BM - Diet and obesity Flashcards

1
Q

Definition of obesity

A

“Accumulation of fat stores to an extent that compromises health.”

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2
Q

Why is there a high level of interest in fat as a culture?

A

The ‘obesity epidemic’ is a recurring theme within the media. So we might assume that the British population is more informed than ever on the topic.

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3
Q

What are studies on our perception of overweight?

A
  1. Study 1: Researchers at UCL carried out a study among obese adults to find out how they perceived their own weight they uncovered some surprising results .The researchers looked at data from two surveys, conducted 5 years apart in 2007 and 2012, in which 657 obese persons were asked to select a descriptor for their own body weight. They could choose from the options: very underweight, underweight, about right, overweight, very overweight, obese. The results showed that the proportion of obese adults selecting the term ‘obese’ to describe their body size was very low in both sexes: 13% of women in 2007 and 11% of women in 2012, and less than 10% of men at both time points.
    Study 1: Now, of course the term ‘obese’ goes hand-in-hand with stigmatisation, which might well explain the reluctance to use it. The researchers did take this into consideration and went on to look at whether people were more likely to use the less controversial term ‘very overweight’. However, among women there was actually a decrease in the use of the term ‘very overweight’ over time. The majority of the adult obese population of Great Britain do not identify themselves as either ‘obese’ or even ‘very overweight’.
  2. Study 2: Overweight children are at an increased risk of premature mortality and disease in adulthood.Looked at the extent to which parental and objective weight status cut-offs diverge. 2976 children in England 4-5 and 10-11 years old. A third of parents underestimate their child’s BMI. Other evidence suggests that parents who recognise their child’s weight status are more likely to perceive potential health risks. The earlier you become obese, the worse your health outcome over time.
  3. Study 3: 5,000 young people aged 13 to 15 who had taken part with their families in the annual health survey for England between 2005 and 2012. They had been weighed and measured and had been asked whether they thought they were “about the right weight”, “too heavy” or “too light”. Relatively few ‘normal-weight’ teens think they are too heavy, but many who are overweight do not acknowledge. 39% of overweight teenagers thought they were the right weight. Only 7% of teenagers thought they were overweight.
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4
Q

What is the anthropomorphic measurement of weight?

A

BMI

Formula: weight in kg/height in m2

Adults:
- Underweight: BMI <18.5
- Normal weight: BMI = 18.5 – 24.9
- Overweight: BMI = 25 – 29.9
- Obesity: BMI =/> 30
- Severe (‘morbid’) obesity: BMI =/> 40
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5
Q

What are the 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 an unreliable indicator of actual fat- It fails to account for WHERE fat is located on the body (talk a bit more about that in a minute). There are different implications on health depending on where you are carrying the fat.
  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, and are at higher risk of weight related diseases, at lower BMI scores. 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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6
Q

Weight circumference as a measurement of obesity

A
Central obesity is of greater risk to your health as opposed to someone who is pear shaped.

Men
Overweight: WC > 37 inches (94 cm)
Obesity: WC > 40 inches (102 cm)

Women
Overweight: WC > 32 inches (80 cm)
Obesity: WC > 35 inches (88 cm)

Ethnic specific values for waist circumference have also been defined.
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7
Q

Waist to height ratio as a measurement of obesity…

A
  • Waist should be less than half your height, so values under 0.5
  • Meta-analysis of 31 studies involving of over 30,000 people in several ethnic groups, shows the superiority of WHtR over WC and BMI for detecting cardiometabolic risk factors in both sexes.
  • Call for Waist-to-height ratio to be considered as a screening tool.
  • Ashwell, M., Gunn, P., & Gibson, S. (2012). Waist‐to‐height ratio is a better screening tool than waist circumference and BMI for adult cardiometabolic risk factors: systematic review and meta‐analysis.Obesity reviews,13(3), 275-286.
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8
Q

