As the New Year commences, millions of Americans resolve to lose weight.
This desire extends beyond cosmetic appearance as the public learns that surplus body fat markedly shortens longevity.
What’s missing is a before-meal strategy that enables people to eat sensibly without every excess calorie converting to storage fat.
In 2012, a study was published showing that people consuming 350 mg of green coffee bean extract before meals lost an average of 17.6 pounds while reducing body fat.1
What few comprehend is that the glucose-lowering effect of green coffee bean extract not only facilitates weight loss, but may lower vascular risks as well.
By way of example, another 2012 study found that heart attack risk increased 69% in a risk group who had only modestly elevated after-meal blood glucose levels.2
No one disputes that diabetics suffer higher incidences of virtually every disease. What researchers are confirming is that even non-diabetics with high normal glucose face shortened life spans.3
The encouraging news is that the obesity-inducing impact of after-meal glucose surges can be mitigated if one commits to “preparing their body to eat” before each meal.
In 1950, Americans spent an average 30% of their income on food.4
Food cost outlays have since dropped to 10% as more efficient ways of growing and processing foods have evolved.5 This makes excess calorie consumption affordable to most everyone in modern societies.
A consequence of food becoming so cheap is that people eat too much, causing obesity rates to explode.
One can easily draw a correlation to the reduction in food costs as a percentage of average income and the increased amounts of body fat people carry. There is more to the story, however.
Tobacco use has plummeted from over 45% in the 1950s to around 19% today.6,7 People who smoke cigarettes weigh less because they usually consume fewer calories. Nicotine also boosts metabolic rate which facilitates burning of body fat.
For decades, nicotine was the drug of choice for large segments of society. Nicotine was smoked throughout the day to induce pleasurable effects in the brain. As smoking rates declined, consumption of high-glycemic calories has become a drug substitute, as people turn to “feel good” food to replace the brain chemical alteration that previous generations derived from nicotine (tobacco).
Obesity-related disease has now overcome the epidemic ill effects caused by cigarette smoking. Just think, while 19% of the population still smokes, almost 70% are now overweight or obese, placing them at sharply higher risks of degenerative disease.8
Unless aggressive interventions are instituted, a public health disaster of unprecedented magnitude is upon us.
Consequences of After-Meal Glucose Surges
Glucose levels rise in your blood after a meal and if you are healthy, glucose will quickly drop back to pre-meal ranges. If glucose rises too much and stays elevated too long, however, a tremendous amount of tissue damage is inflicted.9-11
Diabetics have sharply higher rates of cardiovascular disease compared to non-diabetics.12,13 Yet, even in many not considered diabetic, cardiovascular death rates are 40% higher when fasting glucose levels are above 85 mg/dL.3
The Honolulu Heart Program found that the risk of coronary artery disease correlated with glucose levels measured one hour after a 50-gr oral glucose load. The incidence of fatal coronary artery disease was twice as high in patients with after-meal glucose levels between 157-189 mg/dL compared to those under 114 mg/dL.14
The Whitehall Study of British male civil servants showed that blood glucose levels of 96 mg/dL or higher two hours after a meal were associated with a two-fold increase in mortality from coronary artery disease.15
The Oslo Study indicated that risk of fatal stroke in diabetic patients increased by 13% for each 18 mg/dL elevation in after-meal glucose.16 This is corroborated by a 2012 study showing a 69% increase in heart attack risk in a risk group based on after-meal glucose levels that were only 18 mg/dL above healthy ranges.2
In an interesting study where after-meal glucose spikes were impeded, heart attacks rates dropped an astounding 91%.17 Even when someone suffers a heart attack, the amount of damage to the heart muscle is significantly reduced when steps are taken ahead of time to reduce post-meal glucose surges.18-19
The consistent finding from the scientific literature is that people with higher glucose levels suffer sharply higher vascular disease rates.
