The prevalence of T2DM in this study was 16.9%, lower than that in the National Health and Morbidity Survey (NHMS) 2019 (18.3%) and a study conducted in Penang (19.6%) [25, 26]. However, the prevalence was higher than that reported by the NHMS in 2023, 2015 and 2011 (15.6%, 13.4% and 15.2% respectively) [27,28,29]. Meanwhile, the prevalence of this study is just slightly higher than the one reported by NHMS 2006 (16.6%) [30]. The prevalence of T2DM reported by the NHMS shows descending trend from 16.6% in 2006 to 13.4% in 2015, spiking upwards from 13.4% in 2015 to 18.3% in 2019, but the trend was descending again from 18.3 to 15.6% in 2019 to 2023. The inconsistent trends over the years were due to several factors including changes in socio-demographic and lifestyle (poor diet and physical inactivity) [31, 32]. Ramadas also concluded that the low adherence to nutritional guidelines, limited access to healthcare services in rural areas, and socio-cultural barriers to adopt healthier lifestyles are the main challenges in managing T2DM in Malaysia [32].
An elevated prevalence of inadequate dietary vitamin A intake (22.8%) was observed among this study population compared to the RNI [33]. A previous study conducted in Malaysia reported ≤ 27.9% prevalence of inadequate dietary vitamin A intake by adults aged 18 to 59 years old [34]. However, the prevalence of inadequate dietary vitamin A intake in this study was relatively low compared to the United States (45.2%) and China (> 83.3%) population [35, 36]. The discrepancy may be due to the abundance of vitamin-A rich local fruit and vegetables available in Malaysia such as water spinach, pumpkin, mango and papaya. Furthermore, animal products such as eggs, liver and fish were widely consumed by this population that may contribute to adequate intake of vitamin A among Malaysian population [5, 37]. A subsequent finding of this study was an insignificant difference of dietary vitamin A intake between the T2DM groups. Nevertheless, the multiple logistic regression indicated that dietary vitamin A intake higher than the RNI could benefit by reducing the prevalence of T2DM in Malaysian population. This aligns with the role of vitamin A, particularly its metabolites form of retinoic acid to control insulin sensitivity, support pancreatic β-cell function, and impose the antioxidant and anti-inflammatory properties [7, 38]. A gene network leading to glucose uptake, lipid metabolism, and immune response is also influenced by retinoid receptor signaling namely retinoic acid receptor (RAR) and retinoid X receptor (RXR). Besides, Valdés-Ramos et al. suggesting the regulation of retinol binding protein 4 (RBP4), a retinol transporter in bloodstream and adipokine, may offer understanding on the broader metabolic effects of vitamin A [7]. Overall, these mechanisms highlight the adequate dietary vitamin A intake could contribute to protection against T2DM in high-risk population such as Malaysian.
This study population has inadequate intake of vitamin B-complex (B6, B9, and B12) compared to the RNI [33]. There is a notably high prevalence of inadequate dietary vitamin B-complex intake observed in this study, specifically 80.5% (vitamin B12), 98.3% (vitamin B6), and 100% (vitamin B9). A recent study in Malaysia with 88 healthy subjects have reported approximately 32% and 53% prevalence of inadequate dietary vitamin B6 and B12 respectively [39]. In general, the prevalence of inadequacy among Malaysian population was high compared to the American population with only 11.1%, 12.1% and 4.0% prevalence of inadequate dietary vitamin B6, B9, and B12 intake, respectively [36]. The main source of vitamin B-complex were green leafy vegetables, legumes and dairy products, which are less consumed by Malaysian adults compared to Americans [40]. Apart from that, this current study found that there is a significant lower dietary vitamin B-complex intake among T2DM group compared to the other counterpart. Further statistical tests revealed that there is a significant inverse association between higher dietary B-complex intake level with the prevalence of T2DM. These findings were supported by previous studies that concluded deficiency of vitamin B-complex (B6, B9, and B12) was associated with the risk of T2DM [7, 11, 12]. This is due to raised homocysteine levels when there is an insufficiency of vitamin B-complex [12]. Increased homocysteine levels are involved in T2DM development together with β-cell dysfunction and insulin resistance [11, 12]. These adverse outcomes are also caused by oxidative stress and inflammation [12]. Moreover, mechanisms including enhanced tryptophan catabolism through the kynurenine pathway, reduced rate of adipogenesis, impaired lipid metabolism, and reduced capability to counteract advanced glycation end-product (AGE) formation might all contribute to promoting diabetes [11]. Mascolo and Verni also suggested that vitamin B6 acts as an antioxidant by counteracting the formation of reactive oxygen species (ROS) and AGEs to reduce the risk of T2DM [11]. Meanwhile, vitamin B9 could improve glycaemic control by reducing glycosylated haemoglobin fasting blood glucose, serum insulin, and insulin resistance as well as homocysteinemia in T2DM patients [7, 12]. Taken together, the adequate dietary vitamin B is required to protect and manage T2DM conditions by maintaining these biological mechanisms.
