colorectal cancer risk

How Sugar Harms Your Gut and Increases Colorectal Cancer Risk

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Sugar can damage our intestines and even increase the risk of colorectal cancer.

In this series, we will explore the good and bad sweeteners, uncover the unexpected outcomes of cutting out sugar, and discover the ultimate way to achieve this.

Here’s a fact you may find hard to believe or might not want to accept: Sugar can damage our intestines and even increase the risk of colorectal cancer.

Sugar Increases the Risk of 2 Colonic Diseases

Inflammatory bowel disease (IBD) is widely regarded as the intestinal disorder most directly associated with sugar.

Crohn’s disease and ulcerative colitis are the two main types of inflammatory bowel diseases. These conditions can be highly debilitating, often leading to symptoms such as persistent diarrhea, abdominal pain, rectal bleeding, bloody stools, weight loss, and fatigue.

IBD has become increasingly prevalent in recent times.

A narrative review published in Clinical Gastroenterology and Hepatology in 2022 highlighted that multiple epidemiological data indicate a direct correlation between the high consumption of sugar in Western diets and an increased risk of IBD.

The journal Inflammatory Bowel Diseases published a large-scale study that revealed, based on surveys of more than 366,000 adults from various European countries, that individuals who consumed the highest amounts of sugar and soft drinks had a 1.68 times higher incidence of ulcerative colitis compared to those who consumed the least. Moreover, another review showed that for every additional 10 grams of sugar consumed per day, the risk of Crohn’s disease increased by approximately 1 percent.

Additionally, numerous population-based studies have indicated that about 10 percent of patients with IBD believe that consuming sugary foods can trigger disease flare-ups and worsen symptoms. The previously mentioned 2022 narrative review also pointed out that Crohn’s disease patients often reported increased sugar consumption prior to feeling ill.

How Does Sugar Trigger Intestinal Inflammation

A high-sugar diet can lead to significant changes in gut microbial composition in a very short period. Bacteria that thrive on simple sugars multiply rapidly, whereas those dependent on fibers, such as Bacteroides, may decrease in number. Bacteroides are highly beneficial for both the human body and gut health, partly due to their ability to break down dietary fiber into short-chain fatty acids.

Short-chain fatty acids are essential for the gut, serving as vital nutrients for intestinal mucosal cells. They not only support the gut’s immune and barrier functions but also stimulate gut repair, thus alleviating gut inflammation. In a high-sugar diet, short-chain fatty acids in the gut are rapidly depleted.

A decrease in the levels of short-chain fatty acids has been observed in the guts of patients with IBD.

A high-sugar diet can also lead to a reduction in the quantity of Akkermansia bacteria, beneficial microbes that regulate mucus layer thickness and support intestinal barrier function.

At the same time, sugar promotes the rapid growth of harmful bacteria.

An experiment published in Science Translational Medicine in 2020 revealed that sucrose-fed mice exhibited a significant increase in mucin-degrading bacteria in their intestines, resulting in the thinning of the intestinal mucus layer, aggravating colitis.

“It is direct evidence that eating sugar makes your body highly sensitive to developing colitis,” Hasan Zaki, an assistant professor in the pathology department at the University of Texas Southwestern Medical Center, said during an interview with The Epoch Times. “All of this can happen within a few days.”

A high-sugar diet also leads to an increase in the relative abundance of Proteobacteria in the gut. These bacteria carry toxic lipopolysaccharides, leading to inflammation and the impairment of intestinal epithelial integrity.

Sugar not only disrupts the balance of gut bacteria but also decreases overall microbial diversity. The production of short-chain fatty acids also relies on a diverse gut bacterial environment and the cooperation of different bacterial species.

Contributes to Leaky Gut

Sugar can lead to increased intestinal permeability, commonly referred to as “leaky gut.”

It may also alter the architecture of the intestinal mucosa, leading to the thinning of the gut and the production of high levels of reactive oxygen species, ultimately causing damage.

Substances that shouldn’t typically enter the body, such as bacterial lipopolysaccharides, entering the bloodstream from the gut can lead to endotoxemia, exacerbating both local and systemic chronic inflammation.

