Life Extension Magazine®

Issue: Oct 2010

Aggressive Actions Needed to Avert Obesity Crisis

As a catastrophic obesity epidemic unfolds before our eyes, conventional medicine’s inadequate response shocks the conscience. One third of the American population is obese—with another third overweight. This guarantees an imminent health and economic disaster as these individuals succumb to diseases requiring high cost medical care. The best the federal government can suggest is diet, exercise, and dangerous prescription drugs. Sadly overlooked are irrefutable data showing that excess fat accumulation in aging humans is reversible with an aggressive multi-modal attack. Find out 27 correctable causes that underlie age-related weight gain, along with clinically validated regimens that effectively target these factors.

By William Faloon.

William Faloon 
William Faloon
Integrated Medicine Optimizes Brain Function—Naturally

The impending medical catastrophe caused by today’s obesity epidemic reminds me of the 1950s.

Back then, one scientific report after another confirmed the diseases inflicted by cigarette smoking. Yet it was not until 1964 that any kind of substantive step was taken to reduce tobacco consumption.1 Even today (46 years later), smoking remains a leading cause of premature death.2

As deadly as cigarettes are, the explosive increase in the number of overweight/obese individuals is projected to create an even greater economic and health disaster.

Similar to the deferred effects of cigarette smoking, medical costs associated with obesity-related diseases are mostly postponed. This means that society has only begun to pay the enormous healthcare expenses that will accrue as overweight individuals succumb to cancer,3-6 vascular occlusion,7,8 kidney failure,9 diabetes,10 arthritis,11 early senility,12 and other illnesses.

The federal government’s meager steps to combat this calamity have failed. The evidence can be seen by the fact that nearly three times more Americans are obese today compared to 1960. A more startling statistic is that six times more Americans are morbidly obese (body mass index 40 and above) than in 1960.13

Obese individuals (body mass index 30 and above) now comprise over one-third of the American population. Another one-third is overweight (body mass index of 25-29).13 The majority of Americans are thus destined to suffer higher incidences of degenerative diseases than this nation’s healthcare system can afford.

As it relates to longevity, excess body fat robs victims of quality and quantity of life.14 What you will be surprised to learn is that factors that underlie age-related weight gain also preclude the optimal expression of our longevity genes.

This issue of Life Extension Magazine® describes validated methods aging people can use to simultaneously shed excess fat pounds, reduce disease risk, and turn on youth-promoting “longevity genes.”

Doctors Fail to Recognize Obesity As a Multi-factorial Disorder

The US Department of Agriculture released data showing that Americans consumed an extra 331 calories a day in 2006 compared to 1978.15

Doctors Fail to Recognize Obesity As a Multi-factorial Disorder

If that number does not sound like a lot, just look how it quickly adds up. An extra 331 calories per day equals 2,317 calories each week or 120,000 extra calories in a year. This amount of excess food intake translates into roughly 34 pounds of stored body fat!

The government is using this data to explain why so many Americans suffer excess weight problems. The government only has the story partially right.

What is not recognized by conventional experts is that maturing humans lose the metabolic capacity to utilize even the limited number of calories they may be ingesting. When we use the term “metabolic capacity,” we are referring to a constellation of deleterious changes that arise during aging that predispose us to accumulate excess body fat.

A young person can eat a reasonable amount of food and efficiently convert these calories into energy with minimal residual fat storage. As that same person ages, they suffer a multitude of changes that impact body weight regulation such as hormone imbalance, insulin insensitivity, mitochondrial dysfunction, and decline in resting energy expenditure.16-19

This means that even if we don’t consume a single calorie more at 45 years old compared to our food energy consumption at 25 years old, our aging physiology predisposes us to weight gain.

Tackling the Problem Head On

If there is one truth that has been learned over the past 30 years, it is that there is no “magic bullet” that singlehandedly can be counted on to reverse age-associated weight gain. An understanding of the mechanisms involved in excess fat storage reveals why the advice to “just eat less” is doomed to fail over the long term.

Life Extension has been on a multi-decade crusade to validate effective methods of inducing fat loss. We have identified nutrients, hormones, and drugs that have demonstrated efficacy in peer-reviewed scientific publications, yet are overlooked by mainstream physicians.

We have funded millions of dollars in laboratory and clinical research to develop formulations to combat the obesity-inducing factors that plague the aging population.

The public still does not understand, however, that weight gain is the result of a myriad of metabolic and physiologic factors. The encouraging news is that scientifically supported methods exist to correct many of the mechanisms that predispose us to accumulate excessive body fat.

