Life Extension Magazine February 2011
Take Control of Your Blood Sugar Levels With Targeted Nutrient Compounds
By Alonzo Brody
By Alonzo Brody
Over fifty years ago scientists conclusively established that low levels of chromium directly contribute to high blood sugar and pre-diabetic complications.1
Yet today, anywhere between 25-50% of the American population suffers from chromium deficiency.2 This is likely the result of modern commercial farming methods that have depleted the soil of valuable chromium and industrial food processing that depletes natural chromium from whole foods. Compounding the danger is the reality that your body’s capacity to absorb chromium declines with age.
These alarming facts highlight a widespread, stealth threat that rampant nutritional insufficiencies may be undermining even the best efforts to optimize blood glucose levels.
As Life Extension® members are well aware, excess glucose not only increases degenerative disease risk, but also adversely impacts longevity genes required for extended life span.
In published studies, chromium deficiency has been shown to induce early-stage diabetic complications and hasten the onset of full-blown diabetes.3-5
The encouraging news is that a targeted set of novel nutritional compounds has been identified that optimizes your body’s ability to keep a tight rein on glucose levels.
In this article, you will learn of a cutting-edge chromium complex that enhances your body’s ability to utilize glucose as you age. You will also discover the proven power of additional nutrients to protect against the system-wide damage inflicted by surplus glucose.
Chromium: The Master Blood Sugar Regulator
Studies on chromium have consistently demonstrated improvement in blood sugar levels, insulin sensitivity, and lipid profiles.6-9 More recent research reveals how it works: chromium favorably modulates your cells’ internal communication centers (intracellular signaling systems) to effectively lower blood glucose.
Every cell in your body uses an internal communications system that must function properly in order to establish and maintain optimal blood glucose absorption and metabolism. Such intracellular signaling is especially critical to cells’ ability to detect and respond to elevated glucose levels in the blood.
When cells detect these elevations, an array of biomolecular processes is set in motion that will determine how well they will manage the increased sugar burden. Chromium is now recognized to be vital to this process, enabling cellular uptake and breakdown of blood sugar—and effectively lowering glucose levels in the blood.10,11
The clinical literature is rich with data supporting chromium’s singular ability to lower blood sugar levels and increase insulin sensitivity.
In a 2009 study, diabetic patients given chromium experienced reductions in their total insulin requirements, along with reductions in fasting and afternoon glucose levels.12 Recent studies show that supplementation with chromium and biotin can improve glycemic control in overweight to obese diabetic patients when taken along with their regular medication.13
Chromium also exerts its positive effects on blood sugar selectively—which means it does not induce dangerously low blood sugar levels like some drugs, but rather kicks into gear only when blood sugar levels become too high.14,15
Scientists recognize that control of blood sugar in the immediate period following a meal (the postprandial period) is perhaps more important than at any other time. This is the interval when blood sugar can dangerously spike in the body, inflicting low-level, cumulative damage to multiple physiological systems over time. Chromium has been shown to dramatically reduce total exposure to glucose during the postprandial period in most subjects.16
Chromium’s multitargeted actions not only keep sugar levels low, they also prevent the formation of advanced glycation end products, or AGEs.5,12,17,18 Most notably, chromium helps bring down levels of hemoglobin A1c, the advanced glycation end product associated with long-term exposure to elevated sugar concentrations.18
These benefits are accompanied by healthy reductions in abnormal lipid levels and increases in artery-cleansing high-density lipoprotein (HDL) in the blood.9 The combination of chromium and biotin has also been shown to favorably affect a biomarker called the atherogenic index: the ratio of triglycerides to HDL that is associated with increased cardiovascular risk.19
The improvement in insulin signaling by chromium is also associated with decreased production of specific pro-inflammatory cytokines. These cell-signaling molecules play a mutually reinforcing role in prolonging and worsening impaired glucose control.11,20
Potent Organic Blood Sugar Stabilizers: Amla and Shilajit
Chromium is a highly reactive metal ion, requiring balance through additional organic materials in order to stabilize and enhance its effects. Two traditional remedies for obesity and its consequences have more recently been shown to synergistically enhance chromium’s beneficial action.
