De Vany and insulin 'sunburn'?

[Patrick Yeung]

Okay, so ive been thinking about this. Who cares?

Okay, so the genetic damage may be permanent, but your body is still growing and building well into its 20s if youre healthy.

If you have kids, I bet most had em before they were 35, and the genetic damage could not have been that extensive and really affect their childern's genes could it?

And, so long as you stop and dont contiune down that path, you should be okay.

[Patrick Yeung]

Originally Posted by Grissim Connery

every once and a while i invite a bunch of people over and we just bake a ton of crap. it's really fun and great, but i always wonder whether it would be more advantageous to use splenda as opposed to sugar just to avoid insulin issues. i have a strongly ingrained fear towards artificial sweeteners, but i always wonder whether the insulin spike could potentially be just as bad as the effects of some artifical sweetener. i have noticed that if i eat something with splenda, i generally feel satisfied very quickly, whereas if i eat something with for reals sugar, i just crave more and more.

I thought artificial sweetners would also cause insulin spikes. Theyve done studies that show subjects injesting them then having the same craving effects as sugar.

Besides, they dont bake well. Molecually, it wont work the same as sugar would in say... a batch of brownies. Thought, ive herad it will in some applications or with modifications.

[Grissim Connery]

i've gotten away with splenda in baking situations. it behaves pretty similarly, but i tend to make things that are easier to present. cookies, macaroons, etc. as opposed to cake and such. i hate when a cake doesn't turn out right, so i don't like to gamble with splenda

[Garrett Smith]

Patrick,
The Pottenger "Cat Study", while it has its flaws, shows that genetic damage and nutritional deficiencies accumulate over generations.

I don't think splurging here and there is much of an issue. However, diabetic parents are setting their children up (both by nature and nurture) to be future diabetics.

The Genetics of Diabetes, from the American Diabetes Association

Type 2 diabetes: your child's risk

Type 2 diabetes runs in families. In part, this tendency is due to children learning bad habits eating a poor diet, not exercising--from their parents. But there is also a genetic basis.

In general, if you have type 2 diabetes, the risk of your child getting diabetes is 1 in 7 if you were diagnosed before age 50 and 1 in 13 if you were diagnosed after age 50.

Some scientists believe that a child's risk is greater when the parent with type 2 diabetes is the mother. If both you and your partner have type 2 diabetes, your child's risk is about 1 in 2.

People with certain rare types of type 2 diabetes have different risks. If you have the rare form called maturity-onset diabetes of the young (MODY), your child has almost a 1-in-2 chance of getting it, too.

Note that the first bolded paragraph might be inferred to imply that the sooner the diabetes shows up, the greater the genetic damage, hence the higher risk in the children.

Note that the second bolded paragraph might be inferred to imply that the genetic damage can come from both the father or mother--but the "soup" that the fetus develops in is more important.

[Grissim Connery]

as i stated before, i'm iffy about artificial sweeteners in general, but i was curious as to whether sucralose had an effect on insulin. this is some stuff i found real quick. thought i'd post it.

Lack of effect of sucralose on glucose homeostasis in subjects with type 2 diabetes.
Grotz VL, Henry RR, McGill JB, Prince MJ, Shamoon H, Trout JR, Pi-Sunyer FX.

Medical and Nutritional Affairs, McNeil Nutritionals, New Bruswick, NJ 08903-2400, USA. lgrotz@mspus.jnj.com

OBJECTIVE: To investigate the effect of 3-months' daily administration of high doses of sucralose, a non-nutritive sweetener, on glycemic control in subjects with type 2 diabetes. DESIGN: A multicenter, double-blind, placebo-controlled, randomized study, consisting of a 6-week screening phase, a 13-week test phase, and a 4-week follow-up phase. SUBJECTS/SETTING: Subjects with type 2 diabetes (age range 31 to 70 years) entered the test phase of this study; 128 subjects completed the study. The subjects were recruited from 5 medical centers across the United States and were, on average, obese. INTERVENTION: Subjects were randomly assigned to receive either placebo (cellulose) capsules (n=69) or 667 mg encapsulated sucralose (n=67) daily for the 13-week test phase. All subjects blindly received placebo capsules during the last 4 weeks of the screening phase and for the entire 4-week follow-up phase. MAIN OUTCOME MEASURES: Glycated hemoglobin (HbA1c), fasting plasma glucose, and fasting serum C-peptide were measured approximately every 2 weeks to evaluate blood glucose homeostasis. Data were analyzed by analysis of variance using repeated measures. RESULTS: There were no significant differences between the sucralose and placebo groups in HbA1c, fasting plasma glucose, or fasting serum C-peptide changes from baseline. There were no clinically meaningful differences between the groups in any safety measure. CONCLUSIONS: This study demonstrated that, similar to cellulose, sucralose consumption for 3 months at doses of 7.5 mg/kg/day, which is approximately three times the estimated maximum intake, had no effect on glucose homeostasis in individuals with type 2 diabetes. Additionally, this study showed that sucralose was as well-tolerated by the study subjects as was the placebo.

Glycemic effect of a single high oral dose of the novel sweetener sucralose in patients with diabetes.
Mezitis NH, Maggio CA, Koch P, Quddoos A, Allison DB, Pi-Sunyer FX.

