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Glucose Control Support Helps Maintain Healthy Blood Sugar Levels* 

Diabetes is often misunderstood as a simple sugar imbalance that can be readily corrected through medical intervention. In truth, it is a complex metabolic disorder in which a confluence of social, behavioral, dietary, and lifestyle factors unmask an underlying genetic susceptibility. The disease has serious implications for vision, cardiovascular health, and kidney and neural functions. Its expression largely depends on lifestyle issues, including diet, weight management, and physical exercise - a multifaceted combination of factors that makes treatment complex and challenging.

The predominant form of diabetes is type II or non-insulin-dependent diabetes, a disease highly correlated with family history, physical inactivity, obesity, and ethnicity. Traditionally associated with middle age, the incidence of type II diabetes among younger adults and children is rising dramatically. More common in women, especially those with a history of gestational (pregnancy-related) diabetes, its prevalence in America has tripled in the last 30 years. While increasing across all age and ethnic groups, its ascendance among children and adolescents is most worrisome.

Over 90% of diabetics are type II, and it is the rapid increase in this form of the disease that is propelling the global increase in all diabetes cases. While diabetes exhibits a strong hereditary component, its rate of increase is too great to be a consequence of increased gene frequency. Instead, evidence points toward the combined influences of lifestyle, dietary, and environmental factors.2

An Emerging Epidemic:
Diabetes and ChildrenVirtually unknown in children until recently, type II diabetes is now appearing with alarming regularity in overweight and sedentary young people. During the last three decades, the number of overweight children in the US has more than doubled. With this has come a dramatic rise in type II diabetes. In major US urban centers, the percentage of children with newly diagnosed type II diabetes has ballooned from less than 5% in 1994 to 30-50% in recent years.3

Obesity is a hallmark of the disease. A predisposition toward visceral obesity (deposition of abdominal fat) is associated with increased insulin resistance and contributes to its early onset.4 This may explain why 85% of American children who develop type II diabetes are overweight or obese at the time of diagnosis. According to Dr. Arlan Rosenbloom, chair of the American Diabetes Association Consensus Panel, “Type II diabetes in children is an emerging epidemic.”

Insulin Resistance:
the Silent StalkerSyndrome X is the dark force behind type II diabetes. Also known as metabolic syndrome, it is a preclinical stage of the disease, believed to affect up to 25% of North American adults. A constellation of metabolic changes that progress silently over a period of years, Syndrome X is characterized by increased resistance to insulin, the regulatory hormone that suppresses hepatic (liver) glucose output and removes excess glucose from the blood.

The onset of insulin resistance is characterized by a host of related symptoms, including:
hypertension (high blood pressure)
elevated blood triglycerides (fats)
elevated LDL (“bad”) cholesterol
reduced HDL (“good”) cholesterol
accelerated hardening of the arteries
proliferation of cells in the arterial walls
development of abdominal obesity
glycosylation (cross-linking of fats and proteins with glucose)
hyperinsulinemia (high-blood insulin levels).

The syndrome is particularly alarming in children and adolescents because the changes, which in adults are usually spread over a number of years, are compressed into a few short years in young teens.5 The longer a person has the disease, the greater the likelihood of developing long-term disabilities. Unfortunately, physicians are now seeing more young people prematurely develop these life-threatening complications.

The prognosis is not encouraging: approximately one-third to one-half of those diagnosed with insulin resistance will develop diabetes. Of those, two-thirds will eventually die of cardiovascular complications. Compared to non-diabetics, adult diabetics are almost twice as likely to have asthma, three times more likely to have hypertension and heart disease, and four times more likely to suffer a stroke.6


Insulin is produced by highly specialized beta cells in the pancreas, a lobular gland located behind the stomach. The hormone is secreted into the blood in response to elevated blood-sugar levels. Insulin helps the body utilize blood sugar by binding to specialized receptor sites on the cellular surfaces, much like a key fits into a lock. Insulin “unlocks” the receptor and glucose (a molecule too large to pass through) is transported into the cell. Once inside, glucose is used for cellular fuel, and any excess is stored as glycogen (a form of animal starch) or converted to glycerol for the formation of fat.

When blood sugar levels are low, or during times of stress, liver glycogen stores are quickly converted back to glucose by the action of glucagon, another pancreatic hormone. Glucagon also encourages the breakdown of fat in adipose tissue to glycerol and fatty acids. The liver reconverts these to glucose, releasing it into the blood. Through this intricate balancing act, insulin and glucagon perform a central role in regulating the body’s blood-sugar level.

Rising insulin resistance disrupts this balance when the normal levels of insulin no longer unlock the cellular “doors.” The beta cells of the pancreas, in a futile attempt to restore homeostasis, shift into “overdrive” and begin pumping out ever-increasing amounts of insulin. Chronically high levels of insulin further “desensitize” the cellular receptors, leading to even greater insulin resistance. A vicious and damaging cycle ensues—the genesis of type II diabetes.

What defies explanation is what causes insulin resistance in the first place. We know that virtually everyone who develops type II diabetes starts with insulin resistance. We also know that the risk of developing type II diabetes is strongly correlated with central body obesity and the ectopic (abnormal) accumulation of fat. It appears that insulin resistance may not be determined so much by the amount of body fat as by where the fat is located.1 In fact, one of the best predictive markers for insulin resistance is excess body weight, in particular weight around the waist.

McGarry presents a compelling case that the ectopic accumulation of fat in muscle and other peripheral tissues is intimately involved with the onset of insulin resistance and the gradual collapse of pancreatic beta cell function.1 Insulin sensitivity can fall dramatically without the appearance of diabetes, as long as the pancreatic beta cells compensate. It is their inevitable demise (possibly due to lipotoxicity) that leads to increased hyperglycemia, a further rise in blood lipids, and an ever-greater accumulation of fat in the muscle cell. Increasing hyperlipidemia (high blood lipids) in turn exacerbates insulin resistance and degrades liver function.

According to McGarry, in the progression from being overweight to being obese, the liver becomes resistant to insulin and the hormone’s ability to suppress hepatic (liver) glucose production. “Under these conditions, the hyperinsulinemia turns the liver into a ‘fat-producing factory’ with all of its negative downstream effects.”1 Once established, these disturbances in lipid metabolism are devastating to blood sugar balance and weight management. Accel-eration of the cycle and eventual collapse of pancreatic insulin production herald the appearance of diabetes.

The answer to how these metabolic derangements begin may lie in the “thrifty gene hypothesis,” which postulates the presence of a genetic factor designed to promote extra fat deposition.7 Speculation also suggests a defect in the leptin-signaling system, a metabolic pathway that appears to mediate fatty acid metabolism in muscle tissue and acts as a kind of “fuel gauge” to monitor cellular energy status.8 (Leptin, a chemical messenger produced by the adipose, or fat-storing, cells of the body, initiates the breakdown and oxidation of stored fat.)9 Still other research points to the possible development of functional resistance to the actions of the leptin hormone itself.10,11

Whatever the mechanism, a diminished capacity to oxidize fat appears to be a pre-eminent clinical marker for insulin resistance.12-14 This is supported by animal studies, which confirm that dietary lowering of muscle triglycerides improves insulin sensitivity and reverses diabetes.15,16 The fact that two of the most effective preventive programs for diabetes are diet and exercise lends credence to the argument that onset of the disease involves a profound disturbance in lipid dynamics.
The previous clinical definition of insulin resistance syndrome required evidence of insulin resistance. Disturbances in glucose metabolism, however, develop relatively late in the disease’s progression. Consequently, under the old definition, many people in the early stages of insulin resistance went undiagnosed.

The new definition, developed recently by the US National Cholesterol Education Panel,
incorporates five easily measured variables:

abdominal obesity
elevated fasting blood
triglyceride levels
low levels of HDL (“good”) cholesterol
high fasting blood sugar levels
high blood pressure.

