[Fwd: LDN or LDD or Both?-long [was Re: I Am Taking DM]]

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[dextromethorphan_therapy] LDN or LDD or Both?-long [was Re:

I Am Taking DM]

Date:

Sat, 13 Oct 2007 18:57:07 -0500

From:

Jo Drager <mary.jo@...>

Reply-

dextromethorphan_therapy

dextromethorphan_therapy

Dudley Delany" <DudleyDelany@...> wrote:

>> On October 2nd, I took my last dose of the LDN...for a suspected

case of prostate cancer and, on October 3rd, >>started on 1.5 ml nightly

of the "Scot-Tussin Extra Strength DM Cough Suppressant" featured at

>>http://tinyurl.com/2a2hyy...

>...Today I experienced a sign that my prostate cancer is trying to

make a comeback, so tonight I am increasing my >dosage of DM from 4.5 mg

to 6 mg....

Dear Dudley,

I'm not at all sure you need to stop taking LDN to take LDD (low-dose

Dextromethorphan [DXM/DM]), and benefit from both.* In a post dated

9/24/2007, on the big LDN group, Elliot, who is a pharmacist,

suggested the two may be synergistic, pointing out that in many ways

they work differently and noncompetitively.

More and more I'm thinking the same.

While it is true that both LDN and LDD influence neurotransmitter

systems, the neurotransmitters each drug targets differ in

classification, as well as in their names.

LDN raises the levels of a few types of endorphins. Endorphins are only

one set of subgroups of many many many different neuropeptide

neurotransmitters, of which there are more than 100 in mammals.

Neuropeptides are peptides found in neural (nerve) tissue. Peptides are

defined as short protein chains, polypeptides are longer protein chains,

and single proteins are, themselves, large organic compounds made of

chains of amino acids. http://en.wikipedia.org/wiki/Neuropeptide

The only recreational drugs acting on neuropeptide receptors are the

opiates, which target the mu, kappa, and delta opioid receptors for the

body's natural narcotics, the various endorphins. LDN works by

temporarily blocking the mu opioid receptors, which ups the body's

formation of endorphins, starting very next day. This rise in endorphin

levels, (which can increase with time for as long as one's endorphin

levels remain suboptimal), starts signaling the body to reapportion its

mu and delta opioid receptors, which in turn signals the CNS to start

strengthening immune health.

It turns out that low endorphin levels create an imbalance between the

mu and delta opioid receptors, which in turn signals the central nervous

system (CNS) to weaken immune system competence! I find this surprising

and more than somewhat fascinating. It finally gives me the excuse I've

been looking for to work for good feelings for me!

My immune health depends on it!

http://autoimmunedisease.suite101.com/article.cfm/low_dose_naltrexone

LDD also affects certain neurotransmitters but of a different class; it

affects some amine neurotransmitters. You'll recall that a protein is a

large organic compound made of amino acids arranged in a linear chain.

Amines are much smaller organic compounds than even single proteins, and

nitrogen is their key atom. Some amine neurotransmitters are

acetylcholine, noradrenaline, dopamine, serotonin, and histamine.

LDD works in 2 phases. The body converts DXM to DXO (dextrophan), which

is chemically similar to DXM, and reacts with the same receptors in the

body, but with a change in focus. Whereas DXM is strongest at the PCP2

and sigma receptors, DXO primarily targets the NMDA

(N-methyl-d-aspartate) receptors.

PCP2 receptors are dopamine reuptake receptors. DXM temporarily blocks

these, thus raising blood levels of dopamine, another feel-good brain

chemical. This probably is why people with parkinsons's shouldn't use

DXM without consulting a doctor. If LDD increases dopamine levels to the

extent LDN increases endorphins, which is as a multiple of up to a

whopping 200% - 300% of the endorphins one produces without LDN, then

combined with a parkinson's med like levadopa, which also substantially

increases dopamine levels, LDD could cause a dangerous rise in dopamine.

I don't know yet whether this happens, but it bears checking into if you

have parkinsons's.

NMDA receptor antagonists are at least somewhat anesthetic, because one

function of NMDA neurotransmitter systems is to help us feel pain. As an

NMDA antagonist, DXM temporarily blocks neurotransmission of pain.

LDN, otoh, relieves pain by increasing our body's natural narcotics,

the endorphins, which dull pain.

Sigma receptors once were thought to be types of opioid receptors,

because some substances that act on them behave in some ways like some

narcotics, e.g., codeine and DXM both reduce coughing.

But although DXM happens to be chemically related to the opiate agonists

(dextromethorphan is the methyl ether of the d-isomer of the codeine

analog levorphanol), the only morphine-like characteristic

dextromethorphan retains is its cough suppressant property. Studies show

that DXM does not affect either mu, kappa, or delta opioid receptors.

And when the sigma1 receptor was isolated and cloned, it was found to

have no structural similarity to any opioid receptors. At that point,

sigma receptors were separated into their own class of receptors.

http://en.wikipedia.org/wiki/Sigma_receptor

Bottom line:

Temporarily blocking the mu opioid receptors for a few hours each night

is the key to how LDN modulates the immune system back to health. I'm

not far enough in my LDD research to have an opinion one way or the

other whether it's actions also modulate the immune system but if yes,

they do so by mechanisms different from LDN, and so far as I can tell

LDD and LDN don't appear to compete.

Best health,

Jo

*Note: Just as you want a fast-acting form of naltrexone if you take

LDN, you also want a fast-acting form of DXM if you take LDD. Even the

fast-acting form of DXM takes between 4-8 hours to clear the body. There

is a time-release formulation of DXM called Dextromethorphan Polistirex;

you don't want it.