EXCESS IRON IN THE BODY CAN CAUSE DIABETES. ALL DIABETICS SHOULD BE
SCREENED FOR THIS COMMON GENETIC CONDITION BY THEIR DOCTORS.
THE IRON ELEPHANT by Roberta Crawford
( Chapter 7, Page 43/Reprinted with permission of the author):
Untreated Iron Overload Can Give You Diabetes
One day in her doctor’s office in Mississippi Marta started feeling
cold and colder. Nurses wrapped her
in blankets, but she could not get warm. Finally a nurse had to bring
a heater into the office and turn it
full on Marta. The sudden temperature drop had happened before, but
the doctor had not really
believed Marta until this day. This day he hospitalized her.
Hypothyroidism can be a complication of
iron overload.
Looking back at those days, Marta rages that incompetent medical
care–specifically medical ignorance
about iron overload–has ruined her life. Her mother remembers her as
a pretty little kid, a fair delicate
skinned redhead, lively but easily tired.
"If I had seen a Dr. Crosby at age fifteen," she says, "my life would
have been different." Instead of
being disabled, Marta is certain she would now be normal, with
husband, children, career. William H.
Crosby is a world wide authority on hemochromatosis. Marta had met
him at an IOD symposium.
At age twenty-nine Marta completed menopause and thus gave up her
dreams of having children.
Unsuccessful efforts to have a baby have scuttled many a marriage.
Marta gave up on those efforts
because of her many no-name illnesses.
Emotional scars deepened years later when a fiancé jilted her just two
weeks before their wedding.
"Failing libido…low energy…it was too much for him," Marta says.
Health problems mounted. The act of eating became so strenuous that
Marta would have to look for a
place to lie down after meals. It was not that she neglected medical
care. She allowed physicians to
perform dilation and curettage and two laparoscopies. She describes
that procedure as "going in
through the navel and looking around."
Marta started suffering a series of influenses. "I never really got
over one"," she says," they sort of
overlapped." Doctors kept her on constant antibiotics, and for more
than a year prescribed massive
doses of Motrin for painful, crooked fingers. The medication did not
help.
Profoundly exhausted and depressed, Marta visited her mother in
Indiana for two weeks to recuperate.
Friends were startled by her "greenish" color. Marta tried to help
her color by sunbathing at poolside.
Otherwise she slept for days and days. But Marta could not rest away
the deep fatigue.
Back to Mississippi and back to doctors. "Well, your liver enzymes
are elevated," said a doctor, "but if it
were anything serious you’d be dead." When Marta asked for a second
opinion, the doctor became
defensive. "Why: You don’t think I can take care of you?" Marta
nevertheless sought help from an
internist.
Finally a urine check revealed sugar. Diabetes was diagnosed. Iron
overload was then detected at last.
Marta’s first migraine headache struck while she was in the hospital.
Since then the headaches–"three
day killers"–have become a weekly way of life.
Now Marta occupies herself with twice weekly phlebotomies to unload
the iron and with managing her
diabetes. She reflects on what has happened to her family. Her
younger sister, Marybeth, working in
television in New Jersey, then received a belated diagnosis as well.
Marybeth’s blood tests had also
revealed elevated liver enzymes that were ignored. At age eleven
Marybeth underwent treatment for
hepatitis. The family’s doctor was the same man who had treated their
father, dead of a stroke, enlarged
heart and enlarged liver at fifty-eight. His sickly brother had died
at fifty-four; the father of the two
brothers had died at fifty-five.
One thing that makes Marta grind her teeth is a notation that she saw
on medical records: "doubt
hemochromatosis." This note was entered not once but twice over the
years. Why was the suspicion not
followed up? she cries.
Clinical manifestations of diabetes in a hemochromatosis patient are
indistinguishable from those of any
diabetes.. Severity depends upon the amount of iron load and whether
the diabetes is discovered early or
late in the course of iron accumulation. You can expect improvement
in about half of all patients when
you unload the iron aggressively. Some patients are able to reduce or
discontinue insulin injections. This
outcome depends on the vigor of therapy.
Harold was a successful building contractor with an attractive wife
and three sons. The family divided
their time between Palm Beach and Bar Harbor, Maine. One day it
happened. Harold received the
unhappy diagnosis that he had diabetes. He was a man of means. He
could afford the best in medical
care, so Harold immediately checked in at the Joslin Clinic in Boston.
Blood sugar is difficult to regulate when the underlying cause of
pancreas damage in excess iron, unless
that iron is removed. Harold’s doctors at the clinic did not ask, "is
iron involved?"
It is preferable, of course, to find the iron before pancreas damage,
but every diabetic should be carefully
evaluated for iron. When physicians do not suspect iron overload,
they do not look for it; when they do
not look for iron overload, they do not find it.
The clinic gave Harold diet instructions and he went home to manage
the diabetes. But the diabetes was
unmanageable. Harold collapsed and ended in the hospital, where
hemochromatosis was finally
diagnosed.
Too late. Harold at that time had three months left of life.
Death certificates that list diabetes as the cause of death often omit
the real underlying cause:
hemochromatosis. No. The real cause is ignorance. You can
successfully treat hemochromatosis when
you detect it early.
"My grandmother and mother both died of diabetes," says a new
hemochromatosis patient thoughtfully.
The diabetes that often develops in iron overloaded individuals used
to be called bronze diabetes because
of the skin pigmentation that sometimes occurs. Iron can darken the
skin. However, it is a mistake to
rule out a diagnosis on the basis of light skin. Excess iron presents
many variables.
Most people who suffer iron caused diabetes are unaware they are iron
overloaded.
———————————————————————————————-
Note: It is estimated that 10% of all diabetics have iron overload
caused diabetes. This cause can be
ruled out by the doctor by performing the following blood work: serum
iron, TIBC, serum ferritin, and
percent of saturation.
Sandra Thomas, National Director of Public Education
Iron Overload Diseases Association, Inc. (non-profit)
About the Author:
Roberta Crawford is the founder/president of the Iron Overload
Diseases Association, Inc. (non-profit),
the international clearinghouse for information on iron
overload/hemochromatosis, a genetic disease of
high iron storage in the body. Roberta Crawford, who has iron
overload, wrote THE IRON
ELEPHANT. This book is intended to help the reader look at iron with
new eyes, to see iron in a new
light, and to gain understanding of the proper place of iron in human
health. This book should not be
substituted for the advice and treatment of a physician but rather
should be used as enhancement of the
reader’s understanding of iron . The author and publisher disclaim
responsibility of any adverse effects
resulting from the information presented here.
The following information is based on research and studies done by the
leading doctors and researchers in
the nation/world in the field of hemochromatosis and other iron
loading diseases:
IRON OVERLOAD ALERT
MORE THAN ONE MILLION AMERICANS HAVE UNDETECTED IRON OVERLOAD
WHAT IS IT?
The most common iron overload disease is hemochromatosis, a condition
of defective metabolism for
iron. Not a blood disease! The body lacks the ability to refrain
from absorbing excess iron from a regular
diet. Unlike other nutrients, iron is not excreted.
WHAT DOES IT DO?
Excessive iron injures organs and can result in a variety of
disorders: cancer (especially of the
male/female reproductive organs), heart disease/failure, arthritis,
chronic fatigue, diabetes (especially
"bronze diabetes" where the skin turns bronze or gray in color without
exposure to sunlight),
cirrhosis/cancer of the liver, impotence, sterility, infertility,
early menopause, and early death. The
patient may have any combination of these symptoms. Iron overload
should be diagnosed before overt
symptoms appear–routine testing will accomplish this mission. Iron
overload is lethal unless it is (1)
detected and equally vital, (2) adequately treated.
HOW DO YOU GET IT?
Genes that cause the metabolic defect are recessively inherited, the
most common abnormal gene known.
One out of 8 people carries the single gene (person is a carrier) and
one in 200 carries both genes (person
has hemochromatosis). Day by day the affected individual absorbs too
much iron, which accumulates in
organs and tissue.
Repeated blood transfusions, iron medication and extreme dietary iron
also result in iron damage to the
body.
Some anemias are iron-loading anemias. Low hemoglobin does not mean
low iron!
HOW DO YOU FIND OUT?
Measure SI (serum iron) and TIBC (Total Iron Binding Capacity)
TESTING
Mathematically divide TIBC into SI
Normal value 12-50%
Measure serum ferritin. Normal value: 5-150
(Labs vary. Most set normal limits too high)
If you test high: begin treatment
If you test low: you must search for
(1) chronic internal blood loss (ulcers?)
(2) tumor
(3) infection
Cancer cells and bacteria require iron for growth. These cells remove
iron from circulation and can
result in low saturation. At the same time ferritin (storage iron)
may spike, indicating cancer or
infection.
ALTERNATIVE TO LIVER BIOPSY
Treatment confirms the diagnosis! If a liver biopsy is performed, the
tissue must be properly stained to
…
read more »
HEMOCHROMATOSIS/IRON OVERLOAD FACT SHEET
1.) A genetic condition of abnormal iron metabolism that permits too
much absorption of iron from an
ordinary diet. It is NOT a blood disease. It is possible for someone
who has never had an iron pill in
their life, to have iron overload.
2.) Frequency (incidence in the general population) of the abnormal
gene is: 1 in 200 people has
hemochromatosis (double gene) and 1 in 8 people is a carrier of
hemochromatosis (single gene)
3.) Most affected people DO NOT KNOW they are accumulating dangerous
stores of iron. Tragically
underdiagnosed, no race, age, or gender is immune.
4.) The excess iron injures body organs and KILLS unless detected in
time for adequate removal.
5.) When the excess iron IS detected early and is ADEQUATELY removed,
the individual can enjoy a
normal life span in normal health.
6.) Iron damage may cause heart irregularities/failure; chronic
fatigue; cirrhosis/cancer of the liver;
arthritis; impotence/sterility/infertility, early menopause; diabetes
(bronze diabetes, a darkening, graying
of the skin not caused by sun exposure); or other forms of cancer
(cancer thrives on iron).
7.) The iron-overloaded person may be anemic at the same time. There
are several types of anemia that
are iron-loading!
8.) A simple blood test can indicate iron levels. They must be proper
iron measures: Total Iron Binding
Capacity (TIBC) together with Serum Iron. Divide TIBC into Serum Iron
to get the percentage of
transferrin saturation. Serum Ferritin. A new test, Serum
Ferritin-Iron Assay, hopefully will be available
through MetPath Labs in several months.
