Endorphins or Brain Inflammation?

[Guest guest]

Hi ,

Just thought I'd throw my two cents in as an unqualified community health

researcher (that last bit

so you can factor a credibility rating for what I'm about to say, lol).

My thoughts are ... both fever and inflammation are the body's warning signs

that something's wrong.

Fever is a sign of infection. The body temperature is raised to kill the

infection.

Inflammation also involves body temperature.

Both are linked to the body's immune system and immune responses.

Fever should be temporary - inflammation should be temporary - as in spraining a

wrist - as in a

minor allergic response.

When inflammation is not temporary, that is, it is extended over longer terms

.... longer term damage

results.

The human body is truly miraculous at healing - cells are constantly renewed and

replaced - but it

is much harder to heal damage from extended or recurrent periods of inflammation

(depending on the

location, type, and severity of the damage) - a wrist, a heart valve, several

hundred neurons.

I suspect most, if not all, chronic and critical disease begins with extended

periods or recurring

episodes of inflammation - the catalyst for which could be anything - an

extended allergic response,

a prolonged poor diet, chemical exposure, a car accident, long term use of

drugs, or extended

periods of stress, etc.

[For this reason I'd like to see researchers and doctors focus and collaborate

on early warning

signs and possible causes (translational medicine). This is one area I feel

could prove of major

benefit to society in the longer term.]

Back to the subject and still thinking out loud ...

Endorphins are the body's natural pain killers.

Inflammation causes pain. To kill pain, you must reduce inflammation.

It's possible LDN (via increasing endorphins - the body's natural pain killers)

reduces

inflammation - thereby effecting pain relief - thereby giving the body

'time-out' to heal -

including replacing damaged cells.

The increase in endorphins would have additional important benefits because

endorphins are 'feel

good' hormones and anything that makes us 'feel good' speeds healing - which is

why we should all

make time every day to have a good chuckle - isn't that right Cap'n Caveman?

Regards,

Cris

www.casehealth.com.au

www.casehealth.com

Endorphins or Brain Inflamation?

Posted by: " maxwell98king " wjkeeman@... maxwell98king

Date: Mon Oct 23, 2006 1:06 pm (PDT)

Hi, not to confuse the endorphin question but maybe LDN works by

reducing disease causing brain inflamation and endorphins are a marker

on how effective naltrexone is. The report below from the National

Inastitutes of Health show that naloxone/naltrexone, an opioid recetor

antagonist, can exihbit neuro-protection when administered to diseased

rats (during daytime I would guess).

While I take LDN at night, I am not a great believer in the night time

theory. Because of these scientific research papers on opioid

antagonists, which seem to be neuro-protective at very low doses, I

believe the explanation lies in these reports which, for me, are hard

to grasp.

Until there are clinical trials with LDN on people, it's all theory.

The reports on Dr. Bihari's patients are now quite old and I don't

expect to see any further updates.

Is there any news on Dr. Myra Gironi and her LDN MS trials?

From the NIH:

Introduction

During the development of neurodegenerative diseases such as

Parkinson's disease, Alzheimer's disease, multiple sclerosis, AIDS

dementia complex, and amyotrophic lateral sclerosis, as well as during

post-traumatic brain injuries and ischemia, inflammation in the

central nervous system is frequently observed (McGeer et al., 1988;

Dickson et al., 1993; Raine, 1994; Matyszak, 1998). One of the major

characteristics of the neuroimmune responses is the activation of the

resident immune cells of the brain, the microglia, through a process

termed reactive microgliosis (Dickson et al., 1993; Kreutzberg, 1996).

Activated microglia secrete a variety of proinflammatory and cytotoxic

factors, including nitric oxide (NO), tumor necrosis factor-alpha

(TNF-alpha ), interleukin-1beta (IL-1beta ), arachidonic acid,

eicosanoids, and reactive oxygen species (Merrill et al., 1992;

Minghetti and Levi, 1998). Combinations of these glia-released factors

were neurotoxic in vitro and are thought to actively participate in

the progression of neurodegenerative diseases in vivo (Boje and Arora,

1992; Banati et al., 1993; Raine, 1994; Bronstein et al., 1995;

Kreutzberg, 1996; Jeohn et al., 1998). More recently, it has been

reported that peroxynitrite, formed from NO and superoxide, may be a

more direct and significant cytotoxic intermediate (Beckman et al.,

1993). However, the exact mechanisms of action responsible for the

cytotoxicity for these numerous factors are still largely unknown.