Percentage body fat as a measurement of obesity…

A
  • Callipers- straight forward tells you exactly to mm or inch how much fat is on your body.
  • Bodystat and tanita- impedance measures. Firstly person’s height and weight and age, gender is noted. Small electrical current circulated the devices measures the impedance or resistance to the signal as it travels through the water that is found in muscle and fat. The more muscle a person has, the more water their body can hold. The greater the amount of water in a person’s body, the easier it is for the current to pass through it. The more fat, the more resistance to the current
  • Hydrostatic weighing- considered a gold standard and is highly accurate- but expensive and uncomfortable. People must empty their lungs as much as possible before entering the tub and must hold their breath underwater.
  • Bod Pod also expensive but also considered a gold standard. It is as accurate as hydrostatic weighing.. It can detect small changes in body fat and lean body mass (i.e., muscle, bones and organs). Utilising a technique called air displacement plethysmography the client sits comfortably in a chamber for two to three minutes whilst the volume of air displaced by the body is measured and used to calculate body fat percentage.
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9
Q

What are the health consequences of obesity?

A

Mortality and adiposity

359,387 participants from nine countries in the European Prospective Investigation into Cancer and Nutrition (EPIC) (which we will talk about more later)

Adjusted Relative Risk of Death among Men and Women in the European Prospective Investigation into Cancer and Nutrition (EPIC cohort-), according to BMI & Waist Circumference

Solid lines indicate relative risks, and dashed lines represent 95% CI

Stratification according to center and age at recruitment and additional adjustment for smoking status, educational level, alcohol consumption, physical activity, and height.
Famous J shaped associated. Risk higher in those of low and high body fat

Lowest risks of death related to BMI were observed at a BMI of 25.3 for men and 24.3 for women.

In this study both waist circumference and BMI useful for predicting death

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10
Q

Where can there be physical consequences of obesity?

A
lungs
heart
head
liver
uterus
ovaries
legs
general body
testes
bowels
kidney
pancreas
breasts
throat
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11
Q

About obesity and cardiovascular disease…

A
  • Leading cause of death worldwide
  • Second biggest cause of death in the UK – but gender difference!

CVD group of diseases affect the circulatory system the most common of which are CHD and stroke.

CVD is the leading cause of death worldwide and the in the UK. According to the WHO it accounts for approximately 30% of worldwide deaths every year

CVD was the most common cause of death in the UK for women (28% of all female deaths), but not for men, where cancer is now the most common cause of death (32% of all male deaths).

Downward trend in CVD since the 1970s. In 2009 CVD cost the NHS £8.7 billion and the economy £19 billion.

Putting in stents has become increasingly common, having doubled in the last decade. This is part of why CVD is decreasing (but it is still the biggest killer!).

In the UK, mortality from CVD has been falling since the early 1970s->
Mortality has been declining in all regions of the UK
In England, death rates from heart attack have halved since 2002.
This decline is thought to be attributable to reductions in smoking, improved hospital treatment and better management of blood pressure and cholesterol (Smolina, Wright, Rayner, & Goldacre, 2012).
Over 92,000 percutaneous coronary interventions (PCI) were carried out in the UK in 2012, more than twice as many as a decade ago
Despite downward trends in mortality the economic costs of CVD are vast.
In 2009, the overall cost of CVD to the UK economy was an estimated £19 billion

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12
Q

What is the burden of diabetes?

A
  • Increasing in prevalence globally and in the UK
  • Type II diabetes: 85-95% of cases
  • Undiagnosed diabetes is a problem (45% of sufferers don’t know they have it!)
  • Extremely costly to health systems

T2D- chronic disease that is becoming increasing more prevalent globally.
Figure from IDF Diabetes Atlas - yearly report on worldwide trends in T2D. 382m adults worldwide (8.3% of adult population).
- Worldwide set to rise beyond 592m in next 25 years.
UK 3.2 million adults (6%) set to rise to 5 million in next 10 years (Diabetes UK)
Type II diabetes accounts for the majority of cases of diabetes and is the cause of the huge increase in prevalence in diabetes
Undiagnosed diabetes- 45% of people with diabetes are not aware that they have this serious health condition
Burden of diabetes is enormous - It is the 4th or 5th leading cause of death in most high income countries according to WHO and IDF
- Extremely costly to health systems. Accounts for almost 11% of worldwide health expenditure.
- 10% of the NHS budget

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13
Q

What are the complications of obesity?

