Life Extension Magazine®

Woman holding glucose test meter to finger of hand

Overlooked Dangers of Insulin and Glucose Spikes

With age, cells become insulin resistant and lose their ability to efficiently process glucose. Two plant extracts have been shown to slash after-meal insulin by 56% and after-meal glucose by 15% in human trials.

Scientifically reviewed by: Dr. Amanda Martin , DC, in October 2024. Written by: Michael Downey.

After a meal, blood-glucose levels increase and our pancreas responds by secreting insulin.

In youth, there is a delicate balance that drives glucose into cells mostly for energy production. Once blood-glucose levels drop to a fasting range, insulin production subsides.

With age, a sedentary lifestyle, and a diet featuring refined carbohydrates and simple sugars, our cells become insulin resistant, which allows blood-glucose levels to rise.

Rising glucose levels trigger the pancreas to release more insulin to counter the glucose—creating a vicious cycle.1

These factors promote weight gain and other metabolic disturbances.

As weight accumulates, fat cells pour out cytokines, which generate inflammation throughout the body.2,3

The medical term for this condition is hyperinsulinemia. It sets the stage for age-related diseases like atherosclerosis, hypertension, lipid abnormalities, type II diabetes, obesity, and cancer.4-15

Two plant extracts have been identified that block damaging insulin and glucose surges. In human trials, one of these extracts slashed after-meal insulin by 56% and after-meal glucose by 15%.

After-meal spikes in blood glucose are an important indicator of glycemic control. One of these plants extracts completely reversed the glucose surge within two hours.

Since insulin is required to sustain life, the public mistakenly sees this hormone in a favorable light.

As you will learn in this article, too much insulin not only contributes to weight gain, but to a multitude of diseases associated with obesity.

Excess blood levels of the hormone insulin occur in response to poor dietary choices, lack of physical activity and normal aging.

The medical term that defines the pancreas over-secreting insulin is hyperinsulinemia.

Excess insulin remaining in the blood after a meal has been identified as a major cause of nonalcoholic fatty liver disease.16,17

Hyperinsulinemia is an independent risk factor for kidney disease among metabolic syndrome patients.18

High insulin blood levels are predictive of type II diabetes and strongly associated with obesity.19,20

What you need to know

  • Modern medicine’s reliance on fasting plasma-glucose tests for yearly examinations means that lethally high after-meal insulin and glucose levels are often missed for years.
  • By the time glucose abnormalities are caught, excess insulin has likely already caused immense damage.
  • Fortunately, maqui-berry extract has been verified in human studies to delay glucose absorption—crushing after-meal insulin by up to 56% and glucose by 15%—and to lower HbA1c readings by 0.3% (from 5.65% to 5.35%).
  • Additionally, human research demonstrates that a natural clove extract inhibits hepatic glucose release, reversing after-meal glucose within two hours.

Link Between Elevated Insulin and Cancer

Insulin and Cancer  

A number of published studies indicate that high insulin levels drive the development and progression of many types of malignancies.2,21,22

Human studies implicate high insulin levels in at least seven common cancers:

  • Colorectal cancer: 17% to 42% greater risk of precancerous adenomas23-25
  • Breast cancer: 2- to 3-fold higher risk27
  • Stomach cancer: 69% to 101% higher risk26
  • Endometrial cancer: 45-fold greater risk for type I endometrial (uterine lining) cancer28
  • Ovarian cancer29
  • Prostate cancer: 2.55-fold risk of malignancies30 and a 5.62-fold risk of locally advanced tumors31
  • Liver cancer: 2.4-fold risk among those with both hepatitis B and high insulin levels.32

Elevated insulin levels are associated with the development of more aggressive and metastatic cancers that carry a grim prognosis.33,34

These alarming figures have inspired researchers to find out why there’s such a close connection between high insulin levels and cancer. And in just the past few years, researchers have uncovered mechanisms behind this deadly insulin/cancer connection.

