The causes of cardiovascular disease are not fully understood, but it is believed that both diet and lifestyle factors play an important role in the aetiology. Risk factors for cardiovascular disease include hypertension, changes to blood lipid profiles, obesity, as well as elevated plasma homocysteine and blood glucose levels. The metabolic syndrome is a disorder characterised by insulin resistance that is increasingly being associated with cardiovascular disease. As insulin sensitivity is reduced through fatty acid accumulation in muscle cells, abnormal partitioning of energy results in increased abdominal fat accumulation, which results in inflammation and free radical generation that can then damage arteries and raise blood pressure, which ultimately leads to the development of cardiovascular disease. Poor quality diets are though to contribute to increases in serum fatty acids, and lack of exercise is thought to prevent oxidation of these fatty acids following accumulation in muscle cells.
Researchers1 have investigated the ability of lifestyle to cause changes in the risk of cardiovascular disease, in obese subjects with a body mass index of over 30kg/m2. For 26 weeks, 17 individuals were assigned to receive a low calories diet and exercise regimen that produced a ≈750 kcal/day calorie deficit, and advice from a dietician specialising in obesity. The low calorie diet contained 30% of energy from fat, 50% from carbohydrate and 20% from protein. This subjects were also administered a multivitamin and mineral supplement in order to ensure the diet provided the minimum quantities of recommended nutrients. Exercise consisted of 90 minutes of supervised flexibility, endurance, and strength work on 3 non-consecutive days per week. The control group were instructed to maintain their usual diet and exercise programmes for the length of the study.
The results showed that the treatment group lost an average of 8.2 kg of body weight compared to no significant change (0.7kg) in the body weight of the control group. Beneficial changes in the waist circumference, (1cm versus -10cm), plasma glucose levels (4mg/dL versus ‑4mg/dL), serum triglycerides (0mg/dL versus -45mg/dL), systolic blood pressure (-2mmHg versus ‑10mmHg), diastolic blood pressure (0mmHg versus -8mmHg), C-reactive protein (0.8mg/L versus -2.5mg/L) and interleukin 6 (1.6 pg/mL and -2.4 pg/mL) were seen between the control and treatment groups, respectively. Concentrations of serum free fatty acid decreased significantly in the treatment group (99µmol/L) compared to the control group (10µmol/L). Overall, the number of subjects in the treatment group with metabolic syndrome fell by 59%, whereas the control group had no reduction in cases, suggesting that insulin resistance had fallen only in the treatment group.
These results suggests that changes to lifestyle habits can result in short-term weight loss and improvements in some of the main risk factors for cardiovascular disease. Interestingly, the serum free fatty acid concentration of the treatment group was reduced, which suggests that insulin sensitivity may have improved. Further evidence for this was the reduction in the number of individuals clinically classified as having metabolic syndrome (just over half). Reductions in C-reactive protein also suggests that systemic inflammation was reduced following dietary and exercise intervention. Importantly, a multivitamin and mineral supplement was administered to the treatment group, but not the control group. This is a confounding variable as it makes it difficult to differentiate the role played by correction of underlying vitamin deficiencies from the weight loss attained. The researchers did not also measure or comment on homocysteine levels, an independent risk factor for cardiovascular disease.
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