OBESITY AND GENETICS
Biological explanations for obesity, including genetic explanations.
Eating Disorders/Obesity
Let’s start with some trivia
What are the “World’s Unhealthiest Foods”?
The "unhealthiest" foods tend to be those that least resemble their original natural ingredients and have the most added refined and artificial additives. Prime examples are the "white foods"-white sugar, white flour, and white fat, and the gamut of foods in which they are the principal ingredients.
"White sugar" includes refined sugar cane or sugar beets that have virtually all B vitamins, minerals, antioxidants, and other essential nutrients removed. Corn syrup is also a "white sugar," made from processed cornstarch and devoid of other nutrients.
"White flour," analogously, is whole wheat flour minus its nutrient-packed wheat germ and fibrous bran. Nutritionally speaking, white flour a ghost-like shadow of its original whole grain.
"White fat" can include rendered animal lard, vegetable oils "hydrogenated" to make them hard at room temperature, and refined tropical fats such as cottonseed oil. Hydrogenation is a chemical process that transforms natural fats into more saturated "trans"-fatty acids that do not occur naturally and are strongly associated with cardiovascular disease.
Foods having "whites" as their primary ingredients are frighteningly ubiquitous! Examples include soft drinks, most breads, crackers, pasta, pastries and pastry fillings, cakes, frostings, margarine and bread spreads, jellies, sweets and candies, frozen dinners, hamburger and hotdog buns, snacks, doughnuts, pizzas, pies, candy bars, and cookies-all of which are common snacks and convenience foods. Indeed, many of these combine all three whites- white sugar, flour, and fat! Furthermore, these foods frequently contain artificial colours, artificial flavours, preservatives, texturising and processing agents, and other additives that further detract from their nutritional stature and health.
The world’s fattest countries: USA, Cook (pacific Islands), UK, Australia
There are currently 1.6 billion overweight adults in the world, according to the World Health Organization. That number will grow by 40% over the next ten years. Just 7% of people in eastern Asia were obese, compared to 36% of people seeing their doctors in Canada, 38% of women in Middle Eastern countries and 40% in South Africa.
Canada and South Africa led in the percentage of overweight people, with an average BMI of 29 among both men and women in Canada and 29 among South African women.
Obese is defined as having a BMI greater than or equal to 30.
} 1 in 2 adults in the US were either overweight or obese in the 1990s (Tataranni, 2000)
} In the UK, there is an upward trend in obesity
◦ 1\2 women and 2\3 men are either overweight or obese
} Obesity shortens life by an average of 9 years (National Adult Office, 2001)
} Mokdad et al. (1999) refer to an “obesity epidemic.”
} The World Health Organization increases risks of
◦ Type 2 diabetes
◦ High blood pressure
◦ Reduced life expectancy
} Masso-Gonzalez (2009) estimated the incidence of diabetes in the UK between 1996 and 2005
◦ Type 1 was constant
◦ Type 2 increased from 46% to 56%
} The most common ways to define obesity are
◦ BMI (Body Mass Index)
◦ Waist circumference
◦ Measuring the thickness of fatty tissue using callipers
} BMI is calculated by dividing a person’s weight by their height squared
} BMI of less than 18.5=underweight
} BMI over 25=overweight
} BMI over 30=obese
} BMI over 40=morbidly obese
Biological Explanations for Obesity: Genetic explanations.
FAMILY STUDIES
Genetic explanations focus on genes through family and adoption studies (identical and non-identical twins). Specific genes that may affect physiology and psychological features, such as intelligence and mental order, may also be examined. Neural explanations can include dysfunctions of the brain and nervous system, including structures such as the hypothalamus and neurotransmitters such as serotonin and dopamine.
Genetic Explanation for Obesity Research seems to suggest a genetic basis for obesity as some individuals appear more genetically predisposed to become obese than others. There does not appear to be a single gene responsible, but genetic explanations suggest multiple genes that make an individual more vulnerable to developing the disorder. Twin studies into obesity have reported heritability ranges of 40% to 75%. A meta-analysis by Maes et al. (1997) involving 75,000 individuals found heritability estimates for BMI in 74% of identical twins and only 32% in non-identical twins.