The herb amla (Indian gooseberry) directly impacts a host of biochemical and gene-regulating processes that positively influence factors related to high blood sugar and metabolic syndrome. Traditional preparations containing amla have long been known to lower blood sugar in diabetic animals and humans, but until recently the mechanisms were unclear.33,34
We now know that amla extracts are powerful antioxidants.35,36 They inhibit digestive enzymes that would otherwise convert starch to sugar, helping to reduce blood sugar loads following a meal.35 In pre-clinical models, an herbal combination containing amla reduces lipid peroxidation, the free radical damage to cell membranes that plays a critical role in atherosclerosis and the development of insulin resistance.37
Amla extract also shields tissues from damage inflicted by excess glucose at multiple levels and it prevents production of sugar alcohols that wreak havoc on the vulnerable ocular (eye) structures and other tissues in diabetics.38,39 Amla extracts are showing additional promise in preventing the metabolic syndrome in animal models.40
Additional balance is provided by shilajit, a complex mixture of organic and inorganic compounds rich in fulvic acid. Studies have shown that shilajit has remarkable effects on the ways in which our mitochondria utilize energy from sugar and fats.41
Fulvic acid acts as a molecular “chaperone,” shuttling electrons efficiently along their pathways within mitochondria.42-44 This enhances the efficiency of mitochondrial respiration and speeds blood sugar metabolism.45
The compound of chromium plus amla and shilajit thus acts to optimize the way your body takes up and distributes glucose between and within cells, assuring rapid removal of glucose from the bloodstream and efficient utilization of glucose within cells.
Blocking Carbohydrate Breakdown with Seaweed Extracts
A complementary strategy in the battle against elevated glucose is to limit the amount of glucose the body has to process. Many doctors counsel their patients to reduce their total carbohydrate intake, but this strategy provides only partial protection for most people. Another approach is to blunt the conversion of starches into their component sugars in the gastrointestinal tract. This can be accomplished safely and effectively by introducing natural enzyme inhibitors that halt carbohydrate metabolism in the gut. The most attractive targets are the sugar-producing alpha-amylase and alpha-glucosidase enzymes.
Extracts from a variety of seaweeds have inhibitory effects on these enzymes.46-49 Animal studies have revealed that inhibiting these enzymes lowers blood sugar levels.50,51 Not only are the polyphenols found in these seaweeds powerful tools in reducing elevated glucose, they are also potent antioxidants.52,53
These seaweed extracts stimulate differentiation of fat cells, preventing them from replicating and reducing the release of harmful fat-related cytokines.54,55 They achieve this effect in part through their upregulation of the important PPAR metabolic sensing system and also through increased expression of the GLUT4 glucose transporter.54,55
Cinnamon: A Clinically Documented Glucose Fighter
Cinnamon’s traditional uses have been related to obesity and to the conditions we now recognize as diabetes and the metabolic syndrome. The polyphenols in water-soluble cinnamon extracts act on multiple targets to enhance insulin sensitivity, lower blood sugar, and limit damage by advanced glycation end products.56,57 Collectively, these effects contribute to reduction in the risks for the metabolic syndrome.58
Cinnamon polyphenols are powerful antioxidants that exert direct protective effects on cells and tissues.59 In recent years, we’ve learned that cinnamon also potently increases the number and activity of glucose transport complexes that enable cells to take up glucose in the presence of insulin.60,61
Cinnamon also upregulates production of the metabolic sensors known as PPARs, which are being investigated by pharmaceutical companies as sources for anti-diabetic drug development.62 PPARs represent another mechanism by which cells recognize increased glucose concentrations and act to lower them. Increased PPAR activity contributes to improved insulin sensitivity.
