Category: Gene

In a modern world, longevity is convinced as one of the most important parts for human-beings, more and more people want to have a long lifespan. Scientists are dedicating on which parts would be more important in human lifespan, genes or behavior. Some people believe that our genes depend on our parents, most of the diseases are caused by family inheritance, family history is one of the strongest risk factors for common disease such as cancer, diabetes, heart disease and so on. However, a good life behavior can change even the whole life of a people. And I am firmly believed that good life behavior is more important than genes.

In the first place, I have seen an article, which described a twin; their parents are both fat, so it means that the twin will both have the genes that associate with fat. And they were adopted by different families and have different growth environments, and the result is one of the twins, inherit her parents, another one is opposite to her parents. Though many years research the scientists finally found that the twin have experienced the similar situation. Both of them like to eat, and easy to get hungry. Also, they both easy to gain their weight, and their brain always tell them that they need to stay relax, eat more and avoid doing any exercise. When they all group up, one had similar size with her parents followed, but the other one was forced to take physics exercise every day, it happened for a long while, that result such a totally different body size. And it is easy to know the slim one has a longer lifespan than the other one. In this example, it obviously that people who have a good behavior is more important than genes.

Furthermore, genes can always be changed when we don’t know and we cannot control. What we can operate is our behavior. Though the physical traits and behaviors you born with and what you get experienced are both important during your life. Your characteristic can influent your experiences and your experiences can impact your characteristics. Your behavior will change when you experience more. Genes are easy to be changed, for example, when a woman pregnant the behavior of the woman can also make a different to the new-born baby. In some situation genes may play an importance part, it determines the basic way for most of your physics condition like tall range, IQ, the disease which you have when you born and so on. However, these could not make a key decision in your whole life. The acquired change can lead a person to their way. How we face with the difficulty is mostly depend on what we have experience and what we think about it, which is not related to genes. It is totally different that the optimistic and negative people face with the same problem, the optimistic can always lead the ending well. On the contrary, the negative people will give up which lead a worse ending.

To sum up, good life behavior is more important than genes for a long and health life. Why inherit genes estimate can just be a reference is that genes’ change is not sure and have a wide range. We are not sure when and where would be the genes changed. Not all longevity people have a perfect gene system, but almost all of them have good behavior that can help their long and health life. We cannot change our genes which is talented, but we can try to perfect our life behavior that help us with a longer lifespan.

This essay aims to answer this question by evaluating the role of genetic responsibility in doctor-patient confidentiality in the context of individuals suffering from Huntington disease (HD). HD is an uncurable and progressive neurological disorder characterised by late onset of motor, cognitive and behavioural changes. HD is an autosomal dominant disorder where an individual offspring has a 50% chance of inheriting the HD causing allele (Caron et al., 2018). Genetic responsibility is the responsibility of one’s genetic information to self and family as it is both individual yet transgenerational familial information (Statement, 1998). Several criteria must be met before the doctor makes a choice to disclose or not to disclose. The criteria are attempts were made to encourage disclosure, to warn them about the genetic risks it has to at-risk relatives and to ascertain an individual has the mental capacity to make an informed choice (Statement, 1998, Wusthoff, 2003).

The Declaration of Geneva outlines the duties and ethical principles of doctors: patient’s autonomy and non-maleficence (Parsa-Parsi, 2017). Presently, patient’s autonomy is one of the key cornerstones of medical ethics. Respect for autonomy in genetic responsibility stipulates one’s right to choose who and what degree they would like their relatives to know about their genetic information (Wusthoff, 2003). Doctors can educate the patient on the implications for at-risk relatives but they are bound to the ethical duty of doctor-patient confidentiality (Statement, 1998).

“Primum non nocere,” is the obligation of non-maleficence where one should prevent from taking actions that constitutes harm (Hakimian, 2000). Doctors should factor in the possibility that some relatives might not want to know this genetic information and hence disclosure would result in more harm. Disclosure may cause psychological, social and financial harm as they could be subjected to genetic stigma or are unable to obtain employment and/or insurance (Statement, 1998). Findings by Penziner et al. demonstrated that this fear is very real and prevalent where 90% of employed HD participants revealed their HD status but nearly all would not disclose this information to future employers (Penziner et al., 2008). Study by Oster et al. cited that the main concern for relatives to remain untested is the fear of losing health insurance. Additionally, 41.6% chose to pay from their own expenses for testing to hide their genetic risks from their insurer (Oster et al., 2008). Especially in the case of HD where there is no cure, some individuals would rather be ignorant to the risks. Lastly, American Society of Human Genetics dictates that disclosure is allowed when the disclosed information is used to prevent harm and the harm is serious and imminent. However, since HD is a progressive untreatable disease, International Huntington Association render it impermissible to disclose this genetic information without consent (Godard et al., 2006).

On the contrary, it can be debated that a doctor has a duty to warn at-risk relatives even if this breaches the patient’s confidentiality. Individuals in favour sees this duty as a duty to prevent foreseeable harm (Godard et al., 2006). Even though knowing one is tested positive for HD does not prevent this disease from manifesting, it prevents the transmission of HD to future generations through informed reproductive choices (Hakimian, 2000). Findings from Decruyenaere et al. showed that 1/3 chose not to have children and 1/3 chose prenatal diagnosis after performing predictive testing (Wusthoff, 2003). Furthermore, knowing one’s risk of HD permits them to make certain health and employment choices. If they begin to exhibit symptoms of HD like depression and irritability, early interventions can be made to tackle these manageable manifestations (McCusker and Loy, 2017) Hence, it can be argued that at-risk relatives cannot make these decisions if they are unaware of their genetic risk. From this viewpoint, the autonomy of at-risk relatives is equally important and knowledge is favoured over ignorance as doctors are expected to benefit the patients (Godard et al., 2006).

Lastly, disagreements were made against the restrictive requirement that the threat must be serious and imminent to permit disclosure. However, many genetic diseases including HD require time to manifest (Bell and Bennett, 2001). Additionally, can knowing the degree of likelihood of having HD and the likelihood that genetic predisposition leads to actual manifestation dictate the seriousness of the disease (Lemmens and Austin, 2001)? These considerations are controversial as it is difficult to reasonably answer these questions with precision.

Based on the above discussion, I have concluded that in the context of HD, a doctor should not disclose a patient’s genetic diagnosis to at-risk relatives without consent. If a patient is mentally capable of understanding the genetic risks and attempts has been made by the doctor to encourage disclosure, I believe the doctor should respect the patient autonomous decision. I do recognise that some individuals might debate that a patient refusal to disclosure would be unfair to the autonomous decision making of at-risk relatives. Often, when individuals make such a claim, it is in the context that the disease can be prevented or treated with early interventions. However, with HD being an uncurable disease, an individual might place their at-risk relatives in more harm as they need to bear the genetic discrimination that comes with HD. Knowing one’s risk of HD might affect their employment and insurance opportunities. In addition, HD is a chronic disease with a late onset of symptoms, individuals can lead a relatively normal life before tell-tale signs were to appear. Therefore, not knowing one’s genetic risk of HD might prevent them from facing such genetic discrimination since young. It is important to note that as genetic techniques get more advanced, it would be easier to study the genetic components of disease. Therefore, we might be able to find treatments for diseases with genetic components. Hence, this recommendation might not stand and we would need to review it.

Genetic therapy is the use of the delivery of nucleic acid regeneration cells to a patient’s somatic cells to prevent or treat the disease. In the last few years, much research has been done worldwide in the field of genetic cancer treatment. In the current situation, there are many types of cancer treatments like viral replication, tumor suppression, tumor immunogenicity, suicidal gene therapy, etc. Cancer is a disease caused by mutations in cells that remain unprotected and lead to cell growth and division. There are more than 100 types of cancer. Viral vectors can produce tumor anti future research genes (proteins found in tumor cells) to stimulate the body’s immune response.

Therefore, vector development remains an important area for future research.The ultimate goal of gene therapy is to develop genetically modified non-toxic genes that can insert and deliver foreign genes to specific types of cells such as cancer cells. Over the past two decades, much research has been done in the field of genetic engineering around the world explicitly in the use of cancer. Virus vectors are biological systems found in mutations that can transmit their genes to infected cells. Many viruses like retrovirus, adenovirus, herpes simplex virus [HSV], adeno-associated virus [AAV], and poxvirus have been modified to eliminate their toxins and maintain their high genetic transmission capacity.

