Bacteria and Thyroid Disease

[Guest guest]

http://bmj.bmjjournals.com/cgi/eletters/326/7384/295

Streptococci induce Rheumatism and Thyroiditis21 March 2003

Friedrich Flachsbart,

General medicine

37085 Gvttingen

Send response to journal:

Re: Streptococci induce Rheumatism and Thyroiditis

Email Friedrich Flachsbart

Dear Sir,

the connections between acute respiratory infections, acute rheumatic fever

and hyperthyreoidism were first described by v. Basedow, 28. March 1840.

The connections between acute respiratory infections, acute rheumatic fever

and diabetes mellitus were first described by Ebstein, 1876.

And Veil again focussed these lines of evidence to the central point:

Induction by streptococcal infection.

We only have to look into the old books to find the new things.

W. H. Veil: Der Rheumatismus und die streptomykotische Symbiose. Enke,

Stuttgart, 1939.

All the best to You

Yours

Friedrich Flachsbart

Competing interests: None declared

Biochemists already know how Bacteria induce Thyroid Dysfunction23 March

2003

Trevor G Marshall, PhD,

Research Director

Sarcinfo, Thousand Oaks California, 91360-1122

Send response to journal:

Re: Biochemists already know how Bacteria induce Thyroid Dysfunction

Email Trevor G Marshall, PhD

Biochemists have known for some time that the Thyroid and Parathyroid are

both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D

(1,25-D) [1]. There is an excellent drawing illustrating the systemic

effects of this steroid available online from University of California,

Riverside, Dept of Biochemistry (click here to view it). Unfortunately,

clinical medicine has been slow to use this knowledge, and this secosteroid

is rarely measured, even today.

I have some 1,25-D data which demonstrates that between 20% and 50% of

euthyroid patients are suffering from undiagnosed inflammation, most

probably as the result of an undiagnosed immune condition. This data would

indicate that a significant percentage of the population could be at risk.

The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It

is a component of the immune system's Th1 inflammatory response. Angiotensin

II is also involved. We have recently proposed a working description of the

Th1 endocrine biochemistry [2]

The Th1 inflammatory cycle is mounted in response to infection. It has been

shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and

lipopeptides [3]. Most folks' immune systems seem to neutralize the

infective agent and recover, but a proportion of the population does not

manage to immediately kill all the bacteria, and those which remain continue

to secrete lipopolysaccharide and lipopetides. Consequently, the body's

immune reaction is sustained for long periods, sometimes for life. A small

proportion of these continuing immune reactions are severe enough to cause

the most chronic immune disease, Sarcoidosis [4]. We have found that

measuring the elevated production of 1,25-D steroid gives a reliable

indication of the degree of immune dysfunction.

We have achieved excellent results using antibiotics to induce remission in

chronic sarcoidosis, but, at this point, have been unable to get our results

through peer-review. Give it time... maybe another decade or two...

Half a century ago, McPherson Brown reported positive results with

antibiotics in Rheumatoid Arthritis [5], but, despite significant popular

acclaim [6] his discovery has still not been acknowleged by the mainstream

clinical community.

'Therapeutic probe' with some older antibiotics is now reliably curing

autoimmune' disease, and this has given reasonable confirmation that the

so-called 'autoimmune' diseases are actually due to Cell Wall Deficient

bacteria [7,8]. These are species of resistant bacteria (including strep

species) which have developed resistance to the antibiotics whose mode of

attack on the organism is destruction of the cell walls (such as the

penicillins). I would therefore caution against using the " auto " -immune word

as the immune system is clearly reacting to a simulus, not to itself.

Unfortunately I suspect it may take a very long time for this pathogenesis

to be recognized, and fully adopted into clinical practice.

It is becoming clear that recognition of the (relatively simple)

biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and

1,25-D will take equally as long to transition from the realm of Molecular

Biochemistry into clinical practice.

Guy Scadding first noted the links between this secosteroid's metabolism and

Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, " we

only have to look into the old books to find the new things " . Unfortunately,

most of these old books were burned during the 'wonder-drug' and 'Evidence

Based Medicine' revolutions...

Biochemists have known for some time that the Thyroid and Parathyroid are

both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D

(1,25-D) [1]. There is an excellent drawing illustrating the systemic

effects of this steroid available online from University of California,

Riverside, Dept of Biochemistry (click here to view it). Unfortunately,

clinical medicine has been slow to use this knowledge, and this secosteroid

is rarely measured, even today.

I have some 1,25-D data which demonstrates that between 20% and 50% of

euthyroid patients are suffering from undiagnosed inflammation, most

probably as the result of an undiagnosed immune condition. This data would

indicate that a significant percentage of the population could be at risk.

