3 replies to this topic

[R.S.]

So let's say I eat a piece of white bread, a high glycemic food. How long after eating it will my pancreas begin producing insulin to curb blood sugar levels?

[SweetJade1980]

So let's say I eat a piece of white bread, a high glycemic food. How long after eating it will my pancreas begin producing insulin to curb blood sugar levels?

LOL, why didn't anyone else take this question?

As soon as your food has been broken down, glucose will reach the liver and the liver will tell the pancreas to release insulin. However, small amounts of Insulin is contstantly present in the blood stream. Whenever you consume 100mg of Glucose your pancrease releases more Insulin. In a normal person blood glucose levels peak in 1 hr and then are back to normal by the 2nd hour. For someone with Type I or II Diabetes or Insulin Resistance this may be not be the case.

So we've always heard that Insulin Resistance means that we aren't sensitive to normal amounts of insulin, right? Well that could be for a multitude of reasons, and sometimes....the reason may be that the insulin we produce is defective. Hence why you may have heard that some Type II Diabetics, IRs, and even acne patients improve on Insulin injections!

What? How can that be? Well, it has to do with our bodies' feedback mechanisms. If something is defective your body will keep producing and producing until the desired affect has been achieved (...or it won't be able to produce at all). Yet since it's defective that effect won't occur....but a cascade of other undesirable effects will (inflammation, excess androgens, etc). So by taking Insulin injections you are beating your pancreas to the punch! That way you aren't producing too much defective insulin, you are getting good insulin that works to get the sugar where it needs to go, and those cascade of other events will occur at a more normal level. LOL, so Insulin is not always the bad guy.

Now the problem comes in with Insulin and IGF-1 (can also be defective), when these hormones or growth factors aren't defective. In which case the problem may be that our Insulin and IGF-1 receptors on our liver, muscle, and adipose (fat) cells are defective (or already full). If this is the case, the pancrease is going to keep continuously secreting enough Insulin in order to get the job done. Thus, the cascade of unwanted effects will also follow.

Now, something I discovered the other day, may answer the question of how sugar can be inflammatory. We know there are different ways that sugar can spark inflammation through insulin, but just the process of metabolizing sugar also has it's own end result!. I've heard about AGEs a few times but never really investigated until I came across this article below the other night. It talks about how Glycated Insulin is associated with diseases such as Diabetes, Insulin Resistance etc and that Glycated Insulin will be present in the blood stream after a meal before regular insulin appears!

Horm Metab Res. 2006 Feb;38(2):94-7. Related Articles, Links


Meal-dependent regulation of circulating glycated insulin in type 2 diabetic subjects.

McKillop AM, Lindsay JR, Au S, Mahood KI, O'Harte FP, Flatt PR, Bell PM.

School of Biomedical Sciences, University of Ulster, Coleraine, Northern Ireland. am.mckillop@ulster.ac.uk

There is mounting evidence that elevated circulating concentrations of glycated insulin play a role in insulin resistance in type 2 diabetes. This study evaluated the secretion of glycated insulin in response to enteral stimulation in type 2 diabetic subjects. Following a mixed meal (450 kcal; 44 % carbohydrate; 40 % fat; 16 % protein), glycated insulin rose 10-fold to peak (60 min) at 104.5 +/- 25.0 pmol/l (p < 0.001), representing 22 % total circulating insulin. The response paralleled early rises in insulin and C-peptide, which peaked at 90 min and were more protracted. Maximum glucose concentrations were observed at 50 min. These data indicate that type 2 diabetic subjects exhibit a rapid meal-induced release of glycated insulin from readily releasable pancreatic beta-cell stores, which might contribute to impaired glucose homeostasis following enteral nutrition.

PMID: 16523409 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

Ann N Y Acad Sci. 2005 Jun;1043:452-60. Related Articles, Links


Advanced glycation in health and disease: role of the modern environment.

Vlassara H.

Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA. helen.vlassara@mssm.edu

It is believed that intracellular and extracellular advanced glycation (AGEs) or lipoxidation end products (ALEs), together with dysregulated glucose and lipid metabolism, are important contributors to oxidant or carbonyl stress, enhanced cellular redox-sensitive transcription factor activity, and impaired innate immune defense, causing over time inappropriate inflammatory responses. However, neither the magnitude nor the persistent nature of this increased prooxidant state are completely understood. A significant correlation has been found between ingested and circulating AGEs in humans in recent years. Based on animal studies, the injurious impact of diet-derived AGEs to vascular and kidney tissues is estimated to rival or even exceed that caused by hyperglycemia or hyperlipidemia. Consistent with this view, dietary AGE restriction has been associated with suppression of several immune defects, insulin resistance, and diabetic complications, whether genetically or diet induced, despite persistent diabetes. These findings are in support of clinical evidence from subjects with diabetes or vascular or kidney disease. Most recently, evidence from animal studies points to AGE restriction as an effective means for extending median life span, similar to that previously shown by marked caloric restriction. We conclude that excessive AGE consumption, in the current dietary/social structure, represents an independent factor for inappropriate oxidant stress responses, which may promote the premature expression of complex diseases associated with adult life, such as diabetes and cardiovascular disease.

Publication Types:
Review

PMID: 16037266 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum


In layman's terms (didn't think I'd hear about Maillard browning in anything other than nutrition):

ANTIOXIDANTS-PREVENTION AGAINST AGING

BENFOTAMIN--CARAMELIZATION OF THE FLESH [eww]

Its not just any antioxidant...you need ones which fight... Advanced Glycation Endproducts, or "AGEs" as they're appropriately called, are the end result of the complex chemical process through which the structure of proteins is warped by exposure to sugars or by other, much more reactive molecules. AGE chemistry is the cause of the "browning" you see when you roast a chicken or make toast, but the same "browning" chemistry is at work in your body every day of your life. In your arteries. In your kidneys. In your heart, your eyes, your skin, your nerves. In every cell, the sugar that your body uses for fuel is busily at work at this very moment, caramelizing your body through exactly the same chemical processes that caramelize onions or peanut brittle. Its this chemistry which changes nerve tissue and facilitates the change in senses in aging.

Glycation math is simple: more sugar equals more AGE'd proteins. As a result, people with diabetes begin to feel the effects of glycation at much younger ages than do people with more normal blood sugar levels. Watching people with diabetes age is like watching "normal" aging played on fast-forward.

Slowly, imperceptibly, AGE reactions create chemical handcuffs which gum up your proteins, deactivate your enzymes, trigger unhealthy biochemical signaling in your cells, and damage your DNA. Aging you. This is also partially why low carbohydrate diets work well for some people and those with neurological problems such as autism, Alzheimer's, and even heavy metal toxicity.

Two Ways to AGE

There are two major ways that AGEs can form inside the body. One way is through a simple series of chemical reactions known as the "Maillard Pathway," known from food chemistry for a century.

But more recently, scientists have come to understand another pathway of AGE formation - a distinctly biological pathway, which only occurs within your cells because of the body's metabolism of carbohydrates.

When blood sugar levels rise, some key kinds of cell - including nerve cells (neurons) and the cells that make up the fine blood cells of the retina of the eye and the filtering units (glomeruli) of the kidney - are also flooded with glucose. The resulting high sugar levels within these cells cause a logjam in the normal cellular metabolism of glucose

This backlog results in a buildup within the cell of super-reactive glucose-metabolic intermediates known as triosephosphates. And once that happens, the excess triosephosphates attack the surrounding proteins, lipids, and DNA, causing AGE damage from within the heart of the cell. It's these cells are thus the most vulnerable to the complications of diabetes and other functional disorders.

Drugs do exist which can inhibit the formation of AGE, but none are available on the market as yet, and one of the most promising candidate (aminoguanidine) has shown signs of toxicity in human trials so therefore appears to have been abandoned by its developers.