The limitations associated with viral vectors, for their safety especially immune defenses and their limited ability of transgenic substances have encouraged research workers to focus more on non-burgeoning carriers as another means of carrying viruses. Vein-free vectors are usually cationic in nature.Gene treatment has had a bad 10 years. In fact, it started badly before the 1990S and began with two unauthorized trials in the early 70S and early 80S. First, an attempt was made to treat two young girls with arginase defense syndrome using Vivo gene therapy with the wild-type shope papillomavirus in the hope that the viral arginase would replace an enzyme that was not present in patients. The second was ex vivo therapy for β-thalassemia bone marrow transplant using asthma-globin-treated bone marrow cells in two patients. There is no real follow-up because both trials were discontinued but apparently did not improve or harm patients.

Restorative vaccines epitomize a feasible option for treating late-stage cancer with effectual tumor viral therapy and the patient’s immunity. Recent clinical tests have provided encouraging outcomes leading to the adoption of the first curative cancer vaccine by the U.S. Food and drug administration. These breakthroughs not only provide a new way to treat and manage cancer but also open the way for meaningful evolution and improvement of future drugs through effective anti-cancer antidotes.Tumor suppressor genes can be grouped into the following categories: caretaker genes, gatekeeper genes, and more recently landscaper genes. Part of a tumor or anti-oncogene is a cell that controls the cell during cell division and recurrence when the uncontrollable cell can lead to cancer when the type of stress plant changes leading to loss or reduction of its function through another genetic mutation. This may allow the cell to grow abnormally of human cancer compared with activation of plant genetic stress can be subdivided into new genes and new care improved genes ensure gene sequence. DNA sequence and those genetic mutations allow genetic mutations to accumulate at present gatekeepers by directly controlling cell growth by inhibiting cell growth apoptosis in retaining genes that control growth by contributing to the environment where mutations can create an environment that promotes uncontrolled growth.

Therapeutic approaches based on mutations in cancer cells include regeneration of gene mutations in deficient genes. Genetic therapy p53 provides an attractive strategy to test the viability of this technique.Suicide genetic therapy is a therapeutic strategy, in which gene mutations are performed in cancer cells. Suicide gene therapy is based on the introduction into tumor cells of a viral or a bacterial gene, which allows the conversion of a non-toxic compound into a lethal drug. Although suicide gene therapy has been successfully used in a large number of in vitro and in vivo studies, its application to cancer patients has not reached the desirable clinical significance. Side effects of this treatment are still present, as major problems doctors have to deal with in clinical practice. Although unspecified cytotoxic agents form an effective treatment against cancer cells, they also tend to kill normal cells, rapidly differentiating. On the other hand, genetic therapies are both under investigation, and some have already been planned for clinical practice. Several approaches have been investigated to find a targeted treatment for cancer cells, while not affecting normal cells.

Adeno associated virus type 2 (AAV) is a non-viral DNA virus used as a eukaryotic gene transfer vector in vitro and in vivo AAV has a variety of features that can make it useful in human gene therapy the AAV virus does not require an increase in host cells. We can show selections related to active cell division of both wild AAV species and AAV vector. AAV vector tends to persist in infected cells for a long time without adverse effects on the wildlife species that normally congregate in the same chromosome region nineteen while removed AAV vectors interact in some way in the cell genome can also continue in the form of episomal cells. AAV carriers used to transfer various cell types to in vitro epithelial bone marrow cells and lymphocyte cells.Oncolytic virotherapy is an arising therapy that utilizes antiretroviral drugs that keep butchering disorder late advances join the chance of a solitary virotherapy therapy with the accessibility of remedies that breath life into the spread of intratumoral tainting systems to refresh the shielded reaction to oncolytic illnesses and the presence of the intratumoral pollution the major clinical achievement was the coordination of stage 3 herpes simplex defilement therapy utilizing talimogene laherparepvec (imlygic) of metastatic melanoma challenges in the field to pick the champs in a developing number of intelligent stages and arranging things and anticancer security to improve clinical-level models and to pass on defilements that think about more requesting orders than can be masculine.

For my inquiry, I wanted to determine whether genetics are related to the fact that women are more prone to knee injuries than men. Specifically, Anterior Cruciate Ligament tears (ACL) in athletes. Through numerous articles I discovered a lot of information relating genetics to ACLs. Recent studies have hypothesized that genetics do in fact have relations to a higher probability in an ACL tear.

More specifically, people with “weaker knees” meaning less muscle mass and weaker ligaments due to collagen build up, are more prone to getting a tear. (Team Arivale, 2017) Collagen, is what makes up our ligaments and tendons. It was determined that people who have a specific collagen variant are less likely to result in injury. This type being COL1A1. This does not mean necessarily that those whose ligaments are made up of COL1A1 are immune to tears, there are still other risk factors involved that can result in injury. The COL5A1 variant is found to be involved in a higher risk of ACL tears. Women specifically were tested and found that those who carried the COL5A1 variant were at a much higher risk for an ACL tear. (Team Arivale, 2017) This information still didn’t give me a full understanding of if gender plays a roll genetically into the susceptibility of knee injuries, so I dug deeper.

Women generally tend to have higher estrogen levels due to frequent hormonal changes during menstrual cycles. The higher amount of hormones could possibly lead to injury, although this has not yet been proven. Females also have a wider pelvis, which effects the alignment of our knees and ankles. This could mean a much more narrow gap inside the knee, leaving a smaller amount of room for the ACL to travel through. (Mclure, 2012) Women are also more flexible than men which leaves us with loose ligaments, as well we tend to have less powerful muscles and smaller muscles mass compared to males which is a contributing factor to the likelihood of females being at a higher risk. (Shmerling, 2015) Obviously genetics are not the only contributing factor, as females move their bodies differently than men. The way we change direction, jump and land are all different but the cause of this is also genetic. For example, women tend to land more upright and take off and change direction using the same foot. (Mclure, 2012) Through many thorough articles I have discovered that the likelihood of a female undergoing an ACL tear is much more likely than a male and that genetics do play a role in that. Although, nothing can be 100% proven and therefore we cannot blame the likelihood solely on genetics.

Evidence 1: Are ACL tears hereditary?

The links between ACL tears and genetics are all within the type of collagen buildup of the tendons and ligaments in our bodies. As explained before, those whose collagen makeup is of the COL1A1 variant, are less likely to result in an ACL injury. If this variant is passed onto offspring, they would also be at a lesser risk of the specified injury. (Team Arivale, 2017) This does not mean they couldn’t possibly ever suffer from one, it just means their risk factor is slightly lowered than most. Although, if someone with the COL5A1 variant, being the collagen type linked to weaker knees, leaving a higher possibility for injury passed that onto their offspring, the child would then most likely be at risk as well. Therefore, the possibility of a potential ACL tear/injury or lower-risk factor is hereditary, but it does not guarantee the outlook for that person. Someone with the COL5A1 collagen makeup could go through their entire life without suffering an ACL ailment, as well as someone with the COL1A1 variant could undergo an ACL related injury. This concludes that ACL tears alone, are not hereditary but it is the likelihood based upon the buildup of your collagen. (Team Arivale, 2017)

Evidence 2: Are ACL tears completely genetically related, or instead does it have to do with the movements during contact sports?

My research has shown me that quick jerky movements during sports and physical activity are factors that contribute to ACL tears. Sharp turns with planted feet, suddenly slowing down and changing direction, landing funny from jumping, and suddenly stopping. (ScienceDaily, 2012) The contact aspect of some sports can be a contributor as well. Full blows to the knee during sports due to tackles are plausible causes of ACL tears. (ScienceDaily, 2012) Again, the likelihood of tearing your ACL goes back into genetics meaning that genetics and movement are correlated. It’s not solely and completely genetically related, it connects to the different movements or scenarios that may cause injury. Movement is a large component in the tearing of ACLs, but is not the direct fault of the injury.

Overall, ACL tears are more commonly to be found in women based upon our genetic makeup and the ways our bodies move differently compared to men. The cause for the higher risk is not from genetics alone but a combination of many factors. Even though ACL tears are more common in women, there are still things we can to do gain some control and try to prevent it from happening ourselves. Things like strengthening exercises and informational workshops are extremely helpful when it comes to ACL tear prevention. (Shmerling, 2015)

Abstract

This experiment was performed to determine the factors that influence the tas2r38 gene has on the PTC bitter taste receptor’s genotype was determined by electrophoresis using PCR and DNA extraction. The class data C allele frequency is slightly over 50% which matches with the map which shows similar frequency’s. Which suggests that there is a correlation between the SNPs and the bitter taster ability.