Why Insulin Promotes Cancer

High levels of insulin trigger rapid cell division, while at the same time elevated blood sugar and fat levels provide metabolic fuel for tumor expansion.2,35

In response to chronically elevated insulin/glucose some cells lose control of their DNA regulatory genes—which is the hallmark of malignancy. This sequence of events is believed to promote cancer, at least in colon cells and possibly in those throughout the body.2

By its very nature, insulin is a growth factor, which means it naturally stimulates cell growth. The problem is that once a cancer cell has emerged, too much insulin results in overstimulation. This results in greater proliferation, migration, and invasiveness of cancer cells—all of the factors that make them so deadly.33,36

These cancer-promoting effects of insulin were shown vividly when scientists injected colon cancer cells into mice and then fed them either a normal or high-calorie diet. The high-calorie-diet mice had elevated levels of insulin and other growth-promoting molecules. As a result, their tumors grew to twice the size of tumors in the normal-diet group—in just 17 days.37

Another reason excess insulin promotes cancer is because it causes damaging oxidative stress.

When researchers applied a small amount of insulin to cell cultures, enough oxidative stress was generated from just a single exposure to damage DNA strands.34,36 When they extended the exposure to six days, the amount of insulin required to induce similar damage was reduced by a factor of 10.36 This demonstrates how chronically elevated insulin rapidly escalates DNA damage.

Studies have also revealed a close relationship among body size, type II diabetes, and many cancers.2,21 A diet rich in readily digested sugars and carbohydrates, for example, has been shown to increase the risk of developing a common form of breast cancer (estrogen receptor-negative) by 36%-41%.35

The connection between high insulin levels and cancer adds a strong rationale to suppress after-meal insulin and glucose surges.

In a timely development, scientists have demonstrated two plant extracts that target after-meal insulin and glucose levels.

Maqui-Berry Extract Slashes After-Meal Insulin and Glucose

Maqui Berries
Maqui Berries

Maqui-berry extracts have been shown to decrease after-meal rises in both glucose and insulin.

Research suggests that a proprietary extract of maqui berries contains potent compounds known as delphinidins.

Delphinidins stimulate a peptide that lowers after-meal blood glucose and can help moderate insulin spikes. The peptide stimulated by maqui-derived delphinidins is glucagon-like peptide-1 (GLP-1).38

GLP-1 slows and delays stomach-emptying, so glucose from a meal reaches the absorptive tissue in the small intestine later, and in lower quantities, than it would otherwise.39,40

In a human trial, ten volunteers were enlisted whose fasting glucose levels were normal (under 100 mg/dL) but whose after-meal glucose levels, after a standard white rice meal, were between 100 mg/dL and 125 mg/dL (considered altered glucose tolerance).41

Participants took either a placebo or 200 mg of maqui-berry extract 30 minutes before eating a small meal of 75 grams (about 2.5 ounces) of white rice, calculated to produce a rise in after-meal glucose levels.

The placebo group’s after-meal glucose levels peaked after one hour, at about 115 mg/dL.

By contrast, the after-meal glucose levels in the maqui-berry group had only risen to 98 mg/dL after one hour, a 15% difference. As an added benefit, their glucose levels did not peak for a full two hours after the meal. Even then, they reached a high of about 107 mg/dL.41

The effect on insulin levels was more dramatic. After the meal, insulin concentrations in the placebo group rose steadily until they reached an average of 25.33 µIU/ml after one hour. In sharp contrast, the maqui-extract group’s insulin levels increased much more slowly, reaching an average of only 11.22 µIU/ml after an hour—a compelling 56% lower insulin level!41

In fact, insulin levels in the maqui-extract group did not peak until a full hour and a half after the meal. Even then, it peaked at a much lower level than the placebo group.41

Maqui-Berry Extract Reduces Long-Term Glucose Levels

A separate study showed that maqui-berry extract can impact chronically elevated glucose levels as well.42

For the study, a group of newly identified prediabetic individuals took 180 mg of standardized maqui-berry extract every morning for 90 days. Follow-up tests occurred at 30, 60, and 90 days.42

On follow-up testing days, researchers measured the participants’ hemoglobin A1c (HbA1c) blood levels. Unlike an after-meal glucose reading, which tells you what your glucose levels are at that moment in time, the HbA1c measures how high glucose has been over the past three to four months. The normal value for HbA1c is 5.6% or lower.43

The researchers documented that maqui-berry extract reduced HbA1c levels by 0.3% (from 5.65% to 5.35%).42

No serious adverse events were observed in either of these clinical trials.41,42

Clove Extract Prevents Glucose Spikes

Cloves
Cloves

Clove extract is an excellent complement to maqui berry because of its impressive ability to control after-meal blood glucose.

