Tag Archives: diabetes

Sugar and Alcohol: Your Liver Can’t Tell The Difference

Dr. David Unwin, Fellow of the Royal College of General Practitioners (FRCGP) together with fellow researchers recently completed a study showing low carb diets significantly reduce fatty liver, weight and blood sugar. Trialing a low carb approach over a year, they found rapid improvements in liver function among other positive effects.

“My interest in abnormal liver, and particularly GGT blood results began when I noticed that in our family practice of 9,000 patients well over a 1,000 had an abnormal GGT result,” said Dr. Unwin. “I could predict which patients would have lost weight -before they came into my consulting room from the improvement in GGT blood results alone- so began to wonder about raised GGT levels, Diabetes and non-alcoholic fatty liver disease (NAFLD): Was dietary carbohydrate a link?”

Before we get to the summary, let’s breakdown some of the statistics.

  • Approximately 30 million children and adults have diabetes in the United States. Out of that number, nearly 95% have type 2 diabetes according to the American Diabetes Association.1
  • The National Conference of State Legislatures (NCSL) reports obesity affects more than one-third of adults and 17% of youth in the United States. This equates to 78 million adults and 12 million children suffering from the obesity epidemic. As adopters of the Paleo diet well know, obesity increases risk for heart disease, type 2 diabetes, and cancer among other debilitating health conditions, like non-alcoholic fatty liver disease (NAFLD).2
  • The American Liver Foundation reports (NAFLD) affects up to 25% of Americans, where risk is directly correlated to being overweight or obese, having diabetes, high cholesterol or high triglycerides.3

As the cost of health care continues to skyrocket, Dr. Unwin has decreased his prescribing budget £15,000-£30,000 a year by prescribing a low carb diet to patients who in two years’ time decreased average blood sugar by 10% and is now below the national average in the UK4 and US.

“I would say sugar is definitely rather like alcohol for the liver, and would point out that starchy foods like bread and pasta are a rich source of glucose,” said Dr. Unwin.

Well, thankfully the Paleo diet is devoid of breads, pastas, grains, pseudo grains, and processed sugars. When we focus upon lean meats, fish, poultry, veggies, and fruits, nuts, and seeds in moderation, a Paleo prescription is the best, cost effective investment you can make for your health.

Summary* presented ahead of publication in Diabetes in Practice September 15, 2015.

Unwin DJ1, Cuthertson DJ2, Feinman R3, Sprung VS2 (2015) A pilot study to explore the role of a low-carbohydrate intervention to improve GGT levels and HbA1c. Diabesity in Practice 4 [in press]

1Norwood Surgery, Norwood Ave, Southport. 2Department of Obesity and Endocrinology, Institute of Ageing & Chronic Disease, University of Liverpool, UK. 3Professor of biochemistry and medical researcher at State University of New York Health Science Center at Brooklyn, USA.

Working title: Raised GGT levels, Diabetes and NAFLD: Is dietary carbohydrate a link?  Primary care pilot of a low carbohydrate diet

Abnormal liver function tests are often attributed to excessive alcohol consumption and/or medication without further investigation. However they may be secondary to non-alcoholic fatty liver disease (NAFLD). NAFLD is now prevalent in 20-30% of adults in the Western World. Considering the increased cardiovascular and metabolic risk of NAFLD, identification and effective risk factor management of these patients is critical.

Background Excess dietary glucose leads progressively to hepatocyte triglyceride accumulation (non-alcoholic fatty liver disease-NAFLD), insulin resistance and T2DM. Considering the increased cardiovascular risks of NAFLD and T2DM, effective risk-factor management of these patients is critical. Weight loss can improve abnormal liver biochemistry, the histological progression of NAFLD, and diabetic control. However, the most effective diet remains controversial.

Aim We implemented a low-carbohydrate (CHO) diet in a primary health setting, assessing the effect on serum GGT, HbA1c levels (as proxies for suspected NAFLD and diabetic control), and weight.

Design  69 patients with a mean  GGT of 77 iu/L (NR 0-50) and an average BMI of 34.4Kg/m2 were recruited opportunistically and advised on reducing total glucose intake (including starch), while increasing intake of  natural fats, vegetables and protein.

Method Baseline blood samples were assessed for GGT levels, lipid profile, and HbA1c. Anthropometrics were assessed and repeated at monthly intervals. The patients were provided monthly support by their general practitioner or practice nurse, either individually or as a group.

Results After an average of 13 months on a low-CHO diet there was a 46% mean reduction in GGT of 29.9 iu/L (95% CI= -43.7, -16.2; P<0.001), accompanied by average reductions in weight [-8.8Kg (95% CI= -10.0, -7.5; P<0.001)],and HbA1c [10.0mmol/mol (95% CI= -13.9, -6.2; P<0.001)].

Conclusions We provide evidence that low-carbohydrate, dietary management of patients with T2DM and/or suspected NAFLD in primary care is feasible and improves abnormal liver biochemistry and other cardio-metabolic risk factors. This raises the question as to whether dietary carbohydrate plays a role in the etiology of diabetes and NAFLD, as well as obesity. Over the study period and given a choice not a single patient opted to start antidiabetic medication, losing weight instead. This helps explain why our practice is the only one in the Southport and Formby CCG to have static diabetes drug costs for three years running.

*Note: The summary displayed above is not the official abstract from Diabetes in Practice.

David Unwin | The Paleo Diet

David Unwin is the senior partner and GP trainer at the Norwood Surgery, Southport, a seaside resort in the North West of England. He is an expert clinical adviser in diabetes for the Royal College of General Practitioners, and has a special interest in the Solution Focused psychological approach to the consultation. David lives on a farm with his wife, son and their sheep, turkeys, hens -and a very large pig!

 

 

REFERENCES

[1] //www.diabetes.org/diabetes-basics/statistics/infographics.html?loc=db-slabnav

[2] //www.ncsl.org/research/health/obesity-statistics-in-the-united-states.aspx

[3] //www.liverfoundation.org/abouttheliver/info/nafld/

[4] //diabetesdietblog.com/2015/07/15/you-only-need-one-arrow-dr-unwin-proves-it-again/

Artificial Sweeteners | The Paleo Diet

Introduction: Evolutionary Perspective

It’s pretty clear that if we follow the example of our hunter gatherer ancestors, artificial sweeteners should not be part of contemporary Stone Age diets. In my book, The Paleo Diet Revised (2010)1 I warned against drinking artificially sweetened soft drinks and further strengthened my opposition to all artificial sweeteners in 2012 with The Paleo Answer.2 Over the past few years numerous epidemiological (population), animal, tissue and human studies have demonstrated the adverse health effects of these synthetic chemicals. A particularly powerful study just published in the October 2014 issue of Nature3 provides a convincing argument against the use of artificial sweeteners in our food supply. If you consume artificial sweeteners in the form of sodas or foods once in a blue moon, they will have little or no adverse effects upon your long term health. However, I would never recommend that you drink artificially sweetened beverages or foods on a daily or even weekly basis, as they may promote insulin resistance,3, 4 obesity in adults5-7, 30-33 and children,8-11, 32, 44 metabolic syndrome diseases,12-18, 33 migraine headaches,19-23 adverse pregnancy outcomes,24-26 childhood allergies,24 and certain cancers.27-29

Artificial Sweeteners

The table* below shows the five artificial sweeteners that the U.S. Food and Drug Administration (FDA) has approved for consumption.

Artificial Sweeteners: Agents of Insulin Resistance, Obesity and Disease | The Paleo Diet

*Note that the artificial sweetener cyclamate was banned in the U.S. in 1969, but is still available in certain countries outside of the U.S.

In addition to these artificial sweeteners, the FDA has sanctioned a sugar substitute, stevia, as a dietary supplement since 1995. Stevia is a crystalline substance made from the leaves of a plant native to central and South America and is 100 to 300 times sweeter than table sugar. A concentrated derivative of stevia leaves called rebaudioside A was recently (2008) authorized by the FDA and goes by the trade names of Only Sweet, PureVia, Reb-A, Rebiana, SweetLeaf, and Truvia.