Critical Need to Impede Calorie Absorption
Doctors are so used to seeing elevated blood sugar that they seldom comment when fasting glucose levels approach or modestly exceed 100 mg/dL. Not only do these slightly higher blood glucose levels increase disease risk, but they contribute to excess storage of body fat.20
There is a tiny percentage of the population that practices rigid calorie restriction. These individuals maintain fasting glucose under 86 mg/dL and meticulously guard against after-meal meal glucose surges. Their reward for eating around 1,500-1,800 calories a day is reductions in almost every disease risk and a probable reversal of certain aging processes. Calorie restriction favorably restores gene expression that promotes youthful cellular function.21
Life Extension® has advocated moderate to intense calorie restriction since its inception in 1980. We are well aware, however, that even dedicated health conscious individuals cannot consistently under eat.
So to achieve some of the benefits of calorie restriction without suffering chronic hunger, most aging people should “prepare their body to eat” by ingesting compounds before meals that impede sugar absorption and reduce the creation of surplus glucose in their liver from other foods.
Your Liver Converts Protein Into Glucose
Animal and human studies show that those who chronically under eat have markedly lower blood glucose and insulin levels.22,23 Excess insulin contributes to the same degenerative diseases as do high glucose. High insulin also causes excess storage of cellular fat that precludes successful long term weight loss.
People who consistently overeat often have chronically elevated blood glucose, which results in the pancreas secreting a continuous flow of insulin.24-26
Even when one reduces consumption of high-glycemic carbohydrates (sugars and starches), the liver continues to synthesize glucose from the protein-based foods one eats.27,28 The pancreas of course steps up insulin production to reduce this liver-generated glucose.
The vast majority of aging people thus suffer chronically elevated glucose and insulin blood levels. The tragic result can be seen in today’s soaring epidemic of obesity.
The take home lesson is that to achieve health benefits associated with low glucose-insulin blood levels; one must reduce after-meal surges of glucose into the bloodstream AND suppress the synthesis of glucose by the liver (gluconeogenesis).
Fortunately, a variety of nutrients and/or drugs (when taken before meals) can both impede glucose absorption and slash the amount of glucose synthesized in the liver. A further benefit to these nutrients (and/or drugs) is improvement in muscle cell insulin sensitivity, thus further reducing blood glucose/insulin levels.
Confirmation of Sugar’s Lethal Danger
A headline 2012 news story reported that if a person drinks just one 12-ounce sugar sweetened beverage a day, their risk of having a heart attack increases by 20%.29
This finding should not surprise Life Extension® members who have already learned that post-meal spikes in blood glucose increases risk of virtually every age-related disorder.
For example, a study we previously reported on showed that an increase of 63 mg/dL in after-meal glucose increases risk of a heart attack by two-fold or 200%.30
This consistent stream of published data is telling us to avoid any kind of sweetened beverage. This includes naturally sweetened drinks like orange juice that provide little in the way of beneficial polyphenols (like those found in pomegranate juice), but do cause glucose blood levels to spike.
What to Do If You Can’t Resist Sweets
Diets comprising of starches and simple sugars cause the majority of the population to suffer dangerously high glucose-insulin levels.24
As we age, even carbohydrate restriction does not always get us to optimal fasting glucose levels (under 86 mg/dL) because we tend to convert other foods into sugar (via gluconeogenesis).
For the past four years, I have made it a strict habit to take several glucose regulating agents before virtually every meal. The result is that a recent fasting glucose test came in at 81 mg/dL and I’ve shed considerable abdominal fat.
I cannot emphasize enough, based on the totality of the scientific evidence, the critical need to protect your bloodstream before meals against deadly glucose surges.
Drugs That Safely Lower Blood Glucose
For those who prefer to have their doctors prescribe them medications, there are two with proven blood glucose lowering effects.
The first is the glucosidase-inhibiting drug called acarbose. Glucosidase is one of the digestive enzymes that convert ingested sugars into glucose.17,31,32 Taking 25-100 mg of acarbose immediately before one eats will reduce the post-meal glucose surge. Some people complain about intestinal upset with acarbose. It should also be used with caution in those who are hypoglycemic, but otherwise is safe.
The second prescription drug to lower glucose is metformin. By inhibiting gluconeogenesis in the liver, metformin lowers blood glucose-insulin levels.33-37 Metformin also functions by other beneficial mechanisms.38-41 For three decades, Life Extension® provided evidence that metformin is a broad-spectrum anti-aging drug, yet most doctors are ignorant of its multiple benefits and often refuse to prescribe it to non-diabetics.
