An inappropriate lifestyle has proved to be the downfall of many elderly individuals. One such notable victim was Thomas Parr, born in 1483; later in life known as the ‘olde, olde, very olde man of Shropshire’. He first married and became a father at the age of 80 years, had a child out of wedlock at 105 and was still working in the fields at 130 years old.1 His secret was said to be a diet of “subrancid cheese and milk in every form, coarse and hard bread and small drink, generally sour whey.”2,3 At the age of 152, Parr became a celebrity and was invited to London as a guest of King Charles 1, and was regally wined and dined, but never reached 153. The cause of death, according to the great surgeon, William Harvey, who performed his autopsy, was the rich diet and polluted air of London probably contributing to his demise.3
Epidemiology of obesity
Levels of obesity in the population increase with age until around 70 years, after which prevalence declines due to a number of factors including concurrent illness, such as chronic obstructive pulmonary disease (COPD) and malignant disease causing weight loss; failure to thrive of the elderly; and the fact that obese individuals tend to die prematurely. However, with improving healthcare and public health, life expectancy is increasing and it can be anticipated that the peak age for obesity will increase as will both the clinical and economic burden for an extra decade.
The weight of men peaks earlier than women, possibly due to lower life expectancy, and deterioration in health at an earlier age.4 In contrast, when Body Mass Index (BMI) is plotted and the prevalence of obesity is diagnosed by waist circumference, a different picture is revealed that shows increases are unabated with age, probably demonstrating the vagaries of the different measuring techniques. The higher rate of obesity as defined by waist circumference probably represents those individuals displaying sarcopenia, with loss of muscle mass, in favour of an expanded visceral adipocyte mass. To further complicate the picture, height reduction in the elderly due to changes in bone and disc composition affects the interpretation of measurements. If a subject decreases in stature due to loss in vertebral bone, there is a corresponding increase in BMI.5
HSE data also reveal increasing levels of obesity in immigrant and deprived populations, demonstrating the health inequalities of obesity, and raising the possibility that, as both subsections of the population are increasing, the obesity epidemic will worsen imminently.
The Foresight Report, published in 2007 by the Department of Trade and Industry suggests that by 2050, 60% of men and 50% of women could be clinically obese, and that without action, obesity-related diseases will cost an extra £45.5 billion per year to the economy.6 A recent report by McKinsey7 revealed that obesity has a similar Global Economic Impact as armed violence, war and terrorism combined. In response, over recent months, major figures in Government, Public Health England and the NHS have started to become serious about obesity and its ramifications.
Clinical aspects of obesity
Rather than being merely a cosmetic or social issue, the seriousness of an expanded adipocyte mass lies in the profound deleterious effect it has on all the systems of the body. This is by its mechanical presence, hormonal and psychological ramifications, but mainly in its metabolic influence centred on the production of pro-inflammatory cytokines, reduced adiponectin, and the induction of insulin resistance. Excess body weight in the elderly correlates strongly with chronic ill health, poor quality of life, functional decline, disability, and dependency.8
The most widely accepted comorbidity of obesity is type 2 diabetes and approximately 20% of the population develop diabetes by the age of 75.9 Over the age of 65 years, diabetes or glucose intolerance was present in 30–40% of Framingham Study subjects.10 The fact that half of subjects are unaware that they have the condition11 emphasises the importance of screening for diabetes in the elderly obese population.
The improvement of identification and management of diabetes, especially over the last decade, paradoxically, is being offset by enhanced life expectancy, and therefore increased likelihood of long-term microvascular, microvascular and other complications. These include the more traditionally recognised conditions such as cardiovascular disease, retinopathy, nephropathy and neuropathy, as well as less readily associated ones such as cardiac autonomic neuropathy,12 Charcot neuroarthropathy,13 periodontal disease14 and falls.15 Elevated BMI is not only associated with a diagnosis of diabetes, but is also linked with progressively higher risk for all diabetes complications, especially in women.
