Sorry to burst your bubble, I guess I did come off a little harsh and if I were to do that with you I'd have to do the same with every rep that practices the same marketing strategy but that ofcourse would be a never ending battle.
I did do some research although I'm sure there's much more you can teach me about Drive. But please notice in my post that I said it works "but it's not the best" for his purposes. Out of all the ingredients it seems only 1-2 directly contribute to fat loss the main one being forskolin which despite all the research on it has had limited feedback in the real world when applied to fat loss although I will admit it seems to aid fat loss, no doubt. But most of the users I've heard from tend to think of it as aiding fat loss in the long run and and perhaps avoiding fat gain when on a bulk. Also there seems to be research that indicates that Forskolin can in fact be detrimental to one's health:
Psychopharmacology (Berl). 1992;106(1):136-42. Related Articles, Links
Noradrenergic receptor mechanisms in neophobia.
Steketee JD, Silverman PB, Swann AC.
Department of Psychiatry and Behavioral Sciences, University of Texas Medical School, Houston.
We have previously demonstrated that depletion of forebrain norepinephrine (NE) led to an attenuation of neophobia in a novel environment, as defined by a greater preference for novel food over familiar food. To study further the role of forebrain NE in neophobia we chronically infused noradrenergic receptor ligands or forskolin into the lateral ventricles of sham and 6-hydroxydopamine dorsal bundle lesioned rats. Chronic NE infusions into lesioned animals reversed the lesion-induced shift in relative food preference. The beta receptor agonist isoproterenol had moderate effects similar to those of NE in lesioned and sham animals. Phenylephrine, an alpha-1 agonist, was without effect. Forskolin, an adenylate cyclase activator, mimicked the effects of NE infusions. These data suggest a role for noradrenergic stimulation of adenylate cyclase in neophobia.
Ofcourse we know nothing about the dose used but it's still food for thought...
Cell Signal. 2005 Sep;17(9):1111-24. Epub 2005 Feb 25.
Early immune response and regulation of IL-2 receptor subunits.
Hughes-Fulford M, Sugano E, Schopper T, Li CF, Boonyaratanakornkit JB, Cogoli A.
Northern California Institute for Research and Education, San Francisco, CA, United States.
[email protected]
Affymetrix oligonucleotide arrays were used to monitor expression of 8796 genes and probe sets in activated T-cells; analysis revealed that 217 genes were significantly upregulated within 4 h. Induced genes included transcription factors, cytokines and their receptor genes. Analysis by semi-quantitative RT-PCR confirmed the significant induction of IL-2, IL-2R(gamma) and IL-2R(alpha). Forty-eight of the 217 induced genes are known to or predicted to be regulated by a CRE promoter/enhancer. We found that T-cell activation caused a significant increase in CREB phosphorylation furthermore, inhibition of the PKC pathway by GF109203 reduced CREB activation by 50% and inhibition of the PKA pathway caused a total block of CREB phosphorylation and significantly reduced IFN(gamma), IL-2 and IL-2R(alpha) gene expression by approximately 40% (p<0.001). PKC(theta) plays a major role in T-cell activation: inhibition of PKC significantly reduced the expression of IFN(gamma), IL-2 and IL-2R(alpha). Since PKC blocked activation of CREB, we studied potential cross-talk between the PKC and the PKA/MAPK pathways, PMA-stimulated Jurkat cells were studied with specific signal pathway inhibitors. Extracellular signal-regulated kinase-2 (ERK2) pathway was found to be significantly activated greater than seven-fold within 30 min; however, there was little activation of ERK-1 and no activation of JNK or p38 MAPK. Inhibition of the PKA pathway, but not the PKC pathway, resulted in inhibition of ERK1/2 activation at all time points, inhibition of MEK1 and 2 significantly blocked expression of IL-2 and IL-2R(alpha). Gene expression of IL-2R(alpha) and IFN(gamma) was dependent on PKA in S49 wt cells but not in kin- mutants. Using gel shift analysis, we found that forskolin activation of T-cells resulted in activation of AP1 sites; this increase in nuclear extract AP1 was significantly blocked by MEK1 inhibitor U0126. Taken together, these results suggest that the PKA in addition to PKC and MAPK pathways plays a role in early T-cell activation and induction of IL-2, IL-2R(alpha) and IFN(gamma) gene expression.
PMID: 15993752
Forskolin potentiaties Histamine-induced BBB pearmability:
Pharmacol Res Commun. 1985 Apr;17(4):395-404. Related Articles, Links
Evidence for the involvement of histamine in the regulation of blood-brain barrier permeability.
Gulati A, Dhawan KN, Shukla R, Srimal RC, Dhawan BN.
Role of histaminergic mechanisms in the regulation of blood-brain barrier (BBB) was assessed in dog. Histamine increased the entry of sodium fluorescein from the blood to the cerebrospinal fluid (CSF) in a dose-dependent manner. Histamine receptor antagonists, mepyramine (H1) and metiamide (H2) per se did not affect the entry of dye in the CSF. Mepyramine failed to affect the change induced by histamine whereas metiamide completely blocked the histamine-induced entry of sodium fluorescein in CSF. 2-Methyl histamine, a specific H1-agonist, did not affect the barrier permeability. However, 4-methyl histamine, a specific H2 receptor agonist significantly increased the permeability of BBB. This increase was blocked by metiamide. Forskolin, a stimulant of adenylate cyclase, also increased the entry of dye in the CSF which could be significantly blocked by metiamide. It is concluded that histamine increases the permeability of BBB by affecting H2-receptors linked to adenylate cyclase.
PMID: 4040247
) and recover from the stress of your cut.
