Dietary sugar intake as a risk factor for early-onset colorectal cancer in young New Zealanders

New Zealand continues to experience some of the highest incidence and mortality rates of colorectal cancer (CRC) worldwide, with more than 3,500 new diagnoses and 1,200 CRC-related deaths reported in 2020.¹ Of increasing concern is the steady rise in early-onset colorectal cancer (EOCRC), defined as CRC diagnosed before the age of 50. EOCRC incidence in New Zealand is increasing by approximately 26% per decade, with an even sharper rise of 36% per decade among Māori.¹ Most of these cancers are sporadic and increasingly recognised as associated with extrinsic (and therefore modifiable) risk factors.²

It has been 10 years since David Wishart proposed a compelling argument for a metabolic, rather than purely genetic, basis for the global increase in cancer, citing alterations in metabolic pathways as key drivers of carcinogenesis.³ The finding that metabolic profiling of biopsied CRC tumours and matched normal tissue can discriminate normal from malignant samples, as well as colon from rectal cancers, supports this hypothesis.⁴ To date, a range of relevant metabolites have been identified,^5,6 including urinary glucose levels.⁷ This gains significance given there is increasing evidence that the metabolic dysregulation associated with obesity and type 2 diabetes mellitus (T2DM) may also contribute to the pathogenesis of EOCRC.⁸

Sugar, a term commonly used to describe simple carbohydrates such as glucose, fructose and galactose, is normally metabolised in the small intestine and absorbed into the bloodstream, resulting in an insulin response that promotes cellular uptake of glucose.⁹ Elevated fasting glucose levels and glycosylated haemoglobin (HbA_1c), markers of acute and chronic dysglycemia respectively, are reported in CRC patients.¹⁰ Moreover, elevated HbA_1c levels in non-diabetic adults, especially those aged 40–50 years, appear to support a link between excessive dietary sugar intake and increased risk of colon carcinogenesis.¹¹ Collectively, these studies reinforce the idea that lifestyle changes reflected in altered metabolic profiles are likely contributing to rising CRC risk in younger populations,² particularly with regards sugar consumption.

In the past century, sugar intake has tripled worldwide, largely driven by the introduction of sugar-sweetened beverages (SSBs).¹² SSB consumption among young people has risen steadily since the 1980s.¹³ Despite the World Health Organization (WHO) advising that added sugars should comprise no more than 10% of daily caloric intake (approximately 50–60 grams per day),¹⁴ many SSBs (including fruit drinks, energy drinks, sports drinks and carbonated beverages) contain enough glucose, fructose and sucrose to exceed this limit within a single serving.¹⁵ As a result, sugar intake among young people who reportedly consume SSBs on a regular basis often frequently surpass these recommended guidelines. This gains significance with evidence that regular consumption of SSBs (≥2 servings per day) is associated with an increased risk of EOCRC by as much as 32%.¹⁶

Mechanistically, the link between excess dietary sugar and CRC risk relates to cancer-specific pathways involving energy metabolism, lipid metabolism, inflammation and immune regulation.¹⁷ Notably, the association appears strongest for cancers of the colon¹⁰ and, more specifically, the proximal colon,¹⁸ supporting the hypothesis that unabsorbed sugars exceeding the small intestine’s absorptive capacity can transit into the proximal colon.¹⁹ Colonocytes that line the epithelial barrier are normally shielded from the gut microbiota by a constitutively expressed inner mucus layer.²⁰ While glucose intake can alter the composition of the gut microbiota,²¹ emerging evidence suggests that dysglycemia-induced thinning or dysfunction of the mucus barrier (occurring even in the absence of dysbiosis) may compromise epithelial protection,^22,23 increasing the risk of carcinogenesis.

In New Zealand, SSBs are the leading contributor of added sugar among both children and adults²⁴ and therefore likely play a significant role in childhood and adolescent obesity, particularly among Māori.²⁵ Being overweight or obese, especially during childhood, is a recognised risk factor for future CRC.^25–27 Approximately one in eight New Zealand children is now obese, helping to explain the persistent rise in EOCRC incidence.²⁸ Childhood obesity is also strongly associated with the development of metabolic disorders such as dysglycemia, impaired glucose tolerance and T2DM later in life.²⁸ However, while high SSB intake clearly promotes weight gain,²⁹ animal studies show that high-glucose or high-fructose diets can induce adverse changes in the colonic microenvironment even in the absence of weight gain.²¹ Consistent with this, increased SSB consumption does not always correlate with higher body fat percentages in young New Zealanders.¹⁴

The identification of glucose-related metabolic biomarkers offers a promising avenue for early risk assessment in primary care settings. Simple, low-cost measurements such as glucose or HbA_1c levels could help general practitioners identify patients at elevated metabolic risk long before symptoms arise, potentially facilitating earlier diagnostic evaluation with faecal immunochemical testing (FIT) and, when indicated, colonoscopy. Given that childhood obesity and metabolic disorders frequently persist into adulthood, intervention efforts must begin early and be culturally responsive, particularly for Māori communities who bear a disproportionate burden of EOCRC.

In summary, the growing body of evidence linking metabolic dysregulation, excessive dietary sugar intake and EOCRC underscores an important and potentially preventable public health challenge for New Zealand. The association between SSB consumption and increased CRC risk, particularly among young individuals, reflects broader shifts in diet, metabolic health and lifestyle over recent decades. Importantly, the mechanistic pathways involved, including dysglycemia-related impairment of the proximal colonic environment and disruption of the protective barriers, provide biologically plausible foundations for this relationship.

As evidence continues to accumulate, the need for public health intervention becomes increasingly clear. Ultimately, reducing SSB consumption, one of the most modifiable contributors to excessive dietary sugar intake, represents an achievable and impactful strategy to mitigate the rising burden of EOCRC and metabolic disease in young New Zealanders.