Obesity Flashcards
What happens when weight is stable
When weight stable
E in = E out + E stored
What happens in weight gain
Weight gain
E in exceeds E out
Increase intake
Decrease expenditure
When does obesity occur
Obesity can only occur when energy intake remains higher than energy expenditure for an extended period of time.
Excess energy intake is stored as fat
When is fat detrimental
In excess
What is meant by energy homeostasis
Energy homeostasis = in a steady state, the energy intake must equal the energy expenditure.
What is total energy expenditure equal to
Heat produced + work on environment ( at rest all energy expenditure is equal to heat produced that is thermogenesis)
What can daily energy expenditure be split into
The RMR (RMR-sum of the sleeping metabolic rate and energy cost of arousal) which represents 50-70% of daily EE
RMR correlates best with fat free mass, and therefore RMR generally correlates with body
The thermic effect of food, which represents 5-15 %of daily EE
The energy cost of physical activity (sum of spontaneous PA and unrestricted/voluntary physical activity), which represents 20-40% of daily EE.
Why is it harder to lose weight the more you lose
§ REE is proportional to lean fat body mass (LBM) and so 100kg people may have 2800 REE while 80kg may have 2000 REE.
o This means its much harder to lose weight the more you lose – i.e. first 10kg easier than next 10kg.
What does BMR correlate with
BMR correlates with body weight. Reason is because the increase in weight is not just fat, usually about 25% is lean tissue - comprising heart, skeletal muscle, enlargement of digestive tract and liver.
Cases of obese patients with low BMR have yet to be found.
Energy expended on a fixed activity is always higher for people carrying extra weight, so total EE in obese persons is generally higher than lean.
Evidence that low levels of PA are a familial trait, which may predispose to obesity.
Describe a different view of the equation
Looking at the equation in a different way – the enegy expenditure sie of the eqn can be subdivided into obligatory EE – which is what all cells of the body need to maintain function – this forms between 50-70% of EE in humans.
Adapytive thermogenesis covers the energy converted into heat as a result of body temperature regulation – not particularly important in humans since we have methods to counteract these changes in temperature ie. Clothes and heating within buildings etc.
The majority of energy expenditure is in the form of REE/BMR and so exercise etc. will only affect a small portion of our energy expenditure (while REE represents like 65-70%).
Describe adaptive thermogenesis
variable, regulated by the brain
responds to temperature and diet
occurs in adipocyte mitochondria, skeletal muscle and other sites
Describe the use of BMI to measure energy stores
o Weight & height measurements – i.e. BMI (2530 = obese).
§ Note – measurements of BMI have different ranges depending on ethnicity (Asians lower bounds).
§ Also be aware the muscle weighs more than fat and so the values may be misleading.
List the range for BMI
18.5 Underweight
18.5-24.9 Healthy weight
25–29.9 Overweight
30-34.9 Obese (class1 obesity)
35-39.9 Severe obesity (class 2 obesity)
40-50 Morbid obesity (class 3 obesity)
50-60 Super obesity
>60 Super-morbid obesity
How do the values of BMI differ for Asian populations
<18.5 Underweight 18.5-22.9 Healthy weight 23-24.9 Pre-obese (overweight) 25-29.9 Obese > 30 Severe obesity
What was BMI derived from
Life insurance tables- how much they cost the health service
Describe another method for assessing energy stores
o Regional adiposity/energy partitioning.
§ Central adiposity is much more strongly associated to CVD.
§ “Waist: hip” ratio – Associated to the “Metabolic Syndrome”
§ Now in the UK, around 65% of the population is ‘overweight’ and so it is ‘normal’ to be overweight.
Describe the situation in 2004
In 2004, 10% 6- 10 year old boys and girls
5% of 11-15 year old boys, and 11% of 11-15 year old girls are obese.
Across the under 20 age group as a whole, 10% of females and 8% males are obese.
If we include those who are overweight and obese this is 35% for females and 28% for males.
These figures do not include any adjustment to allow for bias in non-respondents to the survey and may actually under-represent the proportion of obese teenagers.