A
  1. Chronic hyperglycaemia of diabetes is linked to long-term damage, dysfunction and failure of various organs.
  2. The harmful effects of diabetes can be divided into microvascular and macrovascular complications
  3. Microvascular complications (damage to small blood vessels)
    • Retinopathy damage to the eyes is the biggest cause of blindness
    • Nephropathy damage to the kidney can lead to kidney failure
    • Neuropathy can lead to foot ulcers and is the biggest cause of amputation

The macrovascular complications encompass various cardiovascular diseases- and are the focus of my PhD but I think it is important to highlight the other deleterious side effects of this disease.

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14
Q

What are the microvascular consequences of obesity?

A

retinopathy
nephropathy
neuropathy

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15
Q

What are the microvascular consequences of obesity?

A

stroke
coronary heart disease
peripheral vascular disease

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16
Q

What is the relationship of obesity with cancer?

A

• The link between body weight and cancer is firmly established
• Meta-analysis 89 prospective studies:
• Overweight and obesity associated with increased risk of breast, colorectal, endometrial, kidney, and ovarian cancers
• Association between weight and oesophagealcancer in men only
• Mixed associations for pancreatic and prostate cancer

Guh (2009) on reading list
The link between body weight and cancer is firmly established and based on a large body of consistent evidence
• Pancreatic cancer not associated with overweight but linked with obesity
• Prostate cancer associated with overweight only

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17
Q

What other physical conditions are associated with obesity?

A

• Meta-analysis 89 prospective studies:
• Overweight and obese BMI increase the likelihood of developing asthma, gallbladder disease, osteoarthritis and chronic back pain
• For gallbladder disease WC is a better predictor of risk than BMI
• The associations get stronger as BMI increases

Gallbladder disease WC is a better predictor than BMI.

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18
Q

How does adipose tissue act as an endocrine organ?

A

Biomedical science students- I’m sure you know a lot about this but adipose tissue is an active endocrine organ
Intra-abdominal fat is key

White adipose tissue is highly complex and is composed of various cell types that interact dynamically with each other through the secretion of adipokines, including hormones, cytokines and chemokines. This tissue is now recognized as being equivalent to an endocrine organ

Abdominal fat release substances collectively known as adipokines (e.g. hormones, enzymes and cytokines) into the circulation

Adipokines associated with:
insulin resistance
dyslipidaemia [raised LDL cholesterol, triglycerides, lowered HDL cholesterol and raised blood pressure]
inflammation

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19
Q

About diet and Cardiovascular Disease?

A

• High-sodium diet increases risk of hypertension, which is a risk for CVD
• Strong evidence high consumption of trans fats causally contributes to CVD (through atherosclerosis), weaker evidence for saturated fat
• Strong evidence that vegetables, nuts & Mediterranean diet (RCT) are protective
• Moderate evidence for the protective effect of fruits, fish, whole grains, fibre and alcohol
“Evidence for most nutrients or foods too modest to be conclusive”

Dietary patterns also influence risk of coronary heart disease.
Ecological data from the Seven Countries Study showed a strong positive association (r=0.73) between saturated fatty acid intake and CHD incidence,although a much lower correlation was observed for total fat (r=0.39), suggesting that not all types of fat (ie, polyunsaturated fatty acids) are associated with an increased CHD risk.
Little direct evidence from RCTs mostly longitudinal cohort BUT RCT for Med Diet high in fv, whole grains, fish etc. and reduced CVD

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20
Q

About sugar and 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”. ADA
• However, sugary drinks have been linked to 30% increase risk of diabetes
– (26% adjusting for BMI!)

1. 2015 meta-analysis by Wang and colleagues, eight studies published between 2004 -2014 . A total of 286,697 participants. Majority of studies in US but also 2 in EU and 1 in Japan
2. Estimated that the risk of diabetes associated with high consumption of SSBs is 1.30 times that for low consumption. 
3. Evidence from the European Prospective study in 8 European countries, showed that one sugar-sweetened soft drink daily was associated with a risk of developing diabetes
4. June 2015, the scientific journalCirculationpublished a study estimating that sugary drinks are linked to 180,000 deaths worldwide per year; of these, 133,000 were from diabetes.
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21
Q

About diet and cancer…

A

• Early research 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
– BUT 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 and some evidence for other cancers, including oesophagus, liver, kidney, and prostate

Research in the 80s and early 90s suggested that a third of cancers could be avoidable by changes to diet

AND we did see early that there is overall a very consistent relationship between the majority of cancers and measures of adiposity
Few specific food or drinks have been convincingly linked to cancerà diet consists of many different foods, nutrients and minerals

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22
Q

What was the EPID cohort?

