Carbohydrate-restricted Diet for The Therapeutic Paradigm
Robert Su, Virginia Pain Clinic
31 December 2009
Robert Su, Pharm.B., M.D. Author, Carbohydrates Can Kill www.carbohydratescankill.com E-mail: carbohydratescankill@verizon.net
Congratulations to Doctors Node and Inoue on their excellent work to produce such an interesting and educational article.
In my literature review and personal experimentations, I have observed an axis of the excessive consumption of carbohydrates especially those high in glycemic indices and glycemic loads, the daily repeated postprandial hyperglycemia, the repeated postprandial inflammation with both acute and chronic pathological effects on cells, tissues, and organs. [1., 2, 3] The pathological role of hyperglycemia at least includes (1) inflammatory and pro-inflammatory, (2) vasoconstrictive (and hypertensive), (3) pro-thrombotic, (4) arteriosclerotic and atherosclerotic, and (5) glycosylative and pro-glycation. [4]
Inflammation by both acute and chronic or repeated postprandial hyperglycemia (during the period of hours immediately after the beginning of each meal) [5, 6, 7] illustrates why the readings of fasting blood glucose test and glucose tolerance test (at the end of the two-hour period), as well as hemoglobin A1c are ineffective in predicting the risks of diseases including diabetes mellitus, arteriosclerosis and atherosclerosis, neurodegenerative diseases such as Alzheimer’s disease, cancers, and many others. The mass of the pancreatic beta cells starts to decrease, during an individual’s life regardless of his age, when the magnitude of hyperglycemia, on either the vertical or horizontal scale, or both, is so enormous that inflammation, as a consequence, permanently damages the beta cells (apoptosis.) Without halting the repeated postprandial hyperglycemia, the size of apoptosis would exceed the size of regeneration of the mass of the pancreatic beta cells. [8, 9] By the time when either or both the readings of fasting blood glucose and glucose tolerance test is abnormal, about 40-60% of the individual’s beta cells are already damaged or dead; and he is now diagnosed with diabetes mellitus. [10] During the same time, other tissues or organs are also assaulted by inflammation and have begun the pathological process. Studies have even shown atherosclerosis occurs in infancy. [11., 12, 13] The prognosis of his disease(s) will largely depend on the effectiveness of controlling his blood glucose level at all time not just on the readings of the fasting blood glucose and/or the two-hour post glucose tolerance test.
Hemoglobin A1c is a result of glycation between blood glucose and the globin of hemoglobin. The higher the blood glucose level the greater the hemoglobin A1c will be. Because of a lifespan of 60-90 day for hemoglobin, an individual’s hemoglobin A1c largely reflects an averaged level of his blood glucose over a period, not an acute fluctuation of his blood glucose during a short period of hours. Having known the consequent inflammation of hyperglycemia, which is capable of triggering an acute vascular event or others, hemoglobin A1c is ineffective as a predicting biomarker for acute heart attack or stroke.
I have emphasized that, regardless of an individual’s state of health, everyone needs an annual or semiannual series of blood glucose tests, started at the pre-prandial or fasting and continued for two or three hours of the postprandial at a 15-minute interval. These tests will help both assess the functions of his pancreatic beta cells, and evaluate the impacts of his foods on the blood glucose level. In my opinion when the readings are over 120 mg% (a red flag when over 150 mg%), [14., 15, 16] he should avoid the foods high in glycemic index and glycemic load for preventing his progression towards diabetes mellitus. The tests are beneficial for both preventive medicine and personal health education.
Having understood the relationships between the carbohydrate foods excluding the non-digestible fibers, the amount of monosaccharides in the small intestine for absorption, the level of blood sugars (mainly glucose here for illustration), [17] the level of inflammation as a result of hyperglycemia, [18, 19, 20, 21, 22] and the risks of diseases, we have employed many pharmacological products in both disease prevention and management. For examples, we have observed positive results, at least for a short period of time, with certain anti-inflammatory drugs, hypoglycemic agents for increasing insulin secretion or facilitating the peripheral glucose uptake, as well as insulin preparations in cases of insulin dependent diabetes mellitus.