Lacking until now has been a comprehensive program that enables doctors and patients to work together to design individualized programs that not only facilitate weight loss, but also reduce cardiovascular risk factors such as triglycerides, glucose, LDL, and C-reactive protein.

Even more fascinating is new evidence that a proper weight loss program can enhance the expression of our longevity genes.20 What this means is that aging humans now have a roadmap to lose unsightly body fat and slash disease risk, while adding healthy decades to their life spans.

Despite overwhelming documentation that age-associated weight gain can be reversed, no one has put all the pieces of the puzzle together until now.

The Life Extension® Weight Loss Guide

The Life Extension® Weight Loss Guide

Life Extension has accumulated hard data about why Americans are getting fatter every year and what scientific steps can be taken to help reverse this frightening trend.

We realized, however, the urgent need to amalgamate this information into a user-friendly book that can be utilized to target the multiple obesity factors aging humans face.

We are pleased to announce the publication of the Life Extension® Weight Loss Guide, a reference book that compiles the research and clinical trials our organization has painstakingly assembled over the past three decades.

This book will sell in stores for $29.95. As a Life Extension® member, we are discounting the price by 70%, so you pay only $8.99.

It is our sincere desire that the Life Extension® Weight Loss Guide will initiate a scientific renaissance in the interventions that aging humans and their doctors employ to induce sustained reductions of body fat. You can order a copy of this book today by calling 1-800-544-4440.

New Multi-Ingredient Powdered Drink Combats Several Weight Gain Inducers

For many Life Extension members, the use of various nutrient formulas has been an important weight management tool. While thousands have used these products with success, some have not been able to achieve results.

As part of our ongoing clinical research, we set out to produce a powdered drink mix formula incorporating several proven fat-loss agents. The objective was to help our most treatment-resistant overweight members achieve their desired weight management goals—individuals who have previously tried innumerable weight management programs, nutrients, and pharmaceutical agents without success.

Furthermore, we wanted to test this new multi-ingredient powdered formula against a similar capsule formula to be certain that the powder formula with one new ingredient worked in treatment-resistant study subjects who previously failed to achieve their desired weight management results.

Figure 1: Weight loss over time
Figure 1: Weight loss over time

The findings were quite remarkable.

In treatment-resistant overweight study subjects, the new Calorie Control Weight Management powdered drink formula, mixed with water and consumed 15-30 minutes prior to the two largest meals of the day, generated, on average, 65% greater weight loss over 8 weeks in comparison with treatment-resistant study subjects given the capsule form. [See Figure 1 to the right]

In addition to achieving greater mean (average) weight loss over the eight-week study period, treatment-resistant overweight and obese study subjects also achieved greater categorical weight loss.

Figure 2: Categorical weight loss (10 lbs.)
Figure 2: Categorical weight loss (10 lbs.)

This meant that by week eight, 58% of treatment-resistant study subjects who consumed the new Calorie Control Weight Management powdered drink formula were able to lose greater than 10 pounds as compared with only 22% of those using the capsule formula. For the greater than 12 pounds threshold, the results were equally impressive for the new powdered formula, with 41% of study subjects losing greater than 12 pounds by week eight in comparison with only 11% given the capsule formula. [See Figure 2 to the right and 3 below]

These results are all the more impressive because they occurred with treatment-resistant individuals who struggled with excess body weight and failed multiple past weight management programs, nutrients, and pharmaceutical interventions… yet were able to finally start achieving their weight management goals with this new Calorie Control Weight Management powdered drink formula.

Figure 3: Categorical weight loss (12 lbs.)
Figure 3: Categorical weight loss (12 lbs.)

Descriptions of the published scientific studies that support the ingredients in the new Calorie Control Weight Management Formula appear in the first article of this month’s issue.

Rather than relying solely on clinical trials conducted by others, the Life Extension Foundation® went a step further and conducted our own open-label, randomized clinical study in treatment-resistant volunteers. Our findings support the benefits of the ingredients in the Calorie Control Weight Management Formula.

We now have a potent front-line weapon to be used in a comprehensive program to rid surplus fat pounds.

An Epidemic with Catastrophic Ramifications

A 120-page government report released earlier this year paints a grim picture if today’s obesity epidemic is not brought under control.96

For example, one out of every three young Americans (ages 2 to 19) is already overweight or obese. This group has not yet even encountered most of the age-related obesity inducers described at the end of this article, indicating that an epidemic of gargantuan proportions will soon be upon us.

