Hepatotoxicity
The frequency of adverse reactions to kava, particularly liver injury, is not known. Based upon reported cases, the estimated frequency of clinically apparent liver injury due to kava is less than 1:1,000,000 daily doses. However, spontaneous reporting is believed to capture less than 1% of severe adverse events from the use of dietary supplements. Between 50 and 100 cases of clinically apparent liver injury have been published or discussed in the literature. Advocates of the herbal have strongly rejected these numbers, disputing both their accuracy and the causality assessment process. Still, there seem to be convincing evidence in some cases of severe hepatitis ending in fulminant hepatic failure, requiring liver transplantation, and even leading to death. Patients typically present with fatigue, nausea, elevations in serum aminotransferase levels, and jaundice 2 to 24 weeks after starting use of the product. The pattern of enzyme elevations is hepatocellular with marked elevations in serum aminotransferase and minimal increases in alkaline phosphatase levels. In some cases, features of immunoallergic hepatitis (rash, fever, eosinophilia, and recurrence on reexposure) are present. Liver biopsy findings include focal hepatocellular necrosis, lobular inflammation and intrahepatic cholestasis. In more severe cases there is massive or submassive necrosis.
--> http://livertox.nih.gov/KavaKava.htm
not sure about finding a prami supplier. it's called "pramistar" in the EU. im a little reluctant to recommend it though, skeptical of long-term side effects. you could also go the natural route:
The committee highlights curcumin as one flavonoid for which there is substantial evidence of neuroprotectant effects in animal models of TBI...
Therefore, the consumption of flavonoid-rich foods, such as berries and cocoa, throughout life holds a potential to limit the neurodegeneration associated with a variety of neurological disorders and to prevent or reverse normal or abnormal deteriorations in cognitive performance.
the lappaconitine havent tried, but it looks good. lithium i would do 1/4 of a tab, maybe you try 1 full tab and see if theres side effects. i would personally taper off at a doc's advice then start the lithium fresh, but it seems many redditors like to combine them. PJ recommended royal jelly. royal jelly, bilobalide (ginkgo), naringin (in oranges/grapefruits), nobiletin (same foods), ibogaine and exercise all induce GDNF. ginkgo also has NGF, BDNF, as well as neuromodulatory or adaptogenic properties.
a little searching also turned up Prostaglandin D2 as a relevant factor. i found one guy suggesting quercetin + jojoba + lecithin. didnt look into mechanisms or other testimonies, so take it with a grain of salt.
Newly Discovered Factor in Androgenetic Alopecia. The Cure is Near? Washington: Researchers have discovered an abnormal amount of a protein called Prostaglandin D2 in the bald scalp of men with male pattern baldness.
The discovery by researchers at Perelman School of Medicine at the University of Pennsylvania may lead directly to new treatments for the most common cause of hair loss in men.
In both human and animal models, researchers found that a prostaglandin known as PGD2 and its derivative, 15-dPGJ2, inhibit hair growth.
The PGD2-related inhibition occurred through a receptor called GPR44, which is a promising therapeutic target for androgenetic alopecia in both men and women with hair loss and thinning.
Male pattern baldness strikes 8 of 10 men under 70 years old, and causes hair follicles to shrink and produce microscopic hairs, which grow for a shorter duration of time than normal follicles.
Researchers took an unbiased approach when scanning for potential biological causes of baldness, looking in scalp tissue from balding and non-bald spots from men with male pattern baldness and then corroborating findings in mouse models.
They found that levels of PGD2 were elevated in bald scalp tissue at levels 3 times greater than what was found in comparative haired scalp of men with androgenetic alopecia.
When PGD2 was added to cultured hair follicles, PGD2-treated hair was significantly shortly, while PGD2``s derivative, 15-dPGJ2, completely inhibited hair growth.
“Although a different prostaglandin was known to increase hair growth, our findings were unexpected, as prostaglandins haven`t been thought about in relation to hair loss, yet it made sense that there was an inhibitor of hair growth, based on our earlier work looking at hair follicle stem cells,” said George Cotsarelis, MD, chair and professor of Dermatology, and senior author on the studies.
In a Penn study published last year, underlying hair follicle stem cells were found intact, suggesting that the scalp was lacking an activator or something was inhibiting hair follicle growth.
Prostaglandins are well characterized for their role in many bodily functions – controlling cell growth, constricting and dilating smooth muscle tissue – and a different prostaglandin (F2alpha) is known to increase hair growth.
Researchers found that as PGD2 inhibits hair growth, other prostaglandins work in opposition, enhancing and regulating the speed of hair growth.
While these studies looked at AGA in men, the researchers noted that prostaglandins may represent a common pathway shared by both men and women with AGA.
Future studies, potentially testing topical treatments that may target GPR44, can determine whether targeting prostaglandins will benefit woman with AGA as well.
perhaps also things to optimize LDL/HDL, and phosphatidylcholine/serine is prudent. the mere addition of a phosphatidyl donor could resolve limiting steps in the generation of many necessary brain membrane lipids. also consider MCTs or refined coconut oil, in addition to your fish oil. i may be getting ahead of myself here, but even something like exercise and ketogenic diet might give a little boost. i would personally use the keto sparingly tho. last words, you can also use valerian in place of kava if it's just to treat insomnia, and not anxiety.
Role of Lipids in Brain Injury and Diseases.
Adibhatla RM1, Hatcher JF. (2007)
Lipid metabolism is of particular interest due to its high concentration in CNS. The importance of lipids in cell signaling and tissue physiology is demonstrated by many CNS disorders and injuries that involve deregulated metabolism. The long suffering lipid field is gaining reputation and respect as evidenced through the Center of Biomedical Research Excellence in Lipidomics and Pathobiology (COBRE), Lipid MAPS (Metabolites And Pathways Strategy) Consortium sponsored by NIH, European initiatives for decoding the lipids through genomic approaches, and Genomics of Lipid-associated Disorder (GOLD) project initiated by Austrian government. This review attempts to provide an overview of the lipid imbalances associated with neurological disorders (Alzheimer's, Parkinson's; Niemann-Pick; Multiple sclerosis, Huntington, amyotrophic lateral sclerosis, schizophrenia, bipolar disorders and epilepsy) and CNS injury (Stroke, traumatic brain injury; and spinal cord injury) and a few provocative thoughts. Lipidomic analyses along with RNA silencing will provide new insights into the role of lipid intermediates in cell signaling and hopefully open new avenues for prevention or treatment options.
Edited by gamesguru, 16 June 2016 - 05:08 PM.