Erectile dysfunction (ED) is defined as the persistent inability to attain or maintain an erection sufficient to permit satisfactory sexual activity (Hatzimouratidis et al., 2016). Penile erection is a complex neurovascular phenomenon, and ED may result from various abnormalities arising from vasculogenic, neurogenic, hormonal, anatomical, drug-induced and psychogenic causes (Zhengyan et al., 2014). Endothelial dysfunction (EDys) has been found to be central to atherosclerosis which is one of the most common causes of ED (Gandaglia et al., 2014; Shah et al., 2016). EDys has also been linked to various risk factors like hypertension, diabetes, smoking and other oxidative stressors (Vlachopoulos et al., 2007). Thus, ED has been suggested to be an early marker of cardiovascular disease (CVD) (Shah et al., 2016). Endothelial cells have nitric oxide synthase (eNOS) which is responsible for the formation of nitric oxide (NO) which acts as a relaxing factor and plays a major role in activation and maintenance of the erection process (Aversa et al., 2010). Hyperhomocysteinaemia (HHcy) has a marked inhibitory effect on eNOS and promotes NOS uncoupling (Zhang et al., 2016). Folic acid (FA) has been demonstrated to play an important role in the metabolism of NO by potentially inverting NOS uncoupling (Stoll et al., 2010; Yang et al., 2014). FA supplementation has been found to improve endothelial dysfunction in patients with DM or hypertension (Cui et al., 2017; Hamidi Madani et al., 2013). Compared to the western countries, Asian population differ in genetic makeup, dietary and lifestyle profiles. It has also been found that nutritional deficiencies in FA account for increased