I was quite excited about this and was trying to understand it here in public when I received a PM from a friend telling me that I had put my big foot down right in the middle of some very sensitive negotiations over patent issues that needed to be resolved to move it toward clinical trials.

I have now been told that those negotiations have gone well and that trials should begin this year! And that it is safe to talk about it again. So, it being Christmas, a little hope for us all makes a good present.

I know more than I did, so I am going to try to clear up some of the confusion. First, we are talking about two different but similar discoveries by the same team led by P.S. Whitton. One is that urocortin acting upon CRF receptors triggered repair. Unfortunately, urocortin does not cross the BBB, plus there are a lot of unknowns about it to be followed up.

The other, and far more exciting, was the discovery that the receptors for a peptide called Glucagon-Like Peptide-1 (GLP-1) triggered similar repair when activated by either GLP-1 itself or an agonist (mimic). The diabetic drug Ex-4, derived from our friend the Gila Monster, is such a mimic and has already passed through many hoops for its diabetic uses that won't have to be repeated. Also, it readily passes the BBB and lasts several hours while GLP-1 lasts only minutes. So, we unexpectedly have a half-approved cure that really cured rats. Not only did it cure rats with PD caused by injecting one particular toxin, it also cured rats with PD caused by a second type of toxin. That is, it cured it in two unrelated models. That's good.

GLP-1 is produced in your gut when you eat and triggers insulin production in the pancreas. But its receptors are found other places including the brain. It also fits into some pretty specific spots in the PD puzzle. For example, two things that have been shown to stop PD are fasting and exercise. If you have ever fasted, after a day or so you aren't hungry. GLP-1 controls appetite. Exercise not only slows PD, it also increases production of GLP-1.

There is quite a bit more, including some white rat opportunities that increase GLP-1, but it looks better than anything that I have seen thus far.

So Merry Christmas!

...and have been "coincidentally" suggested as helpful in PD at one time or another-
1- Exercise
2- Fasting
3- Coconut oil
4- Ginseng
5- Glutamine
6- Whey

Thank you Rick for sharing all of this, very promising and offers hope at a great time, since several things that looked so good have "failed" (no need to remind everyone, we all know what they are/were).

I think you and all here that self-experiment should get a t-shirt that says "Lab Rat" on it, Lordy knows it is well-deserved!

Link from 9/10/2007:
http://neurotalk.psychcentral.com/sh...ghlight=byetta

Link listed in response to this topic on 10/27/08 is incorrect--madelyn






Talent hits a target no one else can hit; Genius hits a target no one else can see. Arthur Schopenhauer

Thanks, Rick. I have glutamine in my lab room, and I'm tempted to take a bit, but I won't!

Thanks for the birthday present; I'm a Christmas eve baby. HUGE snow storm in NYC when I was born. Cars not allowed on the road, but the cop let me go home. Darn, I miss my dad.

After sifting through the options and considering cost, effectiveness, and PD-specific conflicts, it looks like the coconut oil is my choice. Of its eight major components, seven bump up GLP-1 levels. It also provides an explanation for the report in the other thread of the Tampa doctor whose husband benefited from it. I wonder, too, if fish oil has a similar action in addition to anti-inflammatory effects. There seems to be a pattern leading to certain fats.

Much has been made of the fact that Inuits ("Eskimos") have little heart disease. Does anyone know if they have much PD?

Fish oil does seem to double GLP-1 levels, at least under the conditions described below. Somewhere in the last year I read a news story about the lone survivor of a mining accident in West Virginia who was virtually brain dead. In desperation, his GP pumped him full of fish oil for several weeks and he was making a strong recovery. Interesting.


1: Regul Pept. 1999 Apr 30;80(3):101-6.

Inhibition of human gastric lipase by intraduodenal fat involves glucagon-like
peptide-1 and cholecystokinin.

Wøjdemann M, Riber C, Bisgaard T, Sternby B, Larsen S, Rehfeld JF, Holst JJ,
Olsen O.

Department of Surgery, Rigshospitalet, National University Hospital, Copenhagen,
Denmark. rh01977@rh.dk

Seven healthy volunteers were intubated with two double lumen nasogastric tubes,
one in the stomach, the other in the duodenum. This system allows simultaneous
sampling of gastric juice and separate intraduodenal perfusion with a dietary fat
(fish oil, 1269 kJ). Gastrin-17 was infused i.v. at a rate of 40 pmol/kg/h
throughout the study. Gastric lipase was measured at 15-min intervals as activity
(tributyrin) and as immunoreactivity (ELISA). Infusion of gastrin-17 resulted in
a stable increase in the plasma concentration from a basal concentration of 8.3
+/- 0.8 pmol/l to 41.4 +/- 4.2 pmol/l. Perfusion with fat reduced gastric lipase
activity from 24.2 +/- 5.3 to 7.2 +/- 2.5 kU/l (P < 0.05), and immunoreactivity
from 0.7 +/- 0.1 to 0.42 +/- 0.1 mg/l (P < 0.05). After termination of fat
perfusion, gastric lipase secretion increased again, though not reaching
preinhibitory concentrations. During the intraduodenal perfusion with fat the
plasma concentrations of glucagon-like peptide-1 (GLP-1) and cholecystokinin
(CCK) increased from 6.9 +/- 0.5 to 15.1 +/- 1.5 pmol/l (P < 0.05) and from 1.2
+/- 0.4 to 3.8 +/- 0.9 pmol/l (P < 0.05). This study reveals a negative effect of
fat in the duodenum on gastric lipase secretion. This effect may be mediated by
GLP-1 and/or CCK.


PMID: 10425652 [PubMed - indexed for MEDLINE]

http://www.setma.com/article.cfm?ID=292


"The recent return home of the only survivor of the Sago mine disaster, Randall McCloy Jr., seems miraculous and it was. Yet, there is a sound basis for his recovery. McCloy, who had suffered heart, kidney, and liver failure in addition to brain failure, returned home less than four months after the mining disaster. One of the principle reasons for this recover was Dr. Bailes’ administering of very high doses of Omega 3 Fish Oil to McCloy.

McCloy received (and continues to take) 15 grams per day of EPA and DHA. Although a seemingly extraordinarily high dose, McCloy’s blood levels of these fatty acids were constantly monitored to maintain them within a therapeutic zone to maximize the reduction of systemic inflammation without compromising the body’s ability to fight infection.

The implications of Randall McCloy’s remarkable recovery have widespread medical importance, not only for brain trauma patients, but also for any patient with neurological disorders. It has been demonstrated by Harvard Medical School that high-dose fish oil has significant benefits in treating bipolar depression, and a recent study demonstrated the same levels used by Dr. Bailes in treating Randall McCloy also demonstrated significant improvement in children with ADHD. Maybe this is why our grandmother called fish oil "brain food."

any further information about this topic? madelyn

...Tom Isaacs' Parkinson's Trust was funding a hush-hush clinical trial. I have been trying to catch Tom in his office long enough to get an update with little success. I'll report once I know more.