Evolutionary explanations for food preference

Our preferences were shaped in the environment of evolutionary adaptedness (EEA) — a world in which food was scarce and some plants were poisonous.

• Preference for sweet and fatty foods. Sweetness signals ripe fruit and readily available energy; fat is the most energy-dense nutrient. In a world of scarcity, an appetite for both was adaptive. It is maladaptive now, in an environment where such foods are abundant — a mismatch that contributes directly to obesity.
• Preference for salt. Sodium is essential for nerve and muscle function and could not be stored, so a taste for salt was adaptive.
• Bitterness aversion. Many plant toxins taste bitter, so an innate aversion to bitterness protected against poisoning. Children's rejection of green vegetables fits this pattern.
• Neophobia — a wariness of new foods, most pronounced in early childhood, when a child is newly mobile and could eat something dangerous. It is adaptive: the safest food is the one you have eaten before and survived.
• Taste aversion learning (the Garcia effect). Garcia and Koelling (1966) found that rats which were made ill (by radiation or a drug) some time after consuming a novel-tasting solution developed a powerful and long-lasting aversion to that taste — after only one pairing, and despite a delay of hours between the taste and the illness. This 'one-trial learning' violates the usual rules of classical conditioning, which require repeated pairing and close contiguity. Crucially, rats could associate taste with illness but not light or noise with illness. This is biological preparedness: we are evolutionarily prepared to make exactly the associations that keep us alive.

Evaluation: the Garcia effect is powerfully supported and has real-world application — it explains the food aversions that patients develop during chemotherapy, and has been used to deter coyotes from attacking livestock by baiting carcasses with a nausea-inducing agent. But the evolutionary account struggles to explain cultural variation: chillies are painfully aversive on first exposure, yet are staples in many cuisines. Nor can it easily explain why some people relish extremely bitter foods (coffee, dark chocolate). It also runs the risk of being an untestable 'just-so' story, since a plausible adaptive account can be invented after the fact for almost any preference.

Why one trial?

The role of learning in food preference

• Classical conditioning. A neutral food paired with something already liked comes to be liked itself. This is why flavour-flavour learning works: pairing a vegetable with a sweet sauce increases liking for the vegetable. Advertisers exploit this by pairing products with attractive imagery and music.
• Operant conditioning. Eating a food that reduces hunger, or that tastes good, is positively reinforced, so the behaviour is repeated. Parents who use dessert as a reward for eating vegetables inadvertently teach the child that the vegetable is the price and the dessert is the prize — which typically reduces long-term liking for the vegetable.
• Social learning theory. Children imitate the eating behaviour of models. Parents are the most important: children can only eat what is provided, and parental attitudes are copied. Peers matter increasingly with age, and the media provides high-status models and abundant food advertising.
• Cultural influences. Food preferences vary enormously by culture and are transmitted through the family. Norms about what is edible (insects, offal, pork) are learned, not innate.

Evaluation: a purely learning-based account is contradicted by the powerful evidence for innate preferences — newborns show a preference for sweet tastes before they can have learned anything, and neophobia and bitterness aversion appear without instruction. The best conclusion is interactionist: innate biases set the starting point, and learning and culture shape the detail. Much of the research is also correlational — the fact that children's preferences resemble their parents' could reflect shared genes as much as shared learning, which is a genuine confound.

The dual-centre model, ghrelin and leptin

Eating is governed by homeostasis — the maintenance of a stable internal state. Blood glucose falling below a set point triggers hunger.

The dual-centre model of the hypothalamus:

• Lateral hypothalamus (LH) — the 'ON' switch, or feeding centre. Stimulation of the LH causes an animal to eat; damage to it (a lesion) causes aphagia — a refusal to eat, potentially to the point of starvation. It acts partly via the neurotransmitter neuropeptide Y (NPY), which is a powerful appetite stimulant.
• Ventromedial hypothalamus (VMH) — the 'OFF' switch, or satiety centre. Stimulation of the VMH causes an animal to stop eating; damage to it causes hyperphagia — over-eating and gross obesity.

Hormones

• Ghrelin — the hunger hormone, secreted by the stomach when it is empty. Ghrelin levels rise before a meal and fall afterwards. It signals the arcuate nucleus of the hypothalamus, stimulating the release of NPY and thus appetite.
• Leptin — the satiety hormone, secreted by fat cells (adipose tissue). The more fat a person carries, the more leptin circulates, so leptin acts as a long-term signal of energy stores, inhibiting NPY and reducing appetite. Rare genetic leptin deficiency produces severe childhood obesity, which can be treated by giving leptin.
• CCK (cholecystokinin) — released by the small intestine when food arrives, promoting short-term satiety and slowing the emptying of the stomach.