During the recent years, we have also tried to reduce the amount of monosaccharides from being absorbed into the circulation, which directly boosts the blood glucose level. As cited in Doctors Node and Inoue’s article, we are using alpha-glucosidase inhibitors to reduce the postprandial blood sugar level. In addition, we have also discovered a benefit of the gastric by-pass surgery for lowering the diabetic patients’ blood glucose levels. [23] The alpha-glucosidase inhibitors block the release of the pancreatic amylase. The gastric by-pass surgery reroutes a majority of polysaccharides and disaccharides of the foods into a very short, last part of the small intestine for decreasing the contact time between the polysaccharides and disaccharides and the pancreatic enzymes, As a result, the surgery cuts the amount of polysaccharides and disaccharides to be converted into monosaccharides for absorption. [24] There might be some biochemical factors, which were possibly responsible for lowering the blood glucose level by both the alpha-glucosidase inhibitors and the gastric bypass surgery. However, both approaches restrict the amount of carbohydrates from being digested and absorbed, and consequently reduce the blood glucose level. Their success is also critically depending on the consumption of monosaccharides such as simple sugars in the individual’s foods, because neither approach can deter the absorption of monosaccharides. In short, they are either a biochemical or surgical form of restricting carbohydrate foods. However, their side effects and complications cannot be ignored.
Instead of letting the individual risk his health and life and take in many carbohydrate foods, andw sending a majority of polysaccharides and disaccharides into the colon for waste, it is logical for him to restrict carbohydrate foods daily in the first place, especially those high in glycemic indices and glycemic loads. As a result, he will have a stable, low normal range of blood glucose level at all time, sustain a very low level of inflammation, and improve his risks of vascular failure, diabetes mellitus, and many diseases.
References:
1 Su RK. “Carbohydrates Can Kill.” Carbohydrates Can Kill. Pages 328-332. http://www/carbohydratescankill.com 2 Su RK. “Inflammation, Inflammation & Inflammation!” Carbohydrates Can Kill. Pages 337-344. http://www/carbohydratescankill.com 3 Esposito K, et al. “ Inflammatory Cytokine Concentrations Are Acutely Increased by Hyperglycemia in Humans Role of Oxidative Stress.” Circulation, Published online Volume 106, Number 16, Pages 2067-2072. September 30, 2002, http://circ.ahajournals.org/cgi/content/full/106/16/2067 4 Su RK. “Role of Hyperglycemia” Carbohydrates Can Kill. Pages 347-354. http://www/carbohydratescankill.com 5 Su RK. “Diabetes Mellitus and Insulin Resistance.” Carbohydrates Can Kill. Pages 50. http://www/carbohydratescankill.com 6 Su RK. “Everyone Needs Annual Blood Glucose Screening.” Carbohydrates Can Kill. Pages 364-367. http://www/carbohydratescankill.com 7 Koichi Node and Teruo Inoue, “Postprandial hyperglycemia as an etiological factor in vascular failure.” Cardiovascular Diabetology 2009, 8:23doi:10.1186/1475-2840-8-23 http://www.cardiab.com/content/8/1/23, 8 Eizirik DL, Korbutt GS, and Hellerström C. “Prolonged exposure of human pancreatic islets to high glucose concentrations in vitro impairs the beta-cell function.” Journal of Clinical Investigation, Volume 90, Number 4, Pages 1263–1268. October 1992. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=443168 or “Video: If Diabetes Mellitus is Preventable.” http://www.carbohydratescankill.com 9 Akirav E. et al. “Beta-cell Mass and Type 1 Diabetes: Going, Going, Gone?” Diabetes. November 2008 vol. 57 no. 11 2883-2888 http://diabetes.diabetesjournals.org/content/57/11/2883.full.pdf+html 10 Leonardi O, et al. “Beta-cell apoptosis in the pathogenesis of human type 2 diabetes mellitus.” European Journal of Endocrinology. (2003) 149 99–102. http://www.eje-online.org/cgi/reprint/149/2/99.pdf 11 Tanaka K, Masuda J, Imamura T, Sueishi K, Nakashima T, Sakurai I, Shozawa T, Hosoda Y, Yoshida Y, Nishiyama Y, et al “A nation-wide study of atherosclerosis in infants, children and young adults in Japan.” Atherosclerosis. 