Under the new definition, a person with any three of these conditions is classified as having insulin resistance syndrome. To assess whether the new criteria could predict excess risk for heart disease and diabetes, researchers found that the risk of coronary heart disease—and, more strikingly, diabetes—rose as the number of metabolic abnormalities increased. Men with four to five features of the syndrome had almost four times the risk of coronary heart disease and 25 times the risk of diabetes compared to those with no abnormalities. The study also confirmed that C-reactive protein, an inflammatory marker, was significantly elevated in men with metabolic syndrome compared to those without metabolic syndrome.17

Current guidelines suggest that people are diabetic if their fasting glucose levels exceed 126 mg/dL (7.0 mmol/L). Levels over 109 mg/dL indicate a prediabetic state and levels below 109 are considered normal. While significantly improved from the previously used glucose tolerance test, these recommendations may still be too lenient. In October 2003, the American Diabetes Association further reduced the cut-off for impaired glucose tolerance from 109 to 100 mg/dL, meaning anyone with fasting glucose levels above 100 would be classified as prediabetic. More recently, the Life Extension Foundation has prescribed optimal fasting glucose levels of less than 86 mg/dL.18 This recommendation is based on clinical evidence that higher fasting levels can progressively and markedly increase cardiovascular risk.19

Lowering the bar on fasting glucose levels is a good thing, as it is estimated that up to one-half of diabetes sufferers have not been diagnosed.20 Screening for diabetes should begin at 45 years of age and should be repeated every three years in persons without risk factors and more frequently in individuals with risk factors.21

Fortunately, insulin resistance and type II diabetes lend themselves to a holistic approach to disease management. Lifestyle modifications can have a remarkable impact on prevention and treatment. Controlling insulin resistance—not the high blood sugar levels caused by it—is the key to success.

With a death toll second only to smoking, obesity claims the lives of nearly 300,000 Americans each year.22 According to the American Diabetes Association, “Obesity is now reaching epidemic proportions in the US and elsewhere.” From 1991 to 2001, obesity in America increased 74% while the prevalence of diabetes increased 61%. The tripling of type II diabetes incidence over the last 30 years owes much to this surge in obesity.

A recent study by researchers at the Centers for Disease Control and Prevention investigated the links between obesity, diabetes, high blood pressure, high cholesterol, asthma, and arthritis. Compared to adults of a healthy weight, obese adults had twice the risk for high cholesterol, three times the risk for asthma, four times the risk for arthritis, and over six times the risk for hypertension.23 The strongest correlation was between obesity and diabetes: obese people exhibited over seven times the risk for diabetes compared with people of normal weight.

The good news is that up to 90% of type II diabetes cases can be prevented with simple lifestyle changes, including diet, exercise, and smoking cessation.24 The Diabetes Prevention Program, a multi-center trial involving over 3,200 people with impaired glucose tolerance, was the first large-scale study to demonstrate conclusively that weight loss can effectively delay type II diabetes. Results showed that lifestyle intervention, consisting of calorie reduction and 30 minutes a day of mild exercise, reduced risk by 58%—almost double that conferred by the oral diabetes drug metformin (Glucophage®). The results were so convincing that the study was concluded earlier than planned. The authors surmise that up to 10 million Americans can sharply lower their risk of diabetes through simple attention to diet, exercise, and lifestyle modification.25 These findings are supported by the earlier work of Dr. Roy Walford, who demonstrated that caloric restriction aggressively lowers both fasting glucose and blood insulin levels.18

Growing evidence suggests that C-reactive protein may also play a role in the development of central body obesity and the onset of type II diabetes.26 Abdominal fat is a major source of this inflammatory agent, and the increased risk of atherosclerosis and insulin resistance associated with visceral obesity may well be a consequence of enhanced C-reactive protein secretion. The surest and safest way to remedy the situation is to lose weight. Women who completed a 12-week restricted-calorie diet lost an average of 17.4 pounds and reduced their C-reactive protein levels by 26%.27

One thing is certain:
people who are overweight are already in a prediabetic state and need to take corrective action before the damage is done. Unfortunately, most diagnoses occur far too late in the game.

While opinions differ as to which ratio of carbohydrates, proteins, and fats is optimal in preventing and treating diabetes, it is safe to say that carbohydrates create insulin. As more carbohydrates are consumed, more insulin is produced. Today’s obesity and diabetes epidemics reflect that too many people are asking their bodies to run on the wrong grade of fuel—refined carbohydrates. In the 1980s, Americans consumed an average of 12 pounds of sugar each year; today, US per-capita sugar consumption is an astounding 150+ pounds per year.28

Stanford’s Dr. Gerald Reaven suggests that a diet consisting of 45% carbohydrates, 40% “good” fats, and 15% protein will benefit individuals with insulin resistance. According to Reaven, only when healthy fats replace carbohydrates will insulin levels drop and clusters of symptoms associated with insulin resistance abate.29 Unfortunately, the standard diabetic diet recommended by most physicians is very high in carbohydrates, which raises blood sugar, stimulates insulin production, and almost guarantees that the diabetic will be a patient for life.

People need to pay attention not only to their total carbohydrate load, but also to the types of carbohydrates they eat. High-glycemic foods—such as white rice, white flour-based products, pasta, starchy vegetables, and many processed foods—are quickly converted to blood sugar when digested, causing insulin levels to spike. Conversely, the carbohydrates found in low-glycemic foods, such as asparagus, broccoli, cabbage, green beans, and other low-starch vegetables and fruits, are converted slowly to blood sugar and create a more gradual rise in blood insulin levels. Avoiding “white foods” is a simple recipe that can help you avoid trouble.
While total fat intake does not appear to influence the risk of diabetes, consuming trans-saturated fats (trans fats), the hydrogenated or partially hydrogenated oils so ubiquitous in processed and fast foods, can greatly increase your risk for diabetes. A recent study showed that a minuscule 2% increase in calories from trans-fatty acids raised the risk of diabetes in women by 39%; conversely, a 5% increase in calories from polyunsaturated (good) fats reduced the risk for diabetes by 37%.30

If nothing else, simply replacing trans-fats in the diet with polyunsaturated fats will reduce the risk of diabetes dramatically. Dietary fats that are considered to be beneficial include extra virgin olive oil, fish oil, almond oil and almond butter, avocados, nuts, and seed oils such as sesame, pumpkin, sunflower, and flax.

Eating a diet rich in soluble and insoluble fiber improves insulin sensitivity and reduces circulating insulin levels. Fiber impedes gastric emptying and the passage of food through the gut, slows the breakdown of high-glycemic starchy foods, and delays glucose uptake into the blood. In a recent study reported in the New England Journal of Medicine, researchers conclude that a high-fiber diet significantly improves glycemic control, decreases insulin levels, and lowers plasma lipid concentrations in as little as six weeks.31
Exercise improves cardiovascular function and the body’s ability to metabolize glucose. Weight loss through exercise and diet correlates to a return to normal levels of insulin resistance and may be the single most effective approach to treating insulin resistance and reducing the risk of diabetes.32 Conditioned muscles are more responsive to insulin and blood sugar balance than non-conditioned muscles,28 possibly due to an increase in the number of insulin receptors on the muscle cell.

Physical exercise burns calories, and as energy expenditure is increased, the incidence of diabetes is found to decrease. Moreover, this protective effect appears to be most pronounced in individuals who are at greatest risk for developing the disease.33 Physically fit people also secrete less insulin. Results from the Nurses’ and Physicians’ Health Studies, conducted in the early 1990s, reveal that insulin response is more attenuated in physically fit individuals than in people who are less fit.34,35 Researchers recently demonstrated that when individuals are introduced to a regular exercise program, they experience a striking decrease in their risk of developing diabetes.36 In fact, regular exercise, when combined with weight loss, can reduce the insulin requirements of type II diabetics by up to 100%.37

A low-glycemic, reduced-calorie diet with healthy fats and fiber, along with regular exercise, is a safe and effective means to prevent and treat diabetes, as well as to shed excess weight.

The Role of Supplements:Beyond a healthy diet, considerable evidence demonstrates the efficacy of daily nutritional supplementation as a way to prevent and treat diabetes. The following dietary supplements have been found to be particularly beneficial.

