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Aspirin Reduces Blood Glucose
This would go along with the increased iron hypothesis because aspirin
is proposed to be simply a substance produced by a plant to grab iron.
Published: 06:20 EST, April 29, 2008
* w w w .physorg . com /news128668808.html
Aspirin-like compounds increase insulin secretion in otherwise healthy
obese people
Aspirin-like compounds (salicylates) can claim another health benefit:
increasing the amount of insulin produced by otherwise healthy obese
people. Obesity is associated with insulin resistance, the first step
toward type 2 diabetes.
Aspirin and other salicylates are known to reduce blood glucose in
diabetic patients. New research accepted for publication in the
Journal of Clinical Endocrinology & Metabolism reveals a similar
beneficial effect among obese individuals by increasing the amount of
insulin secreted into the bloodstream.
"The administration of a salicylate led to the lowering of serum
glucose concentrations," said Jose-Manuel Fernandez-Real of the
Institut d'Investigacio Biomedica de Girona and CIBEROBN
Fisiopatologia de la Obesidad, Spain, and lead author of the study.
"These findings highlight the importance of further research on the
possible therapeutic benefit of aspirin in the fight against type 2
diabetes."
For their study, Fernandez-Real and his colleagues evaluated the
effects of triflusal (a derivative of salicylate) on 28 subjects (nine
men and 29 women). The average age of the participants was 48 years
old and their average Body Mass Index (BMI) was 33.9. A BMI of over 30
is considered obese. During three, four-week treatment periods, the
study participants received a 600 mg dose, a 900 mg dose, or a placebo
once per day.
The researchers found that administration of triflusal led to
decreased fasting serum glucose. Contrary to their expectations,
insulin sensitivity did not significantly change during the trial.
Insulin secretion, however, significantly increased in relation to the
dose size.
In conjunction with the human studies, the researchers also conducted
laboratory studies on insulin-producing cells (known as islets of
Langerhans) from mice and humans. The researchers observed that
triflusal significantly increased the insulin secreted by these
cells.
"Aspirin therapy has been recognized to improve glucose tolerance and
to reduce insulin requirements in diabetic subjects," said Fernandez-
Real. "To our knowledge, this is the first study to show that
salicylates lowered serum glucose in non-diabetic obese subjects. We
believe that this effect was due to a previously unsuspected increase
in insulin secretion rather than enhanced insulin sensitivity."
Source: The Endocrine Society
-----------------------------------------------
Iron Imbalance in Brain May Cause Migraine
Updated: Fri, Sep 28 6:22 PM EDT
By Will Boggs, MD
NEW YORK (Reuters Health) - Abnormalities in the way the brain's pain
control center handles iron may lead to the development of migraine
attacks and headaches, according to a study by Kansas researchers.
During migraine, a portion of the brain known as the periaqueductal
gray matter (PAG) may fail to "switch on" to prevent pain, Dr. K.
Michael Welch of the University of Kansas Medical Center in Kansas
City told Reuters Health.
"In migraine, a trigger such as stress activates the PAG but it does
not switch on because it is dysfunctional," he explained, "or else
switches on an abnormal part."
The result? "Pain instead of no pain," according to Welch.
His team studied levels of iron in the PAG of patients with either
migraine headaches or recurrent, non-migraine headaches and compared
them to levels in people without headache or migraine.
Changes in iron levels can reflect changes in the way the cells of the
PAG work, the authors pointed out.
According to the report, published in a recent issue of the journal
Headache, iron levels in the PAG were significantly increased in
patients with migraine and those with headache compared to the
headache-free group.
In fact, the researchers pointed out, the longer patients had
experienced headaches, the higher the iron levels in the PAG were,
though iron levels at the beginning of their illness were still
clearly higher than normal.
Increased iron levels may be both a cause of migraine attacks and a
result of repeated headaches, the investigators noted.
"Thus, we believe that the increased (iron levels) in our migraine
groups reflect impaired iron (balance), possibly associated with
(nerve) dysfunction or damage," the authors concluded.
"Perhaps the PAG abnormality is essential to the cause of the headache
in migraine," Welch said. "The gradual deposition of iron increases
dysfunction, and headaches coalesce from episodic to continuous."
How, then, might one minimize the damage from increased iron stores?
Welch advised, "Treat episodes quickly and prevent (attacks) whenever
possible."
SOURCE: Headache 2001;41:629-637.
------------------------------------------------------------
* en.wikipedia.org/wiki/Salicylic_acid
Salicylic acid is an enol of a =E2-keto carbonic acid and therefore
forms purple complexes with iron(III) salts.
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
is proposed to be simply a substance produced by a plant to grab iron.
Published: 06:20 EST, April 29, 2008
* w w w .physorg . com /news128668808.html
Aspirin-like compounds increase insulin secretion in otherwise healthy
obese people
Aspirin-like compounds (salicylates) can claim another health benefit:
increasing the amount of insulin produced by otherwise healthy obese
people. Obesity is associated with insulin resistance, the first step
toward type 2 diabetes.
Aspirin and other salicylates are known to reduce blood glucose in
diabetic patients. New research accepted for publication in the
Journal of Clinical Endocrinology & Metabolism reveals a similar
beneficial effect among obese individuals by increasing the amount of
insulin secreted into the bloodstream.
"The administration of a salicylate led to the lowering of serum
glucose concentrations," said Jose-Manuel Fernandez-Real of the
Institut d'Investigacio Biomedica de Girona and CIBEROBN
Fisiopatologia de la Obesidad, Spain, and lead author of the study.
"These findings highlight the importance of further research on the
possible therapeutic benefit of aspirin in the fight against type 2
diabetes."
For their study, Fernandez-Real and his colleagues evaluated the
effects of triflusal (a derivative of salicylate) on 28 subjects (nine
men and 29 women). The average age of the participants was 48 years
old and their average Body Mass Index (BMI) was 33.9. A BMI of over 30
is considered obese. During three, four-week treatment periods, the
study participants received a 600 mg dose, a 900 mg dose, or a placebo
once per day.
The researchers found that administration of triflusal led to
decreased fasting serum glucose. Contrary to their expectations,
insulin sensitivity did not significantly change during the trial.
Insulin secretion, however, significantly increased in relation to the
dose size.
In conjunction with the human studies, the researchers also conducted
laboratory studies on insulin-producing cells (known as islets of
Langerhans) from mice and humans. The researchers observed that
triflusal significantly increased the insulin secreted by these
cells.
"Aspirin therapy has been recognized to improve glucose tolerance and
to reduce insulin requirements in diabetic subjects," said Fernandez-
Real. "To our knowledge, this is the first study to show that
salicylates lowered serum glucose in non-diabetic obese subjects. We
believe that this effect was due to a previously unsuspected increase
in insulin secretion rather than enhanced insulin sensitivity."
Source: The Endocrine Society
-----------------------------------------------
Iron Imbalance in Brain May Cause Migraine
Updated: Fri, Sep 28 6:22 PM EDT
By Will Boggs, MD
NEW YORK (Reuters Health) - Abnormalities in the way the brain's pain
control center handles iron may lead to the development of migraine
attacks and headaches, according to a study by Kansas researchers.
During migraine, a portion of the brain known as the periaqueductal
gray matter (PAG) may fail to "switch on" to prevent pain, Dr. K.
Michael Welch of the University of Kansas Medical Center in Kansas
City told Reuters Health.