1988 Aug;72(2-3):143-56 http://www.ncbi.nlm.nih.gov/pubmed/3214466?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed 12 Gerald S. Berenson, M.D., Sathanur R. Srinivasan, Ph.D., Weihang Bao, Ph.D., William P. Newman, M.D., Richard E. Tracy, M.D., Ph.D., Wendy A. Wattigney, M.S., for The Bogalusa Heart Study “Association between Multiple Cardiovascular Risk Factors and Atherosclerosis in Children and Young Adults.” New England Journal of Medicine, June 4, 1998, Number 23, Vol. 338:1650-1656 http://content.nejm.org/cgi/content/abstract/338/23/1650 13 osé Milei, MD PhD,1 Giulia Ottaviani, MD PhD,2 Anna Maria Lavezzi, MD,2 Daniel R Grana, VMD,1 Inés Stella, MD,1 and Luigi Matturri, MD PhD2 “Perinatal and infant early atherosclerotic coronary lesions.” Canadian Journal of Cardiology. 2008 February; 24(2): 137–141. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2644569 14 Williams LS, et al. “Effects of admission hyperglycemia on mortality and costs in acute ischemic stroke.” Neurology Volume 59, Pages 67-71. 2002. http://www.neurology.org/cgi/content/abstract/59/1/67 15 Capes SE, et al. “Stress Hyperglycemia and Prognosis of Stroke in Nondiabetic and Diabetic Patients. A Systematic Overview.” Stroke. Volume 32, Pages 2426-2432. 2001. http://stroke.ahajournals.org/cgi/reprint/32/10/2426.pdf 16 Thomas MC, et al. “Early peri-operative hyperglycaemia and renal allograft rejection in patients without diabetes.” Nephrology (BioMed Central). Volume 1, Number 1. 2000. Published online October 4, 2000. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=29098 17 Su RK. “The Digestion of Different Nutrients.” Carbohydrates Can Kill. Pages 9-12. http://www/carbohydratescankill.com 18 Seshadri P, et al. “A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity.” American Journal of Medicine, Volume 117, Issue 6, Pages 398-405. September 15, 2004. http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=15380496 19 Thomas MC, et al. “Early peri-operative hyperglycaemia and renal allograft rejection in patients without diabetes.” Nephrology (BioMed Central). Volume 1, Number 1. 2000. Published online October 4, 2000. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=29098 20 Yudkin JS, Stehouwer CDA, Emeis JJ and Coppack SW. “C-Reactive Protein in Healthy Subjects: Associations With Obesity, Insulin Resistance, and Endothelial Dysfunction. A Potential Role for Cytokines Originating From Adipose Tissue.” Arteriosclerosis, Thrombosis, and Vascular Biology, (the American Heart Association, Inc.) Volume 19, Number 4, Pages 972-978. 1999. http://atvb.ahajournals.org/cgi/content/full/19/4/972?ijkey=bc7ff94a637764853fbee0ded041fcffb04b0cff 21 Esposito K, et al. “ Inflammatory Cytokine Concentrations Are Acutely Increased by Hyperglycemia in Humans Role of Oxidative Stress.” Circulation, Published online Volume 106, Number 16, Pages 2067-2072. September 30, 2002, http://circ.ahajournals.org/cgi/content/full/106/16/2067 22 Liu S, et al. “Relation between a diet with a high glycemic load and plasma concentrations of high-sensitivity C-reactive protein in middle-aged women.” American Journal Clinical Nutrition. Volume 75, Number 3, Pages 492–8. 2002. http://www.ajcn.org/cgi/content/abstract/75/3/492 23 Cummings DE, et al. “Role of the bypassed proximal intestine in the anti-diabetic effects of bariatric surgery.” Surgery for Obesity and Related Diseases. 2007; 3(2): 109–115. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702249/pdf/nihms%2D21334.pdf/?tool=pmcentrez 24 Su RK. “Speaking of Diabetic Diet.” Carbohydrates Can Kill. Pages 332-337. http://www/carbohydratescankill.com
Cardiovascular Diabetology
Carbohydrate-restricted Diet for The Therapeutic Paradigm
31 December 2009
Robert Su, Pharm.B., M.D. Author, Carbohydrates Can Kill www.carbohydratescankill.com E-mail: carbohydratescankill@verizon.net
Congratulations to Doctors Node and Inoue on their excellent work to produce such an interesting and educational article.
