The prevention of mental disorders follows the public health understanding of prevention, occurring at three levels, namely, primary, secondary and tertiary [5]. Primary prevention aims to reduce the onset of mental disorders, thus reducing incidence. Secondary and tertiary prevention do not reduce incidence, but seek to lower the prevalence of established cases. Secondary prevention is concerned with early detection and treatment of mental disorders and tertiary prevention aims to reduce relapse and disability as well as enhance rehabilitation and morbidity. Secondary and tertiary prevention thus do not aim to reduce incidence, but together with primary prevention and treatment, share the common goal of reducing the burden of mental disorders [6].

Mental health promotion overlaps with primary prevention and is essentially concerned with promoting optimal mental and behavioural health and psycho-physiological development [7, 8]. Both mental health promotion and primary prevention aim to reduce risk factors for mental ill health as well as strengthen protective factors for mental well-being. They are thus interrelated. Promoting mental health may have an effect on reducing the incidence of mental disorders, as positive mental health is protective against mental disorders. Mental disorder prevention may use mental health promotion strategies. Both concepts may thus be present in the same intervention, but have different and complementary outcomes [9].

The scope of this chapter is limited to primary prevention, although the relationship between mental health promotion, the different levels of prevention and with treatment is often blurred. For example, treatment of depression in adults may prevent the onset of mental disorders in their children, and treatment of childhood depression can help to prevent depression in adulthood [6].

Primary prevention interventions can be universal, selective or indicated. Universal interventions target the whole population, with the assumption that the intervention is likely to benefit the entire population. Selective interventions target individuals or groups whose risk of developing a mental disorder is elevated as a result of biological, social or psychological risk factors. Indicated prevention programmes target individuals having preclinical minimum but detectable signs of mental illness that do not warrant a diagnosis of a mental disorder. Selective and indicated interventions are likely to show more focused benefits, given the elevated risk among the target groups for the development of disorders. Gordon [10] understands primary prevention as being aimed at people who do not show any suffering, discomfort or disability from the disorder to be prevented. Consequently, it has been suggested that indicated primary prevention overlaps with secondary prevention or early intervention for symptoms that may be part of the initial or prodromal phase of a disorder [11]. The importance of indicated prevention is, however, underscored by findings that the longer the duration of a disorder, the more difficult it is to treat [12]. Thus, even if it is considered early intervention, indicated prevention is likely to have better outcomes than delayed treatment.

Primary prevention interventions are essentially concerned with reducing risk and strengthening protective factors for the development of mental disorders. Risk factors refer to conditions that increase the probability of onset of a mental disorder, as well as greater severity and duration of the disorder. By contrast, protective factors serve to improve a person’s resilience to risk factors through modifying, mediating, ameliorating or altering conditions to promote more adaptive responses to environmental stressors [13].

As indicated in the Section ‘Recent evidence from advances in developmental neuroscience’, developmental neural plasticity is most prominent during prenatal development and early infancy. During this period, the brain develops rapidly and environmental influences can affect basic neurodevelopmental processes such as neuronal migration, synaptogenesis, synaptic pruning and myelination. Together with epidemiological and life course studies, there is an emerging body of evidence on the impact of the following risk factors on these neurodevelopmental processes.

Prenatally, micronutrient deficiencies, especially low vitamin folic acid and iodine can affect brain development causing irreversible neurocognitive deficits [17, 18]. Vitamin folic acid deficiency has been associated with disorders in the formation of the neural tube [6]. Iron deficiency can also cause neurocognitive deficits and poor socio-emotional development in children [17, 18]. Epidemiological studies indicate increased risk of schizophrenia in children born during famines. This is thought to be a result of deprivation of essential micronutrients causing disruptions in brain development [19]. Prenatal exposure to infectious diseases such influenza, rubella and toxoplasmosis can also affect neural developmental processes increasing risk for mental retardation, schizophrenia and autism [6].

Prenatal and postnatal exposure to environmental toxins such as lead, arsenic, pesticides, tobacco smoke and alcohol also negatively affects the developing brain, placing the developing foetus and infant at risk for neurocognitive deficits. For example, alcohol prenatally can result in foetal alcohol syndrome (FAS) associated with facial anomalies, growth retardation and abnormalities in the central nervous system, which can cause neurocognitive and social deficits in children, as well as substance abuse in adulthood [20, 21]. Prenatal and postnatal exposure to lead and prenatal exposure to tobacco smoke can result in attention deficit and conduct disorder in school-going children [22, 23]. Premature birth and low birth weight are also risk factors for a number of disorders including schizophrenia, autism and learning disabilities [6]. Anoxia as a consequence of birth trauma, is associated with brain malfunction, which can cause a range of mental and physical disabilities [20].

Postnatally, the development of a secure attachment relationship between an infant and his/her caregiver is essential for healthy development [20]. Disturbances in early infant–caregiver relationships such as loss of primary attachment figures, caregiver depression, as well as abuse and neglect can result in disturbances in social and emotional development and interpersonal attachments later in life in the form of behavioural disorders, anxiety, depression and attention problems [20]. This is thought to be a result of the development of abnormalities in stress-response hormone production [6]. Deprivation in cognitive and psychosocial stimulation during infancy has also been found to be associated with cognitive and socio-emotional impairment [20]. The development of synapses or connections between neurons reaches its peak during infancy; the synapse being the primary site of information transfer in the nervous system. Cognitive and socio-emotional impairment during this period is thought to be as a result of synaptic pruning, whereby some synaptic connections that are unused as a result of lack of environmental stimulation are pruned. Given plasticity persists throughout childhood and adulthood, regeneration of neurons and synapses is possible, but is contingent on environmental stimulation [6].

Many of these risk factors during prenatal development and infancy are more prevalent in scarce-resourced contexts. Iron deficiency anaemia is widespread in LMICs, and associated with dietary deficiency as well as helminthic infestations, malaria and diarrheal disease [17]. A third of children in LMICs under the age of 5 years have stunted growth for their age, a measure of chronic under-nutrition [17]. LMICs also have a much higher rate of infectious diseases such as HIV/AIDS and malaria that can result in neurocognitive deficits if untreated [4]. Raised lead exposure affects about 40% of children in LMICs [17].

Preschool children (3–5 years) begin to start regulating their attention, emotions, motor behavior and cognitions, developing a sense of a distinct self-identity [20]. They begin to be exposed to influences beyond the family and the development of social relatedness and self-regulatory control, which form the building blocks for healthy cognitive and social competence, are important developmental tasks. Exposure to undue stress such as child maltreatment, family conflict/violence or parental loss/separation can interfere with the emerging self-regulatory processes, resulting in regressive behaviours such as bed-wetting and anxiety in preschool children.