YouTubeExplain genetic, neurochemical, hormonal, structural and immune explanations of major depressive disorder, compare them with PTSD, and evaluate them through causality, measurement, perspective and responsibility.
Each is in the Psychology glossary, with every other term in the subject.
A reduced ability to feel pleasure or interest in activities a person used to enjoy; one of the two core symptoms of major depressive disorder.
A small signalling protein released by immune cells; pro-inflammatory cytokines such as IL-6 and TNF-α promote inflammation and can affect mood and behaviour.
The hypothesis that the symptoms of schizophrenia, especially hallucinations and delusions, are linked to excessive dopamine activity in certain pathways of the brain.
The hypothesis that long-lasting activation of the immune system and raised pro-inflammatory cytokines contribute to the development of depression in some people.
The hypothesis that depression is caused by low levels or reduced activity of monoamine neurotransmitters, especially serotonin and noradrenaline, in the brain.
Describe the main symptoms of major depressive disorder and why biological explanations of it are studied.
Explain genetic explanations of depression, using evidence from twin, molecular and gene–environment studies.
Explain the monoamine hypothesis of depression and evaluate the evidence for and against it.
Explain how HPA axis dysregulation, reduced hippocampal volume and inflammation may contribute to depression.
Compare and contrast biological explanations of depression with those of post-traumatic stress disorder.
Discuss how biological factors interact with cognitive and sociocultural factors in mental health disorders.
Evaluate biological explanations with reference to causality, measurement, perspective and responsibility.
Biological explanations of mental health disorders look for causes in the body: in genes, in chemical messengers in the brain, in stress hormones, in brain structure and in the immune system. They are studied because major depressive disorder is one of the most common and disabling health conditions in the world: about 4% of the world’s population, some 322 million people, have depression at any one time, and it is about 1.5 times as common in women as in men.
Sources: WHO, Depression fact sheet (2023 estimates).
Biological explanations draw on several approach terms: genetic inheritance, chemical messengers, neurotransmission and the diathesis-stress model. Each gives part of the picture, and each has to be combined with cognitive and sociocultural factors, because no single biological cause of depression has been found. The debate about how much a biological explanation can explain is a debate about
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Everyone feels sad at times. Major depressive disorder (MDD) is different in its severity, its duration and its effect on daily life. In the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), a diagnosis requires at least five of nine symptoms for at least two weeks, nearly every day, causing significant distress or impairment. At least one of the five must be depressed mood or a marked loss of interest or pleasure in activities.
Kind of symptom | Examples |
|---|---|
Emotional | Depressed mood; loss of interest or pleasure (anhedonia) |
Cognitive | Feelings of worthlessness or excessive guilt; poor concentration; indecisiveness; recurrent thoughts of death or suicide |
Physical | Changes in sleep (insomnia or sleeping too much); changes in appetite or weight; fatigue and loss of energy |
Behavioural | Slowed movement and speech, or restlessness and agitation; withdrawal from others |
Several features of depression shape the search for causes. It often runs in families, which suggests genes. It includes physical symptoms such as disturbed sleep and appetite, which suggests changes in the brain and body. Episodes often follow stressful events, which suggests an environmental trigger. It also often recurs, and many people who recover have further episodes. A good biological explanation must account for all of these, and also for why most people who experience severe stress do not become depressed.
YouTubeGenetic explanations propose that some people inherit a greater vulnerability to depression. Research on genetic inheritance estimates this vulnerability by comparing relatives who share different proportions of their genes: if monozygotic twins, who share almost all their genes, are more often both depressed than dizygotic twins, who share about half, genetic factors are implicated. The statistic that results, heritability, estimates how much of the variation in depression risk within a population is associated with genetic differences.
Family studies show that depression runs in families: in a meta-analysis by Sullivan, Neale and Kendler (2000), first-degree relatives of people with depression had about 2.8 times the odds of depression themselves. Twin studies then separate genes from family environment. The same meta-analysis combined five twin studies and estimated the heritability of major depression at 37%, with almost no effect of the environment shared by siblings and 63% due to the individual-specific environment (and measurement error).
Depression is therefore moderately heritable: genes contribute, but most of the variation in who becomes depressed is linked to experiences that are specific to each person, such as their own life events, relationships and illnesses. Recurrent depression appears to be more familial than a single episode.
