Obesity Flashcards

1
Q

State the proportion of obese, and overweight people in Scotland. Are these figures increasing/decreasing/constant ?

How many overweight or obese people are there in the world ?

A

29% obese
65% overweight (includes obese)

Increasing

> 2.1 billion people (30% of global population) are overweight or obese

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2
Q

Identify the three countries with the greatest rate of obesity.

Is the rate of increase in obesity greater or lesser than in other countries ?

A

USA
Mexico
England

3 countries with greatest rate of obesity, have greater increase in rate of obesity

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3
Q

Describe the economic costs of obesity.

A
  • Global economic impact from obesity: $2.0 trillion, equivalent to global impact from smoking or armed violence, war and terrorism
  • 2-7% of all health-care spending in developed economies
  • Personal, social, economic costs partly because obesity leads to multiple chronic health conditions
  • Decreased life expectancy (up to 20 yrs depending on severity of obesity)
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4
Q

Describe the role of the GP in obesity.

A

GPs important:
• More obese patients visit GPs frequently c.f. healthy weight counterparts

What can GPs do:
• Primary care practitioners - well placed to implement weight loss and obesity prevention programs opportunistically
• Interventions shown to be effective
– partnerships (e.g. between primary care practice and commercial weight loss organisation)
– communication based interventions
• NHS SIGN + NICE guidelines - doctors regularly screen for obesity
and recommend interventions to o/wt and obese patients within primary care

• Yet, weight discussion often unsuccessful and seldom occurs in primary care consultations

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5
Q

Explain why weight discussions are often unsuccessful and seldom occur in primary care consultations.

A
  • Embarrassment -Lack of adequate training/support
  • Dr doesn’t think patient has motivation
  • Sensitive topic
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6
Q

When weight WAS discussed in primary care, who is it that raised the issue ?

A

In few times where weight was discussed,
it was practioner who raised the issue with patient
(often patient closing down the discussion)

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7
Q

Describe the impact of brief interventions for obesity in primary care.

A
  • RCT showed that: Both advice only, and support (e.g. referral to weight management group) helped patients lose weight (however, support more so) (each patient was give 30 seconds of one of the two)
  • So interventions are acceptable (according to patients) + useful
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8
Q

What is obesity ?

A

Excess adiposity

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9
Q

State formula for BMI. What is the main problem of BMI as a tool to estimate obesity ?

A

Body mass index (BMI) = Wt (kg)/ht (m)2

• Proxy measure (fat mass + fat-free mass) BUT still useful population level measure of o/wt and obesity across gender and age for adults

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10
Q

Identify the main measures used for obesity.

A
  • BMI

- Waist circumference (reasonable indicator of intra- abdominal or visceral fat)

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11
Q

What are the NICE cut offs in terms of increased risk of health problems for waist circumference ?

A

NICE cut offs: males wc >94cm or females wc ≥ 80cm at ↑ed risk
health problems

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12
Q

What BMIs is obesity ? Overweight ?

A

Obesity is classified as BMI more or equal to 30kg/m2.
Class I is 30 to 34.9 kg/m2.
Class II is 35.0 to 39.9 kg/m2.
Class III is 40 and above.

Overweight is anything from 25 kg/m2 to above (includes pre-obesity and the three classes of obesity)

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13
Q

Identify co-morbidities of obesity.

A
Stroke
Heart Disease
Diabeters
Cancer
Psychological problems (depression, reduced self confidence
anxiety, reduced quality of life, body 
dissatisfaction, may lead into eating 
disorders)
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14
Q

How is obesity defined in children ? WHa

A

• Arbitrary ref values (85th, 95th centiles for population), which vary worldwide

• IOTF: adult cut offs (BMI 25, 30) be linked to BMI centiles for children to provide child cut-offs (International standards, based on mean of international centiles)
‒ aim to define internationally acceptable cut off points for child obesity and overweight (helps compare different countries and come up with strategy applicable to all countries)
-e.g.
if 19.8 BMI as male aged 10 overweight child

• International cut offs reformulated to allow BMI to be expressed as a centile or SD score
- very minor changes in existing cut-offs

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15
Q

Draw a graph of BMI vs age for overweight, and obese males, and females respectively up to age 18. Explain the differences between males and females.

A

Refer to graph on page 3

More linear in males, more concave in females (probably due to early puberty)

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16
Q

What is the percentage of children at risk of overweight (including obesity) in Scotland?
Percentage of children at a health weight ?

