Essay Sample on Seasonal Moods: Exploring the Correlation Between Photoperiods and Emotions

Introduction

The seasonal moods changes, especially in winter, have always been a debate by many scholars across the world. Some do not comprehend the association and the relationship between the despair or emotions and the photoperiods in winter (Lam & Levitan, 2000). Such view the relationship is metaphoric while for others it is argued that there is a clear correlation between the length of the daylight in winter and the personal moods. The distinct association between the two was only understood in very recent researches(Mugnusson, 2000). One of the known mood change associated with changes in the seasons is the Seasonal Affective Disorder.

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The study of the Seasonal Affective Disorder provides interesting implications of how the environmental cues affect the brain which is the regulating organ of the nervous system. The Seasonal Affective Disorder is often complicated, and sometimes it is thought to be a recurring depression in winter (Lam et al., 2000). However, it is recorded that especially more vulnerable people often experience the disorder during winter. Such vulnerable people often have lower light associated depression threshold. People often react differently to seasonal changes (Mugnusson, 2000). For instance, among thirty-five million Americans, ten million may often experience Seasonal Affective Disorder while the remaining twenty-five million with subsyndromal Seasonal Affective Disorder(Lam et al., 2000). Although most of the people in the northern hemispheres often undergo some mild depressions associated with the seasonal changes, about ten percent are diagnosed with Seasonal Affective Disorder.

Several pieces of research have shown a relationship between the genetic composition, the brain and the changes in moods and disorders related to the changes in the dark-light cycles (Lam et al., 2000). The gene polymorphism together with the seasonal changes has substantial impacts on the behavior and the moods of the affected patients. Individuals with close relatives experiencing seasonal disorders can also suffer from the condition. This is because the seasonal disorder is genetically inherited. The patient's biological clock can contribute to the severity of the seasonal mood changes. Various physiological conditions of the body such as the circadian rhythm change often contribute immensely to this phenomenon (Mugnusson, 2000). Furthermore, research has shown that availability and lack of sunlight affect the production and subsequent release of certain chemicals in the brain. Imbalances in the brain chemicals result in an awful feeling and a low mood, especially during winter. Weight gains, depressions often characterize seasonal Affective disorder, and lack of energy among others (Lam & Levitan, 2000).

Several treatment methods have been proposed to deal with seasonal disorders and mood changes during winter. Some of these treatment methods include psychotherapy, medications, and light therapy. Also referred to as phototherapy, light therapy the patient sits in a single lightbox (Mugnusson, 2000). They are then exposed to very bright lights within the first hour of each day. Phototherapy mimics the natural light condition of the outdoor. The change in brain chemicals is linked with the individuals' moods (Lam & Levitan, 2000).

Some medication can also be offered to the patients including the extended version of bupropion, which facilitates the prevention of the depressive episodes for people with the history of mood changes during winters. Psychotherapy, which is referred to as talk therapy, is the other avenue to treat such conditions (Mugnusson, 2000). Cognitive behavioral therapy helps in the identification and the engagement of the patients to manage stress and help them cope with the situation.

The Concept of Gene and Chromosomal Mutation

Scientists have described gene mutations as the permanent change or alteration in the DNA sequence that builds up the gene. Mutations often have size variations and can affect any part of the single and large chromosomes (Baba, Ara, Hasegawa, Takai, Okumura, Baba, & Mori, 2006). Gene mutations are classified into hereditary mutations and the somatic or the acquired mutation. Unlike the somatic mutations, gene mutations are often inherited from the parents and can present throughout the lives of the offsprings in almost all the cells of the body (Van Der Zwaag, Van Rijsingen, Asimaki, Jongbloed, Van Veldhuisen, Wiesfeld,...& Christiaans, 2012). Such mutations are described as germline mutations since they occur in the reproductive cells, i.e., the egg and the sperm cell. Upon the uniting of the cells from both the parents, the resultant mass of the cell comprises the genetic makeup of both the parents (Kaelin et al., 2005). Suppose the DNA from the parents have contains a mutagen then the fertilized egg will contain the mutation.

