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Behavioural Medicine > Diet, Obesity and Healthy Related Outcomes > Flashcards

Diet, Obesity and Healthy Related Outcomes Flashcards

1
Q

How do we measure BMI and what are the cut offs?

A

weight (kg)/ height (m^2)

Underweight - <18.5
Normal - 18.5-24.9
Overweight - 25-29.9
Obese - 30 and up 
Severe 'morbidly' obese 40 and up
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2
Q

What are the latest figures of overweight and obesity for men and women?

A

Latest figures - 2018

~7 out of 10 men are overweight or obese (67%)

More than 4 in 10 men are obese (26%)

2% of men are morbidly obese

6 in 10 women are overweight or obese (60%)

~ 3 in 10 women are obese (29%)

4% of women are morbidly obese

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3
Q

What are some problems with BMI?

A
  1. Famously fails to distinguish between fat and muscle- tall man at 6’2” estimated BMI over more than 30
  2. BMI is a unreliable indicator of actual fat- It fails to account for WHERE fat is located on the body
  3. BMI does not apply equally to people of all ethnicities- Asians have higher weight-related disease related risks- possible explanation is body fat. South Asians higher levels of body fat. Blacks have lower levers of body fat and higher lean muscle mass lower risk of obesity-related disease. International debate whether cut points for overweight and obesity should be lower cutoffs. China and Japan define overweight as a BMI of 24 or higher and obesity a BMI of 28 or higher; in India, overweight is defined as a BMI of 23 or higher, and obesity, a BMI of 27 or higher
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4
Q

How do we define overweight and obesity using waist circumference?

A

MEN:
Overweight: WC > 37 inches (94 cm)
Obese: WC > 40 inches (102 cm)

WOMEN:
Overweight: WC >32 inches (80cm)
Obese: WC > 35 inches (88cm)

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5
Q

Describe trends in waist circumference since 1993.

A

There has been an increase in mean waist circumference among both men and women since 1993.

There are well documented links between high levels of central adiposity in adults, as measured by waist circumference, waist-to-height or waist-to-hip ratio and risk of obesity-related conditions including type 2 diabetes, hypertension and heart disease. These links remain even once BMI is adjusted for, demonstrating that measures of central adiposity are independent predictors of future obesity-related ill health.

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6
Q

What are health consequences of obesity for men and women?

A 
Male deaths (2018)
1. Heart disease
2. Dementia
3. Lung cancer
4. Chronic lower respiratory disease
5. Cerebrovascular disease 
Influenza and pneumonia

Female deaths (2018)

  1. Dementia
  2. Heart disease
  3. Cerebrovascular disease
  4. Chronic lower respiratory disease
  5. Influenza and pneumonia
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7
Q

Expand on cardiovascular disease as a health consequence of obesity.

A

Umbrella term for a range of diseases

Heart disease and stroke are the leading causes of death worldwide

Confirmed link between obesity and cardiovascular disease

Mortality rates from heart disease and stroke have been falling over the past decades

Cost to NHS over 9 billion yearly

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8
Q

Expand on diabetes as a health consequence of obesity.

A

Huge increase in the prevalence of diabetes

Type 2 diabetes accounts for the majority of cases

Obesity is the main risk factor for type 2 diabetes

One of the leading causes of death worldwide (4th)

Undiagnosed diabetes is a cause for concern

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9
Q

Expand on cancer as a health consequence of obesity.

A

Link between weight and cancer is firmly established

2nd biggest preventable cause of cancer

Meta-analysis 89 studies on overweight and obesity

Increased risk of 13 cancers

2 of the most common types– breast & bowel cancer

3 of the hardest to treat – pancreatic, oesophageal & gallbladder cancers

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10
Q

Expand on dementia as a health consequence of obesity.

A

Emerging evidence in this area

2020 study of over 6000 adults from the English Longitudinal Study of Ageing with 11-year follow-up

Obesity linked with a 31% increased risk of dementia than those with BMI in normal range

Women with abdominal obesity (based on waist circumference) had a 39% increased risk of dementia

No association with waist circumference in men

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11
Q

What are the pathways linking obesity and health?

A

Direct pathway
Obesity has a direct impact on our physiology

Indirect pathway
Obesity associated with poor health behaviour which in turn impacts health

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12
Q

Expand on the direct pathway.

A

see ppt slide 25

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13
Q

Expand on the indirect pathway with sleep and obesity

A 
Sleep  
Short sleep (< 6hours per night) & poor sleep quality increases the risk of obesity

Sleep and metabolic change
Decreased glucose tolerance & decreased insulin sensitivity

Increased evening concentrations of cortisol

Increased levels of ghrelin & decreased levels of leptin

Ghrelin increases hunger signalling

Leptin reduces hunger signalling

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14
Q

Expand on the indirect pathway with diet and CVD.