Introduction

The study of the variation in the ability to taste phenylthiocarbamide(PTC) was first discovered by A.J Fox in the 1930s when he and his co-worker discovered that they tasted different things (Fox, 1932 ). This then led to the discovery that some people could taste PTC, these people are called tasters and some people could not and these were called non-tasters. This was then studied further to estimate the frequency of taster and non-taster allele across the populations all over the world (Guo & Reed, 2001 ). Also, PTC has a strong correlation with the ability to taste naturally occurring substances like toxins (HARRIS & KALMUS, 1949 ) (Wooding, et al., 2004).

The full name for the gene TAS2R38 is taste 2 receptors number 38 and is located at 7q34 complement and is 1,143bp long and with only one exon and it controls the ability to taste glucosinolates, a family of bitter-tasting compounds found in plants of the Brassica and this is controlled by a protein which is found in the tongue and is a seven-transmembrane g protein-coupled receptor. ( National Center for Biotechnology Information, 2018).

These three SNP make up the haplotypes PAV which is used to refer to tasters and AVI which is used to refer to non-tasters. The aim of the study is to find out what my genotype is at position 145 of TAS2R38 and find out about my bitter-taste ability’s and what my phenotype is. Another aim of the study is to test whether the class data will help support the correlation between the bitter taste ability and the SNP.

Materials and Methods

DNA extraction

The subjects were UK university students, because they were over the age of 18 and alive consent had to be given for the DNA to be extracted and analysed. This is in accordance with the human tissue act 2004(section 45 schedule 4) which states that consent must be obtained unless for cases or the prevention of crime. Consent was insured by making the subjects sign a consent form and privacy was ensured by the students all having an anonymous number.

The subject’s cheek was swabbed with a buccal swab 5-6 times to ensure that there was plenty of DNA cells. It was then placed in a 1.5ml Eppendorf tube which has 200ul of Phosphate Buffered Saline solution (PBS). This was then left so the PBS can lyse the extracted DNA.

20ul of proteinase K and 400μl lysis buffer (from Gene Jet Whole Blood DNA Purification Kit) was pipetted into the PBS and was incubated at 56oc for 10 minutes because this is the optimum temperature for the proteinase K to start to digestive native proteins which happened between 50-60 oc (Farrell Jr. , 2010).

The Buccal tip is then squeezed to get as much liquid out as possible then disposed of.200ul of ethanol is then pipetted into the tube and inverted, this is to ensure all the liquids are mixed properly. The Gene JET Genomic DNA Purification Columns are then secured to a collection tube. Then all the liquid from the Eppendorf tube is pipetted into the purification column and is placed in the centrifuge for 1min at 8000rmp. This is to help purify the DNA because it will bind to the collection tube while the waste goes into the collection tube.

The flow-through is disposed of and the collection tube secured,500ul of wash buffer I(from Gene Jet Whole Blood DNA Purification Kit ) was pipetted into the spin column and centrifuged for 1 min at 10,000 rpm. When finished the flow through is disposed of,500ul wash buffer II (from Gene Jet Whole Blood DNA Purification Kit )was pipetted into the column and centrifuged for 3mins at the max speed (≥13,000 rpm)

The purification tube is then filled with 50ul of elution buffet I(from Gene Jet Whole Blood DNA Purification Kit ) in the centre of the membrane to eluate genomic DNA. This is then left at room temp for 2 mins so the DNA can dissolve the buffer. Then it is centrifuged for 1min at 10,000rmp.

DNA amplification

Two PCR tubes are handed out to each subject; one is for the PCR and one is the negative control. 12.5μl of PCR master mix(made by Promega) is added to each. The PCR master mix is made up of Taq Polymerase, dNTPs, MgCl2 and reaction buffers. Then 2.5μl of distilled water,2.5μl forward primer (PTC145-F) into each tube and 2.5μl reverse primer (PTC145-R) were pipetted into each tube.

Then 5μl of the subject extracted DNA was pipetted into tube 1 and 5μl of distilled water is added to the negative control into tube 2.these are then both vortexed to ensure all is mixed well.

They are then placed in the PCR machine where it runs cycles of 95°C for 3 mins then 35 cycles of (95°C 30s, 58°C 45s, 72°C 45s), 72°C 5 min.

This is the DNA amplified.

Digestion

Digestion of 500 ng PCR product with 10 U of HaeIII enzyme by NEB (excess enzyme to make it cuts) at 37°C for 2 hours on a thermocycler and inactivated at 80°C for 30 min.

Electrophoresis and genotyping

The gel(2% agarose gel in TBE with GelRed solution) had to be checked and the comb removed.2ul of blue loading dye was added and mixed to all the undigested and digested PCR product. Then 12 of a DNA size marker was added to the far left. This is to help after the electrophoresis to count the ladder position and location. Then the samples were loaded into the gel wells. The electrophoresis tank was then connected to the power supply and ran for 30 minutes at 130v. This is then taken to the gel analysis system which will adjust the focus and brightness and switch to the UV light and the image from this is then saved.

DISCUSSION

My results were inconclusive. This means that I don’t know my genotype, however, I did predict my phenotype based on my experience and on research. It was stated that tasters would find cruciferous vegetable that contains either isothiocyanates and gitorin bitter because the there structure is similar to the structure of PTC (Wooding, et al., 2004). There is also research that states that PTC tasters are less likely to smoker being (38.4%) than in non-smokers (43.1%) (Risso, et al., 2016).AVI non-tasters were reported to have higher alcohol use than either intermediate and taster (Duffy, et al., 2004 ). Based on the research I predicted I was a taster. I predicted this because I don’t smoke or drink and I think that cabbage and broccoli are slightly bitter. This is backed up by the global diversity of the TAS2R38 PAV, AVI and AAI haplotypes from populations (Risso, et al., 2016).

I had troubles that made it so that my experiment didn’t work. One trouble was that the liquid kept bubbling which means I could have not put the right amount of my DNA or other material in the tubes which means that the PCR didn’t work and that the electrophoresis couldn’t happen. Next time I will hold the pipette all the way down and make sure to not release the lever before I have to.

Another problem was that there might not have been enough DNA for the PCR or electrophoresis to work this is because I could have not scraped my cheeks with the buccal swab enough times.Next time I will make sure to swipe more times to be certain there is enough DNA on the buccal swab.

The last problem is that on the first time I could have made it so that the liquid was pipetted under the well or on top of the well in the electrophoresis meaning that it wouldn’t show as ladders clearly when it was scanned. Next time I will make sure I’m in the well and not on top of it before I pipette the DNA.

There were some ethical considerations that had to be considered before the experiment could take place.one of the ethical issues is a person’s right to privacy and this was dealt with by each student being given a random number to put on their samples and this ensured that the result was kept anonymise. Another issue was consent which had to be given because everyone was over 18,competent and alive. This issue was handled by ensuring that everyone signed a consent form.

In conclusion I believe that the data all confirm that the TAS2R38 gene does affect the ability to the bitter taste receptor and I believe that it is a useful gene as it helps to detect the bitter taste of toxins and some poisons. The class data also helped with accepting the distribution of tastes, intermediate and non-tasters across the globe.

References

1. National Center for Biotechnology Information, 2018. TAS2R38 taste 2 receptor member 38 [ Homo sapiens (human) ]. [Online] Available at: https://www.ncbi.nlm.nih.gov/[Accessed 30 12 2018].
2. Duffy, V. B. et al., 2004 . Bitter Receptor Gene (TAS2R38), 6-n-Propylthiouracil (PROP) Bitterness and Alcohol Intake. Alcoholism: Clinical and Experimental Research, 28(11), p. 1629–1637.
3. Farrell Jr. , R. E., 2010. Resilient Ribonucleases. In: RNA Methodologies: Laboratory Guide for Isolation and Characterization . s.l.:Academic Press, pp. 155-172.
4. Fox, A. L., 1932 . The Relationship between Chemical Constitution and Taste. PNAS, 18(1), p. 115–120.
5. Guo, S.-W. & Reed, D. R., 2001 . The genetics of phenylthiocarbamide perception. Annals of Human Biology, 28(2), p. 111–142.
6. HARRIS, H. & KALMUS, H., 1949 . Chemical specificity in genetical differences of taste sensitivity.. Annals Of Eugenics, 15(1), pp. 32-45.
7. Risso, D. S. et al., 2016. Genetic Variation in the TAS2R38 Bitter Taste Receptor and Smoking Behaviors. PLOS One, 11(10).
8. Risso, D. S. et al., 2016. Global diversity in the TAS2R38 bitter taste receptor: revisiting a classic evolutionary PROPosal. Scientific Reports, 6(1).
9. Rodriguez, , S., Gaunt , T. R. & Day, I. N. M., n.d.
10. Rodriguez, S., Gaunt , T. R. & Day, I. N. M., 2009. Hardy-Weinberg Equilibrium Testing of Biological Ascertainment for Mendelian Randomization Studies. American Journal of Epidemiology, 169(4), pp. 505-514.
11. Wooding, S. et al., 2004. Natural Selection and Molecular Evolution in PTC, a Bitter-Taste Receptor Gene. American Journal of Human Genetics, 74(4), p. 637–646.

