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Sunday Science by Go_UnPro Episode 1: 2025_11_02 · Go Un-Pro

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Welcome to Sunday Science,
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where we dive into a few recent scientific articles and their
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translation into our modern lives.
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Here is your host,
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Brent W.
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Lartz,
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MD.
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All right!
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Today we are having our first episode of Sunday Science from Go On Pro.
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This is dated November 2nd,
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2025.
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We're going to discuss how your diet,
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your microbiome,
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and genetics can cause colon cancer in young people.
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Not only that,
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but it could have been your diet and your microbiome in childhood
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that could have started all the whole process here.
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Colon cancer causes approximately 1.
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9 million cases per year and 900,
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000 deaths.
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It is the second leading cause of cancer deaths.
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globally while being the fourth most common diagnosed cancer.
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What does that mean?
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If it's the second leading cause of cancer deaths but the fourth most
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common diagnosed cancer,
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it means it could be somewhat more deadly than a couple of other types of cancer.
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In the U.
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S.,
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154,
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000 new cases occurred in 2023,
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and the incidence is declining,
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and there are 52,
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900 deaths in the year 2023.
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Deaths also declining,
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likely related to increased screening and increased lifestyles better lifestyles.
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Five-year survival of localized colon cancer is 91 and for all stages,
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it is 65%.
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Factors including a sedentary lifestyle,
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diet high in processed.
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foods and red meat,
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smoking,
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lack of exercise,
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ethanol,
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genetics,
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inflammatory bowel disease,
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and certainly the outcomes of these cancers are associated with access to care.
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Early colon cancer statistics: the incidence is rising in those under age 50,
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and 55 years of 10% of colon cancer is in patients who are under age 50,
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rising approximately 2% per year,
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and that's a 51% increase since 1994.
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Approximately 7,
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000 to now more than 15,
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000 cases per year in those under age 50.
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Potentially another statistic that is bantered about is 20% of those
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under age 55; colon cancer is rising as well.
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It used to be that this was only seen in young persons.
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If they had a genetic familial basis for colon cancer,
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these are persons with a couple of different genetic illnesses,
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one called familial adenomatous polyposis.
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That syndrome is autosomal dominant in about 50% of the cases,
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and most of the rest are new mutations that we can now determine.
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These persons have colons that are filled with polyps,
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and hence,
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if you have a colon filled with polyps by the time you're age 30 or 40,
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all the more likelihood you're going to get colon cancer; and hence,
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some of these persons have their colons taken out prophylactically
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prevent colon cancer.
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However,
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now most of these,
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or at least some of these.
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cases of early colon cancer are potentially linked to the microbiome.
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Early colon cancer is now the deadliest cancer in young men,
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and it is the second most deadly cancer in young women.
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Often,
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this is related to a delay in diagnosis because,
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at age 40,
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before we were less likely to have a uh tests to diagnose and/ or
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screen for these illnesses,
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because it was very uncommon.
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But given the increased prevalence and insulin incidence of these diseases,
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we are now seeing the screening ages dropping uh,
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to what they used to be.
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Um,
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54% of patients with early cancer were misdiagnosed as hemorrhoids,
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uh,
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irritable bowel syndrome,
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et cetera.
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36 saw three or more doctors before their diagnosis,
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and the symptoms of which change in bowel habits,
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bleeding,
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abdominal pain.
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Um,
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now we have screened and a recommendation to screen at age 45 or
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sooner if you have risk factors.
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Um,
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there are genetic and environmental causes.
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The type and the pattern and the location of the mutations causing
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these colon cancers depend on the chemical and potentially tobacco
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and other carcinogens have a certain pattern of mutations that are
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associated with them.
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And these are being discovered and have been discovered for many years,
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but now we're finding a particular type of mutation.
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Um,
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that is associated with your bacteria in your intestine.
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Let's talk a little bit about the mutations in colon cancer.
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The first we're going to talk about is adenomatous polyposis coli
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tumor suppressive gene.
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When you get a mutation in this gene,
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you will acquire a benign adenoma.
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This mutation in this gene is present present in over 80% of colorectal cancer.
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Its function is to maintain homeostasis of the gut epithelium.
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So you can see why this particular mutation would potentially cause
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inflammation and then cause polyps and then cause an adenoma.
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Epidermal growth factor receptor mutations then potentially.
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can add on to that mutation for colorectal cancer progression.
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And then subsequent mutations,
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there are multiple ones: KRAS,
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PTEN,
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and TP53 are a few of the other mutations.
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Screening for colon cancer,
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the gold standard is colonoscopy,
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but there are also a couple of other tests.