"In migraine, a trigger such as stress activates the PAG but it does
not switch on because it is dysfunctional," he explained, "or else
switches on an abnormal part."
The result? "Pain instead of no pain," according to Welch.
His team studied levels of iron in the PAG of patients with either
migraine headaches or recurrent, non-migraine headaches and compared
them to levels in people without headache or migraine.
Changes in iron levels can reflect changes in the way the cells of the
PAG work, the authors pointed out.
According to the report, published in a recent issue of the journal
Headache, iron levels in the PAG were significantly increased in
patients with migraine and those with headache compared to the
headache-free group.
In fact, the researchers pointed out, the longer patients had
experienced headaches, the higher the iron levels in the PAG were,
though iron levels at the beginning of their illness were still
clearly higher than normal.
Increased iron levels may be both a cause of migraine attacks and a
result of repeated headaches, the investigators noted.
"Thus, we believe that the increased (iron levels) in our migraine
groups reflect impaired iron (balance), possibly associated with
(nerve) dysfunction or damage," the authors concluded.
"Perhaps the PAG abnormality is essential to the cause of the headache
in migraine," Welch said. "The gradual deposition of iron increases
dysfunction, and headaches coalesce from episodic to continuous."
How, then, might one minimize the damage from increased iron stores?
Welch advised, "Treat episodes quickly and prevent (attacks) whenever
possible."
SOURCE: Headache 2001;41:629-637.
------------------------------------------------------------
* en.wikipedia.org/wiki/Salicylic_acid
Salicylic acid is an enol of a =E2-keto carbonic acid and therefore
forms purple complexes with iron(III) salts.
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
"This would go along with the increased iron hypothesis because aspirin
is proposed to be simply a substance produced by a plant to grab iron."
There is no such "iron hypothesis" with which to agree.
Jesus ate a mediterranean diet.
is proposed to be simply a substance produced by a plant to grab iron."
There is no such "iron hypothesis" with which to agree.
Jesus ate a mediterranean diet.
On Apr 30, 6:31 am, pa...@ferris . com wrote:
There is no such "iron hypothesis" with which to agree.
<<
Explain the clinical trial .. then .. since it has been PROVEN iron in
excess causes diabetes .. where is the iron coming from.
You talk the big talk but cannot seem to come up with even a ..
pathetic .. explanation.
How come.
Eh ..
Because .. ?
You are a stupid .. medical .. professional .. who cannot seem to do
anything but experiments which would make Mengele .. cringe.
You kill kids .. old people and pregnant women and fetuses
Isn't that .. right ..
* w w w .clinicaltrials.gov/show/NCT00230087
Iron Depletion Therapy for Type 2 DM and NAFLD
This study is currently recruiting patients.
Verified by National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK) March 2006
Sponsored by: National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK)
Information provided by: National Institute of Diabetes and Digestive
and Kidney Diseases (NIDDK)
ClinicalTrials.gov Identifier: NCT00230087
Purpose
The purpose of this study is to find out whether lowering the amount
of
iron in the body will result in less resistance to insulin and
improved
liver function in patients with type 2 diabetes mellitus and
non-alcoholic fatty liver disease. This may result in better diabetes
control and/or a decrease in the amount of liver fat.
Condition Intervention Phase
Non-Alcoholic Fatty Liver Disease
Diabetes Mellitus
Procedure: iron depletion by phlebotomy
Phase II
MedlinePlus related topics: Diabetes
Study Type: Interventional
Study Design: Treatment, Non-Randomized, Open Label, Uncontrolled,
Single Group Assignment, Efficacy Study
Official Title: Iron Depletion Therapy for Patients With Type 2
Diabetes Mellitus and Non-Alcoholic Fatty Liver Disease
Further study details as provided by National Institute of Diabetes
and
Digestive and Kidney Diseases (NIDDK):
Primary Outcomes: · Improved insulin sensitivity as determined by:;
(1) hyperinsulinemic euglycemic clamp method; (2) HOMA model-
determined by the OGTT method
Secondary Outcomes: · Change in serum aminotransferase levels; ·
Change in levels of serum, plasma and urinary markers of oxidative
stress; · Changes in intrahepatic and intraabdominal fat content as
determined by CT scan; · Change in serum levels of proinflammatory
cytokines (ie IL-6, TnF-aR2)
Expected Total Enrollment: 15
Study start: September 2005; Expected completion: January 2008
Last follow-up: October 2007; Data entry closure: December 2007
Nonalcoholic fatty liver disease (NAFLD) is a common liver disease in
the United States. NAFLD can lead to severe liver disease in some
patients. Patients with NAFLD develop resistance to the normal action
of insulin. Insulin is important for processing sugar and fat and
increased resistance to insulin leads to fat in the liver. There is a
correlation between the amount of iron in a person's body and the
ability of insulin to work properly. Several small studies suggest
that
removal of iron may improve both diabetes and NAFLD by lowering
insulin
resistance.
The goal of this pilot study is to determine the effect of iron
depletion on insulin sensitivity in patients with type 2 diabetes
mellitus and non-alcoholic fatty liver disease. This study will be
performed as an ancillary P&F study to the NASH CRN; all participants
will be recruited from the NASH CRN Database Study. Secondary outcome
measures will include the effect of iron depletion on hepatic
necroinflammation, markers of oxidative stress and intrahepatic fat
content. Insulin resistance will be directly measured using a two-
step
hyperinsulinemic euglycemic clamp procedure, before and after iron
depletion by phlebotomy. Oral glucose tolerance tests will also be
performed in order to evaluate the efficacy of using the indirect,
but
less cumbersome, HOMA model to derive values of insulin resistance in
this patient cohort. This study will advance our understanding of the
role of body iron stores in the pathophysiology of type 2 diabetes
mellitus and non-alcoholic fatty liver disease. If iron depletion
results in improved insulin sensitivity, reduced hepatic
necroinflammation and/or intrahepatic fat content, a large scale,
randomized, controlled trial of iron depletion in patients with type
2
diabetes mellitus and non-alcoholic fatty liver disease will be
planned.
Eligibility
Ages Eligible for Study: 18 Years - 65 Years, Genders Eligible
for Study: Both
Criteria
Inclusion Criteria
Histological evidence of NAFLD and enrollment in NASH CRN Database
Study
Type 2 DM treated with diet or a stable dose of non-insulin
sensitizing
oral hypoglycemic agents for > 3 mo.
Hemoglobin HbA1c level = 8 %
Serum ALT levels =1.3 x ULN
Between 18-65 years of age
Exclusion Criteria
Hereditary hemochromatosis or hepatic iron overload defined as any of
the following:
2+ iron on hepatic iron staining
Hepatic Iron Index = 1.9
C282Y homozygous or C282Y/H63D compound heterozygous HFE genotype
Use of insulin or thiazolidinediones for the treatment of diabetes
Use of anti-NASH drugs (thiazolidinediones, vitamin E, UDCA, SAM-e,
betaine, milk thistle, gemfibrozil, anti-TNF therapies, probiotics)
Serum ferritin <50µg/L
Serum transferrin-iron saturation <10 %
Hemoglobin <10 mg/L
Hematocrit <38 %
Voluntary blood donation or therapeutic phlebotomy within the
previous
twelve months (except routine lab tests)
Pregnant or lactating women
Prior history of coronary artery disease, myocardial infarction,
exertional dyspnea or chronic chest pain at rest.
