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 Citation 5 is too old to even bother with... Lets look at a publication that discusses cholesterol translocation into mito and its control at a much finer level of detail - some 12 yrs later. You might as well learn something while you're reading my rather hot tempered posts. You wanna play in my backyard, fine. http://endo.endojournals.org/cgi/content/full/144/8/3368Inhibition of Cyclooxygenase-2 Activity Enhances Steroidogenesis and Steroidogenic Acute Regulatory Gene Expression in MA-10 Mouse Leydig Cells. XingJia Wang, Matthew T. Dyson, Youngah Jo and Douglas M. Stocco. Endocrinology Vol. 144, No. 8 3368-3375 (2003). To study the mechanism for the regulatory effect of arachidonic acid (AA) on steroidogenesis, the role of cyclooxygenase (COX) in steroid production and steroidogenic acute regulatory (StAR) gene expression was investigated. Although stimulation with 0.05 mM dibutyryl cAMP (Bt2cAMP) did not increase StAR protein or progesterone in MA-10 mouse Leydig cells, the addition of 1 µM of the COX inhibitor indomethacin increased StAR protein expression and progesterone production by 5.7-fold and 34.3-fold, respectively. In the presence of indomethacin, the level of Bt2cAMP required for maximal steroidogenesis was reduced from 1.0 mM to 0.25 mM. Similar results were obtained in studies on StAR promoter activity and in Northern blot analyses of StAR mRNA expression, suggesting that inhibition of COX activity enhanced StAR gene transcription. COX2 (an inducible isoform of COX) was constitutively detected in MA-10 cells. Although SC560, a selective COX1 inhibitor, did not affect steroidogenesis, the COX2 inhibitor NS398 significantly enhanced Bt2cAMP-stimulated StAR protein expression and steroid production. Overexpression of the COX2 gene in COS-1 cells significantly inhibited StAR promoter activity. The results of the present study suggest that inhibition of COX2 activity increases the sensitivity of steroidogenesis to cAMP stimulation in MA-10 Leydig cells. You can read the paper if you want. It sez exacty what I have aready pointed out... You turn on the AA pathwway, you fuck up transport of cholesterol and screw up steroidogenesis. Bottom line, AA is anti testosterone control. This is getting fun. Next... proud hyperborean
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| QUOTE (Vetteman @ Nov 24 2005, 09:16 PM) | What is a "kiddie winkie"? 
Yeah, but can I lose fat and gain muscle by taking it?
Anecdotal evidence says yes. Science says no?
If I train extra hard and have a really good diet while taking it I should see good results, right? |
You are butting into my rebuttal, you dog! The answer to your question is more complex than is indicated by these citations I am in the middle of reading and commenting on... Go back up a couple of posts and see my original citation on the HIGHY complex nature of AA on various cell systems. Does anybody even bother to read these citations *I* post?? Oh yeah...you asked about kiddie winkies.. A scottish slang term for kids, as in the younger crowd. I should probaby edit that out...but, I am now missing my gym time, and getting a bit riled. As I mentioned to you privately, the only reason I am posting here is that I feel driven to do so, as one would, seeing a kid step out in front of a speeding car. You instinctively want to pull them back to safety. Were I to tell Larry Marnett that (pretty much the father of the AA pathway) that folks were actually taking this stuff as a supplement, he would fucking laugh out loud. He's studying its expression on cancer cell surfaces. It causes cells to become mobile under certain conditions. Now that would right away put up my antennae, if I were considering taking it... Know what i mean, Verne?? proud hyperborean
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So the rest of the citations are even older than the last one...1990.. Lets start to look at a few others... http://www.ncbi.nlm.nih.gov/entrez/query.f...0&dopt=AbstractMetabolism of exogenous and endogenous arachidonic acid in cancer. Phinney SD. Adv Exp Med Biol. 1996;399:87-94. Epidemiologic evidence in humans and controlled trials in animal models indicate that total dietary fat increases the risk of cancer. The animal evidence indicates that the greatest efficacy in promoting carcinogenesis is achieved with omega-6 fatty acids with little or no effect from either the omega-3 or monounsaturated fatty acid families. Epidemiologic studies