Nutrition sits at the intersection of many of the major risk factors for metabolic and cardiovascular disease: obesity, insulin resistance, diabetes, hypertension and dyslipidaemia. This is particularly important in Bahrain, where the prevalence of diabetes and cardiometabolic burden is substantial. Cardiovascular disease remains a leading cause of mortality in Bahrain, while the Southwest and North Africa (SWANA) region has the world’s highest age-standardised incidence and prevalence of coronary heart disease, alongside high rates of dyslipidaemia, hypertension and diabetes (source: WHO data for Bahrain).

There are two features that make the Gulf Cooperation Council (GCC) distinctive. First is the paradox of coexistence of abundance and deficiency. We have increasingly calorie-rich food environments and widespread availability of highly processed foods, yet deficiencies in nutrients such as vitamin D remain remarkably common. Second is the speed of dietary transition: reformulated "sugar-free," "diet" and "keto" products have moved into everyday diets faster than the evidence base on them has matured. Taken together, these two features put the GCC in an unusual position: the early adoption of reformulated products is faster here than in most global regions, while the research that tells us what those products do excludes the GCC population.

Dr Nitya Kumar started to investigate sucralose consumption and vitamin D deficiency to try to understand the dynamic between nutritional and preventive health. The two research projects began with quite different questions but ultimately address the same issue: are some of our assumptions about nutrition too simplistic?

Sucralose is particularly interesting because it is widely marketed and perceived as a healthier alternative to sugar, especially by people concerned about weight or diabetes. Yet emerging evidence suggested that a substance providing virtually no calories might still influence insulin physiology.

Vitamin D presents almost the opposite paradox. In a region with abundant year-round sunshine, deficiency remains extremely common. Me and my colleagues wanted to understand whether this deficiency was also associated with the very cardiometabolic problems that are highly prevalent in MENA populations.

Both studies therefore examine nutritional exposures that appear straightforward on the surface but become much more complex when we study their metabolic effects.

Our sucralose review challenged the idea that non-nutritive does not necessarily mean metabolically inactive. Among 16 studies examining insulin response, eight reported increased insulin responses following sucralose exposure. More strikingly, six of eight studies examining insulin sensitivity reported reductions. The evidence was not completely consistent, so it would be inappropriate to conclude that sucralose inevitably causes insulin resistance. However, there is enough evidence to question the assumption that sucralose is metabolically inert, particularly with habitual consumption and in people already at risk of diabetes.

For vitamin D, we reviewed 17 studies across nine SWANA countries. Vitamin D deficiency was consistently associated with greater adiposity, and pooled analyses found that deficient individuals had higher BMI, total cholesterol and average blood sugar level (HbA1c). One important thing to note is that our findings demonstrate that low vitamin D and higher heart disease risk tend to appear in the same people, which is not the same as showing that one causes the other. However, most studies were observational, largely cross-sectional and there was heterogeneity across them.

Dr Nitya Kumar commented: "From our research, the lesson for me is the following: I think the key is to resist binary messages about foods or nutrients being either 'good' or 'bad'. We should communicate both the findings and the uncertainty."

Our sucralose study does not mean that every sugar-free product is unhealthy without stating what it is being compared against: water, sugar, or placebo, and the answers differ. Our findings do not imply that a diet drink is worse than the sugared version, rather, it is not “metabolically inert” as plain water. In other words, “Zero calories” do not necessarily mean “zero metabolic effects”.

Similarly, our findings regarding vitamin D supplements tell us that nutritional exposures can have effects that are more complex than their labels suggest.

Good public communication on nutritional exposures should distinguish association from causation, acknowledge uncertainty and put findings into context. For readers, the useful next step is a conversation rather than a change: ask a clinician or dietitian about your overall intake of sucralose, and about testing vitamin D levels before supplementing.

From a research perspective, if world region-specific evidence was available, it would change three things:

• Clinically, it would let us counsel patients or the general public with specificity instead of generality: cumulative sweetener intake is not currently something most clinicians ask about, largely because there is no mg-per-serving figure on the label to ask about. Mandatory declaration of sweetener content by dose would make that conversation possible.
• At population level, it would sharpen targeting. Our data suggest women and individuals with higher adiposity carry a disproportionate share of vitamin D deficiency, which argues for screening and food-fortification strategies aimed at those groups rather than blanket supplementation.
• As for personalisation, ethnicity appears to matter mechanistically. Two comparable four-week sucralose trials reached opposite conclusions in Thai and Turkish populations, and populations at elevated baseline risk of insulin resistance may respond differently to identical exposures. However, almost all of this literature has been generated elsewhere.

Until we have sufficiently large and representative longitudinal cohorts study specific to national populations, much of our understanding of nutrition, metabolism and cardiometabolic disease is currently based on evidence derived from other populations. As a result, applying findings from predominantly European, North American or other populations may not fully capture Bahrain or the region's disease trajectories or identify risk factors that are particularly important in SWANA. Establishing well-characterised, diverse longitudinal cohorts across national populations would therefore be critical to generating locally relevant evidence and enabling more precise nutrition strategies.