WEEK 6 OBESITY Flashcards
What is overweight and obesity defined as?
- When energy intake is more than energy expended through physical activity
What is the most common calculation for weight status in adults and what is the formula?
- BMI
- BMI= weight in kg/height (m^2)
What is the prevalence in Australia (2017) of overweight and obesity in children?
- 1 in 5 children (20%) from 2-4 yrs
- 11% had overweight and 9 % had obesity
Does childhood obesity affect a similar proportion of males and females?
- YES
Why is obesity known as a wicked problem?
- Because it is difficult or impossible to solve
- We need to know what matters, what works (in the real world) and what translates.
- Must think in new and different ways
What are 4 reasons why a wicked problem in general is difficult to solve?
- incomplete or contradictory knowledge
- the number of people and opinions involved
- Large economic burden
- the interconnected nature of these problems with other problems
e. g. Poverty being linked with education, and nutrition being linked with poverty.
What are two of the main factors in relation to obesity being a wicked problem?
- Double burden of malnutrition (drives of under and over nutrition are in women and children sharing common elements like poverty and food security)
- Access to obesity prevention is inequitable (lots of children are at risk of failing to reach their full potential due to the impact of developmental risks on health., wellbeing and productivity throughout life.
Are obesity related behaviours established in early childhood and do they track through to adulthood?
- YES and YES
What is the rough time period that is viewed as a crucial period for child obesity prevention?
- First 2000 days (5 years)
Is obesity much harder to reverse than prevent?
Yes
True or false. A meta-analysis showed children with obesity have a five fold increase risk of having obesity in adulthood….
TRUE
Do we have any reliable tools to determine risk and protective profiles from infancy, to develop evidence-based interventions that will assist parents, educators, and health promotion practitioners to reduce the prevalence of excessive weight gain in the formative preschool years?
- NO
Is there a link between higher weight status and cancers?
- YES
What are three implications of childhood obesity beyond physical health?
- Negatively impacting self esteem and mental health
- Long term education
- Quality of life
Are the causes of obesity simple or complex?
- they are complex, extending from genetic to social-cultural factors.
What type of theory has been used to summarise the complex interplay between these multidimensional contributors to excess child weight development and inform childhood obesity research?
- Ecological systems theory (quality and the context of a child’s environment)
What is Ecological systems theory?
- It places the parent and child factors as the most PROXIMAL influences on the development of overweight and obesity during early childhood.
How is ecological systems theory integrated with the early obesity risk in the first 2000 days?
- This involves the early mother/caregiver- child interactions: biological, behavioral, and psychosocial interactions.
What are three reasons why high quality parent-child interactions ‘matter’ to child development?
- responsive, sensitive parenting, helps to build trust in the relationship- child knows their parent can comfort/support them in times of stress
- High quality interactions impact on the neurophysiological structures (sleep, stress response, appetite), thus supporting optimal development of self-regulation
- Stress response, sleep and appetite are implicated in energy regulation and eating behavior (cortisol slows metabolism, stress eating etc)
What are examples of child-level factors?
- Age
- Gender
- Temperament
- Self-regulation
- Eating behaviour
Do cross sectional studies give an idea of causation?
- NO
- Because the data is collected at one time point
What are the multi-level social-ecological interactions that shape parent/caregiver actions- in terms of childhood overweight/obesity?
- Health equity
- Political, economic and social drivers of inequities (including racism-related stressors, not soley race/ethnicity)
What are three integrating perspectives for addressing early childhood obesity prevention?
- Childhood development (incorporates ages ad stages of child dev, quality of caregiver interactions)
- Health equity (drivers of social determinants of health)
- Critical race theory
What is critical race theory?
- recognizes current and historical factors that drive widening inequities in obesity rates and disproportionate burden experienced by historically disadvantaged populations.
What is a BMI b/w 35 and 40 classified as?
Obese
What is a BMI>40 classified as?
- Morbidly obese
What is the normal BMI range between?
- 18.5 and 25
As of 2017-2018, what was the % of adult Australians with overweight and obesity?
- 67% (compared to 38% in 1990)
- This equates to 5, 844, 200 Australians
Is overweight/ obesity classed as an epidemic?
- YES
What is overweight and obesity considered to be the leading cause of?
- Preventable death
What are examples of things that obesity is linked with?
- high blood pressure
- High blood sugar
What are 8 factors that may contribute to Obesity?
- Genetics/epigenetics
- Lifestyle eating/exercise patterns
- Socioeconomic status
- Psychological factors
- Cultural background
- Age
- Hormonal, metabolic, and physiological factors
- Sleep disturbances
Is the determination of body composition mono or polygenic?
- Polygenic (>600 genes)
Is the heritability of BMI low or high?
- Quite high (50-90%)
Has a genetic predisposition to Obesity been proven?
- YES
Are monogenic forms of obesity common?
- NO they are rare e.g. Ob-/Ob- gene
What is the most common syndromic cause of Obesity?
