Monash University Overweight and Obesity Part 1 PDF

NUTRITION, DIETETICS & FOOD OVERWEIGHT AND OBESITY: PART 1 1. Defining and measuring overweight and obesity 2. Obesity and chronic...

NUTRITION, DIETETICS & FOOD OVERWEIGHT AND OBESITY: PART 1 1. Defining and measuring overweight and obesity 2. Obesity and chronic disease risk 3. Biological, environmental and psychological factors contributing to BMI Dr Alan McCubbin Semester Two, 2024 OVERWEIGHT AND OBESITY | 1 COPYRIGHT COMMONWEALTH OF AUSTRALIA - Copyright Regulations 1969. This material has been reproduced and communicated to you by or on behalf of Monash University pursuant to Part VB of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Cover image: Shutterstock All other figures as cited. OVERWEIGHT AND OBESITY – PART 1 | 2 On the surface, overweight and obesity looks pretty straightforward. People have a higher BMI due to excess body fat, caused by eating too much and not moving enough. A lifestyle choice. But when you start looking in more depth, you realise that things are far more complicated than that. Yes, body fat relates to energy balance, which relates to energy intake and expenditure. But energy intake and expenditure are not merely “lifestyle choices” – they are complex phenomenon with biological, psychological, and sociological drivers. This section around overweight and obesity attempts to unpack that complexity, examine the drivers of increasing BMI in the population, and whether obesity is a symptom, a disease, a risk factor, or a combination of these. DEFINITION AND MEASUREMENT OF OVERWEIGHT AND OBESITY The World Health Organisation defines obesity as “abnormal or excessive fat accumulation that presents a risk to health.1” The key here is “presents a risk to health” – this is potentially quite different to how you might normally think about obesity as a number, shape or general appearance. The WHO does categorise overweight and obesity based on Body Mass Index (BMI) values regardless of the presence or absence of other health conditions, but the cut-offs for each category were designed to reflect different levels of chronic disease risk. 𝑊𝑒𝑖𝑔ℎ𝑡 (𝑘𝑔) 𝐵𝑜𝑑𝑦 𝑀𝑎𝑠𝑠 𝐼𝑛𝑑𝑒𝑥 (𝑘𝑔/𝑚2 ) = 𝐻𝑒𝑖𝑔ℎ𝑡 (𝑚)2 Category BMI Range Underweight < 18.5-24.9 kg/m2 Normal or Healthy Weight 18.5-24.9 kg/m2 Overweight 25-30 kg/m2 Obese Class I 30-35 kg/m2 Obese Class II 35-40 kg/m2 Obese Class III >40 kg/m2 OVERWEIGHT AND OBESITY – PART 1 | 3 Some publications have suggested different category cut-offs for Asian populations, given research has suggested that disease risk increases in Asian populations at a lower BMI compared to other population groups. This was reviewed by WHO in 2004 2: “ …the proportion of Asian people with a high risk of type 2 diabetes and cardiovascular disease is substantial at BMIs lower than the existing WHO cut-off point for overweight (≥ 25 kg/m2). – WHO Expert Consultation, 2004. ” Ultimately however, the working group decided that clearly different cut-offs could not be established based on disease risk, and the decision was made not to create separate cut- off values, although many other research groups and organisations disagree and have implemented different values: “ …available data do not necessarily indicate a clear BMI cut-off point for all Asians for overweight or obesity... The consultation (therefore) agreed that the WHO BMI cut-off points should be retained as (per) international classifications. – WHO Expert Consultation, 2004. ” Defining childhood obesity BMI cut-offs work well for adults, but not children, because the changes in muscle mass from birth to adulthood move the BMI point where excess body fat becomes a potential health concern. You should already be familiar with growth charts for children and adolescents. The BMI chart can be used for defining childhood overweight and obesity based on BMI percentiles: Category BMI Percentile Range Underweight < 5th percentile Normal or Healthy Weight 5th - 85th percentile Overweight 85th - 95th percentile Obese > 95th OVERWEIGHT AND OBESITY – PART 1 | 4 Is BMI actually a good method to define overweight and obesity? BMI is often highly criticised, especially on social media and in the gym and fitness industry, as not being a good indicator of body fatness and health risk. These criticisms often cite extremely lean, muscular male physiques that would meet the WHO