Despite the positive responses above to using nicotine for cutting, I'd urge caution in respects to other aspects of the bodybuilding lifestyle and/or being a male. I've previously read about nicotine's affects on fertility so I decided to do a PubMed search on "nicotine AND testosterone." Fifty hits came up and the highlights were:
- Increase in prolactin. Some bros on this board are already taking AAS that increases prolactin so nicotine may be throwing fuel on the proverbial fire in regards to prolactin induced gyno (debatable topic).
- Affects on libido. Most of us on this board are male so this should be of concern.
- The combination of no libido, decreased sperm count, and consequently no fertility. Some of the bros on this board are trying to start families so using nicotine for cutting could have an impact on starting a family.
- smoking leads to a secretory dysfunction of the Leydig cells. Some bros on this board are already taking AAS that affects the HPTA axis so once again nicotine may be throwing fuel on the proverbial fire.
- Significant decrease in testosterone response to human chorionic gonadotropin (hCG). Some bros on this board are taking hCG during or after their AAS cycle so cutting with nicotine could be hurting their recovery.
~Todd
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Effects of intravenous cocaine and cigarette smoking on luteinizing hormone, testosterone, and prolactin in men.
Mendelson JH, Sholar MB, Mutschler NH, Jaszyna-Gasior M, Goletiani NV, Siegel AJ, Mello NK.
Alcohol and Drug Abuse Research Center, Harvard Medical School/McLean Hospital, Belmont, MA 02478, USA.
[email protected]
Cocaine and nicotine have a number of similar behavioral and neurobiological effects. This study compared the acute effects of cocaine and cigarette smoking on luteinizing hormone (LH), testosterone (T), and prolactin. Twenty-four men who met American Psychiatric Association Diagnostic and Statistical Manual criteria for cocaine abuse or nicotine dependence were given intravenous cocaine (0.4 mg/kg) or placebo-cocaine, or smoked a low or high nicotine cigarette under controlled conditions.
Placebo-cocaine or low nicotine cigarette smoking did not change LH, T, or prolactin. Peak plasma levels of 254 +/- 18 ng cocaine/ml and 22.6 +/- 3.4 ng nicotine/ml were measured at 8 and 14 min, respectively.
LH increased significantly after both i.v. cocaine and high nicotine cigarette smoking (P < 0.01). These LH increases were significantly correlated with increases in cocaine and nicotine plasma levels (P < 0.001-0.003), and high nicotine cigarette smoking stimulated significantly greater increases in LH release than i.v. cocaine (P < 0.05).
Testosterone levels did not change significantly after either cocaine or after high nicotine cigarette smoking. After i.v. cocaine, prolactin decreased significantly and remained below baseline levels throughout the sampling period (P < 0.05-0.01).
After high nicotine cigarette smoking, prolactin increased to hyperpro-lactinemic levels within 6 min and remained significantly above baseline levels for 42 min (P < 0.05-0.03). The rapid increases in LH and reports of subjective "high" after both i.v. cocaine and high nicotine cigarette smoking illustrate the similarities between these drugs and suggest a possible contribution of LH to their abuse-related effects.
Publication Types:
Clinical Trial
Controlled Clinical Trial
PMID: 12893845 [PubMed - indexed for MEDLINE]
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Prevention of chronic alcohol and nicotine-induced azospermia, sterility and decreased libido, by a novel tri-substituted benzoflavone moiety from Passiflora incarnata Linneaus in healthy male rats.
Dhawan K, Sharma A.
Pharmacognosy Division, University Institute of Pharmaceutical Sciences, Panjab University, - 160014, Chandigarh, India.
[email protected]
Excessive long term consumption of alcohol and nicotine have serious detrimental effects upon the libido, fertility, and sperm count in male species. The present work describes the beneficial effects of a novel tri-substituted benzoflavone moiety (BZF) isolated from Passiflora incarnata Linneaus, the phyto-chemical isolation, spectroscopic elucidation, and multifarious biological activities of which have recently been reported by the authors. The BZF moiety has been reported to increase libido, sperm count, and sexual fertility in 2 years old male rats at 10 mg/kg, po dose, in the one of our previous studies. Presently, the BZF moiety has been evaluated against chronic ethanol- and nicotine-induced decrease in libido, sexual fertility and mating efficiency in healthy male rats. The male rats were given ethanol (3 g/kg, po) A, nicotine (2 mg/kg, sc) N, alcohol-nicotine combinations (AN) alone, and also with 10 mg/kg po dose of BZF (concurrent administrations).
