Diabetes, Insulin and Peat Plan Adjustments

[Asimov]

Read the 50 or comments of diabetics saying "I went low carb, hba1c dropped X points, got off insulin". Go there and tell them how ******* retarded they are.

I'm sure anonymous internet comments are what we should base our conclusions on. Those people are ******* retarded, you and them don't get why low carb works in the short term. Here's a pro-tip, your eating barely any carbs hahaha. It won't help you ever be able to eat more carbs, the opposite actually. I guarantee most of those "50 commenters" can't pass a OGTT.

Still waiting on those 80 studies that show honey is superior to fruits, that's pretty important info

Of course they can't pass an OGTT....they're ******* diabetics They can't tolerate glucose......which is exactly ******* why I'm saying they SHOULDN'T consume glucose. Do you even realize how massively you're contradicting yourself??? You're saying flat out "those people can't tolerate glucose....so they should consume a bunch of glucose". It astounds me that people would hold your advice with any regard. You're genuinely not very intelligent.

Just because you are starving yourself of sugar(low carb) and blood sugar levels go down does not mean you "cured" your diabetes. It means you are starving yourself of sugar. :2cents

I agree. But what it does do is...

A) allows the diabetic to get OFF insulin (which is a worthwhile goal in and of it's self)
B) allows them to improve body composition (which is a worthwhile goal in and of it's self)
C) reduce systemic inflammation, and
D) (most importantly) buy them some healthy time to reduce iron levels which improves the bodies response to insulin, allowing them actually CURE diabetes

As I mentioned, high iron levels are the most likely cause of diabetes, not carbs (this is important, because this thread turned into a debate about sugar consumption. However, my MAIN point was that high iron is the driver of diabetes.) The low carbs are a temporary fix to keep your blood sugar values in control while you attack the root cause of the problem. It's no different than putting a cast on a broken arm. Yes....the cast is compensating for a physiological problem. And no, it has NOTHING to do with healing the problem. What it does is sets up a safe environment where your body can fix the problem without risking further damage.

These are things that staying on a high sugar diet will NOT do. As evidence by diabetes support groups across the country, the people who eat high carbohydrates never do as well as those who go low carbohydrate. Studies and informal observation has shown the same thing time and time again: those on high carbohydrate diets use more insulin, gain more fat, and are generally less healthy than those who go low carb. The root cause of the problem is iron and liver damage, but in between the time when you start your diet and your liver repairs, low carb is absolutely the way to go for the best quality of life.

So I reiterate for the original poster: Phlebotomy, copper, low carb consumption save pure fructose and/or honey, vitamin E and C supplementation, and lots and lots and lots of saturated fat.

 

[Jenn]

Just because you are starving yourself of sugar(low carb) and blood sugar levels go down does not mean you "cured" your diabetes. It means you are starving yourself of sugar. :2cents

What he said.

High blood sugar is NOT the problem, it is merely a symptom. The problem is the sugar is not completing its cycle, not getting into the cells that need it. True diabetics are sugar starved and protein deficient. Just because you eat it, doesn't mean your body can use it. For a lot of people, simply increasing potassium (in a USABLE form) and making sure to have it WITH the sugar makes a huge difference. For some people, it is possible to have so much damage from PUFA's that even the potassium doesn't help in the beginning. The body NEEDS potassium to get the glucose into the cells. The muscles don't need potassium to utilize glucose, so that why "diabetics" respond so well to excercise.

A serving of wheat contains 50-100 mg of potassium and is only glucose (if it's actually digested properly). A serving of OJ is 450+- mg and is half glucose and half fructose. It is balanced, grain is not. So reducing GRAINS can be very beneficial for a diabetic. The SAD is a grain based diet. Not all carbs are created equal and behave differently in the body.

Insulin is a protein made by the pancreas. Insulin production is a MINOR part of what the pancreas does. Enzyme production and pH maintenance of the intestines is it's main job.

Avoiding PUFA's and focusing on gelatin (to repair PUFA damage) and enough potassium are crucial. Niacinimide is good, most diabetics are deficient.

 

[jyb]

Avoiding PUFA's and focusing on gelatin (to repair PUFA damage) and enough potassium are crucial. Niacinimide is good, most diabetics are deficient.

Did you have anything specific in mind when saying gelatin repairs pufa damage? I only know vaguely from RP articles that it acts like an anti-serotonin and prevents further damage from tryptophan, and I've read on this forum that it helps heal the gut.

 

[Mittir]

Avoiding PUFA's and focusing on gelatin (to repair PUFA damage) and enough potassium are crucial. Niacinimide is good, most diabetics are deficient.

Did you have anything specific in mind when saying gelatin repairs pufa damage? I only know vaguely from RP articles that it acts like an anti-serotonin and prevents further damage from tryptophan, and I've read on this forum that it helps heal the gut.