Since 1980 the number of people consuming artificially sweetened products in the U.S. has more than doubled.32, 33 Today, at least 46 million Americans regularly ingest foods sweetened by these chemicals – mainly in the form of soft drinks, or in a huge number of artificially sweetened products, including baby food.32, 33

Artificial Sweeteners and Obesity

If you were to ask most people why they drink artificially sweetened beverages, the resounding answer would be to enjoy a sweet drink without all the drawbacks of sugar laden sodas. Doesn’t everyone know that soft drinks sweetened with sugar promote obesity, type 2 diabetes and the Metabolic Syndrome (high blood pressure, high blood cholesterol and heart disease)? Of course, and the standard line of thought goes something like this, “if we remove refined sugars from our diets and replace them with artificial sweeteners, we would all be a lot healthier.” I can agree with the first and last parts of this argument, but not the second.

A number of large epidemiological studies5-7; 8-11, 44 and animal experiments34-43 indicate that artificially sweetened beverages may actually not be part of the solution to the U.S. obesity epidemic, but rather may be part of the problem.30-33 Unexpectedly, a series of large population based studies, including the San Antonio Heart Study6 examining 3,682 adults over a 7-8 year period; the American Cancer Society Study7 including 78,694 women; and the Nurses’ Health Study5 of 31,940 women have clearly demonstrated strong associations between increased intakes of artificial sweeteners and obesity. Alarmingly, these effects have been observed in children8, 11, 44 as well as in adults, and were utterly unanticipated because most artificial sweeteners were previously thought to be inert and not react with our gut or metabolism in an unsafe manner.30-33, 45

Laboratory Animal Experiments

In the course of the past few years, animal experiments have reversed these erroneous assumptions. Rats allowed to eat their normal chow consumed more food and gained more weight when artificial sweeteners were added to their diet.34-43 The best available evidence indicates that artificial sweeteners when consumed by either laboratory animals or humans promote weight gain by altering the normal gut bacterial biome3, 45 which in turn adversely affects glucose and insulin metabolism and consequently appetite. Who would have ever thought that a mass marketed product which supposedly was designed to help us lose weight may have actually caused exactly the opposite result? But wait, there is more.

Cancer

In 1958 the federal government deemed both saccharin and cyclamate as “generally recognized as safe (GRAS)” artificial sweeteners. Eleven years later the FDA banned cyclamate and announced its intention to ban saccharin in 1977 because of worries over increased cancer risks from both of these chemicals. Consumer protests eventually led to a moratorium from congress on the ban for saccharin, but unfortunately it is still with us today. Aspartame was sanctioned for use as a sweetener by the FDA in 1996, followed by sucralose (1999), neotame (2002), and acesulfame (2003). You may think that anytime chemical additives such as artificial sweeteners were permitted into our food supply, they would have been thoroughly tested and conclusively shown to be safe. Unfortunately, this is not always the case, and the potential toxicity of some of these sweetening compounds are widely disputed in the scientific community, particularly in light of newer, more carefully controlled animal studies.27-29

A series of more recent experiments29 from Dr. Soffritti’s laboratory in Bologna, Italy have shown that even low doses of aspartame given to rats over the course of their lives leads to increased cancer rates. This study is important, because many people may consume much higher concentrations of this chemical by drinking artificially sweetened beverages on a daily basis for years and years.

Migraines

Aspartame has also been shown to trigger migraine headaches in certain people because it breaks down into a compound called methanol (otherwise known as wood alcohol) in our bodies. And it’s not just aspartame that may prove dangerous to our health when we ingest these synthetic concoctions on a regular basis. Recent animal experiments27 have revealed that saccharin, acesulfame as well as aspartame caused DNA damage in mice bone marrow. Frequently, it is difficult to translate results from animal experiments into, meaningful recommendations for humans, because large epidemiological studies generally don’t show artificial sweeteners to be risk factors for cancer. Does this mean that these compounds are completely safe? Absolutely not.

Pregnancy

A 2010 prospective study25 of 59,334 pregnant women from Denmark showed for the first time that consumption of artificially sweetened soft drinks significantly increased the risk for pre-term delivery (less than 37 weeks). This condition shouldn’t be taken lightly, as it represents the leading cause of infant death. An interesting outcome of this study was that only artificially sweetened beverages increased the risk for pre-term delivery – and not sugar sweetened soft drinks. A follow-up study confirmed these results.26 Am I recommending that pregnant women consume sugary soft drinks? Emphatically no! But these studies indicate that sugar sweetened drinks may be less harmful to your developing fetus than are artificially sweetened soft drinks.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

REFERENCES

1. Cordain L. The Paleo Diet. John Wiley & Sons, NY New York, 2010.

2. Cordain L. The Paleo Answer. John Wiley & Sons, NY New York, 2012

3. Suez J, Korem T, Zeevi D, Zilberman-Schapira G, Thaiss CA, Maza O, Israeli D, Zmora N, Gilad S, Weinberger A, Kuperman Y, Harmelin A, Kolodkin-Gal I, Shapiro H, Halpern Z, Segal E, Elinav E. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. 2014 Oct 9;514(7521):181-6

4. Horwitz DL, McLane M, Kobe P. Response to single dose of aspartame or saccharin by NIDDM patients. Diabetes Care. 1988 Mar;11(3):230-4.

5. Colditz GA, Willett WC, Stampfer MJ, London SJ, Segal MR, Speizer FE. Patterns of weight change and their relation to diet in a cohort of healthy women. Am J Clin Nutr. 1990 Jun;51(6):1100-5

6. Fowler SP, Williams K, Resendez RG, Hunt KJ, Hazuda HP, Stern MP. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity (Silver Spring). 2008 Aug;16(8):1894-900.

7. Stellman SD, Garfinkel L. Artificial sweetener use and one-year weight change among women. Prev Med. 1986 Mar;15(2):195-202.

8. Blum JW, Jacobsen DJ, Donnelly JE. Beverage consumption patterns in elementary school aged children across a two-year period. J Am Coll Nutr. 2005 Apr;24(2):93-8.

9. Forshee RA, Storey ML. Total beverage consumption and beverage choices among children and adolescents. Int J Food Sci Nutr. 2003 Jul;54(4):297-307

10. Striegel-Moore RH, Thompson D, Affenito SG, Franko DL, Obarzanek E, Barton BA, Schreiber GB, Daniels SR, Schmidt M, Crawford PB. Correlates of beverage intake in adolescent girls: the National Heart, Lung, and Blood Institute Growth and Health Study.J Pediatr. 2006 Feb;148(2):183-7.

11. Brown RJ, de Banate MA, Rother KI. Artificial sweeteners: a systematic review of metabolic effects in youth. Int J Pediatr Obes. 2010 Aug;5(4):305-12

12. Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR Jr. Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care. 2009 Apr;32(4):688-94.

13. Cohen L, Curhan G, Forman J. Association of sweetened beverage intake with incident hypertension. J Gen Intern Med. 2012 Sep;27(9):1127-34.

14. Gardener H, Rundek T, Markert M, Wright CB, Elkind MS, Sacco RL. Diet soft drink consumption is associated with an increased risk of vascular events in the Northern Manhattan Study. J Gen Intern Med. 2012 Sep;27(9):1120-6.

15. Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs JB, D’Agostino RB, Gaziano JM, Vasan RS.Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation. 2007 Jul 31;116(5):480-8.

16. Lutsey PL, Steffen LM, Stevens J. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Circulation. 2008 Feb 12;117(6):754-61

17. Fagherazzi G, Vilier A, Saes Sartorelli D, Lajous M, Balkau B, Clavel-Chapelon F.
Consumption of artificially and sugar-sweetened beverages and incident type 2 diabetes in the Etude Epidemiologique aupres des femmes de la Mutuelle Generale de l’Education Nationale-European Prospective Investigation into Cancer and Nutrition cohort. Am J Clin Nutr. 2013 Mar;97(3):517-23

18. Greenwood DC, Threapleton DE, Evans CE, Cleghorn CL, Nykjaer C, Woodhead C, Burley VJ. Association between sugar-sweetened and artificially sweetened soft drinks and type 2 diabetes: systematic review and dose-response meta-analysis of prospective studies. Br J Nutr. 2014 Sep 14;112(5):725-34.

19. Abegaz EG, Bursey RG. Formaldehyde, aspartame, migraines: a possible connection. Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9

20. Bigal ME, Krymchantowski AV. Migraine triggered by sucralose–a case report. Headache. 2006 Mar;46(3):515-7

21. Jacob SE, Stechschulte S. Formaldehyde, aspartame, and migraines: a possible connection. Dermatitis. 2008 May-Jun;19(3):E10-1.