Similar to dietary vitamin A intake, dietary vitamin C intake was also recorded as a non-negligible prevalence of inadequacy (28.8%) among this study population compared to the RNI [33]. Mirnalini et al. has reported that adults aged 18 to 59 years old shows ≤ 37.1% prevalence of dietary vitamin C inadequacy among Malaysian population [34]. However, previous studies conducted in the United States and China reported higher prevalence of inadequate dietary vitamin C intake, estimated at 45.9% and > 58.5% respectively [35, 36]. The inconsistency may be due to equatorial climate in Malaysia supporting the year-round farming of vitamin C-rich fresh fruits and leafy vegetables such as guava, mango, papaya, cabbage, and spinach. Meanwhile, seasonal variation in the United States and China limits year-round fresh fruit availability especially during winter season. This circumstance led to dependence on pickled or cooked fruits and vegetables that may reduce the vitamin C content due to food processing and heat sensitivity. Another noteworthy result of this study was the significant lower dietary vitamin C intake among those with T2DM compared to those without T2DM. The finding was further complimented by multiple logistic regression that shows higher odds of T2DM prevalence for those consuming dietary vitamin C lower than RNI. These results are consistent with the physiological role of vitamin C as the antioxidant and anti-inflammatory agent, β-cell function protection and modulation of oxidative stress pathways [7, 41, 42]. Previous observational studies support an inverse association between vitamin C intake and T2DM risks, but interventional studies remain indecisive [7, 41, 42]. Meanwhile, a recent study conducted in India has found that T2DM patients showed lower plasma ascorbate levels compared to controls, despite consuming adequate dietary vitamin C [43]. The study has concluded that the lower plasma ascorbate level among T2DM patients was due to disease related oxidative stress and impaired vitamin C uptake, rather than dietary inadequacy [43]. On the whole, these results showed that adequate vitamin C intake is vital in preventing and managing T2DM disease.
This study revealed that there is an inadequate dietary vitamin E intake compared to the RNI with 91.3% prevalence of inadequacy among Malaysian population [33]. The finding was comparable with the Chinese and American population that recorded prevalence of inadequate dietary vitamin E intake of > 83.3% and 83.7%, respectively [35, 36]. Despite regional differences in food choices and availability, the inadequate vitamin E intake remains notably prevalent across the population. The main dietary sources of vitamin E are edible vegetable oil in the form of tocopherol (wheat germ oil, sunflower oil, and palm oil) or α-tocopherol (olive oil) [44]. Besides, unprocessed seeds, nuts, cereal grains, green leafy vegetables and fatty portion of meats contain lower level of vitamin E compared to the edible vegetable oil [33]. It is reasonable to conclude that the limited dietary sources of vitamin E is the main reason for the high prevalent of inadequate vitamin E across the global population. Another important finding of this study was a significant lower dietary vitamin E intake in T2DM group compared to non-T2DM group. The finding was consistent with a previous study conducted in Nigeria that reported that plasma vitamin E was significantly lower in the T2DM group compared to the controls [45]. On top of that, further statistical analysis shows a significant higher prevalence of T2DM among those taking dietary vitamin E at lower levels compared to the highest quartile. The present findings were in agreement with Valdés-Ramos et al. which concluded that high concentrations of α-tocopherol (a form of vitamin E in human plasma) were associated with a decreased risk of diabetes in the general population [7]. This might be due to the role of α-tocopherol as an antioxidant in the body, neutralizing free radicals and thus protecting cellular membranes and lipoproteins from oxidative damage [7, 46]. At large, these findings highlight that adequate dietary vitamin E intake plays an important role in protection against T2DM risk and condition.