Stark examples of the costs related to obesity come from this 120-page government report. In 2006 for example, an additional $1,429 in medical costs was spent treating each obese adult American compared to those of normal weight. Annual losses to US businesses due to obesity were $12.8 billion in absenteeism and $30 billion in lost productivity.

In 1980, there were 5.6 million diagnosed cases of diabetes. By 2007, this number shot up to 17.4 million.97 Diabetics are at substantially increased risk for virtually every degenerative disorder.

According to economists, the annual medical costs of obesity in America went from $78.5 billion in 1998 to $147 billion in 2008.98 As I stated at the beginning of this article, therapeutic costs relating to obesity are significantly delayed, meaning this nation faces staggering healthcare expenditures as the population ages and falls ill to obesity-induced diseases.

Over the last thirty years, a record number of artificial sweeteners, artificial fats, and prescription weight-loss drugs have been approved by the FDA. None of this has stopped the relentless surge in the number of overweight and obese Americans.

Don’t Fall Victim to Institutional Ignorance!

As a member of the Life Extension Foundation, you do not have to suffer from the blatant failings of our conventional institutions.

27 Correctable, Obesity-Inducers
Click Here
Don’t Fall Victim to Institutional Ignorance!

When you turn this page, you’ll see a striking graphic highlighting 27 inducers of unwanted fat storage. The first article in this issue describes how the new Calorie Control Weight Management Formula attacks 12 of these 27 causes of weight gain, making it an important weapon in a comprehensive program to reduce body mass.

The article Low Testosterone Promotes Abdominal Obesity in Aging describes the multiple beneficial effects that occur when aging men restore free testosterone to youthful ranges. Not only does testosterone facilitate reduction in abdominal fat, but it also reduces blood glucose levels by improving insulin sensitivity.

The article Critical Need to Control Fasting and After-Meal Glucose Levels outlines the importance of maintaining tight glucose control and reveals methods to not only lose weight, but to also turn on one’s youth-promoting longevity genes.

Every component of Life Extension’s weight loss protocols are supported by findings from the peer-reviewed scientific literature, yet conventional doctors and the federal government wallow in a state of ignorance as they desperately warn of an impending obesity crisis, but offer no practical approaches to avert it.

As you’ll learn in this issue of Life Extension Magazine, age-related weight gain is reversible when the multiple underlying inducers of obesity are thwarted.

For longer life,

For Longer Life

William Faloon

The Multiple Factors Involved In Age-related Weight Gain

Many of you are familiar with a graphic we previously made titled the 17 Daggers of Arterial Disease. The purpose of this image was to show 17 correctable risk factors that predispose people to heart attack.

To highlight 27 correctable inducers of age-associated obesity, we have created on the (27 Correctable Obesity-Inducers Image above) a new illustration that shows multiple daggers pointed at an obese torso. Any one of these obesity-inducers (daggers) can cause or contribute to surplus fat accumulation. In the real world, the cumulative effects of many of the following obesity inducers subjects aging individuals to uncontrolled weight gain:

1. Loss of leptin sensitivity (induces hunger and inhibits release of stored fat from adipocytes)21-24

2. Low adiponectin (increases fat storage in adipocytes and inhibits insulin sensitivity)25,26

3. Excess glycerol-3 phosphate dehydrogenase activity (facilitates conversion of glucose to stored fat—triglycerides—in adipocytes)27

4. Excess amylase activity (digestive enzyme that enables dietary carbohydrates sugars to be rapidly absorbed)28-32

5. Excess lipase activity (enables too many dietary fats to be absorbed)24,33-36

6. Excess calorie intake (overwhelms body’s ability to use calories for energy production)37-41

7. Postprandial hypertriglyceridemia (too much fat remaining in the blood long after meals)36,42

8. Postprandial hyperglycemia (too much glucose remaining in the blood long after meals)26,37,43-49

9. Deficient resting energy expenditure (enables fat accumulation in lieu of calorie burning)24,50

10. Elevated C-reactive protein (binds to leptin and neutralizes leptin’s anti-obesity effects in the body)51

11. Loss of insulin sensitivity (inhibits utilization of glucose in energy producing cells and promotes excess fat storage in adipocytes)26,52-54

12. Insufficient fiber intake (enables rapid rise in blood glucose after meals and postprandial hyperglycemia and hyperinsulinemia)55-60

