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Chemobrain in Colon Cancer
Chemobrain in colon cancer is a serious, life-altering side effect. I say this because I have struggled with chemobrain since my diagnosis of an incurable blood cancer called multiple myeloma.
When a friend, Bernie Davis, was diagnosed with colon cancer, I researched the common side effects of treatments for this prevalent cancer. Sure enough, according to research, both oxaliplatin and 5-fluorouracil (5-FU) are prescribed for colon cancer, and they both can cause chemobrain.
In my experience, the solution is to identify those therapies, conventional or non-conventional, that have been shown to reduce or even completely mitigate this side effect.
What non-conventional therapies have been shown to mitigate oxaliplatin and 5-fluorouracil-induced chemobrain in colon cancer survivors?
Short answer up front: there’s no single proven “cure” for oxaliplatin/5-FU chemobrain in colon-cancer survivors, but multiple non-pharmacological (non-conventional) approaches have shown benefit for chemotherapy-related cognitive impairment (CRCI) in cancer survivors — and several of those approaches have mechanistic or (preclinical + clinical) evidence specifically relevant to 5-FU / oxaliplatin.
The strongest, most reproducible options are exercise, cognitive rehabilitation / computerized cognitive training, mind-body therapies (mindfulness / CBT), and diet / gut-microbiome approaches (including emerging probiotic / omega-3 hypotheses). Below I summarize the evidence and practical takeaways.
What the evidence shows (by therapy)
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Exercise (aerobic + resistance, structured programs)
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Multiple reviews and randomized trials show that supervised or structured exercise programs improve self-reported cognitive function after chemotherapy and sometimes objective tests (effects vary by study and outcome). Exercise also improves fatigue, mood and sleep — all of which strongly influence “brain fog.” Exercise has biological plausibility (reduced neuroinflammation, improved neurogenesis/perfusion). PubMed+1
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Cognitive rehabilitation / computerized cognitive training
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Several randomized and controlled trials (group training, Attention Process Training, computerized “brain training”) produced improvements in subjective cognitive function and some objective domains (processing speed, working memory). These interventions are among the most evidence-backed non-drug treatments for CRCI. PubMed+1
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Mind-body therapies — mindfulness, MBSR, CBT for cognition
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Mindfulness-based stress reduction (MBSR) and cognitive behavioral interventions for cognitive complaints have shown durable improvements in self-reported cognition, anxiety, and quality of life in cancer survivors. They’re low risk and commonly recommended. PMC+1
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Dietary patterns, omega-3s and the MIND diet
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Observational and mechanistic work links Mediterranean / MIND-style diets and omega-3 fatty acids with better cognitive outcomes after cancer treatment; randomized trials in cancer patients are sparse, but the biology (anti-inflammatory, neuroprotective) supports the approach as an adjunct. SpringerLink+1
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Gut-microbiome modulation (probiotics, prebiotics, diet)
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Chemotherapies such as 5-FU disrupt the gut microbiome; preclinical and emerging human data support the idea that restoring microbiome balance can reduce neuroinflammation and behavioral/cognitive symptoms. Human RCT evidence is early but promising in other cancer populations. PMC+1
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Preclinical / drug-specific findings (oxaliplatin & 5-FU)
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Animal models using 5-FU and oxaliplatin have reproduced cognitive deficits and show that physical activity (and some anti-inflammatory nutritional strategies in animals) can mitigate those deficits — i.e., there is direct mechanistic evidence linking exercise to protection from 5-FU/oxaliplatin neurotoxicity (but human colon-cancer-specific RCTs are limited). PubMed+1
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Strength of evidence & limitations
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Most high-quality RCT evidence for CRCI comes from mixed-cancer cohorts (many breast-cancer studies). Direct RCT evidence that specifically enrolls colon-cancer survivors treated with oxaliplatin+5-FU is limited. So recommendations are extrapolated from broader CRCI literature plus specific preclinical work on oxaliplatin/5-FU. The overall conclusion: these non-pharmacological interventions are low-risk, plausibly effective, and recommended as frontline approaches, but large colon-cancer-specific trials are still needed. PMC+1
Safety & caveats
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Supplements (high-dose omega-3, herbal remedies) can interact with chemo/anticoagulants — always check with your oncologist. Probiotics are generally safe for most survivors but should be used cautiously in those with severe immunosuppression or central lines. Wiley Online Library
Chemobrain from oxaliplatin and 5-fluorouracil is a known side effect. Bernie Davis has the opportunity to explore therapies before, during and after conventional treatments with the goal of reducing or preventing this side effect altogether.
Scroll down the page and post a comment or your experiences with chemobrain.
Thank you,
David Emerson
- Cancer Survivor
- Cancer Coach
- Director PeopleBeatingCancer
Neurocognitive Effects of Chemotherapy for Colorectal Cancer: A Systematic Review and a Meta-Analysis of 11 Studies
Purpose
Chemotherapy-related cognitive impairment (CRCI) is a controversial concept not much explored on colorectal cancer patients.
Materials and Methods
We identified 11 prospective studies: eight studies on 696 colorectal cancer patients who received chemotherapy and three studies on 346 rectal cancer patients who received neoadjuvant chemoradiotherapy. Standardized mean differences (SMDs) of neuropsychological test results and the cognitive quality-of-life scale were calculated using random effect models. A meta-regression was conducted to investigate the association between mean study population age and effect sizes.
Results
The association between chemotherapy and cognitive impairment was not clear in colorectal cancer patients (SMD, 0.003; 95% confidence interval, −0.080 to 0.086). However, a meta-regression showed that older patients are more vulnerable to CRCI than younger patients (β=–0.016, p < 0.001).
Conclusion
Chemotherapy has an overall positive negligible effect size on the cognitive function of colorectal patients. Age is a significant moderator of CRCI.
Cognitive dysfunction in chemobrain: Molecular mechanisms and therapeutic implications
Abstract
Chemotherapy-induced cognitive impairment (CICI), commonly referred to as chemobrain, is a prevalent side effect of cancer treatment that severely affects survivors’ quality of life. Chemotherapeutic agents, including:
- cisplatin,
- doxorubicin,
- and paclitaxel,
cross the blood-brain barrier (BBB) and induce neurotoxicity, resulting in cognitive dysfunction. These agents trigger reactive oxygen species (ROS) generation, cause mitochondrial dysfunction, and induce DNA damage, all of which impair synaptic plasticity and neurogenesis.
Mitochondrial dysfunction is central to chemobrain, as it disrupts ATP production, increases oxidative stress, and leads to neuronal apoptosis. Furthermore, mitochondrial DNA (mtDNA) damage caused by agents like cisplatin impairs oxidative phosphorylation, exacerbating neuronal degeneration.
The molecular mechanisms of chemobrain likely involve several key players, including NAMPT-dependent NAD+ depletion and increased levels of Cyclooxygenase-2 (COX-2), which collectively exacerbate oxidative stress and neuroinflammation. Another important molecular target is the Adenosine A2A receptor (A2AR).
When activated, it contributes to synaptic dysfunction and cognitive decline, particularly in chemotherapy-related cognitive deficits in the hippocampus. This review explores the complex interplay of these core pathologies in chemobrain and discusses how targeting these pathways could offer a therapeutic strategy to alleviate cognitive impairments in cancer survivors.
Chemobrain in colon cancer Chemobrain in colon cancer Chemobrain in colon cancer