Lower Your Serum Insulin Level to Reduce the Risk of Cancer, Diabetes, and Live Longer.
- David S. Klein, MD FACA FACPM
- Oct 1
- 7 min read
Why Lowering Insulin Matters: Inflammation, Cancer Risk, and Insulin Resistance—What the General Public Should Know
Most of us recognize insulin as the hormone that helps move glucose from the blood into our cells. Less widely appreciated is the fact that persistently elevated insulin—often called hyperinsulinemia—is not benign. It is part of a broader metabolic picture that fuels chronic, “smoldering” inflammation, accelerates insulin resistance, and is epidemiologically linked with higher risks for several cancers. The encouraging news is that everyday choices—what we eat, how we move, how we sleep—can lower insulin levels and shift that biology in our favor.
This essay lays out, in plain language, why insulin matters and how to act on it—grounded in clinical and mechanistic research.
In short, the insulin level, the greater the harm.
Insulin is a powerful growth and storage signal. In the right context—after a meal—it helps muscles and the liver absorb glucose, promotes glycogen storage, and tempers the liver’s own glucose output. When insulin is chronically elevated, however, tissues become less responsive (insulin resistance), the pancreas compensates by producing even more insulin, and a self‐reinforcing cycle develops. Over time, that cycle intertwines with inflammatory pathways and adverse cell-growth signals. Reviews over the last decade synthesize evidence that hyperinsulinemia is implicated in metabolic inflammation, aging biology, and cancer-promoting processes. E-DMJPMC
Excess energy intake—especially ultra-processed foods rich in refined starches and sugars—promotes fat storage in adipose tissue. As fat cells enlarge, they release danger signals and attract immune cells (particularly macrophages). Those immune cells and stressed adipocytes secrete cytokines like TNF-α, IL-6, and MCP-1, which activate inflammatory cascades (NF-κB, JNK). The result is chronic low-grade inflammation that further impairs insulin signaling in liver, muscle, and fat, raising insulin levels still more. This bidirectional loop—sometimes called metaflammation—is now a central model for obesity-related insulin resistance. Nature+1PMC
Clinically, you can sometimes “see” the loop using simple markers. Waist circumference tracks visceral adiposity; high triglycerides with low HDL suggest hepatic insulin resistance; high-sensitivity CRP (hs-CRP) is one marker of systemic inflammation. While no single test tells the whole story, the pattern often points to the same biology.
Cancer risk and progression are influenced by many factors, but one repeatedly observed theme is the insulin/IGF-1 axis. Insulin and insulin-like growth factors activate PI3K–AKT–mTOR and MAPK pathways that promote cell survival and proliferation; chronically elevated signaling may create a more permissive environment for tumor initiation and growth. Epidemiologic studies link higher fasting insulin or C-peptide (a proxy for endogenous insulin secretion) with greater risk of colorectal and certain endocrine-related cancers, and diabetes itself is associated with increased colorectal cancer risk. Mechanistic reviews and large observational syntheses converge on this axis as biologically plausible and clinically relevant, though causality and effect sizes vary by tumor type and study design. PMC+1PubMed
The prudent takeaway is not that insulin “causes” cancer in a simple linear way, but that metabolic health—lower fasting insulin, less visceral adiposity, improved insulin sensitivity—likely shifts risk in the right direction.