Even when identical twins were reared apart and experienced similar environmental influences, their BMI was more similar than non-identical twins reared together in similar environments (Stunkard et al., 1990).
Adoption studies have looked at individuals who have been adopted as infants and raised by biologically unrelated families. This allows researchers to attempt to separate the influence of biological parents (genetics) and adoptive parents (environment). Stunkard et al. (1986) examined 540 adult adoptees and their biological and adoptive parents. The research found a strong relationship between the weight category (i.e. underweight, overweight or obese) of adopted individuals and their biological parent's weight category; however, no significant relationship with their adoptive parent’s w’s weight category.
Evidence from twin and adoption studies supports the notion that genetics are crucial in determining body mass index (BMI) and the propensity for obesity.
Twin Studies: Twin studies offer valuable insights into the heritability of obesity. The substantial difference in heritability estimates between identical (monozygotic) and non-identical (dizygotic) twins underscores the genetic influence on body weight. Identical twins, who share 100% of their genes, exhibit more similar BMI patterns than non-identical twins, even when raised in different environments. This suggests that genetic factors are a significant contributor to obesity.
Adoption Studies: Adoption studies provide a unique perspective by comparing adopted individuals with their biological and adoptive parents. The findings that adopted individuals' weight categories correlate more strongly with their biological parents than with their adoptive parents emphasize the genetic underpinnings of obesity. These studies demonstrate that, despite environmental variations, the genetic contribution to obesity is substantial.
A variety of genetic theories, including the thrifty gene hypothesis, polygenic determination, and the examination of specific obesity-related genes, support the concept that some individuals are genetically predisposed to accumulate excess body fat. These theories contribute to our understanding of why obesity can vary significantly among individuals, even within the same environment.
Thrifty Gene Hypothesis
The thrifty gene hypothesis posits that certain individuals carry genetic variations that enhance the efficiency of food utilization and energy storage. Originally proposed by James V. Neel in the 1960s, this theory suggests that these genes were advantageous during historical periods of feast and famine, allowing individuals to store fat during times of abundance and survive on these stores during periods of scarcity. In modern societies, where food is abundant and often high in calories, these genes may predispose individuals to obesity.
Polygenic Determination
Obesity is now considered polygenic, which is influenced by the interaction of multiple genes rather than a single genetic cause. Studies have identified numerous genetic loci associated with body mass index (BMI) and other obesity-related traits. For instance, a study by Locke et al. (2015) identified 97 genes associated with variations in BMI. However, these genes account for only a small fraction of BMI variation, suggesting that many more obesity-related genes are yet to be discovered. This polygenic nature underscores the complexity of genetic contributions to obesity, involving metabolism, fat storage, and appetite regulation.
Specific Obesity-Related Genes
Research has also focused on identifying specific genes that contribute to obesity. For example, variations in the FTO (fat mass and obesity-associated) gene have been consistently linked to obesity risk in various populations. The FTO gene is thought to influence energy intake and food preference, particularly for high-calorie foods. However, like other genetic factors associated with obesity, the effect sizes of these genes are relatively small, indicating that no single gene is solely responsible for obesity.
POLYGENIC DETERMINATION
Polygenic determination offers a nuanced understanding of the genetic influences on obesity, suggesting that rather than being controlled by a single gene, obesity results from the interplay of multiple genes. This complexity reflects the varied aspects of obesity, such as the distribution of body fat and overall body mass index (BMI), which are influenced by many genetic factors working in concert with environmental influences.
Polygenic Nature of Obesity
Multiple Genes Involved: Research, including the study by Adam Locke et al. (2015), underscores the polygenic nature of obesity by identifying numerous genes associated with BMI variations. These findings highlight the complex genetic landscape underlying obesity, where each gene contributes a small effect to the overall risk.