definition for “overweight” based on BMI. Overall though this scenario of abnormally high muscle mass is not common across the entire population. The NHMRC Clinical practice guidelines for the management of overweight and obesity suggest that BMI is a useful tool for evaluating populations or groups of people, more so than individuals 3: “ Health researchers have found BMI to be a good indicator for the health and lifespan of adults – not necessarily for an individual, but for a group of people who have the same BMI. – NHMRC Clinical Practice Guidelines for the Management of Overweight and Obesity in Adults, Adolescents, and Children in Australia, 2013. ” Obesity prevalence and changes over time The proportion of the population who meet the BMI-defined criteria for overweight and obesity is increasing over time. Australian data does not go back this far, but US data shows a noticeable rise in obesity prevalence beginning around the late-1970s, a trend that continues to this day. Figure Source: Centres for Disease Control & Prevention; 2018 [updated 2018 Sep 5]. Available from: https://www.cdc.gov/nchs/data/hestat/obesity_adult_15_16/obesity_adult_15_16.htm OVERWEIGHT AND OBESITY – PART 1 | 5 In Australia, prevalence of overweight has actually declined slightly since 1990. However, this decline has occurred because these people have now become classified as obese, not because they moved back into the healthy weight range: Prevalence of overweight and obese persons aged 18 and over, 1995 to 2022 (%) 45 40 35 30 25 20 15 10 5 0 1995 2007-08 2011-12 2014-15 2017-18 2022 Overweight Obese Severely Obese Figure redrawn from: AIHW. Overweight and Obesity [Internet]. Canberra, ACT: AIHW; 2024 [updated 2024 Jun 17; cited 2024 Jul 9]. Available from: https://www.aihw.gov.au/reports/overweight- obesity/overweight-and-obesity/contents/overweight-and-obesity Other methods of measuring and quantifying obesity or body fatness There are a range of other, more precise methods of measuring body fat available. We won’t revisit the body composition assessment methods in detail here, but the key point is that a measurement of % body fat, or body fat in kg as a component of body composition, is not helpful without clear criteria about what level of % body fat poses a health risk, since the point of defining obesity relates to its role as a risk factor for illness. What is more relevant is measuring body fat distribution, as this has clear links with chronic disease risk. As a general rule, greater body fat distribution around the abdominal region increases the likelihood of increased visceral adipose tissue, which is most strongly associated with disease risk. This can be assessed practically through the use of waist circumference, waist:height ratio, or regional body fat measures from DXA assessment. OVERWEIGHT AND OBESITY – PART 1 | 6 The following cut-offs are suggested for waist circumference in relation to increased disease risk: Men Women Caucasian Asian * Women Asian * Not at risk < 94 cm < 90 cm < 80 cm < 80 cm Increased risk 94 – 102 cm Not given 80 - 88 cm Not given Greatly increased risk ≥102 cm Not given ≥ 88 cm Not given * South Asian, Chinese & Japanese people. Table source: NHMRC. Clinical practice guidelines for the management of overweight and obesity in adults, adolescents, and children in Australia. 2013. Another method proposed is the waist:height ratio (WHtR) 4: 𝑊𝑎𝑖𝑠𝑡 𝐶𝑖𝑟𝑐𝑢𝑚𝑓𝑒𝑟𝑒𝑛𝑐𝑒 (𝑐𝑚) 𝑊𝐻𝑡𝑅 = 𝐻𝑒𝑖𝑔ℎ𝑡 (𝑐𝑚) with the following suggested cut-offs for increased chronic disease risk Men Women Diabetes risk > 0.52 > 0.53 Cardiovascular disease > 0.53 > 0.50 Hypertension > 0.50 > 0.50 Hyperlipidaemia > 0.49 > 0.49 Metabolic syndrome > 0.50 > 0.49 Overall suggested target < 0.50 < 0.50 Table source: Browning et al. A systematic review of waist-to-height ratio as a screening tool for the prediction of cardiovascular disease and diabetes: 0.5 could be a suitable global boundary value. Nutr Res Rev. 2010; 23(2):247-69. OVERWEIGHT AND OBESITY – PART 1 | 7 Modern DXA scanners and software can provide regional assessments of body fat. Among these regions are the android and gynoid regions: From this, the android:gynoid ratio can be calculated. A higher ratio (i.e., more android fat relative to gynoid fat) is associated with increased chronic disease risk, including Type 2 Diabetes 5. OVERWEIGHT, OBESITY, AND CHRONIC