22. Lipton RB, Newman LC, Cohen JS, Solomon S. Aspartame as a dietary trigger of headache. Headache. 1989 Feb;29(2):90-2

23. Newman LC, Lipton RB. Migraine MLT-down: an unusual presentation of migraine in patients with aspartame-triggered headaches. Headache. 2001 Oct;41(9):899-901.
Araújo JR, Martel F, Keating E. Exposure to non-nutritive sweeteners during pregnancy and lactation: Impact in programming of metabolic diseases in the progeny later in life. Reprod Toxicol. 2014 Sep 28;49C:196-201.

24. Maslova E, Strøm M, Olsen SF, Halldorsson TI. Consumption of artificially-sweetened soft drinks in pregnancy and risk of child asthma and allergic rhinitis.PLoS One. 2013;8(2):e57261.

25. Halldorsson TI, Strøm M, Petersen SB, Olsen SF. Intake of artificially sweetened soft drinks and risk of preterm delivery: a prospective cohort study in 59,334 Danish pregnant women. Am J Clin Nutr. 2010 Sep;92(3):626-33.

26. Englund-Ögge L1, Brantsæter AL, Haugen M, Sengpiel V, Khatibi A, Myhre R, Myking S, Meltzer HM, Kacerovsky M, Nilsen RM, Jacobsson B. Association between intake of artificially sweetened and sugar-sweetened beverages and preterm delivery: a large prospective cohort study. Am J Clin Nutr. 2012 Sep;96(3):552-9.

27. Bandyopadhyay A, Ghoshal S, Mukherjee A. Genotoxicity testing of low-calorie sweeteners: aspartame, acesulfame-K, and saccharin. Drug Chem Toxicol. 2008;31(4):447-57

28. Belpoggi F, Soffritti M, Padovani M, Degli Esposti D, Lauriola M, Minardi F. Results of long-term carcinogenicity bioassay on Sprague-Dawley rats exposed to aspartame administered in feed. Ann N Y Acad Sci. 2006 Sep;1076:559-77.

29. Soffritti M, Belpoggi F, Tibaldi E, Esposti DD, Lauriola M. Life-span exposure to low doses of aspartame beginning during prenatal life increases cancer effects in rats. Environ Health Perspect. 2007 Sep;115(9):1293-7

30. Ferreira AV1, Generoso SV, Teixeira AL. Do low-calorie drinks ‘cheat’ the enteral-brain axis? Curr Opin Clin Nutr Metab Care. 2014 Sep;17(5):465-70.

31. Swithers SE, Martin AA, Davidson TL. High-intensity sweeteners and energy balance. Physiol Behav. 2010 Apr 26;100(1):55-62

32. Yang Q. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010 Jun;83(2):101-8.

33. Swithers SE. Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements. Trends Endocrinol Metab. 2013 Sep;24(9):431-41.

34. Swithers SE, Davidson TL. A role for sweet taste: calorie predictive relations in energy regulation by rats. Behav Neurosci. 2008 Feb;122(1):161-73.

35. Swithers SE, Baker CR, Davidson TL. General and persistent effects of high-intensity sweeteners on body weight gain and caloric compensation in rats. Behav Neurosci. 2009 Aug;123(4):772-80

36. Swithers SE, Martin AA, Clark KM, Laboy AF, Davidson TL. Body weight gain in rats consuming sweetened liquids. Effects of caffeine and diet composition. Appetite. 2010 Dec;55(3):528-33

37. Feijó Fde M1, Ballard CR, Foletto KC, Batista BA, Neves AM, Ribeiro MF, Bertoluci MC. Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. Appetite. 2013 Jan;60(1):203-7.

38. Swithers SE, Sample CH, Davidson TL. Adverse effects of high-intensity sweeteners on energy intake and weight control in male and obesity-prone female rats. Behav Neurosci. 2013 Apr;127(2):262-74.

39. Pierce WD, Heth CD, Owczarczyk JC, Russell JC, Proctor SD. Overeating by young obesity-prone and lean rats caused by tastes associated with low energy foods. Obesity (Silver Spring). 2007 Aug;15(8):1969-79.

40. von Poser Toigo E, Huffell AP, Mota CS, Bertolini D, Pettenuzzo LF, Dalmaz C.
Metabolic and feeding behavior alterations provoked by prenatal exposure to aspartame. Appetite. 2014 Dec 24. pii: S0195-6663(14)00774-0.

41. Polyák E, Gombos K, Hajnal B, Bonyár-Müller K, Szabó S, Gubicskó-Kisbenedek A, Marton K, Ember I. Effects of artificial sweeteners on body weight, food and drink intake. Acta Physiol Hung. 2010 Dec;97(4):401-7

42. Malaisse WJ, Vanonderbergen A, Louchami K, Jijakli H, Malaisse-Lagae F. Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets. Cell Signal. 1998 Nov;10(10):727-33

43. Swithers SE, Laboy AF, Clark K, Cooper S, Davidson TL. Experience with the high-intensity sweetener saccharin impairs glucose homeostasis and GLP-1 release in rats. Behav Brain Res. 2012 Jul 15;233(1):1-14

44. Berkey CS, Rockett HR, Field AE, Gillman MW, Colditz GA. Sugar-added beverages and adolescent weight change. Obes Res. 2004 May;12(5):778-88.

45. Schiffman SS. Rationale for further medical and health research on high-potency sweeteners. Chem Senses. 2012 Oct;37(8):671-9.

Paleo Diet Lowers Blood Sugar

Hello Dr. Cordain!

My name is Chuck Mullen. I am a 63 year old man, and have been active in sports all my life! In May of 2014, I had a routine visit with my doctor. Although I have always looked healthy, I wasn’t feeling right. My blood work revealed that my blood sugar was 300, and my A1C was 12. Oh, by the way, my blood pressure was 160/100. My doctor immediately put me on insulin and gave me medicine to normalize my blood pressure. I was devastated to say the least! A friend of mine told me about your book, The Paleo Diet, so I immediately ordered it. I have been naive for 62 and a half years in my eating. I am a teaching tennis pro and would drink gallons of sports drinks and eat lots of carbs. Boy, have I been wrong!I am very disciplined; I do not drink, or smoke and never have. I started on the Paleo Diet within the week.

I was off the insulin and the blood pressure medicine! I became a fanatic about checking my blood glucose levels, which were back to normal. I had a follow up appointment six weeks later with my doctor. When I went in, his nurse took all my vitals and ran a blood test. My doctor came in and sat down, looked at the numbers and said, “looks like the insulin is working…” My blood sugar dropped to 104. I said I had not taken any insulin in four weeks. After shaking his head in disbelief, he said your blood pressure medicine is working fine, 116/70. I mentioned I wasn’t taking that either. He thought I was joking! “What are you doing, then?” I told him about the Paleo Diet, and shaking his head again, he said, “You were a full blown diabetic six weeks ago, and now your normal without medicine!” He ran another test to check my A1C, which dropped to 7 from 12. Again in disbelief, he said that if they can drop the A1C and sugar in six weeks with meds by 1 point, it’s considered a success.

It’s amazing what doctors don’t know; but if one doctor wants to learn, perhaps others do as well. You probably saved my life, Dr. Cordain! By the way, the girls say I look 15 years younger! I weigh what I weighed when I graduated high school in 1970. I am looking forward to the next 50 years! Thanks again.

Chuck

Let’s Face It: Halloween Haunts Diabetics

Halloween treats are hardly Paleo. One bite-sized candy bar can contain anywhere from 10 – 30g of carbohydrate. And it’s not fibrous carbs or safe starches; it’s usually sugar. Pop two or three of these and, you’re looking at potentially 2-6 more units of insulin injections to maintain blood glucose control, let alone the risks of inducing hypoglycemia. One comprehensive review showed that this may induce up to a two-fold increased risk for severe hypoglycemia.2 It has long been known that the best strategy for diabetics is carbohydrate restriction, especially restricting sugar intake, not increasing the insulin to counteract large sugar boluses. With symptoms ranging from tachycardia and sweating, to stupor and coma, hypoglycemia isn’t a laughing matter.1

Furthermore, one study even showed a 71% increased risk of cardiovascular mortality in younger diabetic patients, and a threefold increased risk of hypoglycemia.4 While trick-or-treating one day out of the year will not be the end-all, it’s not without risks. If you must have your Halloween treats, keep it to a minimum, and if you’re diabetic, monitor your blood glucose. Choose dark chocolate over pure sugar confections, which have a healthy dose of dietary fat to attenuate the spike in blood glucose.