In an exciting study, investigators found that a water-soluble extract of the clove flower bud (Syzygium aromaticum) reduced after-meal blood sugar.44

Clove extract contains polyphenols that can regulate glycogen phosphorylase, the enzyme responsible for releasing glucose into the bloodstream that is stored in the liver and muscles in the form of glycogen.45

This typically happens under stress or low nutrient availability, But with aging, too much stored glucose is often chronically released from liver stores.

Inhibiting glycogen phosphorylase with clove can help block excess glucose release into the bloodstream.

These benefits were seen when clove extract was given to diabetic mice, where it suppressed both blood-glucose elevations and HbA1c readings.45

But would it reduce after-meal glucose spikes in humans as well?

To answer that question, scientists divided a group of healthy volunteers into two groups according to baseline glucose levels: one with normal glucose levels and one with high-glucose. All subjects received 250 mg of clove extract daily for 30 days.44

Random blood-glucose levels were measured before supplementation, and again on days 12, 24, and 30. Additional blood draws were done two hours after a typical lunch.44

For both groups, glucose readings fell significantly at day 12—and they continued to drop throughout the study until the after-meal glucose values were about the same level as the before-meal values!44

The high-glucose group showed greater improvement, indicating greater benefit for this at-risk population. No one experienced abnormally low blood-glucose, making clove extract safer than hypoglycemic drugs that can trigger dangerously low readings.44

Summary

Summary  

With aging, a sedentary life, and ingestion of sugars and starch, after-meal insulin and glucose spikes can escalate to a chronic state of hyperinsulinemia, a risk for multiple age-related diseases including cancer.

Most individuals rely on a fasting blood glucose test from annual physical exams, but high after-meal insulin levels can be missed for many years.

When glucose abnormalities are finally detected, severe insulin-driven damage has likely already occurred.

Human studies have validated two plant extracts that can reverse this trend.

Maqui-berry extract has been shown to slash after-meal insulin up to 56%, glucose by 15%, and HbA1c by 0.3% (from 5.65% to 5.35%).

And clove extract reverses after-meal glucose surges within two hours.

Inasmuch as excess insulin and glucose levels promote disease and accelerate aging, these two plant extracts provide powerful support for a healthy longevity program.

If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.

