What does current research reveal about the key drivers behind the rising incidence of colorectal cancer in younger adults, and why does this trend represent an urgent public health concern?
Modern medicine continues to look to Paul Ehrlich’s magic bullet as the answer to cancer. Yet, it is modern science that dispels the magic bullet of causation and treatment of cancer with a multisystem failure as the cause. As a result, a multi-system failure approach must also meet treatment.
All aspects of medicine look to the magic bullet of cancer causation and cancer treatment. Whether natural, holistic, integrative, or conventional, this holy grail remains the focus of the quest against cancer. This strategy is a reductionist trap across the divide.
The real divide is not between conventional and natural medicine. It is between reductionist thinking and systems thinking. Both camps repeatedly search for their own version of the magic bullet. Both look for the needle in the haystack of heterogeneity.
Heterogeneity is the concept that things are not the same. Heterogeneity is a foundational principle in biology. Patients are heterogeneous. Tumors with the same name are heterogeneous. The same tumor in two different patients behaves differently—that’s heterogeneity. Heterogeneity exists within the same tumor. Even different metastatic sites are heterogeneous. There is an old adage: the more things change, the more they are the same. Here, the more heterogeneous the biology of cancer proves to be, the more we think all cancers are the same.
The future solutions of cancer care will not be found in either conventional medicine or natural medicine alone. It will belong to systems medicine—an approach that integrates evidence-based pharmaceuticals, nutrition, metabolism, immunology, microbiome science, lifestyle interventions, local therapies, and precision combinations, recognizing that no single intervention is likely to be sufficient for most patients.
UPFs
I recently had the opportunity to travel to China. I left with many questions, but one specific to the question posed here is, “Is China about 20-30 years behind the U.S.?” China appears to be following many of the same nutrition, metabolic, and cancer trends that the United States experienced decades earlier. Could the pace and pattern differ due to cultural, dietary, and environmental factors?
One of the greatest contrasts between modern-day America and traditional China is how food is viewed. Today, the average American adult obtains more than half of their daily calories from ultra-processed foods (UPFs). To be exact, approximately 55% of total daily calories are obtained from UPFs. A more startling statistic is that it shows an upward trend: children and adolescents consume an average of 62% of their daily calories from UPFs.
In China, consumption of UPFs is increasing rapidly, yet it still represents only a fraction of total calories for most adults. According to the China Health and Nutrition Survey (1997-2011), UPFs generally account for only 4-10% of total daily caloric intake nationally. Despite the low percentage, China’s UPF intake has increased from < 2% of daily calorie intake to 10% today. An increase in obesity, metabolic syndrome, type II diabetes, and obesity-associated cancers in China appears to mirror the increase in UPFs.
Take-home: Americans consume roughly 6-10 times as many UPFs as the average Chinese adult.
What are UPFs? Ultra-processed foods are industrialized formulations manufactured largely from refined substances extracted from foods or synthesized ingredients, often containing little intact whole food, categorized as NOVA group 4.
What is NOVA? NOVA is not an acronym but actually the name of the grouping system for processed foods. It is a food classification system developed by researchers at the University of São Paulo that categorizes foods based on the extent and purpose of processing, rather than their nutrient content or carcinogenicity alone. It is widely used in nutrition and public health research to study dietary patterns and chronic disease. The four NOVA groups of processed foods include:
- NOVA Group 1 – Unprocessed or Minimally Processed Foods (cleaning, washing, trimming, chilling, freezing)
- NOVA Group 2 – Processed Culinary Ingredients (pressing, milling, refining, grinding)
- NOVA Group 3 – Processed Foods (canning, bottling, smoking, baking, fermentation)
- NOVA Group 4 – Ultra-Processed Foods (UPFs)
Ultra-processed food intake in the U.S. parallels the obesity risk and obesity-associated cancers. I think it is safe to question if UPFs are even food at all. Clearly, the changing demographics of cancer are multi-factorial. The magic-bullet approach need not apply.
A few UPFs are labeled as carcinogenic, but it is the cumulative exposure to emulsifiers, artificial sweeteners, flavor enhancers, food colorings, packaging-derived chemicals, modified starches, refined carbohydrates, and others that leads to cumulative damage, cumulative failure, and loss of resilience. As a whole, UPFs are not labeled as carcinogens. Numerous prospective cohort studies and meta-analyses have reported an association between higher UPF consumption and increased risk of the following:
- Colorectal cancer
- Breast cancer
- Pancreatic cancer
- Overall cancer incidence and mortality
Ultra-processed foods frequently contain flavor enhancers, artificial colors, emulsifiers, stabilizers, preservatives, sweeteners, modified starches, protein isolates, industrial seed oils—all the food groups we never knew existed. The problem is UPFs are refined, manufactured, extracted, synthesized, and do not resemble food at any level, but they rarely exist in isolation. In fact, UPFs often contain 10-30 different UPF ingredients.