The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It

is a component of the immune system's Th1 inflammatory response. Angiotensin

II is also involved. We have recently proposed a working description of the

Th1 endocrine biochemistry [2]

The Th1 inflammatory cycle is mounted in response to infection. It has been

shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and

lipopeptides [3]. Most folks' immune systems seem to neutralize the

infective agent and recover, but a proportion of the population does not

manage to immediately kill all the bacteria, and those which remain continue

to secrete lipopolysaccharide and lipopetides. Consequently, the body's

immune reaction is sustained for long periods, sometimes for life. A small

proportion of these continuing immune reactions are severe enough to cause

the most chronic immune disease, Sarcoidosis [4]. We have found that

measuring the elevated production of 1,25-D steroid gives a reliable

indication of the degree of immune dysfunction.

We have achieved excellent results using antibiotics to induce remission in

chronic sarcoidosis, but, at this point, have been unable to get our results

through peer-review. Give it time... maybe another decade or two...

Half a century ago, McPherson Brown reported positive results with

antibiotics in Rheumatoid Arthritis [5], but, despite significant popular

acclaim [6] his discovery has still not been acknowleged by the mainstream

clinical community.

'Therapeutic probe' with some older antibiotics is now reliably curing

autoimmune' disease, and this has given reasonable confirmation that the

so-called 'autoimmune' diseases are actually due to Cell Wall Deficient

bacteria [7,8]. These are species of resistant bacteria (including strep

species) which have developed resistance to the antibiotics whose mode of

attack on the organism is destruction of the cell walls (such as the

penicillins). I would therefore caution against using the " auto " -immune word

as the immune system is clearly reacting to a simulus, not to itself.

Unfortunately I suspect it may take a very long time for this pathogenesis

to be recognized, and fully adopted into clinical practice.

It is becoming clear that recognition of the (relatively simple)

biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and

1,25-D will take equally as long to transition from the realm of Molecular

Biochemistry into clinical practice.

Guy Scadding first noted the links between this secosteroid's metabolism and

Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, " we

only have to look into the old books to find the new things " . Unfortunately,

most of these old books were burned during the 'wonder-drug' and 'Evidence

Based Medicine' revolutions...

1. Norman AW, D, ED, Okamura WH, Fletterick RJ:

Three-dimensional model of the ligand binding domain of the nuclear receptor

for 1alpha,25-dihydroxy-vitamin D. J Cell Biochem 1999 Sep 1; 74(3):323-33

[PubMed Abstract]

Note: There is an excellent colored image of this Thyroid 1,25-D receptor at

URL http://biochemistry.ucr.edu/faculty/norman.html

2. Marshall TG, Marshall FE: New Treatments Emerge as Sarcoidosis Yields Up

its Secrets. Clinmed 2003 Jan 27;2003010001. clinmed.netprints

org/cgi/content/full/2003010001 (accessed 27 Jan 2003) [Full Text]

3. M|hlradt PF, Kiess M, Meyer H,S|ssmuth R, Jung G. Structure and Specific

Activity of Macrophage-Stimulating Lipopeptides from Mycoplasma hyorhinis.

Infect Immun 1998 Oct; 6(10): 804-10 [Full Text]

4. Marshall TG, Marshall FE: Brown, et al, ACCESS Study finds Bacterial

Pathogens in Sarcoidosis Patients. [Electronic Letter] Chest 2003: Feb 12.

Available from URL http://www.chestjournal.org/cgi/eletters/123/2/413#96

5. Brown TMcP, Wichelhausen RH, LB, Merchant WR: The in-vivo action

of aureomycin on pleuropneumonia-like organisms associated with various

rheumatic diseases. J Lab Clin Med 1949; 34: 1304-1410

6. The Road Back Foundation: Rheumatic Treatment and Research. Available

from URL http://www.roadback.org

7. Cantwell AR Jr: Variably acid-fast bacteria in a case of systemic

sarcoidosis and hypodermitis sclerodermiformis. Dermatologica 1981;

163(3):239-48 [PubMed Abstract]

8. Almenoff PL, A, Lesser M, Mattman LH: Growth of acid fast L forms

from the blood of patients with sarcoidosis. Thorax 1996 May; 51(5):530-3

[PubMed Abstract]

9. Scadding JG: Sarcoidosis, with special reference to lung changes. BR Med

J 1950; 1: 745-753

Competing interests: None declared

[Guest guest]

Thanks for all the postings for those too exhausted to do the research. Now to

muddle through them with the brain fog.

Frannie

Bacteria and Thyroid Disease

http://bmj.bmjjournals.com/cgi/eletters/326/7384/295

Streptococci induce Rheumatism and Thyroiditis21 March 2003

Friedrich Flachsbart,

General medicine

37085 Gvttingen

Send response to journal:

Re: Streptococci induce Rheumatism and Thyroiditis

Email Friedrich Flachsbart

Dear Sir,

the connections between acute respiratory infections, acute rheumatic fever

and hyperthyreoidism were first described by v. Basedow, 28. March 1840.

The connections between acute respiratory infections, acute rheumatic fever

and diabetes mellitus were first described by Ebstein, 1876.

