Title: Obesity, undernutrition, and cardiovascular disease in the elderly


Key words: obesity, undernutrition, CVD, cardiovascular disease, diabetes, age, inactivity, excess carbohydrate, type 2 diabetes, lipid profile, low carbohydrate, fats, cholesterol, LDL, atherogenic, hypertension, arteriosclerosis, weight loss, triglycerides, fish oils, polyunsaturated fats, mono-unsaturated, hyperlipidaemia, hyperglycaemia, postprandial, insulin resistance, glyceamic index, glucose, lipids, men, women, pancreas, hyperinsulinaemia, post-menopausal, visceral adipose, visceral fat, insulin sensitivity, antioxidants, vitamin C, vitamin E, B6, folate, B12, dietary intervention, saturated fat, intake, unrefined cereals, fruit, vegetables, homocyteine, multivitamin, multimineral, exercise, soya, sterol, stanol, butter, margarine, statins,  


Date: Sept 2006


Category: Life changes


Nutrimed Module:


Type: Article


Author: Morgan, G


Obesity, undernutrition, and cardiovascular disease in the elderly

Obesity, undernutrition and cardiovascular disease are increasing problems in an increasingly elderly population. The World Health has reported that the worldwide incidence of obesity has doubled within the last 10 years (WHO 1998). In the UK, the prevalence of poor nutrition in the elderly has been well documented (Finch 1998), and the incidence of diabetes and related cardiovascular disease within the population continues to grow (Mann 2002). How are we to interpret these findings and what can be done about it? This review will look at the research that has been done within this area and suggest potential nutritional strategies to treat an ever-increasing problem.


Sugar versus fat

Obesity remains one of the best predictors of cardiovascular disease. Age leads to increasing levels of physical handicap and inactivity, which is associated with both of these conditions. Opposing the prevailing theory of excess fat intake as the cause of obesity, Yudkin (Yudkin 1969) originally proposed the theory that excess carbohydrate consumption led to increased weight, abnormal lipid profiles and, indirectly, to type 2 diabetes and cardiovascular disease. Low carbohydrate diets subsequently became the mainstay for the dietary management of diabetes. The results of the Seven Countries Study (Keys 1970), which showed fats to play a pivotal role in the aetiology of cardiovascular disease, was later to eclipse Yudkin’s work in demonstrating the important part played by carbohydrates in the aetiology of cardiovascular disease. Both fats and carbohydrates play a part, as became apparent.


The Atherogenic Lipid Profile

Elevated plasma total cholesterol, LDL cholesterol, triglyceride and low HDL cholesterol levels are the hallmark of the atherogenic lipid profile, a profile linked to obesity, hypertension and arteriosclerosis, the major markers of cardiovascular disease (Griffin 1994). A high intake of saturated fat has been linked to both raised cholesterol levels, obesity and cardiovascular disease (Keys 1970). Weight loss itself has been independently associated with reductions in cholesterol levels and heart disease (Dattilo 1992). Cholesterol, however, acts as a poor marker of cardiovascular disease, triglyceride levels being a better predictor (Reardon 1985, Austin 1991, Griffin 1994). In the Framingham study, 90% of the cardiovascular cases had elevated triglyceride levels of over 1.5 mmol/l. (Castelli 1986). Elevated triglyceride levels increase with age and have been reported to be associated with a 3-fold increase in the rate of cardiovascular disease (Griffin 1994).


Fish oils, rich in n-3 polyunsaturated fatty acids, have been shown to reduce plasma triglyceride levels and reduce cardiac morbidity (Harris 1989, Burr 1989, Gissi 1999, Minihane 2000). In addition, replacing saturated with all forms of polyunsaturated fats improves the lipid profile and has been shown to be beneficial (Hjermann 1981, de Lorgeril 1994, Mann 2002). More recently, mono-unsaturated fatty acids have, in particular, been demonstrated to produce an even more favourable profile, with increased levels of HDL cholesterol (Katan 1997, Vessby 2001).


Postprandial hyperglycaemia and hyperlipidaemia

Research has now confirmed the link between insulin insensitivity or resistance and the atherogenic lipid profile. Meta-analysis of this research has shown that high glucose loads, particularly through the consumption of foods with a high glycaemic index, leads to both prolonged hyperglycaemia and hyperlipidaemia in the postprandial phase and the development of insulin resistance and pancreatic exhaustion, progressing to type 2 diabetes and cardiovascular disease (Coutinho 1999, Ludwig 2002). Prolonged elevated triglyceride levels in this phase are characteristic (Griffin 1994). Studies giving food with a low glycaemic index have led to weight loss and reduction in the markers for the above diseases (Slabber 1994, Ludwig 2002). Elevated levels of both glucose and lipids have been shown to be directly toxic to the beta-cells of the pancreas (Unger 1995). Impaired glucose tolerance in men has been associated with an increased rate of cardiovascular disease (Balkau 1998). Relatively sharp falls in blood glucose during the postprandial phase, an expression of hyperinsulinaemia provoked by a high glucose load, leads to ‘binging’ on energy-dense carbohydrates during this period and has been linked to the obesity associated with type 2 diabetes and cardiovascular disease (Ludwig 2002).