9.) LOW iron means investigate the cause: cancer? Internal bleeding?
Chronic infection? It is dangerous
to take iron without knowing the reason for the iron deficiency.
10.) When iron overload is discovered, it is imperative to unload the
excess iron as FAST AS POSSIBLE
by weekly or twice weekly bleedings. If severely anemic, an iron
chelator must be used instead of
bleedings, usually Desferal is the drug.
11.) All blood relatives of the iron-overloaded individual must be
checked and monitored for the rest of
their lives. This includes men, women (pre and post menopausal) and
children.
For more information on iron overload/hemochromatosis, please contact:
Sandra Thomas, National Director of Public Education, IOD
E-mail: KGMQ…@prodigy.com StarLad…@aol.com
Internet: starl…@emi.net
WWW Page: http://www.emi.net/~iron_iod/
Or write/call directly:
Iron Overload Diseases Association, Inc. (non-profit)
Roberta Crawford, Founder/President
433 Westwind Drive, North Palm Beach, Florida 33408-5123
Telephone: (407) 840-8512 or (407) 840-8513
- Hide quoted text — Show quoted text -
starl…@emi.net wrote:
>EXCESS IRON IN THE BODY CAN CAUSE DIABETES. ALL DIABETICS SHOULD BE
>SCREENED FOR THIS COMMON GENETIC CONDITION BY THEIR DOCTORS.
>THE IRON ELEPHANT by Roberta Crawford
>( Chapter 7, Page 43/Reprinted with permission of the author):
>Untreated Iron Overload Can Give You Diabetes
>One day in her doctor’s office in Mississippi Marta started feeling
>cold and colder. Nurses wrapped her
>in blankets, but she could not get warm. Finally a nurse had to bring
>a heater into the office and turn it
>full on Marta. The sudden temperature drop had happened before, but
>the doctor had not really
>believed Marta until this day. This day he hospitalized her.
>Hypothyroidism can be a complication of
>iron overload.
>Looking back at those days, Marta rages that incompetent medical
>care–specifically medical ignorance
>about iron overload–has ruined her life. Her mother remembers her as
>a pretty little kid, a fair delicate
>skinned redhead, lively but easily tired.
>"If I had seen a Dr. Crosby at age fifteen," she says, "my life would
>have been different." Instead of
>being disabled, Marta is certain she would now be normal, with
>husband, children, career. William H.
>Crosby is a world wide authority on hemochromatosis. Marta had met
>him at an IOD symposium.
>At age twenty-nine Marta completed menopause and thus gave up her
>dreams of having children.
>Unsuccessful efforts to have a baby have scuttled many a marriage.
>Marta gave up on those efforts
>because of her many no-name illnesses.
>Emotional scars deepened years later when a fiancé jilted her just two
>weeks before their wedding.
>"Failing libido…low energy…it was too much for him," Marta says.
>Health problems mounted. The act of eating became so strenuous that
>Marta would have to look for a
>place to lie down after meals. It was not that she neglected medical
>care. She allowed physicians to
>perform dilation and curettage and two laparoscopies. She describes
>that procedure as "going in
>through the navel and looking around."
>Marta started suffering a series of influenses. "I never really got
>over one"," she says," they sort of
>overlapped." Doctors kept her on constant antibiotics, and for more
>than a year prescribed massive
>doses of Motrin for painful, crooked fingers. The medication did not
>help.
>Profoundly exhausted and depressed, Marta visited her mother in
>Indiana for two weeks to recuperate.
>Friends were startled by her "greenish" color. Marta tried to help
>her color by sunbathing at poolside.
>Otherwise she slept for days and days. But Marta could not rest away
>the deep fatigue.
>Back to Mississippi and back to doctors. "Well, your liver enzymes
>are elevated," said a doctor, "but if it
>were anything serious you’d be dead." When Marta asked for a second
>opinion, the doctor became
>defensive. "Why: You don’t think I can take care of you?" Marta
>nevertheless sought help from an
>internist.
>Finally a urine check revealed sugar. Diabetes was diagnosed. Iron
>overload was then detected at last.
>Marta’s first migraine headache struck while she was in the hospital.
>Since then the headaches–"three
>day killers"–have become a weekly way of life.
>Now Marta occupies herself with twice weekly phlebotomies to unload
>the iron and with managing her
>diabetes. She reflects on what has happened to her family. Her
>younger sister, Marybeth, working in
>television in New Jersey, then received a belated diagnosis as well.
>Marybeth’s blood tests had also
>revealed elevated liver enzymes that were ignored. At age eleven
>Marybeth underwent treatment for
>hepatitis. The family’s doctor was the same man who had treated their
>father, dead of a stroke, enlarged
>heart and enlarged liver at fifty-eight. His sickly brother had died
>at fifty-four; the father of the two
>brothers had died at fifty-five.
>One thing that makes Marta grind her teeth is a notation that she saw
>on medical records: "doubt
>hemochromatosis." This note was entered not once but twice over the
>years. Why was the suspicion not
>followed up? she cries.
>Clinical manifestations of diabetes in a hemochromatosis patient are
>indistinguishable from those of any
>diabetes.. Severity depends upon the amount of iron load and whether
>the diabetes is discovered early or
>late in the course of iron accumulation. You can expect improvement
>in about half of all patients when
>you unload the iron aggressively. Some patients are able to reduce or
>discontinue insulin injections. This
>outcome depends on the vigor of therapy.
>Harold was a successful building contractor with an attractive wife
>and three sons. The family divided
>their time between Palm Beach and Bar Harbor, Maine. One day it
>happened. Harold received the
>unhappy diagnosis that he had diabetes. He was a man of means. He
>could afford the best in medical
>care, so Harold immediately checked in at the Joslin Clinic in Boston.
>Blood sugar is difficult to regulate when the underlying cause of
>pancreas damage in excess iron, unless
>that iron is removed. Harold’s doctors at the clinic did not ask, "is
>iron involved?"
>It is preferable, of course, to find the iron before pancreas damage,
>but every diabetic should be carefully
>evaluated for iron. When physicians do not suspect iron overload,
>they do not look for it; when they do
>not look for iron overload, they do not find it.
>The clinic gave Harold diet instructions and he went home to manage
>the diabetes. But the diabetes was
>unmanageable. Harold collapsed and ended in the hospital, where
>hemochromatosis was finally
>diagnosed.
>Too late. Harold at that time had three months left of life.
>Death certificates that list diabetes as the cause of death often omit
>the real underlying cause:
>hemochromatosis. No. The real cause is ignorance. You can
>successfully treat hemochromatosis when
>you detect it early.
>"My grandmother and mother both died of diabetes," says a new
>hemochromatosis patient thoughtfully.
>The diabetes that often develops in iron overloaded individuals used
>to be called bronze diabetes because
>of the skin pigmentation that sometimes occurs. Iron can darken the
>skin. However, it is a mistake to
>rule out a diagnosis on the basis of light skin. Excess iron presents
>many variables.
>Most people who suffer iron caused diabetes are unaware they are iron
>overloaded.
>———————————————————————————————-
>Note: It is estimated that 10% of all diabetics have iron overload
>caused diabetes. This cause can be
>ruled out by the doctor by performing the following blood work: serum
>iron, TIBC, serum ferritin, and
>percent of saturation.
>Sandra Thomas, National Director of Public Education
>Iron Overload Diseases Association, Inc. (non-profit)
>About the Author:
>Roberta Crawford is the founder/president of the Iron Overload
>Diseases Association, Inc. (non-profit),
>the international clearinghouse for information on iron
>overload/hemochromatosis, a genetic disease of
>high iron storage in the body. Roberta Crawford, who has iron
>overload, wrote THE IRON
>ELEPHANT. This book is intended to help the reader look at iron with
>new eyes, to
…
read more »
In article <DIKp5z….@emi.net>, <starl…@emi.net> wrote:
> HEMOCHROMATOSIS/IRON OVERLOAD FACT SHEET
I’ve seen this posting for the third or fourth time now. While I have no
reason to question that hemochromatosis may be a dangerous condition that
may go undiagnosed many times and that this fact alone may deserve more
attention, I’m getting a little irritated by those repetitive postings in
a very short interval.
This type of posting behaviour can usually be explained by
- technical problems (unlikely in this case)
- (possibly momentary) lack of control of the technology involved
- an urge to bring a message to the masses, usually preceived as some
kind of missionary activity
- an attempt to make money before the true motivation is revealed
Needless to say, people suspecting one of the last two reasons (and
particularly the last one, since following the advice might then not only
be useless but would even encourage further abuse), aren’t likely to ask
for the tests proposed in the posting to be performed, even if they would
have been motivated to do so after seeing the posting for the first one
or two times.
If your motivations are sincere, then I’m afraid you were overshooting and
you may have done your cause a disservice.
- Werner, wishing back the good old days before the Internet was a
commercial success
—
_________________________________________________________________________
/ Werner Almesberger, DI-LRC,EPFL,CH werner.almesber…@lrc.di.epfl.ch /
/_IN_R_133__Tel_+41_21_693_6621__Fax_+41_21_693_6610_____________________/
I have answered this gentleman privately via e-mail, but I shall also
do so publicly, IOD is a non profit organization whose sole mission is
to save lives by identifying hemochromatosis patients and educating
the public and medical community.
I serve as a non-paid volunteer for this organization and have done so
for the past ten years.
Anyone wishing more information, may e-mail me or contact our office
directly.
The repeated posts will not be continued, however, I shall continue to
post life saving information on this subject. Those who wish to read
and act upon it may do so.
Sandra Thomas, National Director of Public Education
Iron Overload Diseases Association, Inc. (non-profit)
- Hide quoted text — Show quoted text -
almes…@lrc.epfl.ch (Werner Almesberger) wrote:
>In article <DIKp5z….@emi.net>, <starl…@emi.net> wrote:
>> HEMOCHROMATOSIS/IRON OVERLOAD FACT SHEET
>I’ve seen this posting for the third or fourth time now. While I have no
>reason to question that hemochromatosis may be a dangerous condition that
>may go undiagnosed many times and that this fact alone may deserve more
>attention, I’m getting a little irritated by those repetitive postings in
>a very short interval.