Evidence of myocardial infarction as determined by an ECG
Location and Contact Information
Please refer to this study by ClinicalTrials.gov identifier
NCT00230087
Jim E Nelson, PhD 206-221-4537 jam...@medicine.washington.edu
Virginia Mugford, BS 206-221-4538
virgin...@medicine.washington.edu
Washington
University of Washington Medical Center, Seattle, Washington,
98195, United States; Recruiting
Jim Nelson, PhD 206-221-4537 jam...@medicine.washington.edu
Study chairs or principal investigators
Kris V Kowdley, MD, Principal Investigator, University of
Washington
More Information
Study ID Numbers: DK 61728-S1
Last Updated: March 6, 2006
Record first received: September 29, 2005
ClinicalTrials.gov Identifier: NCT00230087
Health Authority: United States: Federal Government
ClinicalTrials.gov processed this record on 2006-06-28
U.S. National Library of Medicine, Contact NLM Customer Service
National Institutes of Health, Department of Health & Human Services
Copyright, Privacy, Accessibility, Freedom of Information Act
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
There is no such "iron hypothesis" with which to agree.
<<
Explain the clinical trial .. then .. since it has been PROVEN iron in
excess causes diabetes .. where is the iron coming from.
You talk the big talk but cannot seem to come up with even a ..
pathetic .. explanation.
How come.
Eh ..
Because .. ?
You are a stupid .. medical .. professional .. who cannot seem to do
anything but experiments which would make Mengele .. cringe.
You kill kids .. old people and pregnant women and fetuses
Isn't that .. right ..
* w w w .clinicaltrials.gov/show/NCT00230087
Iron Depletion Therapy for Type 2 DM and NAFLD
This study is currently recruiting patients.
Verified by National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK) March 2006
Sponsored by: National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK)
Information provided by: National Institute of Diabetes and Digestive
and Kidney Diseases (NIDDK)
ClinicalTrials.gov Identifier: NCT00230087
Purpose
The purpose of this study is to find out whether lowering the amount
of
iron in the body will result in less resistance to insulin and
improved
liver function in patients with type 2 diabetes mellitus and
non-alcoholic fatty liver disease. This may result in better diabetes
control and/or a decrease in the amount of liver fat.
Condition Intervention Phase
Non-Alcoholic Fatty Liver Disease
Diabetes Mellitus
Procedure: iron depletion by phlebotomy
Phase II
MedlinePlus related topics: Diabetes
Study Type: Interventional
Study Design: Treatment, Non-Randomized, Open Label, Uncontrolled,
Single Group Assignment, Efficacy Study
Official Title: Iron Depletion Therapy for Patients With Type 2
Diabetes Mellitus and Non-Alcoholic Fatty Liver Disease
Further study details as provided by National Institute of Diabetes
and
Digestive and Kidney Diseases (NIDDK):
Primary Outcomes: · Improved insulin sensitivity as determined by:;
(1) hyperinsulinemic euglycemic clamp method; (2) HOMA model-
determined by the OGTT method
Secondary Outcomes: · Change in serum aminotransferase levels; ·
Change in levels of serum, plasma and urinary markers of oxidative
stress; · Changes in intrahepatic and intraabdominal fat content as
determined by CT scan; · Change in serum levels of proinflammatory
cytokines (ie IL-6, TnF-aR2)
Expected Total Enrollment: 15
Study start: September 2005; Expected completion: January 2008
Last follow-up: October 2007; Data entry closure: December 2007
Nonalcoholic fatty liver disease (NAFLD) is a common liver disease in
the United States. NAFLD can lead to severe liver disease in some
patients. Patients with NAFLD develop resistance to the normal action
of insulin. Insulin is important for processing sugar and fat and
increased resistance to insulin leads to fat in the liver. There is a
correlation between the amount of iron in a person's body and the
ability of insulin to work properly. Several small studies suggest
that
removal of iron may improve both diabetes and NAFLD by lowering
insulin
resistance.
The goal of this pilot study is to determine the effect of iron
depletion on insulin sensitivity in patients with type 2 diabetes
mellitus and non-alcoholic fatty liver disease. This study will be
performed as an ancillary P&F study to the NASH CRN; all participants
will be recruited from the NASH CRN Database Study. Secondary outcome
measures will include the effect of iron depletion on hepatic
necroinflammation, markers of oxidative stress and intrahepatic fat
content. Insulin resistance will be directly measured using a two-
step
hyperinsulinemic euglycemic clamp procedure, before and after iron
depletion by phlebotomy. Oral glucose tolerance tests will also be
performed in order to evaluate the efficacy of using the indirect,
but
less cumbersome, HOMA model to derive values of insulin resistance in
this patient cohort. This study will advance our understanding of the
role of body iron stores in the pathophysiology of type 2 diabetes
mellitus and non-alcoholic fatty liver disease. If iron depletion
results in improved insulin sensitivity, reduced hepatic
necroinflammation and/or intrahepatic fat content, a large scale,
randomized, controlled trial of iron depletion in patients with type
2
diabetes mellitus and non-alcoholic fatty liver disease will be
planned.
Eligibility
Ages Eligible for Study: 18 Years - 65 Years, Genders Eligible
for Study: Both
Criteria
Inclusion Criteria
Histological evidence of NAFLD and enrollment in NASH CRN Database
Study
Type 2 DM treated with diet or a stable dose of non-insulin
sensitizing
oral hypoglycemic agents for > 3 mo.
Hemoglobin HbA1c level = 8 %
Serum ALT levels =1.3 x ULN
Between 18-65 years of age
Exclusion Criteria
Hereditary hemochromatosis or hepatic iron overload defined as any of
the following:
2+ iron on hepatic iron staining
Hepatic Iron Index = 1.9
C282Y homozygous or C282Y/H63D compound heterozygous HFE genotype
Use of insulin or thiazolidinediones for the treatment of diabetes
Use of anti-NASH drugs (thiazolidinediones, vitamin E, UDCA, SAM-e,
betaine, milk thistle, gemfibrozil, anti-TNF therapies, probiotics)
Serum ferritin <50µg/L
Serum transferrin-iron saturation <10 %
Hemoglobin <10 mg/L
Hematocrit <38 %
Voluntary blood donation or therapeutic phlebotomy within the
previous
twelve months (except routine lab tests)
Pregnant or lactating women
Prior history of coronary artery disease, myocardial infarction,
exertional dyspnea or chronic chest pain at rest.
Evidence of myocardial infarction as determined by an ECG
Location and Contact Information
Please refer to this study by ClinicalTrials.gov identifier
NCT00230087
Jim E Nelson, PhD 206-221-4537 jam...@medicine.washington.edu
Virginia Mugford, BS 206-221-4538
virgin...@medicine.washington.edu
Washington
University of Washington Medical Center, Seattle, Washington,
98195, United States; Recruiting
Jim Nelson, PhD 206-221-4537 jam...@medicine.washington.edu
Study chairs or principal investigators
Kris V Kowdley, MD, Principal Investigator, University of
Washington
More Information
Study ID Numbers: DK 61728-S1
Last Updated: March 6, 2006
Record first received: September 29, 2005
ClinicalTrials.gov Identifier: NCT00230087
Health Authority: United States: Federal Government
ClinicalTrials.gov processed this record on 2006-06-28
U.S. National Library of Medicine, Contact NLM Customer Service
National Institutes of Health, Department of Health & Human Services
Copyright, Privacy, Accessibility, Freedom of Information Act
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
On Apr 30, 7:10 am, ironjustice <teamtan...@hotmail . com > wrote: kill
kids .. old people and pregnant women and fetuses <<
Might as well throw in more groups of people they kill on a regular
basis ..