Metformin can be safely used by virtually everyone as long as they don’t have significant impairment of heart, kidney, or liver function and are not hypoglycemic.
Metformin and acarbose are sold as low-cost generic drugs, but many consumers are wary of prescription drugs and choose natural approaches instead. Fortunately, there are affordable nutrients that function in analogous ways to acarbose and metformin.
Natural Glucose Lowering Agents
Human clinical trials show markedly lower increases in after-meal blood glucose when green coffee berry extract is taken before an oral glucose loading test.42,43
One compelling study showed that people not taking green coffee extract had glucose levels of 130 mg/dL one-hour after sugar ingestion. In study subjects taking 400 mg of green coffee extract, glucose levels dropped to 93 mg/dL after sugar ingestion.44 The difference between having a post-load glucose reading of 93 mg/dL compared to 130 mg/dL is about a 70% reduction in heart attack risk.30
Green coffee bean extract lowers blood glucose by inhibiting carbohydrate digestive enzymes(similar to the drug acarbose) and suppressing creation of glucose in the liver (like metformin.)45-47
For many aging people, taking a green coffee bean extract capsule before each meal may be all they need to achieve healthier fasting and after-meal glucose levels.
Those seeking to reduce glucose readings down to those who practice aggressive calorie restriction should seek a green coffee extract supplement that also provides chromium,48-50 green tea extract,51-55 and Irvingia.56-58
Unique Weight-Loss Mechanisms
Chlorogenic acid in green coffee extract antagonizes glucose absorption.60 It apparently does so by shifting the glucose uptake to more distal regions of the small intestine.60 It also seems to inhibit amylase, the enzyme that breaks down starch into sugar.61
What makes chlorogenic acids in green coffee extract particularly unique is that they inhibit glucose-6-phosphatase, an enzyme that promotes glucose synthesis and release in the liver (gluconeogenesis).46,47 This lowers blood sugar levels and helps promote weight loss.
Chlorogenic acid has been shown to specifically reduce after-meal glucose peaks associated with carbohydrate ingestion.62 This lowers insulin activity and reduces fat accumulation63,64 —both associated with favorable body mass changes.
Additional research has confirmed that compounds in coffee decrease adipose (fat) tissue.64
Together, these glucose-lowering and anti-adipose mechanisms make green coffee extracts an exciting natural way to help combat unwanted body fat.
Preliminary Findings on Green Coffee Extract
A human study showed that daily consumption of coffee rich in the compounds that are found abundantly in green coffee beans resulted in a lower calorie intake—which caused reduced weight and body fat.65
In a 12-week, placebo-controlled study, scientists tested the efficacy of green coffee bean extract. Thirty overweight or obese human volunteers took either the extract or a placebo, dissolved in instant coffee. The extract produced an average 11 pound weight loss. This was paralleled by a decrease in glucose absorption and an increase in glucose utilization. The researchers reported that the lower availability of glucose that results from these effects would cause the body to increase the metabolism of fat reserves, which would eventually decrease body fat and mass.66
A 2011 review and meta-analysis of published and unpublished clinical human studies on green coffee bean extract concluded that there was an overall significant decrease in body weight. However, the scientists concluded that further rigorous research was needed to conclusively establish the weight-loss efficacy of the extract.67
Dynamic Weight Loss Results
To determine conclusively whether green coffee bean extract has an anti-obesity benefit, scientists set up a randomized, double-blind, placebo-controlled, linear dose, crossover study on humans.1
In a crossover study, participants are cycled through different phases of treatment and placebo. In this case, subjects took a high dose of green coffee bean extract for 6 weeks, a lower dose green coffee bean extract for 6 weeks, and a placebo for 6 weeks in a randomized, double-blind manner. Between phases, there was a 2-week “washout” period, making the entire study 22 weeks long.1
Crossover studies are considered sound, because each person in the test group serves as his or her own control. This improves the chances of getting an accurate result, because it eliminates the possibility of the outcome reflecting a difference between the active and control groups. To ensure the findings were more representative, the investigation enlisted both men and women.
