Sugar intake is associated with progression from islet autoimmunity to type 1 diabetes: the Diabetes

http://ht.ly/O1htC

Diabetologia. 2015 Jun 7. [Epub ahead of print]
[h=1]Sugar intake is associated with progression from islet autoimmunity to type 1 diabetes: the Diabetes Autoimmunity Study in the Young.[/h]Lamb MM1, Frederiksen B, Seifert JA, Kroehl M, Rewers M, Norris JM.
[h=3]Author information[/h]

[h=3]Abstract[/h][h=4]AIMS/HYPOTHESIS:[/h]Dietary sugar intake may increase insulin production, stress the beta cells and increase the risk for islet autoimmunity (IA) and subsequent type 1 diabetes.
[h=4]METHODS:[/h]Since 1993, the Diabetes Autoimmunity Study in the Young (DAISY) has followed children at increased genetic risk for type 1 diabetes for the development of IA (autoantibodies to insulin, GAD or protein tyrosine phosphatase-like protein [IA2] twice or more in succession) and progression to type 1 diabetes. Information on intake of fructose, sucrose, total sugars, sugar-sweetened beverages, beverages with non-nutritive sweetener and juice was collected prospectively throughout childhood via food frequency questionnaires (FFQs). We examined diet records for 1,893 children (mean age at last follow-up 10.2 years); 142 developed IA and 42 progressed to type 1 diabetes. HLA genotype was dichotomised as high risk (HLA-DR3/4,DQB1*0302) or not. All Cox regression models were adjusted for total energy, FFQ type, type 1 diabetes family history, HLA genotype and ethnicity.
[h=4]RESULTS:[/h]In children with IA, progression to type 1 diabetes was significantly associated with intake of total sugars (HR 1.75, 95% CI 1.07-2.85). Progression to type 1 diabetes was also associated with increased intake of sugar-sweetened beverages in those with the high-risk HLA genotype (HR 1.84, 95% CI 1.25-2.71), but not in children without it (interaction p value = 0.02). No sugar variables were associated with IA risk.
[h=4]CONCLUSIONS/INTERPRETATION:[/h]Sugar intake may exacerbate the later stage of type 1 diabetes development; sugar-sweetened beverages may be especially detrimental to children with the highest genetic risk of developing type 1 diabetes.


PMID: 26048237 [PubMed - as supplied by publisher]

 

So I shouldn't have put Coke in her bottle? Damn! Now you tell me.

(where's the eye rolling icon when you need it?)

 

Thanks for sharing this, Ellen. This is interesting for those of us with non-T1 kiddos, although I don't actually know my younger child's HLA genotype and whether he falls in this risk bucket. TrialNet doesn't provide that information, does it?

 

The liver can turn 25 grams of fructose into glycogen and glucose per day if its not all at once. After that, it gets turned into triglycerides, or spills into the blood. Both of those are bad. The triglycerides build on fructose (and also those built on linoleic acid (high omega-6 plant oils) are easy to oxidize and oxidized triglycerides are the ROOT nutritional cause of CHD, and inflammation). There is basically proof that beta cells are killed by oxidative species like oxidized and glycated triglycerides (lipotoxicity) along with glucotoxicity. Fructose in the blood, even a trace is also very bad. Usually you have about 1% as much fructose as glucose in the blood, but it has 10x the glycosylating capacity. So if you have 1 mg/dl of fructose in the blood it is like having an extra 10 mg/dl of glucose.

Sucrose as well as sugar from vegetables and fruits will basically all yield 45-55% fructose. Prior to my dealing with diabetes, I would have strongly recommended that people eat a diet that nets no more than 25 grams of fructose per day for these reasons. Milk sugar can be factored in separately but that would basically set a limit on non milk "sugar" at 50 grams a day (25 net fructose +/-). When liver glycogen is empty the liver can use it faster, so it may get worse as the day goes on.

Also the 25 gram limit can be raised to match exercise because liver glycogen gets used up in exercise. If you burn 500 cals in exercise, and 40% is from carbs (moderate intensity) then that would be 200 cals or 50 grams from carbs you could add back in. Most cutting edge sports nutritionists would say that 1/3 of those 50 grams should be from fructose and 2/3 from glucose. So an hour of jogging or hard practice might earn you about 15-20 grams of net fructose on the day.