Causes

Obesity is characterized as a chronic condition as the result of an excess amount of body fat and it is defined by body mass index (BMI). A person’s BMI is determined by their height and weight (Balentine, 2019). However, to properly understand the impact of obesity, we need to look at what actually causes obesity in the first place:

One of the main causes is genetic influence. Several genes contribute to weight gain and body fat distribution; in fact, over 400 different genes are connected to being overweight or obese – they affect appetite, satiety, metabolism and even the tendency to use eating as a way to cope with stress (Harvard Medical School, 2009). The genetic causes of obesity can be broadly classified into different sections. Monogenic obesity is caused by a single gene mutation (Thaker, 2017). For example, mutations in the genes encoding leptin and leptin receptors were found in two severely obese cousins, and further research showed that leptin and leptin receptor – deficient patients exhibited severe weight gain, which resulted in severe obesity (Farooqi & O’Rahilly, 2006). This result is understandable as leptin is a hormone that regulates appetite, food intake and satiety, and so clearly, an absence would lead to constant hunger and weight gain. Another section is syndromic obesity, which is obesity that is associated with clinical phenotypes, which can include organ-system specific abnormalities and intellectual disability. The two most common forms of syndromic obesity are Bardet-Biedl syndrome and Prader Willi syndrome (Thaker, 2017). Bardet-Biedl syndrome is a genetic condition where mutations damage the structure and function of cilia and can cause vision loss, learning difficulties and abnormal weight gain. (Genetics Home Reference, 2020). Prader Willi syndrome is a genetic disorder due to the loss of function of specific genes and causes restricted growth and constant hunger, ultimately leading to type 2 diabetes and obesity (Genetics Home Reference, 2020). However, whilst genes do play a significant role in the development of the body, the Harvard School of Public Health (HSPH) claim that genes associated with obesity play a small part in the overall risk (Legg, 2016). This means that even if a person carries a gene linked to obesity, they do not necessarily become obese, and vice versa, leading to the belief that genetics have a smaller role in obesity compared to others such as environmental.

There are also many environmental influences on obesity. For example, urbanization has a large role in an obesogenic environment. Studies have shown that in communities that have low economic infrastructure and unsafe/inaccessible play areas, children are unable to perform the physical activity required for healthy development and so obese individuals are more prevalent in these areas (Pirgon & Aslan, 2015). It is common knowledge that physical activity is a must in order to live a healthy and balanced lifestyle, and so by not having the adequate structures for this, adults and children alike are practically being denied the right to live healthily, especially if they cannot afford luxuries such as a gym membership or a nearby leisure centre. Moreover, areas that have been highly urbanized, for example some major cities in Turkey, have diminished access to physical and sporting activities, and this leads to more people living a sedentary lifestyle, which increases the risk of obesity – in the UK , people are 20% less active now than in the 1960s, which is correlated with the increase of obesity over the past years (Fenton, 2017). This is in opposition to areas that have more parks and walking areas, where it is easier for children to lose weight (Pirgon & Aslan, 2015), showing that in order to help prevent an increase in obesity, consideration of public health and activity needs to be taken in urban planning of communities.

Obesity can also be linked to economic disparities as obesity is not evenly distributed across socio-demographic groups. In the UK, obesity rates are highest for children from the most deprived areas (Fenton, 2017). In these areas (which happen to be situated in a highly obesogenic environment), calorie-rich foods are available all around: meal deals in supermarkets, cheap sweets at the corner store and most importantly, fast food restaurants. Public Health England (PHE) has found that 17% of all fast food outlets are in the top 10% most deprived areas in the UK, similar to results showing that areas with the lowest earnings, such as Huddersfield, have the highest density of fast food restaurants (Magrini, 2018). This increase in consumption of out-of-home meals that have a high fat, sugar and salt content lead to an increase in obesity, especially in socially deprived areas, which would also probably not have any proper access to a form a physical activity.

Another thing that may prevent people from being physically active is technology. Research has shown that there is a relationship between screen media exposure and obesity. One example is a longitudinal study of a sample of US 10 – 15 year-olds, where there was a strong relationship between the number of hours that television was watched per day and the prevalence of overweight (Gortmaker, et al., 1996). The reason for this effect on obesity is that technology displaces physical activity as it takes up people’s time, especially if they work jobs that require them to be sitting around computers for most of the day, leading them to a sedentary lifestyle. However, it is difficult to accurately measure the relationship between screen time and physical activity – studies where screen time is reduced have only increased the amount of physical activity by a small portion (Ramsey Buchanan, et al., 2016), suggesting that displacement of physical activity is not a strong enough link between screen time and obesity. In fact, there is more evidence to support that screen media increases energy intake as children consume up to a third of their daily calorie intake in front of the screen (Robinson, et al., 2017). This could be because of how foods, especially more calorie-dense foods, are marketed on television advertisements, movies and social media etc., which encourages children to consume more food, and this, with the addition of less physical activity, would eventually result in obesity.

There are many other causes of obesity such as psychological trauma, where overeating is used as a coping mechanism to deal with events from the past (Leon & Roth, 1977), the side effects of medication such as antidepressants and some oral contraceptives, and hormone levels. Nevertheless, by covering some of the main causes of obesity, it will be much easier to be able to understand and evaluate its effects along with the effects of weight bias.

Costs

It is obvious that one of the largest impacts that obesity has on society is its costs. Obesity itself does not have a large impact on the costs, but rather it is the obesity and overweight – related health issues that do. In 2014/2015, the NHS spent around £6.1 billion on these issues (Fenton, 2017), which includes diabetes, coronary heart disease and even cancer. Cancer itself costs £9.4 billion (NHS, 2011), and so an increase in obesity (and eventually cancer) would lead to an increase of costs for the NHS. Data shows that there was an 18% increase in admissions for obesity treatment such as sleeve gastrectomy (reducing stomach size by 15%) or conditions or even complicated by obesity, including heart disease and cancer (Boseley, 2018) and with the NHS already under so much pressure due to being understaffed, an ageing population and the lack of beds, the increase in obesity-related health illnesses will put even more of a strain on the NHS, possibly even taking them into further debt. The most shocking (possibly even upsetting) element of all this is that obesity is a highly preventable disease; although there are genetic elements to becoming overweight, like we saw before, it is mostly due to the obesogenic environment that a majority of the world’s urban population lives in, and therefore there could have been the possibility that the cost of obesity and overweight-related issues could have been reduced, placing less pressure on the NHS and using some of these funds on other segments of healthcare and society e.g. the police service.

It is also shown that the amount spent on the treatment of obesity and diabetes is greater than amount spent on police, fire service and judicial system combined (Fenton, 2017). This clearly would lead to a rise in crime, the chance that calls do not get answered as quickly and officers are not as fast as responding to emergencies (Dodd, 2018) causing fewer crimes such as thefts from being investigated and so fewer offenders are brought to justice, making some areas less safe. We can therefore clearly see how this large economic cost can even lead to societal impacts, showing the damaging impact obesity has on society in relation to its costs, yet this estimate may not be entirely true.

On one hand, it is possible that the costs of obesity on the NHS have been largely miscalculated. The estimates may not be balanced cost-effective analyses, where £3.6 billion is saved on pensions and healthcare from the 7.1% of early deaths attributable to high BMIs (Owens, 2019) which means that the costs may actually be £2.47 billion per year – 2.3% of the estimated budget. The almost “exaggeration” of the estimate could be seen as propaganda put out by public health campaigners and politicians in order to gain media attention and cause an uproar, and though their intentions are good, these tactics incite a climate of resentment against obese people (BBC, 2015), which evidently enforces weight bias within society. However, on the other, there is not much research to back these claims up, and so the NHS’s original £6.1 billion spent on obesity-related illnesses estimate is considered to be the correct one.