>This type of posting behaviour can usually be explained by
> – technical problems (unlikely in this case)
> – (possibly momentary) lack of control of the technology involved
> – an urge to bring a message to the masses, usually preceived as some
> kind of missionary activity
> – an attempt to make money before the true motivation is revealed
>Needless to say, people suspecting one of the last two reasons (and
>particularly the last one, since following the advice might then not only
>be useless but would even encourage further abuse), aren’t likely to ask
>for the tests proposed in the posting to be performed, even if they would
>have been motivated to do so after seeing the posting for the first one
>or two times.
>If your motivations are sincere, then I’m afraid you were overshooting and
>you may have done your cause a disservice.
>- Werner, wishing back the good old days before the Internet was a
> commercial success
>–
> _________________________________________________________________________
> / Werner Almesberger, DI-LRC,EPFL,CH werner.almesber…@lrc.di.epfl.ch /
>/_IN_R_133__Tel_+41_21_693_6621__Fax_+41_21_693_6610_____________________/
In article <RAOUL.95Nov23223…@al-burro.mit.edu>,
ra…@al-burro.mit.edu (Nico Garcia) wrote:
> STARLADY KNOWS NOTHING ABOUT TYPE I DIABETES
> BELIEVING HER WILL CONFUSE TYPE I DIABETICS, WHO HAVE A COMPLETELY
> DIFFERENT PATHAOLOGY
Nico,
I sure hope you do as you promise and follow up on getting some information
about this disease before someone else who knows as little as you do about
it actually listens to you.
Hemochromatosis is a condition wherein the body absorbs and stores abnormal
amounts of iron. This condition can lead to fatal levels of iron
deposition in the organs (most frequently the PANCREAS, liver, and heart)
from diets that contain no more than "normal" amounts of iron. It can be
hereditary or acquired (most commonly in cases of anemias that require
frequent transfusions). The hereditary form is autosomal recessive and is
one of the most common hereditary diseases of people of European descent.
The symptoms of iron overload are general in nature and gradual in
appearance.
My family became "experts" on the disease the hard way. In April 1993 my
son was diagnosed with type l diabetes. Please note here, all you experts
out there who feel that you know everything there is to know about type 1,
that it can also be caused by excess levels of iron being deposited in the
pancreas. These deposits kill beta cells thus causing the pancreas to no
longer produce insulin – hence, type 1 diabetes.
Two months later, in June 1993, my son (age 25) ended up in the hospital
with congestive heart failure. He was transferred to MGH in Boston for
diagnosis of the cause and determination of a treatment plan. Tissue
stains from a heart biopsy showed an extremely high level of iron which was
the cause of his cardiomyopathy that led to congestive heart failure.
Diagnosis was hereditary hemochromatosis leading to diabetes and
cardiomyopathy. For those of you who still do not believe, I refer you to
the August 18,1994 issue of the new England of Medicine case records from
Mass General concerning my son’s case.
To continue the saga of hemochromatosis, my son received a heart/liver
transplant (the liver was also a goner due to the iron) in August 1993.
They had considered throwing in a pancreas too while they were at it. But
the consensus was that the pancreas was optional (as diabetes can be
controlled with insulin) so it was an unnecessary complication on something
that was going to be a tricky proposition in the first place.
My son’s case was unusual in that he had accumulated enough iron to do
extensive damage at such an early age. Damage is not usually seen in men
until their mid-40′s and in women until about ten years later. According
to the National Organization for Rare Disorders, "Many patients are
diagnosed on autopsy because they appear to be healthy adults who die
suddenly." My son was diagnosed and treated at one the top hospitals in
the country, and the doctors there put the possibility of hemochromatosis
being the ultlimate diagnosis at the very bottom of their list going into
things. It was a possibility, but not a probability. Even hot shots can
be suprised once in a while.
If anyone out there would like to know more about this subject, I suggest
that they contact the Iron Overload Diseases Assoc. at 407-840-8512 (and
8513). Or visit their web page at http://www.emi.net/~iron_iod/
Regards,
Marianne D’Angelo
Thanks to Marianne for commenting on diabetes and iron storage.
Unfortunately, many of us find out about this connection the hard way.
I too have diabetes in the family. My maternal great grandfather and
grandfather both had diabetes and died from it, undiagnosed at the
time, no doubt, of hemochromatosis. My mother was the first in the
family to be diagnosed with hemochromatosis, although she had not
developed diabetes (yet) but had other health problems as a result.
Unfortunately, the public and the medical community are not as aware
of this potentially lethal but treatable condition as they should be.
Too many people are being injured and dying needless deaths due to
lack of diagnosis and treatment.
For more info, please email me (starl…@emi.net) or contact the IOD
office directly: (407) 840-8512. Inquiries from the public as well as
medical professionals are most welcome.
Sandra Thomas, National Director of Public Education, IOD
- Hide quoted text — Show quoted text -
r…@tiac.net (Marianne D’Angelo) wrote:
>In article <RAOUL.95Nov23223…@al-burro.mit.edu>,
>ra…@al-burro.mit.edu (Nico Garcia) wrote:
>> STARLADY KNOWS NOTHING ABOUT TYPE I DIABETES
>> BELIEVING HER WILL CONFUSE TYPE I DIABETICS, WHO HAVE A COMPLETELY
>> DIFFERENT PATHAOLOGY
>Nico,
>I sure hope you do as you promise and follow up on getting some information
>about this disease before someone else who knows as little as you do about
>it actually listens to you.
>Hemochromatosis is a condition wherein the body absorbs and stores abnormal
>amounts of iron. This condition can lead to fatal levels of iron
>deposition in the organs (most frequently the PANCREAS, liver, and heart)
>from diets that contain no more than "normal" amounts of iron. It can be
>hereditary or acquired (most commonly in cases of anemias that require
>frequent transfusions). The hereditary form is autosomal recessive and is
>one of the most common hereditary diseases of people of European descent.
>The symptoms of iron overload are general in nature and gradual in
>appearance.
>My family became "experts" on the disease the hard way. In April 1993 my
>son was diagnosed with type l diabetes. Please note here, all you experts
>out there who feel that you know everything there is to know about type 1,
>that it can also be caused by excess levels of iron being deposited in the
>pancreas. These deposits kill beta cells thus causing the pancreas to no
>longer produce insulin – hence, type 1 diabetes.
>Two months later, in June 1993, my son (age 25) ended up in the hospital
>with congestive heart failure. He was transferred to MGH in Boston for
>diagnosis of the cause and determination of a treatment plan. Tissue
>stains from a heart biopsy showed an extremely high level of iron which was
>the cause of his cardiomyopathy that led to congestive heart failure.
>Diagnosis was hereditary hemochromatosis leading to diabetes and
>cardiomyopathy. For those of you who still do not believe, I refer you to
>the August 18,1994 issue of the new England of Medicine case records from
>Mass General concerning my son’s case.
>To continue the saga of hemochromatosis, my son received a heart/liver
>transplant (the liver was also a goner due to the iron) in August 1993.
>They had considered throwing in a pancreas too while they were at it. But
>the consensus was that the pancreas was optional (as diabetes can be
>controlled with insulin) so it was an unnecessary complication on something
>that was going to be a tricky proposition in the first place.
>My son’s case was unusual in that he had accumulated enough iron to do
>extensive damage at such an early age. Damage is not usually seen in men
>until their mid-40′s and in women until about ten years later. According
>to the National Organization for Rare Disorders, "Many patients are
>diagnosed on autopsy because they appear to be healthy adults who die
>suddenly." My son was diagnosed and treated at one the top hospitals in
>the country, and the doctors there put the possibility of hemochromatosis
>being the ultlimate diagnosis at the very bottom of their list going into
>things. It was a possibility, but not a probability. Even hot shots can
>be suprised once in a while.
>If anyone out there would like to know more about this subject, I suggest
>that they contact the Iron Overload Diseases Assoc. at 407-840-8512 (and
>8513). Or visit their web page at http://www.emi.net/~iron_iod/
>Regards,
>Marianne D’Angelo
HEMOCHROMATOSIS/IRON OVERLOAD FACT SHEET
1.) A genetic condition of abnormal iron metabolism that permits too
much absorption of iron from an
ordinary diet. It is NOT a blood disease. It is possible for someone
who has never had an iron pill in
their life, to have iron overload.
2.) Frequency (incidence in the general population) of the abnormal
gene is: 1 in 200 people has
hemochromatosis (double gene) and 1 in 8 people is a carrier of
hemochromatosis (single gene)
3.) Most affected people DO NOT KNOW they are accumulating dangerous
stores of iron. Tragically
underdiagnosed, no race, age, or gender is immune.
4.) The excess iron injures body organs and KILLS unless detected in
time for adequate removal.
5.) When the excess iron IS detected early and is ADEQUATELY removed,
the individual can enjoy a
normal life span in normal health.
6.) Iron damage may cause heart irregularities/failure; chronic
fatigue; cirrhosis/cancer of the liver;
arthritis; impotence/sterility/infertility, early menopause; diabetes
(bronze diabetes, a darkening, graying
of the skin not caused by sun exposure); or other forms of cancer
(cancer thrives on iron).
7.) The iron-overloaded person may be anemic at the same time. There
are several types of anemia that
are iron-loading!
8.) A simple blood test can indicate iron levels. They must be proper
iron measures: Total Iron Binding
Capacity (TIBC) together with Serum Iron. Divide TIBC into Serum Iron
to get the percentage of
transferrin saturation. Serum Ferritin. A new test, Serum
Ferritin-Iron Assay, hopefully will be available
through MetPath Labs in several months.
9.) LOW iron means investigate the cause: cancer? Internal bleeding?
Chronic infection? It is dangerous
to take iron without knowing the reason for the iron deficiency.
10.) When iron overload is discovered, it is imperative to unload the
excess iron as FAST AS POSSIBLE
by weekly or twice weekly bleedings. If severely anemic, an iron
chelator must be used instead of
bleedings, usually Desferal is the drug.
11.) All blood relatives of the iron-overloaded individual must be
checked and monitored for the rest of
their lives. This includes men, women (pre and post menopausal) and
children.