In human studies, cinnamon supplementation lowers blood sugar and increases insulin sensitivity.63 It blunts the spike in glucose levels following ingestion of a sugar-rich meal, and at the same time lowers insulin spikes.64,65
Cinnamon also helps to increase satiety, the feeling of being full that prevents us from eating more than we should.66
Cinnamon has also been shown to lower blood pressure, enhancing its anti-metabolic syndrome effects.67 The combination of reduced blood sugar, reduced blood pressure, and improved body composition promises tremendous health benefits in adults with early metabolic syndrome but without signs of diabetes.68
These effects powerfully lower the body’s total exposure to excess glucose. But cinnamon also acts to prevent glucose-induced tissue damage, reducing protein glycation and preventing the cumulative effects of AGEs.69 Cinnamon supplements have shown promise, for example, in reducing diabetic neuropathy, the painful and debilitating nerve injury that results from glycation of neural proteins.70 And cinnamon’s polyphenols have anti-inflammatory, antimicrobial, antitumor, cholesterol-lowering, and immunomodulatory effects that contribute to our overall disease risk reduction.71 Specifically, cinnamon extracts have been shown to reduce levels of the fat tissue-derived inflammatory cytokines that increase our risk of cardiovascular disease.72
Up to 50% of the American population is deficient in chromium, one of the principal nutrients the body needs to control blood sugar levels. A novel chromium complex has been identified that optimizes your body’s ability to break down and convert blood sugar into energy at the cellular level.
The organic compounds amla (Indian gooseberry) and shilajit work synergistically to enhance chromium’s glucose-lowering effects. Amla shields cells from damage inflicted by high blood sugar, while shilajit boosts efficient cellular metabolism of glucose.
In human studies, cinnamon supplementation lowers blood sugar and increases insulin sensitivity.
Cinnamon polyphenols activate cells’ glucose detection systems, enabling them to act more quickly to counter high blood sugar. Cinnamon also induces the feeling of being full (satiety) to prevent overconsumption and the after-meal spikes in blood sugar and insulin that result. Extracts of brown seaweed help prevent glucose elevations by blocking digestive enzymes and limiting glucose absorption from the intestine.
Taken together, these nutrients provide aging individuals with potent natural mechanisms to suppress fasting blood glucose levels to optimal ranges (below 86 mg/dL) while blunting dangerous after-meal glucose spikes.
If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at
1. Mertz W, Angino EE, Cannon HL, Hambidge KM, Voors AW. Chromium. In: US National Committee for Geochemistry. Subcommittee on the Geochemical Environment. Geochemistry and the Environment. Volume I. The Relation of Selected Trace Elements to Health and Disease. Washington, D.C.: National Academy of Sciences; 1974:29-35.
2. Available at http://www.drweil.com/drw/u/ART02868/chromium.html. Accessed November 20, 2010.
3. Striffler JS, Polansky M, Anderson RA. Overproduction of insulin in the chromium-deficient rat. Metabolism. 1999;48(8):1063-8.
4. Vincent JB. Mechanisms of chromium action: low-molecular-weight chromium-binding substance. J Am Coll Nutr. 1999 Feb;18(1):6-12.
5. Terpilowska S, Zaporowska H. The role of chromium in cell biology and medicine. Przegl Lek. 2004;61 Suppl 3:51-4.
6. Anderson RA, Cheng N, Bryden NA, Polansky MM, Chi J, Feng J. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes. 1997 Nov;46(11):1786-91.
7. Linday LA. Trivalent chromium and the diabetes prevention program. Med Hypotheses. 1997 Jul;49(1):47-9.
8. Bahijiri SM, Mira SA, Mufti AM, Ajabnoor MA. The effects of inorganic chromium and brewer’s yeast supplementation on glucose tolerance, serum lipids and drug dosage in individuals with type 2 diabetes. Saudi Med J. 2000 Sep;21(9):831-7.