And Veil again focussed these lines of evidence to the central point:

Induction by streptococcal infection.

We only have to look into the old books to find the new things.

W. H. Veil: Der Rheumatismus und die streptomykotische Symbiose. Enke,

Stuttgart, 1939.

All the best to You

Yours

Friedrich Flachsbart

Competing interests: None declared

Biochemists already know how Bacteria induce Thyroid Dysfunction23 March

2003

Trevor G Marshall, PhD,

Research Director

Sarcinfo, Thousand Oaks California, 91360-1122

Send response to journal:

Re: Biochemists already know how Bacteria induce Thyroid Dysfunction

Email Trevor G Marshall, PhD

Biochemists have known for some time that the Thyroid and Parathyroid are

both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D

(1,25-D) [1]. There is an excellent drawing illustrating the systemic

effects of this steroid available online from University of California,

Riverside, Dept of Biochemistry (click here to view it). Unfortunately,

clinical medicine has been slow to use this knowledge, and this secosteroid

is rarely measured, even today.

I have some 1,25-D data which demonstrates that between 20% and 50% of

euthyroid patients are suffering from undiagnosed inflammation, most

probably as the result of an undiagnosed immune condition. This data would

indicate that a significant percentage of the population could be at risk

The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It

is a component of the immune system's Th1 inflammatory response. Angiotensin

II is also involved. We have recently proposed a working description of the

Th1 endocrine biochemistry [2]

The Th1 inflammatory cycle is mounted in response to infection. It has been

shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and

lipopeptides [3]. Most folks' immune systems seem to neutralize the

infective agent and recover, but a proportion of the population does not

manage to immediately kill all the bacteria, and those which remain continue

to secrete lipopolysaccharide and lipopetides. Consequently, the body's

immune reaction is sustained for long periods, sometimes for life. A small

proportion of these continuing immune reactions are severe enough to cause

the most chronic immune disease, Sarcoidosis [4]. We have found that

measuring the elevated production of 1,25-D steroid gives a reliable

indication of the degree of immune dysfunction.

We have achieved excellent results using antibiotics to induce remission in

chronic sarcoidosis, but, at this point, have been unable to get our results

through peer-review. Give it time... maybe another decade or two...

Half a century ago, McPherson Brown reported positive results with

antibiotics in Rheumatoid Arthritis [5], but, despite significant popular

acclaim [6] his discovery has still not been acknowleged by the mainstream

clinical community.

'Therapeutic probe' with some older antibiotics is now reliably curing

autoimmune' disease, and this has given reasonable confirmation that the

so-called 'autoimmune' diseases are actually due to Cell Wall Deficient

bacteria [7,8]. These are species of resistant bacteria (including strep

species) which have developed resistance to the antibiotics whose mode of

attack on the organism is destruction of the cell walls (such as the

penicillins). I would therefore caution against using the " auto " -immune word

as the immune system is clearly reacting to a simulus, not to itself.

Unfortunately I suspect it may take a very long time for this pathogenesis

to be recognized, and fully adopted into clinical practice.

It is becoming clear that recognition of the (relatively simple)

biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and

1,25-D will take equally as long to transition from the realm of Molecular

Biochemistry into clinical practice.

Guy Scadding first noted the links between this secosteroid's metabolism and

Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, " we

only have to look into the old books to find the new things " . Unfortunately,

most of these old books were burned during the 'wonder-drug' and 'Evidence

Based Medicine' revolutions...

Biochemists have known for some time that the Thyroid and Parathyroid are

both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D

(1,25-D) [1]. There is an excellent drawing illustrating the systemic

effects of this steroid available online from University of California,

Riverside, Dept of Biochemistry (click here to view it). Unfortunately,

clinical medicine has been slow to use this knowledge, and this secosteroid

is rarely measured, even today.

I have some 1,25-D data which demonstrates that between 20% and 50% of

euthyroid patients are suffering from undiagnosed inflammation, most

probably as the result of an undiagnosed immune condition. This data would

indicate that a significant percentage of the population could be at risk

The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It

is a component of the immune system's Th1 inflammatory response. Angiotensin

II is also involved. We have recently proposed a working description of the

Th1 endocrine biochemistry [2]

The Th1 inflammatory cycle is mounted in response to infection. It has been

shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and

lipopeptides [3]. Most folks' immune systems seem to neutralize the

infective agent and recover, but a proportion of the population does not

manage to immediately kill all the bacteria, and those which remain continue

to secrete lipopolysaccharide and lipopetides. Consequently, the body's

immune reaction is sustained for long periods, sometimes for life. A small

proportion of these continuing immune reactions are severe enough to cause

the most chronic immune disease, Sarcoidosis [4]. We have found that

measuring the elevated production of 1,25-D steroid gives a reliable

indication of the degree of immune dysfunction.

We have achieved excellent results using antibiotics to induce remission in

chronic sarcoidosis, but, at this point, have been unable to get our results

through peer-review. Give it time... maybe another decade or two...

