Free Shipping on All Orders $75 Or More!

Your Trusted Brand for Over 35 Years

Life Extension Magazine

<< Back to July 2013

Stop Starch-Induced Glucose Surges

July 2013

By Scott Rackinow

Shield Your Body from Chronically Elevated Insulin
Shield Your Body from Chronically Elevated Insulin

Anyone whose blood sugar is not under optimum control is exposed to the dangers of chronically elevated insulin levels. That’s because your body will pump out insulin so long as blood sugar levels are above normal—and can result in an insulin level that may be dangerously elevated in its effort to keep blood sugar at a normal level, making it a truly hidden danger.

Insulin, of course, is a useful and necessary hormone. It is responsible for driving blood sugar into cells, where it’s burned for energy. Without properly regulated amounts of insulin we couldn’t survive.

But insulin, like many hormones, has multiple functions. The little-known “dark side” of insulin is that it is a powerful growth factor.41 And in the healthy adult body, there’s limited usefulness in growth factors. Excessive growth factor production triggers cell replication in places we don’t want it. Insulin and other growth factors are implicated, for example, in cancer, where unregulated cellular reproduction produces deadly malignancies.42And imbalanced growth factors, including insulin, are also implicated in the thickening and poor responsiveness of smooth muscle cells lining arterial walls, contributing to cardiovascular disease.41

Excessive insulin production is the result of insulin resistance, which is another way to say “prediabetes.” High insulin levels are associated with a 37% increase in the risk of dying from cancer—whether or not you have diabetes.40,43 Doctors are finally learning to pay attention to insulin levels as well as to blood sugar levels when evaluating new treatments and when advising their patients. And they are starting to seek therapies that increase insulin sensitivity and lower overall insulin levels.44

Most antidiabetic drugs aim only to drive down blood sugar levels and have no effect on insulin; others are actually intended to increase your insulin levels in the attempt to reduce blood sugar. But transglucosidase works in part by lowering insulin levels as blood sugar normalizes.

In human studies in which healthy subjects with evidence of insulin resistance ate a test meal of white rice (high in starch), placebo recipients saw their insulin levels rise along with their after-meal blood sugars (the expected response), while those receiving transglucosidase had small decreases in insulin over the same time period.6 And in patients with diabetes, who already had elevated insulin levels, 12 weeks of transglucosidase supplementation led to significant drops in insulin concentration overall. These are remarkable findings, given that these subjects made no other changes in their diets or lifestyles.

Reduce the Impact of Diabetes

Another clinical study looked at patients who already had type II diabetes, and the researchers found that the benefits of transglucosidase are just as exciting for those with full-blown diabetes as they are for prediabetics.22

Diabetics not only have elevated blood sugar and often high insulin levels, but also have detectable evidence of advanced glycation end products in the form of hemoglobin A1c (HbA1c). This blood test is an indication of total blood sugar levels over an approximate two to three-month period.

Patients in the study received total daily doses of 900,000 units of transglucosidase, 2.7 million units of transglucosidase, or a placebo.22 Both doses produced respectable reductions in hemoglobin A1c, lowering it by an average 0.18 and 0.21%, respectively (normal measurements for this test should not exceed 5.5%).

Patients’ insulin concentrations fell significantly as well, by 2.79 and 3.59 mIU/mL, respectively.22 And while transglucosidase does not replace metformin if internal overproduction of glucose by the liver is the culprit behind elevated fasting glucose (>85 mg/dL) or elevated HbA1C (>5.5%), its dramatic insulin reductions are similar to those seen with the drug metformin, which can reduce fasting insulin by about 38% in obese, insulin-resistant people.39,40

But the benefits of transglucosidase for diabetics don’t end there. The patients taking transglucosidase also had significant increases in a beneficial cytokine called adiponectin and significant reductions in triglycerides and diastolic blood pressure.22

On the other hand, the placebo patients experienced significant increases in their body mass index (a measure of total weight for height) and also had increases in markers of fat-induced liver damage. Neither group of patients taking transglucosidase had such changes.22

If you already have type II diabetes, the availability of this novel enzyme is excellent news. It means that supplementing with transglucosidase not only helps protect against dangerous glycation reactions taking place in your tissues (which will cause heart, kidney, nerve and eye disease, given time), but also blunts excessive insulin levels (which raise your risk of cancer and cardiovascular diseases). In addition, it can also help protect you from further weight gain and other measures of poor health. And it’s all done without taking a single drug.