- Prader-willi syndrome
What are the symptoms of prader-willi syndrome?
- Hypotonia
- Hypogonadism
- Obesity (major one- excessive appetite- insatiable)
- CNS and endocrine gland dysfunction
What is the genetic cause of Prader Willi syndrome associated with?
- Lack of expression of paternal chromosome 15q11-q13 genes
What are 65-75% of cases of prader willi syndrome?
- De novo microdeletion of the 15q11-q13 region of teh paternal chromosome
What are 20-30% of cases of Prader willi syndrome associated with?
- maternal uniparental disomy (UPD)
1. Two maternal chromosomes, none from father
2. Associated with advanced maternal age
What are 2-5% of prader willi syndrome cases associated with?
- Imprinting error- epigenetic transference
Which hormone is largely increased in children with prader willi syndrome?
- ghrelin
Which gene is leptin encoded by?
- The Ob gene
What is Leptin directly proportional to?
- The amount of fat in the body
What is the basic role of Leptin?
- To inform the brain how much fat there is in the body
What does a mutation in the ob gene result in?
- Prevents Leptin from being secreted thus can’t reach the brain to let the body know when not to eat
- Mice become “little balls of butter”
What are the symptoms of ob/ob deletion?
- Profound obesity . Glucose intolerant/insulin resistant. - Cold intolerant - Immune dysfunction - No circulating leptin levels.
Is there a treatment for those that are deficient in leptin?
- Yes you can have leptin replacement therapy. This allows the person to return to a relatively normal weight
Without leptin secretion, what does the body believe it is constantly in a state of, and what does this lead to?
- In a constant state of starvation or there is an absence of fat stores.
- This signals to the brain to increase food intake and reduce energy epxenditure
- NO satiation (uncontrollable eating)
- Leads to profound morbid obesity.
If individuals have a mutation in leptin receptor, do they respond to exogenous Leptin therapy?
- NO
- They have elevated circulating levels of Leptin and the brain can’t respond.
What is a potential treatment for the LepR mutation?
- Growth Hormone treatment
- Leads to lipolysis
Is idiopathic obesity monogenic?
- NO it is polygenic (SNPs, epigenetics)
- Many mutations and environmental factors at play
- Increased adiposity= increased circulating levels of leptin
Do we all have a ‘set point’ weight?
- YES
- If you eat too much, the body undergoes compensatory changes in energy expenditure.
- Body weight is thought to be predetermined by the genetic background ‘propensity genes’
Where is the ‘set point’ theory exemplified (experiment example)?
- In hamsters
- They lost body weight when food restricted but as soon as the restriction stopped, they returned to their normal body weight.
- It is evident even with genetic manipulation (e.g. MC4-R KO)
When is set point thought to be established in terms of growth and development?
- Across the pubertal transition
Does the body try to defend/maintain the set point values?
- YES e.g. if you eat less, the body will act to promote hunger and decrease energy expenditure, thus promoting food intake.
Can the body establish a new, lower setpoint?
- NO
- Can only establish a higher setpoint :((
What two factors is the set point determined by?
- genes x environment
What is the process by which we identify susceptibility genes?
- GWAS (genome wide association study)
- This looks at a genome wide set of genetic variants (SNPs) in different individuals to see if any variant is associated with a trait.
- It then relates the SNPs to obesity and tries to make an association
What is one common gene with the SNP study for Obesity?
- FTO (fat mass, and obesity associated gene-protein)
- mRNA demethylase
Which gene was identified as the first known to contribute to obesity and how was this identified?
- FTO
- Identified though GWAS
- Individuals having 2 copies of variant FTO they were 1.67x more likely to be obese
What are the symptoms when FTO is overexpressed in mice?
- Increase body weight
- Drastically increased fat mass.
- Increased food intake.
- Increased preference for high calorie foods.
- Reduced physical activity and energy expenditure.
- Impaired Browning of white adipose tissue.
Is there only 1 FTO variant in humans?
- NO there are multiple variants
- 89 genetic variants within introns 1 and 2 of FTO have been associated with BMI
What is an issue with GWAS data and obesity related genes?
- The GWAS data is present BUT difficult to interpret. This is because a lot of changes occur in non coding regions of the gene.
Does an increased BMI reduce longevity?
- YES e.g. Life expectancy of a 20 year old morbidly obese male is 13 years shorter than a male of normal weight and the same age.
Do people who are considered as ‘healthy fat’ show any of the typical risk factors associated with obesity and the nasty diseases?
- NO
What are the associated diseased with metabolic syndrome?
- Neurological disorders
- PCOS
- Cancer
- Cardiovascular disease
- Type II diabetes
- Stroke
- NASH (Non Alcoholic Liver Disease)
What are some examples of risk factors associated with metabolic syndrome?
- Inflammation
- Oxidative stress
- Abdominal adiposity
- Blood glucose
- Decrease in HDL-L
What type of fat is linked with many adverse events?
- Visceral fat