This study highlighted the insufficient dietary vitamin K intake compared to the RNI and 82.2% prevalence of inadequacy among Malaysian adults [33]. The prevalence recorded in this study was high compared to a recent study conducted in Malaysia reported approximately 50% prevalence of inadequate dietary vitamin K intake in 88 healthy subjects [39]. This inconsistency was likely due to the huge differences in sample size and health status of the participant in this study that includes those with comorbidity of T2DM and hypertension. Meanwhile, Reider et al. reported approximately 55% prevalence of inadequate dietary vitamin K intake by the American population [36]. Higher prevalence of inadequate dietary vitamin K intake among Malaysians compared to the American population was potentially attributable to lower consumption of green leafy vegetables and dairy products, especially milk and cheese observed in this study population [40, 47]. This study also revealed that dietary vitamin K intake was significantly lower among T2DM patients compared to those without T2DM. Moreover, further statistical analysis indicates that there is a significant inverse association between higher intake of dietary vitamin K and the prevalence of T2DM. These findings were supported by the previous studies that demonstrate the evidence for a lower risk of T2DM with increased vitamin K intake [7, 10]. Of the two main forms of vitamin K, namely phylloquinone and menaquinone, menaquinone but not phylloquinone may have a role in decreasing the risk of T2DM [48]. The mechanisms that might be involved in reducing the risk of T2DM include the carboxylation of the vitamin K-dependent protein osteocalcin, anti-inflammatory properties, and lipid-lowering effects [9]. Thus, an adequate dietary vitamin K intake is compulsory in protection and management of T2DM condition.
The multiple logistic regression has found that higher energy intake, age (> 50 years old), urban area, lower SES, medication intake for HPT, family history of T2DM and HPT and comorbidity of HPT were significant confounders for the association between dietary vitamin intake and prevalence of T2DM. T2DM patients usually follow a restricted diet to manage their blood sugar level, that may focus on controlling macronutrients (carbohydrate, protein and fat) which unintentionally reduces the vitamin-dense food but increases energy-dense food consumption. Furthermore, Md Isa et al. had found that T2DM patients in Malaysia preferred higher fat intake rather than protein when carbohydrate intake was restricted [16]. Moreover, the urban residents typically consumed modern diets adapted by their urban lifestyle that is characterized by highly processed, convenience-based foods or frequent meals eaten outside the home, which tend to be richer in animal products but lower intake of vegetable and fruits, and consequently made them more vulnerable to T2DM compared to the rural residents [5, 37]. Those with low SES were linked to their incapability of decision making and affordability to practice healthy lifestyle, balanced dietary intake and also their awareness to manage T2DM condition properly [31, 32]. Meanwhile, those with a family history of T2DM and HPT were more likely to inherit unhealthy lifestyles as families tend to share similar habits and lifestyles, which include dietary intake and physical activity [49]. Regular medication intake for HPT was also a significant covariate due to dietary adjustment requirements in order to optimize the efficiency and minimize the side effects of the medication [50, 51]. The dietary adjustment includes; (1) modification of meal timing intake due to the requirement whether the medication to be taken with or without meal (2) decision to avoid certain food that have potential drug-nutrient interaction which may enhance or reduce the medication efficacy and results in unfavorable effects. For instance, the intake of bitter melon should be carefully considered by T2DM patients who are taking insulin because the food potentially enhances the treatment but may cause severe hypoglycemia [52]. Furthermore, the medication may alter the patient’s ability to taste and smell certain foods and consequently lead to a reduced food intake due to change of taste sensation, lessened sensitivity to flavors, or unpleasant after taste [50, 53]. On top of that, some medications altered appetite directly by suppressing hunger and subsequently restricting food intake [50, 53].
This study discusses the prevalence of dietary vitamin intake inadequacy among the Malaysian population and the association between dietary vitamin intake level and the prevalence of T2DM, together with the potential mechanisms that are involved in this association. However, the limitations of this study should be highlighted. First, this cross-sectional study could not ascertain the cause-and-effect of dietary vitamin intake and T2DM. Second, the dietary recall method used in the FFQ was subject to recall bias, which could underestimate or overestimate the dietary vitamin intake. To overcome this limitation, this study only includes data with plausible energy intake in the range of 500 to 5000 kcal. Therefore, future studies should use the quantification of vitamins in the human body together with prospective methods to delineate the cause-and-effect relationship between dietary vitamin intake and T2DM.