For more information on iron overload/hemochromatosis, please contact:
Sandra Thomas, National Director of Public Education, IOD
E-mail: KGMQ…@prodigy.com StarLad…@aol.com
Internet: starl…@emi.net
WWW Page: http://www.emi.net/~iron_iod/
Or write/call directly:
Iron Overload Diseases Association, Inc. (non-profit)
Roberta Crawford, Founder/President
433 Westwind Drive, North Palm Beach, Florida 33408-5123
Telephone: (407) 840-8512 or (407) 840-8513
- Hide quoted text — Show quoted text -
r…@tiac.net (Marianne D’Angelo) wrote:
>In article <RAOUL.95Nov23223…@al-burro.mit.edu>,
>ra…@al-burro.mit.edu (Nico Garcia) wrote:
>> STARLADY KNOWS NOTHING ABOUT TYPE I DIABETES
>> BELIEVING HER WILL CONFUSE TYPE I DIABETICS, WHO HAVE A COMPLETELY
>> DIFFERENT PATHAOLOGY
>Nico,
>I sure hope you do as you promise and follow up on getting some information
>about this disease before someone else who knows as little as you do about
>it actually listens to you.
>Hemochromatosis is a condition wherein the body absorbs and stores abnormal
>amounts of iron. This condition can lead to fatal levels of iron
>deposition in the organs (most frequently the PANCREAS, liver, and heart)
>from diets that contain no more than "normal" amounts of iron. It can be
>hereditary or acquired (most commonly in cases of anemias that require
>frequent transfusions). The hereditary form is autosomal recessive and is
>one of the most common hereditary diseases of people of European descent.
>The symptoms of iron overload are general in nature and gradual in
>appearance.
>My family became "experts" on the disease the hard way. In April 1993 my
>son was diagnosed with type l diabetes. Please note here, all you experts
>out there who feel that you know everything there is to know about type 1,
>that it can also be caused by excess levels of iron being deposited in the
>pancreas. These deposits kill beta cells thus causing the pancreas to no
>longer produce insulin – hence, type 1 diabetes.
>Two months later, in June 1993, my son (age 25) ended up in the hospital
>with congestive heart failure. He was transferred to MGH in Boston for
>diagnosis of the cause and determination of a treatment plan. Tissue
>stains from a heart biopsy showed an extremely high level of iron which was
>the cause of his cardiomyopathy that led to congestive heart failure.
>Diagnosis was hereditary hemochromatosis leading to diabetes and
>cardiomyopathy. For those of you who still do not believe, I refer you to
>the August 18,1994 issue of the new England of Medicine case records from
>Mass General concerning my son’s case.
>To continue the saga of hemochromatosis, my son received a heart/liver
>transplant (the liver was also a goner due to the iron) in August 1993.
>They had considered throwing in a pancreas too while they were at it. But
>the consensus was that the pancreas was optional (as diabetes can be
>controlled with insulin) so it was an unnecessary complication on something
>that was going to be a tricky proposition in the first place.
>My son’s case was unusual in that he had accumulated enough iron to do
>extensive damage at such an early age. Damage is not usually seen in men
>until their mid-40′s and in women until about ten years later. According
>to the National Organization for Rare Disorders, "Many patients are
>diagnosed on autopsy because they appear to be healthy adults who die
>suddenly." My son was diagnosed and treated at one the top hospitals in
>the country, and the doctors there put the possibility of hemochromatosis
>being the ultlimate diagnosis at the very bottom of their list going into
>things. It was a possibility, but not a probability. Even hot shots can
>be suprised once in a while.
>If anyone out there would like to know more about this subject, I suggest
>that they contact the Iron Overload Diseases Assoc. at 407-840-8512 (and
>8513). Or visit their web page at http://www.emi.net/~iron_iod/
>Regards,
>Marianne D’Angelo
In article <ACDB5F23966849…@rfd.tiac.net>,
Marianne D’Angelo <r…@tiac.net> wrote:
>In article <RAOUL.95Nov23223…@al-burro.mit.edu>,
>ra…@al-burro.mit.edu (Nico Garcia) wrote:
>> STARLADY KNOWS NOTHING ABOUT TYPE I DIABETES
>> BELIEVING HER WILL CONFUSE TYPE I DIABETICS, WHO HAVE A COMPLETELY
>> DIFFERENT PATHAOLOGY
Excuse me: I mis-spelled PATHOLOGY.
>I sure hope you do as you promise and follow up on getting some information
>about this disease before someone else who knows as little as you do about
>it actually listens to you.
I’ve seen notes and articles on it before, thank you. They are
consistent with the the web page STARLADY mentions, although it has no
pointers to more detailed information but is merely the contents of
her article here, which she *keeps posting*. I’ve also written to her
postmaster to complain about the duplicate postings.
>My family became "experts" on the disease the hard way. In April 1993 my
>son was diagnosed with type l diabetes. Please note here, all you experts
>out there who feel that you know everything there is to know about type 1,
>that it can also be caused by excess levels of iron being deposited in the
>pancreas. These deposits kill beta cells thus causing the pancreas to no
>longer produce insulin – hence, type 1 diabetes.
Sigh. We’ve seen multiple definitions of Type I diabetes, which I really
hate: it’s why I hate the "Type I/II" distinction, it gets mis-used.
Did your son lose all beta cells, or merely most? What were his C-peptide
results, if that test has been done since onset? Could this have been
independent of his diabetes in this case? I’m actually curious.
>Two months later, in June 1993, my son (age 25) ended up in the hospital
>with congestive heart failure. He was transferred to MGH in Boston for
>diagnosis of the cause and determination of a treatment plan. Tissue
>stains from a heart biopsy showed an extremely high level of iron which was
>the cause of his cardiomyopathy that led to congestive heart failure.
>Diagnosis was hereditary hemochromatosis leading to diabetes and
>cardiomyopathy. For those of you who still do not believe, I refer you to
>the August 18,1994 issue of the new England of Medicine case records from
>Mass General concerning my son’s case.
Do you mean New England Journal of Medicine? I can check those. This
is interesting. Now, me, if I were examining your son’s case, I’d have
questioned the Type I diagnosis at age 25. It sounds like they
definitely missed the problem, although they may not have had clues to
search further.
>To continue the saga of hemochromatosis, my son received a heart/liver
>transplant (the liver was also a goner due to the iron) in August 1993.
>They had considered throwing in a pancreas too while they were at it. But
>the consensus was that the pancreas was optional (as diabetes can be
>controlled with insulin) so it was an unnecessary complication on something
>that was going to be a tricky proposition in the first place.
*GACK*. I hope he is doing all right. I also know there is some beta
cell work going on at MGH, that we’ve seen mentioned here. Sounds like
your son had a very rough time. He has no insulin production left?
Can he get on this group? I’d be very curious to hear from him about
this.
>My son’s case was unusual in that he had accumulated enough iron to do
>extensive damage at such an early age. Damage is not usually seen in men
>until their mid-40′s and in women until about ten years later. According
>to the National Organization for Rare Disorders, "Many patients are
>diagnosed on autopsy because they appear to be healthy adults who die
>suddenly." My son was diagnosed and treated at one the top hospitals in
>the country, and the doctors there put the possibility of hemochromatosis
>being the ultlimate diagnosis at the very bottom of their list going into
>things. It was a possibility, but not a probability. Even hot shots can
>be suprised once in a while.
MGH is a very, very good research hospital, especially in
surgery. However, I have my personal doubts about their diagnostic
competence and especially their handling of chronic or "uninteresting"
problems. I’ve coped with them on occasion, for emergencies and
research: for experimental procedures I’d go there, but for standard
medicine I’d consider a hospital where I know the staff personally and
they will cooperate with me in treating the problem more quickly and
more individually. They may have improved: it’s been a year since
I visited their ER (I got mugged, had my jaw checked out), but their
idea of triage is pretty sad).
Interesting, though. Is it only older diabetics that can turn out to
be hemochromatosis? From your description, I would suspect this.
>If anyone out there would like to know more about this subject, I suggest
>that they contact the Iron Overload Diseases Assoc. at 407-840-8512 (and
>8513). Or visit their web page at http://www.emi.net/~iron_iod/
No point to reading it. Starlady *keeps posting the entire web page*,
anytime anybody else posts here. There is no detailed information on
it, just that one-page press release style IRON OVERLOAD CAN KILL sort
of tabloid writing.
Shame, really. A simple description of classic symptoms, typical age
of onset, etc., straight out of a medical text, would be very helpful.
Nico Garcia
ra…@mit.edu
My opinions are my own, not MIT’s or my employer’s or my cat’s
(Well, maybe my cat’s….)
Nico Garcia (ra…@ATHENA.MIT.EDU) wrote:
: Sigh. We’ve seen multiple definitions of Type I diabetes, which I really
: hate: it’s why I hate the "Type I/II" distinction, it gets mis-used.
: Did your son lose all beta cells, or merely most? What were his C-peptide
: results, if that test has been done since onset? Could this have been
: independent of his diabetes in this case? I’m actually curious.
: Do you mean New England Journal of Medicine? I can check those. This
: is interesting. Now, me, if I were examining your son’s case, I’d have
: questioned the Type I diagnosis at age 25. It sounds like they
: definitely missed the problem, although they may not have had clues to
: search further.
(Just parenthetically, why would you have questioned a Type I diagnosis
at 25? At that age, Type I is still more commonly diagnosed than Type II….)
: Interesting, though. Is it only older diabetics that can turn out to
: be hemochromatosis? From your description, I would suspect this.
: Shame, really. A simple description of classic symptoms, typical age
: of onset, etc., straight out of a medical text, would be very helpful.
Well, my Merck Manual says:
"Hemochromatosis is rare before middle age. The typical manifestations are
cirrhosis of the liver, bronze skin pigmentation, diabetes mellitus
(overt in 50 to 60% of patients), and cardiomyopathy manifested by
cardiomegaly, heart failure, and arrhythmias or conduction disturbances.
Pituitary failure is common and may be the cause of the frequently
observed testicular atrophy and loss of libido. Abdominal pain,
arthritis, and chondrocalcinosis occur less often. Presumably, all of
these changes are due to parenchymal Fe deposition, although an increased
familial incidence of diabetes mellitus suggests that factors other than
pancreatic siderosis* may play a role. Hepatomas ocur with increased
frequency in patients with long-standing hemochromatosis."
Siderosis = greater than normal deposition of Fe in the tissues,
resulting in tissue injury.
