Cocoa flavanols (CFs) are proposed to decrease the risk of cardiovascular disease (CVD) by reducing blood pressure, and augmenting endothelium-dependent dilatation (EDD), by increasing nitric oxide (NO) bioavailability (1). Evidence suggests EDD is blunted in young South Asian (SA) compared to White European (WE) men (2), consistent with higher CVD risk in SAs (3). Whether EDD is blunted in SA women has received little attention, nor has the effect of CFs on EDD in young women.

Thus, healthy women (11 WE/12 SA, aged 18-26years) completed food frequency and lifestyle questionnaires before undertaking a double-blind, cross-over study, in which they randomly received high-(695mg CFs) and low-flavanol (5.6mg CFs) cocoa drinks across two visits during the low-oestrogen phase of their menstrual cycle. One hour later, near-infrared spectroscopy (NIRS) was applied to the forearm to monitor totalHb (oxyHb+deoxyHb), as an index of forearm blood flow following 2-min arterial occlusion (reactive hyperaemia), 2-min rhythmic handgrip at 60% maximal voluntary contraction (exercise hyperaemia) and during 8-min mental stress (arithmetic) task. Effects of ethnicity and CFs on ∆totalHb were compared by two-way repeated measures ANOVA.

Physical inactivity was more prevalent amongst SAs than WEs (41.7% vs 0% with <1day physical activity/week, p=0.0373). Further, WEs consumed more fibre (WE:19.7±5.67(mean±SD), SA:14.4±5.05g/day, p=0.0269), vitamin C (WE:133±42.3, SA:89.5±44.1mg/day, p=0.0241), and fruit than SAs (WE:7.91±0.680, SA:4.50±0.657times/week, p=0.0017). Peak reactive hyperaemia tended to be higher in WEs (WE:65.5±45.3, SA:42.6±15.9AU, p=0.0595), as was peak exercise hyperaemia (WE:57.1±36.1, SA:31.3±16.1AU, p=0.0113). However, acute CFs had no effect on reactive (high-CF:50.3±38.0, low-CF:55.7±30.7AU, p=0.507), or exercise hyperaemia (high-CF:47.8±36.6, low-CF:39.3±22.0AU, p=0.275).

During mental stress, ∆totalHb was not different between WE and SA women and acute CFs had no effect on this response in either group (p>0.305), in contrast to the augmented forearm vasodilatation reported in men (4).  However, whereas some individual women showed the expected forearm vasodilator response to mental stress, others showed vasoconstriction as reported previously, particularly in SA men (2). Since the proportion of “vasodilators” and “vasoconstrictors” was comparable in WE and SA women (both 50%), effects of CFs were tested in these subgroups.  There was no effect of CFs in “vasodilators”, but the mean decrease in totalHb was attenuated in “vasoconstrictors” (p=0.005), consistent with CFs promoting vasodilation.

These findings indicate that both reactive and exercise hyperaemia are blunted in young SA, relative to WE women.  We propose this may partly reflect lower physical activity and cardioprotective nutrient intake in SA women, lifestyle behaviours known to impair EDD. Assuming CFs increase NO availability (1), the lack of effect of acute CFs on reactive, and exercise hyperaemia suggests any contribution NO makes to these responses is small, or already maximal in both young SA and WE women, possibly reflecting influences of oestrogen. The forearm vasodilator response to mental stress is largely NO mediated (5), while exaggerated vasoconstrictor responses to stress are predictive of CVD (2). Against this background, we suggest that irrespective of ethnicity, CFs may be particularly beneficial in increasing NO availability in women whose forearm vasodilator response to mental stress is impaired.