To add to all this, which is excellent by the way, I remember reading an article some time ago about how in our youth, our cells primarily use sodium as the main conductor....but as we age, it switches to calcium. They don't know why, of course, but at least they are looking at it.

In light of some of the rather huge med-tech discoveries lately (talking here about the imaging of a living brain just making the headlines last week, incredible-they can actually see the tau tangles in Alzheimer's and this technology will hopefully be used for PD as well), it seems like they could test the calcium hypothesis fairly easily by injecting some various calcium solutions and seeing what happens in the brain real-time, on the screen.

I noted in the article Laura cited that while most of the research group is in Ireland, one of the members is at Georgia Tech. I think that's pretty hopeful, as that is one of the best engineering schools in the country (no ties there, just what I've heard).

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]

I'm a little skeptical of dr. kidd, writes well but not a MD, researcher or ever been peer reviewed, supplement industry consultant. yet you post his "opinions".

I understand where you are coming from and I am suspicious by nature myself. That's why I like this guy.

P.M Kidd is one of the best. You can download his CV at
www.dockidd.com.

Here is the cover page (It runs to 24 darned pages):

Dr. Parris Kidd was born in Jamaica and earned his B.Sc. degree with First
Class Honors at the University of the West Indies. Subsequently he emigrated
to the USA and earned his PhD in cell biology at the University of California
at Berkeley. In 1983, after serving seven years as a research investigator in
cardiology at the University of California's San Francisco Medical Center
(UCSF) and as a lecturer at Berkeley and at the University of the Pacific, Dr.
Kidd entered the new field of nutritional biomedicine. His first project was to
write Antioxidant Adaptation—Its Role in Free Radical Pathology. Published
in 1985, this 500-page text established nutritional antioxidants as the body’s
premier anti-toxic, anti-inflammatory, and anti-aging substances. It also
established Dr. Kidd as a leading scientist in alternative medicine.
In 1990 Dr. Kidd published Living with the AIDS Virus—A Strategy for
Long-Term Survival. This book discussed the then-limited pharmaceutical
options for managing HIV-1, as well as the evidence that dietary and lifestyle
modification, supplementation with nutrients and herbs, and physical exercise
could help extend lifespan for the person living with AIDS. Dr. Kidd
presented this new integrative approach to disease management
internationally, at community meetings, universities and People with HIV
support groups.
Dr. Kidd subsequently broadened his focus to brain nutrition. In 1994 he
helped introduce the nutrient PhosphatidylSerine (PS) to North America. In
1997 he helped introduce GlyceroPhosphoCholine (GPC). In 2003 he helped
introduce krill omega-3 phospholipids. He has lectured and written
extensively on the uses of these phospholipid nutrients to support attention,
memory and mood, and to salvage declining brain function. Recently he has
published books on PS and GPC.
Dr. Parris Kidd is now internationally recognized as a nutrition educator and
dietary supplement product developer. He remains committed to providing
quality healthcare information rooted in good science. He has published
numerous peer reviewed scientific articles, book chapters, monographs, and
magazine articles on diverse topics in healthcare. He is a Contributing Editor
to the journal Alternative Medicine Review, Science Adviser for Total Health
magazine, and designer of dozens of dietary supplement formulations. Dr.
Kidd’s website at www.dockidd.com carries a number of his educational
contributions as free downloads. Dr. Kidd continues to be a strong advocate of
integrative strategies for health maintenance and disease management.

I have an appointment with my neuro tomorrow to discuss some of this. One of the things I expect is an agreement that I should see an endocrinologist just to figure out what is real. So I started looking at the local endos to see if any stood out. There aren't many in my little town and I didn't have any hopes of anything special. I settled on one that got two favorable ratings. He was the only rated one in town. He had a short bio on his website. Seemed normal enough and it mentioned that had one journal publication to his credit, but no link, no title. I went to Medline and found it from five years ago. Checkit out...


1. Endocr Pract. 2005 Jan-Feb;11(1):37-42.

Urinary calcium excretion in primary hyperparathyroidism: relationship to
25-hydroxyvitamin d status.

Bussey AD, Bruder JM.

Division of Endocrinology, University of Texas Health Science Center, San
Antonio, TX 78284-7877, USA.