As you notice, it doesn’t say anything about whether Type I or II, but if
the definition of Type I is diabetes caused by the destruction of the
beta cells and Type II is a result of excessive insulin resistance, then
it’s likely that the diabetes of hemochromatosis is closer to Type I than
to Type II. True, it’s not CLASSICAL Type I, but not classical Type II,
either, and it would seem likely that patients would respond more like
Type I’s than Type II’s to treatment, for example, they would probably
respond better to insulin than to orals, and they would probably be
sensitive to small insulin doses.
One of the things that this discussion shows is that diabetes is, once
again, just not simple, and there are MORE than the standard 2 types that
everyone talks about. Just because the majority of the flowers in the
garden are red or yellow doesn’t mean they ALL are!
And, Nico, it’s true that StarLady IS posting this a bit too often, but
this IS valid information, and there may be readers out there who NEED to
know it!
Smiles,
._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c-
Natalie A. Sera, AKA Dr. Quack, with all her ducks in a row!!!!
___
Type \/ 3, MI 4x (3Rs and an N) a year and a half!
Proud mother of Josh, age 21
._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._(` ._c- ._c- ._c- ._c- ._c-
Can YOU find the Ugly Duckling?
Carol Haagensen (XEPK…@prodigy.com) wrote:
: This sounds like an interesting disease….one I’m unfamiliar with.
(So please do a little reading up on it! And share your findings!)
: With an elevated SGOT, he should have been
: alerted that something wierd was happening because a diabetic’s SGOT is
: usually LOW, not elevated. Interestingly enough, the SGOT rises
: whenever cells die from any of several organs…but it is abnormally low
: in uncontrolled diabetes…and here’s the kicker!–SGOT is the same thing
: as the amino acid aspartine (Nutrasweet)! In theory, then, diabetics
: would benefit from aspartine!
If the SGOT alone is elevated, the doctors don’t get too excited, because
even a hard day of exercise can elevate it. I’ve had elevated SGOT
several times. If several OTHER enzymes are elevated as well, it’s time
to get worried.
And SGOT is NOT the same thing as aspartine (Nutrasweet) (sic) . It’s an
enzyme. The abbreviation SGOT stands for serum glutamic oxaloacetic
transaminase. However, it’s now most frequently called AST – aspartate
transaminase. Don’t let the fact that it has "aspartate" in the name
confuse you — it’s NOT the same thing.
Thanks for bringing this up — the more we all investigate, the more we
can all learn!
Smiles,
._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c-
Natalie A. Sera, AKA Dr. Quack, with all her ducks in a row!!!!
___
Type \/ 3, MI 4x (3Rs and an N) a year and a half!
Proud mother of Josh, age 21
._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._c- ._(` ._c- ._c- ._c- ._c- ._c-
Can YOU find the Ugly Duckling?
In article <4965v0$…@senator-bedfellow.MIT.EDU>,
ra…@ATHENA.MIT.EDU (Nico Garcia) wrote:
Nico,
I refuse to get into a spitting contest with you. If you have a problem
with the diagnosis of my son’s case, I suggest that you take it up with the
editorial board at the New England Journal of Medicine for printing a case
record which you find inferior. As I stated previously, the issue is
8/18/94 — pages 460-66 to be precise.
I hope that your response is due to your own lack of information, and not
due to arrogance impeding an admission of that lack. The posting of the
consequences of iron overload in this newsgroup is entirely appropriate, as
one of the complications of the condition is diabetes. This has been known
for over 100 years. The problem is that it is not possible to know that
iron overload exists unless specific tests are done for it. In iron
overload, diabetes can be one step on the way to further, and ultimately
fatal, complications. I, for one, would appreciate such information in
advance since there is a treatment for hemochromatosis which, once again,
has been known for over 100 years. Just because doctors don’t check for a
specific condition, it doesn’t mean that it doesn’t exist.
> MGH is a very, very good research hospital, especially in
> surgery. However, I have my personal doubts about their diagnostic
> competence and especially their handling of chronic or "uninteresting"
> problems. I’ve coped with them on occasion, for emergencies and
> research: for experimental procedures I’d go there, but for standard
> medicine I’d consider a hospital where I know the staff personally and
> they will cooperate with me in treating the problem more quickly and
> more individually. They may have improved
I’m sure that MGH (which was just ranked by US News and World Report within
the past week as the #3 hospital in the nation) will be concerned by your
assessment of them. And I am sorry for you that they found you
"uninteresting." I can assure anyone that is interested that our family
has found their physicians and staff to be outstanding, cooperative,
supportive, and any number of other superlatives. I would highly recommend
them to one and all.
Normally, I would be happy to refer you to my sons docs for your further
enlightenment, which you so obviously require, but they are very busy
people who do not have time for crackpots. And, as we have to continue to
deal with them on a regular basis, I would prefer to maintain our current
amiable, cooperative relationship. But, if you are truly interested, you
could start by looking up the heads of the cardiology, hematology,
gastroenterology, transplantation, endocrinology, etc. groups. I’m sure
they would be receptive to your questions as to their competence in making
patient evaluations. Have you perhaps missed your calling in life?
BTW, what institution are you affiliated with? I would imagine that
everyone here would like to know what your credentials are.
> it’s been a year since
> I visited their ER (I got mugged, had my jaw checked out), but their
> idea of triage is pretty sad).
I didn’t realize that it was possible to be mugged online. Or do you have
the same charming personality in the real world too?
Regards,
Marianne D’Angelo
In article <496juh$2…@usenetw1.news.prodigy.com>,
XEPK…@prodigy.com (Carol Haagensen) wrote:
> This sounds like an interesting disease….one I’m unfamiliar with. I am
> interested, therefore, why the chemistry panels did not show this
> advancing problem.
> If you have specific
> information about the lab work, I would enjoy reviewing it. Thanks. –
> ch
Carol,
You are right on the mark in saying that the disease is one you’re
unfamiliar with. That is the problem in a nutshell. My son had exhibited
symptoms of iron overload for many years, but since they are so general in
nature and gradual in onset, they were either attributed to something else
or things "corrected" themselves as time went on (and before any diagnosis
was made). He was always seemingly healthy – played Little League
baseball, Pop Warner football; in high school he ran track, wrestled,
played football; played tennis and golf for recreation, etc. Every now and
then something would come up like severe abdominal pains that landed him in
the ER, only to dissipate by the time a doctor saw him; enlarged liver that
would return to "normal"; heart "murmur" that lead to an ultrasound that
would show "nothing"; ultrasound of the gall bladder that would show
nothing; thousands of dollars of bloodwork done in college for widely
fluctuating platelet counts, etc. that were ultimately attributed to
mononucleosis. This went on for years, becoming more frequent as he grew
older — but always looking and acting "healthy." He received what you
would refer to as "good" medical care all his life. He had the same
pediatrician for the first 10 years of his life, the next one for 4 years,
went through several internists is high school because his regular doctor
left town, and spent a great deal of time in the hematology lab of the
medical school of the university he attended (where they looked for such
things as leukemia and ended up saying "probably mono" without ever
considering hemochromatosis).
When he was 25, things finally started to fall apart for good. He went to
a local internist who took one look at him and said he had diabetes. Six
days in the hospital got his diabetes under control and tests showed, among
other things, an enlarged liver, heart irregularities, high triglycerides,
etc. About a month later, after he had improved considerably from having
his diabetes under control, his doctor referred him to an endocrinologist
who found a whole host of other "abnormal" lab results. On his follow-up
visit to his internist, an EKG ( it was about the 8th one they had done
since he had been hospitalized) showed something really bad was going on.
He was sent straight to the ER (no stops along the way) to see a
cardiologist. One look there at an ultrasound, and they picked up the
phone to pass him on to Mass General Hospital.
In short, there were lots of tests done, all showing a lot of things were
"not quite normal," but that doesns’t get you anywhere unless you can tie
them all together. Some of the initial numbers from tests done on his
admittance to MGH appear in the NEJM 8/18/94 issue.
If the patient looks healthy and acts healthy, doctors rightly assume that
he *is* healthy. That makes sense, otherwise you would have to go around
assuming that we are all *sick* just because we look healthy.
I can remember many moons ago reading in Physiology 101 that excess iron
can be toxic. So I would expect that it would be common knowledge among
medical professionals. It probably is, but they don’t go the next step to
realize that it is possible (and not all that uncommon) for the body to
absorb abnormally large amounts of iron from a normal diet. And this can
lead to widespread damage. It is even possible to be anemic while your
body has accumulated and stored huge amounts or iron in various sites.
There is no way of knowing that someone has excess iron unless you test for
that specifically. I can only tell you that after all the tests and
problems my son had, no one diagnosed hemochromatosis until the tissue
stains from his heart biopsy "lit up like a Christmas tree" according to
his cardiologist. At that point, all the residents and fellows ran to
their terminals and began furiously searching Medline to bone up on this
"new" disease.
Hindsight is always 20/20 as they say. But is a waste of time saying that
someone *should have* seen the problem. The *real* problem is that too
many medical professionals are unaware that such a potential problem
exists, therefore they don’t look for it in the first place.
If I had my druthers, my son would have been diagnosed years ago before the
damage was irreversible. But, all things considered, we are very happy to
just have to worry about diabetes (since they elected not to include a
pancreas) and taking immunosuppressants and all that goes along with them.
But it would at least serve some purpose if some other doctor or patient
could learn from my son’s case. That is why I cannot allow a post such as
Mr. Garcia’s to go unanswered. Ignorance can be fatal.
If you are interested in learning more, a good starting reference would be
"Overview of Hemochromatosis" by Lloyd H Smith in The Western Journal of
Medicine, September 1990. It was one of the many references the MGH
fellows were kind enough to share with us in our mutual learning process.
Regards,
Marianne D’angelo
In article <ACDCD0329668142…@rfd.tiac.net> r…@tiac.net (Marianne D’Angelo) writes:
I refuse to get into a spitting contest with you. If you have a problem
with the diagnosis of my son’s case, I suggest that you take it up with the
editorial board at the New England Journal of Medicine for printing a case
record which you find inferior. As I stated previously, the issue is
8/18/94 — pages 460-66 to be precise.
Oh, bite me. Your son’s been through a lot of grief, sharing that is
cool. Bringing new medical information to the group is
wonderful. Including the same damn web page to every posting on the
net, with no personal comment, is really stupid, and that’s what
starlady was doing. A Usenet posting full of
IRON OVERLOAD CAUSES DEATH,
etc., headlines is not useful, which was the original problem. There
was some real data there, which I looked at and have no problem with.
