Will the Increasing Prevalence of Obesity Slow Down the Decline of Coronary Heart Disease?

CHD causes around 82,000 deaths each year with an additional estimated 2.7 million people living with the condition, making it the UK’s largest killer (NHS). The increasing prevalence of obesity in the UK is likely to cause an increase in health complications, including CHD. Audelin et al, (2008) states that 44% of CHD patients entering cardiac rehabilitation were obese and 80% were overweight. Guh et al, (2008) states that prevention of CHD in obese individuals is best achieved through weight loss.

Obesity is normally initiated by an increased energy intake compared to energy expenditure, along with other causes such as genetics, endocrine conditions, drugs, or psychiatric disorders. Obesity is defined as 30-40 Kg/m² and morbidly obese is >40 Kg/m². Metabolic conditions associated with obesity such as metabolic syndrome (MetS) increase the risk of CHD and type 2 diabetes (T2DM). Exercise and dieting with the objective to lose weight is related to a decrease in the risk factors associated with MetS and T2DM (Ades et al, 2009). Jarnal et al, (2009) studied the influence of physical activity and abdominal obesity on the potential of developing CHD, and the variation of different inflammatory biomarkers on healthy men and women over a 10 year period. The results identified that circulating levels of C-reactive protein and fibrinogen were linearly correlated in participants with an increased waist circumference and individuals with an increased risk of CHD. The research found that waist circumference was a valid CHD risk predictor.

CHD results from atherosclerosis of a coronary artery, causing hypoxia to the myocardial cells, manifesting in heart attack and/ or angina. The Framingham risk score (FRS) uses age, gender, systolic blood pressure, hypertension, total and high-density lipo-protein cholesterol levels, smoking, and diabetes as markers for the risk of CHD (Peter et al, 1998). The addition of coronary artery calcium (CAC) scores added significant improvement and reliability to the FRS predictions (Kavousi et al, 2012).

Figure 1 displays the percentage of men and women aged 16 and over, with obesity between the years of 1993 to 2009. Data taken from UK poverty.org.

Figure 2 displays the percentage incidence of men and women with coronary heart disease between the years of 1986 to 2008, Data taken from the British heart foundation.

Some observational evidence indicates an inverse correlation between obesity and CHD mortality, this is known as the ‘obesity paradox’ (Villareal et al, 2005). Unal et al, (2004) analysed the decrease of CHD in the general population of the UK, the conclusion stated the decline was due to a reduction in major risk factors, primarily smoking. The progress of a decline in CHD is moderately offset due to the increasing prevalence of obesity (Adams et al, 2006).

Treatment of obesity is a serious issue, due to its high prevalence and association with morbidity and mortality. Treatment for obesity usually starts with lifestyle changes, such as exercise and personal diet plans, followed by medication, and as a last resort, surgery. Phentermine and topiramate (PHEN/ TPM) is used in the treatment of epilepsy, however weight loss is an unintentional side effect. After 3 months of PHEN/ TPM treatment for obesity, weight loss is tested compared to baseline body weight. The patient will discontinue use of the drug if weight loss is <5%, due to the risk to benefit ratio. The strength to using PHEN/ TPM is due to the short usage period, the patient doesn’t become reliant on medication. Due to the current incline of obesity, further education needs to be conveyed to the general population on the severe health risks. At some point soon I will write a blog to describe and evaluate the history of the pharmacology for obesity.

Wang et al, (2014) looked at the effect of leptin on the risk for developing CHD. Although leptin causes satiety, obese persons display high concentrations of leptin, and are resistant to the effects. The meta-analysis stated that leptin and CHD correlation was not statistically significant, high levels in males should be followed closely. Further research into biomarkers for CHD would help determine individuals with increased risk at an earlier stage, myeloperoxidase (MPO) has been proposed as a risk marker. Zhang et al, (2001) found patients with CHD displayed increased blood MPO activity. Valentina et al, (2008) states that the amount of data defining MPO is relatively low, and MPO is not likely to be specific to CHD.