A

STRONG EVIDENCE
High-sodium diet increases risk of hypertension

Vegetables, nuts & Mediterranean diet (RCT) are protective

High consumption of trans fats causally contributes to atherosclerosis

MODERATE EVIDENCE
Consumption of fruits, fish, whole grains, fibre and alcohol

WEAK EVIDENCE
Consumption of saturated fat and atherosclerosis

But saturated fats linked with bad cholesterol. Red meat often high in salt!

“Evidence for most nutrients or foods too modest to be conclusive”

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15
Q

Expand on the indirect pathway with diet and Type 2 diabetes.

A

“Sugar may be linked to type 2 diabetes by making a significant contribution to becoming overweight…sugar alone in your diet is not enough. Weight is determined by total energy intake”.
Diabetes UK

“The myth that sugar causes diabetes is commonly accepted…one of the biggest risk factors for type 2 diabetes is beingoverweight, and a diet high in calories from any source contributes to weight gain”.
American Diabetes Association

Sugary drinks have been linked to 30% increase risk of diabetes

Effect remains even when taking BMI into account (26% adjusting for BMI)

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16
Q

Expand on the indirect pathway with diet and cancer.

A

Early evidence
Estimated 32- 35% of cancer was avoidable by diet change

But few specific food items have been convincingly linked to cancer

EPIC cohort (EU)
Fruit & vegetables reduce mouth, larynx, oesophagus, lung & bowel cancer risk
No effect on lymphoma, breast, prostate or ovarian cancers
NIH-AARP study (US)
Fruit and vegetable consumption and reduced risk of head and neck cancers
Strong link between red meat and colorectal cancer
Red meat consumption also linked with oesophagus, liver, kidney, and prostate cancers

17
Q

What are the emotional consequences of obesity in young people and adults?

A

YOUNG PEOPLE

  • Body dissatisfaction
  • Slightly lower self-esteem in community samples
  • No consistent evidence of higher rates of depression in community samples
  • Higher rates of depression in clinical populations

ADULTS
Body dissatisfaction
No consistent differences in self-esteem
Higher rates of depression at the higher grades of obesity
Higher rates of depression in clinical populations

18
Q

What are the social consequences of obesity?

A

Educational access

  • Lower college attendance
  • Lower teacher ratings of ability for obese girls
  • Bullying and teasing at school

Marriage and social position

  • Less likely to get married
  • Downward socioeconomic status trajectory for obese women

Employment

  • Employers less willing to take obese people as employees
  • Obese employees earn less and are less likely to get a promotion

Social stereotyping

  • Unattractive
  • Weak-willed

Discrimination
- Out of 2,944 participants less than 5% reported weight discrimination
<1% of ‘normal weight’ reported discrimination
36% of ‘morbidly obese’ individuals reported discrimination

  • Weight discrimination associated with 0.95kg weight gain over 4 year follow-up
19
Q

What is the annual probability of achieving normal weight?

A

Annual probability of achieving normal weight (n=278, 982):

Obese man: 1 in 210
Obese woman: 1 in 124

Morbidly obese man: 1 in 1290
Morbidly obese woman: 1 in 677

20
Q

Expand on lifestyle interventions as a treatment for obesity.

A

Multi-factorial interventions that are tailored according to patient needs and risk factor status

Promoting healthy habits, dietary counselling, exercise training, and behavioural change targets

Meta-analytic evidence:
Analysis of 17 interventions that had a minimum observation period of 1 year

Lifestyle interventions resulted in significant reductions in weight compared with standard care

On average participants lose about 3.5 kg which is maintained for 3 years

21
Q

Expand on behavioural therapy as a treatment for obesity.

A

Nutrition and exercise advice
e.g. Easy nutritional swaps e.g. Beeken top 10 tips

Functional analysis of behaviour
Self-monitoring of eating and activity
Evaluation of positive and negative cognitions
Stimulus control in relation to food and activity choices
Self-reinforcement of behaviour change
Cognitive restructuring 
Reward good behaviour
Relapse prevention
22
Q

Expand on functional analysis of behaviour and behaviour chain

A

Functional analysis of behaviour:

  • Classical conditioning is central
  • 2 stimuli repeatedly paired will become linked
  • Eating cookies whilst watching TV –> turning on TV triggers craving for cookies
  • Identify and distinguish cues

Behaviour chain:
- One behaviour, linked to another, can contribute to an overeating episode.

  • What appears to be an unexpected dietary lapse can be traced to a whole series of small decisions and behaviours.
  • The behaviour chain also reveals where the individual can intervene in the future to prevent unwanted eating. Thus, the individual might avoid bringing cookies into the house or at least store them out of sight to reduce impulse eating.
23
Q

Expand on self monitoring as a behavioural therapy treatment option for obesity,

A

Most important component of behavioural treatment

People can underestimate calorie intake by 40-50% per day

Detailed records of: 
Food intake
Physical activity
Weight
Mood (positive and negative)

Reveals patterns such as calories from soft drinks
Monitors internal triggers (e.g. mood modification & “what the hell effect’)
Targets for intervention in the behaviour chain

24
Q

Expand on cognitive restructuring.