Kendler, Gatz, Gardner and Pedersen (2006) aimed to estimate the heritability of lifetime major depression in the largest twin sample studied up to that time, and to test three questions that earlier studies had left open: whether genes matter more for depression in women than in men, whether the same genes are involved in both sexes, and whether the role of genes had changed across generations born in different decades.
The study used the Swedish Twin Registry, a national register of twins born in Sweden. Lifetime major depression was assessed by personal interview, using modified DSM-IV criteria, in 42,161 twins, including 15,493 complete pairs, from three birth cohorts spanning 1900–1958. The pairs included MZ and DZ twins of the same sex and DZ pairs of opposite sexes.
The researchers compared how often MZ and DZ co-twins were both affected and fitted statistical twin models that divide the variation in risk into genetic effects, shared environment and individual-specific environment. Opposite-sex DZ pairs were the key to the second question: if the genes that influence depression were exactly the same in men and women, opposite-sex DZ pairs would resemble each other as much as same-sex DZ pairs.
The heritability of major depression was significantly higher in women (42%) than in men (29%).
The genetic risk factors for depression in men and women were only moderately correlated, which suggests that some genes act differently, or only, in one sex.
There were no significant differences in the roles of genes and environment across the three birth cohorts, from twins born in 1900 to twins born in 1958.
The individual-specific environment accounted for most of the remaining variation, as in earlier studies.
Sources: Kendler, K. S., Gatz, M., Gardner, C. O. and Pedersen, N. L. (2006). A Swedish national twin study of lifetime major depression. _American Journal of Psychiatry, 163(1), 109–114._
Kendler and colleagues concluded that lifetime major depression is moderately heritable, with estimates similar to those of earlier studies; that genes matter more for women than for men; and that some genetic risk factors are sex-specific. The stability across cohorts suggests that the balance of genes and environment did not change over six decades of Swedish history, despite large social changes.
The sample was very large and drawn from a national register, so it was far more representative than samples recruited through clinics or advertisements. Depression was assessed by interview using standard criteria, not by a single questionnaire. However, lifetime depression was measured by asking people, some of them in old age, to remember past episodes. Recall of episodes decades earlier is unreliable, and errors of this kind are counted as individual-specific environment, which may lower the estimate of heritability. The twin method also relies on the equal environments assumption: if MZ twins were treated more alike than DZ twins, heritability would be overestimated.
Opposite-sex DZ twins share about half their varying genes, like same-sex DZ twins. If exactly the same genes influenced depression in men and women, opposite-sex pairs would be as similar in depression risk as same-sex DZ pairs. They were less similar, which is why Kendler and colleagues concluded that the genetic risk factors were only moderately correlated across the sexes.
The sample was Swedish and almost entirely of European ancestry. Sweden has a welfare system that reduces some environmental differences, such as access to health care, and heritability is higher when environments are more similar. The sex difference could also be partly due to measurement: men may be less willing to report depressive symptoms in an interview, which would make their diagnoses less reliable and lower their heritability estimate.
A heritability of 42% describes variation in a population. It does not show which genes are involved or how they act, and it does not mean that 42% of a particular woman’s depression is genetic. Genes may act indirectly, for example by influencing personality traits that make stressful events more likely or harder to cope with.
Twin registers hold personal health information on tens of thousands of people. Their use depends on informed consent, strict confidentiality and anonymised data. Communicating the results also requires care: a finding that depression is “partly genetic” can be heard by the public as “depression is in the genes”, which can increase fatalism.
Molecular genetics looks for the specific genes behind the heritability of depression. Early research tested candidate genes chosen for their biological role, especially the serotonin transporter gene. Large genome-wide association studies have since shown that depression is highly polygenic. Howard et al. (2019) combined data on 807,553 people (246,363 cases and 561,190 controls) and identified 102 independent genetic variants associated with depression; 87 of them were confirmed in an independent sample of over 1.3 million people. The genes involved were linked to synaptic structure and neurotransmission, and to prefrontal brain regions.
Each of these variants changes risk by a tiny amount, and together they explain only a small part of the heritability estimated from twins. Most of the samples were of European ancestry, so the results may not apply equally to other populations. There is no single “depression gene” and no genetic test that can diagnose depression.