Even in healthy individuals, a candy bar containing 45g of carbohydrate (mostly sugar) can spike blood glucose by up to 30 points.3

Diabetics and Sugar

Applied Physiology, Nutrition, and Metabolism, 2013, 38:484-489, 10.1139/apnm-2011-0226

Again, it’s only one day out of the year, but diabetic patients + candy = no bueno. The risks and consequences of hyper- and hypoglycemia are much greater.

The good news: a Paleo Diet does wonders for insulin sensitivity.6 In the figure below, the filled symbols represent glucose tolerance prior to the study, and the open symbols after 12 weeks.

Diabetics and Sugar

Diabetologia. 2007 Sep;50(9):1795-807. Epub 2007 Jun 22.

The Paleo Diet is the optimal “diabetes diet” in type 2 diabetic patients.5 If that doesn’t say a lot, I don’t know what does!

William Lagakos, Ph.D.
@caloriesproper
CaloriesProper

William Lagakos, Ph.D.Dr. William Lagakos received a Ph.D. in Nutritional Biochemistry and Physiology from Rutgers University where his research focused on dietary fat assimilation and integrated energy metabolism. His postdoctoral research at the University of California, San Diego, centered on obesity, inflammation, and insulin resistance. Dr. William Lagakos has authored numerous manuscripts which have been published in peer-reviewed journals, as well as a non-fiction book titled The Poor, Misunderstood Calorie which explores the concept of calories and simultaneously explains how hormones and the neuroendocrine response to foods regulate nutrient partitioning. He is presently a nutritional sciences researcher, consultant, and blogger.

REFERENCES

1. Ahren B. Avoiding hypoglycemia: a key to success for glucose-lowering therapy in type 2 diabetes. Vasc Health Risk Manag. 2013;9:155-163.

2. Boussageon R, Bejan-Angoulvant T, Saadatian-Elahi M, Lafont S, Bergeonneau C, Kassai B, . . . Cornu C. Effect of intensive glucose lowering treatment on all cause mortality, cardiovascular death, and microvascular events in type 2 diabetes: meta-analysis of randomised controlled trials. BMJ. 2011;343:d4169.

3. Dugan K, Campbell B, Dufour F, Roman S, Woodall C, McAdams M, . . . Wilborn CD. Acute glycemic and blood lipid response to the ingestion of a candy bar-like protein supplement compared with its candy bar counterpart. Appl Physiol Nutr Metab. May 2013;38(5):484-489.

4. Giorgino F. Intensive glucose-lowering results in increased cardiovascular mortality in younger but not older individuals with type 2 diabetes. Evid Based Med. Jul 15 2014.

5. Jonsson T, Granfeldt Y, Ahren B, Branell UC, Palsson G, Hansson A, . . . Lindeberg S. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovascular diabetology. 2009;8:35.

6. Lindeberg S, Jonsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjostrom K, Ahren B. A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Diabetologia. Sep 2007;50(9):1795-1807.

Sugar Is Killing Us

It’s no surprise a vast majority of the world recognizes sugar is destroying our health and ruining our lives.1, 2, 3, 4 Over the last 30 years, we’ve seen disease rates skyrocket, alongside our climbing intake of sugar.5, 6, 7, 8, 9 Our concern for this creeping information wavers and takes a backseat to social media, “selfies” and celebrities.10, 11

The growing concern around sugar deserves not only immediate attention, but immediate action.12, 13, 14 Unfortunately, the roadblocks are endless.15, 16 The least of which, is the food industry itself.17 Take, for example, the makers of orange juice, a product which contains a whopping 21g of sugar in a mere 8oz glass,18 and is traditionally the standard American breakfast beverage.

The addictive properties of sugar are well-documented, as are the risks of consuming too much.19, 20 And yet, we can’t seem to stop ourselves.21, 22 Sugar is often added to products surreptitiously, without our consent.23 It is also marketed – quite heavily – towards children.24, 25 We must put a stop to this. Our children are our future, and if they are obese, cognitively impaired, and sick – how much of a future do they really have?

So why sugar is so detrimental? The biochemistry says it all.20 As sugar enters the bloodstream, insulin is secreted.26 The more sugar you eat, the more insulin you secrete. High sugar diets can lead to insulin resistance.27 This condition is one of the hallmarks of obesity and overweight humans everywhere.28 If you consume too much sugar, you’re bound to experience hypoglycemia, commonly referred to as your “sugar crash.”29 This leaves your body craving more sugar – and the addictive process perpetuates.30

Sugar is Killing Us | The Paleo Diet

Sagittal, Coronal and Axial Representations of Glucose-related Regional Grey (A) and White (B) Matter Volumes.
doi:10.1371/journal.pone.0073697.g002

It’s a simple model, but one which we are all familiar with.36 Stress also leads us to overeat.31, 37 And we do not over-consume just any calories, but rather we eat neurologically-rewarding foods.38 This means foods that are either: high in sugar, or foods high in sugar and fat.39 In a study from 2010, researchers showed a disruption of sensitivity to brain-stimulation reward (BSR) from eating high fat and/or high carbohydrate food.40 So you become accustomed to the rewards of these foods, and crave them more.41

The rates of diabetes both nationally, and worldwide, have skyrocketed.42 This is not debatable. Guess what else has skyrocketed, in conjunction with diabetes rates? You guessed it: sugar consumption. There are now obese newborns.43, 44

All of these problems and conditions can be linked directly to sugar intake, and yet, you may be blindsided by how much sugar you’re consuming in the first place. A recent study showed food manufacturers not disclosing the actual values of fructose corn syrup on their product labels.45 Does this bother you? It should.

Sugar is Killing Us | The Paleo Diet

Besides the physiologic effects of too much sugar, there are vast and damning economic effects.32 Take, for example, that diabetes alone costs the United States $245 billion per year.46 This is a rise of 41% in a mere five years. That is an absolutely terrifying figure. Have I scared you yet?

How about the fact that higher glucose levels are associated with lower memory and reduced hippocampal microstructure?47 Or, how about the study from the New England Journal of Medicine, which showed that higher glucose levels may be a risk factor for dementia.48 What was interesting (and alarming) about this finding, was that this was the risk for those without diabetes. This means that you can be taking in “normal” amounts of sugar, not exhibit symptoms of diabetes, and still be risking dementia. Act and don’t turn a blind eye. Save your health.

Sugar is Killing Us | The Paleo Diet

N Engl J Med. Aug 8, 2013; 369(6): 540–548.

Other studies have shown, unsurprisingly, that sugar consumption promotes weight gain in children and adults.33 All behaviors have a biochemical basis. ADHD, ADD, et al, are all likely partially due to a poor diet.49, 50 A diet that, almost always, is high in sugar.51, 52 Since studies have shown that intense sweetness surpasses cocaine reward, it is not surprising that many Americans cannot stop consuming sugar.53 But, in order to help stop alarmingly rising healthcare costs, they must stop their gluttonous consumption, and re-focus their diet on whole, real foods, all part of a Paleo Diet.

Other studies have shown that most US adults consume more added sugar than is recommended,34 and that this overconsumption leads to increased risk for cardiovascular disease mortality.54 This is literally the smoking gun that shows that sugar is killing us. Other studies have shown that higher levels of sugar also lower fitness.55 And another interesting study showed that junk food alone made rats lazy.56 Does this give you food for thought? Perhaps you should prioritize a change to your diet?

Insulin, which is secreted in order to deal with sugar in the bloodstream, blocks leptin signaling.35 Leptin is the “satiety” hormone, which helps to tell our hypothalamus to stop eating.57 Since we are now secreting 2-3 times the amount of insulin than we used to, you can see, directly, how this has resulted in disastrous consequences for our world’s health.58 And why are we secreting more insulin? Quite simply, to deal with all the sugar we are over-consuming. It is not a complicated formula, but it is a formula that is bankrupting our nation, and making so many sick and overweight.

Prevention is paradigm. Avoid a high-sugar diet, become leaner, think faster, and feel better. There is not a single better thing you can do, diet-related, that will help you to improve your health. A Paleo Diet, which is intrinsically low in sugar, high in nutrient-dense foods, and filled with micronutrients, is the best path to wellness.

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References

1. Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature. 2012;482(7383):27-9.

2. Available at: //www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html. Accessed September 13, 2014.

3. Available at: //www.telegraph.co.uk/foodanddrink/healthyeating/9987825/Sweet-poison-why-sugar-is-ruining-our-health.html. Accessed September 13, 2014.

