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Re: LDN as it used to be, Back to basic!

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Yes what I said was crap but not my calculations: GIGO.

I am taking about 18 nanograms per kg of body mass and of course

I don't weigh 240 kg but 240 lbs.

Even Dr. Bihari said:

> at levels several times above 10 mg, at

> which these drugs have been generally administered in the past for

> other purposes, especially narcotic addiction, the effects of the

> preferential blocking action against Mu over Delta receptor sites

> disappears, since the amount of the drug is large enough to cause

at

> least substantial blocking of Delta sites while the Mu sites remain

> fully blocked.

I think the word several is very ambiguous. It *is* enough to cause

substantial blocking of the Delta sites if that is what they are.

Complete blocking actually. I am saying above 4,5 is actually

dangerous if you have low endorphin anyway. Even 4 was dangerous

for me but that is just an anecdote.

Concentration once the stuff is fully distributed in your body, *is*

dependent on body mass. A person who has half as much mass will have

twice as concentrated a dose.

For those who care, that is 2.25 mg, not 4.5. Many females weigh

half what I do or less. If they and I both take 4.5 mg they are

taking twice what I take, or what would be 9mg for me.

I should think the dosage should be given for a specific weight to

reduce the confusion. You are free to believe it doesn't matter and

it may not, but if it does you may cause an exacerbation. I think I

have.

-Sullivan

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Like the person on RemedyFind, I also think, and told the MsClinic,

that I stopped the exacerbation with LDN. If true this would save

a lot of bottles of cortisone!

They believed me (!) as far as not putting me on cortisone. Said

cortisone will not stop an exacerbation just speed up recovery.

-Sullivan

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Where are these calculations coming from?

And, has this theory been prooved?

Unfortunately we all agree no one could jet bother to run medical

trial on Naltrexone. However doctors like Bihari and Lawrence have

hundreds of patients taking up to 4.5mg and reporting no MS

progression and relevant improvements. I have my sister that started

LDN with 3.5mg and then passed to 4.5mg. She then decided to stick to

4.5mg because she is feeling great. Even Dr. Lawrence was strongly

recommending switching to 4.5mg ASAP since the benefit of 4.5mg was

much greater than 3mg.

I am really sorry to hear your complaining (was for taking 4 mg of

LDN, wasn't it?) but you should be really sure of this theory before

scaring others.

Are we sure 100% that taking LDN in liquid form accurate enough? (In

Italy, 50mg liquid Naltrexone (Antaxone) comes in a 20ml bottle.

Therefore, to have 3mg on LDN you take 1.2ml and for 4.5mg you take

1.8ml of it. Is it the same for you? Are you taking now 0.8ml of

liquid Naltrexone?)

Attributing LDN efficiency all down to the body mass is a bit

reductive way to measure the necessary dosage....

Don't you think that things like what you're eating or if you take

alcohol or if you take other drugs at the same time, equally matter?

I already wrote that my sister stopped drinking alcohol (when she was

on 3.5mg of Naltrexone) because she had twice a bad day the morning

after.

Please read this:

(http://www.muhealth.org/~pharm204/pharmacodynamics_and_pharmacok.html

)

=======================================================

The intensity of a biological response produced by a drug is related

to the concentration of the drug at the site of action, which is in

turn affected, by a variety of factors grouped together under the

heading PHARMACOKINETICS. There are 4 pharmacokinetic phases which

all affect drug concentration at the site of action . These phases

are:

1. Absorption: The ability of a drug to enter the blood

stream. It is expressed as a rate (amount per time e.g. g/min,

cc/hour) and indicates the speed with which the drug leaves its site

of administration and the degree to which this occurs. Absorption is

affected by the physiochemical properties of the drug - a drug's

size, shape and charge all affect how well it will be absorbed (if

you'd like to review the effect of pH on drug charge click here),

the types of transporters - remember that most drugs move by passive

diffusion (i.e. from areas of high to areas of low concentration).