A

72%

28%

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17
Q

What is the prevalence of child obesity in Scotland ?

A

13%

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18
Q

Identify possible consequences of childhood obesity.

A
  • Pulmonary: Sleep apnoea; Asthma
  • Orthopaedic: Ankle sprains; Increased risk of fractures
  • Neurological: Idiopathic intracranial hypertension
  • Gastroenterological: Cholelithiasis; Liver steatosis/non-alcoholic fatty liver
  • Endocrine: Type 2 diabetes; Polycystic ovary syndrome
  • Cardiovascular: Hypertension; Dyslipidaemia
  • Psychological: Depression; Low self esteem

These are consequences we used to just see in adults, now in children as well.

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19
Q

Briefly define the Foresight obesity systems map.

A

Map which identifies all the pathways which contribute to obesity, at the center of which is energy imbalance.

20
Q

Identify all the factors which contribute to energy imbalance in obesity.

A

1) Modifiable:
- Diet
- Activity

2) Environmental and social influences
- Individual/biological susceptibility
- Dietary and physical activity patterns
- Socioeconomic status and age

21
Q

Identify tools to understand genotype in obesity.

A
  • Genetic screening
  • Parental obesity
  • TEE (total energy expenditure)/REE (resting energy expenditure)
  • Body composition
22
Q

Identify tools to understand phenotype in obesity.

A
  • COMP-X (proxy for how well we adjust to different energies and food. Those with precise COMP X, will adjust correctly to different amounts of energy from food)
  • EAH (eating in absence of hunger)
  • SSS (Sensory-specific satiety, “decline in pleasantness associated with a food as it is eaten relative to a food that has not been eaten”)
  • Diet records
  • Activity monitors
  • Activity Q
23
Q

Which of energy expenditure (activity) or intake (diet) is more important in obesity ?

A

Both v important

24
Q

Identify factors in activity which correlate with a higher prevalence of obesity.

A

Increase in sedentary behavior (cars, TV for children) correlated with increase in obesity (so sedentary lifestyle predisposes to obesity)

25
Q

Describe the relationship between sensory variety and obesity.

A

increasing the variety of sensorialy distinct foods, virtually identical in composition, can increase food and energy intake and in the short to medium term can alter energy balance (and increase body weight)

26
Q

Identify factors which can affect energy intake.

A
  • Intake of sensorialy distinct foods
  • Sugar sweetened beverages
  • Larger portion sizes

All contribute to increased energy intake

27
Q

Describe the link between portion sizes and the increase in obesity in the last few years.

A
  • Over time, portion distortion has occurred (one portion perceived as being supposed to be larger than it actually is)
  • Large portions of energy dense (ED) food facilitates over consumption – Portion size effect (PSE)
  • Without compensation, the PSE may promote overconsumption and weight gain over time (if not compensating with larger energy expenditure)
28
Q

Describe the genetic link to obesity.

A

Explored through familial, twin, family, functional studies.

1) Monogenic forms of obesity
– rare (<5%)
– single gene disorders (gene mutations e.g. LEP, LEPR, MC4R)
– seems to be disruption in repetitive pathway rather than energy expenditure pathway, leading notably to hyperphagia (excessive urge and drive to eat)

2) Polygenic/ common forms of obesity
– complex interactions between genes and environment
• gene-gene
• gene-environment
– this results in individual variation in obese phenotype

29
Q

Give a specific example of gene - environment interaction in the pathogenesis of obesity.

A

Pima Indians

1) Pima in Arizona
- Typical American lifestyle
- Typical American diet
- High prevalence of obesity

2) Pima in Sierra Madre Mountains of Mexico
• traditional methods of farming, cooking, fetching water
• largely unaffected by labour saving devices
• Much lower prevalence of obesity

Overall, genetic profiles of these two groups almost identical (have thrifty genotype), but gene-environment interactions are different (i.e. group 1 is in a permissive environment) so group 1 develops obesity but not group 2.

30
Q

Define thrifty genotype.

A

Thrifty genes are those which enable individuals to efficiently collect and process food to deposit fat during periods of food abundance in order to provide for periods of food shortage (feast and famine)

I.E. GENETIC PREDISPOSITION

31
Q

Define thrifty phenotype.

