of the organism (Hochberg et al.,
2011; Lane et al., 2014). But if the resulting phenotype is a poor match for conditions after birth, or if
adaptation constrains capacity to withstand later challenges, ospring are at risk (Godfrey, Gluckman &
Hanson, 2010).
Factors at conception that can aect the development of the embryo include maternal nutrition and infections.
Poor maternal nutrition at conception can have a major impact on the developmental program, altering the rate
of cell division and subsequent prenatal and postnatal nutritional development (Chavatte-Palmer et al., 2016;
Lane et al., 2014). Maternal infections during this very early stages of development can also produce
epigenetic changes, altering the immune functioning of the child (Lane et al., 2014).
Epigenetic changes can occur throughout pregnancy. Hormones and nutrients that cross the placenta can be
aected by the mother’s body composition, metabolism, and long-term lifestyle (Gluckman et al., 2009). The
foetus is sensitive to hormonal and other physiological indicators of maternal stress, and heightened exposure
to stress in the womb is associated with greater reactivity to stress after birth, as well as longer-term problems
with emotional and cognitive functioning. In general, prenatal stress exposure makes children more reactive to
challenge and threat (Thompson, 2014). In addition, maternal stress and toxin exposure during pregnancy, and
maternal-infant interactions after birth have been linked to changes in the ospring’s epigenetic state
(Champagne, 2008, 2011; Skinner, Manikkam, & Guerrero-Bosagna, 2010; Thompson, 2014). Even natural
variations in the quality or quantity of maternal care can have a long-term impact the ospring’s brain and
behaviour (Champagne, 2011). The prevalence of these eects suggests that epigenetic eects are a central
mechanism by which environmental experiences, both positive and negative, become biologically embedded
and ‘get under the skin’ (Keating, 2016).
Epigenetic changes can also occur during the postnatal period. For instance, stressors such as poverty in early
childhood can alter the programming of the immune system (McDade, 2012; Miller et al., 2009, 2011; Miller &
Chen, 2013; Raposa et al., 2014; Ziol-Guest, Duncan, Kalil & Boyce, 2012). Because the immunological system
is developing during this time, changes get embedded in a manner that persists across the lifespan and makes
the person more susceptible to diseases. The mechanism involved is the epigenetic modification of genes
expressed in the brain that shape neuroendocrine and behavioural stress responsivity throughout life (Weaver,
2009). A harsh family climate – characterised by conflict, a lack of warmth, inadequate parenting, and
household chaos – alters key immune cells and produces a chronic inflammatory state in the body (Miller &
Chen, 2010; Miller et al., 2011a, 2011b; Raposa et al., 2014). Hormonally, early stress confers altered patterns
of endocrine and autonomic discharge. Acting together with other exposures and genetic liabilities, the
resulting inflammation promotes other pathogenic mechanisms that ultimately foster chronic disease (Miller et
al., 2011).
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There is now also evidence that epigenetic changes can be inherited. This means that the experiences of
parents and even grandparents can be transmitted across generations and contribute to non-genomic
transmission of disease risk across generations (Gapp & Bohacek, 2017; Gluckman, Hanson, & Buklijas, 2010;
Gluckman, Hanson, & Low, 2011; Hansen et al., 2011; Heindel, 2015; Kundakovic & Champagne, 2015; Lane et
al., 2014; Low, Gluckman, & Hanson, 2012; Moore, 2015; Wang, Liu & Sun, 2017). When parents have been
exposed to adverse experiences (including nutrition, environmental toxins, abusive behaviour, and social
stress) that have produced changes to their epigenome, these changes can sometimes be passed on to their
children, with powerful eects on their physiological, metabolic and cellular functions (Gapp & Bohacek, 2017;
Wang et al., 2017). While this is not a universal eect, when it does occur children receive genes that are in an
active or ‘switched on’ state rather than a dormant or latent state. Thus, the long-term consequences of
adverse environmental conditions during the first 1000 days may not be limited to one generation, but may
lead to poor health in the generations to follow, even if these individuals develop in optimal conditions
themselves (Roseboom & Watson, 2012; Wang et al., 2017).
Perhaps most damaging is when parents have experienced trauma, as a result of childhood abuse, family
violence, war and so on. The impact of this intergenerational trauma on development during the first 1000
days is significant. The adverse impact of parental trauma can be transferred to the child through a range of
influences, including: epigenetic changes resulting from the trauma exposure itself, the caregiver’s mental
health as a result of the trauma (Schwerdtfeger, Werner, Peters, & Oliver, 2013), and the co-morbidities (e.g.
drug and alcohol abuse) that often result from trauma (Cohen, Hien & Batchelder, 2008). For example, parents
of infants who have experienced sustained trauma are more likely to (amongst other things): use punitive,
aggressive, and physical forms of discipline (Gara, Allen, Herzog, & Woolfolk, 2000; Appleyard & Osofsy, 2003);
while children of parents who have experienced sustained trauma are more likely to (amongst other things)
have insecure and disorganised attachment during infancy (which is also associated with depressive symptoms
in childhood and later life) (Lee & Hankin, 2009; Hankin, 2005; Bosquet et al., 2014).
In addition to this, research has shown that long-term behavioural responses to stress and epigenetic
alterations in adult children of traumatised parents can be facilitated by in utero eects (Boersma et al., 2014),
variations in early postnatal care, and/or other early life experiences that are influenced by parental exposure
to trauma (Yehuda et al., 2015; Champagne & Meaney, 2006). In a recent study of holocaust survivors, Yehuda
and colleagues (2015) found that genetic modifications as a result of trauma are capable of being passed onto
children, aecting subsequent generations.
Recently, another form of biological embedding – telomere eects – has been identified. This involves
biologically embedding at a cellular level.
2.2.4 Telomere eects
Telomeres are the caps at the end of each of our chromosomes, and can be likened to the plastic tips at the
end of shoelaces (Blackburn & Epel, 2012, 2017; Blackburn, Epel & Lin, 2015; Prescott, 2015) (See figure 1).
Telomeres Telomeres
(protective tips)
Paired strands
of DNA
Figure 1. Telomeres (Telomerase Activation Sciences, 2011). http://www.tasciences.com/what-is-a-telomere/
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Telomeres play a vital role in determining our health and longevity. Over the course of our lives, our cells divide
numerous times, and the function of the telomeres is to stop the DNA from unravelling during this process. Our
telomeres shorten with each division of our cells, and when they become too short, the cells stop dividing
altogether, which causes our tissues to degenerate and ultimately die (Jaskelio et al, 2011). These senescent
cells (cells that no longer divide and grow) can also leak pro-inflammatory substances that make us more
vulnerable to pain and chronic illness as we age. Thus, shortened telomeres not only shape our health-span
(how long we live a healthy life), but also our disease-span (how long we live with disease that interferes with
our quality of life) (Blackburn & Epel, 2017).
Telomeres are shaped by our genes, but also respond to how we live – the foods we eat, our responses to
emotional challenges, the amount of exercise we get, whether we were exposed to childhood stress, and even
the level of trust and safety in the neighbourhood (Blackburn & Epel, 2017). Chronic stress is known to be
associated with shortened telomeres in adults, and evidence is accumulating that this is also true of such
exposures early in life, and that the eect is dose-dependent (i.e. the more severe and sustained the stress,
the shorter the telomeres) (Brown et al., 2009; Oliveira et al., 2016; Price et al., 2013). In a study of Romanian
children, Drury and colleagues (2011) found that those who had been placed in institutional care for long
periods before the age of five had significantly shorter telomeres than other children their age.
Cellular aging begins in the womb. Telomere length can be directly transmitted from mother to child at the
point of conception: if the mother’s telomeres are short throughout her body (including those in the egg) when
she contributes the egg, the baby’s telomeres will also be short – from the moment the baby starts developing
(Blackburn & Epel, 2017). The developing child’s telomeres can be further shaped by the mother’s nutrition and
stress levels during the pregnancy. Fathers can also transmit shortened telomeres, although not to the same
extent as mothers (Blackburn & Epel, 2017).
There is a sense in which parents can not only transmit both epigenetic changes such as shortened telomeres,
but also the environments that produced these changes:
Organisms always develop in specific contexts, and organisms that survive and
reproduce will normally conceive the next generation in contexts like those in
which they developed. In this way, individuals of the next generation are
typically born into environments that are, in many ways, much like the
environments their parents were born into; as a result, they then have similar
experiences. And having inherited their parents’ DNA and (in a sense) their
parents’ developmental environments, the ospring then typically develop the
characteristics that helped their parents survive, doing so in the same way
their parents did.
(Moore, 2015)
As Blackburn & Epel (2017) point out, this means that social disadvantage can be transmitted across
generations: if the parents’ telomeres were shortened by chronic stress, poverty, unsafe neighbourhoods, or
chemical exposures, they can pass these shortened telomeres on directly to their children. As these children
grow, they are likely to be exposed to poverty and stress, which will erode their telomeres further. They will
pass these on to their own children, so that each new generation of babies has shorter telomeres than the
previous one. Thus, Blackburn and Epel (2017) argue, ‘From the first moments of birth, telomeres may be a
measure of social and health inequalities.
Fortunately, as we will see later, telomere shortening can be slowed, prevented or even reversed through
exposure to positive environments, so the impact of early adverse experiences or inheritance can
becounteracted.
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2.2.5 Synaptic pruning
The second mechanism whereby environmental experiences become biologically embedded is synaptic pruning
(Keating, 2016; Webb et al., 2001). While a baby is born with billions of brain neurons, it has relatively few
synapses4. The initial surge in synaptic connections between brain neurons occurs after birth as the child goes
through a process of rapid learning. During this period billions of neurons in the brain send electrical signals to
communicate with each other, and it is these connections that become the foundation of brain development.
Connections are strengthened through recurrent use, and our experiences and environment determine which
connections are used most. Connections that are used more become stronger and enduring, while those that
are not used become weak and eventually fade away through a process called synaptic pruning (Shonko &
Phillips, 2000; Center on the Developing Child at Harvard University (CDCHU), 2016.
Well used circuits create pathways for strong connections in and between areas of the brain that are
responsible for motor skills, sight, emotions, behavioural regulation, logic, language, and memory during the
early critical period of development. Although dierent areas of the brain are responsible for each dierent
function, they are all interrelated and one form of skill cannot completely develop without support from others.
In other words, what comes first forms a foundation for everything that comes later (Sweatt, 2009; CDCHU,
2016). Building more advanced language, cognitive, social, and emotional skills on a weak foundation is
significantly more challenging with age, even if a conducive environment is restored in later life (CDCHU,
2016). As circuits develop successively, dierent experiences are critical at dierent ages and if one stage is
not developed appropriately, this will inevitably undermine the appropriate development of the next stage and
so on (CDCHU, 2016).
The primary way that these brain connections are reinforced and strengthened is through the child’s
interaction with his/her care giver(s) through a process of ‘serve and return’ (CDCHU, 2016). Children pursue
interactions through facial expressions, gestures, babbling, and words, and adults who are responsive ‘return’
these ‘serves’ with similar vocalising, gestures, and emotional engagement (CDCHU, 2016). However, if the
caregiver’s response is unreliable, inappropriate, or absent, the developing brain’s architecture can be disrupted
as a result of this under-stimulation. This then adversely impacts later stages of development, learning,
behaviour and health outcomes (Reis, Collins, & Berscheid, 2000; Meaney, 2001; Champagne, Francis, Mar &
Meaney, 2003; CDCHU, 2016).
2.2.6 Developmental origins of health and disease
What makes this new knowledge about developmental plasticity and programming so important is the
evidence that experiences during the first 1000 days can have lifelong eects. This is the Developmental
Origins of Health and Disease (DOHaD) hypothesis (Barouki et al., 2012; Gluckman & Hanson, 2004; Gluckman,
Hanson & Beedle, 2007; Halfon et al., 2014; Heindel, 2007; Heindel & Vandenberg, 2015; Prescott, 2015;
Rosenfeld, 2015; Rubin, 2016). This hypothesis maintains that environmental exposures to stress,
undernutrition or environmental toxins during critical periods of development can have long-term eects on
health and wellbeing by ‘programming’ organs, tissues, or body system structures or functions in ways that
increase the risk of metabolic, cardiovascular, immunological, and neurobehavioral disorders, and even cancer.
4 A synapse is what allows information to flow from one brain cell (neuron) to another.
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Our development from single cells to highly complex multi-celled organisms is an extraordinarily delicate and
complex process, and can be disrupted by numerous factors, such as disease or environmental toxins (Davies,
2014; Prescott, 2015). As Prescott (2015) describes it,
During the months before our birth, most of our major structures and body
functions are put in place. Small or subtle happenings in this period can have
slow ripple eects that may not be revealed for many years. Key organs, such
as the brain, the heart, the kidneys and the lungs are all formed in this period.
In many cases the full quota of cells in these organs is fixed at birth (in the
heart and kidney) or soon after (the brain and lungs). Even unnoticed, early
adverse events might reduce the quota of heart-muscle cells, or the number of
functional kidney units (nephrons), or the lung capacity that we are born with.
And much of that is set for life. Once these organs are formed, we can’t grow
new heart muscle or nephrons, although stem-cell research is trying hard to
overcome these biological limitations.
Protection for the foetus is provided by two protective barriers, the blood–brain barrier in the foetus itself and
the placental barrier (Wong, Wais & Crawford, (2015). Both barriers develop during early pregnancy and act as
filters to regulate the flow of specific nutrients and substances. The blood-brain barrier acts as a barrier to
protect the development and function of neurons. These develop early: in the developing human brain, the
growth of neurons begins in the embryonic period at about 6 weeks’ gestation, peaks at 14 weeks, and is
largely complete by 25 weeks. Meanwhile, the placenta acts as a selective filter for potentially harmful
substances circulating in the maternal blood (Wong et al., 2015). Until relatively recently, it was thought that
the foetus was completely protected from the mother’s physical and emotional environment by these twin
barriers (Gluckman et al., 2007; Paul, 2010). However, we now know that, while the placenta provides some
protection against infection and maternal cortisol, there is free exchange between the embryonic and maternal
blood systems, and the placental wall (which is thinnest in the first trimester when the foetus is developing
most rapidly) does not protect the foetus against drugs, alcohol, smoking, environmental toxins or severe
maternal stress (Coe & Lubach, 2008; Wong et al., 2015).5 As Donald (1979) memorably stated, ‘The first 38
weeks of life spent in the allegedly protected environment of the amniotic sac are medically more eventful and
more fraught with danger and accident than the next 38 years in the life span of most human individuals.
5 This exchange between the embryonic and maternal blood systems provides opportunities for the prevention of disease – eg. adding folic acid during the
early conception period to prevent spina bifida.
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The DOHaD hypothesis maintains that the foetus not only registers these changes in the intrauterine
environment, but also uses this information as a kind of ‘weather forecast’ from their mothers that prepares
them for the type of world in which they will have to live, and alters its phenotype6 accordingly (Barker, 2004;
Coe & Lubach, 2008; Gluckman & Hanson, 2005; Gluckman et al., 2009; Robinson, 2013). This process of
predictive adaptation works in the interests of the foetus and infant when the antenatal and postnatal
environments are both optimal and stable, as this ensures that any changes to the phenotype do not
compromise later health and development. However, when these environments are less than optimal and when
the prenatal and postnatal environments do not match, predictive mismatches (discussed below) can occur
(Bateson, Gluckman & Hanson, 2014; Gluckman & Hanson, 2005; Prescott, 2015).7 Adult conditions such as
coronary heart disease, stroke, diabetes, and cancer that once were regarded solely as products of adult
behaviour and lifestyles are now seen as being linked to processes and experiences occurring in pregnancy or
infancy (Heindel, 2007; Moore, 2014a).
By now, the evidence underpinning the DOHaD hypothesis is suciently robust for it to be considered a
paradigm rather than a hypothesis (Hanson et al., 2011; Heindel & Vandenberg, 2015; Heindel et al., 2015;
Prescott, Millstein, Katzman & Logan, 2016; Rubin, 2016). There is a flourishing field of research focusing on the
developmental origins of health and disease, with its own professional associations internationally
(International Society for Developmental Origins of Health and Disease) and nationally (DOHaD Society of
Australia and New Zealand) (Prescott et al., 2016).
2.3 Summary
The brain is not a stand-alone bodily system, but is intricately connected to other major bodily systems,
(including the immune, endocrinal, metabolic, cardiovascular, enteric and musculoskeletal systems) which shape
and are shaped by each other. What is ‘learned’ in the prenatal and first two to three years of life aects not
only the neurological system but also the other bodily systems to which the brain is connected, with profound
consequences over the life course.
One key concept which captures how early life shapes lifelong health and development is developmental
plasticity, and refers to our capacity to adapt to dierent social and physical environments. This capacity is at
its greatest in the first 1000 days. During development, there are brief critical periods during which a system
or organ has to mature. While most systems mature in utero, brain development occurs mostly in the first two
years after birth and is strongly shaped by a child’s social and physical experiences. This is a form of
developmental plasticity, known as neuroplasticity, and refers to the biological capacity of the central nervous
system to change structurally and functionally in response to experience, and adapt to the environment. While
changes made might be adaptive for the immediate environment, they can come with long-term costs, both
psychologically and physically.
Children are able to adapt to their environments because the foetus (and infant) respond to cues such as
nutrition or hormones, by adapting their phenotype to their particular environment. This is called biological
embedding. Two central mechanisms underlie this adaptation process: epigenetic eects, which refers to
changes in the function of genes as a result of environmental factors; and synaptic pruning, which refers to the
process of removing underused synapses in the brain, aecting synaptic connections in and between areas of
the brain that are responsible for cognitive, social and emotional development.
6 Where the genotype represents the genetic makeup of an organism, the phenotype is the outcome of the interaction between the genotype and the
environment, and is the organism’s actual physical form and behaviour.
7 Other models of how the foetus adapts to changes in the intrauterine environment include the thrifty phenome hypothesis (Hales & Barker, 1992; Wells,
2011) and the maternal capital hypothesis (Wells, 2010, 2012). Regardless of the exact form that adaptation takes, the end results are the same – long
term eects on developmental health and wellbeing.
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Telomere eects are another way in which biological embedding occurs. Telomeres are the caps at the end of
each chromosome and they play a vital role in determining our health and longevity. Over the course of our
lives, our cells divide numerous times, and the function of the telomeres is to stop our DNA from unravelling
during this process. Telomeres are shaped by our genes, but also respond to how we live and when they
become too short, because of toxic stress or other adverse life factors, our cells stop dividing and can leak
pro-inflammatory substances that make us more vulnerable to pain and chronic illness as we age. Telomere
length can be directly transmitted from mother to child but can also be further shaped by the mother’s
nutrition and stress levels during the pregnancy.
What makes this new knowledge about developmental plasticity and programming so important is the
evidence that experiences during the first 1000 days can have lifelong eects. This is the Developmental
Origins of Health and Disease (DOHaD) hypothesis, which maintains that environmental exposures such as
stress or undernutrition / overnutrition during critical periods of development can have long-term eects on
health and wellbeing by ‘programming’ organs, tissues, or body system structures or functions. The DOHaD
hypothesis maintains that this starts even before birth, where the foetus uses the intrauterine environment to
‘predict’ the type of world it will be born into, and alters its phenotype accordingly. This predictive adaptation is
in the interests of the foetus and infant when the antenatal and postnatal environments are both optimal,
however, when these environments are less than optimal and when the prenatal and postnatal environments
do not match, predictive mismatches (discussed in section 3) can occur.
~ ~ ~
The second major body of evidence reshaping our understanding of early development relates to the social and
environmental changes that have occurred over the past half century or so, and the impact of these on health
and wellbeing.