Half a century ago, McPherson Brown reported positive results with

antibiotics in Rheumatoid Arthritis [5], but, despite significant popular

acclaim [6] his discovery has still not been acknowleged by the mainstream

clinical community.

'Therapeutic probe' with some older antibiotics is now reliably curing

autoimmune' disease, and this has given reasonable confirmation that the

so-called 'autoimmune' diseases are actually due to Cell Wall Deficient

bacteria [7,8]. These are species of resistant bacteria (including strep

species) which have developed resistance to the antibiotics whose mode of

attack on the organism is destruction of the cell walls (such as the

penicillins). I would therefore caution against using the " auto " -immune word

as the immune system is clearly reacting to a simulus, not to itself.

Unfortunately I suspect it may take a very long time for this pathogenesis

to be recognized, and fully adopted into clinical practice.

It is becoming clear that recognition of the (relatively simple)

biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and

1,25-D will take equally as long to transition from the realm of Molecular

Biochemistry into clinical practice.

Guy Scadding first noted the links between this secosteroid's metabolism and

Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, " we

only have to look into the old books to find the new things " . Unfortunately,

most of these old books were burned during the 'wonder-drug' and 'Evidence

Based Medicine' revolutions...

1. Norman AW, D, ED, Okamura WH, Fletterick RJ:

Three-dimensional model of the ligand binding domain of the nuclear receptor

for 1alpha,25-dihydroxy-vitamin D. J Cell Biochem 1999 Sep 1; 74(3):323-33

[PubMed Abstract]

Note: There is an excellent colored image of this Thyroid 1,25-D receptor at

URL http://biochemistry.ucr.edu/faculty/norman.html

2. Marshall TG, Marshall FE: New Treatments Emerge as Sarcoidosis Yields Up

its Secrets. Clinmed 2003 Jan 27;2003010001. clinmed.netprints

org/cgi/content/full/2003010001 (accessed 27 Jan 2003) [Full Text]

3. M|hlradt PF, Kiess M, Meyer H,S|ssmuth R, Jung G. Structure and Specific

Activity of Macrophage-Stimulating Lipopeptides from Mycoplasma hyorhinis

Infect Immun 1998 Oct; 6(10): 804-10 [Full Text]

4. Marshall TG, Marshall FE: Brown, et al, ACCESS Study finds Bacterial

Pathogens in Sarcoidosis Patients. [Electronic Letter] Chest 2003: Feb 12

Available from URL http://www.chestjournal.org/cgi/eletters/123/2/413#96

5. Brown TMcP, Wichelhausen RH, LB, Merchant WR: The in-vivo action

of aureomycin on pleuropneumonia-like organisms associated with various

rheumatic diseases. J Lab Clin Med 1949; 34: 1304-1410

6. The Road Back Foundation: Rheumatic Treatment and Research. Available

from URL http://www.roadback.org

7. Cantwell AR Jr: Variably acid-fast bacteria in a case of systemic

sarcoidosis and hypodermitis sclerodermiformis. Dermatologica 1981;

163(3):239-48 [PubMed Abstract]

8. Almenoff PL, A, Lesser M, Mattman LH: Growth of acid fast L forms

from the blood of patients with sarcoidosis. Thorax 1996 May; 51(5):530-3

[PubMed Abstract]

9. Scadding JG: Sarcoidosis, with special reference to lung changes. BR Med

J 1950; 1: 745-753

Competing interests: None declared

[Guest guest]

Thanks for all the postings for those too exhausted to do the research. Now to

muddle through them with the brain fog.

Frannie

Bacteria and Thyroid Disease

http://bmj.bmjjournals.com/cgi/eletters/326/7384/295

Streptococci induce Rheumatism and Thyroiditis21 March 2003

Friedrich Flachsbart,

General medicine

37085 Gvttingen

Send response to journal:

Re: Streptococci induce Rheumatism and Thyroiditis

Email Friedrich Flachsbart

Dear Sir,

the connections between acute respiratory infections, acute rheumatic fever

and hyperthyreoidism were first described by v. Basedow, 28. March 1840.

The connections between acute respiratory infections, acute rheumatic fever

and diabetes mellitus were first described by Ebstein, 1876.

And Veil again focussed these lines of evidence to the central point:

Induction by streptococcal infection.

We only have to look into the old books to find the new things.

W. H. Veil: Der Rheumatismus und die streptomykotische Symbiose. Enke,

Stuttgart, 1939.

All the best to You

Yours

Friedrich Flachsbart

Competing interests: None declared

Biochemists already know how Bacteria induce Thyroid Dysfunction23 March

2003

Trevor G Marshall, PhD,

Research Director

Sarcinfo, Thousand Oaks California, 91360-1122

Send response to journal:

Re: Biochemists already know how Bacteria induce Thyroid Dysfunction

Email Trevor G Marshall, PhD

Biochemists have known for some time that the Thyroid and Parathyroid are

both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D

(1,25-D) [1]. There is an excellent drawing illustrating the systemic

effects of this steroid available online from University of California,

Riverside, Dept of Biochemistry (click here to view it). Unfortunately,

clinical medicine has been slow to use this knowledge, and this secosteroid

is rarely measured, even today.

