obesity genetic factors Flashcards
Statistics for the genetic causation of obesity
A study by Zhang and Lin (2023) conducted a meta-analysis and highlighted that children with one obese parent have an increased risk of becoming obese, with odds ratios indicating a significantly higher likelihood of obesity in offspring when both parents are obese
It is important to research this as parents and children often share environment and genetic consititution
Adoptee studies
smoller et al., 1986= found a strong relationship between the weight class of the adoptee and their biological parents weight class, but no relationship with their adoptive parents weight class. Interestingly also was stronger relationship with the biological mother than fathers weight.
A 2021 study conducted by Kesternich et al. found that the weight status of biological parents significantly influenced the weight of adopted children, while no significant relationship was observed with the adoptive parents’ weight status
Twin studies
identical twins reared apart are more similar in weight than nonidentical twins reared together, genetic factors accounted for 66-70=5 of the variance in their body weight, suggesting a strong genetic component in obesity (Stunkard et al., 1990)
Allison et al., 1996- concluded 50% of the total variance found in BMI resulted from genetic factors
Longitudinal Studies on Twin Weight Similarity: Hopper et al. (2016) revisited findings from the Minnesota Study of Twins Reared Apart, reporting that genetic influences account for approximately 66-70% of the variance in BMI among separated identical twins.
Fat cell theory
Number of fat cells (genetic) can also effect the tendency to be obese.
Healthy weighted indivuals hvae around 25-35 billion fat cells (fat cells are important to store fat in periods of energy surplus and to tell the brain when to eat/not eat), mildly obese people have the same number of fat cells but they differ in size and weight (enlarged).
Severly obese people have up to 100-125 billion fat cells (Sjostorm 1980). Research has shown that if people are born with more fat cells, there are more cells immediatly to fill up when existing number of cells have been used, therefore it is easier to gain weight.
Number of Fat Cells (Hyperplasia): Fat cells primarily develop during childhood and adolescence. The total number of fat cells (adipocytes) an individual has is typically determined by the time they reach early adulthood. After this point, the number generally remains stable throughout adulthood, even if a person loses weight.
Size of Fat Cells (Hypertrophy): Once adulthood is reached, fat cells can still expand to store more fat (hypertrophy). In response to excessive calorie intake, these existing fat cells grow larger, and eventually, the body may also produce new fat cells if the existing ones reach their maximum capacity.
2. Implications for Obesity:
People with obesity may have both a higher number of fat cells (fat cell hyperplasia) and larger fat cells (fat cell hypertrophy). Studies show that both processes contribute to obesity.
Once fat cells are created, they rarely disappear, even with significant weight loss. Instead, they shrink in size but remain in the body, making long-term weight maintenance challenging.
This helps explain why individuals who have been obese for long periods often struggle to maintain weight loss, as their fat cells are primed to refill.
Supporting Studies
a. Fat Cell Number and Obesity:
A landmark study by Spalding et al. (2008) in Nature found that the number of fat cells in adults is relatively constant, regardless of whether they gain or lose weight. This study indicated that people who become obese often maintain a high number of fat cells, even after weight loss. The researchers observed that while the size of fat cells decreases with weight loss, the number does not, which means that the tendency to regain weight could be influenced by the body’s desire to refill these cells.
b. Fat Cell Hypertrophy in Obesity:
A 2009 study published in Obesity Reviews by Lundgren et al. highlighted that in the early stages of obesity, fat cell hypertrophy (enlargement of existing fat cells) predominates. As weight gain continues, the body can start producing new fat cells through hyperplasia to accommodate additional fat storage.
c. Childhood Obesity and Fat Cell Theory:
Another critical aspect of the fat cell theory relates to childhood obesity. Research published by Knittle et al. (1979) in The Journal of Clinical Investigation demonstrated that individuals who were obese as children have a higher number of fat cells compared to those who developed obesity later in life. This suggests that early intervention is crucial because fat cell number is established early in life and remains stable in adulthood.
d. Fat Cell Turnover:
While the number of fat cells remains constant, they undergo continual turnover. A study published in Nature by Arner and Spalding (2010) showed that fat cells are regularly renewed throughout life, but this turnover is not related to weight changes. Obese individuals have the same rate of fat cell renewal as lean individuals, but the absolute number of fat cells is higher in people with obesity
Metabolic rate theory
resting metabolic rate is found to be highly heritable (Bouchard et al., 1990)- one theory of obesity is lower metabolic rates.
