Re: darlenesb2000@... sent you a link to content of interest

[Guest guest]

Darlene,

Thank you very much for posting this latest info. What I found

interesting is the iodine deficiency that many experience and I have

read a little bit about a year or so ago. I HIGHLY recommend male

and female to read this information along with hypothyrodism. These

suppliments may help many. I pasted some of the information below,

but please go to the links and read further.

In the United States, iodine has been voluntarily supplemented in

table salt in the 1920's. I thought all salt was iodized and I just

checked mine and it states that it is not iodized right on the front

label. This is great, they take out the good stuff and add other

toxins like aspertame in some food products. Now does that make

sense?

PLEASE check it out.

KC

Background

Iodine is a chemical element. It is found in trace amounts in the

human body, in which its only known function is in the synthesis of

thyroid hormones. Severe iodine deficiency results in impaired

thyroid hormone synthesis and/or thyroid enlargement (goiter).

Population effects of severe iodine deficiency, termed iodine

deficiency disorders (IDDs), include endemic goiter, hypothyroidism,

cretinism, decreased fertility rate, increased infant mortality, and

mental retardation.

Iodine is primarily obtained through the diet but is also a

component of some medications, such as radiology contrast agents,

iodophor cleansers, and amiodarone. Worldwide, the soil in large

geographic areas is deficient in iodine. Twenty-nine percent of the

world's population living in approximately 130 countries is

estimated to live in areas of deficiency (see Table). This occurs

primarily in mountainous regions such as the Himalayas, the European

Alps, and the Andes, where iodine has been washed away by glaciation

and flooding. Iodine deficiency also occurs in lowland regions far

from the oceans, such as central Africa and eastern Europe. Those

who consume only locally produced foods in these areas are at risk

for IDD.

Iodine Deficiency Characteristics

Iodine Deficiency None Mild Moderate Severe

Median urine iodine, mcg/L >100

50-99

20-49

<20

Goiter prevalence <5%

5-20%

20-30%

>30%

Neonatal thyroid stimulating hormone (TSH),

>5 IU/mL whole blood <3%

3-20%

20-40%

>40%

Cretinism 0

0

+

+

Adapted from the World Health Organization (WHO)/United Nations

Children's Fund (UNICEF)/International Council for Control of Iodine

Deficiency Disorders (ICCIDD).

Normal dietary iodine intake is 100-150 mcg/d. The US Institute of

Medicine (IOM) recommended dietary allowance (RDA) is 150 mcg/d of

iodine for adults and adolescents, 220 mcg/d for pregnant women, 290

mcg/d for lactating women, and 90-120 mcg/d for children aged 1-11

years. The adequate intake for infants is 110-130 mcg/d. In areas

where iodine is not added to the water supply or food products meant

for humans or domesticated animals, the primary sources of dietary

iodine are saltwater fish, seaweed, and trace amounts in grains. The

upper limit of safe daily iodine intake is 1100 mcg/d for adults,

and it is lower for children.

In the United States, iodine has been voluntarily supplemented in

table salt (70 mcg/g). Salt was selected as the medium for iodine

supplementation because intake is uniform across all socioeconomic

strata, intake is uniform across seasons of the year,

supplementation is achieved using simple technology, and the program

is inexpensive. The estimated annual cost of iodine supplementation

of salt in the United States is $0.04 per person. Other major

sources of dietary iodine in the United States are egg yolks, milk,

and milk products because of iodine supplementation in chicken feed,

the treatment of milk cows and cattle with supplemental dietary

iodine to prevent hoof rot and increase fertility, and the use of

iodophor cleaners by the dairy industry.

In the early 1900s, the Great Lakes, Appalachian, and northwestern

regions of the United States were endemic regions for IDD, but since

the iodization of salt and other foods in the 1920s, dietary iodine

levels generally have been adequate. However, sustaining these

iodization programs has become a new concern. The National Health

and Nutrition Examination Survey (NHANES), NHANES III, demonstrated

that the median US urinary iodine excretion fell from 320 mcg/d to

145 mcg/d between the early 1970s and the early 1990s and that some

subsets of the population may be at increased risk for moderate IDD.