9. Bahijri SM. Effect of chromium supplementation on glucose tolerance and lipid profile. Saudi Med J. 2000 Jan;21(1):45-50.
10. Vincent JB. Quest for the molecular mechanism of chromium action and its relationship to diabetes. Nutr Rev. 2000 Mar;58(3 Pt 1):67-72.
11. Chen WY, Chen CJ, Liu CH, Mao FC. Chromium supplementation enhances insulin signalling in skeletal muscle of obese KK/HlJ diabetic mice. Diabetes Obes Metab. 2009 Apr;11(4):293-303.
12. Pohl M, Mayr P, Mertl-Roetzer M, et al. Glycemic control in patients with type 2 diabetes mellitus with a disease-specific enteral formula: stage II of a randomized, controlled multicenter trial. JPEN J Parenter Enteral Nutr. 2009 Jan-Feb;33(1):37-49.
13. Albarracin CA, Fuqua BC, Evans JL, Goldfine ID. Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. Diabetes Metab Res Rev. 2008 Jan-Feb;24(1):41-51.
14. Ryan GJ, Wanko NS, Redman AR, Cook CB. Chromium as adjunctive treatment for type 2 diabetes. Ann Pharmacother. 2003 Jun;37(6):876-85.
15. Cefalu WT, Rood J, Pinsonat P, et al. Characterization of the metabolic and physiologic response to chromium supplementation in subjects with type 2 diabetes mellitus. Metabolism. 2010 May;59(5):755-62.
16. Frauchiger MT, Wenk C, Colombani PC. Effects of acute chromium supplementation on postprandial metabolism in healthy young men. J Am Coll Nutr. 2004 Aug;23(4):351-7.
17. Jain SK, Patel P, Rogier K. Trivalent chromium inhibits protein glycosylation and lipid peroxidation in high glucose-treated erythrocytes. Antioxid Redox Signal. 2006 Jan-Feb;8(1-2):238-41.
18. Keszthelyi Z, Past T, Koltai K, Szabo L, Mozsik G. Chromium (III)-ion enhances the utilization of glucose in type-2 diabetes mellitus. Orv Hetil. 2003 Oct 19;144(42):2073-6.
19. Geohas J, Daly A, Juturu V, Finch M, Komorowski JR. Chromium picolinate and biotin combination reduces atherogenic index of plasma in patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized clinical trial. Am J Med Sci. 2007 Mar;333(3):145-53.
20. Jain SK, Rains JL, Croad JL. High glucose and ketosis (acetoacetate) increases, and chromium niacinate decreases, IL-6, IL-8, and MCP-1 secretion and oxidative stress in U937 monocytes. Antioxid Redox Signal. 2007 Oct;9(10):1581-90.
21. Clodfelder BJ, Emamaullee J, Hepburn DD, Chakov NE, Nettles HS, Vincent JB. The trail of chromium(III) in vivo from the blood to the urine: the roles of transferrin and chromodulin. J Biol Inorg Chem. 2001 Jun;6(5-6):608-17.
22. Chen G, Liu P, Pattar GR, et al. Chromium activates glucose transporter 4 trafficking and enhances insulin-stimulated glucose transport in 3T3-L1 adipocytes via a cholesterol-dependent mechanism. Mol Endocrinol. 2006 Apr;20(4):857-70.
23. Lund S, Holman GD, Schmitz O, Pedersen O. Contraction stimulates translocation of glucose transporter GLUT4 in skeletal muscle through a mechanism distinct from that of insulin. Proc Natl Acad Sci U S A. 1995 Jun 20;92(13):5817-21.
24 James DE, Brown R, Navarro J, Pilch PF. Insulin-regulatable tissues express a unique insulin-sensitive glucose transport protein. Nature. 1988 May 12;333(6169):183-5.
25. James DE, Strube M, Mueckler M. Molecular cloning and characterization of an insulin-regulatable glucose transporter. Nature. 1989 Mar 2;338(6210):83-7.
