Re: LDN for Type 1 diabetes - dawn phenomenon on LDN - Armour thyroid reformulation (Hashimotos's)

[Guest guest]

Hi Jim, I have read somewhere that LDN w/ alpha lopic acid, ala, can reverse some of the damages of diabeties, ie neuropathy.

I certainly encourage your search for understanding, science, research is like

my love life, several failures hopfully followed by one mistake and you have it.

press on, and stay vertical, david a

[low dose naltrexone] LDN for Type 1 diabetes - dawn phenomenon on LDN - Armour thyroid reformulation (Hashimotos's)

Hi,

(Sorry for the long and somewhat technical and highly hypothetical discussion. The main questions about what others have noticed is at the end)

** Diabetes and Dawn Phenomenon (DP) **

I'm using LDN in hopes that it will do something for my Type 1 diabetes. It is late onset, and low-carb managed, and I think I may still be honeymooning after about 5 years.. Except that the LDN seems to be screwing that up. I don't think this is a "real" DP though, I think the LDN is causing an imbalance between how the beta cells (insulin) and alpha cells (glucagon) are reacting to other hormones and neuro-endocrine signaling.

I've never bought the idea that non-diabetics "just create enough insulin to counter the DP" - which is described as being anywhere from 50-150 points - within about 3 hours (according to Dr. K. Bernstein in his book IRRC). I think that the alpha and beta cells are acting in concert to move glucose first from storage (glycogen in the liver and other places) first into the blood (glucagon) and then into cells (insulin). Nice neat mechanism, and I think it's all controlled mainly by the neuro-endocrine meshwork surrounding the islets and presumably "co-ordinating" in some way all the cells in the islets (one type of which, the "PP cells" we don't really know what do - I'm not sure if we know what the gamma cells do either).

But some Type 1's have a honeymoon that has no DP - which would require a compromised pancreas (enough to need insulin) to be able to create enough endogenous insulin within only an hour or two to counter 50-100 points of BG rise. I just don't think that's possibly, given that even low-carb meals cannot be dealt with that quickly, and so require bolus to remain (relatively) normo-glycemic).

I think the DP is mediated by the neuro-endocrine meshwork, and as long as there is some meshwork and some beta cells still functioning - the meshwork, beta, and alpha cells can adjust themselves to the lowered capacity of the beta cells in Type 1 (the alpha cells either become relatively resistant to whatever signal neural part is creting, or that signal is just created less.

But if the LDN is:

1) Possibly allow some regeneration of beta cells or differentiation of ductal cells

2) Maybe also allowing the beta cells which are alive to function "better". I think the autoimmunity not only kills beta cells, but also "impedes" the function of ones that are still alive - possibly by knocking out the normal Phase 1 insulin response feedback loop, which depends on ICA512 (which is attacked), or possibly by auto-antibodies latching onto insulin itself

I think there is some debate as to whether actual insulin auto-antibodies form. I they did and attached and drew T-cells to insulin systemically, it would appear to almost be able to shut the entire system down, and drive the immune system - and the attendant sickness behavior - to an extra-ordinarily high level, which doesn't seem to happen. Unless the auto-antibodies do not call forth T-cells, and so pro-inflammatory cytokines are never main. Auto-antibodies can exist without T-cell involvement for some reason. This has even been observed (and created) in NOD mice in the lab (Razaci 2006 I believe about TRPV1+ neurons)

3) Most hypothetically (in terms of the "DP" I have seen), by altering the "balance" that existed between the small beta cell population and (presumably) full alpha-cell population. The beta cells function better, and/or respond better to signals from the meshwork, while the alpha cells are still "down-regulated" with reference to those signals It takes about 6 weeks for the meshwork to regrow - confirmed in islet transplant patients using immuno-suppressants.

If this hypothesis is true (and I'm now so far out on a limb of the hypothesis tree that it breaks..): The beta cells produce more insulin, which produces a drop. The alpha cells at some point "notice" this (via normal hypo-gycemic sensing means) and produce glucagon.

But I the alpha cells may "overshoot" and produce hyperglycemia, relative to human normal of about 81. If the beta-cells production of amylin is also compromised (which may or may not be controlled by the meshwork's hypothetical role in the DP, or tied in any way to insulin production.. Amylin isn't there to "fine tune" the action of glucagon.

