SSE sent me a bottle of this to give feedback on and I've been taking it for several days now.

It's been helpful WRT reducing minor aches at 4 caps but it isn't nearly strong enough for DOMS,IOW there is no chance of mistaking this for the narcotic that the name was grifted from.

My mother has some pretty severe lower back problems so I've given her the bottle,I'll post how she fares with it.I know that she does not like taking de-rugs for pain so if this could help to lower required dosages I'd be impressed.I will post her doctor's diagnosis of her condition when I update with her feedback.

In for the review from Mom.

Solid update Colin, make sure the accurate dosage is taken, dosing is WEIGHT-DEPENDENT.

I have chronic pain issues and take real vicodin and tramadol as a result of my condtion.
I will be following this thread.
Anything that would allow me to take less drugs would be of interest to me.

Update?

Mine hasn't shown up yet..

Send me PM with shipping info, let me check.

Colin, DOMS is not regulated by the same pathways as other pain, lookie here:

J Physiol. 2007 Nov 15;585(Pt 1):287-94. Epub 2007 Oct 11.

Central modulation of exercise-induced muscle pain in humans.

Ray CA, Carter JR.

Heart & Vascular Institute H047, Penn State College of Medicine, The Milton S. Hershey Medical Center, 500 University Drive, Hershey, PA 17033-2390, USA. caray@psu.edu

The purpose of the current study was to determine if exercise-induced muscle pain is modulated by central neural mechanisms (i.e. higher brain systems). Ratings of muscle pain perception (MPP) and perceived exertion (RPE), muscle sympathetic nerve activity (MSNA), arterial pressure, and heart rate were measured during fatiguing isometric handgrip (IHG) at 30% maximum voluntary contraction and postexercise muscle ischaemia (PEMI). The exercise trial was performed twice, before and after administration of naloxone (16 mg intravenous; n = 9) and codeine (60 mg oral; n = 7). All measured variables increased with exercise duration. During the control trial in all subjects (n = 16), MPP significantly increased during PEMI above ratings reported during IHG (6.6 +/- 0.8 to 9.5 +/- 1.0; P < 0.01). However, MSNA did not significantly change compared with IHG (7 +/- 1 to 7 +/- 1 bursts (15 s)(-1)), whereas mean arterial blood pressure was slightly reduced (104 +/- 4 to 100 +/- 3 mmHg; P < 0.05) and heart rate returned to baseline values during PEMI (83 +/- 3 to 67 +/- 2 beats min(-1); P < 0.01). These responses were not significantly altered by the administration of naloxone or codeine. There was no significant relation between arterial blood pressure and MSNA with MPP during either IHG or PEMI. A second study (n = 8) compared MPP during ischaemic IHG to MPP during PEMI. MPP was greater during PEMI as compared with ischaemic IHG. These findings suggest that central command modulates the perception of muscle pain during exercise. Furthermore, endogenous opioids, arterial blood pressure and MSNA do not appear to modulate acute exercise-induced muscle pain.
PMID: 17932155 [PubMed - indexed for MEDLINE]

I can not emphasize how true this is in real world applications. As I noted above, I have chronic stomach problems and use both tramadol and vicodin to relieve the pain caused by it. I take vicodin 7.5/750. One pill is enough to relieve all but the worst pain, in which case I can take another.
When I have severe DOMs and I am suffering from my condition, the vicodine will completely relieve my stomach pain. However, it provides no relief from my DOMs. For example, if my legs were extremely sore prior to taking the vicodin, they would still be sore and I would still be walking funny after taking the vicodin.

Any update?

Not yet but I'll be seeing my family this weekend so I'll post how she's been faring shortly.She's been on it at 2 caps twice per day since the 22nd so I should be able to post up some thorough feedback.I'll update with her medical diagnosis as well.

Well,my mother has told me Vicodene has been somewhat helpful WRT general pain/getting around,as of the past several days.

Nothing profound,so far as when she feels an acute pain she hasn't swayed from dropping her pharm (5mg percocet).

She said it was about on par with the Sesathin liquid I gave her a while back,which she discontinued taking because she grew tired of dealing with the "yuck" taste.