And this is not an anti fruit issue at all. Fruit nets about the same fructose per gram of sugar as "sugar" and fruit is not really high in sugar. A Banana with 20 grams of carbs will have only about 14 grams of sugar and 7 grams of net fructose so you could easily eat 3 1/2 bananas a day without exceeding the livers ability to clear fructose toxicity.

Also, it suggests to me that Omega-6 are going to have a similar effect on beta cell destruction. Please people, cut out high omega-6 plant oils. Even if they don't harm beta cells, they are probably THE fat-related dietary cause of heart disease and inflammatory issues. Saturated fat can not even form oxidized triglycerides and monounsaturates are also very hard to get to form oxidized TGs.

 

Soooo your day job is.....electrician?

 

Yep, that's why my daughter has T1D: I fed her too much sugar. It's the parent's fault...

 

Just mho, but this kind of research doesn't make me feel parent-blamed in the least (my daughter had maybe 6 sugar-sweetened beverages total in the two years that she lived before diagnosis!)

T1D rates are rising across the industrialized world at a breakneck pace of 3-5% per year, and are rising particularly quickly in very young children. It's pretty clear that there are environmental factors at play. At a population level, studies like DAISY are valuable to untangle what those environmental triggers might be.

I say this as a parent who made a futile attempt to head off celiac in my daughter, having followed circa-2010 infant feeding guidelines for babies at high familial risk of developing CD, guidelines that have since been retracted. So I absolutely know that research like this can only provide tentative and partial answers, and I don't pretend that any one intervention would prevent T1D developing in my other kids. Still, a healthy skepticism doesn't mean the research shouldn't be done to shed light on what in our environment might be causing the epidemic of autoimmunities like T1D, particularly if one day studies like this might yield recommendations that slow the growth of T1D at the population level.

 

While I'm confident that the research and statistical analysis done in this study were sound, and the results accurate, I'm none too happy about the fact that what we (as parents of children with T1D) have been trying to set straight for the "diabetes-uneducated" for so long (that we didn't cause our child's T1D by feeding them too much sugar), now has some significant grounding in truth.

It will be much more difficult to set this misperception straight with data like these...

 

It has been known for over a decade that wheat based diets promote leaky gut syndrome which greatly increases the likelyhood of many autoimmune diseases or syndromes. T1D almost certainly gets turned on through a compromised gut lining and the number one food item that compromises the gut lining is Psyllium fiber (grain fiber), along with other proteins and lignins which are particularly high in wheat among the grains. Another is fructose and artificial sweeteners that harm the good intestinal bacteria. Another is reduced and non-fat milk as milk fat is strongly protective against leaky gut. Also protective of leaky gut is potato starch, cellulose and pectin fiber, fermented full fat milk and vegetables.

 

Leaky gut? I thought that was a condition that wasn't accepted by the vast majority of physicians. Most hits I get from google are from woo-sites. Care to explain?

 

I knew that medicine was way behind cutting edge nutrition, but not that far. http://www.thedailybeast.com/articl...eal-may-be-the-cause-of-several-diseases.html

This one may be considered "commercial" but it is fully cited: http://perfecthealthdiet.com/2010/0...i-healing-the-gut-by-eliminating-food-toxins/

I will add the citations here in case its a site no-no.

References

[1] Fujimura KE et al. Role of the gut microbiota in defining human health. Expert Rev Anti Infect Ther. 2010 Apr;8(4):435-54. http://pmid.us/20377338.

[2] Ruas-Madiedo P et al. Mucin degradation by Bifidobacterium strains isolated from the human intestinal microbiota. Appl Environ Microbiol. 2008 Mar;74(6):1936-40. http://pmid.us/18223105.

[3] Bode L. Human milk oligosaccharides: prebiotics and beyond. Nutr Rev. 2009 Nov;67 Suppl 2:S183-91. http://pmid.us/19906222. Hat tip Dr. Art Ayers.