Central obesity

In men progressive obesity tends to be centripetal, distinguishing it from the peripheral obesity seen in women. In spite of the loss of protection provided by oestrogens, post-menopausal women continue to display lower rates of cardiovascular disease into old age. This has been linked to the absence of the male morphological type of obesity. Further analysis shows this to this to be due to an increase in male visceral adipose tissue rather than the increase in subcutaneous adipose tissue displayed in women. The male pattern has been directly linked to impaired insulin sensitivity and cardiovascular disease (Despres 1993, Lemieux 1994, Couillard 1999). In contrast, female subcutaneous tissue has been shown to retain an oxidative capacity which allows it to clear triglycerides from the blood in the postprandial phase (Lemieux 1994). In rats, a diet with a high glycaemic load, in the presence of poor fat oxidative power, progresses to obesity (Pawlak 2000). A similar process in humans probably leads to the visceral fat deposition characteristic of the male pattern of obesity.


Oxidative stress

Cardiovascular disease is known to have an inflammatory aetiology and to be mediated by oxidative stress (Ross 1999). Recent work has shown that a delayed postprandial phase is associated with increased free radical activity, antioxidant depletion, vascular endothelium damage and the development of atherosclerotic lesions, impaired endothelial function, raised blood pressure and myocardial and peripheral ischaemia (Lefebve 1998, Ceriello 2000). Studies have also shown that antioxidants, such as vitamin C and E, taken with food help to abort the oxidative stress chain reaction occurring during the postprandial phase (Title 2000).


Raised homocysteine levels, associated with ageing, have also been linked to vascular endothelium damage and cardiovascular disease and shown to be associated with vitamin B12, folate and vitamin B6 deficiency, all common in the elderly (Graham 1997, Homocysteine Lowering Trialists Collaboration 1998). There is thus considerable evidence that addressing these nutritional issues will be able to help to disrupt important metabolic pathways leading to atherosclerosis and heart disease.



Dietary intervention programmes have now been shown conclusively to lead to weight loss, correction of abnormal lipid profiles, and a reduction in the incidence of type 2 diabetes and cardiovascular disease (Shaomei 1999, McCauley 2002). Programmes, such as the American National Cholesterol Education Program (Shaomei 1999), have achieved these results by implementing the lessons learnt from lipid and other research. Reducing saturated fat intake, increasing the ratio of polyunsaturated fats in the diet, encouraging increased consumption of oily fish, unrefined cereals, and fresh fruit and vegetables help to bring this about. Further refinements could be made by increasing monounsaturated oil consumption, in the form of olive oil (Katan 1997), and by increasing consumption of folate-rich green leafy vegetables in order to reduce homocysteine levels (Jacques 1999). Multivitamin/mineral supplementation is recommended, particularly for those institutionalised individuals, in view of their poor antioxidant and nutritional status. Such measures have all been shown to be more effective when combined with an exercise regime (Shaomei 1999, McCauley 2002).


Apart from the above lifestyle measures, two other dietary innovations would be beneficial. Replacing meat, especially red meat, with soya-based protein has been shown to regularise abnormal lipid profiles. Consumption of 50G per day of soya protein leads to falls in total cholesterol and triglycerides of around 10%, independent of weight loss (Anderson 1995). 30G of soya would amount to 2 cups of soya milk and one portion of a soya- based protein substitute meal per day, which, realistically, could be incorporated into the daily diet. Replacement of butter or margarines with sterol and stanol-containing spreads would also be beneficial. Consumption of 25g/day of these spreads leads to a reduction in cholesterol levels, equivalent to about one third of that produced by statin drugs (Law 2000). Their only drawback is their cost, which at around £70 a year, may preclude their widespread use.



Obesity, poor nutrition and cardiovascular disease form a triad that is closely associated with old age. Dietary intervention and exercise remain the treatment of choice but sadly, due to motivational issues, lack of social support and insufficient provision of informed medical care, an integrated management programme is rarely able to be provided. Government sponsored nutritional education programmes need to be addressed to both health workers and the population at large in order that the enormous cost of managing the obesity related diseases of diabetes and cardiovascular disease can be curbed and the health of the population maintained into old age.  




1. WHO (1998) Obesity: preventing and managing the global epidemic. Report of a WHO consultation on obesity. Geneva: World Health Organisation

2. Finch S, et al. (1998) National Diet and Nutrition Survey: People aged 65 years and over. Vol. 1: Report of the Diet and Nutrition Survey. London: H.M. Stationery Office

3. Mann JI (2002) Diet and risk of coronary heart disease and type2 diabetes. The Lancet 360: 783-789

4. Yudkin J, Watson RH (1969) Sugar and ischaemic heart disease. BMJ 4:110-11

5. Keys A (1970) Coronary heart disease in seven countries. Circulation Suppl 11-186-1-198

6. Griffin BA, et al. (1994) Role of plasma triglyceride in the regulation of plasma low density lipoprotein (LDL) subfractions: relative Contribution of small, dense LDL to coronary heart disease risk. Atherosclerosis 106: 241-53