Participants were restricted to those who were classified as obese or pre-obese, because people who have these conditions are subject to obesity’s metabolic effects and find weight loss difficult to achieve.
To further ensure that any effect on weight, body fat or BMI could be solely attributed to the extract, there were no significant changes in dietary calories or in the dietary percentages of carbohydrates, fat, and proteins at any time during the study. There were also no significant changes in exercise. The daily 350 mg capsules of green coffee bean extract were the only intervention, although in a non-study situation, people seeking weight reduction would ideally combine green coffee bean extract with lower calorie consumption and greater physical activity to promote maximum weight loss.
During the high-dose phase, subjects took 350 mg of extract, three times daily. The lower dose phase included 350 mg of extract, taken twice daily.1 The placebo phase involved a 350 mg dose three times daily of an inert capsule containing an inactive substance.1
The striking results were published in January 2012.
Over the 22-week trial, investigators found that all subjects experienced a reduction in body weight, BMI, and body fat during both the high-dose and low-dose phases of the study, but not in the placebo phase!
After 12 weeks of administering 350 mg green coffee bean extract three times a day the scientists found that:1
- Weight decreased by over 17.6 pounds on average—with some subjects losing more than 22.7 pounds!
- BMI decreased by an average of 2.92!
- Body fat percentage decreased by an average 4.44%, with some subjects dropping their body fat percentage by 6.44%!
- Heart rate decreased by a significant average of 2.56 beats per minute!
The substantial anti-obesity impact was clearly reflected in the finding that a remarkable 37% of participants who were assessed as having pre-obesity (25-30 BMI) at the start of the study had their condition reversed to the normal-weight range!1
A study follow-up showed that, contrasting with food-restriction diets, a surprising 87.5% of the test subjects were able to maintain their weight loss after completing the study.1 No side effects were observed.
This and other studies demonstrate the importance of “preparing your body to eat” by taking green coffee bean extract before each meal. The dual effects of reducing after-meal glucose and inducing meaningful weight loss make it a supplement that virtually every aging person should take before eating.
Novel Approach to Reverse Fat Accumulation
Reversing obesity requires attacking it on several fronts, including exercise, diet, and novel interventions such as aggressively lowering glucose and insulin blood levels.
The good news is that scientists have confirmed that green coffee bean extract can inhibit certain obesity-inducing processes. Coffee compounds can reduce body fat,64,66,72 improve lipid profiles,73-75 reduce blood glucose,73,76 and can decrease the absorption of calories!46,66 There are many diet plans that people may be involved with right now. By taking 350 mg of green coffee bean extract before each meal, the fat loss effects may be augmented.1
In the study showing weight loss of 17.6 pounds after 12 weeks, the human subjects were not told to make any significant changes in calorie composition, calorie intake, or exercise habits!1 It is important to understand, however, that people who take the time to participate in weight loss studies want to see results, and may instinctively cut some calories and become more active even when they are told not to.
To optimize this natural approach, overweight and obese individuals should take green coffee bean extract and other nutrients like chromium and green tea extract before each meal.
Save Money While Supporting Research
Every time you purchase a Life Extension® product, you contribute to research aimed at extending healthy human life span. Life Extension® continues to fund a record number of scientific projects, while battling incompetent bureaucrats who seek to suffocate medical innovation.
During our 24th annual winter Super Sale, all Life Extension® formulas are discounted so that members can obtain up-to-date versions at the lowest prices of the year.
Until January 31, 2013, members take advantage of Super Sale discounts to stock up on cutting–edge formulas designed to circumvent the underlying mechanisms of aging…including deadly surplus storage of fat pounds.
For longer life,
- Vinson JA, Burnham BR, Nagendran MV. Randomized, double-blind, placebo-controlled, linear dose, crossover study to evaluate the efficacy and safety of a green coffee bean extract in overweight subjects. Diabetes Metab Syndr Obes. 2012;5:21-7.
- Benn M, Tybjaerg-Hansen A, McCarthy MI, Jensen GB, Grande P, Nordestgaard BG. Nonfasting glucose, ischemic heart disease, and myocardial infarction: a Mendelian randomization study. J Am Coll Cardiol. 2012 Jun 19;59(25):2356-65.
