“Clinical Developmental & Health Psychology – Lecture 1 (UNIVERSITY OF AMSTERDAM)”

People with a mental disorder tend to have higher mortality and have lower reproductive success.

The paternal age effect refers to increased risk of a mental disorder when the father is older when he has the child. It is possible that females with mental disorders have higher reproductive success than males with a mental disorder because of females are not always fertile and thus have more of a choice of whether to reproduce.

The mental disorder paradox refers to mental disorders being common (1), having high heritability (2) and people with mental disorders having lower reproductive success but mental disorders not having been eliminated through natural selection. There are three general resolutions for this paradox:

  1. Ancestral neutrality
    This states that mental disorders have a negative effect on reproductive success in modern times but this was not the case in ancestral times (e.g. schizophrenia was seen as divinity; anxiety served a purpose).
  2. Balancing selection
    This states that mental disorders have a negative effect on reproductive success but this is counterbalanced by positive effects (e.g. people with schizophrenia are more creative; people with autism have better systematic thinking).
  3. Polygenic mutation-selection balance
    This states that mental disorders are the result of unavoidable mutations in one of the many genes that underlie human behaviour. The mental disorders consist of a lot of genes meaning that the random variations cannot be selected out, which means that mental disorders cannot be filtered out through natural selection.

It is possible that people with a mental disorder themselves have lower reproductive success but family members with the genes but not with the disorder only have the positive effects (e.g. higher creativity). This could enhance their reproductive success (i.e. higher inclusive fitness), which keeps the genes of a mental disorder present in the population. However, this does not appear to be the case.

High comorbidity would be expected if a lot of genes underly mental disorders. As this is the case, this provides support for the polygenic mutation-selection balance hypothesis. Furthermore, it is possible that many genes for mental disorders are recessive as there is an association between inbreeding and mental disorders. The heritability of mental disorders could be explained in the polygenic mutation-selection balance because mutations can take a long time before they are eliminated.

Developmental psychopathology refers to the focus on the interplay of personal and environmental factors in the origin of mental disorders. This includes genotype-environment interactions, epigenetic encoding of life events and neurobiological factors. Computational psychiatry refers to mathematical models of cognitive and neural processes (e.g. decision making) to identify the mechanisms involved in mental disorders.

Evolutionary psychopathology uses biological models and concepts to understand the functions of the neural and psychological processes involved in mental disorders and how they have been shaped by selection processes. Evolutionary psychopathology does not necessarily regard mental disorders as dysfunctions. It is possible that behaviours that decrease well-being are not maladaptive by default. The potential fitness benefits of behaviour need to be considered.

Mental disorders tend to lead to lower reproductive success. Undesirable conditions can lead to dysfunctional or functional mechanisms. The dysfunctional mechanisms are considered in the polygenic mutation-selection balance. The functional mechanisms that are currently maladaptive are considered in ancestral neutrality. The functional mechanisms that are currently adaptive can have both maladaptive and adaptive outcomes for the single individual.

There are trade-offs in individuals. This means that one skill is overdeveloped, leading to another skill being underdeveloped (e.g. mechanistic cognition is good in autism at the cost of mentalistic cognition). There are several evolutionary conflicts (e.g. genes from father and mother; long-term or short-term mating).

Differential susceptibility refers to a difference in susceptibility to the environment. This generally expresses itself as either being sensitive to the effects of experience (i.e. orchids) or not being very sensitive to the effects of experience (i.e. dandelions). The orchids are more susceptible to adverse conditions but also more responsive to safe and supportive conditions. According to an evolutionary perspective, individual differences in susceptibility are an adaptive response to unpredictable fluctuations in the environment. It is possible that early adversity does not impair development but adaptively shapes it. Psychopathological conditions may also arise due to biologically adaptive but undesired behavioural strategies.

The two main problems of classification of mental disorders are comorbidity and heterogeneity within disorders.

Life history theory refers to the way organisms allocate time and energy to the activities that comprise their life cycle. The life history-related traits covary along a fast-slow continuum (e.g. reproduce early or late in life). Limited resources during development is associated with fast traits. The fast-slow distinction can demonstrate that some mental disorders are adaptive responses to maladaptive environments.

There are several disorders that tend to follow the fast spectrum (e.g. ADHD) and disorders that follow the slow spectrum (e.g. autism; depression). It is possible to classify disorders along this spectrum.

It may be useful to classify mental disorders based on the fast and slow continuum (i.e. following the life history theory).

Evolutionary mismatch refers to psychological mechanisms which developed in pre-modern times are no longer matched to the environment as it did during the development of the mechanism (i.e. psychological mechanisms do not match the modern environment). This may be the case because people live in environments that differ from the ones in which they evolved.

Mismatch can be classified along source (1), type (2), cause (3) and consequences (4). The causes of a mismatch are changes in input (1), changes in input intensity (2), input being replaced by novel or fake cues with similar attributes (3) and change in the consequence of output (4). A mismatch can be positive for an organism. The different causes of mismatches lead to different consequences for individuals and reproductive fitness. Predictions about mismatch consequences can be made by understanding the mechanism’s functional features.

A forced mismatch occurs when a new environment is imposed on an organism. A hijacked mismatch occurs when a novel stimulus is favoured by a certain mechanism over stimuli that the mechanism evolved to process.

For example, in ancient times, sugar was rare so humans developed a mechanism of eating the sweetest things when they could. However, nowadays, sugary foods are always present, meaning that people could eat a lot of sugar, following the previously developed mechanism which is now leading to maladaptive outcomes (e.g. obesity).

It appears as if evolutionary mismatch is linked to mental disorders as evolutionary mismatch may make people more vulnerable to mental disorders.

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