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Yet Another Reason to Not Eat Beef: Cancer-Causing Mutations

I stopped eating beef 5 years ago, following a trip to Costa Rica just days after being diagnosed with breast cancer. Our daughter had been urging us to give up red meat for more than a decade, but a lecture and slide show on the effect of cattle ranching on Costa Rica’s spectacular biodiversity, right after my diagnosis, finally did the trick. So compelling were the environmental and human health reasons to no longer eat beef that I barely dwelled on the obvious animal cruelty aspect.

Back home, I wrote about another anti-beef argument here at DNA Science: a sugar (a type of sialic acid) on our cell surfaces that is slightly different than versions on muscle cells of cattle and pigs. The cells of these animals make an enzyme that dismantles their form of sialic acid, but our cells don’t. As a result, the human immune system reacts to cow and pig muscle cells bearing sialic acid with its inflammatory response. Over time, thanks to hamburgers and steaks and ribs, risks of cardiovascular disease, arthritis, and cancer rise.

A few days ago, my husband and I returned from a second trip to Costa Rica. This time, we saw firsthand the stark difference between cattle grazing land and the plants-upon-plants-upon-plants that make up natural ecosystems. At a cloud forest conservation and restoration site near Carara National Park on the central Pacific coast, naturalist Edwin Ramirez gave a riveting presentation on efforts to reclaim pastureland and coax back the natural biodiversity. He has spent the past three decades restoring the forest, and he led our group on a hike through it.

Eating beef has long been associated with increased cancer risk. The grilled meat releases heterocyclic aromatic amines (HAAs), which are absorbed into the bloodstream and sent to the liver, where they’re metabolized into mutagens – chemical compounds that raise the risk of certain cancers. Broccoli and brussels sprouts have an anti-cancer effect because they produce glucosinolates. These molecules activate “xenobiotic metabolizing enzymes” that divert HAAs down a different, non-mutagenic pathway.

A recent report in Cancer Discovery from Marios Giannakis, MD, PhD, of Harvard Medical School and the Dana-Farber Cancer Institute and colleagues, fleshes out the mutational steps from a meat-heavy diet that trigger cancer-causing mutations in cells of the colon and rectum. The research provides a mechanism behind the long-noted link between eating red meat and increased colorectal cancer risk.

The International Agency for Research on Cancer declared processed meat carcinogenic and red meat probably carcinogenic to humans in 2015. And experiments in non-human animals linked eating red meat to formation of carcinogenic compounds in the colon.

“What (was) missing (was) a demonstration that colorectal cancers from patients have a specific pattern of mutations that can be attributed to red meat. Identifying these molecular changes in colon cells that can cause cancer would not only support the role of red meat in colorectal cancer development, but would also provide novel avenues for cancer prevention and treatment,” Giannakis said.

The researchers sequenced DNA from normal cells and colorectal cancer cells from 900 patients who were part of a nationwide investigation. The study also collected information on diet, lifestyle, and other health-related factors for several years before the cancer diagnoses.

Sequencing the DNA revealed several “mutational signatures” in cancer cells, including a set of mutations that indicate alkylation. This form of DNA damage arises from adding a methyl group (CH3). The alkylating signature was detected at a much higher level among participants who’d consumed a lot of processed or unprocessed red meat before cancer diagnosis, but not in people who’d eaten only fish or poultry. And the distal end of the colon was much more likely to have this form of DNA damage than the proximal (more internal) end.

Specifically, the study found that mutations in the genes KRAS and PIK3CA drive development of colorectal cancer. Patients who had the alkylating signature in their cancer cells face a 47 percent greater risk of death from the disease compared to patients with other mutations.

Said Giannakis, “These findings suggest that red meat consumption may cause alkylating damage that leads to cancer-causing mutations in KRAS and PIK3CA, promoting colorectal cancer development. Our data further support red meat intake as a risk factor for colorectal cancer and also provide opportunities to prevent, detect, and treat this disease.”

The finding has practical implications. Testing for these mutations in cells from stool samples could be used to identify people who are genetically predisposed to be at higher risk of developing colorectal cancer, alerting them to cut meat from their diets. The signature might also be used in earlier cancer detection or as a biomarker for prognosis.

The genetic links between eating a diet high in red meat and development of colorectal cancer present compelling justification for change. But even if that weren’t so, plant-based foods are so incredibly varied and abundant that consuming muscle tissue from animals just isn’t necessary.

CODA

Investigating the link between eating red meat and developing colorectal cancer provides a terrific example of the process of scientific inquiry, from association to correlation to possible cause.

• People who eat a lot of red meat have a higher likelihood of developing colorectal cancer: association.
• The more red meat in the diet, the higher the cancer risk: correlation.
• Cancer-causing mutations are more likely in the cancer cells of patients who eat a lot of red meat: evidence of a mechanism that might explain the association and correlation, revealing a possible cause.

But striking evidence isn’t proof. A different explanation might elude us, right now. For science is never final. The media’s misplaced focus on scientific “proof” may be contributing to the spread of misinformation about how the natural world, and technology, work.


Discussion
  1. This article conflates effects of processed meat with red meat and fails to differentiate people who consume only red meat from those that eat red meat and those that eat processed meat and red meat.

    These distinctions are important as there is very clear evidence that processed meat which had nitrates or nitrites added as preservative – produce nitrous amines during cooking that unprocessed red meat does not.

    Nitrosamines are highly carcinogenic and are responsible majority of cancer risk from processed meat. Failing to separate this large carcinogenic risk that forms the majority of risk in diets including both red meat and processed meat grossly inflates the implied risk from eating red meat.

    Overall the article reads as one written with highly selective facts to support conclusions drawn in advance. Thus the article suffers from confirmation bias.

    In addition the conclusions presented do not fit with what we see in populations who eat red meat or even high amounts of red meat. For example. Hunter gatherer populations who have v low incidence of colorectal cancer.

    1. Thank you. I focused on the sialic acid and new cancer gene findings because the nitrosamine link has been known for decades. I should have mentioned that. But this is a blog, and my intent was not to be comprehensive. Just to discuss new findings and how they affect me. So yes, if it was a journal article reporting research, there would have been confirmation bias. The sialic acid finding shouldn’t matter whether meat is processes or treated or not. That is what convinced me.

  2. Why is ‘was’ written in brackets?

    “What (was) missing (was) a demonstration that colorectal cancers……”

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