I have some 1,25-D data which demonstrates that between 20% and 50% of

euthyroid patients are suffering from undiagnosed inflammation, most

probably as the result of an undiagnosed immune condition. This data would

indicate that a significant percentage of the population could be at risk

The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It

is a component of the immune system's Th1 inflammatory response. Angiotensin

II is also involved. We have recently proposed a working description of the

Th1 endocrine biochemistry [2]

The Th1 inflammatory cycle is mounted in response to infection. It has been

shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and

lipopeptides [3]. Most folks' immune systems seem to neutralize the

infective agent and recover, but a proportion of the population does not

manage to immediately kill all the bacteria, and those which remain continue

to secrete lipopolysaccharide and lipopetides. Consequently, the body's

immune reaction is sustained for long periods, sometimes for life. A small

proportion of these continuing immune reactions are severe enough to cause

the most chronic immune disease, Sarcoidosis [4]. We have found that

measuring the elevated production of 1,25-D steroid gives a reliable

indication of the degree of immune dysfunction.

We have achieved excellent results using antibiotics to induce remission in

chronic sarcoidosis, but, at this point, have been unable to get our results

through peer-review. Give it time... maybe another decade or two...

Half a century ago, McPherson Brown reported positive results with

antibiotics in Rheumatoid Arthritis [5], but, despite significant popular

acclaim [6] his discovery has still not been acknowleged by the mainstream

clinical community.

'Therapeutic probe' with some older antibiotics is now reliably curing

autoimmune' disease, and this has given reasonable confirmation that the

so-called 'autoimmune' diseases are actually due to Cell Wall Deficient

bacteria [7,8]. These are species of resistant bacteria (including strep

species) which have developed resistance to the antibiotics whose mode of

attack on the organism is destruction of the cell walls (such as the

penicillins). I would therefore caution against using the " auto " -immune word

as the immune system is clearly reacting to a simulus, not to itself.

Unfortunately I suspect it may take a very long time for this pathogenesis

to be recognized, and fully adopted into clinical practice.

It is becoming clear that recognition of the (relatively simple)

biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and

1,25-D will take equally as long to transition from the realm of Molecular

Biochemistry into clinical practice.

Guy Scadding first noted the links between this secosteroid's metabolism and

Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, " we

only have to look into the old books to find the new things " . Unfortunately,

most of these old books were burned during the 'wonder-drug' and 'Evidence

Based Medicine' revolutions...

Biochemists have known for some time that the Thyroid and Parathyroid are

both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D

(1,25-D) [1]. There is an excellent drawing illustrating the systemic

effects of this steroid available online from University of California,

Riverside, Dept of Biochemistry (click here to view it). Unfortunately,

clinical medicine has been slow to use this knowledge, and this secosteroid

is rarely measured, even today.

I have some 1,25-D data which demonstrates that between 20% and 50% of

euthyroid patients are suffering from undiagnosed inflammation, most

probably as the result of an undiagnosed immune condition. This data would

indicate that a significant percentage of the population could be at risk

The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It

is a component of the immune system's Th1 inflammatory response. Angiotensin

II is also involved. We have recently proposed a working description of the

Th1 endocrine biochemistry [2]

The Th1 inflammatory cycle is mounted in response to infection. It has been

shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and

lipopeptides [3]. Most folks' immune systems seem to neutralize the

infective agent and recover, but a proportion of the population does not

manage to immediately kill all the bacteria, and those which remain continue

to secrete lipopolysaccharide and lipopetides. Consequently, the body's

immune reaction is sustained for long periods, sometimes for life. A small

proportion of these continuing immune reactions are severe enough to cause

the most chronic immune disease, Sarcoidosis [4]. We have found that

measuring the elevated production of 1,25-D steroid gives a reliable

indication of the degree of immune dysfunction.

We have achieved excellent results using antibiotics to induce remission in

chronic sarcoidosis, but, at this point, have been unable to get our results

through peer-review. Give it time... maybe another decade or two...

Half a century ago, McPherson Brown reported positive results with

antibiotics in Rheumatoid Arthritis [5], but, despite significant popular

acclaim [6] his discovery has still not been acknowleged by the mainstream

clinical community.

'Therapeutic probe' with some older antibiotics is now reliably curing

autoimmune' disease, and this has given reasonable confirmation that the

so-called 'autoimmune' diseases are actually due to Cell Wall Deficient

bacteria [7,8]. These are species of resistant bacteria (including strep

species) which have developed resistance to the antibiotics whose mode of

attack on the organism is destruction of the cell walls (such as the

penicillins). I would therefore caution against using the " auto " -immune word

as the immune system is clearly reacting to a simulus, not to itself.

