Summary

This document outlines the aim of a lecture on obesity, defining obesity and explaining measurement methods. It covers prevalence in various populations, and discusses medical and financial costs.

Full Transcript

Obesity I Appetite: The psychology of eating and drinking 1 1 Introduction • The aim of this lecture is to: – Outline what obesity is – Outline how obesity is measured – Describe its prevalence (i.e., % in population) • In the US, Worldwide, Australia and NSW • With respect to ethnicity, age and...

Obesity I Appetite: The psychology of eating and drinking 1 1 Introduction • The aim of this lecture is to: – Outline what obesity is – Outline how obesity is measured – Describe its prevalence (i.e., % in population) • In the US, Worldwide, Australia and NSW • With respect to ethnicity, age and SES – Examine its medical and financial costs to individuals and society 2 2 What is obesity? • The body utilises fat cells for long-term energy storage • We have 2 types of fat cell • Brown fat cells (BAT) are used to generate heat and are located either side of the spinal column (shoulders) • BAT are rich in mitochondria (hence high energy use) and are not directly implicated in obesity • BAT cells contain 30-50% fat • BAT constitute 5% of the body mass of babies to generate heat • The distinction between the 2 types may not be absolute 3 3 White fat cells • White fat cells have several functions: – They insulate the body • A person with 2mm of subcutaneous fat will feel as comfortable at 15C as a person with 1mm will feel at 16C – They cushion the internal organs – They form the bodies long-term energy store • Each white fat cell is 85% fat • This is stored in a single large vacuole • It is not currently known whether obesity is the result of the progressive enlargement of a set number of white fat cells or enlargement plus the addition of new white fat cells – White fat cells serve an important endocrine function • • • • Leptin Resistin (producing insulin resistance in a variety of cell types) Fasting-inducing Adipose Factor (akin to Leptin in action) The full variety of this endocrine role is not as yet fully elucidated 4 4 White fat cells • Around 20% of an average weight woman and around 15% of an average weight man is composed of white fat cells • This represents roughly 1 months store of energy • White fat cells are distributed in different ways in men and women • Women more on hips/thighs and men more on the waist • Subcutaneously and around organs in both • When we ingest more energy than we use we are in positive energy balance • It is under these conditions that we start to turn this excess energy into fat which is stored in the white fat cells • It is this process which can ultimately result in obesity 5 5 Measurement of obesity • The aim of all forms of obesity measurement is to estimate the proportion of a person’s body which is made of fat (i.e., white fat cells) • The most frequently used measure is the Body Mass Index (BMI) or Quetelet’s index. • To calculate your BMI you divide your weight in Kilograms by the square of your height in Metres – For an average Australian man weighing 85 Kg and 1.79 M tall – Their BMI = 85/(1.79 x 1.79) = 85/3.2 = 26.6 • What does this mean? 6 6 BMI* for adults • • • • BMI’s below 18.5 are in the underweight range BMI’s of 18.5-24.9 are in the normal range BMI’s of 25.0-29.9 are in the overweight range BMI’s above 30 are in the obese range – Moderate obesity 30.0-34.9 – Severe obesity 35.0-39.9 – Very severe obesity 40.0+ (or Morbid obesity) • There is some argument about where cut-offs fall (*WHO classification scheme, 1998) 7 7 Pro’s and Con’s of BMI • For – – – – Easy to use Can be measured remotely Accurate Correlates with adiposity (r = 0.4 to 0.9) • Against – Takes no account of fat distribution (abdominal vs. other) – Takes no account of variation in muscle mass (e.g., many professional athletes have BMIs in 25-32 range) – Influenced by age – Influenced by trunk to leg length 8 8 Other measures • Skin fold thickness (Calipers) – Stomach and top of arm/leg – Does not provide measure of general adiposity – Difficulty of definition • Waste circumference – Around stomach (or waist to hip ratio) – Good for estimating a separate risk factor for heart disease and stroke • Excess risk occurs in men with waists 94cm+ and in women with waists 80cm+ – Does not provide measure of general adiposity – Difficulty of definition, especially in the obese • Bioelectrical impedance – Indirectly estimates % body fat by measuring the resistance to flow of electricity through the body – Very sensitive to hydration status of body – Only provides a rough overall measure of body fat • Other measures – Ultrasound, Chemical [metabolic rate], Computerised Tomography/MRI 9 9 Prevalence • There is a consensus that we are in the midst of an obesity epidemic – This is affecting men and women, (and boys and girls), to a similar extent, which is why most of the statistics to come are not divided by gender • For reasons