26. Pattar GR, Tackett L, Liu P, Elmendorf JS. Chromium picolinate positively influences the glucose transporter system via affecting cholesterol homeostasis in adipocytes cultured under hyperglycemic diabetic conditions. Mutat Res. 2006 Nov 7;610(1-2):93-100.
27. Eyster CA, Olson AL. Compartmentalization and regulation of insulin signaling to GLUT4 by the cytoskeleton. Vitam Horm. 2009;80:193-215.
28. Lauritzen HP. In vivo imaging of GLUT4 translocation. Appl Physiol Nutr Metab. 2009 Jun;34(3):420-3.
29. Leney SE, Tavare JM. The molecular basis of insulin-stimulated glucose uptake: signalling, trafficking and potential drug targets. J Endocrinol. 2009 Oct;203(1):1-18.
30. Wu YT, Sun Z, Che SP, Wang X, Wang Y, Guo G. Regulation of chromium on gene expression of skeletal muscles in diabetic rats. Wei Sheng Yan Jiu. 2005 Mar;34(2):184-7.
31. Qiao W, Peng Z, Wang Z, Wei J, Zhou A. Chromium improves glucose uptake and metabolism through upregulating the mRNA levels of IR, GLUT4, GS, and UCP3 in skeletal muscle cells. Biol Trace Elem Res. 2009 Nov;131(2):133-42.
32. Wang YQ, Yao MH. Effects of chromium picolinate on glucose uptake in insulin-resistant 3T3-L1 adipocytes involve activation of p38 MAPK. J Nutr Biochem. 2009 Dec;20(12):982-91.
33. Manjunatha S, Jaryal AK, Bijlani RL, Sachdeva U, Gupta SK. Effect of Chyawanprash and vitamin C on glucose tolerance and lipoprotein profile. Indian J Physiol Pharmacol. 2001 Jan;45(1):71-9.
34. Babu PS, Stanely Mainzen Prince P. Antihyperglycaemic and antioxidant effect of hyponidd, an ayurvedic herbomineral formulation in streptozotocin-induced diabetic rats. J Pharm Pharmacol. 2004 Nov;56(11):1435-42.
35. Nampoothiri SV, Prathapan A, Cherian OL, Raghu KG, Venugopalan VV, Sundaresan A. In vitro antioxidant and inhibitory potential of Terminalia bellerica and Emblica officinalis fruits against LDL oxidation and key enzymes linked to type 2 diabetes. Food Chem Toxicol. 2010 Oct 14.
36. Rao TP, Sakaguchi N, Juneja LR, Wada E, Yokozawa T. Amla (Emblica officinalis Gaertn.) extracts reduce oxidative stress in streptozotocin-induced diabetic rats. J Med Food. 2005 Fall;8(3):362-8.
37. Patel SS, Shah RS, Goyal RK. Antihyperglycemic, antihyperlipidemic and antioxidant effects of Dihar, a polyherbal ayurvedic formulation in streptozotocin induced diabetic rats. Indian J Exp Biol. 2009 Jul;47(7):564-70.
38. Suryanarayana P, Kumar PA, Saraswat M, Petrash JM, Reddy GB. Inhibition of aldose reductase by tannoid principles of Emblica officinalis: implications for the prevention of sugar cataract. Mol Vis. 2004 Mar 12;10:148-54.
39. Suryanarayana P, Saraswat M, Petrash JM, Reddy GB. Emblica officinalis and its enriched tannoids delay streptozotocin-induced diabetic cataract in rats. Mol Vis. 2007;13:1291-7.
40. Kim HY, Okubo T, Juneja LR, Yokozawa T. The protective role of amla (Emblica officinalis Gaertn.) against fructose-induced metabolic syndrome in a rat model. Br J Nutr. 2010 Feb;103(4):502-12.
41. Meena H, Pandey HK, Arya MC, Ahmed Z. Shilajit: A panacea for high-altitude problems. Int J Ayurveda Res. 2010 Jan;1(1):37-40.