13. Serotonin deficit (causes carbohydrate binging)61,62

14. Testosterone deficit (men) (contributes to abdominal obesity)63-65

15. Estrogen-progesterone imbalance (women) (contributes to fat accumulation in waist-hips)66

16. Thyroid deficit (precludes efficient cellular utilization of ingested calories)67

17. Decreased physical activity (worsens insulin sensitivity and slows metabolic rate)68-70

18. Fasting hyperinsulinemia (precludes release of stored body fat and increases appetite)71-73

19. Excess gluconeogenesis (causes chronically elevated glucose levels even when fasting)26,74-76

20. Insomnia/insufficient sleep (contributes to hunger and insulin resistance)77-79

21. Polycystic ovary syndrome (women) (associated with weight gain, excess testosterone blood levels, and insulin resistance)80-82

22. Cortisol excess (contributes to increased appetite, insulin resistance, and visceral obesity)85,86

23. Medications (antidepressants, antipsychotics, anti-epileptics, corticosteroids, sulfonylureas, and beta blockers) (associated with insulin resistance and weight gain)85,86

24. Psychological dysfunction (e.g. binge eating, depression) (abnormal emotional and psychological patterns of eating that can lead to weight gain)72,87,88

25. Insufficient vitamin D (associated with insulin insensitivity)89-91

26. Poor dietary choices (chronically engorges blood stream with dangerous fats and sugars—often cooked at high temperatures—that bloat adipocytes)92,93

27. Excess glucosidase activity (digestive enzyme that facilitates conversion of ingested carbohydrates into blood glucose)94,95

The new Calorie Control Weight Management Formula helps neutralize the first 12 on this list of 27 obesity inducers, representing an important initial step to correcting pathologic mechanisms that predispose to age-induced weight gain.

The Life Extension® Weight Loss Guide provides a comprehensive roadmap that overweight and obese humans can follow to circumvent other obesity inducers to not only shed body fat, but also add quality years to their life span.

For example, men with low free testosterone levels may find it impossible to lose significant inches off their abdomen. In women, excess testosterone has the opposite effect and can create abdominal obesity. Fortunately there are low-cost medications that can safely increase free testosterone in men and decrease it in women. These are all fully described in the Life Extension® Weight Loss Guide book available at the member discount price of $8.99 by calling 1-800-544-4440.

References

1. Available at: http://profiles.nlm.nih.gov/NN/Views/Exhibit/narrative/smoking.html. Accessed May 31, 2010

2. Available at: http://www.who.int/tobacco/health_priority/en/index.html. Accessed May 31, 2010.

3. Reeves GK, Pirie K, Beral V, et al. Cancer incidence and mortality in relation to body mass index in the Million Women Study: cohort study. BMJ. 2007 Dec 1;335(7630):1134.

4. Calle EE, Kaaks R. Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nat Rev Cancer. 2004 Aug;4(8):579-91.

5. Schapira DV, Kumar NB, Lyman GH. Estimate of breast cancer risk reduction with weight loss. Cancer. 1991 May 15;67(10):2622-5.

6. Pan SY, DesMeules M, Morrison H, Wen SW. Obesity, high energy intake, lack of physical activity, and the risk of kidney cancer. Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2453-60.

7. Calabro P, Yeh ET. Intra-abdominal adiposity, inflammation, and cardiovascular risk: new insight into global cardiometabolic risk. Curr Hypertens Rep. 2008 Feb;10(1):32-8.

8. Bodary PF, Iglay HB, Eitzman DT. Strategies to reduce vascular risk associated with obesity. Curr Vasc Pharmacol. 2007 Oct;5(4):249-58.

9. Rosa EC, Zanella MT, Ribeiro AB, Kohlmann JO. Visceral obesity, hypertension and cardio-renal risk: a review. Arq Bras Endocrinol Metabol. 2005 Apr;49(2):196-204.

10. Lacquemant C, Vasseur F, Lepretre F, Froguel P. Adipocytokins, obesity and development of type 2 diabetes. Med Sci (Paris). 2005 Dec 21; Spec No:10-8.

11. Gandhi R, Wasserstein D, Razak F, Davey JR, Mahomed NN. BMI independently predicts younger age at hip and knee replacement. Obesity (Silver Spring). 2010 Apr 8.

12. Dahl A, Hassing LB, Fransson E, et al. Being overweight in midlife is associated with lower cognitive ability and steeper cognitive decline in late life. J Gerontol A Biol Sci Med Sci. 2010 Jul 3;29(6):543-52.

