IB Psychology SLTopic 1 — Mental Health DisordersPaper 1 & 2Biological approach~10 min read
How Genes Contribute to Depression
Depression often runs in families. Your first thought might be “so it must be in the genes” — but families share more than DNA. They share houses, money worries, habits and stress. This page shows you how psychologists try to separate those two things, and why the answer is never a clean 100%.
📚 What you need to know
Major depressive disorder (MDD) is diagnosed from a set list of symptoms, not from one bad week.
The genetic explanation sits on the nature side of the nature–nurture debate.
Heritability means how much of the difference between people can be traced to genes.
Concordance rate = if one twin has MDD, what is the chance the other one does too.
MZ twins share 100% of their DNA; DZ twins share about 50%, like ordinary siblings.
You must be able to name McGuffin et al. (1996) and say what its numbers actually prove.
Concordance is never 100%, so genes alone cannot be the whole story.
What counts as depression?
Before you argue about causes, you need to know what is being explained. Clinicians look for a cluster of symptoms that has lasted a while and is getting in the way of normal life:
Long periods of feeling low, hopeless or worthless, or being unusually irritable.
Losing interest in things that used to be enjoyable.
Appetite changes, with weight going up or down.
Sleeping far too little or far too much.
Trouble deciding things, and very low motivation.
Thoughts about death or about ending one’s life.
Notice that this is a list of symptoms, not a cause. Two people can both be diagnosed with MDD and have almost nothing in common in how they got there. Keep that in your back pocket — it becomes a strong evaluation point later.
A note before you carry on. This topic can hit close to home for some students. If any of it is describing how you have been feeling lately, please talk to someone you trust — a parent, a teacher, your school counsellor, or your doctor. You are allowed to ask for help before things get bad.
The logic behind twin studies
Here is the problem. Your family gives you genes and an environment at the same time. If depression is common in your family, you cannot tell which one did it.
Twins give researchers a way in. Identical (monozygotic, MZ) twins come from one egg, so their DNA is the same. Non–identical (dizygotic, DZ) twins come from two eggs, so they are genetically just normal siblings who happen to share a birthday. Both types usually grow up in the same house at the same time.
The reasoning in one line
Same home for both pairs → if MZ concordance is higher than DZ, the extra similarity must come from the extra shared DNA
So the comparison is the point. A high MZ figure on its own means nothing. It is the gap between MZ and DZ that carries the argument.
Read the chart as a subtraction. Doubling the shared DNA roughly doubled the chance of both twins being affected — but it did not push the bar anywhere near the top.
🔬 McGuffin et al. (1996)
The twin study you should quote for genetic explanations of MDD
AIM
To compare how often both twins in a pair had MDD, in MZ pairs against DZ pairs.
PARTICIPANTS
177 twins who had been treated for depression at the Maudsley Hospital in London between 1948 and 1986. These first twins are called the probands. Their same-sex twin siblings were then traced and used as the comparison group.
PROCEDURE
Clinicians assessed each twin’s mental state using interviews and standard tests, and medical records were used as extra evidence. The researchers doing the assessing did not know whether a pair was MZ or DZ, and did not know whether the twin had a diagnosis — a double blind setup.
RESULTS
Concordance was 46% in MZ pairs and 20% in DZ pairs. When one MZ twin had a short depressive episode, the other one often had a similar episode too.
CONCLUSION
Genes make a real contribution to who develops MDD, but they clearly do not decide it on their own.
The blind assessment is worth a mark on its own. If the clinician knew a twin was identical to a depressed person, they might unconsciously look harder for symptoms. Removing that removes researcher bias — say that in an evaluation and you sound like you actually understand method, not just numbers.
What 46% really tells you
Students lose marks here by treating 46% as a win for genetics and stopping. Push it further.
🧩 Three things the number is telling you
Genes matter. 46% against 20% is a big difference, and the only systematic difference between the groups is DNA.
Genes are not enough. If depression were purely genetic, MZ concordance would have to be 100%. It never is, in any study. So something else has to be pulling one twin down and not the other.
The same genotype can give different phenotypes. Two people with identical DNA can end up with different outcomes, because life happened differently to each of them.