Describe obesity as a disease of ageing
As we age, the proportion of people who are overweight and obese increases
What happens to people who gain weight at key measuring points
Hard to stop their path- they will become overweight or obese
What does genetic background predict
Risk to the environment- environment is a major factor for change
Describe the impact of obesity for the low-middle income countries
Devastating
problems with malnutrition and now also the complications of obesity (T2DM, hypertension)- more strain on the health system
Summarise the epidemiology of BMI in the UK
Highest in age group 55-64
Ethnic groups – highest in Caucasian and Bangladeshi1
Regional variation – Scotland and North England highest2
Smokers: lower BMI but greater central obesity3
Higher in social class 5 – men and women1
Describe the variation of BMI amongst smokers and different ethnic groups
Smokers – data on WHR that smoker, despite being leaner than non-smokers, have more central obesity than non-smokers.
The highest WHR among smokers was found to be dose dependent, being greatest in those smoking 20 or more cigs / day.
Ethnic Group –Varies depending on age. BMI not found to be higher in different ethnic groups, but we know that south asians are more likely to have abdominal obesity and a higher risk of developing type 2 DM.
Describe the genetic contribution to obesity
60% inheritable but explain only 5% of obesity
Describe the impact of obesity on non-communicable diseases
Obesity drives most of the non-communicable diseases (T2DM, cancer, hypertension)- affects every field of medicine
List the Orexigenic / anabolic molecules
expressed by genes in the CNS
Neuropeptide Y (NPY) Agouti gene related peptide (AGRP) Agouti-related transcript (ART) Melanin-concentrating hormone (MCH) Dopamine
List the Anorectic / catabolic molecules
expressed by genes in the CNS
Leptin receptor (LEPR) Pro-opiomelanocortin (POMC) Melanocortin receptor 4 (MCR4) Corticotropin releasing hormone (CRH) Serotonin receptor subtype 2C (5-HT2C) Glucagon-like peptide 1 receptor (GLP-1R)
Describe the Prentice and Jebb studies
Prentice and Jebb have graphically documented two indicators of inactivity (hours per week of TV viewing and cars per household) against the current secular trend in obesity in Britain. A strong relationship exists.
At the same time, similar data for total energy consumption and fat intake show downward trends (bad science- didn’t take into account food consumed between meals).
Points convincingly towards reduced energy expenditure, as a result of increased availability of labour saving devices, as a major contributor to obesity.
Numerous studies show that those who remain active or increase their physical activity level, or perhaps more importantly who reduce their sedentary pursuits like tv viewing
TV viewing is a surrogate for daily activity- linked to weight gain over time
What do our genes protect against
Malnutrition- appetite regulation
excess energy is new
survival was eating food in contact- and to use the energy efficiently
this works against us in an environment of excess energy as we store it
Describe the regulation of feeding
Average human eats 900,000 kcals per year.
A 0.02% error would result in an extra 3500 kcals per year
This would result in an extra 1lb weight gain per year
Describe the economic costs of obesity
Costs of treating obesity £49m Other direct costs of up to £1.2bn (2.6% of total NHS budget) Other indirect costs of up to £1.07bn Premature mortality accounts for £1.1bn Sickness absence accounts for 18m days/yr (= up to £1.45bn)
Total direct + indirect costs = up to £3.7bn
(= 42% increase in just 6 years)
The Foresight report (Oct07) - cost estimates suggest that by 2022 the costs of obesity may increase by up to £30bn per year
Describe the link of obesity to other medical conditions
Obesity is known to lead to both chronic and severe medical problems.
Biggest killer – coronary heart disease
Biggest impact on morbidity and quality of life – diabetes
Ostearthritis – weight bearing joints
Infertility: in women as PCOS and men are more likely to be impotent
Cancers: breast, endometrial
Describe IHD
This is the main cause of premature death among the obese.
Hypertension, coronary thrombosis and congestive heart failure are all significantly commoner among obese people than normal weight control
Obese women are over 3 times more likely to have an MI cf. Non-obese women.
And both men and women are twice as likely to experience angina.
Describe T2DM
Obese people are up to 80 times more likely to develop diabetes than those who are of a normal weight.
Describe the link between obesity and cancers
breast, endometrial, stomach, and colon.
Obesity is thought to increases risk of developing cancer primarily through its effect on hormones
Describe the link between obesity and gallstones
Formed when the bile contains too much cholesterol or bilirubin or not enough bile salts, or when the gall bladder does not empty properly.
Increasing weight – increased prevalence
Describe the link between obesity and osteoarthritis
Hips, knees and spine.
Overweight adults are more than twice as likely as their peers to devlelop osteoarthritis in their hips and knees.
Describe the link between obesity and mental health
Obese women – less likely to be hired
More likely to have their performance rated negatively
Less likely to be promoted
Depression
What else is obesity linked to
Sleep apnoea
Infertility
Gout
