Re: FW: High-protein diets not advised for diabetics

[Guest guest]

Ok...a little research to back these claims that this diet is dangerous

would be nice....

I'm a dietitian myself and this is the same old argument I've heard from

my profession for the past 10 years regarding high protein diets. No

research to back this up though.

The point is, losing weight (by whatever means) and KEEPING it off

(whether by the traditional ADA diet, low carbing, exercise, etc. etc.)

greatly lessens the dangers of heart disease, kidney failure, stroke,

etc. etc.

Gail

[Guest guest]

> I don't think this one can be accurate

> because on Atkins my blood sugars normalize

> completely. ...

> I would like to see more on the other reports

> though.

Here are the abstracts for the two references [12, 13] that I gave on

the subject of relation between high protein diet and insulin

resistance:

Abstract for [12] is at:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

cmd=Retrieve & db=PubMed & list_uids=8923841 & dopt=Abstract

J Clin Endocrinol Metab 1996 Nov;81(11):3938-43

Effect of dietary protein intake on insulin secretion and glucose

metabolism in insulin-dependent diabetes mellitus.

Linn T, Geyer R, Prassek S, Laube H

Diabetology and Metabolism Unit, Justus Liebig University, Giessen,

Germany.

Adult-onset insulin dependent diabetes mellitus (IDDM) is associated

with significant residual insulin secretion. The process leading to

the ultimate destruction of B cells may be influenced, among other

factors, by the quality and amount of ingested protein. Using a

standardized food questionnaire, we matched 13 individuals with

normal protein (NP; 0.74 0.08 g/kg.day) and high protein (HP; 1.87

0.26 g/kg.day) intake from a sample of 117 newly diagnosed IDDM

patients according to sex, age, body mass index, and energy intake.

Nondiabetic control subjects were also selected. Dietary habits did

not change significantly over an observation period of 1 yr. Glucagon-

stimulated C peptide was significantly higher in the NP compared to

the HP group (0.71 0.06 vs. 0.50 0.04 nmol/L; P < 0.002). NP food was

associated with higher overall insulin sensitivity in both patients

and nondiabetic subjects. Hepatic glucose output was significantly

increased in individuals with HP intake [HP IDDM, 14.8 0.6 vs. NP

IDDM, 12.7 0.7 (P < 0.01); HP control, 12.2 0.5 vs. NP control, 10.9

0.5 (P < 0.01 mumol/kg.min). Insulin-mediated suppression of hepatic

glucose production was impaired in diabetic patients with high

protein intake, but not in patients with normal protein diet.

Gluconeogenesis estimated from 13C enrichment in breath and plasma

was increased in individuals on a HP diet. We conclude that a NP diet

is accompanied by delayed progression of the continuous loss of

endogenous insulin in IDDM. This phenomenon is possibly due to

decreased insulin demand on the B cells and/or reduced hepatic

glucose production favoring enhanced insulin sensitivity.

PMID: 8923841, UI: 97082605

Abstract for [13] is at:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Display & DB=PubMed

Metabolism 1996 Dec;45(12):1483-6

A moderate increase in daily protein intake causing an enhanced

endogenous insulin secretion does not alter circulating levels or

urinary excretion of dehydroepiandrosterone sulfate.

Remer T, Pietrzik K, Manz F

Research Institute of Child Nutrition, Dortmund, Germany.

To study the effect of a moderate increase in insulin secretion

produced by an increased daily protein intake on

dehydroepiandrosterone sulfate (DHEAS), a balanced randomized

crossover trial consisting of three strictly controlled dietary

regimens was performed in six healthy male volunteers. The basic diet

( contained 50 g protein/d; diets P and M (also basic diets) were

enriched with either 32 g protein/d (P) or 10 mmol L-methionine/d

(M). Methionine was given (as a specific nonprotein source of

endogenously derived sulfate) to control for possible confounding

effects on DHEAS due to an increased sulfate supply. At the end of

each 4-day diet period, blood and 24-hour urine samples were

collected. Fasting plasma levels of testosterone, cortisol, insulin-

like growth factor-I (IGF-I), and insulin, as well as urinary output

of total (hot acid-cleaved) testosterone conjugates and 3alpha-

androstanediol glucuronide, did not show significant changes in

response to dietary manipulations. Endogenous sulfate availability

(as reflected by renal sulfate output per 24 hours) approximately

doubled with diets P and M. However, plasma levels (6.3 1.5, 6.8 1.8,

and 6.9 2.1 micromol/L for B, P, and M, respectively) and urinary

excretion (8.8 9.8, 9.4 11.2, 8.0 8.3 micromol/d) of DHEAS remained

unaffected. Considering the clear increments (P < .01) in urinary C-

peptide excretion with diet P (20.4 10.3 nmol/d) versus diets B and M

(12.6 5.1 and 13.2 3.6 nmol/d), respectively, our results suggest

that a moderately strong diet-induced increase in daily insulin

secretion does not alter urinary and plasma levels of DHEAS.

I hope that you can draw some conclusion from those.

Regards

Thornton

Pforzheim, Germany