Genes are thought to work mainly by changing how a person responds to stress, as in the diathesis-stress model. Caspi et al. (2003) reported that people with a short allele of the serotonin transporter gene were more likely to become depressed after stressful life events.
The finding inspired a great deal of research, but large studies did not confirm it: Border et al. (2019), using samples of up to 443,264 people, found no clear evidence for any of 18 popular candidate genes, or their interaction with stress, in depression. The idea of gene–environment interaction is still supported by twin research, but no specific genetic variant has been shown to explain who becomes depressed under stress.
The monoamine hypothesis is the oldest neurochemical explanation of depression. Monoamines are a group of neurotransmitters that includes serotonin, noradrenaline and dopamine. The hypothesis proposes that depression is caused by reduced activity of these neurotransmitters in the brain, especially serotonin. In its popular form it is known as the “chemical imbalance” theory.
The hypothesis grew out of chance observations with drugs in the 1950s. A drug used to treat tuberculosis (iproniazid) was found to lift mood, and it increased monoamine levels by blocking the enzyme that breaks them down. Reserpine, a blood-pressure drug that depletes monoamines, was reported to make some patients depressed, although later reviews found this evidence mixed. Researchers reasoned backwards: if raising monoamines relieves depression and lowering them causes it, depression might be caused by low monoamines.
The figure shows the reasoning behind modern antidepressants. After serotonin is released into the synapse and binds to receptors, a transporter carries it back into the presynaptic neuron (reuptake). Selective serotonin reuptake inhibitors (SSRIs), such as fluoxetine, block this transporter, so more serotonin remains in the synapse. If low serotonin caused depression, increasing it should relieve symptoms.
Drug effects. Antidepressants that increase monoamine activity are, on average, more effective than placebo in treating depression, although the difference is modest and varies between people. This was long treated as the main evidence for the hypothesis.
Tryptophan depletion. Serotonin is made from tryptophan, an amino acid in food. Tryptophan depletion studies give people a drink that lacks tryptophan, which lowers serotonin for a few hours. Delgado et al. (1990) found that 14 of 21 patients who had recovered from depression on antidepressants relapsed temporarily after depletion.
However, a meta-analysis by Ruhé, Mason and Schene (2007) found that depletion did not lower mood in healthy volunteers. It lowered mood slightly in healthy people with a family history of depression and more in people who had previously been depressed.
If low serotonin caused depression, lowering it should make anyone feel worse. Depletion affects only people who are already vulnerable, which suggests that serotonin is involved in a vulnerability or in maintaining recovery rather than being the cause of depression.
The time lag. SSRIs increase serotonin in the synapse within hours, yet improvements in mood usually take two to six weeks. If low serotonin were the cause, mood should improve as soon as serotonin rises. The delay suggests that the drugs work through slower, downstream changes, such as changes in receptor sensitivity or in neuroplasticity, not by correcting a shortage.
The treatment–aetiology fallacy. The fact that a treatment works does not show what caused the problem. Aspirin relieves a headache, but headaches are not caused by a lack of aspirin. In the same way, the fact that SSRIs help some depressed people does not show that their depression was caused by low serotonin.
Direct evidence. Moncrieff et al. (2022) carried out an umbrella review of the main areas of serotonin research, including serotonin and its breakdown products in body fluids, serotonin receptors and transporters, tryptophan depletion and serotonin transporter gene studies. They concluded that these areas provide no consistent evidence that depression is associated with, or caused by, lowered serotonin activity. Some evidence suggested that long-term antidepressant use may itself lower serotonin levels, which complicates studies of patients.
The review was widely reported and strongly debated. Critics argued that “no consistent evidence for low serotonin” is not the same as “serotonin plays no role”, that the review did not consider all relevant evidence, and that whether antidepressants help does not depend on the hypothesis being true. Many researchers now accept that the simple chemical imbalance idea is not supported, while still studying how serotonin systems are involved in some forms of depression and in how antidepressants work.
YouTubeThe monoamine hypothesis is one example of a common pattern: a neurochemical explanation inferred from the effects of drugs. The dopamine hypothesis of schizophrenia followed the same route. Amphetamines, which increase dopamine activity, can produce psychotic symptoms such as hallucinations and delusions, and the first antipsychotic drugs, which reduce psychotic symptoms, block dopamine receptors.