This reduction in US dietary iodine intake likely was a result of

the removal of iodate conditioners in store-bought breads, widely

publicized recommendations for reduced salt and egg intake for blood

pressure and cholesterol control, and the increasing use of

noniodized salt in manufactured or premade convenience foods. The

most recent NHANES survey of 2001-2002 showed that US dietary iodine

intake has stabilized.

Pathophysiology

Dietary iodine is taken up readily through the gut in the form of

iodide. From the circulation, it is concentrated in the thyroid

gland by means of an energy-dependent sodium-iodate symporter. In

the follicle cells of the thyroid gland, 4 atoms of iodine are

incorporated into each molecule of thyroxine (T4) and 3 atoms into

each molecule of triiodothyronine (T3). These hormones are essential

for neuronal development, sexual development, and growth and for

regulating the metabolic rate, body heat, and energy.

When dietary iodine intake is inadequate for thyroid hormone

synthesis, the serum T4 level initially falls and a number of

processes ensue to restore adequate thyroid hormone production. The

pituitary gland senses low levels of circulating T4 and releases

more TSH. TSH stimulates the growth and metabolic activity of

thyroid follicular cells. TSH stimulates each cell to increase

iodine uptake and thyroid hormone synthesis and secretion. Increased

TSH levels and reduction of iodine stores within the thyroid result

in increased T3 production relative to T4 production. T3 is 20-100

times more biologically active than T4 and requires fewer atoms of

iodine for biosynthesis.

These processes tend to conserve iodine stores and help maintain

normal thyroid function. In addition, thyroid hormones are

deiodinated in the liver, and the iodine is released back into the

circulation for reuptake and reuse by the thyroid gland. Even under

these circumstances, iodine is passively lost in the urine, with

additional small (10%) losses from biliary secretion into the gut.

Therefore, enlargement of the thyroid gland begins as an adaptive

process to low iodine intake. Iodine deficiency is the most common

cause of goiter in the world. The goiter initially is diffuse but

eventually becomes nodular. Some nodules may become autonomous and

secrete thyroid hormone regardless of the TSH level. These

autonomous nodules have been demonstrated to frequently contain TSH-

activating mutations. Initially, thyroid hormone output by the

normal thyroid surrounding the autonomous nodules is reduced to

maintain euthyroidism. Autonomous nodules may cause hyperthyroidism.

High levels of iodine, such as those found in radiographic contrast

dyes or amiodarone, may cause hyperthyroidism in the setting of

nodular goiter with " hot " or autonomous nodules or hypothyroidism in

the setting of autoimmune thyroid disease. If the total output of

thyroid hormone by the autonomous nodules exceeds that of the normal

thyroid gland, the patient becomes biochemically hyperthyroid. This

condition is known as a toxic multinodular goiter.

When iodine deficiency is more severe, thyroid hormone production

falls and the patient experiences a hypothyroid condition. Adults

have the usual signs and symptoms of hypothyroidism (see

Hypothyroidism), while hypothyroidism in the fetus and in young

children prevents central nervous system development and maturation,

with permanent mental retardation, neurological defects, and growth

abnormalities known as cretinism.

Frequency

United States

Early in the 20th century, the Great Lakes, Appalachian, and

northwestern regions of the United States were endemic for IDD, but

since the iodization of salt and other foods in the 1920s, dietary

iodine levels generally has been adequate. National survey data

suggest that average US dietary iodine intake fell dramatically from

1971-1990 and then stabilized. Urinary iodine values of less than 50

mcg/L are found in 11.1% of the total population, 7.3% of pregnant

women, and 16.8% of reproductive-aged women.