References

  1. Wolever TM. Dietary carbohydrates and insulin action in humans. Br J Nutr. 2000;83 Suppl 1:S97-102.
  2. Gunter MJ, Leitzmann MF. Obesity and colorectal cancer: epidemiology, mechanisms and candidate genes. J Nutr Biochem. 2006;17(3):145-56.
  3. Khan S, Shukla S, Sinha S, et al. Role of adipokines and cytokines in obesity-associated breast cancer: therapeutic targets. Cytokine Growth Factor Rev. 2013;24(6):503-13.
  4. Burnol AF, Morzyglod L, Popineau L. [Cross-talk between insulin signaling and cell proliferation pathways]. Ann Endocrinol (Paris). 2013;74(2):74-8.
  5. Balkau B, Kahn HS, Courbon D, et al. Hyperinsulinemia predicts fatal liver cancer but is inversely associated with fatal cancer at some other sites: the Paris Prospective Study. Diabetes Care. 2001;24(5):843-9.
  6. Chu NF, Spiegelman D, Hotamisligil GS, et al. Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men. Atherosclerosis. 2001;157(2):495-503.
  7. Godsland IF, Crook D, Walton C, et al. Influence of insulin resistance, secretion, and clearance on serum cholesterol, triglycerides, lipoprotein cholesterol, and blood pressure in healthy men. Arterioscler Thromb. 1992;12(9):1030-5.
  8. Goldstein BJ. Insulin resistance as the core defect in type 2 diabetes mellitus. Am J Cardiol. 2002;90(5a):3g-10g.
  9. Karhapaa P, Malkki M, Laakso M. Isolated low HDL cholesterol. An insulin-resistant state. Diabetes. 1994;43(3):411-7.
  10. Ko GT, Cockram CS, Woo J, et al. Obesity, insulin resistance and isolated low high-density-lipoprotein cholesterol in Chinese subjects. Diabet Med. 2001;18(8):663-6.
  11. Modan M, Halkin H, Almog S, et al. Hyperinsulinemia. A link between hypertension obesity and glucose intolerance. J Clin Invest. 1985;75(3):809-17.
  12. Mykkanen L, Kuusisto J, Haffner SM, et al. Hyperinsulinemia predicts multiple atherogenic changes in lipoproteins in elderly subjects. Arterioscler Thromb. 1994;14(4):518-26.
  13. Nilsen TI, Vatten LJ. Prospective study of colorectal cancer risk and physical activity, diabetes, blood glucose and BMI: exploring the hyperinsulinaemia hypothesis. Br J Cancer. 2001;84(3):417-22.
  14. Salonen JT, Lakka TA, Lakka HM, et al. Hyperinsulinemia is associated with the incidence of hypertension and dyslipidemia in middle-aged men. Diabetes. 1998;47(2):270-5.
  15. Wilcox G. Insulin and insulin resistance. Clin Biochem Rev. 2005;26(2):19-39.
  16. Kawano Y, Cohen DE. Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease. J Gastroenterol. 2013;48(4):434-41.
  17. Hurjui DM, Nita O, Graur LI, et al. The central role of the non alcoholic fatty liver disease in metabolic syndrome. Rev Med Chir Soc Med Nat Iasi. 2012;116(2):425-31.
  18. Sarafidis PA, Ruilope LM. Insulin resistance, hyperinsulinemia, and renal injury: mechanisms and implications. Am J Nephrol. 2006;26(3):232-44.
  19. Johnson MS, Figueroa-Colon R, Huang TT, et al. Longitudinal changes in body fat in African American and Caucasian children: influence of fasting insulin and insulin sensitivity. J Clin Endocrinol Metab. 2001;86(7):3182-7.
  20. Erion KA, Corkey BE. Hyperinsulinemia: a Cause of Obesity? Curr Obes Rep. 2017;6(2):178-86.
  21. Bao B, Wang Z, Li Y, et al. The complexities of obesity and diabetes with the development and progression of pancreatic cancer. Biochim Biophys Acta. 2011;1815(2):135-46.
  22. Fierz Y, Novosyadlyy R, Vijayakumar A, et al. Insulin-sensitizing therapy attenuates type 2 diabetes-mediated mammary tumor progression. Diabetes. 2010;59(3):686-93.
  23. Kim EH, Kim HK, Bae SJ, et al. Fasting serum insulin levels and insulin resistance are associated with colorectal adenoma in Koreans. J Diabetes Investig. 2014;5(3):297-304.
  24. Jiang B, Zhang X, Du LL, et al. Possible roles of insulin, IGF-1 and IGFBPs in initiation and progression of colorectal cancer. World J Gastroenterol. 2014;20(6):1608-13.
  25. Tsai CJ, Giovannucci EL. Hyperinsulinemia, insulin resistance, vitamin D, and colorectal cancer among whites and African Americans. Dig Dis Sci. 2012;57(10):2497-503.
