Caffeine

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Caffeine is the most widespread psychoactive drug in the world [1] and is contained in large quantities in coffee and, in lower concentration, in other beverages that are regularly consumed to temporally ward of drowsiness or increase mental performance.

The main mechanism [2] at work with caffeine to achieve the alleviation of drowsiness is by blocking adenosine receptors in the brain, due to a similar chemical structure as adenosine[3], that are a part of the sleep regulation mechanism.

While caffeine both does induce a number of scientifically validated positive and negative effects on humans for a short time after consumption, withdrawal symptoms are possible in the case of caffeine dependence and are recognized by the ICD-11 and DSM-5.

There are large genetically based differences in caffeine clearance time in the body[4], which might account for anecdotal accounts of varying sensitivity and prolonged effects of caffeine after ingestion.

Caffeinated beverages

Average caffeine content in beverages[5][6][7][8][9]

Product Serving size Caffeine(mg/serving) Caffeine(mg/L)
Percolated coffee 207 mL (7.0 US fl oz) 80–135 386–652
Drip coffee 207 mL (7.0 US fl oz) 115–175 555–845
Coffee, decaffeinated 207 mL (7.0 US fl oz) 5–15 24–72
Green tea 236 mL (8.0 US fl oz) 25 106
Black tea 236 mL (8.0 US fl oz) 42 178
Coca-Cola 355 mL (12.0 US fl oz) 34 96
Mountain Dew 355 mL (12.0 US fl oz) 54 154
Pepsi Zero Sugar 355 mL (12.0 US fl oz) 69 194
Red Bull 250 mL (8.5 US fl oz) 80 320

Note: Caffeine content in tea can vary significantly based on leaf type and steeping time.

Detailed info on Green tea and Black tea.

Recommendations

For the purpose of adapting to Polyphasic sleep, the community discourages the intake of caffeinated beverages due to the ability of caffeine to disrupt sleep, decrease the amount of SWS sleep[10] in a sleep block and mask sleep deprivation symptoms during the adaptation period. The long half life of caffeine (particularly as contained in coffee), significantly outlasts both the perceptible cognitive boost and the inevitable following caffeine crash, proceeding to effect the next sleep block in a subtle but negative way.

References

  1. Burchfield G (1997). Hopes M (ed.). "What's your poison: caffeine". Australian Broadcasting Corporation. Archived from the original on 26 July 2009. Retrieved 15 January 2014.
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769007/
  3. "The structure of caffeine is very similar to adenosine, which allows it to bind to (all) the A1, A2a, A2b, and A3 ARs."Julius Schuster,Ellen in Progress in Neuro-Psychopharmacology and Biological PsychiatryS.Mitchell
  4. "CYP1A2 gene polymorphism has been shown to alter the expression or activity of the CYP1A2 enzyme (Rasmussen et al., 2002), which subsequently results in a large individual variability of caffeine clearance." in "Progress in Neuro-Psychopharmacology and Biological Psychiatry" by JuliusSchuster, Ellen S.Mitchell
  5. "Caffeine Content of Food and Drugs". Nutrition Action Health Newsletter. Center for Science in the Public Interest. 1996. Archived from the original on 14 June 2007. Retrieved 3 August 2009.
  6. "Caffeine Content of Beverages, Foods, & Medications". The Vaults of Erowid. 7 July 2006. Retrieved 3 August 2009.
  7. "Caffeine Content of Drinks". Caffeine Informer. Retrieved 8 December 2013.
  8. Chin JM, Merves ML, Goldberger BA, Sampson-Cone A, Cone EJ (October 2008). "Caffeine content of brewed teas". Journal of Analytical Toxicology. 32 (8): 702–4. doi:10.1093/jat/32.8.702. PMID 19007524
  9. Richardson B (2009). "Too Easy to be True. De-bunking the At-Home Decaffeination Myth". Elmwood Inn. Archived from the original on 27 December 2011. Retrieved 12 January 2012.
  10. Adenosine analogs and sleep in rats. Radulovacki M, Virus RM, Djuricic-Nedelson M, Green RD J Pharmacol Exp Ther. 1984 Feb; 228(2):268-74.[1]

See also

Caffeine half-life calculator


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