One study showed that for women, being slightly overweight led to higher risk of cardiovascular, cerebrovascular, renal, and lower extremity complications. For men, slightly overweight status was not significant for developing diabetes complications. For women in the upper range of overweight, the risk also increased for cardiovascular, renal, ocular, and lower extremity complications. Men too achieved greater risk compared to men with normal BMI.16
Rates of cardiovascular disease are increased in association with central obesity,17 independent of diabetes, partially due to the pro-inflammatory environment, including endothelial dysfunction and blood hypercoagulability, promoted by adipocytokines produced by visceral adipocytes such as TNFα and PAI-1.18
Obstructive sleep apnoea is also associated with obesity and much more prevalent in the elderly.19 However, there are comorbidities which, although not unique to the elderly, have specific ramifications for this group. Chronic venous insufficiency,20 for example, is linked with obesity; in one study 45.2% of leg ulcer sufferers were obese, whilst only 27.2% had non-insulin dependent diabetes.21 Varicose veins are also more common in obese subjects.22
Framingham demonstrated links between obesity and osteoarthritis, stating ‘cross-sectional data show that obesity or as yet unknown factors associated with obesity cause knee osteoarthritis.’23 There also seems to be a connection between obesity and inflammatory arthritis.24
Findings from NHANES25 suggest that obesity is associated with depression mainly among persons with severe obesity. Functional aspects of obesity include breathless on daily activities and climbing the stairs, and inability to manage simple personal hygiene tasks, and cutting toenails.
Sarcopenia refers to reduced muscle mass in the elderly, caused by, or causing limited mobility and linked with diverse medical conditions as well as falls.26 Irwin Rosenberg proposed the term in 1989, from the Greek ‘sarx’—flesh and ‘penia’—loss, to describe this age-related decrease of muscle mass.27
For the diagnosis of sarcopenia, the European Working Group on Sarcopenia in Older People (EWGSOP)28 recommends using the presence of both low muscle mass and low muscle function (strength or performance). Sarcopenia with limited mobility is defined as a person with muscle loss whose walking speed is equal to or less than 1m/s or who walks less than 400m during a six-minute walk. Also who has a lean appendicular mass corrected for height squared of 2 standard deviations or more below the mean of healthy persons between 20 and 30 years of age of the same ethnic group. The limitation in mobility should not clearly be a result of otherwise defined specific diseases of muscle, peripheral vascular disease with intermittent claudication, central and peripheral nervous system disorders, or cachexia. Clinically significant interventions are defined as an increase in the six-minute walk of at least 50 meters or an increase of walking speed of at least 0.1 m/s.29 When obesity and sarcopenia coincide, the result is sarcopenic obesity;30 at any given BMI, an elderly individual will have a higher percentage of body fat at the expense of muscle, than a younger person. Increased physical activity in the elderly can produce beneficial effects on muscle strength, endurance, and well-being31 and is therefore a vital component of weight management in this age group. The expression ‘dynapenic obesity’ describes the combined effect of obesity and low muscle strength, which has the effect of increasing the risk of incident type 2 diabetes in older adults.32
A 10% weight loss is associated with clinically significant reductions in hypertension, lipids mortality,33 sleep apnoea34 and other comorbid conditions. The Look-AHEAD study35 intended to answer the ultimate question: does weight loss by lifestyle changes reduce cardiovascular mortality? The study looked at 5,000 patients with type 2 diabetes for 13.5 years following intensive initial treatment, then less intensive subsequent input. Four-year data revealed impressive weight loss, and improvement in surrogate markers, in particular, a 23% reduction in insulin users from baseline. Remarkably, despite these outstanding results, Look-AHEAD was halted for reasons of ‘futility’ due to a lower than expected event rate.
