I know it sounds insane, but nicotine can be used to achieve your weight loss goals. I do want to preface this with the benefits are small and unless you have both your training and diet optimized you won’t see much out of it. With that said, here is a (pretty long) review I wrote about it, WITH GRAPHS!

Introduction

Nicotine is one of the most common drugs used today. The prevalence of use in athletic endeavors is surprisingly high (especially among baseball), some research has shown between 34-39% in professional baseball players (Connolly et al. 1988; Ernster et al. 1990 ) and as high as 57% among collegiate counterparts (Gingiss and Gottlieb 1991). It is unknown whether this heightened use is cultural, tradition, or simply just because of Nicotine’s inherent addictive properties (Epping-Jordan et al. 1998). There is a lack in consistency in the current body of evidence on the effects on athletic performance in terms of both physical and psychological aspects for performance-oriented athletes. An even larger dearth exists pertaining to athletes in aesthetic endeavors and weight class controlled sports (bodybuilders, wrestlers, gymnasts etc.); however, from basic and animal models extrapolations can be made with reasonable confidence.

Due to nicotine’s stimulant qualities some potential benefits of use include greater endurance, power outputs, increased strength, improved reaction times, pain tolerance, and weight loss/control benefits. These potential benefits are not coupled without a laundry list of problems such as heighted anxiety, cancer, or possible detriments to all of the performance measures listed above. Pertaining to cancer, there is no question that smoking and other forms of tobacco use are associated with cancer and carcinogenic compounds; however it must be included that certain forms of nicotine use are not associated with cancer (Murray et al. 2009). Nicotine replacement therapy alone was found to not be a significant predictor of cancer (p=0.57) and when it was entered with smoking it remained non-significant (p=0.25). To take this information and say that smokeless tobacco using athletes will not get cancer is inaccurate; however, it does lead one to think that nicotine is not the carcinogenic substance within tobacco products.

The purpose of this review is to explain and investigate applied effects of nicotine consumption within the scope of athletic performance along with potential weight control and physique oriented outcomes. Discussion and practical applications are also provided.

Structure Function and Excretion

Nicotine (C 10 H 14 N 2 ) is the primary alkaloid in tobacco products; it is also an agonist at neuronal nicotinic acetylcholine receptors. This means that due to a similar structure and shape nicotine can take the place of acetylcholine in terms of neural transmission. Nicotine readily diffuses across the skin (transdermal patches), the lungs (smoking), and mucous membranes (nasal spray, chew, or gum). From these sites, nicotine gets into the blood stream through diffusion. Nicotine then can transverse the blood brain barrier where, through neural transmission and up-regulation, stimulates the sympathetic nervous system (SNS), promote heighted heart rate, blood pressure, increase metabolic rate, and block the release of insulin (sometimes promoting acute hyperglycemia) (Pomerleau 1992). All of these outcomes are congruent with the fight or flight nature of the SNS.

After the effects of nicotine have worn off the body excretes this substance primarily through the liver (~80%). The process is done via the cytochrome P450 2A6 (CYP2A6) pathway in which nicotine is converted to cotinine (Benowitz 1996). Following this, cotinine is excreted through (primarily) urine and saliva. The half-life of cotinine is 24 hours, thus when measuring nicotine levels cotinine is the primary chemical of concern.

Physical Performance

Those who use nicotine-containing substances (especially smokers) are often thought to be less physically fit. This assumption is reasonably valid; however, it is false to think that just because there may be a correlation that this goes to causation. There are several other factors that are not taken into account. Perhaps one with a predisposition to smoke also has a predisposition to have low activity levels, thereby influencing a correlation. An unbiased, peer-reviewed evidence based perspective is the only way to truly understand the true effects of nicotine on physical performance.