Dosing Enzymes
Dosing Enzymes

*Unlike many other nutrients, enzymes are dosed according to their unit of activity. One enzymatic unit is the amount of enzyme needed to convert one micromole (µmol) of a substance per minute. This is not to be confused with the International Unit (IU), which is an unrelated measure of other biologically active substances such as vitamin D.

Because transglucosidase is an enzyme, the dosages are measured in “units of enzyme activity” not milligrams or International Units (IU). A 450,000 unit dose is typically the amount found in one capsule.


Chronically elevated glucose and insulin levels, especially those immediately following a meal, should be a major concern of any adult—even if you have no known history of high blood sugar. High insulin and glucose blood levels are at least as dangerous as high cholesterol when it comes to increased risk of cardiovascular disease.

In addition, chronically elevated glucose and insulin sharply elevate cancer rates. That’s why it’s important to take all possible steps to prevent dietary starch from converting into deadly sugar calories.

Transglucosidase is a groundbreaking supplement that is the first of its kind. Its dual mechanism of action helps manage high blood sugar and excess insulin by blocking the release of harmful sugar from starch…converting it instead into beneficial fiber.

This is a medical breakthrough capable of mitigating the growing diabetes epidemic—and is a critical new tool in our kit for managing dangerous metabolic conditions.

If your fasting glucose is over 85 mg/dL (which most adults are), or you have other indicators of glucose impairment such as elevated hemoglobin A1c or elevated fasting insulin, take transglucosidase before your two heaviest starch-containing meals of the day.

Human clinical trials have established its value in healthy as well as diabetic individuals. And that translates to lower risks for cancer, vision problems, and heart disease.

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

Doggie Diabetes
Doggie Diabetes

Diabetes is common in dogs as well as people. Fortunately, transglucosidase can help manage glucose levels in dogs as well as in humans. When researchers in Japan studied transglucosidase in animals, they found that the results were virtually identical with what we’ve seen in human studies.21

Healthy non-diabetic control dogs receiving transglucosidase experienced lower total after-meal glucose and insulin levels compared with those receiving the control diet alone. And the usual “spike” in after-meal glucose levels was virtually eliminated, allowing the dogs to maintain normal glucose concentrations of 85 to 95 mg/dL.21


