Printer Friendly

Deadly carbohydrates the lethal sugar/cancer connection.

A new study shows what researchers have suspected for years--consuming carbohydrates dramatically increases the risk for a common type of breast cancer, a kind that is notoriously hard to treat. (1)

The study, published earlier this year in Cancer Epidemiology, Biomarkers & Prevention, revealed that postmenopausal women treated for breast cancer were:

* Two times more likely to have recurrence if their carbohydrate intake remained stable or increased after surgery,

* 70% more likely to have a recurrence if their tumors tested positive for " insulin-like growth factor-1," or IGF-1 (IGF-1 increases in response to excess carbohydrate intake),

* Likely to have a 5-fold increase in the risk of recurrence if they had the combination of an IGF-1 receptor-positive tumor plus a stable or increased carbohydrate intake. (1)

While the study focused on reducing future cancer recurrences, it has tremendous implications for women who have not yet experienced breast cancer, and for that matter, for everyone concerned about preventing cancers in the future.

A powerful way to reduce cancer risk is to get control of your intake of refined carbohydrates, IGF-1, and insulin levels. (2) Yet despite the known risks of excess carbohydrate intake (obesity, cancer, and vascular disease), cutting out carbs can be challenging for most people.

This article investigates the connections between carbohydrate intake and breast cancer risk. It then explores recent data showing how consuming and absorbing too many carbohydrates is associated with elevations in IGF-1, which increases the risk of breast cancer recurrence. It concludes with real-world solutions to help mitigate the adverse impact of excessive carbohydrate intake.

The Breast Cancer/Carbohydrate Connection

There is growing interest among the scientific community in the relationship between carbohydrate consumption and cancer, with a special focus on breast cancer.

Diets high in readily digested carbohydrates (like those found in most processed foods) are associated with increased cancer risks. Women who consume great amounts of foods with a high glycemic index (the rate at which carbohydrates raise blood sugar levels) have a 57% increased risk of breast cancer, while those who eat food with a high glycemic load (a product of the glycemic index and the total available carbohydrate content of a food) have as much as a 153% increase in risk. (3)

This increased risk has been specifically identified in people who are overweight or obese. Overweight women, for example, are 35% more likely to get breast cancer if they eat a lot of foods with a high glycemic index. (4) Asian women whose primary carbohydrate source is white rice are 19% more likely to develop breast cancer with every 100-gram (about 3 ounces) increment in their rice intake per day. But those who eat brown rice, a slower-digesting starch, are 24% less likely to develop breast cancer with every 100-gram increment of rice consumed per day. (5) When glucose levels get so high that they enter the diabetic range, breast cancer risk grows to twice that of postmenopausal women with normal sugar levels. (6)

In addition to increasing the risk of developing breast cancer in postmenopausal women, glycemic load and total carbohydrate consumption are also associated with the worst kinds of breast cancer, namely those lacking receptors for estrogen and progesterone molecules. (7) Triple negative breast cancers--in which cancer cells do not contain receptors for estrogen, progesterone, or HER2--cannot be treated with treatments that oppose hormone actions. This leaves patients to suffer through more deadly, and often less effective, treatment options, thereby lowering survival rates substantially. (8)

On the other hand, the Nurses' Health Study, a large, women's health-focused research project, demonstrated that women who followed a diet high in vegetables and low in carbohydrates were 19% less likely to develop estrogen receptor negative breast cancer. (9)

Carbohydrates And Cancer Risk

There is a deeper problem with high carbohydrate consumption, even when blood sugar levels don't rise.

High-carbohydrate diets produce chronic elevations of insulin as the body tries to deal with the excess sugar. (4) Protein glycation caused by excess glucose also contributes to insulin resistance, raising blood glucose levels and potentially insulin levels as a result. (10) Because insulin is a growth factor, elevated insulin levels represent a potential breast cancer threat because it appears to stimulate breast cancer cells to grow and reproduce. (11)

Studies now reveal another danger--one that goes beyond glycation and insulin levels--which raises a woman's risk for breast cancer in relation to her carbohydrate intake.

