The historical context of food scarcity and the necessity for physical labour have significantly shaped human metabolism and our current struggles with obesity. Metabolism efficiency, which once served as an evolutionary advantage, now contributes to weight challenges in the modern world. This shift underscores the complex interplay between biological adaptations and contemporary lifestyles.

HISTORICAL ADAPTION

Historically, an efficient metabolism that required less energy (food) to perform physical tasks was advantageous. In times when food supply was inconsistent and physical labour was essential for survival, individuals with a more efficient metabolism were more likely to survive and reproduce. These conditions favoured storing excess energy as fat, which could be used during periods of scarcity.

MODERN CHALLENGES

With consistent food supply and technological advancements reducing physical exertion in daily tasks, the same metabolic efficiency has become a predisposing factor for obesity. High-calorie foods are readily available today, and much of the population leads a sedentary lifestyle. For individuals with an efficient metabolism, consuming more calories than are expended is easier, leading to weight gain.

NEURAL EXPLANATIONS

Neural explanations for obesity highlight the significant role of the brain's regulatory systems in managing energy balance, appetite, and food intake. Dysfunctions in neurotransmitter systems like serotonin and dopamine and abnormalities in the hypothalamus provide insight into the neurobiological underpinnings of obesity.

SEROTONIN AND OBESITY

Serotonin is crucial for regulating appetite and satiety signals within the hypothalamus. Abnormally low levels of serotonin can lead to disrupted satiety cues, resulting in overeating as the body fails to receive accurate signals to stop eating. This dysfunction may stem from genetic predispositions, environmental stressors, or other disorders like depression, highlighting the complex interaction between the brain's chemistry and obesity.

DOPAMINE’S ROLE

Dopamine, associated with the brain's reward system, also plays a vital role in obesity. It's linked to the pleasure derived from eating and the anticipatory cues associated with food. Studies, such as those by Gene-Jack Wang et al., demonstrate that individuals with obesity often have fewer dopamine D2 receptors, leading to diminished reward responses to food intake. This deficiency in reward response may drive individuals to overeat as a compensatory mechanism to achieve the expected pleasure from eating, akin to behaviors observed in addiction.

THE SUGAR RUSH

Chasing Serotonin and Dopamine

There is a second component to sugar addiction: not only are sugars (‘carbohydrates’) metabolically addictive, but they are most likely physically addictive too. Because sugar pumps up Dopamine and Serotonin levels in the short-term—but, like any addictive drug, the reward diminishes over time, while the compulsion to eat ‘carbohydrates’ (sugar) remains. So we eat more and more ‘Carbohydrates’ (sugar) to recreate that dopamine rush and subsequent serotonin contentment…but as we gain weight, we get less and less of that reward. All we get is the sugar spike and subsequent metabolic crash. (Viking 1999), likens the biochemical effects of carbohydrates to those of alcohol and cocaine. The more you eat, the more you want; addicts cannot control their intake.

Bad eating habits: Eating too quickly: A study conducted by Maruyama et al. and published in the British Medical Journal in 2002 supports the thesis that eating quickly is linked to obesity. Maruyama’s study found that those who ate more quickly were significantly more likely to be overweight. In addition, the study found that those who ate until feeling full were also more likely to be overweight. It was concluded that eating quickly and eating until full could have a greater impact on being overweight.



HYPOTHALAMIC DYSFUNCTION

The hypothalamus, particularly the arcuate nucleus, is central to the regulation of appetite and body weight. It monitors energy levels and integrates signals related to food intake and energy expenditure. Dysfunctions or maladaptations in this area can lead to imbalances in energy homeostasis, contributing significantly to obesity. The arcuate nucleus's role in adjusting food intake relative to physical activity underscores the importance of the hypothalamus in maintaining a healthy weight.

HORMONAL EXPLANATIONS

Hormones also play a major role in hunger and obesity. Recent reports have described leptin, a hormone released by fat cells. Although leptin is absent in a strain of genetically obese mice, it is not in obese humans (Gura, 1997). Many obese people become Leptin resistant; if Leptin is not uptaken by the body, it increases appetite. See earlier discussions on Leptin (e.g., how Leptin resistance is caused by grains and sugar). This Western obsession with carbohydrates has devastating consequences for weight gain. Firstly, carbs increase appetite, secondly, although eating carbs may decrease Ghrelin more quickly than protein and thus kill hunger pangs, the effects are short-lived and appetite returns quickly.