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3. Global factors influencing health and
development
3.1 Social climate change and its impact on families
Over the last several decades we have experienced a series of social, economic, demographic and technological
changes that are unprecedented in their rapidity and scale. Dubbed the ‘Great Acceleration’ (McNeil & Engelke,
2015; Steen et al., 2015), these changes have dramatically altered the conditions under which we are living
(Friedman, 2016; Keeley, 2015; Li, McMurray & Stanley, 2008; Putnam, 2015; Silbereisen & Che, 2010; Trask,
2010; Wells, 2009) and the social and physical health problems we are experiencing (Kearns, Beaty & Barnett,
2007; Li et al., 2008; Palfrey, Tonniges, Green & Richmond, 2005).
These changes arise from the same fundamental factors that have contributed to global climate change and
constitute a form of social climate change (Moore, 2014a) that has resulted in changes to the conditions under
which families raise their children, as well as changes in families themselves (Bauman, 2011; Cassells, Toohey,
Keegan, & Mohanty, 2013; Giddens, 2002; Golombok, 2015; Hayes, Weston, Qu & Gray, 2010; Parke, 2013;
Richardson & Prior, 2005; Trask, 2010; Wells, 2009). For example, there have been dramatic changes in
employment opportunities and conditions for families (Richardson & Prior, 2005), with more parents working
full-time, in shift work, doing non-standard hours, working longer hours, more unemployed families, and more
children being raised in poverty (Hayes et al., 2010; Richardson & Prior, 2005). Moreover, the search for cheap
housing (Zhu, 2014) and secure employment has led to families moving away from the communities in which
they were raised, leaving many families isolated and lacking supportive personal networks (extended family,
friends or other families of young children).
Australian governments of all political persuasions have done (and continue to do) much to protect families
from the adverse eects of these social and economic changes. Despite this, the problems persist. One of the
main reasons that tackling this widening gap has proven to be so challenging is that the nature of the
problems facing society and governments have altered – they are now more likely to be ‘wicked’ problems
(Australian Public Services Commission, 2007; Head & Alford, 2008; Moore & Fry, 2011; Rittel and Webber,
1973; Weber & Khademian, 2008). Wicked problems are complex and intractable and cannot be resolved using
traditional governance and leadership models, nor by service-driven approaches (Grint, 2010; Moore & Fry,
2011). Examples of wicked problems include child protection, family violence, Aboriginal disadvantage, social
exclusion, health inequalities, entrenched poverty, and obesity. Some wicked problems (e.g. poverty and child
abuse) while not new, have become more of a concern because of increased awareness regarding their adverse
consequences on child development, and the complex nature of their underlying causes.
3.2 The mismatch hypothesis
Evidence is now accumulating that some of the physical and mental health problems that are now prevalent
arise from, a mismatch between human evolutionary capacities and modern environments (Kearns et al., 2007;
Lieberman, 2013a).
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There are two forms of mismatch that can result in disease: predictive mismatch and evolutionary mismatch. As
discussed in the previous section, predictive mismatch occurs when our bodies make adaptations based on
predictions regarding the kind of environments we are going to be living in, and the environments do not match
the predictions. Evolutionary mismatch, however, occurs when our bodies encounter conditions for which they
were not evolutionarily adapted (Gluckman and Hanson, 2006; Gibson, 2009; Hanson and Gluckman, 2014;
Lieberman, 2013). While many of the recent social and environmental changes that have occurred have been
beneficial (e.g. greater availability of food, improved sanitation, and scientific medicine, leading to lower infant
mortality and increased longevity), other changes have created conditions for which our bodies were not
designed, with damaging eects upon our physical and mental health. Lieberman (2013) argues that the net
eect of these changes has been to reduce or eliminate a number of the normal sources of stress which human
bodies require for healthy development – removing extremes of heat and cold, feast and famine, exercise and
rest. When we do not experience these normal sources of stress during development, then our bodily systems
– including our metabolic, immune, endocrinal, cardiovascular and muscular-skeletal systems – fail to develop
properly, leading to the emergence of mismatch diseases in adult life, if not before.
This mismatch between our evolutionary capacities and our modern living environments has led to a major
change in the nature of the physical and mental health problems that people experience. Such issues are now
far more likely to be chronic rather than acute conditions, and are known as non-communicable diseases
(NCDs) (Prescott, 2015) or mismatch diseases (Lieberman, 2013). Over the last half century or so, there has
been a huge growth in the incidence of these conditions. Nearly two thirds of deaths worldwide are
attributable to NCDs (Bloom et al., 2011), and vast numbers of people are living with disabilities caused by
mismatch diseases. According to the Australian Institute of Health and Welfare (2015a), about half of all
Australians have a chronic disease, and around 20 per cent have at least two.8 Mismatch diseases account for
the bulk of health care spending throughout the world (Lieberman, 2013), and are now seen as a major global
threat to humanity, not only to our health, but to the social and economic advancement of all nations
(Prescott, 2015; United Nations, 2011).
Mismatch environmental influences during the first 1000 days have been shown to aect our susceptibility
to a wide range of the non-communicable diseases and conditions in later life (Balbus et al., 2013; Barouki et
al., 2012; Gibson, 2009; Heindel et al., 2015; Lieberman, 2013; Prescott, 2015). They include allergies,
immune and autoimmune diseases, neurodevelopmental and neurodegenerative diseases/dysfunctions,
arthritis and osteoporosis, inflammatory bowel disease, some cancer types, infertility, changes in timing of
puberty, depression, and psychiatric disorders such as schizophrenia (Barouki et al., 2012; Heindel et al.,
2015; Prescott, 2015).
Other evidence suggests that mismatch diseases can also result from the impact that changed living
conditions have had on the human microbiome.
8 These calculations are based on the incidence of eight chronic diseases: arthritis, asthma, back problems, cancer, chronic obstructive pulmonary disease,
cardiovascular disease, diabetes and mental health conditions.
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3.2.1 The role of the microbiome
Vast numbers of bacteria, viruses, and fungi (collectively known as the microbiome) live in and on the human
body and play an important role in maintaining our health and wellbeing (Haahtela, et al., 2013; Blaser, 2014a;
Collen, 2015; Dietert, 2016; Mayer, 2016; Relman, 2012). Microbes outnumber our human cells and therefore
the genes that are transmitted from parents to infant are predominantly microbial9. It has been estimated that
only 1 per cent of genetic transfer is human (Mayer, 2016), with the genes of microbes – the ‘second human
genome’ (Relman, 2012) – making up the rest. Thus, rather than being a single stand-alone species, humans are
more properly understood to be superorganisms made up of thousands of biologically diverse species (Dietert,
2016). The microbiome contributes significantly to individual dierences between us: while humans are
relatively homogeneous in their genetic makeup, we vary greatly in the composition of microbiomes, with only
a third of the microbiome’s constituent genes found in a majority of healthy individuals (Human Microbiome
Project Consortium, 2012; Lloyd-Price, Abu-Ali, & Huttenhower, 2016).
The diverse ecology of microbes that make up the microbiome has coevolved with our species over millennia
(Haahtela et al., 2013; Logan, Jacka & Prescott, 2016). These microbes provide us with essential services in
exchange for being housed and fed. In particular, it is the bacteria in our gut that play a critical role in our
physical and even our mental health (Blaser, 2014a; Haahtela, et al., 2013; Mayer, 2016). The beneficial
functions they perform include helping digest food components that our guts cannot process (including
essential elements in breastmilk), regulating our bodies’ metabolisms, producing hormones, detoxifying
dangerous chemicals we ingest with our food, training and regulating the immune system, and preventing the
invasion and growth of dangerous pathogens (Mayer, 2016).
By virtue of its ability to confer an extensive set of protective and functional benefits to its human host, the
gut microbiome can be considered a microbial or metabolic ‘organ’, and maintaining the proper health and
functionality of this ‘organ’ is of significant importance (Huang et al., 2013). In short, it is the microbiome that
helps keep us healthy (Blaser, 2014a). The brain, the gut, and the microbiome are in constant close
communication, and function as parts of a single integrated system – the brain-gut-microbiome axis (Mayer,
2016). The first 1000 days are particularly crucial in shaping the architecture of this axis: both the brain and
the microbiome are still developing, and changes during this period tend to persist for life. The consequences
may not emerge until later in life, when the diversity and resilience of the gut microbiome decreases, making
us vulnerable to degenerative diseases such as Alzheimer’s or Parkinson’s disease (Mayer, 2016).
Any change in the abundance, or composition or diversity of these micro-organisms can have significant health
consequences. For instance, it may lead to failures to regulate and restore appropriate immune and inflammatory
responses (Haahtela et al., 2013; Huang et al., 2013; Weng & Walker, 2013), which can contribute to chronic
inflammatory conditions such as inflammatory bowel disease and asthma, and may even play a role in the
development of conditions such as autism spectrum disorder, psychiatric disorders such as depression, and
neurodegenerative conditions such as Parkinson’s disease (Dash, Clarke, Berk & Jacka, 2015; Haahtela et al.,
2013; Huang et al., 2013; Mayer, 2016; Vuong & Hsiao, 2017; Zheng et al., 2016). Since the trac on the brain-
gut-microbiome axis is two-way, our mental states can shape the composition of our gut bacteria. For instance,
one study found that the infants of mothers who experience cumulative stress during pregnancy show marked
disturbances in the composition of their gut bacteria, and subsequently have more health problems, such as
infant gastrointestinal symptoms and allergic reactions (Zijlmans et al., 2015).
Disturbances of the composition of the microbiome – known as dysbiosis – can take several forms: a loss of
beneficial microbes, an expansion of harmful microbes, or a loss of overall microbial diversity (Logan, 2015; Logan
et al., 2016; Petersen & Round, 2014). Logan (2015) suggests that the conditions promoting dysbiosis are
unequally distributed across society, with those living in socioeconomically deprived conditions where grey space
(as opposed to green space) is the dominant environmental feature being more likely to be experiencingdysbiosis.
9 Recent estimates (Sender, Fuchs & Milo, 2016a, 2016b) suggest that, rather than vastly outnumbering the cells in the human body, the ratio of bacteria
in the human microbiome to cells in the body is roughly 1:1. However, this does not include other microbes such as viruses, fungi and parasites.
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The two sources of microbial exposure that are important for human health and development – environmental
and human microbiota – have both become less diverse as a result of modern lifestyle changes. In addition,
environmental changes such as urbanisation, higher exposure to chemicals and less exposure to green spaces,
have reduced our exposure to a diverse range of plant, animal and microbial life. This has been linked with a
range of mismatch diseases, including allergies, and Type 1 diabetes (Haahtela et al., 2013) and asthma (Huang
& Boushey, 2015; Noval Rivas, Crother & Arditi, 2016). Our developmental health is also at risk because parts
of our ancestral microbiome are disappearing (Blaser, 2014b). This is due to a range or factors, including
overuse of antibiotics (in treating humans and in promoting the growth of the animals we eat) (Anderson et al.,
2017; Hersh & Kronman, 2017), overuse of caesarean section births when not strictly necessary, the
widespread use of sanitisers and antiseptics, and the shift to a Westernized high-fat high-carbohydrate high-
fructose diet (Albenberg & Wu, 2014; Huang et al., 2013; Sonnenburg & Sonnenburg, 2014). As Mayer (2016)
notes, it is easier to reduce gut microbial diversity in adults than it is to increase it above the level established
in the first 1000 days.
Although the womb was thought to provide a sterile environment for the foetus, we now know that some
bacteria are able to cross the placenta (Rodriguez et al., 2015), although we know very little about the nature
and impact of microbes that do so. What we do know is that, from birth onwards, infants are rapidly colonised
by a remarkably wide diversity of bacteria. In the case of the colonisation of the gut, the composition of gut
microbiota in infants is markedly dierent from those in adults, but becomes progressively more adult-like as
the infant acquires more microbes from the people around them, and reaches an adult-like form by the age of
three (Yatsunenko et al., 2012). Thus, the transition from no microbiota to an adult-like microbiome is all
accomplished during the first 1000 days or so of life (Blaser, 2014a; Logan et al., 2016).
Just as the human epigenome is developmentally programmed by the early environment, so too is the human
microbiome (Logan et al., 2016). In the postnatal period, microbial colonisation is influenced by factors such as
gestational age, antibiotic exposure, delivery mode (caesarean section delays and laters the establishment of
the gut microbiome), breastfeeding, formula milks, timing and types of solid foods, and genetic factors (Logan
et al., 2016; Rodriguez et al., 2015).The importance of acquiring a full complement of microbiota in the early
years is captured in the self-completion hypothesis – which maintains that the single, most pivotal sign in
distinguishing a life course of health versus that filled with disease is a successful and timely ‘seeding’ with an
optimal complement of microbiota (Dietert, 2014; Dietert & Dietert, 2012; Dietert, 2016). There appears to be
a narrow developmental window for eective seeding surrounding birth, and the completion of the full
microbiome over the next two and a half to three years shapes their gut microbiome for a lifetime (Mayer,
2016; Wopereis et al., 2014). The immune dysregulation created by missing gut microbes during key periods of
immune maturation can remain into adulthood (Dietert, 2014) and act as a biomarker of specific health risks
(Dietert, 2014).
The microbiome evidence is another form of mismatch. The developing immune system appears to be
particularly susceptible to modern environmental change, with the most common and earliest developing
non-communicable diseases being immune-related conditions such as allergies (Prescott, 2013) and obesity
(Segovia, Vickers & Reynolds, 2017).
3.2.2 Allergies
Australia has one of the highest rates of allergic diseases in the world (Prescott, 2015), with the latest
generation of infants experiencing an epidemic of potentially life-threatening food allergies which were
uncommon in their parents and rare in their grandparents. In just ten years there has been a five-fold rise in
serious (anaphylactic) food allergies in pre-schoolers (Mullins, 2007). The ‘Healthnuts’ study (Osborne et al.,
2011) of over 2,000 Melbourne infants found that more than 10 per cent of one year olds now have a food
allergy. Even more have other allergic conditions, such as eczema. There also appears to be more severe
disease, earlier onset and delayed resolution. Common food allergies, such as egg and milk allergy, which were
previously transient in early childhood, are becoming increasingly persistent (Osborne et al., 2011).
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Research shows that the very early postnatal period is a critical time for immune development and allergy
prevention (Prescott, 2011). In the days following birth, there is an enormous influx of bacteria in an infant’s
gut, which stimulates the local immune system and the processes that prevent bacteria from ‘infecting’ or
‘invading’ (Prescott, 2011). A perfect balance develops where ‘friendly’ bacteria have a home and are fed by the
infant; and in return, they ensure that he/she has a healthy immune system and that less friendly bacteria are
kept away (Prescott, 2011).
Progressive modernisation and cleaner living appears to have altered the balance between humans and their
friendly gut microbes (Prescott, 2011). This has been a strong element in the ‘hygiene hypothesis’, which
proposes that there may be an association between the change in exposure to microbes and the increased
incidence of allergies (Warner, 2003). Infants who go on to develop allergic disease are known to have lower
levels of ‘friendly’ bacteria in the first week of life (Björkstén et al., 2001; Kalliomäki et al., 2001), and higher
levels of disease-producing bacteria (Böttcher et al., 2000). Newer studies also show reduced diversity of the
gut bacteria in infants who go on to develop allergic disease (Sjögren et al., 2009). Collectively, this evidence
strongly suggests that the pattern of colonisation of bacteria in the first few weeks of life may influence the
patterns of immune development in later life.
3.2.3 Obesity
A second major mismatch condition is obesity. Like diabetes and other non-communicable diseases, obesity is
characterised by chronic low-grade inflammation, which in turn contributes to further disease progression, in
part by changing homeostatic set points (such as insulin sensitivity or blood pressure) (Medzhitov, 2008).
Obesity is a complex condition with multiple causes (Campbell, 2016). While not a disease in itself, obesity is a
major risk factor for the development of Type 2 diabetes (Franks & McCarthy, 2016) and other adverse health
outcomes. Childhood obesity is of significant concern given that it has been described as reaching epidemic
proportions in recent times (Segovia et al., 2017; Young, Johnson, & Krebs, 2012), and because patterns of
weight gain, metabolism, and even the total numbers of fat cells in our bodies are determined in early life
(Prescott, 2015).
Some of the key prenatal influences on the development of childhood obesity include the mother’s smoking
habits during pregnancy (Oken, Levitan & Gillman, 2008); the mother’s weight gain during pregnancy (Oken et
al., 2007; Segovia et al., 2017); and the mother’s blood sugar levels during pregnancy, particularly, whether she
develops pregnancy-related (gestational) diabetes (Hillier et al., 2007; Harvard School of Public Health, 2016).
However, environmental influences do not stop with birth. Instead, they simply shift from a small, confined
space largely controlled by the mother’s genes, lifestyle, and physiology, to an unbounded environment with
equally influential eects (Harvard School of Public Health, 2016). There are three variable postnatal factors
during infancy that impact weight in later life: how rapidly an infant gains weight, initiation and length of
breastfeeding, and the duration of infant sleep. The first two of these factors (rapidity of infant weight gain
and initiation and length of breastfeeding) are discussed in section 6.1.2 (Nutrition in infancy) of this report.
Research shows an association between restricted sleep and weight gain in adults (Singhal, 2007), and there is
now reason to believe that a similar association may hold true for infants (Harvard University School of Public
Health, 2016). In a study of 915 children, infants who slept fewer than 12 hours a day were twice as likely to
be overweight at age 3, compared with infants who slept more than 12 hours a day (Demerath et al., 2009).
Influences associated with shorter infant sleep duration include maternal depression during pregnancy, early
introduction of solid foods (before 4 months), and infant TV viewing (Karaolis-Danckert et al., 2006). The
mechanisms underlying the association between sleep duration and obesity are unclear (Taheri, 2006).
However, studies in adults have shown that sleep restriction can lead to changes in the levels of certain
hormones responsible for the control of hunger and appetite (Spiegel, Tasali, Penev &Van Cauter, 2004).
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Several studies suggest that childhood obesity increases the risk of food allergies (Castro-Rodriguez et al.,
2001; Gold, Damokosh, Dockery, & Berkey, 2003), while others suggest that allergic inflammation may impact
metabolism (and increase the likelihood of obesity). In other words, the relationship between allergy and
obesity may operate in both directions (Prescott, 2015). The connection between metabolism and the immune
system occurs at many levels; hormonal interactions, sensing of nutrients by immune cells, and in the gut
bacteria (Prescott, 2015).
Early life holds the keys to how and why allergies and obesity develop, and is the best opportunity to reverse
the allergy epidemic (Prescott, 2011). Thus, in considering environmental factors that may be driving the rise
in allergic disease, we must particularly consider their eects in pregnancy and the early postnatal period
(Prescott, 2011). On the basis of the proposed interplay between our modern dietary patterns and cleaner
environments, prebiotic and probiotic bacteria have both been used to prevent allergy in early life
(Prescott,2015).
3.3 Summary
Social and environmental changes over the past half century or so have resulted in a social climate change that
has transformed the conditions under which families raise their children, as well as changes in families
themselves. Dramatic changes to things such as employment and housing have significantly contributed to a
rise in the conditions that are known to adversely impact child health and wellbeing, such as poverty and social
isolation. To that end, it is becoming increasingly evident that the complex and entwined nature of these
‘wicked’ problems is such that traditional governance and service-driven approaches are no longer eective in
driving change.
The drastic rise in some of today’s most commonly occurring health problems is believed to be influenced by
this social climate change, which has resulted in a mismatch between human evolutionary capacities and
modern environments. This is referred to as the mismatch hypothesis and can be broken into two categories:
predictive mismatch (which occurs when our bodies make adaptations based on predictions regarding the kind
of environments we are going to be living in, and the environments do not match the predictions) and
evolutionary mismatch (which occurs when our bodies encounter conditions for which they were not
evolutionarily adapted or designed). This mismatch between our evolutionary capacities and our modern living
environments has given rise to chronic physical and mental health conditions that are known as non-
communicable diseases and conditions.
