Do genetic and environmental contributions to obesity need to sum to 100%? I often hear non-scientists and scientists alike saying something like “Pink eye is 37 % genetic, therefore it is 63 % environmental”. I’d like you to stop and think about whether this is true. To help with you thinking about this I’ve constructed 3 Venn diagrams, labelled A, B and C where genetic contribution is beige, environmental contribution is pink and being obese is in yellow. Which of these Venn diagrams best explains obesity incidence and do the genetic and environmental risks sum to 100%. To help you think about this you might want to ask yourself what is the % contribution of the environment for someone to suffer from phenylketonuria, what is the genetic contribution. If you don’t know what phenylketonuria is look it up, Wikipedia is fine. What symptoms does someone with phenylketonuria have if the follow a strict diet? Does this mean it is 100% environmental? Is it also 100% inherited?

Question

BlackTom AI · Accepted Answer

Heritability is a population statistic and genes and environment can interact, so the correct diagram is C.

1) Relevant concepts
- Heritability estimates the proportion of variance in a trait in a population attributable to genetic differences, not a per‑person “% genetic” cause.  
- Many traits (including obesity) are complex: genetic susceptibility and environmental exposure interact (gene × environment).  
- Phenylketonuria (PKU) illustrates interaction: pathogenic PAH mutations are necessary (genetic), but neurotoxic symptoms occur only if dietary phenylalanine is not restricted (environment).

2) Step‑by‑step reasoning
- If a disorder required only genes (no environmental trigger) the phenotype would appear regardless of environment — that would look like a purely genetic circle.  
- If a disorder required only environment the phenotype would appear regardless of genotype — that would look purely environmental.  
- PKU: genotype is necessary (you won’t get PKU without the mutations) but the phenotype is prevented by environmental change (low‑Phe diet). That shows dependence on both factors — i.e., the phenotype lies in the overlap of genetics and environment.  
- Obesity is similar for most people: genetic susceptibility raises risk but an “obesogenic” environment (high caloric access, sedentary lifestyle) is usually required to produce the phenotype. Thus obesity cases primarily lie where genetic susceptibility and environment overlap.

3) Calculations
- No numerical calculation applies. Important point: you cannot algebraically sum “% genetic” + “% environmental” = 100% when effects overlap or interact — overlap would be double‑counted and heritability is population‑specific.

4) Why C is correct
- Diagram C places the obesity (yellow) region inside the intersection of genetics (beige) and environment (pink), reflecting that both usually contribute and that the phenotype depends on their interaction (matches PKU logic and modern obesity understanding).

5) Why A and B are incorrect
- A implies obesity arises independently within separate genetic‑only and environment‑only domains (purely additive, no interaction) — not consistent with PKU or typical obesity.  
- B implies obesity largely independent of one or both factors or only marginally overlapping, failing to capture the usual gene × environment dependence.

6) Conclusion
- Therefore diagram C best explains obesity incidence, and genetic and environmental “percent contributions” do not simply sum to 100%. This matches the provided answer: b. C.

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