A

Reduced fetal growth is strongly associated with a number of chronic conditions later in life. This increased susceptibility results from adaptations made by the fetus in an environment limited in its supply of nutrients.

32
Q

Graph BMI vs obesogenic environment for:

  • Genetically resistant
  • Slight genetic predisposition
  • Strong genetic prediposition
  • Genetically obese
A

Refer to graph on page 6.
-Genetically resistant remains lean regardless of environment

-Slight genetic predisposition
-Strong genetic prediposition
-Genetically obese
With more permissive environment, all these three have increased BMI (but different rates of increase)

33
Q

Identify genes involved in monogenic forms of obesity, and the chromosomes each is located on.

A

LEP (ch 7)
LEPR (ch 1)
POMC (ch 2)

34
Q

To what extent is leptin therapy adequate for obesity ?

A

Leptin therapy only works for monogenic forms of obesity with defect in Leptin gene.

BUT monogenic forms of obesity account for less than 5% of obesities (so not actually an effective treatment)

35
Q

Define leptin.

A

“hormone predominantly made by adipose cells that helps to regulate energy balance by inhibiting hunger”

36
Q

Identify common gene variants predisposing to polygenic obesity.

A
  • Peroxisome proliferator-activated receptor (PPARG ) (Pro12ala), role in insulin sensitivity and adipocyte differentiation
  • Uncoupling Proteins (UCPs), role in energy balance
  • Beta adrenergic receptors (B3-Trp64Arg), role in energy balance through stimulation of thermogenesis and lipid mobilisation
  • FTO (fat mass and obesity associated)
37
Q

What is the significance of Genome-wide association studies (GWAS) in obesity ?

A

Genome-wide association studies (GWAS) identify new obesity loci:

• Whole genome studies
- systematic analysis of genome
- powered to detect small effects
by testing in large populations (10,000-‐100000 individuals)
- e.g. FTO gene, Melanocortin 4 receptor (MC4R)

38
Q

Where the FTO gene located ?

A

• Chromosome 16

39
Q

Describe the link between the FTO gene and obesity.

A

• Encodes a protein with 2-oxoglutarate-dependent nucleic acid demethylase activity
• Role in fatty acid metabolism, DNA repair, post-translational changes
• Expressed in brain, pancreatic islet, adipose tissue, adrenal glands
-putative role in hypothalamic-pituitary-adrenal (HPA) axis (implicated in body
weight and satiety regulation)
-increases in hypothalamic expression of FTO are associated with the regulation of energy intake (FTO risk variants (i.e. AT or AA whereas TT is wildtype) are associated with increased energy intake, and to preference for fat intake)
• Polymorphisms on FTO gene robustly linked to BMI and obesity in adults and children (i.e. FTO variants predispose to obesity. Homozygous for risk allele has therefore been linked with higher body weights)

40
Q

If a gene is established as having a correlation with obesity, what are possible ways this susceptibility could be mediated ?

A

• Within energy balance framework, susceptibility could be mediated through:

  • weak appetite regulation leading to changes in eating behaviour e.g. increased energy intake
  • or through diminished energy expenditure
41
Q

Define obsogenic.

A

Promoting excessive weight gain

42
Q

Identify the WHO dietary recommendations for populations and individuals.

A
  • Promotion of exclusive breastfeeding
  • Avoid adding sugars/starches to formula
  • Allow child to regulate food intake rather than feeding until the plate is empty
  • Promote an active lifestyle, limit TV viewing
  • Promote intake of fruit and vegetables

• Limit salt (sodium) consumption

These are modifiable factors.

43
Q

Identify the main points of the WHO Global strategy on diet, physical activity (PA), health.

A

Promote and protect health through healthy eating and PA:

  1. Reduce risk factors for chronic diseases that stem from unhealthy diets and PA through public health actions
  2. Increase awareness and understanding of the influences of diet and PA on health an the positive impact of preventive interventions
  3. Develop, strengthen and implement global, regional, national policies and action plans to improve diets and increase PA that are sustainable, comprehensive and actively engage all sectors
  4. Monitor science and promote research on diet and physical activity
44
Q

What is the first step in the Obesity Care Pathway ?

A

Tier 1, population-wide intervention and prevention initiatives. From a clinical POV, providing information and guidance on healthy eating and physical activity.

45
Q

Identify the components of energy balance.

A
  • Energy intake (proteins, carbs, fats)

- Energy expenditure (activity, thermal effect of food, basal metabolic rate)