The dopamine hypothesis has better direct support than the serotonin hypothesis of depression, from brain imaging that finds increased dopamine release in some people with schizophrenia, but it faces similar criticisms: antipsychotics do not help all patients, they do not treat the negative symptoms (such as social withdrawal) well, and drug effects do not prove a cause.
A second biological explanation focuses on the body’s stress system. When a person faces a stressor, the HPA axis (hypothalamic–pituitary–adrenal axis) is activated: the hypothalamus releases a hormone (CRH) that signals the pituitary gland, which releases another hormone (ACTH) that signals the adrenal glands to release cortisol. Cortisol mobilises energy and helps the body cope. Normally, cortisol then acts on receptors in the brain, including in the hippocampus, to switch the response off again. This is negative feedback.
The HPA explanation proposes that in many people with depression this system is overactive: the feedback loop is weakened, cortisol stays high for long periods, and prolonged high cortisol affects mood, sleep, appetite and the brain regions that regulate the stress response. The explanation fits the diathesis-stress model well, because it describes a biological route from stressful experience to depression.
Stetler and Miller (2011) combined 361 studies with 18,454 participants. Depressed people tended to have higher cortisol than non-depressed people, a moderate effect (d = 0.60), and higher levels of ACTH. However, the cortisol effect was almost halved (d = 0.33) when only methodologically adequate studies were included, and it was much larger in older inpatients and in severe forms of depression with melancholic or psychotic features than in younger outpatients. HPA overactivity is therefore found in some kinds of depression and some patients, not in depression as a whole.
The evidence also leaves the direction of cause open. High cortisol might contribute to depression, but being depressed (with poor sleep, worry and inactivity) could also raise cortisol. Early adversity may play a part in both: research on the epigenetics of stress suggests that childhood maltreatment can change the expression of the genes for cortisol receptors, which would make the stress response harder to switch off in adulthood.
The hippocampus, a structure in the temporal lobe involved in memory and in switching off the stress response, is one of the regions most consistently linked to depression. It is rich in cortisol receptors, and animal research shows that prolonged high levels of stress hormones can damage hippocampal neurons and reduce the growth of new ones.
Videbech and Ravnkilde (2004) combined 12 MRI studies with 351 patients with unipolar depression and 279 healthy controls. On average, hippocampal volume was 8% smaller on the left and 10% smaller on the right in the patients. A larger number of depressive episodes was associated with a smaller right hippocampus, which suggested that the reduction may build up with repeated episodes.
The ENIGMA consortium has since pooled MRI data from many research groups to give much larger samples. Schmaal et al. (2016) compared 1,728 patients with MDD and 7,199 controls from 15 samples worldwide. Patients had significantly smaller hippocampi, but the difference was small (about 1.2%, d = −0.14). It was driven by patients with recurrent depression and by those whose depression began at age 21 or younger; patients in their first episode did not differ from controls.
The difference between the two estimates (8–10% against about 1%) illustrates a general pattern in brain imaging research: small early studies tend to overestimate effects, and very large pooled studies give smaller but more reliable ones. The ENIGMA results also suggest that a smaller hippocampus is more likely to be linked to the course of the illness (recurrence, early onset) than to depression in general.
A newer explanation links depression to the immune system. When the body fights an infection, immune cells release signalling proteins called cytokines. Some of these cause inflammation and also act on the brain, producing “sickness behaviour”: fatigue, loss of appetite, sleep changes, withdrawal and low mood. These overlap strongly with the symptoms of depression.
The inflammation hypothesis proposes that, in some people, long-lasting low-grade inflammation contributes to depression. Dowlati et al. (2010) combined 24 studies and found significantly higher concentrations of two pro-inflammatory cytokines, TNF-α and IL-6, in people with major depression than in controls; other cytokines did not differ.
The hypothesis can explain why depression is more common in people with chronic physical illnesses that involve inflammation, and it links depression to stress, because chronic stress also raises inflammation. However, the evidence is mostly correlational; not all depressed people show inflammation; obesity, smoking and poor sleep raise both inflammation and depression risk, so they are possible confounding variables; and treatments that target inflammation are still being tested.
Comparing two disorders shows which biological factors are specific to one disorder and which are general vulnerabilities. Post-traumatic stress disorder is a useful comparison because it always follows an identifiable trauma. This makes it possible to ask whether a biological difference was present before the trauma or was caused by it.