This danger is posed by a growth factor so closely related to insulin that it is called " insulin-like growth factor-1," or IGF-1. IGF-1 now appears to be a culprit that links high-carbohydrate intake to cancer risks throughout the body, but with special relevance for breast and possibly prostate cancers. (1,12)

How IGF-1 Increases Breast Cancer Risk

Serum levels of IGF-1 are associated with breast cancer risk in premenopausal women, and the higher the IGF-1, the greater the risk. (6,13) Studies show this risk increase to be between 60 to 86%, compared to women with lower levels. For premenopausal women 50 or younger, this increased risk grows to 150%. (14,15)

Some studies, however, demonstrate about a 38% increase in breast cancer risk in women older than 50 with high IGF-1 concentrations. (16,17)

IGF-1 has a strong impact on breast cancer because two of its functions, promoting tissue growth and suppressing programmed cell death (apoptosis), are hallmarks of malignant cells. The actions of IGF-1 are necessary for growth and development through childhood. (18) But in adults, higher levels of IGF-1 can pose problems, including increasing cancer risk and shortening life span. (19)

IGF-1 is a protein hormone similar in structure to insulin. (20) It is a growth factor involved in normal mammary gland development and promotes healthy cell proliferation, growth, and reproduction and thereby helps the developing mammary gland form correctly. (21)

In adults, increased carbohydrate consumption appears to raise IGF-1 production and increase the risk of cancer. (19,22) In children, IGF-1 appears to be more beneficial, since rapid cell replication and cell survival is desired. (20,23) In addition to stimulating cell growth and division, IGF-1 appears to suppress apoptosis, (24,25) one of the body's many defense mechanisms against cancer. When this protective mechanism fails, abnormal, precancerous cells survive and reproduce instead of being naturally removed from healthy tissue. (14,26)

These two mechanisms--growth promotion and diminished apoptosis--are hallmarks of malignant cells. That's why high levels of IGF-1, with its ability to promote tissue growth and suppress apoptosis, are a potent cancer promoter. (14,22,27) Lab research shows that when developing mammary cells are exposed to high levels of IGF-1, it causes the cells to form large sphere-like clumps with sustained proliferative activity, abnormal changes suggestive of carcinogenesis. (21)

IGF-1 can promote cancer through its local effects on specific cell types. Making matters worse, cancers that develop under IGF-1 stimulation are often resistant to chemotherapy and radiation. (28,29) Recent evidence suggests IGF-1 and estrogen work together to promote cancer in human breast tissue. (30)

How Inhibiting IGF-1 Reduces Cancer Risk

On its own, IGF-1 is not the problem. Like most signaling molecules, IGF-1 exerts specific actions on cells only when it binds to specific IGF-1 receptors. IGF-1 receptors are found in many tissues. This increased IGF-1 signaling and receptor expression is recognized as one factor in breast cancers becoming resistant to treatment. (29)

IGF-1 receptor levels are higher in other cancers as well, including prostate cancer. High IGF-1 levels, along with reduced levels of the main serum-binding protein IGF-BP3 (insulin-like growth factor binding protein 3) in the blood predispose men to developing prostate cancer. (31) As with breast cancers, increased IGF-1 signaling is associated with prostate cancers becoming independent of hormonal control. This makes them much more difficult to treat with conventional anti hormone therapies. (32)

Fortunately, in studies that used antibody molecules to inhibit IGF-1 binding to IGF-1 receptors, several factors needed for cancer progression were inhibited, including protein synthesis, cell growth, and survival. (33) Furthering this point, people with a congenital IGF-1 deficiency have significantly reduced rates of cancer. (19)

In addition, research shows that the antidiabetic drug metformin (which has multiple health-promoting benefits) suppresses IGF-1 signaling in human pancreatic cancer cells in culture. (34)

Research has shown that women with plasma IGF-1 levels less than 120 ng/mL are more likely to survive breast cancer. (35) In fact, lowering IGF-1 plasma levels has now been recommended to: (35)

* Reduce the risk of developing breast cancer in high-risk women,

* Slow breast cancer progression in patients in the early stages of their disease,

* Lower the risk of breast cancer recurrence, and

* Increase the probability of surviving breast cancer.

For these reasons, Big Pharma is keenly pursuing drugs that inhibit IGF-1 receptor binding or signaling for use against a variety of cancers, though to date many of these study results have been miserable. (26,36-39)

Fortunately, there are a number of natural ways to reduce the damage caused by IGF-1.

Reduce Your Body's Exposure To Carbohydrates And IGF-1

The most direct way to reduce your body's exposure to the carbohydrates that induce IGF-1 activity and its related cancer risk is to eat a diet containing fewer carbohydrates and simple sugars. However, this is challenging for many people, particularly those who are also trying to reduce consumption of animal proteins and fats. (40) Similarly, you can lower overall exposure to carbohydrate breakdown by consuming a diet high in fiber (which is not readily broken down by the intestine); but again, high-fiber diets can be unappealing and uncomfortable for many people. (40)

A more palatable and practical option to reduce carbohydrate exposure is to use specific nutrients that limit or slow starch breakdown in the intestine, which in turn reduces blood sugar levels and insulin levels. [(40)] By reducing these levels, you can "turn down the volume" on the IGF-1 system and gain more control of your dietary risk for cancer. (23,41,42)

Table 1 (next page) offers examples of some of the nutrients known to be most effective at reducing your body's exposure to excessive dietary carbohydrate, potentially modulating IGF-1 and insulin levels.