- Bjornholt JV, Erikssen G, Aaser E, et al. Fasting blood glucose: an underestimated risk factor for cardiovascular death. Results from a 22-year follow-up of healthy nondiabetic men. Diabetes Care. 1999 Jan;22(1):45-9.
- Available at: http://www.bls.gov/opub/uscs/1950.pdf. Accessed October 31, 2012.
- Available at: http://www.ers.usda.gov/data-products/food-expenditures.aspx. Accessed October 31, 2012.
- Available at: http://healthland.time.com/2011/11/17/are-smokers-today-more-addicted-than-in-the-past/. Accessed October 31, 2012.
- Available at: http://www.gallup.com/poll/109048/us-smoking-rate-still-coming-down.aspx. Accessed October 31, 2012.
- Available at: http://www.cdc.gov/nchs/fastats/overwt.htm. Accessed October 31, 2012.
- Ceriello A. Mechanisms of tissue damage in the postprandial state. Int J Clin Pract Suppl. 2001 Sep;(123):7-12.
- Vlassara H. Advanced glycation end-products and atherosclerosis. Ann Med. 1996 Oct;28(5):419-26.
- Ceriello A. Impaired glucose tolerance and cardiovascular disease: the possible role of post-prandial hyperglycemia. Am Heart J. 2004 May;147(5):803-7.
- Timmer JR, Hoekstra M, Nijsten MW, et al. Prognostic value of admission glycosylated hemoglobin and glucose in nondiabetic patients with ST-segment-elevation myocardial infarction treated with percutaneous coronary intervention. Circulation. 2011 Aug 9;124(6):704-11.
- Norhammar A, Schenck-Gustafsson K. Type 2 diabetes and cardiovascular disease in women. Diabetologia. 2012 Sep 4. [Epub ahead of print]
- Donahue RP, Abbott RD, Reed DM, et al. Postchallenge glucose concentration and coronary heart disease in men of Japanese ancestry. Honolulu Heart Program. Diabetes. 1987 Jun;36(6):689-92.
- Fuller JH, Shipley MJ, Rose G, et al: Coronary-heart-disease risk and impaired glucose tolerance. The Whitehall Study. Lancet. 1980 Jun 28; 1(8183):1373-6.
- Haheim LL, Holme I, Hjermann I, et al: Nonfasting serum glucose and the risk of fatal stroke in diabetic and nondiabetic subjects. 18-year follow-up of the Oslo Study. Stroke. 1995 May;26(5):774-7.
- Zeymer U. Cardiovascular benefits of acarbose in impaired glucose tolerance and type 2 diabetes. Int J Cardiol. 2006 Feb 8;107(1):11-20.
- Minatoguchi S, Zhang Z, Bao N, et al. Acarbose reduces myocardial infarct size by preventing postprandial hyperglycemia and hydroxyl radical production and opening mitochondrial KATP channels in rabbits. J Cardiovasc Pharmacol. 2009 Jul;54(1):25-30.
- Frantz S, Calvillo L, Tillmanns J, et al. Repetitive postprandial hyperglycemia increases cardiac ischemia/reperfusion injury: prevention by the alpha-glucosidase inhibitor acarbose. FASEB J. 2005 Apr;19(6):591-3.
- Parks EJ, Parks EJ. Changes in fat synthesis influenced by dietary macronutrient content. Proc Nutr Soc. 2002 May;61(2):281-6.
- Raffoul JJ; Guo Z; Soofi A; Heydari AR. Caloric restriction and genomic stability. J Nutr Health Aging. 1999 3(2):102-10.
- Martins C, Morgan LM, Robertson MD. Effects of restrained eating behaviour on insulin sensitivity in normal-weight individuals. Physiol Behav. 2009 Mar 23;96(4-5):703-8.
- Heilbronn LK, de Jonge L, Frisard MI, et al. Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial. JAMA. 2006 Apr 5;295(13):1539-48.
- Heller RF, Heller RF. Hyperinsulinemic obesity and carbohydrate addiction: the missing link is the carbohydrate frequency factor. Med Hypotheses. 1994 May;42(5):307-12.