But picture every person on first encountering that posting, who
doesn’t know the actual risk of it, or hasn’t had a chance to look for
details of it. It’s tabloid sensationalism. Data, like your
description of your son’s case, is far more effective, especially in
this forum.
I hope that your response is due to your own lack of information,
and not
due to arrogance impeding an admission of that lack. The posting of the
consequences of iron overload in this newsgroup is entirely appropriate, as
one of the complications of the condition is diabetes. This has been known
for over 100 years. The problem is that it is not possible to know that
Well, yeah. That’s cool. It’s the style, and the lack of data. For
example: what is typical age of complications from iron overload, from
your own note? 30′s or older? That’s not classically Type I. So isn’t
the possibility of diabetes-induced hemochromatosis far more likely
for Type II, and extremely unlikely for Type I? And by treating the
iron overload, can the beta cell function be restored or preserved?
I’ve talked to MGH doctors and nurses about Type I vs. Type II and the
change in diagnostic labels from adult-onset and juvenile-onset. They
were *very* sloppy about insulin independence being different from
adult-onset, and sloppiness with the labels has gotten very common
everywhere. And if you see them for other problems (such as ER or
orthopedic surgery), I would monitor my diabetes myself, because they
didn’t *watch* it. Left me sick as a dog when I broke my leg and they
treated me there.
iron overload exists unless specific tests are done for it. In iron
overload, diabetes can be one step on the way to further, and ultimately
fatal, complications. I, for one, would appreciate such information in
advance since there is a treatment for hemochromatosis which, once again,
has been known for over 100 years. Just because doctors don’t check for a
specific condition, it doesn’t mean that it doesn’t exist.
Well, yeah. Now, are there any additional symptoms of hemochromatosis
that we can watch for, to help us convince the doctor to look further?
I’m sure that MGH (which was just ranked by US News and World Report within
the past week as the #3 hospital in the nation) will be concerned by your
assessment of them. And I am sorry for you that they found you
"uninteresting." I can assure anyone that is interested that our family
has found their physicians and staff to be outstanding, cooperative,
supportive, and any number of other superlatives. I would highly recommend
them to one and all.
You have, frankly, a fascinating case. They are wonderful for that sort
of work. Organ transplants are considered exciting work, especially things
like livers that are life-saving and don’t happen often, and are difficult.
Try a broken leg, simple contusions or lacerations, or a bad insulin
reaction. They make very pretty stitches, but they lie about what
procedure they’re about to do, they didn’t check levels of anesthesia
before proceeding, they ignored my blood work when flat on my back for
the broken leg, assumed "diabetic" meant "lo-calorie diet", and wound
up making me sick as a dog until my sister (an endocrinologist in town
for a convention) happened to visit and raised bloody hell. Then the
Demerol wore off, I read my chart, and *I* raised bloody hell.
Or waiting an hour for their "stat" lab work to come back to confirm
that the glucose level is back up. By that point, you could miss lunch
and it could be coming back down again!
Normally, I would be happy to refer you to my sons docs for your further
enlightenment, which you so obviously require, but they are very busy
people who do not have time for crackpots. And, as we have to continue to
deal with them on a regular basis, I would prefer to maintain our current
amiable, cooperative relationship. But, if you are truly interested, you
could start by looking up the heads of the cardiology, hematology,
gastroenterology, transplantation, endocrinology, etc. groups. I’m sure
they would be receptive to your questions as to their competence in making
patient evaluations. Have you perhaps missed your calling in life?
Nope. In fact, I know some staff there personally. My dad also did
some radiation treatment research there years ago. If you want names,
ask off the group. The problem for me, perhaps, was that I was dealing
with surgeons. Surgery is famous for getting bone-heads of medical
schools, especially osteopathy. While the heads of departments tend to
be very good (especially at big hospitals like MGH), the heads do not
handle standard cases. So the
BTW, what institution are you affiliated with? I would imagine that
everyone here would like to know what your credentials are.
Bio-electric engineering from MIT. I’ll mention my job off the group in
private email if you want.
I didn’t realize that it was possible to be mugged online. Or do you have
the same charming personality in the real world too?
Marianne, I was giving a buck to a wino near Park St. station (I was
in a good mood). Some guy leaped out and grabbed my wallet, and a
struggle ensued (I was no longer in a good mood). He got some cash, I
got his shirt, and stayed to pick up my glasses when he ran off. Got my
jaw checked out at the ER, which took 3 hours to get an X-ray, another 2
hours to get it looked at, on a *very* slow night there.
This, of course, is stupid. "First come, first serve" is idiocy when
the delay for the first cases handled make the later cases *worse*,
which has happened to me. And for non-life-threatening, this was what
they seemed to use. Setting aside a small section of the available
staff for the quick, easy cases would improve crowding, get more
people out the door faster, and handle simple cases properly before
complications set in, such as the end of shock or infection.
Nico Garcia
ra…@mit.edu
My opinions are my own, not MIT’s or my employer’s or my cat’s
(Well, maybe my cat’s….)
In article <ACDCD0399668142…@rfd.tiac.net> r…@tiac.net (Marianne D’Angelo) writes:
[Long detailed description of her son's case omitted]
Now, *this* was very helpful. Good. Thank you.
In fact, I ask the group to forgive me if I have been grumpy out here lately.
While I stand by most of my assertions, I realize that I have been out of
sorts and less than politic about my suggestions and questions.
I have, not an excuse, but a reason. I visited my suddenly terminally
ill father this week to talk to him and make some good-byes, and that
also meant dealing with family members I haven’t seen in 20 years for
good reason. I’m feeling a bit grumpy.
Nico Garcia
ra…@mit.edu
My opinions are my own, not MIT’s or my employer’s or my cat’s
(Well, maybe my cat’s….)
js…@scs.unr.edu (Joshua I. Sera) wrote:
snip snip
>As you notice, it doesn’t say anything about whether Type I or II, but
if
>the definition of Type I is diabetes caused by the destruction of the
>beta cells and Type II is a result of excessive insulin resistance, then
>it’s likely that the diabetes of hemochromatosis is closer to Type I
than
>to Type II. True, it’s not CLASSICAL Type I, but not classical Type II,
>either, and it would seem likely that patients would respond more like
>Type I’s than Type II’s to treatment, for example, they would probably
>respond better to insulin than to orals, and they would probably be
>sensitive to small insulin doses.
snip snip
Just to clarify. I believe this kind of diabetes would more correctly be
termed diabetes *insipitus"…and is technically different than a type 1
or type 11.
–ch]
r…@tiac.net (Marianne D’Angelo) wrote:
snip snip
I am truly sorry to hear about your difficulties. Obviously, this has
been many years of stress and worry for you. As you mentioned in one of
your posts, this is not a common disease…and I’ve never run into it,
either. Elusive symptoms and fluctuating bloodwork, no doubt, lead to a
delayed diagnosis. We’ll just have to hope that your message is there if
someone else is having similar problems/symptoms. Good luck to you and
your family.
–ch
Carol Haagensen (XEPK…@prodigy.com) wrote:
: Just to clarify. I believe this kind of diabetes would more correctly be
: termed diabetes *insipitus"…and is technically different than a type 1
: or type 11.
Carol, what in the WORLD are you talking about???? Diabetes insipidus is
another beastie altogether and has NO connection with what we have been
discussing! Would you like the lecture now, or would you like the chance
to get out your nursing books and reviewing what you should have learned
about it?
Natalie A. Sera, a TEACHER, not a health professional
js…@scs.unr.edu (Joshua I. Sera) wrote:
- Hide quoted text — Show quoted text -
>Carol Haagensen (XEPK…@prodigy.com) wrote:
>: Just to clarify. I believe this kind of diabetes would more correctly
be
>: termed diabetes *insipitus"…and is technically different than a type
1
>: or type 11.
>Carol, what in the WORLD are you talking about???? Diabetes insipidus is
>another beastie altogether and has NO connection with what we have been
>discussing! Would you like the lecture now, or would you like the chance
>to get out your nursing books and reviewing what you should have learned
>about it?
>Natalie A. Sera, a TEACHER, not a health professional
If I am in error, I’m sure that you, and others, will let me know…as I
am always impressed with the wealth of knowledge of this usenet group.
It was my understanding the "insipitus" was a different brand of diabetes
than the type I or Type II. Since the diabetes being discussed on this
thread did not seem to conform to either "brand", then I thought that
this could be a case of insipidus rather than type I or II. As you may
be aware, the insipitus brand of diabetes is caused by trauma to the
pituitary gland…which *I* think is a reasonable supposition when we are
talking about a systemic disorder that caused "diabetes" in this case, as
well as numerous other organ disfunctions. I doubt very sincerely if the
docs who treated the iron induced "diabetic" patient tore apart his
pancreas to determine if the beta cells had really died, or if it was a
form of insipitus diabetes. I apologize if I was not clear in my post.
However, if you had read the post to which I reponded, where the post-er
was in a quandry over which *kind* of diabetes was involved, I think it
was a logical conclusion that there was *another* kind of ddiabetes that
had not been considered. By the way, a mark of a good teacher is
listening. :)
–ch
In article <499ue9$…@usenetw1.news.prodigy.com>,
XEPK…@prodigy.com (Carol Haagensen) wrote:
>Obviously, this has been many years of stress and worry for you. As you mentioned in >one of your posts, this is not a common disease…and I’ve never run into it,
> either. Elusive symptoms and fluctuating bloodwork, no doubt, lead to a
> delayed diagnosis. We’ll just have to hope that your message is there if
> someone else is having similar problems/symptoms. Good luck to you and
> your family.
> –ch
Carol,
Thank you for your concern and good wishes. But the whole point of my
original response has been missed. Iron overload is not a *rare* disease,
it is *rarely diagnosed.* The two are completely different.
Every source that discusses the disease states that it is a common
hereditary trait in people of European descent. The fact that physicians
do not routinely test for it does not mean that it is uncommon. It merely
reflects what they have *not* been taught in medical school.