These treatments were given for 30 days. At the end of treatments, it was observed that rat groups A, N, and AN had no libido (evaluated by mounting behaviour), declined sperm count, and consequently no mating efficiency or fertility (upon pairing with pro-estrus female rats). However, the rats which were given 10 mg/kg BZF along-with nicotine (NP group), alcohol (AP group), and alcohol-nicotine combination (ANP) exhibited significant libido-oriented mounting behaviour, increased sperm count (significantly comparable to the control group), and increased fertilization potential. The rats having decreased sperm count, libido and fertilization potential due to chronic administration of alcohol, nicotine and alcohol-nicotine combinations, i.e., rats of A, N, and AN groups were again subdivided and were given 10 mg/kg BZF for 7 days. This treatment confirmed that BZF speeds up the restoration of sexuality in rats upon cessation of the administration of substances like alcohol, nicotine and alcohol-nicotine combinations, which have severe detrimental effects upon male sexuality, fertility and vigour. BZF, the strongest inhibitor of aromatase enzyme, when administered concurrently with substances like alcohol and nicotine restores sexual virility, libido and vigour in male rats by maintaining the blood-testosterone levels to be high.
PMID: 12408873 [PubMed - indexed for MEDLINE]
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Comment: this abstract may be out of context since it's discussing chronic administration of nicotine and cutting with nicotine is approximately equivalent to one cigarette. Therefore, this abstract was not quoted in highlights, but thought it was good to see some of the problems highlighted by chronic administration
Nicotine administration induced changes in the gonadal functions in male rats.
Kavitharaj NK, Vijayammal PL.
Department of Biochemistry, University of Kerala, Karyavattom, Thiruvananthapuram, Kerala, India.
Nicotine is reported to have toxic effects on gonadal functions, in addition to its established role in the pathogenesis of atherosclerosis and lung cancer. So nicotine-induced biochemical changes were studied in liver and testes. Chronic administration of nicotine was found to produce enhanced synthesis of cholesterol, triglycerides, phospholipids and free fatty acids in the liver and testes. The activity of the lipogenic enzymes was high in liver but unaltered in testes. The testosterone and estradiol levels in the serum were lower. As the changes brought about by chronic administration of nicotine were counteracted by mecamylamine, a known inhibitor of nicotine, it was proven that nicotine is having a specific gonadotoxic effect.
PMID: 9831825 [PubMed - indexed for MEDLINE]
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Effects of smoking on testicular function and fertilizing potential in rats.
Yamamoto Y, Isoyama E, Sofikitis N, Miyagawa I.
Department of Urology, Tottori University School of Medicine, Yonago, Japan.
We evaluated the effects of smoking on testicular function and fertilizing potential in rats. Twenty rats (group A) were exposed to the smoke of 20 cigarettes for 1 h per day. Ten rats (group B) were exposed to the smoke of 40 incense sticks for 1 h per day, and an additional 10 rats served as a control group (group C). After 10 weeks of daily exposure, serum levels of nicotine and cotinine were assessed, and a mating test was conducted. Five days later, serum concentrations of testosterone before and after human chorionic gonadotropin (hCG) stimulation, gonadotropins, and epididymal sperm content and motility were evaluated. In addition, in vitro fertilization was carried out. Nicotine and cotinine were detected in group A, but not in groups B and C. Basal serum testosterone and gonadotropin concentrations did not differ significantly among the three groups, but
the testosterone response to hCG stimulation was significantly lower in group A than in groups B and C. Group A showed significant reductions in epididymal sperm content and motility, and in fertility in vivo and in vitro. These findings suggest that smoking leads to a secretory dysfunction of the Leydig cells, and also a deficiency in sperm maturation and spermatogenesis. In addition, smoking has a detrimental effect on sperm fertilizing potentials in vivo and in vitro.
PMID: 9537696 [PubMed - indexed for MEDLINE]
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Inhibitory role of cholinergic agonists on testosterone secretion by purified rat Leydig cells.
Favaretto AL, Valenca MM, Picanco-Diniz DL, Antunes-Rodrigues JA.