13. Available at: http://www.downeyobesityreport.com/category/fact-sheets/. Accessed June 2, 2010.

14. Conway B, Rene A. Obesity as a disease: no lightweight matter. Obes Rev. 2004 3:145-51.

15. Available at: http://blogs.wsj.com/health/2010/05/12/white-house-obesity-report-suggests-more-pe-is-not-enough/. Accessed June 2, 2010.

16. Abate N, Haffner SM, Garg A, Peshock RM, Grundy SM. Sex steroid hormones, upper body obesity, and insulin resistance. J Clin Endocrinol Metab. 2002 Oct;87(10):4522-7.

17. Unoki H, Bujo H, Yamagishi S, Takeuchi M, Imaizumi T, Saito Y. Advanced glycation end products attenuate cellular insulin sensitivity by increasing the generation of intracellular reactive oxygen species in adipocytes. Diabetes Res Clin Pract. 2007 May;76(2):236-44.

18. Alfonzo-Gonzalez G, Doucet E, Bouchard C, Tremblay A. Greater than predicted decrease in resting energy expenditure with age: cross-sectional and longitudinal evidence. Eur J Clin Nutr. 2006 Jan;60(1):18-24.

19. Ames BN. Delaying the mitochondrial decay of aging. Ann N Y Acad Sci. 2004 Jun;1019:406-11.

20. Palacios OM, Carmona JJ, Michan S, et al. Diet and exercise signals regulate SIRT3 and activate AMPK and PGC-1alpha in skeletal muscle. Aging (Albany NY). 2009 Aug 15;1(9):771-83.

21. Chessler SD, Fujimoto WY, Shofer JB, Boyko EJ, Weigle DS. Increased plasma leptin levels are associated with fat accumulation in Japanese Americans. Diabetes. 1998 Feb;47(2):239-43.

22. Scarpace PJ, Zhang Y. Leptin resistance: a prediposing factor for diet-induced obesity. Am J Physiol Regul Integr Comp Physiol. 2009 Mar;296(3):R493-500.

23. 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.

24. Klaus S, Pultz S, Thone-Reineke C, Wolfram S. Epigallocatechin gallate attenuates diet-induced obesity in mice by decreasing energy absorption and increasing fat oxidation. Int J Obes (Lond). 2005 Jun;29(6):615-23.

25. Yatagai T, Nagasaka S, Taniguchi A, et al. Hypoadiponectinemia is associated with visceral fat accumulation and insulin resistance in Japanese men with type 2 diabetes mellitus. Metabolism. 2003 Oct;52(10):1274-8.

26. Oben JE, Ngondi JL, Blum K. Inhibition of Irvingia gabonensis seed extract (OB131) on adipogenesis as mediated via down regulation of the PPARgamma and leptin genes and up-regulation of the adiponectin gene. Lipids Health Dis. 2008 Nov 13;7:44.

27. Wise LS, Green H. Participation of one isozyme of cytosolic glycerophosphate dehydrogenase in the adipose conversion of 3T3 cells. J Biol Chem. 1979 Jan 25;254(2):273-5.

28. Ngondi JL, Djiotsa EJ, Fossouo Z, Oben J. Hypoglycaemic effect of the methanol extract of Irvingia gabonensis seeds on streptozotocin diabetic rats. Afr J Trad CAM. 2006;3(4):74–7.

29. Zhang XQ, Yang MY, Ma Y, Tian J, Song JR. Isolation and activity of an alpha-amylase inhibitor from white kidney beans. Yao Xue Xue Bao. 2007 Dec;42(12):1282-7.

30. Udani J, Singh BB. Blocking carbohydrate absorption and weight loss: a clinical trial using a proprietary fractionated white bean extract. Altern Ther Health Med. 2007 Jul-Aug;13(4):32-7.

31. Wolfram S, Wang Y, Thielecke F. Anti-obesity effects of green tea: from bedside to bench. Mol Nutr Food Res. 2006 Feb;50(2):176-87.

32. Kusano R, Andou H, Fujieda M, Tanaka T, Matsuo Y, Kouno I. Polymer-like polyphenols of black tea and their lipase and amylase inhibitory activities. Chem Pharm Bull (Tokyo). 2008 Mar;56(3):266-72.

33. Juhel C, Armand M, Pafumi Y, Rosier C, Vandermander J, Lairon D. Green tea extract (AR25) inhibits lipolysis of triglycerides in gastric and duodenal medium in vitro. J Nutr Biochem. 2000 Jan;11(1):45-51.

