To Cheat or Not To Cheat: Tryptophan Hydroxylase 2 SNP Variants Contribute to Dishonest Behavior
Qiang Shen1, Meijun Teo2, Eyal Winter3
1College of Economics and Management, Zhejiang University of TechnologyHangzhou, China; Department of Management Science and Engineering, School of Management, Zhejiang UniversityHangzhou, China.
Frontiers in Behavioral Neuroscience
|May 21, 2016
Summary
Genetic variations in the tryptophan hydroxylase 2 (TPH2) gene, crucial for brain serotonin production, are linked to individual differences in deceptive behavior. This neurogenetic study sheds light on the biological underpinnings of lying.
Area of Science:
- Neuroscience
- Behavioral Genetics
- Psychology
Background:
- Deception, or lying, is a complex human behavior studied across disciplines like philosophy, theology, economics, psychology, and neuroscience.
- While heredity influences deceptive behavior, specific genes and neurotransmitter pathways involved remain largely unexplored.
- Understanding the neurobiological basis of deception is crucial for various scientific fields.
Purpose of the Study:
- To investigate the genetic underpinnings of individual differences in deceptive behavior.
- To explore the role of specific neurotransmitter pathways in deception.
- To identify potential genetic markers associated with lying.
Main Methods:
- A neurogenetic strategy was employed to study deception.
- Deception was modeled using an incentivized die-under-cup task in a laboratory setting.
- Single nucleotide polymorphism (SNP) variants in the tryptophan hydroxylase 2 (TPH2) gene were analyzed.
Main Results:
- Provisional evidence suggests that SNP variants in the TPH2 gene are associated with individual differences in deceptive behavior.
- TPH2 encodes the rate-limiting enzyme for brain serotonin biosynthesis, implicating the serotonin pathway in deception.
- This exploratory study provides initial insights into the genetic contribution to lying.
Conclusions:
- The TPH2 gene and its associated serotonin pathway may play a role in modulating deceptive behavior.
- Further research is warranted to confirm these findings and elucidate the precise mechanisms.
- This study opens avenues for understanding the neurogenetic basis of deception.
Related Concept Videos
01:29Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu
102
Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
102
01:11Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
65
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
65
01:27Principles of Pharmacogenetics: Types of Genetic Variants
86
The human genome is over 99.9% identical between individuals, yet genetic differences exist at millions of bases. The human genome contains approximately 3 million variant positions per individual, many of which are heterozygous, contributing to genetic diversity and individual traits. Genetic variations include single-nucleotide polymorphisms (SNPs), insertions, deletions, and copy number variations (CNVs).SNPs, the most common variation, involve single-base changes in DNA. These can be...
86
01:05Single Nucleotide Polymorphisms-SNPs
19.7K
A single nucleotide polymorphism or SNP is a single nucleotide variation at a specific genomic position in a large population. It is the most prevalent type of sequence variation found in the human genome. Point mutations that occur in more than 1% of the population qualify as SNPs. These are present once every 1000 nucleotides on an average in the human genome. Replacement of a purine with another purine (A/G) or a pyrimidine with another pyrimidine (C/T) is known as a transition. In contrast,...
19.7K
01:28Pharmacogenetics of Phase I Enzymes: Cytochrome P450 Isozymes
108
Cytochrome P450 (CYP450) enzymes are a superfamily of heme-containing monooxygenases that play a pivotal role in Phase I drug metabolism by catalyzing oxidation and reduction reactions.These enzymes transform lipophilic xenobiotics into more hydrophilic metabolites, facilitating subsequent Phase II conjugation and eventual excretion. The CYP450 family is classified into families (e.g., CYP1–CYP3) and subfamilies (e.g., CYP2A, CYP2C), based on amino acid sequence homology.CYP450...
108
01:16Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters
104
The pharmacogenetics of drug transporters is increasingly recognized as a critical factor influencing interindividual variability in drug absorption, distribution, and elimination. These membrane-bound proteins regulate drugs' movement across cellular barriers by actively pumping them out (efflux) or facilitating their uptake (influx). Among the major transporter families, ATP-binding cassette (ABC) and solute carrier (SLC) transporters play particularly prominent roles. Genetic polymorphisms...
104