Evaluation: the model is supported by lesion studies in animals, but it is now known to be far too simple. Lesions to the VMH also damage a nearby region, the paraventricular nucleus, so the classic hyperphagia finding may not be caused by VMH damage at all. Most obese people, moreover, have high — not low — levels of leptin, which suggests the problem is leptin resistance rather than leptin deficiency, and explains why leptin therapy has been disappointing as a treatment for obesity. And homeostasis alone cannot explain why we eat when we are not hungry, or stop when food is still available — psychological and social factors are essential.

Lesion the hypothalamus

Explanations for anorexia nervosa

Anorexia nervosa — a serious eating disorder characterised by a significantly low body weight, an intense fear of gaining weight, and a distorted perception of one's own body. It has the highest mortality rate of any psychiatric disorder.

Biological explanations

• Genetic. Anorexia runs in families. Holland et al. (1988) studied 45 pairs of twins where one had anorexia, and found a concordance rate of 56% for MZ twins compared with 5% for DZ twins — a substantial genetic component. It is polygenic.
• Neural. Serotonin and dopamine are both implicated. High serotonin levels are associated with the anxiety characteristic of anorexia; altered dopamine activity in the striatum may explain why anorexic patients associate food with anxiety rather than pleasure, and why they can find self-starvation rewarding.

Psychological explanations

• Family systems theory (Minuchin et al., 1978) — the specification names three concepts. Enmeshment: family members are over-involved in each other's lives, with no clear boundaries, so the young person has no separate identity. Autonomy: because the enmeshed family denies the adolescent any independence, the normal developmental task of separating from the family is blocked. Control: refusing food becomes the one domain in which she can exert control over her own life. The family is also typically overprotective, rigid and conflict-avoiding.
• Social learning theory — anorexia is learned by modelling and reinforcement. Thin models in the media are seen to be rewarded with status and attention (vicarious reinforcement); praise for weight loss directly reinforces restriction.
• Cognitive explanations — distortions (a genuinely distorted perception of body size) and irrational beliefs ('if I eat that, I will become fat'), maintained by black-and-white thinking about food.

Evaluation: family systems theory has been criticised for blaming parents on very weak evidence, and much of it is based on retrospective accounts from families already in crisis — the 'enmeshment' may be a consequence of having a critically ill child rather than a cause. The cultural evidence is important: Becker et al. (2002) studied adolescent girls in Fiji before and after the introduction of Western television and found a marked increase in disordered eating attitudes and in dieting after television arrived — strong support for social and media influences. But note that the vast majority of girls exposed to thin media models do not develop anorexia, so media exposure cannot be a sufficient cause: a diathesis-stress account is more plausible.

Biological and psychological explanations for obesity

Biological explanations for obesity

• Genetic. Twin and adoption studies show a substantial heritable component; adopted children's weight correlates more closely with their biological than their adoptive parents.
• Leptin resistance and abnormalities in the hypothalamic circuits described earlier.
• The thrifty gene hypothesis (Neel) — genes that promote efficient fat storage were adaptive in the feast-and-famine EEA and are maladaptive in an environment of permanent abundance.

Psychological explanations for obesity

• Restraint theory (Herman and Polivy). Paradoxically, attempting to restrain eating makes over-eating more likely. Cognitive restraint requires constant vigilance and depletes self-control, so restrained eaters are prone to disinhibition.
• The boundary model (Herman and Polivy). We eat between a hunger boundary and a satiety boundary. Dieters impose a cognitive 'diet boundary' well below their satiety boundary. Once they cross it — by eating a forbidden food — the 'what-the-hell effect' takes over and they eat all the way up to the satiety boundary, ending up eating more than a non-dieter. This explains why breaking a diet so often ends in a binge.
• Disinhibition — restraint is broken by emotional distress, alcohol, or the presence of highly palatable food.

Neural explanations for obesity — beyond leptin resistance, imaging research implicates the dopamine reward system: some obese individuals show reduced D2 receptor availability in the striatum, so ordinary amounts of food are less rewarding and more must be eaten to obtain the same reward. This parallels the reward-deficiency account of addiction.

Evaluation: restraint theory is well supported by laboratory 'preload' studies, in which restrained eaters given a milkshake preload then eat more ice cream than non-restrained eaters given the same preload. But restraint theory has a serious problem: it cannot explain anorexia, where restraint plainly does not lead to over-eating and can be sustained for years. The biological and psychological explanations are complementary, and obesity is best understood as the interaction of a genetic vulnerability with an obesogenic environment — an environment engineered to deliver cheap, energy-dense, highly palatable food.

The what-the-hell effect

Which hormone?

Leptin and obesity

Neophobia

Learning explanations

Evaluating family systems theory

Evolutionary logic

Restraint theory's limits

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Term and meaning

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The big ideas to know

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