MOTHER’S WEIGHT

Developmental variables also influence adult weight. Too little or too much to eat early in development affects adult weight. Maternal starvation during pregnancy affects children's adult body weight. In

1944, during World War II, the retreating German armies virtually isolated a part of the Netherlands (Holland), resulting in a severe winter famine. When the young men born there in the spring of 1945 were drafted 18 years later, they were more likely to be overweight than were young men from other parts of the Netherlands (Ravelli et al., 1976; Stein et al., 1975).

Having too much to eat as a baby can also increase adult body weight. People who were fed too much as babies are more likely to be overweight than adults, apparently because early overfeeding makes the developing body produce extra fat cells, which need to be filled.

Breastfeeding may reduce the chance of developing obesity. A recent study reported that the longer a child had been breastfed, the lower his/her chance of becoming obese at age 5 to 6 (von Kries et al., 1999). However, this is a correlational study, so breastfeeding may be confounded with other variables, such as socioeconomic status, which also correlates with obesity

PRENATAL EXPOSURE

Epidemiological studies have established a connection between prenatal alcohol exposure and an increased risk of alcoholism later in life, suggesting that early exposure can have long-lasting effects on preference and behaviour beyond the well-documented risks to fetal health and brain development (Abate et al., 2008). This implies that prenatal experiences can influence future taste preferences and potentially addictive behaviours.

The concept of prenatal learning extends to dietary preferences beyond alcohol. Research involving rats has indicated that a maternal diet high in fat and sugar can predispose offspring to similar dietary preferences (Bayol et al., 2007). Studies show that offspring of rats fed a diet rich in "junk" food during pregnancy displayed alterations in brain reward pathways, specifically in opioid signalling, making them less sensitive to the rewards of high-fat, high-sugar foods. Consequently, these offspring needed to consume more such foods to achieve the pleasurable dopamine "rush" associated with eating (Ong and Muhlhausler, 2011; Gugusheff et al., 2013).

Furthermore, the theory that breastfeeding can influence early taste preferences is plausible since babies directly consume milk, providing immediate and direct exposure to various flavours in the mother's diet. This direct form of exposure may reinforce the preferences established prenatally, further emphasizing the importance of maternal dietary choices during both pregnancy and lactation periods in shaping infant taste preferences and potentially long-term dietary habits.

The theory that our food preferences are shaped even before birth suggests a fascinating aspect of human development. According to research, a pregnant mother's diet can influence her unborn child's future food preferences through the flavours transmitted via amniotic fluid. Studies have indicated that from as early as 12 weeks into gestation, a fetus begins to swallow amniotic fluid, and by 28 weeks, it develops a significant sense of smell. This early exposure could potentially familiarize babies with certain flavours even before birth.

Evidence from both animal and human studies supports the idea of prenatal taste learning. For example, newborns have been shown to recognize and prefer the smell of their amniotic fluid, suggesting early learning about food odours and tastes that occurs in the womb.

BREASTFEEDING

Mennella and her colleagues at Monell have also shown that nursing babies detect flavours like garlic, ethanol (from alcoholic drinks) and vanilla in their mothers' milk. A baby who has never tasted garlic will suckle longer the first time their mother eats it, presumably gathering extra information about this new flavour. Compared with babies whose mothers took garlic placebo pills, the “garlic babies” spent more time attached to the breast. "[Mother's milk] is one of the first ways babies learn," Mennella thinks.

Breast-fed babies whose mothers eat a wide range of foods are more likely to embrace new foods later on, her research has shown, and infants fed on harsh-tasting formulas remain more tolerant of bitter and sour at age 4 or 5. Mennella thinks this may hint at how individual flavour preferences begin developing. "Our olfactory memories are oldest, most resistant to change," she says. "I think that underlies why certain foods are preferred—they are associated with things that occur early in life."

Rats also learn what to eat. Mother's milk can be flavoured by adding flavours to the food the mother eats. Rat pups born to rat mothers that ate a flavoured food grew up preferring that flavour. Young rats also learn what to eat by smelling the breath of older rats returning to the nest after eating. Rats are less comparable.

Studies have shown that the diets of pregnant rats, especially those high in fats and sugars from foods like potato chips and doughnuts, can significantly influence the food preferences of their offspring (Bayol et al., 2007). This effect extends to altering the brain's reward system in these offspring, specifically the pathways associated with opioid signalling.

Further research indicates that the reward system in their offspring's brains changes when pregnant rats consume a diet laden with "junk food" components—such as cookies, cheese puffs, sweetened breakfast cereals, and processed meats. The offspring from mothers on a "junk food" diet exhibit a reduced sensitivity to the rewards typically triggered by high-fat, high-sugar foods. Consequently, these offspring need to consume larger quantities of such foods to achieve the dopamine-induced "rush" that contributes to the pleasurable experience of eating (Ong and Muhlhausler, 2011; Gugusheff et al., 2013).