[4] Ames BN, Gold LS. Paracelsus to parascience: the environmental cancer distraction. Mutation Research 2000 Jan 17; 447(1):3-13. http://pmid.us/10686303

[5] Cummings JH. The effect of dietary fibre on fecal weight and composition. Pp 547–73 in: Spiller GA, ed. Handbook of dietary fibre in human nutrition. 2nd ed. Boca Raton, FL: CRC Press, 1993.

[6] Bernardo D et al. Is gliadin really safe for non-coeliac individuals? Production of interleukin 15 in biopsy culture from non-coeliac individuals challenged with gliadin peptides. Gut 2007 Jun;56(6):889-90. http://pmid.us/17519496.

[7] Drago S et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scand J Gastroenterol. 2006 Apr;41(4):408-19. http://pmid.us/16635908.

[8] Not T et al. Celiac disease risk in the USA: high prevalence of antiendomysium antibodies in healthy blood donors. Scand J Gastroenterol. 1998 May;33(5):494-8. http://pmid.us/9648988.

[9] Sollid LM, Jabri B. Is celiac disease an autoimmune disorder? Curr Opin Immunol. 2005 Dec;17(6):595-600. http://pmid.us/16214317.

[10] Singh MM et al Wheat gluten as a pathogenic factor in schizophrenia. Science. 1976 Jan 30;191(4225):401-2. http://pmid.us/1246624. Dohan FC et al 1984 Is schizophrenia rare if grain is rare? Biol Psychiatry. 1984 Mar;19(3):385-99. http://pmid.us/6609726.

[11] Lorenzsonn V, Olsen WA. In vivo responses of rat intestinal epithelium to intraluminal dietary lectins. Gastroenterology. 1982 May;82(5 Pt 1):838-48. http://pmid.us/6895878.

[12] Sjölander A et al. Morphological changes of rat small intestine after short-time exposure to concanavalin A or wheat germ agglutinin. Cell Struct Funct. 1986 Sep;11(3):285-93. http://pmid.us/3768964.

[13] Mellanby E. (March 15 1919) An experimental investigation on rickets. The Lancet 193(4985):407-412.

[14] Carpenter KJ, Lewin WJ. A critical review: A reexamination of the composition of diets associated with pellagra. J Nutr 1985 May;115(5):543–552. http://pmid.us/3998856.

[15] Biagi F et al. A milligram of gluten a day keeps the mucosal recovery away: a case report. Nutr Rev. 2004 Sep;62(9):360-3. http://pmid.us/15497770.

[16] Kordás K et al. Phytohaemagglutinin inhibits gastric acid but not pepsin secretion in conscious rats. J Physiol Paris. 2001 Jan-Dec;95(1-6):309-14. http://pmid.us/11595455. Pusztai A et al. Kidney bean lectin-induced Escherichia coli overgrowth in the small intestine is blocked by GNA, a mannose-specific lectin. J Appl Bacteriol. 1993 Oct;75(4):360-8. http://pmid.us/8226393. Prykhod’ko O et al. Precocious gut maturation and immune cell expansion by single dose feeding the lectin phytohaemagglutinin to suckling rats. Br J Nutr. 2009 Mar;101(5):735-42. http://pmid.us/18644165.

[17] Pusztai A et al. Inhibition of starch digestion by alpha-amylase inhibitor reduces the efficiency of utilization of dietary proteins and lipids and retards the growth of rats. J Nutr. 1995 Jun;125(6):1554-62. http://pmid.us/7782910.

[18] Haeney MR et al. Soya protein antibodies in man: their occurrence and possible relevance in coeliac disease. J Clin Pathol. 1982 Mar; 35(3):319-22. http://pmid.us/7040491.

[19] IBD in EPIC Study Investigators. Linoleic acid, a dietary n-6 polyunsaturated fatty acid, and the aetiology of ulcerative colitis: a nested case-control study within a European prospective cohort study. Gut. 2009 Dec;58(12):1606-11. http://pmid.us/19628674.

[20] John S et al. Dietary n-3 polyunsaturated fatty acids and the aetiology of ulcerative colitis: a UK prospective cohort study. Eur J Gastroenterol Hepatol. 2010 May;22(5):602-6. http://pmid.us/20216220.

[21] Bergheim I et al. Antibiotics protect against fructose-induced hepatic lipid accumulation in mice: role of endotoxin. J Hepatol. 2008 Jun; 48(6): 983-92. http://pmid.us/18395289.