in humans indicate a positive association between meat intake and colon cancer, but a negative association with chicken and fish. There is also a negative association between non-steroidal anti-inflammatory drug (NSAID) intake and colon cancer. Red meat is a potentially significant source of dietary arachidonic acid, which is the primary substrate for the eicosanoids whose production is blocked by NSAIDs. Thus there is a positive association between carcinogenesis and dietary intake of both the omega-6 fatty acid precursor linoleic acid and its product arachidonic acid, and a negative association with use of a drug blocking its metabolism to eicosanoids. Another potentially important factor in arachidonate metabolism is variation in its endogenous distribution. We have recently reported abnormal distribution of arachidonic acid between lipid fractions in human obesity, and parallel abnormalities in animal models of genetic obesity. This implies a potential role for variation in the endogenous distribution of arachidonic acid in the etiology of cancers which have increased incidence in human obesity. This paper addresses the role of arachidonate intake, its endogenous production, and its distribution within lipid fractions in carcinogenesis. proud hyperborean
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Antagonism of Arachidonic Acid Is Linked to the Antitumorigenic Effect of Dietary Eicosapentaenoic Acid in ApcMin/+ Mice. Melissa B. Hansen Petrik, Michael F. McEntee*, Chun-Hung Chiu and Jay Whelan. (Journal of Nutrition 130:1153-1158 (2000). The multiple intestinal neoplasia (ApcMin/+) mouse possesses a germline mutation at codon 850 of the adenomatous polyposis coli (Apc) gene resulting in the formation of a nonfunctional truncated gene product. Following a somatic mutation of the remaining wild-type allele, mice spontaneously develop ~40–50 tumors throughout the intestinal tract. This mouse model has been used to study intestinal tumorigenesis because this mutation is analogous to the inherited APC mutation in humans with familial adenomatous polyposis (FAP). These individuals characteristically develop numerous adenomas throughout their intestinal tracts. Only a few studies have evaluated the effects of dietary fatty acids on tumorigenesis in this animal model with varying results, and none have linked these effects to alterations in arachidonic acid (AA) metabolism. This study was designed to evaluate the antitumorigenic effect of dietary (n-3) polyunsaturated fatty acids (PUFA) in the ApcMin/+ mouse model and to determine whether these effects are related to inhibition of AA metabolism. Male ApcMin/+mice were fed diets supplemented with eicosapentaenoic acid (EPA), AA or a combination of AA + EPA. Mean tumor number in the EPA group was 68% lower (P < 0.05) compared with the control group, whereas AA supplementation did not significantly alter tumor load. The reduction in tumor load coincided with significant reductions in intestinal AA content and levels of prostaglandins. However, supplementing AA to the EPA diet (AA + EPA) abolished the antitumorigenic effect of EPA, increased tissue AA content fourfold and prostaglandin production two- to fourfold. These results indicate that AA is involved in tumorigenesis and suggest that EPA’s ability to reduce tumor load in ApcMin/+ mice is related to reductions in tissue AA content or its metabolism. Antagonism means to block binding. DHA is a conversion product of omega-3 fats (first step) along with EPA. Its been shown to be important for brain cell membrane intregrity and is also a potent antioxidant in brain. Here, it was shown to block tumorigenesis (tumor formation), and tumor formation was restored by the addition of AA. So, natural protective substances in food that might forestall tumor formation are blocked by exogenous AA. Ooopsy daisy. proud hyperborean