Julie Mennella's research involving pregnant women consuming carrot juice during pregnancy found that infants exposed to carrot flavor in utero showed a greater acceptance for carrot-flavored cereal compared to those without such exposure. This points to prenatal learning as a factor in shaping dietary preferences.

However, various factors can confound these findings, such as whether a baby is breastfed or bottle-fed and other foods introduced during weaning. The research raises questions about how these prenatal flavour experiences translate into long-term food preferences, considering potential genetic influences and the role of early dietary exposure post-birth.

Critically assessing these studies, it's clear that while prenatal exposure to flavours can influence initial taste preferences, the complexity of human taste development is influenced by a myriad of genetic, environmental, and cultural factors. Further research is needed to fully understand the mechanisms behind prenatal taste programming and its impact on lifelong eating habits.

While sensitive, our taste buds rely heavily on integrating other senses, such as smell and sight, to perceive and distinguish flavours fully. Research indicates that these senses significantly influence our expectations and perceptions of taste. Experiments, where participants were blindfolded, have shown difficulties in identifying subtle differences in flavours, such as different types of sweets, suggesting that people struggle to identify flavours accurately without visual cues or prior knowledge (schemas) of what they are eating.

This raises questions about the sensitivity of taste buds, especially in newborns who have not yet developed complex schemas for flavours. It suggests that the ability of babies to detect specific flavours, like a carrot in amniotic fluid, may not solely depend on the taste buds' sensitivity but also on the integration with the sense of smell and, potentially, even the visual aspects associated with eating after birth.

The detectability of specific flavours, such as carrot juice, in amniotic fluid, among other flavours a mother might consume, is a subject of debate. While some studies support prenatal exposure to flavours through amniotic fluid, the extent to which these flavours are distinct and memorable enough to influence a baby's future food preferences remains unclear

HORMONES AND EATING SPEED

A study published this year in the Journal of Clinical Endocrinology and Metabolism explored the possible causal effects of eating speed. The study’s author, Kokkinos, conjectured that the speed at which a person eats might affect hormone levels, which might explain the difference in satiety ratings between those who eat quickly and those who eat slowly, e.g., it takes 20 minutes for the food to register in the brain. Hence, if you eat quickly, you eat more in that twenty minutes than someone who eats slowly. Research shows fat people eat quickly.

RESEARCH

Experiments with rats and humans have shown that when large amounts of very tasty foods are available, subjects will overeat and become obese (Bobroff & Kissileff, 1986; Jordan & Spiegel, 1977; Sclafani & Springer, 1976).

The incidence of morbid obesity has been a problem only in the last twenty-five years, although this research is correlational only. Countries that tend to have morbid obesity are also modern individualistic countries with easy access to fatty foods, fast foods and carbohydrates. Other theories explaining this statistic seem inadequate, e.g. mutation of genes could not have occurred so quickly.

CONCLUSIONS

Although many aspects of human eating behaviour may have helped humans survive in a natural environment, these same aspects of human eating behaviour are frequently maladaptive in our current environment, where highly preferred foods are also easily and cheaply available. In our current environment, these behaviours contribute significantly to our population being overweight and obese and suffering from various health problems associated with overeating. There is a mismatch between some aspects of the environment in which we evolved and currently exist.

EVALUATION

Much of the research on neural mechanisms is convincing and has a good experimental design. Consider ghrelin studies and leptin studies, for instance.

Low-calorie diets fail with alarming consistency. This adds credibility to all the above theories.

The government needs to change its dieting advice. Low calorie does not work.

The government must restrict food industries and fast food chains, increasing taxes or requiring health warnings on their products.

Reductionist. It all boils down to survival and reproduction. Does not consider culture, learning lifestyle, or other biological factors. Plus, it can’t just be evolutionary; as it is only countries in the West that have obesity problems, people in collectivist cultures are not so obese. It must be our environment, e.g., toxic environment, plentiful food. ‘‘Genes load the gun, the environment pulls the trigger’’ In other words, modern lifestyle causes us problems with our evolutionary food preferences. So, ET must also be combined with a psychological lifestyle explanation for it to make cultures obese. Evolutionary theory alone in collectivist cultures is still a generally adaptive way of life as food is scarce. Advertisers, fast food chains, manufacturers, and supermarkets create havoc with these evolutionary mechanisms in modern societies. (Bray, 1998). Therefore, ET and lifestyle change can explain the rapid rise in obesity over the last twenty-fifty years, as it only seems to occur in countries where food availability is easy (fast and cheap, sweet, refined carbohydrate food).