International

Internationally, 2.2 billion people worldwide are at risk for IDD.

Of these, 30-70% have goiter and 1-10% have cretinism.

Mortality/Morbidity

Mild-to-moderate IDD can cause thyroid function abnormalities and

endemic goiter (see Image 2).

In areas with severe endemic IDD, rates of miscarriage and infant

mortality are increased. Cretinism is rare, but populations in which

severe iodine deficiency is prevalent are at risk for reduced

intelligence and mental retardation. In fact, iodine deficiency is

the leading cause of preventable mental retardation worldwide.

Whether iodine deficiency causes an increased risk for thyroid

cancer is unclear, but a higher proportion of more aggressive

thyroid cancers (ie, follicular thyroid carcinoma) and an increased

thyroid cancer mortality rate are found in areas where iodine

deficiency is endemic.

The clinical disorders of iodine deficiency tend to be more profound

in geographic areas associated with coexisting selenium and vitamin

A deficiencies and in regions where goitrogens such as cassava or

millet are major staples of the diet.

Race

No racial differences exist; prevalence is affected only by

geographic area and diet.

Sex

After age 10 years, the prevalence of goiter is higher in girls than

in boys in areas of iodine deficiency. No sex-based difference is

observed in the incidence of cretinism.

Age

Patients of any age can be affected by iodine deficiency. The most

devastating complications of IDD occur when iodine is deficient

during fetal and neonatal growth.

>

> darlenesb2000@... sent you a link to the following content:

>

> Mold Madness: Neurotoxins Overlooked 3

> http://www.corepsychblog.com/2007/04/mold_madness_ne_1.html

>

> The sender also included this note:

>

> Dr. : Mold Madness Neurotoxins Overlooked 3

>

> --

> Sent via a FeedFlare link from a FeedBurner feed.

> http://www.feedburner.com/fb/a/publishers/feedflare

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[Guest guest]

KC, your are quite welcome. I am looking forward to Dr. 's next piece on

Mold Madness Neurotoxins Overlooked 4 once he post's it. This information is

very important for everyone to read. Take care and Happy Easter to everyone.

Darlene

tigerpaw2c <tigerpaw2c@...> wrote: Darlene,

Thank you very much for posting this latest info. What I found

interesting is the iodine deficiency that many experience and I have

read a little bit about a year or so ago. I HIGHLY recommend male

and female to read this information along with hypothyrodism. These

suppliments may help many. I pasted some of the information below,

but please go to the links and read further.

In the United States, iodine has been voluntarily supplemented in

table salt in the 1920's. I thought all salt was iodized and I just

checked mine and it states that it is not iodized right on the front

label. This is great, they take out the good stuff and add other

toxins like aspertame in some food products. Now does that make

sense?

PLEASE check it out.

KC

Background

Iodine is a chemical element. It is found in trace amounts in the

human body, in which its only known function is in the synthesis of

thyroid hormones. Severe iodine deficiency results in impaired

thyroid hormone synthesis and/or thyroid enlargement (goiter).

Population effects of severe iodine deficiency, termed iodine

deficiency disorders (IDDs), include endemic goiter, hypothyroidism,

cretinism, decreased fertility rate, increased infant mortality, and

mental retardation.

Iodine is primarily obtained through the diet but is also a

component of some medications, such as radiology contrast agents,

iodophor cleansers, and amiodarone. Worldwide, the soil in large

geographic areas is deficient in iodine. Twenty-nine percent of the

world's population living in approximately 130 countries is

estimated to live in areas of deficiency (see Table). This occurs

primarily in mountainous regions such as the Himalayas, the European

Alps, and the Andes, where iodine has been washed away by glaciation

and flooding. Iodine deficiency also occurs in lowland regions far

from the oceans, such as central Africa and eastern Europe. Those

who consume only locally produced foods in these areas are at risk

for IDD.