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Okey dokey. you got me pissed now... I told you, I've been following this field for longer than some of you been on this planet. This page http://www.med.wayne.edu/cancerbiology/faculty/keqin.htmLists recent publications by a faculty member up at Wayne State U. Thats where Larry got his start as a post doc, alongside Ken Honn. And yep, here is his protege. Now you just look down thru her pubs and tell me if you see a pattern between AA and cancer cell migration.. (bark of laughter). ang, K. and Honn, K.V. 1997. Lipoxygenase metabolites and cancer metastasis. Adv Exp Med Biol. 422:71-84. Nie, D., Hillman G.G., Geddes, T., Tang, K., Pierson, C., Grignon, D.J., and Honn, K.V. 1998. Platelet-type 12-lipoxygenase in a human prostate carcinoma stimulates angiogenesis and tumor growth. Cancer Research, 58: 4047-4051. Tang, K. and Honn, K.V. 1999. 12(S)-HETE in cancer metastasis. Adv Exp Med Biol. 447:181-91. Tang, K., Nie, D., Cai, Y., and Honn, K.V. 1999. The ?4 integrin subunit rescues A431 cells from apoptosis through a PI3K/Akt kinase signaling Pathway. Biochem Biophy Res Comm. 264: 127,132. Nie, D., Hillman, G.G., Geddes, T., Tang, K., Pierson, C., Grignon, D.J. and Honn, K.V. 1999, Platelet-type 12-lipoxygenase regulates angiogenesis in human prostate carcinoma. Adv Exp Med Biol. 469:623-30. Tang, K., Nie, D. and Honn KV. 1999. Role of autocrine motility factor in a 12-lipoxygenase dependent anti-apoptotic pathway. Adv Exp Med Biol. 1999;469:583-90. Nie, D., Tang, K., Digio, C., and Honn, K.V. 2000. Eicosanoid regulation of angiogenesis: role of endothelial arachidonate 12-lipoxygenase. Blood. 95:2304-2311. Nie, D., Lamberti, A., Zacharek, A., Li, L., Szekeres, K., Tang, K., Chen, Y., and Honn, K.V. 2000. Thromboxane A2 regulation of endothelial cell migration, angiogenesis and tumor metastasis. Biochem Biophys Res Comm. 267: 245-251. Tang, K., Finley, R.L. Jr., Nie, D., and Honn, K.V. 2000. Identification of 12-lipoxygenase interaction with cellular proteins by yeast two-hybrid screening. Biochemistry. 39: 3185-3191. Szekeres, K., Tang, K., Trikha, M., and Honn, K.V. 2000. Eicosanoid activation of extracellular signal-regulated kinase 1/2 in human epidermoid carcinoma cells. J Biol Chem. 275: 38831-38841. Nie, D., Tang, K., Szekeres, K., Li, L., and Honn, K.V. 2000. Eicosanoid regulation of angiogenesis in human prostate carcinoma and its therapeutic implications. Ann N Y Acad Sci. 95: 165-167. Nie, D., Lamberti, M., Zacharek, A., Li, L., Szekeres, K., Tang, K., Chen, Y., and Honn, K.V. 2000. Thromboxane A (2) regulation of endothelial cell migration, angiogenesis, and tumor metastasis. Biochem Biophys Res Commun. 267: 245-251. Nie, D., Tang, K., Szekeres, K., Trikha, M. and Honn, K.V. 2000. Role of eicosanoids intumor growth and metastasis. Advances in Eicosanoid Research (C.S.Serhan, ed) Spring, Berlin. pp201-217. Nie, D., Che, M., Grignon, D., Tang, K. and Honn, K.V. 2001. Role of eicosanoids in prostate cancer progression. Cancer and metastasis Review. 20:195-206. Pidgeon, G.P., Tang, K., Rice, R.L., Li, L., Taylor, J.D., and Honn, K.V. 2003. Over-expression of leukocyte-type 12-lipoxygenase promotes W256 tumor cell survival by enhanced avb5 expression. Internal J. Cancer. 105:459-271. Pidgeon, G.P., Tang, K., Cai, Y., Piasentin, E., and Honn, K.V. 2003. Over-expression of platelet- type 12-lipoxygenase promotes tumor survival by enhancing vitronectin-specific integrin expression. Cancer Res. 63: 4258-4267. Nie, D., Nemeth, J., Qiao, Y., Tang, K., Hilman, G.G., Cher, M., Grignon, D., and Honn, K.V 2003. Increased metastatic potentials in human prostate carcinoma cells by Overexpression of arachidonate 12-Lipoxygenase. Clin Exp Metastasis. 20: 657-663. Nie, D., Che, M., Zacharek, A., Qiao, Y., Li, L., Lamberti, M., Tang, K., Cai, Y., Guo, G., Grignon, D., and Honn, K.V. 2004. Differential expression of thromboxane synthase in prostate carcinoma: Role in tumor cell motility. American Journal of Pathology. 164: 429-439. Tang, K., Finley Jr., R.L., Nie, D., Cai, Y., Lamberti, M.P., Fridman, R., Carey, T.E., Crissman, J.D., and Honn, K.V. Regulation of Arachidonate 12-Lipoxygenase by physical interaction with Integrin ?4 Subuint. (in preparation for re-submission) Tang, K., Nie, D., Cai, Y.L., Lamberti, M.P., and Honn, K.V. 12-Lipoxygenase effects on androgen-stimulated prostate cancer cell growth and motility. Manuscript in preparation proud hyperborean