As you can see from Table 1, there are many options for gaining control of your body's exposure to excess carbohydrates. Note that these products act by several different mechanisms; this is a critical and widely recognized factor in the effectiveness of these natural supplements.


Many people have shifted away from animal proteins and fats toward a more carbohydrate-rich diet in an effort to improve their health and longevity.

Unfortunately, diets high in carbohydrates, especially sugars and refined starch, raise cancer risk. This is, in part, due to higher levels of IGF-1, a growth factor that promotes cell replication and slows programmed cell death--two major components of cancer development.

High levels of IGF-1 are strongly associated with breast cancers, and perhaps others. In addition, tumors promoted by IGF-1 are more likely than other tumors to be resistant to standard hormone treatments, increasing the need for more toxic chemotherapy.

You can help control IGF-1 levels by restricting intake of refined carbohydrates (white starches) and increasing intake of dietary fiber. Many people find these dietary interventions difficult to sustain.

An alternative to these dietary shifts is to use natural supplement formulas that reduce the ability of dietary carbohydrates to reach your bloodstream, thereby lowering blood sugar, improving insulin sensitivity, and potentially reducing the body's production of cancer-promoting IGF-1.

Several such supplements exist in multi-ingredient formulas, thus providing broad-spectrum blood sugar modulating mechanisms. By choosing an appropriate supplement formula regimen to be taken before carbohydrate- and starch- containing meals, you may reduce cancer risks associated with elevated blood glucose, insulin, and IGF-1.

If you have any questions on the scientific content of this article, please call a Life Extension[R] Health Advisor at 1-866-864-3027.


Carbohydrates And Breast Cancer Risk

* Americans' high consumption of carbohydrates puts them at increased risk for many cancers, especially breast cancers.

* Insulin-like growth factor (IGF-1) and insulin are underlying culprits associated with carbohydrate intake and cancer.

* IGF-1 promotes rapid cell replication while reducing normal programmed cell death, two major factors associated with cancer development.

* Studies show a close relationship between carbohydrate consumption, IGF-1, and breast cancer risk.

* You can reduce your carbohydrate and IGF-1-related cancer risk by selecting appropriate nutraceuticals that reduce carbohydrate breakdown and absorption.

* If you are one of the many who find it hard to cut down on carbohydrates in your diet, it is time to turn to some of the many natural dietary supplements that may limit your exposure to these cancer risk factors.


Studies show that reducing insulin and IGF-1 signaling not only decreases cancer risk, but can also extend life span in many organisms. IGF-1 receptors in the brains of mammals have been shown to control life span through several mechanisms including control of energy metabolism and modified stress resistance. (85) Studies show that humans with genetic deficiencies in growth factors including IGF-1 are reported to have increased life span. (19,86-89)

Some researchers believe one of the reasons calorie restriction is so effective at extending life span is because it triggers a reduction in insulin/IGF-1 signaling, part of which involves reducing cancer risk. (90,91) This is supported by the recent observation that combining IGF-1 inhibition with calorie restriction in animals with cancer produced a significant decrease in tumor weight. (92)


(1.) Emond JA, Pierce JP, Natarajan L, et al. Risk of Breast Cancer Recurrence Associated with Carbohydrate Intake and Tissue Expression of IGF-1 Receptor. Cancer Epidemiol Biomarkers Prev. 2014 Jul;23(7):1273-9.

(2.) Boyd DB. Insulin and cancer. Integr Cancer Ther. 2003 Dec;2(4):315-29.

(3.) Sieri S, Pala V, Brighenti F, et al. Dietary glycemic index, glycemic load, and the risk of breast cancer in an Italian prospective cohort study. Am J Clin Nutr. 2007 Oct;86(4):1160-6.

(4.) Lajous M, Boutron-Ruault MC, Fabre A, Clavel-Chapelon F, Romieu I. Carbohydrate intake, glycemic index, glycemic load, and risk of postmenopausal breast cancer in a prospective study of French women. Am J Clin Nutr. 2008 May;87(5):1384-91.

(5.) Yun SH, Kim K, Nam SJ, Kong G, Kim MK. The association of carbohydrate intake, glycemic load, glycemic index, and selected rice foods with breast cancer risk: a case-control study in South Korea. Asia Pac J Clin Nutr. 2010;19(3):383-92.

(6.) Krajcik RA, Borofsky ND, Massardo S, Orentreich N. Insulin-like growth factor I (IGF-I), IGF-binding proteins, and breast cancer. Cancer Epidemiol Biomarkers Prev. 2002 Dec;11(12):1566-73.

(7.) Romieu I, Ferrari P, Rinaldi S, et al. Dietary glycemic index and glycemic load and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Am J Clin Nutr. 2012 Aug;96(2):345-55.