42. Klapper L, McKnight DM, Fulton JR, et al. Fulvic acid oxidation state detection using fluorescence spectroscopy. Environ Sci Technol. 2002 Jul 15;36(14):3170-5.
43. Royer RA, Burgos WD, Fisher AS, Unz RF, Dempsey BA. Enhancement of biological reduction of hematite by electron shuttling and Fe(II) complexation. Environ Sci Technol. 2002 May 1;36(9):1939-46.
44. Kang SH, Choi W. Oxidative degradation of organic compounds using zero-valent iron in the presence of natural organic matter serving as an electron shuttle. Environ Sci Technol. 2009 Feb 1;43(3):878-83.
45. Visser SA. Effect of humic substances on mitochondrial respiration and oxidative phosphorylation. Sci Total Environ. 1987 Apr;62:347-54.
46. Kim KY, Nguyen TH, Kurihara H, Kim SM. Alpha-glucosidase inhibitory activity of bromophenol purified from the red alga Polyopes lancifolia. J Food Sci. 2010 Jun;75(5):H145-50.
47. Apostolidis E, Lee CM. In vitro potential of Ascophyllum nodosum phenolic antioxidant-mediated alpha-glucosidase and alpha-amylase inhibition. J Food Sci. 2010 Apr;75(3):H97-102.
48. Kim KY, Nam KA, Kurihara H, Kim SM. Potent alpha-glucosidase inhibitors purified from the red alga Grateloupia elliptica. Phytochemistry. 2008 Nov;69(16):2820-5.
49. Zhang J, Tiller C, Shen J, et al. Antidiabetic properties of polysaccharide- and polyphenolic-enriched fractions from the brown seaweed Ascophyllum nodosum. Can J Physiol Pharmacol. 2007 Nov;85(11):1116-23.
50. Heo SJ, Hwang JY, Choi JI, Han JS, Kim HJ, Jeon YJ. Diphlorethohydroxycarmalol isolated from Ishige okamurae, a brown algae, a potent alpha-glucosidase and alpha-amylase inhibitor, alleviates postprandial hyperglycemia in diabetic mice. Eur J Pharmacol. 2009 Aug 1;615(1-3):252-6.
51. Lamela M, Anca J, Villar R, Otero J, Calleja JM. Hypoglycemic activity of several seaweed extracts. J Ethnopharmacol. 1989 Nov;27(1-2):35-43.
52. Iwai K. Antidiabetic and antioxidant effects of polyphenols in brown alga Ecklonia stolonifera in genetically diabetic KK-A(y) mice. Plant Foods Hum Nutr. 2008 Dec;63(4):163-9.
53. Ruperez P, Ahrazem O, Leal JA. Potential antioxidant capacity of sulfated polysaccharides from the edible marine brown seaweed Fucus vesiculosus. J Agric Food Chem. 2002 Feb 13;50(4):840-5.
54. Kim SN, Choi HY, Lee W, Park GM, Shin WS, Kim YK. Sargaquinoic acid and sargahydroquinoic acid from Sargassum yezoense stimulate adipocyte differentiation through PPARalpha/gamma activation in 3T3-L1 cells. FEBS Lett. 2008 Oct 15;582(23-24):3465-72.
55. Kang SI, Jin YJ, Ko HC, et al. Petalonia improves glucose homeostasis in streptozotocin-induced diabetic mice. Biochem Biophys Res Commun. 2008 Aug 22;373(2):265-9.
56. Cao H, Polansky MM, Anderson RA. Cinnamon extract and polyphenols affect the expression of tristetraprolin, insulin receptor, and glucose transporter 4 in mouse 3T3-L1 adipocytes. Arch Biochem Biophys. 2007 Mar 15;459(2):214-22.
57. Lu Z, Jia Q, Wang R, et al. Hypoglycemic activities of A- and B-type procyanidin oligomer-rich extracts from different Cinnamon barks. Phytomedicine. 2010 Sep 17.