Recent studies show that obesity is often associated with lower metabolic rates, reinforcing earlier findings. For instance, a 2021 study by Martins et al. demonstrated that metabolic adaptation occurs in response to low-energy diets, leading to a reduction in metabolic rate, which can hinder weight loss efforts in obese individuals
Another study by Pontzer et al. (2021) published in Science highlighted that metabolic rates change throughout life but are influenced significantly by body composition. Obese individuals generally have a lower resting metabolic rate due to differences in fat-free mass, which burns more calories than fat
These studies confirm that lower metabolic rates in obese individuals can contribute to difficulties in weight management
HOWEVER- NO STRONG evidence- contradicting evidence
Some studies indicate that obese individuals may have higher metabolic rates due to the increased energy demands of maintaining a larger body mass. For instance, Johnstone et al. (2005) found that fat-free mass, which is higher in obese individuals, strongly influences metabolic rate, thus leading to higher energy expenditure in some cases
to explain- obese people may have lower metabolic rates to start with, which results in weight gain, and this weight gain itself results in an increase in metabolic rate (Ravussin 1989)
LEPTIN
Leptin levels are high in obese people and low in anorexia sufferers, leptin levels fall when someone loses weight (Ferron et al., 1997)
Leptin resistance- found on other card
Montague et al.,1997- found children with a defect in the OB gene, these children were then given daily dosage of leptin, which resulted in weight loss and less food intake (Farooqi et al., 1999)
Evaluative points to the genetic basis to obesity
research in lowered metabolic rate and high fat cells has mostly been refuted.
genetics of appetite control still remain in research
sample size of genetic studies are small, and the problem of the environement is still prevelent. Twin studies assume the environment for twins is constant and that only the genetic makeup of nonidentical twins is different, however it is possible identical twins are brought up more similarly because they are identical, in addition adoptee children often go to homes of parents who are similar to their biological parents
also identification of indivdual genes responsible for obesity is problmeatic, as most genes function by interacting with other genes and also the environement.
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Therefore we need to research our ever changing environment the impact this has on obesity.
SET POINT THEORY- Kennedy 1953
The set point model is a theory that explains how the body regulates weight, appetite, and energy expenditure to maintain a predetermined, stable body weight, often called the “set point.” According to this theory, each individual has a biologically programmed set point—a weight range that the body naturally gravitates towards. This range is maintained by physiological mechanisms that control appetite and energy expenditure through feedback systems in the brain, particularly the hypothalamus
Biological Weight Regulation:
The body defends a certain weight (set point) by adjusting hunger, metabolism, and energy expenditure.
When body weight decreases below the set point (due to dieting or weight loss), the body responds by increasing hunger and slowing down metabolism to restore weight.
Conversely, when body weight increases above the set point (due to overeating), the body may increase energy expenditure or reduce appetite to return to the set point.
Role of the Hypothalamus:
The hypothalamus in the brain plays a central role in regulating hunger and satiety through hormones like leptin and ghrelin.
Adaptive Mechanisms:
The body employs adaptive thermogenesis, a process where metabolic rate decreases during periods of calorie restriction, making weight loss harder. This is why people often hit “weight plateaus” when trying to lose weight.
When weight is regained, the body may increase its energy efficiency, making it harder to maintain weight loss over the long term
Levitsky 2002, set point theory has been rejected as an adequate explanation of obesity. It cannot explain the sudden increase prevalence in obesity over the latter half of the 21st century
settling point theory
adapted from the set point theory. Biology offers a range of weight status called the setlling point. An individual lies within their settling point is controlled by environmental cues. But with obesity rising, it would mean this settling point is very big.