  1. German JB, Dillard CJ. Saturated fats: what dietary intake? Am J Clin Nutr. 2004 Sep;80(3):550-9.
  2. Available at: Accessed April 3, 2013.
  3. Daly ME, Vale C, Walker M, Littlefield A, Alberti KG, Mathers JC. Acute effects on insulin sensitivity and diurnal metabolic profiles of a high-sucrose compared with a high-starch diet. Am J Clin Nutr. 1998 Jun;67(6):1186-96.
  4. Raben A, Holst JJ, Madsen J, Astrup A. Diurnal metabolic profiles after 14 d of an ad libitum high-starch, high-sucrose, or high-fat diet in normal-weight never-obese and postobese women. Am J Clin Nutr. 2001 Feb;73(2):177-89.
  5. Brand-Miller JC, Stockmann K, Atkinson F, Petocz P, Denyer G. Glycemic index, postprandial glycemia, and the shape of the curve in healthy subjects: analysis of a database of more than 1,000 foods. Am J Clin Nutr. 2009 Jan;89(1):97-105.
  6. Sasaki M, Joh T, Koikeda S, et al. A novel strategy in production of oligosaccharides in digestive tract: prevention of postprandial hyperglycemia and hyperinsulinemia. J Clin Biochem Nutr.2007 Nov;41(3):191-6.
  7. Ao Z, Simsek S, Zhang G, Venkatachalam M, Reuhs BL, Hamaker BR. Starch with a slow digestion property produced by altering its chain length, branch density, and crystalline structure. J Agric Food Chem. 2007 May 30;55(11):4540-7.
  8. Available at: > 12/978293375.Bc.r.html. Accessed Feb 26, 2013.
  9. Available at: Accessed April 4, 2013.
  10. Liljeberg HG, Akerberg AK, Björck IM. Effect of the glycemic index and content of indigestible carbohydrates of cereal-based breakfast meals on glucose tolerance at lunch in healthy subjects. Am J Clin Nutr. 1999 Apr;69(4):647-55.
  11. Verzijl N, DeGroot J, Ben ZC, et al. Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: a possible mechanism through which age is a risk factor for osteoarthritis. Arthritis Rheum. 2002 Jan;46(1):114-23.
  12. Del Turco S, Basta G. An update on advanced glycation endproducts and atherosclerosis. Biofactors.2012 Jul-Aug;38(4):266-74.
  13. Sell DR, Monnier VM. Molecular basis of arterial stiffening: role of glycation- a mini-review. Gerontology.2012;58(3):227-37.
  14. Cerf ME. Beta cell dynamics: beta cell replenishment, beta cell compensation and diabetes. Endocrine.2013 Mar 13.
  15. Cerf ME. Beta cell dysfunction and insulin resistance. Front Endocrinol (Lausanne). 2013;4:37.
  16. Kuhl H. Breast cancer risk in the WHI study: the problem of obesity. Maturitas.2005 May 16;51(1):83-97.
  17. Moyad MA. Obesity, interrelated mechanisms, and exposures and kidney cancer. Semin Urol Oncol. 2001 Nov;19(4):270-9.
  18. Sandovici I, Hammerle CM, Ozanne SE, Constancia M. Developmental and environmental epigenetic programming of the endocrine pancreas: consequences for type 2 diabetes. Cell Mol Life Sci. 2013 Mar 6.
  19. Abdelmoneim SS, Hagen ME, Mendrick E, et al. Acute hyperglycemia reduces myocardial blood flow reserve and the magnitude of reduction is associated with insulin resistance: a study in nondiabetic humans using contrast echocardiography. Heart Vessels.2012 Nov 23.
  20. Reaven G. Insulin resistance and coronary heart disease in nondiabetic individuals. Arterioscler Thromb Vasc Biol. 2012 Aug;32(8):1754-9.
  21. Sako T, Mori A, Lee P, et al. Supplementing transglucosidase with a high-fiber diet for prevention of postprandial hyperglycemia in streptozotocin-induced diabetic dogs. Vet Res Commun. 2010 Feb;34(2):161-72.
  22. Sasaki M, Imaeda K, Okayama N, et al. Effects of transglucosidase on diabetes, cardiovascular risk factors and hepatic biomarkers in patients with type 2 diabetes: a 12-week, randomized, double-blind, placebo-controlled trial. Diabetes Obes Metab.2012 Apr;14(4):379-82.
  23. Ota M, Okamoto T, Wakabayashi H. Action of transglucosidase from Aspergillus niger on maltoheptaose and [U-(13)C]maltose. Carbohydr Res. 2009 Mar 10;344(4):460-5.
  24. Beerens K, Desmet T, Soetaert W. Enzymes for the biocatalytic production of rare sugars. J Ind Microbiol Biotechnol.2012 Jun;39(6):823-34.
