IB Psychology SLTopic 2 — Health ProblemsPaper 1 & 2Biological approach~10 min read
Stress, Cortisol and Weight Gain
Everyone says stress makes people eat badly, as if it were a matter of willpower giving way. The biology says something more interesting: stress changes the hormones that tell you when you are hungry and when you are full. The signal itself gets distorted.
📚 What you need to know
Cortisol is a hormone produced in the adrenal cortex when the HPA axis is activated by stress.
HPA = hypothalamus–pituitary–adrenal.
Cortisol normally regulates the immune system and suppresses inflammation, which is useful.
Under chronic stress, excess cortisol over-suppresses the immune system and lowers resistance to illness.
Stress and obesity have a two-way relationship.
Three hormones to name: leptin (fullness), ghrelin (hunger), neuropeptide Y (appetite).
Kumar et al. (2022) is the study — a literature review, not an experiment.
Cortisol and the immune system
Start here, because it is the part examiners ask about most reliably and students learn least well.
🧩 What cortisol does, in order
The body meets a stressor, and the HPA axis activates.
The adrenal cortex releases cortisol into the bloodstream.
In the short term, cortisol regulates the immune system and suppresses inflammation. This is beneficial.
Under chronic stress, cortisol keeps building up.
That leads to over-suppression of the immune system, so resistance to illness drops.
The immune system, mainly white blood cells, defends the body against harmful antigens such as bacteria, viruses and cancerous cells. Stress does not directly cause infection. What it does is reduce the immune system’s ability to fight antigens, which makes infection more likely.
The example that makes it stick. This is why so many students go down with a cold during exam season, when stress levels and cortisol are both high. You did not catch it because you were tired. You caught it because your defences were quietly turned down.
How stress feeds into weight gain
Stress can lead to obesity, and obesity can raise stress levels. It is a two-way relationship, which is why the diagram below is a loop rather than an arrow.
Two mechanisms are involved:
Self-regulation weakens. Stress reduces people’s ability to control their behaviour generally, including resisting fatty or sugary foods.
Appetite hormones are disrupted. Stress interferes with leptin, which signals fullness to the brain, ghrelin, which signals hunger, and neuropeptide Y, which regulates appetite. Disruption to these makes overeating more likely.
Note where the loop can be interrupted. You cannot easily switch off the HPA axis, but stress itself can be managed — which is exactly the conclusion Kumar’s review reached about treatment.
Here is the sentence that lifts an answer: stress does not only make people want to eat more, it changes the information the brain is getting about hunger and fullness. Framing it as a signalling problem rather than a willpower problem is both more accurate and more compassionate, and examiners notice the difference.
🔬 Kumar et al. (2022)
Pulling twenty years of research together
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
Obesity treatment is more effective when stress is also targeted. Stress is a major factor in obesity, though biological and sociocultural factors also play a role. Research shows people eat more under stress because of the cortisol awakening response. Many people self-medicate with comfort food during stress, which increases BMI over time. Recognising and addressing stress-eating is key to breaking the cortisol–stress–obesity cycle.
CONCLUSION
Stress and obesity are closely connected, so they should be studied and treated together rather than separately.
What a literature review can and cannot tell you
A literature review does not collect new data. It gathers existing studies and looks for patterns across them. That has a real advantage: you get a comprehensive appreciation of a complex issue, drawing on cognitive, sociocultural and biological research at once, rather than one narrow explanation.
The corresponding weakness is that a review is only as good as the studies inside it, and the reviewer chooses which studies go in. That is where confirmation bias becomes a genuine threat to validity.
Evaluating the explanation
Strengths
Strong biological evidence for the cortisol–stress link makes the obesity findings convincing.
Stress management strategies such as walking, meditation or a warm bath are accessible and practical for most people.
A review draws on cognitive, sociocultural and biological research, giving a holistic picture.
It produces a clear treatment implication: target stress alongside weight.
Limitations
Tackling stress-related eating is difficult because eating is pleasurable, making behaviour change hard to sustain.
Individual differences are not accounted for. Not everyone eats more when stressed — some lose their appetite instead.
That limits the explanation, since stress does not affect all people in the same way.
A review collects no new data and depends on which studies were selected.
Linking to the concepts
Measurement: a literature review is a good way of gaining a comprehensive appreciation of a complex issue such as stress-related obesity, because it avoids relying on one narrow and possibly limited explanation of a health problem.
Bias: confirmation bias is a real threat to validity in a review. The researcher must practise reflexivity, making sure their own biases, prejudices and preconceived ideas do not lead them to select only the data that supports their hypothesis.
EXAM ANSWER
Discuss one biological explanation of one health problem. [22 marks]
Start with the physiology, in sequence
Stress activates the HPA axis; the adrenal cortex releases cortisol; chronic elevation over-suppresses the immune system.
Connect it to the health problem
Cortisol disrupts leptin, ghrelin and neuropeptide Y, so hunger and fullness signals become unreliable, while self-regulation weakens.
Evidence
Kumar et al.: a review of research from 2000 to 2020 concluding obesity treatment is more effective when stress is targeted too.
Evaluate on individual differences
Not everyone eats more under stress; some lose appetite. So the model describes a tendency, not a rule.
Conclude: a strong mechanism that still needs the person’s contextindividual differences is the sharpest criticism of any biological explanation
💡 Exam tips
Spell out HPA in full at least once. It costs nothing and signals precision.
Name all three appetite hormones with what each one does. Three quick, specific marks.
Use the exam-season cold example. It is concrete and shows you understand the immune link.
Describe the relationship as two-way. Treating it as a one-way arrow loses the point of the topic.
Evaluate the method, not just the finding — a literature review has its own distinct strengths and weaknesses.
This page connects to the depression pages through stress and to the culture pages through food environments. Say so if there is room.
⚠ Common mix-ups
Swapping leptin and ghrelin. Ghrelin makes you hungry, leptin says stop.
Saying stress causes infection. It lowers resistance; the antigens do the rest.
Calling cortisol harmful. It is normally useful. The problem is chronic excess.
Calling Kumar an experiment. It is a literature review, with all that implies.
Claiming everyone overeats under stress. Some people lose their appetite, and that is a named limitation.
Forgetting the loop runs both ways. Weight gain can itself become a stressor.
Up next: Drug Treatments for Depression — the start of Prevention and Treatment. We have spent two topics explaining why things go wrong. Now we look at what actually gets done about it, and how well it works.
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