"Young, fit climbers or trekkers"
"Many climbers have died of HAPE when they were mistakenly treated for
pneumonia"
I guess this might be all the pneumonia .. COPD .. bronchitis we see
down here .. on level ground caused by erythrocytosis ..
* w w w .basecampmd . com /expguide/hape.shtml
HAPE - High Altitude Pulmonary Edema
Another form of severe altitude illness is High Altitude Pulmonary
Edema, a potentially deadly condition that develops because the lung
arteries develop excessive pressure in response to low oxygen,
resulting in overflow of fluid in the lungs. Though it often occurs
with AMS, it is not felt to be related and the classic signs of AMS
may be absent. Signs and symptoms of HAPE include any of the
following:
- Extreme fatigue
- Breathlessness at rest
- Fast, shallow breathing
- Cough, possibly productive of frothy or pink sputum
- Gurgling or rattling breaths
- Chest tightness, fullness, or congestion
- Blue or gray lips or fingernails
- Drowsiness
HAPE usually occurs on the second night after an ascent, and is more
frequent in young, fit climbers or trekkers.
In some persons, the hypoxia of high altitude causes constriction of
some of the blood vessels in the lungs, shunting all of the blood
through a limited number of vessels that are not constricted. This
dramatically elevates the blood pressure in these vessels and results
in a high-pressure leak of fluid from the blood vessels into the
lungs. Exertion and cold exposure can also raise the pulmonary blood
pressure and may contribute to either the onset or worsening of HAPE.
Immediate descent is the treatment of choice for HAPE; unless oxygen
is available delay may be fatal. Descend to the last elevation where
the victim felt well upon awakening. Descent may be complicated by
extreme fatigue and possibly also by confusion (due to inability to
get enough oxygen to the brain); HAPE frequently occurs at night, and
may worsen with exertion. These victims often need to be carried.
It is common for persons with severe HAPE to also develop HACE,
presumably due to the extremely low levels of oxygen in their blood
(equivalent to a continued rapid ascent).
HAPE usually resolves rapidly with descent, and one or two days of
rest at a lower elevation may be adequate for complete recovery. Once
the symptoms have fully resolved, cautious re-ascent is acceptable.
Summary of HAPE treatment
DESCENT, rest, oxygen, rehydration, and for severe cases, nifedipine,
salmeterol, acetazolamide, sildenafil or tadalafil and dexamethasone
may be used. Nifedipine, acetazolamide, sildenafil/tadalafil and
dexamethasone have all been shown to lower the pulmonary hypertensive
response to hypoxia, but they are prescription medicines for a good
reason -- they may be hazardous to use without appropriate medical
supervision and advice. Salmeterol is more commonly used as an asthma
medication, but it also can hasten the body's ability to re-absorb
edema fluid that clogs up the airways in HAPE. It is also a
prescription medication in most of the world.
HAPE can be confused with a number of other respiratory conditions:
High Altitude Cough and Bronchitis are both characterized by a
persistent cough with or without sputum production. There is no
shortness of breath at rest, no severe fatigue. Normal oxygen
saturations (for the altitude) will be measured if a pulse oximeter is
available.
Pneumonia can be difficult to distinguish from HAPE. Fever is common
with HAPE and does not prove the patient has pneumonia. Coughing up
green or yellow sputum may occur with HAPE, and both can cause low
blood levels of oxygen. The diagnostic test (and treatment) is descent
- HAPE will improve rapidly. If the patient does not improve with
descent, then consider antibiotics. HAPE is much more common at
altitude than pneumonia, and more dangerous; many climbers have died
of HAPE when they were mistakenly treated for pneumonia.
Asthma might also be confused with HAPE. Fortunately, asthmatics seem
to do better at altitude than at sea-level. If you think it's asthma,
try asthma medications, but if the person does not improve fairly
quickly assume it is HAPE and treat it accordingly..
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
> On Apr 30, 6:31 am, pa...@ferris . com wrote:
> There is no such "iron hypothesis" with which to agree.
> <<
>
> Explain the clinical trial .. then .. since it has been PROVEN iron in
> excess causes diabetes .. where is the iron coming from.
> You talk the big talk but cannot seem to come up with even a ..
> pathetic .. explanation.
> How come.
> Eh ..
> Because .. ?
> You are a stupid .. medical .. professional .. who cannot seem to do
> anything but experiments which would make Mengele .. cringe.
>
> You kill kids .. old people and pregnant women and fetuses
>
> Isn't that .. right ..
>
> * w w w .clinicaltrials.gov/show/NCT00230087
>
> Iron Depletion Therapy for Type 2 DM and NAFLD
>
> This study is currently recruiting patients.
> Verified by National Institute of Diabetes and Digestive and Kidney
> Diseases (NIDDK) March 2006
>
> Sponsored by: National Institute of Diabetes and Digestive and Kidney
> Diseases (NIDDK)
> Information provided by: National Institute of Diabetes and Digestive
> and Kidney Diseases (NIDDK)
> ClinicalTrials.gov Identifier: NCT00230087
>
> Purpose
>
> The purpose of this study is to find out whether lowering the amount
> of
> iron in the body will result in less resistance to insulin and
> improved
> liver function in patients with type 2 diabetes mellitus and
> non-alcoholic fatty liver disease. This may result in better diabetes
> control and/or a decrease in the amount of liver fat.
> Condition Intervention Phase
> Non-Alcoholic Fatty Liver Disease
> Diabetes Mellitus
> Procedure: iron depletion by phlebotomy
> Phase II
>
> MedlinePlus related topics: Diabetes
>
> Study Type: Interventional
> Study Design: Treatment, Non-Randomized, Open Label, Uncontrolled,
> Single Group Assignment, Efficacy Study
>
> Official Title: Iron Depletion Therapy for Patients With Type 2
> Diabetes Mellitus and Non-Alcoholic Fatty Liver Disease
>
> Further study details as provided by National Institute of Diabetes
> and
> Digestive and Kidney Diseases (NIDDK):
> Primary Outcomes: · Improved insulin sensitivity as determined by:;
> (1) hyperinsulinemic euglycemic clamp method; (2) HOMA model-
> determined by the OGTT method
> Secondary Outcomes: · Change in serum aminotransferase levels; ·
> Change in levels of serum, plasma and urinary markers of oxidative
> stress; · Changes in intrahepatic and intraabdominal fat content as
> determined by CT scan; · Change in serum levels of proinflammatory
> cytokines (ie IL-6, TnF-aR2)
> Expected Total Enrollment: 15
> Study start: September 2005; Expected completion: January 2008
> Last follow-up: October 2007; Data entry closure: December 2007
>
> Nonalcoholic fatty liver disease (NAFLD) is a common liver disease in
> the United States. NAFLD can lead to severe liver disease in some
> patients. Patients with NAFLD develop resistance to the normal action
> of insulin. Insulin is important for processing sugar and fat and
> increased resistance to insulin leads to fat in the liver. There is a
> correlation between the amount of iron in a person's body and the
> ability of insulin to work properly. Several small studies suggest
> that
> removal of iron may improve both diabetes and NAFLD by lowering
> insulin
> resistance.
