Posted by casse on January 9, 2010, at 12:57:58
In reply to Re: LDN Low Dose Naltrexone Questions, posted by Elroy on January 8, 2010, at 15:45:12
I was glad to see you give due credit to Dr. Zagon. I regard him as the foremost expert on LDN.
What I discovered in the 6 months I've used LDN is that whether I take 2.5 mg (the highest I've taken) or the very low dose I've been using, I still experience agitation. What I will try now that I seem to have found an antidepressant that works very well for anxiety symptoms (tianeptine), is to ramp up LDN quickly to 1.5mg again and continue to increase until I'm at 3 mg. I may have to wait for a few weeks to do that as I might need surgery in a couple of weeks.
I've read that naltrexone raises cortisol and noradrenaline levels ( albiet at the 25-50mg doses used in the studies on which the abstracts were based ). I just can't help wondering if some people experience an increase in cortisol even at a low dose. It has been my suspicion that elevated cortisol and noradrenaline are responsible for the irritability and agitation, not the LDN pr.se.. BUT, what I can say for absolute certain is that when I use LDN, I feel much the same way the next morning as a dose of vicodin would make me feel. Awful.
I have a rudimentary understanding of homeostasis and the action of LDN. I'm familiar with all of the books you recomended, but haven't read them yet. Most of my information comes from scientific abstracts, lowdosenaltexone.org , and Dr. Zagon's posted research. I wasn't aware that Dr. Chris Steel, was considered an expert although he's definitely a high profile advocate. I must read more about his experience with LDN.
Maybe there have been studies using doses lower than 1.5 mg that I'm not aware of. Or maybe one of the books you recommend will explain why doses lower than 1.5 mg can't be effective, but with the dissention out there regarding dose, I would have thought someone would have made direct reference to it by now. I guess I won't know until I read them myself, and You've given me more incentive to do so. Thank you for that. Perhaps doing so will bridge some of the gaps in my understanding and answer some nagging questions I have.But I think it's an oversimplification to say that more endorphins will equal elevated mood. A study at U of M found that many of the women subjects with antidepressant resistant Major Depressive Disorder had exaggerated activation of the mu opioid system during emotional challenges, yet the binding potential of endorphins was diminished. Read both the article and the abstract.
Article:
http://www.anxietyinsights.info/overactive_brain_endorphin_system_linked_to_depression.htmAbstract:
http://archpsyc.ama-assn.org/cgi/content/abstract/63/11/1199This begs the question of whether more is better. If there is a reduction in binding potential, there may be a chemical deficiency preventing activation of mu receptors, and subsequently, no relief, or euphoria. Since I have MDD and have had poor success with antidepressants, I wonder if this applies to me. If I am understanding this correctly it isn't a matter of deficiency but rather, possible resistance to endorphins at the mu receptors. I also wonder how kappa receptors might play into this, since their activation is significantly involved in dysphoric symptoms.
I'm just throwing this out there in case someone has a handle on it. I don't' have the answers.
And I appreciated your excellent analogy Elroy.
All the best...
Casse
poster:casse
thread:919880
URL: http://www.dr-bob.org/babble/20100103/msgs/933028.html