A rise in the consumption of refined sugars in food and beverages has often been implicated in the epidemic of obesity, type 2 diabetes and cardiovascular diseases. While most added sugars are consumed as the disaccharide sucrose or in the form of its two constituent monosaccharides (glucose and fructose), it is its fructose moiety which, despite its classification as a low-glycemic sugar, is viewed as the more harmful sugar component. Indeed, chronic studies comparing diets containing fructose in substitution for glucose have demonstrated a more adverse lipid profile and greater cardiometabolic risks.

During the past decade, there has been increasing interest in the potential beneficial effects of galactose, a low-glycemic sugar monosaccharide which in combination with glucose constitutes the disaccharide lactose. Although galactose is absorbed at the same rate as glucose, most of it is taken up by the liver where it is metabolized to other substrates (glucose, lactate or fatty acids) that are readily metabolized by extrahepatic cells. Consequently, as the release of galactose in the form of glucose into the blood is delayed, it could provide an energy source of choice with a low-glycemic index and a low-insulinemic response. Indeed, several studies in healthy humans have shown that the ingestion of galactose elicits only small increases in plasma glucose and insulin, which are not different from those in response to fructose ingestion

This specific metabolic fate of galactose has formed the basis of interest in this low-glycemic sugar with respect to its potential impact on exercise performance and more recently for weight control. In the latter context, several acute studies have shown that ingestion of galactose leads to increased satiety. Furthermore, a chronic study involving intermittent intake of sugary drinks in women has shown that intake of galactose in substitution for glucose resulted in increased fat mobilization and oxidation, which would be consistent with the much lesser impact of galactose than glucose ingestion on circulating insulin. These studies have led to the proposal that diets with galactose as a source of carbohydrates could be useful in the management of obesity and type 2 diabetes

Little is known, however, about the impact of galactose ingestion on the cardiovascular system. By contrast, it has repeatedly been demonstrated that the ingestion of glucose and fructose drinks is characterized by specific haemodynamic responses in healthy young and older people [18]. Unlike drinking glucose, which decreases total peripheral resistance by an insulin-mediated release of nitric oxide accompanied by a metabolic vasodilation leading to an increase in cardiac output (CO), thereby resulting in little or no change in blood pressure (BP), the ingestion of fructose elicits a significant increase in BP that results from a more modest increase in CO but without a decrease in TPR. These differential BP responses to glucose and fructose ingestion have been attributed to their differential effects on insulin secretion, and to the well-known effect of insulin not only in enhancing sympathetic activation of cardiac contractility (hence contributing to the increased CO), but also in stimulating peripheral vasodilatation and hence decreasing TPR [20]. In this context, the question arises as to whether ingestion of galactose, which like fructose has only a mild stimulatory effect on insulin release,would also lead to higher BP. In testing this hypothesis, the aim of our study here was to investigate, using comprehensive and continuous cardiovascular monitoring, potential differences in BP and haemodynamics between galactose, glucose and fructose in a cross-over study design in young men.

Galactose resembles glucose in its marginal impact on BP, which contrasts with the significant BP-elevating effect of fructose ingestion. Furthermore, it has a much less pronounced effect on cardiac workload than glucose. Galactose thus presents the interesting characteristics of a low-glycemic sugar with mild cardiovascular effects.