Mismatch diseases can also result from the impact that changed living conditions have had on our microbiome
(the collection of bacteria, viruses, and fungi that live in and on our body). Our microbiome is critical to our
health and is in constant communication with our gut and brain, all three of which function as an integrated
system. Changes in the abundance, composition, or diversity of our microbiome can result in significant health
consequences. The two sources of microbial exposure that are important for human health and development –
environmental and human microbiota – have both become less diverse as a result of modern lifestyle changes,
such as urbanisation and less exposure to green spaces.
Acquiring a full complement of microbiota in the first 1000 days is central to optimal health throughout the
lifespan. This is known as the self-completion hypothesis. There appears to be a narrow developmental
window for eective ‘seeding’ surrounding birth, and the completion of the full microbiome over the next two
and a half to three years of life, which shapes the gut microbiome for a lifetime. Two of the most common and
earliest developing non-communicable diseases/conditions are inflammatory conditions such as allergies
andobesity.
~ ~ ~
The third body of evidence that is reshaping our understanding of early development concerns the social
determinants of health.
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4. Social determinants of health
Our health and broader life outcomes are not exclusively based on our genetic or biological disposition
(Hertzman et al., 2010; Bambra et al., 2010; Goldfeld et al., 2012). Rather, they are strongly shaped by the
social, economic and environmental conditions into which we are born, grow, live, and age (WHO Commission on
the Social Determinants of Health, 2008). These social conditions, known as the social determinants of health,
ultimately work through biological pathways to shape our health and wellbeing. Key social determinants
include (but are not limited to): socioeconomic status, educational attainment, employment status, poverty,
geographic location, disability, gender, and social connectivity.
Our social determinants have the power to shape our lives for better or worse (Halfon, Larson & Russ, 2010;
Marmot Review, 2010), unilaterally assigning us to a social standing that impacts our economic resources,
status and autonomy (Moore, McDonald & McHugh-Dillon, 2014a; VicHealth, 2013). Social determinants play a
critical role in the first 1000 days (Bronfenbrenner, 1979; Barker, 1994; Wadsworth, 1997; Hertzman, 2000;
Shonko & Philips, 2000), as it is during this period that a number of vital skills and abilities develop (Moore,
McDonald & McHugh-Dillon, 2015; Dyson et al., 2010; Hertzman, 2010; Strategic Review of Health Inequalities
in England post-2010 Committee, 2010; Shonko, 2012).
Social determinants are often interrelated and/or co-existing. For example, we know that families who
experience adversity often do so as a result of multiple determinants and in multiple areas of their life
(Bromfield, Lamont, Parker, & Horsfall, 2010; Oroyemi et al., 2009). As such, social determinants should be
understood as a set of correlating and interactive factors that may or may not lead to adversity within the
family (Olsson & Hwang, 2003).
Social determinants are also transmitted across generations. Several researchers in dierent fields have
observed that parents not only transmit genetic and epigenetic characteristics, but also the environments that
produce those characteristics (Blackburn & Eppel, 2017; Lieberman, 2013; Moore, 2015). According to
Blackburn and Eppel (2017), the evidence from telomere syndrome families suggests that it is possible for the
eects of social disadvantage to accumulate over the generations. Social disadvantage is associated with
poverty, worse health and shorter telomeres, and parents whose telomeres are shortened by this disadvantage
may directly transmit those shorter telomeres to their babies in utero. Those children will be born with
telomeres shortened by their parents’ life circumstances. As these children grow up, they are also exposed to
poverty and stress, and their telomeres will erode even further. In a downward spiral, each generation directly
transmits its ever-shortening telomeres to the next.
Lieberman (2013) makes a similar argument about the spread of mismatch diseases, describing an insidious
feedback loop that promotes the spread of these diseases. We get sick from non-infectious mismatch diseases
caused by our bodies being poorly or inadequately adapted to the novel environments we have created, then
we fail to address the novel environmental factors responsible for the mismatch, which then allows the disease
to remain prevalent or sometimes to become more common or severe. Lieberman calls this phenomenon
dysevolution and argues that this is not a form of biological evolution, because it does not involve a direct
transfer of mismatch diseases from one generation to the next. Instead, it is a form of cultural evolution,
because it involves a transfer of behaviours and environments that promote mismatch diseases in the next
generation, that is, our children (Jablonka & Lamb, 2014; Lieberman, 2013).
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4.1 Social gradient eects in health and wellbeing
Research shows that the lower one’s social standing in life (e.g. persistent unemployment or chronic
homelessness), the worse the long-term health and wellbeing outcomes are likely to be (Adler & Stewart,
2010; WHO, 2010). This global phenomenon is referred to as the social gradient in health and is evident from
the very top of the socioeconomic spectrum to the very bottom. Social gradients represent more than just
disparities between the poor and the wealthy, they also represent disparities within similar cohorts. That is, at
any given point along the socioeconomic continuum, one is likely to experience inferior health outcomes to
those above them (Shepherd, Li & Zubrick, 2012; Marmot & Wilkinson, 2006). For example, the Australian
Socio-Economic Index of Disadvantage for Areas (SEIFA) illustrates a notable discrepancy between health
outcomes according to level of disadvantage — with outcomes becoming progressively worse with increased
disadvantage (ABS, 2010).
It is impossible to eectively address existing social gradients in health without first addressing the social
determinants of health. One of the most significant social determinants of child health and wellbeing is
poverty.
4.2 Poverty10
Research by the Australian Institute of Health and Welfare (AIHW) found that in 2013-14, approximately
70,000 Australian children received support from homelessness services (AIHW, 2010).
A significant body of evidence highlights the strong correlation between poverty in the first 1000 days and
adverse health and wellbeing outcomes in later life (Goldfeld & West, 2014; Kruk, 2013; Hertzman et al., 2010;
Marmot Review, 2010; Khanam et al., 2009). Evidence is now emerging of the eects of poverty on brain
development (Barch et al., 2016; Hair, Hanson,Wolfe & Pollak; 2015; Luby et al., 2013; Luby 2015). One of
these studies (Barch et al., 2016) found that areas of the brain responsible for learning, memory, and regulation
of stress and emotions were connected to other parts of the brain in a ‘weaker’ way in children from low income
families, as compared to children from higher income families. The level of this weakness varied according to
the degree and length of poverty the child had been exposed to (Barch et al., 2016). These findings indicate
there is a clear and coherent risk trajectory in which caregiving nurturance shapes the development of key
brain regions in the context of poverty and that the development of these brain structures in turn shapes
academic outcomes (Luby, 2015). Moreover, research shows that while children from high income families with
developmental delays are likely to catch up to their peers in later life, children of low income families are much
less likely to do so and in fact, the gap between them and their more auent counterparts is likely to grow
exponentially (Feinstein, 2003).
It is worth noting that while persistent poverty in the first 1000 days has a cumulative negative impact on
development, prolonged poverty during later stages of life is less likely to have a significant impact on future
life outcomes (Dickerson & Popli, 2012). Equally, relieving poverty (particularly in the first 1000 days) has been
shown to increase birth weight and other outcomes, which can reduce the likelihood of negative outcomes in
later life (Strully et al., 2010). For example, Costello and colleagues (2003) found that even a minor increase in
income amongst families experiencing poverty resulted in decreased rates of childhood mental ill health
(Costello, Compton, Keeler & Angold, 2003).
10 Here, the terms ‘poverty’, ‘low income’ and ‘economic hardship’ will be used interchangeably. Furthermore, the term ‘financial distress’ will be used to refer
to the behavioural and emotional response that parents experience when facing economic hardship (Starkey et al., 2013).
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4.2.1 Poverty in pregnancy
Starting from pregnancy, the experience of poverty begins to shape the unborn child’s life. Women in the most
economically disadvantaged areas of Australia are less likely to receive antenatal care in their first trimester of
pregnancy, compared to women in the most economically advantaged areas (55 per cent versus 68 per cent)
(AIHW, 2015a). Moreover, poverty in pregnancy is associated with increased use of tobacco, alcohol and other
drugs; and poor nutrition and obesity — all of which have been shown to increase the likelihood of health and
developmental vulnerabilities in children (Penman-Aguilar, Carter, Snead & Kourtis, 2013; Bailey, 2006; Weis et
al., 2004; Conde-Agudelo, Rosas-Bermundez & Kafury-Goeta, 2006).
Poverty is also likely to increase a mother’s exposure to psychological stressors, such as domestic violence and
homelessness, which impacts the body’s normal regulation of hormones during pregnancy and increases the
likelihood of foetal growth delay and preterm birth (Weinstock 2005). Research shows that pre-term babies
face an increased risk of various short and long-term health and well-being adversities (Luciana, 2003; Platt,
2014), such as depression, infectious and non-infectious respiratory problems, neonatal jaundice, epilepsy,
cerebral palsy, visual impairments, cognitive impairment and developmental coordination disorder (Moore et al.,
2015; Patton et al., 2004).
4.2.2 Poverty in infancy
The existing correlation between poverty in infancy and adverse outcomes in later life is not a random
occurrence. Research into the influence of poverty on child development has primarily been guided by three
key theories:
1. That economic hardship can contribute greatly to psychological distress in parents and hence negatively
impact their care-giving capacity (Conger & Conger, 2002).
The relationship between financial distress and depression / anxiety is strongly supported by research
(Green et al., 2005; Prawitz et al. 2006; Zimmerman &Katon, 2005; Coiro, 2001). A UK study by Green and
colleagues (2005) found that families in the lowest income quintile were three times as likely than those
in the highest income quintile to experience mental ill health (including depression and anxiety) (Green et
al., 2005), and nine times more likely to experience a psychiatric disorder (Marmot, 2010).
Parental psychological distress is the primary connecting factor between economic hardship and less
responsive and/or hostile parenting behaviours (Mistry et al., 2002; Solantaus et al., 2004; Parke et al.,
2004; Gersho et al., 2007). In a meta-analysis of 46 studies, Lovejoy and colleagues (2000) found a
strong correlation between depressive symptoms in mothers and disengaged (e.g. withdrawn, ignoring)
and hostile (e.g. mean and angry) parenting (Lovejoy, Graczyk, O’Hare & Neuman, 2000). Findings also
showed that the eects of parental depression were strongest amongst low income mothers of infants.
When infants and young children interact with a disengaged or irritable caregiver, the anxiety that is
created in them can cause their body to increase production of potentially harmful stress hormones
(Dawson & Ashman, 2000; NSCDC, 2014). If this bodily reaction occurs often and over a sustained period
of time, it can aect the child’s brain development and interfere with his/her ability to learn and increase
the likelihood of mental ill health in later life (NSCDC, 2005). A 20 year longitudinal study by Weissman
and colleagues (2006)found that children of parents with depression were three times more likely to
experience anxiety disorders, major depression, and substance dependence in later life (Weissman et al.,
2006).
2. That families with greater financial resources have the capacity to make greater investments in the
development of their child, where disadvantaged families may only be able to invest in the child’s more
immediate needs (Bradley & Corwyn, 2002; Evans, 2004; Corcoran & Adams, 1997; Duncan & Magnuson,
2003; Linver et al., 2002).
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Investments in child development relate to degree of family support, access to learning materials available
in the home and the family’s standard of living (adequate food, housing, clothing, medical care, etc.).
Research shows that children who experience poverty are less likely to live in cognitively stimulating
environments, have less access to books, fewer age-appropriate toys, fewer informal learning settings,
fewer educational materials, and spent more time in front of the television (Bradley & Corwyn, 2002;
Duncan & Brooks-Gunn, 1997; Evans, 2004).
Linver and colleagues (2002) found that the correlation between family income and child cognitive
development is noticeably reduced when investments (e.g. language stimulation, providing books and
other learning materials, and exposing the child to learning experiences outside the home) are introduced
to the child’s everyday environment. Moreover, the level of parental investment was shown to
significantly dominate the association between income and child behaviour problems at 3 and 5 years of
age (Linver, Brooks-Gunn & Kohen, 2002).
3. That children who are born into (and have a prolonged experience of) poverty are more likely to
experience prolonged stress (Evans & Kim, 2012).
Research shows that children who experience persistent poverty in the first 1000 days are more likely to
display symptoms that are consistent with anxiety (higher blood pressure; irregular cortisol production;
irregular metabolic activity; and poorer immune functioning) (Evans & Kim, 2012; Blair et al., 2011; Miller,
Chen & Parker, 2011a). This is because children who live in poverty are more likely to have co-occurring
exposure to family distress and separation, maternal depression, family and domestic violence, reduced
parental responsiveness, and increased use of physical discipline (Bradley & Corwyn, 2002; Conger &
Donnellan, 2007; Grant et al., 2003). They are also more likely to live in homes that are overcrowded; in
neighbourhoods that are less connected and have less social supports; and be exposed to more toxins,
crime and trac (Evans, 2004; Evans & Kim, 2012; Evans & Kim, 2010; Samero, Seifer, & McDonough,
2004).
During the first 1000 days, the neural circuits responsible for managing stress are particularly malleable
(NSCDC, 2014). A child’s early experiences determine how these circuits are activated and controlled in
the future. Prolonged and excessive toxic stress during this period can impact the developing brain
circuits and hormonal systems in a way that leads to poorly controlled stress response systems; ones that
are overly reactive or slow to shut down when faced with challenges throughout the lifespan (NSCDC,
2014; Loman & Gunner, 2010). For example, research shows that children who experienced persistent
poverty in early life are more likely to exhibit non-adaptive coping strategies (disengagement and
avoidance) in later life (Evans & Kim, 2012). Non-adaptive strategies are associated with higher levels of
internalising (depression and anxiety) and externalising (aggression and impulsive) behaviours
(Wadsworth & Achenbach, 2005; Compas et al., 2001).
Because children depend on their caregivers to meet their every need, the experience of poverty impacts
them in multiple and concurrent ways, during the most critical period of their life. The quality of care that
a child receives, the number and quality of learning opportunities it has, and the level and duration of
stress that it experiences, are all significantly influenced by the experience and duration of poverty.
There is evidence for each of these theories, and the link between poverty in infancy and adverse outcomes in
later life may be a product of all three pathways. While much has been learned, we have yet to fully understand
the relative strength of these dierent influences or how they fit together. Further research is needed to
settle these questions.
Aboriginal children experience poverty at significantly higher rates than their non-Aboriginal counterparts
(ACOSS, 2014), and this is only one of a number of social determinants that inequitably aect
Aboriginalpeople.
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4.3 Social determinants and Aboriginal11 health
Provided the necessary social conditions are in place, Aboriginal culture is a protective force for Aboriginal
children, families and communities. Aboriginal parents have strong cultural practices in family life and child
rearing, and know how to keep their children safe and to raise them to be active contributors to family and
community life (Lohar, Butera & Kennedy, 2014). However, the eects of intergenerational trauma, cultural
disconnection and family disruption among many Aboriginal communities, are increasingly being recognised as
factors which can have significant adverse outcomes for some Aboriginal children (Council of Australian
Governments [COAG], 2009).
Faced with all the evidence regarding the challenges confronting Aboriginal populations and the poor health
and other outcomes they experience, it is easy to lose sight of the strengths of Aboriginal culture and the
resilience of many Aboriginal communities and people. This may partly reflect a tendency to focus unduly on
the negatives. As Nguyen and Cairney (2013) note, current government frameworks that collect data about
Aboriginal people often focus on deficits, disadvantage and dysfunction. These frameworks gather statistical
information for the purposes of policy analysis and program development and therefore use indicators that are
important to policy, but lack a wellbeing perspective that recognises the strengths and resilience of Aboriginal
and Torres Strait Islander people or reflects their worldviews, perspectives and values. The definition of
wellbeing developed by the Social Health Reference Group for the National Aboriginal and Torres Strait Islander
Health Council and National MentalHealth Working Group (2004) highlights the importance of connection to
land, culture, spirituality, ancestry, family and community, and how these aect the individual. As stated by
Zubrick et al. (2014),
There are unique aspects of Aboriginal culture that can have a significant
influence on Aboriginal health and that enables Aboriginal people to maintain
spirituality central to the Indigenous notion of health. Connection to land,
spirituality and ancestry, kinship networks, and cultural continuity are
commonly identified by Aboriginal people as important health-protecting
factors. These are said to serve as sources of resilience and as a unique
reservoir of strength and recovery when faced with adversity, and can
compensate for, and mitigate against, the impact of stressful circumstances on
the social and emotional wellbeing of individuals, families and communities.
In the case of Aboriginal populations and children, the social determinants explanation of inequities in health
outcomes is more complicated.
11 In this section, the term “Aboriginal” refers to Aboriginal and Torres Strait Islander Australians. Based on 2011 Census data, around 3 per cent of the
Australian population (approximately 670 000 people) were estimated as being Aboriginal (Steering Committee for the Review of Government Service
Provision, 2014). According to Boulton (2016), these fall into two demographic layers: approximately 80 per cent live in urban centres on the east coast,
while the remaining 20 per cent live in small towns and remote communities across the tropical north of the country and through the Central and
Western deserts. The health and developmental outcomes for these two populations can dier significantly.
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The social determinants of Aboriginal health include (but are not limited to) social status, employment, poverty,
housing, education, the experience of racism, and intergenerational trauma12 (Gee et al., 2014; Muid, 2006).
The available data indicates that all of these factors have a disproportionately large impact on the health and
wellbeing of the Aboriginal population (ABS, 2011, 2012a, 2012b; AIHW, 2015b, 2015c; Gracey & King, 2009).
Additionally, a growing body of evidence highlights a significant relationship between a robust anity with
traditional cultures and improved health and wellbeing outcomes amongst Aboriginal peoples (Colquhoun &
Dockery, 2012; Wexler, 2009; Fleming & Ledogar, 2008). For example, applying data from the 2002 National
Aboriginal and Torres Strait Islander Survey (NATSISS), Dockery (2009, 2010) found that greater attachment to
traditional culture is associated with a range of improved outcomes for Aboriginal peoples (e.g. self-assessed
health, educational attainment, employment status, incarceration rates and alcohol abuse).
Aboriginal children experience poverty at significantly higher rates than their non-Aboriginal counterparts
(ACOSS, 2014). Furthermore, Aboriginal mothers are more likely to experience higher-risk pregnancies
(including teenage pregnancy), with maternal mortality for Aboriginal women being double that of other
Australian women (Humphrey et al., 2015; Chandler et al., 2003). Despite these alarming rates, only around
half of Aboriginal women will receive antenatal care in their first trimester of pregnancy — compared with the
national average of two-thirds (Harris & Wells, 2016). Aboriginal women are also more likely to experience
domestic and family violence during pregnancy (Taft, Watson, & Lee, 2004) and use alcohol and tobacco during
pregnancy (ABS, 2016). In 2015, almost four in ten Aboriginal children aged 0–3 years had a birth mother who
had smoked or chewed tobacco during pregnancy, and about one in ten had a birth mother who drank alcohol
during pregnancy (ABS, 2016). Aboriginal children continue to be over-represented in the out-of-home-care
system: they are seven times more likely than non-Aboriginal children to have involvement with child
protection services (AIHW, 2016) and eleven times more likely to be placed in out-of-home care (often with
non-Aboriginal families outside of their community) (AIHW, 2015b). Evidence shows that these numbers are
steadily increasing (AIHW, 2016).
Given the above, it is not surprising that Aboriginal children have some of the poorest health and
developmental outcomes in Australia. On average, Aboriginal children have poorer outcomes than non-
Aboriginal children on almost all standard indicators of wellbeing (Harris & Wells, 2016; Productivity
Commission, 2016). Infants of Aboriginal mothers continue to die at almost double the rate of infants born to
non-Aboriginal mothers and are twice as likely to be born with low birth weight (AIHW, 2015b; Holland, 2015).