Not only would the cost of obesity include the NHS’s estimate, but also the approaches to reducing obesity. One major example is the sugar tax, officially named the “Soft Drinks Industry Levy”, which was introduced to the UK in 2018 as part of the government’s obesity strategy which aims to reduce sugar consumption by persuading companies to reformulate their high sugar brands and avoid paying the levy. There are obviously many benefits of the sugar tax as it provides incentive to reduce the consumption on sugary drinks, which enables higher spending on health care as it raises revenue and encourages companies to produce healthier snacks, but some economists see it as a regressive tax, where a higher percentage is taken from low-income groups and can also lead to job losses (Pettinger, 2019). However, these arguments are weak as people do not need to buy sugary drinks, they can always switch to alternatives to avoid the tax. Also, everyone, including those on low incomes, will benefit from the increased spending on healthcare and a better quality of life. Between April and October of 2018, £154 million was raised to fund school sports programs and breakfast clubs to help combat childhood obesity (Rathbone Greenbank Investments, 2019). The sugar tax provides strong social and economic benefits and will encourage a healthier lifestyle to help reduce the increase of obesity with minimal economic disruption. From this, we can conclude that there are efforts being put in place in order to reduce the economic impacts of obesity.

There are also many other techniques that the government is putting in place to reduce obesity as it is suggested that obesity prevention could result in cost savings. For example, food labels are clearer and more consistent so that people are able to understand what are in the products they are consuming (Diabetes UK, n.d.). They are restricting price promotions on unhealthy foods so as to convince the public that unhealthy food is not the cheaper option; this is significantly important for those in low income families as they are then able to buy healthier foods instead of opting to buy what is on a deal. There are many more incentives put in place to reduce the costs, and although it is not a cure for increasing health expenditures, obesity prevention could possibly be a cost-effective way of improving mental health. We can then clearly see that since there are efforts put in place to reduce the costs, and so in the near future, the cost of obesity-related illnesses could be reduced.

Overall, we can see that obesity costs a lot on the NHS, and due to the increase of overweigh-related diseases, more pressure will be placed on the NHS. As shown in Figure 1, along with smoking and war, obesity is one of the most expensive manmade burdens that needs to be confronted before allowing the costs to become insurmountable as it is already 3% of the UK’s GDP. Weight bias, however, does not really have an impact on the economy and costs, but it does have an impact on other parts of society.

Physical Health

It is common knowledge that obesity impacts physical health and leads to many illnesses. One example of this is obstructive sleep apnea (OSA), which is a breathing problem that happens during sleep where the throat closes completely and the airway collapses, stopping air from travelling to and from the lungs for ten seconds or more, at least a hundred times a night. Research shows that there is a linear correlation between OSA and obesity (Jehan, et al., 2017) and that at least 45% of obese subjects suffer from it (Young, et al., 1993), showing that as weight increases, the risk for obstructive sleep apnea also increases. The narrowing of the upper respiratory muscles in obese individuals occurs due to the accumulation of fatty tissues, and the obstruction of breathing due to the narrowing of the upper airway leads to a marked increase of pressure in the thorax, triggering apnea. OSA interferes with a person’s life, causing them to become more tired and fatigued throughout the day, making it more difficult to concentrate on work and can even make people feel moody and quick-tempered, which can damage people’s relationships with their peers. A lack of sleep weakens the immune system, leaving those with OSA more vulnerable to illness. However, the most significant danger of OSA is that it could lead to metabolic syndrome, a disorder that includes high blood pressure, abnormal cholesterol levels and high blood sugar, all of which would lead to a higher risk of heart disease. Having OSA increases the risk of high blood pressure as sudden drops in blood oxygen levels that occur during sleep apnea increase the blood pressure and can strain the cardiovascular system (Mayo Clinic Staff, 2018). All of this evidence is important in demonstrating how obesity can lead to many other conditions that can have grave impact on a person’s life.

There is also a link between obesity and asthma. Epidemiological studies of asthma and obesity have clearly shown that obesity is more likely to occur in obese patients, and this does not differ between the sexes (Sutherland, 2014). There is also evidence of a dose-responsive relationship, with the odds of developing asthma increasing as BMI increases (Beuther & Sutherland, 2011). There are also physiological mechanisms e.g. obesity alters lung mechanics, leading to symptoms of dyspnea, which is shortness of breath. The reduced airflow and a change in the compliance of the respiratory system is linked to a combination of excess soft-tissue weight compressing on the rib cage and fatty infiltration of the chest wall. These alterations lead obese individuals to breathe in reduced lung volumes, which may be one cause in the increase of dyspnea as there is an increase work of breathing (Sutherland, 2014). The asthma and dyspnea, like the obstructive sleep apnea, can have a very negative effect on a person’s life, as even simple activities such as walking up the stairs become a daily challenge. However, there is data that suggests that asthma might be over diagnosed in the obese population. Obese patients report more dyspnea and asthma-like symptoms than non-obese patients, which leads to misdiagnosis. Consequently, over diagnosis leads to an increase in the prevalence of asthma in developed countries (Aaron, et al., 2008), meaning that more healthcare services and money is spent on asthma, even though it is not required.

Do you know if you are in good health? Maybe BMI can tell you the answer. BMI values can be obtained by dividing weight(kg) by the square of height(m). The BMI values in the range of 18.5-30 are normal, but the values up to 30 are defined as obesity. If you are obese, I’m sorry to inform you that you need to change. In fact, obesity is one of the most important public health problems in the 21st century. Even in 2013, obesity was considered a disease in the United States. Today’s society believes that obesity is mainly caused by these factors: unhealthy eating behavior, medical conditions, genetics, and habits.

As society develops, people’s lives have become rich, accompanied by unhealthy eating behavior. However, unhealthy eating behavior is one of the most important factors leading to obesity. Among them, overeating is a primary cause. Modern people are under pressure from all aspects of their lives. A survey shows that people with high social pressure consume more calories. Physiologically speaking, higher-calorie foods bring greater pleasure to the brain, thereby alleviating stress. In addition, most people do not have strong self-discipline; they hardly limit their calorie intake. This leads to the second point of unhealthy eating behavior – picky eating. People enjoy eating high-calorie food even though it makes them fat since most junk food tastes better than healthy food. The brain’s incentive mechanism makes it increasingly hard for people to resist junk food. Then people not only get fatter and fatter but also will be malnutrition. in today’s society, unhealthy eating behavior is the most common cause of obesity. Because it could happen to any of us.

Medical condition is also a major cause of obesity. Conditions can be broken down into two categories — mental and physical. In today’s society, psychological problem has become a prevailing issue that troubles many people. Many people have different degrees of depression and mental illness. In fact, depression and mental illness do not directly contribute to obesity, but treatment drugs do. Some drugs can affect the appetite regulation center of the human brain while treating mental problems. As a result, the body cannot control its appetite and begins to gain weight. Similarly, there are some drugs that have calming effects. This reduces physical activity and leads to fat hoarding. On the other hand, physical diseases can also lead to obesity. Hypothyroidism will reduce thyroid hormone secretion. However, the function of thyroid hormones is to stimulate the body to consume energy for heat production. When the thyroid hormone is lowered, the body stores more fat on the premise of eating the same food, which leads to obesity. Of course, there are also some physical injuries that can lead to obesity. Take my brother for example. He was badly injured in a car accident. He had to stay in bed for three months. During those three months, he consumed much more nutrition than usual in order to recover as soon as possible. Because of the muscle tissue damage and decreased hormone secretion, he gained weight very quickly. By the end of his recovery, he gained 30 kilograms. Obviously, diseases can cause obesity very easily. And at this time, there is no way to prevent obesity.