4. Moreira PI. High-sugar diets, type 2 diabetes and Alzheimer’s disease. Curr Opin Clin Nutr Metab Care. 2013;16(4):440-5.

5. Ford ES, Giles WH, Mokdad AH. Increasing prevalence of the metabolic syndrome among u.s. Adults. Diabetes Care. 2004;27(10):2444-9.

6. Seaquist ER. Addressing the burden of diabetes. JAMA. 2014;311(22):2267-8.

7. Available at: //www.cdc.gov/nchs/data/databriefs/db122.htm. Accessed September 13, 2014.

8. Available at: //wholehealthsource.blogspot.com/2012/02/by-2606-us-diet-will-be-100-percent.html. Accessed September 13, 2014.

9. Johnson RK, Appel LJ, Brands M, et al. Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation. 2009;120(11):1011-20.

10. Available at: //www.newsherald.com/opinions/letters-to-the-editor/too-many-americans-are-selfish-and-self-absorbed-1.195653. Accessed September 13, 2014.

11. Available at: //www.today.com/id/30312181/ns/today-today_books/t/me-me-me-americas-narcissism-epidemic/#.VBTMylbD_IU. Accessed September 13, 2014.

12. Available at: //well.blogs.nytimes.com/2014/02/19/learning-to-cut-the-sugar/. Accessed September 13, 2014.

13. Available at: //blogs.kqed.org/newsfix/2014/09/12/berkeley-is-talking-about-sugar-and-the-conversation-isnt-sweet/. Accessed September 13, 2014.

14. Available at: //www.telegraph.co.uk/news/worldnews/europe/netherlands/10314705/Sugar-is-addictive-and-the-most-dangerous-drug-of-the-times.html. Accessed September 13, 2014.

15. Available at: //www.nytimes.com/2010/07/03/nyregion/03sodatax.html. Accessed September 13, 2014.

16. Available at: //www.publicintegrity.org/2009/11/04/2758/food-lobbys-war-soda-tax. Accessed September 13, 2014.

17. Available at: //www.npr.org/blogs/thesalt/2013/02/26/172969363/how-the-food-industry-manipulates-taste-buds-with-salt-sugar-fat. Accessed September 13, 2014.

18. Available at: //www.orangejuicefacts.com/nutrition.html. Accessed September 13, 2014.

19. Ahmed SH, Guillem K, Vandaele Y. Sugar addiction: pushing the drug-sugar analogy to the limit. Curr Opin Clin Nutr Metab Care. 2013;16(4):434-9.

20. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

21. Gearhardt A, Roberts M, Ashe M. If sugar is addictive…what does it mean for the law?. J Law Med Ethics. 2013;41 Suppl 1:46-9.

22. Available at: //www.ars.usda.gov/is/AR/archive/jun00/sugar0600.htm. Accessed September 13, 2014.

23. Available at: //www.webmd.com/food-recipes/features/sugar-shockers-foods-surprisingly-high-in-sugar. Accessed September 13, 2014.

24. Available at: //www.cbsnews.com/news/cdc-kids-consume-too-much-sugar-mostly-from-processed-foods/. Accessed September 13, 2014.

25. Lythgoe A, Roberts C, Madden AM, Rennie KL. Marketing foods to children: a comparison of nutrient content between children’s and non-children’s products. Public Health Nutr. 2013;16(12):2221-30.

26. Daly M. Sugars, insulin sensitivity, and the postprandial state. Am J Clin Nutr. 2003;78(4):865S-872S.

27. Musselman LP, Fink JL, Narzinski K, et al. A high-sugar diet produces obesity and insulin resistance in wild-type Drosophila. Dis Model Mech. 2011;4(6):842-9.

28. Gallagher EJ, Leroith D, Karnieli E. Insulin resistance in obesity as the underlying cause for the metabolic syndrome. Mt Sinai J Med. 2010;77(5):511-23.

29. Hofeldt FD. Reactive hypoglycemia. Endocrinol Metab Clin North Am. 1989;18(1):185-201.

30. Yang Q. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010;83(2):101-8.

31. Oliver KG, Huon GF, Zadro L, Williams KD. The role of interpersonal stress in overeating among high and low disinhibitors. Eat Behav. 2001;2(1):19-26.

32. Available at: //www.forbes.com/sites/aroy/2012/04/23/trustees-medicare-will-go-broke-in-2016-if-you-exclude-obamacares-double-counting/. Accessed September 13, 2014.

33. Malik, Vasanti S., Matthias B. Schulze, and Frank B. Hu. “Intake of sugar-sweetened beverages and weight gain: a systematic review.” The American journal of clinical nutrition 84.2 (2006): 274-288.

34. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med. 2014.

35. Kellerer M, Lammers R, Fritsche A, et al. Insulin inhibits leptin receptor signalling in HEK293 cells at the level of janus kinase-2: a potential mechanism for hyperinsulinaemia-associated leptin resistance. Diabetologia. 2001;44(9):1125-32.

36. Available at: //www.huffingtonpost.co.uk/2013/07/26/why-is-sugar-so-addictive_n_3643965.html. Accessed October 2, 2014.

37. Greeno CG, Wing RR. Stress-induced eating. Psychol Bull. 1994;115(3):444-64.

38. Available at: //www.cnn.com/2012/02/08/health/healthy-eating-tips-stress/. Accessed October 2, 2014.

39. Torres SJ, Nowson CA. Relationship between stress, eating behavior, and obesity. Nutrition. 2007;23(11-12):887-94.

40. Epstein DH, Shaham Y. Cheesecake-eating rats and the question of food addiction. Nat Neurosci. 2010;13(5):529-31.

41. Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010;13(5):635-41.

42. Weeratunga P, Jayasinghe S, Perera Y, Jayasena G, Jayasinghe S. Per capita sugar consumption and prevalence of diabetes mellitus–global and regional associations. BMC Public Health. 2014;14:186.

43. Soubry A, Murphy SK, Wang F, et al. Newborns of obese parents have altered DNA methylation patterns at imprinted genes. Int J Obes (Lond). 2013.

44. Available at: //healthland.time.com/2012/11/29/predicting-obesity-at-birth/. Accessed October 2, 2014.

45. Walker RW, Dumke KA, Goran MI. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition. 2014;30(7-8):928-35.

46. Available at: //www.diabetes.org/advocacy/news-events/cost-of-diabetes.html. Accessed September 29, 2014.

47. Kerti L, Witte AV, Winkler A, Grittner U, Rujescu D, Flöel A. Higher glucose levels associated with lower memory and reduced hippocampal microstructure. Neurology. 2013;81(20):1746-52.

48. Crane PK, Walker R, Hubbard RA, et al. Glucose levels and risk of dementia. N Engl J Med. 2013;369(6):540-8.

49. Millichap JG, Yee MM. The diet factor in attention-deficit/hyperactivity disorder. Pediatrics. 2012;129(2):330-7.

50. Johnson RJ, Gold MS, Johnson DR, et al. Attention-deficit/hyperactivity disorder: is it time to reappraise the role of sugar consumption?. Postgrad Med. 2011;123(5):39-49.

51. Kanoski SE, Davidson TL. Western diet consumption and cognitive impairment: links to hippocampal dysfunction and obesity. Physiol Behav. 2011;103(1):59-68.

52. Crescenzo R, Bianco F, Coppola P, et al. Fructose supplementation worsens the deleterious effects of short-term high-fat feeding on hepatic steatosis and lipid metabolism in adult rats. Exp Physiol. 2014;99(9):1203-13.

53. Lenoir M, Serre F, Cantin L, Ahmed SH. Intense sweetness surpasses cocaine reward. PLoS ONE. 2007;2(8):e698.

54. Schmidt LA. New unsweetened truths about sugar. JAMA Intern Med. 2014;174(4):525-6.

55. Ruff JS, Suchy AK, Hugentobler SA, et al. Human-relevant levels of added sugar consumption increase female mortality and lower male fitness in mice. Nat Commun. 2013;4:2245.

56. Blaisdell AP, Lau YL, Telminova E, et al. Food quality and motivation: a refined low-fat diet induces obesity and impairs performance on a progressive ratio schedule of instrumental lever pressing in rats. Physiol Behav. 2014;128:220-5.