On the other hand, some companies are selling supplements are marketed as "AGE-inhibitors." But while many of the herbs and other nutrients may be valuable, and many even inhibit AGEing in a test tube, there's no evidence that most of these "AGE-blocking" antioxidants have any effect on prevention against AGEing in your body at the dosages used.
Just more myths and aging....possibly.

Examples include thyme extract, inositol, acetyl-L-carnitine, taurine, and a whole host of antioxidants (including n-acetyl-cysteine (NAC) and flavonoids, such as quercetin and resveratrol).
http://www.y2khealthanddetox.com/bft.html

For those of you that want a more technical explanation, here's an excerpt:

Protein glycation and AGE formation are accompanied by increased free radical activity that contributes to the bimolecular damage in diabetes (1, 13, 23). AGEs act as mediators and can initiate a wide range of abnormal responses in cells and tissues such as the inappropriate expression of growth factors, alterations in growth dynamics, accumulation of extra-cellular matrix and initiation of cell death (21, 23), through decreased solubility, elasticity and enzymatic affinities in long-living proteins such as collagen (8, 15).

http://www.jyi.org/research/re.php?id=575

Maillard reaction products in food as pro-inflammatory and pro-arteriosclerotic factors of degenerative diseases, 2005

http://www.ncbi.nlm.nih.gov/entrez/query.f...l=pubmed_docsum

Now some articles I came across mentions the use of Benfatomine, a form of B1 and there's also a form of B6 that's supposed to be good as well. Otherwise I think I saw some info on Carnosine. I guess one day that's something else to research I hope my much longer than anticipated answer, helped you out a bit....

Of course, I'd appreciate further clarification from our other members

Take care!

[SweetJade1980]

To further answer your "how soon" response, I know that Semi-Refined Wheat will have a more rapid and increased insulin response than will Semi-Refned Rice. This is because, well the authors of the study theorized it was due to their different types of starch.

There are two types of starch:

Amylose - Slowly metabolized. Found in 20% of plant foods.

Amylopectin - Quickly metabolized and found over 80% of plant foods.

Otherwise, I'm not really the person to ask about Glycemic Levels, because other than straight sugar(s), I don't really look at food in that sense. My body doesn't react to foods in that way, at least not in terms of the symptoms I'm able to visibly see or feel.

Glycemic Loads, Index, or Insulin Index for me is most relevant when we are talking about 100% Fruit Juice, ADDED sugars, and Dairy (I'm extremely sensitive). Otherwise the foods I think I can eat and the foods I know I must avoid, don't really fall into the above with regards to how one should treat a Glucose Intolerance (Diabetes, Insulin Resistance). Hence, why you are hearing me speak more about chronic inflammation, food intolerances and how the two can impair glucose metabolism.

Although, this fall semester I will be studing Advanced Nutrition, Diet Therapy I, among some other courses, and doing some Field Experience so you can probably ask me this question again I'll be able to give you a much more proper, ADA approved, educated response!

Take care.


P.S. Here's the article (there's 2 on pubmed covering this)

Cornell-China study suggests rice-based diet
FOR RELEASE: March 25 1996
Contact: Susan Lang
Office: (607) 255-3613
E-mail: SSL4@cornell.edu

ITHACA, N.Y. -- A diet based on wheat foods such as pasta, bread and cereal may be contributing to this nation's soaring rates of diabetes, obesity, high blood pressure, high cholesterol and coronary heart disease, according to a new Cornell University study.

On the other hand, rice-based diets, and to a lesser extent fish and green vegetables, appear to lower the level of blood values associated with the risk of these diseases. These findings, published in the January 1996 issue of the American Journal of Clinical Nutrition, come from the Cornell-China-Oxford Project on Nutrition, Health and Environment, a massive survey across the far reaches of China that investigates more diseases and dietary characteristics than any other study to date.