Additionally, the accumulation of sugar in the colon increases the intestinal osmotic load, which retains excess water in the intestines. This also accelerates the fermentation rate of gut microbiota, resulting in bloating, abdominal pain, and intestinal dysfunction.

How Sugar Harms Your Gut and Increases Colorectal Cancer Risk

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Sugar can damage our intestines and even increase the risk of colorectal cancer.

This is Part 10 in the series “The Ultimate Guide to Kicking Sugar”

In this series, we will explore the good and bad sweeteners, uncover the unexpected outcomes of cutting out sugar, and discover the ultimate way to achieve this.

Here’s a fact you may find hard to believe or might not want to accept: Sugar can damage our intestines and even increase the risk of colorectal cancer.

Sugar Increases the Risk of 2 Colonic Diseases

Inflammatory bowel disease (IBD) is widely regarded as the intestinal disorder most directly associated with sugar.

Crohn’s disease and ulcerative colitis are the two main types of inflammatory bowel diseases. These conditions can be highly debilitating, often leading to symptoms such as persistent diarrhea, abdominal pain, rectal bleeding, bloody stools, weight loss, and fatigue.

IBD has become increasingly prevalent in recent times.

A narrative review published in Clinical Gastroenterology and Hepatology in 2022 highlighted that multiple epidemiological data indicate a direct correlation between the high consumption of sugar in Western diets and an increased risk of IBD.

The journal Inflammatory Bowel Diseases published a large-scale study that revealed, based on surveys of more than 366,000 adults from various European countries, that individuals who consumed the highest amounts of sugar and soft drinks had a 1.68 times higher incidence of ulcerative colitis compared to those who consumed the least. Moreover, another review showed that for every additional 10 grams of sugar consumed per day, the risk of Crohn’s disease increased by approximately 1 percent.

Additionally, numerous population-based studies have indicated that about 10 percent of patients with IBD believe that consuming sugary foods can trigger disease flare-ups and worsen symptoms. The previously mentioned 2022 narrative review also pointed out that Crohn’s disease patients often reported increased sugar consumption prior to feeling ill.

How Does Sugar Trigger Intestinal Inflammation?

A high-sugar diet can lead to significant changes in gut microbial composition in a very short period. Bacteria that thrive on simple sugars multiply rapidly, whereas those dependent on fibers, such as Bacteroides, may decrease in number. Bacteroides are highly beneficial for both the human body and gut health, partly due to their ability to break down dietary fiber into short-chain fatty acids.

Short-chain fatty acids are essential for the gut, serving as vital nutrients for intestinal mucosal cells. They not only support the gut’s immune and barrier functions but also stimulate gut repair, thus alleviating gut inflammation. In a high-sugar diet, short-chain fatty acids in the gut are rapidly depleted.

A decrease in the levels of short-chain fatty acids has been observed in the guts of patients with IBD.

A high-sugar diet can also lead to a reduction in the quantity of Akkermansia bacteria, beneficial microbes that regulate mucus layer thickness and support intestinal barrier function.

At the same time, sugar promotes the rapid growth of harmful bacteria.

An experiment published in Science Translational Medicine in 2020 revealed that sucrose-fed mice exhibited a significant increase in mucin-degrading bacteria in their intestines, resulting in the thinning of the intestinal mucus layer, aggravating colitis.

“It is direct evidence that eating sugar makes your body highly sensitive to developing colitis,” Hasan Zaki, an assistant professor in the pathology department at the University of Texas Southwestern Medical Center, said during an interview with The Epoch Times. “All of this can happen within a few days.”

A high-sugar diet also leads to an increase in the relative abundance of Proteobacteria in the gut. These bacteria carry toxic lipopolysaccharides, leading to inflammation and the impairment of intestinal epithelial integrity.

Sugar not only disrupts the balance of gut bacteria but also decreases overall microbial diversity. The production of short-chain fatty acids also relies on a diverse gut bacterial environment and the cooperation of different bacterial species.

Contributes to Leaky Gut

Sugar can lead to increased intestinal permeability, commonly referred to as “leaky gut.”

It may also alter the architecture of the intestinal mucosa, leading to the thinning of the gut and the production of high levels of reactive oxygen species, ultimately causing damage.