DISEASE RISK We’ve already had a look at a few cut-offs for body composition that imply increase disease risk. The next section will provide evidence for this link. Overweight, obesity and disease burden We discussed disease burden in a previous session – it’s the loss of quantity and/or quality of life that results from (in this case) one or more chronic diseases. The Australian Institute of Health and Welfare in 2019 published a comprehensive review of the burden of disease in Australia, including the proportion (%) of total disease burden that could be attributed to individual risk factors, including tobacco smoking, illicit drug use, alcohol, OVERWEIGHT AND OBESITY – PART 1 | 8 physical inactivity, domestic violence, unsafe sex, dietary risks (not BMI), environmental exposures (sun, pollution, occupational hazards), high blood pressure, blood glucose, cholesterol, impaired kidney function, iron deficiency and low bone density. Overweight and obesity accounted for 8.4% of the disease burden (out of the 37.5% that could be explained by all risk factors combined). Only tobacco smoking (9.3%) accounted for a greater proportion of the attributable disease burden. This review further segmented the disease burden data to calculate the % of attributable burden for individual types of chronic diseases. Overweight and obesity produced the following values 6: Total % attributable % of attributable burden burden (all risk factors) Cancer 7.8 43.5 Cardiovascular disease 19.3 65.2 Musculoskeletal 10.9 17.7 Mental Illness - 33.4 Injuries - 42.5 Respiratory 8.0 51.4 Neurological 9.0 23.6 Gastrointestinal 1.4 19.1 Endocrine disorders (including diabetes) 44.6 98.0 Infections - 13.7 Kidney diseases 35.6 89.2 OVERWEIGHT AND OBESITY – PART 1 | 9 What’s the mechanism? If we appreciate that overweight and obesity are large contributors to the burden of major chronic diseases (especially cardiovascular disease and Type 2 diabetes), the obvious question then is, how? We understand from the allostatic load model that various stressors (including those caused by obesity) can lead to cellular dysfunction, and eventually organ system dysfunction (i.e., disease). But we can potentially go further into explaining these mechanisms on a disease-specific level. The exact mechanisms that link obesity to the pathophysiology of Type 2 diabetes are still not entirely understood, but there are several inter-related mechanisms proposed 7: Greater adipose tissue/adipocytes, especially visceral adipocytes, contribute to: o An excessive release of pro-inflammatory cytokines TNF-α and IL-6, which can interfere with normal insulin signalling processes (requiring greater insulin production) and the function of β-cells in the pancreas, which are responsible for producing insulin. o Greater circulating levels of the hormone leptin, supresses the release of another hormone, adiponectin, from the adipocytes. Adiponectin has an anti-inflammatory role (helping to offset those pro-inflammatory cytokines), a direct role in facilitating insulin action (insulin sensitivity), and a role in optimising the function of mitochondria. Increased fat deposition within muscle, pancreas, liver and other tissues (ectopic fat), as well as overall excess substrate availability (including carbohydrate) are also associated with mitochondrial dysfunction, although the exact mechanisms aren’t clear. Mitochondrial dysfunction results in increased production of reactive oxygen species (ROS), and impaired substrate metabolism, which leads to insulin resistance in the cell. The insulin resistance increases the demand for insulin production in the pancreas, but the ectopic fat in the pancreas impairs the function of the β-cells which are responsible for producing insulin. This mismatch eventually leads to an increased blood glucose concentration, the criteria for diagnosis of diabetes. As you can see, it’s complex, and there’s a lot we still don’t know. For the purpose of this unit, simply understand that: excess adipose tissue and fat deposits in organ tissues this, as well as an overall excess of adipose tissue and energy substrates available to cells, creates oxidative stress and inflammation, and these lead to a series of things to go wrong in the adipocytes and organ tissues (e.g. muscle, liver and pancreas) that result in insulin resistance and an impairment in the