In addition to this, Aboriginal children overall have lower levels of participation in Early Childhood Education
and Care (ECEC) services, which has been shown to improve children’s lifelong outcomes across all areas of
health and wellbeing (Sims, 2011). However, despite the fact that research has identified a range of complex
and co-occurring reasons for lower Aboriginal engagement with ECE (in particular, a dearth in the availability of
culturally appropriate services and supports), the educational experiences of Aboriginal Australians is often
framed from a ‘deficit’ viewpoint (where a lack of Aboriginal engagement with mainstream educational
institutions is seen as the ‘problem’) (Krakouer, 2016).
Not surprisingly, Aboriginal children are twice as likely as their non-Aboriginal counterparts to be
developmentally vulnerable across all developmental domains (Australian Government, 2015). Vulnerabilities
at school entry track through to poor literacy and numeracy outcomes across all schooling years (Australian
Curriculum Assessment and Reporting Authority, 2012; Falster et al., 2016). In older Aboriginal Australians,
this trajectory of disadvantage is likely to lead to poor educational attainment and life opportunities,
unemployment, poor health and premature mortality, and over-representation in the criminal justice system
and out- of-home-care (Falster et al., 2016; Thomson, De Bortoli & Buckley, 2013; Weatherburn, 2014).
While we know that the ‘traditional’ social gradients in health contribute significantly to the disparities between
Aboriginal and non-Aboriginal children, there are additional factors (unique to the experience of Aboriginal
Australians) that also play a contributing role. The following sections will explore these in further detail.
12 Resulting as an aftermath of colonisation (i.e. the stolen generation, disposition of land, culture and language, displacement and more).
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Social gradients and Aboriginal health
As discussed, inequities in health outcomes are often reflective of inequities in social, economic and political
status. However, the association between ‘traditional’ social determinants (e.g. education, housing, income etc.)
and health are likely to be more complex for Aboriginal children for a number of reasons. One is that
marginalisation and discrimination are often deeply embedded in the lives of Aboriginal people, limiting the
likelihood of health benefits that are typically associated with improved income, education, etc. (Gracey & King,
2009). Another reason is that the generational marginalisation of Aboriginal people can impact optimal
development in a number of ways, placing some Aboriginal children at a greater disadvantage from the
beginning of life and limiting the acquisition of skills that can be drawn upon for the benefits of health at all
levels of the gradient (Shepherd, 2012). Finally, kinship, spirituality, connection to traditional lands and cultural
continuity play a central role in the health and wellbeing of Aboriginal Australians (Poroch et al., 2009).
However, these factors are not captured in our ‘traditional’ understanding of the social determinants of health
(Boulton, 2016; Currie, 2009; Muntaner, Eaton, Miech & O’Campo, 2004; Shepherd, 2012).
Boulton (2016) argues that understanding the origins of Aboriginal child ill-health requires a wider time frame.
We need to understand that the immediate consequences of disadvantage — the social determinants of ill-
health such as lack of education, unemployment, overcrowding and poverty — are far down the pathway of
causality. In other words, these social determinants are themselves the result of far-distant historical factors.
The historical and ongoing circumstances of colonisation and the profound and sustained marginalisation of
Aboriginal peoples are credible explanations for a much less consistent social gradient within Aboriginal
populations (Shepherd et al., 2012). Racism13, materialised in the marginalisation of a group of people, is
acknowledged as having a detrimental impact on the health of Aboriginal (and other minority groups)
throughout the world (Priest et al., 2012; Priest et al., 2011). Racism can impact health in a number of ways.
Specifically: it can reduced access to optimal health determinants such as quality education and employment;
diminish a positive self-identity; increase stress, substance misuse and self-harm; decrease access to social
supports; and have detrimental eects on cultural identity (Paradies et al., 2009). Moreover, the experience of
racism can restrict access to cultural activities, which are found to be protective factors for Aboriginal people’s
overall health and wellbeing (Bals, Turi, Skre & Kvernmo, 2011).
The range of human rights violations that Aboriginal Australians have experienced (and continue to
experience) as a result of colonisation is extensive. These include the eects of policies such as separation of
Aboriginal children from their families (Australian Human Rights Commission, 1997). Unequivocal evidence
supports that this has resulted in the experience of first hand and second hand trauma amongst Aboriginal
families (Nutton & Fast, 2015; Royal Commission into Aboriginal Deaths in Custody, 1991; Waxler, 2009;
Wesley-Esquimaux & Smolewski, 2004; Wilczynski et al., 2007). Ongoing firsthand (e.g. experiences of the
child protection system) and secondary exposure to traumatic experiences induces intergenerational trauma
(Atkinson, Nelson & Atkinson, 2010), which Muid (2006) defines as: “the subjective experiencing and
remembering of events in the mind of an individual or the life of a community, passed from adults to children in
cyclic processes as collective emotional and psychological injury over the life span and across generations”
(Muid, 2006, p. 36). Much like culture, trauma (and its symptoms) can become ‘normalised’ in a population and
transformed into a way of life (Duran & Duran, 1995). Intergenerational trauma closely correlates with social
gradients, as the impact of trauma greatly imprints on all parts of a person’s life (and that of their children).
The interruption between family and community, characterised by breakdown of social norms (evident for
example, in the increase of family violence and drug and alcohol abuse), is particularly related to adverse
health outcomes amongst Aboriginal families and children (Stanley, Tomison & Pocock, 2003). The Aboriginal
and Torres Strait Islander Social Justice Commissioner (ATSISJC) summarises this as ‘internalised colonialism’ or
‘lateral violence’ (ATSISJC, 2011), where rather than directing its anger toward its oppressor, the oppressed
directs its anger internally – toward its own cultural group (Osborne, Baum & Brown, 2013).
13 Racism is conceptualised as comprising avoidable and unfair phenomena that lead to inequalities in power, resources and opportunities across racial or
ethnic groups. It can be expressed through beliefs and stereotypes, prejudices and discrimination, and occurs at many social levels, including
interpersonally and systemically, and as internalised racism (Berman & Paradis, 2010).
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The social determinants of health, particularly relating to poverty and the systematic discrimination of
Aboriginal Australians, help us to understand the foundations upon which disparities in health and wellbeing
outcomes of Aboriginal and non-Aboriginal children are formed. While there is limited evidence which directly
relates to the social determinants of Aboriginal children health (particularly in the first 1000 days), the fact
that Aboriginal children are significantly more likely to be born with low birthweight, amplifies the early start
and consequences of socioeconomic disadvantage.
Much work is underway to redress inequities between Aboriginal and non-Aboriginal children. For example, The
First 1000 Days Australia model, led by Professor Kerry Arabena at the University of Melbourne, is building a
coordinated, comprehensive, culturally informed strategy to strengthen Aboriginal families to address their
children’s needs. This model incorporates a research program that is premised on culture being the main
protective factor in ensuring the health and wellbeing of Aboriginal families (Arabena, Howell-Muers, Ritte, &
Munro-Harrison, 2015; Arabena, Ritte & Panozzo, 2016).
4.4 Summary
Our health and broader lifelong outcomes are strongly shaped by the social, economic and environmental
conditions into which we are born, grow, live, and age. These conditions, which are almost always interrelated
and co-occurring, are referred to as the social determinant of health. Starting in the first 1000 days, our social
determinants have the power to shape our lives for better or worse, assigning us to a social standing that
impacts our economic resources, status and autonomy.
The lower a child’s social standing in life, the worse their health and wellbeing outcomes are likely to be. This is
known as the social gradient eect in health and wellbeing and occurs from the very top of the socioeconomic
spectrum to the very bottom. Social gradients represent more than just disparities between the poor and the
wealthy, they also represent disparities within similar cohorts. It is impossible to eectively address existing
social gradients in health without first addressing the social determinants of health. Poverty is perhaps the
most powerful social determinant of child health and wellbeing.
A prolonged experience of poverty in the first 1000 days has been shown to adversely impact health and
wellbeing outcomes over an entire lifespan. Poverty impacts a child’s development in three primary ways:
1. It places significant psychological distress on a child’s caregiver(s) and hence negatively impacts their
care-giving capacity.
2. It makes it challenging for caregivers to make greater investments in the development of their child.
Families who live in poverty are less likely to be able to aord or access learning materials, and their
standard of living (adequate food, housing, clothing, medical care, etc.) is also more likely to be low.
3. It means that children are more likely to be exposed to ongoing traumatic experiences (such as
homelessness, domestic violence and reduced parental responsiveness). Prolonged toxic stress during this
period can impact the developing brain and hormonal systems, with lifelong consequences.
Children from low income families with developmental delays are less likely to catch up to their peers in later
life. However, relieving poverty has been shown to increase birth weight and have other positive impacts on
child health and development.
Aboriginal children are significantly more likely to experience sustained poverty than their non-Aboriginal
counterparts, and have significantly higher adverse health and development outcomes. Vulnerabilities at
school entry track through to poor literacy and numeracy outcomes across all schooling years, and eventually
this trajectory of disadvantage is likely to lead to poor educational attainment and life opportunities,
unemployment, poor health and premature mortality.
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The association between ‘traditional’ social determinants (e.g. education, income etc.) and health are likely to
be more complex for Aboriginal children due to a number of reasons, including marginalisation and the
experiences of racism that are often deeply embedded in the lives of Aboriginal Australians. These experiences
place Aboriginal children at a greater disadvantage from the beginning of life, and limit health and wellbeing
outcomes at all levels of the gradient. Additionally, our ‘traditional’ understanding of the social determinants of
health do not capture things such as kinship and connection to traditional lands and cultural continuity, which
play a central role in the health and wellbeing of Aboriginal Australians.
The historical circumstances of colonisation and the profound and sustained marginalisation of Aboriginal
peoples has resulted in the experience of first hand and intergenerational trauma amongst Aboriginal families.
Much like culture, trauma (and its symptoms) can become ‘normalised’ in a population and transformed into a
way of life. The interruption between family and community, characterised by breakdown of social norms
(evident for example, in the increase of family violence), is particularly related to adverse health outcomes
amongst Aboriginal children.
~ ~ ~
What we have described so far has pertained to the biological and social mechanisms of development and
change. However, these do not relate to the actual early life experiences that influence health and wellbeing
outcomes. These are the subject of the next section.
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5. Child, family, community and
environmental factors shaping health
and development
This section reviews some of the primary child, family, community and environmental factors that influence
development in the first 1000 days. These include: child characteristics (such as temperament), the relational
environment (such as parent engagement), and the physical environment (such as housing).
5.1 Child characteristics
5.1.1 Temperament
Temperament refers to individual dierences in the regulation of experience which emerge early in life and
remain moderately stable across development (Kagan, 2012; Lewis & Olsson, 2011; Rothbart, 1989, 2012).
These distinct patterns of feelings and behaviours shape the child’s aective, attentional and motor responses
in various situations. For example, temperament can aect young children’s mood and emotions, how they
approach and react to situations, and their level of fear, frustration, sadness and discomfort (Encyclopedia on
Early Childhood Development, June 2012; Rothbart, 1989).
The influence of temperament on developmental pathways and outcomes are now widely recognised
(Rothbart, 2011; Rothbart & Bates, 2006). For example, Lewis and Olsson (2011) found that stressful family
environments experienced in the infant’s first year of life and high reactive, avoidant, and impulsive
temperament styles directly and independently contribute to anxiety and depressive symptoms in children at 4
years of age. Children’s temperamental traits show only modest stability during infancy and toddlerhood and
show a rather large increase in stability by around 3 years of age (B. W. Roberts & DelVecchio, 2000), as
executive attention develops further.
Biological foundation of temperament
The biological foundation of a temperamental bias (a bias towards certain temperamental characteristics) is
usually, but not always, genetic (Kagan, 2012). In some cases it is the result of severe stress or infection in the
pregnant mother which aects the foetus.
The behaviours in infants and young children that are most often attributed to a temperamental bias are
unusually high or low levels of irritability, motor activity, smiling, ease of regulating these responses, and a
consistent tendency to approach or to avoid unfamiliar people, objects, and places (Kagan, 2012).
Temperamental bias does not determine a particular future trait because life experiences aect the bias and
create a pool of possible personality traits. By the second year of a child’s life, the child’s temperamental biases
and the products of experience have integrated. This integration makes it dicult to detect the early
temperamental biases of most children, because the same behaviour could be the partial result of a
temperamental bias or the product of experience alone. For example, not all shy children inherit a
temperamental bias favouring that quality (Kagan, 2012).
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Interplay between temperament and environment
There is evidence to suggest that children dier in the extent to which they are influenced—for better and for
worse—by their environmental experiences, due to ‘vulnerability’ in their make-up. This vulnerability may be
behavioural (e.g. dicult temperament) or genetic (Bakermans-Kranenburg & van IJzendoorn, 2007, 2010,
2011; Belsky, Bakermans-Kranenburg, & van IJzendoorn, 2007; Ellis et al., 2011). Children with such ‘risk’
characteristics are thought to be disproportionately aected by poor rearing influences, while more likely to
benefit from highly supportive environments (Boyce & Ellis, 2005).
Hartman and Belsky (2015) found that temperamental and genetic characteristics played a role in
distinguishing children that were either more or less susceptible to parental influences. In particular, two
temperamental patterns have emerged as being indicators of heightened susceptibility to rearing: negative
emotionality, and a highly sensitive personality (Hartman & Belsky, 2015). By contrast, less susceptible
individuals are less aected by rearing conditions, whether they are positive or negative. For example, Belsky
(2005) observed that highly negatively emotional (low adaptability, high activity, and low emotional
regulation) infants were disproportionately more susceptible to rearing. This was also a quality that was
identified as moderating the impact of early experiences. For example, quality of maternal discipline (gentle
guidance versus forceful control) has been shown to influence substantially more variance in the self-control of
infants and toddlers who display greater negative emotionality (Kochanska, 1993).
5.1.2 Dierential susceptibility
The association between certain genetic profiles and increased susceptibility to environmental conditions
(GXE) reveal that some children are more influenced by their environmental conditions than others as a
function of the presence or absence of specific genetic characteristics (Caspi & Shiner, 2006). Specifically,
“susceptibility genes” have been identified and shown to influence the risk for problematic developmental
outcomes in the presence of adverse environmental conditions. For example, one study found that certain
genetic characteristics moderate the relationship between child maltreatment and antisocial behaviour
(Cicchetti, Rogosch, & Thibodeau, 2012), while another found this to be the case between maternal prenatal
depression on child emotional dysregulation (Babineau et al., 2015).
In addition to moderating the eects of stressful environmental conditions, dierential susceptibility has also
been shown to moderate development in supportive environments. That is, children who are disproportionately
vulnerable to adversity are also disproportionately more likely to benefit from highly supportive environments
(Belsky et al., 2007; Boyce & Ellis, 2005). For example, in a longitudinal study of infants, maternal insensitivity
when children were 10 months of age predicted externalising problems more than 2 years later, but only for
children carrying the ‘risk’ gene (Bakermans-Kranenburg & van IJzendoorn, 2006). Moreover, while children
carrying the “risk” gene displayed the most externalising behaviour of all children when mothers were judged
insensitive, they also manifested the least externalising behaviour when mothers were judged as
highlysensitive.
As we have seen, a child’s temperamental bias, coupled with early life experiences, can influence their
development and lifelong outcomes for better or worse. While early life experiences are hugely significant for
all children, for those who are disproportionately influenced by their environment, due to ‘risk’ characteristics,
the nature and quality of their interpersonal relationships play a particularly vital role in determining their
lifelong health and wellbeing outcomes.
The following section reviews the evidence relating to the role of family and caregivers in the development
and wellbeing of a child, beginning in the first 1000 days, with continued eects across the lifespan.
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5.2 Parental and family characteristics
As noted earlier, families have become much more diverse in their structure over the past decades, and many
new family forms have emerged: lesbian mother families; gay father families; families headed by single
mothers by choice; and families created by assisted reproductive technologies such as in vitro fertilisation, egg
donation, sperm donation, embryo donation and surrogacy (Golombok, 2015; Parke, 2013). Concerns have been
expressed about the possible impact of these new family structures on child development, but these have
proven to be unfounded.
The research evidence shows that children in these various new family forms are just as likely as children in
‘traditional’ families to do well or have problems. What matters is not how the family is constituted but the
quality of parenting, the child’s own personal characteristics and, importantly, the social and physical
environment in which they are raised (including societal attitudes). Research shows that the quality of family
relationships and the wider social environment are more influential in a child’s psychological development than
are the number, gender, sexual orientation, or biological relatedness of their parents or the method of their
conception (Golombok, 2015). While it is true that the psychological adjustment of children in single-mother
families are more at risk of psychological problems than are children from homes where the father is present,
this dierence is largely accounted for by factors that often accompany single parenthood, such as economic
hardship, maternal depression and lack of social support, as well as factors that preceded the transition to a
single-parent home, such as parental conflict (Golombok, 2015).
5.2.1 Neurobiology of interpersonal relationships
As noted in the section on Interplay between temperament and environment, temperament-related behaviour
and parenting behaviour influence one another, and are independently associated with child socio-emotional
development. Children’s self-regulatory diculties are more likely to lead to externalising problems when
parents use inconsistent discipline strategies or are low in firm discipline (Bates, Pettit, Dodge, & Ridge, 1998;
Lengua, Wolchik, Sandler, & West, 2000).
The notion that infants with dicult temperaments may be more susceptible to the eects of parenting than
infants with less dicult temperaments is consistent with the larger dierential susceptibility hypothesis,
which proposes that children may dier in the degree to which parenting qualities aect aspects of child
development (Stright, Gallagher, & Kelley, 2008). For example, children who have high levels of fearfulness are
less likely to have internalizing and externalizing problems if their parents are high in warmth and in gentle
discipline strategies (Kochanska, 1997; Sentse et al., 2009).
A child’s development is significantly shaped by the nature of their relationship or attachment with their
primary caregiver during infancy (Benoit, 2004). A consistently responsive and nurturing relationship between
the child and its caregiver encourages a secure attachment and facilitates the development of future
relationships throughout the child’s life, while providing a safe foundation for learning.
5.2.2 Parent-child attachment and parenting style
To learn eectively, children need to feel calm, safe and protected (US Department of Health and Human
Services, 2001). When this attachment process is interrupted, the child’s brain places an emphasis on
developing neuronal pathways that are associated with survival, before those that are essential to future
learning and growth (US Department of Health and Human Services, 2001).
Attachment research during childhood demonstrates that infants are born with a range of attachment
behaviours that seek proximity to and safety in supportive others (attachment figures). In this view, proximity
and safety seeking is a way for the child to maintain or increase its positive feelings and minimise or regulate
its stress feelings and defensive states (Bowlby, 1988).
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Although there are various sub-categories of attachment styles, they can essentially be broken down into two
overarching styles: secure attachment and insecure attachment.
Secure attachment is defined by a sense of attachment security, comfort with closeness and interdependence,
and confidence in support seeking and other positive ways of managing stress. This occurs in infants whose
caregiver(s) respond to their distress in a consistent, caring, and timely manner (e.g. picking up and comforting
the infant). In this instance the infant can feel secure in their knowledge that they can express negative
emotion and prompt a comforting response from the caregiver (Van Ijzendoorn, Schuengel & Bakermans-
Kranenburg 1999). Here, the infant’s strategy for dealing with distress is ‘organised’ and ‘secure’ — they seek
proximity to and maintain contact with the caregiver until they feel safe (Benoit, 2004). A secure attachment is
aligned with enhanced developmental outcomes in later life in areas such as self-reliance, self-ecacy,
empathy, and social competence (Goldberg, 2000).