A

The European Prospective Investigation into Cancer and Nutrition (EPIC) study is one of the largest cohort studies in the world, with more than half a million (521 000) participants recruited across 10 European countries and followed for almost 15 years.

EPIC was designed to investigate the relationships between diet, nutritional status, lifestyle and environmental factors, and the incidence of cancer
NIH-AARP
National Institute of Health- American Association of Retired Persons

People aged aged 50-71 years, and who resided in one of six states (California, Florida, Pennsylvania, New Jersey, North Carolina, and Louisiana) or in two metropolitan areas (Atlanta, Georgia and Detroit, Michigan). The questionnaire included a dietary section as well as some lifestyle questions. Over 500,000 people returned the questionnaire, again v large study

Positive association between red and processed meat and colorectal cancer was convincing on the basis of the results of 16 cohort studies and 71 case-control studies. Update 2011 only served to strengthen the evidence in favour of a link between red and processed meat intake and colorectal cancer

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23
Q

What are the emotional consequences of obesity?

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 in community samples
• Higher rates of depression at the higher grades of obesity
• Higher rates of depression in clinical populations

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24
Q

About discrimination and social exclusion from 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 SES 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
25
Q

Evidence on fat shaming…

A

‘In your day-to-day life, how often have any of the following things happened to you?’
1. You are treated with less respect or courtesy
2. You receive poorer service than other people in restaurants and stores
3. People act as if they think you are not clever
4. You are threatened or harassed
5. You receive poorer service or treatment than other people from doctors or hospitals

Results
• 2,944 participants less than 5% reported weight discrimination.
• Range: less than 1% of ‘normal weight’ to 36% of ‘morbidly obese’ individuals.
• People who reported weight discrimination gained 0.95kg over the 4 year period whereas those who did not lost 0.71kg.

One has only to glance at the ‘comments’ section of news reports discussing obesity to realise that obese people are openly subjected to labelling and stereotyping, and some outright abusive attacks.

But does this ‘fat shaming’ help ppl lose weight?
2,944 UK adults over four years who participated in the English Longitudinal Study of Ageing (ELSA), a study of adults aged 50 or older. Participants are weighed and measured every four years, and asked questions on a range of topics every two years.

Participants who reported discrimination in any of the situations were asked to indicate the reason(s) they attributed their experience.

The researchers considered participants who attributed experiences of discrimination to their weight as cases of perceived weight discrimination.

Men and women reported similar levels of weight discrimination

However, because this study looked only at the relationship of perceived stigma and weight gain, we cannot conclude that stigma caused weight gain – it could also be that weight gain increased perceived stigma, or that a third factor influenced both weight gain and stigma. To conclusively establish whether stigma indeed causes weight gain, we would have to run a controlled experiment with at least two groups of similarly overweight people, where one group is subjected to stigma over a period of time, and the other one is not, and then measure their weight at the end of the study. Of course, such an experiment would be highly unethical, given theeffects of stigma on psychological health. Another limitation of this study was that discrimination was assessed two years after the initial weight measurements and two years before the final measurements, although the researchers controlled statistically for this

26
Q

What are the possible causes of obesity?

A

1 - genetics
2 - obesogenic Environment
3 - psychology and eating behaviour

27
Q

What are the genetic causes of obesity?

A

Different study designs to explore the genetics of obesity.

• Quantitative genetic studies
– E.g. twin studies
• Molecular genetic studies
– E.g. Genome-wide association studies (GWAS)

There are a number of different methods that can be used to determine the likelihood that genetic variation plays a role in disease risk. The approach that you take largely depends on the question that you want to answer.

If you are starting out, and you have no idea whether genes are involved at all you would begin by conducting a quantitative genetic study: this will tell you the extent to which genes are involved at all, versus the environment.