In 2012, a 13-year follow up paper to the landmark Diabetes Prevention Study was published. The original paper famously demonstrated a 58% reduction in cumulative incidence of diabetes in subjects with impaired glucose tolerance, with intensive lifestyle intervention. The follow-up study demonstrated a ‘legacy’ effect—those people who initially underwent intensive lifestyle treatment benefited from a long-term 32% reduction in the cumulative incidence of diabetes, despite lapses in diet and physical activity after the premature culmination of the trial.36
The obesity paradox
Clearly, obesity is associated with comorbidities including diabetes, cardiovascular disease, obstructive sleep apnoea, cancer, and many others in the elderly population. Equally clearly, weight loss confers protection against their onset and may improve these conditions. It is counter-intuitive, therefore, that, although obesity is implicated in their cause, its presence seems to be protective against adverse outcomes once they have occurred. “The idea that a known risk factor somehow transforms into a ‘protective’ agent after an occurrence of a vascular clinical event is both surreal and troubling”.37 This phenomenon is known as the ‘Obesity Paradox’; an example of so-called ‘reverse epidemiology’.38
There is an increasing body of data contradicting traditional weight loss assumptions in elderly individuals, suggesting that although excess weight clearly contributes to various comorbid conditions, once those conditions have occurred, excess weight may improve subsequent outcomes.39 Evidence from studies including 30,000 chronic heart failure patients suggests that overweight and obese patients with heart failure had reductions in CV (–19% and –40%, respectively) and all-cause (–16% and –33%, respectively) mortality during 2.7-year follow-up.40 A similar pattern occurs in acutely decompensated heart failure; higher BMI is associated with lower in-hospital mortality.
A meta-analysis of 250,000 patients with coronary artery disease, cardiovascular and total mortality outcomes were better in overweight and ‘mildly’ obese patients compared with ‘normal’ weight.41 The INVEST study of 22,500 individuals with hypertension plus coronary artery disease, showed a lower risk of death or major cardiovascular events in overweight and obese subjects compared with normal weight.42 The Scottish Coronary Revascularisation Register concurred:43 among patients undergoing PCI for CAD, raised BMI was associated with enhanced 5-year survival.
Another study showed that overweight and obesity are associated with improved short- and long-term survival after acute myocardial infarction, resulting in moderate gains in life expectancy relative to normal-weight patients.44 These findings suggest that higher BMI confers a protective advantage over the entire remaining lifespan in older patients with acute myocardial infarction. Other publications have shown that higher percentage body fat predicts better prognoses in HF patients, and possibly CHD mortality.45 Meta-analysis has also shown that a BMI of 33.4-60—too high for there to be any doubt of excess adiposity—there is significantly higher LV ejection fraction, with significant BNP decreases in the highest BMI quartile.46
Recent studies specifically on body fat assessed by dexa-scan show that with established CV diseases, including advanced HF, higher levels of BMI and Body Fat appear to be protective,47 except in extreme obesity (BMI) >40),48 however there is emerging contradictory evidence that benefits might only be short-lived.49 Subjects with peripheral vascular disease benefit in a similar fashion; mortality decreases with increasing BMI, possibly explained by the presence of COPD inducing weight loss.50 An unexpected survival benefit has been reported in sleep apnoea associated with obesity.51
Obese and overweight CVA subjects have significantly better survival than their counterparts;52 obesity is associated with a lower stroke and mortality rate in elderly anticoagulated atrial fibrillation patients.53 Obesity is also linked with lower mortality in pre-capillary and disproportional post-capillary pulmonary hypertension patients.54 In addition, it is a risk factor for end stage renal failure, but its presence may improve outcomes.55
Studies of dementia, including Alzheimer’s disease, demonstrate a similar pattern: obesity in middle age is related to greater dementia risk in later life,56 but when later life materialises, the risks are reversed.57 Less controversially, low BMI is associated with an increased fracture risk, whereas a high BMI is protective in all ages, and with all, but mainly hip fracture.58 Early research suggests that higher BMI may have a protective effect against mortality in vascular patients with lower limb ulcers.59 To add to the uncertainty, a recent JAMA paper suggests that individuals diagnosed with type 2 diabetes with relatively low BMIs fared less well in terms of mortality than overweight and obese people.
However, the obvious reaction that obesity might be somehow protective against diabetes, needs scrutiny, being entirely counter-intuitive. Possible explanations include the use of BMI rather than direct measures of adiposity being misrepresentative, or that patients carrying excess weight are identified younger, enabling enhanced prevention by cholesterol and blood pressure optimisation; low to normal weight may be caused by intercurrent disease, failure to thrive of the elderly, excess alcohol intake or smoking, and weight loss may be unintentional. Furthermore, BMI may be high because of athletic build and muscularity—protective against CVD—in contrast to increased adiposity, known to be harmful.