Insecure attachment arises when caregivers are unavailable, unresponsive or unpredictable in responding to
the child’s needs, proximity seeking fails to relieve distress, and alternative strategies for emotional regulation
(other than proximity seeking) are developed (Mikulincer et al., 2003). Extended separation from the
attachment figure leads to a sequence of reactions: an initial intense activation of the attachment system
(including crying for and searching for the attachment figure); despair and apathy; and detachment (including
avoidance of the caregiver, even on their return). However, despite this apparent lack of concern, infants with
avoidant attachment patterns have been shown to have more physiological arousal than other infants,
indicating that they have learned to supress their distress (Goldberg, 2000). Insecure attachments are often
associated with an increased likelihood of developing social and emotional maladjustment in later life
(Benoit,2004).
Parenting style in the first 1000 days is central to establishing the child’s attachment style (Kochanska, Coy,
Tjebkes, & Husarek, 1998), and therefore overall his/her health and wellbeing outcomes in later life (Waldfogel,
2006). Parenting style relates to the emotional context that caregivers create to communicate with the child
(Rodrigo, Byrne & Rodriguez, 2014).
The three primary parenting styles — aection or warmth; behavioural control; and psychological control — have
each been associated with varying child social and emotional outcomes (Zarra-Nezhad et al., 2014). For
example, warm, responsive and supportive parenting has been shown to promote the development of
children’s emotion regulation and social skills (Hart et al., 2003). Also parental behavioural control (e.g. setting
limits and showing consistency in discipline) has been associated with adaptive child development and low
levels of externalising problem behaviour (Barber, 1996; Hart et al., 2003). However, negative parenting
characteristics, including strictness, neglect, control, punishment, and lack of support will potentially lead to
subsequent child behavioural and emotional problems in later life (Sadiq Sangawi, Adams & Reissland, 2015).
5.2.3 Contribution of fathers/male caregivers
While research on parenting often focuses primarily on the role of mothers or families in general, growing
evidence supports the critical and unique role of fathers/male caregivers14 in early childhood development
(Cabrera, Shannon, Tamis-LeMonda, 2007). A 2008 systematic review found that father engagement positively
impacted social, behavioural, psychological and cognitive outcomes in children (Sarkadi, Kristiansson, Oberklaid
& Bremberg, 2008). Specifically, greater father involvement has been linked to: greater levels of cognitive and
social competence; increased capacity for empathy; positive self-control and self-esteem; better interactions
with siblings; and better academic progress (Wilson & Prior, 2011).
14 In the remainder of this section, fathers will be used to mean fathers and male caregivers.
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Whilst both parents play important roles in the early development of child security and attachment, research
suggests that some influences are more distinct among fathers or mothers. For example, evidence supports
that fathers play a more prominent role in facilitating play exploration which fosters emotional and behavioural
self-regulation, whilst mothers are more likely to provide comfort in times of distress (Lamb, 2002). Moreover,
research indicates that fathers play a distinct (as in dierent to mothers) role in children’s socialisation.
Specifically, fathers who model positive behaviours such as accessibility, engagement and responsibility
contribute to: better psychosocial adjustment; better social competence and maturity; and more positive child/
adolescent-father relationships (Wilson & Prior, 2011).
Conversely, poor father-child relationships and fathering behaviours can have a lasting eect on a child’s social
adjustment and relationships, associated with inferior adult social functioning; significantly reduced likelihood
of secure adjustment; and a significantly greater risk of avoidant or dependent attachment styles (Goodwin &
Styron, 2012). Moreover, poor quality early father-child relationships have been associated with an increased
likelihood of mental health disorders such as depression, bipolar, anxiety disorders and phobias (regardless of
socio-economic status and perceived quality of childhood maternal relationship) in later life (Goodwin &
Styron,2012).
It is evident that a child’s interaction with their caregiver is perhaps the most powerful determinant of their
future health and wellbeing. Regardless of the diversity of family structures, what is most important is the
quality of care that the child receives. This is true for all children, but particularly so for children with
temperaments that make them more susceptible to the eects of parenting. When a child is exposed to
persistent trauma in the first 1000 days, regardless of their temperament, they are significantly more likely to
experience a lifetime of poor health and wellbeing. The evidence for this is discussed in the section below.
5.3 Adverse interpersonal relationships and sustained trauma
While it is clear that positive health and developmental outcomes for children depend on caregiving that is
responsive, warm and consistent, the evidence is equally as clear that unresponsive and harsh or punitive
parenting in the early days is likely to result in adverse health and developmental outcomes throughout the life
course (WHO, 2011; Hertzman & Boyce, 2010; Hart & Rubia, 2012; McLaughlin, Sheridan & Lamber, 2014).
Over the last decades overwhelming evidence has established a strong dose–response (response that varies
based on levels of exposure) between exposure to adverse early experiences such as abuse and neglect, and
increased likelihood of: cognitive and language diculties, lower educational attainment, unemployment,
poverty, homelessness, becoming victims or perpetrators of violence in later life, early mortality, heart disease,
diabetes, liver disease, cancer, depression, anxiety, eating disorders, obesity, and suicide (Liu et al., 2013; Sethi
et al., 2013; Fortin et al., 2014; Hart, Smith, Gruer & Watt, 2010).
5.3.1 Child abuse and neglect: an Australian snapshot
In 2014-15, 1 in 35 Australian children received child protection services, 73 per cent of whom were repeat
clients with at least one previous child protection involvement (AIHW, 2016), highlighting the sustained nature
of abuse and/or neglect in the overwhelming majority of cases. Infants (under the age of one) were the most
likely age group to receive child protection services across Australia, while children who live in the most
disadvantaged areas of Australia (an overwhelming majority of whom are Aboriginal) are also more likely to
receive child protection services than any other cohort (AIHW, 2016).
There has been a consistent increase in the number of notifications and substantiations over the last 5 years,
with a 6 per cent increase in the last 12 months alone (AIHW, 2016). Alarmingly, research shows that these
figures are likely to under-represent the number of child maltreatment (including fatal) incidents (Schnitzer,
Gulino, & Yuan, 2013; Sheldon-Sherman, Wilson, & Smith, 2013).
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5.3.2 Adverse early life experiences and poor lifelong outcomes: the linking
mechanisms
There are three key linking mechanisms through which sustained exposure to abuse and/or neglect increase
the likelihood of ill (physical and mental) health and early mortality:
1. It disrupts the progression of critical developmental processes (namely the stress response and brain
development).
The experience of toxic stress in the first 1000 days can result in significant harm to the body’s stress
response and cause the continuous production of stress hormones (Loman & Gunner, 2010). This ongoing
‘wear and tear’ on the body’s stress response can seriously harm development, and ultimately health and
well-being outcomes, in a number of ways (Centre on the Developing Child, 2012; Cicchetti & Rogosch, 2001;
Andrews & Neises, 2012). Changes to the body’s stress response can increase the risk for physical ill health,
such as asthma, hypertension, heart disease and diabetes (Swanson, Entringer, Buss & Wadhwa, 2009), and
has been linked to depression, anxiety, and disruptive behaviours in later life (Alink, Cicchetti, Kim, & Rogosch,
2012).
Similarly, chronic activation of the stress response can have concurrent adverse impacts on other regulatory
systems, including the immune system. Studies have found that chronic childhood trauma is associated with
excessive immune cell production, which can enhance the production of inflammatory cells, associated with
increased feelings of anxiety (Reichenberg et al., 2001; VanZomeren-Dohm et al., 2013). High levels of
inflammatory cells can also cause damage to the brain by decreasing brain growth, resulting in potential mental
ill health and developmental delays (VanZomeren-Dohm et al., 2013; Andrews & Neises, 2007; Woods et al.,
2005; Reichenberg et al., 2001).
Moreover, areas of the brain that are aected by high levels of immune cells are also involved in the regulation
of anxiety and interpretation of fear responses, fear memories, and the recovery of traumatic memories
(VanZomeren-Dohm et al., 2013). As such, disruptions to brain development during critical periods of
development can lead to a disrupted fear response and ultimately behavioural dysregulation, common in
traumatised children (VanZomeren-Dohm et al., 2013; Yehuda & LeDoux, 2007).
Trauma also impacts the child’s developing brain. As we saw in the section on Synaptic pruning, a child’s brain
architecture can be dramatically disrupted as a result of under-stimulation (due to neglect) and also lead to
epigenetic changes that interrupt the appropriate development of systems that manage the child’s stress
response in later life and can result in increased risk of adult ill health (Szyf, 2009; Bagot et al., 2009; CDCHU,
2016).
2. It impacts the way in which children relate to and interpret the world around them.
Prolonged exposure to neglect and/or abuse can cause a child to become more aware of and sensitive to
stressors in their environment, where stressors become more prominent and/or threatening than they are likely
to be (VanZomeren-Dohm et al., 2013). Research shows that children who are exposed to chronic abuse and/or
neglect become hypervigilant toward perceived environmental threats and are more likely to interpret a neutral
situation as hostile (Pollak & Kistler, 2002; Pollak, Cicchetti, Hornung & Reed, 2000). While the ability to detect
a violent parent’s anger will help the child know when to avoid contact with the parent, making it an adaptive
tactic for survival, studies have shown that threat recognition comes at the expense of other emotions (Pollak
& Kistler, 2002; VanZomeren-Dohm et al., 2013). This is because the disproportionate allocation of attention
and cognitive resources used for threat detection leads to reduction in the ability to process and understand
other emotional states in later life (Pollak et al., 2000).
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The long-term impact of this is significant and includes an increase in the likelihood of engaging in disruptive
social relationships and behaviours in later life (Kim-Spoon, Cicchetti & Rogosch, 2012; VanZomeren-Dohm et
al., 2013). For example, abuse in early childhood has been shown to increase the likelihood of adult criminal
behaviour by 28 per cent and violent crime by 30 per cent (Widom & Maxfield, 2001). This disruption in the
child’s response to stress is also likely to contribute to the development of adverse risk behaviours that lead to
adverse health and well-being outcomes in later life (VanZomeren-Dohm et al., 2013).
3. It is likely to result in the development of negative risk behaviours in later life that lead to an increase in
the likelihood of risk factors that undermine health and well-being outcomes.
The strong correlation between certain lifestyle factors that are known to significantly increase the likelihood
of adult morbidity and mortality (known as health risk behaviours) has been widely established (Fortin et al.,
2014; Hart, Smith, Gruer & Watt, 2010; Anda, Butchart, Felitti &Brown, 2010; Campbell, Rebekah, Walker &
Egede, 2016). Such risk factors relate (but are not limited) to: smoking, obesity, high-risk sexual behaviours,
unintended pregnancy, alcohol and drug abuse, and perpetration of violence (Fortin et al., 2014; The Center on
the Developing Child, 2010).
A significant body of evidence demonstrates that a leading cause of engaging in such adverse health risk
behaviours is sustained exposure to abuse and neglect in early childhood (The National Scientific Council on
the Developing Child, 2010; Felitti et al., 1998; Campbell, Rebekah, Walker & Egede, 2016; Huang et al., 2015;
Ng, Skorupski, Frey & Wolf-Wendel, 2013). In their landmark study, Felitti and colleagues (1998) found that risk
behaviours such as alcohol and drug abuse were used for their immediate physiological or psychological
benefits as a coping device and that when such behaviours were adapted as a coping mechanism, they tended
to be used chronically, further enhancing their negative health impact (Felitti et al., 1998).
The correlation between abuse and neglect in early childhood and adverse health risk behaviours are echoed
by other such studies (Mersky, Topitzes & Reynolds, 2013; Fortin et al., 2014; The National Scientific Council
on the Developing Child, 2010) that have found a significant increase in the number of risk factors as a result
of prolonged exposure to one or more adverse childhood experiences (ACEs). Evidence also shows that
prolonged exposure to traumatic experiences in childhood is associated with increased risk for self-destructive
behaviours such as self-mutilation and suicide attempts (Corcoran et al., 2006; Read et al., 2001; Widom,
1998).
Evidence surrounding the lifelong negative impacts of adverse early life experiences is significant. While
traumatic early life experiences are often the result of abuse and neglect, one of the most influential factors
that increase the likelihood of child abuse and neglect are family and domestic violence. This is discussed in
the sections below.
5.4 Impact of family and domestic violence
Overwhelming evidence supports the correlation between children’s exposure to family and domestic violence
and the increased likelihood of adverse lifelong outcomes (Humphreys, 2008; Margolin & Gordis, 2000; Zeanah
et al., 1999; Mathias, Mertin, & Murray, 1995; Cummings & Davies, 1994). Marshall and Watt (1999) found that
interpersonal conflict was the strongest risk factor for behavioural problems, significantly associated with
externalising and internalising behaviours and social and attention problems, when children were assessed at
the age of five. They also found that more frequent and intense episodes of conflict increased the likelihood of
childhood behavioural problems. But how early in a child’s life is exposure to family conflict and violence likely
to have an impact?
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5.4.1 Domestic violence in pregnancy
Pregnancy is recognised as a period of high risk for the onset or worsening of domestic violence (Taft 2002;
WHO 2000). Pregnant women who are victims of domestic violence are more likely to experience all forms of
violence including physical assault (Catalano, 2013), sexual assault (WHO, 2011) and psychological aggression
(Martin, et al., 2004). Violence during pregnancy can also be more extreme: women who experience domestic
violence during pregnancy are likely to be hit in the abdomen (WHO, 2011); and likely to be hit more frequently
(Martin et al., 2004), posing significant risk of harm to the mother and unborn child.
High levels of maternal stress can also result in an increase in the mother’s cortisol production which can enter
the foetus’s brain via the placenta and the umbilical veins (Sandman et al., 1999). Although the placenta can
inactivate a proportion of maternal cortisol, sustained stress adversely aects the growing brain. Maternal
anxiety during the earlier part of the prenatal period is associated with lower birth weight, shorter gestational
age and smaller infant head circumference at birth, suggesting a decrease in brain growth due to high levels of
prenatal maternal stress (Lou et al., 1994).
Studies have also found a strong correlation between domestic violence during pregnancy and poor emotional
regulation and academic outcomes in school (Durand, Schrailber, Franca-Junior & Barros, 2011); behavioural
problems during infancy (Flach et al., 2011); poor maternal attachment (Quinlavin & Evans, 2005); an increase
in internalising problems from as early as 24 months (McFarlane et al., 2014); and aggressive behaviours at
school (Durand, Schrailber, Franca-Junior & Barros, 2011).
5.4.2 Domestic violence during infancy and early childhood
Research shows that abuse during pregnancy strongly predicts abuse immediately following birth (Huth-Bocks,
Levendosky & Bogat, 2002). One study found that 95% of women who were subjected to violence during
pregnancy were also subjected to violence within the first three months postpartum, with 52% requiring
medical care for injuries sustained as a result of domestic violence (Stewart, 1994).
Witnessing violence can be extremely distressing even for infants. Threats to a caregiver is one of the most
psychologically destructive traumas for children (Scheeringa & Zeanah, 1995). Infants who hear or witness
anger and/or violence, or a parent being hurt can show symptoms of Posttraumatic Stress Disorder (PTSD),
including eating problems, sleep disturbances, lack of typical responses to adults and loss of previously acquired
developmental skills (Bogat et al., 2006, De Bellis & Thomas, 2003, Schore, 2001). Infants and toddlers who
witness adult verbal conflict or violence against a family member, and/or whose mothers experience domestic
violence during pregnancy are also more likely to demonstrate increased externalising behaviours (lower levels
of social competence, diculties with peer relationships, aggressiveness, and disruptive behaviour) in later life
and greater child adjustment diculties (Levendosky et al., 2006; McDonald et al., 2007).
The degree to which domestic violence aects parenting capacity is also likely to influence emotional
outcomes in children exposed to domestic violence (Graham-Bermann & Levendosky, 1998). During times of
distress, an infant will seek the protection and proximity of his caregiver by applying strategies that will gain
the caregiver’s attention. An infant’s ability to self-regulate emotions during times of stress, anger or trauma
can be significantly compromised in the long run if a caregiver does not appropriately respond to this need
(Kaufman & Henrich, 2000).
There is overwhelming evidence that exposure to family and domestic violence during infancy and early
childhood can negatively impact brain development, and ultimately other domains such as emotional regulation
(Carpenter & Stacks 2009; Laing 2000; McIntosh 2003; Perry 2005). The impact of chronic stress and trauma
on the developing brain has been discussed in the section on Adverse interpersonal relationships and
sustained trauma.
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As we have seen, the experiences that a child has within their familial environment, including the quality and
nature of care they receive, and the people and things they are exposed to (as a direct result of their
caregiver’s actions and/or lifestyle) plays a fundamental role in shaping their future health and life outcomes.
However, while quality of care is pivotal to the child’s wellbeing, it is not the only factor that helps shape
future outcomes. The community (including social supports) that a child grows up in and their physical
environment (such as their housing conditions) are also extremely important in shaping their future health
andwellbeing.
5.5 Community environments
Over the past few decades, communities in Australia and other developed nations have been steadily
fragmenting, and people’s sense of community has fragmented also (Barnes, Katz, Korbin & O’Brien, 2006;
Hughes et al., 2007; Leigh, 2010). Nowadays, there may be little sense of community tied to locality,
particularly in larger urban centres. There is also less trust and reciprocity, and more concerns about personal
safety (Leigh, 2010).
There are many reasons for this fragmentation (Blau & Fingerman, 2009; Leigh, 2010). These include a partial
erosion of traditional family and neighbourhood support networks, due to factors such as increased family
mobility and the search for aordable housing. The continued population growth combined with the steady
shift to cities is outstripping the capacity of cities to provide the basic physical and social infrastructure to
support families adequately. But there are also factors such as increases in the speed and ease of transport
and of communication methodologies that have enabled people to have contacts with much more widely
spread social networks and reduced their reliance on people in their immediate neighbourhoods (Hughes et al.,
2007; Leigh, 2010; Wellman, 2001).
These changes in communities are important because both the social and physical environments of a
community are known to have an impact on people’s health and wellbeing (Barnes, Katz, Korbin & O’Brien,
2006; Edwards & Bromfield, 2009; Goldhagen, 2017; Pebley & Sastry, 2004; Pinker, 2015; Popkin, Acs & Smith,
2010; Sustainable Development Commission, 2009). There is evidence that our immediate social networks —
those people we mix with on a regular basis — have a significant influence on our ideas, emotions, health,
relationships, behaviour, and even our politics (Christakis & Fowler, 2009; US Department of Health and Human
Services, 2011). Even ‘consequential strangers’ — people outside our circle of family and close friends, such as
casual acquaintances — are important for personal and community wellbeing (Blau & Fingerman, 2009).
5.5.1 Social supports15
Social supports have a particularly significant role during periods of stress or major life transition.
Social supports during pregnancy
Pregnancy is a time of significant life change and requires significant psychological adjustment and support
(Robles & Kiecolt-Glaser, 2003; Elsenbruch et al., 2007). The perception and experience of insucient support
has a visibly detrimental eect on not only maternal psychological wellbeing, but also adverse health and
wellbeing outcomes for the child (Dibaba et al., 2013; Grote et al., 2010; Dunkel Schetter & Lobel, 2011;
WHO,2009).
15 The terms ‘social supports’, ‘social connections’ and ‘social relationships’ are used interchangeably and refer to three categories of family support:
practical (having someone who can oer a lift, or help look after your child, etc.); emotional (having someone who will listen and provide emotional
comfort and reassurance, particularly during a stressful situation, etc.); and advice and information (having someone to contact who can help and/or
provide advice if the baby is not feeding/sleeping, etc) (McArthur & Winkworth, 2016).