  26. Hidaka A, Sasazuki S, Goto A, et al. Plasma insulin, C-peptide and blood glucose and the risk of gastric cancer: the Japan Public Health Center-based prospective study. Int J Cancer. 2015;136(6):1402-10.M
  27. Kabat GC, Kim M, Caan BJ, et al. Repeated measures of serum glucose and insulin in relation to postmenopausal breast cancer. Int J Cancer. 2009;125(11):2704-10.
  28. Shan W, Ning C, Luo X, et al. Hyperinsulinemia is associated with endometrial hyperplasia and disordered proliferative endometrium: a prospective cross-sectional study. Gynecol Oncol. 2014;132(3):606-10.
  29. Otokozawa S, Tanaka R, Akasaka H, et al. Associations of Serum Isoflavone, Adiponectin and Insulin Levels with Risk for Epithelial Ovarian Cancer: Results of a Case-control Study. Asian Pac J Cancer Prev. 2015;16(12):4987-91.
  30. Pandeya DR, Mittal A, Sathian B, et al. Role of hyperinsulinemia in increased risk of prostate cancer: a case control study from Kathmandu Valley. Asian Pac J Cancer Prev. 2014;15(2):1031-3.
  31. Yun SJ, Min BD, Kang HW, et al. Elevated insulin and insulin resistance are associated with the advanced pathological stage of prostate cancer in Korean population. J Korean Med Sci. 2012;27(9):1079-84.
  32. Chao LT, Wu CF, Sung FY, et al. Insulin, glucose and hepatocellular carcinoma risk in male hepatitis B carriers: results from 17-year follow-up of a population-based cohort. Carcinogenesis. 2011;32(6):876-81.
  33. De Marco P, Romeo E, Vivacqua A, et al. GPER1 is regulated by insulin in cancer cells and cancer-associated fibroblasts. Endocr Relat Cancer. 2014;21(5):739-53.
  34. Othman EM, Hintzsche H, Stopper H. Signaling steps in the induction of genomic damage by insulin in colon and kidney cells. Free Radic Biol Med. 2014;68:247-57.
  35. Romieu I, Ferrari P, Rinaldi S, et al. Dietary glycemic index and glycemic load and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Am J Clin Nutr. 2012;96(2):345-55.
  36. Othman EM, Leyh A, Stopper H. Insulin mediated DNA damage in mammalian colon cells and human lymphocytes in vitro. Mutat Res. 2013;745-746:34-9.
  37. Algire C, Amrein L, Zakikhani M, et al. Metformin blocks the stimulative effect of a high-energy diet on colon carcinoma growth in vivo and is associated with reduced expression of fatty acid synthase. Endocr Relat Cancer. 2010;17(2):351-60.
  38. Kato M, Tani T, Terahara N, et al. The Anthocyanin Delphinidin 3-Rutinoside Stimulates Glucagon-Like Peptide-1 Secretion in Murine GLUTag Cell Line via the Ca2+/Calmodulin-Dependent Kinase II Pathway. PLoS One. 2015;10(5):e0126157.
  39. Imeryuz N, Yegen BC, Bozkurt A, et al. Glucagon-like peptide-1 inhibits gastric emptying via vagal afferent-mediated central mechanisms. Am J Physiol. 1997;273(4 Pt 1):G920-7.
  40. Näslund E, Bogefors J, Skogar S, et al. GLP-1 slows solid gastric emptying and inhibits insulin, glucagon, and PYY release in humans. Am J Physiol. 1999;277(3 Pt 2):R910-6.
  41. Hidalgo J, Flores C, Hidalgo MA, et al. Delphinol(R) standardized maqui berry extract reduces postprandial blood glucose increase in individuals with impaired glucose regulation by novel mechanism of sodium glucose cotransporter inhibition. Panminerva Med. 2014;56(2 Suppl 3):1-7.
  42. Alvarado J, Schoenlau F, Leschot A, et al. Delphinol(R) standardized maqui berry extract significantly lowers blood glucose and improves blood lipid profile in prediabetic individuals in three-month clinical trial. Panminerva Med. 2016;58(3 Suppl 1):1-6.
  43. Available at: http://www.mayoclinic.org/tests-procedures/a1c-test/details/results/rsc-20167939. Accessed 19 April, 2017.
  44. Supplier Internal Study. Effect of Clovinol on Random Blood Sugar Levels - A Pilot Study. Data on File. 2017.
  45. Sanae F, Kamiyama O, Ikeda-Obatake K, et al. Effects of eugenol-reduced clove extract on glycogen phosphorylase b and the development of diabetes in db/db mice. Food & Function. 2014;5(2):214-9.