OBJECTIVE: To determine the prevalence of vitamin D deficiency in patients with
primary hyperparathyroidism (PHPT) and evaluate the relationship between urinary
calcium excretion and serum 25-hydroxyvitamin D (25-OH-D) levels in patients with
PHPT. METHODS: We present a case report and a review of the medical records of
patients with PHPT. Of 75 patients with PHPT substantiated by hypercalcemia and
increased levels of intact parathyroid hormone (iPTH), 35 were identified with
laboratory evaluation of vitamin D levels and 24-hour urinary calcium excretion.
These study subjects were stratified as 25-OH-D deficient, insufficient, or
replete (on the basis of serum values of <15, 15 to 25, or >25 ng/mL,
respectively). Total 24-hour urinary calcium excretion and the fractional
excretion of calcium (FECa) were analyzed as a function of 25-OH-D status.
RESULTS: Of the 35 study subjects, 14 (40%) and 13 (37%) had 25-OH-D deficiency
or insufficiency, respectively. Those patients with a 25-OH-D level <15 ng/mL had
higher serum iPTH concentrations as well as lower urinary calcium excretion and
FECa. No significant correlations were found, however, between 25-OH-D status and
iPTH concentrations (r = -0.21; P = 0.23), total 24-hour urinary calcium
excretion (r = 0.07; P = 0.7), or FECa (r = 0.04; P = 0.8). CONCLUSION: Vitamin D
deficiency (25-OH-D levels <15 ng/mL) was common in our population of patients
with PHPT. Urinary calcium excretion was not significantly altered by 25-OH-D
deficiency in patients with newly recognized PHPT. Measurements of total urinary
calcium excretion and FECa can be reliably used to rule out familial benign
hypocalciuric hypercalcemia in the initial evaluation of PHPT, regardless of
25-OH-D status. Determining 25-OH-D concentrations best assesses the vitamin D
status.

PMID: 16033734 [PubMed - indexed for MEDLINE]

We've come to a more rocky place now, full of polyps, things broken down, unidentified pain, at the same time as arthritis,weak bones, plus our lengthy and narrow exit pipery. There are many ways to get a stomach ache.

Getting things to pass would logically need a moist and large enough pathway and uncluttered circuitry. Where is the clean up commttee?

I 'm in over my head not quite sure how it happened. lol i am really learning from this thread tho and am researching toward another contribution.

Wow, Rick that is what I call serendipity! I'll be curious to see if he mentions any relation between PD and thyroiditis. I too plan on seeing an endocrinologist just as a follow up to our discussion and the fact that I largely started feeling like crap a few months post partum and it has worsened if anything. The symptoms point toward hypothyroidism like weight gain, fatigue, depression...yet I am having attacks very similar to what you experience which is result of hyperthyroidism. Talk about confusing!

My pregnancy and that of many other YO moms hold secrets to all this too. In fact, in researching how most women I know who have had babies while having PD and permanently worsened (me included)as a result, I ran right into all this thyroid info and when I hit parathyroid it gelled even more with PD.

One or two scarce articles even dare broach the effect of pregnancy on PD. The lone researcher in this area has suggested our PD is worsened by rapidly fluctuating hormones. Maybe this is so, but estrogen is supposed to be neuroprotective, so I could see a symptom exacerbation as our estrogen drops rather quickly after delivery, but I would then think we might return to baseline, but this is not the case. I'd say estrogen might still be a factor but something else is working against us, and I started thinking "thyroid".

About thyroid and pregnancy:

Many women develop thyroiditis post partum. It begins as hyperthyroidism and the thyroid never recovers from the inflammatory autoimmune attack (our immune system is stunted in favor of fetal develop) and we then become hypothyroid. It can disappear within a year or remain a permanent state for some women and clinically this autoimmune form is indistinguishable from Hoshimoto's Disease. Even more interesting...look at these case reports- longstanding, untreated Hashimoto's hypothyroidism can turn into neurodegenerative disease like cerebellar degeneration that looks like Ataxia, Parkinsonism, and MSA. In other words there is clear evidence that what begins as an autoimmune attack on the thyroid ends as an autoimmune attack in the person's brain. I can say that in seeing four different neurologists, not one ever asked if my thyroid had been checked.

I am not at all saying that my PD is not what it is, but I do wonder now if I developed a thyroid problem from pregnancy and untreated it has impacted the PD. I will be suggesting this to my PD mama friends; clearly it can do this. I am most definitely having all things thyroid checked very soon.

Oh, one last anecdote of interest...patients with untreated or under
treated hypothyroid report experiencing "brain fog".

Please report back after your neurology visit.

Laura

I went to see my GP today as my vitamin D and calcium levels are low - she's agreed to give me vitamin D injections and is referring me to an endocrinologist. Not sure how successful my quest will be using conventional medicine but am considering seeing someone who practises something similar to functional medicine who can test my parathyroid, thyroid and cortisol levels more thoroughly than the NHS.

Trixiedee

Saw the new neuro today. In a nutshell - "Cut back on the Requip, see the endo, and come back in six weeks. "

Blood work from three weeks ago (and in first stages of an attack) was low normal (3.5 with norm 3.5 to 5.0) which is about what would be expected in my scenario.

Next step is to get my GP to arrange an appointment with the endo. Have a call in for that purpose.

I had my children at 33 and 35 yrs of age. Never started menstrual periods again, was diagnosed hyperthyroid - later that became hypothyroid. just having young onset menopause increases risk for pd.

paula