(8.) Hoeferlin LA, C EC, Park MA. Challenges in the treatment of triple negative and HER2-overexpressing breast cancer. J Surg Sci. 2013 Dec;1(1):3-7.

(9.) Fung TT, Hu FB, Hankinson SE, Willett WC, Holmes MD. Low-carbohydrate diets, dietary approaches to stop hypertension-style diets, and the risk of postmenopausal breast cancer. Am J Epidemiol. 2011 Sep 15;174(6):652-60.

(10.) Farrar JL, Hartle DK, Hargrove JL, Greenspan P. A novel nutraceutical property of select sorghum (Sorghum bicolor) brans: inhibition of protein glycation. Phytother Res. 2008 Aug;22(8): 1052-6.

(11.) Mulligan AM, O'Malley FP, Ennis M, Fantus IG, Goodwin PJ. Insulin receptor is an independent predictor of a favorable outcome in early stage breast cancer. Breast Cancer Res Treat. 2007 Nov;106(1):39-47.

(12.) Roberts CT. IGF-1 and prostate cancer. Novartis Found Symp. 2004;262:193-9.

(13.) Hankinson SE, Willett WC, Colditz GA, et al. Circulating concentrations of insulin-like growth factor-I and risk of breast cancer. Lancet. 1998 May 9;351(9113): 1393-6.

(14.) Wu MH, Chou YC, Chou WY, et al. Relationships between critical period of estrogen exposure and circulating levels of insulin-like growth factor-I (IGF-I) in breast cancer: evidence from a case-control study. Int J Cancer. 2010 Jan 15;126(2):508-14.

(15.) Schernhammer ES, Holly JM, Pollak MN, Hankinson SE. Circulating levels of insulin-like growth factors, their binding proteins, and breast cancer risk. Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):699-704.

(16.) Rinaldi S, Peeters PH, Berrino F, et al. IGF-I, IGFBP-3 and breast cancer risk in women: The European Prospective Investigation into Cancer and Nutrition (EPIC). Endocr Relat Cancer. 2006 Jun;13(2):593-605.

(17.) Kaaks R, Johnson T, Tikk K, et al. Insulin-like growth factor I and risk of breast cancer by age and hormone receptor status-A prospective study within the EPIC cohort. Int J Cancer. 2014 Jun 1; 134(11):2683-90.

(18.) Yakar S, Rosen CJ, Beamer WG, et al. Circulating levels of IGF-1 directly regulate bone growth and density. J Clin Invest. 2002 Sep;110(6):771-81.

(19.) Melnik BC, John SM, Schmitz G. (2011). Over-stimulation of insulin/IGF-1 signaling by western diet may promote diseases of civilization: lessons learnt from laron syndrome. NutrMetab. 2011;8(1):41.

(20.) Laron Z. Insulin-like growth factor 1 (IGF-1): a growth hormone. J Clin Pathol: Mol Pathol. 2001;54:311-16.

(21.) Gajewska M, Zielniok K, Debski B, Motyl T. IGF-I retards proper development of acinar structures formed by bovine mammary epithelial cells via sustained activation of Akt kinase. Domest Anim Endocrinol. 2013 Oct;45(3):111-21.

(22.) Kaaks R. Nutrition, insulin, IGF-1 metabolism and cancer risk: a summary of epidemiological evidence. Novartis Found Symp. 2004;262:247-60; discussion 260-8.

(23.) Runchey SS, Pollak MN, Valsta LM, et al. Glycemic load effect on fasting and post-prandial serum glucose, insulin, IGF-1 and IGFBP-3 in a randomized, controlled feeding study. Eur J Clin Nutr. 2012 Oct;66(10):1146-52.

(24.) Romieu I, Ferrari P, Rinaldi S, et al. Dietary glycemic index and glycemic load and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Am J Clin Nutr. 2012 Aug;96(2):345-55.

(25.) Hellawell GO, Turner GD, Davies DR, Poulsom R, Brewster SF, Macaulay VM. Expression of the type 1 insulin-like growth factor receptor is up-regulated in primary prostate cancer and commonly persists in metastatic disease. Cancer Res. 2002 May 15;62(10):2942-50.

(26.) Robertson JF, Ferrero JM, Bourgeois H, et al. Ganitumab with either exemestane or fulvestrant for postmenopausal women with advanced, hormone-receptor-positive breast cancer: a randomised, controlled, double-blind, phase 2 trial. Lancet Oncol. 2013 Mar;14(3):228-35.

(27.) Vadgama JV, Wu Y, Datta G, Khan H, Chillar R. Plasma insulin-like growth factor-I and serum IGF-binding protein 3 can be associated with the progression of breast cancer, and predict the risk of recurrence and the probability of survival in African-American and Hispanic women. Oncology. 1999 Nov;57(4):330-40.