Artichoke Leaves:

Artichokes are packed with phytonutrients such as quercetin, rutin, gallic acid, and cynarin, all working to protect against many health risks including cancer, heart disease, liver dysfunction, high cholesterol, and diabetes.38  In 2004, the United States Department of Agriculture conducted its largest, most comprehensive study analyzing the antioxidant content of the most commonly consumed foods. To the surprise of many, artichokes ranked in the top four vegetables and seventh overall.39 Throughout this article you’ll learn about the numerous ways that incorporating artichokes into your diet can benefit your health and well-being.

High cholesterol is associated with an increased risk for coronary heart disease and atherosclerosis. Artichokes and artichoke leaf extract reduce cholesterol levels. The efforts to study this idea date back all the way to the 1970s, when scientists began examining cynarin and cholesterol in their labs.41

In a 12-week, double-blind study, 75 patients received placebo or 1,280 mg standardized artichoke leaf daily. At the end of the 12 weeks, the treated group recorded a modest reduction in total cholesterol of 4.2%.42

To further demonstrate the artichoke’s heart-healthy powers, scientists set up a randomized, placebo-controlled study to examine the effect of artichoke leaf extract in patients with high cholesterol. All participants showed positive results. Over 6 weeks, participants were split up, with half receiving artichoke extract and the rest a placebo. The patients receiving artichoke were shown to have an 18.5% reduction in cholesterol level.43

Digestive Health

The high concentration of cynarin in artichokes not only affects cholesterol, but also can contribute to aiding in digestive health. Cynarin is known to stimulate the production of bile, which enables us to digest fats and absorb vitamins from our food, making artichokes an excellent way to start any meal.40

Studies have shown that artichoke leaf extract can be very helpful for people suffering from irritable bowel syndrome (IBS) and dyspepsia, or upset stomachs. In a study done at the University of Reading in the United Kingdom, 208 adults who suffered from IBS and dyspepsia were monitored over a two-month period of intervention with artichoke leaf extract. Results showed a 26.4% reduction in IBS incidence among the participants at the end of the trial. A significant shift of self-reported bowel patterns away from “alternating constipation/diarrhea” toward “normal” was observed as well. Dyspepsia symptoms also decreased by 41% after treatment, and in general, the participants noted a 20% increase in quality of life after treatment.44

Liver Function

The boost in bile production you gain from eating artichokes can also be attributed to cynarin, which can be very beneficial to the health of your liver. The bile that your liver produces helps to remove dangerous toxins and digest fats. Artichokes also contain the flavonoid silymarin, a powerful liver protectant. Silymarin averts the process of lipid peroxidation from occurring in the cell membranes of the tissues of the liver, making the artichoke an ideal weapon in your arsenal to help you obtain optimal liver function.45

References:
1. McGarry JD. Banting lecture 2001: dysregu- lation of fatty acid metabolism in the etiolo- gy of type 2 diabetes. Diabetes. 2002 Jan;51(1):7-18.
2. Rosenbloom A, Arslanian S, Brink S, et al. Type 2 diabetes in children and adolescents. Diabetes Care. 2000 Mar;23(3):381-9.
3. Rocchini AP. Childhood obesity and a dia- betes epidemic. N Engl J Med. 2002 Mar;346(11):854-5.
4. Widen E, Lehto M, Kanninen T, Walston J, Shuldiner AR, Groop LC. Association of a polymorphism in the beta 3-adrenergic- receptor gene with features of the insulin resistance syndrome in Finns. N Engl J Med. 1995 Aug;333(6):348-51.
5. Grundy SM, Howard B, Smith S Jr, Eckel R, Redberg R, Bonow RO. Prevention Conference VI: Diabetes and Cardiovascular Disease: executive summary: conference proceeding for healthcare pro- fessionals from a special writing group of the American Heart Association. Circulation. 2002 May;105(18):2231-9.
6. Stagnitti MN. Statistical Brief #34: The Prevalence of Obesity and Other Chronic Health Conditions among Diabetic Adults in the U.S. Community Population, 2001. Medical Expenditure Panel Survey. Agency for Healthcare Research and Quality, Department of Health and Human Services webpage. Available at: http://www.meps.ahrq.gov/PrintProducts/ PrintProd_Detail.asp. Accessed Jan 30, 2004.
7. Neel JV. Diabetes mellitus: a “thrifty” genotype rendered detrimental by “progress”? Am J Hum Genet. 1962 Dec;14:353-62.
8. Minokoshi Y, Kim YB, Peroni OD, et al. Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase. Nature. 2002 Jan;415(6869):339-43.
9. Deus P. Leptin: The next big thing. Mind and Muscle Magazine [serial online]. Oct 26, 2001; Issue 3. Available at: http://mindand muscle.net/magazine/i3leptin.html. Accessed February 12, 2004.
10. Sinha MK, Caro JF. Clinical aspects of lep- tin. Vitam Horm. 1998;54:1-30.
11. Eiden S, Daniel C, Steinbrueck A, Schmidt I, Simon E. Salmon calcitonin—a potent inhibitor of food intake in states of impaired leptin signalling in laboratory rodents. J Physiol. 2002 Jun;541(Pt 3):1041-8.
12. Astrup A, Buemann B, Christensen NJ, Toubro S. Failure to increase lipid oxidation in response to increasing dietary fat content in formerly obese women. Am J Physiol. 1994 Apr;266(4 Pt 1):E592-E599.
13. Froidevaux F, Schutz Y, Christin L, Jequier E. Energy expenditure in obese women before and during weight loss, after refeed- ing, and in the weight-relapse period. Am J Clin Nutr. 1993 Jan;57(1):35-42.
14. Ravussin E, Lillioja S, Knowler WC, et al. Reduced rate of energy expenditure as a risk factor for body-weight gain. N Engl J Med. 1988 Feb;318(8):467-72.
15. Man ZW, Hirashima T, Mori S, Kawano K. Decrease in triglyceride accumulation in tis- sues by restricted diet and improvement of diabetes in Otsuka Long-Evans Tokushima fatty rats, a non-insulin-dependent diabetes model. Metabolism. 2000 Jan;49(1):108-14.
16. Ohneda M, Inman LR, Unger RH. Caloric restriction in obese pre-diabetic rats prevents beta-cell depletion, loss of beta-cell GLUT 2 and glucose incompetence. Diabetologia. 1995 Feb;38(2):173-9.
17. Sattar N, Gaw A, Scherbakova O, et al. Metabolic syndrome with and without C- reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation. 2003 Jul;108(4):414-9.
18. Faloon W. What you don’t know about blood sugar. Life Extension Magazine. January 2004:11-20.
19. 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 nondia- betic men. Diabetes Care. 1999 Jan;22(1):45-49.
20. Harris MI, Hadden WC, Knowler WC, Bennett PH. Prevalence of diabetes and impaired glucose tolerance and plasma glu- cose levels in US population aged 20-74 yr. Diabetes. 1987 Apr;36(4):523-34.
21. Mayfield J. Diagnosis and classification of diabetes mellitus: new criteria. Am Fam Physician. 1998 Oct;58(6):1355-70.
22. Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB. Annual deaths attributable to obesity in the United States. JAMA. 1999 Oct;282(16):1530-8.
23. Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity- related health risk factors, 2001. JAMA. 2003 Jan;289(1):76-9.
24. Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes mel- litus in women. N Engl J Med. 2001 Sep;345(11):790-7.
25. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or met- formin. N Engl J Med. 2002 Feb;346(6):393-403.
26. Lemieux I, Pascot A, Prud’homme D, et al. Elevated C-reactive protein: another compo- nent of the atherothrombotic profile of abdominal obesity. Arterioscler Thromb Vasc Biol. 2001 Jun;21(6):961-7.
27. Heilbronn LK, Noakes M, Clifton PM. Energy restriction and weight loss on very- low-fat diets reduce C-reactive protein con- centrations in obese, healthy women. Arterioscler Thromb Vasc Biol. 2001 Jun;21(6):968-70.
28. Challem J, Berkson B, Smith M. Syndrome X. New York: John Wiley & Sons; 2000.
29. Reaven GM. Syndrome X. New York: Simon and Schuster; 2000.
30. Salmeron J, Hu FB, Manson JE, et al. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr. 2001 Jun;73(6):1019-26.
31. Chandalia M, Garg A, Lutjohann D, von Bergmann K, Grundy SM, Brinkley LJ. Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus. N Engl J Med. 2000 May;342(19):1392-8.
32. Greiger L. Syndrome X. Heart Information Network webpage. Available at: http://www.heartinfo.com/nutrition/ syndx072999.htm. Accessed Nov 15, 2000.
33. Helmrich SP, Ragland DR, Leung RW, Paffenbarger RS, Jr. Physical activity and reduced occurrence of non-insulin-depen- dent diabetes mellitus. N Engl J Med. 1991 Jul;325(3):147-52.
34. Manson JE, Rimm EB, Stampfer MJ, et al. Physical activity and incidence of non- insulin-dependent diabetes mellitus in women. Lancet. 1991 Sep;338(8770):774-778.
35. Manson JE, Nathan DM, Krolewski AS, Stampfer MJ, Willett WC, Hennekens CH. A prospective study of exercise and inci- dence of diabetes among US male physi- cians. JAMA. 1992 Jul;268(1):63-7.
36. Uusitupa M, Louheranta A, Lindstrom J, et al. The Finnish Diabetes Prevention Study. Br J Nutr. 2000 Mar;83(Suppl 1):S137-42.
37. Nieman DC. Fitness and Sports Medicine. 3rd ed. Palo Alto, CA: Bull Publishing; 1995.
38. Available at: http://www.oceanmist.com/health/antioxidant.aspx. Accessed June 20, 2011.
39. Available at: http://www.eurekalert.org/pub_releases/2004-06/aas-lus061504.php. Accessed June 21, 2011.
40. Grotto D. 101 Foods That Could Save Your Life. New York: Bantam Bell; 2008.
41. Heckers H, Dittmar K, Schmahl FW, Huth K. Inefficiency of cynarin as therapeutic regimen in familial type II hyperlipoproteinaemia. Atherosclerosis. 1977 Feb;26(2):249-53.
42. Bundy R, Walker AF, Middleton RW, Wallis C, Simpson HC. Artichoke leaf extract (Cynara scolymus) reduces plasma cholesterol in otherwise healthy hypercholesterolemic adults: a randomized, double blind placebo controlled trial. Phytomedicine. 2008 Sep;15(9):668-75.
43. Englisch W, Beckers C, Unkauf M, Ruepp M, Zinserling V. Efficacy of Artichoke dry extract in patients with hyperlipoproteinemia. Arzneimittelforschung. 2000 Mar;50(3):260-5.
44. Bundy R, Walker AF, Middleton RW, Marakis G, Booth JC. Artichoke leaf extract reduces symptoms of irritable bowel syndrome and improves quality of life in otherwise healthy volunteers suffering from concomitant dyspepsia. J Alter Complement Med. 2004 Aug;10(4):667-9.
45. Available at: http://www.foodforyourhealing.com/foods-for-liver-health/. Accessed June 19, 2011.