Dysbiosis
Most look to obesity as a root cause of disease. Yet, it is a biomarker of root dysfunction. It is a canary in the coal mine that pivots from a biomarker of dysfunction to a contributor to dysfunction and disease. It is the gut-microbiome axis that funnels together the immune system and metabolic impact:
- Reduced gut microbial diversity
- Dysbiosis
- Increased Pathobionts
- Decreased SCFA production (butyrate, propionate, acetate)
- Altered bile acid signaling
- Breakdown of gut epithelial barrier
- Increased leaky gut
- Kynurenine/IDO1 (Indoleamine 2,3-dioxygenase 1)-mediated immune suppression
- Increased LPS → TLR4 activation
- Increased chronic systemic inflammation
- Increased inflammaging
- Increased senescence
- Promoting a Senescence-Associated Secretory Phenotype
- Increased chronic systemic inflammation
- Accelerated cell aging
The result is an alteration in the immune axis with significant consequences for the tumor-immune microenvironment. An increase in myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), and regulatory T cells (Tregs) promotes immunosuppression. As a result, the activity of CD8+ T cells and natural killer (NK) cells is decreased. This promotes increased immune-desert and immune-excluded phenotypes in cancer. This impact is separate from the impact of chemotherapy and radiation on the immune system—separate, yet stacked.
The end result, no pun intended, is a change in the demographics of cancer, here colorectal.
Obesity
The immune system originates in the gut. Moreover, the gut metabolome, functional or dysfunctional, is more important than the taxa. Any intervention or therapy that modulates the immune system must take into account the gut environment. Early-onset cancers and obesity-associated cancers are clear evidence of the disruption of the microbiome-immune-metabolic axis.
Two core convergent epidemiological signs must be considered. First, early-onset cancers (ages 20-49) are rising across multiple tumor types. According to a recent British Medical Journal article, eleven tumors are rising disproportionately in young adults:
- Colorectal
- Breast
- Ovarian
- Endometrial
- Pancreatic
- Liver
- Kidney
- Gallbladder
- Thyroid
- Multiple myeloma
- Oral
In parallel, the Centers for Disease Control (CDC) in the U.S. has shown that thirteen obesity-associated cancers are increasing in conjunction with increasing age-adjusted mortality rates. The thirteen obesity-associated cancers include the following:
- Colorectal
- Endometrial
- Esophageal adenocarcinoma
- Gastric cardia
- Liver
- Gallbladder
- Pancreatic
- Kidney
- Thyroid
- Ovarian
- Multiple myeloma
- Meningioma
The alarming mortality rates highlighted by the CDC point to an alarming change in demographics in cancer. Age-adjusted mortality rates in obesity-associated cancers have increased from 3.73 per million in 1999 to 13.52 per million in 2020. That is a 3.6-fold increase in mortality in obesity-associated cancers in one generation. Independent data from the CDC and BMJ demonstrate a parallel trend. We ignore them at our own peril. A lack of curiosity will allow this peril to become reality.
An analysis of overlap provides key insights. Ten of the eleven cancers between the BMJ and CDC directly overlap:
- Colorectal
- Breast
- Ovarian
- Endometrial
- Pancreatic
- Liver
- Kidney
- Gallbladder
- Thyroid
- Multiple myeloma
Ninety-one percent of early-onset cancers are obesity-associated. Currently, 74% of U.S. adults are either obese or overweight. The future trend provides no reason for optimism, as 21.2% of those aged 2-19 are obese, with greater than 70% maintaining obesity beyond the age of 30. The adolescent obesity rate cannot be properly framed without proper context. Pre-pandemic, the adolescent obesity rate was at 19.3%. The rise in childhood obesity from 19.3% to 21.1% represents more than excess weight—it reflects large-scale disruptions in the gut microbiome, immune programming, metabolism, obesity, and future disease risk, particularly the aforementioned 10 cancer risks.
These parallel data points cannot be interpreted through the prism of cancer incidence alone. It reflects more aggressive tumor biology. Moreover, it reflects altered human and tumor metabolism and reduced tumor immune competence.
Ultimately, a compromised immune system is at the root of the changing demographics of cancer, yet the root is not single, but the roots are numerous.
Apply to work with Dr. Nathan Goodyear by clicking here.
References:
Li, H., Boakye, D., Chen, X., Hoffmeister, M., & Brenner, H. (2021). Association of body mass index with risk of early-onset colorectal cancer: Systematic review and meta-analysis. The American Journal of Gastroenterology, 116(11), 2173–2183. https://doi.org/10.14309/ajg.0000000000001393 — PubMed
Noiman, A. N., Fryar, C. D., Saif, N. T., & Afful, J. (2025). Prevalence of overweight, obesity, and severe obesity among children and adolescents ages 2–19 years: United States, 1963–1965 through August 2021–August 2023. NCHS Health E-Stat, 112, 1–7. https://doi.org/10.15620/cdc/174645 — CDC/NCHS report
Simmonds, M., Llewellyn, A., Owen, C. G., & Woolacott, N. (2016). Predicting adult obesity from childhood obesity: A systematic review and meta-analysis. Obesity Reviews, 17(2), 95–107. https://doi.org/10.1111/obr.12334 — PubMed
U.S. Census Bureau. (2026). Annual estimates of the resident population by single year of age and sex for the United States: April 1, 2020 to July 1, 2025. Population Estimates Program. — Population estimates tables
Lauby-Secretan, B., Scoccianti, C., Loomis, D., Grosse, Y., Bianchini, F., & Straif, K. (2016). Body fatness and cancer—Viewpoint of the IARC Working Group. The New England Journal of Medicine, 375(8), 794–798. https://doi.org/10.1056/NEJMsr1606602