Re: Oh Well


Hi_Therre wrote:
Just back from the ol foot doc (podiatrist), and the news was not
good. The damned nail fungus is about the same as it was four months
ago. For the past 2 1/2 years I've been fighting this god damned nail
fungus, and it still exists. We are at a stalemate with the damned
thing. Spent well over a thousand dollars, and no end in sight. The
foot doc is making a good living off my misery. Got to be a better
way of dealing with this damned problem. I've used vicks, Penlac,
Lamisil, and most recently - Sporanox. Sporanox has not improved
anything, but it has emptied my wallet. The doc says that I am most
likely one of those poor miserable bastards that cannot eliminate nail
fungus from their body. Some people can not be cured of it.

Anybody have any ideas we haven't tried? No, I do not mean dipping my
feet in bleach, vinegar, urea, or any other stupid voodoo solution. I
need a solution to this damned problem. I can't keep pouring bucks in
a never ending problem.
_____________________________________
http://www.healthdiabeticsoftware.com/ Free

You most likely will have to target the 'underlying' cause .. which is
... the inability of the body to sequester the PROMOTIONAL .. factor ..
iron ..

Increased iron in the body is being TARGETED in infection elimination
... and yeast / fungus .. NEED .. iron ..

"acquisition of iron is a CRUCIAL pathogenetic event"

So the upcoming trial of iron depletion in diabetes .. may .. be ..
JUST what you are looking .. for ..

http://www.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...@xxxxxxxxxxxxxxxxxxxxxxx
Virginia Mugford, BS 206-221-4538
virgin...@xxxxxxxxxxxxxxxxxxxxxxx


Washington
University of Washington Medical Center, Seattle, Washington,
98195, United States; Recruiting
Jim Nelson, PhD 206-221-4537 jam...@xxxxxxxxxxxxxxxxxxxxxxx


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

----------------------------------------------------
Acta Microbiol Immunol Hung. 2005;52(2):185-97. Related Articles, Links


Iron gathering of opportunistic pathogenic fungi. A mini review.


Nyilasi I, Papp T, Tako M, Nagy E, Vagvolgyi C.


HAS-USZ Microbiology Research Group, Department of Microbiology,
University
of Szeged, P.O. Box 533, H-6701 Szeged, Hungary.


Iron is an essential nutrient for most organisms because it serves as a

catalytic cofactor in oxidation-reduction reactions. Iron is rather
unavailable because it occurs in its insoluble ferric form in oxides
and
hydroxides, while in serum of mammalian hosts is highly bound to
carrier
proteins such as transferrin, so the free iron concentration is
extremely low
insufficient for microbial growth. Therefore, many organisms have
developed
different iron-scavenging systems for solubilizing ferric iron and
transporting it into cells across the fungal membrane. There are three
major
mechanisms by which fungi can obtain iron from the host: (a)
utilization of a
high affinity iron permease to transport iron intracellularly, (b)
production
and secretion of low molecular weight iron-specific chelators
(siderophores),
(c) utilization of a hem oxygenase to acquire iron from hemin. Patients
with
elevated levels of available serum iron treated with iron chelator,
deferoxamine to remedy iron overload conditions have an increased
susceptibility of invasive zygomycosis. Presumably deferoxamine
predisposes
patients to Zygomycetes infections by acting as a siderophore]. The
frequency
of zygomycosis is increasing in recent years and these infections
respond
very poorly to currently available antifungal agents, so new approaches
to
develop strategies to prevent and treat zygomycosis are urgently
needed.
Siderophores and iron-transport proteins have been suggested to
function as
virulence factors because the acquisition of iron is a crucial
pathogenetic
event. Biosynthesis and uptake of siderophores represent possible
targets for
antifungal therapy.


PMID: 16003938 [PubMed - in process]


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