Cinnamon:
Is rich in bioactive compounds that help regulate blood sugar levels. This isn’t the cinnamon you’d use to flavor your cappuccino, by the way. It’s a related species called Cinnamomum cassia—and scientists around the world are now discovering its glucose-lowering power.1-4

Extract of this form of cinnamon triggers cell signaling proteins inside the pancreas, bringing the secretion and regulation of insulin levels into greater balance. This helps to restore your body’s natural ability to control blood sugar as you age.

Cinnamon acts as an insulin sensitizer, triggering proteins that lower insulin resistance at the cellular level.7 It has also been shown to thwart advanced glycation end products (AGEs) which are implicated in diabetic complications, atherosclerosis, and Alzheimer’s disease.5,6 A recent in vivo study found cinnamon accomplishes this anti-glycation effect in part through its antioxidant scavenging capabilities.9

Cinnamon also triggers genes in muscle and fatty tissue that transfer glucose out of the bloodstream and into energy producing cells, effectively lowering blood glucose. This quenches the highly reactive oxidant and inflammatory inferno in your body stoked by chronic glucose overexposure.

An abundance of animal studies published in 2010 7-10 confirm that cinnamon polyphenols can significantly reduce fasting glucose levels, improve pancreatic function, and enhance insulin sensitivity—even in diabetic models.

In one recent study, researchers examined the effect of cinnamon extract on mice that were divided into a control diabetic group and cinnamon extract-treated group.10 For 12 weeks, the researchers measured blood glucose and other markers of diabetes. They found fasting blood glucose and two hour postprandial (after-meal) blood glucose levels in the cinnamon-treated group were significantly lower than those in the control group. These findings led the researchers to conclude:

“Our results suggest that cinnamon extract significantly increases insulin sensitivity, reduces serum, and hepatic lipids, and improves hyperglycemia and hyperlipidemia.”10

In humans, the literature is similarly rich with data underscoring cinnamon’s potent, multimodal effects. Researchers have documented compelling results for those afflicted with metabolic syndrome, type 2 diabetes, and polycystic ovary syndrome (a known causative factor in insulin resistance, obesity, and diabetes in women).11

In controlled human studies in these populations, cinnamon extracts have been shown to induce profoundly beneficial, broad-spectrum effects on markers of glucose tolerance across the board.14 They improve blood sugar levels, insulin sensitivity, cholesterol and antioxidant status, blood pressure, lean body mass, and gastric emptying.14 Clinicians examining cinnamon’s therapeutic potential in diabetic individuals have reported declines in fasting blood glucose anywhere between 10-29%.12,13

1. Yu YB, Dosanjh L, Lao L, Tan M, Shim BS, Luo Y. Cinnamomum cassia bark in two herbal formulas increases life span in Caenorhabditis elegans via insulin signaling and stress response pathways. PLoS One. 2010 Feb 22;5(2):e9339

2. Imparl-Radosevich J, Deas S, Polansky MM, et al. Regulation of PTP-1 and insulin receptor kinase by fractions from cinnamon: implications for cinnamon regulation of insulin signaling. Horm Res. 1998 Sep;50(3):177-82.

3. Qin B, Nagasaki M, Ren M, Bajotto G, Oshida Y, Sato Y. Cinnamon extract (traditional herb) potentiates in vivo insulin-regulated glucose utilization via enhancing insulin signaling in rats. Diabetes Res Clin Pract. 2003 Dec;62(3):139-48.

4. Qin B, Nagasaki M, Ren M, Bajotto G, Oshida Y, Sato Y. Cinnamon extract prevents the insulin resistance induced by a high-fructose diet. Horm Metab Res. 2004 Feb;36(2):119-25.

5. Dearlove RP, Greenspan P, Hartle DK, Swanson RB, Harbrove JL. Inhibition of protein glycation by extracts of culinary herbs and spices. J Med Food. 2008 Jun;11(2):275-81.

6. Peng X, Chao J, Sun Z, 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.

7. Ping H, Zhang G, Ren G. Antidiabetic effects of cinnamon oil in diabetic KK-Ay mice. Food Chem Toxicol. 2010 Aug-Sep;48(8-9):2344-9.

8. Cao H, Graves DJ, Anderson RA. Cinnamon extract regulates glucose transporter and insulin-signaling gene expression in mouse adipocytes. Phytomedicine. 2010 May 27.

9. Anand P, Murali KY, Tandon V, Murthy PS, Chandra R. Insulinotropic effect of cinnamaldehyde on transcriptional regulation of pyruvate kinase, phosphoenolpyruvate carboxykinase, and GLUT4 translocation in experimental diabetic rats. Chem Biol Interact. 2010 Jun 7;186(1):72-81.

10. Kim SH, Choung SY. Antihyperglycemic and antihyperlipidemic action of Cinnamomi Cassiae (Cinnamon bark) extract in C57BL/Ks db/db mice. Arch Pharm Res. 2010 Feb;33(2):325-33.

11. 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 1;4(3):685-93.

12. Kirkham S, Akilen R, Sharma S, Tsiami A. The potential of cinnamon to reduce blood glucose levels in patients with type 2 diabetes and insulin resistance. Diabetes Obes Metab. 2009 Dec;11(12):1100-13.