34. Di Pierro F, Borsetto Menghi AM, Barreca A, Lucarelli M, Calandrelli A. Highly bioavailable green tea: Clinical study on obese subjects. Integr Nutr. 2008;11(2):1-14.

35. Kobayashi M, Ichitani M, Suzuki Y, et al. Black-tea polyphenols suppress postprandial hypertriacylglycerolemia by suppressing lymphatic transport of dietary fat in rats. J Agric Food Chem. 2009 Aug 12;57(15):7131–6.

36. Rossner S, Sjostrom L, Noack R, Meinders AE, Noseda G. Weight loss, weight maintenance, and improved cardiovascular risk factors after 2 years treatment with orlistat for obesity. Obes Res. 2000 Jan;8(1):49-61

37. 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.

38. Larson-Meyer DE, Heilbronn LK, Redman LM, et al. Effect of calorie restriction with or without exercise on insulin sensitivity, beta-cell function, fat cell size, and ectopic lipid in overweight subjects. Diabetes Care. 2006 Jun;29(6):1337-44.

39. 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.

40. Barger JL, Kayo T, Vann JM, et al. A low dose of dietary resveratrol partially mimics caloric restriction and retards aging parameters in mice. PLoS One. 2008 Jun 4;3(6):e2264.

41. Joseph JA, Fisher DR, Cheng V, Rimando AM, Shukitt-Hale B. Cellular and behavioral effects of stilbene resveratrol analogues: implications for reducing the deleterious effects of aging. J Agric Food Chem. 2008 Nov 26;56(22):10544-51.

42. Ceriello A, Taboga C, Tonutti L, et al. Evidence for an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial dysfunction and oxidative stress generation: effects of short- and long-term simvastatin treatment. Circulation. 2002 Sep 3;106(10):1211-8.

43. Ceriello A. Impaired glucose tolerance and cardiovascular disease: the possible role of post-prandial hyperglycemia. Am Heart J. 2004 May;147(5):803-7.

44. Chong MF, Fielding BA, Frayn KN. Mechanisms for the acute effect of fructose on postprandial lipemia. Am J Clin Nutr. 2007 Jun;85(6):1511-20.

45. Hosoda K , Wang MF , Liao ML , et al. Antihyperglycemic effect of oolong tea in type 2 diabetes. Diabetes Care. 2003 26:1714-8.

46. Fukino Y, Ikeda A, Maruyama K, Aoki N, Okubo T, Iso H. Randomized controlled trial for an effect of green tea-extract powder supplementation on glucose abnormalities. Eur J Clin Nutr. 2008 Aug;62(8):953-60.

47. Ngondi JL, Fossouo Z, Djiotsa EJ, Oben J. Glycaemic variations after administration of Irvingia gabonensis seeds fractions in normoglycemic rats. Afri J Trad Cam. 2006;3(4):94-101.

48. Poppitt SD, van Drunen JD, McGill AT, Mulvey TB, Leahy FE. Supplementation of a high-carbohydrate breakfast with barley beta-glucan improves postprandial glycaemic response for meals but not beverages. Asia Pac J Clin Nutr. 2007 16(1):16-24.

49. Li Y, Wen S, Kota BP, et al. Punica granatum flower extract, a potent alpha-glucosidase inhibitor, improves postprandial hyperglycemia in Zucker diabetic fatty rats. J Ethnopharmacol. 2005 Jun 3;99(2):239-44.

50. Pasiakos SM, Mettel JB, West K, et al. Maintenance of resting energy expenditure after weight loss in premenopausal women: potential benefits of a high-protein, reduced-calorie diet. Metabolism. 2008 Apr;57(4):458-64.

51. Chen K, Li F, Li J, et al. Induction of leptin resistance through direct interaction of C-reactive protein with leptin. Nat Med. 2006 Apr;12(4):425-32.

52. Jeanrenaud B. Hyperinsulinemia in obesity syndromes: its metabolic consequences and possible etiology. Metabolism. 1978 Dec;27(12 Suppl 2):1881–92.

53. Petersen KF, Shulman GI. Etiology of insulin resistance. Am J Med. 2006 May;119(5 Suppl 1):S10-6.

54. Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R. Effects of a low-insulin-response, energy-restricted diet on weight loss and plasma insulin concentrations in hyperinsulinemic obese females. Am J Clin Nutr. 1994;60(1):48-53.

