Obesity Lecture PDF

Obesity II Appetite: The psychology of eating and drinking 1 1 Introduction In this second lecture on obesity we will examine – The causes of obesity Environmental (external caus...

Obesity II Appetite: The psychology of eating and drinking 1 1 Introduction In this second lecture on obesity we will examine – The causes of obesity Environmental (external causes of over-eating and reduced- activity) Genetic predispositions (internal causes of the above) In addition we will look at the contention that the obesity epidemic and its health consequences are over-hyped by scientists and drug companies Finally, we will explore some other correlates of the rise in obesity which might offer some rather unexpected explanations of its cause (e.g., smoking, delayed pregnancy, psychoactive drugs) 2 2  The causes of the obesity epidemic The basic cause of obesity is simple and well understood Energy intake simply outstrips energy expenditure There are two key factors in the last four decades that have contributed to this – (1) The development of an obesogenic environment – (2) A preexisting genetic disposition to become obese Notice how disposition to become obese does not become important until one is placed in an obesogenic environment (i.e., no inmate got fat in Auschwitz) the genetic component 3 3 The obesogenic environment The obesogenic environment has developed over the last forty years It is evident in most industrialised nations (and now in developing nations as well) but especially in North America, Europe and Australia It is intimately connected to all aspects of our daily lives It is characterised by a reduction in physical activity and an increase in the availability and consumption of processed foods Processed foods are highly palatable, 4 they're high in either salt and or sugar 4  Physical activity In the last 40 years people in Western nations have reduced physical activity through increasing car usage and TV viewing The advent of digital media has added to the number of sedentary leisure activities, increasing peoples total screen time exposure (and hence the amount of time they are inactive) 5 5 Physical activity Occupation – Most occupations have become less physically demanding – This is a consequence of increasing mechanisation and a shift in the type of work we do, namely away from manufacturing/agriculture to service industries In the 1950’s around 55% of the labour force in the US were involved in jobs which had a physical component Today, only 32% of the labour force are in such jobs – One consequence of this is that we expend less energy at work, on average, than in the past (see figure) 6 6 Think of the impact that urban design has on obesity Travel to work In the US, less than 10% of trips outside the home are made on foot or bicycle Obesity rates tend to be higher in areas which are primarily reliant upon the car Think of the impact that urban design has on obesity – Size of gardens, ‘cul-de-sac’ effect, walking vs. car distance Poor neighbourhoods also have fewer parks and people are often more reluctant to use them because of fear of crime Whilst in the past we may have walked to work, people now use their car, often by necessity This again reduces energy expenditure 7 7 Leisure activity The main leisure activity of Westerners is TV In 1960 the average person watched 13hrs/wk, now it is 26hrs/wk (and this does not include other devices) The amount of time spent watching TV is moderately correlated with obesity More TV = less physical activity = greater obesity This relationship is particularly pronounced in children and is also associated with snacking In addition, children are also the target for TV advertising for high fat/sweet foods Young children are unable to discern the difference between an advert and ‘factual’ TV 8 8  Physical activity - cause or correlation? The evidence we have reviewed suggests an association (at the population level) between obesity and activity Is there any stronger (causal) evidence? – Longitudinal studies come closest to addressing this In Finland a 5yr follow-up study of 12,000 people found that physical activity at baseline was the best predictor of weight gain at follow-up (i.e., no exercise put you at greater risk) Similar findings have been obtained in the US Nurses study (prospective longitudinal study of 68,000 nurses) and with longer follow-up periods (10yrs) Overall, the consilience of evidence points to one conclusion - less physical activity contributes to higher rates of obesity 9 9 School In the US during the 1980’s (and later in other Western nations) there was a strong drive to cut costs in public education – This led to the loss of school exercise programs – The sale of school playing fields – The introduction of fast-food into school canteens (outsourcing of catering) – Fast-food advertising in schools (revenue) – Exclusive contracts to provide soft-drinks (vending machines etc) in schools – Similar story in the UK (with school lunches such as turkey twizzlers [right], chips & coke) 10 10  Demographic shifts Many families (irrespective of their composition) have all their adult member/s working – A consequence of this is a greater reliance upon processed food (restaurants, fast-food, TV dinners, etc) Processed food is typically higher in fat, sugar and salt, and the consumer has little or no control over the ingredients in that food 11 11 Processed foods Most processed foods are highly palatable – So you are likely to eat more of them than blander foods and consume them in preference to healthier alternatives – They contain larger quantities of fat, sugar and salt Often this fat is in the form of ‘trans-fats’that are advantageous due to long shelf life but have adverse effects on blood cholesterol Fat has more calories than sugar and protein, so eating an extra gram of fat is far more deleterious for weight control than an extra gram of sugar or protein Eating foods that contain lots of added sugar may have several negative effects on the body (it may: spike blood sugar, up-regulate fat production, cause inflammation, and shorten inter-meal intervals) Excess salt intake appears to contribute