that should now be clear, most large scale studies rely upon using BMI • We will look at data from large scale surveys in the US, Worldwide, Australia and NSW • We will start with the US 10 10 Prevalence data in the USA • The CDC (Centre for Disease Control) provides the worlds most comprehensive set of data on body weight • These data come from the Behavioral Risk Factor Surveillance System (BRFS) which is a telephone interview conducted with a representative sample of Americans in all states every year • Note that the CDC slides to follow just show obesity (BMI 30+) – The first set of slides cover 1990-2006, where you can see the epidemic unfolding before your very eyes (and the epidemic really starts in the early 1980s) – and so I’m going to scroll through these fairly quickly – This is followed by data from 2007 and from 2019, which we will look at in a little more detail (and noting the legend changes too) • Studies consistently show that telephone surveys systematically underestimate levels of obesity and overweight (by around 5%) so these are conservative estimates • This view is supported by the National Health and Nutrition Examination Survey (NHANES) which actually measures people and indicates broadly similar results 11 11 Obesity Trends* Among U.S. Adults BRFSS, 1990 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 12 <10% 10%–14% Obesity Trends* Among U.S. Adults BRFSS, 1991 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 13 Obesity Trends* Among U.S. Adults BRFSS, 1992 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 14 <10% 10%–14% 15%–19% Obesity Trends* Among U.S. Adults BRFSS, 1993 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 15 Obesity Trends* Among U.S. Adults BRFSS, 1994 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 16 <10% 10%–14% 15%–19% Obesity Trends* Among U.S. Adults BRFSS, 1995 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 17 Obesity Trends* Among U.S. Adults BRFSS, 1996 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 18 <10% 10%–14% 15%–19% Obesity Trends* Among U.S. Adults BRFSS, 1997 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% ≥20% 19 Obesity Trends* Among U.S. Adults BRFSS, 1998 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 20 <10% 10%–14% 15%–19% ≥20% Obesity Trends* Among U.S. Adults BRFSS, 1999 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% ≥20% 21 Obesity Trends* Among U.S. Adults BRFSS, 2000 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 22 <10% 10%–14% 15%–19% ≥20% Obesity Trends* Among U.S. Adults BRFSS, 2001 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% ≥25% 23 Obesity Trends* Among U.S. Adults BRFSS, 2002 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 24 <10% 10%–14% 15%–19% 20%–24% ≥25% Obesity Trends* Among U.S. Adults BRFSS, 2003 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% ≥25% 25 Obesity Trends* Among U.S. Adults BRFSS, 2004 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 26 <10% 10%–14% 15%–19% 20%–24% ≥25% Obesity Trends* Among U.S. Adults BRFSS, 2005 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30% 27 Obesity Trends* Among U.S. Adults BRFSS, 2006 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data 28 <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30% BRFSS L: 2007 R: 2019 29 29 SES, Age, Ethnicity & Obesity in the US 30 30 Child and adolescent obesity in the US 31 31 Overweight and obesity in the OECD Note that this graph includes both overweight (BMI 25-30) and obese people (BMI 30+) 32 32 Obesity around the world 33 33 Obesity in Australia Note that the reported % overweight includes the obese Latest figures: 67% overweight, 31% obese 34 34 Childhood obesity and overweight in Australia 2016 35 35 Adult overweight & obesity – NSW 36 36 Health Care Costs • In Australia estimates suggest that direct health costs from obesity are 10.7 Billion Aus$ per year • Normal weight direct health costs per year per person = $1472 • Obese direct health costs per year per person = $2788 – In addition, indirect government costs exceed 10 Billion Aus$ for obesity • In the US direct health care costs for the obese have risen from 52 Billion US$ in 1995 to 178 Billion US$ in 2012 (current estimate, 210 Billion US$) – Amongst children/adolescents in the US, obesity-related direct health care costs tripled between 1980 and 1998 – Amongst US adults, for cardiovascular disease alone, 17% of all direct medical costs were related to overweight and obesity 37 37 Medical consequences • Diabetes – Type I diabetes (IDDM - Insulin dependent diabetes) is not weight related, occurs due to loss of islet cells in the pancreas and thus no insulin (>10% of diabetics) – Type II diabetes (NIDDM – Non-insulin dependent diabetes) is directly related to body weight • Type II diabetes is now very common – In the US in 1958 there were 1.5M diabetics – In the US in 2015 there were 20M (with probably another 7.5M undiagnosed) – Much more common in African Americans, with 1 in 4 women over 55 in this group with