Excess adiposity may act as a protective ‘metabolic reserve’; some individuals may only suffer from a condition because of their obesity, and therefore suffer a less malign form of the illness than someone who receives the diagnosis despite being lean. For example, type 2 diabetes is unusual in lean individuals, so might represent a more sinister manifestation of the disease. People may have been diagnosed later in the course of the illness because of their leanness, or may have lost weight because of previously undiagnosed diabetes. However, the number of studies supporting the obesity paradox is growing and possible confounders identified and accounted for, but evidence is still strong.
The Edmonton Obesity Staging System60 is now widely accepted, defining severity of obesity not by size, but by score on four scales: physical disease, mental health, social and functional abilities. Thus a person can be ‘morbidly obese’ by traditional parlance, but if fully fit and functional they are EOSS stage zero. Another individual may have BMI of 31, but suffer diabetes with retinopathy, unable to work or drive and therefore be depressed and EOSS stage 4.
The system ensures that everyone is treated on their own merits. Overall, in the elderly mortality increases with decreasing BMI as discussed earlier, therefore patients should be carefully chosen for their suitability for weight loss, and fully assessed and comorbid disease managed as a priority, before weight loss is implemented if deemed appropriate.
In a recent follow-up of the landmark Tromsø61 and HUNT62 studies, BMI <25 in elderly individuals is linked to increased mortality, although a modest increase in mortality is found with increasing BMI; overweight individuals had lowest mortality.
Bariatric surgery is now routinely carried out in patients aged 55, often in those aged over 60 years, and less commonly, but increasingly in those aged over 70 years in very closely scrutinised circumstances. Ultimately, palliative care for obesity has been mooted; a person might be so obese, and unwell, that losing weight would be impossible and futile, so that priorities should be maintaining quality of life in comfortable, cared-for, safe environments.
Conflict of interest; none declared
1. The old, old, very old man. Or The age and long life of Thomas Par. John Taylor. Pub Gosson, London 1635
2. Keynes G. The Life of William Harvey. (Oxford 1966) 220–25
3. Doughty BP. Old Parr: or how old is old? South Med J 1988; 81(7): 906–8
4. Haslam DW, James WPT. Obesity. Lancet 2005; 366:
5. Dympna Gallagher, D, Visser M, Sepulveda D, et al. How Useful Is Body Mass Index for Comparison of Body Fatness across Age, Sex, and Ethnic Groups? Heymsfield Am. J Epidemiol 1996; 143(3): 228–39
6. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/287943/07-1469x-tackling-obesities-future-choices-summary.pdf (accessed 14/04/16)
7. http://www.mckinsey.com/industries/healthcare-systems-and-services/our-insights/how-the-world-could-better-fight-obesity (accessed 14/04/16)
8. Kyrou I, Tsigos C. Obesity in the Elderly Diabetic Patient. Is weight loss beneficial? Diabetes Care 2009; 32(Suppl 2): S403–S409
9. Harris MI, Flegal KM, Cowie CC, et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in US. adults. Diabetes Care 1998; 21(4): 518–7
10. Wilson P, Kannel W. Obesity, Diabetes, and Risk of Cardiovascular Disease in the Elderly. The American Journal of Geriatric Cardiology 2002; 11(2): 119–24
11. Meneilly G, Tessier D. Diabetes in Elderly Adults. J Gerontol A Biol Sci Med Sci 2001; 56 (1): M5-M13
12. Maser R, Lenhard M. Cardiovascular Autonomic Neuropathy Due to Diabetes Mellitus: Clinical Manifestations, Consequences, and Treatment. JCEM DOI: http://dx.doi.org/10.1210/jc.2005-0754
