Eating and weight regulation

We eat for energy. Energy is available in 3 forms; glucose (simple sugar, byproducts of carbohydrates), amino acids (broken down from proteins), and lipids (fats).

Food is processed via digestion. Food and water enter the mouth, pass down the esophagus and then reach the stomach. Substances then appear in the first part of the intestine, the duodenum. In the stomach and the intestine, food is broken down and chemically changed.

Absorptive phase: when the gastrointestinal tract is full and nutrients are absorbed from the digestive system. Glucose and amino acids are the principle source of energy for cells during this phase. Excess nutrients are stored.

Fasting (or post-absorptive phase): phase during which nutrients are not available from the digestive system. Glucose, amino acids, and fatty acids are derived from glycogen, protein, and adipose tissue during this phase. Two types of cells receive nutrition: neurons (glucose only), and non-neural cells (glucose or fatty acids).

Energy can be obtained through a variety of routes. Body cells can metabolise fats or glucose. Brain cells can only metabolise glucose.

Chemical messengers influence on eating: hunger signals are secreted by the stomach wall. Ghrelin is one of the signals that triggers feelings of hunger as mealtimes approach. In dieters who lose weight, ghrelin levels increase which may be one reason its so hard to stay on a diet. 
Satiety signals are produced by adipose (fat) tissue; leptin suppresses appetite as its level increase. When body fat decreases, leptin levels fall, and appetite decreases. A rise in blood sugar levels after a meal stimulates the pancreas to secrete insulin. Insulin suppresses appetite by acting on the brain. The hormone PYY is secreted by the small intenstine after meals, acting as an appetite suppressant.

Ghrelin: hormone secreted from the stomach when its empty. It signals hunger - increasing before meals and decreasing after. It travels through the vagal nerve.

Hunger signals are triggered by glucoprivation: fall in the level of glucose available to cells, detected by the liver and hypothalamus where glucose receptors signal lack of glucose and trigger hunger, and lipoprivation: fall in the level of fatty acids available to cells, detected by the liver. Can also have a combination of the 2.

Gastric factors in various parts of the digestive system:

• Stomach: contains nutrient receptors; an animal will keep eating if food doesn't get to the stomach or if it is emptied before digestion (e.g with a gastric fistula). The stomach detects nutrients, not volume. If food in stomach is replaced with saline solution, an animal still feels hungry
• Intestine: CCK (cholecystokinin) is a peptide hormone secreted in the duodenum which is involved in the breakdown of fats. Food in the gut causes the release of CCK, which sends a satiety message to the brain. PYY (peptide YY) is released after a meal, in proportion to the calories ingested
• Liver: last stage of satiety occurs here. It signals to the brain that food and nutrients have been digested
• Leptin is released by fat tissue as a satiety signal. More leptin = less appetite

Eating is controlled by a network of interacting brain regions which contain detectors of nutrient state and other information. These regions include: cortex, hypothalamus, and the brainstem. The vagus nerve links the brain with several organs via its endings, which are sensitive to nutrient-related events in the liver, stomach, and pancreas.

The cortex contains systems involved in taste perception and in the appreciation of food. The orbitofrontal cortex (OFC) is part of the prefrontal cortex and is linked to the encoding of the reward value of food. The OFC is linked to the subjective hedonic value of food. These systems communicate with the nucleus of the solitary tract. Hypothalamus contains the arcuate nucleus which is important as it has receptors for ghrelin, leptin, insulin, and serotonin 

Dual centre hypothesis: the hypothalamus contains 2 distinct, independently operating centres, one responsible for satiety, the other for hunger. Hunger centre in the lateral hypothalamic (LH) area, satiety centre in the ventral medial hypothalamus (VMH). If the LH is lesioned, there is no interest in food and refusal to eat. If the VMH is lesioned, overeating and rapid weight gain occurs. However if the LH is stimulated, besides overeating, other behaviours are observed too, so LH may be involved in arousal rather than just eating. Also, lesions restricted to the VMH alone don't cause overeating, this is more likely if lesions involve the VMH plus other areas.

Set-point theory (Nisbett, 1972): individuals engage in eating behaviour to maintain internal homeostasis. The system aims for a set-point or target. Therefore, if energy levels are below that target, we eat. If set-point is reached, we stop eating. But what exactly is the system trying to maintain - glucose levels? Body fat levels?

Glucoprivation and lipoprivation can be experimentally induced and will stimulate eating up to when the set-point is reached, supporting set-point theory. However, in everyday life, drops in glucose and fat levels aren't large enough to induce eating. We eat even when glucose levels are high, and external factors such as sight and smell also cause eating.

Positive-incentive theories: eating is a response to positive incentives and to the anticipated pleasure of the food rather than a unique response to deprivation or energy deficit. Different foods have different incentive values - also due to social and environmental factors. High incentive values are usually for foods that are rich in sodium, vitamins & minerals, energy, and sweet and fatty foods.

Environmental factors include

• time of day
• portion size
• distractions

Social factors

• cultural habits
• eating with others

Satiety is specific to the taste of food recently digested (Clifton et al, 1987). We get full faster if meals are limited to one food type. It's a special case of the principle of habituation (Epstein et al, 2009). Cognitive processes linked to specific brain areas influence sensory specific satiety. Eating as habituation encourages variety in the diet, and reduces the possible accumulation of toxin that may be associated with a particular food. However, it may contribute to body weight increase and obesity because more sugar-rich and variety-rich food is available

A circadian rhythm is roughly a 24 hour cycle in the physiological processes of humans and non-humans. Circadian rhythms are important for feeding patterns (McHill et al, 2017). Eating at certain times of the day, which partly depends on sleep habits, may lead to optimal body functionality via clock synchronisation (Hart et al, 2013). Synchronising all the clocks in the body (e.g eating and sleeping) is essential for the body to function at its best.