In 3,250 Chinese women living in widely dispersed rural counties, the researchers examined the relationship of various foods with a specific set of biochemical blood tests that have been shown to be commonly linked with diabetes, obesity, high blood pressure and coronary heart disease -- otherwise collectively known as the "insulin resistance syndrome."

"We found that the pattern of blood biochemistries of people in the northern part of China who eat a predominantly wheat- based diet resemble those in people with insulin resistance," said Jeffrey Gates, who has a doctorate in health sciences and works in Cornell's Division of Nutritional Sciences; he collaborated with T. Colin Campbell, the Cornell biochemist and director of the China project, Banoo Parpia, Cornell research associate, and Chen Junshi of the Chinese Academy of Preventive Medicine in Beijing.

This pattern includes higher insulin, higher triglycerides, and lower sex hormone binding globulin (a measure of insulin resistance).

"The Chinese women in the south, on the other hand, eat a rice-based diet and have a pattern of blood values that would be considered low risk," Gates added.

In the past couple of decades, many studies have pointed to insulin as being a common factor linking such diverse disorders as high blood pressure, diabetes and coronary heart disease. Recent research also has discovered that sex hormone binding globulin (SHBG), a relatively unknown blood protein, is a reasonably good indicator of insulin resistance. Low levels of SHBG are consistently linked to high levels of insulin in the body. Sustained high levels of insulin are, in turn, associated with the development of the chronic diseases mentioned above.

The Cornell researchers, therefore, looked at SHBG, triglycerides, cholesterol, insulin, testosterone, glucose and 21 different food groups. Factors commonly associated with insulin resistance, such as meat consumption, smoking, and weight were controlled for in the analysis.

"Though other foods such as fish and green vegetables were associated with changes in blood parameters studied, the strong effects of rice and wheat on SHBG were remarkable and unexpected," Gates said. "Women in the northern, wheat- eating counties consistently had low HDL levels, high triglycerides, and low SHBG, all suggestive of insulin resistance. Evidently, rice and wheat can have significantly different effects on the important biochemical parameters we measured." Interestingly, both the rice and wheat consumed in these Chinese regions are semi-refined. Gates stressed, however, that while rice and wheat appear to make the biggest impact on SHBG and insulin, certain other foods in the Chinese meal also have an important effect on SHBG and insulin changes in the blood, and thus ultimately, on those diseases associated with insulin resistance.

Gates speculates that "the differing effects of wheat and rice on SHBG and insulin may be due to the difference in amylose content, a particular kind of starch." Other researchers have found that some rice varieties have higher amylose content than wheat; some rices, on the other hand, have comparable levels.

"Several recent studies have shown that starches with higher amylose content slow down glucose absorption and thus reduce the insulin response of the meal," Gates added. "Clearly, the effects of wheat or rice on insulin response must not be isolated from the important influence of other dietary and lifestyle factors such as fat and exercise. However, this study lends support to the idea that certain starches may play an important role in the development of insulin resistance and thus increase an individual's risk for diabetes, hypertension, and coronary artery disease." -30-
http://www.news.cornell.edu/releases/March....wheat.ssl.html

SHBG is a protein that binds Free Androgens/Testosterone so that they aren't active in the body. So in a system where androgen levels are high (i.e. Hyperandrogenism), SHBG levels will be low. Just like this article stated, in a system where Insulin levels are high, SHBG levels will also be low. Thus why some studies mention using SHBG levels as a marker for Insulin Resistance

Of course this also depends on the age and gender of the individual as these diets regulate hormones based on what's appropriate at a given time in life.

(It's a study that hasn't been further replicated and because of it's age, I wonder if maybe they got something wrong. Then again look at the results some of us have acheived....so why no clinically controlled replications?)

[LuckyMan]

For those of you that want a more technical explanation...

rubber sheep Its too variable to give a very accurate answer but roughly for white bread, it's about 15-20 mins.