>
> The goal of this pilot study is to determine the effect of iron
> depletion on insulin sensitivity in patients with type 2 diabetes
> mellitus and non-alcoholic fatty liver disease. This study will be
> performed as an ancillary P&F study to the NASH CRN; all participants
> will be recruited from the NASH CRN Database Study. Secondary outcome
> measures will include the effect of iron depletion on hepatic
> necroinflammation, markers of oxidative stress and intrahepatic fat
> content. Insulin resistance will be directly measured using a two-
> step
> hyperinsulinemic euglycemic clamp procedure, before and after iron
> depletion by phlebotomy. Oral glucose tolerance tests will also be
> performed in order to evaluate the efficacy of using the indirect,
> but
> less cumbersome, HOMA model to derive values of insulin resistance in
> this patient cohort. This study will advance our understanding of the
> role of body iron stores in the pathophysiology of type 2 diabetes
> mellitus and non-alcoholic fatty liver disease. If iron depletion
> results in improved insulin sensitivity, reduced hepatic
> necroinflammation and/or intrahepatic fat content, a large scale,
> randomized, controlled trial of iron depletion in patients with type
> 2
> diabetes mellitus and non-alcoholic fatty liver disease will be
> planned.
>
> Eligibility
>
> Ages Eligible for Study: 18 Years - 65 Years, Genders Eligib=
le
> for Study: Both
> Criteria
> Inclusion Criteria
>
> Histological evidence of NAFLD and enrollment in NASH CRN Database
> Study
> Type 2 DM treated with diet or a stable dose of non-insulin
> sensitizing
> oral hypoglycemic agents for > 3 mo.
> Hemoglobin HbA1c level = 8 %
> Serum ALT levels =1.3 x ULN
> Between 18-65 years of age
> Exclusion Criteria
>
> Hereditary hemochromatosis or hepatic iron overload defined as any of
> the following:
>
> 2+ iron on hepatic iron staining
> Hepatic Iron Index = 1.9
> C282Y homozygous or C282Y/H63D compound heterozygous HFE genotype
> Use of insulin or thiazolidinediones for the treatment of diabetes
> Use of anti-NASH drugs (thiazolidinediones, vitamin E, UDCA, SAM-e,
> betaine, milk thistle, gemfibrozil, anti-TNF therapies, probiotics)
> Serum ferritin <50µg/L
> Serum transferrin-iron saturation <10 %
> Hemoglobin <10 mg/L
> Hematocrit <38 %
> Voluntary blood donation or therapeutic phlebotomy within the
> previous
> twelve months (except routine lab tests)
> Pregnant or lactating women
> Prior history of coronary artery disease, myocardial infarction,
> exertional dyspnea or chronic chest pain at rest.
> Evidence of myocardial infarction as determined by an ECG
> Location and Contact Information
>
> Please refer to this study by ClinicalTrials.gov identifier
> NCT00230087
>
> Jim E Nelson, PhD 206-221-4537 jam...@medicine.washingto=
n.edu
> Virginia Mugford, BS 206-221-4538
> virgin...@medicine.washington.edu
>
> Washington
> University of Washington Medical Center, Seattle, Washingto=
n,
> 98195, United States; Recruiting
> Jim Nelson, PhD 206-221-4537 jam...@medicine.washington.edu
>
> Study chairs or principal investigators
>
> Kris V Kowdley, MD, Principal Investigator, University of
> Washington
>
> More Information
>
> Study ID Numbers: DK 61728-S1
> Last Updated: March 6, 2006
> Record first received: September 29, 2005
> ClinicalTrials.gov Identifier: NCT00230087
> Health Authority: United States: Federal Government
> ClinicalTrials.gov processed this record on 2006-06-28
>
> U.S. National Library of Medicine, Contact NLM Customer Service
> National Institutes of Health, Department of Health & Human Services
> Copyright, Privacy, Accessibility, Freedom of Information Act
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian! * tinyurl . com /2r2nkh
>
> Man Is A Herbivore! * tinyurl . com /a3cc3
>
> DEAD PEOPLE WALKING * tinyurl . com /zk9fk
kids .. old people and pregnant women and fetuses <<
Might as well throw in more groups of people they kill on a regular
basis ..
"Young, fit climbers or trekkers"
"Many climbers have died of HAPE when they were mistakenly treated for
pneumonia"
I guess this might be all the pneumonia .. COPD .. bronchitis we see
down here .. on level ground caused by erythrocytosis ..
* w w w .basecampmd . com /expguide/hape.shtml
HAPE - High Altitude Pulmonary Edema
Another form of severe altitude illness is High Altitude Pulmonary
Edema, a potentially deadly condition that develops because the lung
arteries develop excessive pressure in response to low oxygen,
resulting in overflow of fluid in the lungs. Though it often occurs
with AMS, it is not felt to be related and the classic signs of AMS
may be absent. Signs and symptoms of HAPE include any of the
following:
- Extreme fatigue
- Breathlessness at rest
- Fast, shallow breathing
- Cough, possibly productive of frothy or pink sputum
- Gurgling or rattling breaths
- Chest tightness, fullness, or congestion
- Blue or gray lips or fingernails
- Drowsiness
HAPE usually occurs on the second night after an ascent, and is more
frequent in young, fit climbers or trekkers.
In some persons, the hypoxia of high altitude causes constriction of
some of the blood vessels in the lungs, shunting all of the blood
through a limited number of vessels that are not constricted. This
dramatically elevates the blood pressure in these vessels and results
in a high-pressure leak of fluid from the blood vessels into the
lungs. Exertion and cold exposure can also raise the pulmonary blood
pressure and may contribute to either the onset or worsening of HAPE.
Immediate descent is the treatment of choice for HAPE; unless oxygen
is available delay may be fatal. Descend to the last elevation where
the victim felt well upon awakening. Descent may be complicated by
extreme fatigue and possibly also by confusion (due to inability to
get enough oxygen to the brain); HAPE frequently occurs at night, and
may worsen with exertion. These victims often need to be carried.
It is common for persons with severe HAPE to also develop HACE,
presumably due to the extremely low levels of oxygen in their blood
(equivalent to a continued rapid ascent).
HAPE usually resolves rapidly with descent, and one or two days of
rest at a lower elevation may be adequate for complete recovery. Once
the symptoms have fully resolved, cautious re-ascent is acceptable.
Summary of HAPE treatment
DESCENT, rest, oxygen, rehydration, and for severe cases, nifedipine,
salmeterol, acetazolamide, sildenafil or tadalafil and dexamethasone
may be used. Nifedipine, acetazolamide, sildenafil/tadalafil and
dexamethasone have all been shown to lower the pulmonary hypertensive
response to hypoxia, but they are prescription medicines for a good
reason -- they may be hazardous to use without appropriate medical
supervision and advice. Salmeterol is more commonly used as an asthma
medication, but it also can hasten the body's ability to re-absorb
edema fluid that clogs up the airways in HAPE. It is also a
prescription medication in most of the world.
HAPE can be confused with a number of other respiratory conditions:
High Altitude Cough and Bronchitis are both characterized by a
persistent cough with or without sputum production. There is no
shortness of breath at rest, no severe fatigue. Normal oxygen
saturations (for the altitude) will be measured if a pulse oximeter is
available.
Pneumonia can be difficult to distinguish from HAPE. Fever is common
with HAPE and does not prove the patient has pneumonia. Coughing up
green or yellow sputum may occur with HAPE, and both can cause low
blood levels of oxygen. The diagnostic test (and treatment) is descent
- HAPE will improve rapidly. If the patient does not improve with
descent, then consider antibiotics. HAPE is much more common at
altitude than pneumonia, and more dangerous; many climbers have died
of HAPE when they were mistakenly treated for pneumonia.