[22] Stephen AM et al. Effect of changing transit time on colonic microbial metabolism in man. Gut. 1987 May;28(5):601-9. http://pmid.us/3596341.

[23] Quoted in Science Daily, http://www.sciencedaily.com/releases/2006/08/060823093156.htm. Hat tip Dr. Michael Eades.

[24] Burr ML et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet. 1989 Sep 30;2(8666):757-61. http://pmid.us/2571009. Hat tip Stephan Guyenet.

[25] Berti I et al. Usefulness of screening program for celiac disease in autoimmune thyroiditis. Dig Dis Sci. 2000 Feb;45(2):403-6. http://pmid.us/10711459.

[26] Mainardi E et al. Thyroid-related autoantibodies and celiac disease: a role for a gluten-free diet? J Clin Gastroenterol. 2002 Sep;35(3):245-8. http://pmid.us/12192201.

 

http://www.healthline.com/health-news/leaky-gut-implicated-in-multiple-sclerosis-092514

 

You posted an article which to great extent contained commentary from a "Paleo Mom", an ad for a book, a gish gallop of studies that for the most part doesn't seem to have anything to do with leaky gut, but with intestinal microbiology in general. Then you finished up with what appears to have been a study in mice of an "MS-like" condition (as opposed to real MS in real people). An interesting theory and a couple of studies showing some signs of support for said theory isn't enough to accept it as proven science. I see kids everywhere whose parents are forcing restrictive diets on them based on dubious science at best and pure fads at worst. Medical science is slow to accept new theories for a reason: If we jump on everything that looks "interesting", chances are very high we get steered in the wrong direction most of the time.

Sorry, but you hit on a pet peeve of mine. This will be my last remark on this.

 

http://www.ncbi.nlm.nih.gov/pubmed/19538307?dopt=AbstractPlus
http://www.ncbi.nlm.nih.gov/pubmed/7635964?dopt=AbstractPlus
http://www.ncbi.nlm.nih.gov/pubmed/11082037?dopt=AbstractPlus

Leaky gut is far less dubious than the idea that humans should be consuming large amounts of cereal grains or a carbohydrate based diet in the first place. The grain based diet was pure social propoganda. The 55-70% carb diet was pure propoganda. People never ate that way outside the US and before 1900. Doctors don't want to have to tell their patients that the 70% carb diet they recommended in the 80s took 10 years off of their lives. Or that whole eggs, milk and beef fat are actually NOT causes of atherosclerosis.

I guess in 25 years we can look back on this thread a laugh a little.

 

Leaky gut, by whatever name you'd like to call it, does seem to have some science behind it. Dr. Alessio Fassano of the Center for Celiac Research has presented talks on this at Friends for Life. See http://www.ncbi.nlm.nih.gov/pubmed/22109896

I think that the whole premise of sugar intake "maybe" contributing to type 1 is not relevant for those of us whose child was diagnosed as a toddler. We did not feed our daughter much sugar at all, especially sweetened beverages. In fact, she did not have any soda/cola until she was 5 when Diet Coke was served at a JDRF (then JDF) event.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507568/

 

"Woo-sites". Perfect! Mind if I use this term (if it was yours originally?)


There are far too many woo sites on the Net. Remember to always consider the source. It stands repeating: Just because it's on the Internet doesn't mean it's true!

 

No, woo-sites is a widely used term. I didn't come up with it. Actually, woo-sites play an important role as a quick sanity check of theories. If Naturalnews, GreenMedInfo or RealFarmacy appear on the first page of Google hits, my skepticism kicks into overdrive.

 

Yup, it's a big MAYBE. What most people don't realize is that a single study pointing in a certain direction doesn't mean that it's necessarily a done deal. More often than not, someone trying to replicate the results using a slightly different method will get different results. At this point, I would be very cautious reading too much into it. It would be very unfortunate if parents started blaming themselves for their children's T1D when there's no strong proof (yet) that it was caused by anything they did.

 

"Woo" or "Woo Woo" is wildly used in the skeptic community. Please use it fill tilt. I think it originated with the sound of the SciFy sound of the Theremin used in movies. It's the sound I hear in my head when "Dr." Oz speaks.