to hypertension – Soft drinks consumption is independently associated with obesity and it results in incomplete caloric compensation Soft drink consumption is a risk factor for Type II diabetes and osteoporosis 12 12  Variety Rats given a large variety of palatable foods become obese (cafeteria diets) Humans are in a similar situation – Palatable foods are available at any time in most places – Supermarkets stock an incredible variety of different foods – New products constantly come on-line In the US… – 1978: 400 new snack food products / year – 1978: 380 new bakery products / year – 1993: 2250 new snack food products / year – 1993: 1500 new bakery products / year – 2010: 5550 new snack food products / year 13 13 Portion size Portion sizes have increased If people are given larger portions they eat more Similarly, for a given portion size, if packaging size is increased, consumption also increases Mean portion sizes in the US are (outlet for outlet) 25% larger than in Europe As also are plate sizes, recipe book portions and even guide books focus more on portion size in the US 14 14  Supersizing Supersizing is a common marketing ploy where by a small extra cost is accompanied by an extra-large size portion This ploy is very profitable This an extract from a 2017 Royal Society of Public Health report about super-sizing in the UK Most people in the UK (78% surveyed) say they are asked in restaurants, fast food outlets and stores at least once a week if they want to “go large”, opting for more food or bigger portions. Those who succumb to upselling get an extra 55% more calories on average by paying just a fraction more: scaling up the meal or the coffee or buying a cut-price chocolate bar raises the average cost by 17%. Young people aged 18-24 are the most likely to experience upselling, consuming an extra 750 calories a week that could potentially lead them to put on 5 kg of extra weight per year. Restaurant staff speaking anonymously describe how they are trained and incentivised to upsell. One cafe worker says that if they are asked for a latte, “I will reply with ‘Large?’” The confidence of insinuating that a large is what a typical customer orders often nudges the customer into ordering the bigger and slightly more expensive drink. If somebody asks for a cake, the response is: “Is that with cream or ice cream today?”. 15 15 Is it really the environment? The evidence is very strong that it is – Notably obesity has been increasing in the last 40 years which is clearly too short a time for genetic changes to occur Pima Indians – In the US they have very high rates of obesity (mean BMI=33.4; 80-85% obese) and diabetes – Genetically similar Pima Indians living in rural Mexico have both lower rates of obesity (mean BMI=24.9) and diabetes – The primary difference between these two genetically similar populations is diet and exercise Migration studies – US residents of African, Caribbean & Latin American descent all have significantly higher BMI’s, than their relatives in their country of origin – In all of these studies, where genetically similar groups are compared in their new or native country, what differs is diet and exercise 16 16  The environment – and genes All of the environmental factors reviewed above interact to generate what has been termed an obesogenic environment However, some people still manage to remain thin in this environment while others gain weight Thus, some individuals appear more susceptible to the obesogenic environment than others - that is they may have a genetic predisposition to weight gain 17 17 Genetic susceptibility to weight gain Body weight is affected by many factors which are likely to be influenced by our genetic make up It should not be surprising then to find that genetic influences on bodyweight are ‘polygenic’ Twin, adoption and family studies all show that an individual’s risk of obesity (all measures) is increased when that person’s relative/s are obese – Having one obese parent increases a child’s risk of being obese by 40%, two obese parents by 80% – Identical twins raised apart (vs raised together) suggest that around 70% of the variance in body weight is controlled by genetic factors – Adoption studies indicate that a child resembles their biological parents in weight, not their adopted parents and this holds especially so for the biological mother 18 It's been suggested that individuals who later become obese are born with more fat cells than those who 18 don't become obese down the line.  Genetic predisposition Genetic influences that predispose to obesity operate on: Energy balance - Thermogenesis, Liver metabolism (of fat) Feeding behaviour – Fat preferences, Leptin resistance, Craving Skeletal muscle growth - Rate of growth Satiety regulation - Serotonin levels, POMC levels Fat cell numbers/differentiation – Obese individuals may be born with more (BMI < 30 have around 20-25 billion fat cells; BMI 30+ have around 100-125 billion) In other words many if not all of the pathways that we know to be involved in regulating body weight 19 19 Is there really anything to worry about? Several books (e.g. Fat Politics) and influential media articles (see front cover of Time - Right) have suggested that the consequences of the obesity epidemic are over-inflated and the causes wrong This is argued to occur because scientists want grant money for their research on appetite and drug companies want to sell (what would be) highly profitable slimming pills (But do not forget to examine the motivations of these critics!) Is their any merit to these claims? 