Asthma might also be confused with HAPE. Fortunately, asthmatics seem
to do better at altitude than at sea-level. If you think it's asthma,
try asthma medications, but if the person does not improve fairly
quickly assume it is HAPE and treat it accordingly..
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
> On Apr 30, 6:31 am, pa...@ferris . com wrote:
> There is no such "iron hypothesis" with which to agree.
> <<
>
> Explain the clinical trial .. then .. since it has been PROVEN iron in
> excess causes diabetes .. where is the iron coming from.
> You talk the big talk but cannot seem to come up with even a ..
> pathetic .. explanation.
> How come.
> Eh ..
> Because .. ?
> You are a stupid .. medical .. professional .. who cannot seem to do
> anything but experiments which would make Mengele .. cringe.
>
> You kill kids .. old people and pregnant women and fetuses
>
> Isn't that .. right ..
>
> * w w w .clinicaltrials.gov/show/NCT00230087
>
> Iron Depletion Therapy for Type 2 DM and NAFLD
>
> This study is currently recruiting patients.
> Verified by National Institute of Diabetes and Digestive and Kidney
> Diseases (NIDDK) March 2006
>
> Sponsored by: National Institute of Diabetes and Digestive and Kidney
> Diseases (NIDDK)
> Information provided by: National Institute of Diabetes and Digestive
> and Kidney Diseases (NIDDK)
> ClinicalTrials.gov Identifier: NCT00230087
>
> Purpose
>
> The purpose of this study is to find out whether lowering the amount
> of
> iron in the body will result in less resistance to insulin and
> improved
> liver function in patients with type 2 diabetes mellitus and
> non-alcoholic fatty liver disease. This may result in better diabetes
> control and/or a decrease in the amount of liver fat.
> Condition Intervention Phase
> Non-Alcoholic Fatty Liver Disease
> Diabetes Mellitus
> Procedure: iron depletion by phlebotomy
> Phase II
>
> MedlinePlus related topics: Diabetes
>
> Study Type: Interventional
> Study Design: Treatment, Non-Randomized, Open Label, Uncontrolled,
> Single Group Assignment, Efficacy Study
>
> Official Title: Iron Depletion Therapy for Patients With Type 2
> Diabetes Mellitus and Non-Alcoholic Fatty Liver Disease
>
> Further study details as provided by National Institute of Diabetes
> and
> Digestive and Kidney Diseases (NIDDK):
> Primary Outcomes: · Improved insulin sensitivity as determined by:;
> (1) hyperinsulinemic euglycemic clamp method; (2) HOMA model-
> determined by the OGTT method
> Secondary Outcomes: · Change in serum aminotransferase levels; ·
> Change in levels of serum, plasma and urinary markers of oxidative
> stress; · Changes in intrahepatic and intraabdominal fat content as
> determined by CT scan; · Change in serum levels of proinflammatory
> cytokines (ie IL-6, TnF-aR2)
> Expected Total Enrollment: 15
> Study start: September 2005; Expected completion: January 2008
> Last follow-up: October 2007; Data entry closure: December 2007
>
> Nonalcoholic fatty liver disease (NAFLD) is a common liver disease in
> the United States. NAFLD can lead to severe liver disease in some
> patients. Patients with NAFLD develop resistance to the normal action
> of insulin. Insulin is important for processing sugar and fat and
> increased resistance to insulin leads to fat in the liver. There is a
> correlation between the amount of iron in a person's body and the
> ability of insulin to work properly. Several small studies suggest
> that
> removal of iron may improve both diabetes and NAFLD by lowering
> insulin
> resistance.
>
> The goal of this pilot study is to determine the effect of iron
> depletion on insulin sensitivity in patients with type 2 diabetes
> mellitus and non-alcoholic fatty liver disease. This study will be
> performed as an ancillary P&F study to the NASH CRN; all participants
> will be recruited from the NASH CRN Database Study. Secondary outcome
> measures will include the effect of iron depletion on hepatic
> necroinflammation, markers of oxidative stress and intrahepatic fat
> content. Insulin resistance will be directly measured using a two-
> step
> hyperinsulinemic euglycemic clamp procedure, before and after iron
> depletion by phlebotomy. Oral glucose tolerance tests will also be
> performed in order to evaluate the efficacy of using the indirect,
> but
> less cumbersome, HOMA model to derive values of insulin resistance in
> this patient cohort. This study will advance our understanding of the
> role of body iron stores in the pathophysiology of type 2 diabetes
> mellitus and non-alcoholic fatty liver disease. If iron depletion
> results in improved insulin sensitivity, reduced hepatic
> necroinflammation and/or intrahepatic fat content, a large scale,
> randomized, controlled trial of iron depletion in patients with type
> 2
> diabetes mellitus and non-alcoholic fatty liver disease will be
> planned.
>
> Eligibility
>
> Ages Eligible for Study: 18 Years - 65 Years, Genders Eligib=
le
> for Study: Both
> Criteria
> Inclusion Criteria
>
> Histological evidence of NAFLD and enrollment in NASH CRN Database
> Study
> Type 2 DM treated with diet or a stable dose of non-insulin
> sensitizing
> oral hypoglycemic agents for > 3 mo.
> Hemoglobin HbA1c level = 8 %
> Serum ALT levels =1.3 x ULN
> Between 18-65 years of age
> Exclusion Criteria
>
> Hereditary hemochromatosis or hepatic iron overload defined as any of
> the following:
>
> 2+ iron on hepatic iron staining
> Hepatic Iron Index = 1.9
> C282Y homozygous or C282Y/H63D compound heterozygous HFE genotype
> Use of insulin or thiazolidinediones for the treatment of diabetes
> Use of anti-NASH drugs (thiazolidinediones, vitamin E, UDCA, SAM-e,
> betaine, milk thistle, gemfibrozil, anti-TNF therapies, probiotics)
> Serum ferritin <50µg/L
> Serum transferrin-iron saturation <10 %
> Hemoglobin <10 mg/L
> Hematocrit <38 %
> Voluntary blood donation or therapeutic phlebotomy within the
> previous
> twelve months (except routine lab tests)
> Pregnant or lactating women
> Prior history of coronary artery disease, myocardial infarction,
> exertional dyspnea or chronic chest pain at rest.
> Evidence of myocardial infarction as determined by an ECG
> Location and Contact Information
>
> Please refer to this study by ClinicalTrials.gov identifier
> NCT00230087
>
> Jim E Nelson, PhD 206-221-4537 jam...@medicine.washingto=
n.edu
> Virginia Mugford, BS 206-221-4538
> virgin...@medicine.washington.edu
>
> Washington
> University of Washington Medical Center, Seattle, Washingto=
n,
> 98195, United States; Recruiting
> Jim Nelson, PhD 206-221-4537 jam...@medicine.washington.edu
>
> Study chairs or principal investigators
>
> Kris V Kowdley, MD, Principal Investigator, University of
> Washington
>
> More Information
>
> Study ID Numbers: DK 61728-S1
> Last Updated: March 6, 2006
> Record first received: September 29, 2005
> ClinicalTrials.gov Identifier: NCT00230087
> Health Authority: United States: Federal Government
> ClinicalTrials.gov processed this record on 2006-06-28
>
> U.S. National Library of Medicine, Contact NLM Customer Service
> National Institutes of Health, Department of Health & Human Services
> Copyright, Privacy, Accessibility, Freedom of Information Act
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian! * tinyurl . com /2r2nkh
>
> Man Is A Herbivore! * tinyurl . com /a3cc3
>
> DEAD PEOPLE WALKING * tinyurl . com /zk9fk
In article
<0201dfbd-9939-4d7a-a5d8-a1c26adf1814@b9g2000prh.googlegroups . com >,
ironjustice <teamtanner@hotmail . com > wrote:
> This would go along with the increased iron hypothesis because aspirin
> is proposed to be simply a substance produced by a plant to grab iron.