Anyway, what I've noticed was an almost immediate reduction of "sickness fatigue" - although that is also influenced by the autoimmune thyroiditis (immune response close to the brain..?). My "carb tolerance" per unit insulin went WAY up it seemed, and my night basal shot (I take two of Levemir - one on waking and then one at about 4-6 PM) started to go down, but not the morning shot for some reason, or not by much. I presume the effect on the morning shot is because the two overlap some).

First the night shot dropped by about a unit, and the morning by about 1/2 unit. Now the night shot seems to have dropped another 1/2 unit, and I'm not sure if anything will happen to the morning shot. I also seem - when these "reductions" happen" - to have temporary need of a small third shot in the middle of the day of about 1/2-1 unit Levemir. This may be to help stabilize things until.. Maybe the neural meshwork/endogenous production is stabilizing. This lasts maybe 2 weeks..

I don't really know on that "duration" point of the third shot. It's only happened once, and my records are a mess - if I want to find anything in them - they are quite detailed, but not computerized or easy to read looking for something. I keep think "why" should spend 4 weeks making a good computer program to store them digitally - when I'll be staring to try to actually get rid of this damn disease within about 3 weeks.. This feeling has been going on for the the past 4 a half years.. My parents have no conception that diabetes can actually be cured (which it can..), or that it causes more problems than "just blood sugar and then need for insulin.. Ha no big deal.."

(Yeah, try MS for a couple months and you'd know what I'm talking about when I talk about sickness behavior. Then - take my #$@%! advice and start on LDN pronto!)

** Armour thyroid reformulation **

As for the thyroiditis, I haven't noticed any real change in it - mainly because I can't get a thyroid med that actually works. The "new" Forest formulation has almost no glucose, which appears to have been replaced with micro-crystalline cellulose - and it doesn't work at all. As it doesn't for hundreds if not thousands of others.. The FDA nor Forest must know but seem to care - as usual it seems.. Erfa (from Canada) is supposedly equivalent to the old formulation of Armour, but it isn't quite (it still crumbles a bit rather than "snaps" in a pill cutter like the old Armour did. Anyway, I think my month-long "experiment" with the "new Armour" (to placate my mother - who doesn't believe Forest would not listen to patients complaints, or that the FDA would not listen to their complains and light a fire under Forest's metaphorical behind until they changed the damn formulation back to what it was - and what they already know how to produce..

My next shot is either to hope that a T3 dietary supplement made by RLC Labs (who also make Westhroid which is FDA approved) can get rid of an rT3-dominant situation I think may have built up during the few weeks on the "new" Armour.. Then maybe the Erfa will work at the old doses of (old) Armour. If not.. I guess find a good compounding pharmacy who can and will make a compound that is exactly like the old Armour - made of Thyroid USP, glucose/dextrose, micro-crystalline cellulose (if there was any), probably some kind of phosphate and some kind of stearate (all drugs seem to have some stearate compound them).

The price will be higher.. (MUCH higher than the ERFA is..), but.. I might be on (or at least closer to) to road to real health (minus the adrenal insufficiency which is why I can't really do any exercise.. The cortisol supplementation I think is just "hold that at bay" - I don't think the adrenals will really heal until either/and 1) HBOT treatment, 2) I get my damn thyroid function normalized at the cellular level.. And keep it there!! Not just the "thyroid" at the blood level, and certainly not TSH which is three "levels" away from actual cellular function. And maybe even more levels than that - assuming T4->(3 DIOs)->T3->(BBB and maybe a more efficient DIO)->pit T3 level and then TSH secretion (that is, if the pit cellular receptors are working correctly, and the "inter-pit" feedback loop between T3 and TSH is also working correctly...)

So I've never really had normal temperatures, and presumably not normal T3/T4 levels either - so the LDN didn't seem to have any effect on it at all - certainly not on my thyroid dose - which wasn't enough to begin with and didn't work.

** Questions **

I'm just wondering if anyone else has used LDN for Type 1, and what their experience was? And whether a day dose might work for it - or perhaps even better?

While Type 1 is autoimmune like MS), but it is a different autoimmunity that MS, which might influence things - especially since MS is a brain autoimmunity, and LDN works (presumably) on chemicals or processes that are produced in the brain, while Type 1 is a peripheral autoimmunity (although it does attack the neural meshwork of the islets - via the S-100-beta antigen and pre-Schwann cells). Thyroiditis may be a different matter - it's autoimmunity is very close to the CSF, and the thyroid also has a large number of nerves running through it.

Jim