A low-GI diet may have beneficial effects on thrombolytic function. The activity of plasminogen activator inhibitor-1, a thrombolytic factor that increases clot and plaque formation, has been found to be 53% lower after 24 days on a low -GI diet compared with a high-GI diet in twenty subjects with type 2 diabetes [50].
Long-term studies are clearly required, as recently, an increased plasma homocysteine level (+6.6%) was observed in individuals that follow strictly a low- carbohydrates diet for several months [51]. In contrast, a low-fat diet induced a decrease of plasma homocysteine by 6–8%. This may be an important observation as the relationship between total plasma homocysteine and CVD is dose dependent and independent of other risk factors. In humans, the effects of homocysteine on endothelial and vascular function and blood coagulation provide explanations for increased CVD risk [15,52,53].
The effects of increased body fatness on cardiovascular function can be predicted. Total body oxygen consumption is increased because of an expanded lean tissue mass and metabolically active adipose tissue, and this is accompanied by an absolute increase in cardiac output. The total blood volume in obesity is increased in proportion to body weight. This increase in blood volume contributes to an increase to the left ventricular pre-load and an increase in resting cardiac output. The increased demand for cardiac output is achieved by an increase in stroke volume: an increase in stroke volume results from an increase in diastolic filling of the left ventricle. This thickening of the wall with dilatation results in eccentric hypertrophy. The cardiovascular adaptation to the increased intravascular volume of obesity may not completely restore normal homodynamic function. Marked systolic dysfunction occurs when the ventricle can no longer adapt to volume overload. Dilatation of the left ventricle cavity radius leads to a decline in ventricular contractility. A combination of systolic and diastolic dysfunction progresses to heart failure [46,54]. Hyperglicaemia exacerbates oxidative stress, which is associated with inflammation, increased blood pressure, accelerated clot formation and decreased endothelium-dependent blood flow [47,55], and which may also worsen insulin resistance [56].
Conclusion
Long term compliance to a low-GI diet may induce favorable metabolic effects.
A diet high in fruits and vegetables, whole grains and low fat dairy products are important for weight loss.
Reduced hyperinsulinaemia associated with a low-GI diet may reduce CVD risk through effects on oxidative stress, blood pressure, serum lipids, coagulation factors, inflammatory mediators, endothelial function and thrombolytic function [47,49,55-57].
Based on associations between these metabolic parameters and risk of disease, further controlled studies on low-GI diet and metabolic disease are needed [58,59].
Data from long term clinical trials on the metabolic effects on different diets are needed in this area.
'