>
> Published: 06:20 EST, April 29, 2008
> * w w w .physorg . com /news128668808.html
>
> Aspirin-like compounds increase insulin secretion in otherwise healthy
> obese people
>
> Aspirin-like compounds (salicylates) can claim another health benefit:
> increasing the amount of insulin produced by otherwise healthy obese
> people. Obesity is associated with insulin resistance, the first step
> toward type 2 diabetes.
>
> Aspirin and other salicylates are known to reduce blood glucose in
> diabetic patients. New research accepted for publication in the
> Journal of Clinical Endocrinology & Metabolism reveals a similar
> beneficial effect among obese individuals by increasing the amount of
> insulin secreted into the bloodstream.
>
> "The administration of a salicylate led to the lowering of serum
> glucose concentrations," said Jose-Manuel Fernandez-Real of the
> Institut d'Investigacio Biomedica de Girona and CIBEROBN
> Fisiopatologia de la Obesidad, Spain, and lead author of the study.
> "These findings highlight the importance of further research on the
> possible therapeutic benefit of aspirin in the fight against type 2
> diabetes."
>
> For their study, Fernandez-Real and his colleagues evaluated the
> effects of triflusal (a derivative of salicylate) on 28 subjects (nine
> men and 29 women). The average age of the participants was 48 years
> old and their average Body Mass Index (BMI) was 33.9. A BMI of over 30
> is considered obese. During three, four-week treatment periods, the
> study participants received a 600 mg dose, a 900 mg dose, or a placebo
> once per day.
> The researchers found that administration of triflusal led to
> decreased fasting serum glucose. Contrary to their expectations,
> insulin sensitivity did not significantly change during the trial.
> Insulin secretion, however, significantly increased in relation to the
> dose size.
>
> In conjunction with the human studies, the researchers also conducted
> laboratory studies on insulin-producing cells (known as islets of
> Langerhans) from mice and humans. The researchers observed that
> triflusal significantly increased the insulin secreted by these
> cells.
>
> "Aspirin therapy has been recognized to improve glucose tolerance and
> to reduce insulin requirements in diabetic subjects," said Fernandez-
> Real. "To our knowledge, this is the first study to show that
> salicylates lowered serum glucose in non-diabetic obese subjects. We
> believe that this effect was due to a previously unsuspected increase
> in insulin secretion rather than enhanced insulin sensitivity."
Decreasing glucose by increasing insulin is just trading one evil for
another. Unless you are actually diabetic and not producing enough
insulin, what you want are substances that increase insulin
sensitivity and glucose uptake WITHOUT increasing insulin.
The reasons to take aspirin remain to be that's it's anti-inflammatory
and an AGE inhibitor/blocker/breaker (I forget which).
<0201dfbd-9939-4d7a-a5d8-a1c26adf1814@b9g2000prh.googlegroups . com >,
ironjustice <teamtanner@hotmail . com > wrote:
> This would go along with the increased iron hypothesis because aspirin
> is proposed to be simply a substance produced by a plant to grab iron.
>
> Published: 06:20 EST, April 29, 2008
> * w w w .physorg . com /news128668808.html
>
> Aspirin-like compounds increase insulin secretion in otherwise healthy
> obese people
>
> Aspirin-like compounds (salicylates) can claim another health benefit:
> increasing the amount of insulin produced by otherwise healthy obese
> people. Obesity is associated with insulin resistance, the first step
> toward type 2 diabetes.
>
> Aspirin and other salicylates are known to reduce blood glucose in
> diabetic patients. New research accepted for publication in the
> Journal of Clinical Endocrinology & Metabolism reveals a similar
> beneficial effect among obese individuals by increasing the amount of
> insulin secreted into the bloodstream.
>
> "The administration of a salicylate led to the lowering of serum
> glucose concentrations," said Jose-Manuel Fernandez-Real of the
> Institut d'Investigacio Biomedica de Girona and CIBEROBN
> Fisiopatologia de la Obesidad, Spain, and lead author of the study.
> "These findings highlight the importance of further research on the
> possible therapeutic benefit of aspirin in the fight against type 2
> diabetes."
>
> For their study, Fernandez-Real and his colleagues evaluated the
> effects of triflusal (a derivative of salicylate) on 28 subjects (nine
> men and 29 women). The average age of the participants was 48 years
> old and their average Body Mass Index (BMI) was 33.9. A BMI of over 30
> is considered obese. During three, four-week treatment periods, the
> study participants received a 600 mg dose, a 900 mg dose, or a placebo
> once per day.
> The researchers found that administration of triflusal led to
> decreased fasting serum glucose. Contrary to their expectations,
> insulin sensitivity did not significantly change during the trial.
> Insulin secretion, however, significantly increased in relation to the
> dose size.
>
> In conjunction with the human studies, the researchers also conducted
> laboratory studies on insulin-producing cells (known as islets of
> Langerhans) from mice and humans. The researchers observed that
> triflusal significantly increased the insulin secreted by these
> cells.
>
> "Aspirin therapy has been recognized to improve glucose tolerance and
> to reduce insulin requirements in diabetic subjects," said Fernandez-
> Real. "To our knowledge, this is the first study to show that
> salicylates lowered serum glucose in non-diabetic obese subjects. We
> believe that this effect was due to a previously unsuspected increase
> in insulin secretion rather than enhanced insulin sensitivity."
Decreasing glucose by increasing insulin is just trading one evil for
another. Unless you are actually diabetic and not producing enough
insulin, what you want are substances that increase insulin
sensitivity and glucose uptake WITHOUT increasing insulin.
The reasons to take aspirin remain to be that's it's anti-inflammatory
and an AGE inhibitor/blocker/breaker (I forget which).
On May 4, 8:06 am, noname <nos...@aol . com > wrote:Decreasing glucose by
increasing insulin is just trading one evil for
another. Unless you are actually diabetic and not producing enough
insulin, what you want are substances that increase insulin
sensitivity and glucose uptake WITHOUT increasing insulin. <<
This was done in obese people.
Chances are very high they have pre-diabetes / metabolic syndrome and
therefore pretty much can be considered to BE .. diabetic.
This in no way reflects on those not in this 'category' / pre/
andormetabolic/diabetic .. until of course they too contract the
disease category.
Sooo .. contrary to what you seem to be trying to imply .. ? .. the
underlying cause is still the iron and removing said iron seems to
improve ones' recovery as evidenced in many recent studies culmonating
in a very large clinical trial sponsoiron depred by the NIH of iron
depletion for diabetes and / or non-alcoholic
fatty liver disease .. ?
Yep ..
New research accepted for publication in the
Journal of Clinical Endocrinology & Metabolism reveals a similar
beneficial effect among **obese individuals** by increasing the amount
of
insulin secreted into the bloodstream
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
> In article
> <0201dfbd-9939-4d7a-a5d8-a1c26adf1...@b9g2000prh.googlegroups . com >,
>
>
>
>
>
> ironjustice <teamtan...@hotmail . com > wrote:
> > This would go along with the increased iron hypothesis because aspirin
> > is proposed to be simply a substance produced by a plant to grab iron.
