To review what started me off in this particular direction- a suspicion that I had been dealing with something more than just PD for at least the last five years lead to the study ofrapid onset effects of channelopathies and the possible role in my PD and maybe all PD. In turn this lead me to a particular type of channelopathy linked to the thyroid (endocrine). It differs from the others in two ways- 1) it is the most common by a factor of ten, and 2) unlike the others, it is not inherited but is acquired.

The hyperthyroidism it links to is typically set off by a high stress period, as it was in my case. It can and does coexist with PD in the individual and can be masked by the PD. You may have it in some form or you may develop it.

In the limited trials that have been done, treating the thyroid problem produced great improvements in the PD without exception. The following study links stress and the endocrine system to the Th1/Th2 balance of the immune system which, in turn, determines how the microglia in your substantia nigra (the immune system) behave.

There are a thousand details to be filled in, but it comes back to stress. At least for some of us, modern society is killing us. A combination of high expectations internalized in childhood (the Parkinson's personality) combined with the destruction of the social safety net by the Industrial Revolution combined with an immune response reacting to social and environmental factors breaks us down, year by year.


1. Ann N Y Acad Sci. 2006 Nov;1088:382-95.

The role of stress in the clinical expression of thyroid autoimmunity.

Tsatsoulis A.

Department of Endocrinology, University of Ioannina, 45110, Ioannina, Greece.
atsatsou@cc.uoi.gr

During stress, activation of the hypothalamic-pituitary-adrenal axis and the
sympathoadrenal system leads to increased secretion of glucocorticoids and
catecholamines, respectively, in order to maintain homeostasis. Recent evidence
suggests that stress hormones, acting on antigen-presenting immune cells, may
influence the differentiation of bipotential T helper (Th) cells away from Th1
and toward a Th2 phenotype. This results in suppression of cellular immunity and
potentiation of humoral immunity. Thyroid autoimmunity is clinically expressed as
Hashimoto's thyroiditis (HT) and its variants (sporadic or postpartum
thyroiditis) or as Grave's disease (GD). The different phenotypic expression of
thyroid autoimmunity is largely dependent on the balance of Th1 versus Th2 immune
response. A predominantly Th1-mediated immune activity may promote apoptotic
pathways on thyroid follicular cells leading to thyroid cell destruction and HT.
Conversely, predominance of Th2-mediated immune response may induce
antigen-specific B lymphocytes to produce anti-TSH receptor (TSHr) antibodies
causing GD. The weight of evidence from epidemiological and case-control studies
supports an association between stress and GD. On the other hand, there is little
information available on the effect of stress on HT, but there is evidence for an
increase in postpartum thyroiditis, following the cellular immune suppressive
effect of pregnancy. Whether stress has a causative effect on GD remains elusive.
Circumstantial evidence supports the hypothesis that stress may influence the
clinical expression of thyroid autoimmunity in susceptible individuals favoring
the development of GD by shifting the Th1-Th2 balance away for Th1 and toward
Th2. Conversely, recovery from stress or the immune suppressive effect of
pregnancy may induce a Th2 to Th1 "return shift" leading to autoimmune (sporadic)
or postpartum thyroiditis, respectively.

PMID: 17192582 [PubMed - indexed for MEDLINE]

and this one


1. Altern Med Rev. 2003 Aug;8(3):223-46.

Th1/Th2 balance: the hypothesis, its limitations, and implications for health and
disease.

Kidd P.

One theory of immune regulation involves homeostasis between T-helper 1 (Th1) and
T-helper 2 (Th2) activity. The Th1/Th2 hypothesis arose from 1986 research
suggesting mouse T-helper cells expressed differing cytokine patterns. This
hypothesis was adapted to human immunity, with Th1- and Th2-helper cells
directing different immune response pathways. Th1 cells drive the type-1 pathway
("cellular immunity") to fight viruses and other intracellular pathogens,
eliminate cancerous cells, and stimulate delayed-type hypersensitivity (DTH) skin
reactions. Th2 cells drive the type-2 pathway ("humoral immunity") and
up-regulate antibody production to fight extracellular organisms; type 2
dominance is credited with tolerance of xenografts and of the fetus during
pregnancy. Overactivation of either pattern can cause disease, and either pathway
can down-regulate the other. But the hypothesis has major inconsistencies; human
cytokine activities rarely fall into exclusive pro-Th1 or -Th2 patterns. The
non-helper regulatory T cells, or the antigen-presenting cells (APC), likely
influence immunity in a manner comparable to Th1 and Th2 cells. Many diseases
previously classified as Th1 or Th2 dominant fail to meet the set criteria.
Experimentally, Th1 polarization is readily transformed to Th2 dominance through
depletion of intracellular glutathione, and vice versa. Mercury depletes
glutathione and polarizes toward Th2 dominance. Several nutrients and hormones
measurably influence Th1/Th2 balance, including plant sterols/sterolins,
melatonin, probiotics, progesterone, and the minerals selenium and zinc. The
long-chain omega-3 fatty acids EPA (eicosapentaenoic acid) and DHA
(docosahexaenoic acid) significantly benefit diverse inflammatory and autoimmune
conditions without any specific Th1/Th2 effect. Th1/Th2-based immunotherapies,
e.g., T-cell receptor (TCR) peptides and interleukin-4 (IL-4) injections, have
produced mixed results to date.

PMID: 12946237 [PubMed - indexed for MEDLINE]