Small Fraction of BMI Variation: Although numerous genes have been linked to BMI, they account for a small percentage of BMI variation. This suggests that the genetic basis of obesity is not only polygenic but also influenced by interactions between these genes and environmental factors such as diet and physical activity.
Missing Heritability: The concept of "missing heritability" refers to the gap between the heritability of obesity estimated by family and twin studies and the proportion of variance explained by identified genetic variants. This gap indicates that many more genes likely contribute to obesity risk but remain unidentified. The search for these genes continues, hoping to unravel the full genetic complexity of obesity.
Evaluation of Polygenic Determination
Strengths: Polygenic determination provides a more accurate representation of the genetic complexity of obesity. It moves beyond simplistic, single-gene explanations to encompass the disorder's multifactorial nature, acknowledging numerous genes' small but significant contributions.
Limitations: Despite identifying many genes associated with obesity, the polygenic model has yet to explain the disorder's genetic basis fully. The small effect sizes of identified genes and the vast number of undiscovered genes challenge our understanding and ability to predict obesity risk based on genetics alone.
Implications for Treatment and Prevention: Recognizing obesity as a polygenic condition highlights the limitations of solely genetic-based interventions. Effective strategies for managing and preventing obesity will likely require personalized approaches considering an individual's unique genetic makeup and environmental and lifestyle factors.
In summary, polygenic determination underscores the complexity of genetic contributions to obesity, emphasizing the need for comprehensive research and multifaceted approaches to treatment and prevention. Understanding the interplay between the multitude of genes and their interaction with environmental factors is crucial for developing more effective strategies to combat obesity.
Evaluation of Biological Explanations
Evaluating genetic explanations for obesity highlights the complex interplay between genetic predispositions and environmental factors in developing this condition. While genetics undeniably play a role in obesity, the limitations of twin studies and the changing impact of genetic influences across a person’s lifespan suggest that environmental factors also play a significant role.
Limitations of Twin Studies
Shared Environment: Twin studies, particularly those involving identical twins, often struggle to disentangle the effects of shared genetics from shared environments. The assumption that identical and non-identical twins experience equally similar environments has been questioned, potentially leading to an overestimation of genetic influence.
Treatment Differences: Identical twins may be treated more similarly by their environment than non-identical twins, not just within families but also by friends, teachers, and society. This similarity in treatment could inflate the perceived genetic contribution to obesity.
Genetic Influence and Age
Variability with Age: The impact of genetics on BMI appears to fluctuate with age. Genetic influences are pronounced during childhood, but as individuals age and gain more autonomy over their lifestyle choices, the environmental contribution to obesity becomes more significant. This suggests that genetic predispositions are modulated by lifestyle factors, which can either mitigate or exacerbate the risk of obesity.
The Surge in Obesity Rates
Rapid Environmental Changes: The dramatic increase in obesity rates over the last few decades cannot be explained solely by genetic factors, as the human genome has not undergone significant changes in this short period. Instead, environmental changes, including increased availability and consumption of high-calorie foods, decreased physical activity, and lifestyle changes, are likely driving this trend.
Diathesis-Stress Model
Interaction of Genes and Environment: The diathesis-stress model offers a more comprehensive explanation by suggesting that environmental stressors activate genetic predispositions to obesity. The modern food environment, characterized by easy access to energy-dense foods and sedentary lifestyles, may act as a trigger for individuals genetically predisposed to obesity.
Leptin Regulation and Genetic Basis
Mixed Evidence on Leptin Genes: Research into genes regulating leptin, a hormone critical for appetite and weight regulation, has yielded mixed results. While leptin plays a crucial role in weight management, the lack of consistent evidence linking specific genes to obesity underscores the multifactorial nature of this condition. It suggests that other factors, beyond genetics, significantly contribute to obesity.
In conclusion, while genetic factors contribute to the risk of developing obesity, they do not act in isolation. The interaction between genetic predispositions and environmental factors is critical in understanding the prevalence and escalation of obesity. This emphasizes the need for comprehensive approaches to obesity prevention and treatment that consider both genetic vulnerabilities and modifiable lifestyle factors.
