Re: Data on negative outcomes of High Protein Low Carb diets (was diabetes treatments of yesterday)
- From: Alan S <loralgtweightandcarbs@xxxxxxxxx>
- Date: Mon, 29 Oct 2007 08:34:09 +1100
On Sun, 28 Oct 2007 15:59:49 -0500, Jefferson
<fwroy@xxxxxxxxxxxxxxxxxxxx> wrote:
Hi Randy:(8-iso-PGF2
Here's some recent data on negative outcomes of "Low Carb, High
Protein" diets.
I think you are going to need to develop a better argument. All of these
articles do not support your contention. Also reduced IGF-1 levels are
not always a good thing for health.
The title to that relates to the link above. See the statement that
European Journal of Clinical Nutrition (2007) 61, 575-581
Full paper available here - http://www.nature.com/ejcn/journal/v61/n5/pdf/1602557a.pdf
includes the capitalized NONSIGNIFICANT below.
"Low-carbohydrate–high-protein diet and long-term
survival in a general population cohort"
The study was conducted for ten years and had a good size sample. "From
the remaining 26,331 volunteers, 3,387 (13%) were excluded, because at
enrollment had coronary artery disease, diabetes mellitus, cancer or a
combination of these diseases." The subjects were not people with
diabetes or coronary artery disease. Sorry, the wrong population for
this newsgroup.
"Results: During 113 230 persons years of follow-up, there were 455
deaths. In models with energy adjustment, higher intake of
carbohydrates was associated with significant reduction of total
mortality, whereas higher intake of protein was associated with
NONSIGNIFICANT increase of total mortality (per decile, mortality ratios
0.94 with 95% CI 0.89 –0.99, and 1.02 with 95% CI 0.98 –
1.07 respectively)." There was an increase risk of .13 from the lowest
to the highest quintile.
(SNIPPED)
Conclusion: Prolonged consumption of diets low in carbohydrates and
high in
protein is associated with an increase in total mortality.
2. High Protein diets increase IGF which might have negative
consequences:
See: http://www.hon.ch/News/HSN/536486.html
Calorie restriction was a big part of the low-protein, low-calorie diet
diet. The Western diet was likely to be high carbohydrate. Also note
That "people in the first group averaged a daily intake of 0.73 grams of
protein per kilogram of body weight. The runners ate 1.6 grams, and
sedentary people ate 1.23 grams of protein a day. The recommended daily
allowance for protein intake is 0.8 grams, Fontana said. That's about
three ounces of protein per day for a 220-pound man." An average size
man is 70 kilograms (2.2 x 70=154 lbs.) .73x70=51 grams and 1.6x70=112
grams.
"Results: BMI was lower in the low-protein, low-calorie diet (21.3 ±
3.1) and runner (21.6 ± 1.6) groups than in the Western diet (26.5 ±
2.7; P < 0.005) group. Plasma concentrations of insulin, free sex
hormones, leptin, and C-reactive protein were lower and sex
hormone–binding globulin was higher in the low-protein, low-calorie diet
and runner groups than in the sedentary Western diet group (all P <
0.05). Plasma insulin-like growth factor I (IGF-I) and the concentration
ratio of IGF-I to IGF binding protein 3 were lower in the low-protein,
low-calorie diet group (139 ± 37 ng/mL and 0.033 ± 0.01, respectively)
than in the runner (177 ± 37 ng/mL and 0.044 ± 0.01, respectively) and
sedentary Western (201 ± 42 ng/mL and 0.046 ± 0.01, respectively) diet
groups (P < 0.005).
Conclusions: Exercise training, decreased adiposity, and long-term
consumption of a low-protein, low-calorie diet are associated with low
plasma growth factors and hormones that are linked to an increased risk
of cancer. Low protein intake may have additional protective effects
because it is associated with a decrease in circulating IGF-I
independent of body fat mass."
Long-term low-protein, low-calorie diet and endurance exercise modulate
metabolic factors associated with cancer risk -
http://www.ajcn.org/cgi/content/abstract/84/6/1456
Note that in the following article the term IGF was not found using the
Adobe search routine. The loss of weight alone would have reduced
inflammation and insulin resistance caused by fat (adipose) deposits.