In conclusion, the steady decrease in CHD is optimistic, due to better treatment and a decrease in risk factors. However, obesity is a serious health concern and reduction in this condition is important, to decrease the onset of CHD and other diseases. Sorry for the long first post.

References

Adams KF, Schatzkin A, Harris TB, Kipnis V, Mouw T, Ballard-Barbash R,Hollenbeck A, Leitzmann MF (2006) Overweight, obesity, and mortality in a large prospective cohort of persons 50 to 71 years old. N Engl J Med 2006;355:763-778

Ades PA, Savage PD, Toth MJ, et al.(2009) High-calorie-expenditure exercise: a new approach to cardiac rehabilitation for overweight coronary patients. Circulation. 2009;119:2671–267

D.P. Guh, W. Zhang, N. Bansback et al. (2009) The incidence of co-morbidities related to obesity and overweight: a systematic review and meta-analysis, BMC Public Health, 9 (2009), p. 88

D.T. Villareal, C.M. Apovian, R.F. Kushner et al. (2005) Obesity in older adults: technical review and position statement of the American Society for Nutrition and NAASO, Obes Res, 13 (2005), pp. 1849–1863

Jarnal S, Benoit J, Arsenault, Melanie C, Philippa J, Ewa Ninio, Nicholas J Wareham, John J P Kastelein, Kay-Tee Knaw and S Matthijs Boekholdt. (2009) Inflammatory biomarkers, physical activity, waist circumference, and risk of future coronary heart disease in healthy men and women. European heart journal vol 32, issue 3, pp 336-344

Kavousi M, Elias-Smale S, Leening MJ, Vliegenthart R, Verwoert GC, Krestin GP, Ouderk M, De Maat MP, Leebeek FW, Mattace-Raso FU, Lindemans J, Hofman A, Steyerberg EW, Van der Lugt A, Witteman JC (2012) Evaluation of newer risk markers for coronary heart disease risk classification : a cohort study. Ann intern Med 156: 438-44.

Loria V, Dato I, Biasucci L. (2008). Myeloperoxidase: A new biomarker of inflammation is ischemic heart disease and acute coronary syndromes

M.C. Audelin, P.D. Savage, P.A. Ades, (2008) Changing clinical profile of patients entering cardiac rehabilitation/secondary prevention programs: 1996 to 2006, J Cardiopulm Rehabil Prev, 28 (2008), pp. 299–306

NHS (2012) Coronary heart disease. http://www.nhs.uk/Conditions/Coronary-heart-disease/Pages/Introduction.aspx. [11 Mar 2014]

Palmer, G. Obesity. http://www.poverty.org.uk/63/index.shtml#def [14 Mar 2014]

Peter W F, Wilson MD, Ralph B, D’Agostino PhD, Daniel Levy, Albert M Belanger, William B, Kannel MD. (1998) Prediction of coronary heart disease using risk factor categories. Framingham Heart Study. 97: 1837-1847

Scarborough P, Wickramasinge K (2011) Trends in coronary heart disease 1961-2011. BHF London. file:///C:/Users/Nathan/Downloads/BHF%20Trends%20in%20Coronary%20Heart%20Disease.pdf (Online) [10 Mar 2014]

Unal B, Critchley JA, Capewell S, (2004) Explaining the decline in coronary heart disease mortality in England and Wales between 1981 and 2000. Circulation2004;109:1101-1107

Wang, J, San-Bao C, Feng S, Xiao-Lu N. (2014) Leptin and coronary heart disease: A systematic review and meta-analysis. Athersclerosis volume 223, issue 1, pages 3-10.

Zhang R, Brennan M-L, Fu X, (2001). Association between myeloperoxidase levels and risk of coronary artery disease. Journal of the American Medical Association.2001;286(17):2136–2142.