However, some cultures and individuals do not put on weight. Are there individual differences? Not all people gain weight. Sixty-four per cent of the UK are overweight. Why aren’t the other 36? Are genetic factors involved, too? Some people may have inherited more Leptin production, etc.

Co-evolution? Some cultures are more prone to gaining weight. Or maybe people have different constitutions because they evolved in different places. (co-evolution) For instance, people from Africa, Southeast Asia and Polynesia are especially prone to obesity because they are more likely to have inherited the genes that encourage the storage of fat, Jeffrey Friedman, an obesity specialist at the Rockefeller University in New York, writes in the journal Science.’ The difference in obesity rates between ethnic groups could have something to do with their respective genetic histories. "For people who lived in times of privation, such as hunter-gatherers, food was only sporadically available, and the risk of famine was ever-present.” In such an environment, genes predisposing to obesity increase energy stores and provide a survival advantage in times of famine. This is the so-called thrifty gene hypothesis," he says, explains why obesity often runs in the family

EVALUATION: Jeffrey Friedman

simple, effective explanations

There is evidence that certain ethnic groups are more predisposed to obesity

reduce the risk of stigmatisation of obese individuals

BUT might reduce the effectiveness of dieting

doesn’t explain why obesity is on the increase today, whereas our gene pool has remained constant

doesn’t explain why geographical relocation to an obesogenic environment often causes individuals to gain weight

it is still unclear how genes are involved in obesity and to what extent.

People in collectivist societies also put on weight. Moreover, although obesity has never been as problematic as it is now, people have been obese throughout history. Other theories must also be considered to work with EP or in isolation. For instance, the medical community has long documented how refined Carbohydrates increase appetite and cause damage to Leptin, Ghrelin, etc. While most of us are guilty of savouring an occasional snack, eating too many carbohydrates or junk foods can lead to more hunger. The more carbohydrates you eat, like white bread and chips, the more glucose you will generate. Your body produces large amounts of insulin to manage this excess glucose. We must combine neural, evolutionary and lifestyle theories to understand.

Deterministic? We have no choice but to eat past satiety or like fat. However, 36% of people in the UK are not overweight. Some people are Successful dieters; others can eat healthily and avoid fat, sugars, and refined carbohydrates.

Obesity costs employers over 13 billion dollars a year. Employees are missing millions of work days due to illness related to obesity. Obesity costs the taxpayer millions in terms of money spent treating it in the NHS. There is a need to put money and time into something more productive and healthy! Never mind the many deaths it causes!

Psychology is a science that finds it difficult to isolate variables. How can you possibly isolate everything and determine the absolute causes of obesity? There are too many factors, such as Ghrelin, Leptin, glucose, the thrifty gene, etc. It would also be expensive.

Can obesity be linked to psychological causes, too? For example, operant conditioning, eating everything and being seen as good; social learning theory, copying obsessive parents’ eating habits; and psychodynamic causes, e.g., eating too much as a way of hiding pain/oral complex/ sexual problems.

Not all carbs that make us fat lack fibre. See the article below:

 Let us return to the “carbohydrates are making us fat” issue. Historical carbohydrate intake data make it glaringly obvious that blaming all carbohydrates for current obesity rates is grossly misguided.

A study from the American Journal of Clinical Nutrition, which displays the average per capita intake of calories and macronutrients (fat, protein, and carbohydrates) in the United States between 1909 and 1997, is rather interesting, especially since it disproves much of the central arguments made by fervent low-carb eaters. For starters, many in the low-carb camp like to make the statement that calories are irrelevant (according to them, calories from fat and protein “don’t count” because they do not lead to weight gain). This study shows that “until 1980, the total energy intake remained relatively constant. Then, between 1980 and 1997, energy intake increased by > 500 kcals/day.” In addition, wouldn’t you know the early 1980s was when obesity rates began to rise? Now, yes, approximately 80% of these extra calories came from carbohydrates. Specifically, that study points out that carbohydrates went from comprising 48 per cent of the diet to 54 per cent of the American diet. However, it also states that “from 1963 to 1997, total fat consumption increased nearly 30%, protein consumption increased 8%, and total energy consumption increased 9%”. Therefore, we are looking at a caloric increase from all macronutrients. Let us take a closer look at carbohydrates, though. The “It’s the Carbohydrates, stupid!” advocates point out that carbohydrate consumption in the United States has increased over the past fifty years. Yes, absolutely. Set the clock back another fifty years, and the “blame the carbohydrates” mentality does not hold much weight.