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Experiencing social support during pregnancy reduces the likelihood of maternal stress, depression and risk
taking behaviours during and after pregnancy (Kawachi & Berkman, 2001; Rini et al., 2006; Robles & Kiecolt-
Glaser, 2003;). Social supports during pregnancy can vary based on the mother’s particular needs during her
pregnancy, labour, delivery, and the postpartum period (Gjerdingenm, Froberg & Fontaine, 1991). For example,
informational supports (such as prenatal classes) are associated with reduced physical pain and complications
during labour and delivery (Firouzbakht, Nikpour, Khafri, 2014; Gjerdingenm et al., 1991), while support during
labour and delivery is associated with the shorter duration of labour, less use of pain medications, and fewer
caesarean sections and instrumental deliveries (Hodnett et al., 2011).
Moreover, studies have shown that the level of social supports during pregnancy can impact a woman’s
protective behaviours during this period: A German study by Elsenbruch and colleagues (2007) found that 33
per cent of women who had low social supports smoked during their first trimester of pregnancy compared to
only 17 per cent of women who reported having high social supports (Elsenbruch et al., 2007).
Social supports in infancy
Parental social supports play a significant role in the health and wellbeing of children in a number of ways. It
facilitates the child’s contact with other caring adults and helps build positive attachment relationships, and
plays a significant role in modelling relational skills for children (US Department of Health and Human Services,
2011). Social support also greatly aects parental care-giving capacity by promoting positive mental health
and resilience during challenging periods (Green, Furrer, & McAllistar, 2007; Palamaro et al., 2012).
Importantly, positive social support reduces the likelihood of child maltreatment (Bishop & Leadbeater, 1999):
the risk of child maltreatment increases when parents (particularly those who are experiencing concurrent
vulnerabilities such as poverty, depression, unemployment etc.) have limited social supports (MacLeod &
Nelson, 2000). Finally, social support helps families to access family and/or early intervention services (Kang,
2012). This is in part due to the notion that without adequate social networks, the opportunity to be
‘introduced’ to services may be limited (Winkworth, McArthur, Layton, & Thompson, 2010; Winkworth et al.,
2010).
5.6 Physical environment16
Research continues to demonstrate the direct (cognitive, social, emotional, and biological outcomes) and
indirect (parent’s caregiving capacity) impact of physical environments on children’s development (Evans, 2006;
Evans & Hygge, 2007; Evans & Lepore, 1993).
5.6.1 Housing17
Access to stable and adequate housing is a basic human need (Maslow, 1948). It has a significant impact on
the health and wellbeing of families and children as it provides a safe environment, autonomy, and security
which is needed for full participation in social, educational, economic, and community life (AIHW, 2010; Vic DHS
2006; Wise 2003).
16 Physical environment refers to factors such as housing, access to parks and safe places for play, access to green spaces and natural environments and
level of road trac at the expense of pedestrian safety and comfort.
17 Housing refers to a dwelling that is safe, secure, aordable, and appropriate. It also encompasses issues relating to housing mobility, homelessness,
neighbourhood characteristics, and over-crowding.
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Young children are particularly vulnerable to inadequate housing as they are physiologically more susceptible
to environmental hazards (e.g. mould, allergens and tobacco smoke); spend more time in the home and as such
have more exposure to environmental hazards; are more susceptible to physical features of a home that can
cause injury; and have limited communication abilities and control over their environment (AIHW, 2014).
Research has linked negative home environments during the first 1000 days with a host of developmental
issues, including (but not limited to): inferior language development; behaviour problems; insucient school
readiness; aggression, anxiety and depression; and impaired cognitive development (Evans et al., 2010;
Vernon-Feagans, Garrett-Peters, Willoughby & Mills-Koonce, 2011).
Longer-term eects have also been documented, including (but not limited to): decreased likelihood of high
school graduation; increased likelihood of teen parenthood; increased likelihood of adult unemployment;
decreased income; and higher rates of poverty (Duncan, Ziol-Guest & Kalil, 2010; Pungello et al., 2010).
Aordability
Cost of housing is often the largest and least flexible item in a family budget and low-income households are
particularly vulnerable to housing stress, given that they tend to spend a greater proportion of their income on
housing (AIHW, 2010). An Australian analysis of housing aordability stress (Stone & Reynolds, 2016) found
that rates of stress have been increasing, especially among those living in rental accommodation. Focusing on
children, this study found that 41 per cent of children from two-parent low-income families living in rented
accommodation were experiencing housing aordability stress, a rate that jumps to 67 per cent with single
parent families. While parents can buer their children from the adverse eects of this source of stress, it is
hard to sustain.
High housing costs can aect child wellbeing through the experience of family financial or material hardship
(Harkness & Newman, 2005). Families who allocate a disproportionate amount of their income to housing have
to cut back on other basic needs such as food, clothing, and heating (Lippman, 2005). Lack of aordable
housing can also impact parenting capacity and mental health. Family stress can be related to housing
aordability where housing costs are the main source of economic hardship and/or family conflict (Leventhal &
Newman, 2010). Parents facing financial hardship face an increased risk of chronic stress, depression and
partner conflict, which, in turn, correlates with more inconsistent, unsupportive, and punitive parenting styles
(Leventhal & Newman, 2010). As we have seen, poor quality interactions between parent and child is related
to greater likelihood of poor health and emotional and educational set-backs in later life (Harkness & Newman,
2005; Leventhal & Newman, 2010).
Homelessness
Homelessness may only occur once, may be episodic, or be chronic, however, on any dimension it is
incompatible with a safe and nurturing environment for children (Nooe & Patterson, 2010). Homelessness is a
complex problem that places children at increased risk of long-term poverty, homelessness in adulthood,
unemployment, chronic ill-health, and other forms of disadvantage and social exclusion (AIHW, 2010).
While data on the health and development of homeless children are limited, studies in the Unites States show
that homeless children face a greater risk of experiencing learning, developmental and behavioural problems.
Infants and toddlers may experience delays in physical and mental development (Cooper, 2001; Horn & Jordan,
2007; Hicks-Coolick, Burnside-Eaton & Ardith, 2003). One Australian study of homeless pre-schoolers reported
that about 50 per cent suered significant emotional developmental delays (Dockery et al., 2010).
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Compared with children from low-income households that have never been homeless, children from homeless
families are twice as likely to be hospitalised and make significantly more visits to hospital emergency
departments (Weinreb, Goldberg & Perlo, 1998). A higher incidence of asthma and other respiratory problems,
infectious diseases, trauma related injuries, lead poisoning, chronic diarrhoea, visual and neurological deficits,
delayed immunisations, tooth decay, ear and skin infections, conjunctivitis, and mental health problems and
behavioural disorders have also been found (Cooper, 2001; Karim, Tischler, Gregory & Vostanis, 2006; Weinreb,
Goldberg & Perlo, 1998; Yu, 2008).
Moreover, parents in homeless families are likely to suer from depression and stress which may mean they
are unable to give their children enough attention or aection (AIHW, 2010). The inability of parents to provide
suitable housing can also lead to intervention by child protection agencies and the placement of children in
foster care, which can cause further stress for these children (Dockery et al., 2010). Homeless parents typically
have smaller social networks and higher levels of relationship conflict, accidents and violence (Nooe &
Patterson, 2010). They are also at an increased risk for alcohol and drug dependence, depression,
schizophrenia and suicide (Nooe & Patterson, 2010).
Homelessness also impacts a family’s housing mobility (the frequency housing movement). The absence of a
secure home can make it challenging for a child to establish a sense of identity and can result in diculty for
the child to establish bonds (e.g. friends, parks) that make them feel secure and develop healthy social habits
(Roy, Maynard & Weiss, 2004). Continuous moving may also change social connections by eliminating a family’s
close social networks that provide emotional support and information about the community.
Research shows that renters, particularly those on low incomes, experience higher levels of mobility and that
the negative eects of mobility are magnified with increased moves when changes in schools and residential
mobility are combined (Leventhal & Newman, 2010). Jellyman & Spencer (2010) found an increased likelihood
of behavioural problems in children where the total number of lifetime moves exceeded three (Jellyman &
Spencer, 2008). Unaordable housing can increase chronic mobility, particularly among low-income families,
and homelessness can also eventuate from chronic mobility (Auh, Cook, Crull & Fletcher, 2006).
Dwelling characteristics
Children’s development also depends on the environments in which they live and interact, including the quality
of their environment and the interactions between the child and other people in the environment
(AIHW,2010).
Household income impacts the quality, type and size of housing a family can aord. Often the most aordable
housing is also that of least quality, in terms of both the dwelling and neighbourhood (AIHW, 2010). The
quality of housing can be compromised due to its age, inadequate maintenance, lack of basic amenities and
poor design, and can lead to indoor air quality hazards including mould growth and the presence of toxic
substances such as lead paint or asbestos (Cooper, 2001). Because younger children spend more time inside
the home compared with adolescents, there may be a stronger association between housing quality and
physical health for younger children (Leventhal & Newman 2010).
Exposure to environmental allergens also has strong and critical eects during infancy and early childhood and
respiratory health may be determined by such exposure during the first year of life (Salam et al., 2004). Poor
quality housing is usually situated in lower socioeconomic neighbourhoods and risk factors associated with
these neighbourhoods also contribute to unfavourable child outcomes (Cooper, 2001; Dockery et al., 2010).
Overcrowding
Overcrowding refers to the minimum acceptable living area per person or the average number of people per
dwelling. The adverse eects of overcrowding on children can persist throughout life, impacting future
socioeconomic status and wellbeing; children are also at a greater risk of finding themselves in similar
situations as their parents, leading to the intergenerational transmission of social disparity (Solari &
Mare,2007).
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This is because the lack of space that children experience when living in crowded conditions can negatively
impact their sense of autonomy, social behaviour, health, developmental outcomes, and school performance
(Dockery et al., 2010). It can negatively impact their sleep patterns due to dierent schedules of household
members that can lead to diculty concentrating during the day and negatively aect mood and behaviour
(Solari & Mare, 2007). Children in overcrowded houses are also less likely to have sucient space for play and
may also experience greater risk of abuse due to the greater diculty they face in removing themselves from
potentially volatile situations (Bartlett, 1997). Moreover, when parents have to cope with overcrowding it
impacts their parenting behaviour and can lead to increased conflict between children and parents, as well as
influence marital conflict (Dockery et al., 2010; Evans et al., 1998).
5.6.2 Built environments
Over 90 per cent of Australians live in urban environments (Easthope & Tice, 2011), and neighbourhoods are a
key setting in which children begin their lives. To date, the evidence indicates that the way we design and build
neighbourhoods have a range of personal and social benefits (Goldhagen, 2017), such as promoting healthier
lifestyles and contributing to reducing the risk of non-communicable disease (Sallis, Floyd, Rodríguez & Saelens,
2012; Villanueva et al., 2016). Societal changes over decades have dramatically reduced the need for physical
activity in daily life while creating ubiquitous barriers to physical activity (Sallis et al., 2012). Features of the
built environment that promote healthier lifestyles include easy access to facilities, services, and social
infrastructure, parks and recreational facilities, stores selling fresh produce) (Ulmer, Chapman, Kershaw, &
Campbell, 2014; Villanueva et al., 2016). On the other hand, a poorly designed neighbourhood has less
connected street networks and limited access to shops and services, but an oversupply of fast food restaurants
(Ulmer et al., 2014; Villanueva et al.,2016).
Most of the research on the relationship between the built environment and health has focused onchildren’s
physical activity and obesity, and the impact on child development is less well understood. Nevertheless, it is
plausible that children’s regular physical activity also benefits their cognitive, emotional and psychosocial
development (Villanueva et al., 2016). Moreover, as Ulmer and colleagues (2014) note, at an individual level,
the eect size of built environment interventions is likely to be small, but these benefits are important
because they are experienced by many people, which creates a population-level exposure with sustainable
public health benefits.
5.6.3 Natural environments
Access to nature and green space can have a significant impact on children’s life-long development (Strife &
Downey, 2009; Kellert, 2002; Grineski, 2006). Such access provides children with various cognitive, emotional,
and physical benefits, including (but not limited to): better educational attainment, reduced stress and
aggression, and lower risk of obesity (Faber Taylor & Kuo, 2006; Kellert, 2002; Louv, 2007; Stretesky & Lynch,
2002). Conversely, children’s lack of exposure to nature is linked to a decline in their mental and physical
health (Faber Taylor, Kuo, & Sullivan, 2001; Goldman & Koduru, 2000; Petty, Peacock, Sellens, & Grin, 2005;
Senier, Mayer, Brown, & Morello-Frosh, 2007).
Exposures to nature and environmental factors have a wide range of health and social benefits (Frumkin et al.,
2017). They can even have an impact on a parent’s care-giving capacity, by playing a significant role in coping
with and recovering from stress and mental fatigue (Berto, 2014). Green spaces have also been shown to
increase social interactions between families and children, promoting social trust and community perceptions
of safety (Coley, Sullivan, & Kuo, 1997; Kuo, Bacaicoa, & Sullivan, 1998). Children living in poverty are more
likely to lack access to natural environments as well as to be exposed to environmental hazards (Chakraborty &
Armstrong, 2001; Derezinski, Lacy & Stretesky, 2003; Lester, Allen, & Hill, 2001).
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The community and physical environments that children experience in the first 1000 days shape their later life
outcomes, for better or worse. The level of social supports that a child’s caregiver(s) has access to, drastically
impacts their caregiving capacity; while a child’s physical environments (including the quality and nature of
their housing and the natural environments they can access) have the power to aect multiple and concurrent
health and wellbeing outcomes throughout the lifespan.
Another significant aspect of a child’s physical environment, which has significant consequences, beginning in
the first 1000 days, is the level and nature of environmental toxins in the environment.
5.6.4 Environmental toxins and their eects
Environmental toxins in pregnancy
During the first 1000 days, the brains of infants and children are uniquely sensitive to environmental
neurotoxicants at levels far below those that are known to harm adults (Heyer & Meredith, 2017; International
Scientific Committee of the International Conference on Fetal Programming and Developmental Toxicity, 2007;
Landrigan & Miodovnik, 2011; Miodovnik, 2011; National Research Council, 1993). Early life exposures to toxic
chemicals are important causes of disease and neurodevelopmental disorders (Heyer & Meredith, 2017;
Landrigan & Miodovnik, 2011; Landrigan et al., 2005; Martin & Dombrowski, 2008; Wong et al., 2015; Woodru
et al., 2004), with eects across the lifespan (Landrigan, 2016).
There are tens of thousands of synthetic chemicals currently used in developed nations, although not all of
these are produced in significant quantities (Collaborative on Health and the Environment, 2007; Gray, 2008).
For the majority of these chemicals, there is no toxicological screening data and there is little information on
the potential eects on learning and development. While it is possible that some of these chemicals have
beneficial eects, many do not. At least 200 industrially applied or produced chemicals have been associated
with neurotoxicity in humans, and exposure to these modifying compounds, through consumer products or
environmental pollution, poses serious threats to public health (Heyer & Meredith, 2017). Harmful exposures
can start as early as in utero (Martin & Dombrowski, 2008; Schettler, 2010; WHO, 2017). Because of the
omnipresence of chemicals in our daily life, pregnant women have continuous contact with chemicals in food,
water, air, and consumer products (Wang et al., 2016). Despite the fact that the foetus is carried inside the
mother’s womb, the mother’s chemical body burden is shared with her foetus; many substances easily cross
the placenta and the foetal blood brain barrier to reach the developing brain (Grandjean and Landrigan, 2006;
Wong et al., 2015). As a result, the next generations are born ‘‘pre-polluted’’ owing to these preconception and
pre-birth exposures (Wang et al., 2016). Evidence of these exposures comes from analyses of the umbilical
cords of newborn babies showing they contain an average of two hundred industrial chemicals (Murphy, 2010).
The brains of infants and children are uniquely sensitive to environmental neurotoxicants at levels far below
those that are known to harm adults (Miodovnik, 2011). The foetus’ small size and immature state of
development mean that it is more vulnerable to environmental toxins during the prenatal period than at any
other time in its life (Murphy, 2010). This is because they are exposed to larger doses relative to the body
weight at a time when organ systems are being formed and rapid growth of neurological structures is occurring
(International Scientific Committee of the International Conference on Foetal Programming and Developmental
Toxicity, 2007; Martin & Dombrowski, 2008; Schettler, 2010; Wang, Padula, Sirota & Woodru, 2016).
Exposures to substances such as lead that have minimal or no discernible impacts in adults can permanently
alter brain development and function in a child (Schettler, 2010).
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These chemical exposures, especially during critical and sensitive windows of development such as pregnancy,
can contribute to preterm birth (Burris, Baccarelli, Wright & Wright, 2016) and lead to a myriad of health
consequences that can manifest across individuals’ lifespans and potentially be transmitted to future
generations (Wang et al., 2016). Four underlying mechanisms that produce these adverse outcomes have been
proposed (Heyer & Meredith, 2017): oxidative stress, immune system dysregulation, altered neurotransmission
and thyroid hormone disruption. Based on a review of the evidence regarding a range of environmental toxins,
Heyer and Meredith (2017) estimated the period during which exposure to each toxicant was most likely to
increase the risk of developing neurodevelopmental disorders such as ADHD, autism spectrum disorders, and
schizophrenia. They found that the sensitive time-windows for the majority of toxicants occur between
conception and birth.
Experimental evidence suggests that developmental exposure to persistent organic pollutants (POP) and to
some non-persistent pesticides may disrupt metabolic regulation of glucose metabolism and insulin secretion,
and thereby contribute to the current epidemic of obesity and metabolic disorders (Cummins, 2012; Debost-
Legrand et al., 2016). These chemical pollutants are known as obesogens, and they can cause epigenetic
changes in the embryo, thereby favouring the development of fat cells at the expense of other cell types (such
as bone), making weight increase more likely (Cummins, 2012).
Some commonly encountered chemicals can disrupt the function of hormones and other chemical messengers
that are vital to normal human development and function. Known as endocrine disruptors, these chemicals
interfere with the body’s key signalling pathways and can cause harm, especially during foetal and early life
development (Gore et al., 2015; Schettler, 2010). The Endocrine Society’s most recent Scientific Statement on
Endocrine-Disrupting Chemicals (Gore et al., 2015) explains why such disruption can have long-term eects
ondevelopment:
During embryonic development, organogenesis and tissue dierentiation
proceed through a series of tightly regulated and temporally coordinated
events at the cellular, biochemical, and molecular levels, ultimately resulting in
a functional, mature structure. Development is an Einbahnstrasse (one-way
street), and thus natural substances such as hormones as well as
environmental changes, including exposures to exogenous environmental
chemicals, alter this unidirectional process. These latter perturbations may
impart structural and functional changes that can profoundly deflect the
developmental trajectory, often leading to lifelong phenotypic changes such as
increased endocrine disease propensity.
Chemicals known to have endocrine disruption eects include bisphenol A., phthalates, atrazine,
polychlorinated biphenyls and polybrominated diphenyl ethers (PCBs), and DDT. Other types of chemicals
known to have adverse eects upon development include perfluoroalkyl substances, phenols, pesticides, and
metals (Wang et al., 2016).
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Air pollution
Various types of air pollution are known to have an adverse impact on health, including combustion sources
that include diesel- and gasoline-powered motor vehicles, coal-fired power plants, residential heating, cooking,
and tobacco smoking (Bostrom et al., 2002). Research has tied exposure to trac-related air pollution during
pregnancy to a host of adverse birth outcomes, including premature delivery, low birth weight, and heart
malformations (Currie & Walker, 2011; Perera et al., 2009; Trasande, Malecha & Attina, 2016). Exposure to high
levels of air pollution during pregnancy — particularly during third trimester — can double a woman’s risk of
having a child with autism, with the risk increasing proportionally with exposure to greater amounts of fine
particulate matter in the air (Raz et al., 2015). Perera (2017) argues that the evidence is clear that developing
children, and especially poor children, now bear a disproportionate burden of disease from both environmental
pollution and climate change due to fossil fuel combustion. By sharply reducing our dependence on fossil fuels
we would achieve highly significant health and economic benefits for our children, with both immediate and
long-term benefits (Perera, 2017).