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So lets look at colon cancer risk associated with certain polymorhisms of the two primary enzymes in the AA pathways (first two steps) . Two pretty dang recent papers, by the way... Arachidonate lipoxygenase (ALOX) and cyclooxygenase (COX) polymorphisms and colon cancer risk. Julie E. Goodman, Elise D. Bowman1, Stephen J. Chanock, Anthony J. Alberg4 and Curtis C. Harris. Carcinogenesis 2004 25(12):2467-2472. In the human colon, arachidonic acid is metabolized primarily by cyclooxygenase (COX) and arachidonate lipoxygenase (ALOX) to bioactive lipids, which are implicated in colon cancer risk. Several polymorphisms in ALOX and COX genes have been identified, including G-1752A, G-1699A and Glu254Lys in ALOX5; Gln261Arg in ALOX12; Leu237Met and Val481Ile in COX1; and C-645T and Val511Ala in COX2. Because of the significant role of arachidonic acid metabolism in colon cancer, we hypothesized that these polymorphisms could influence susceptibility to colon cancer. We addressed this hypothesis in African-Americans and Caucasians using colon cancer cases (n = 293) and hospital- (n = 229) and population-based (n = 304) control groups. Polymorphisms did not differ between the control groups (P > 0.05); thus, they are combined for all analyses presented. ALOX5 Glu254Lys and COX2 C-645T and Val511Ala allele frequencies differed between Caucasians and African-American controls (P < 0.001). The ALOX5 –1752 and –1699 polymorphisms were in linkage disequilibrium (P < 0.001) and associated with a decreased risk in Caucasians in ALOX5 haplotype analyses (P = 0.03). Furthermore, an inverse association was observed between A alleles at positions –1752 and –1699 of ALOX5 and colon cancer risk in Caucasians, but not in African-Americans. Caucasians with A alleles at ALOX5 –1752 had a reduced odds of colon cancer versus those with G alleles [odds ratio (OR) (GA versus GG), 0.63; 95% confidence interval (CI), 0.39–1.01; OR (AA versus GG), 0.33; 95% CI, 0.07–1.65, Ptrend = 0.02]. Similar results were observed for ALOX5 G-1699A [OR (GA versus GG), 0.59, 95% CI, 0.37–0.94; OR (AA versus GG), 0.27, 95% CI, 0.06–1.32, Ptrend = 0.01]. Statistically significant associations with colon cancer were not observed for the other polymorphisms investigated. We have shown for the first time that a haplotype containing ALOX5 G-1752A and G-1699A in a negative regulatory region of the promoter may influence colon cancer risk in Caucasians. Colorectal adenoma risk is modified by the interplay between polymorphisms in arachidonic acid pathway genes and fish consumption. Christine L.E. Siezen, Astrid I.M. van Leeuwen, Nicolien R. Kram, Manon E.M. Luken1, Henk J. van Kranen and Ellen Kampman. Carcinogenesis 2005 26(2):449-457 Associations between polymorphisms in genes (SNPs) involved in the arachidonic acid (AA) pathway and colorectal adenomas have been investigated in a Dutch case control study including 384 cases and 403 polyp-free controls. Twenty-one polymorphisms in seven candidate genes were studied and a potential modifying effect of fish consumption was considered. A protective effect on colorectal adenomas was found for the CT genotype of SNP H477H in PPAR{gamma} and the GC genotype of SNP V102V in COX-2 (OR 0.63, 95% CI 0.45–0.89 and OR 0.65, 95% CI 0.46–0.92, respectively) compared with the homozygous major genotypes. An increase in adenoma risk was observed for the TC genotype of SNP c.2242T->C in COX-2 (OR 1.47, 95% CI 1.07–2.00) compared with the TT genotype. Analysis with estimated haplotypes confirmed these associations and revealed three additional associations with COX-2, sPLA2 and 15LOX haplotypes. Fish consumption modified the associations with COX-2 and PPAR{delta} genotypes. For SNP c.-789C->T in PPAR{delta} the major genotype showed a decrease in adenoma risk for those in the highest tertile of fish consumption ( T3), as compared with the lowest tertile (T1) (OR 0.65, 95% CI 0.41–1.02). Protective effects were also observed for SNPs V102V and c.2242T->C in COX-2 and high fish intake. The interaction between fish consumption and c.2242T->C was statistically significant, with an OR for the TT genotype and high fish consumption of 0.52 (95% CI 0.27–1.01) as compared with low fish intake. These results indicate that SNPs in genes involved in the AA pathway are associated with colorectal adenoma risk. Some of these associations are modified by fish consumption. Now, if you're eyes were glazing over reading thru these abstracts, the last line should jump out at you. One - they found control regions associated with a genotype in white folks that positively correlates for tendency to form colon adenoma (a MAJOR killer among American white boys) and consumption of fish oils (protective). And they tell you what? Do not comsume fish oils while taking AA as a supp?? <laughing my ass off and recloaking> proud hyperborean
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Guru
Group: Advanced Members
Posts: 1095
Member No.: 32634
Joined: 18-June 04
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| QUOTE (Vetteman @ Nov 25 2005, 12:16 AM) | What is a "kiddie winkie"?