(28.) Arnaldez FI, Helman LJ. Targeting the insulin growth factor receptor 1. Hematol Oncol Clin North Am. 2012 Jun;26(3):527-42.

(29.) Jones HE, Goddard L, Gee JM, et al. Insulin-like growth factor-I receptor signalling and acquired resistance to gefitinib (ZD1839; Iressa) in human breast and prostate cancer cells. Endocr Relat Cancer. 2004 Dec;11(4):793-814.

(30.) Sarfstein R, Pasmanik-Chor M, Yeheskel A, et al. Insulin-like growth factor-I receptor (IGF-IR) translocates to nucleus and autoregulates IGF-IR gene expression in breast cancer cells. J Biol Chem. 2012 Jan 20;287(4):2766-76.

(31.) Hellawell GO, Turner GD, Davies DR, Poulsom R, Brewster SF, Macaulay VM. Expression of the type 1 insulin-like growth factor receptor is up-regulated in primary prostate cancer and commonly persists in metastatic disease. Cancer Res. 2002 May 15;62(10):2942-50.

(32.) Galet C, Gray A, Said JW, et al. Effects of Calorie Restriction and IGF-1 Receptor Blockade on the Progression of 22Rv1 Prostate Cancer Xenografts. Int J MolSci. 2013;14(7):13782-95.

(33.) Evdokimova V, Tognon CE, Benatar T, et al. IGFBP7 binds to the IGF-1 receptor and blocks its activation by insulin-like growth factors. Sci Signal. 2012 Dec 18;5(255):ra92.

(34.) Karnevi E, Said K, Andersson R, Rosendahl AH. Metformin-mediated growth inhibition involves suppression of the IGF-I receptor signalling pathway in human pancreatic cancer cells. BMC Cancer. 2013; 13:235.

(35.) Vadgama JV, Wu Y, Datta G, Khan H, Chillar R. Plasma insulin-like growth factor-I and serum IGF-binding protein 3 can be associated with the progression of breast cancer, and predict the risk of recurrence and the probability of survival in African-American and Hispanic women. Oncology. 1999 Nov;57(4):330-40.

(36.) Fagan DH, Uselman RR, Sachdev D, Yee D. Acquired resistance to tamoxifen is associated with loss of the type I insulin-like growth factor receptor: implications for breast cancer treatment. Cancer Res. 2012 Jul 1;72(13):3372-80.

(37.) Fu P, Ibusuki M, Yamamoto Y, et al. Insulin-like growth factor-1 receptor gene expression is associated with survival in breast cancer: a comprehensive analysis of gene copy number, mRNA and protein expression. Breast Cancer Res Treat. 2011 Nov;130(1):307-17.

(38.) Ma CX, Suman VJ, Goetz M, et al. A phase I trial of the IGF-1R antibody Cixutumumab in combination with temsirolimus in patients with metastatic breast cancer. Breast Cancer Res Treat. 2013 May;139(1):145-53.

(39.) Warshamana-Greene GS, Litz J, Buchdunger E, Garcia-Echeverria C, Hofmann F, Krystal GW. The insulin-like growth factor-I receptor kinase inhibitor, NVP-ADW742, sensitizes small cell lung cancer cell lines to the effects of chemotherapy. Clin Cancer Res. 2005 Feb 15;11 (4): 1563-71.

(40.) Preuss HG. Bean amylase inhibitor and other carbohydrate absorption blockers: effects on diabesity and general health. J Am Coll Nutr. 2009 Jun;28(3):266-76.

(41.) Pasanisi P, Bruno E, Manoukian S, Berrino F. A randomized controlled trial of diet and physical activity in BRCA mutation carriers. Fam Cancer. 2014 Jun;13(2):181-7.

(42.) Klement RJ, Kammerer U. Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutr Metab (Lond). 2011 Oct 26;8:75.

(43.) Kaats GR, Keith SC, Keith PL, Leckie RB, Perricone NV, Preuss HG. A combination of l-arabinose and chromium lowers circulating glucose and insulin levels after an acute oral sucrose challenge. Nutr J. 2011;10:42.

(44.) Shibanuma K, Degawa Y, Houda K. Determination of the transient period of the EIS complex and investigation of the suppression of blood glucose levels by L-arabinose in healthy adults. Eur J Nutr. 2011 Sep;50(6):447-53.

(45.) Preuss HG, Echard B, Bagchi D, Perricone NV! Comparing effects of carbohydrate (CHO) blockers and trivalent chromium on CHO-induced insulin resistance and elevated blood pressure in rats. J Am Coll Nutr. 2013;32(1):58-65.

