Nicotine Patch

Nicotine

  • Drugs
  • Updated August 24, 2016

Nicotine is an addictive substance found in tobacco products that can act as both a stimulant and a relaxant. Nicotine is available as gums, inhalers, lozenges, nasal sprays, patches, and e-cigarettes and is often sold as a smoking cessation aid. While tobacco is unquestionably dangerous—and smoking tobacco likely increases the risk of dementia—nicotine therapy may offer protection against cognitive decline or dementia, though the evidence is mixed.

Evidence

The quality of the available research is limited because information on long-term nicotine use in humans comes entirely from the use of tobacco. Our search found:

• 1 meta-analysis of 41 randomized controlled trials examining cognitive outcomes in healthy adults, along with 2 pilot randomized trials in healthy nonsmokers
• 3 randomized controlled trials in Alzheimer's disease patients
• 2 randomized controlled trials in patients with mild cognitive impairment or age-associated memory impairment
• 2 clinical trials in older adults
• Numerous preclinical studies

Potential Benefit

Smoking tobacco is likely to increase the risk of dementia, and the evidence is mixed on whether nicotine treatment may protect against cognitive decline or dementia. In healthy adult non-smokers, nicotine has improved aspects of fine motor skills, attention, and memory in short clinical trials [2]. However, these effects may be unrelated to the risk of dementia or long-term cognitive decline. For older adults with mild cognitive impairment, nicotine therapy in two small trials led to improvements in some aspects of cognition but not others [3][4]. A new trial is underway with support from the National Institute of Aging and the Alzheimer's Drug Discovery Foundation to more conclusively test the effects of transdermal nicotine patches for patients with mild cognitive impairment [5].

In preclinical research, nicotine worsened some aspects of Alzheimer’s disease [6][7] and protected against others [8-10].

APOE4 Carriers:

Nicotine was reported to promote cognition to a greater extent for APOE4 carriers, based on a handful of experiments with healthy adults [11-13], but older smokers with APOE4 were the most likely to have impaired cognition and low brain metabolism [14]. However, APOE4 status did not alter the association of smoking history on disease progression or biological markers of Alzheimer’s disease [15]. For more information on what the APOE4 gene allele means for your health, read our APOE4 information page.

For Dementia Patients

It is uncertain whether Alzheimer's patients might benefit from nicotine therapy. A handful of clinical trials suggested that they are not likely to benefit but a 2001 meta-analysis by the Cochrane Collaboration, an independent global health network, concluded that these trials were of poor quality [16].

Safety

Nicotine therapy not provided through tobacco is well-tolerated but there are some safety concerns such as impaired sleep, addiction, interactions with other drugs, gastrointestinal symptoms, and possible cardiovascular effects. Nicotine poisoning or overdose can occur and children are especially vulnerable [17]. Some individuals may have health conditions that substantially increase the risks of side effects. Most experts agree that nicotine is highly addictive [18], although some scientists argue that tobacco is addictive but not because of nicotine [19]. Nicotine interacts with many other drugs so the use of other medications can impact the safety of nicotine treatment.

NOTE: This is not a comprehensive safety evaluation or complete list of potentially harmful drug interactions. It is important to discuss safety issues with your physician before taking any new supplement or medication.

How to Use

Nicotine replacement therapy is marketed to help people stop using tobacco. It is available as patches, gum, and lozenges that can typically be purchased over the counter and as inhalers and nasal sprays that require a doctor’s prescription. In small clinical trials, the dose of nicotine that improved some aspects of cognition ranged from 5 to 15 mg/day [3][4][20]. Higher doses likely have greater risk of sleep side effects [18].

References

  1. Swan GE, Lessov-Schlaggar CN (2007) The effects of tobacco smoke and nicotine on cognition and the brain. Neuropsychology review 17, 259-273.
  2. Heishman SJ, Kleykamp BA, Singleton EG (2010) Meta-analysis of the acute effects of nicotine and smoking on human performance. Psychopharmacology 210, 453-469.
  3. Newhouse P, Kellar K, Aisen P et al. (2012) Nicotine treatment of mild cognitive impairment: a 6-month double-blind pilot clinical trial. Neurology 78, 91-101.
  4. White HK, Levin ED (2004) Chronic transdermal nicotine patch treatment effects on cognitive performance in age-associated memory impairment. Psychopharmacology 171, 465-471.
  5. Aisen P, Newhouse P Memory Improvement Through Nicotine Dosing (MIND) Study (MIND). Clinicaltrials.gov.
  6. Deng J, Shen C, Wang YJ et al. (2010) Nicotine exacerbates tau phosphorylation and cognitive impairment induced by amyloid-beta 25-35 in rats. European journal of pharmacology 637, 83-88.
  7. Oddo S, Caccamo A, Green KN et al. (2005) Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease. Proceedings of the National Academy of Sciences of the United States of America 102, 3046-3051.
  8. Brown D, Ramlochansingh C, Manaye KF et al. (2013) Nicotine promotes survival of cells expressing amyloid precursor protein and presenilin: implication for Alzheimer's disease. Neuroscience letters 535, 57-61.
  9. Inestrosa NC, Godoy JA, Vargas JY et al. (2013) Nicotine prevents synaptic impairment induced by amyloid-beta oligomers through alpha7-nicotinic acetylcholine receptor activation. Neuromolecular medicine 15, 549-569.
  10. Xue MQ, Liu XX, Zhang YL et al. (2014) Nicotine exerts neuroprotective effects against beta-amyloid-induced neurotoxicity in SH-SY5Y cells through the Erk1/2-p38-JNK-dependent signaling pathway. International journal of molecular medicine 33, 925-933.
  11. Evans S, Dowell NG, Tabet N et al. (2013) Nicotine effects on attentional reorienting in mid-age adults, and interactions with apolipoprotein E status. Journal of psychopharmacology 27, 1007-1014.
  12. Evans S, Gray MA, Dowell NG et al. (2013) APOE E4 Carriers show prospective memory enhancement under nicotine, and evidence for specialisation within medial BA10. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 38, 655-663.
  13. Marchant NL, King SL, Tabet N et al. (2010) Positive effects of cholinergic stimulation favor young APOE epsilon4 carriers. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 35, 1090-1096.
  14. Durazzo TC, Mattsson N, Weiner MW et al. (2016) Interaction of Cigarette Smoking History With APOE Genotype and Age on Amyloid Level, Glucose Metabolism, and Neurocognition in Cognitively Normal Elders. Nicotine Tob Res 18, 204-211.
  15. Sabbagh MN, Tyas SL, Emery SC et al. (2005) Smoking affects the phenotype of Alzheimer disease. Neurology 64, 1301-1303.
  16. Lopez-Arrieta JM, Rodriguez JL, Sanz F (2001) Efficacy and safety of nicotine on Alzheimer's disease patients. The Cochrane database of systematic reviews, CD001749.
  17. Nicotine replacement therapy to quit smoking. American Cancer Society.
  18. Stolerman IP, Jarvis MJ (1995) The scientific case that nicotine is addictive. Psychopharmacology 117, 2-10; discussion 14-20.
  19. Frenk H, Dar R (2011) If the data contradict the theory, throw out the data: Nicotine addiction in the 2010 report of the Surgeon General. Harm reduction journal 8, 12.
  20. Min SK, Moon IW, Ko RW et al. (2001) Effects of transdermal nicotine on attention and memory in healthy elderly non-smokers. Psychopharmacology 159, 83-88.