13. Mang B, Wolters M, Schmitt B, et al. Effects of a cinnamon extract on plasma glucose, HbA, and serum lipids in diabetes mellitus type 2. Eur J Clin Invest. 2006 May;36(5):340-4.

Dandelion root, has been traditionally used to help support liver detoxification.  It is also used to aid digestion and as a mild diuretic.

Garcinia: HCA (hydroxycitric acid) is a close relative of citric acid, the agent that gives citrus fruits their characteristic tart flavor. HCA is obtained as a 50% standardized extract of Garcinia cambogia, a small fruit from southern India, where it has been used for centuries as a food preservative, flavoring agent, and digestive aid. HCA is a safe, natural supplement for weight management.1

When calorie intake exceeds the body’s energy needs, the excess glucose is converted into glycogen, which is stored in the liver and muscles for future conversion into energy. Weight gain occurs after the body’s capacity for glycogen storage is reached. At this point, glucose from excessive calorie intake is converted into acetyl coenzyme A via a metabolic pathway involving the enzyme ATP-citrate lyase and then into fat molecules, which are stored in fat cells. HCA is a competitive inhibitor of ATP citrate lyase, a key enzyme which facilitates the synthesis of fatty acids, cholesterol and triglycerides. HCA may reduce the synthesis of fatty acids in humans during a persistent excess of energy intake as carbohydrate.2

It has been suggested that HCA promotes weight loss by increasing serotonin levels, reducing hunger and appetite, and suppressing carbohydrate conversion into fat by inhibiting ATP-citrate lyase,3-9* thus regulating fat and obesity related genes.10 HCA may also attenuate the increases in oxidative stress, and insulin resistance.11

1. J Med. 2004;35(1-6):33-48.2. Physiol Behav. 2006 Jul 30;88(4-5):371-81.3. J Agric Food Chem. 2002 Jan 2;50(1):10-22.4. Med Hypotheses. 1988 Sep;27(1):39-40.5. Curr Concepts Nutr. 1983;12:139-67.6. Acta Biochim Pol. 1976;23(2-3):227-34.7. Lipids. 1974 Feb;9(2):121-8.8. Lipids. 1974 Feb;9(2):129-34.9. J Biol Chem. 1971 Feb 10;246(3):629-32.10. DNA Cell Biol. 2007 Sep;26(9):627-39.11. Mol Cell Biochem. 2007 Oct;304(1-2):93-9.

Green tea: Contains health-promoting polyphenols including epigallocatechin-3-gallate (EGCG), a powerful antioxidant which has been the subject of extensive scientific research. The antioxidant activity of EGCG is about 25–100 times that of vitamins C and E.1 One cup of green tea provides roughly 200 mg of polyphenols2 and has antioxidant effects that are greater than a serving of broccoli, spinach, carrots or strawberries.

1. Mutat Res. 2006 Dec 10;611(1-2):42-53. 2. Altern Med Rev. 2000 Aug;5(4):372-5.

Olive Leaf: Many of the validated benefits of the Mediterranean diet derive from heart-healthy compounds contained in the olive fruit, including the polyphenols tyrosol and hydroxytyrosol.1-4 When it comes to olive’s power to support blood pressure already within a healthy range, research shows the bioactive compound oleuropein5-8 is primarily responsible.

The problem is that optimal amounts of oleuropein are not found in the fruit. The highest concentrations of oleuropein are contained in the olive leaf 9-13—a part of the plant that is neither readily available nor commonly consumed.

1.Anal Chim Acta. 2007 Feb 5;583(2):402-10. 2. J Agric Food Chem. 2007 Sep 5;55(18):7609-14. 3. Lipids. 2001 Nov;36(11):1195-202. 4. Eur J Cancer. 2000 Jun;36(10):1235-47.5. Phytother Res. 2008;22:1239-42.6. Benolea® EFLA 943. Unpublished study. October 11, 2011.7. J Ethnopharmacol. 2008 Nov 22;120(2):233-40.8. Int J Food Sci Nutr. 2005 Dec;56(8):613-20.9. Handbuch Phytotherapie. Stuttgart, Germany: Wissenschaftliche Verlagsgesellschaft; 2003.10. J Pharm Belg. 1996 Mar-Apr;51(2):69-71.11. Therapie. 1999 Nov-Dec;54(6):717-23.12. Ann Pharm Fr. 2000 Jul;58(4):271-7.13. Arznei-forschung. 1972 Sep;22(9):1476-86.

Watercress was renown in herbal history as a spring-cleaning herb for purifying the blood and toning the whole system. Many of the great herbalists wrote of the revitalizing powers of watercress. Early Romans revered the health benefits of watercress, while the Greeks believed it was valuable brain food and strengthened the nervous system. Persian King Xerxes fed watercress to his soldiers, to keep up strength and stamina.

Therapeutic uses have included: coughs, head colds, bronchial ailments, tuberculosis, asthma, emphysema, stress, pain, arthritis, stiff back and joints, diabetes, anemia, constipation, cataracts, failing eye sight, night blindness, leukemia, cancer, hemorrhaging, heart conditions, eczema, scabies, body deodorizer, edema, bleeding gums, weight loss, indigestion, alcoholism, intestinal parasites, circulation, sluggish menstruation, lack of energy, kidney and gall stones, as a brain and nerve strengthener; ailments of the spleen, thyroid, and liver; to normalize cholesterol and blood pressure; for improved memory, for mental function decline and to retard ageing; for failing or scant milk supply of nursing mothers; to regulate flow of bile, health of glands and the functions of body metabolism. It is one of the best sources of the element iodine, other than seaweed, such as kelp. Iodine is important to the function of the thyroid gland. The leaves used as a poultice are applied for relief from enlarged prostate gland.

Watercress contains more sulfur than any other vegetable, except horseradish. Sulfur rich foods play an important part in protein absorption, blood purifying, cell building and in healthy hair and skin.

The potassium content of watercress is valued for weight loss, as its diuretic action draws excess fluid down and out of the body. Dieters will benefit with eating high potassium foods and eliminating or cutting back on high sodium foods, including salt. The rich calcium content of watercress has been encouraged for soft teeth and weak bone conditions.

B17 is a vitamin found in some plants that are used for human consumption. This is where watercress comes in, as it has approximately 98mg of vitamin B17 per 100 grams of leaves.

Also, noteworthy is the fact that watercress is a food with alkalinity of 8.1 in metabolic reaction, making it valuable in our daily diet; to counteract an acidic system, caused by overall consumption of too many acid foods, processed foods, stresses and pollutants in the environment. Watercress is a powerful cleanser of the body, especially the bloodstream. It has properties that help dissolve fatigue-causing fibrin, coagulated in the blood vessels.

Watercress being a Brassicaceae plant and in the same family as mustard, has the typical pungent flavor due to the chemical compounds known as isosalfocyanic glucosides.


Constituents:
volatile oil, glycosides, fibre, protein with animo acids arginine, histidine, isoleucine, leucine, lysine, threonine, phenylalinine, methionine, tryptophan, valine, folic acid, courmarins

Vitamins:
A , B1, B2, B3, B5, B6, B17, C, D, E, K

Minerals:
calcium, phosphorus, potassium, iron, sodium, magnesium, copper, manganese, florine, sulphur, chlorine, iodine, germanium, silica, zinc

Health benefits of Watercress
This rich flavored green leafy vegetable is store house of many phytonutrients that have health promotional and disease prevention properties.*

One of the very low calorie green leafy vegetables (11 kcal per 100 g raw leaves) and very low in fats; recommended in cholesterol controlling and weight reduction programs.*

Cress leaves and stems contain gluconasturtiin, a glucosinolate compound that gives peppery flavor. Research studies suggest that the hydrolysis product of gluconasturtiin, 2-phenethyl isothiocyanate (PEITC), is believed to be cancer preventing by inhibition of phase I enzymes (mono-oxygenases and cytochrome P450s).*

Fresh cress has more concentration of ascorbic acid (vitamin C) than some of fruits and vegetables. 100 g of leaves provide 47 mg or 72% of RDA of vitamin C.  As an anti-oxidant, vitamin C helps to quench free radicals and reactive oxygen species (ROS) through its reduction potential properties. Lab studies suggests that regular consumption of foods rich in vitamin C helps maintain normal connective tissue, prevent iron deficiency, and also helps body develop resistance against infectious agents by boosting immunity.*

It is one of the excellent vegetable sources for vitamin-K; 100 g provides over 200% of daily recommended intake. Vitamin K has potential role bone health by promoting osteotrophic (bone formation and strengthening) activity. Adequate vitamin-K levels in the diet helps limiting neuronal damage in the brain; thus, has established role in the treatment of patients suffering from Alzheimer's disease.*

Cress is also excellent source of vitamin-A and flavonoids anti-oxidants like ß carotene, lutein and zeaxanthin.