If you conduct a study like this and find out that genes are playing an important role in shaping the disease risk you might then want to go on to do a molecular genetic study where you try and identify the actual genetic variants that may be involved. Historically, these began with candidate gene studies, then we went on to use linkage studies, and the current trend is genome-wide association studies…

28
Q

Twin studies in obesity…

A

16,000 families with twin births in 1994-96
5000 pairs assessed for weight at ages 4,7 and 10 and appetite at age 10
214 pairs visited at age 4 & 10 to assess weight and appetite

Twins Early Development Study (or TEDS), which includes more than 16000 families with twins born in 1994 to 1996 in England and Wales. Weight was measured in 5000 pairs at 4, 7 and 10 years and appetite at age 10, using parent reported questionnaires.
In order to collect much more detailed data, and to validate the parent-reported data, researcher measures were taken in a subsample of 214 pairs of twins at home when they 4 and then again when they were 10 years old.

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.

29
Q

Is body weight heritable?

A

yes very

30
Q

What was GWAS?

A

Polygenic obesity and risk score adiposity

More than 32 common genetic variants have now been identified for indices of adiposity through GWAS genome-wide association studies. And it is possible to aggregate these together into a polygenic obesity risk score. This has been done in TEDS, and the graph shows the regression line for BMI (in blue) and waist (in red), plotted against genetic risk of obesity, at age 10. As you can see, genetic risk of obesity (along with other complex phenotypes) is normally distributed in the sample, and as genetic risk of obesity increases, so does BMI and waist circumference. At age 10, the 28 SNPs together explain about 3% of the variance. However, nearly 100 additional SNPs have recently been identified which doubles the variance explained.

31
Q

What is the genome wide complex trait analysis?

A

Missing heritability problem à Twin studies indicate that weight is highly heritable but polygenic risk scores explain very little of the variance in weight.

Genome-wide Complex Trait Analysis (GCTA) estimates the additive genetic effect of common SNPs

37% of the twin-estimated heritability (30/82%) can be explained by additive effects of multiple common SNPs

• Genome-wide Association Studies (GWAS) have made significant headway in identifying single-nucleotide polymorphisms (SNPs) that are related to body weight indexed by BMI
• However, even in combination, the 32 established SNPs explain <3%of the variation in BMI in either adults or children
• The mismatch between the high heritability estimates from twin studies and the small proportion of variation explained through GWAS findings have come to be known as the problem of ‘missing heritability’
• Part of the missing heritability is likely to be due to rare genetic variants and some non-additive genetic effects. GWAS analyses that only capture additive effects of common SNPs.
• A second possibility is that there are multiple additional common genetic variants that contribute to the effect observed in twins studies, but they have such small effect sizes that they cannot be detected even in the huge data sets used in contemporary GWAS analyses.
• A novel approach called Genome-wide Complex Trait Analysis (GCTA) takes advantage of the fact that the degree of genetic resemblance for common SNPs at the whole-genome level is normally distributed among unrelated individuals.The purpose of GCTA is not to identify specific SNPs related to the target phenotype (in this obesity), but rather to estimate the total additive genetic effect of the common SNPs. Its value relative to GWAS comes from the fact that the GCTA estimate includes the effect of SNPs well below the current GWAS threshold.

32
Q

What is the obesogenic environment?

A
Food environment
	– Availability
	– Cost
	– Variety
	– Portion sizes
	– High energy density (kcal/g)
	– High fat
	– Low fibre (not filling)
	– Food advertising

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

So children not only inherit genes from their parents they also inherit to a certain extent their environment. Of course environment plays a role in ‘missing heritability’ and obesity has been rising faster than genes can explain.

33
Q

What is the relation of high availability and low cost of food with obesity?

A

The Foresight report highlighted that energy intake per day has increased steadily between 1969-71 and 2003-05 in high-income countries such as the US and the UK.

34
Q

Food energy supply and obesity in the US

A

Swinburn and colleagues predicted the changes in weight from the changes in estimated energy intakes in US children and adults between 1970s and 2000s. The increased US food energy supply (adjusted for wastage and assumed to be proportional to energy intake) was apportioned to children and adults and inserted into equations that relate energy intake to body weight derived from doubly labelled water studies. The weight increases predicted from the equations were compared to the weight increases measured in representative US surveys over the same period.