However, in the somatic or the acquired mutation, the mutation occurs sometimes in the life of a person. Environmental variations and conditions such as exposure to Ultraviolet rays of the sun may result in somatic mutation (Baba et al., 2006). However, a somatic mutation can also occur when the DNA itself in the cell division process experiences an error. This kind of mutation can never b transferred to the next generations unlike the case of hereditary mutation (Van Der Zwaag et al., 2012).

Moreover, there is a new kind of gene mutation referred to as the de novo mutation. It is neither somatic nor hereditary (Van Der Zwaag et al., 2012). This type of mutation can often appear in the reproductive cells but absent in the rest of the person's cells. This mutation can be absent in the individual gametes of the parents but are experienced soon after fertilization of the eggs. This kind of mutation can be used to explain the reason why a child may experience mutation in all the cells yet the parents do not have the mutation in their cells (Baba et al., 2006). Mutations can occur either in the chromosomes or in the genes. The mutation experienced in the genes is called the gene mutation while that experienced in the chromosome is referred to as chromosomal mutations (Kaelin et al., 2005). Gene mutation involves the alteration in the sequence of the nucleotides that are found within the DNA chain. The information in the DNA is altered and results in variations in the proteins produced. For example, in the case of Sickle cell anemia, the mutation results in a slight change in the protein molecule that forms the hemoglobin. Many scientists argue that such mutations can be caused by radiations such as the x-rays, the gamma rays, cosmic and ultraviolet rays among others. Additionally, certain chemicals referred to as mutagens may result in the alteration of the nucleotide within the DNA molecules. The chemical mutagens include formaldehyde, nitrous acid, ethyl ethane, etc.

Chromosomal mutations, on the other hand, result from the alteration in the structure of a part or the whole chromosome (Van Der Zwaag et al., 2012). These structural variations can be due to chemicals, radiations and in some cases even viral infections. Changes are experienced in the chromosomes in the process of cell division (Kaelin et al., 2005). Autosomal disorders such as cystic fibrosis and sickle cell anemia are caused when the genes are situated on one of the autosomes (Baba et al., 2006). These disorders are either recessive or dominant. Autosomal recessive portrays one of the several ways in which diseases and disorders can be passed through the family lineage (Kaelin et al., 2005). It occurs in the presence of two abnormal gene copies.

Autosomal dominance is the inheritance patterns whereby the individual has a single copy of the gene mutant and one other normal gene within the pair of the autosomal chromosomes (Baba et al., 2006). The probability of the individuals with autosomal dominant disorder passing the disorder to the next generation is often a half (Van Der Zwaag et al., 2012).

References

Baba, T., Ara, T., Hasegawa, M., Takai, Y., Okumura, Y., Baba, M., & Mori, H. (2006). Construction of Escherichia coli K12 inframe, singlegene knockout mutants: the Keio collection. Molecular systems biology, 2(1). Doi 10.1038/msb4100050.

Kaelin Jr, W. G. (2005). The concept of synthetic lethality in the context of anticancer therapy. Nature reviews cancer, 5(9), 689.https://www.nature.com/articles/nrc1691

Lam, R. W., & Levitan, R. D. (2000). Pathophysiology of seasonal affective disorder: a review. Journal of Psychiatry and Neuroscience, 25(5), 469.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1408021/

Magnusson, A. (2000). An overview of epidemiological studies on the seasonal affective disorder. Acta Psychiatrica Scandinavica, 101(3), 176-184.Doi: 10.1034/j.1600-0447.2000.101003176.x

Van Der Zwaag, P. A., Van Rijsingen, I. A., Asimaki, A., Jongbloed, J. D., Van Veldhuisen, D. J., Wiesfeld, A. C. ...& Christiaans, I. (2012). Phospholamban R14del mutation in patients diagnosed with dilated cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy: evidence supporting the concept of arrhythmogenic cardiomyopathy. European journal of heart failure, 14(11), 1199-1207.Doi:10.1093/eurjhf/hfs119.