In my literature review and personal experimentations, I have observed an axis of the excessive consumption of carbohydrates especially those high in glycemic indices and glycemic loads, the daily repeated postprandial hyperglycemia, the repeated postprandial inflammation with both acute and chronic pathological effects on cells, tissues, and organs. [1., 2, 3] The pathological role of hyperglycemia at least includes (1) inflammatory and pro-inflammatory, (2) vasoconstrictive (and hypertensive), (3) pro-thrombotic, (4) arteriosclerotic and atherosclerotic, and (5) glycosylative and pro-glycation. [4]
Inflammation by both acute and chronic or repeated postprandial hyperglycemia (during the period of hours immediately after the beginning of each meal) [5, 6, 7] illustrates why the readings of fasting blood glucose test and glucose tolerance test (at the end of the two-hour period), as well as hemoglobin A1c are ineffective in predicting the risks of diseases including diabetes mellitus, arteriosclerosis and atherosclerosis, neurodegenerative diseases such as Alzheimer’s disease, cancers, and many others. The mass of the pancreatic beta cells starts to decrease, during an individual’s life regardless of his age, when the magnitude of hyperglycemia, on either the vertical or horizontal scale, or both, is so enormous that inflammation, as a consequence, permanently damages the beta cells (apoptosis.) Without halting the repeated postprandial hyperglycemia, the size of apoptosis would exceed the size of regeneration of the mass of the pancreatic beta cells. [8, 9] By the time when either or both the readings of fasting blood glucose and glucose tolerance test is abnormal, about 40-60% of the individual’s beta cells are already damaged or dead; and he is now diagnosed with diabetes mellitus. [10] During the same time, other tissues or organs are also assaulted by inflammation and have begun the pathological process. Studies have even shown atherosclerosis occurs in infancy. [11., 12, 13] The prognosis of his disease(s) will largely depend on the effectiveness of controlling his blood glucose level at all time not just on the readings of the fasting blood glucose and/or the two-hour post glucose tolerance test.
Hemoglobin A1c is a result of glycation between blood glucose and the globin of hemoglobin. The higher the blood glucose level the greater the hemoglobin A1c will be. Because of a lifespan of 60-90 day for hemoglobin, an individual’s hemoglobin A1c largely reflects an averaged level of his blood glucose over a period, not an acute fluctuation of his blood glucose during a short period of hours. Having known the consequent inflammation of hyperglycemia, which is capable of triggering an acute vascular event or others, hemoglobin A1c is ineffective as a predicting biomarker for acute heart attack or stroke.
I have emphasized that, regardless of an individual’s state of health, everyone needs an annual or semiannual series of blood glucose tests, started at the pre-prandial or fasting and continued for two or three hours of the postprandial at a 15-minute interval. These tests will help both assess the functions of his pancreatic beta cells, and evaluate the impacts of his foods on the blood glucose level. In my opinion when the readings are over 120 mg% (a red flag when over 150 mg%), [14., 15, 16] he should avoid the foods high in glycemic index and glycemic load for preventing his progression towards diabetes mellitus. The tests are beneficial for both preventive medicine and personal health education.
Having understood the relationships between the carbohydrate foods excluding the non-digestible fibers, the amount of monosaccharides in the small intestine for absorption, the level of blood sugars (mainly glucose here for illustration), [17] the level of inflammation as a result of hyperglycemia, [18, 19, 20, 21, 22] and the risks of diseases, we have employed many pharmacological products in both disease prevention and management. For examples, we have observed positive results, at least for a short period of time, with certain anti-inflammatory drugs, hypoglycemic agents for increasing insulin secretion or facilitating the peripheral glucose uptake, as well as insulin preparations in cases of insulin dependent diabetes mellitus.