>
> > Published: 06:20 EST, April 29, 2008
> > * w w w .physorg . com /news128668808.html
>
> > Aspirin-like compounds increase insulin secretion in otherwise healthy
> > obese people
>
> > Aspirin-like compounds (salicylates) can claim another health benefit:
> > increasing the amount of insulin produced by otherwise healthy obese
> > people. Obesity is associated with insulin resistance, the first step
> > toward type 2 diabetes.
>
> > Aspirin and other salicylates are known to reduce blood glucose in
> > diabetic patients. New research accepted for publication in the
> > Journal of Clinical Endocrinology & Metabolism reveals a similar
> > beneficial effect among obese individuals by increasing the amount of
> > insulin secreted into the bloodstream.
>
> > "The administration of a salicylate led to the lowering of serum
> > glucose concentrations," said Jose-Manuel Fernandez-Real of the
> > Institut d'Investigacio Biomedica de Girona and CIBEROBN
> > Fisiopatologia de la Obesidad, Spain, and lead author of the study.
> > "These findings highlight the importance of further research on the
> > possible therapeutic benefit of aspirin in the fight against type 2
> > diabetes."
>
> > For their study, Fernandez-Real and his colleagues evaluated the
> > effects of triflusal (a derivative of salicylate) on 28 subjects (nine
> > men and 29 women). The average age of the participants was 48 years
> > old and their average Body Mass Index (BMI) was 33.9. A BMI of over 30
> > is considered obese. During three, four-week treatment periods, the
> > study participants received a 600 mg dose, a 900 mg dose, or a placebo
> > once per day.
> > The researchers found that administration of triflusal led to
> > decreased fasting serum glucose. Contrary to their expectations,
> > insulin sensitivity did not significantly change during the trial.
> > Insulin secretion, however, significantly increased in relation to the
> > dose size.
>
> > In conjunction with the human studies, the researchers also conducted
> > laboratory studies on insulin-producing cells (known as islets of
> > Langerhans) from mice and humans. The researchers observed that
> > triflusal significantly increased the insulin secreted by these
> > cells.
>
> > "Aspirin therapy has been recognized to improve glucose tolerance and
> > to reduce insulin requirements in diabetic subjects," said Fernandez-
> > Real. "To our knowledge, this is the first study to show that
> > salicylates lowered serum glucose in non-diabetic obese subjects. We
> > believe that this effect was due to a previously unsuspected increase
> > in insulin secretion rather than enhanced insulin sensitivity."
>
> Decreasing glucose by increasing insulin is just trading one evil for
> another. Unless you are actually diabetic and not producing enough
> insulin, what you want are substances that increase insulin
> sensitivity and glucose uptake WITHOUT increasing insulin.
>
> The reasons to take aspirin remain to be that's it's anti-inflammatory
> and an AGE inhibitor/blocker/breaker (I forget which).- Hide quoted text -=
>
> - Show quoted text -
increasing insulin is just trading one evil for
another. Unless you are actually diabetic and not producing enough
insulin, what you want are substances that increase insulin
sensitivity and glucose uptake WITHOUT increasing insulin. <<
This was done in obese people.
Chances are very high they have pre-diabetes / metabolic syndrome and
therefore pretty much can be considered to BE .. diabetic.
This in no way reflects on those not in this 'category' / pre/
andormetabolic/diabetic .. until of course they too contract the
disease category.
Sooo .. contrary to what you seem to be trying to imply .. ? .. the
underlying cause is still the iron and removing said iron seems to
improve ones' recovery as evidenced in many recent studies culmonating
in a very large clinical trial sponsoiron depred by the NIH of iron
depletion for diabetes and / or non-alcoholic
fatty liver disease .. ?
Yep ..
New research accepted for publication in the
Journal of Clinical Endocrinology & Metabolism reveals a similar
beneficial effect among **obese individuals** by increasing the amount
of
insulin secreted into the bloodstream
Who loves ya.
Tom
Jesus Was A Vegetarian!
* tinyurl . com /2r2nkh
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
> In article
> <0201dfbd-9939-4d7a-a5d8-a1c26adf1...@b9g2000prh.googlegroups . com >,
>
>
>
>
>
> ironjustice <teamtan...@hotmail . com > wrote:
> > This would go along with the increased iron hypothesis because aspirin
> > is proposed to be simply a substance produced by a plant to grab iron.
>
> > Published: 06:20 EST, April 29, 2008
> > * w w w .physorg . com /news128668808.html
>
> > Aspirin-like compounds increase insulin secretion in otherwise healthy
> > obese people
>
> > Aspirin-like compounds (salicylates) can claim another health benefit:
> > increasing the amount of insulin produced by otherwise healthy obese
> > people. Obesity is associated with insulin resistance, the first step
> > toward type 2 diabetes.
>
> > Aspirin and other salicylates are known to reduce blood glucose in
> > diabetic patients. New research accepted for publication in the
> > Journal of Clinical Endocrinology & Metabolism reveals a similar
> > beneficial effect among obese individuals by increasing the amount of
> > insulin secreted into the bloodstream.
>
> > "The administration of a salicylate led to the lowering of serum
> > glucose concentrations," said Jose-Manuel Fernandez-Real of the
> > Institut d'Investigacio Biomedica de Girona and CIBEROBN
> > Fisiopatologia de la Obesidad, Spain, and lead author of the study.
> > "These findings highlight the importance of further research on the
> > possible therapeutic benefit of aspirin in the fight against type 2
> > diabetes."
>
> > For their study, Fernandez-Real and his colleagues evaluated the
> > effects of triflusal (a derivative of salicylate) on 28 subjects (nine
> > men and 29 women). The average age of the participants was 48 years
> > old and their average Body Mass Index (BMI) was 33.9. A BMI of over 30
> > is considered obese. During three, four-week treatment periods, the
> > study participants received a 600 mg dose, a 900 mg dose, or a placebo
> > once per day.
> > The researchers found that administration of triflusal led to
> > decreased fasting serum glucose. Contrary to their expectations,
> > insulin sensitivity did not significantly change during the trial.
> > Insulin secretion, however, significantly increased in relation to the
> > dose size.
>
> > In conjunction with the human studies, the researchers also conducted
> > laboratory studies on insulin-producing cells (known as islets of
> > Langerhans) from mice and humans. The researchers observed that
> > triflusal significantly increased the insulin secreted by these
> > cells.
>
> > "Aspirin therapy has been recognized to improve glucose tolerance and
> > to reduce insulin requirements in diabetic subjects," said Fernandez-
> > Real. "To our knowledge, this is the first study to show that
> > salicylates lowered serum glucose in non-diabetic obese subjects. We
> > believe that this effect was due to a previously unsuspected increase
> > in insulin secretion rather than enhanced insulin sensitivity."
>
> Decreasing glucose by increasing insulin is just trading one evil for
> another. Unless you are actually diabetic and not producing enough
> insulin, what you want are substances that increase insulin
> sensitivity and glucose uptake WITHOUT increasing insulin.
>
> The reasons to take aspirin remain to be that's it's anti-inflammatory
> and an AGE inhibitor/blocker/breaker (I forget which).- Hide quoted text -=
>
> - Show quoted text -