Polycyclic Aromatic Hydrocarbons
Polycyclic Aromatic Hydrocarbons (PAHs) are a group of over 100 dierent chemicals that are formed during
the incomplete burning of coal, oil and gas, garbage, or other organic substances like tobacco or charbroiled
meat. Perera et al. (2006) found that high prenatal exposure to PAHs was associated with lower mental
development at age three, with implications for school performance. In a comparative study between Krakow
(Poland), and New York (USA), Choi et al. (2006) found an adverse reproductive eect of relatively low PAH
concentrations. Given foetal growth impairment has been linked to child developmental and health problems,
the researchers concluded that substantial health benefits would result from global reduction of PAH emissions
(Choi et al., 2006).
Other pollutants
Pollutants under scrutiny include not just PAHs, but other pollutants that are universally present such as
carbon monoxide. One American study found that the infants and young children of women living in areas with
severe air pollution had three times the incidence of heart malformations and valve defects (Ritz et al., 2002).
Another study (Ritz, Wilhelm, Hoggatt, & Ghosh, 2007) found that pregnant women living in areas with high
carbon monoxide or fine particle levels have a risk of preterm birth that is 10 to 25 per cent higher than those
who live in neighbourhoods with cleaner air. It has also been established that rates of asthma are increased in
children exposed to second-hand cigarette smoke and to fine particulate air pollution (Federal Interagency
Forum on Child and Family Statistics, 2010; United States Environmental Protection Agency). Even more
concerning is that risk of respiratory death is increased in infants exposed to fine particulate air pollution
(Woodru, Darrow, & Parker, 2008).
Environmental toxins in infancy
Infants are particularly vulnerable to environmental toxin exposure for several reasons (Heyer & Meredith,
2017; Miodovnik, 2011):
Certain chemicals are shown to accumulate in maternal adipose tissue and breast milk and can be
transmitted by breast feeding (Grandjean and Landrigan, 2006). Children may also undergo higher
contamination levels from environmental pollutants. This is because they have relatively greater energy
demands than adults due to development and therefore, relative to bodyweight they breathe air more
rapidly and are reported to ingest a higher proportion of water, fruit, and vegetables in their diet than
adults based on dietary analysis patterns (Heyer & Meredith, 2017).
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Children are inherently at an increased risk of exposure because they spend more time indoors and
outdoors crawling and playing on the ground, thereby increasing levels of contact with potentially
contaminated dust and soil or toxic residues on toys and other objects. As a result, levels of
environmental toxicants in the blood and brains of babies and young children may be many times higher
than those of adults living in the same environment (Heyer & Meredith, 2017; Miodovnik, 2011).
Children’s metabolic pathways are immature (National Research Council, 1993) and a child ’s ability to
metabolise toxic chemicals is dierent to that of an adult (Atterberry, Burnett, & Chambers, 1997; Pastor,
Sadd & Morello-Frosch, 2002). Children’s early developmental processes are easily disrupted (National
Research Council, 1993). They also have more time than adults to develop chronic diseases. Many
diseases thought to be triggered by toxic chemicals, such as cancer and neurodegenerative diseases, are
now understood to evolve through multistage, multiyear processes that may be initiated by exposures in
infancy (Landrigan et al., 2006).
One of the sources of exposure to environmental toxins is through many new synthetic materials, such as food
packaging, that infants and children come in contact with (Landrigan & Goldman, 2011).
Food packaging
Chemicals used in the packaging, storage, and processing of foodstus may harm health over the long term
(Muncke, Myers, Scheringer, and Porta, 2014). This is because most of these substances are not inert and can
leach into the foods we eat. People who eat packaged or processed foods are likely to be chronically exposed
to low levels of these substances throughout their lives (Muncke et al., 2014).
Constant exposure to an estimated 4000 ‘food contact materials’ in food packaging is common for most people
in modern society (Cribb, 2014). These materials are a significant source of chemical food contamination,
although current testing methods do not cover the risks which this low-level, lifelong exposure may cause, and
therefore legally they are not considered as contaminates (Cribb, 2014). Understanding the immediate and
long-term impacts of these exposures is essential to the prevention of chronic disease (Muncke, Myers,
Scheringer, & Porta, 2014).
One of the conclusions to be drawn from this brief review of the evidence regarding the impact of environmental
toxins on development concerns the importance of the timing of the exposures. As stated by the International
Scientific Committee of the International Conference on Foetal Programming and Developmental Toxicity (2007),
Research into the environmental influence on developmental programming of
health and disease has therefore led to a new paradigm of toxicologic
understanding. The old paradigm, developed over four centuries ago by
Paracelsus, was that “the dose makes the poison”. However, for exposures
sustained during early development, the most important issue is that “the
timing makes the poison”. This extended paradigm deserves wide attention to
protect the foetus and child against preventable hazards.
This call for prevention has been echoed by others (Haugen, Schug, Collman & Heindel, 2015; Heyer & Meredith,
2017; Landrigan & Goldman, 2011). Given the mounting evidence of the eects of environmental exposures in
the first 1000 days, Haugen and colleagues (2015) argue that the DOHaD paradigm should be expanded from
its historical focus on nutrition to include environmental exposures to chemicals. The adverse eects of
exposure to environmental toxins are preventable if the eects are recognised and appropriate action taken
(Landrigan & Goldman, 2011). A notable example of this in Australia was the removal of lead from petrol.
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5.7 Summary
A child’s temperament, the quality of care they receive and the relationships they experience, the communities
in which they reside, and the physical environments which they occupy, all have significant and lifelong
consequences on the quality of their health and wellbeing.
The biological foundation of a temperamental bias (a bias towards certain temperamental characteristics) is
usually, but not always, genetic (Kagan, 2012). In some cases it is the result of severe stress or infection in the
pregnant mother which aects the foetus.
While a child’s temperament is shaped by genetic susceptibilities, the development of temperamental traits are
greatly influenced—for better and for worse—by their environmental experiences. However, some children are
more influenced by their environmental conditions than others due to the presence (or absence) of specific
genetic characteristics. This is known as dierential susceptibility. Children with such ‘risk’ genes are thought
to be disproportionately aected by poor rearing influences, while more likely to thrive in highly
supportiveenvironments.
The quality of a child’s interpersonal relationships in the first 1000 days plays the most significant role in
shaping a child’s lifelong outcomes. While there is no evidence to suggest that the structure of a child’s family
(e.g. whether they are raised by same-sex parents) impacts future health and wellbeing, the quality of their
relationships, and attachment with their caregiver is of upmost importance. Infants seek proximity to, and safety
in their caregiver as a way of maintaining or increasing their positive feelings and minimising or regulating their
stress states. An interrupted attachment process means that the child’s brain places an emphasis on developing
neuronal pathways that are associated with survival, before those that are essential to learning and growth.
Parenting style in the first 1000 days is central to a child’s attachment style. The most positive parenting style
is one that is characterised by responsiveness, warmth, sensitivity, acceptance, predictability, consistency and
a lack of harsh, punitive forms of discipline.
Evidence also supports the unique role of male caregivers in early childhood development: associated with
positive social, emotional and cognitive developmental outcomes. Conversely, poor father-child relationships
and fathering behaviours can have lasting eects on areas such as social adjustment and increase likelihood of
mental ill health in later life.
When positive and secure attachments are not created, and the child is exposed to significant and persistent
adverse experiences, this is likely to result in poor health and development outcomes throughout the life
course. There are three key reasons for this:
1. Trauma disrupts the progression of critical developmental processes (namely the stress response and
brain development).
2. Trauma impacts the way in which children relate to and interpret the world around them.
3. Trauma is likely to result in the development of negative risk behaviours in later life that significantly
increase the likelihood of adult morbidity and mortality.
A child’s exposure to domestic violence is one primary way that trauma can take place. Domestic violence
during pregnancy poses significant risk of harm to the mother and unborn child, while exposure after birth can
be extremely distressing for an infant and negatively impact brain development and regulatory systems.
Domestic violence also significantly impacts a parent’s caregiving capacity.
A caregiver’s sense of community and access to social supports can also impact child development, as they
greatly impact a parent’s caregiving capacity. Social support during pregnancy reduces the likelihood of
maternal stress, depression and risk taking behaviours during and after pregnancy, and decreases the risk of
child maltreatment after birth.
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The child’s physical environment is also significant to their lifelong health and wellbeing. The most obvious of
these is housing, as children are particularly vulnerable to inadequate housing (the structural quality of the
house, housing aordability, homelessness and continued housing mobility). For example, lack of appropriate
housing impacts a caregiver’s mental health, which in turn impacts their caregiving capacity; while
overcrowding can negatively impact their sleep patterns and also put them at greater risk of abuse.
Access to nature and green space can also significantly impact a children’s development, by providing (or
denying) them the opportunity to access spaces that are conducive to thriving cognitive, emotional, and
physical development. Children living in poverty are more likely to lack access to natural environments as well
as to be exposed to environmental hazards.
The presence of environmental toxins during and after pregnancy grossly impact a child’s health and wellbeing.
Infants and children are more vulnerable to environmental toxins because they are exposed to larger doses
relative to the body weight at a time when organ systems are being formed, and can permanently alter brain
development and function in a child. Toxins such as air pollutants, carbon monoxide and even food packaging
can be damaging to the child’s developing organ systems.
~ ~ ~
While we have thus far reviewed the evidence surrounding the biological, child, family, community and
environmental factors that shape health and development in the first 1000 days, the following section
examines some of the most influential individual level factors of child health and development.
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6. Individual level factors influencing
child health and development
6.1 Nutrition
There is now clear evidence that early life nutrition in the foetus, infant and young child can have profound
eects on long-term health (Davies et al., 2016a, 2016b). From preconception to adulthood, our dietary intake
has the ability to shape the individual or population health trajectories for better or worse (Gluckman et al.,
2011; Langley-Evans & McMullen, 2010). Over the past decades, research has shown that good nutrition is
central to optimal health and development outcomes and disease prevention. Conversely, excessive intake of
energy or insucient intake of protective nutrients, especially during critical periods of development, is
associated with poor health and contributes to health disparities (Herman, Taylor Baer, Adams et al., 2014).
The presence or lack of good nutritional status of the mother and/or child is a critical factor in ‘programming’
the child for healthy development and positive long-term health and wellbeing outcomes. Foetal and early-life
nutrition has been linked to setting the risk for conditions such as coronary heart disease, Type-2 diabetes,
osteoporosis, asthma, lung disease and some forms of cancer (British Medical Association, 2009).
6.1.1 Nutrition in preconception and pregnancy
It is now well established that maternal nutrition can aect the ospring’s epigenetic state and have lifelong
eects on: the child’s mental health (Sarris et al., 2015 & Jacka et al., 2013); food/flavour preferences
(Gugushe, Ong & Muhlhausler, 2011; Vucetic et al., 2010); satiety, muscle mass and insulin resistance (Low et
al., 2012; Vaiserman, 2014). This is because the foetus uses nutritional input from its mother to anticipate the
kind of nutritional world it will be born into, and adjusts its phenotype accordingly (Moore et al., 2014a). This
was discussed in section 2.3.2 (the Mismatch hypothesis).
Research shows that the developmental induction of risks in an obesogenic environment (environmental
influences that promote obesity) is considerably influenced by maternal nutritional status at conception, during
pregnancy, and during weaning (Low et al., 2012). Women who are overweight or obese before pregnancy are
at greater risk of developing hypertensive disorders such as pre-eclampsia during pregnancy, and giving birth
to larger infants who are at increased risk of developing obesity in later life (World Health Organization, 2010).
Overweight and obesity can also increase the risk of stillbirth, dicult delivery, haemorrhage and birth defects
(Arabin & Stupin, 2014).
Weight gain during pregnancy can also aect the immediate and future health of infants: while excessive
gestational weight gain can increase birth weight and postpartum weight retention, inadequate gestational
weight gain can increase the likelihood of poor foetal development (Siega-Riz et al., 2009; ACOG Committee
opinion, 2013).
Increasing evidence is also pointing toward a relationship between paternal obesity and adverse health
outcomes in the ospring (McPherson, Fullston, Aitken & Lane, 2014). Paternal obesity impairs sex hormones,
basic sperm function, and molecular composition (Ng et al., 2010; Sermondade et al., 2013) which results in
disturbed embryo development and health, and an increased subsequent ospring disease burden (Fariello et
al., 2012; Ribas-Maynou et al., 2012). However, some studies have shown that the reversibility of obesity-
induced parental programming may be possible with diet and exercise interventions (Chen, Gong, & Xu, 2013;
Ibrahim et al., 2012; Saez Lancellotti et al., 2013; Stephens & Polotsky, 2013).
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6.1.2 Nutrition in infancy
The speed of postnatal growth is at its highest during infancy — a time when the infant is entirely dependent
on others to meet its nutrient needs (Robinson, 2015). Inadequate nutrition and restriction of growth during
this period can result in permanent stunting (Scientific Advisory Committee on Nutrition, 2011) in addition to
having potential for lifelong deficits in neurological functioning (Innis, 2014). Excessive and rapid weight gain
in infancy, however, is also a concern and has been linked to obesity in later life, as well as a number of risk
factors for cardiovascular disease (Brands, Demmelmair & Koletzko, 2014 ; Weng et al., 2012).
Exclusive breastfeeding has been shown to at least modestly protect against excessive early infant gain and
later obesity, an eect that may result from dierences in composition of weight gain between breast-fed and
formula-fed infants (Young et al., 2012). Moreover, the method of infant feeding (i.e. suckled directly at the
breast or via a bottle) can also aect infant growth patterns. When feeding at the breast, the pace and volume
of intake are controlled by the infant, but the caregiver maintains more control when bottle feeding (Crow,
Fawcett, & Wright, 1980). Infants fed from a bottle (vs. fed at the breast) consume more milk, protein, and
energy (Heinig et al, 1993; Isomura et al., 2011; Sievers, Oldigs, Santer, & Schaub, 2002), potentially resulting
in greater weight gain (Dewey et al., 1993; Haisma et al., 2003; Heinig et al., 1993). Removing control from the
infant may also impact the infant’s ability to interpret satiety cues and self-regulate food intake accordingly
(Dewey & Lonnerdal, 1986; Disantis, Collins, Fisher, & Davey, 2011; Li, Fein, & Grummer-Strawn, 2010;
Matheny, Birch, & Picciano, 1990). These mechanisms are thought to occur regardless of what is in the bottle
(i.e., breastmilk vs. formula).
Duration of breastfeeding
Research suggests that the initiation and duration of breastfeeding during infancy can also influence obesity
in later life (Stettler, Zemel, Kumanyika, & Stallings, 2002). A longer duration of breastfeeding has been
associated with decreased likelihood of obesity in later life (Harder, Bergmann, Kallischnigg, & Plagemann,
2005). Harder et al. (2005) found that the risk of obesity was reduced by 4 per cent for each month of
breastfeeding, with this eect lasting up to a duration of breastfeeding of 9 months. Breast milk has also been
found to decrease the likelihood of developing allergies in later life as it contains many immune factors
(Prescott, 2011) and substances that promote favourable colonisation of the gut with friendly bacteria.
(Prescott, 2011).
Introduction of complementary foods and drinks
Complementary feeding commences when breast milk alone is no longer sucient to meet the nutritional
requirements of infants, and other foods and liquids are needed, along with breast milk (WHO, 2016). The
timely introduction of appropriate complementary foods are critical in ensuring optimal growth and wellbeing
(UNICEF Innocenti Research Centre, 2005). If complementary foods or drinks are introduced too early or are not
given safely in the correct quantity at the optimum time, growth rates can falter dramatically and lead to
growth restriction and even stunting — associated with an under-developed brain (Michaelsen, Weaver, Branca
& Robertson, 2010).
Complementary foods are often introduced at approximately 6 months of age, although some infants may need
complementary foods earlier, but not before 4 months of age (Michaelsen et al., 2010). Complementary feeding
should be a process of introducing foods, while maintaining breastfeeding. Highly salted foods should not be
given during the complementary feeding period, nor should salt be added to food during this period
(Michaelsen et al., 2010).
Evidence shows that obesity, diabetes, cardiovascular morbidity, and neuropsychiatric diseases can all be
considered paediatric diseases. As such, disease prevention must start with improved nutrition (and reduced
exposure to environmental chemicals) during development.
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Davies and colleagues (2016) show that there are now significant data to support the hypothesis that early
life nutrition in the foetus, infant and young child can have profound eects on long-term health. As the
findings of further research become available, recommendations on optimizing early life nutrition should be
formulated and made widely available as part of the preventative health policy agenda in Australia.
The other two primary individual level factors that significantly impact health and development in the first
1000 days, and beyond, are substance use and significant maternal stress. Evidence surrounding these are
discussed in the below sections.
6.2 Substance use
6.2.1 Alcohol
Exposure to alcohol in the uterus is the leading cause of cognitive impairment and neurodevelopmental
disorders (Centers for Disease Control and Prevention, 2002; Eustace, Kang, & Coombs, 2003), and the most
common preventable cause of birth defects. Although the risk of birth defects increases with frequent
maternal alcohol intake, alcohol exposure throughout pregnancy and before pregnancy is confirmed to have
detrimental consequences for foetal brain development and growth and increases the likelihood of pre-term
delivery and physical malformations (AIHW, 2016).
According to the 2013 National Drug Strategy Household Survey, 49 per cent of Australian women did not
consume alcohol while pregnant, but over 50 per cent of pregnant women consumed alcohol before they knew
they were pregnant, and 25 percent continued to drink even after they knew they were pregnant (AIHW,
2013).
Foetal alcohol spectrum disorder (FASD)
The eects of alcohol on the embryo or foetus produce a spectrum of disorders that aect physical, learning
and behavioural outcomes (Abel, 2012; Burd, Cotsonas-Hassler, Marsolf, & Kerbeshian, 2003). The range of
eects is collectively termed ‘foetal alcohol spectrum disorder’ (FASD) and can include abnormalities in the
formation of the face, intellectual and learning disabilities, deficits in executive functioning, memory problems,
speech and language delays, inattention, hyperactivity, internalising and externalising behavioural problems,
and social impairments that remain apparent to varying degrees throughout life (Coles et al., 1997; Jacobson &
Jacobson, 2002; Kingsbury & Tudehope, 2006). In adults, FASD is associated with high rates of mental health
problems, alcohol and other drug misuse, and inappropriate sexual behaviour (Streissguth et al. 2004).
Studies show that overall, lower levels of alcohol are needed to produce behavioural anomalies than are
needed to produce physical eects, and some brain regions are more susceptible to alcohol than other regions
(Randall, 2001). Scanning of the brains of children with prenatal alcohol exposure has showed increased
incidence of abnormalities in areas of the brain that are responsible for motor movement learning, behaviours,
cognition and emotional regulation (Mattson & Riley, 1998; Mattson, Schoenfeld, & Riley, 2001). FASD is known
to be under-recognised in Australia, and eorts have been made to develop criteria that can help with early
identification (Watkins et al., 2014).
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Threshold for risk
There is inconsistent data about the eect of social (i.e. ‘light’) alcohol consumption on pregnancy outcomes
(Kalter, 2003). However, based on available research evidence, it cannot be stated that light drinking in
pregnancy has been established to be safe. In particular, any messages implying that light drinking might be
safe should not be disseminated without also providing a threshold or cut-o above which there is an increase
in risk (Sayal, 2009). Safe recommendations should focus not just on the average amount of alcohol consumed,
but also on patterns of consumption. Patterns more accurately reflect blood alcohol levels, as problems may
develop even at low levels of alcohol consumption if binge drinking takes place and high blood alcohol levels
are present in the critical phases of foetal development (Goransson et al., 2003).
