Obesity lecture Flashcards
what is obesity?
1) Obesity is a chronic, life-threatening disease
2) An excessive accumulation of body fat sufficient to impair health
3) Independent risk factor - for at least 30 common health conditions
According to WHO, what are the BMI boundaries for the following and state the risk of co-morbidity for each:
1) normal
2) overweight
3) obese
4) severe obese
5) morbidly obese:
1) normal: 18.5-24.9
2) overweight: 25.29.9 - mild increase
3) obese : 30-34.9- moderate
4) severe obese: 35-39.9- severe
5) morbidly obese: over 40 - very severe
what is the formula used to calculate BMI?
BMI = Weight (kg)/Height (m)2
The measurement of waist circumference provides information about the distribution of body fat and is a measure of risk for conditions such as coronary heart disease (CHD). what size waist in men and women put them at increased risk of co-morbidity’s ?
1) men : increased risk over 94cm, Substantially
increased risk at over 102cm
2) women: increased risk at 88cm and substantially over 88cm
list some of the implications of obesity
1) heart disease
2) cancer
3) stroke
4) asthma
5) sleep apnoea
6) Type 2 diabetes
7) liver disease
8) reproductive problems
outline what causes obesity
1) Individual’s lifestyle choice
2) Abundant cheap palatable food, aggressively advertised and available 24/7, little need for physical activity at home or work
3) It is determined by genetic factors
Define: energy balance and outline the terms positive and negative energy balance
1) energy balance: State in which energy intake, in the form of food and /or drinks, matches the energy expended
2) Positive energy balance: Energy in > energy out
- Results in weight gain
3) Negative energy balance: Energy in < energy out
- Results in weight loss
list the components of daily energy expenditure and explain how they are different in a sedentary Person and an active person
1) Thermic effect of feeding: this is the same in a Sedentary Person as well as a active person
- energy expenditure above the resting metabolic rate, due to the cost of processing food for use in storage
2) Energy expenditure of physical activity: this is more in a physically active person
3) Resting energy expenditure- the amount of energy you use just existing: this makes up most of the sedentary Person daily energy expenditure.
- amount of energy, required for a 24-hours by the body during resting conditions.
list the factors that influence resting energy expenditure (REE)
1) Body composition
2) Gender
3) Age
4) Height, weight
5) Hormones e.g. thyroid hormone
6) Body temperature
7) Pregnancy
8) Fasting/malnutrition
what is yo-yo dieting?
1) Weight loss -> Loss of muscle mass -> reduced BMR -> Reduced requirements
- the problem is: when you loose weight you also loose muscle mass, muscle normally burns energy. so your reducing your BMR which reduces your requirements for energy
- best way to loose weight therefore is to gain more muscle so you loose more weight while resting
what is BMR?
Basal metabolic rate (BMR) is the amount of energy expended while at rest in a neutrally temperate environment, in the post-absorptive state (meaning that the digestive system is inactive, which requires about twelve hours of fasting).
what is The Barker Hypothesis ?
Adverse environments in foetal life and early childhood establish increased risk of disease in adult life
Describe how adverse environments in foetal life can lead to metabolic syndrome.
1) suboptimal maternal nutrition, placental abnormalities, other maternal factors (stress, infection, drugs)
2) all of the above lead to changes in fetal gene expression
3) leads to altered fetal growth metabolism
4) reduced birth weight: this now leads to conflicting postnatal environment- if the baby is born underweight the mother might over feed the child to rectify this and this leads to the child being overweight
5) metabolic syndrome
outline the The Barker Hypothesis
1) Under-nutrition in gestation induces programming of the pancreatic beta cells, muscle, liver, adipose tissues and neuroendocrine axis
2) Mismatch of poor prenatal environment and rich postnatal environment leads to maladaptation
3) increases risk of obesity, glucose intolerance and coronary heart disease in adult life
list the Evidence supporting the Genetic Influence of obesity.
1) Familial aggregation: Familial clustering of obesity in families
2) Twin studies: Greater concordance among monozygote compared with dizygote twins
- evidence where twins have been raised separately
how many genes may influence adiposity? and what factors do these genes influence?