Substances that shouldn’t typically enter the body, such as bacterial lipopolysaccharides, entering the bloodstream from the gut can lead to endotoxemia, exacerbating both local and systemic chronic inflammation.

Additionally, the accumulation of sugar in the colon increases the intestinal osmotic load, which retains excess water in the intestines. This also accelerates the fermentation rate of gut microbiota, resulting in bloating, abdominal pain, and intestinal dysfunction.

The Ultimate Guide to Kicking Sugar

Inhibits Gut Regeneration

The colon’s regeneration rate is rapid, with intestinal stem cells continuously dividing while old cells are continually shed. However, a study published in 2023 revealed that a high-sugar diet can disrupt this mechanism. The study also found that sugar directly affects the proliferation of colonic epithelial cells, inhibiting their growth, and this damage intensifies with higher sugar concentrations.

Furthermore, a high-sugar diet can alter the colon’s innate immune function and reduce the number of intestinal immune cells, diminishing their responsiveness to tissue damage.

Mr. Zaki emphasized the importance of recognizing the harm that sugar inflicts on the human body, stating: “We spend a lot of money to deal with those diseases, but that’s not the solution.

“I think we should have some kind of policy from governments to make sure that we understand that sugar is harmful, just like smoking is harmful.”

The Strong Connection Between Sugar and Colorectal Cancer

Sugar is also associated with the occurrence, recurrence, and mortality rates of colorectal cancer.

In a prospective cohort study involving stage three colon cancer patients, it was found that individuals who consumed two or more servings of sugar-sweetened beverages per day experienced a 67 percent increased risk of colon cancer recurrence or mortality compared to those who consumed less than two servings monthly. The risk increased even further, reaching 122 percent, for patients who were both overweight and less physically active.

An older case-control study conducted by University of Utah researchers revealed that both high sugar intake and a high glycemic index diet increase the risk of developing colon cancer by more than 50 percent.

“Consuming large amounts of sugar leads to an increase in stored energy in the form of fat, indirectly raising the risk of colon cancer,” said Dr. Jeremy Kortmansky, associate professor of clinical medicine (medical oncology) at Yale School of Medicine, chief network officer at Smilow Cancer Hospital, and clinical director of the gastrointestinal medical oncology division at Yale Cancer Center, during an interview with The Epoch Times.

The indirect connection between sugar consumption, obesity, and cancer can be explained in several ways. According to Dr. Kortmansky, one particularly compelling theory involves the relationship between obesity and insulin resistance. Obese individuals often have higher insulin levels, which can stimulate cancer’s insulin-like growth factor receptors, thus activating pathways that promote cancer development and growth. This interferes with intestinal cell growth and division, resulting in abnormal cell renewal in which old cells fail to die off.

As for the theory suggesting that sugar-induced inflammation increases the risk of cancer, Dr. Kortmansky explained that inflammation in the body often leads to local damage and DNA changes in cells. Normally, inflammation would cause these problematic cells to die, but if they survive, there’s a potential risk of cancer development.

Additionally, there are some studies that establish a direct connection between sugar and cancer.

An animal study published in Nature in 2019 confirmed that high-fructose corn syrup directly promotes the growth and progression of colorectal cancer tumors, and this effect is independent of obesity. Lewis Cantley, the lead researcher of the study and a professor at Harvard Medical School’s Department of Cell Biology, emphasized during an interview with The Epoch Times that this effect might also apply to humans.

“Consumption of high-fructose corn syrup dramatically increased in the 1960s. Over the following 20 years, there was a dramatic increase in colorectal cancer in relatively young adults,” he pointed out, noting that such people typically have KRAS mutations. KRAS mutations are oncogenes with the highest mutation rate among cancers and are linked to cancers with high mortality rates.

“We showed that giving mice high-fructose corn syrup orally had the same effect of enhancing colorectal cancers in the context of KRAS mutations.”

Just 5 to 25 grams of fructose can saturate the absorption capacity of the small intestine, after which fructose enters and comes into direct contact with the colonic lumen of the proximal colon.