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You've all heard of these tests that are,
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um,
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found on commercials during multiple different,
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uh,
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broadcasts on,
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uh,
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cable TV.
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Uh,
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or there's also a blood DNA test.
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The difference is the colonoscopy is the gold standard,
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and this is the only way that you can remove some of these,
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uh,
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pre-cancerous polyps before they develop cancer.
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Uh,
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the stool for DNA tests are good.
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tests at screening for precancerous but they do miss some of these.
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And they're also their specificity is not,
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you could have false positives.
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Um now there is a microbiome length.
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And here's where we're going to talk about this.
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There is,
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uh,
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there are colibactin-producing E.
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coli that are not the same strains that cause diarrhea.
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And you think about your hamburger or other types of food based caused by E.
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coli.
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These are different strains.
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Colibactin is a DNA mutagen and it is causes certain mutation patterns.
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And those mutation patterns can be detected in colon cancer.
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And hence we're going to be talking about that later,
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uh,
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in Some of these new articles we're going to be talking about three new articles,
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um,
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that are related to this.
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It is possibly related to exposure as a child because it takes a
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long time for these mutations to build up and also for them to now
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then acquire other mutations,
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um,
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requiring,
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uh,
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that are required to develop colorectal cancer.
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Up to 68% of colorectal colonized colorectal cancers are colonized with PKS E.
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coli.
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This is the colibactin-producing E.
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coli,
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also called PKS-positive E.
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coli.
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All right,
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we're going to be talking about first,
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um,
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an article in the Lancet Microbiome which was published in April of 2025.
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This,
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um,
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article had examined the genomes of 981 bowel cancer patients,
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their cancer cells in 11 countries.
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Under 40 cancer diagnosis,
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if you were diagnosed at age 40 or less,
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you were 3.
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3 times more likely have colobactin mutations.
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If you were greater than 70 and you had colon cancer,
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it is more prevalent,
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this colobactin mutations countries that had higher rates of early onset cancer.
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These polyketide synthase positive E.
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coli strains produced E.
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coli,
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produced colobactin and hence then developed the colon cancer potentially.
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Another article from Nature Microbiology from 2025 studied dietary
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fiber and its inhibition of colobactin.
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They studied mice with three different types of either a low carb,
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low fiber diet,
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high fat,
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high sugar diet,
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or normal chow.
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The PKS positive bacteria induced senescence associated secretory phenotype,
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which further potentiated by inflammatory triggers,
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and mismatch repair deficient modelwas associated with increases in
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those PKS positive bacteria.
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The low carb,
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low fiber diet was associated with a higher amount of PKS positive bacteria.
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The high fat,
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high sugar diet and the normal chow were associated with low amount
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of PKS positive bacteria comparatively.
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One issue here is,
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what if you had a low carb,
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high fiber diet instead?
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of a high-fat,
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high-sugar diet or some other types of diets.
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Certainly,
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there are more than one type of different diet that you could study in this situation.
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Frontiers in Microbiology article from 2025 also showed that inulin,
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which potentially we think of inulin as being a good thing in our
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diet because it is a fiber that decreases inflammation in most patients.
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However,
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this article investigated inulin,
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um,
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because it was found potentially to be protective,
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but it also has tumor-promoting effects.
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This article showed that there was a if you had a combination of
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pks-positive bacteria instilled into these mice that were prone.
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to develop cancer.
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They were APC mutated mice.
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Then they were treated with DSS to stimulate tumors.
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If those pks positive mice were also then given inulin,
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then it promoted tumors in those mice.
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If a strain of E.
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coli deficient in colibactin,
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same pks positive mice,
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but they did not produce colibactin.
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If that was introduced,
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instead of the tumors were found.
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If you gave a paraprobiotic,
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which was pasteurized E.
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coli,
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same strain defect,
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actually a Nissl strain,
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which was a pasteurized paraprobiotic that also inhibited the tumor agenesis.
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Very confounding results here,
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suggesting that it's not just the pks positive but potentially.
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Maybe the um competition in the intestines of these mice with either other strains of E.
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coli or a paraprobiotic that has good factors produced by certain
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probiotic strains that was tumor-protective.
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Other colon cancer issues,
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you certainly need a driver mutation.
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And so that driver mutation may be these colibactin-induced
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mutations that were induced as a child.
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And then you need pro-cancer passenger pro-progression bacteria.
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So there are certain bacteria that induce the either directly
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producing compounds that cause DNA damage or inflammation that causes that damage.
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And then,
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once there is a mutation causing a tumor.