57. Myers MG, Cowley MA, Münzberg H. Mechanisms of leptin action and leptin resistance. Annu Rev Physiol. 2008;70:537-56.

58. Larsson H, Ahrén B. Glucose intolerance is predicted by low insulin secretion and high glucagon secretion: outcome of a prospective study in postmenopausal Caucasian women. Diabetologia. 2000;43(2):194-202.

Does Non-Allergenic Milk Exist? | The Paleo Diet

Dear Paleo Diet Team,

In the 1997 work entitled “Food and Low Incidence of Insulin Dependent Diabetes Mellitus (IDDM) in Iceland” (L. Thorsdottir and O. Reykdal) have suggested that the incidence of IDDM is lower in Iceland than in other human genetic related nations of Scandinavia.

Since milk proteins alleles frequencies in the Nordic cattle breeds varies and preliminary (at that time) results indicated that Beta Casein A1 was particularly low in Iceland milk, they have speculated that IDDM was caused by Beta Casein A1 and its bioactive peptide BCM-7.

My opinion is that Diabetes mellitus is not caused by one single factor alone, but perhaps there are also other factors involved.

I would like to know your opinion on that matter if possible, since cattle breeding association in Brazil, of a particular breed that produces A2 milk, is applying to official agencies to market their milk with the allegation of “non-allergenic milk.”

One of their main allegations is based on data that BCM-7 alone would be the “villain” in the milk, with which I totally disagree, since milk allergies are a multifactorial health problem.

Your attention would be greatly appreciated.

Jose Luiz M Garcia

Pedro Carrera Bastos’ Response:

Dear Mr. Garcia,

Cow’s milk (CM), as you know, has several proteins, but we can group these proteins into two major ones: whey proteins and caseins. 1 Caseins represent about 80% of the total protein content of CM, as seen in this table. 1

6.12.14-table1Caseins in CM (and also in goat’s milk) are divided into: alphaS1, alphaS2, beta and kappa.2

Following digestive proteolysis of beta-caseins in the human gut (and also after food processing, such as milk fermentation and microbial cheese ripening) there will be a release of bioactive peptides called beta-casomorphins (BCMs). 3 BCMs contain 4-11 amino acids and, more importantly, they are resistant to further proteolysis and express opioid like activity. This means they could potentially bind various opioid receptors in the human nervous system, and also in the gastrointestinal, immune and endocrine systems.3

Beta caseins (as well as the other caseins in CM) are encoded by genes found on bovine chromosome 63 and there are 12 recognized genetic variants of beta-casein: A1, A2, A3, B, C, D, E, F, H1, H2, I and G. A1 and A2 are the most common forms of beta-casein found in dairy cattle in western countries.3

Beta-caseins are proteins with 209 amino acids and the difference between A1 and A2 lies in just one amino acid at position 67: histidine in A1 and proline in A2.3, 4 Apparently, “ancestral cattle” (as well as goats, yak and most sheep) contained the A2 version of beta-casein gene and not the A1 version, which is a single nucleotide polymorphism (SNP) that appeared 5,000 to 10,000 years ago only in Bos taurus, being present today in breeds, such as Holstein, Friesian and Ayrshire.4, 5

The main premise behind the A1/A2 hypothesis is that beta-casein A1, but not A2, will originate the opioid like peptide beta-casomorphin-7 (BCM-7).3, 4 BCM-7 (which contains 7 amino acids) resists further digestion in the human gut, could be absorbed by some individuals, like babies and people with intestinal hyperpermeability, and can influence gut function without being absorbed into the bloodstream.3, 4 The proponents of this hypothesis claim that after being absorbed, BCM-7 could increase low-density lipoprotein oxidation and bind to opioid receptors in the nervous, immune and endocrine systems.3-6

This in vitro and animal data combined with epidemiological studies led to the hypothesis that beta-casein A1 is implicated in Autism and Schizophrenia,3, 4 Type 1 Diabetes,3-5 Cardiovascular Disease,3-6 Sudden Infant Death Syndrome,3 and perhaps even in Metabolic Syndrome (because it could cause insulin resistance).6

In the last years, some important scientific papers have been published criticizing the epidemiological and animal data, and particularly the lack of intervention studies supporting the above causality.5, 7, 8

Having said that, I believe the A1/A2 hypothesis should not be readily dismissed. It deserves to be better studied in animal models and, more importantly, in randomized controlled trials. Nevertheless, when it comes to Type 1 Diabetes (T1D), multiple lines of evidence strongly suggest various CM proteins, and not just beta-casein (which could yield BCM-7), are involved.

Beta-lactoglobulin (BLG)

BLG is a protein found in the whey fraction of CM (but apparently not in the whey of human’s milk) that has structural homology with the human protein glycodelin, which is responsible for the modulation of T-lymphocytes.9 This means that BLG could generate antibodies to glycodelin, and indirectly lead to autoimmunity in genetically susceptible children,9 especially if introduced early in life when there is increased intestinal permeability.9, 10

Bovine serum albumin (BSA)

This is another protein present in the whey fraction of CM. Antibodies against a specific peptide derived from BSA, called ABBOS, have been found repeatedly in the majority of patients with T1D.11-13 This is relevant because there is molecular mimicry between the peptide ABBOS and a beta-cell surface protein p69, one of the autoantigens attacked by T cells in T1D patients.11

Bovine insulin (BI)

CM, human’s milk, and presumably milk from all mammals contains insulin.10 Immunity to BI is common in children who consume cow’s milk or who have been exposed to infant formulas containing cow’s milk.10 Because BI differs from human insulin by only three amino acids, it can generate antibodies against human insulin in genetically susceptible individuals with increased intestinal permeability and other gut dysfunctions10 and/or enteral virus infections in their early years.10, 14

A recent randomized controlled trial (RCT) confirmed the role of BI in T1D.15 In this pilot trial, infants with genetic susceptibility for T1D were assigned to either a “normal” CM based formula, a whey-based hydrolyzed formula, or a whey-based formula “essentially free of bovine insulin” and it was found that the insulin-free formula reduced the cumulative incidence of autoantibodies by age 3 years.15

Interestingly, the RCT gives more support to the role of CM proteins in T1D. In this trial, 230 infants with genetic susceptibility to T1D and at least one family member with T1D received either a casein hydrolysate formula or a conventional, CM-based formula (control) whenever breast milk was not available during the first 6 to 8 months of life. The casein hydrolysate formula, as compared with the control, was associated with a decreased risk of positivity for at least one diabetes-associated autoantibody.16

In conclusion, the available evidence cannot firmly confirm or refute a causal role of BCM-7 in T1D. Nevertheless, even if a causal role is confirmed, drinking CM without beta-casein A1 could still represent a risk for people with genetically susceptibility for T1D, since there are various other potential problematic proteins in CM.

Best wishes,

Pedro Bastos, MA, MS, Ph.D. candidate in Medical Sciences at Lund University, Sweden;

Pedro Bastos | About The Paleo Diet TeamPedro Bastos provides consultations, research, and advice to The Paleo Diet community. He is a member of the New York Academy of Sciences, the International Society for the Study of Fatty Acids and Lipids, and the Nutrition Society. Pedro is a certified personal trainer and strength and conditioning instructor, and he holds post-graduate diplomas in exercise and health (from School of Sport Science of Rio Maior, Portugal) and in biochemistry and orthomolecular medicine (from Fernando Pessoa University, Portugal). He received his master’s degree in human nutrition and food quality through Universitat de les Illes Balears (Spain). His research interests are dairy products and human health, nutrition and chronic inflammatory/auto-immune diseases, role of micronutrients in human health, prevention of osteoporosis and sarcopenia, nutrition and liver adenomas, and the role of nutrition in sports injury prevention.

REFERENCES

1. Chandan RC. Milk composition, physical and processing characteristics. In Hui YH, Chandan RC, Clark S, et al. Handbook of Food Products Manufacturing – Health, Meat, Milk, Poultry, Seafood, and Vegetables. John Wiley & Sons; 2007: 347-377

2. Park YW, Haenlein GFW. Handbook of milk of non-bovine mammals. Blackwell Publishing; 2006

3. Kamiński S, Cieslińska A, Kostyra E. Polymorphism of bovine beta-casein and its potential effect on human health. J Appl Genet. 2007;48(3):189-98.