During the recent years, we have also tried to reduce the amount of monosaccharides from being absorbed into the circulation, which directly boosts the blood glucose level. As cited in Doctors Node and Inoue’s article, we are using alpha-glucosidase inhibitors to reduce the postprandial blood sugar level. In addition, we have also discovered a benefit of the gastric by-pass surgery for lowering the diabetic patients’ blood glucose levels. [23] The alpha-glucosidase inhibitors block the release of the pancreatic amylase. The gastric by-pass surgery reroutes a majority of polysaccharides and disaccharides of the foods into a very short, last part of the small intestine for decreasing the contact time between the polysaccharides and disaccharides and the pancreatic enzymes, As a result, the surgery cuts the amount of polysaccharides and disaccharides to be converted into monosaccharides for absorption. [24] There might be some biochemical factors, which were possibly responsible for lowering the blood glucose level by both the alpha-glucosidase inhibitors and the gastric bypass surgery. However, both approaches restrict the amount of carbohydrates from being digested and absorbed, and consequently reduce the blood glucose level. Their success is also critically depending on the consumption of monosaccharides such as simple sugars in the individual’s foods, because neither approach can deter the absorption of monosaccharides. In short, they are either a biochemical or surgical form of restricting carbohydrate foods. However, their side effects and complications cannot be ignored.
Instead of letting the individual risk his health and life and take in many carbohydrate foods, andw sending a majority of polysaccharides and disaccharides into the colon for waste, it is logical for him to restrict carbohydrate foods daily in the first place, especially those high in glycemic indices and glycemic loads. As a result, he will have a stable, low normal range of blood glucose level at all time, sustain a very low level of inflammation, and improve his risks of vascular failure, diabetes mellitus, and many diseases.
References:
1 Su RK. “Carbohydrates Can Kill.” Carbohydrates Can Kill. Pages 328-332. http://www/carbohydratescankill.com
2 Su RK. “Inflammation, Inflammation & Inflammation!” Carbohydrates Can Kill. Pages 337-344. http://www/carbohydratescankill.com
3 Esposito K, et al. “ Inflammatory Cytokine Concentrations Are Acutely Increased by Hyperglycemia in Humans Role of Oxidative Stress.” Circulation, Published online Volume 106, Number 16, Pages 2067-2072. September 30, 2002, http://circ.ahajournals.org/cgi/content/full/106/16/2067
4 Su RK. “Role of Hyperglycemia” Carbohydrates Can Kill. Pages 347-354. http://www/carbohydratescankill.com
5 Su RK. “Diabetes Mellitus and Insulin Resistance.” Carbohydrates Can Kill. Pages 50. http://www/carbohydratescankill.com
6 Su RK. “Everyone Needs Annual Blood Glucose Screening.” Carbohydrates Can Kill. Pages 364-367. http://www/carbohydratescankill.com
7 Koichi Node and Teruo Inoue, “Postprandial hyperglycemia as an etiological factor in vascular failure.” Cardiovascular Diabetology 2009, 8:23doi:10.1186/1475-2840-8-23 http://www.cardiab.com/content/8/1/23,
8 Eizirik DL, Korbutt GS, and Hellerström C. “Prolonged exposure of human pancreatic islets to high glucose concentrations in vitro impairs the beta-cell function.” Journal of Clinical Investigation, Volume 90, Number 4, Pages 1263–1268. October 1992. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=443168 or “Video: If Diabetes Mellitus is Preventable.” http://www.carbohydratescankill.com
9 Akirav E. et al. “Beta-cell Mass and Type 1 Diabetes: Going, Going, Gone?” Diabetes. November 2008 vol. 57 no. 11 2883-2888 http://diabetes.diabetesjournals.org/content/57/11/2883.full.pdf+html
10 Leonardi O, et al. “Beta-cell apoptosis in the pathogenesis of human type 2 diabetes mellitus.” European Journal of Endocrinology. (2003) 149 99–102. http://www.eje-online.org/cgi/reprint/149/2/99.pdf