  25. Cani PD. Crosstalk between the gut microbiota and the endocannabinoid system: impact on the gut barrier function and the adipose tissue. Clin Microbiol Infect. 2012 Jul;18 Suppl 4:50-3.
  26. Costa GT, Guimaraes SB, Sampaio HA. Fructo-oligosaccharide effects on blood glucose: an overview. Acta Cir Bras.2012 Mar;27(3):279-82.
  27. Di Bartolomeo F, Startek JB, Van den Ende W. Prebiotics to fight diseases: Reality or fiction? Phytother Res. 2012 Dec 27.
  28. Mallappa RH, Rokana N, Duary RK, Panwar H, Batish VK, Grover S. Management of metabolic syndrome through probiotic and prebiotic interventions. Indian J Endocrinol Metab.2012 Jan;16(1):20-7.
  29. Molinaro F, Paschetta E, Cassader M, Gambino R, Musso G. Probiotics, prebiotics, energy balance, and obesity: mechanistic insights and therapeutic implications. Gastroenterol Clin North Am. 2012 Dec;41(4):843-54.
  30. Kurimoto M, Nishimoto T, Nakada T, Chaen H, Fukuda S, Tsujisaka Y. Synthesis by an alpha-glucosidase of glycosyl-trehaloses with an isomaltosyl residue. Biosci Biotechnol Biochem. 1997 Apr;61(4):699-703.
  31. A high-fiber diet may help you live longer. Mayo Clin Health Lett.2012 Jun;30(6):4.
  32. Marlett JA, McBurney MI, Slavin JL. Position of the American Dietetic Association: health implications of dietary fiber. J Am Diet Assoc. 2002 Jul;102(7):993-1000.
  33. Ajani UA, Ford ES, Mokdad AH. Dietary fiber and C-reactive protein: findings from national health and nutrition examination survey data. J Nutr.2004 May;134(5):1181-5.
  34. Liu S, Willett WC, Manson JE, Hu FB, Rosner B, Colditz G. Relation between changes in intakes of dietary fiber and grain products and changes in weight and development of obesity among middle-aged women. Am J Clin Nutr.2003 Nov;78(5):920-7.
  35. Sluijs I, van der Schouw YT, van der AD, et al. Carbohydrate quantity and quality and risk of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) study. Am J Clin Nutr.2010 Oct;92(4):905-11.
  36. Silva FM, Steemburgo T, de Mello VD, Tonding SF, Gross JL, Azevedo MJ. High dietary glycemic index and low fiber content are associated with metabolic syndrome in patients with type 2 diabetes. J Am Coll Nutr. 2011 Apr;30(2):141-8.
  37. Transglucosidase improves the gut microbiota profile of type 2 diabetes mellitus patients. Presented at Digestive Disease Week. 2013 May 18-21. Orlando, FL
  38. Kumar V, Sinha AK, Makkar HP, de Boeck G, Becker K. Dietary roles of non-starch polysaccharides in human nutrition: a review. Crit Rev Food Sci Nutr.2012;52(10):899-935.
  39. Freemark M, Bursey D. The effects of metformin on body mass index and glucose tolerance in obese adolescents with fasting hyperinsulinemia and a family history of type 2 diabetes. Pediatrics.2001 Apr;107(4):E55.
  40. Jalving M, Gietema JA, Lefrandt JD, et al. Metformin: taking away the candy for cancer? Eur J Cancer. 2010 Sep;46(13):2369-80.
  41. Breen DM, Giacca A. Effects of insulin on the vasculature. Curr Vasc Pharmacol. 2011 May;9(3):321-32.
  42. Muhidin SO, Magan AA, Osman KA, Syed S, Ahmed MH. The relationship between nonalcoholic fatty liver disease and colorectal cancer: the future challenges and outcomes of the metabolic syndrome. J Obes.2012;2012:637538.
  43. Dankner R, Shanik MH, Keinan-Boker L, Cohen C, Chetrit A. Effect of elevated basal insulin on cancer incidence and mortality in cancer incident patients: the Israel GOH 29-year follow-up study. Diabetes Care.2012 Jul;35(7):1538-43.
  44. Fierz Y, Novosyadlyy R, Vijayakumar A, Yakar S, LeRoith D. Insulin-sensitizing therapy attenuates type 2 diabetes-mediated mammary tumor progression. Diabetes.2010 Mar;59(3):686-93.
  45. Holt SH, Miller JC, Petocz P. An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods. Am J Clin Nutr.1997 Nov;66(5):1264-76.
  46. Holt SH, Miller JC, Petocz P, Farmakalidis E. A satiety index of common foods. Eur J Clin Nutr. 1995 Sep;49(9):675-90.