Does A Popular Dr. Oz-Endorsed Diet Supplement Promote Diabetes?

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Does A Popular Dr. Oz-Endorsed Diet Supplement Promote Diabetes?

Garcinia cambogia extract is a widely known weight loss supplement, often touted by celebrity TV personality Dr. Oz.  But is this dietary supplement as safe as he claims? 



Garcinia cambogia extract (GCE) is a popular diet supplement. Typically, GCE has been described as a safe dietary supplements in the marketplace, supposedly devoid of any serious side effects. The perusal of the medical literature, however, reveals it bestows a number of physiological mechanisms that indicate the supplement nourishes the development, continuance, or aggravation of diabetes. Some of the biological effects of GCE, such as the inhibition of endogenous cholesterol synthesis, the manipulation of the ATP citrate lyase enzyme, and a decrease in metabolic glucose consumption, are shared with statin drugs whose prolonged use has been associated with a significantly increased risk of diabetes.



Garcinia cambogia extract is a widely known weight loss supplement. It gained increasing notoriety after charming celebrity personality Dr. Oz had promoted it on his popular TV show some time back with his characteristic propensity of resorting to provocative language, calling it the "holy grail" and a "breakthrough" in weight loss, apparently devoid of significant adverse effects.1 In that particular TV episode of Oz' show (where he originally advertised the alleged value of the diet pill) the claim is made that garcinia cambogia extract is also beneficial for diabetics.

While leveraging of Dr. Oz' enormous popularity and influence, vendors and websites selling the garcinia diet pill typically make similar positive weight loss-related assertions about the supplement. And some marketers are also pronouncing that the garcinia cambogia diet product is advantageous in diabetes because it allegedly improves glucose control.

Highly authoritative medical sites, too, tend to proclaim that garcinia cambogia extract is generally safe. Although some of these medical sources note that the weight loss product could be somewhat problematic in diabetics because it may lower blood glucose levels when taken in conjunction with certain diabetes medications.


Garcinia Cambogia Extract Raises Blood Glucose Content

Against the backdrop of this customary portrayal of garcinia cambogia extract (GCE) as a quite harmless product is a sizable volume of medical data that indicates the diet supplement promotes hyperglycemia (high blood sugar concentration), a principal clinical manifestation of diabetes.

Research experiments found that hyperglycemia is largely a ramification of an overproduction of glucose in the liver (gluconeogenesis) and the subsequent release of glucose into the blood stream (glycogenolysis), dissenting from the common proposition that insulin resistance is mainly responsible for the excess sugar in the blood.2-6

Stress hormones, such as cortisol, release fat stores (lipolysis) and recruit protein from tissues (proteolysis), activating gluconeogenesis.2,7,8 Diabetics have elevated levels of cortisol in the blood and, as expected, an increased grade of gluconeogenesis.9 Garcinia cambogia extract, akin to cortisol, turns on gluconeogenesis.10-12


Exacerbating the hyperglycemia-spurring state of a heightened cortisol value, the blood content of thyroid hormones (e.g., T3) are depressed in diabetes.9 T3 stimulates cellular glucose uptake and its metabolic disposal ("sugar burning"),9 assisting in the regulation of homeostatic blood glucose levels and helping to decrease excessive sugar levels in the blood, and, therefore, opposes the development or sustainment of hyperglycemia. Contrary to the action of T3, garcinia cambogia supplements shift metabolic respiration to fat burning, away from "sugar burning",13-15 which antagonizes the anti-hyperglycemic effect of T3 and advances the pro-hyperglycemic activity of cortisol, respectively.


The hormone insulin is the chief substance of blood sugar control and is synthesized by the beta-cells in the pancreas.2 An insulin deficiency triggers gluconeogenesis through glucagon activation.2,16 The major "active" ingredient of GCE, hydroxycitric acid, inhibits the enzyme ATP citrate lyase.2,10-13 The curtailment of this enzyme by hydroxycitric acid or blood fats (e.g, mobilized by lipolysis) leads to beta-cell destruction and impairs the release of insulin.15,17,18 Unsurprisingly, and as mentioned, among garcinia cambogia side effects is that the diet pill activates gluconeogenesis.10-12 Diabetics have reduced activity of ATP citrate lyase in beta-cells compared to normal people,19 which suggests that garcinia cambogia extract may worsen the diabetic condition (e.g., hyperglycemia) in individuals with diabetes. An insulin deficit, in turn, raises cortisol,2 enabling, enforcing, and sustaining a hyperglycemic state in a vicious cycle via interactions between depressed T3, high cortisol, and GCE.