ability to produce insulin to meet demand. OVERWEIGHT AND OBESITY – PART 1 | 10 As for cardiovascular disease, the underlying processes of oxidative stress and inflammation are similar to Type 2 diabetes. The oxidative stress can also increase the risk of damage to the endothelial lining of arteries, and together with effects on the liver that increase LDL-cholesterol production, can lead to the processes of atherosclerosis 8. Atherosclerosis is the main process resulting in ischaemic heart disease, stroke, and peripheral vascular disease, and will be discussed in more detail in that section of the unit. Figure: Potential mechanisms explaining the link between obesity (especially abdominal obesity) and the increased risk of cardiovascular disease and type 2 diabetes. OVERWEIGHT AND OBESITY – PART 1 | 11 Collectively, these biological processes lead to the combination of factors known as metabolic syndrome: “ …the central features of the metabolic syndrome are insulin resistance, visceral adiposity, atherogenic dyslipidemia and endothelial dysfunction. These conditions are interrelated and share common mediators, pathways and pathophysiological mechanisms. ” – Huang PL. A comprehensive definition for metabolic syndrome. Dis Model Mech. 2009; 2(5-6): 231–237. There are different criteria used to define Metabolic Syndrome. Most are based on a combination of factors that can be measured clinically, including BMI, waist circumference, insulin resistance, fasting glucose, fasting triglycerides, and elevated blood pressure. Regardless of the exact criteria used, the point is that a combination of things are occurring as a result of obesity and other forms of allostatic stress, and these are all major risk factors for Type 2 diabetes and various forms of cardiovascular disease. Obesity and cancer risk With so many different types of cancers, the mechanisms for why obesity increases their risk is tricky. Overall, a few potential mechanisms have been described that may be relevant to multiple cancer types: Chronic, low-grade inflammation, as already described (allostatic stress), may also increase the risk of DNA damage and telomere shortening. This has been linked with an increased risk of oesophageal, gallbladder, liver, and some other cancers. Adipocytes produce estrogen, so excess adipose tissue can increase the risk of developing estrogen-sensitive cancers like breast, endometrial, ovarian, and some other cancers. High circulating insulin and Insulin-like Growth Factor 1 (IGF-1) (due to insulin resistance) may increase the risk of colorectal, kidney, prostate, and endometrial cancers. Adipokines (cytokines specifically released from adipocytes) may stimulate or inhibit cell growth and regulation, increasing general cancer cell growth. Excess adipose tissue may also influence growth factors like mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) that enhance the rate of cancerous cell growth. OVERWEIGHT AND OBESITY – PART 1 | 12 The figure below shows which cancers obesity has been identified as a risk factor for: OVERWEIGHT AND OBESITY – PART 1 | 13 Can you have a high BMI and still be healthy? Given that the definition of obesity relates to increased health risk, is it possible to have a high BMI but no chronic disease risk? This question was investigated in one of the longest running epidemiological datasets ever created: the US National Health and Nutrition Examination Survey (NHANES). Currently, about 5,000 Americans that are representative of the overall US population are examined every year, using a combination of surveys, blood samples and physical examination. The NHANES dataset is frequently used by other researchers due to its standardised collection, large sample size, comprehensive list of measured variables, and long timeframe (the study started in the early 1960s). Researchers examined a cross-sectional sub-set of the NHANES data collected between 1999-2004 to investigate the prevalence of metabolic abnormalities (elevated blood pressure, triglyceride or glucose levels, insulin resistance, systemic inflammation, and decreased HDL-Cholesterol). Participants were grouped based on BMI category (normal weight, overweight and obese). As seen in the figure, the prevalence of metabolic abnormalities significantly increased with each BMI category. Despite this, one third of obese participants did not have any of the metabolic abnormalities studied. Whether this is because they have not yet developed these factors, or simply got lucky, is hard to know. But it does suggest that having a BMI >30 kg/m2 does not guarantee a poor health outcome, but definitely increases the likelihood. Figure source: Wildman RP. et al. The obese without cardiometabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering: prevalence and correlates of 2 phenotypes among the US population (NHANES 1999-2004). Arch Intern Med. 2008. 