It is also rich in B-complex group of vitamins such as riboflavin, niacin, vitamin B-6 (pyridoxine), thiamin and pantothenic acid that are essential for optimum cellular metabolic functions.*

It is also rich source of minerals like copper, calcium, potassium, magnesium, manganese and phosphorus. Potassium in an important component of cell and body fluids that helps controlling heart rate and blood pressure by countering effects of sodium. Manganese is used by the body as a co-factor for the antioxidant enzyme superoxide dismutase. Calcium is required as bone/teeth mineral and in the regulation of heart and skeletal muscle activity.*

Acta Poloniae Pharmaceutica; Investigation of Antioxidant Properties of Nasturtium Officinale (Watercress) Leaf Extracts; Ozen Tevfki; March 2009
Effect of hydroalcoholic extracts of Nasturtium officinale leaves on lipid profile in high-fat diet rats./ Selfollah Bahramikla and Razieh Yazdanparast / J Ethnopharmacol. 2008 Jan 4;115(1):116-2 / doi:10.1016/j.jep.2007.09.015)
Nasturtium officinale reduces oxidative stress and enhances antioxidant capacity in hypercholesterolaemic rats / Razieh Yazdanparast et al / Chemico-Biological Interactions Vol 172, Issue 3, 15 April 2008/ doi:10.1016/j.cbi.2008.01.006
Decrease of plasma and urinary oxidative metabolites of acetaminophen after consumption of watercress by human volunteers / Clinical pharmacology and therapeutics / 1996, vol. 60, no6, pp. 651-66
An Experimental Model for Study of the Hepatoprotective Activity of Nasturtium Officinale (Watercress) Against Acetaminophen Toxicity using in Situ Rat Liver System / Alireza Ebadollahi Natanzi / uropean Journal of Scientific Research • ISSN 1450-216X Vol.38 No.4 (2009), pp 556-564
Platelet Aggregatory Effects of Nasturtium officinale and Solanum torvum Extracts / H Moriyama et al / Nat Med • VOL.57;NO.4;PAGE.133-138(2003) /
Activity against drug resistant-tuberculosis strains of plants used in Mexican traditional medicine to treat tuberculosis and other respiratory diseases / Maria del Rayo Camacho-Corona et al / Phytotherapy Research • Volume 22 Issue 1, Pages 82 – 85

Blueberry Leaf: The phytochemical composition of Blueberry leaf has been studied at the Georgian Institute of Plant Biochemistry for decades (Durmishidze et al. 1981). The investigation of phytochemical composition indicates blueberry leaf contains large amounts of caffeoylquinic 3,5-diccafeylqunic, neochlorogenic, 4-caffeoylquinic, 3coumaroylqunic and caffeic acid (Mzhavanadze et al. 1972). The concentration of these two major phenolic compounds in the extract can reach as high as 15-20% dry weight. In addition to chlorogenic and caffeic acids, the following compounds have been identified in blueberry leaf:
Coumaric Acid, Salidroside, Tyrosol, Ericolin, Rutin, Arbutin, Anthocyanosides, Quercetin

The content of chlorogenic and caffeic acids in blueberry leaf is dependent on vegetation period. The maximum level of chlorogenic and caffeic acids observed in young spring leaf extract were 15-20%, while their concentrations are dramatically reduces to 3% in mature leaves (Mshavanadze, 1971; Durmishidze et al. 1981). Traditionally, the Caucasian Blueberry leaf is harvested in early spring to assure the maximum yield and the highest concentration of chlorogenic and caffeic acids, which guarantees its efficacy. In fact, blueberry leaf extract has been standardized to a minimum of 18% chlorogenic and caffeic acids.

Chlorogenic Acid
To better understandand appreciate fully the health-promoting properties of blueberry leaf extract it is important to describe the pharmacological properties of its major constituent, chlorogenic acid. Researchers have reported that chlorogenic acid possess pharmacologically relevant health promoting properties, particularly in lowering plasma glucose and in treatment of diabetes. Among more than a dozen positive physiological actions of chlorogenic acid, the plasma glucose lowering properties are the most impressive.

Diabetes: Animal Studies
Cirnarella et al. (1996) studied the therapeutic action of the blueberry leaf extract on streptozotocindiabetic rats for 4 days. Plasma glucose levels were consistently found to drop by about 26% at two different stages of diabetes. Unexpectedly, plasma triglyceride (TG) was also decreased by 39% following treatment. The present findings indicate that the active constituent(s) of blueberry leaves may prove potentially useful for treatment of dyslipidaemiae associated with impaired TG-rich lipoprotein clearance. Therefore, the reduction in blood sugar by 26% recently reported by Cirnarella et al. (1996) is a rather expected result. The present findings indicate that active constituents of blueberry leaf extract may prove potentially useful for treatment of high blood sugar and plasma triglyceride level (Cirnarella et al. 1996).

Human Clinical Study: Diabetes Patients
In a second clinical trial the effect of blueberry leaf extract on plasma glucose level was studied in patients with Type II Diabetics (Abidoff 1999). Twenty-nine patients with type II diabetes, average age of 50 years, were selected to participate in a double-blind, placebo-controlled, 60-days trial. Sixty days before beginning the drug phase of clinical study patients underwent a period of diet counseling and surveillance. Their dietary intakes were standardized to contain 40-45% total calories from carbohydrates. Patients in the study were asked to maintain their medications throughout the dietary and drug phase of the trial. On admission and at two-week intervals throughout the study, patients were evaluated for fasting glucose, triglycerides serum values. Food record analysis, body mass index, and a symptom questionnaire were also included at the laboratory intervention times. After the initial dietary run-in phase, subjects were randomly assigned to receive 200mg of standardized blueberry leaf extract powder in capsule form or a placebo, to be taken three times a day in 200ml of water before meals. During the initial period of diet counseling there was no significant change in fasting blood glucose values for either of the groups. However, beginning with week 6 and continuing to the end of the trial, those individuals taking the blueberry leaf extract showed a significant reduction in mean plasma glucose levels, from approximately 169 mg/dL to 136 mg/dL (p < 0.01). Furthermore, by the end of the clinical study, those taking the blueberry leaf extract showed a reduction of triglyceride and LDL values from 179 ±95 mg/dL to 130 ±53 mg/L (p < 0.005) and 141 ±47 mg/dL to 115 ±34 mg/dL (p < 0.01) respectively. All patients tolerated well blueberry leaf extract even at 400mg, three times a day (1200mg/day).

Results of the clinical trial are confirmed, well know and previously described phenomenon that blueberry leaf extract possess antidiabetic properties. The use of blueberry leaf extract may provide a first line approach to the reduction of blood glucose in type II diabetic patients before other prescriptive avenues are employed. Improvement in total cholesterol and LDL level observed in various studies is possibly due to the protective role of caffeic and chlorogenic acids in LDL oxidation that was recently described in scientific literature.