Finally, I have to mention genetics and habits. Although this is rare, it does cause obesity. Some people are unlucky because they are naturally fatter than others. This is a genetic problem. Generally speaking, if a person’s parents are obese, then the person is more likely to be obese. However, the fundamental problem is gene expression. As of 2006, more than 41 of sites on the human genome have been linked to the development of obesity when a favorable environment is present. (Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss, 2006) People with two copies of the FTO gene (fat mass and obesity-associated gene) have been found on average to weigh 3–4 kg more and have a 1.67-fold greater risk of obesity compared with those without the risk allele. (FTO: the first gene contributing to common forms of human obesity, 2008) The differences in BMI between people that are due to genetics vary depending on the population examined from 6% to 85%. (Genetic epidemiology of obesity, 2007) When different obesity genes are expressed at the same time, they can cause significant obesity. Then, habits and customs are one of the reasons. The sedentary lifestyle is also one of the reasons why the number of obese people is increasing. For example, a survey showed that 27% of people in Canada with sedentary lifestyles suffer from obesity, but only 19.6% of people with normal activities suffer from obesity. Being sedentary reduces their metabolism and presses the nervous system, resulting in fat accumulation. Essentially, the main cause of obesity in this group is not to exercise and live in single lifestyle. If such people change their lifestyle, they will lose weight thus leading to obesity.

In a word, unhealthy eating behaviors, medical conditions genetics, and habits are very likely to be obesity. However, obesity can cause not only a bad body shape but also many serious diseases, such as diabetes, hypertension, cardiovascular and cerebrovascular diseases, and so on. Obesity patients who are too severe are even at risk for their lives. Surveys have shown that, on average, severe obesity (BMI greater than 40) reduces life expectancy by 10 years. Of course, there are also many ways to avoid obesity. The most important part is to establish a good concept of healthy life and supplement the basic knowledge of healthy life. On this basis, as long as scientific diet, hard exercise, and good habits are adjusted, obesity will be farther and farther away from people.

Genes have been in control of human traits since humans have been a species. However, what genes control beyond physical traits is not as well known. Therefore this prompts the question to what extent genes affect happiness. This question is becoming more prevalent with the rise in genetic editing and what could be done with genetic engineering to further push the human race. This question ties into the stimulus material “Genes, Economics, and Happiness” which goes into depth about genes and their links to happiness in ways such as money and social class. Genes Economics and Happiness also talks about DNA strands that are the direct cause of happiness and whether or not scientists have the technology to determine what exact genes affect human emotions. Another study shows that genes play a major role in the regulation of your own brain’s serotonin and dopamine levels(Ebstein et al 1996; Hamer 1996) which could prove that genes could not only affect your happiness directly but indirectly as well. Serotonin is one of the chemicals in the brain that is linked to overall happiness and well-being in a person(Medical News Today). But as genes have been studied to affect a person’s happiness it has also been stated that genes can cause depression or lower happiness levels as well( Dennis S. Charney). This question has been looked at from many perspectives/lenses such as economic, social, medical, and scientific with different arguments following suit mainly about how much genes affect an individual’s happiness. The exact amount genes play in one’s personality is still unknown and the main argument is how much do genes affect a person’s happiness and life evaluation. This question has been answered in many different ways but the one thing that is hard to have a solid standpoint on is what gene exactly affects happiness and how much genes really play in one’s happiness.

From a medical perspective, the exact amount genes play into one’s happiness is unknown but one of the more widespread ideologies is the 50-10-40% formula(Sonja Lyubomirksy). Which states that 50% of how happy you are is genetics, 10% is your state of mind, and the last 40% is one’s environment. This formula shows how much of your happiness is believed to be inherited or predetermined by one’s genetics which relates to the philosophy of “Genes. Economics, and Happiness” in the fact that genes do play a role in happiness but differ in their findings and motives with genes economics and happiness not finding the exact gene that effects happiness but narrowing down by a sizable amount. The article also states that it is believed that at the very least genes play at least a 33% role in one’s happiness and very well could be higher but they do not believe that it could be lower. This is not always true as for some individuals the environment may play more of a role in one’s attitude or play less of a role but this scale is the most widespread. Although immense amounts of research have been done on how genes affect a person’s happiness or life satisfaction etc. Studies also show genes affect people’s anger and tolerance levels as well. In a study done by Yinghui Guo, Huiyun Zhang, Jie Gao Sheng, Wei Chunhong, SongPeng, and Sun Mingqi Qiao they studied rats’ behaviors and how they reacted to certain events. The study found multiple genes that were linked to depression, anger management, and irritability(yinghui Guo) meaning that genes may play a lot larger roles in how people obtain their emotions and behaviors. These all show how genes can directly affect a person’s emotions whether it’s in a positive aspect like being overall happier.

From an economic perspective, genes do affect your socioeconomic status which in turn could affect a person’s life satisfaction and or happiness overall. One of the biggest genetic studies in recent years was done by a group of Harvard economists(New York Times) This group’s goal was to find out how successful a person could be just from someone’s genes. The study had a ranking system that ranked people’s chances at success on a scale with the top of the rankings having a 57 percent chance at graduating with a bachelor’s degree and the bottom of the scale having a 12 Percent chance at graduation with a bachelor degree ( Ward, Jacob). Having any form of a college degree more than doubles one’s odds of obtaining a job as well as increases the chance of obtaining a high-paying job(Napach Bernice), a high-paying job is considered to be $65,000 yearly(USA Today). This ties into people becoming poverty-struck when unable to find a job due to not having a steady income or simply not making enough money although working full time. A study states “In conclusion of this study they’ve found that there is an indirect effect on happiness because people with higher income levels do have a higher probability of finding employment and report higher levels of happiness.” It also is very difficult to escape poverty with only 56% getting out after one year(Stevens Ann) and after 7 years a 17% chance to escape poverty. This ties into happiness because people who are in poverty seem to exert lower happiness levels and overall less energy. The stimulus material “Genes, Economics and Happiness” also talks about economics and genes, mainly discussing the happiness gene but also talks about the income of the people they selected for the study. However, some studies have directly linked income to genes. But whether genes affect one’s income directly is a controversial topic because of all the different things that could affect it like what kind of environment you are born into, what kind of diseases you are born with, how much your parents influence your life, etc. However, some studies have concluded genes do affect one’s income in a direct manner and make some people more likely to just make less money solely from their genes alone. An example of this is a study done by Jay Gould he believed that some countries were in a poverty state because of the citizen’s genetic makeup. This study however came under heavy fire due to the fact that many found it to be racist and genetic determinism. However, some people believe this paper to be very valuable to the opening of the now very popular study of genes and how they affect people on a more important level.

Genes do not only control how happy you are but how you obtain happiness as well. In the stimulus material “The Happiness Project” the author talks about how he is happy because his daughter was happy when he took her to Disneyland. Nations that have a certain allele in the fatty acid amide hydrolase state that they perceive things in a happier state of mind and overall believe themselves to be happier than others(Springer). According to a study done by WebMD, it states” People with a gene variation including one or two A’s were found to have less optimism, mastery, and self-esteem, and more symptoms of depression than people with a variation including two G’s.” Studies have also found that genes can affect whether or not a person is optimistic or pessimistic(Mann Denise). This in turn can affect a person’s happiness because it is proven that people who are optimistic tend to be happier and healthier than those who are not (LoveEquals). This applies to people who are pessimistic as well meaning that pessimistic people tend to be unhappier because of the negative outlook they have on life. One may argue that being pessimistic or optimistic does not necessarily determine a person’s attitude or personality and this statement is true but people who have these personalities are more often than not going to fall into being unhappier or happier.

Lastly not only do genes affect our happiness but life evaluation as well. In the stimulus material “High income improves evaluation of life but not emotional well-being”, Life evaluation refers to the thoughts that people have about their life when they think about it. Since genes have been shown to affect a person’s income this in turn affects a person’s life evaluation as well. The stimulus material “High income improves evaluation of life but not emotional well-being” talks about how income can make people evaluate their lives in a more positive light. However, having a higher income does not show any improvement in a person’s well-being consistently. Though some may say this all depends on a person’s situation and how much money means to them during a certain period of time the study used people from many different ranges of income. Life evaluation is not only affected by happiness but is indirectly affected by it in many ways. Some forms are Marriage, Income, Family, and Environment which all are not exactly happiness but can contribute to a person’s happiness or make a person not as happy as well. Environment plays one of the biggest roles in one life evaluation because of how some people perceive money. If a rich person acquires something they don’t need they will acquire as much happiness as someone who is not as rich when they acquire something that they do need like a car or something like that.

