[Homesteadingfamily] Re: Cookware for prepping

On Mon, 15 Nov 2010 13:35:53 -0800
Strumpets Delight <strumpetsdelight@gmail.com> wrote:

> Do you have documentation of these claims Eric?

The best source I know about what can happen from too much iron
is an aritcle in the CDC's Emerging Infectious Diseases journal
a few years ago. It does a very good summary.

----------------------------------------------------

From http://www.cdc.gov/ncidod/EID/vol5no3/weinberg.htm:

Iron Loading and Disease Surveillance
Eugene D. Weinberg
Indiana University, Bloomington, Indiana, USA

...

Excessive iron in specific tissues (iron loading) promotes
infection, neoplasia, cardiomyopathy, arthropathy, and a
profusion of endocrine and possibly neurodegenerative
disorders.

...

... Moreover, in infectious diseases, inflammatory
diseases, and illnesses that involve ischemia and
reperfusion, iron causes reactions that produce superoxide
radicals. ...

... To survive and replicate in hosts, microbial pathogens
must acquire host iron. Highly virulent strains possess
exceptionally powerful mechanisms for obtaining host iron
from healthy hosts. In persons whose tissues and cells
contain excessive iron, pathogens can much more readily
procure iron from molecules of transferrin that are
elevated in iron saturation. In such cases, even microbial
strains that are not ordinarily dangerous can cause
illness. Markedly invasive neoplastic cell strains can
glean host iron more easily than less malignant strains or
normal host cells. Moreover, iron-loaded tissues are
especially susceptible to growth of malignant cells.

...

Table 1. Iron loading in specific tissues and increased
risk for disease

Tissue type Disease
----------------------- ---------------------------------
Alveolar macrophages Pulmonary neoplasia and
infection

Anterior pituitary Gonadal and growth dysfunction

Aorta; carotid and Atherosclerosis
coronary arteries

Colorectal mucosa Adenoma, carcinoma

Heart Arrhythmia, cardiomyopathy

Infant intestine Botulism, salmonellosis, sudden
death

Joints Arthropathy

Liver Viral hepatitis, cirrhosis,
carcinoma

Macrophages Intracellular infections

Pancreas Acinar and beta cell necrosis,
carcinoma

Plasma and lymph Extracellular infections

Skeletal system Osteoporosis

Skin Leprosy, melanoma

Soft tissue Sarcoma

Substantia nigra Parkinson's disease

...

Table 2. Microbial genera with strains whose growth in body
fluids, cells, tissues, and intact vertebrate hosts is
stimulated by excess iron

...

Excessive iron is correlated with synovial damage in
rheumatoid arthritis and with impaired glucose metabolism
in diabetes. The association of Chlamydia pneumoniae and
excessive iron with cardiovascular disease is well
established. Growth of this pathogen is strongly suppressed
by iron restriction.

----------------------------------------------------------

Take a look at table 2. As much as I'd like to put it
here, trying to format it to fit is pretty tough.

----------------------------------------------------------

Now keep in mind that much of this is from too much iron. The
problem is that there is no magical line between too much and
not too much. So just a little excessive iron that may affect
one condition might not have much affect on other conditions.

Some other sources on the Internet you might want to read
include:

http://articles.latimes.com/1992-09-09/news/mn-156_1_heart-attacks

According to the report, men with high amounts of iron
in their bodies had twice as much risk of heart attacks
as men with lower amounts of iron--after known heart
disease risk factors, such as cholesterol levels and
smoking, were taken into account.

...

A decade ago, Sullivan theorized that women are
protected against heart attacks until after menopause
because of the large amounts of iron they lose each
month in menstrual blood. Despite the exclusion of
women from the Finnish study, Sullivan called the
findings "especially relevant" to his theory.

The Finnish researchers, led by Dr. Jukka T. Salonen
and Riitta Salonen said their findings raise the
question of whether current dietary recommendations for
iron intake should be revised for men and possibly for
post-menopausal women.

...