4. Woodford K. Devil in the Milk: Illness, health and politics of A1 and A2 milk. Craig Potton Publishing; 2007.

5. Merriman TR. Type 1 diabetes, the A1 milk hypothesis and vitamin D deficiency. Diab Res Clin Pract. 2008:1–8.

6. Lindeberg. Food And Western Disease: Health and Nutrition from an Evolutionary Perspective. Wiley-Blackwell; 2010.

7. Truswell AS. The A2 milk case: a critical review. Eur J Clin Nutr. 2005; 59: 623–631.

8. Clemens RA. Milk A1 and A2 peptides and diabetes. Nestle Nutr Workshop Ser Pediatr Program. 2011;67:187–195.

9. Goldfarb MF. Relation of time of introduction of cow milk protein to an infant and risk of type-1 diabetes mellitus. J Proteome Res. 2008 May;7(5):2165-7

10. Vaarala O. Is it dietary insulin? Ann N Y Acad Sci. 2006 Oct;1079:350-9.

11. Karjalainen J, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. N Engl J Med. 1992 Jul 30;327(5):302-7.

12. Pérez-Bravo F, et al. Duration of breast feeding and bovine serum albumin antibody levels in type 1 diabetes: a case-control study. Pediatr Diabetes. 2003 Dec;4(4):157-61.

13. Banwell B, et al. Abnormal T-cell reactivities in childhood inflammatory demyelinating disease and type 1 diabetes. Ann Neurol. 2008 Jan;63(1):98-111.

14. Mäkelä M, et al. Enteral virus infections in early childhood and an enhanced type 1 diabetes-associated antibody response to dietary insulin. J Autoimmun. 2006 Aug;27(1):54-61.

 15. Vaarala O, et al. Removal of Bovine Insulin From Cow’s Milk Formula and Early Initiation of Beta-Cell Autoimmunity in the FINDIA Pilot Study. Arch Pediatr Adolesc Med. 2012 Jul 1;166(7):608-14.

 16. Knip M, et al. Dietary intervention in infancy and later signs of beta-cell autoimmunity. N Engl J Med. 2010 Nov 11;363(20):1900-8.

Mediterranean Diet | The Paleo Diet

Dr. Cordain,

Yours and Maelán Fontes Villalba’s position is both convincing and very interesting. But you agree that there are also studies showing protective effect of whole-grains?

I have another hypothesis – maybe complementary to yours: Perhaps it is before all drastic technological treatments applied to raw food edible materials that have rendered them deleterious for health via modified compounds not adapted to our genetics. Otherwise, our ancestors had a very low life expectancy: this an important point. And, if cereal grains were so bad, why are they edible? Don’t forget also that we have to consider wholegrains in the context of a whole diet. Finally, our ancestors seemed to eat lots of meat: maybe they were submitted to acidosis? And what do we know about diet-related chronic diseases at this ancient periods?

However, your genetic argument remains strong, I agree.

Friendly yours,

Anthony FARDET, Ph.D.
Chargé de Recherches (Research scientist)
Human Nutrition Research Center, Auvergne
Clermont-Ferrand/Theix Research Center
France

Dr. Cordain’s Response

Dear Dr. Fardet,

Thank you for keeping an open scientific mind — in regard to your comments, it is ironic that the range of diets to which our species has been conditioned to over the vast expanse of evolutionary experience is now beyond the reach of many of the world’s people.

France and French people have developed a cultural tradition of foods and eating/lifestyle habits which on the surface (in large population studies) appear to be healthier than in many parts of Europe and in the rest of the world. In France, on a population wide basis, French bread and other forms of wheat are consumed daily, as is wine, cultured cheese, and butter. Let’s not forget fresh veggies, fruit, fish, olives and olive oils — particularly in the South of France. Moreover, American style fast food is typically shunned by at least the older French population. Additionally, meals are consumed over long time periods with multiple dishes consumed in relaxed settings. These dietary patterns typically result in reduced total caloric intakes over a 24 hour period. This manner of meals pretty much describes the Mediterranean Diet which likely is healthier than the typical US Diet or the typical non-Mediterranean European Diet — both of which appear to accelerate all chronic diseases of western civilization.

Could the French or Mediterranean Diet be the healthiest way to stave off the chronic diseases which impact most western societies or is there a healthier alternative? Contrast the Mediterranean Diet and its associated morbidity and mortality rates for all causes combined to the Japanese Diet, or better yet to contemporary Paleo Diets. We now have preliminary data that the Paleo Diet is more nutritionally dense than the Mediterranean Diet and maintains multiple nutritional characteristics superior to the French, Mediterranean or Japanese Diets. The therapeutic data for contemporary Paleo Diets is now available. You can find these studies if you diligently look for them on MEDLINE.

Let me now address a few other concerns you have offered:

1. “Otherwise, our ancestors had a very low life expectancy: this an important point.”

Although this issue may represent an intuitive “flash point,” the best and most correct data would suggest otherwise. First, your characterization that, “our ancestors had a very low life expectancy” is not necessarily correct and is moreover misleading. Let me give you a simple example. If we have a population of 4 people (2 adults who die at age 80 and who give birth to 2 children who die in childbirth), then the average life expectancy of this population is quite low (160 years/4 = 40 years). Hence, “average lifespan” really only represents the average age at death. What is more important is to characterize the “average age” of the entire living population.

These statistics are calculated regularly by life insurance companies in the western world and are called Life Tables. Life Tables therefore reflect the living population and not those who have died only compared to the living. At least 4 life table studies of hunter gatherers show that a good percentage of the population survives into old age (>60 yrs.). These facts are rather surprising given that in their world, there was no modern medicine, sanitation or contemporary health practices, and that mortality comes not from chronic diseases (as in the western world) but rather from accidents, trauma, snake bikes, warfare and the stresses of living outdoors for an entire lifetime. Mortality and morbidity among hunter gatherers (even the elderly) do not show them sufferings the signs or symptoms of chronic disease found in western populations, and this should be the take home point. Let’s adopt the best of their worlds — leave the worst behind and take the best that the modern world has to offer.

2.”If cereal grains were so bad, why are they edible?”

Again, I encourage you to read my paper, “Cereal Grains: Humanity’s Double Edged Sword’ — Cordain, L. Cereal Grains: Humanity’s Double Edged Sword. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73.

Cereal grains (whole wheat, rye, barley, oats, corn, maize, sorghum, millet, etc.) are not generally edible (or very poorly digestible) by humans (or almost any other primate) in their natural state without cooking. As a species, we have a poor/limited ability to hydrolyze raw grain starches into sugars and metabolize them and degrade their raw proteins into amino acids in our guts for absorption. Hence whole, uncooked grains consumed by humans and by virtually all primates (except for a single species of baboon [Gelada]) represent a food source which was rarely or never never consumed. See my paper cited above for the scientific references.

Accordingly, until humans developed fire, cereal grains would have never been a significant food source. More importantly, the ability to start fires “at will” is the crucial issue here. This technology likely developed in Europe (only) about 300,000 to 250,000 years ago, but occurred not “at will”, but more likely by collecting natural and lightning caused fires. To star a fire “at will” results from 4 or 5 technological advances which probably occurred only after the appearance of behaviorally modern humans (~200,000 ago or less).

More importantly, the cell walls of cereal grains must be broken down by mechanical means (milling) before fire and heating are effective to hydrolyze cereal grain starches and thereby make them available for human nutritional absorption. Important in this concept is that the first crude cereal milling stones do not appear in the archaeological record until about 15,000-25.000 years ago in the mid-east. The fossil, nutritional and physiological data indicate that cereal grains would have been rarely or never used as food sources by our species until very recently in human evolution, simply because they were indigestible.

3. “Don’t forget also that we have to consider whole-grains in the context of a whole diet.”

Consider reading these two papers:

1. Cordain L. The nutritional characteristics of a contemporary diet based upon Paleolithic food groups. J Am Neutraceut Assoc 2002; 5:15-24.

2. Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, Brand-Miller J. Origins and evolution of the western diet: Health implications for the 21st century. Am J Clin Nutr 2005;81:341-54

When cereal grains displace lean meats, fish, seafood, eggs, organ meats, fresh vegetables, and fresh fruits, they dilute the trace nutrient (vitamin, mineral, phytochemical) concentration of the 13 nutrients most lacking in the typical western diet. Hence, in the context of a whole diet, the inclusion of cereal grains makes all nutritional considerations worse.

4. “Finally, our ancestors seemed to eat lots of meat: maybe they were submitted to acidosis?”