1) >300 genes may influence adiposity
2) Genetic factors influence: body size and shape, body fat distribution, metabolic rate, brain chemistry
- Thrifty metabolism gene allows for inc fat storage to protect against famine
- Heritability of obesity estimated at ~ 40-60%
explain the cycle of feast and famine
1) Those that were better at fuel storage or utilization more likely to survive during famine
2) Over generations, we developed genetically to be exceptionally efficient at the intake and utilization of fuel
outline the likelihood of a child being obese in the following circumstances:
1) No obese parents
2) One obese parent
3) Two obese parents
1) no obese parents; Child =10% chance of obesity
2) one obese parent: Child = 40% chance of obesity
3) two obese parents: Child = 80% chance of obesity
explain why the rapid rise in obesity in last 30 years cannot be explained by genetics
1) There is no single gene except in rare circumstances
2) there are a lot of genes responsible and other factors going on.
3)
what were the outcomes of the Food4Me Study?
personalised nutrition increased dietary behaviour. so generic dietary advice should be avoided .there was no impact from understanding the phenotype and genotype as this did not lead to better outcomes for the individuals
what is Energy homeostasis? and what are the two types of feedback signals?
1) Energy homeostasis is a balance between energy input, as food intake, and energy expenditure.
2) short term and long term
outline the short term feedback signal of energy homoeostasis
1) Operates on a meal-to-meal basis
2) Determines the amount of food ingested in a single meal
3) Satiety factors include nervous signals initiated in the GI tract
outline the long term feedback signal of energy homoeostasis
1) Work over periods of weeks to years to regulate our energy intake & expenditure
2) Modulated by adipose tissue mass; major mediators are leptin and insulin
what is the control centre for apatite regulation?
1) The hypothalamus: receives and integrates neural, metabolic and humoral signals from the periphery
Describe how appetite is regulated
1) Ghrelin (hunger hormone), peptides found in the GI tract ( PYY, CCK, GLP-1, Oxm, PP)
- these feed into the neuropeptide transmitter which then feeds into the receptorsm (Y1 & Y5) to stimulate feeding. then then leads to increased food intake and decreased expenditure.
2) peptides which reduce feeding behaviour: insulin, leptin
- this feeds into the POMC/CART which feeds into the MC3 & MC4 receptor to suppress feeding and increase expenditure
with regards to leptin answer the following questions:
1) where is it secreted from?
2) what is its role?
3) where does it act ?
4) role in weight gain and weight loss?
1) Secreted by adipocytes in proportion to the amount of stored fat
- Diurnal variation: peak at night
2) Primary way brain knows how much body fat is stored
- Regulates long term body weight rather than short term appetite
3) Acts in the CNS to suppress food intake
4) during weight gain the fat cells swell in size because of the increased leptin. this leads to decreased food intake and increased energy expenditure
- during weight loss leptin decreases to increase food intake and decrease energy expenditure
list the role of the following Gut Hormones in Regulating Appetite:
1) Secretin
2) GIP
3) Motilin
4) Cholecystokinin
5) ghrelin
6) gastrin
7) insulin and glucagon
8) pancreatic polypeptide
9) amylin
10) GLP 1,2
11) oxyntomodulin
12) PYY336
1) Secretin: pancreatic exocrine secretion
2) GIP: incretin activity
3) Motilin: GI mortality
4) Cholecystokinin: gall bladder constriction, GI mortality, pancreatic exocrine secretion
5) ghrelin: hunger, growth hormone release
6) gastrin: acid secretion
7) insulin and glucagon: glucose homeostasis
8) pancreatic polypeptide: gastric mortality, feeling full
9) amylin: glucose homoeostasis, GI mortality
10) GLP 1: incretin activity, feeling full
11) GLP 2: GI mortality and growth
11) oxyntomodulin: feeling full, acid secretion
12) PYY336: feeling full
Ghrelin
1) where is it secreted from?
2) when do levels of ghrelin rise and fall?
3) what is the role of Ghrelin?
4) which syndrome has a characteristic high level of ghrelin?
5) what mediates its activity?
1) Peptide hormone secreted by gastric mucosa
2) Levels rise just before meals and fall after
3) to Increases food intake
- Ghrelin administration in rats strongly stimulates feeding
4) High Ghrelin levels in Prader-Willi syndrome
5) Orexigenic (appetite stimulating) effects of ghrelin mediated through hypothalamus
- stimulates NPY neurons
list some cognitive influences Overriding Hunger and Satiety
presence of others, favourite foods, time of day, free or abundant food, moods (bored/anxious), stress
what is the purpose of Regulation of energy balance?
Regulation of energy balance primarily acts to protect us against starvation so with the changes to our environment over recent years, we are becoming increasingly obese as a nation
what is the influence of genetic based variations on a obesogenic environment?