(46.) Evock-Clover CM, Polansky MM, Anderson RA, Steele NC. Dietary chromium supplementation with or without somatotropin treatment alters serum hormones and metabolites in growing pigs without affecting growth performance. J Nutr. 1993 Sep;123(9):1504-12.

(47.) No authors listed. Diabetes Educ. 2004;Suppl:2-14.

(48.) Frauchiger MT, Wenk C, Colombani PC. Effects of acute chromium supplementation on postprandial metabolism in healthy young men. J Am Coll Nutr. 2004 Aug;23(4):351-7.

(49.) Wang ZQ, Qin J, Martin J, et al. Phenotype of subjects with type 2 diabetes mellitus may determine clinical response to chromium supplementation. Metabolism. 2007 Dec;56(12):1652-5.

(50.) Sharma S, Agrawal RP, Choudhary M, Jain S, Goyal S, Agarwal V Beneficial effect of chromium supplementation on glucose, HbA1C and lipid variables in individuals with newly onset type-2 diabetes. J Trace Elem Med Biol. 2011 Jul;25(3):149-53.

(51.) Landin-Wilhelmsen K, Wilhelmsen L, Lappas G, et al. Serum insulin-like growth factor I in a random population sample of men and women: relation to age, sex, smoking habits, coffee consumption and physical activity, blood pressure and concentrations of plasma lipids, fibrinogen, parathyroid hormone and osteocalcin. Clin Endocrinol (Oxf). 1994 Sep;41(3):351-7.

(52.) Ho L, Varghese M, Wang J, et al. Dietary supplementation with decaffeinated green coffee improves diet-induced insulin resistance and brain energy metabolism in mice. NutrNeurosci. 2012 Jan;15(1):37-45.

(53.) Lecoultre V, Carrel G, Egli L, et al. Coffee consumption attenuates short-term fructose-induced liver insulin resistance in healthy men. Am J Clin Nutr. 2014 Feb;99(2):268-75.

(54.) Song SJ, Choi S, Park T. Decaffeinated green coffee bean extract attenuates diet-induced obesity and insulin resistance in mice. Evid Based Complement Alternat Med. 2014;2014:718379. Epub 2014 Apr 10.

(55.) Omoruyi F, Adamson I. Digestive and hepatic enzymes in streptozotocin-induced diabetic rats fed supplements of dikanut (Irvingia gabonensis) and cellulose. Ann Nutr Metab. 1993;37(1): 14-23.

(56.) Ngondi JL, Oben JE, Minka SR. The effect of Irvingia gabonensis seeds on body weight and blood lipids of obese subjects in Cameroon. Lipids Health Dis. 2005;4:12.

(57.) 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;7:44.

(58.) 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;8:7.

(59.) Ross SM. African mango (IGOB131): a proprietary seed extract of Irvingia gabonensis is found to be effective in reducing body weight and improving metabolic parameters in overweight humans. Holist Nurs Pract. 2011 Jul-Aug;25(4):215-7.

(60.) Duerr RL, McKirnan MD, Gim RD, Clark RG, Chien KR, Ross J. Cardiovascular effects of insulin-like growth factor-1 and growth hormone in chronic left ventricular failure in the rat. Circulation. 1996;93(12):2188-96.

(61.) Miyahara C, Miyazawa M, Satoh S, Sakai A, Mizusaki S. Inhibitory effects of mulberry leaf extract on post- prandial hyperglycemia in normal rats. J Nutr Sci Vitaminol (Tokyo). 2004 Jun;50(3):161-4.

(62.) Zhong L, Furne JK, Levitt MD. An extract of black, green, and mulberry teas causes malabsorption of carbohydrate but not of triacylglycerol in healthy volunteers. Am J Clin Nutr. 2006 Sep;84(3):551-5.

(63.) Tanabe K, Nakamura S, Omagari K, Oku T. Repeated ingestion of the leaf extract from Morus alba reduces insulin resistance in KK-Ay mice. Nutr Res. 2011 Nov;31(11):848-54.

(64.) Lim HH, Lee SO, Kim SY, Yang SJ, Lim Y Anti-inflammatory and antiobesity effects of mulberry leaf and fruit extract on high fat diet-induced obesity. Exp Biol Med (Maywood). 2013 Oct;238(10):1160-9.

(65.) Nazari M, Hajizadeh MR, Mahmoodi M, Mirzaei MR, Hassanshahi G. The regulatory impacts of Morus Alba leaf extract on some enzymes involved in glucose metabolism pathways in diabetic rat liver. Clin Lab. 2013;59(5-6):497-504.

(66.) Wu T, Qi X, Liu Y, et al. Dietary supplementation with purified mulberry (Morus australis Poir) anthocyanins suppresses body weight gain in high-fat diet fed C57BL/6 mice. FoodChem. 2013 Nov 1;141(1):482-7.