6.2.2 Illicit drugs and other psychoactive substances
Illicit drugs and other psychoactive substances in pregnancy
The adverse eects of substance abuse can be considerable, and include premature birth, foetal distress,
physical and/or mental retardation, birth defects and withdrawal symptoms upon birth (Russell 1995).
Treatment resulting in separation could also have implications for infant–maternal attachment (Love &
Tsantefski, 2006). In the longer term, the eects of in utero exposure to drugs and alcohol include (but are not
limited to) increased risk of sudden infant death syndrome (SIDS), impulsivity, learning disabilities, antisocial
behaviour and neurological deficits (Dore, Doris and Wright 1995).
The illicit nature of much substance use makes it dicult to establish the prevalence of substance use in
pregnancy. However, Australian (Thomas, 1988) and international (Goode, 2000; McElhatton, 2000; Scully et
al., 2004; Marcellus, 2002; Greenfield, Manwani, & Nargiso, 2003) research indicates that drug use in
pregnancy is a serious and rapidly growing social problem (Love & Tsantefski, 2006). Consistent with
international research, Victorian maternity units have recorded steadily increasing rates of substance use in
pregnancy (Murphy, 2000). As these reports are based on self-disclosure of substance use, they are likely to
underestimate prevalence (Love & Tsantefski, 2006).
Australian research (Swift, Copeland, & Hall, 1996) has also shown that of the women seeking treatment for
substance dependence, approximately half are mothers, and most are using two or more drugs at, or near, the
same time. These women also had a range of other co-occurring physical and psychological health concerns
such as hepatitis, eating disorders and suicide attempts (Swift et al., 1996), and reported higher rates of
negative childhood experiences, psychological distress, lower levels of perceived social support, homelessness
and domestic violence (Harmer, Sanderson, & Mertin, 1999).
Illicit drugs and other psychoactive substances in infancy
It is well established that children who are raised in families with parental substance misuse often have poor
developmental outcomes (Dawe, Harnett, & Frye, 2008). However, parental substance abuse often co-exists
with other risk factors (such as domestic violence, low income, and transience) and it is the sum of these
various influences that determines the child’s lifelong outcomes (Dawe et al., 2008).
While it is dicult to obtain accurate data, it has been estimated that approximately 13 per cent of Australian
children aged 12 years or less are exposed to an adult who is a regular binge drinker (Dawe et al., 2008).
Additionally, just over 2.3 per cent of children aged 12 years or under are estimated to be living in a household
containing at least one daily cannabis user and 0.8 per cent are estimated to be living with an adult who used
methamphetamine at least monthly. However, these figures are widely acknowledged to be underestimated,
given the self-reporting nature of data collection (Dawe et al., 2008).
Substance misuse by parents of very young children can compromise parental care in several ways, including
intoxication, drowsiness and impaired attention, withdrawal symptoms, and engaging in illegal and
dangerousactivities.
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When a parent is intoxicated, their ability to provide adequate care and protection to an infant is significantly
compromised: intoxication will severely impair a parent’s ability to provide a regular routine, clean environment
(Dawe et al., 2008) and be responsive and sensitive to a child’s emotional and developmental needs.
Substances that result in a state of extreme drowsiness and impaired concentration and attention, such as
alcohol and heroin, clearly impact parental supervision, increasing risk of injury, neglect or harm by others.
Regular use of substances such as amphetamines are also associated with a state of agitation, psychosis,
restlessness and impaired judgement (Dawe et al., 2008). These states are clearly incompatible with sensitive
and responsive parenting and may indeed increase the risk of neglect and abuse (Dawe et al., 2008).
A parent who is dependent on a substance will experience withdrawal symptoms when they are unable to use.
While the experience of withdrawal varies across substance classes, such a physical state has the potential to
impair the parent’s ability to focus on the needs of their child over their own immediate physical and
psychological distress (Dawe et al., 2008).
Illicit drugs such as opioids and amphetamine-type substances often require engagement in a range of illegal
activities, such as theft or prostitution, in order to support the habit (Dawe et al., 2008). The use of these
substances also comes with risks of exposure to injecting and other paraphernalia, association with other
adults who use substances and, for some children, exposure to a physically dangerous environment when
substances are being manufactured and/or not safely disposed. Child death reviews conducted by the Victorian
Child Death Review Committee have consistently noted the high prevalence of parental substance misuse
among deaths of infants known to the Victorian Child Protection Service (Victorian Child Death Review
Committee, 2012).
Besides compromising parental care in various ways, alcohol or drug misuse can also increase the likelihood of
child maltreatment by increasing the risk of violent tendencies (Flanzer 1993). Drugs such as crack, cocaine,
heroin, LSD and marijuana have been proposed as direct causal factors that ‘reduce inhibitions, unleash violent
tendencies, and/or directly elicit violent behaviour’ (Gelles 1993, p.183). Research shows that drugs (and
alcohol) can lower the inhibitions that keep people from acting upon physically or sexually violent impulses
(Araji & Finkelhor 1986). Furthermore, frustration tolerance may be lowered by alcohol or drugs, leaving a
parent more likely to physically abuse a child when under their influence. Substance abuse may also diminish
any shame or guilt a perpetrator feels after maltreating a child (Hayes & Emsho 1993). The failure to
experience negative emotions or inhibitors may perpetuate maltreatment as it minimises the negative
consequences for the oender following an assault.
Co-morbidity
Over 50 per cent of heroin users, 20 per cent of amphetamine users, 16.5 per cent of cannabis users and 11
per cent of high-risk alcohol users reported diagnosis or treatment for mental illness in the past 12 months
(Australian Institute of Health and Welfare, 2005, p. 99). When women are considered separately from men, the
rates of co-morbid conditions are even higher, including trauma-related conditions (Conners et al., 2003;
Najavitis, Weiss, & Shaw, 1997). Moreover, many families with parental substance abuse also experience low
income/poverty, report high rates of unemployment, have unstable accommodation, and experience social
isolation (Conners et al., 2003; Powis, Gossop, Bury, Payne, & Griths, 2000), compounding the eects of
parental substance misuse.
Social isolation is a key feature of the lives of families with parental substance abuse. Typically, women with
substance misuse problems feel unable to attend a range of community activities that are often the building
blocks of community connectedness and support. Parents who have limited social support and live socially
isolated lives are at greater risk for poor parenting practices. This is especially the case when these problems
are further compounded by other risk factors, such as parental mental health problems and
socioeconomicdisadvantage.
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6.2.3 Toba c co
There is conclusive evidence that smoking causes compromised fertility, and that parental smoking potentially
has long-term and serious consequences for child health (Mitchell, Devlin, & Mannes, 2006). In 2010, 11.7% of
pregnant women smoked before knowing they were pregnant, while 7.7% reported that they smoked after
they knew they were pregnant. However, underreporting of smoking during pregnancy is a common practice,
given the social stigma associated with smoking during pregnancy. High rates of underreporting have been
reported in intervention trials (Mitchell et al., 2006).The likelihood of smoking during pregnancy was higher
among teenagers, women in disadvantaged circumstances and Aboriginal women (Laws, Li, & Sullivan, 2010).
Smoking in pregnancy
Within minutes of inhalation of tobacco smoke, wherever the blood flows, many of the more than 4000
chemicals from tobacco smoke also rapidly flow (US Department of Health and Human Services, 2004). Nicotine
induces the narrowing of the blood vessels, which aects the function of the placenta, restricting blood flow
and reducing the supply of nutrients and oxygen to the foetus (US Department of Health and Human Services,
2004). There is growing evidence that smoking during pregnancy aects the normal development of the brain
systems that regulate oxygen uptake and heart function, increasing the risk of stillbirth, neonatal death and
SIDS (British Medical Association, 2004). Blood vessel constriction and high levels of carbon monoxide in the
blood caused by smoking may induce hypoxia (oxygen deficiency), which has been implicated in placental
abruption. Hypoxia can also result in the enlargement of the placenta, causing it to extend over the cervix, as
seen in placenta praevia. Smoking during pregnancy has also been linked to the development of childhood
obesity (Oken, Levitan & Gillman, 2008).
Dose-response relationships exist between maternal smoking during pregnancy and stress or abstinence signs
in the baby, including central nervous system visual stress and greater excitability (Law et al., 2003). These
findings may indicate neonatal withdrawal from nicotine. Another study (Godding et al., 2004) found
neurotoxic eects of maternal smoking in pregnancy, impacting a newborn’s neurobehavioral outcomes, such
as childhood learning disabilities.
Whether eective pharmacotherapies such as nicotine replacement therapy (NRT) are safe to use in pregnancy
is still unknown. Nicotine itself has the potential to disturb the development of the embryo or foetus and there
is no known safe level of nicotine that can be administered during pregnancy. Given that the ratio of potential
benefit to harm is not conclusive, most recommendations are to consider pharmacotherapy only after
psychosocial intervention has failed (Fiore and the Clinical Practice Guideline Treating Tobacco Use and
Dependence 2008 Update Panel, 2008; Melvin et al, 2000).
Exposure to environmental tobacco smoke (ETS) or passive smoking during pregnancy is associated with a
wide range of complications during gestation as well as in the perinatal and neonatal periods. Specifically,
there is a high risk for preterm, low birth weight, small for gestational age infants, as well as for sudden infant
death syndrome (Simón et al., 2017). Simón and colleagues (2017) studied the eect of the progressive
introduction of smoke-free legislation in Spain, and found that even partial smoking bans resulted in reductions
in preterm birth rates and low birth weight, with even greater reductions following the reduction of
comprehensive bans (Collaco, Wilson & McGrath-Morrow, 2017).
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Smoking in infancy
Exposure to environmental tobacco smoke (ETS) during infancy and childhood has also been associated with
slower rates of growth in lung function and increased risk of asthma, middle ear disease and respiratory
disease (British Medical Association, 2004). Some studies have found that compared to children of non-
smokers, the children of smokers have a poorer performance at school, with lower scores in cognitive tests and
greater likelihood of behavioural problems, including hyperactivity and shorter attention spans (British Medical
Association, 2004). Exposure to environmental tobacco smoke (ETS) or passive smoking may also influence
breastfeeding, with non-smoking women who are exposed to ETS stopping breastfeeding sooner than those
who are not exposed (British Medical Association, 2004).
Nicotine distributes rapidly to and from breast milk. As maternal plasma nicotine concentration rises and falls,
breast milk concentration also rises and falls. The mean elimination half-life of nicotine in breast milk is 95
minutes (Dempsey and Benowitz 2001). Mothers who smoke are less likely to start breastfeeding their babies
than non-smoking mothers, and tend to breastfeed for a shorter time. Breast milk production is also lower in
smokers than in non-smokers. In breastfeeding mothers who smoke, milk output is reduced by more than 250
mL/day compared with non-smoking mothers.
6.3 Stress
Researchers have consist ently found that various types of chronic stress are linked to — and probably cause
— shorter telomeres (Blackburn & Epel, 2012). Telomere short ness and stress have independently been
associated with several common conditions, such as cardiovascular disease and diabetes. These associations
are so widespread and consistent that even without a detailed understanding of the biochemical pathways
involved, the message is clear. Failure to alleviate severe stress caused by prolonged threats such as violence,
financial hardship, abuse and emotional neglect, particularly in children, will result in exponentially higher costs
further down the line — personal, economic and otherwise.
6.3.1 Stress in pregnancy
As discussed, the prenatal period is a time of rapid change and extreme vulnerability for the foetus. It is during
this period that the foetus is described as being in a state of ‘programming’: the process by which an event or
insult during a sensitive developmental period has a long-lasting or permanent influence. The eects of
programming depend on the timing of the exposure and on the developmental stage of organ systems. One
primary risk factor for health outcomes resulting from foetal programming is prenatal exposure to maternal
stress (Davis & Sandman, 2010).
During pregnancy, maternal stress impacts the foetal nervous system and reduces foetal growth and length of
gestation. High levels of maternal anxiety are significantly associated with increased risk of intrauterine
growth restriction (Ding et al., 2014; Grote et al., 2010). Poor growth in utero is a major risk factor for a number
of subsequent health problems in the child’s later years, being linked to conditions such as heart disease,
hypertension, and low birth weight, which increases the risk of developing conditions such as obesity and
diabetes (Massin, Withofs, Maeyns, & Ravet, 2001; Shankaran, Das, & Bauer, 2006). Maternal stress levels are
also associated with poorer birth outcomes, including preterm delivery, lower birth weight and gestational age,
smaller head circumference, and poorer neurological scores at birth (Dole et al., 2003; Glover & O’Connor, 2006;
Glynn, Dunkel Schetter, Hobel, & Sandman, 2008; Glynn, Wadhwa, Dunkel Schetter, & Sandman, 2001; Hobel &
Culhane, 2003).
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Similarly, a growing body of evidence has revealed that maternal gestation stress can negatively impact a
range of health and developmental outcomes in infancy and early childhood (Monk, 2001; Ruiz & Avant, 2005;
Talge, Neal, & Glover, 2007; Tegetho et al., 2011, Greene, Olsen, Schaner, & Meinlschmidt, 2011). These
include cognitive development, language development, behavioural and emotional development, and physical
and neuromuscular maturation.
Cognitive and language development. There is evidence that maternal elevated stress and anxiety during
pregnancy is associated with delayed infant cognitive development (Brouwers, van Baar, & Pop, 2001;
Buitelaar et. al., 2003; Glover & O’Connor, 2006; Huizink et al., 2003; Sandman, Davis, Buss, & Glynn, 2012) and
that this may persist well into adolescence (Mennes, Stiers, Lagae, & Van den Bergh, 2006). Maternal
gestational stress, particularly in early pregnancy, has also been linked to lower language outcomes in infancy
and early childhood (Henrichs et al., 2011; Laplante et al., 2004).
Behavioural and emotional development. A growing body of research indicates a correlation between maternal
stress and child emotional and behavioural problems after birth (de Weerth, van Hees, & Buitelaar, 2003; Glover
& O’Connor, 2006; O’Connor, Heron, Golding & Glover, 2003; Robinson et al., 2008; Sandman et al., 2012). For
example, Robinson et al. (2008) found that the experience of multiple stress events in pregnancy was
predictive of clinically significant levels of behavioural problems in the pre-school years after adjustment for
multiple other risk factors. These eects were equally balanced across internalising and externalising
symptoms. These eects can be very long-lasting. Epigenetic changes (facilitated in utero) relating specifically
to the regulation of stress hormones have been found in adult children of parents with PTSD or other stress-
related disorders (Yehuda et al., 2015).
Physical and neuromuscular maturation. Maternal stress in pregnancy also has an impact on children’s physical
and neuromuscular maturation (Buitelaar et al., 2003; Ellman et al., 2008; Grace, Bulsara, Robinson & Hands,
2016; Huizink et al., 2003; Sandman et al., 2012). Stress has an accumulative eect on the developing foetal
motor system, especially in late pregnancy when the cerebellar cortex (the area of the brain responsible for
regulating motor movements) is growing most rapidly. The negative eects of maternal gestational stress on
ospring motor development becomes more evident as the child becomes older (Grace et al., 2016). The
continued growth of the neurological systems throughout the first decade (Gramsbergen, 2003) may explain
why the full impact on these systems is not evident until after puberty.
6.4 Summary
The most significant individual level factors in the first 1000 days which influence child health and
development relate to nutrition, substance use and the experience of significant stress.
The presence or lack of good nutritional status of the mother and/or child is a critical factor in ‘programming’
the child for healthy development and positive long-term health and wellbeing outcomes. Women who are
overweight or obese before pregnancy are at greater risk of complications during pregnancy, and giving birth to
larger infants, who are at increased risk of developing obesity in later life. While excessive weight gain during
pregnancy can also increase birth weight, inadequate gestational weight gain can increase the likelihood of
poor foetal development.
After birth, factors such as excessive and rapid weight gain (and inadequate sleep) have been shown to
contribute to childhood obesity. Exclusive breastfeeding has been shown to modestly protect against this,
while the initiation and duration of breastfeeding can also influence this. Breast milk has also been found to
decrease the likelihood of developing allergies in later life.
Complementary feeding (introduced at approximately 6 months of age) can commence when breast milk alone
is no longer sucient to meet the nutritional requirements of infants, and other foods and liquids are needed,
along with breast milk. Because obesity, diabetes, cardiovascular morbidity, and neuropsychiatric diseases can
all be considered paediatric diseases, disease prevention must start with improved nutrition.
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Substance use in the first 1000 days is another noteworthy individual level factor which significantly impacts
child health and wellbeing. Exposure to alcohol in the uterus is the leading cause of cognitive impairment and
neurodevelopmental disorders, and the most common preventable cause of birth defects. The eects of alcohol
on the embryo or foetus produce a spectrum of lifelong disorders that aect physical, learning and behavioural
outcomes, the range of which is collectively termed ‘foetal alcohol spectrum disorder’ (FASD). Based on available
research evidence, it cannot be stated that light drinking in pregnancy has been established to besafe.
The adverse eects of substance use can be considerable, and include (but are not limited to) premature birth,
physical and/or mental retardation and birth defects. Pregnant women who are substance dependant are also
more likely to present with co-occurring physical and psychological health concerns such as hepatitis, eating
disorders and suicide attempts, increasing the risk of harm to their child before and after birth. Substance
misuse after birth compromises parental care in several ways, including intoxication, drowsiness and impaired
attention, withdrawal symptoms, and engaging in illegal and dangerous activities. These all impact a
caregiver’s capacity to respond to the child’s immediate and long-term health, safety and wellbeing needs.
Exposure to tobacco in the first 1000 days is also detrimental to the health and wellbeing of the child. Within
minutes of inhalation of tobacco smoke, wherever the blood flows, many of the more than 4000 chemicals
from tobacco smoke also rapidly flow. Nicotine also restricts blood flow to the placenta and reduces the supply
of nutrients and oxygen to the foetus. Following birth, exposure to environmental tobacco smoke in childhood
is associated with slower rates of growth in lung function and increased risk of asthma (amongst various other
adverse outcomes).
Toxic stress is the third major individual level factor that impacts health in the first 1000 days, and beyond.
Toxic stress during pregnancy impacts the foetal nervous system and reduces foetal growth and length of
gestation. Poor growth in utero is a major risk factor for a number of subsequent health problems in the child’s
later years, including: physical and neuromuscular maturation; behavioural and emotional development; and
cognitive development. Toxic stress can also impact a parent’s caregiving capacity and risk taking behaviour,
once the child is born.
~ ~ ~
So far, we have reviewed the evidence relating to the various factors and mechanisms through which child
health and development can be influenced, for better or worse. The following section highlights the evidence
surrounding how a child’s experiences in the first 1000 days translates to outcomes in later life, and how
long-lasting those eects are.
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7. Beyond the first 1000 days
In considering how children’s early life experiences are linked to later life outcomes, it is important to note that
development is not simply interactional but is transactional. Rather than development being simply the product
of an interaction between a child’s genetic / epigenetic characteristics and the various caregiving and other
environments they experience, it involves a dynamic transactional process whereby the child shapes the
environment at the same time as the environment shapes the child (Bornstein, 2009; Mandy & Lai, 2016;
Samero, 2009). Thus, infants and parent bring distinctive characteristics to their exchanges, but each also
changes as a result of their interactions with one another, and both therefore enter the next interaction as
changed individuals. This means that development is a function of the individual and the individual’s
environment and not of either alone (Bornstein, 2009).
With this consideration in mind, we will now explore several of the developmental pathways linking
development during the first 1000 days and later outcomes.
7. 1 Pathways to later outcomes
Four key ways in which early childhood experiences can have long-term eects have been identified (Boivin &
Hertzman, 2012; Hertzman & Power, 2003; Keating & Hertzman, 1999; Shonko, Boyce & McEwen, 2009).
They are:
biological embedding
accumulation eects
developmental escalations of risk over time
triple hit eects.