The Science of Bodyweight (Laura) Flashcards
1
Q
Criteria fo food addiction
A
- Tolerance: increasing amounts of food needed to be satisfied
- Distress and dysphoria during eating
- Persistent desire for food and unsuccessful attempts to curtail amount eaten
- Great deal of time spent eating
2
Q
How do we measure food addiction
A
- Yale food addiction scale
- Self report questionnaire
- Symptom count
- Used extensively over last decade but mostly cross sectionally
- Limited predictive power
3
Q
What is BMI?
A
A formula that allows us to make weight comparisons across people
4
Q
What is the BMI equatioin
A
weight (kg)/height^2 (m)
- Allows a measure of weight that takes into account the variation due to height
- Z scores used for children to take account of age and growth in height
5
Q
History of BMI
A
- Health insurance companies in North America concerned to know the risk of certain people needing a health insurance payout
- The tables were created with relative scarcity of women and racial and ethnic minorities in underlying datasets
- 1900s: Normal weight tables, Medico-actuarial standards of weight (Dubliin, 1912)
- 1937: Body frame (small, medium and large) was added to the tables (Dublin and Lotha)
- Keys (1972) found the Quetelet index from 1832 and renamed it Body Mass Index
6
Q
Strengths of BMI
A
- Simple and low cost (Kennedy, Shea and Sun, 2012)
- Even though self-report weight is often under-estimated and height is over-estimated (Ng et al. 2011) there is a correlation between self-report and measured BMI (Pursey, Burrows, Stanwell, and Collins, 2014)
- Correlated with direct measures of body fat such as underwater weighing (densitometry) and dual energy x-ray absorptiometry (DEXA) (Rothman, 2008)
7
Q
Criticisms of BMI
A
- Does not adequately account for age, gender or race, especially in terms of standard cut-offs (Kennedy, Shea and Sun, 2012)
- E.g. greater bone mineral density and muscle mass in black people compared to white people may account for higher BMIs in black population (Strings, 2019 and Wagner and Heyward, 2000)
- Indirect measure of body fat: does not reflect changes in body fat and muscle mass
8
Q
What are the trends in body weight?
A
- In 2016, globally, 1.9 billion adults were overweight, of whom 650 million had obesity
- In 2016 there were 41 million children under 5 and 340 million aged 5-19 with overweight or obesity
- In 2016, for moderate and severe underweight (8.4% in girls and 12.4% in boys) in most regions this number shows a decreasing trend despite population growth
9
Q
What are the risk factors associated with child obesity and overweight?
A
- Type 2 diabetes
- Incidence of metabolic syndrome in youth
- Obesity as an adult
(Biro and Wien, 2010)
10
Q
What are the risk factors associated with adult obesity and overweight?
A
- Cardio-vascular disease (Ortega, Lavie, and Blair, 2016)
- Type 2 diabetes (Mokdad et al., 2003)
- Some cancers (Font-Burgada, Sun and Karin, 2016)
11
Q
Key assumptions on whether there is a genetic disposition to overweight/obesity
A
- Considering the principles of natural selection, if there are genes which pre-dispose humans or some humans to a bodyweight classified as obesity then at some point there must have been a fitness benefit to have such genes
- Modern humans share their DNA and anatomy with Cr-Magnon humans from 28,000 years ago
12
Q
What is the thrifty gene hypothesis
Neel (1962)
A
- Originally proposed as an explanation for type 2 diabetes but was quickly expanded to apply to obesity
- Suggested that genes that predispose to type 2 diabetes had previously been advantageous
- Individuals who carried more fat would be better able to survive times of famine
- But in times when food is abundant this adaptation prepares humans for a famine that never comes
13
Q
Criticism of the thrifty gene hypothesis
A
- By this logic, all humans would have obesity after so many generations of such strong selective force but this is not the case (Speakman, 2007)
- Benyshek and Watson (2006) suggest that the problem with this approach is that famine was not such a frequent feature of our evolutionary past and only an issue since agriculture became dominant 12,000 years ago (over a much shorter time thrifty genes haven’t spread so far in the population)
- Speakman (2016) argues that the selection pressure would have to be huge to have spread as far as it has in 12,000 years but famines have just not exerted that influence
14
Q
What is the drifty gene hypothesis?
