Genetic Polymorphisms in the Human Population - Essay Example

Nicotine is the major constituent of cigarettes that causes addiction. Addiction is a complicated urge by the body because of overreliance on certain activity or drug product. Scientists have been trying to discover scientific ideas proofing the condition of addiction. Genetic factors are the commonly proposed factors by researchers and scientists to play a significant part in development of addiction. According to the paper cyp2a6, the population being studied gives its unique variants of CYP2A6, which are linked to cigarette smoking. Therefore, many articles evaluate the association between genetic polymorphisms with cigarette smoking and nicotine addiction (Amos, Spitz & Cinciripini, 2010). The purpose of my paper is to evaluate the proof that smoking and nicotine addiction is determined by several genetic polymorphisms in human population.

From the article nicotine-dependence-in-Chinese-population, usage of tobacco has been one of the causes of mortality in the world. The usage of tobacco can be prevented especially before addiction to prevent high mortality. About 80% of smokers are found in developing nations such as Mexico (Organization, 2016). Tobacco consumption is a big problem in such developing countries. Several studies and research have been done in the developing countries. A genetic association study was carried out in Mexico to compare light smokers, heavy smokers and non-smokers.

The results confirmed that CYP2A6 gene was confirmed to have about 80% of nicotine metabolism among the smokers and tobacco users (Pérez-Rubio et al., 2017). This gene is known of having high level of polymorphic. This led to the determination of more than one haplotypes. The haplotypes are in the official nomenclature for CYP genes. SNPs and other mutations were discovered in CYP2A6. The number of alleles can be determined using information such as gene duplications, gene deletions and variations of the copy number.

A study was also carried out in nuclear families with smoking members to investigate on a number of tobacco related phenotypes. Seven chromosomes were observed in DSM-IV- like ND. Other experiments had the same results. Heterogeneity inherent in ND is very necessary when analyzing the results. Some other results of previous experiments could not be trusted because they were from alcohol fields. In this case FTND was assessed from individuals who have been smoking for a long period of time. This can be explained to be a lifetime assessment of ND severity (Pérez-Rubio et al., 2017). This has physiological basis. This study however could not prove the heterogeneity across chromosomes for indices of ND.

According to the article chipping-away-at-the-genetics-of-smoking-behavior-mini-review, smoking affects gene of the users at all the different stages of smoking (Amos, Spitz & Cinciripini, 2010). It may not necessarily affect all genes. It may affect specific enzymes or constituent of a gene. Its effects may thus be transmitted or inherited. Families whose parents have been heavy smokers for a long period of time may suffer the problem of addiction. The children of such families may be addicted to smoking just after using it for a short period of time. Children may be born with diseases similar to those that affect heavy smokers. The genes in their body are already affected through inheritance from their parents ("Genome-wide meta-analyses identify multiple loci associated with smoking behavior", 2010). Smoking in the presence of a pregnant woman is hazardous because the women inhales and ingests it to the baby. Research suggests that babies with smoking parents have a high chance of being born with birth defects. In most cases these children are born with heart defect or brain issues. Smoking affects both smokers and nonsmokers. Partial smokers are nonsmokers and they include pregnant women. If a woman ingests smoke from a smoker, it goes directly to the mother’s circulation system, which is transferred to the fetus. Such cases result to complications in different stages of fetal development.

The latest experiment was carried out to evaluate the duty of genetic influences in stopping smokers from using tobacco. Carmelli came up with evidence that genes are involved in relapse (Amos, Spitz & Cinciripini, 2010). Heritability approximates show that it is very difficult to quit smoking and show failed cessation. The latest outcomes encourage people on the significance of considering phenotypic complexity of ND in investigations concerning genes. They support the consideration of applying ND in the genetic experiments.

The art of measurement of ND has adjusted from one global measure to multiple measures. It implies scientists have discovered and confirmed its importance in genetic experiments and investigations. Having multiple measures has enabled its usage in many investigations worldwide Different constituents of ND are very important in understanding the architecture of ND (Wen et al., 2017).

Individual SNP-based association analysis used the PLINK program. The objective was to show linear regression for FTND. Those who smoke in the family were used as covariates. The process was repeated with those who do not smoke in the family as covariates (Wen et al., 2017). The two experiments gave similar outcomes. This implies that both the genes of the smokers and non-smokers in the family were affected. This may be through inheritance from their parents or the non-smokers being passive smokers.

It is important to understand the pathophysiology of tobacco and nicotine addiction because the process relies on the identification of certain characteristics. The established criteria for nicotine addiction depends on the psychoactive effects, compulsive use and drug-reinforced behaviour. Overdependence on drugs often results in euphoria effects, physical dependence, and tolerance (Pérez-Rubio et al., 2017). Certain phenotypes inspire other measurements of nicotine dependence. These phenotypes express a trait based on environmental influence and genetics. Valid measurements of different phenotype dependence are important for research because it examines how these phenotypes are related to smoking behaviours and whether the same phenotypes are related to specific neurobiological measures of addiction. Different factors contribute to alcohol addiction. These factors include; effects of the product like the pharmacokinetics, the response of the user, which includes physiologic response and genetic susceptibility, and lastly, the environmental setting which involves accessibility and availability of the drug.

Nicotine addiction and smoking depend on the content of nicotine ingested and the way which it is ingested. The faster the delivery, the faster the rate of absorption, which means the greater the potential for addiction (Wen et al., 2017). Nicotine is readily absorbed into the lungs, mucosa, and skin, which means that nicotine taken in higher contents has a high risk of addiction. If an individual has suppressed nicotine genes, then if exposed to series of nicotine and smoking, the person might develop genetic signs of nicotine addiction. Research suggests that there is strong evidence for genetic influence on smoking behaviours. The genetic study on smoking behaviours has generated less evidence than addiction due to alcoholism (Pérez-Rubio et al., 2017). Behavioural genetics studies are important in isolating the phenotypes responsible for genetic smoking behaviours.