11 Tanaka K, Masuda J, Imamura T, Sueishi K, Nakashima T, Sakurai I, Shozawa T, Hosoda Y, Yoshida Y, Nishiyama Y, et al “A nation-wide study of atherosclerosis in infants, children and young adults in Japan.” Atherosclerosis. 1988 Aug;72(2-3):143-56 http://www.ncbi.nlm.nih.gov/pubmed/3214466?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed
12 Gerald S. Berenson, M.D., Sathanur R. Srinivasan, Ph.D., Weihang Bao, Ph.D., William P. Newman, M.D., Richard E. Tracy, M.D., Ph.D., Wendy A. Wattigney, M.S., for The Bogalusa Heart Study “Association between Multiple Cardiovascular Risk Factors and Atherosclerosis in Children and Young Adults.” New England Journal of Medicine, June 4, 1998, Number 23, Vol. 338:1650-1656 http://content.nejm.org/cgi/content/abstract/338/23/1650
13 osé Milei, MD PhD,1 Giulia Ottaviani, MD PhD,2 Anna Maria Lavezzi, MD,2 Daniel R Grana, VMD,1 Inés Stella, MD,1 and Luigi Matturri, MD PhD2 “Perinatal and infant early atherosclerotic coronary lesions.” Canadian Journal of Cardiology. 2008 February; 24(2): 137–141. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2644569
14 Williams LS, et al. “Effects of admission hyperglycemia on mortality and costs in acute ischemic stroke.” Neurology Volume 59, Pages 67-71. 2002. http://www.neurology.org/cgi/content/abstract/59/1/67
15 Capes SE, et al. “Stress Hyperglycemia and Prognosis of Stroke in Nondiabetic and Diabetic Patients. A Systematic Overview.” Stroke. Volume 32, Pages 2426-2432. 2001. http://stroke.ahajournals.org/cgi/reprint/32/10/2426.pdf
16 Thomas MC, et al. “Early peri-operative hyperglycaemia and renal allograft rejection in patients without diabetes.” Nephrology (BioMed Central). Volume 1, Number 1. 2000. Published online October 4, 2000. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=29098
17 Su RK. “The Digestion of Different Nutrients.” Carbohydrates Can Kill. Pages 9-12. http://www/carbohydratescankill.com
18 Seshadri P, et al. “A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity.” American Journal of Medicine, Volume 117, Issue 6, Pages 398-405. September 15, 2004. http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=15380496
19 Thomas MC, et al. “Early peri-operative hyperglycaemia and renal allograft rejection in patients without diabetes.” Nephrology (BioMed Central). Volume 1, Number 1. 2000. Published online October 4, 2000. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=29098
20 Yudkin JS, Stehouwer CDA, Emeis JJ and Coppack SW. “C-Reactive Protein in Healthy Subjects: Associations With Obesity, Insulin Resistance, and Endothelial Dysfunction. A Potential Role for Cytokines Originating From Adipose Tissue.” Arteriosclerosis, Thrombosis, and Vascular Biology, (the American Heart Association, Inc.) Volume 19, Number 4, Pages 972-978. 1999. http://atvb.ahajournals.org/cgi/content/full/19/4/972?ijkey=bc7ff94a637764853fbee0ded041fcffb04b0cff
21 Esposito K, et al. “ Inflammatory Cytokine Concentrations Are Acutely Increased by Hyperglycemia in Humans Role of Oxidative Stress.” Circulation, Published online Volume 106, Number 16, Pages 2067-2072. September 30, 2002, http://circ.ahajournals.org/cgi/content/full/106/16/2067
22 Liu S, et al. “Relation between a diet with a high glycemic load and plasma concentrations of high-sensitivity C-reactive protein in middle-aged women.” American Journal Clinical Nutrition. Volume 75, Number 3, Pages 492–8. 2002. http://www.ajcn.org/cgi/content/abstract/75/3/492
23 Cummings DE, et al. “Role of the bypassed proximal intestine in the anti-diabetic effects of bariatric surgery.” Surgery for Obesity and Related Diseases. 2007; 3(2): 109–115. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702249/pdf/nihms%2D21334.pdf/?tool=pmcentrez
24 Su RK. “Speaking of Diabetic Diet.” Carbohydrates Can Kill. Pages 332-337. http://www/carbohydratescankill.com
Competing interests
None