Practical ways to lower insulin and calm inflammation
1) Choose a dietary pattern that blunts insulin spikes—and is sustainable
Two broad strategies consistently help:
Mediterranean-style eating. High in vegetables, legumes, nuts, fish, olive oil, and minimally processed whole grains, this pattern is associated with lower insulin resistance and improved cardiometabolic markers—independent of weight loss. Recent syntheses show better HOMA-IR and post-challenge insulin sensitivity with higher adherence. PMCBioMed Central
Lower glycemic load (GL) approaches. Emphasizing fiber-rich carbohydrates, intact whole grains, legumes, and reduced refined starch/sugar leads to smaller post-meal glucose and insulin excursions. A large evidence review suggests low-GI/GL dietary patterns produce modest but meaningful improvements in glycemic control, lipids, blood pressure, adiposity, and inflammation—particularly in people with diabetes. PMC
No single macronutrient ratio fits everyone, and trials differ on whether lowering glycemic index/load independently reduces inflammatory cytokines. That said, prioritizing fiber-rich, minimally processed foods is a robust, pragmatic way to reduce both insulin demand and inflammatory tone. PubMed
A word on intermittent fasting (IF) and time-restricted eating (TRE). IF can lower fasting insulin and improve insulin sensitivity for many people, in part by extending periods of low insulin (“metabolic switching”). A major review and randomized trials—especially early time-restricted feeding—support improvements in insulin sensitivity and related risk markers. However, IF is not universally superior to other calorie-controlled approaches; the “best” method is the one you can sustain safely. New England Journal of MedicineNature
Fiber is your friend. Soluble fiber slows glucose absorption, feeds the gut microbiome, and yields short-chain fatty acids that improve insulin signaling and inflammatory tone. Recent reviews and trials show that higher fiber intake—particularly from whole foods—supports insulin sensitivity and glycemic control. MDPI
2) Move your body—consistently
Regular physical activity is a potent insulin sensitizer. Meta-analytic data show that aerobic and combined (aerobic + resistance) programs lower fasting insulin and HOMA-IR; resistance-only programs can still help (especially for muscle mass and glucose disposal), but combined training generally produces the most reliable improvements in insulin biology. Aim for at least 150–300 minutes/week of moderate aerobic activity plus 2–3 sessions/week of resistance training. PMC
3) Lose a little (or a lot) of visceral fat
Even 5–10% weight loss can substantially reduce fasting insulin and inflammation, with larger losses (when appropriate and safe) yielding larger metabolic dividends. In people with prediabetes, an intensive lifestyle program targeting ~7% weight loss and regular activity cut progression to type 2 diabetes by 58% over ~3 years—far outperforming metformin in that trial—underscoring how strongly lifestyle affects insulin resistance risk. New England Journal of Medicine
4) Sleep like it’s your job
Short or disrupted sleep impairs insulin signaling after just a night or two, and chronic sleep curtailment promotes weight gain and insulin resistance via appetite hormones and sympathetic activation. Guarding 7–9 hours of regular, high-quality sleep is a practical, under-appreciated insulin-lowering intervention. The Lancet
5) Tame chronic stress
Psychophysiologic stress raises counter-regulatory hormones (cortisol, catecholamines) that antagonize insulin. Mind-body practices, social connection, and exposure to daylight and nature are not mere niceties; they alter autonomic tone and can lower cardiometabolic risk over time. (Pair this with the sleep guidance above for compounding benefits.)
How (and whether) to measure insulin
Glucose-centric tests (fasting glucose, oral glucose tolerance, HbA1c) are standard. Fasting insulin and HOMA-IR can add context, especially in earlier stages when glucose still looks “normal.” C-peptide sometimes helps when teasing out endogenous insulin production (e.g., differentiating pancreatic reserve in diabetes phenotypes) and has been used in research on cancer risk, but it’s not a routine cancer screen. Discuss with your clinician which tests, if any, will change management for you personally.
In my practice, I check insulin levels simultaneously with glucose and HgA1c. By doing this, I get a good view into past metabolic activity with the HgA1c, present situation with the blood glucose, and future issues with the Insulin level.
Safety and special situations
If you’re on glucose-lowering medications (especially insulin or sulfonylureas), dietary shifts and fasting protocols require medical supervision to avoid hypoglycemia. People with eating disorders, frailty, pregnancy, or certain endocrine conditions need tailored plans. For many, the safest and most sustainable first steps are Mediterranean-style meals, more daily movement, better sleep, and stress hygiene.
A pragmatic 6-week blueprint
Plate pattern at each meal: half non-starchy vegetables; a palm-sized portion of protein; a thumb-sized portion of healthy fat; and a fist-sized portion of intact, fiber-rich carbs (or fruit).