Unfortunately I suspect it may take a very long time for this pathogenesis

to be recognized, and fully adopted into clinical practice.

It is becoming clear that recognition of the (relatively simple)

biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and

1,25-D will take equally as long to transition from the realm of Molecular

Biochemistry into clinical practice.

Guy Scadding first noted the links between this secosteroid's metabolism and

Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, " we

only have to look into the old books to find the new things " . Unfortunately,

most of these old books were burned during the 'wonder-drug' and 'Evidence

Based Medicine' revolutions...

1. Norman AW, D, ED, Okamura WH, Fletterick RJ:

Three-dimensional model of the ligand binding domain of the nuclear receptor

for 1alpha,25-dihydroxy-vitamin D. J Cell Biochem 1999 Sep 1; 74(3):323-33

[PubMed Abstract]

Note: There is an excellent colored image of this Thyroid 1,25-D receptor at

URL http://biochemistry.ucr.edu/faculty/norman.html

2. Marshall TG, Marshall FE: New Treatments Emerge as Sarcoidosis Yields Up

its Secrets. Clinmed 2003 Jan 27;2003010001. clinmed.netprints

org/cgi/content/full/2003010001 (accessed 27 Jan 2003) [Full Text]

3. M|hlradt PF, Kiess M, Meyer H,S|ssmuth R, Jung G. Structure and Specific

Activity of Macrophage-Stimulating Lipopeptides from Mycoplasma hyorhinis

Infect Immun 1998 Oct; 6(10): 804-10 [Full Text]

4. Marshall TG, Marshall FE: Brown, et al, ACCESS Study finds Bacterial

Pathogens in Sarcoidosis Patients. [Electronic Letter] Chest 2003: Feb 12

Available from URL http://www.chestjournal.org/cgi/eletters/123/2/413#96

5. Brown TMcP, Wichelhausen RH, LB, Merchant WR: The in-vivo action

of aureomycin on pleuropneumonia-like organisms associated with various

rheumatic diseases. J Lab Clin Med 1949; 34: 1304-1410

6. The Road Back Foundation: Rheumatic Treatment and Research. Available

from URL http://www.roadback.org

7. Cantwell AR Jr: Variably acid-fast bacteria in a case of systemic

sarcoidosis and hypodermitis sclerodermiformis. Dermatologica 1981;

163(3):239-48 [PubMed Abstract]

8. Almenoff PL, A, Lesser M, Mattman LH: Growth of acid fast L forms

from the blood of patients with sarcoidosis. Thorax 1996 May; 51(5):530-3

[PubMed Abstract]

9. Scadding JG: Sarcoidosis, with special reference to lung changes. BR Med

J 1950; 1: 745-753

Competing interests: None declared

[Guest guest]

Thanks for all the postings for those too exhausted to do the research. Now to

muddle through them with the brain fog.

Frannie

Bacteria and Thyroid Disease

http://bmj.bmjjournals.com/cgi/eletters/326/7384/295

Streptococci induce Rheumatism and Thyroiditis21 March 2003

Friedrich Flachsbart,

General medicine

37085 Gvttingen

Send response to journal:

Re: Streptococci induce Rheumatism and Thyroiditis

Email Friedrich Flachsbart

Dear Sir,

the connections between acute respiratory infections, acute rheumatic fever

and hyperthyreoidism were first described by v. Basedow, 28. March 1840.

The connections between acute respiratory infections, acute rheumatic fever

and diabetes mellitus were first described by Ebstein, 1876.

And Veil again focussed these lines of evidence to the central point:

Induction by streptococcal infection.

We only have to look into the old books to find the new things.

W. H. Veil: Der Rheumatismus und die streptomykotische Symbiose. Enke,

Stuttgart, 1939.

All the best to You

Yours

Friedrich Flachsbart

Competing interests: None declared

Biochemists already know how Bacteria induce Thyroid Dysfunction23 March

2003

Trevor G Marshall, PhD,

Research Director

Sarcinfo, Thousand Oaks California, 91360-1122

Send response to journal:

Re: Biochemists already know how Bacteria induce Thyroid Dysfunction

Email Trevor G Marshall, PhD

Biochemists have known for some time that the Thyroid and Parathyroid are

both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D

(1,25-D) [1]. There is an excellent drawing illustrating the systemic

effects of this steroid available online from University of California,

Riverside, Dept of Biochemistry (click here to view it). Unfortunately,

clinical medicine has been slow to use this knowledge, and this secosteroid

is rarely measured, even today.