168(15):1617-1624. https://doi.org/10.1001/archinte.168.15.1617 OVERWEIGHT AND OBESITY – PART 1 | 14 Obesity and mental health Whilst the focus of obesity and health risk has focussed on metabolic chronic diseases, there is another potentially large impact of overweight and obesity – on mental health. We will discuss the evidence for the links between diet quality and mental health later in the unit, but this refers to the social stigma and discrimination faced by people with a higher BMI. This includes bullying and teasing that can lead to school refusal in children and social isolation in adults, as well as body image disturbance. So powerful are the impacts of social stigma and discrimination with overweight and obesity, that obese people often achieve less educational and economic attainment through their life compared to healthy weight peers. As future health professionals, it is your responsibility to understand the social stigma and discrimination faced by overweight and obese people, and ensure such biases (often unconscious or unintended) don’t influence your work. For more information on this, watch the videos available on Moodle. The following section should also help put this into context. SUMMARY ▪ Overweight and obesity are defined based on BMI cut-offs that are designed to indicate levels of disease risk. ▪ Being obese significantly increases the risk of several chronic diseases, although not everyone who meets the BMI criteria for obesity will experience these health issues. Treat the individual and their health risk, not the number. ▪ The mechanisms that link increase adiposity (especially abdominal adiposity) to disease outcomes is still not fully understand, but aligns with the concepts in the overall allostatic load model, with increased energy intake and adipose tissue both potential forms of allostatic stress. ▪ Being in a positive energy balance that results in obesity is immensely complex. ▪ We still don’t fully understand the relative contributions of biological, environmental, societal, and psychological factors, but clearly it’s not a simple answer. ▪ Complex causes are going to require complex solutions, or sledgehammers (to be continued…) OVERWEIGHT AND OBESITY – PART 1 | 15 READING AND RESOURCES References: 1. World Health Organization. Obesity [Internet]. Geneva, Switzerland: WHO; 2019 [not dated; cited 2024 Jul 26]. Available from: https://www.who.int/topics/obesity/en/ 2. WHO Expert Consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. Lancet. 2004; 363(9403):157- 63. DOI: https://doi.org/10.1016/s0140-6736(03)15268-3 3. NHMRC. Clinical practice guidelines for the management of overweight and obesity in adults, adolescents, and children in Australia. 2013. Melbourne: NHMRC. https://www.nhmrc.gov.au/about-us/publications/clinical-practice-guidelines- management-overweight-and-obesity 4. Browning et al. A systematic review of waist-to-height ratio as a screening tool for the prediction of cardiovascular disease and diabetes: 0.5 could be a suitable global boundary value. Nutr Res Rev. 2010; 23(2):247-69. DOI: https://doi.org/10.1017/s0954422410000144 5. Aucouturier J et al. Effect of android to gynoid fat ratio on insulin resistance in obese youth. Arch Pediatr Adolesc Med. 2009; 163:1826–31. DOI: https://doi.org/10.1001/archpediatrics.2009.148 6. AIHW (2019). Australian Burden of Disease Study: impact and causes of illness and death in Australia 2015. Australian Burden of Disease series no. 19. Cat. no. BOD 22. Canberra: AIHW 7. Kahn S. et al. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature. 2006; 444(7121):840-6. DOI: https://doi.org/10.1038/nature05482 8. Van Gaal L. et al. Mechanisms linking obesity with cardiovascular disease. Nature. 2016; 444(7121):875-880. DOI: https://doi.org/10.1038/nature05487 OVERWEIGHT AND OBESITY – PART 1 | 16