Yeah, but can I lose fat and gain muscle by taking it?
Anecdotal evidence says yes. Science says no?
If I train extra hard and have a really good diet while taking it I should see good results, right? |
shes not saying it doesnt work (it does), shes saying that it also happens to cause cancer. This was hashed over on avant over a year ago, and I think llewellyn won the argument somehow. He's the one who's read every study ever published involving arachidonic acid, I think he'd best explain why he thinks these studies that trouble are citing do not apply. I think Par Deus also agreed with this assessment, although I do not know why. maybe he'll see this and chime in. I personally have no family history of any kind of cancer, so I remain more than willing to roll the dice on this one. I again ask, does anybody have any bottles of X-factor they are willing to sell, or, trade for legal steroids? C'mon, baby needs a new pair of shoes... or a pair of biceps...
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| QUOTE (trouble @ Nov 24 2005, 11:49 PM) | bottom line: inhibits test production in testes - leydig cells.
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Not quite. AA >regulates< testosterone production in the testes. The purpose of the first few abstracts were to display that AA has a very unique relationship with steriodogenesis in the testes. "...Leydig tumor cells were treated with various concentrations of quinacrine (an inhibitor of arachidonic acid production). Incubation of the cells with quinacrine resulted in dose-dependent decreases in steroid production..." http://www.ncbi.nlm.nih.gov/entrez/query.f...3565&query_hl=1"The effect of inhibitors and products of arachidonic acid metabolism on rat testicular steroidogenesis has been investigated...The LH-stimulated increase in secretion of testosterone and progesterone was also inhibited by indomethacin and NDGA...The metabolites of lipoxygenase (15-HPETE, 15-HETE, 5-HPETE and 5-HETE) and cyclooxygenase (PGF2 alpha) pathways stimulated 3 beta-HSD and 17 beta-HSD activity and enhanced the secretion of progesterone and testosterone. It is concluded that arachidonic acid metabolites are intratesticular factors which can regulate LH-stimulated testicular steroidogenesis." http://www.ncbi.nlm.nih.gov/entrez/query.f...9939&query_hl=1Indomethacin inhibits arachidonic acid and thereby inhibits testosterone. The metabolites of lipoxygenase (products of AA) "enhanced the secretion of...testosterone." Pretty simple. I think 'trouble' misread that study or is clueless, or both. "which results in the release of arachidonic acid and the formation of leukotrienes, which stimulate steroidogenesis in the Leydig cell." http://www.ncbi.nlm.nih.gov/entrez/query.f...9882&query_hl=1"Lipoxygenase metabolites of arachidonic acid were shown to stimulate gonadotrophin release dose-dependently in rat pituitary cells." http://www.ncbi.nlm.nih.gov/entrez/query.f...9770&query_hl=1"In men, obesity has generally been associated with reduced plasma testosterone levels and with elevation of the plasma free fatty acids (FFAs). In this study, we investigated the effects of saturated FFAs including palmitic acid (PA) and stearic acid (SA), and polyunsaturated FFA arachidonic acid (AA) on the survival of rat testicular Leydig cell cultured in vitro. PA and SA markedly suppressed Leydig cell survival in a time- and dose-dependent manner. In contrast, AA stimulated the cell proliferation at 5-10 times of physiological concentration...These results indicate that PA and SA induce apoptosis in testicular Leydig cells by ceramide production and these apoptotic effects may be a possible mechanism for reproductive abnormalities in obese men, and AA can partly prevent the apoptotic effect induced by saturated FFA." http://www.ncbi.nlm.nih.gov/entrez/query.f...033&query_hl=17"Moreover, exogenous AA induced a dose-dependent increase of testosterone secretion which was inhibited by NDGA. Our results strongly support the previous concept that the lipoxygenase pathway is involved in the mechanism of action of LH on testis Leydig cells." http://www.ncbi.nlm.nih.gov/entrez/query.f...535&query_hl=17
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Guru
Group: Advanced Members
Posts: 3544
Member No.: 49238
Joined: 2-November 04
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| QUOTE (RepubCarrier @ Nov 24 2005, 03:12 PM) |
Diesel, I know you think it was effective, but do you think it was worth the price? $100 for 50 days is quite a hefty price. |
If you look at the review most people say its worth the money.