- Zhang X, Zhang G, Zhang H, Karin M, Bai H, Cai D. Hypothalamic IKKbeta/NF-kappaB and ER stress link overnutrition to energy imbalance and obesity. Cell. 2008 Oct 3;135(1):61-73.
- Danielsson A, Fagerholm S, Ost A, et al. Short-term overeating induces insulin resistance in fat cells in lean human subjects. Mol Med. 2009 Jul-Aug;15(7-8):228-34.
- Basu R, Chandramouli V, Dicke B, Landau B, Rizza R. Obesity and type 2 diabetes impair insulin-induced suppression of glycogenolysis as well as gluconeogenesis. Diabetes. 2005 Jul;54(7):1942-8.
- Kim DH, Perdomo G, Zhang T, et al. FoxO6 integrates insulin signaling with gluconeogenesis in the liver. Diabetes. 2011 Nov;60(11):2763-74.
- de Koning L, Malik VS, Kellogg MD, Rimm EB, Willett WC, Hu FB. Sweetened beverage consumption, incident coronary heart disease, and biomarkers of risk in men. Circulation. 2012 Apr 10;125(14):1735-41, S1.
- Gerstein HC, Pais P, Pogue J, Yusuf S. Relationship of glucose and insulin levels to the risk of myocardial infarction: a case-control study. J Am Coll Cardiol. 1999 Mar;33(3):612-9.
- D'Elia JN, Salyers AA. Contribution of a neopullulanase, a pullulanase, and an alpha-glucosidase to growth of Bacteroides thetaiotaomicron on starch. J Bacteriol. 1996 Dec;178(24):7173-9.
- Oyama T, Saiki A, Endoh K, et al. Effect of acarbose, an alpha-glucosidase inhibitor, on serum lipoprotein lipase mass levels and common carotid artery intima-media thickness in type 2 diabetes mellitus treated by sulfonylurea. J Atheroscler Thromb. 2008 Jun;15(3):154-9.
- Caton PW, Nayuni NK, Kieswich J, Khan NQ, Yaqoob MM, Corder R. Metformin suppresses hepatic gluconeogenesis through induction of SIRT1 and GCN5. J Endocrinol. 2010 Apr;205(1):97-106.
- Otto M, Breinholt J, Westergaard N. Metformin inhibits glycogen synthesis and gluconeogenesis in cultured rat hepatocytes. Diabetes Obes Metab. 2003 May;5(3):189-94.
- Perriello G, Misericordia P, Volpi E, Santucci A, Santucci C, Ferrannini E, Ventura MM, Santeusanio F, Brunetti P, Bolli GB. Acute antihyperglycemic mechanisms of metformin in NIDDM. Evidence for suppression of lipid oxidation and hepatic glucose production. Diabetes. 1994 Jul;43(7):920-8.
- Saxena P, Prakash A, Nigam A. Effect of metformin therapy on 2-h post-glucose insulin levels in patients of polycystic ovarian syndrome. J Hum Reprod Sci. 2010 Sep;3(3):139-42.
- Verma S, Bhanot S, McNeill JH. Metformin decreases plasma insulin levels and systolic blood pressure in spontaneously hypertensive rats. Am J Physiol. 1994 Oct;267(4 Pt 2):H1250-3.
- Isakovic A, Harhaji L, Stevanovic D, et al. Dual antiglioma action of metformin: cell cycle arrest and mitochondria-dependent apoptosis. Cell Mol Life Sci. 2007 May;64(10):1290-302.
- Xie Y, Wang YL, Yu L, et al. Metformin promotes progesterone receptor expression via inhibition of mammalian target of rapamycin (mTOR) in endometrial cancer cells. J Steroid Biochem Mol Biol. 2011 Sep;126(3-5):113-20.
- Ben Sahra I, Regazzetti C, Robert G, et al. Metformin, independent of AMPK, induces mTOR inhibition and cell-cycle arrest through REDD1. Cancer Res. 2011 Jul 1;71(13):4366-72.
- Micic D, Cvijovic G, Trajkovic V, Duntas LH, Polovina S. Metformin: its emerging role in oncology. Hormones (Athens). 2011 Jan-Mar;10(1):5-15.
