. Author manuscript; available in PMC: 2011 Jul 1.

Published in final edited form as: Parkinsonism Relat Disord. 2010 Mar 20;16(6):370–375. doi: 10.1016/j.parkreldis.2010.02.012

Table 2.

Risk of Parkinson’s disease associated with NAT2 slow and fast acetylators.

NAT2	Genotype	%Cases (n)	%Controls (n)	RR (95% CI)¹	Adj RR (95% CI)²	Interaction with Caffeine^*	Interaction with PMH^@
WOMEN
All
	Fast	40(59)	44(298)	1.00 (Ref)	1.00 (Ref)	0.32	0.85
	Slow^#	60(90)	57^{^}(387)	1.13 (0.77, 1.64)	1.11 (0.76, 1.62)
PMH Ever
Users
	Fast	38 (37)	44(183)	1.00 (Ref)	1.00 (Ref)
	Slow^#	62(60)	56(230)	1.14 (0.72, 1.82)	1.13 (0.71, 1.80)
Never
Users
	Fast	42 (16)	40(76)	1.00 (Ref)	1.00 (Ref)
	Slow^#	58 (22)	60 (115)	1.21 (0.55, 2.66)	1.23 (0.55, 2.73)

MEN
	Fast	42 (54)	39 (206)	1.00 (Ref)	1.00 (Ref)	0.73
	Slow^#	58 (76)	61 (327)	0.87 (0.59, 1.30)	0.84 (0.56, 1.26)

Caffeine modeled as a linear variable in mg/day

slow acetylators defined as possessing 2 or more mutant alleles of NAT2 G286E (rs1799931), NAT2 I114T (rs1801280), NAT2 R197Q (rs1799930)

adjusted for matching factors (age, source of DNA (blood or buccal smear), race)

adjusted for matching factors (age, source of DNA (blood or buccal smear), race) with additional adjustment for smoking in pack years. Analyses among ever and never users of PMH included an additional interaction term between smoking and use of PMH

PMH modeled as dichotomous (never/ever users)

^{^}

Numbers do not sum to 100% because of rounding.