Speakman (2008)
A
- Questions the assumption that evolution only works through natural selection (lots of processes that lead to genetic change)
- One of these is called Genetic drift (non-adaptive evolutionary change)
- Body weight in many animals is well regulated between a lower level and an upper level
- The lower level is selected for by starvation risk: genes to prevent starvation are advantageous
- The upper level is selected for by risk of predation: genes to avoid becoming prey
- Around 2 to 2.5 million years ago the predation risk that regulated the upper limit disappeared
- Disappeared due to social behaviours that allowed for warning of predator risks and weapons/fire to protect oneself from predator
- Without selection pressure genes were subject to random mutation and genetic drift
15
Q
Genetic drift definition
A
A change in the frequency of a particular variant of a gene (allele) due to chance rather than reproductive success as in natural selection
16
Q
Criticisms of drifty gene hypothesis
A
- Obesity epidemic has not been around for the last 20,000 years when it should have been is we have the same genetic architecture as. Cro-Magnon humans
- Speakman argues that this is because there was not the abundance of food available at that point so there would have been insufficient food for bodyweight to increase up towards the ‘drifted’ upper level
- This was not the case due to an abundant food supply
17
Q
An overarching criticism of evolutionary theories of bodyweight
Selleyah (2019)
A
- Many of the evolutionary theories tend to treat humans as a homogenous block and fail to account for differences in obesity across populations in terms of ethnicities
- Selleyah offers a theory that does account for this
- This is a maladaptive scenario where genes that provided cold adaptation. rather than heat adaptation also conferred higher metabolic rates (providing a way go burn off excess energy even when food is abundant)
18
Q
What is the ‘obesogenic’ environment?
A
An environment that promotes gaining weight and one that is not conducive to weight loss
19
Q
Features of the obesogenic envirnment
A
- Large portion sizes
- Energy dense foods
- Highly palatable foods
- Many eating opportunities
- Food variety
20
Q
How has the food environment changed across history?
A
- Advent of agriculture 12,000 years ago
- Rise of slave trade in early 17th century saw a rise in sugar production
- In 1660 England imported 1200 barrels of sugar from Barbados, but by 1700, 50000 barrels were imported
- Speakman (2016) argues that one of the reasons why. this environmental change didn’t result in the rising rates of obesity we have seen over the last few 50 years is because this abundance was restricted to wealthier portions of the population who did have bodyweights that would be considered obese
21
Q
Gene environment interaction definition
A
A different effect of a genotype on disease risk in persons with different environmental exposures
22
Q
G x E: Classic example (Pima people)
Schulz, Bennett, Ravussin, Kidd, Esparza and Valencia (2006)
A
- Pima people are Native Americans living in two areas, (1) Gila River, Arizona, USA (2) Sierra Madre Mountains, Mexico
- Both populations have been DNA tested to establish their genetic similarity to each other by comparison to. other Native American populations
- High prevalence of type 2 diabetes of Pima people in USA (world’s highest recorded prevalence - 51%)
23
Q
What is polygenic risk score?
A
Calculation which reflects how many trait-relevant SNPs a person has and their strength of influence
24
Q
How do genes affect bodyweight (Finnish study)
A
- Finnish cohort study
- 5024 participants
- Genotyping conducted on every participant
- 90 of 97 loci used to calculate polygenic risk score
- Appetite traits measured by questionnaire
25
Q
What is ghrelin?
A
- Hunger hormone
- Expressed mainly by stomach but also by duodenum, jejunum, ileum, colon, lung, heart, pancreas, kidney, testis, pituitary and hypothalamus
- Secreted by the stomach and reaches the brain by crossing the blood-brain barrier
- Transmits its signal through the vagal nerve
- Stimulating the activity of NPY/AGRP neurons and decreasing the activity of POMC and CART neurons makes ghrelin increase appetite and food intake
26
Q
What happens if you don’t have ghrelin?
A
Zigman et al (2005)
- Mutant mice without the ghrelin gene, or ghrelin receptor gene
- Still eat normally and maintain body weight
- Do not gain weight when fed at a high fat palatable diet (obesogenic environment)