Fat is an endocrine hormone the secretes TNFa and other negative
biochemicals (except adiponectin)that result in increased CRP, ROS,
hydrogen peroxide levels. Even after treatment the obese subjects still
had BMI >30%. The article emphasizes caloric restriction or diet and
exercise, but not protein.
"Obese men (N=31), 15 of whom had metabolic syndrome were placed on a
high-fiber, low-fat diet in a 3-week residential program where food was
provided ad libitum and daily aerobic exercise was performed. In each
subject, pre- and post-intervention fasting blood was drawn for
circulating levels of serum lipids, glucose and insulin (for estimation
of insulin sensitivity), oxidative stress generating enzyme
myeloperoxidase (MPO) and marker 8-isoprostaglandin F2
),
the inflammatory protein C reactive protein (CRP), soluble intracellular, CRP, sICAM-1, sP-selectin,
adhesion molecule (sICAM)-1 as an indicator of endothelial activation,
sP-selectin as a marker of platelet activation, the chemokine macrophage
inflammatory protein-1D (MIP-1D) and total matrix metalloproteinase-9
(MMP-9). Using subject sera and human aortic endothelial cell (HAEC)
culture systems, vascular cell adhesion molecule-1 (VCAM-1) cell
surface abundance and monocyte chemotactic protein-1 (MCP-1), nitric
oxide (NO), superoxide, and hydrogen peroxide production were measured
in vitro by fluorometric detection. Also determined in vitro was
serum-induced, monocyte adhesion and monocyte chemotatic activity (MCA).
After 3 weeks, significant reductions (p<0.05) in BMI, all serum lipids
and lipid ratios, fasting glucose, insulin, homeostasis model assessment
for insulin resistance, MPO, 8-iso-PGF2
MIP-1D, and MMP-9 were noted. In vitro, serum-stimulated cellular VCAM-1
expression, MCP-1 production, and fluorometric detection of superoxide
and hydrogen peroxide production decreased, while a concomitant increase
in NO production was noted (all p<0.01). Additionally, both monocyte
adhesion (p<0.05) and MCA (p<0.01) decreased. Nine of 15 were no longer
positive for metabolic syndrome post-intervention. Intensive lifestyle
modification may ameliorate novel CAD risk factors in men with metabolic
syndrome factors prior to reversal of obesity.
Keywords: atherosclerosis, lipids, inflammation, cell adhesion
molecules, nitric oxide"
A populare and sucessful medical low carb appoach increases this very
same hormone (IGF)
See:http://jap.physiology.org/cgi/reprint/01292.2005v1
This article does not refer to IGF-1. Age also makes a difference in
the healthiness of IGF-1 signaling. "Reduced IGF-I signaling is involved
in muscle atrophy and results from decreased muscle exercise, reduced
growth hormone and insulin levels, reduced vitamin D, ..." Reasons for
the degeneration of aging skeletal muscle: a central role for IGF-1
signaling - http://www.springerlink.com/content/rmjtb6pqhvcq274g/
"Circulating levels of insulin-like growth factor 1 protein (IGF-I)
decline with advancing age, and IGF-I is thought to be causally related
to the loss of muscle mass and strength that occurs with age.
Furthermore, exogenous growth hormone administration increases
circulating IGF-I levels, which have been shown to increase muscle mass
and possibly strength. Yet, it seems that circulating levels of IGF-I
are not as important for muscle growth as are the isoforms of IGF-I
produced by skeletal muscle, which act in an autocrine/paracrine
fashion." Muscle strength response to strength training is influenced by
insulin-like growth factor 1 genotype in older adults -
http://jap.physiology.org/cgi/content/full/98/6/2147
It appears that Krom knows more than you do about IGF-1.
As many are probably aware, consistent low calorie diets are the only
method to be found to reduce all diseasse and increase life span
across the complete animal spectrum. This applies to amebas, spiders,
rats, dogs, monkeys and very likely humans.
Low calorie diets are one thing but reducing calories can occur by
reducing any of the macronutrients. Keeping proteins and fats constant
while reducing carbohydrates is a case in point. There is at least one
study that positively supports the latter approach.
Frank
Thanks Frank. Glad I read all the replies before posting.
Better than anything I could have said.
I haven't finished reading the detail, but I'm still
searching for the figures on diabetics among the "cohorts".
Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com
Psyllium, Fibre, Muesli and Nuts
.
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