Iodine Deficiency Characteristics

Iodine Deficiency None Mild Moderate Severe

Median urine iodine, mcg/L >100

50-99

20-49

<20

Goiter prevalence <5%

5-20%

20-30%

>30%

Neonatal thyroid stimulating hormone (TSH),

>5 IU/mL whole blood <3%

3-20%

20-40%

>40%

Cretinism 0

0

+

+

Adapted from the World Health Organization (WHO)/United Nations

Children's Fund (UNICEF)/International Council for Control of Iodine

Deficiency Disorders (ICCIDD).

Normal dietary iodine intake is 100-150 mcg/d. The US Institute of

Medicine (IOM) recommended dietary allowance (RDA) is 150 mcg/d of

iodine for adults and adolescents, 220 mcg/d for pregnant women, 290

mcg/d for lactating women, and 90-120 mcg/d for children aged 1-11

years. The adequate intake for infants is 110-130 mcg/d. In areas

where iodine is not added to the water supply or food products meant

for humans or domesticated animals, the primary sources of dietary

iodine are saltwater fish, seaweed, and trace amounts in grains. The

upper limit of safe daily iodine intake is 1100 mcg/d for adults,

and it is lower for children.

In the United States, iodine has been voluntarily supplemented in

table salt (70 mcg/g). Salt was selected as the medium for iodine

supplementation because intake is uniform across all socioeconomic

strata, intake is uniform across seasons of the year,

supplementation is achieved using simple technology, and the program

is inexpensive. The estimated annual cost of iodine supplementation

of salt in the United States is $0.04 per person. Other major

sources of dietary iodine in the United States are egg yolks, milk,

and milk products because of iodine supplementation in chicken feed,

the treatment of milk cows and cattle with supplemental dietary

iodine to prevent hoof rot and increase fertility, and the use of

iodophor cleaners by the dairy industry.

In the early 1900s, the Great Lakes, Appalachian, and northwestern

regions of the United States were endemic regions for IDD, but since

the iodization of salt and other foods in the 1920s, dietary iodine

levels generally have been adequate. However, sustaining these

iodization programs has become a new concern. The National Health

and Nutrition Examination Survey (NHANES), NHANES III, demonstrated

that the median US urinary iodine excretion fell from 320 mcg/d to

145 mcg/d between the early 1970s and the early 1990s and that some

subsets of the population may be at increased risk for moderate IDD.

This reduction in US dietary iodine intake likely was a result of

the removal of iodate conditioners in store-bought breads, widely

publicized recommendations for reduced salt and egg intake for blood

pressure and cholesterol control, and the increasing use of

noniodized salt in manufactured or premade convenience foods. The

most recent NHANES survey of 2001-2002 showed that US dietary iodine

intake has stabilized.

Pathophysiology

Dietary iodine is taken up readily through the gut in the form of

iodide. From the circulation, it is concentrated in the thyroid

gland by means of an energy-dependent sodium-iodate symporter. In

the follicle cells of the thyroid gland, 4 atoms of iodine are

incorporated into each molecule of thyroxine (T4) and 3 atoms into

each molecule of triiodothyronine (T3). These hormones are essential

for neuronal development, sexual development, and growth and for

regulating the metabolic rate, body heat, and energy.

When dietary iodine intake is inadequate for thyroid hormone

synthesis, the serum T4 level initially falls and a number of

processes ensue to restore adequate thyroid hormone production. The

pituitary gland senses low levels of circulating T4 and releases

more TSH. TSH stimulates the growth and metabolic activity of

thyroid follicular cells. TSH stimulates each cell to increase

iodine uptake and thyroid hormone synthesis and secretion. Increased

TSH levels and reduction of iodine stores within the thyroid result

in increased T3 production relative to T4 production. T3 is 20-100

times more biologically active than T4 and requires fewer atoms of

iodine for biosynthesis.