55. Kromhout D, Bloemberg B, Seidell JC, Nissinen A, Menotti A. Physical activity and dietary fiber determine population body fat levels: the Seven Countries Study. Int J ObeS Relat Metab Disord. 2001 Mar;25(3):301-6.

56. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA. 1997 Feb 12;277(6):472-7.

57. Salmeron J, Ascherio A, Rimm EB, et al. Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care. 1997 Apr;20(4):545-50.

58. Sierra M, Garcia JJ, Fernández N, Diez MJ, Calle AP, Sahagún AM. Effects of ispaghula husk and guar gum on postprandial glucose and insulin concentrations in healthy subjects. Eur J Clin Nutr. 2001 Apr;55(4):235-43.

59. Ou S, Kwok K, Li Y, Fu L. In vitro study of possible role of dietary fiber in lowering postprandial serum glucose. J Agric Food Chem. 2001 Feb;49(2):1026-9.

60. Liu S, Willett WC, Manson JE, et al. Relation between changes in intakes of dietary fiber and grain products and changes in weight and development of obesity among middle-aged women. Am J Clin Nutr. 2003 Nov;78(5):920-7.

61. Breum L, Rasmussen MH, Hilsted J, Fernstrom JD. Twenty-four-hour plasma tryptophan concentrations and ratios are below normal in obese subjects and are not normalized by substantial weight reduction. Am J Clin Nutr. 2003 May;77(5):1112-8.

62. Heraief E, Burckhardt P, Wurtman JJ, Wurtman RJ. Tryptophan administration may enhance weight loss by some moderately obese patients on a protein-sparing modified fast (PSMF) diet. Int J Eating Disord. 1985; 4(3):281-92.

63. Tsai EC, Boyko EJ, Leonetti DL, Fujimoto WY. Low serum testosterone level as a predictor of increased visceral fat in Japanese-American men. Int J Obes Relat Metab Disord. 2000 Apr;24(4):485-91.

64. Marin P, Krotkiewski M, Bjorntorp P. Androgen treatment of middle-aged, obese men: effects on metabolism, muscle and adipose tissues. Eur J Med. 1992 Oct;1(6):329-36.

65. Marin P, Oden B, Bjorntorp P. Assimilation and mobilization of triglycerides in subcutaneous abdominal and femoral adipose tissue in vivo in men: effects of androgens. J Clin Endocrinol Metab. 1995 Jan;80(1):239-43.

66. Lee JR, Hanley J, Hopkins V. What Your Doctor May Not Tell You About Premenopause: Balance Your Hormones and Your Life from Thirty to Fifty. New York, NY: Warner Books;1999.

67. Pedersen O, Richelsen B, Bak J, et al. Characterization of the insulin resistance of glucose utilization in adipocytes from patients with hyper- and hypothyroidism. Acta Endocrin. 1998 Oct;119(2):228-34.

68. Hamburg NM, McMackin CJ, Huang AL, et al. Physical inactivity rapidly induces insulin resistance and microvascular dysfunction in healthy volunteers. Arterioscler Thromb Vasc Biol. 2007 Dec;27(12):2650-6.

69. Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta Physiol (Oxf). 2008 Jan;192(1):127-35.

70. Solomon TP, Haus JM, Kelly KR, et al. Randomized trial on the effects of a 7-d low-glycemic diet and exercise intervention on insulin resistance in older obese humans. Am J Clin Nutr. 2009 Nov;90(5):1222-9.

71. 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.

72. Alemzadeh R, Langley G, Upchurch L, Smith P, Slonim AE. Beneficial effect of diazoxide in obese hyperinsulinemic adults. J Clin Endocrinol Metab. 1998 Jun;83(6):1911-5.

73. Westerterp-Plantenga M, Diepvens K, Joosen AM, Berube-Parent S, Tremblay A. Metabolic effects of spices, teas, and caffeine. Physiol Behav. 2006 Aug 30;89(1):85-91.

74. Gastaldelli A, Toschi E, Pettiti M, et al. Effect of physiological hyperinsulinemia on gluconeogenesis in nondiabetic subjects and in type 2 diabetic patients. Diabetes. 2001 Aug;50(8):1807-12.

75. 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.

76. Furukawa Y. Enhancement of glucose-induced insulin secretion and modification of glucose metabolism by biotin. Nippon Rinsho. 1999 Oct;57(10):2261-9.

77. Spiegel K, Knutson K, Leproult R, Tasali E, Van Cauter E. Sleep loss: a novel risk factor for insulin resistance and type 2 diabetes. J Appl Physiol. 2005 Nov;99(5):2008-19.