In terms of the long-term effects of tobacco use, Bolinder et al. (2003) investigated how smokers, smokeless tobacco users, and non smoking middle-aged men (35-60 yrs.) compared in maximal oxygen consumption. Some findings were to be expected. When compared to the non-smokers, the smokers had a significantly lower maximal oxygen uptake (p>0.001). However, there was no difference in maximal uptake between the smokeless tobacco users and non-users. There was however a difference in blood pressure and heart rate at resting (immediately before the test) and sub-maximal workloads. These results are similar to that of Weisman (1996), who found no statistical difference in maximal oxygen consumption between smokers (both abstaining and smoking) and non-smokers in a female military population. There were marginal differences between groups, but nothing approached significance.

Pertaining to anaerobic performance Weisman (1996) found no difference between smokers and non-smokers in performance on a Wingate test. However, it was found that smokers who were abstaining from smoking performed significantly better for maximal power outputs (p≤0.05). Thus, this data indicates that nicotine (or smoking) could have ergolytic effects on anaerobic performance. Meier (2006) tested this hypothesis in an athletic population (collegiate football players). The sample size was small (n=12) however there was no difference when the athletes either chewed nicotine gum vs. a placebo in a within subject design. From other research, there are no reported effects of smokeless tobacco on reaction time, maximum voluntary force or rate of force generation (Escher et al. 1998). However, when the nicotine users abstained the voluntary force and rate of generation was improved.

From the lack of evidence, one cannot say that smokeless nicotine has adverse effects on maximal oxygen uptake, power, reaction time, and force generation. Escher et al. (1998) even hypothesized that there may be a potential ergogenic effect from nicotine abstention following prolonged use.

Psychophysiological Performance

There is a scarcity in the literature pertaining to psychophysiological measures in the context of athletic and sport performance. The only measures that have been taken into account are rate of perceived exertion (RPE), state anxiety inventory (STAI) or improved pain tolerance. A reasonable assumption would be that since nicotine increases heart rate and blood pressure during rest and submaximal exertion (Bolinder et al. 2003) that these physical manifestations of stress could become psychological in nature as well, and the heighted SNS arousal would down regulate feelings of pain. However the body of research only partially supports these ideas.

Pertaining to RPE there were no differences between level of nicotine administered (nasal spray) and RPE for low to moderate workloads on a cycle ergometer (Perkins et al. 1991). As before there were differences in heart rate and blood pressure and this time the level of nicotine was shown to be dose dependant. STAI also appears to be increased by nicotine consumption (Landers et al. 1992). However, this did not cause detriments to complex cognitive performance, which were measured by the Stroop task (executive function inhibition test) and an assortment of math problems. The authors even postulated that nicotine consumptions aided participants in these complex cognitive tasks. Pain tolerance was also affected; however the findings indicate that the changes are gender specific. After transdermal nicotine administration, pain tolerance was only increased in males where females received little to no benefit (Jamner 1998).

From this evidence, it appears that nicotine consumption has little adverse psychophysiological effects. RPE at low intensities is not increased, and since maximal physiological capacities aren’t changed it is reasonable to assume that RPE would remain unaffected at higher intensities. STAI is increased, but it is coupled with improved complex performance. Pain tolerance is either unaffected of is improved (for males).

Weight loss/control

The research into why smokers tend to have lower bodyweight than non-smokers (Williamson et al 1991) is currently not well understood; however, from rodent, basic, and some human research some light is shed on these potential mechanisms.

Leptin, a hunger-regulating hormone produced by adipose tissue, is one potential mechanism. Those who chew nicotine gum were found to have higher circulating leptin levels than a control (Eliasson and Smith 1999). Higher leptin levels are associated with higher satiety, thereby leading to less food consumption. On the other side of this equation is ghrelin, which stimulates the hunger response and is produced by the stomach. Ghrelin stimulates follows up the chain and stimulates neuropeptide Y (NPY) which stimulates the hypothalamus and increases the desire to seek out and consume nutrients. In rodent models, nicotine administration has been shown to down regulate NPY (Frankish et al. 1995). Thus, this is a double pronged attack on energy consumption. The hormones that down regulate hunger are stimulated and the mechanisms increasing hunger are blunted, logically this would lead to less overall food consumption if these mechanisms are held true in human models.