My son’s first roommate post-op was a liver transplant in his 60′s. His
wife’s brother was in the VA hospital at that time, in critical condition
because his hemochromatosis-induced diabetes was out of control. He was
not expected to live much longer. Out of the brother’s six children, two
had inherited the double recessive gene and were being treated with
phlebotomies. At our local hospital, there were 17 people coming in for
regular phlebotomies in 1993. According the head of the hematology group,
most of them had been diagnosed through employment-required physicals. The
person at the New England Organ Bank who received the notification that a
donor had become available for my son has followed his case with great
interest since that time. Why? Because both she and her brother have been
diagnosed with hemochromatosis and are being treated. Several months ago a
friend called me in a panic — her mother-in-law had been diagnosed with
severe heart complications due to iron overload. The mother-in-law had
told her that the doctor said that it was imperative for her family’s
health that all blood relatives be tested because the probability was very
high that others would also have hemochromatosis. My friend’s family
doctor pooh-poohed the other physician’s suggestion. She had no idea where
to go and hoped that I could help her find a way to get her three sons
tested. I referred her to my son’s PCP who is now very familiar with the
disease, although before my son came along he too had been unaware of it.
I’m just one person living in a small town of 15,000 people — and I know
of at least 24 people being treated. It is not a rare disease. The point
is that too many people with hemochromatosis are like my son — it isn’t
diagnosed until they are in nearly terminal condition due to its
complications. The treatment is easy – phelbotomies. The test is simple –
a blood test that costs about $50. My son’s "ultimate" treatment cost
about $500,000. And, no, he didn’t suffer ill health for years before
being diagnosed. He suffered many symptoms, but none of them were
disabling in any way and frequently seemed to "clear up" spontaneously. If
anything, his problem was that he seemed far too healthy to be sick.
One complication of hemochromatosis is diabetes. A definite percentage of
people that become diabetic, do so because of excess iron that has been
deposited in their pancreases. That could potentially mean some members of
*this* newsgroup. And that’s why I responded to Mr. Garcia’s dismissal of
the problem initially. Each of you deserves the option to decide for
yourselves whether iron overload could possibly apply to your case.
And as for how hemochromatosis-induced diabetes is treated — my son has,
from day one of his diagnosis, been treated solely with insulin. No oral
medications would be used (and have never been considered) because his
pancreas does not produce insulin. Oral medications, as you all know, help
your body better utilize the insulin that it already produces. It is not
an appropriate medication for my son’s hemochromatosis-induced diabetes. I
hope this clarifies some confusion that seems to exist.
Regards,
Marianne D’Angelo
In article <49ak1d$…@silver.scs.unr.edu>,
js…@scs.unr.edu (Joshua I. Sera) wrote:
> what in the WORLD are you talking about???? Diabetes insipidus is
> another beastie altogether and has NO connection with what we have been
> discussing!
> Natalie A. Sera, a TEACHER, not a health professional
Natalie,
Thank you for helping to clarify what seems to be a common misconception.
Regards,
Marianne D’Angelo
In article <ACDF91CF96689F…@rfd.tiac.net>,
Marianne D’Angelo <r…@tiac.net> wrote:
>*this* newsgroup. And that’s why I responded to Mr. Garcia’s dismissal of
>the problem initially.
I don’t think he did dismiss the problem. He was bothered by the initial
posts (not yours) because they were sensationalistic and repetitive, with
(at first, at any rate) few or no pointers to further information. (He
was also pricklier than usual.)
Rachel
—
Rachel Meredith Kadel or, for the adventurously inclined, Bean-na-Sidhe
rka…@fas.harvard.edu
Honorary Fellow of Brad’s School of Piano Tuning and Bible Technology
In article <49f2sh$…@usenetw1.news.prodigy.com>,
Carol Haagensen <XEPK…@prodigy.com> wrote:
>This is one a subject that I would like to ask. On another post, there
>was some interest in whether or not your son was a Type I or Type II.
>Obviously, if he is only on insulin and an apparent "no insulin
>production", I would rule out Type II. However, with a systemic trauma
>caused by the iron, I wondered if the pituitary had been involved either
>instead of, or as well as, the pancreas…therefore, a diagnosis of
>insipitus diabetes rather than Type I. I doubt that this makes much
>difference, as the treatment would be similar…but, it is with curiosity
>and an attempt to learn about this and its overall effects that initiated
>the question.
The only thing that diabetes insipidus has in common with diabetes mellitus
is the symptom of excess urine. The treatments are not at all the same.
Diabetes insipidus is a disorder of the regulation of water in body. It
has nothing to do with blood sugar. There is no way that any competent
medical practitioner would confuse the two. Diabetes insipidus is treated
with vasopressin nasal spray – not with insulin.
Please, let us all try to be minimally accurate in postings such as this.
It is a disservice to the readership to be throwing out red herrings
that can be corrected with just a little research before posting.
–
Steve Kirchoefer
Naval Research Laboratory
Washington, DC 20375-5347
In article <49cg0f$1…@usenetw1.news.prodigy.com>,
XEPK…@prodigy.com (Carol Haagensen) wrote:
> Since the diabetes being discussed on this thread did not seem to conform to either >"brand", then I thought that this could be a case of insipidus rather than type I or >II. As you may be aware, the insipitus brand of diabetes is caused by trauma to the
> pituitary gland…which *I* think is a reasonable supposition when we are
> talking about a systemic disorder that caused "diabetes" in this case, as
> well as numerous other organ disfunctions. I doubt very sincerely if the
> docs who treated the iron induced "diabetic" patient tore apart his
> pancreas to determine if the beta cells had really died, or if it was a
> form of insipitus diabetes.
> –ch
This whole discussion began in response to a post regarding iron overload
because somewhere in the range of 40-60% of people who do have excess iron
become diabetic. And somewhere along the way, everyone has become
distracted for some reason by the question of whether such people are
actually type 1 or type 2. But if you never heard of the disease and have
no idea how it works, how can you make that determination? And if you
could, would it really matter if your endocrinologist is going to treat it
as type 1?
The suggestion that IOD-induced diabetes is a result of *trauma* to the
pituitary is incorrect. While the pituitary is one part of the endocrine
system where the excess iron is frequently deposited, that is not the point
of origin of the diabetes – it is, rather, the iron deposited in the
pancreas as has been frequently stated here. No, they did not "tear apart
his pancreas to determine if the beta cells had really died." No need, the
disease was first described in 1889 and in the ensuing 100+ years, the
medical profession has had ample opportunity to study the its effect on
various parts of the body. One thing that has been determined is that in
the islet cells, iron is selectively deposited in the B cells. To quote
Lloyd Smith once again in The Western Journal of Medicine, "Patients with
hemochromatosis and diabetes are subject to all the degenerative
complications associated with diabetes, consistent with the duration and
severity of the altered carbohydrate metabolism. With removal of iron by
phlebotomy, as many as one third of patients exhibit improvement in
carbohydrate intolerance, as evidenced by a reduced requirement for
insulin. Complete reversal of insulin requirement does not occur, nor
would it be expected in view of the selective destruction of islet B
cells." And to repeat myself, treatment of IOD-induced diabetes is with
insulin, not with oral medications.
That is why you might want to pay attention to this discussion. If your or
your family’s medical history fits the parameters of any of this
discussion, there is the *possibility* that you have IOD. The really
*terrific* news if you were to be so diagnosed is that, with treatment, you
not only could avoid increased complications from IOD in the future, but
you also could possibly experience an improvement in your diabetes
management. In my son’s case, this has not proven to be true, his pancreas
has accumulated too much iron for improvement and his beta cells are
goners. But there’s always the promise of islet cell transplants in the
future.
While I’m at it here, I’ll give one more try at explaining the frequency of
hereditary IOD. This information comes from the 6/3/93 NEJM.
"Hemochromatosis has been defined as a rare disorder characterized by
cirrhosis, diabetes, changes in skin pigmentation, endocrine failure, heart
failure, and arthropathy….It is now clear that autopsy studies and
calculations based on the recognition of clinical symptoms greatly
underestimated the frequency of the homozygous genotype….Collectively
the published screening studies have established three points. First,
hemochromatosis is not rare. It is probably among the most common
inherited metabolic abnormalities. Second, hemochromatosis can be detected
before any clinical signs or symptoms of disease develop…Third, a new
definition of hemochromatosis is necessary, a definition requiring only
homozygosity for the mutant allele…estimates that hemochromatosis occurs
in 5 U.S. whites per 1000. It is assumed that organ damage will occur in a
substantial proportion of homozygotes….Iron overload is rare in
homozygous persons under the age of 20….elevations of [iron] have been
found at ages as young as two years."
To extrapolate those numbers, that means there may be as many as 1.6
million people with hemochromatosis and another 24-32 million carriers of
the gene in this country alone. However, fewer than 250,000 cases have
diagnosed in the U.S.(per the National Organization for Rare Disorders).
That leaves an awful lot of unidentified cases.
Regards.
Marianne D’Angelo
- Hide quoted text — Show quoted text -
>The only thing that diabetes insipidus has in common with diabetes
mellitus
>is the symptom of excess urine. The treatments are not at all the same.
>Diabetes insipidus is a disorder of the regulation of water in body.
It
>has nothing to do with blood sugar. There is no way that any competent
>medical practitioner would confuse the two. Diabetes insipidus is
treated
>with vasopressin nasal spray – not with insulin.
>Please, let us all try to be minimally accurate in postings such as this.
>It is a disservice to the readership to be throwing out red herrings
>that can be corrected with just a little research before posting.
>–
>Steve Kirchoefer
>Naval Research Laboratory
swki…@chrisco.nrl.navy.mil (Steve Kirchoefer) wrote:
Well, now I know the difference. Thanks for the information. However, I
doubt that "red herrings" will be eliminated by all who post on this
newsgroup "by a little research". I thought that was one of the benefits
of reading, and following threads, on this groups…the assimilation of
information. The day I become perfect, and all knowledgeable, as well as
everyone else, we wouldn’t need a newsgroup, support, doctors, or even
each other! –ch
js…@scs.unr.edu (Joshua I. Sera) wrote:
>896689f…@rfd.tiac.net> <49f2sh$…@usenetw1.news.prodigy.com>:
>Distribution: world
big snip snip
Thank you. LOL.
I have become *quite* informed about insipitus in the last 24 hours,
including a primer from my colleagues when I made the same blunder at
work by asking the "stupid" question. (I don’t believe any question is
"stupid.") Anyway, I stand corrected, and a measure of humility
increased. Thank you for your patience, and your attempts to educate.