58. Qin B, Panickar KS, Anderson RA. Cinnamon: potential role in the prevention of insulin resistance, metabolic syndrome, and type 2 diabetes. J Diabetes Sci Technol. 2010 May;4(3):685-93.
59. Roussel AM, Hininger I, Benaraba R, Ziegenfuss TN, Anderson RA. Antioxidant effects of a cinnamon extract in people with impaired fasting glucose that are overweight or obese. J Am Coll Nutr. 2009 Feb;28(1):16-21.
60. Kim W, Khil LY, Clark R, et al. Naphthalenemethyl ester derivative of dihydroxyhydrocinnamic acid, a component of cinnamon, increases glucose disposal by enhancing translocation of glucose transporter 4. Diabetologia. 2006 Oct;49(10):2437-48.
61. Kim W, Khil LY, Clark R, et al. Naphthalenemethyl ester derivative of dihydroxyhydrocinnamic acid, a component of cinnamon, increases glucose disposal by enhancing translocation of glucose transporter 4. Diabetologia. 2006 Oct;49(10):2437-48.
62. Sheng X, Zhang Y, Gong Z, Huang C, Zang YQ. Improved Insulin Resistance and Lipid Metabolism by Cinnamon Extract through Activation of Peroxisome Proliferator-Activated Receptors. PPAR Res. 2008;2008:581348.
63. Solomon TP, Blannin AK. Effects of short-term cinnamon ingestion on in vivo glucose tolerance. Diabetes Obes Metab. 2007 Nov;9(6):895-901.
64. Hlebowicz J, Hlebowicz A, Lindstedt S, et al. Effects of 1 and 3 g cinnamon on gastric emptying, satiety, and postprandial blood glucose, insulin, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, and ghrelin concentrations in healthy subjects. Am J Clin Nutr. 2009 Mar;89(3):815-21.
65. Solomon TP, Blannin AK. Changes in glucose tolerance and insulin sensitivity following 2 weeks of daily cinnamon ingestion in healthy humans. Eur J Appl Physiol. 2009 Apr;105(6):969-76.
66. Mettler S, Schwarz I, Colombani PC. Additive postprandial blood glucose-attenuating and satiety-enhancing effect of cinnamon and acetic acid. Nutr Res. 2009 Oct;29(10):723-7.
67. Akilen R, Tsiami A, Devendra D, Robinson N. Glycated haemoglobin and blood pressure-lowering effect of cinnamon in multi-ethnic Type 2 diabetic patients in the UK: a randomized, placebo-controlled, double-blind clinical trial. Diabet Med. 2010 Oct;27(10):1159-67.
68. Ziegenfuss TN, Hofheins JE, Mendel RW, Landis J, Anderson RA. Effects of a water-soluble cinnamon extract on body composition and features of the metabolic syndrome in pre-diabetic men and women. J Int Soc Sports Nutr. 2006;3:45-53.
69. Peng X, Ma J, Chao J, et al. Beneficial effects of cinnamon proanthocyanidins on the formation of specific advanced glycation endproducts and methylglyoxal-induced impairment on glucose consumption. J Agric Food Chem. 2010 Jun 9;58(11):6692-6.
70. Bahceci S, Aluclu MU, Canoruc N, et al. Ultrastructural evaluation of the effects of cinnamon on the nervus ischiadicus in diabetic rats. Neurosciences (Riyadh). 2009 Oct;14(4):338-42.
71. Gruenwald J, Freder J, Armbruester N. Cinnamon and health. Crit Rev Food Sci Nutr. 2010 Oct;50(9):822-34.
72. Qin B, Polansky MM, Anderson RA. Cinnamon extract regulates plasma levels of adipose-derived factors and expression of multiple genes related to carbohydrate metabolism and lipogenesis in adipose tissue of fructose-fed rats. Horm Metab Res. 2010 Mar;42(3):187-93.