The evidence on genetic influence on smoking behaviour is stronger that genetic influence on alcoholism. The genetic behaviour of smoking depends on persistence and initiation. Shared environmental influences often trigger certain smoking genes, which affect people whose family has a history of nicotine and tobacco addicts. Both genetic and environmental factors have a role in nicotine addiction. However, there are different heritability coefficient of smoking behaviours across different populations. For example, a comparison of smoking behaviours between white Americans and African Americans. The genetic influence on smoking behaviour is a major risk factor in populations with higher prevalence of smoking like China. Some of the genes that are specific for nicotine dependence include nAChRs (Pérez-Rubio et al., 2017). It is evident that if a crossmatch is done between a man and woman and the siblings portray these traits; chances are the sibling might exhibit certain nicotine and smoking addiction behaviours. Identification of CHRNA5-CHRNA3-CHRNB4 locus is important in studying different smoking phenotypes like cigarettes smoked per day (Wen et al., 2017). Nicotine addiction can arise from the locus CHRNA5, CHRNA3, and CHRNB4 genes. This means people with these genes are strongly associated with nicotine and cigarette addiction. It is inborn, and they can no prevent the behaviours. Some of the environmental factors are responsible for triggering these addiction problems. If someone is exposed to large doses of nicotine, then the genetic composition of the individual might change. The change can be transmitted to offspring’s, who will exhibit similar addictions when exposed to certain environmental factors.

Nicotine dependence is significantly heritable. Evidence suggests that different sections of the genome contain genes that relate to nicotine dependence and variation of these genes depend on nicotine dependence. Measures associated with smoking cessation can be measured based on the heritable traits and genetic variation of an individual. There are different challenges associated with studying the relative contribution of environmental factors and genetics on nicotine dependence. These challenges include better understanding of changing interplay between environment and genes in nicotine dependence etiology, understanding the nicotine dependence phenotype, and developing molecular methods that address different data. Smoking behaviour and nicotine behaviors between different individuals is attributed to various environmental and genetic factors (Wen et al., 2017).

The importance of studying if genes contribute to certain nicotine addiction behaviors is to understand the etiology of these dependence behaviors. Another goal is to identify functional genetic variants to smoking behaviors (Amos, Spitz & Cinciripini, 2010). Cigarette smoking is the most common form of tobacco use, which in the process nicotine is also used. Nicotine dependence is highly heritable due to the transmission of certain phenotypes within the gene. There are different methods of assessing nicotine dependence. The first method involves creating questionnaires for people to answer and the second is through research on the genetic composition of different families that use nicotine to determine if the offspring inherited the same trait. The heaviness of smoking index is an indication that the genetic composition of an individual can be altered and transferred to offsprings.

It is important to understand the biology behind the process of ingesting tobacco/smoking until the tobacco causes dependence in the human body. The process is important in studying if genes are responsible for certain smoking and nicotine dependence behaviors. If someone inhales nicotine, the smoke crosses the blood-brain barrier and attaches to the nicotinic acetylcholine receptors (nAChRs) in the brain (Wen et al., 2017). If the nAChRs are activated, mesocorticolimbic dopamine is stimulated to produce the effects of nicotine. Stimulation of dopamine neurons by nicotine increases the firing rate of terminal dopaminergic fields. The process creates excitement. Continuous use of nicotine makes nAChRs to be dependent on nicotine and in the process creates addiction. This process has the effect on the certain genetic composition of the cell, which is the reason people using nicotine developed mutations in their genes. These mutations can result in diseases like cancers or create a heritable gene that is nicotine dependent. Scientific research explains that it is not clear how genes may contribute to nicotine addiction but evidence on CYP group of enzymes is enough to explain habits like nicotine addiction can be heritable. The CYP group of enzymes speed up the metabolism of nicotine and DRD2 genes which regulate dopamine process.

Research suggests that tobacco consumption can be influenced by genetic variations in the cytochrome P-450, which is a group of enzymes. These enzymes metabolize nicotine to cotinine. Any alteration of these enzymes contributes to abnormal metabolism that results in genetic variation that is associated with nicotine dependence (Amos, Spitz & Cinciripini, 2010). Most addictive drugs interfere with dopaminergic receptors, which is the reason continuous effects of nicotine on the mesolimbic dopaminergic systems interferes with a normal genetic composition of the body.

In conclusion, Smoking affects both the smokers and other non-smokers in the human populations. Most people are passive smokers and they do not realize. Inheritance of genes in case the non-smoker has a blood relationship with the smoker is another way one can become nicotine addict or a smoker. Smoking is addictive and the effects can be passed one from parents to off springs. Smoking should be avoided since its addiction is determined by several genetic polymorphisms in human beings. Despite exhibiting smoking traits, most people begin smoking through peer pressure (Wen et al., 2017). It begins during teenage hood and extends to the rest of their lives. Few people quit smoking after they realize it is not helping them or after they are diagnosed with a chronic disease like cancer. Smoking is addictive and most people find it difficult to quit smoking because of the nicotine content. There are different programs that help people to reduce their smoking habits. It is difficult to quit smoking instantly but a person can start step by step. Another way of preventing smoking is by suppressing the genes that trigger smoking (Pérez-Rubio et al., 2017). Match making and marrying people with inferior smoking genes can result in an offspring that has less chance of smoking. A large percentage of the population smokes as a result of learning the habit from parents or peers. Therefore, smoking can be prevented as long as the correct information is passed from one person to another. There are rare cases of smokers that associate their habits to genetic inheritance, but studying these genes is a way of creating a solution.