Parallels Between The Diabetogenic Properties of Statin Drugs & Garcinia Cambogia Extract

By blocking ATP citrate lyase, garcinia cambogia extract also impedes the body's production of cholesterol, decreasing blood cholesterol levels.13,20 Analogously, the putative primary beneficial effect of the highly profitable statin medications is their ability to inhibit internal cholesterol synthesis.

Research evidence uncovered that the body reacts defensively to the tampering of cholesterol production, augmenting the flow of the vital material from the blood stream into tissues.21 The resulting increased amount of LDL cholesterol inside cells (including pancreatic beta-cells) is thought to increase the load of inflammation -thus, incurring pancreatic injury- because LDL cholesterol is susceptible to oxidative insults.22,23 It has been suggested in the medical literature that this is one of the processes accounting for the significantly higher risk of diabetes from statin therapy.21,23

Another potential mechanism of how cholesterol-lowering agents that inhibit the endogenous production of the vital material can foster diabetes revolves around the fact that (a) beta-cells require cholesterol and the ability to adequately produce the substance for proper insulin secretion and (b) the research observation in connection with statins that the strangling of cholesterol biosynthesis leads to defective insulin secretion from beta cells.24,25 The impairment of insulin secretion by statin medications is among the proposed mechanisms accounting for the association between these drugs and diabetes.21

Significant reductions in total cholesterol and LDL cholesterol had been recorded after the consumption of GCE in human subjects.26 The administration of hydroxycitric acid, the putative key ingredient in GCE, was found to diminish glucose-induced insulin secretion.27,28

As aforecited, in people with type 2 diabetes, the viability of  ATP citrate lyase in pancreatic beta-cells is atrophied compared to non-diabetic individuals.19 While hydroxycitrate-GCE blocks ATP citrate lyase,2,10-13 statins enhance the inhibition of that enzyme,29 which lends support to the notion that the combined ingestion of the two agents synergistically exacerbates their individual diabetogenic potentials.

Furthermore, both statins and GCE reduce cellular glucose consumption,13,14,30 inciting the development of hyperglycemia.31 Decreased metabolic glucose oxidation is one of the physiological attributes that are thought to cause an increase in the incidence of diabetes from statin therapy.23,30



These, and other, relevant research data do not corroborate the perspective that garcinia cambogia extract has a rather solid safety profile as generally and uniformly claimed by both marketers of the diet supplement and respected bodies and resources of medical advice.

On the contrary, these scientific data raise legitimate concerns and eligible arguments about the diabetogenic potential of garcinia cambogia extract to initiate the disease in non-diabetics or agitate it in diabetics, respectively.

(NOTE: A substantially longer, more elaborate version of Rolf Hefti's article is available on his website at



1. & [accessed 1-Jan-2015]


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7. Millet L, Barbe P, Lafontan M, et al: Catecholamine effects on lipolysis and blood flow in human abdominal and femoral adipose tissue. J Appl Physiol (1985). 1998 Jul;85(1):181-8.


8. de Glisezinski I, Larrouy D, Bajzova M, et al: Adrenaline but not noradrenaline is a determinant of exercise-induced lipid mobilization in human subcutaneous adipose tissue. J Physiol. 2009 Jul 1;587(Pt 13):3393-404. doi: 10.1113/jphysiol.2009.168906.


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10. McCarty MF: Utility of metformin as an adjunct to hydroxycitrate/carnitine for reducing body fat in diabetics. Med Hypotheses. 1998 Nov;51(5):399-403.


11. McCarty MF: Promotion of hepatic lipid oxidation and gluconeogenesis as a strategy for appetite control. Med Hypotheses. 1994 Apr;42(4):215-25.


12. McCarty MF: Inhibition of citrate lyase may aid aerobic endurance. Med Hypotheses. 1995 Sep;45(3):247-54.


13. Preuss HG, Rao CV, Garis R, et al: An overview of the safety and efficacy of a novel, natural(-)-hydroxycitric acid extract (HCA-SX) for weight management. J Med. 2004;35(1-6):33-48.


14. Ishihara K, Oyaizu S, Onuki K, et al: Chronic (-)-hydroxycitrate administration spares carbohydrate utilization and promotes lipid oxidation during exercise in mice. J Nutr. 2000 Dec;130(12):2990-5.