Gelatin has tons of special health benefits. I found several articles showing gelatin( a rich source of glycine) improving many diabetic problems. Gelatin helps to boost Glutathione in diabetes patients. Selenium is also needed to increase Glutahione . Diabetics are very low in Glutathione, it is a major anti-oxidant. Thus it helps to protect against free radicals and lipid peroxidation damages done by PUFA. Gelatin also lowers high blood pressure and free fatty acids. You can get tons of good article if you search 'Glycine + Diabetes , glycin + glutathione etc)


Diabetes Care. 2011 Jan;34(1):162-7. doi: 10.2337/dc10-1006. Epub 2010 Oct 7.
Glutathione synthesis is diminished in patients with uncontrolled diabetes and restored by dietary supplementation with cysteine and glycine.
Sekhar RV, McKay SV, Patel SG, Guthikonda AP, Reddy VT, Balasubramanyam A, Jahoor F.
SourceTranslational Metabolism Unit, Baylor College of Medicine, Houston, Texas, USA. [email protected]


Abstract
OBJECTIVE: Sustained hyperglycemia is associated with low cellular levels of the antioxidant glutathione (GSH), which leads to tissue damage attributed to oxidative stress. We tested the hypothesis that diminished GSH in adult patients with uncontrolled type 2 diabetes is attributed to decreased synthesis and measured the effect of dietary supplementation with its precursors cysteine and glycine on GSH synthesis rate and oxidative stress.

RESEARCH DESIGN AND METHODS: We infused 12 diabetic patients and 12 nondiabetic control subjects with [²H₂]-glycine to measure GSH synthesis. We also measured intracellular GSH concentrations, reactive oxygen metabolites, and lipid peroxides. Diabetic patients were restudied after 2 weeks of dietary supplementation with the GSH precursors cysteine and glycine.

RESULTS: Compared with control subjects, diabetic subjects had significantly higher fasting glucose (5.0 ± 0.1 vs. 10.7 ± 0.5 mmol/l; P < 0.001), lower erythrocyte concentrations of glycine (514.7 ± 33.1 vs. 403.2 ± 18.2 μmol/l; P < 0.01), and cysteine (25.2 ± 1.5 vs. 17.8 ± 1.5 μmol/l; P < 0.01); lower concentrations of GSH (6.75 ± 0.47 vs. 1.65 ± 0.16 μmol/g Hb; P < 0.001); diminished fractional (79.21 ± 5.75 vs. 44.86 ± 2.87%/day; P < 0.001) and absolute (5.26 ± 0.61 vs. 0.74 ± 0.10 μmol/g Hb/day; P < 0.001) GSH synthesis rates; and higher reactive oxygen metabolites (286 ± 10 vs. 403 ± 11 Carratelli units [UCarr]; P < 0.001) and lipid peroxides (2.6 ± 0.4 vs. 10.8 ± 1.2 pg/ml; P < 0.001). Following dietary supplementation in diabetic subjects, GSH synthesis and concentrations increased significantly and plasma oxidative stress and lipid peroxides decreased significantly.

CONCLUSIONS: Patients with uncontrolled type 2 diabetes have severely deficient synthesis of glutathione attributed to limited precursor availability. Dietary supplementation with GSH precursor amino acids can restore GSH synthesis and lower oxidative stress and oxidant damage in the face of persistent hyperglycemia

The metabolic response to ingested glycine1–3

Mary C Gannon, Jennifer A Nuttall, and Frank Q Nuttall
ABSTRACT
Background: The metabolic effects of dietary protein are complex.
In persons with type 2 diabetes, protein ingestion results in
little or no increase in plasma glucose concentrations but a stimulation
of insulin and glucagon secretion. Furthermore, when protein
is ingested with glucose, a synergistic effect on insulin secretion
is observed. The most potent protein is gelatin, which consists
of 30% glycine residues.
Objective: The objective of the present study was to determine
whether glycine per se stimulates insulin secretion or reduces the
glucose response when ingested with glucose.
Design: Nine healthy subjects were tested on 4 separate occasions.
Plasma glucose, insulin, glucagon, and glycine concentrations
were measured at various times during a 2-h period after the
ingestion of 1 mmol glycine/kg lean body mass, 25 g glucose,
1 mmol glycine/kg lean body mass + 25 g glucose, or water only,
given in random order.
Results: Plasma concentrations of glycine and glucagon were elevated
after the ingestion of glycine, as expected. The serum insulin
concentration also was slightly elevated after the ingestion of
glycine alone. When glycine was ingested with glucose, the
plasma glucose area response was attenuated by > 50% compared
with the response after the ingestion of glucose alone. The dynamics
of the insulin response after the ingestion of glycine plus glucose
were modestly different from those after the ingestion of glucose
alone, but the area response was not significantly different.
Conclusion: The data are compatible with the hypothesis that oral
glycine stimulates the secretion of a gut hormone that potentiates the
effect of insulin on glucose removal from the circulation. Am J
Clin Nutr 2002;76:1302–7.
KEY WORDS Glycine, insulin, glucose, glucagon, gut
hormones, incretin, amino acids

 

[Asimov]

High blood sugar is NOT the problem, it is merely a symptom. The problem is the sugar is not completing its cycle, not getting into the cells that need it. True diabetics are sugar starved and protein deficient.

If by "true diabetrics" you mean people with Type I diabetes, then you're correct.

However, what you're describing is not the pathology of Type II diabetes, which is what the original poster has. T2DM patients, by diagnosis, aren't sugar starved, they're sugar stuffed.

The treatments are very very different.