The purpose of this site is to collect lab research by medical doctors about herbs that are proven to treat illnesses and counter the false attacks on herbs by the medical industry and false claims by alternative medicine. I let the science tell the facts.
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GABA Date Written 2007
Author Joe Holmes Date Revised  

Report number 5 below shows it will kill prostrate cancer.

GABA is a CRH inhibitor. It is suggested that if one takes GABBA that they carefully listen to their body and if ones mood flattens or depression symptoms increase it could mean ones CRH is too low and to stop taking GABA. If it does not flatten CRH it is probably not a problem for you to take GABA.

GABA acts as a neurotransmitter and helps normalize insulin secretion. See item 2. GABA helps insulin pass through small pores in the pancreas. Item 3. GABA signaling as a novel target for the treatment and prevention of pancreatic cancer. Item 5.

1. "There are several different neurotransmitters (baseballs). The main ones are called Noradrenaline (NA), which is sometimes referred to as "norepinehprine", Dopamine (DA), Serotonin (5HT), and GABA.(1)

2. "O'Sullivan EP, Behan LA, King TF, Hardiman O, Smith D.Department of Diabetes and Endocrinology, Beaumont Hospital, Dublin 9, Ireland. Antibodies against glutamic acid decarboxylase (GAD) are involved in the pathophysiology of stiff-person syndrome (SPS) and type 1 diabetes. GAD catalyses the conversion of glutamate to gamma-aminobutyric acid (GABA). GABA acts as a neurotransmitter between neurones, while in pancreatic beta cells it plays an integral role in normal insulin secretion, hence the clinical presentation of muscular spasms in SPS and insulin deficiency in diabetes. Despite this apparent major overlap in pathophysiology, SPS only rarely occurs in individuals with type 1 diabetes. We report the case of a 41-year-old man presenting with a simultaneous diagnosis of both these conditions. His case is unusual in that it is the first reported case in the literature of these conditions occurring in someone with celiac disease (CD) and dermatitis herpetiformis. We discuss why SPS and type 1 diabetes co-exist in only a minority of cases and speculate on the underlying mechanism of the association with CD and dermatitis herpetiformis in our patient. PMID: 19150172

3. "Eliasson L, Abdulkader F, Braun M, Galvanovskis J, Hoppa MB, Rorsman P.Department of Clinical Sciences in Malmö, Unit of Islet Cell Exocytosis, Lund University Diabetes Centre, Clinical Research Centre, Malmö SE-205 02, Sweden. Pancreatic beta-cells secrete insulin by Ca(2+)-dependent exocytosis of secretory granules. beta-cell exocytosis involves SNARE (soluble NSF-attachment protein receptor) proteins similar to those controlling neurotransmitter release and depends on the close association of L-type Ca(2+) channels and granules. In most cases, the secretory granules fuse individually but there is ultrastructural and biophysical evidence of multivesicular exocytosis. Estimates of the secretory rate in beta-cells in intact islets indicate a release rate of approximately 15 granules per beta-cell per second, 100-fold higher than that observed in biochemical assays. Single-vesicle capacitance measurements reveal that the diameter of the fusion pore connecting the granule lumen with the exterior is approximately 1.4 nm. This is considerably smaller than the size of insulin and membrane fusion is therefore not obligatorily associated with release of the cargo, a feature that may contribute to the different rates of secretion detected by the biochemical and biophysical measurements. However, small molecules like ATP and GABA, which are stored together with insulin in the granules, are small enough to be released via the narrow fusion pore, which accordingly functions as a molecular sieve. We finally consider the possibility that defective fusion pore expansion accounts for the decrease in insulin secretion observed in pathophysiological states including long-term exposure to lipids. PMID: 18511483

4. "Morgado C, Pinto-Ribeiro F, Tavares I. Instituto de Histologia e Embriologia, Faculdade de Medicina, Universidade do Porto, Portugal. Painful diabetic neuropathy is associated to hyperexcitability and spontaneous hyperactivity of spinal cord neurons. The underlying pathophysiological mechanisms are not clear. Increases in excitatory neurotransmission at the spinal cord, involving glutamate and SP, seem to account for the abnormal neuronal activity, but inhibitory influences were never evaluated. This study aims to analyse the expression of GABA, its synthesizing enzyme glutamic acid decarboxylase (GAD) and the potassium chloride cotransporter (KCC2), in the spinal dorsal horn of streptozotocin (STZ)-induced diabetic rats. Four weeks after saline or STZ (60mg/kg) injection, animals were sacrificed and the spinal segments L2-L3 were removed and immunoreacted for GABA, GAD and KCC2, or processed for western blotting for KCC2. Densitometric quantification was performed in the superficial dorsal horn (laminae I, II and III) of immunoreacted sections and in the immunoblots. STZ rats presented a significant increase of GABA expression in laminae II and III when compared with control animals, while no differences were detected in GAD expression. A significant decrease in KCC2 expression was detected by immunohistochemistry in laminae I and II, which was confirmed by immunoblotting. Increased GABA levels, along with decrease in KCC2 expression, may underlie the abnormal neuronal activity detected in the spinal cord of diabetic rats. Reduction in KCC2 expression was shown to lead to increases in intracellular chloride concentration and, in such condition, GABA binding to GABA(A) receptor induces membrane depolarization, provoking neuronal excitation rather than inhibition. Based on these findings, we propose that a loss of GABA-mediated inhibitory tone at the spinal cord may result in neuronal hyperexcitability and spontaneous hyperactivity during diabetes.
PMID: 18457921 (GABA may reduce diabetic neuropathy)

5. "GABA B receptor is a novel drug target for pancreatic cancer. Schuller HM, Al-Wadei HA, Majidi M. Experimental Oncology Laboratory, Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee 37996, USA.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer death. Smoking, diabetes, and pancreatitis are risk factors. It has been shown that the growth of PDAC and pancreatic duct epithelial cells is regulated by beta-adrenoreceptors (beta-ARs). The activity of beta-ARs in the central nervous system is counteracted by gamma-aminobutyric acid (GABA) via GABA B receptor-mediated inhibition of adenylyl cyclase. The aim of the study was to investigate if GABA B R inhibits beta-AR signaling in PDAC and pancreatic duct epithelial cells, thus blocking driving forces of cancer progression, such as cell proliferation and cell migration. METHODS: Intracellular cAMP was measured by immunoassays, DNA synthesis by BrdU incorporation assays, activation of ERK1/2 by ERK activation assays, and Western blots and metastatic potential by cell migration assays in the human PDAC cell lines PANC-1 and BXPC-3 and immortalized human pancreatic duct epithelial cells HPDE6-C7. The expression of norepinephrine, PKAR IIalpha, and GABA in PDAC microarrays was assessed by immunohistochemistry. RESULTS.: Stimulation of the GABA B R by GABA or baclofen inhibited isoproterenol-induced cAMP signaling below base levels. ERK1/2 activity in response to isoproterenol was blocked by GABA, an effect enhanced by transient overexpression of the GABA B R and abolished by GABA B R knockdown. DNA synthesis and cell migration were stimulated by isoproterenol, responses blocked by GABA and baclofen. Norepinephrine and PKAR IIalpha were overexpressed while GABA was underexpressed in human PDAC tissue arrays. CONCLUSIONS: The data suggest the stimulation of GABA B R signaling as a novel target for the treatment and prevention of pancreatic cancer. Cancer 2008. (c) 2007 American Cancer Society. PMID: 18098271


PMID: 19150172

3 PMID: 18511483
4 PMID: 18457921
5 PMID: 18098271



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