However some drugs also ulitize carrier-mediated transporters for

active transport process and facilitated diffusion, nature of the

absorbing surface, blood flow to the site of absorption, drug

concentration (i.e. dose; the easiest way to increase a drug

response is to increase the dose), dose form and the route of

administration

2. Distribution is defined as the movement of a drug throughout

the body to various tissue sites. Distribution is affected by the

physiochemical properties of the drug, cardiac output and blood flow,

the blood brain barrier and drug reservoirs (if you want to review

the effects of drug reservoirs on drug distribution click here)

3. Biotransformation reactions alter the chemical structure of a

drug. Biotransformation occurs primarily in the liver and involves

the enzymatic breakdown of drugs. The goal of biotransformation is

to increase the charge on drugs and target them for excretion (i.e.

increase their solubility in urine (water)) not necessarily to

inactivate them. Thus while biotransformation reactions convert

active drugs to inactivate metabolites, they also convert active

drugs into active metabolites and inactive drugs into active

metabolites.

4. Excretion is the removal of drugs and biotransformation

products from the body. This occurs primarily in the kidney.

==========================================================

Drug concentration is one aspect only of the entire story. You would

agree with me that it is equally risky that someone taking a very low

dose of Naltrexone could not take enough of it all the times.

Also, let me clarify that high dose of Naltrexone (like 50mg daily as

in therapy for opioid dependencies) doesn't develop MS.

Ciao,

Max

> Yes what I said was crap but not my calculations: GIGO.

>

> I am taking about 18 nanograms per kg of body mass and of course

> I don't weigh 240 kg but 240 lbs.

>

> Even Dr. Bihari said:

>

> > at levels several times above 10 mg, at

> > which these drugs have been generally administered in the past

for

> > other purposes, especially narcotic addiction, the effects of the

> > preferential blocking action against Mu over Delta receptor sites

> > disappears, since the amount of the drug is large enough to cause

> at

> > least substantial blocking of Delta sites while the Mu sites

remain

> > fully blocked.

>

> I think the word several is very ambiguous. It *is* enough to cause

> substantial blocking of the Delta sites if that is what they are.

>

> Complete blocking actually. I am saying above 4,5 is actually

> dangerous if you have low endorphin anyway. Even 4 was dangerous

> for me but that is just an anecdote.

>

> Concentration once the stuff is fully distributed in your body,

*is*

> dependent on body mass. A person who has half as much mass will

have

> twice as concentrated a dose.

>

> For those who care, that is 2.25 mg, not 4.5. Many females weigh

> half what I do or less. If they and I both take 4.5 mg they are

> taking twice what I take, or what would be 9mg for me.

>

> I should think the dosage should be given for a specific weight to

> reduce the confusion. You are free to believe it doesn't matter

and

> it may not, but if it does you may cause an exacerbation. I think

I

> have.

>

> -Sullivan

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Hi Masimo, Thank you for bringing us back to earth, and bringing

back method to our madness....please excuse the expression, but

there has been a little mental masterbation going on here.

Your sister has been responding well to the 4.5mg and some of us

respond well to the 3mg dose (the original opti-dose) and I think we

should quit playing with the doseage....I admit I have, and to no

avail. I just have to get used to the truth, that LDN will not cure

my MS....it will only stop the progression. It is hard to accept

though, since so many here are in remission due to LDN, and we all

would love to have that, but alas for some of us, it is not to be.

Thank you again for posting and I wish the best for you and your

sister.

Sally

--- In low dose naltrexone , " maxbtm " <maxbtm@y...>

wrote:

> The " ideal " LDN dosage is obviously dependent individual by

> individual but it has nothing to do with body size or sex.

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Hello:

Then why do these very dose response curves on this page you refer me

to have on one axis dose marked very clearly in units of mg per

kg mass of body weight?

I agree that there are other factors which affect efficacy.

I have not drunk any alcohol while I have been on LDN for instance.

There are no calculations. I have figured out using my own mass

(240 lbs = 108 kg) that I am taking 2mg/108 kg = .018 mg / kg =

18 nanograms per kilogram.

I am not trying to scare anybody. I told you it was anecdotal.

But believe me it did happen. I have also seen many complaints

of stiff legs which you would see if you had MS yourself and took

LDN, could easily be a symptom. I have had them too and it ain't

the filler (distilled water). High dose cannot cause anybody to

develop MS but it can cause worsening of symptoms and *may* cause new

attacks.

I am using a 50mg tablet and 50ml of water of which I measure in a

new syringe marked from 0-3 ml. One ml = 1 mg.