For children, the measured weight gain was 4.0kg and the predicted weight gain for the increased energy intake was identical at 4.0kg. For adults, the measured weight gain was only 8.6kg whereas the predicted weight gain was somewhat higher (10.8kg). The authors concluded that the increases in energy intake were more than sufficient to completely explain the weight gain in the US population. A reversal of the increased energy intake of ~ 500kcal/day for adults and 350kcal/day for children would be required to return to the mean body weights of the 1970s.

35
Q

Increasing portion sizes consumed by children

A

One of the hypothesised reasons for the increased energy intake is increases in portion sizes over the last 30 years.

This graph shows the average portion size consumed by children in the US from nationally representative surveys across four decades.

The average portion sizes of foods consumed by children increased significantly for all foods studied except desserts between 1977-78 and 2003-2006.

36
Q

Increasing portion sizes sold in the US

A

This graph shows the increases in portion sizes of foods sold by supermarkets, restaurants and fast food outlets over the same period. Portion sizes sold by fast food outlets have increased significantly since 1977-88.

37
Q

What is the biological basis for eating?

A

• Hungerà biological survival mechanism (calorie requirements, neurotransmitter & hormones levels etc.)
• Born with innate food preferences
– Preference for sweet and dislike for bitter

38
Q

What is the psychological basis for eating?

A
There are many other reasons for eating other than biological need:
	– Learned associations and preferences
	– Cognitions
	– Hedonic reasons
	– Environmental and social factors
39
Q

What are the models of eating disorder?

A
  1. Developmental model
  2. Cognitive model
  3. Weight concern and body dissatisfaction
40
Q

What is the development model of eating behaviour?

A

Emphasis on learning
Exposure
– People show neophobia but this reduces after exposure – takes 8-10 exposures to a food to change someones view of it and more common in men than women
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
Can you think of problems with this model?
Exposure model
• Neophobia - More common in males
• Evolutionary adaptive process- ties into dislike of bitter
• Reduces after exposure -> research suggests 8-10 exposures are required to change preferences significantly.
• ‘Learned safety’ explanation-> food has not resulted in any negative consequences also supported by the fact that neophobia decreases with age
Social learning- modelling other ppls behaviour

Food dudes research- older children consuming refused food. Changed food preferences and increased fruit and vegetable intake
• Parental feeding styles impact children’s eating behaviours- foods purchased for the house, exposure, habits and preferences. Association between mother’s ‘health motivation’ and quality of children’s diet. BUT some studies show dieters feed children more of the food they are denying themselves. Mother and daughter weight concern and eating style
Not only parentsà media superfoods, health risks of beef

Association
Control food presented as a reward children eat more than neutral food. ‘if you eat your veg you can have a pudding etc.’ Increasing preference for sweet treat
Control-> making restricted food more desirableà children will overeat when given free choice. BUT difference between overt and covert. Overt e.g. firm with how much child should eat ‘covert’ not buying unhealthy foods. Higher overt increased intake of unhealthy food. Covert decreased intake of unhealthy foods.
Problems with the model-> 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

41
Q

What is the cognitive model of eating behaviour?

A

Emphasis on beliefs and attitudes
– Framework for explaining, predicting and changing behaviour
– Many different ones à most eating research uses social cognition models
– Theory of planned behaviour

Many different ones in the health psychology field- also well as explaining and predicating could also be used for changing behaviour and areas to target in interventions
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

Problems
- 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

42
Q

About weight concern and body dissatisfaction…

A

Emphasis on the meaning of food and weight
Food has many meanings…..
Comfort, boredom, pleasure, celebration,
treat, family love, religion, culture etc.
Food can change weight and shape….
Meanings such as attractiveness, control & success

Body dissatisfaction higher in females. Most women think they are fatter than they actually are.
Most women and girls want to be thinner

Negative emotions-> individuals with eating disorders show greater dissatisfaction than those without, dieters have greater dissatisfaction than non-dieters
So body dissatisfaction conceptualised as discrepancy between actual size and reality, actual size and ideal and negative emotions regards body size and shape.