I have some 1,25-D data which demonstrates that between 20% and 50% of

euthyroid patients are suffering from undiagnosed inflammation, most

probably as the result of an undiagnosed immune condition. This data would

indicate that a significant percentage of the population could be at risk

The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It

is a component of the immune system's Th1 inflammatory response. Angiotensin

II is also involved. We have recently proposed a working description of the

Th1 endocrine biochemistry [2]

The Th1 inflammatory cycle is mounted in response to infection. It has been

shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and

lipopeptides [3]. Most folks' immune systems seem to neutralize the

infective agent and recover, but a proportion of the population does not

manage to immediately kill all the bacteria, and those which remain continue

to secrete lipopolysaccharide and lipopetides. Consequently, the body's

immune reaction is sustained for long periods, sometimes for life. A small

proportion of these continuing immune reactions are severe enough to cause

the most chronic immune disease, Sarcoidosis [4]. We have found that

measuring the elevated production of 1,25-D steroid gives a reliable

indication of the degree of immune dysfunction.

We have achieved excellent results using antibiotics to induce remission in

chronic sarcoidosis, but, at this point, have been unable to get our results

through peer-review. Give it time... maybe another decade or two...

Half a century ago, McPherson Brown reported positive results with

antibiotics in Rheumatoid Arthritis [5], but, despite significant popular

acclaim [6] his discovery has still not been acknowleged by the mainstream

clinical community.

'Therapeutic probe' with some older antibiotics is now reliably curing

autoimmune' disease, and this has given reasonable confirmation that the

so-called 'autoimmune' diseases are actually due to Cell Wall Deficient

bacteria [7,8]. These are species of resistant bacteria (including strep

species) which have developed resistance to the antibiotics whose mode of

attack on the organism is destruction of the cell walls (such as the

penicillins). I would therefore caution against using the " auto " -immune word

as the immune system is clearly reacting to a simulus, not to itself.

Unfortunately I suspect it may take a very long time for this pathogenesis

to be recognized, and fully adopted into clinical practice.

It is becoming clear that recognition of the (relatively simple)

biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and

1,25-D will take equally as long to transition from the realm of Molecular

Biochemistry into clinical practice.

Guy Scadding first noted the links between this secosteroid's metabolism and

Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, " we

only have to look into the old books to find the new things " . Unfortunately,

most of these old books were burned during the 'wonder-drug' and 'Evidence

Based Medicine' revolutions...

Biochemists have known for some time that the Thyroid and Parathyroid are

both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D

(1,25-D) [1]. There is an excellent drawing illustrating the systemic

effects of this steroid available online from University of California,

Riverside, Dept of Biochemistry (click here to view it). Unfortunately,

clinical medicine has been slow to use this knowledge, and this secosteroid

is rarely measured, even today.

I have some 1,25-D data which demonstrates that between 20% and 50% of

euthyroid patients are suffering from undiagnosed inflammation, most

probably as the result of an undiagnosed immune condition. This data would

indicate that a significant percentage of the population could be at risk

The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It

is a component of the immune system's Th1 inflammatory response. Angiotensin

II is also involved. We have recently proposed a working description of the

Th1 endocrine biochemistry [2]

The Th1 inflammatory cycle is mounted in response to infection. It has been

shown, in-vitro, that gram-negative bacteria release lipopolysaccharides and

lipopeptides [3]. Most folks' immune systems seem to neutralize the

infective agent and recover, but a proportion of the population does not

manage to immediately kill all the bacteria, and those which remain continue

to secrete lipopolysaccharide and lipopetides. Consequently, the body's

immune reaction is sustained for long periods, sometimes for life. A small

proportion of these continuing immune reactions are severe enough to cause

the most chronic immune disease, Sarcoidosis [4]. We have found that

measuring the elevated production of 1,25-D steroid gives a reliable

indication of the degree of immune dysfunction.

We have achieved excellent results using antibiotics to induce remission in

chronic sarcoidosis, but, at this point, have been unable to get our results

through peer-review. Give it time... maybe another decade or two...

Half a century ago, McPherson Brown reported positive results with

antibiotics in Rheumatoid Arthritis [5], but, despite significant popular

acclaim [6] his discovery has still not been acknowleged by the mainstream

clinical community.

'Therapeutic probe' with some older antibiotics is now reliably curing

autoimmune' disease, and this has given reasonable confirmation that the

so-called 'autoimmune' diseases are actually due to Cell Wall Deficient

bacteria [7,8]. These are species of resistant bacteria (including strep

species) which have developed resistance to the antibiotics whose mode of

attack on the organism is destruction of the cell walls (such as the

penicillins). I would therefore caution against using the " auto " -immune word

as the immune system is clearly reacting to a simulus, not to itself.

Unfortunately I suspect it may take a very long time for this pathogenesis

to be recognized, and fully adopted into clinical practice.

It is becoming clear that recognition of the (relatively simple)

biochemistry whereby bacteria affect the thyroid and parathyroid via Th1 and

1,25-D will take equally as long to transition from the realm of Molecular

Biochemistry into clinical practice.

Guy Scadding first noted the links between this secosteroid's metabolism and

Immune Disease in the BMJ back in 1950 [9]. I agree with Dr. Flachsbart, " we

only have to look into the old books to find the new things " . Unfortunately,

most of these old books were burned during the 'wonder-drug' and 'Evidence

Based Medicine' revolutions...