In conclusion, Genes do affect a person’s happiness in many different ways, whether it’s how they feel happiness, how happy in general a person is, how they look at life, or just how happy they feel as an individual. With the rising popularity of genetic editing a possible outcome of discovering the “happiness gene” could be directly editing this gene making the world an overall happier place. This doesn’t necessarily mean making everyone experience only what’s considered happy emotions, however, if the world became overall more happy then it would make it a better place making things such as war and conflict a lot less likely. Another outcome of determining what gene makes people happy is it makes medication more easily personalized. For example, if your child is born without inheriting certain happiness genes they may be more susceptible to being depressed or suicidal making it easier for doctors to get Medicine to the children who need it faster and more consistently. However, since this is all in theory it is unknown how long or how accurate this method could be. So a child could be incorrectly prescribed medicine and this could lead to many problems for a child’s mental and physical health. Overall further funding and time should be put into researching genes as the benefits from locating what genes make people happy to what extent they do to help further the understanding of the genetics of humans and how to further advance it.

References:

1. Charney, Dennis S., and Husseini K. Manji. “Life Stress, Genes, and Depression: Multiple Pathways Lead to Increased Risk and New Opportunities for Intervention.” Science Signaling, American Association for the Advancement of Science, 23 Mar. 2004, stke.sciencemag.org/content/2004/225/re5.abstract.
2. De Neve, Jan-Emmanuel, et al. “Genes, Economics, and Happiness.” Journal of Neuroscience, Psychology, and Economics, U.S. National Library of Medicine, Nov. 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3858957/.
3. “Genes May Contribute to Making Some Nations Happier than Others.” ScienceDaily, ScienceDaily, 14 Jan. 2016, www.sciencedaily.com/releases/2016/01/160114113520.htm.
4. Guo, et al. “Study of Genes Associated with the ‘Anger-in’ and ‘Anger-out’ Emotions of Humans Using a Rat Model.” Experimental and Therapeutic Medicine, Spandidos Publications, 1 Apr. 2015, www.spandidos-publications.com/etm/9/4/1448.
5. Kahneman, Daniel. Does Money Buy Happiness? Sept. 2010, wws.princeton.edu/sites/default/files/content/docs/news/Happiness_Money_Summary.pdf.
6. “Transitions into & out of Poverty in the United States.” UC Davis Center for Poverty Research, poverty.ucdavis.edu/policy-brief/transitions-out-poverty-united-states.
7. Springer. “Genes May Contribute to Making Some Nations Happier than Others.” ScienceDaily, ScienceDaily, 14 Jan. 2016, www.sciencedaily.com/releases/2016/01/160114113520.htm.
8. Stevens, Ann. “Transitions into & out of Poverty in the United States.” UC Davis Center for Poverty Research, poverty.ucdavis.edu/policy-brief/transitions-out-poverty-united-states.
9. Ward, Jacob. “The ‘Geno-Economists’ Say DNA Can Predict Our Chances of Success.” The New York Times, The New York Times, 16 Nov. 2018, www.nytimes.com/interactive/2018/11/16/magazine/tech-design-economics-genes.html.

Genes have been in control of human traits since humans have been a species. However, what genes control beyond physical traits is not as well known. Therefore this prompts the question to what extent genes affect happiness. This question is becoming more prevalent with the rise in genetic editing and what could be done with genetic engineering to further push the human race. This question ties into the stimulus material “Genes, Economics, and Happiness” which goes into depth about genes and their links to happiness in ways such as money and social class. Genes Economics and Happiness also talks about DNA strands that are the direct cause of happiness and whether or not scientists have the technology to determine what exact genes affect human emotions. Another study shows that genes play a major role in the regulation of your own brain’s serotonin and dopamine levels(Ebstein et al 1996; Hamer 1996) which could prove that genes could not only affect your happiness directly but indirectly as well. Serotonin is one of the chemicals in the brain that is linked to overall happiness and well-being in a person(Medical News Today). But as genes have been studied to affect a person’s happiness it has also been stated that genes can cause depression or lower happiness levels as well( Dennis S. Charney). This question has been looked at from many perspectives/lenses such as economic, social, medical, and scientific with different arguments following suit mainly about how much genes affect an individual’s happiness. The exact amount genes play in one’s personality is still unknown and the main argument is how much do genes affect a person’s happiness and life evaluation. This question has been answered in many different ways but the one thing that is hard to have a solid standpoint on is what gene exactly affects happiness and how much genes really play in one’s happiness.

From a medical perspective, the exact amount genes play into one’s happiness is unknown but one of the more widespread ideologies is the 50-10-40% formula(Sonja Lyubomirksy). Which states that 50% of how happy you are is genetics, 10% is your state of mind, and the last 40% is one’s environment. This formula shows how much of your happiness is believed to be inherited or predetermined by one’s genetics which relates to the philosophy of “Genes. Economics, and Happiness” in the fact that genes do play a role in happiness but differ in their findings and motives with genes economics and happiness not finding the exact gene that effects happiness but narrowing down by a sizable amount. The article also states that it is believed that at the very least genes play at least a 33% role in one’s happiness and very well could be higher but they do not believe that it could be lower. This is not always true as for some individuals the environment may play more of a role in one’s attitude or play less of a role but this scale is the most widespread. Although immense amounts of research have been done on how genes affect a person’s happiness or life satisfaction etc. Studies also show genes affect people’s anger and tolerance levels as well. In a study done by Yinghui Guo, Huiyun Zhang, Jie Gao Sheng, Wei Chunhong, SongPeng, and Sun Mingqi Qiao they studied rats’ behaviors and how they reacted to certain events. The study found multiple genes that were linked to depression, anger management, and irritability(yinghui Guo) meaning that genes may play a lot larger roles in how people obtain their emotions and behaviors. These all show how genes can directly affect a person’s emotions whether it’s in a positive aspect like being overall happier.

From an economic perspective, genes do affect your socioeconomic status which in turn could affect a person’s life satisfaction and or happiness overall. One of the biggest genetic studies in recent years was done by a group of Harvard economists(New York Times) This group’s goal was to find out how successful a person could be just from someone’s genes. The study had a ranking system that ranked people’s chances at success on a scale with the top of the rankings having a 57 percent chance at graduating with a bachelor’s degree and the bottom of the scale having a 12 Percent chance at graduation with a bachelor degree ( Ward, Jacob). Having any form of a college degree more than doubles one’s odds of obtaining a job as well as increases the chance of obtaining a high-paying job(Napach Bernice), a high-paying job is considered to be $65,000 yearly(USA Today). This ties into people becoming poverty-struck when unable to find a job due to not having a steady income or simply not making enough money although working full time. A study states “In conclusion of this study they’ve found that there is an indirect effect on happiness because people with higher income levels do have a higher probability of finding employment and report higher levels of happiness.” It also is very difficult to escape poverty with only 56% getting out after one year(Stevens Ann) and after 7 years a 17% chance to escape poverty. This ties into happiness because people who are in poverty seem to exert lower happiness levels and overall less energy. The stimulus material “Genes, Economics and Happiness” also talks about economics and genes, mainly discussing the happiness gene but also talks about the income of the people they selected for the study. However, some studies have directly linked income to genes. But whether genes affect one’s income directly is a controversial topic because of all the different things that could affect it like what kind of environment you are born into, what kind of diseases you are born with, how much your parents influence your life, etc. However, some studies have concluded genes do affect one’s income in a direct manner and make some people more likely to just make less money solely from their genes alone. An example of this is a study done by Jay Gould he believed that some countries were in a poverty state because of the citizen’s genetic makeup. This study however came under heavy fire due to the fact that many found it to be racist and genetic determinism. However, some people believe this paper to be very valuable to the opening of the now very popular study of genes and how they affect people on a more important level.

Genes do not only control how happy you are but how you obtain happiness as well. In the stimulus material “The Happiness Project” the author talks about how he is happy because his daughter was happy when he took her to Disneyland. Nations that have a certain allele in the fatty acid amide hydrolase state that they perceive things in a happier state of mind and overall believe themselves to be happier than others(Springer). According to a study done by WebMD, it states” People with a gene variation including one or two A’s were found to have less optimism, mastery, and self-esteem, and more symptoms of depression than people with a variation including two G’s.” Studies have also found that genes can affect whether or not a person is optimistic or pessimistic(Mann Denise). This in turn can affect a person’s happiness because it is proven that people who are optimistic tend to be happier and healthier than those who are not (LoveEquals). This applies to people who are pessimistic as well meaning that pessimistic people tend to be unhappier because of the negative outlook they have on life. One may argue that being pessimistic or optimistic does not necessarily determine a person’s attitude or personality and this statement is true but people who have these personalities are more often than not going to fall into being unhappier or happier.