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Chlorogenic acid and hydroxynitrobenzaldehyde: new inhibitor of hepatic glucose 6-phosphatase. Arch Biochem Biophys 15; 339(2): 315-22

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Azuma K, Ippoushi K, Nakayama M, Ito H, Higashio H, Terao J (2000) Absorption of Chlorogenic Acid and Caffeic Acid in Rats after Oral Administration J Agric Food Chem 20; 48 (11): 5496-5500

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Cheng JT, Liu IM (2000) Stimulatory effect of caffeic acid on alpha1A-adrenoceptors to increase glucose uptake into cultured C2C12 cells. Naunyn Schmiedebergs Arch Pharmacol 362 (2): 1227

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Hsu FL, Chen YC, Cheng JT (2000) Caffeic acid as active principle from the fruit of Xanthium strumarium to lower plasma glucose in diabetic rats. Planta Med; 66(3): 228-30

Huang MT, Smart RC, Wong CQ, Conney AH (1988) Inhibitory effect of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on tumor promotion in mouse skin by 12-tetradecanoylphorbol-13- acetate. Cancer Res1; 48(21): 5941-6

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Kerry N, Rice-Ewans C (1999) Inhibition of peroxynitrite-mediated oxidation of Dopamine by flavonoid and phenolic antioxidants and their structural relationships. Journal of Neuroscience, 73, N1 pp. 247-253

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Kitts DD, Wijewickreme AN (1994) Effect of dietary caffeic and chlorogenic acids on in vivo xenobiotic enzyme systems. Plant Foods Hum Nutr. 45(3): 287-98

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Bean Pod, Phaseolus vulgaris, Bulgaria Therapeutic actions: Diuretic. Nutrients: Amino acids, tyrosine, tryptophan, arginine, choline, betaine, and vitamin B. It has been effective in lowering blood sugar levels and can be used (with the concurrence of a doctor) for mild cases of diabetes.

Black Walnut Hulls:
Supports the Natural Balance of Healthy Intestinal Flora within the GI Tract
Supports Healthy Intestinal Environment

 

Fenugreek seeds:  Contain nutrients such as B vitamins, Vitamin C, and Beta Carotene.

In animal and several small, human trials, fenugreek seeds have been found to lower fasting serum glucose levels, both acutely and chronically. Gupta et al reported the results of a small randomized, controlled, double-blind trial to evaluate the effects of fenugreek seeds on glycemic control.18 Twenty-five patients with newly diagnosed type 2 diabetes received either 1 g daily of a hydroalcoholic extract of fenugreek seeds or “usual care” (dietary discretion and exercise). After two months, mean fasting blood glucose levels were reduced in both groups without significant differences between groups (148.3 mg/dL to 119.9 mg/dL in the fenugreek group versus 137.5 mg/dL to 113.0 mg/dL in the “usual care” group). There were no significant differences between groups in mean glucose tolerance test values at the study’s end. The authors did note differences between groups in the area under the curve for blood glucose and insulin levels. This study suggests that fenugreek seed extract and diet/exercise may be equally effective strategies for attaining glycemic control in type 2 diabetes.

1. Morcos SR, Elhawary Z, Gabrial GN. Proteinrich food mixtures for feeding the young in Egypt. 1. Formulation. Z Ernahrungswiss 1981;20:275-282.

2. Yoshikawa M, Murakami T, Komatsu H, et al. Medicinal foodstuffs. IV. Fenugreek seed. (1): structures of trigoneosides Ia, Ib, IIa, IIb, IIIa, and IIIb, new furostanol saponins from the seeds of Indian Trigonella foenum-graecum L. Chem Pharm Bull (Tokyo) 1997;45:81-87.

3. Patil SP, Niphadkar PV, Bapat MM. Allergy to fenugreek (Trigonella foenum graecum). Ann Allergy Asthma Immunol 1997;78:297-300.

4. Ribes G, Sauvaire Y, Baccou JC, et al. Effects of fenugreek seeds on endocrine pancreatic secretions in dogs. Ann Nutr Metab 1984;28:37-43.  

5. Ribes G, Sauvaire Y, Da Costa C, et al. Antidiabetic effects of subfractions from fenugreek seeds in diabetic dogs. Proc Soc Exp Biol Med 1986;182:159-166.

6. Sauvaire Y, Petit P, Broca C, et al. 4- Hydroxyisoleucine: a novel amino acid potentiator of insulin secretion. Diabetes 1998;47:206-210.

7. Raghuram TC, Sharma RD, Sivakumar B, et al. Effect of fenugreek seeds on intravenous glucose disposition in non-insulin dependent diabetic patients. Phytother Res 1994;8:83-86.

8. Ajabnoor MA, Tilmisany AK. Effect of Trigonella foenum graceum on blood glucose levels in normal and alloxan-diabetic mice. J Ethnopharmacol 1988;22:45-49.

9. Amin R, Abdul-Ghani AS, Suleiman MS. Effect of Trigonella feonum graecum on intestinal absorption. Proc. of the 47th Annual Meeting of the American Diabetes Association (Indianapolis U.S.A.). Diabetes 1987;36:211a.

10. Stark A, Madar Z. The effect of an ethanol extract derived from fenugreek (Trigonella foenum-graecum) on bile acid absorption and cholesterol levels in rats. Br J Nutr1993;69:277-287.

11. Petit P, Sauvaire Y, Ponsin G, et al. Effects of a fenugreek seed extract on feeding behaviour in the rat: metabolic-endocrine correlates. Pharmacol Biochem Behav 1993;45:369-374.

12. Al-Habori M, Al-Aghbari AM, Al-Mamary M. Effects of fenugreek seeds and its extracts on plasma lipid profile: a study on rabbits. Phytother Res 1998;12:572-575.

Jambolan seed (also known as Syzygium jambolanum and Syzygium cumini) or jambul is a plant native to India, ranging from the foot of the Himalayas southward. It grows readily in other tropical climates and has been carried to eastern Africa, Brazil, and southeast Asia. Jambul is in the Myrtaceae family. It is a relative of Syzygium aromaticum (cloves) but cloves are apparently not utilized to treat diabetes in traditional herbal medical systems. The area of origin may make a huge difference as one study showed that eugenia fruit grown in Brazil lacked the hypoglycemic effect found in Indian jambul.1 Traditionally the jambul fruits, leaves, seeds, and bark are all used in ayurvedic medicine. The tasty fruits are also consumed as food. The bark contains tannins and carbohydrates, accounting for its long- term use as an astringent to combat ailments like dysentery.2A glycoside in the seed, jamboline, is considered to have antidiabetic properties.2 Older French research shows that the seeds have a significant hypoglycemic effect in diabetic rabbits.3 The seeds have also shown anti- infl ammatory effects in rats and antioxidant properties in diabetic rats.4,5 Older reports from Indian medical journals suggest jambul seed and bark can be benefi cial in humans with diabetes.6,7 Controlled clinical trials are awaited to determine more completely the mechanism of action of jambul, its degree of effi cacy, and to confi rm its safety. E. jambolana Lam., E. unifl ora L., and E. puncifolia (Humb., Bonpl L and Kunt) DC are used in traditional medicine for diabetes. Older studies report that water extracts of jambul leaves do not lower serum glucose levels in diabetic rats or in normal humans.8,9

This may be why most of the reports on traditional use of jambul in diabetic patients in India focus on use of the seeds or bark or it may refl ect the extractability of par tic u lar constituents. For instance, the aqueous extract of E. puncifolia leaves had an anorexic effect, whereas the alcohol extract improved the diabetic state in streptozotocin- induced rats.10 But, in another study, E. jambolana leaf extract also had a hypoglycemic action in diabetic rats.11 In any event, the seed powder of E. jambolana had a hypoglycemic action in streptozotocin- diabetic rats.12,13 Its effect may be per sistent, as in one study, homeostasis was maintained in the rats for two weeks after the cessation of treatment.14 In alloxan- diabetic rabbits the water extract of E. jambolana fruit pulp was more effective than the ethanol extract at reducing fasting blood glucose and improving blood glucose levels in the glucose tolerance test. E. jambolana also increased blood insulin levels in both diabetic and severely diabetic rabbits.15,16 Another study also found that E. jambolana seed extract reduced blood glucose, glycosylated hemoglobin, and increased plasma insulin.17 However, yet another study found that E. jambolana fruit combined with bitter melon decreased insulin levels that were raised in diabetic rats fed a fructose diet.18Again, as mentioned above in the discussion of gymnema, the importance of this effect in patients with insulin re sis tance is unknown. Ayurvedic texts suggest that 1–3 g of seed powder per day is an average dose.19 Additionally, juice of ripe fruits in the amount of 0.5– 2 tsp (2.5– 10 ml) at least three times daily have been recommended for treatment of diabetes.2 A tincture of bark or seed might be attempted at a dose of 3–5 ml three times daily, though the optimal extract and dose are unknown. No side effects are mentioned in the traditional reports, but high- tannin bark extracts may cause mild gastrointestinal upset in some people unless taken with food.