Portion size: decreasing portion-size increases snack intake. This is typically not balanced out by eating less at meal time.

Distractions: TV dinners are less hungry and eat smaller food portions, but the food intake is more frequent and the energy intake overall is higher

Presence of others: increased meal size in social situations e.g de Castro & de Castro (1989): diary study showed positive relationship between amount of food eaten and number of people present; meals eaten with others were 44% bigger than those eaten alone.

Obesity: when BMI is 20% above the ideal weight. BMI is a basic measurement of body fat based on just height and weight. In 2011, 24.8% of adults were obese, and 16.3% of children were obese. It is estimated that by 2050, the obesity rate will be 60% in men, 50% in women, and 25% in children.

Obesity is thought to have a strong genetic component and a smaller environmental component. Twin studies showed that a child's risk of becoming overweight is mostly down to nature, not nurture (Wardel et al, 2008). Variations in a child's body mass index and waist circumference are attributable to genes (77%) and environment (23%). Heritability of obesity is 70% when there are 2 obese parents, 40% with one, and with none, 10%.

Set-point theory: obese individuals may have a higher lipostatic set-point than non obese individuals. This is equivalent to being stuck with a fixed biologically determined set-point.

Leptin: lack of leptin may cause obesity. It correspond to obesity in animals, with leptin injections being linked to weight loss in obese mice. Could also be a lack of leptin receptors.

However, is obesity is mainly down to genetics, why is it on the rise? Genes don't change that fast, so it is still confusing as to how obesity prevalence can rise. Also, genetic theories cannot explain why obesity is higher in certain cases, like in poeple who watch more TV. There is evidence that obesity is not just due to genetics (Symonds et al, 2011).

Methodological issues: according to BMI, 25 is overweight and 30+ is obese. A relatively small shift in bodyweight is enough to push a lot of people over the BMI category of obesity. BMI does not take gender differences or non-liner changes in body weight the occur with age into account.

Environment's role: Ravussinet et al (1990) showed the role of the environment in a study on Pima Indians in Arizona. Nearly 1000 years ago, the tribe split into 2 groups, with one remaining in what is now the US. The other group settled in the mountains of Mexico. The American Pima adopted the modern American lifestyle and diet, making them 26kg heavier than their Mexican cousins (on average), and also increased their cholesterol levels.

Settling-point theory (Hill, Pagliassotti & Peters, 1994): obese people are more sensitive to food-related stimuli in the social and physical environment, which influences their energy intake.

Thrifty genotype (Neel, 1962): in early evolutionary history, thrifty genes promoting efficient fat deposition were advantageous because they allowed survival in periods of famine. In modern society, these genes are disadvantageous because they promote fat deposition in preparation for a famine that's unlikely to come. The end result is widespread obesity and diabetes.

Medical consequences of obesity:

• Diabetes
• Heart disease
• High blood pressure
• Arthritis
• Indigestion
• Gallstones
• Some cancers
• Snoring and sleep apnoea
• Infertility

In financial terms, obesity costs the NHS £6.4bn per year (in 2015).

It can also have psychosocial effects: discrimination and negative attitudes, mental illness, and stress.

Anorexia is the condition in which someone tries to keep their weight as low as possible, which may be through restricting the amount of food eaten, and/or doing excessive exercise.

Biological factors: Twin studies show that 50-80% of variance in anorexia can be explained by genetic factors, showing a biological basis. They may also experience altered satiety/hunger hormones, like having high levels of ghrelin and low levels of leptin.

Psychological factors: childhood anxiety is an important genetically-mediated pathway towards the development of anorexia

Social factors: social isolation, family dynamics, and maternal criticism can all have an effect. Social messages promoting a specific type of body image can be damaging.

There is no one gene identified to cause anorexia. Rather, genetically heritable personality traits and social factors predispose certain individuals to anorexia. There is a broader phenotype featuring perfectionism, rigidity, tendency to behavioural constraint.

Minnesota Starvation Study (Keys et al, 1950): 36 young men underwent very restrictive caloric intake for 6 months. Following the restricted diet, volunteers experiences were the same as those of patients with eating disorders. Standardised personality testing revealed that semi-starvation resulted in significant increase on the depression, hysteria, and hypochondriasis scales.

Anorexia affects the whole body

• Hair thins and gets brittle (also in nails)
• In the brain: can't think right, fear gaining weight, sad, moody, irritable, bad memory, fainting
• Low blood pressure, slow heart rate, palpitations
• Weak muscles, swollen joints, bone loss and fractures
• Kidney stones and failure
• Low potassium, magnesium and sodium
• Constipation and bloating
• Periods stop and there are problems with growing
• Skin bruises and dries easily, growth of fine downy hair all over the body, feel cold easily

Costs the NHS between £3.9 and 4.6bn.

Anorexia is reinforced because eating less food is linked to reward. Sufferers experience:

• Corticotropin-releasing factor. This is released when food intake is reduced
• This activates the pituitary-adrenal axis
• This in turn enhances dopamine release from the ventral striatum
• Ventral striatum acts as a reward system

Obesity and anorexia: both imply unbalanced eating, and both result in abnormal body weight. Both multi-factorial disorders.

Obesity is more strongly related to genetic abnormalities than anorexia. Anorexia has a strong emotional component. Social and cultural influences play a different role in obesity and anorexia.