IB Psychology HLTopic 1 — Health ProblemsPaper 1 & 2Biological approach~9 min read
Stress, Cortisol and Weight Gain
Everybody has noticed that stress changes how they eat. What is less obvious is that the same hormone doing the changing is also the reason people get ill during exam season. This page follows cortisol from the brain to the biscuit tin, and shows why stress and weight form a loop rather than a straight line.
📘 What you need to know
Cortisol is a hormone produced in the adrenal cortex when the hypothalamus–pituitary–adrenal (HPA) axis is activated by stress.
Normally cortisol is helpful: it regulates the immune system and suppresses inflammation.
Under chronic stress, excess cortisol builds up and over-suppresses the immune system, lowering resistance to illness.
Stress does not directly cause infection — it reduces the immune system’s ability to fight antigens, which makes infection more likely.
The cortisol-awakening response (CAR) is the natural rise in cortisol after waking, and research links it to eating more under stress.
Stress disrupts appetite hormones: leptin (fullness), ghrelin (hunger) and neuropeptide Y (appetite regulation).
Stress and obesity form a two-way relationship: stress can lead to weight gain, and weight can add stress.
From threat to hormone
Follow the arrows down the left, then read the right-hand panel. The same hormone explains both the immune effect and the appetite effect, which is why the two so often appear together.
Get the wording exactly right in the exam: stress does not cause infection. It lowers the immune system’s ability to fight antigens, which makes infection more likely. That distinction is worth a mark on its own.
The appetite hormones
Hormone
Its normal job
What stress does
Leptin
Signals fullness to the brain
Disrupted, so the stop signal gets weaker
Ghrelin
Signals hunger
Disrupted, so hunger signals fire when they should not
Neuropeptide Y
Regulates appetite
Disrupted, so overall appetite control weakens
The two-way relationship
Stress affects self-regulation — the ability to control your own behaviour. Under pressure it becomes harder to resist food that is fatty or sugary, partly because willpower is a limited resource and stress is already using it up, and partly because the hormone signals telling you when to stop have been disrupted.
Then it runs the other way. Weight gain can itself become a source of stress, through health worries, social judgement or self-criticism. That feeds back into the CAR and the cycle continues.
The loop
chronic stress → raised cortisol → disrupted appetite signals → weight gain → more stress
Research support: Kumar et al. (2022)
Aim: to examine the link between stress and obesity.
Method: a literature review of journal articles on stress, cortisol and obesity published between 2000 and 2020.
Results: stress emerged as a major factor in obesity, though biological and sociocultural factors also play a part. Research showed people eat more under stress in connection with the CAR, and many people self-medicate with comfort food during stress, which raises BMI over time. Obesity treatment was more effective when stress was targeted directly.
Conclusion: stress and obesity are closely connected and should be studied and treated together rather than separately.
Why a literature review is a sensible method here. Stress-related obesity has cognitive, sociocultural and biological pieces, and no single study covers all three. Pulling together twenty years of research gives a holistic view that one experiment could never produce. The cost is that you are relying on other people’s designs and definitions.
Evaluation
Strengths
Strong biological evidence. The cortisol–stress link is well established physiologically, which makes the obesity findings more convincing than a purely correlational account.
The findings point at a practical intervention. If stress is part of the mechanism, then stress management — walking, meditation, better sleep routines — is accessible and low-cost for most people.
It explains something other models cannot. Neither social learning nor culture explains why the same person eats differently in a calm week and a stressful one.
Limitations
Individual differences are not accounted for. Not everyone eats more under stress; some people lose their appetite entirely. That limits how far the explanation generalises.
Behaviour change is genuinely hard here. Eating is pleasurable, so tackling stress-related eating is difficult to sustain.
Confirmation bias threatens a literature review. Researchers may select the studies that fit their expectations, which is why reflexivity matters.
Reductionist if used alone. Cortisol is one strand; income, food availability, culture and social networks are all still in play.
EXAM QUESTION
Discuss one biological explanation of one health problem. [22]
Step 1: trace the HPA axis in orderHypothalamus, pituitary, adrenal cortex, cortisol. Then note the normal useful role of cortisol.Step 2: explain what chronic stress changesOver-suppressed immune system; leptin, ghrelin and neuropeptide Y disrupted; self-regulation weakened.Step 3: state the two-way relationship explicitlyStress raises weight, weight raises stress. Draw the loop.Step 4: use Kumar, then evaluateLiterature review 2000–2020, stress a major factor, treatment better when stress targeted. Then individual differences and confirmation bias.Strongest evaluation: some people undereat under stress
Link to concepts
Measurement
A literature review is a good way to build a comprehensive picture of a complex issue, because it draws on cognitive, sociocultural and biological research at once. That produces a holistic understanding rather than one narrow explanation of a health problem — which is exactly what a multifactorial issue needs.
Bias
Confirmation bias is the main threat to validity in a review. Researchers must practise reflexivity so their own expectations do not shape which studies they include and which they quietly leave out.
💡 Exam tip
Write the HPA axis in order, using the full names once and the abbreviation afterwards.
Name all three appetite hormones with their function. That level of detail is rare and it stands out.
Use the word bidirectional or “two-way” for the stress–weight relationship.
The individual-differences criticism is the strongest one available, because it is a fact about the phenomenon rather than about a study design.
Explain what a literature review is and what it costs. That is a methodological point, and methodological points score.
Link forward: this page pairs with the social learning page to give a multifactorial answer on obesity.
⚠ Common mix-up
Saying stress causes illness directly. It lowers immune resistance; the antigen still does the work.
Swapping leptin and ghrelin. Leptin says full, ghrelin says hungry.
Treating cortisol as purely harmful. Normal cortisol regulates the immune system and reduces inflammation.
Calling the CAR the same thing as stress. It is the natural rise in cortisol after waking.
Presenting the relationship as one-way. The loop is the point.
Treating a literature review as weak by default. It has real strengths; the weakness is specifically confirmation bias and dependence on others’ methods.
Up next: Drug Treatments for Depression — that completes Health Problems. We now move into Prevention and Treatment, starting with the drugs that come straight out of the monoamine hypothesis.
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