The loss of the function and subsequently the integrity of a specific

subset of neurons, namely, the dopaminergicrgic neurons in the

substantia nigra of the brain, is the hallmark of the pathology of

Parkinson's disease. Inflammation along with increased oxidative

stress in the midbrain appears to precede the eventual loss of

dopaminergicrgic neurons (McGeer et al., 1988; Jenner and Olanow,

1996). Therefore, reducing the severity of inflammation and decreasing

the intensity of oxidative stress may help to preserve the nigral

dopaminergicrgic neurons.

In the course of studying the role of the opioid system in the

neuroimmune responses in the brain, we have discovered that

(-)-naloxone, a nonselective opioid receptor antagonist, inhibits the

lipopolysaccharide (LPS)-induced cytokine release and nitrite

production in murine mixed cortical glia cultures (Das et al., 1995;

Kong et al., 1997). We set out to investigate effects of naloxone on

the inflammation-mediated damage to dopaminergicrgic neurons in the

rat mesencephalic neuron-glia culture system. The underlying mechanism

of action for the protective effects of naloxone was analyzed in

relation to the activity of microglia. In this report, we show that

naloxone protects dopaminergicrgic neurons from LPS-induced damage

through inhibition of microglia activation and subsequent release of

superoxide free radicals.

Abstract

Degeneration of dopaminergicrgic neurons in the substantia nigra of

the brain is a hallmark of Parkinson's disease and inflammation and

oxidative stress are closely associated with the pathogenesis of

degenerative neurological disorders. Treatment of rat mesencephalic

mixed neuron-glia cultures with lipopolysaccharide (LPS)-activated

microglia, resident immune cells of the brain, to release

proinflammatory and neurotoxic factors tumor necrosis factor-alpha ,

interleukin-1beta , nitric oxide, and superoxide and subsequently

caused damage to midbrain neurons, including dopaminergic neurons. The

LPS-induced degeneration of the midbrain neurons was significantly

reduced by cotreatment with naloxone, an opioid receptor antagonist.

This study focused on understanding the mechanism of action for the

protective effect of naloxone on dopaminergic neurons because of

relevance to Parkinson's disease. Both naloxone and its opioid

receptor inactive stereoisomer (+)-naloxone protected the dopaminergic

neurons with equal potency. Naloxone inhibited LPS-induced activation

of microglia and release of proinflammatory factors, and inhibition of

microglia generation of superoxide free radical best correlated with

the neuroprotective effect of naloxone isomers. To further delineate

the site of action, naloxone was found to partially inhibit the

binding of [3H]LPS to cell membranes, whereas it failed to prevent

damage to dopaminergic neurons by peroxynitrite, a product of nitric

oxide and superoxide. These results suggest that naloxone at least in

part interferes with the binding of LPS to cell membranes to inhibit

microglia activation and protect dopaminergic neurons as well as other

neurons in the midbrain cultures from inflammatory damage.

http://jpet.aspetjournals.org/cgi/content/full/293/2/607?maxtoshow= & HITS=10 & hits\

=10 & RESULTFORMAT= & searchid=1115227473067_1759 & stored_search= & FIRSTINDEX=0 & minsco\

re=5000 & journalcode=jpet

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3b. Re: Endorphins or Brain Inflamation?

Posted by: " Dave Carlin " davizona@... outtabodyexperience

Date: Mon Oct 23, 2006 1:15 pm (PDT)

Interesting, there is a guy on the GoodShape forum who believes that LDN works,

but not the way that

Dr Bihari believes it did. His thoughts were alway directed towards inflammation

as well! Very

interesting post.