13. Vinik A, Strotmeyer E, Nakave A, et al. Diabetic Neuropathy in Older Adults. Clin Geriatr Med 2008; 24(3): 407
14. Negrato C, Ariza O, et al. Periodontal disease and diabetes mellitus. J Appl Oral Sci 2013; 21(1): 1–12.
15. Schwartz A, Hillier T, Sellmeyer D, et al. Diabetes Care 2002; 25(10): 1749–54.
16. Gray N, Picone G, Sloan F, et al. The Relationship between BMI and Onset of Diabetes Mellitus and its Complications. South Med J 2015; 108(1): 29–36
17. Sahakyan KR, Somers VK, Rodriguez-Escudero JP, et al. Normal-Weight Central Obesity: Implications for Total and Cardiovascular Mortality. Ann Intern Med 2015; 163(11): 827–35
18. Pieterse C, Schutte R, Schutte AE. Leptin links with plasminogen activator inhibitor-1 in human obesity: the SABPA study. Hypertens Res 2015; 38(7): 507–12
19. Lavie P, Lavie L Unexpected survival advantage in elderly people with moderate sleep apnoea. Journal of Sleep Research 2009; 18(4): 397–403
20. Seidel AC, Belczak CE,Campos MB, et al. The impact of obesity on venous insufficiency. Phlebology 2015; 30: 475–80
21. Jockenhöfer F, Gollnick H, Herberger K, et al. Aetiology, comorbidities and cofactors of chronic leg ulcers: retrospective evaluation of 1 000 patients from 10 specialised dermatological wound care centers in Germany. Int Wound J 2014
22. Onida S, Lane TR, Davies AH. Improving the management of varicose veins. Practitioner 2013; 257(1766): 21-4
23. Felson D, Anderson J, Naimark A, et al. Obesity and Knee Osteoarthritis: The Framingham Study. Ann Intern Med 1988; 109(1): 18–24
24. George MD, Baker JF. The Obesity Epidemic and Consequences for Rheumatoid Arthritis Care. Curr Rheumatol Rep 2016; 18(1): 6
25. Onyike C, Crum R, Lee H, et al. Is Obesity Associated with Major Depression? Results from the Third National Health and Nutrition Examination Survey. Eaton Am J Epidemiol 2003; 58(12): 1139–47
26. Karakelides H, Nair KS. Sarcopenia of aging and its metabolic impact. Curr Top Dev Biol 2005; 68: 123–148
27. Rosenberg I. Summary comments: epidemiological and methodological problems in determining nutritional status of older persons. Am J Clin Nutr 1989;50: 1231–3
28. Cruz-Jentoft A, Baeyens JP, Bauer J, et al. Sarcopenia: European consensus on definition and diagnosis.Report of the European Working Group on Sarcopenia in Older People. Age Ageing 2010; 39(4): 412–23
29. Morley J, et al. The Society on Sarcopenia, Cachexia and Wasting Disorders Trialist Workshop. Sarcopenia With Limited Mobility: An International Consensus. JAMA 2011; 12, (6): 403–409
30. Roubenoff R .Sarcopenic obesity: the confluence of two epidemics. Obes Res 2004; 12: 887–88
31. Elia M. Obesity in the elderly. Obes Res 2001; 9(4): 244S–8S
32. Cuthbertson DJ, Bell JA, Ng SY, et al. Dynapenic obesity and the risk of incident Type 2 diabetes: the English Longitudinal Study of Ageing. Diabet Med 2015
33. Poobalan A, et al Effects of weight loss in overweight /obese individuals and long-term lipid outcomes – a systemic review. Obesity Reviews 2004; 5 (1): 43–50
34. Tuomilehto HP, Seppa JM, Partinen MM, et al. Gylling. Lifestyle intervention with weight reduction: first-line treatment in mild obstructive sleep apnea. Am J Respir Crit Care Med 2009; 179: 320–7
35. The Look AHEAD Research Group. The Look AHEAD Study: A Description of the Lifestyle Intervention and the Evidence Supporting It. Obesity 2006; 14(5): 737–52
36. Lindström J, Peltonen M, Eriksson JG, et al. Improved lifestyle and decreased diabetes risk over 13 years: long-term follow-up of the randomised Finnish Diabetes Prevention Study (DPS). Diabetologia 2013; 56: 284–93
37. Katsnelson M, Rundek T. Obesity Paradox and Stroke. Stroke 2011; 42: 3331–32