(67.) Wu T, Tang Q, Gao Z, et al. Blueberry and mulberry juice prevent obesity development in C57BL/6 mice. PLoS One. 2013;8(10):e77585.

(68.) Naowaboot J, Pannangpetch P, Kukongviriyapan V, Prawan A, Kukongviriyapan U, Itharat A. Mulberry leaf extract stimulates glucose uptake and GLUT4 translocation in rat adipocytes. Am J Chin Med. 2012;40(1):163-75.

(69.) Martinez JA, Marcos R, Macarulla MT, Larralde J. Growth, hormonal status and protein turnover in rats fed on a diet containing peas (Pisum sativum L.) as the source of protein. Plant Foods Hum Nutr. 1995 Apr;47(3):211-20.

(70.) Obiro WC, Zhang T, Jiang B. The nutraceutical role of the Phaseolus vulgaris alpha-amylase inhibitor. Br J Nutr. 2008 Jul;100(1):1-12.

(71.) Nilsson A, Johansson E, Ekstrom L, Bjorck I. Effects of a brown beans evening meal on metabolic risk markers and appetite regulating hormones at a subsequent standardized breakfast: a randomized cross-over study. PLoS One. 2013;8(4):e59985.

(72.) Spadafranca A, Rinelli S, Riva A, et al. Phaseolus vulgaris extract affects glycometabolic and appetite control in healthy human subjects. Br J Nutr. 2013 May 28;109(10):1789-95.

(73.) Zhang S, Zhu M, Shen D. Experimental study on the treatment of diabetes by phloridzin in rats. J Tongji Med Univ. 1998;18(2):105-7, 118.

(74.) Zhao H, Yakar S, Gavrilova O, et al. Phloridzin improves hyperglycemia but not hepatic insulin resistance in a transgenic mouse model of type 2 diabetes. Diabetes. 2004 Nov;53(11):2901-9.

(75.) Simonyi G. New possibility in the oral glucose lowering treatment of type 2 diabetes mellitus: sodium-glucose co-transporter-2 inhibitors. OrvHetil. 2012 May 6;153(18):695-701.

(76.) Paradis ME, Couture P, Lamarche B. A randomised crossover placebo-controlled trial investigating the effect of brown seaweed (Ascophyllum nodosum and Fucus vesiculosus) on postchallenge plasma glucose and insulin levels in men and women. Appl Physiol Nutr Metab. 2011 Dec;36(6):913-9.

(77.) Lordan S, Smyth TJ, Soler-Vila A, Stanton C, Ross RP. The alpha-amylase and alpha-glucosidase inhibitory effects of Irish seaweed extracts. FoodChem. 2013 Dec 1;141(3):2170-6.

(78.) Park JH, Lee SH, Chung IM, Park Y. Sorghum extract exerts an anti-diabetic effect by improving insulin sensitivity via PPAR-gamma in mice fed a high-fat diet. Nutr Res Pract. 2012 Aug;6(4):322-7.

(79.) Poquette NM, Gu X, Lee SO. Grain sorghum muffin reduces glucose and insulin responses in men. Food Funct. 2014 May;5(5):894-9.

(80.) Sasaki M, Joh T, Koikeda S, et al. A novel strategy in production of oligosaccharides in digestive tract: prevention of postprandial hyperglycemia and hyperinsulinemia. J Clin Biochem Nutr. 2007 Nov;41(3):191-6.

(81.) Brison Y, Fabre E, Moulis C, Portais JC, Monsan P, Remaud-Simeon M. Synthesis of dextrans with controlled amounts of alpha-1,2 linkages using the transglucosidase GBD-CD2. Appl Microbiol Biotechnol. 2010 Mar;86(2):545-54.

(82.) Sako T, Mori A, Lee P, et al. Supplementing transglucosidase with a high-fiber diet for prevention of postprandial hyperglycemia in streptozotocin-induced diabetic dogs. Vet Res Commun. 2010 Feb;34(2):161-72.

(83.) Sasaki M, Imaeda K, Okayama N, et al. Effects of transglucosidase on diabetes, cardiovascular risk factors and hepatic biomarkers in patients with type 2 diabetes: a 12-week, randomized, double-blind, placebo-controlled trial. Diabetes Obes Metab. 2012 Apr;14(4):379-82.

(84.) Sasaki M, Ogasawara N, Funaki Y, et al. Transglucosidase improves the gut microbiota profile of type 2 diabetes mellitus patients: a randomized double-blind, placebo-controlled study. BMC Gastroenterol. 2013; 13:81.

(85.) Holzenberger M. Igf-I signaling and effects on longevity. Nestle Nutr Workshop Ser Pediatr Program. 2011;68:237-45; discussion 46-9.