I now can barely walk which is a new experience for me. The strength

in many of my large muscles is gone, making them unuseable. Last

night I fell and got a large goose-egg on my head. While it can be

funny and often is, it can also be dangerous.

If you have convinced everyone that there is no possibility attacks

could be caused by blockading opioid receptors with a high dose of

naltrexone they are safe aren't they? But you have not convinced

me. I think it is of concern that HDN blockades endorphin, and that

auto-immune patients have lowered endorphin production.

I am concerned at the thin-ness on the ground of science attending

the users of LDN. I would like to see the situation rectified. It

may be soon if Bill Gates' philanthropy can be brought to bear in the

third world application which he is more interested in.

However, in the meantime we are all shooting in the dark. Even Dr.

Bihari. If I could read one study on humans that would change the

situation immensely. If you have data on hundreds that in itself is

a large enough sample size to make things different. I have seen

information on only a few tens of MS sufferers. I know people who

are working on small-sample statistics who might even be able to use

the data on tens of patients.

But the studies have not been done.

In the meantime, the page you point me to says:

" combinations of an low opioid dose and an objective analgesic

achieves the same degree of a higher dose of opioid alone "

This applies to endorphin (endogenous morphine) and aspirin, or

endorphin and advil, or endorphin and acetaminophen. Sorry for the

trade names. That means any effect of LDN can be enhanced by the use

of NSAIDs. This is good news, don't you think? Don't all go off

and poison yourselves. Try one tablet.

Nor my theory if you can call it that nor anybody else's theory on

LDN has been proved.

That is my main complaint (a lot more than my MS!). Data I have seen

on doses of naltrexone other than ldninfo.org came from Crain and

Shen on mice and humans, but not with MS, only IBS. I have tried to

contact them but got no response yet.

-Sullivan

> > Yes what I said was crap but not my calculations: GIGO.

> >

> > I am taking about 18 nanograms per kg of body mass and of course

> > I don't weigh 240 kg but 240 lbs.

> >

> > Even Dr. Bihari said:

> >

> > > at levels several times above 10 mg, at

> > > which these drugs have been generally administered in the past

> for

> > > other purposes, especially narcotic addiction, the effects of

the

> > > preferential blocking action against Mu over Delta receptor

sites

> > > disappears, since the amount of the drug is large enough to

cause

> > at

> > > least substantial blocking of Delta sites while the Mu sites

> remain

> > > fully blocked.

> >

> > I think the word several is very ambiguous. It *is* enough to

cause

> > substantial blocking of the Delta sites if that is what they are.

> >

> > Complete blocking actually. I am saying above 4,5 is actually

> > dangerous if you have low endorphin anyway. Even 4 was dangerous

> > for me but that is just an anecdote.

> >

> > Concentration once the stuff is fully distributed in your body,

> *is*

> > dependent on body mass. A person who has half as much mass will

> have

> > twice as concentrated a dose.

> >

> > For those who care, that is 2.25 mg, not 4.5. Many females weigh

> > half what I do or less. If they and I both take 4.5 mg they are

> > taking twice what I take, or what would be 9mg for me.

> >

> > I should think the dosage should be given for a specific weight to

> > reduce the confusion. You are free to believe it doesn't matter

> and

> > it may not, but if it does you may cause an exacerbation. I

think

> I

> > have.

> >

> > -Sullivan

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Hi

What you print below has nothing to do with raising endorphin level

in msers....it has to do with pain management, I believe.

Let's not confuse ourselves with too many unrelated facts. It is

all very interesting, but I want to consentrate on just raising our

endorphin level and fixing our immune systems, so it will quite

attacking our mylin....plain and simple. Find us some scientific

info on that (if there is any) Actually, I think, we are writing

science as we speak...lol

Love, Sally

<chris_sullivan@s...> wrote:

Then why do these very dose response curves on this page you refer

me to have on one axis dose marked very clearly in units of mg per

> kg mass of body weight?

> In the meantime, the page you point me to says:

" combinations of an low opioid dose and an objective analgesic

> achieves the same degree of a higher dose of opioid alone "

This applies to endorphin (endogenous morphine) and aspirin, or

> endorphin and advil, or endorphin and acetaminophen. Sorry for the

> trade names. That means any effect of LDN can be enhanced by the

use of NSAIDs. This is good news, don't you think?

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