–ch
r…@tiac.net (Marianne D’Angelo) wrote:
big snip snip
Thank you for your clarification. I agree that the discussion wandered a
bit with the "type" of diabetes. I’m afraid that was my fault. I think
that subject has already been corrected…I sincerely hope! (My face is
red…and that’s good enough.)
Anyway, you didn’t answer my question….the one that I really wanted
answered. You mentioned a lab test that could determine if Iron overload
was present. However, you did not tell us the "name" of the lab test. I
would like to know it’s name, and it’s normal parameters…if you have
that information.
Also, it sounds as if the only way to properly diagnose this disease is
from this test (God! I hope I didn’t overlook this information, too!
When I’m paying by the minute to read…I skim more than devour the
information.) Anyway, it sounded like if the doctor didn’t already
suspect this disease, then he might not think to run this blood test.
Therefore, I wanted to make sure this was the case…and if not, then
what other abnormalities are present in routine lab work, such as a chem
panel, that might alert someone to its presence? Thanks again.
–ch
Ladies and Gentlemen:
Although I wish this "discussion" had been more to the point, mainly
iron overload/hemochromatosis, I was pleased to see that a true series
of exchanges had taken place here.
I would like to clarify a few things for everyone’s sake.
1.) I am the National Director of Public Education for the Iron
Overload Diseases Association, Inc. (non-profit), the international
clearinghouse for information on iron overload/hemochromatosis. This
is a volunteer postion which I have held for the past ten years. While
everyone is musing about this condition, why not write a letter, send
a fax, send an e-mail to IOD or e-mail to me and request more info,
whether geared for the lay person or the medical professional. That
is what we are here for and we wish that more people would take
advantage of it.
2.) My mother has hemochromatosis, I am a carrier of it. I have first
hand knowledge of what this disease can do (for those of you who like
the personal touch)…..my mother’s ferritin was 4,000+ and after many
incorrect diagnoses, she was finally properly diagnosed and treated.
101 phlebotomies later she is, thank God, doing very well.
3.) I hear several people complaining about the WEB page, otherwise
known as the "Iron Overload Alert" notice, but it seems that those who
are complaining about it have not truly read every word and digested
it as they later post questions which are answered in the page.
Furthermore, if they have questions (or complaints), I personally have
not heard any of them. I have printed my e-mail address (repeatedly
as you have pointed out) and have not received any e-mail that I know
of from this group of people discussing this (except for Marianne
whose son’s problems were caused by H). I would be happy to send more
"detailed" information via e-mail or our IOD office would send
additional information via snail mail or you may call directly and
speak with Roberta Crawford, founder/president of IOD who just
recently returned from Moskow where she lectured on iron loading
anemias..
4.) Did any of you see the segment on CNN this past weekend on iron
overload? I worked on this CNN segment for about six months and IOD
provided Dr. Yip, the patients shown, etc. Here is additional
information on that:
CNN SEGMENT PART 1 & PART 2 ON IRON OVERLOAD ON WWW!!
The CNN segment shown last weekend on iron overload (parts 1 & 2) can
also be found on the World
Wide Web (WWW) at the following address
http://www.cnn.com/HEALTH/index.html
This listing has audio and photos and can be printed out or downloaded
to a file.
More segments are scheduled to be aired this coming weekend…….
IRON OVERLOAD ON CNN!!
CNN HEADLINE NEWS
Week of Sunday, November 26th, 1995
Weekend of December 1, 1995
The Iron Overload Diseases Association, Inc. (non-profit) is pleased
to
announce that CNN Headline News is airing a segment on iron overload
(hemochromatosis) with CNN health reporter Elizabeth Schwartz. Ray
Yip,
MD, of the CDC, and Ron Richardson, an H patient, appear in this
segment.
We hope that you will tune in and watch us spread the word on CNN! We
encourage you to alert your friends and family to watch this health
report,
too!
This segment airs ten minutes after the hour during their health
segment.
The Iron Overload Diseases Association, Inc. is pleased to have
provided
CNN with the name of Dr. Yip and Ron Richardson and much of the
information which was contained in this segment.
5.) For those of you who were disturbed or offended by "tabloid like"
titles to my postings, I have found after a year of posting thousands
of articles on IO on prodigy, the internet, and AOL, that a "medical"
title gets almost no response at all. More alarming, and extremely
acurate, statements like, Iron Kills, National Scandal, are perfectly
accurate and get results and saves lives. When you consider that one
in eight is a carrier and one in 200 has H, it is epidemic in this
country. When you consider that more than a million Americans are
dying of an undiagnosed but treatable disease, it is outrageous. So,
I do what I have to do to get attention. Those doctors or medical
professionals who wish the "scientific" approach are more than welcome
to our stockpile of medical studies. IOD also hosts an annual medical
symposium featuring this topic with the leading doctors speaking. The
1996 symposium will be held in the Spring in St. Louis. Med. pros as
well as the public and med. students are welcome at this symposium.
6.) Because I spend so much time sending out posts, I have repeated
the Iron Alert page alot. I will certainly be happy to post some
other information, of which I have a great deal.
7.) The bottom line here is that EVERYONE should be tested for iron
overload: serum iron, TIBC, serum ferritin, and percent of saturation.
We have two studies to show it is cost effective. While everyone is
debating what KIND of diabetes might be caused by H, they are missing
the most vital point—iron overload can affect newborns, children,
teens, men and women, people of all ages whether or not they have
symptoms. It manifests at different ages. The Merck Manual is
correct in many respects but needs to be brought up to date on many of
its statements. IOD is currently working on updating this material to
send to the Merck Manual in the hopes that their next edition will
reflect the latest information and research. People must not get hung
up on symptoms, only the blood work will truly tell the tale and you
can have IO without any symptoms at all, and that’s the time when you
want to catch it!
8.) And, finally, Nico, I’m sorry that your father was ill, and you
had to face all those relatives, and you got mugged, etc., but why
didn’t you just contact me personally and talk with me? If you
express sympathy and kindness you will receive it back. You don’t need
sarcasm, or put downs, just honest talk. Nico even reported me to my
internet server without ever asking me about what I was doing, or
sharing his misgivings about my postings. I assure you, Nico, and
everyone else, that I am very sincere in my work. I may make mistakes
and be over zealous in my postings, but I have saved lives, I know
this for a fact because I have had people diagnosed and treated as a
result of my postings which is very satisfying indeed. For everyone,
including Nico, please get tested: serum iron, TIBC, serum ferritin,
and percent of saturation. Let me know your results. IOD is here to
help in any way possible.
I don’t want to fight with anyone, I just want to try to save everyone
the pain and suffering that my family, and Marianne’s family, went
through because of a condition which is easy to diagnose and treat
when diagnosed early and treated aggressively.
Anyone wishing further information on iron overload (free of charge),
please
e-mail me or contact the IOD office directly.
Sandra Thomas, (Starl…@emi.net) National Director of Public
Education
Iron Overload Diseases Association, Inc. (non-profit)
433 Westwind Drive, North Palm Beach, Florida 33408
(407) 840-8512
Prodigy: KGMQ01A
Internet: starl…@emi.net
AOL: starlad…@aol.com
In article <49gigt$…@silver.scs.unr.edu>,
js…@scs.unr.edu (Joshua I. Sera) wrote:
> the connection between diabetes mellitus and hemochromatosis is well documented. >Perhaps Marianne can expand on this.
> As far as the discussion of what TYPE of diabetes Marianne’s son has, it
> is true that it doesn’t fall into the CLASSIC definitions of Types I and
> II. Quite possibly it would be best to call it secondary diabetes, in
> that it was caused by another disease (hemochromatosis). But if he
> functions like a Type I, for example needs insulin and is susceptible to
> ketoacidosis, then for all intents and purposes he’s a Type I.
> Natalie A. Sera, Uncertified Medical Educator
It is interesting that practicing endocrinologists seem less concerned
) In both cases,
about finding a separate classification for hemochromatosis-induced
diabetes than some patients seem to be. I have never seen type 1 described
as being caused *exclusively* by an autoimmune response. What everyone is
missing is that hemochromatosis frequently CAUSES type l diabetes. And in
some cases an autoimmune response CAUSES type l diabetes (Does this mean
the disease is secondary to an autoimmune response?
the diabetes is a result of the destruction of beta cells in the pancreas,
there is a genetic tendency (without a doubt in the cases of H-induced
diabetes), patients are susceptible to DKA, and treatment always requires
insulin. In both cases, the "cure" would be a pancreas or islet cell
transplant.
It is true, however, that hemochromatosis is not likely to cause type l in
patients under 20 years of age at least. But every discussion of type l
states that onset up to age 40 is "not uncommon" and can even occur later.
Those over-20-and-up-to-age-40-and- even-later cases are prime ground for
hemochromatosis-induced type 1.
There is currently a great deal of research underway regarding the
autoimmune response and type l onset in hopes of finding a way to prolong
or prevent that onset. But if you happen to have H-induced type 1, it is
even more important to identify that fact because with prompt treatment
with phlebotomies, there has been at least some improvement in the
management of the diabetes in about 30% of cases. And even better yet, if
it is identified that you are absorbing excessive iron early enough (the
tests for which have been covered more than once by the IOD Foundation),
you can be treated with phlebotomies and avoid ANY complications
(including type 1) altogether.
And if you have H-induced type 1 and your beta cells have already been
completely destroyed (as my son’s were) it is absolutely imperative to your
health that you begin treatment as soon as possible. Unlike the autoimmune
response suspected of causing some type 1 cases, your body will not stop
absorbing iron once the beta cells are shot. It just goes right on
absorbing and depositing in the heart (which results eventually in
irreversible damage), the liver (which results in either cirrhosis and/or
liver cancer), the synovial tissues (causing arthritis), and numerous other
sites.
If there are about 1.6 million people in the US alone with hemochromatosis,
and diabetes is a complication in about 40-60% of cases, that means that
somewhere between 640,000 and 960,000 cases of type 1 are due to
hemochromatosis — and only about 250,000 cases of hemochromatosis have
been identified. So if you are type 1 and onset was somewhere after 20
years of age, you should really have your doc test for excess iron. If the
results are negative, great! If they are positive, you will have saved
yourself and your family a great deal of trouble.
Regards,
Marianne D’Angelo