Cancer Companion Guide

The metabolic processes that help your body use food for energy and nourishment are extremely complex. The hormone insulin is a key player. When you eat, sugars from the food enter your bloodstream, which triggers your pancreas to release insulin. That insulin helps the sugar get into your cells to be used for energy. The insulin then ushers any extra sugar to your liver to be stored for later. Insulin also helps your body break down and use lipids, or fats. The amount of insulin in your body goes up and down according to how much sugar is in your bloodstream. But several factors can make your cells resistant to insulin. As a result, your blood sugar and insulin levels will be chronically elevated. Why Obesity and Insulin Resistance Reduce Immunotherapy Effectiveness Short answer: because immunotherapy depends on a metabolically fit immune system — and obesity and insulin resistance reprogram immunity in ways that blunt anti‑tumor response. This article explains how metabolic ...

GLP-1 receptor agonists such as Semaglutide and Tirzepatide have transformed the treatment of obesity and type 2 diabetes. As their use expands globally, a critical question is emerging: Do GLP-1 drugs reduce cancer risk — or is any apparent benefit simply a consequence of weight loss and improved metabolic health? This article reviews: The established link between obesity and cancer The biological mechanisms affected by GLP-1 therapy Human clinical trial data Observational cancer incidence studies Safety signals (including thyroid cancer) What remains unknown All claims below are supported by peer-reviewed sources. 1. Obesity and Cancer: Established Evidence The link between obesity and cancer is well established. The International Agency for Research on Cancer concluded in 2016 that excess body fat increases the risk of at least 13 cancers (1). Key cancers linked to obesity include: Colorectal Postmenopausal breast Endometrial Pancreatic Liver Mechanisms supported by human and transl...

Cancer staging tells us where the tumor is.  Insulin resistance tells us what kind of body the tumor is growing in. Modern oncology places enormous faith in staging systems. TNM categories, AJCC groupings, and increasingly granular molecular subtypes are used to estimate prognosis, guide treatment, and reassure patients. Yet clinicians and patients alike encounter a persistent paradox: Two patients. Same cancer. Same stage. Same treatment. Radically different outcomes. Staging explains part of the story — but not nearly enough. A growing body of evidence suggests that host metabolic health, particularly insulin resistance, often predicts outcomes more reliably than tumor stage alone. This is not an argument against staging. It is an argument that staging is incomplete. What Cancer Staging Measures — and What It Ignores Cancer staging excels at describing tumor geography : Tumor size Lymph node involvement Distant spread What it largely ignores: Insulin and glucose dynamics Inflamma...

Evidence Summary Overall Evidence Grade: A (Strong Clinical Evidence) Multiple randomized controlled trials, meta-analyses, and international oncology guidelines show that exercise, nutrition optimization, vitamin D sufficiency, sleep support, and stress reduction improve cancer-related outcomes when used alongside standard cancer treatments . These interventions are associated with: Improved treatment tolerance Reduced cancer-related fatigue Better quality of life Improved survival in several cancer types These approaches are adjunctive, not curative, and must not replace evidence-based oncology care. What Does the Evidence Say About Lifestyle and Cancer Outcomes? Cancer outcomes are influenced not only by tumor genetics, but also by the biological environment of the patient . Across cancer types, worse outcomes are consistently linked to: Insulin resistance and metabolic dysfunction Chronic systemic inflammation Immune suppression Neuroendocrine dysregulation (stress hormones) Muscl...

Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest human malignancies, with a five-year survival rate stubbornly below 15% despite decades of advances in surgery, chemotherapy, and molecular oncology. Most discussions focus on late diagnosis, aggressive genetics, or therapeutic resistance. Far less attention is paid to a quieter but increasingly evident factor: insulin resistance and metabolic dysfunction . Emerging evidence suggests that pancreatic cancer is not merely influenced by metabolic disease—it may be deeply intertwined with it . Insulin resistance often precedes diagnosis, worsens prognosis, and biologically fuels tumor growth. Yet it remains largely absent from staging systems, risk stratification, and treatment frameworks. A 2023 study from researchers at University of British Columbia’s Faculty of Medicine reveals a direct link between high insulin levels, common among patients with obesity and type 2 diabetes, and pancreatic cancer. The study, published...

1. Current Clinical State: The Limitations of Standard-of-Care (SOC) in Stage 4 PDAC Pancreatic Ductal Adenocarcinoma (PDAC) represents a masterclass in therapeutic resistance. Its aggressive biology is underscored by the fact that over 90% of tumors harbor activating mutations in the KRAS oncogene, driving rapid progression and an inherent resilience to single-agent interventions. In the 2025 landscape, metastatic PDAC remains defined by therapeutic inertia; despite the evolution of multi-agent chemotherapy, the historical failure rates of conventional regimens persist. For patients with stage 4 disease, the strategic necessity to pivot toward novel interventions is no longer a peripheral academic debate but a clinical mandate, given that the historical median survival for metastatic disease often languishes between 3 to 6 months without aggressive intervention. The frontline standards, NALIRIFOX and FOLFIRINOX, represent the peak of fluoropyrimidine-based cytotoxic intensity, yet th...

Pancreatic ductal adenocarcinoma (PDAC) remains among the most treatment-resistant solid tumors. Despite decades of molecular characterization and incremental therapeutic advances, durable responses are rare, and recurrence is nearly universal. Across this landscape, a clear pattern emerges: combination therapies repeatedly outperform single-agent strategies in preclinical studies. Whether framed as targeted drug pairings, multi-agent regimens, or systems-level interventions, contemporary research consistently emphasizes that PDAC cannot be effectively controlled through single-mechanism interventions. This article examines the biological rationale for this convergence, with particular attention to cancer stem cells (CSCs) as a central driver of resistance and relapse. Pancreatic Cancer as an Adaptive System Traditional drug development assumes that disabling a dominant driver is sufficient to halt tumor progression. In PDAC, this assumption is challenged by several features: Extensiv...

Executive Summary In recent years, two seemingly distant worlds of cancer research have begun to converge in unexpected ways. On one side, mainstream oncology is increasingly focused on multi-drug combination strategies designed to block oncogenic drivers and preempt resistance. On the other, interest has grown around repurposed drug combinations — such as ivermectin, fenbendazole, and mebendazole — proposed to exert anticancer effects through metabolic and cellular stress pathways. While these approaches differ profoundly in evidentiary strength, regulatory status, and clinical readiness, they share a common conceptual foundation: cancer is an adaptive system that rarely yields to single-target intervention . Understanding where these strategies align — and where they fundamentally diverge — is essential for separating scientific insight from speculation. Diverse cancer hallmarks targeted by repurposed non-oncology drugs. This figure was created with Biorender.com. Source:  Nat...