Fiber target: work toward ≥30–40 g/day from legumes, vegetables, whole grains, nuts, seeds, and fruit.
Glycemic load swaps: replace refined grains and sugary beverages with water/tea/coffee (minimal sweetener), steel-cut oats or barley, intact brown rice or quinoa, lentils/beans. PMC
Movement “minimum viable dose”: 30 minutes brisk walking most days + two short resistance sessions (push-pull-legs basics). PMC
Sleep routine: fixed sleep/wake times, dim evening light, cool/dark bedroom, morning daylight. The Lancet
Optional TRE trial: consider a 10–12-hour eating window (e.g., 8 am–6 pm) for 3–4 weeks; avoid aggressive fasting if you use insulin/secretagogues or have a history of disordered eating. Nature
Track what matters: waist circumference, fasting triglycerides/HDL ratio, and—if appropriate—fasting insulin or HOMA-IR with your clinician every few months.
Vitamins, Minerals and other Supplements: These will be covered in subsequent Blogs.
Bottom line
Lowering chronically elevated insulin is not about chasing a number; it is about changing the terrain in which inflammation and insulin resistance take root—and where cancer-promoting signals can gain a foothold. Nutrient-dense, lower-GL eating; fiber; consistent movement; adequate sleep; and stress control are the most durable levers we have. They are also the least expensive and the most broadly beneficial across chronic disease domains.
References
Zhang AMY, et al. Hyperinsulinemia in Obesity, Inflammation, and Cancer. Diabetes Metab J. 2021. doi:10.4093/dmj.2020.0250. E-DMJ
Szablewski L. Insulin Resistance: The Increased Risk of Cancers. Int J Mol Sci. 2024. (Open access.) PMC
Li M, et al. Trends in insulin resistance: insights into mechanisms and therapeutics. Signal Transduct Target Ther. 2022. Nature
Guria S, et al. Adipose tissue macrophages and their role in obesity-induced inflammation and insulin resistance. Front Endocrinol. 2023. PMC
Sethi JK, et al. Metabolic Messengers: tumour necrosis factor (TNF). Nat Metab. 2021. Nature
Yu GH, et al. Diabetes and Colorectal Cancer Risk. Cancers (Basel). 2022. PMC
Chen L, et al. Circulating C-peptide level is a predictive factor for colorectal neoplasia. J Gastroenterol Hepatol. 2013 (meta-analysis). PubMed
Zhong W, et al. Obesity and endocrine-related cancer: the important role of the IGF system. Front Endocrinol. 2023. PMC
de Cabo R, Mattson MP. Effects of Intermittent Fasting on Health, Aging, and Disease. N Engl J Med. 2019. New England Journal of Medicine
Xie Z, et al. Randomized controlled trial of early time-restricted feeding: improvements in insulin sensitivity and inflammatory markers. Nat Commun. 2022. Nature
Kazeminasab F, et al. Effects of exercise training on insulin resistance: meta-analysis. BMC Endocr Disord. 2023. PMC
Vetrani C, et al. Mediterranean diet adherence and insulin resistance in overweight/obesity. Nutrients. 2023. PMC
Zheng X, et al. Mediterranean diet and cardiometabolic risk: meta-analysis. BMC Nutr. 2024. BioMed Central
Chiavaroli L, et al. Low-GI/GL dietary patterns: effects on glycemic control, lipids, BP, adiposity, and inflammation. BMJ (systematic review/meta-analysis), 2021. PMC
Diabetes Prevention Program Research Group. Reduction in the Incidence of Type 2 Diabetes with Lifestyle Intervention or Metformin. N Engl J Med. 2002. New England Journal of Medicine
David S. Klein, MD, FACA, FACPM
1917 Boothe Circle, Suite 171
Longwood, Florida 32750
Tel: 407-679-3337
Fax: 407-678-7246









