By Ana Espino | Published on October 15, 2025 | 2 min read
Fasting hyperglycemia (FHG)—defined as elevated blood glucose
levels outside of meals—is a common condition, particularly among individuals
with type 2 diabetes or metabolic syndrome. Its role in the
development of cardiovascular diseases is well established, but its involvement
in oncogenesis remains controversial and poorly understood.
Among current esearch limitations
is the lack of a robust quantification of the level of evidence linking
FHG to specific cancers. Challenges include the complexity of metabolic
mechanisms involved, the variability of epidemiological data, and
the difficulty in isolating the effect of blood glucose from that of
other confounding factors such as body weight, physical activity, and
insulin levels.
The main objective of this
study was to evaluate the strength of evidence linking exposure to
high fasting plasma glucose and the risk of seven major types of cancer,
using the “burden of proof” analytical framework developed by the Institute
for Health Metrics and Evaluation (IHME).
Hyperglycemia — a driver of cancer?
A total of 96 epidemiological
studies, encompassing over 75 million participants worldwide, were
included. The relative risk (RR) was estimated for each cancer type
based on exposure to FHG, defined as a fasting glucose level above 100 mg/dL
(5.6 mmol/L).
The seven cancer types analyzed were
pancreatic, liver, colorectal, breast, ovarian, endometrial, and lung
cancers. The researchers used the Burden of Proof Risk Function (BoPRF)
model to evaluate the strength of causal associations.
The analysis revealed a high
level of evidence for pancreatic, liver, and endometrial cancers,
with a clear dose–response relationship—the higher the fasting glucose
level, the greater the risk of developing these cancers.
Colorectal cancer showed an intermediate level of
evidence, indicating a plausible but less robust association. Conversely, breast,
ovarian, and lung cancers exhibited more heterogeneous or weak results,
with inconsistent associations across populations.
Pancreatic cancer stood out, showing a marked
increase in relative risk (>1.3) even with moderate rises in fasting
glucose, reinforcing the hypothesis of a direct role for hyperglycemia in
pancreatic carcinogenesis. Most included studies were well-adjusted
cohort analyses, strengthening confidence in the findings, though notable
variability remained—likely reflecting contextual or methodological
differences between populations.
Too much sugar, too much risk?
Fasting hyperglycemia, often silent
and overlooked in the absence of clear symptoms, emerges as a credible
risk factor for several metabolically driven cancers. The study
aimed to quantify the strength of this association, and its conclusions
point to a strong, consistent link between elevated glucose levels and pancreatic,
liver, and endometrial cancers.
The association with colorectal
cancer was moderate, while evidence regarding breast, ovarian,
and lung cancers was less convincing.
To deepen understanding, future
studies should integrate precise metabolic biomarkers such as HbA1c,
insulin levels, and inflammatory cytokines. Establishing multicenter
prospective studies with standardized protocols will be essential to
confirm and refine these findings.
Finally, these results should prompt
public health stakeholders to adapt cancer prevention strategies,
incorporating hyperglycemia management—even moderate forms—as a lever for
cancer risk reduction.
Read next: Breast Cancer: The Role of Lifestyle in Reducing Risk
About the author – Ana EspinoPhD in Immunology, specialized in Virology