I asked her what her diagnosis(actual medical condition) was but I can't make out my own handwriting as I jotted it down in the car.Seeing as this has a lot to do with the point of this log i will call her and post up what I should have posted already.

She still has a bit more than a week's worth left of the bottle and SSE/Ross said he was going to send me another two bottles so I'll see how this plays out over the long term.

Sounds good, bottles should arrive shortly.

These haven't arrived,can you please throw me a tracking number?

Well,my mother has told me her pain is mostly around her neck as she has pinched nerves,something about bone encroaching on muscle.She also has a less painful and unrelated situation with her lower back,due to a injury which was the results of moving furniture around 25 years ago.Her cervical bone is connected to her pelvis and this negatively effects the spine,basically another issue with pinched verves,as far as I can tell.

Anyway I'm having her get off of Vicodene as I came across the following abstracts which indicate the active may be problematic if taken with pharmacueticals.So it appears that using Vicodene to cut down on narcotic usage is not an option.

I plan on an aggressive high dosing protocol of the remainder, as well as the two bottles Ross has said are being shipped when they manifest themselves.I'll record any results seen here.

Impact of Andrographis paniculata crude extract on mouse hepatic cytochrome P450 enzymes.
Jarukamjorn K, Don-in K, Makejaruskul C, Laha T, Daodee S, Pearaksa P, Sripanidkulchai BO.

Department of Pharmaceutical Chemistry, Faculty of Pharmaceutical Sciences, Khon Kaen University, Khon Kaen 40002, Thailand. kanok_ja@kku.ac.th

Modulatory influence of Andrographis paniculata crude extract on cytochrome P450 (CYP) enzymes was performed by administration of the crude extract of Andrographis paniculata to ICR male mice. Total hepatic P450 content was not significantly modified by either the aqueous or the alcoholic extracts of Andrographis paniculata. Assessment of hepatic microsomal P450 activities by alkoxyresorufin O-dealkylations noted that both the aqueous and alcoholic extracts of Andrographis paniculata significantly increased ethoxyresorufin O-dealkylase and pentoxyresorufin O-dealkylase activities, while those of methoxyresorufin O-dealkylase activities were not elevated. These results suggested that Andrographis paniculata might effectuate hepatic cytochrome P450 enzymes of which CYP1A1 and CYP2B are the responsive P450 isoforms.

PMID: 16406417 [PubMed - indexed for MEDLINE]


Differential inhibition of rat and human hepatic cytochrome P450 by Andrographis paniculata extract and andrographolide.
Pekthong D, Martin H, Abadie C, Bonet A, Heyd B, Mantion G, Richert L.

Laboratoire de Toxicologie Cellulaire, EA 3921 Optimisation Métabolique et Cellulaire, UFR des Sciences Médicales et Pharmaceutiques, Besançon, France.

The inhibitory effect of Andrographis paniculata extract (APE) and andrographolide (AND), the most medicinally active phytochemical in the extract, on hepatic cytochrome P450s (CYPs) activities was examined using rat and human liver microsomes. For this purpose, CYP1A2-dependent ethoxyresorufin-O-deethylation, CYP2B1-dependent benzyloxyresorufin-O-dealkylation, CYP2B6-dependent bupropion hydroxylation, CYP2C-dependent tolbutamide hydroxylation, CYP2E1-dependent p-nitrophenol hydroxylation and CYP3A-dependent testosterone 6 beta-hydroxylation activities, were determined in the presence and absence of APE or AND (0-200 microM). APE inhibited ethoxyresorufin-O-deethylation activity in rat and human liver microsomes, with apparent Ki values of 8.85 and 24.46 microM, respectively. In each case, the mode of inhibition was noncompetitive. APE also inhibited tolbutamide hydroxylation both in rat and human microsomes with apparent Ki values of 8.21 and 7.51 microM, respectively and the mode of inhibition was mixed type. In addition, APE showed a competitive inhibition only on CYP3A4 in human microsomes with Ki of 25.43 microM. AND was found to be a weak inhibitor of rat CYP2E1 with a Ki of 61.1 microM but did not affect human CYP2E1. In conclusion, it cannot be excluded from the present study that APE could cause drug-drug interactions in humans through CYP3A and 2C9 inhibition.

PMID: 18053665 [PubMed - in process]