- Ong KW, Hsu A, Tan BK. Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes. PLoS One. 2012 7(3):e32718.
- Abidoff MT. Special clinical report on effects of glucose-6-phosphatase on human subjects. Russian Ministry of Health, Moscow, 1999. Unpublished study.
- Nagendran MV. Effect of green coffee bean extract (GCE), High in Chlorogenic Acids, on Glucose Metabolism. Poster presentation number: 45-LB-P. Obesity 2011, the 29th Annual Scientific Meeting of the Obesity Society. Orlando, Florida. October 1-5, 2011.
- Ishikawa A, Yamashita H, Hiemori M, et al. Characterization of inhibitors of postprandial hyperglycemia from the leaves of Nerium indicum. J Nutr Sci Vitaminol (Tokyo). 2007 Apr;53(2):166-73.
- Henry-Vitrac C, Ibarra A, Roller M, Merillon JM, Vitrac X. Contribution of chlorogenic acids to the inhibition of human hepatic glucose-6-phosphatase activity in vitro by Svetol, a standardized decaffeinated green coffee extract. J Agric Food Chem. 2010 Apr 14;58(7):4141-4.
- Andrade-Cetto A, Vazquez RC. Gluconeogenesis inhibition and phytochemical composition of two Cecropia species. J Ethnopharmacol. 2010 Jul 6;130(1):93-7.
- Anderson RA, Cheng N, Bryden NA, et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes. 1997 Nov;46(11):1786-91.
- Lamson DW, Plaza SM. The safety and efficacy of high-dose chromium. Altern Med Rev. 2002 Jun;7(3):218-35.
- Bahijri SM. Effect of chromium supplementation on glucose tolerance and lipid profile. Saudi Med J. 2000 Jan;21(1):45-50.
- Tsuneki H, Ishizuka M, Terasawa M, Wu JB, Sasaoka T, Kimura I. Effect of green tea on blood glucose levels and serum proteomic patterns in diabetic (db/db) mice and on glucose metabolism in healthy humans. BMC Pharmacol. 2004 Aug 26;4:18.
- Venables MC, Hulston CJ, Cox HR, Jeukendrup AE. Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans. Am J Clin Nutr. 2008; 87(3) 778-84.
- Deng ZY, Tao BY, et al. Effect of green tea and black tea on blood glucose, triglycerides, and antioxidants in aged rats. J Agricult Food Chem. 1998 46(10):3875-78.
- Collins QF, Liu HY, Pi J, et al. Epigallocatechin-3-gallate (EGCG), a green tea polyphenol, suppresses hepatic gluconeogenesis through 5’-AMP-activated protein kinase. J Biol Chem. 2007 Oct 12;282(41):30143-9.
- Cao H, Hininger-Favier I, Kelly MA, et al. Green tea polyphenol extract regulates the expression of genes involved in glucose uptake and insulin signaling in rats fed a high fructose diet. J Agric Food Chem. 2007 Jul 25;55(15):6372-8.
- Ngondi JL, Etoundi BC, Nyangono CB, Mbofung CM, Oben JE. IGOB131, a novel seed extract of the West African plant Irvingia gabonensis, significantly reduces body weight and improves metabolic parameters in overweight humans in a randomized double-blind placebo controlled investigation. Lipids Health Dis. 2009 Mar 2;8:7.
- Ngondi JL, Fossouo E, Djiotsa EJ, Oben J. Glycaemic variations after administration of Irvingia gabonensis seeds fractions in normoglycemic rats. Afr J Trad CAM. 2006;3:94-101.
- Adamson I, Okafor C, Abu-Bakare A. A supplement of Dikanut (Irvingia gabonesis) improves treatment of type II diabetics. West Afr J Med. 1990 Apr-Jun;9(2):108-15.
- Zhang Y, Lee ET, Cowan LD, Fabsitz RR, Howard BV. Coffee consumption and the incidence of type 2 diabetes in men and women with normal glucose tolerance: The Strong Heart Study. Nutr Metab Cardiovasc Dis. 2011 Jun;21(6):418-23.
