Home > Archive > Arthritis > March 2005 > Re: psoriatic arthritis & severely underactive thyroid - any advice?!





You are viewing an archived Text-only version of the thread. To view this thread in it's original format and/or if you want to reply to this thread please [click here]

Author Re: psoriatic arthritis & severely underactive thyroid - any advice?!
randall

2005-03-29, 6:25 pm

Hey Ship!

Where did the conversation go today?

Did I trip over someones pride? Was it you?

Do you want to get your gal pal well or not?

Or are you guys inadvertently shilling hulda? lol

Lets pretend you and HER really are into alt
nostrums. And your scientific bent is true!

Here's a gut twister!

Rebuild the good flora in the GUT with this,
www.thewholewhey.com Get the implant and do
the diet and cleanse program and then see what
happens to your alkaline conditions and *LEAKY* guts.

A few pounds (one killo) of good gut flora makes you
happy!

Where does this stuff start?

And whats the relationship of

Milk and melatonin!

Since I wasn't breast fed I can't tell you much about that.
I can tell you how I had to overcome my funky guts as
well as many years of topical psoriasis. But I have a pet
few percent of the stuff to still remind me!

But I've also had melatonin related problems most of my life that a
1mg.
tab every other night or so doesn't completely get rid of. But
certainly helps
so much that i've mentioned it a few dozen times gleefully.

And caused me to wonder why it works up till now.
And science caught up to me. And your crossposted thread
dredged it alll up again and a fresh pubmed and bingo.


http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15775810

The other culprit found in the body of IMIDs folks is LPS,
so lets skew this milk/melatonin/ thing towards endotoxins (LPS),
This first one is for those asthma people, (LPS in Lungs)
(imid = immune mediated inflammatory disorder)
(ALL imids are ramped up by cell wall of endotoxins, aka-LPS)
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15769302
Serial analysis of gene expression in mice with lipopoly-saccharide
(LPS) -induced acute lung injury.

OBJECTIVE: To monitor the systemic gene expression profile in a murine
model of lipopolysaccharide-induced acute lung injury. METHODS: Acute
lung injury was induced by intratracheal injection of
lipopolysaccharide in 3 mice. Another 3 normal mice receiving same
volume of normal saline were taken as the controls. The comprehensive
gene expression profile was monitored by the recently modified long
serial analysis of gene expression. RESULTS: A total of 24670 tags
representing 12168 transcripts in the control mice and 26378 tags
representing 13397 transcripts in the mice with lung injury were
identified respectively. There were 11 transcripts increasing and 7
transcripts decreasing more than 10 folds in the
lipopolysaccharide-treated mice. The most overexpressed genes in the
mice with lung injury included serum amyloid A3, metallothionein 2,
lipocalin 2, cyclin-dependent kinase inhibitor 1A, lactate
dehydrogenase 1, melatonin receptor, S100 calcium-binding protein A9,
natriuretic peptide precursor, etc. Mitogen activated protein kinase 3,
serum albumin, complement component 1 inhibitor, and ATP synthase were
underexpressed in the lung injury mice. CONCLUSIONS: Serial analysis of
gene expression provides a molecular characteristic of acute lung
injury.

PMID: 15769302

LPS turns on the genes that make your symptoms that aim to keep one
alive?

Is lps doing some thing in the brain also?

Can't sleep during the winter? How about someone who falls asleep any
old time?
Wouldn't that lend a clue or two? What does LPS do to your sleep
patterns?


Effects of inflammation produced by chronic lipopolysaccharide
administration on the survival of hypocretin neurons and sleep.

The number of hypocretin-containing neurons is markedly decreased in
most patients with the sleep disorder narcolepsy. It is presently not
known why the loss of hypocretin neurons occurs in these patients. In
the present study, we tested the role of inflammation in the
degeneration of hypocretin neurons. The proinflammagen
lipopolysaccharide (LPS) was infused chronically for 30 days (flow
rate=0.22 microg/h) into the lateral hypothalamus in rats. Compared
with chronic infusions of phosphate-buffered saline (PBS), LPS
infusions produced a decline in the number of hypocretin (29.7%
reduction), melanin concentrating hormone (MCH; 24.7% reduction), and
neuronal nuclear antigen (NeuN)-immunoreactive neurons, as well as a
dense distribution of reactive astrocytes and microglia within the
lateral hypothalamus. LPS infusions also produced a large increase in
the amounts of wakefulness 6 days after the onset of infusion
(72.5+/-8.7% of wakefulness during lights-on period compared with
45.3+/-1.8% in PBS-treated rats). Amounts of wakefulness returned to
control levels in all LPS-treated rats 30 days after the onset of
infusion. A single injection of LPS (1, 5, or 10 microg) did not
produce a significant decline in the number of hypocretin, MCH, or
NeuN-positive neurons. The loss of hypocretin neurons produced by
chronic LPS administration suggests that inflammation may play a role
in the loss of hypocretin neurons in narcolepsy.

PMID: 15306250

Does winter make you SAD? Do you want to be glad?
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15771558
[snip] Although the mechanism(s) behind this disease is not fully
known, one treatment appears to address each of the theories. Light
therapy is a natural, non-invasive, effective, well-researched method
of treatment for SAD. Various light temperatures and times of
administration of light therapy have been studied, and a combination of
morning and evening exposure appears to offer the best efficacy. Other
natural methods of treatment have been studied, including L-tryptophan,
Hypericum perforatum (St. John's wort), and melatonin.

