Editorials

Thyroid function tests and hypothyroidism

BMJ 2003; 326 doi: https://doi.org/10.1136/bmj.326.7384.295 (Published 08 February 2003) Cite this as: BMJ 2003;326:295

Biochemists already know how Bacteria induce Thyroid Dysfunction

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, Thomas 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, Adams D, Collins 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. Mühlradt PF, Kiess M, Meyer H,Süssmuth 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, Robinson 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, Johnson 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

Competing interests: No competing interests

23 March 2003
Trevor G Marshall, PhD
Research Director
Sarcinfo, Thousand Oaks California, 91360-1122