These processes tend to conserve iodine stores and help maintain

normal thyroid function. In addition, thyroid hormones are

deiodinated in the liver, and the iodine is released back into the

circulation for reuptake and reuse by the thyroid gland. Even under

these circumstances, iodine is passively lost in the urine, with

additional small (10%) losses from biliary secretion into the gut.

Therefore, enlargement of the thyroid gland begins as an adaptive

process to low iodine intake. Iodine deficiency is the most common

cause of goiter in the world. The goiter initially is diffuse but

eventually becomes nodular. Some nodules may become autonomous and

secrete thyroid hormone regardless of the TSH level. These

autonomous nodules have been demonstrated to frequently contain TSH-

activating mutations. Initially, thyroid hormone output by the

normal thyroid surrounding the autonomous nodules is reduced to

maintain euthyroidism. Autonomous nodules may cause hyperthyroidism.

High levels of iodine, such as those found in radiographic contrast

dyes or amiodarone, may cause hyperthyroidism in the setting of

nodular goiter with " hot " or autonomous nodules or hypothyroidism in

the setting of autoimmune thyroid disease. If the total output of

thyroid hormone by the autonomous nodules exceeds that of the normal

thyroid gland, the patient becomes biochemically hyperthyroid. This

condition is known as a toxic multinodular goiter.

When iodine deficiency is more severe, thyroid hormone production

falls and the patient experiences a hypothyroid condition. Adults

have the usual signs and symptoms of hypothyroidism (see

Hypothyroidism), while hypothyroidism in the fetus and in young

children prevents central nervous system development and maturation,

with permanent mental retardation, neurological defects, and growth

abnormalities known as cretinism.

Frequency

United States

Early in the 20th century, the Great Lakes, Appalachian, and

northwestern regions of the United States were endemic for IDD, but

since the iodization of salt and other foods in the 1920s, dietary

iodine levels generally has been adequate. National survey data

suggest that average US dietary iodine intake fell dramatically from

1971-1990 and then stabilized. Urinary iodine values of less than 50

mcg/L are found in 11.1% of the total population, 7.3% of pregnant

women, and 16.8% of reproductive-aged women.

International

Internationally, 2.2 billion people worldwide are at risk for IDD.

Of these, 30-70% have goiter and 1-10% have cretinism.

Mortality/Morbidity

Mild-to-moderate IDD can cause thyroid function abnormalities and

endemic goiter (see Image 2).

In areas with severe endemic IDD, rates of miscarriage and infant

mortality are increased. Cretinism is rare, but populations in which

severe iodine deficiency is prevalent are at risk for reduced

intelligence and mental retardation. In fact, iodine deficiency is

the leading cause of preventable mental retardation worldwide.

Whether iodine deficiency causes an increased risk for thyroid

cancer is unclear, but a higher proportion of more aggressive

thyroid cancers (ie, follicular thyroid carcinoma) and an increased

thyroid cancer mortality rate are found in areas where iodine

deficiency is endemic.

The clinical disorders of iodine deficiency tend to be more profound

in geographic areas associated with coexisting selenium and vitamin

A deficiencies and in regions where goitrogens such as cassava or

millet are major staples of the diet.

Race

No racial differences exist; prevalence is affected only by

geographic area and diet.

Sex

After age 10 years, the prevalence of goiter is higher in girls than

in boys in areas of iodine deficiency. No sex-based difference is

observed in the incidence of cretinism.

Age

Patients of any age can be affected by iodine deficiency. The most

devastating complications of IDD occur when iodine is deficient

during fetal and neonatal growth.

>

> darlenesb2000@... sent you a link to the following content:

>

> Mold Madness: Neurotoxins Overlooked 3

> http://www.corepsychblog.com/2007/04/mold_madness_ne_1.html

>

> The sender also included this note:

>

> Dr. : Mold Madness Neurotoxins Overlooked 3

>

> --

> Sent via a FeedFlare link from a FeedBurner feed.

> http://www.feedburner.com/fb/a/publishers/feedflare

>

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