A

Cognitive restructuring

Modify thoughts that undermine weight loss

The impossibility of weight loss – previous failed attempts
Unrealistic eating and weight loss goals
Self-criticism regarding over eating or weight gain

“I’ve blown my diet so I might as well eat what ever I want”

vs

“I’ve over eaten today, but only by about 400 kcals. If I stop now, I can easily make up the difference by cutting back over the next couple of days”

Can help people feel more positive about weight loss

Disappointment -> abandonment of healthy behaviours

Focus on health rather than appearance aspects of weight loss

Improve body image -> help with acceptance of modest weight loss

25
Q

How effective is behavioural therapy and does the review of studies from 1996-2002 say?

A

Effectiveness:

  • Favourable results based on WHO criteria
  • 5-10% reduction in initial weight
  • Dose response relationship between weight loss and treatment duration

Review of studies 1996-2002:

  • Group behavioural approach mean weight loss of 10.7kg (~10% of initial weight)
  • 30 weeks of treatment
  • 80% of patients who begin treatment complete it
26
Q

Give an example of a pharmacological treatment of obesity.

A

ORLISTAT:

Reduced weight by 2.9kg on average (2.5-3.2 kg)
Reduced incidence of diabetes
lowered LDL cholesterol and blood pressure
Improved glycaemic control in those with diabetes
But attrition rates 30-40% on average

27
Q

Expand on the surgical treatment options for obesity and give their mean % weight loss.

A 
Vertical banding - 47.5
Gastric bypass - 61.6
Gastroplasty - 68.2
Duodenal switch - 70.1
Overall: 61.2%
28
Q

What are the areas of interest when discussing causes of obesity?

A
  1. Genetics
  2. Obesogenic environment
  3. Psychology of eating behaviour
29
Q

Expand on genetics as a cause of obesity.

A

And analyses using data from the TEDS twins at age 10 support the observation that weight is heritable. The bar graph shows the monozygotic twin pair correlation in blue and the dizygotic twin pair correlation in red for BMI- STANDARD DEVIATION SCORE (SDS) on the left, and waist-SDS on the right. As you can see, the MZ correlation is far higher than the DZ correlation, indicating a substantial genetic contribution to these two indices of adiposity.
When modelled formally, heritability to be high at 77% for BMI-SDS and 76% for waist circumference

30
Q

Expand on the obesogenic environment as a cause of obesity.

A

FOOD ENVIRONMENT:

  • Availability
  • Cost –> unhealthy food cheaper
  • Variety
  • Portion -> sizes increasing over time
  • High energy density (kcal/g)
  • Low fibre (not filling)
  • Food advertising/labelling

ACTIVITY ENVIRONMENT:

  • Activity environment
  • High cost of activity
  • Labour saving devices
  • Sedentary travel
  • Enjoyable sedentary pastimes
  • High ambient temperatures
31
Q

Expand on psychology and eating behaviour as a cause of obesity.

A

Basis for eating

  • Hunger is biological survival mechanism
  • Born with innate food preferences (sweet rather than bitter foods)
  • But there are many other reasons for eating other than biological need…

Psychological models of eating behaviour

Developmental model

Cognitive model

Weight concern and body dissatisfaction

32
Q

Expand on the developmental model of eating behaviour.

A

Emphasis on learning

Exposure
People show neophobia but this reduces after exposure

Social learning
Importance of modelling and observation
Parental feeding styles and practices are important!

Association
Food as the reward
Food and control- overt & covert differ

33
Q

Expand on the cognitive model.

A
  • Emphasis on beliefs and attitudes
  • Frameworks for explaining, predicting and changing behaviour e.g. Theory of planned behaviour
    see ppt for diagram

In the field of eating behaviour research has suggested that intentions are not particularly good predictors of behaviour per se. So this has driven research looking at the intention-behaviour gap

As intentions are not that good as predictors they have looked at cognitive predictors (i.e. attitude, subjective norms, and perceived behavioural control) of eating behaviour

Attitudes has been found to be a fat intake, salt use, eating in fast food restaurants, low-fat milk, f&v intake.

Attitudes centred around positive vs negative attitudes but also ambivalence ie. presence of both positive and negative attitudes simultaneously e.g. tasty vs fattening

Perceived behaviour control associated with eating behaviour in relation to weight loss and healthy eating
Social norms have NOT been shown to predict eating behaviour

34
Q

What are some problems of the cognitive model?

A
  • Components of model chosen by the researcher based on existing questionnaires important cognitions may be missed
  • Ignore meaning of food and body size
  • Assumes behaviour is rational ignores the role of affect e.g. emotions like guilt, fear of weigh grain, guilt at overeating
  • Ability to predict behaviour is poor- large amount of unexplained variance
35
Q

What are some problems of the developmental model?

A
  • most of the research has taken place in a lab- generalise to naturalistic settings?
  • Food has more diverse meanings than reward and control- more on this later
  • Ignores meaning of weight, body satisfaction, ideas of attractiveness success

Behavioural Medicine (11 decks)

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