38. Kalantar-Zadeh K, Block G; Humphreys M, et al. “Reverse epidemiology of cardiovascular risk factors in maintenance dialysis patients”. Kidney International 2003; 63(3): 793–808
39. Doehner W, Clark A, Anker SD. The obesity paradox: weighing the benefit. European Heart Journal (2010); 31: 146–48
40. Lavie, C. Body Composition and Heart Failure Prevalence and Prognosis: Getting to the Fat of the Matter in the “Obesity Paradox.”Mayo Clin Proc 2010; 85(7): 605-608
41. Romero-Corral A, Montori VM, Somers VK, et al. Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies. Lancet 2006; 368: 666–78
42. Uretsky S, Messerli FH, Bangalore S, et al. Obesity paradox in patients with hypertension and coronary artery disease. Am J Med 2007; 120: 863–70
43. Hastie CE, Padmanabhan S, Slack R, et al. Obesity paradox in a cohort of 4880 consecutive patients undergoing percutaneous coronary intervention. Eur Heart J 2010; 31: 222–26
44. Bucholz EM, Beckman AL, Krumholz HA, Krumholz HM. Excess weight and life expectancy after acute myocardial infarction: The obesity paradox reexamined. Am Heart J 2016; 172: 173–81
45. Lavie CJ, Osman AF, Milani RV, et al. Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Am J Cardiol 2003; 91: 891–94
46. Oreopoulos A, Padwal R, Kalantar-Zadeh K, et al. Body mass index and mortality in heart failure: a meta-analysis. Am. Heart J. 2008; 156(1): 13–22
47. Oreopoulos Mayo Clin Proc 2010; 85(7): 605–608
48. Oga EA, Eseyin OR. The Obesity Paradox and Heart Failure: A Systematic Review of a Decade of Evidence. J Obes 2016
49. Hällberg V, Kataja M, Lahtela J, et al. Obesity paradox disappears in coronary artery bypass graft patients during 20-year follow-up. Eur Heart J Acute Cardiovasc Care 2016
50. Galal W, Gestel Y, Hoeks S et al. The Obesity Paradox in Patients With Peripheral Arterial Disease. Chest 2008; 925
51. Unexpected survival advantage in elderly people with moderate sleep apnoea. Journal of Sleep Research 2009; 18(4): 397–403
52. Vemmos, K. et al. Association between obesity and mortality after acute first-ever stroke: the obesity-stroke paradox. Stroke 2011; 42(1): 30-36
53. Senoo K, Lip GY. Body Mass Index and Adverse Outcomes in Elderly Patients With Atrial Fibrillation: The AMADEUS Trial. Stroke 2016; 47(2): 523–26
54. Zafrir B, Adir Y, Shehadeh W, et al. The association between obesity, mortality and filling pressures in pulmonary hypertension patients; the “obesity paradox”.Respir Med 2012
55. Kalantar-Zadeh K, Abbott KC, Salahudeen AK, et al. Survival advantages of obesity in dialysis patients. Am J Clin Nutr 2005; 81: 543–54
56. Whitmer RA, Gunderson EP, Barrett-Connor E, et al. BMJ 2005; 330(7504): 1360
57. Fitzpatrick A, Kuller, LH, Lopez O, et al. Midlife and Late-Life Obesity and the Risk of Dementia Cardiovascular Health Study. Neurol 2009; 66(3): 336-42
58. De Laet, Kanis JA. Oden A, et al. Osteoporos Int 2005; 16: 1330–38
59. Miller M, Delaney C, Penna D, et al. A 3-year follow-up study of inpatients with lower limb ulcers: evidence of an obesity paradox? J Multidiscip Healthc 2012; 5: 181–16
60. Sharma AM, Kushner RF. A proposed clinical staging system for obesity. Int J Obes (Lond) 2009; 33(3): 289–95
61. Wilsgaard T, Loehr L, Mathiesen E, et al. Cardiovascular health and the modifiable burden of incident myocardial infarction: the Tromsø Study. BMC Public Health 2015; 15: 221
62. Mørkedal B, Vatten L, Romundstad PR, et al. Risk of myocardial infarction and heart failure among metabolically healthy but obese individuals: HUNT (Nord-Trøndelag Health Study), Norway. J Am Coll Cardiol 2014; 63(11): 1071-8