Sullivan suggested that, based on the findings, the
level of iron considered normal may need to be lowered.

http://www.straightdope.com/columns/read/2548/does-giving-blood-reduce-your-chances-of-getting-heart-disease

The iron hypothesis arose from the observation that
premenopausal women have a much lower incidence of heart
disease than men but that after menopause the difference
narrows dramatically. Originally it was thought this had
something to do with sex hormones. However, men given
estrogen suffer more heart disease than normal, and
women who stop menstruating due to surgery but still
have estrogen-producing ovaries suffer increased heart
problems nonetheless.

In 1981, trying to make sense out of this, pathologist
Jerome Sullivan proposed an alternative explanation:
"The greater incidence of heart diseases in men and
postmenopausal women is due to higher levels of stored
iron in these two groups." Evidence: (1) diseases that
cause iron buildup often result in heart failure; (2)
the older a man gets, the more iron he accumulates; (3)
after menopause, stored iron in women rises to the
level found in men; and (4) the types of heart disease
found in affluent countries are rare among impoverished
peoples with iron-deficient diets. Sullivan's
recommended treatment: "regular phlebotomy," medicalese
for having someone extract your blood.

Some later research supported Sullivan's theory. The
most recent study I've seen, published in Heart by
David G. Meyers et al, examined 3,900 male participants
in the Nebraska Diet Heart Study and found that
nonsmokers who had donated blood in the past three
years had a 30 percent lower risk of major heart
problems. (Curiously, donating multiple times during
the three years, as opposed to once or twice, brought no
additional benefit.) Other researchers conjectured that
iron interacts with LDL (bad) cholesterol to promote
atherosclerosis, and there's a lot of stuff about free
radicals and so on that I don't have the heart to
explain.

http://www.ncbi.nlm.nih.gov/pubmed/11087066

Iron is a vital element in life. However, it may
participate in diverse pathological processes by
catalyzing the formation of reactive oxygen free
radicals. During the past decade, considerable evidence
has supported the role of oxidative stress in the
development of atherosclerosis and related
cardiovascular diseases. The oxidation of low-density
lipoprotein (LDL) and lipid is believed to be one of the
crucial events leading to plaque formation in
vasculature. It has been hypothesized that iron-mediated
oxidation is involved in this process. In favor of this
idea, several epidemiological studies have shown that
the level of body iron stores is positively correlated
with the incidence of coronary heart disease in human
populations. However, some studies have yielded
conflicting results. Recently, studies conducted in our
laboratory and others have demonstrated that iron
deposition is prominent in human atherosclerotic
lesions. The iron deposits appear to colocalize with
ceroid, which is an end product of extensively oxidized
lipid and protein complex, in lesions, providing
histological evidence to support the iron hypothesis.
Additional experiments in animals have further revealed
that the severity of atherosclerosis can be markedly
influenced by iron overload or deficiency.
Collectively, these data provide a strong pathological
basis to support the detrimental role of iron in
vascular damage and progression of the disease.

http://www.ncbi.nlm.nih.gov/pubmed/10421276

Strong epidemiological evidence is available that iron
is an important factor in the process of
atherosclerosis. Epidemiological studies, eg,
prospective follow-up studies in blood donors, may
clarify the cardiovascular benefits of iron depletion.
Knowledge of the molecular mechanism of iron-related
cardiovascular disease is still limited.

http://www.jvascnurs.net/article/S1062-0303(00)38179-1/abstract

This article summarizes research conducted during the
last 2 decades that addresses the idea that stored iron
plays a role in the pathogenesis of atherosclerosis and
that iron reduction through phlebotomy may play a role
in the treatment or prevention of atherosclerosis. Body
iron stores rise after adolescence in men and menopause
in women. This rise has been linked to the pathogenesis
of atherosclerosis through iron-induced oxidation of
low-density lipids and foam cell formation. However, the
available evidence on the iron hypothesis remains
circumstantial. Reduction of body iron stores in the
setting of a controlled, prospective intervention trial
is necessary to determine whether the amount of stored
iron is related to clinically meaningful vascular
disease.

-----------------

From what I read once, but don't remember precisely here,
excess iron is necessary for the formation of atheroclerosis --
no excess iron, littoe or no atheroclerosis.

Eric