Common not limited to people with eating disorders!

Dieting-> ‘restraint theory’ dieters/restrained eaters do eat less in lab environment but then evidence for overeating ‘what the hell effect’ also overeating in dieters may be related to attempts at mood modification. Eat more when they have low mood. Also ‘motivational collapse’

Emphasis on the meaning of food and weight

Body dissatisfaction
Research on size estimation, perceptions of reality vs. ideal and negative emotions

Dieting and overeating
Body dissatisfaction related to dieting as well as overeating!
– Dietingà Restraint theory
– Overeating in dieters à Motivational collapse
– Overeating in dieters à‘What the hell effect’
– Overeating in dieters à Mood modification

Body dissatisfaction higher in females. Most women think they are fatter than they actually are.
Most women and girls want to be thinner

Negative emotions-> individuals with eating disorders show greater dissatisfaction than those without, dieters have greater dissatisfaction than non-dieters
So body dissatisfaction conceptualised as discrepancy between actual size and reality, actual size and ideal and negative emotions regards body size and shape.

Common not limited to people with eating disorders!
Dieting-> ‘restraint theory’ dieters/restrained eaters do eat less in lab environment but then evidence for overeating ‘what the hell effect’ also overeating in dieters may be related to attempts at mood modification. Eat more when they have low mood. Also ‘motivational collapse’

43
Q

What is a model for gene-environmental interaction and eating behaviour - a role for appetite…

A

• Eating has a biological basis
• However psychological & psychosocial factors play a major role:
1. Developmental model emphasises learning
2. Cognitive model emphasises beliefs & attitudes
3. Weight control model emphasises meaning of food and weight

So how are genetics, the obesogenic environment and the psychology of eating linked?!

44
Q

Appetite is heritable

A

This suggests an appetite pathway for ‘obesity gene’

Results from another Twin study at UCL called GEMINI as well as TEDS

The observation that a large proportion of the genetic effect on body weight has been expressed by the time children are 4 years old, led Professor Jane Wardle to establish Gemini Study in order to start collecting detailed information on early life characteristics to explore growth trajectories from birth. These twins have had weight collected every 3 months. Data collection started in 2007.

45
Q

What is the government policy?

A

Department of health and NHS perspective

• Department of Health Policy
– Reducing obesity and improving diet
– Giving children a healthy start in life
– Improving outcomes: strategy for cancer
• National Service Frameworks for CHD
• Diabetes National Service Framework

So —->

• All highlight obesity & diet as a key areas for action
• Action to reduce fat, sugar and salt in the diet, and increase fruit and vegetable consumption

46
Q

What are the treatment options for obesity?

A

Behavioural interventions (diet and activity)
Pharmacology
Surgery

47
Q

What are the behavioural interventions for obesity?

A

‘Lifestyle interventions’

Behavioural therapy

48
Q

What are the pharmacological treatment options for obesity?

A

– Orlistat (‘Xenical’ or ‘Alli’) – the only weight loss drug still on the market out fo these three – lipase inhibitor
– Subutramine (withdrawn Jan 2010) – serotonin reuptake inhibitor
– Rimonabant (withdrawn June 2008) – antagonist of the CB1 receptor

49
Q

What are the surgery options for obesity?

A
  • gastric banding
  • vertical banded gastroplasty
  • gastric bypass
50
Q

What is the results of the meta-analysis of lifestyle interventions for obesity, 1995-2005?

A

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

They can include promoting healthy lifestyle habits, dietary counselling, physical exercise training, and behavioural change targets

Meta-analysis of lifestyle interventions
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

  • Lifestyle programs are multi-factorial interventions that are designed for each patient or group of patients according to their risk factor status and the needs of the subjects. These include promoting healthy lifestyle habits, dietary counselling, physical exercise training, and behavioural change targets
  • Galani & Schneider (2007) conducted a systematic review and meta-analysis of 17 ‘lifestyle interventions’ to treat overweight and obesity that had a minimum observation period of 1 year. Compared with standard care lifestyle interventions resulted in significant reductions in weight for 3 years.
51
Q

What is done in behavioural therapy for obesity?