Another set of mechanisms are increased lipolysis and inhibition of fatty acid synthesis (FAS). Lipolysis means break down of fat (lipids) and FAS is term for how the body makes fat tissue. Nicotine activates beta-adrenoceptors via release of catecholamines (epinephrine and norepinephrine) thus leading to the up-regulation in lipid break down, as well as by stimulating (directly) nicotinic cholinergic lipolytic receptors located on adipose cells (Andersson and Arner 2001). Nicotine also appears to stimulate an array of protein kinases that inhibit FAS. The primary routes are through stimulation of LKB1 which leads to stimulation of AMPK, threonine 172, and lastly acetyl-CoA carboxylase (An et al. 2007). This cascade leads to a down regulation in FAS.

Thermogenesis, heat production, is another potential mechanism for how nicotine can promote weight loss or weight storage. Norepinephrine is stimulated by nicotine consumption (Grunberg et al. 1988) and this is necessary for thermogensis. Through a series of events this nicotine stimulated catecholamine release up-regulates uncoupling protein 1 (UCP1) and leads to energy be loosed as heat in rodent adipose tissue (Arai et al. 2001; Yoshida et al. 1999). UCP1 alters oxidative phosporylation from regular ATP synthesis thus leading to dissipation of energy without mechanical work that manifests as heat. Other rodent based research investigates weight gain in young mice along with varying levels of nicotine administration. The results were reported as the food efficiency ratio (weight gain/food intake). The mice given the highest levels of nicotine gained the least weight even when consuming similar levels of food compared to a control (Wager-Srdar et al. 1984). Thus, this extra energy, as the authors hypothesized, was probably being loosed as heat and not being stored. Similar study’s in human smokers shown that after smoking cessation, those who replace the highest percentage of cotinine levels (nicotine’s measured metabolite) have the least weight gain (Doherty et al. 1996).

There is limited human research into this controversial topic; however, the mechanisms are logical as long as nicotine has similar affects on mice and humans. Simpler mechanisms are related to increased energy expenditure during low-moderate activity levels, as well as at rest (Perkins et al 1994; Jessen et al. 2003). The effects seem to be additive with coupled caffeine supplementation. Overall, in some models nicotine augments hunger systems, lipolysis, FAS, thermogenesis, and increases energy expenditure.

Conclusions and practical applications

It must be stressed that nicotine is an addictive substance (Epping-Jordan et al. 1998) however as long as it is consumed via gum the association with cancer is insignificant (Murray et al. 2009). All of that being stated plainly, nicotine (without smoke) does not appear to have adverse affects on maximal oxygen consumption, power outputs, or strength. Nor does it seem to adversely affect RPE, cause debilitating anxiety, and if one is a male the research supports increased pain tolerance. Numerous theoretical mechanisms for weight control/loss have been explained. In terms of ergogenic aids this is where nicotine appears to have the greatest utility. Athletes that are physique oriented (bodybuilders, gymnasts etc.) and weight class oriented (wrestling, weightlifting etc.) could use this to optimize body fat percentages along with a sound diet and exercise plan. The most common guidelines for supplementation were between 1-2 mg of nicotine coupled with 0, 50, or 100 mg of caffeine. However, the benefits past 1 mg of nicotine were minimal and were best coupled with 100 mg of caffeine (Jessen et al. 2003). The benefits in lipolysis and energy expenditure are modest; however, at the highest levels when performance is a greater concern than overall health the modest benefits are the difference between winning and losing.

Self Experiment

I took 1 mg a day (about the same as 1 cigarette) and here were my results after 2 weeks. I was already super lean, but i thought it was pretty cool.

References (Come fight me)

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