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Now you might need passenger progression bacteria.
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And this is another theory that your microbiome is important.
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Fecal transplants from colon cancer mice can transfer the disease to germ-free mice.
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This was discovered in 2013,
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quite a while ago,
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suggesting that there is something about the something in the feces in general,
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the bacteria that then produce back colon cancer in these mice.
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Then there is also evidence that microbial dysbiosis can affect some
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tumorigenesis as well.
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There are short-chain fatty acids that bacteria produce that could stimulate polyps.
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And then there is in persons such as those with Lynch.
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Syndrome,
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which is a syndrome that is prone to develop colon cancer.
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The microbes,
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if they are present in those patients,
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can produce 8-oxoguanine.
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Those 8-oxoguanine lesions produce a mismatch repair system dysfunction and,
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hence,
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your production of colon cancer in those patients.
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And,
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as we talked about,
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dysbiosis causes inflammation,
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and that can lead to colorectal cancer.
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And what do we all need to do about this?
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And this is certainly not that controversial because transformation
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requires acquisition of mutations.
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Those mutations are in suppressors and oncogenes,
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and it begins in the intestinal stem cells and can develop.
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over the course of your life.
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Studies have shown that high-fiber diets low in processed foods and low in red meats,
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and exercise,
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and maintaining a healthy weight is protective from developing colon cancer.
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Carcinogenic microbes colonizing a large portion of humans can
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potentially alter their host genetics but also contribute to the
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carcinogenesis in a host that already is predisposed by their
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genetics or their dietary composition or inflammatory dysregulation.
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Now we have to think about what about as parents?
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Do we really need to think about our children if we are feeding them
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now processed foods and red meats?
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is this the reason why we're now seeing the rapid increase in
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younger patients developing colon cancer?
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Because think about it: from around the year of 2015,
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when we first started to see this increase,
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what is important about that date?
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What is approximately 40 years before that date?
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40 years before 2015 is 1975.
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1975 is when we started really ramping up the processed foods,
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the increased sugars in our diet,
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high fructose corn syrups,
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and multiple of other different dietary changes from the from the
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revolution of processed foods that occurred in this country in 1975.
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Now go to 1985 and the different changes we had.
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then That is approximately 40 years ago.
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Now what's it going to be like when we get to be 40 years from now
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and 40 years from maybe 10 years ago?
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Certainly,
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over the last 10 years we have had an improvement in recognition
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that high fiber diets are important,
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and the prevalence of persons who are eating more vegan food,
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more whole food diets is increasing slowly.
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But what's going to happen 40 years from now?
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Is that percent of individuals with colon cancer,
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is it going to be even higher than now?
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Is it going to be instead of an incidence of of 10 of colon cancers,
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is it going to be 50 of colon cancer?
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We're going to have a wave in 10,
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20 years where Instead of having 15,
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000 cases per year,
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are we going to have 50,
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000,
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or are we going to be having 100,
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000 cases per year and many more deaths until we start screening at age 40 or 35?
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Maybe even to take care of these polyps that were induced by the
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colibactin-producing E.
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coli.
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So something to think about,
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and that microbiome link,
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and what to do about our microbiome: probiotics,
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fiber,
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natural foods,
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whole foods,
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mostly plant-based diets.
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Going to be more and more studies that are going to elucidate the
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effects of these improved dietary changes to see if they make an
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impact on these colon cancer incidences.
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Or here's a question: Is it going to take many more years after that
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to discover that we need to have these whole food diets in the years
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from age zero and maybe in utero to from age zero to 10 years of age
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20 years of age when we're not thinking about our diet when we're
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feeding our kids a lot of red meat and a lot of proteins because we
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need to induce their growth.
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We think they want to be weightlifters,
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football players,
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baseball players.
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So we pile on and take them out for steak and take them out for low
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fiber diet restaurants and fast foods and all of that.
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Is it going to really take until we realize that it's our children
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that we need to protect and not at age 40 and age 50 like myself
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when I'm starting to have a better diet now because I am learning about these things.
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Is it going to take until then before we figure out that it is our
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children that we need to be really impacting in the future?
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Thank you very much for this.
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I will include the references.
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There are approximately five different references here that I'll
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include in the show notes for this.
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Certainly,
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Alberto Martin is one of the important authors of these articles,
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but there are multiple other people,
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including Dr.
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Santos and others who are involved in this.
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There is an organization in the UK and worldwide that is looking
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into these different factors as well.
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And I'll include that in the show notes as well.
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Thank you very much for attending,
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and thank you,
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and have a nice rest of your Sunday.
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