True et al. (1993) studied 4,042 male twin pairs who served in the US military during the Vietnam War era. Genetic factors accounted for about 13–34% of the variation in different PTSD symptoms, even after adjusting for how much combat each twin had seen, and the shared family environment made no detectable contribution. MZ twins were also more alike than DZ twins in their exposure to combat, which suggests that genetically influenced traits affect the likelihood of facing traumatic situations at all, an example of gene–environment correlation.
Smaller hippocampal volume is also found in PTSD. Gilbertson et al. (2002) studied pairs of identical twins in which one twin had been exposed to combat in Vietnam and the other had not. Veterans with severe PTSD had smaller hippocampi, and so did their identical co-twins who had never been in combat. The more severe the veteran’s PTSD, the smaller the hippocampi of both twins. This suggests that a smaller hippocampus is a pre-existing, probably partly genetic, risk factor that makes people more vulnerable to developing PTSD after trauma, rather than only a result of trauma.
The HPA findings differ from depression. Whereas depression is often associated with raised cortisol, PTSD has been associated in some studies with lower cortisol. A meta-analysis by Meewisse et al. (2007) of 37 studies (828 people with PTSD, 800 controls) found no overall difference in basal cortisol, but lower levels in PTSD under certain conditions: in studies that measured cortisol in blood, in samples that included women, in people whose trauma was physical or sexual abuse, and in afternoon samples. The relation between stress hormones and disorders is therefore more complicated than “more stress hormone, more disorder”.
Biological factor | Major depressive disorder | Post-traumatic stress disorder |
|---|---|---|
Genetic influence | Heritability about 37% (twin meta-analysis); about 42% in women and 29% in men in Sweden | Genes explain about 13–34% of variation in symptoms in male veteran twins |
Stress hormones | Cortisol often raised, especially in severe and older inpatients | No overall difference; lower cortisol only under some conditions |
Hippocampus | Smaller, mainly in recurrent and early-onset depression; may be a consequence of episodes | Smaller; twin evidence suggests a pre-existing vulnerability |
Role of the environment | Stressful life events often trigger episodes, but depression can occur without them | A traumatic event is part of the definition of the disorder |
The comparison shows that the same structure or hormone can play different roles in different disorders, and that research designs such as twin studies of discordant exposure can address causality in a way that simple patient–control comparisons cannot.
None of the biological explanations accounts for depression on its own. Each describes a vulnerability or a mechanism that becomes important in combination with other factors. The biopsychosocial model treats a disorder as the product of biological, psychological and social factors acting together, and the diathesis-stress model describes one way in which they combine.
Biological and sociocultural. Stressful life events, poverty and social isolation are among the strongest predictors of depression. Their biological effects (activation of the HPA axis, inflammation) may be the route by which social adversity affects the brain.
Biological and cognitive. Negative thinking patterns, such as those described in Beck’s cognitive model, are themselves partly heritable and may be one way in which genes influence depression. Cognitive therapy can produce changes in brain activity, which shows that the influence runs in both directions.
Culture. How depression is experienced and expressed differs across cultures. In China, for example, distress has often been expressed through physical complaints (somatisation) rather than low mood, and the first genetic variants for depression to be found and replicated came from a study of Chinese women with severe recurrent depression. Biological research needs culturally valid diagnoses to study the same thing across populations.
This interaction is why most psychologists describe depression as a group of related conditions with different combinations of causes, rather than as one disease with one cause. For one person, a strong genetic loading and high cortisol may be central; for another, a severe life event and a lack of social support.
Biological explanations have real strengths. They are based on measurable variables (genes, hormone levels, brain volumes), they are tested with large samples and objective methods, and they have led to treatments such as antidepressants. They also explain why depression runs in families and why it involves physical symptoms such as disturbed sleep and appetite.
Their main weakness is biological reductionism: reducing a complex disorder to one biological level. A purely biological explanation cannot account for why depression is linked to social circumstances such as unemployment or bereavement, why rates differ between countries and social groups, or why psychological therapies are about as effective as medication for many people. The evidence supports a holistic or interactionist perspective in which biological factors are one part of the explanation.