Pepato MT, Mori DM, Baviera AM, et al. Fruit of the jambolan tree (Eugenia jambolana Lam.) and experimental diabetes. J Ethnopharmacol 2005;96:43– 48.

Nadkarni KM, Nadkarni AK. Indian Materia Medica. Bombay, India:Pop u lar Prakashan 1976.

Ratsimamanga AR, Loiseau A, Ratsimamanga- Urverg S, et al. Action of a hypoglycemic agent found in the young bark of Eugenia jambolania [sic] (Myrtaceae) on induced hyperglycemia of the rabbit and continuation of its purifi cation. C R Acad Sci Hebd Seances Acad Sci D 1973;277:2219– 2222 [in French].

Chaudhuri AKN, Pal S, Gomes A, et al. Anti- infl ammatory and related actions of Syzygium cuminii [sic]seed extract. Phytother Res 1990;4:5– 10.

Prince PSM, Menon VP. Effect of Syzigium cumini [sic] in plasma antioxidants on alloxan- induced diabetes in rats. J Clin Biochem Nutr 1998;25:81– 86.

Sepaha GC, Bose SN. Clinical observations on the antidiabetic properties of Pterocarpus marsupium and Eugenia jambolana. J Indian Med Assoc 1956;27:388– 391.

Srivastava Y, Venkatakrishna- Bhatt H, Gupta OP, et al. Hypoglycemia induced by Syzygium cumini Linn seeds in diabetes mellitus. Asian Med J 1983;26:489– 491.

Teixeira CC, Fuchs FD, Blotta RM, et al. Effect of tea prepared from leaves of Syzygium jambos on glucose tolerance in nondiabetic subjects. Diabetes Care 1990;13:907– 908.

Teixeira CC, Pinto LP, Kessler FHP, et al. The effect of Syzygium cumini (L) skeels on postprandial blood glucose levels in nondiabetic rats and rats with streptozotocin- induced diabetes mellitus. J Ethnopharmacol 1997;56:209– 213.

Brunetti IL, Vendramini RC, Januario AM, et al. Effects and toxicity of Eugenia punicifolia extracts in streptozotocin- diabetic rats. Pharmaceut Biol 2006;44:35– 43.

Damasceno DC, Volpato GT, Calderon IDMP, et al. Study of Averrhoa carambola and Eugenia jambolana extracts purchased from manipulation drugstore on the experimental diabetes. Revista Brasileira de Toxicologia 2002;15:9– 14 [in Portuguese].

Sridhar SB, Sheetal UD, Pai MRSM, et al. Preclinical evaluation of the antidabetic effect of Eugenia jambolana seed powder in streptozotocin- diabetic rats. Brazilian J Med Biol Res 2005;38:463– 468.

Ravi K, Sivagnanam K, Subramanian S. Antidiabetic activity of Eugenia jambolana seed kernels on streptozotocin- induced diabetic rats. J Med Food 2004;7:187– 191.

Ravi K, Rajasekaran S, Subramanian S. Hypoglycemic effect of Eugenia jambolana seed kernels on streptozotocin- induced diabetes in rats. Pharmaceut Biol 2003;41:598– 603.

Sharma SB, Nasir A, Prabhu KM, et al. Antihyperglycemic effect of the fruit- pulp of eugenia jambolana in experimental diabetes mellitus. J Ethnopharmacol 2006;104:367– 373.

Sharma SB, Nasir A, Prabhu KM, et al. Hypoglycemic and hypolipidemic effect of ethanolic extract of seeds of Eugenia jambolana in alloxan- induced diabetic rabbits. J Ethnopharmacol 2003;85:201– 206.

Ravi K, Ramachandran B, Subramanian S. Protective effect of Eugenia jambolana seed kernel on tissue antioxidants in streptozotocin- induced diabetic rats. Biol Pharmaceut Bull 2004;27:1212– 1217.

Vikrant V, Grover JK, Tandon N, et al. Treatment with extracts of Momordica charantia and Eugenia jambolana prevents hyperglycemia and hyperinsulinemia in fructose- fed rats. J Ethnopharmacol 2001;76:139– 143.

Kapoor LD. CRC Handbook of Ayurvedic Medicinal Plants. Boca Raton, FL:CRC Press 1990.

Goat's Rue/French Lilac Galega officinalis was the basis for the anti-diabetic medication Metformin (but Metformin is a chemical isolate) 1. "Guanidine is an active ingredient extracted from Galega officinalis ... we observed that guanidine decreased plasma glucose in STZ rats" 2. "Galega officinalis (galega, Goat's Rue, French Lilac) is well known for its hypoglycaemic action and has been used as part of a plant mixture in the treatment of diabetes mellitus ... During phannacological investigations ... a weight reducing effect of galega was discovered ... together with its established hypoglycaemic effects, galega has a novel weight reducing action that, in normal mice, is largely independent of a reduction in food intake. The mechanism of the weight reducing action of galega is unclear but involves loss of body fat" 3.

1- Vuksan V, Sievenpiper JL. Herbal remedies in the management of diabetes. Nutr Metab Cardiovasc Dis. 2005 Jun;15(3): 149-60

2- Chang CH, Tsao CW, Huang SY, Cheng JT. Activation of imidazoline I(2B) receptors by guanidine to increase glucose uptake in skeletal muscle of rats. Neurosci Lett. 2009 Dec 25;467(2):147-9

3- Palit P, Furman BL, Gray AI. Novel weight-reducing activity of  galega officinalis in mice. J Phann Pharmacol. 1999 Nav;51 (II): 1313-9 [28] Burnham TH, et aI, editors. The Review of Natural Products. Facts and Comparisons, St. Louis. 2001: 283:284

 

 

 
Herbal Dietary Supplement
2 fl. oz. (59 ml)

 

Supplement Facts
Serving Size 2 ml (58 drops)
Servings per Container 30

 

Ingredients  Amount per Serving %DV 
Proprietary blend extracts (1:1)  2 ml  **

[Artichoke leaf (Cynara scolymus), Bean pod (Phaseolus vulgaris), Black walnut hulls (Juglans nigra), Blueberry leaf (Vaccinum angustifolium), Cinnamon bark (Cinnamomum cassia), Dandelion root (Taraxacum officinale), Fenugreek seed (Trigonella foenum graecum), Goat’s rue leaf (Galega officinale), Garcinia fruit (Garcinia cambogia), Green tea leaf (Camellia sinensis), Jambolan seed (Syzygium cumini), Olive leaf (Olea europaea), and Watercress herb (Nasturtium officinale)].
 

**Daily Value (DV) not established.

 

Other Ingredients: Certified organic grain alcohol, filtered water.

 

Warning: Do not use if you are pregnant, may become pregnant, or breastfeeding. If you have any blood coagulation disorders, or if you are taking any prescription drug, consult your health care professional before using this product.

• Keep out of reach of children.
• Store in a cool, dry place.
• Shake well before use.

 

Direction: Mix 1 ml (29 drops) of GlucoFase® with water and drink it 30 minutes before each meal twice daily, not exceeding 2 ml (58 drops) per day, or as recommended by a healthcare practitioner.

Caution: Because this product may lower blood glucose, consult your healthcare provider before taking this product if you are taking blood glucose lowering medication.

 

Manufactured for Pathealth Labs, LLC.
Registered formula by: Marcel Moheb PhD
Tracy, California. 95376 US

 

CODE: GLUCOFASE-II

 



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*“These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.”
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