- Johnston KL, Clifford MN, Morgan LM. Coffee acutely modifies gastrointestinal hormone secretion and glucose tolerance in humans: glycemic effects of chlorogenic acid and caffeine. Am J Clin Nutr. 2003 Oct;78(4):728-33.
- Narita Y, Inouye K. Kinetic analysis and mechanism on the inhibition of chlorogenic acid and its components against porcine pancreas alpha-amylase isozymes I and II. J Agric Food Chem. 2009 Oct 14;57(19):9218-25.
- Tunnicliffe JM, Eller LK, Reimer RA, Hittel DS, Shearer J. Chlorogenic acid differentially affects postprandial glucose and glucose-dependent insulinotropic polypeptide response in rats. Appl Physiol Nutr Metab. 2011 Oct;36(5):650-9.
- Loopstra-Masters RC, Liese AD, Haffner SM, Wagenknecht LE, Hanley AJ. Associations between the intake of caffeinated and decaffeinated coffee and measures of insulin sensitivity and beta cell function. Diabetologia. 2011 Feb;54(2):320-8.
- Shimoda H, Seki E, Aitani M. Inhibitory effect of green coffee bean extract on fat accumulation and body weight gain in mice. BMC Complement Altern Med. 2006 Mar 17;6:9.
- Bakuradze T, Boehm N, Janzowski C, et al. Antioxidant-rich coffee reduces DNA damage, elevates glutathione status and contributes to weight control: results from an intervention study. Mol Nutr Food Res. 2011 May;55(5):793-7.
- Thom E. The effect of chlorogenic acid enriched coffee on glucose absorption in healthy volunteers and its effect on body mass when used long-term in overweight and obese people. J Int Med Res. 2007;35(6):900-8.
- Onakpoya I, Terry R, Ernst E. The use of green coffee extract as a weight loss supplement: a systematic review and meta-analysis of randomised clinical trials. Gastroenterol Res Pract. 2011;2011. pii: 382852.
- Available at: http://www.who.int/mediacentre/factsheets/fs311/en/. Accessed on April 24, 2012.
- Adams KF, Schatzkin A, Harris TB, et al. Overweight, obesity, and mortality in a large prospective cohort of persons 50 to 71 years old. N Engl J Med. 2006 August 24;355(8):763-78.
- Available at : http://www.oecd.org/dataoecd/1/61/49716427.pdf. Accessed April 24, 2012
- Moriarty J, Branda M, Olsen Kerry, et al. The Effects of incremental costs of smoking and obesity on health care costs among adults: A 7-year longitudinal study. J Occup Environ Med. 2012 March;54(3):286-91.
- Murase T, Misawa K, Minegishi Y, Aoki M, Ominami H, Suzuki Y, Shibuya Y, Hase T. Coffee polyphenols suppress diet-induced body fat accumulation by downregulating SREBP-1c and related molecules in C57BL/6J mice. Am J Physiol Endocrinol Metab. 2011 Jan;300(1):E122-33.
- Li SY, Chang CQ, Ma FY, Yu CL. Modulating effects of chlorogenic acid on lipids and glucose metabolism and expression of hepatic peroxisome proliferator-activated receptor-alpha in golden hamsters fed on high fat diet. Biomed Environ Sci. 2009 Apr;22(2):122-9.
- Superko HR, Bortz W Jr, Williams PT, Albers JJ, Wood PD. Caffeinated and decaffeinated coffee effects on plasma lipoprotein cholesterol, apolipoproteins, and lipase activity: a controlled, randomized trial. Am J Clin Nutr. 1991 Sep;54(3):599-605.
- Cho AS, Jeon SM, Kim MJ, Yeo J, Seo KI, Choi MS, Lee MK. Chlorogenic acid exhibits anti-obesity property and improves lipid metabolism in high-fat diet-induced-obese mice. Food Chem Toxicol. 2010 Mar;48(3):937-43.
- Bidel S, Hu G, Sundvall J, Kaprio J, Tuomilehto J. Effects of coffee consumption on glucose tolerance, serum glucose and insulin levels: a cross-sectional analysis. Horm Metab Res. 2006;38(1):38-43.