In a clinical preliminary study published in The American Journal of Clinical Nutrition in 2022, an analysis of lesion location was conducted on 2,733 cases of colorectal cancer deaths. The results revealed direct associations between high consumption of sugar-sweetened beverages and total fructose intake and an increased incidence and mortality rate of proximal colon cancer.

Interestingly, this significant relationship didn’t exist in the distal colon or rectum. Researchers believe that these findings provide evidence that dietary sugar can directly contribute to the development of colorectal cancer.

Ultra-Processed Foods Linked to Colorectal Cancer Risk, CV Death

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Making fresh foods available and affordable will promote public heath, editorialists say

A photo of three slices of previously frozen cooked pizza on a plate on a blue plaid tablecloth.

Regular consumption of ultra-processed foods was associated with an increased risk of colorectal cancer, all-cause mortality, and cardiovascular mortality, according to findings from two studies published in The BMJ.

In the first paper, which analyzed three prospective U.S. cohort studies, men in the highest quintile of consumption had a 29% higher risk of developing colorectal cancer compared with those in the lowest (HR 1.29, 95% CI 1.08-1.53, P=0.01), with an even greater association seen for distal colon cancer (HR 1.72, 95% CI 1.24-2.37, P<0.001), reported Fang Zhang, MD, of Tufts University in Boston, and colleagues.

These associations remained significant even after adjusting for BMI and nutritional quality indicators, they noted, and no association between ultra-processed food intake and colorectal cancer was seen among women.

In the second paper, which involved an Italian prospective study, an adjusted multivariable analysis showed a higher risk of all-cause mortality (HR 1.19, 95% CI 1.04-1.35) and cardiovascular mortality (HR 1.32, 95% CI 1.06-1.64) among adults in the highest quarter of the Food Standards Agency Nutrient Profiling System (FSAm-NPS) dietary index compared with the lowest quarter.

When looking at only those who fell within the two highest categories of ultra-processed food intake, based on the NOVA classification system, the associations remained for all-cause mortality (HR 1.19, 95% CI 1.05-1.36) and cardiovascular mortality (HR 1.27, 95% CI 1.02-1.58), reported Marialaura Bonaccio, PhD, of IRCCS Neuromed in Pozzilli, Italy, and colleagues.

In an accompanying editorial, Carlos Monteiro, MD, PhD, and Geoffrey Cannon, MA, both of the University of São Paulo in Brazil, noted that “the overall positive solution includes making supplies of fresh and minimally processed foods … available, attractive, and affordable. And sustaining national initiatives to promote and support freshly prepared meals made with fresh and minimally processed foods, using small amounts of processed culinary ingredients and processed foods.”

“Enacted, this will promote public health. It will also nourish families, society, economies, and the environment,” they added.

Colorectal Cancer

For their study, Zhang and colleagues used data on healthcare workers from three large U.S. prospective cohorts, including 46,341 men from the Health Professionals Follow-up Study from 1986-2014, 67,425 women from the Nurses’ Health Study I from 1986-2014, and 92,482 women from the Nurses’ Health Study II from 1991-2015. The NOVA classification system was used to assess levels of ultra-processed foods, and only physicians were blinded.

Over 24 to 28 years of follow-up, 3,216 cases of colorectal cancer were documented, 1,294 in men and 1,922 in women.

A higher consumption of meat/poultry/seafood-based ready-to-eat products was associated with an increased risk of colorectal cancer in men (HR 1.44, 95% CI 1.20-1.73), as was higher consumption of sugar-sweetened beverages (HR 1.21, 95% CI 1.01-1.44), while ready-to-eat or heat mixed dishes were linked to an increased risk for women (HR 1.17, 95% CI 1.01-1.36).

Interestingly, dairy-based desserts and yogurt were tied to a 17% lower risk of colorectal cancer among women (HR 0.83, 95% CI 0.71-0.97).

Potential explanations for the different patterns between the sexes might be due to the effects of obesity or sex hormones, Zhang and team noted.

They also acknowledged that the self-administered validated food frequency questionnaires used in the study included a limited list of pre-defined foods, which was a limitation to their study.