A

• Advise on behaviours to modify energy balance
– Nutrition and exercise advise
• e.g. easy nutrition swaps, Beeken et al., “Top 10 Tips”
• Strategies to increase control over energy balance behaviours
– Goal-setting in relation to behaviour change
• SMART goals
– Self-monitoring of eating and activity
• Diary

SMART-> Specific, Measurable Achievable, Results-focused, Time-bound

Strategies to increase control over energy balance behaviours
• Stimulus control in relation to food and activity choices
1. Avoidance
• E.g. environment, situation
2. Distraction
• e.g. brushing teeth instead
3. Resistance
• e.g. exposure to stimulus and active control
à willpower is important!
• Evaluation of positive and negative cognitions
– Thought Diary- monitor internal ‘triggers’
– Stop ‘what the hell effect’ and using food for mood modification
• Reward good behaviour
– Reward but not with food!

Avoidance e.g. going to the supermarket hungry

Distraction- emotional eating and stress management. Study brushing teeth makes craving go away in 20 minutes

Specific, measureable, realistic, time defined, can keep track of.

52
Q

What is the effectiveness of behavioural therapy for obesity?

A

Behaviour therapy yields very favourable results as judged by the WHO criteria for success (5-10% reduction in initial weight)

Weight losses have increased threefold over the past 30 years as treatment duration has increased by the same amount

53
Q

Review of studies from 1996-2002 on obesity…

A

Review of studies 1996-2002
• Patients treated with a comprehensive group behavioural approach lose approximately 10.7kg (approx. 10% of initial weight) in 30 weeks of treatment
• Importantly 80% of patients who begin treatment complete it

Weight losses have increased almost threefold over the past 30 years as treatment duration has increased by the same amount. Studies between 1996 and 2002 show that patients treated with a comprehensive group behavioural approach lose approximately 10.7kg (about 10% of initial weight) in 30 weeks of treatment. In addition, about 80% of patients who begin treatment complete it. Thus, behaviour therapy yields very favourable results as judged by the criteria for success (i.e. a 5-10% reduction in initial weight) proposed by the World Health Organisation (WHO).

54
Q

What is fat cell memory?

A

Weight loss does not reduce the number of fat cells, it just shrinks/flattens them

55
Q

About weight regain and metabolic processes…

A

• Fat cell memoryà Weight loss does not reduce the number of fat cells but shrinks/flattens them
• Compensatory metabolic processes resist maintenance of altered body weight
– Decrease in salience of satiety signals,
– Increase in salience of hunger signals
– increase in metabolic efficiency
– Weight loss of 10% or more associated with a reduction in energy expenditure
– caloric disadvantage of about 250 to 400 calories
– E.g. 13.5 stone woman after weight loss needs 2300 to maintain body weight. Woman of same weight who was never overweight can eat 2600 calories a day and maintain weight
.

Treating weight loss is complex. Discussed some of the genetics, environmental influence and psychology. Another issue is fat cell memory

Leibel researched the body’s response to weight loss. For 25 years, tracked about 130 individuals for six months or longer at a stretch.

The research shows that the changes that occur after weight loss translate to a huge caloric disadvantage of about 250 to 400 calories.

If you have been obese, you burn less calories per day than someone of your weight that had never been obese. This is partly why it is so difficult for weight loss to be maintained.

56
Q

What are the outcomes with orlistat at 2 years?

A

It is clear that there is a dose response.

The maximal weight loss is achieved between 6 and 9 months and then there was a slow regain in all groups.

57
Q

What are the effects of orlistat treatment?

A

Reduced weight by 2.9kg on average (2.5- 3.2 kg)
Reduced incidence of diabetes, lowered LDL cholesterol and BP and helped with glycaemic control in individuals with diabetes

BUT

Attrition rates 30-40% on average

These figures are versus placebo

58
Q

About surgical interventions for obesity…

A

Compared to usual care surgery led to significant reduction in body weight (-23% at 2 years, -17% at 10 years, -16% at 15 years and -18% at 20 years). The most effective surgical method is gastric bypass surgery, leading to -26% change in body weight, followed by vertical banded gastroplasty (stomach stapling) and gastric banding.