Genetically-based variations determine our susceptibility or resistance to an obesogenic environment and the ease with which people are able to lose weight
What hormones does adipose tissue produce?
1) Aromatase
2) TNF alpha, IL-6 and leptin, (cytokines)
3) Plasminogen activator inhibitor-1
4) Angiotensin
5) Adiponectin
6) insulin
7) Lipoprotein lipase and apolipoprotein E,
Below is a list of hormones produced by adipose tissue, state the role each hormones has in the body.
1) Aromatase
2) TNF alpha, IL-6 and leptin, (cytokines)
3) Plasminogen activator inhibitor-1
4) Angiotensin
5) Adiponectin
6) Lipoprotein lipase and apolipoprotein E,
1) Aromatase, which is involved in sex hormone metabolism.
2) TNF alpha, IL-6 and leptin, which are collectively termed ‘cytokines’ and are involved in sending messages between cells.
3) Plasminogen activator inhibitor-1, which is involved in the clotting of blood.
4) Angiotensin, which is involved in blood pressure control.
5) Adiponectin, which improves the body’s sensitivity to insulin and so helps to protect against developing type 2 diabetes
6) Lipoprotein lipase and apolipoprotein E, which are involved in storage and metabolism of fat to release energy.
as a result of obesity a person is at a greatly increased risk when they have certain health conditions. list some of the health conditions which have a greatly increased risk of problems as a result of obesity.
Greatly increased (relative risk»_space;5)
1) diabetes
2) gall bladder disease
3) hypertension
4) dyslipidaemia
5) sleep apnoea
6) breathlessness
7) non-alcoholic fatty liver disease
as a result of obesity a person is at a moderately increased risk when they have certain health conditions. list some of the health conditions which have a moderately increased risk of problems as a result of obesity.
Moderately increased (relative risk 2-3)
1) Coronary heart disease
2) Osteoarthritis (knees)
3) Hyperuricaemia and gout
4) GORD
what is Obstructive Sleep Apnoea?
Intermittent cessation of breathing during sleep due to the collapse of the pharyngeal airway, resulting in multiple apnoeic or hypopnoeic events
outline the impact of obesity on asthma
1) 2-3x increased risk of asthma in obese population – mechanism unknown
2) Related to increased inflammation
3) Adverse effect on lung function
- Role of gastro-oesophageal reflux disease
There are some cancers related to obesity. Describe the mechanisms by which adipose tissue may influence cancer risk
- Adipose tissue is an active endocrine organ
- Mechanisms by which adipose tissue may influence cancer risk:
1) Production of sex steroid hormones (e.g., oestrogen, androgens)
2) Effects on insulin sensitivity and production of insulin-like growth factors
3) Actions on other hormones in adipose tissue (e.g., leptin, adiponectin)
4) Increases in oxidative stress and chronic low-grade inflammation that affect the body’s immune response
describe the Health benefits of a modest (10%) weight loss
1) Mortality 20-25% fall in overall mortality, 30-40% fall in diabetes related deaths, 40-50% fall in obesity-related cancer deaths
2) Diabetes: Up to 50% fall in fasting blood glucose
Reduces risk of developing diabetes by over 50%
3) lipids: Fall of 10% total cholesterol, 15% LDL and 30% TG; Increase of 8% HDL
4) Blood pressure: 10 mmHg fall in diastolic and systolic pressures
outline the Treatment options for obesity
1) Lifestyle modification - Behaviour change
2) Medical management:
- Orlistat
- Incretin mimetics (GLP-1 Agonists) e.g. exenatide
3) Surgical management:
- Gastric band
- Gastric bypass
- Sleeve gastrectomy
list some of the behavioural changes that can be recommended to an overweight individual
1) Diet
2) Exercise
3) Medical model: The assumption that abnormal behaviour is the result of physical problems and should be treated medically
4) Behavioural model: lifestyle
outline the Pharmacological management of obesity
1) appetite suppresents
- Phentermine: May help but results in dry mouth,
nausea and constipation.
2) Reduce fat absorption
- Orlistat/Alli: Eating fat causes anal leakage
- Can cause substantial weight loss
Describe the Surgical management of obesity
1) vertical sleeve gastrectomy : stomach made smaller, leads to less absorption
2) adjustable gastric band- restricting the size of the stomach, feel full
3) gastric bypass- restrictive, stomach and first half of intestine made smaller
can the adverse effects associated with obesity be reversed?
The majority of the adverse effects associated with obesity can be reversed or attenuated by weight loss which should be an integral part of the treatment of these morbidities