the disease • Around 1.5M Australians have diagnosed type II diabetes – Much more common in Indigenous Australians & Pacific Islanders 38 38 Type II diabetes - Physiology • The body still secretes insulin, more in fact than in a nonobese individual • Fat (especially around the stomach) appears primarily responsible, although the precise mechanism is not understood • The consequence is insulin resistance • Insulin resistance is characterised by a failure of muscle, fat and liver cells to respond appropriately to insulin • This results in hyperglycemia (i.e., elevated blood sugar levels) 39 39 Type II diabetes - health • Health effects (see earlier lecture as well) – Poorly managed Type II diabetes results in: • Microvascular disease - Increased blood sugar results in less permeable small blood vessels and capillaries, leading to an inadequate supply of oxygen and nutrients to surrounding tissue » Neuropathy (nerve death) » Tissue death leading to ulceration, with infection resulting in amputation of fingers, toes, arms and legs » Blindness (death of retinal tissue) » Renal failure (damage to kidney tissue) • Macrovascular disease – From atherosclerosis » Heightened blood cholesterol (stroke/heart attack) » Accounts for up to 40% of all US heart disease » Heightened blood pressure (stroke/heart attack) » Which can also lead to renal failure 40 40 Type II diabetes • Conclusion – Type II diabetes is caused by excess weight gain and is thus a direct consequence of obesity – The risk of getting Type II diabetes starts to rise linearly with a BMI over 22 – Type II diabetes is a chronic disease and is managed via: • Diet (low GI foods, high fibre foods) and exercise – Modest loss of weight brings marked improvement • Drugs (some cause obesity, others such as Metaformin are effective in combination with lifestyle changes) • Insulin treatment (when the disease can no longer be managed by drugs or lifestyle modifications) 41 41 Heart disease, hypertension, stroke • Independent of diabetes, obesity raises blood pressure and increases plasma levels of ‘bad’ cholesterol resulting in atherosclerosis – Atherosclerosis of the coronary artery leads to blockage, so blood can no longer reach the heart muscle – This causes death of heart tissue from lack of oxygen/nutrients – This leads to “jump-back” of the electrical signal that causes the heart to beat, as the signal cannot propagate through dead tissue – The result is a heart attack – the heart stops beating • Independent of other risk factors, an obese person (BMI=30) has a 3 fold increased chance of a fatal heart attack relative to someone with a BMI < 25 – These effects are compounded by abnormal blood clotting in the obese, which increases the chance of a thrombosis 42 42 Cancer • Obese people are 23% more likely to die from cancer than individuals of normal weight (8% more likely for overweight people) • Of common cancers… – 9% of bowel cancers and 17% of breast cancers can be attributed to obesity • For rarer cancers… – 49% of endometrial cancers, 35% of oesophageal and 35% of kidney cancers can be attributed to obesity • Cancer detection and treatment is more difficult in obese individuals leading to higher mortality 43 43 Other medical conditions • Osteoarthritis – Degenerative diseases of weight bearing joints • Reproductive disorders – Increased risk for pregnancy and of neural tube defects in the foetus – Impotence in men • Sleep apnoea – Fat mass on the neck/face when sleeping can temporarily stop breathing, leading to elevated risk of heart failure – Fat mass on the stomach when sleeping can temporarily stop breathing, leading to elevated risk of heart failure • All of these conditions/risks improve markedly with (even modest) weight loss 44 44 Psychosocial effects • The psychosocial effects of obesity fall most heavily upon children and young adults – Obese children are viewed by their peers as being more lazy, dirty, stupid, ugly and dishonest – Obesity in adolescence (longitudinal studies) reveal poorer educational and social outcomes than in other chronic conditions (e.g., asthma) – Anxiety and depression are far more common in obese than in lean adults and are at levels comparable to those found in chronic pain and cancer sufferers, and quadriplegics • As adults, obese people... – Are less likely to marry; Earn less money; Have fewer educational and career opportunities; and May receive lower quality medical care 45 45 Summary • The proportion of people who are overweight and obese has been increasing for the last 50 years, especially in developed nations • This increase is occurring in all age groups and most worryingly in children and adolescents • This increase is accompanied by significant medical complications, many of which impose major social and financial costs upon society as a whole • Given this barrage of statistics, we might almost forget that we are talking about people - so what is it like to have to live with being obese? 46 46

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