1. Norman AW, D, ED, Okamura WH, Fletterick RJ:

Three-dimensional model of the ligand binding domain of the nuclear receptor

for 1alpha,25-dihydroxy-vitamin D. J Cell Biochem 1999 Sep 1; 74(3):323-33

[PubMed Abstract]

Note: There is an excellent colored image of this Thyroid 1,25-D receptor at

URL http://biochemistry.ucr.edu/faculty/norman.html

2. Marshall TG, Marshall FE: New Treatments Emerge as Sarcoidosis Yields Up

its Secrets. Clinmed 2003 Jan 27;2003010001. clinmed.netprints

org/cgi/content/full/2003010001 (accessed 27 Jan 2003) [Full Text]

3. M|hlradt PF, Kiess M, Meyer H,S|ssmuth R, Jung G. Structure and Specific

Activity of Macrophage-Stimulating Lipopeptides from Mycoplasma hyorhinis

Infect Immun 1998 Oct; 6(10): 804-10 [Full Text]

4. Marshall TG, Marshall FE: Brown, et al, ACCESS Study finds Bacterial

Pathogens in Sarcoidosis Patients. [Electronic Letter] Chest 2003: Feb 12

Available from URL http://www.chestjournal.org/cgi/eletters/123/2/413#96

5. Brown TMcP, Wichelhausen RH, LB, Merchant WR: The in-vivo action

of aureomycin on pleuropneumonia-like organisms associated with various

rheumatic diseases. J Lab Clin Med 1949; 34: 1304-1410

6. The Road Back Foundation: Rheumatic Treatment and Research. Available

from URL http://www.roadback.org

7. Cantwell AR Jr: Variably acid-fast bacteria in a case of systemic

sarcoidosis and hypodermitis sclerodermiformis. Dermatologica 1981;

163(3):239-48 [PubMed Abstract]

8. Almenoff PL, A, Lesser M, Mattman LH: Growth of acid fast L forms

from the blood of patients with sarcoidosis. Thorax 1996 May; 51(5):530-3

[PubMed Abstract]

9. Scadding JG: Sarcoidosis, with special reference to lung changes. BR Med

J 1950; 1: 745-753

Competing interests: None declared

[Guest guest]

Hang in there Frannie... it's hard now... but as you learn more and what

your body needs and things start getting better... you'll find it was SO

worth the effort now!

If you get confused and want someone to go over something with you...

just ask....

Did you guys know that for every person that works up the courage to ask

a question there could be a dozen or more that had the same question but

were too shy to ask?

It can be really hard to ask questions in an open forum like this,

knowing that so many are reading... but for all the info that I've

learned, I'm getting soooo much better at asking questions and trying to

bring up personal observations.. the way I figure it... I can either try

to figure out stuff on my own... or have 2 or 3 hundred others help! I

like having the help!!! hehehehehehe

Topper ()

On Thu, 8 Jan 2004 21:29:46 -0800 " Fran Oyler " writes:

> Thanks for all the postings for those too exhausted to do the

> research. Now to muddle through them with the brain fog.

> Frannie

[Guest guest]

Hang in there Frannie... it's hard now... but as you learn more and what

your body needs and things start getting better... you'll find it was SO

worth the effort now!

If you get confused and want someone to go over something with you...

just ask....

Did you guys know that for every person that works up the courage to ask

a question there could be a dozen or more that had the same question but

were too shy to ask?

It can be really hard to ask questions in an open forum like this,

knowing that so many are reading... but for all the info that I've

learned, I'm getting soooo much better at asking questions and trying to

bring up personal observations.. the way I figure it... I can either try

to figure out stuff on my own... or have 2 or 3 hundred others help! I

like having the help!!! hehehehehehe

Topper ()

On Thu, 8 Jan 2004 21:29:46 -0800 " Fran Oyler " writes:

> Thanks for all the postings for those too exhausted to do the

> research. Now to muddle through them with the brain fog.

> Frannie

[Guest guest]

Hang in there Frannie... it's hard now... but as you learn more and what

your body needs and things start getting better... you'll find it was SO

worth the effort now!

If you get confused and want someone to go over something with you...

just ask....

Did you guys know that for every person that works up the courage to ask

a question there could be a dozen or more that had the same question but

were too shy to ask?

It can be really hard to ask questions in an open forum like this,

knowing that so many are reading... but for all the info that I've

learned, I'm getting soooo much better at asking questions and trying to

bring up personal observations.. the way I figure it... I can either try

to figure out stuff on my own... or have 2 or 3 hundred others help! I

like having the help!!! hehehehehehe

Topper ()

On Thu, 8 Jan 2004 21:29:46 -0800 " Fran Oyler " writes:

> Thanks for all the postings for those too exhausted to do the

> research. Now to muddle through them with the brain fog.

> Frannie