Re: Nutriiveda: Turmeric probably causing seizure reduction

[Guest guest]

Hi there,

Been doing research on Turmeric, since my doctor recommended it for Frozen

Shoulder (I can't take NSAIDS) because of it's anti-inflamatory properties.

Anyway, found a study done in rats that says the active ingredient in Turmeric,

Curcumin, decreases certain kinds of seizures in rats. I'll post the abstract

below.

One thing to know - Turmeric is a mild MAOI - inhibits MAO-A. The way to

increse it's effect is to add black pepper to the active ingredient - Curcumin -

which increases it's absorption by 2000%. Taking Tumeric alone without anything

with it usually doesn't get enough in your system to make a difference one way

or the other (absorption the issue), but sounds like there is something in the

Aryuvedic combination in Nutriiveda that could be boosting it. I'd be curious

what the physicians behind Nutriiveda think about this and if they feel it's

contributing to observations of reduction in seizures.

Also, MAOI's interact with alot of other medications, so I am curious if

Nutriiveda is recommended for someone taking an MAOI? Since Turmeric is an

MAOI, then it could interact, especially if someone is already taking one.

Would it interact with other antidepressants or stimulants a child could be on

for ADD or other things? Just curious. Since MAOI's are an antidepressant,

this might also explain some changes in mood, initial irritability, and also

regression when discontinued.....

Will let you know what the Child Psychiatrist I visit next week says. Will

also cite another article I found about it. Overall it's pretty mild, but am

curious about drug interactions.

Just wanting to share what I found, as information is always beneficial.

Turmeric has been used for thousands of years in Aryuvedic medicine, and has

positive results in many areas - am wondering how it fits in western culture

with our diet and the medications we take (over the counter for colds, etc., and

also prescription) and if we'll run into drug interactions that are less common

in India because fewer people take the medications that are taken in the

west.....

Have a blessed day!

Diane

Curcumin inhibits amygdaloid kindled seizures in rats

DU Peng, LI Xin, LIN Hao-jie, PENG Wei-feng, LIU Jian-ying, MA Yu, FAN Wei ,

WANG Xin

DU Peng Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai

200032, China; LI Xin Department of Neurology, Zhongshan Hospital, Fudan

University, Shanghai 200032, China; LIN Hao-jie Department of Neurology,

Zhongshan Hospital, Fudan University, Shanghai 200032, China; PENG Wei-feng

Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai 200032,

China; LIU Jian-ying Department of Neurology, Zhongshan Hospital, Fudan

University, Shanghai 200032, China; MA Yu Department of Neurology, Zhongshan

Hospital, Fudan University, Shanghai 200032, China; FAN Wei Department of

Neurology, Zhongshan Hospital, Fudan University, Shanghai 200032, China; WANG

Xin Institute of Brain Science, Fudan University, Shanghai 200032, China

Correspondence to: WANG Xin Department of Neurology, Zhongshan Hospital and

Institute of Brain Science, Fudan University, Shanghai 200032, China

(Tel:86-21-64041990 Fax:86-21-64038472 Email:wang-xin@... )

Abstract:

Background Curcumin can reduce the severity of seizures induced by kainate acid

(KA), but the role of curcumin in amygdaloid kindled models is still unknown.

This study aimed to explore the effect of curcumin on the development of

kindling in amygdaloid kindled rats.

Methods With an amygdaloid kindled Sprague-Dawley (SD) rat model and an

electrophysiological method, different doses of curcumin (10

mg & #8729;kg–1 & #8729;d–1 and 30 mg & #8729;kg–1 & #8729;d–1 as low dose groups, 100

mg & #8729;kg–1 & #8729;d–1 and 300 mg & #8729;kg–1 & #8729;d–1 as high dose groups)

were administrated intraperitoneally during the whole kindling days, by

comparison with the course of kindling, afterdischarge (AD) thresholds and the

number of ADs to reach the stages of class I to V seizures in the rats between

control and experimental groups. One-way or two-way ANOVA and Fisher & #8242;s

least significant difference post hoc test were used for statistical analyses.

Results:

Curcumin (both 100 mg & #8729;kg–1 & #8729;d–1 and 300 mg & #8729;kg–1 & #8729;d–1)

significantly inhibited the behavioral seizure development in the (19.80±2.25)

and (21.70±2.21) stimulations respectively required to reach the kindled state.

Rats treated with 100 mg & #8729;kg–1 & #8729;d–1 curcumin 30 minutes before

kindling stimulation showed an obvious increase in the stimulation current

intensity required to evoke AD from (703.3±85.9) µA to (960.0±116.5) µA during

the progression to class V seizures. Rats treated with 300

mg & #8729;kg–1 & #8729;d–1 curcumin showed a significant increase in the

stimulation current intensity required to evoke AD from (735.0±65.2) µA to

(867.0±93.4) µA during the progression to class V seizures. Rats treated with

300 mg & #8729;kg–1 & #8729;d–1 curcumin required much more evoked ADs to reach the

stage of class both IV (as (199.83±12.47) seconds) and V seizures (as

(210.66±10.68) seconds). Rats treated with 100 mg & #8729;kg–1 & #8729;d–1 curcumin

required much more evoked ADs to reach the stage of class V seizures (as

(219.56±18.24) seconds).

Conclusion:

Our study suggests that curcumin has a potential antiepileptogenic effect on

kindling-induced epileptogenesis.

*******************************************************************

Along those same lines, curcumin has shown itself to act like a MAOI drug – one

of the most powerful classes of anti-depressant drugs available. It blocks

monoamine oxidase thereby preventing the brain from breaking down dopamine (read

the Nutrition Wonderland break down on dopamine if you need help). This

mechanism may also help treat Parkinson's disease, as they rely on similar

mechanisms in the brain [8].

The Absorption Problem

Curcumin suffers from a similar problem to most flavonoids we have looked at in

the past: it just doesn't get absorbed into the bloodstream very effectively.

In fact, its present at woefully small amounts in the body. Even after

consuming as much as 12g of turmeric (which is a ton of tumeric), only trace

amounts of curcumin made it into the body [9]. The only way to translate all

this positive research in the lab is to figure out a way to get more curcumin

into the body.

Plenty of researchers are working on this problem though. Cashman at the

Human BioMolecular Research Institute is developing methods to deal with the

bioavailability issue. Dubbed `synthetic curcuminoids`, these compounds his lab

is developing combine the medical benefits of curcumin with a better delivery

vehicle that survives the brutal GI tract that usually destroys natural

curcumin. Some of these synthetic methods employed by the HBRI folks include

nano-particle engineering, cutting edge work that may overcome part of what

holds back this herb today.

A more natural approach may also fix the tumeric absorption problem. The

addition of piperine (an active compound of black pepper) enhances the

anti-depressive effect of turmeric [10]. Simply adding together the compounds

found in nature may multiply the effect of tumeric by up to 2000% by allowing

the body to absorb more curcumin [11]. The complex spice combinations found in

curries backup this theory, as it has been noted Indian cultures who consume

curry regularly have far lower incidences of Alzheimer's as they age.