The average grams of carbohydrate consumed per capita in 1909. That’s right — the same as 1997! Alas, the difference is in the quality of carbohydrates. Total grams of carbohydrates remained the same, but fibre intake plummeted. In other words, what happened after 1980 was an increase in specific sources of carbohydrates: simple/refined carbohydrates: caloric sweeteners (i.e., corn syrup, sugar, etc.) and refined grains (white bread, pasta, rice, etc.

According to figures by the United States Department of Agriculture’s Economic Research Service, “processed potatoes [mainly fries and chips] comprised 64 per cent of total U.S. potato utilization during the 2000s (compared to 35 per cent in the 1960s).”ut fibre intake plummeted Therefore, once again, we are looking at higher intakes of highly processed, fibreless, refined potatoes.

Evaluating neural explanations for obesity reveals a nuanced understanding of how biological factors contribute to this complex condition. While research, such as Ohia et al. (2013) and Ritchie and Noble (2003), provides valuable insights into the roles of serotonin and dopamine in obesity, these explanations also face limitations and challenges in their application and interpretation.

Strengths of Neural Explanations

• Research Support: Studies on serotonin receptors and the DRD2 gene offer compelling evidence linking neural mechanisms with obesity. These findings suggest a biological basis for overeating, providing a clearer picture of obesity's aetiology.

• Potential for Treatment: Understanding the neural underpinnings of obesity opens pathways for developing targeted drug therapies. Addressing serotonin and dopamine deficiencies may mitigate some of the biological factors contributing to obesity.

Limitations of Neural Explanations

• Generalizability of Animal Studies: Research conducted on animals, such as mice, raises questions about the applicability of findings to humans. The physiological and psychological complexities of human obesity may not be fully captured in animal models.

• Correlational Nature: The correlational nature of studies examining neurotransmitter levels and obesity makes it difficult to establish causality. It is unclear whether abnormalities in serotonin and dopamine systems are causes of obesity or consequences of it.

• Overemphasis on Biology: Focusing predominantly on neural explanations may overlook the multifactorial nature of obesity, which includes environmental, psychological, and social determinants. A more holistic approach is necessary to understand and address obesity effectively.

• Individual Differences: Neural explanations may not account for individual variations in obesity. Genetic predispositions, lifestyle choices, and environmental influences also play significant roles in the development and maintenance of obesity.

 EVOLUTIONARY EXPLANATIONS OF OBESITY

Humans evolved in an environment with limited and erratic access to food; several facts about human weight regulation involve maximising stored energy.

Binge eating (or just being plain greedy)

Binge eating: Adaptive in the EEA, as you would never know when your next meal was coming. Those who binged stored fat and survived when food was scarce. In an environment with a limited or erratic food supply, it would be adaptive for animals to take in as much food as possible whenever it is available. Then, if possible, these same animals should retain (as opposed to use) the calories thus consumed as insurance against future periods of food scarcity, e.g., they would store fat. Thus, many of us are prone to overeating when food is abundant.

Impulsive eating (grabbing the quickest option, e.g., choosing fast food over cooking dinner)

It makes evolutionary sense to take food and resources whenever available and not wait for a later delayed benefit. In other words, grab a bag of crisps, order a pizza or buy a ready-made meal over cooking something healthy. In essence, impulsiveness, not self-control, has been naturally selected. Please don’t wait for the fruit to grow bigger; eat it immediately. After all, it may go rotten, get eaten by someone else or you may not see anything else to eat for days. The successful ancestor was the one who took the available food.

Commentary

It is apparent that the above evolutionary heritage again causes problems with our modern-day preferences. Nowadays, food is readily available in modern society, and there is far less uncertainty over death and disease. Therefore, eating a burger and chips as a snack on the run rather than preparing a wholesome meal at home may seem maladaptive. Our evolutionary heritage persists, however, and we engage in maladaptive and impulsive behaviours.

Our love of fast food could also be explained by our busy lifestyle (e.g., a lifestyle explanation, as working Mothers don’t have time to cook).

Liking all the wrong foods!

In our current environment (individualistic and Western cultures only), in which we are surrounded by foods for which we have a high preference, foods that were scarce in the environment in which we evolved, we tend to overeat and gain weight. We have evolved to love foods in the EEA that would have been beneficial to survival, e.g., fat, sugar and carbohydrates were rare in the EEA, so love of them presented no danger to health, but in modern societies, where they are now available in abundance humans seems unable to limit them (Exercise might mitigate some of this weight gain. However, despite ensuing health problems, most adults prefer to conserve energy and not exercise, using labour-saving devices such as elevators and washing machines whenever possible.)

Evolutionary theory cannot be proven because we cannot examine the amount of fat our ancestors stored (they were decomposed). Therefore, it is all speculative and unfalsifiable. Post hoc explanations