Most of the evidence is correlational. Higher cortisol, smaller hippocampi and higher cytokines are found in people with depression, but they could be causes, consequences or results of a third factor such as stress, medication, poor sleep or obesity. Inferring causes from treatment effects, as the monoamine hypothesis did, is a fallacy. Stronger causal evidence comes from prospective studies, twin designs such as Gilbertson et al. (2002) and experiments such as tryptophan depletion, and these often show smaller or more conditional effects.
Major depressive disorder is diagnosed when five of nine symptoms are present, so two people with the same diagnosis can share very few symptoms. If depression is several different conditions, a biological factor present in one subtype will look weak across all patients, as the cortisol findings suggest. Many measures are also indirect: serotonin cannot be measured in the living human brain synapse, so researchers rely on blood levels, breakdown products or imaging of transporters. Cortisol varies across the day, so the time of sampling changes the results.
Most twin, genetic and imaging studies come from Europe, North America and Australia, and most genetic studies use people of European ancestry, so the results may not apply worldwide. Small early studies of candidate genes and brain volume reported larger effects than later large studies, a sign of publication bias and low statistical power. The popularity of the chemical imbalance explanation may also have been increased by the marketing of antidepressants directly to the public in some countries.
Explanations of mental illness affect how people with a disorder are seen by others and how they see themselves. A meta-analysis by Kvaale, Gottdiener and Haslam (2013) of 25 studies found that people who held biogenetic explanations of mental disorders blamed affected people less, but saw them as slightly more dangerous and wanted slightly more social distance from them.
In an experiment, Kemp, Lickel and Deacon (2014) gave people who had experienced depression a fake but credible test result saying that their symptoms were caused by a chemical imbalance. Compared with those told it was not, they did not blame themselves less, felt more pessimistic about recovery, and saw medication as more credible than psychotherapy.
Researchers and clinicians therefore have a responsibility to communicate uncertainty: to explain that biological factors increase vulnerability without making depression permanent or untreatable, and not to present a contested hypothesis as established fact.
Concept | How it applies to biological explanations of depression |
|---|---|
Perspective | A biological perspective explains vulnerability and mechanisms but not social patterns; an interactionist view fits the evidence better |
Causality | Most findings are correlational; treatment effects do not show causes; twin and prospective designs help |
Measurement | Depression is varied; serotonin and cortisol are measured indirectly; small early studies overestimated effects |
Bias | European-ancestry and Western samples; publication bias; marketing of the chemical imbalance idea |
Responsibility | Biogenetic explanations reduce blame but can increase pessimism and social distance |
Change | Biological factors are not fixed: hippocampal volume and HPA activity can change with episodes and treatment |
Major depressive disorder affects about 4% of the world’s population and is about 1.5 times as common in women as in men.
Depression is familial and moderately heritable: about 37% in a twin meta-analysis, and 42% in women and 29% in men in Kendler et al. (2006).
Depression is highly polygenic: a GWAS of over 800,000 people found 102 variants of tiny effect; candidate genes such as 5-HTT have not replicated.
The monoamine hypothesis proposed that low serotonin causes depression; the SSRI time lag, depletion studies and Moncrieff et al. (2022) do not support the simple version.
HPA axis overactivity with raised cortisol is found in some depressed people, mainly in severe forms and older inpatients.
Hippocampal volume is smaller in depression, mainly in recurrent and early-onset cases, possibly as a consequence of repeated episodes.
Raised IL-6 and TNF-α suggest a role for inflammation in some people, but confounds such as obesity and poor sleep are possible.
In PTSD, a smaller hippocampus appears to be a pre-existing vulnerability, according to the co-twin study by Gilbertson et al. (2002), and cortisol is not consistently raised.
Biological explanations are strongest as part of an interactionist, biopsychosocial account; alone they are reductionist and mostly correlational.
Biogenetic explanations can reduce blame but increase pessimism and social distance, so uncertainty must be communicated responsibly.
I can describe the main symptoms of major depressive disorder.
I can explain genetic explanations of depression using twin, GWAS and gene–environment evidence.
I can explain and evaluate the monoamine hypothesis, including the treatment–aetiology fallacy.
I can explain the roles of the HPA axis, the hippocampus and inflammation in depression.
I can describe the aim, method, results and evaluation of Kendler et al. (2006).
I can compare and contrast biological explanations of depression and PTSD.
I can discuss how biological, cognitive and sociocultural factors interact in depression.
I can evaluate biological explanations with reference to causality, measurement, perspective and responsibility.