15. Cheng IS, Huang SW, Lu HC, et al: Oral hydroxycitrate supplementation enhances glycogen synthesis in exercised human skeletal muscle. Br J Nutr. 2012 Apr;107(7):1048-55.


16. Iversen J: Adrenergic receptors and the secretion of glucagon and insulin from the isolated, perfused canine pancreas. J Clin Invest. 1973 Sep;52(9):2102-16.


17. Chu KY, Lin Y, Hendel A, et al: ATP-citrate lyase reduction mediates palmitate-induced apoptosis in pancreatic beta cells. J Biol Chem. 2010 Oct 15;285(42):32606-15.


18. Guay C, Madiraju SR, Aumais A, et al: A role for ATP-citrate lyase, malic enzyme, and pyruvate/citrate cycling in glucose-induced insulin secretion. J Biol Chem. 2007 Dec 7;282(49):35657-65.


19. MacDonald MJ, Longacre MJ, Langberg EC, et al: Decreased levels of metabolic enzymes in pancreatic islets of patients with type 2 diabetes. Diabetologia. 2009 Jun;52(6):1087-91. doi: 10.1007/s00125-009-1319-6.


20. Vasques CA, Schneider R, Klein-Júnior LC, et al: Hypolipemic Effect of Garcinia cambogia in Obese Women. Phytother Res. 2014 Jun;28(6):887-91. doi: 10.1002/ptr.5076. Epub 2013 Oct 17.


21. Sampson UK, Linton MF, Fazio S: Are statins diabetogenic? Curr Opin Cardiol. 2011 Jul;26(4):342-7. doi: 10.1097/HCO.0b013e3283470359.


22. Kruit JK, Kremer PH, Dai L, et al: Cholesterol efflux via ATP-binding cassette transporter A1 (ABCA1) and cholesterol uptake via the LDL receptor influences cholesterol-induced impairment of beta cell function in mice. Diabetologia. 2010 Jun;53(6):1110-9. doi: 10.1007/s00125-010-1691-2.


23. Carter AA, Gomes T, Camacho X, et al: Risk of incident diabetes among patients treated with statins: population based study. BMJ. 2013 May 23;346:f2610. doi: 10.1136/bmj.f2610.


24. Ishikawa M, Okajima F, Inoue N, et al: Distinct effects of pravastatin, atorvastatin, and simvastatin on insulin secretion from a beta-cell line, MIN6 cells. J Atheroscler Thromb. 2006 Dec;13(6):329-35.


25. Xia F, Xie L, Mihic A, et al: Inhibition of cholesterol biosynthesis impairs insulin secretion and voltage-gated calcium channel function in pancreatic beta-cells. Endocrinology. 2008 Oct;149(10):5136-45. doi: 10.1210/en.2008-0161.


26. Preuss HG, Rao CV, Garis R, et al: An overview of the safety and efficacy of a novel, natural(-)-hydroxycitric acid extract (HCA-SX) for weight management. J Med. 2004;35(1-6):33-48.


27. Chen S, Ogawa A, Ohneda M, et al: More direct evidence for a malonyl-CoA-carnitine palmitoyltransferase I interaction as a key event in pancreatic beta-cell signaling. Diabetes. 1994 Jul;43(7):878-83.


28. Guay C, Madiraju SR, Aumais A, et al: A role for ATP-citrate lyase, malic enzyme, and pyruvate/citrate cycling in glucose-induced insulin secretion. J Biol Chem. 2007 Dec 7;282(49):35657-65.


29. Hanai J, Doro N, Sasaki AT, et al: Inhibition of lung cancer growth: ATP citrate lyase knockdown and statin treatment leads to dual blockade of mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K)/AKT pathways. J Cell Physiol. 2012 Apr;227(4):1709-20. doi: 10.1002/jcp.22895.


30. Hamazaki T, Okuyama H, Ogushi Y, Hama R, "Towards a Paradigm Shift in Cholesterol Treatment. A Re-examination of the Cholesterol Issue in Japan", Ann Nutr Metab. 2015;66 Suppl 4:1-116. doi: 10.1159/000381654. Epub 2015 Apr 29. 


31. Sukhija R, Prayaga S, Marashdeh M, et al., "Effect of statins on fasting plasma glucose in diabetic and nondiabetic patients", J Investig Med. 2009 Mar;57(3):495-9. doi: 10.231/JIM.0b013e318197ec8b.

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