7. Dattilo AM, Kris-Etherton PM (1992) Effects of weight reduction on lipids and lipoproteins: a meta-analysis. Am J Clin Nutr 56: 320-28

8. Reardon MF, Nestel PJ, Craig IH, Harper RW (1985) Lipoprotein predictors of the severity of coronary heart disease in men and women. Circulation 71: 881-88

9. Austin MA (1991) Plasma triglycerides and coronary heart disease. Arterioscler Thromb 11: 2-14

10. Castelli WP (1986) The triglyceride issue: a view from Framingham. Am Heart J 112: 432-37

11. Harris WS (1989) Fish oils and plasma lipid and lipoprotein metabolism in humans: a critical review. J Lipid Res 30: 785-807

12. Burr ML, et al. (1989) Effects of changes in fat, fish and fibre intakes on death and myocardial infarction: diet and reinfarction trial. Lancet 2: 757-61

13. Gissi Prevenzione Investigators (1999) Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Lancet 354:477-55

14. Minihane AM, et al. (2000) ApoE polymorphism and fish oil supplementation in subjects with an atherogenic lipoprotein phenotype. Arterioscler Thromb Vasc Biol 20: 1990-97

15. Hjermann I, Holme I, Byre KV, Leren P (1981) Effect of diet and smoking intervention on the incidence of coronary heart disease. Lancet 1: 1305-10

16. de Lorgeril M, et al. (1994) Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet 343: 1454-59

17. Ludwig DS (2002) The glycaemic index: physiological mechanisms Relating to obesity, diabetes, and cardiovascular disease. JAMA 8: 2414-2423

18. Katan MB, Grundy SM, Willett WC (1997) Beyond low-fat diets. N Engl J Med 337: 563-6

19. Vessby B, et al. (2001) Substituting dietary saturated for monounsat- urated fat impairs insulin sensitivity in healthy men and women: the KANWU Study. Diabetologia 44: 312-19

20. Coutinho M, Gerstein HC, Wang Y, Yusuf S (1999) The relationship between glucose and incident cardiovascular events: a metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12.4 years. Diabetes Care 22: 233-240

21. Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R (1994) Effects of a low-insulin-response, energy-restricted diet on weight loss and plasma insulin concentrations in hyperinsulinemic obese females. Am J Clin Nutr 60: 48-53

22. Unger RH (1995) Lipotoxicity in the pathogenesis of obesity- dependent NIDDM: genetic and clinical implications. Diabetes 44: 863-70

23. Balkau B, et al. (1998) High blood glucose concentration is a risk factor for mortality in middle-aged nondiabetic men: 20 year follow up in the Whitehall Study, the Paris Prospective Study, and the Helsinki Policemen Study. Diabetes 21: 360-67

24. Despres J-P (1993) Abdominal obesity as important component of insulin-resistance syndrome. Nutrition 9: 452-59

25. Lemieux S, et al. (1994) Are gender differences in cardiovascular disease risk factors explained by the level of visceral adipose tissue. Diabetologia 37: 757-764

26. Couillard (1999) Gender difference in postprandial lipemia. Importance of visceral adipose tissue accumulation. Arterioscler Thromb Vasc Biol 19: 2448-55

27. Pawlak DB, Denyer DS, Brand-Miller JC (2000) Low post-prandial fat oxidation after a high glycemic index meal leads to increased body fat in chronically fed rats. Obes Res 8: 1285

28. Ross R (1999) Atherosclerosis – an inflammatory disease. N Engl J Med 340: 115-126

29. Lefebve PJ, Scheen AJ (1998) The postprandial state and risk of cardiovascular disease. Diabet Med 15: S63-S68

30. Ceriello (2000) The post-prandial state and cardiovascular disease: relevance to diabetes mellitus. Diabetes Metab Res 16: 125-132

31. Title LM, Cummings PM, Giddens K, Nassa BA (2000) Oral glucose loading acutely attenuates endothelium-dependent vasodilation in healthy adults without diabetes: an effect prevented by vitamins C and E. J Am Coll Cardiol 36: 2185-2191

32. Graham I, et al. (1997) Plasma homocysteine as a risk factor for vascular disease. JAMA 277: 1775-81

33. Homocysteine Lowering Trialists Collaboration (1998) Lowering homocysteine with folic acid based supplements meta-analysis of randomised trials. BMJ 316: 894-98

34. Shaomei Y-P, et al. (1999) Effects of the National Cholesterol Education Program’s Step 1 and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. Am J Clin Nutr 67: 632-46

35. McCauley KA, et al. (2002) Intensive lifestyle changes are necessary to improve insulin sensitivity: a randomised controlled trial. Diabetes Care 25: 445-52

36. Jacques PF, Selhub J, Bostom AG, Wilson PWF, Rosenberg IH (1999) The effect of folic acid fortification on plasma folate and total homocysteine concentrations. N Engl J Med 340: 1449-54

37. Anderson JW, Johnstone BM, Cook-Newell ME (1995) Meta-analysis of the effects of soy protein intake on serum lipids. N Engl J Med 333: 276-82

38. Law M (2000) Plant sterol and stanol margarines and health. BMJ 320: 861-4