20 20  It's an established fact that is widely agreed upon Critics claim… Nobody challenges the idea that we are seeing a massive increase in overweight and obesity What is being challenged are its consequences and its causes The main criticisms are – Excess mortality does not occur until you get in the obese range – Projected death rates from obesity are overstated (i.e. this generations kids will likely lead shorter lives than their parents) – The focus on food and environmental factors (notably lack of exercise) as the cause for obesity is too simplistic These conclusions are based upon correlational evidence There are inconsistencies in these data What we will do is briefly examine these claims Meaning that you can't establish causality 21 21 we know that it's actually lower, it's a BMI of 22 Excess mortality Reanalysis of several databases, which include details of mortality and BMI, do suggest that it is only when you hit a BMI of 30+ that your chances of premature death go up However, increasing BMI (25+) is still associated with increased risk of chronic diseases such as diabetes and heart disease …but if you have a heart attack being overweight seems to enhance survival and indeed being overweight may be beneficial for longevity as long as you are physically fit Even if you develop a chronic disease doctors have become better at managing them so people live longer …nonetheless what this criticism ignores is The reduction in quality of life caused by chronic illness The social and financial burden of managing chronic illness That obesity arises from people progressively gaining weight over time – being overweight is arguably one step along the road to obesity It's not something that happens overnight, people 22 gradually transition from overweight to obese. 22  Kids leading shorter lives This claim was originally based upon projections of obesity As we may become better yet at keeping people alive with the complications that flow from obesity this may be a valid criticism However, no previous generation of doctors have ever encountered obesity and Type II diabetes in children at the rate they are observed today The best thing we can say is that nobody knows what the long term outlook will be for these kids So really nobody knows what happens when you 23 develop type two diabetes when you're 13 or 14 years of age. 23 Are people under-reporting how much they've been eating? What causes obesity? Critics argue that the usual culprits, too much food and not enough exercise, do not adequately explain why we are getting fatter – Paradoxically, some studies even suggest that at an aggregate level people in the West have progressively decreased caloric intake especially over the last 30 years – although this is arguable for many reasons – Similarly, several studies have failed to demonstrate benefits for exercise in children - and these studies spent big money trying to do so – although again one could make various arguments as to why they did not work Do not think that inactivity and overeating are not important - they are - but perhaps their importance has been overstated Could other factors contribute? We will spend the final part of this lecture looking at some alternative ideas 24 24  Other correlates Obesity of the rise in obesity Home temp Chemical pollutants Age @ 1st kid Air con Quit smoking Hours awake 25 25 The less people slept the more likely they were to gain weight Less sleep Obese individuals sleep less which may well be a consequence of obesity, however, several recent findings suggest that lack of sleep may precede obesity… – The US nurses study found There was a linear relationship between amount of time spent asleep and weight gain over the 16 years of the study – Sleep duration and weight gain are linked in kids – Sleep deprived people and animals eat more – Sleep deprivation alters metabolism by reducing plasma leptin levels and increasing ghrelin – In 1960 people slept an average of 8.5hrs/night, a recent US survey suggests this figure is now 7hrs 26 26 When you're hot/cold your body has to work to keep hot or cold, which is why thermoneutrality is problematic. Climate control People in cold and warm countries are now more likely to live in temperatures around ‘thermoneutrality’ (27C) – Both being hot (and thus keeping cool) and being cold (and thus keeping warm) require energy – One study found that being in a room at 22C required 237Kcal more energy (per day) than being in a room at 27C – Whilst no one knows for sure if this too contributes to the obesity epidemic climate control changes mirror the rise in obesity 27 27 Quitting smoking Ex-smokers tend to gain weight During the last 30 years the proportion of non- smokers (in the US) has gone from 64% to 77% Epidemiological studies suggest that this change accounts for around 20% of the increase in obesity in the US It is still better to give up - as you would have to gain 45Kg in weight to equal the risk of dieing from continuing to smoke 28 28 Underweight babies have a higher risk for being obese later in life Pregnancy Maternal metabolic abnormalities during pregnancy increase risk for obesity later in life – During famine (or where the baby is underweight) – Excessive fat intake – Gestational diabetes – Maternal obesity (fertile) Overweight mothers are more fecund – This arguably increases the number of children carrying a genetic propensity for overweight and obesity Mothers are getting older – Having an older mother is an independent risk factor for overweight and obesity 29 29 (of a drug) tending to reduce nervous tension by depressing nerve functions. It's part of the Antipsychotics drug class. Chemicals Certain neuroleptics, anticonvulsants, antihypertensives, HIV medications and diabetes drugs, can all result in weight gain – The use of all these type of drugs has increased (or started) over the period of time that obesity has increased In addition to chemicals we ingest as ‘drugs’ we are also exposed to many chemical pollutants – Although these are at low doses, they accumulate in certain tissues and many appear to exert biological effects even at low doses – Animal studies suggest that some of these chemicals (such as the fire retardant PBDE) result in increased body weight – Other pollutants (PCBs) disrupt endocrine function – Our exposure to such pollutants again mirrors the rise in obesity 30 30  Conclusion The cause of increasing body weight over the last 40 years is a complex phenomenon Clearly eating too much and reduced energy expenditure are major factors (the obesogenic environment), especially when combined with a genetic susceptibility However, it is likely that many other factors contribute too, and we are only just beginning to identify what they may be 31 31