PMID: 15771558

Is Melatonin coming from your Brain? Maybe not,
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15683461
Melatonin was thought to originate primarily from the pineal gland and
to be secreted during the night, but recent studies revealed that
gastrointestinal (GI) tract presents another, many times larger, source
of melatonin that contributes significantly to the circulating
concentration of this indole. Melatonin may exert a direct effect on GI
tissues but its major influence on GI organs seems to occur indirectly,
via the brain-gut axis including peripheral receptors, sensory afferent
(vagal or sympathetic) pathways and central nervous system (CNS) acting
on these organs via autonomic efferents and neuromediators. [snip]
Although exerting certain differences in the mechanism of action on
gastric and pancreatic secretory activities, melatonin derived from its
precursor L-tryptophan, exhibits similar highly protective actions
against the damage of both the stomach and the pancreas and accelerates
the healing of chronic gastric ulcerations by stimulating the
microcirculation and cooperating with arachidonate metabolites such as
prostaglandins, with nitric oxide released from vascular endothelium,
and/or sensory nerves and with their neuropeptides such as calcitonin
gene related peptide. The beneficial effects of melatonin results in
gastro- and pancreato-protection, prevents various forms of gastritis
and pancreatitis through the activation of specific MT2-receptors and
scavenges reactive oxygen species (ROS). Melatonin counteracts the
increase in the ROS-induced lipid peroxidation and preserves, at least
in part, the activity of key anti-oxidizing enzymes such as superoxide
dismutase. It is proposed that melatonin should be considered as the
agent exerting an important role in prevention of gastric and
pancreatic damage and in accelerating healing of gastric ulcers.

PMID: 15683461

You gotta fix those guts. Hulda's zapper doesn't fix those does it?
Paula said she uses it regularly. Is she prolonging an alkaline
condition?

Yes!

How much is to much of a good thing? When it comes to melatonin you may
only
need to take the 1 mg size and cut it into thirds!
http://www.sciencedaily.com/release...50308134331.htm

Some nights I take 3 mg.s and other nights none. And I know folks who
have a problem with 1 mg. anytime. Bad dreams and feeling woozy etc.
But see below for how much you may need.

For all of us in the psoriasis newsgroup there are also P/ melatonin /
serotonin links coming from science recently,
Serotonin and melatonin links to skin biology,
http://groups-beta.google.com/group...254ff51af3e17d6

Just so you don't have to check these links,

http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15677341
The cutaneous serotoninergic/melatoninergic system: securing a place
under the sun.


It was recently discovered that mammalian skin can produce serotonin
and transform it into melatonin. Pathways for the biosynthesis and
biodegradation of serotonin and melatonin have been characterized in
human and rodent skin and in their major cellular populations.
Moreover, receptors for serotonin and melatonin receptors are expressed
in keratinocytes, melanocytes, and fibroblasts and these mediate
phenotypic actions on cellular proliferation and differentiation.
Melatonin exerts receptor-independent effects, including activation of
pathways protective of oxidative stress and the modification of
cellular metabolism. While serotonin is known to have several roles in
skin-e.g., pro-edema, vasodilatory, proinflammatory, and
pruritogenic-melatonin has been experimentally implicated in hair
growth cycling, pigmentation physiology, and melanoma control. Thus,
the widespread expression of a cutaneous seorotoninergic/melatoninergic
syste,m(s) indicates considerable selectivity of action to facilitate
intra-, auto-, or paracrine mechanisms that define and influence skin
function in a highly compartmentalized manner. Notably, the cutaneous
melatoninergic system is organized to respond to continuous stimulation
in contrast to the pineal gland, which (being insulated from the
external environment) responds to discontinuous activation by the
circadian clock. Overall, the cutaneous serotoninergic/melatoninergic
system could counteract or buffer external (environmental) or internal
stresses to preserve the biological integrity of the organ and to
maintain its homeostasis.-Slominski, A. J., Wortsman, J., Tobin, D. J.
The cutaneous serotoninergic/melatoninergic system: securing a place
under the sun.


http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15679607
[snip] In mammals, two types of high-affinity membrane melatonin
receptors, MT1 and MT2 have been identified, which inhibit adenylate
cyclase activity to decrease the intracellular level of cAMP.
Low-affinity membrane receptor MT3/QR2 have also been identified,
though the mechanism has not been cleared yet. Melatonin is also a
natural ligand of nuclear transcription factor ROR(alpha and beta),
which is suggested to regulate cell cycle negatively via target gene
such as p21(WAF/CIP1). Due to its lipophilic structure, melatonin also
enters through both the plasma and nuclear membrane, and acts as a
potent free radical scavenger to protect macromolecules, in particular
DNA [snip]

http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15676032
(Topical melatonin may protect against X-rays/ Sun rays???)

Do you have a hard time sleePing some time?
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=11955797
3-5 mg's of Melatonin may fix that problem.
[snip] Melatonin profiles are a diagnostic tool to distinguish between
several forms of depression, like major depression, winter depression
(SAD), unipolar depression, delayed sleep phase syndrome (DSPS). In
patients with a major depression success with antidepressants
correlated with an increase in their melatonin profiles but only
patients suffering from DSPS can be successfully treated with
melatonin. [snip]

Melatonin to correct skin pigment problems,
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=14592800


Melatonin,
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15357831
Melatonin (5-methoxy N-acetyltryptamine) is a hormone synthesized and
released from the pineal gland at night, which acts on specific high
affinity G-protein coupled receptors to regulate various aspects of
physiology and behaviour, including circadian and seasonal responses,
and some retinal, cardiovascular and immunological functions.[snip]


^^^^^^^^^^^^^^

And now those scientists and you know that the big melatonin
also comes from the gut. All the connections just aren't clear yet!

But if yours is broke, your probably up late wondering why your
such a NIGHT OWL.

Fix and heal the gut and sweet dreams via your
own alternative well functioning mind and body! Why
get hooked on things that don't really cure you?

randall.... that was fun! I hope ship and friends come back again!

Copyright 2003 - 2009 pahealthsystems.com