The available archeaological evidence worldwide, spanning hundreds of thousands of years shows that osteological (bone mineral abnormalities) evidence cannot support your supposition. Rather, osteoporosis, cribra orbitalia and other bone mineral pathologies stemming from dietary induced acidosis only became commonplace following the agricultural revolution and the adoption of cereal grains and plant foods as staples. The physiological and archaeological mechanisms and arguments for these events are fully outlined in my paper, Cereal Grains: Humanity’s Double Edged Sword.

5. “And what do we know about diet-related chronic diseases at this ancient periods?”

As I have pointed out in prior blogs, it is difficult to deduce heart disease from the fossil/bone record. Further, except for bone cancers, the same be held true for cancers. Nevertheless, bone cancers are extremely rare or non-existent in the archaeological human record prior to agriculture. Studies of historically studied hunter gatherers show cardiovascular disease to be rare or non-existent.

Cordain L, Eaton SB, Brand Miller J, Mann N, Hill K. The paradoxical nature of hunter-gatherer diets: Meat based, yet non-atherogenic. Eur J Clin Nutr 2002;56 (suppl 1):S42-S52.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

Modern Paleo | The Paleo Diet

Dear Dr. Cordain and Dr. Fontes Villalba,

I read with great interest your paper entitled: “Carrera-Bastos, P., Fontes-Villalba, M., O’Keefe, J. H., Lindeberg, S. and Cordain, L. (2011). The western diet and lifestyle and diseases of civilization. Research Reports in Clinical Cardiology 2011: 15-35.

The demonstration is quite logical, but I would like to get your opinion on the following issue:

*If the paleolithic diet suits well human genetics and does not lead to chronic diseases – which is true -, and if grain products are not so good for human health, the world has changed with at least 1 billion people living in huge towns worldwide: they cannot realistically have a paleolithic diet going outside to hunt and collect berries! There is a compromise to find between the best and reality of our modern world. In that way, grain cereals and legumes appear as promising foods being cheap, easy to store, with a huge health potential, satiating, etc. Maybe humans before 10,000 years consume grains, but to a lesser extent?*

So, what do you think is the best diet today, in a world with more than 7 billions people and huge cities?

I will be very happy to have your opinion about this issue,

Yours sincerely,

Available I remain,

Anthony FARDET, Ph.D.
Chargé de Recherches (Research scientist)
Human Nutrition Research Center, Auvergne
Clermont-Ferrand/Theix Research Center
France

Maelán Fontes Villalba’s Response:

Hello Dr. FARDET,

Today almost all health authorities and nutritionists believe that cereal grains are healthy for so-called diseases of civilization. This information is derived from epidemiological studies that can not establish cause-effect. Consistently, epidemiological studies show an inverse association between the consumption of cereal grains and western disease, which is not demonstrated by randomized controlled trials. In the women’s health initiative (+48,000 postmenopausal women) those women allocated to the intervention group (eat more than 6 servings/day of wholegrain cereals, 5 servings of fruit/vegetable and <20%en from fat) of whom had a CV event at baseline significantly increased their risk of CV event by 26%. In the DART trial, those men allocated to increase the intake of fiber from wholegrain cereals, increased the risk of death compared to the group who wasn’t advised to increase the intake of fiber.

Some systematic reviews make it clear that we don’t have enough evidence to recommend the intake of cereal grains for the prevention and treatment of cardiovascular disease (Kelly, Cochrane Database of Systematic Reviews, 2007), obesity, (FESNAD-SEEDO, Revista Española De Obesidad, 2011) or diabetes (Priebe, Cochrane Database of Systematic Reviews, 2008). Therefore, I don’t agree with you in that “they have a huge health potential.”

The short-term clinical trials published by my group (Lindeberg, Diabtologia, 2007; Jönsson, Cardiovascular Diabetology, 2009) have shown that a Paleolithic Diet is superior to the Mediterranean and American Diabetes Association diets, respectively.

From an evolutionary standpoint it is very unlikely that we have completed adapted to cereal grains in just 10,000 years (even knowing that human evolution has accelerated since the adoption of agriculture and living in huge cities, probably by pathogens rather than foods). So, there is no body of evidence that demonstrates we have adapted. This information is necessary before performing human experiments showing we are feeding individuals with a food meant for granivorous animals (birds, rodents, etc). And, while “everybody” may think we are adapted, it is very unlikely. The proof simply isn’t there. If we eat the kind of foods we ate during human evolution (>99.9% of our evolution), is there any obvious risk? Not that we are aware of. Are there potential health risk of consuming cereal grains? Yes there are. So, I would stay in the safe side.

Regarding you question about sustainability, I think you can adapt the Standard American Diet to one more suitable for our genetic legacy and improve health. Furthermore, if the world population would eat a diet in accordance with our physiology then the expense in health would be dramatically cut. I am not an expert in this field but I think that famine in the third world is more so a political problem than a problem with food choice itself.

You are right, however, regarding the DART study, the increased risk (18%) was non-significant, but in a Eur J Clin Nutr 2002 Ness, and after statistical adjustment, there was a significant increase of mortality in the first two years, but not the following years.

PastedGraphic-1

Many studies are conducted in ill people with high risk of CVD. If an intervention reduces the risk to that of “normal” westerners, then we could say there was a positive effect, but who wants to be normal? Not me! (see European Heart Journal 2005 Lindeberg). I prefer to have a low risk of western disease.

I agree that the Mediterranean Diet (for example) is better than the Standard American Diet, but is there a better diet? What if we reduce cereal grains in a Mediterranean Diet and increase fruits, tubers and vegetables? Do you improve a diet based on vegetables, fruits, tubers, lean meat, fish, eggs and nut if you include grains?

Dr. Cordain has explained in many lectures that cereals grains are not edible unless you process them. But there are many other reasons (bioactive compounds like exorphins, lectins, saponins, binding to endocrine receptors; antinutrients; protease and amylase inhibitors, etc), why cereal grains can be a problem for most people, besides non-celiac gluten sensitivity (and potential same effect of thousands of proteins in grains).

I am unfamiliar with any study where it has been shown that cereal grains, per se, are protective. As I previously mentioned, there are some studies (with numerous limitations like the PREDIMED study where the control group received much less support and followed a diet similar to that in WHI, where the risk of CVD was reduced, but you cannot say it was because of the intake of cereal grains. On the other hand, the studies comparing healthy diets with and without cereal grains have shown very interesting results. Should we look to the other side, or focus on those interesting data? Well, many people just turn their head to the other way, while we are interested in exploring what happened in those studies (Lindeberg, 2007; Jönsson, 20009; Mellberg, 2014).

The statement that our ancestor lived only until the age of 30 is false. See Kaplan, 2007–>modal age at death is >70 years old in hunter-gatherers. Of course, they are not people from the Paleolithic era but there is no reason to think that it was different then. See also Eaton, 2002 where Dr. Cordain is a co-author (Evolutionary Health Promotion: A Consideration of Common Counterarguments: Preventive Medicine 2002 Eaton).

Regarding meat, it is not true that Paleolithic Diets must necessarily be high in meat. Some hunter-gatherers consume high amounts plants, with carbohydrate being almost 70%en (see the Kitava study).

Best wishes,

Maelán Fontes Villalba, M.S.
www.maelanfontes.com
@maelanfontes

Dr. Cordain’s Response:

Dear Dr. FARDET,

Many thanks for your inquiry. Maelán Fontes has done a good job of summarizing potential health issues with cereal grains in his reply to you. In my paper, “Cereal Grains: Humanity’s Double Edged Sword,” I delve into greater detail on the topic with 55 pages of dialogue and 342 references.

Further, in our paper, “Origins and Evolution of the Western Diet: Health Implications for the 21st Century,” we show how humans have no nutritional requirement for whole grain cereals. In fact, when whole grains are added to the diet they significantly reduce the 13 nutrients most lacking in the US diet.

Further, in our paper “The Nutritional Characteristics of a Contemporary Diet Based upon Paleolithic Food Groups,” you can see how a modern Paleo diet based upon lean meats, fish, seafood, fresh fruits and vegetables and nuts (and devoid of whole grain cereals, dairy products and processed foods) are much more nutrient dense than either the current USDA recommended My Plate diet, or the Mediterrean Diet. The reason for this phenomenon is that the aforementioned foods are more trace nutrient dense than whole grains, dairy products or processed foods for the 13 nutrients most lacking in western diets.

Cheers, I hope these papers provide new learning to further educating yourself on the topic.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

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