78. Donga E, van Dijk M, van Dijk JG, et al. A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8.

79. Wolden-Hanson T, Mitton DR, McCants RL, et al. Daily melatonin administration to middle-aged male rats suppresses body weight, intraabdominal adiposity, and plasma leptin and insulin independent of food intake and total body fat. Endocrinology. 2000 Feb;141(2):487-97.

80. Steckler TL, Herkimer C, Dumesic DA, Padmanabhan V. Developmental programming: excess weight gain amplifies the effects of prenatal testosterone excess on reproductive cyclicity--implication for polycystic ovary syndrome. Endocrinology. 2009 Mar;150(3):1456-65.

81. Carmina E, Bucchieri S, Esposito A, et al. Abdominal fat quantity and distribution in women with polycystic ovary syndrome and extent of its relation to insulin resistance. J Clin Endocrinol Metab. 2007 Jul;92(7):2500-5.

82. Christakou CD, Diamanti-Kandarakis E. Role of androgen excess on metabolic aberrations and cardiovascular risk in women with polycystic ovary syndrome. Womens Health (Lond Engl). 2008 Nov;4(6):583-94.

83. Purnell JQ, Kahn SE, Samuels MH, Brandon D, Loriaux DL, Brunzell JD. Enhanced cortisol production rates, free cortisol, and 11beta-HSD-1 expression correlate with visceral fat and insulin resistance in men: effect of weight loss. Am J Physiol Endocrinol Metab. 2009 Feb;296(2):E351-7.

84. Mattsson C, Olsson T. Estrogens and glucocorticoid hormones in adipose tissue metabolism. Curr Med Chem. 2007 14(27):2918-24.

85. Malone M, Alger-Mayer SA, Anderson DA. Medication associated with weight gain may influence outcome in a weight management program. Ann Pharmacother. 2005 Jul-Aug;39(7-8):1204-8.

86. Verrotti A, la Torre R, Trotta D, Mohn A, Chiarelli F. Valproate-induced insulin resistance and obesity in children. Horm Res. 2009;71(3):125-31.

87. Gaysina D, Hotopf M, Richards M, Colman I, Kuh D, Hardy R. Symptoms of depression and anxiety, and change in body mass index from adolescence to adulthood: results from a British birth cohort. Psychol Med. 2010 Mar 18:1-10.

88. Malone M, Alger-Mayer SA, Anderson DA. The lifestyle challenge program: a multidisciplinary approach to weight management. Ann Pharmacother. 2005 Dec;39(12):2015-20.

89. Nagpal J, Pande JN, Bhartia A. A double-blind, randomized, placebo-controlled trial of the short-term effect of vitamin D3 supplementation on insulin sensitivity in apparently healthy, middle-aged, centrally obese men. Diabet Med. 2009 Jan;26(1):19-27.

90. von Hurst PR, Stonehouse W, Coad J. Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial. Br J Nutr. 2010 Feb;103(4):549-55.

91. Pinelli NR, Jaber LA, Brown MB, Herman WH. Serum 25-hydroxy vitamin D and insulin resistance, metabolic syndrome, and glucose intolerance among Arab Americans. Diabetes Care. 2010 Jun;33(6):1373-5.

92. Gugliucci A, Kotani K, Taing J, et al. Short-term low calorie diet intervention reduces serum advanced glycation end products in healthy overweight or obese adults. Ann Nutr Metab. 2009;54(3):197-201.

93. Braun LT. Cholesterol and triglyceride management: “if I take my medication, can I eat what I want?”. J Cardiovasc Nurs. 2010 May-Jun;25(3):241-6.

94. Tugrul S, Kutlu T, Pekin O, Baglam E, Kiyak H, Oral O. Clinical, endocrine, and metabolic effects of acarbose, a alpha-glucosidase inhibitor, in overweight and nonoverweight patients with polycystic ovarian syndrome. Fertil Steril. 2008 Oct;90(4):1144-8.

95. 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.

96. Available at: http://online.wsj.com/public/resources/documents/obesitymay2010.pdf. Accessed June 4, 2010.

97. Available at: http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm. Accessed July 20, 2010.

98. Available at: http://content.healthaffairs.org/cgi/content/short/hlthaff.28.5.w822. Accessed July 20, 2010.

Subscribe to Life Extension Magazine®

Subscribe Now

Advertise in Life Extension Magazine®

Learn More