Is 10lbs of lean muscle mass plus troubles quotes worth $100?
"It is better to be feared than loved, if you cannot be both. " Niccolo Machiavelli "O Conscience, into what abyss of fears And horrors hast thou [PLINK=1798]driven[/PLINK] me, out of which I find no way, from deep to deeper plunged. " Milton Mod for HLF 
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The fact is, unless you're very cautious in the use of arachidonic acid, the potential negatives outweight the positive gains. You go look at posts in this forum on many antioxidants and supps: sesamin, same-e, omega-3s, milk thistle, Coenzyme Q10, many herbal lignans...all serve as antioxidants, lipid peroxidase inhibitors, antocoagulators, and help prevent oxidative stress effects (the very basis of aging, along with cell turnover control) - and you find in each instance - that AA is the exact opposite in action. If you WANT arachidonic acid, and are interested in side stepping the henious monetary cost for this supp, there are food sources guaranteed to supply you witha hefty dose of AA. Dirt cheap. This post has been edited by Slayer of Souls on Nov 28 2005, 12:09 AM proud hyperborean
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Guru
Group: Advanced Members
Posts: 3544
Member No.: 49238
Joined: 2-November 04
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| QUOTE (trouble @ Nov 27 2005, 05:51 PM) |
The fact is, unless you're very cautious in the use of arachidonic acid, the potential negatives outweight the positive gains. You go look at posts in this forum on many antioxidants and supps: sesamin, same-e, omega-3s, milk thistle, Coenzyme Q10, many herbal lignans...all serve as antioxidants, lipid peroxidase inhibitors, antocoagulators, and help prevent oxidative stress effects (the very basis of aging, along with cell turnover control) - and you find in each instance - that AA is the exact opposite in action.
If you WANT arachidonic acid, and are interested in side stepping the henious monetary cost for this supp, there are food sources guaranteed to supply you witha hefty dose of AA.
Dirt cheap. |
Good point. Lets try and keep this in relation to X-Factor.
"It is better to be feared than loved, if you cannot be both. " Niccolo Machiavelli "O Conscience, into what abyss of fears And horrors hast thou [PLINK=1798]driven[/PLINK] me, out of which I find no way, from deep to deeper plunged. " Milton Mod for HLF
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Sanitized and swuweeky clean. ...but here, which beat the crap out of it disappearing altogether.  thanks slayer.. proud hyperborean
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I'm taking X-Factor right now. I've been using it for almost a week. I take two in the morning and two at night. I haven't noticed anything yet. After reading a few of these X-Factor threads I've become mildly concerned about any potential negative effects. Should I be stacking anything with it? Should I take anything when my cycle is done?
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| QUOTE (Antonio85777 @ Nov 28 2005, 03:26 PM) | | I'm taking X-Factor right now. I've been using it for almost a week. I take two in the morning and two at night. I haven't noticed anything yet. After reading a few of these X-Factor threads I've become mildly concerned about any potential negative effects. Should I be stacking anything with it? Should I take anything when my cycle is done? |
No, you don't need to take anything else while taking X-factor and no PCT is needed.
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X-factor review