The assumption nobody mentions
Twin studies rest on a hidden claim called the equal environments assumption: that MZ pairs and DZ pairs are treated equally similarly by the world around them. That is probably not true. Identical twins are often dressed the same, put in the same class, given the same nickname and treated as a unit. So part of that extra MZ similarity could come from a more similar life, not from more similar DNA.
This does not destroy the study. It just means the genetic effect is probably a bit smaller than the raw numbers suggest. Writing this shows the examiner you can evaluate the method, not just repeat the finding.
Adoption studies fill the gap
Adoption studies come at the same question from the other side. A child who is adopted early gets their genes from one family and their environment from another. If they are more like their biological parents for depression, that points to genes. If they are more like their adoptive parents, that points to upbringing.
Used together, twin and adoption studies are much stronger than either one alone, because the weaknesses do not overlap.
EXAM ANSWER
Explain one genetic explanation of one mental disorder. [9 marks]
Here is the shape of a top-band paragraph. Notice it never just lists the study.
1. Define, don’t describe
MDD is diagnosed from symptoms like low mood, loss of interest and disturbed sleep. The genetic explanation says some people inherit a raised vulnerability to it.
2. Explain the mechanism
Heritability is studied through concordance rates. MZ twins share all their DNA, DZ twins about half, so comparing them separates genes from home life.
3. Bring in the study as evidence
McGuffin et al. found 46% concordance in MZ pairs vs 20% in DZ pairs, with blind assessment to control researcher bias.
4. Say what it proves — and what it doesn’t
The gap supports a genetic contribution. The fact it is not 100% shows genes create vulnerability rather than certainty.
Link back: genes load the gun, environment pulls the triggerthe last line is the one that lifts a 6 into a 9
Strengths and limitations
Strengths
Limitations
Large samples and clear numerical data make findings reliable and easy to compare across studies.
MZ concordance is never 100%, so the explanation is incomplete on its own.
Concordance rates are objective and can be replicated by other research teams.
The equal environments assumption is questionable, so the genetic effect may be overstated.
Blind assessment in McGuffin’s study reduces researcher bias.
It is reductionist — it reduces a complex disorder to inherited biology and ignores stress, poverty and thinking style.
Adoption studies separate genes from environment and back up the same conclusion.
Hospital-based samples like the Maudsley one may only capture more severe cases, so results may not generalise.
Linking to the concepts
Perspective: a purely biological view misses learning, adverse living conditions, and substance misuse, all of which are linked to MDD.
Bias: researchers who expect a genetic result may look harder for symptoms in the co-twin. Blind procedures exist precisely to stop this.
Reductionism: attributing MDD to genes alone is parsimony — picking the simplest theory that fits — which is efficient but can be too simple.
💡 Exam tips
Always quote both numbers. 46% alone is not evidence of anything; 46% versus 20% is.
Use the phrase “genetic vulnerability” or “predisposition” rather than “genetic cause”. It is more accurate and examiners reward it.
Name the design as well as the result: twin study, concordance rate, blind assessment.
Keep one methodological criticism ready (equal environments assumption) and one theoretical one (reductionism). Two different types of criticism scores better than two of the same type.
If the question says “discuss”, you must give both sides. Ending on “genes contribute but do not determine” is a safe, strong close.
You can use this same study for the biological approach, for research methods, and for the nature–nurture debate. Learn it once, use it three times.
⚠ Common mix-ups
Saying 46% of MZ twins have depression. Wrong. It means that in 46% of pairs where one twin already had it, the other did too.
Thinking MZ and DZ twins differ in age or upbringing. They are born together and raised together. Only the shared DNA differs.
Confusing heritability with inevitability. High heritability does not mean you will definitely get the disorder.
Writing “a gene for depression”. There is no single depression gene. Many genes each add a small amount of risk.
Forgetting DZ twins are just siblings. They share about 50% of DNA, exactly like a normal brother or sister.
Treating “reductionist” as an insult. Reductionism also brings scientific clarity and testable predictions. Say both.
Up next: Neurotransmitters and Depression — if genes only create a vulnerability, what is the actual biological machinery they are affecting? That question takes us into the synapse.
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