Lastly not only do genes affect our happiness but life evaluation as well. In the stimulus material “High income improves evaluation of life but not emotional well-being”, Life evaluation refers to the thoughts that people have about their life when they think about it. Since genes have been shown to affect a person’s income this in turn affects a person’s life evaluation as well. The stimulus material “High income improves evaluation of life but not emotional well-being” talks about how income can make people evaluate their lives in a more positive light. However, having a higher income does not show any improvement in a person’s well-being consistently. Though some may say this all depends on a person’s situation and how much money means to them during a certain period of time the study used people from many different ranges of income. Life evaluation is not only affected by happiness but is indirectly affected by it in many ways. Some forms are Marriage, Income, Family, and Environment which all are not exactly happiness but can contribute to a person’s happiness or make a person not as happy as well. Environment plays one of the biggest roles in one life evaluation because of how some people perceive money. If a rich person acquires something they don’t need they will acquire as much happiness as someone who is not as rich when they acquire something that they do need like a car or something like that.

In conclusion, Genes do affect a person’s happiness in many different ways, whether it’s how they feel happiness, how happy in general a person is, how they look at life, or just how happy they feel as an individual. With the rising popularity of genetic editing a possible outcome of discovering the “happiness gene” could be directly editing this gene making the world an overall happier place. This doesn’t necessarily mean making everyone experience only what’s considered happy emotions, however, if the world became overall more happy then it would make it a better place making things such as war and conflict a lot less likely. Another outcome of determining what gene makes people happy is it makes medication more easily personalized. For example, if your child is born without inheriting certain happiness genes they may be more susceptible to being depressed or suicidal making it easier for doctors to get Medicine to the children who need it faster and more consistently. However, since this is all in theory it is unknown how long or how accurate this method could be. So a child could be incorrectly prescribed medicine and this could lead to many problems for a child’s mental and physical health. Overall further funding and time should be put into researching genes as the benefits from locating what genes make people happy to what extent they do to help further the understanding of the genetics of humans and how to further advance it.

References:

1. Charney, Dennis S., and Husseini K. Manji. “Life Stress, Genes, and Depression: Multiple Pathways Lead to Increased Risk and New Opportunities for Intervention.” Science Signaling, American Association for the Advancement of Science, 23 Mar. 2004, stke.sciencemag.org/content/2004/225/re5.abstract.
2. De Neve, Jan-Emmanuel, et al. “Genes, Economics, and Happiness.” Journal of Neuroscience, Psychology, and Economics, U.S. National Library of Medicine, Nov. 2012, www.ncbi.nlm.nih.gov/pmc/articles/PMC3858957/.
3. “Genes May Contribute to Making Some Nations Happier than Others.” ScienceDaily, ScienceDaily, 14 Jan. 2016, www.sciencedaily.com/releases/2016/01/160114113520.htm.
4. Guo, et al. “Study of Genes Associated with the ‘Anger-in’ and ‘Anger-out’ Emotions of Humans Using a Rat Model.” Experimental and Therapeutic Medicine, Spandidos Publications, 1 Apr. 2015, www.spandidos-publications.com/etm/9/4/1448.
5. Kahneman, Daniel. Does Money Buy Happiness? Sept. 2010, wws.princeton.edu/sites/default/files/content/docs/news/Happiness_Money_Summary.pdf.
6. “Transitions into & out of Poverty in the United States.” UC Davis Center for Poverty Research, poverty.ucdavis.edu/policy-brief/transitions-out-poverty-united-states.
7. Springer. “Genes May Contribute to Making Some Nations Happier than Others.” ScienceDaily, ScienceDaily, 14 Jan. 2016, www.sciencedaily.com/releases/2016/01/160114113520.htm.
8. Stevens, Ann. “Transitions into & out of Poverty in the United States.” UC Davis Center for Poverty Research, poverty.ucdavis.edu/policy-brief/transitions-out-poverty-united-states.
9. Ward, Jacob. “The ‘Geno-Economists’ Say DNA Can Predict Our Chances of Success.” The New York Times, The New York Times, 16 Nov. 2018, www.nytimes.com/interactive/2018/11/16/magazine/tech-design-economics-genes.html.

The issues of gene-environment interactions are widely discussed in the field of the modern medicine in relation to the possibilities which can be provided for treating diseases with references to the factor of gene-environment interaction. Researchers pay much attention to examining the interaction between the genetic information and environmental issues as significant factors for developing or preventing definite diseases (Mikail, 2008).

In their article “Multiple Analytical Approaches Reveal Distinct Gene-Environment Interactions in Smokers and Non Smokers in Lung Cancer”, the group of Indian researchers with Rakhshan Ihsan and Pradeep Chauhan present the results of the study which was conducted in order to analyze the correlation between genetic and environmental factors and the development of lung cancer in smokers and non-smokers.

The importance of the investigation depends on the fact the researchers have concentrated on using multiple approaches to discuss the problem.

A. The main objective of the researchers’ study was to examine the cases of lung cancer with references to the multi-analytical approach with the help of which it was possible to analyze the impact of genetic and environmental factors on the disease’s development in complex.

Moreover, the researchers have focused on examining the cancer’s pathogenetic mechanism in relation to smokers and non-smokers. It was necessary to use the multi-analytical approach in order to determine the risk factors for smokers and non-smokers separately according to the problem of gene-environment interaction (Ihsan et al., 2011).

B. To complete the objective of the study, the researchers have determined the sample of 188 persons who suffer from lung cancer. Smokers and non-smokers were included into the group. To control the results of the study, the group of 290 patients was formed. The researchers focused on studying the participants’ history of disease with references to their genotype and such negative habits as smoking (Ihsan et al., 2011).

It was important to analyze the connection between the definite genotype and the risk of lung cancer and the impact of smoking on the disease’s development. The researchers used such approaches as logistic regression (LR), classification and regression tree (CART), and multifactor dimensionality reduction (MDR) in order to present the statistical data in relation to the correlation between genetic and environmental risk factors for the disease’s development (Ihsan et al., 2011).

Using three approaches to analyzing the study’s data, the researchers determined genotypes which are characterized by the high level of risk to lung cancer with references to such factor as smoking. According to the study’s results, smoking can be discussed as one of the most influential factors for the development of lung cancer and for worsening the patient’s state. The researchers have found that CYP1A1*2A polymorphism can be discussed as extremely risky for the development of lung cancer.

Moreover, EPHX1 Tyr113His and SULT1A1 Arg213His types can be considered as associated with the low risks. It was also stated that smokers with EPHX1 113TC (Tyr/His), SULT1A1 213GG (Arg/Arg) genotypes are also at risk to suffer from lung cancer (Ihsan et al., 2011). The usage of three approaches to analyzing the data in relation to the sample and control group is effective for providing the complex picture with references to all the aspects of the problem.

Furthermore, the researchers concentrate on determining not only the impact of smoking on the development of lung cancer but also the effect of such negative habits as tobacco chewing and betel quid chewing on lung cancer in the group of participants. Thus, the genotype distribution was analyzed with references to smoking as the influential environmental factor for causing lung cancer.

C. The previous researches in the field provide the findings according to which the risk of lung cancer’s development is based on definite individuals’ abilities to metabolize carcinogens which can be different in relation to their genotype. However, it is also important to refer to the environmental factors.

The problem is in the fact the singular investigations in relation to genetic factors or environmental factors do not provide the complex picture of the causes for the lung cancer’s development. That is why, it is significant to focus on the multi-analytical approach used for discussing the problem.

The research is useful because of the usage of multiple analytical methods for assessing the risk factors for cancer and their correlation. Thus, the interaction of xenobiotic metabolizing genes and such factors as smoking was examined.

The role of gene-environment interactions for determining the risk factors was supported with the help of several statistical approaches. The significance of the research is accentuated by the possibility to use its results for the further investigations in the field in order to determine the role of genetic and environmental factors in their interaction for provoking lung cancer’s progress.

Moreover, the researchers emphasize the fact that their multi-approach to examining the disease’s causes is more effective in comparison with the traditional LR method (Ihsan et al., 2011). The researches’ results are useful for assessing the connection between genetic polymorphisms and cancer susceptibility with references to such environmental factors as smoking.

References

Ihsan R., Chauhan P. S., Mishra A. K., Yadav D.S., Kaushal M., et al. (2011). Multiple analytical approaches reveal distinct gene-environment interactions in smokers and non smokers in lung cancer. PLOS ONE, 6(12), e29431. doi:10.1371/journal.pone.0029431.

Mikail, C. N. (2008). Public health genomics: The essentials. USA: Jossey-Bass.