Cardiovascular/All-Cause Mortality

In the so-called Moli-sani study, Bonaccio and colleagues examined data on 22,895 participants (mean age 55, 52% women) in Molise, Italy from March 2005 to December 2010.

Over a median follow-up of 12.2 years, 2,205 participants died.

The authors jointly analyzed the the FSAm-NPS — used to derive the Nutri-Score front-of-pack label — and the NOVA classification system to assess mortality, finding that the magnitude of the relationship between the FSAm-NPS dietary index and all-cause mortality was attenuated by 22.3%, which was slightly higher than that for cardiovascular mortality (15.4% attenuated), while mortality risks linked to high ultra-processed food intake were not changed.

“So the problem with ultra-processed products has been suggested to be simply their poor nutrient profiles,” Monteiro and Cannon noted.

Study limitations included possible recall bias from self-reported dietary data, as well as possible social desirability bias, since ultra-processed food intake may have been underreported, Bonaccio and team said.

Cholesterol levels, not statins, influence colorectal cancer risk

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Colorectal cancer
Cancer — Histopathologic image of colonic carcinoid. 

Long-term use of the cholesterol-lowering drugs known as statins does not appear to decrease a patient’s risk of colorectal cancer, suggests a new, large case-control study from Penn Medicine researchers published this week in PLOS Medicine. The observational analysis of over 100,000 patients’ medical records suggests it is cholesterol levels that influence risk, not the much-debated statins, and that “indication bias” may explain the link between the widely-used cardiovascular drugs and risk. Such bias occurs when the indication (high cholesterol, in this case) being treated with a drug is also associated with the outcome of interest (colorectal cancer).

“There appears to be an artificially protective effect of statins,” said Ronac Mamtani, MD, MSCE, an assistant professor of Hematology/Oncology from the Perelman School of Medicine at the University of Pennsylvania and the Abramson Cancer Center, and lead author of the study. “Although the risk of colorectal cancer was lower in statin users versus non-users, when we compared those who continued versus those who discontinued the therapy, such that each group shared the same indication for statin therapy, there was no difference in risk.”

Both statin use and have been linked to a lower colorectal cancer risk, but it has remained unclear which may be responsible for the apparent beneficial effects.

Blood levels were inversely related to colorectal cancer risk: the higher the cholesterol level, the lower the risk for patients, regardless of statin use, the authors found. The researchers also found that an unexplained drop in cholesterol levels one year before a cancer diagnosis increased the risk of cancer in both statin users and non-users.

The findings point to a bigger role of cholesterol levels on cancer risk that could potentially serve as a blood biomarker to help diagnosis colorectal cancer earlier.

Ben Boursi, MD, a postdoctoral fellow in the Perelman School of Medicine, and Yu-Xiao Yang, MD, MSCE, an associate professor of Medicine and Epidemiology at Penn, are senior authors on the paper.

Statins are a common cholesterol-lowering treatment strategy for the management of patients at risk for coronary heart disease. Previous studies have also shown a potential reduction in cancer risk for people who take the drugs; however, they did not account for the blood cholesterol level on cancer risk, the authors said.

In the new study, the researchers compared statin use and blood cholesterol level between 22,163 patients with colorectal cancer and 86,538 patients without colorectal cancer (controls) from a database of electronic records of over 10 million patients from primary care practices in the United Kingdom.

They confirmed findings from previous studies that showed a decreased risk of colorectal cancer in statin users compared to non-users. However, they found that the difference in the risk of colorectal cancer was not significantly different between those patients who continued statin therapy and those who discontinued (OR, 0.98; 95% CI, 0.79-1.22). Furthermore, for every 1 mmol/L (~38.6 mg/dl) increase in total , authors observed a 10 percent decreased risk of colorectal cancer.

Additionally, they observed that decreases in total serum cholesterol (>1 mmol/L) at least a year before the cancer diagnosis were associated with 1.25-fold and 2.36-fold increased of colorectal cancer in users and nonusers, respectively.

“Together, these data demonstrate a complex association between statins, cholesterol, and ,” Mamtani said. “While unexplained decreases in blood total cholesterol should alert physicians to consider colon cancer as one potential explanation, future studies are needed to determine the utility of as a marker for early detection of colon.”