(86.) Barzilai N, Bartke A. Biological approaches to mechanistically understand the healthy life span extension achieved by calorie restriction and modulation of hormones. J Gerontol A Biol Sci Med Sci. 2009 Feb;64(2):187-91.

(87.) Gallagher EJ, LeRoith D. Is growth hormone resistance/IGF-1 reduction good for you? Cell Metab. 2011 Apr 6;13(4):355-6.

(88.) Narasimhan SD, Yen K, Tissenbaum HA. Converging pathways in life span regulation. Curr Biol. 2009 Aug 11;19(15):R657-66.

(89.) Bartke A, Westbrook R. Metabolic characteristics of long-lived mice. Front Genet. 2012;3:288.

(90.) Narasimhan SD, Yen K, Tissenbaum HA. Converging pathways in life span regulation. Curr Biol. 2009 Aug 11;19(15):R657-66.

(91.) Mercken EM, Crosby SD, Lamming DW, et al. Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile. Aging Cell. 2013 Aug;12(4):645-51.

(92.) Galet C, Gray A, Said JW, et al. Effects of calorie restriction and IGF-1 receptor blockade on the progression of 22Rv1 prostate cancer xenografts. Int J Mol Sci. 2013;14(7):13782-95.


Nutrient              Mechanism                 Impact On
                                                Carbohydrate Exposure

L-arabinose (43-45)   Inhibits intestinal       Slows intestinal
                      sucrase (enzyme that      carbohydrate
                      breaks down sucrose       absorption; lowers
                      to glucose and            blood glucose

Chromium (46-50)      Potentiates the           Lowers blood glucose;
                      action of insulin         improves glucose

Coffee (51-54)        Down regulates genes      Reduces blood glucose
                      involved in fat
                      production and
                      stimulates glucose
                      transporter activity

Irvingia gabonensis   Reduces levels of         Reduces absorption,
(African mango;       intestinalcarbohydrate-   blood levels of
Dikanut) (55-60)      digesting                 glucose
                      enzymes; downregulates
                      fat production

Mulberry leaf         Inhibits                  Reduces carbohydrate
extract (61-68)       intestinalcarbohydrate-   absorption; decreases
                      digesting enzymes;        blood glucose
                      supports glucose
                      transporter GLUT4

Phaseolus vulgaris    Inhibits                  Slows carbohydrate
(white kidney bean)   intestinalcarbohydrate-   digestion; suppresses
and other legume      digesting enzymes         hunger/increases
extracts (69-72)                                fullness; reduces
                                                blood glucose

Phloridzin (73-75)    Blocks carrier            Lowers blood glucose
                      proteins that
                      reabsorb glucose from
                      the intestines and

Seaweed               Inhibits                  Appears to reduce
(Ascophyllum          intestinalcarbohydrate-   after-meal blood
nodosum and Fucus     digesting enzymes         glucose
extracts (76,77)

Sorghum (10,78,79)    Activates metabolic       Slows starch
                      sensor PPAR-gamma;        digestion; reduces
                      may inhibit insulin       blood glucose

Transglucosidase      Converts dietary          Slows carbohydrate
(80-84)               sugars and readily        digestion and
                      digested                  absorption; prevents
                      carbohydrates into        after-meal glucose
                      harder-to-digest          increase
                      molecules; improves
                      favorable intestinal
                      microbial population
                      associated with lower
                      diabetes and cancer

Nutrient              Impact On IGF-1/Insulin

L-arabinose (43-45)   Lowers insulin levels; reduces
                      insulin resistance

Chromium (46-50)      Enhances insulin sensitivity;
                      lowers insulin levels

Coffee (51-54)        Improves insulin resistance;
                      IGF-1 levels are lower in
                      women coffee drinkers

Irvingia gabonensis   Decreases body weight, a
(African mango;       contributor to elevated IGF-1
Dikanut) (55-60)

Mulberry leaf         Suppresses body weight gain;
extract (61-68)       reduces insulin resistance

Phaseolus vulgaris    Lowers insulin levels
(white kidney bean)
and other legume
extracts (69-72)

Phloridzin (73-75)    Normalizes glucose tolerance
                      and insulin sensitivity

Seaweed               Improves insulin sensitivity;
(Ascophyllum          reduces insulin levels
nodosum and Fucus
extracts (76,77)

Sorghum (10,78,79)    Improves insulin sensitivity;
                      lowers insulin levels

Transglucosidase      Reduces insulin levels
COPYRIGHT 2014 LE Publications, Inc.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2014 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Report
Author:Martinson, Stephanie
Publication:Life Extension
Geographic Code:1USA
Date:Oct 1, 2014
Previous Article:Assembly line medicine.
Next Article:Unique probiotic targets cardiovascular disease.

Terms of use | Privacy policy | Copyright © 2018 Farlex, Inc. | Feedback | For webmasters