Department of Physiology, Faculty of Medicine of Ribeiro Preto, University of Sao Paulo, Brazil.
The effects of cholinometics on basal or hCG-induced testosterone (T) release by Percoll-purified Leydig cells of the rat were studied. Acetylcholine and carbachol as well as nicotine decreased basal and hCG-induced T secretion. The ganglionic nicotine antagonist hexamethonium promoted a partial reversal of the inhibitory effect of nicotine on basal or hCG-stimulated T secretion. Atropine also reduced the inhibitory effect of carbachol on basal or stimulated androgen release.
These data indicate that, in short-term incubations, testosterone released by purified Leydig cells is inhibited by nicotinic and muscarinic cholinergic agonists, thus supporting the hypothesis that parasympathetic autonomic system may be involved in the negative regulation of testicular androgen secretion.
PMID: 7511424 [PubMed - indexed for MEDLINE]
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Nicotine and cotinine inhibit steroidogenesis in mouse Leydig cells.
Patterson TR, Stringham JD, Meikle AW.
Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132.
Cigarette smoking alters plasma testosterone concentrations in men. The objectives of this study were to determine if nicotine and cotinine, two alkaloid products of cigarettes, affect luteinizing hormone(LH)-stimulated steroidogenesis in isolated adult mouse Leydig cells. Leydig cells from adult Swiss-Webster mice were isolated by linear density gradient and incubated (95% O2, 5% CO2) in minimum essential medium at 37 C for 3 hours with LH (10 ng) and with or without nicotine or cotinine (10(-5)-10(-7) M). Both nicotine and cotinine produced dose response inhibition (P less than 0.05) of LH-stimulated testosterone production (50-70%). The addition of 8-bromo-3',5'-cyclic monophosphate (cAMP, 500 uM) stimulated steroidogenesis comparable to LH in the absence of the alkaloids, but both nicotine and cotinine significantly (P less than 0.05) reduced testosterone production in response to cAMP, suggesting that the alkaloids inhibit testosterone production in response to LH distal to the formation of cAMP. In MEM without calcium, LH-stimulated testosterone synthesis was decreased, and neither nicotine nor cotinine significantly affected steroidogenesis. The addition of a calcium ionophore in MEM with normal calcium content enhanced (P less than 0.05) the inhibitory effects of nicotine and cotinine on LH-responsive steroidogenesis. A calcium channel blocking agent, verapamil, at 10uM significantly (P less than 0.05) reversed the inhibition of LH-stimulated testosterone production produced by both alkaloids when incubated in the medium with a normal calcium concentration.
These results suggest that nicotine and cotinine either affect intracellular calcium content or block the effects of calcium on steroidogenesis in mouse Leydig cells.
PMID: 2154652 [PubMed - indexed for MEDLINE]
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Nicotine and cotinine inhibit rat testis androgen biosynthesis in vitro.
Yeh J, Barbieri RL, Friedman AJ.
Department of Obstetrics and Gynecology, Harvard Medical School, Boston, MA 02115.
The effects of nicotine and cotinine, the major metabolite of nicotine, on testosterone production in rat testis were investigated. Rat Leydig cells were isolated and incubated with nicotine and cotinine. Nicotine produced a dose dependent increase in progesterone levels and a dose-dependent decrease in androstenedione and testosterone concentrations. Cotinine produced a dose-dependent increase in progesterone and androstenedione and a dose-dependent decrease in testosterone levels. The effects of nicotine and cotinine on rat testis mitochondrial cholesterol side chain cleavage enzyme and microsomal 3 beta-hydroxysteroid dehydrogenase-isomerase, 17 alpha-hydroxylase, 17,20-lyase and 17-ketosteroid reductase were examined. Nicotine competitively inhibited 17 alpha-hydroxylase (apparent Ki = 30 microM) and 17,20-lyase (apparent Ki = 18 microM). Cotinine competitively inhibited 17-ketosteroid reductase (apparent Ki = 46 microM). The addition of nicotine to preparations of rat testis microsomes yielded a Type II cytochrome P-450 binding spectrum.
We conclude that nicotine and cotinine competitively inhibit multiple steps in testosterone biosynthesis.
PMID: 2811374 [PubMed - indexed for MEDLINE]