Division of Endocrinology, Diabetes and Nutrition, St. Luke's-Roosevelt Hospital Center, New York, NY 10025, USA. nhm2@columbia.edu

OBJECTIVE: To examine the effect of a single high oral dose of the novel noncaloric sweetener sucralose on short-term glucose homeostasis in patients with IDDM or NIDDM. RESEARCH DESIGN AND METHODS: A total of 13 IDDM and 13 NIDDM patients with glycosylated hemoglobin levels < 10% completed this double-blind cross-over study. After an overnight fast, patients were administered opaque capsules containing either 1,000 mg sucralose or cellulose placebo, followed by a standardized 360-kcal liquid breakfast. Plasma glucose and serum C-peptide levels were measured over the next 4 h. RESULTS: Regardless of the type of diabetes, areas under the curves for changes of plasma glucose and serum C-peptide levels after sucralose administration were not significantly different from those after placebo. During test meals with sucralose, one episode of symptomatic hypoglycemia occurred in each of three IDDM patients, but these episodes were not considered the result of sucralose administration. CONCLUSIONS: The present results support the conclusion that sucralose consumption does not adversely affect short-term blood glucose control in patients with diabetes.

Fujita Y, Wideman RD, Speck M, Asadi A, King DS, Webber TD, Haneda M, Kieffer TJ.

Asahikawa Medical College.

Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are released during meals from endocrine cells located in the gut mucosa and stimulate insulin secretion from pancreatic beta-cells in a glucose-dependent manner. Although the gut epithelium senses luminal sugars, the mechanism of sugar sensing and its downstream events coupled to the release of the incretin hormones are not clearly elucidated. Recently it was reported that sucralose, a sweetener that activates sweet receptors of taste buds, triggers incretin release from a murine enteroendocrine cell line in vitro. We confirmed that immunoreactivity of alpha-gustducin, a key G-coupled protein involved in taste sensing, is co-localized with GIP in rat duodenum. We investigated whether secretion of incretins in response to carbohydrates is mediated via taste receptors by feeding rats the sweet tasting compounds saccharin, acesulfame potassium, D-tryptophan, sucralose, or stevia. Oral gavage of these sweeteners did not reduce the blood glucose excursion to a subsequent intraperitoneal glucose tolerance test. Neither oral sucralose nor oral stevia reduced blood glucose levels in Zucker diabetic fatty rats. Finally, whereas oral glucose increased plasma GIP levels ~4-fold and GLP-1 levels ~2.5-fold post administration, none of the sweeteners tested significantly increased levels of these incretins. Collectively, our findings do not support the concept that release of incretins from enteroendocrine cells is triggered by carbohydrates via a pathway identical to the sensation of 'sweet taste' in the tongue. Key words: GLP-1, GLP-2, K-cell, L-cell.

[Patrick Yeung]

Originally Posted by Grissim Connery

as i stated before, i'm iffy about artificial sweeteners in general, but i was curious as to whether sucralose had an effect on insulin. this is some stuff i found real quick. thought i'd post it.

Well then.... Fine!

No seriously, the article I read was more about how the subjects who had eaten the sweetners would get the same hunger pangs that would be similar to those after a sugar spike.

Arent there different types of sweetners too? I know they are all made differently. Some are sugar derrivatives, and others are completely chemical. Ill have to dig deeper when I get a chance.

And Garret, since Type 2 diabities is reversable/controllable in many cases, its still hard for me to see it as genetically linked. I feel as though a lot of it is more the nurture side than the nature side. Cases of this type of diabities has gone way up in these modern times than has been historically recorded. Too bad they dont have a way to weight the two and show how much of each effects their children.

Thanks though, thats an awesome find.

[Scott Kustes]

Patrick, don't forget about epigenetics...methylations on the genes can determine which are on or off, i.e., which are expressed. DNA itself is only part of the onion.

[Garrett Smith]

Patrick,
I'm very much of the same opinion as you on Type II diabetes and nutrition (nurture).

Genetic "damage" (nature) would simply make it occur with more ease (as in, those susceptible folks would have to keep an even tighter diet than others without it).

Nutrition turns genes on and off, absolutely.

[Joyce Behrendt]

The Pima Indians have a high rate of diabetes.

http://forecast.diabetes.org/magazin...file/work-pima

In my family, my Mom's side is obese and has other symptoms of metabolic syndrome, but no diabetes. My Dad was fairly active and fit, but got type 2 diabetes at 60. Several members of his family, as well as myself and two brothers all have type 2 diabetes. So genetics plays a part in addition to diet. But all those mashed potatoes we ate growing up didn't help either.

[Patrick Yeung]

Yeah but the study was done in 1960s....

Not really sure what you were tryin to get at with it, but theres a lot they arent saying. (i just glanced the article)

I remember watching a video specifically on them because of their diabities and health problems that were begining to develop. Also, many of them were begining to gain a lot of weight. They sourced it to white bread that was being given to them.

Once their lands had been taken, all their natural resources and means of food were gone, and we herded them into camps, they had to eat what we gave them. White flour.

It also had pictures of them like, before and after. THe video went on to show many other native groups falling to the same fate. Look at whats been goin on in the Mediteranian lately. After all the fast food and ice cream parlors started poppin up everywhere, their health has gone to hell, with diabities on the rise.

The video was on Crossfit Endurance, but I cant get to it from work.
(Good thing PM isnt blocked!)