How to avoid obesity related to Plastic Chemical BPA

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This is going to be role in this paper is a research. all the paper it have to be focus as a medical researcher.

  • Medical Researcher – Medical condition expert –Confirms an increased rate of a medical condition upon discovery of the presence of a toxin or the absence of nutrients.
  • Is very important to include the following sections:
  • · Abstract · Background/literature review · Materials and Methods · Results · Conclusion . References (APA formatting) While there most likely will be overlap in the literature review the majority of the papers will focus on each student’s assigned role.
  • All the assignment have to be in APA format
  • Im going to attach you a sample Work is another title but you need to follow the same template.
  • It have to be at less 15 pages plus the references

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1 Running Head: THE DEADLY BLOOM The Deadly Bloom Awesome Student West Coast University CAPS400 Professor Kathryn Ayres March 18th, 2017 2 THE DEADLY BLOOM The Deadly Bloom Abstract Alzheimer’s patients are suspected to have an increase level of Beta-methyl- amino-L-alanine (BMAA). BMAA is an environmental toxin produced by cyanobacteria and is linked to algae blooms. Found in sea creatures such as sharks, fish and shellfish that ingest algae, the neurotoxin is believed to trigger the neurodegenerative disease Alzheimer’s. The examiners performed an autopsy and removed the entire bran from forty deceased bodies. The deceased were separated into a control and experimental group. The experimental group consisted of twenty of the deceased who had diagnoses of Alzheimer’s while living and the remaining twenty had not victims of Alzheimer’s disease. The brains were then placed in a cylinder filled with fluid to distinguish the average volume between the control and experimental group. The results came back to the experimental group suffering from brain atrophy and the control group having no brain atrophy. Medical examiners also used an enzyme-linked immonosorbent assay (ELISA) to disclose the presence of the toxin in the brain tissue of Alzheimer’s patients. The ELISA test proved that BMAA was present in eighteen of the brains of the deceased diagnosed with Alzheimer’s while living. The findings also showed that BMAA was present in three of the healthy brains. To further understand the relation between Alzheimer’s and BMAA scientist should further investigate BMAA. More funding will go towards investigation. The safety information for seafood will contain both a safety summary and a complete toxicological profile. Exposure to BMAA should also decrease to reduce the cost of health care cost to Alzheimer’s. 3 THE DEADLY BLOOM Literature Review Alzheimer’s disease is an illness that affects the brain and includes memory loss causing individuals to forget about loved ones and interfering with social skills. The disease attacks nerve cells of the brain, which then weakens a person’s ability to recall certain aspects of lives (Alzheimer’s Association, n.d). Having this complex illness interferes with daily routines, eating and taking medications have to be reminded by an aid or a family member. Impaired judgments, personality changes, annoyance are some of the symptoms (Web Md, n.d). Pictures, sticky notes are placed on items for remembrance. Ranked number sixth leading cause of death in the United States, Alzheimer’s is irreversible (National Institute on Aging, 2016). Early onset Alzheimer’s occurs in people as young as thirty years old. Late onset Alzheimer’s occurs after sixty years old (NIH Senior Heath, 2015). The disease progresses slowly for some and faster for others. Mental abilities become compromised. Conversations are challenging as a result of compromised mental abilities (Alzheimer’s Association, n.d). It is categorized into three stages, mild, moderate and severe Alzheimer’s. Individuals are diagnosed with the illness during mild Alzheimer’s. Driving and working are capable, however, during this stage a person is experiencing memory lapses. Family members start to take notice of struggles (Alzheimer’s Association, n.d). Close relatives notice difficulties with paying bills handling money and personality changes (National Institute on Aging, 2016). Doctors also detect problems in concentration and memory in this stage (Alzheimer’s Association, n.d). THE DEADLY BLOOM 4 The second stage is moderate Alzheimer’s. “Damage occurs in areas of the brain that control language, reasoning, conscious and sensory processing” (National Institute on Aging, 2016). Individuals require more help than the previous stage. There is an increase in memory loss, an urgency and uncontrollable time use the bathroom. Remembering names, faces and multitasking worsens. “At this stage people have hallucinations, delusions and paranoia” (National Institute on Aging, 2016). More time is spent with family members and not alone. The final stage called severe Alzheimer’s is where assistance is needed at all times. Memory is compromised; people do not remember where they live or family member names, most times are spent in bed “Plaques and tangles spread throughout the brain and brain tissue shrinks” (National Institute on Aging). Joining in conversations does not happen and personalities change dramatically (Alzheimer’s Association, n.d). The ultimate way to diagnose Alzheimer’s is to perform an autopsy. Doctors look at the brain tissues of the deceases to out find whether plaques and tangles exist (NIH Senior Health, 2015). Neurologists can make a diagnosis by asking patients and family members a series of questions about past health; conduct a test to measure memory and a brain scan to look for any abnormalities in the brain (NIH Senior Health, 2015). A person diagnosed with Alzheimer’s can live between ten or twenty years. Depending on the severity some can remain alive for less than three years (Holland, 2016). The cause of Alzheimer’s is genetic for most and idiopathic for others. . “Lateonset Alzheimer’s arises from a complex series of brain changes that occur over decades” (National Institute on Aging, 2016). Alzheimer’s can be inherited from a parent. A child THE DEADLY BLOOM 5 with one parent carrying the gene has a 50/50 chance of inheriting the mutation and develop early onset Alzheimer’s (National Institute of Aging, n.d). A major determinant for late onset Alzheimer’s is the apoliprotein E gene (APOE). “APOE is a cholesterol carrier that supports lipid transport and injury repair in the brain” (Nature Reviews Neurology, 2013). Patients who carry copies of APOE e4 have a higher risk of developing Alzheimer’s disease than patients who are carry APOE 3 (UC Irvine Institute n.d). “APOE lipoproteins bind to several cell-surface receptors to deliver lipids and also to hydrophobic amyloid-B peptide which is thought to initiate toxic events that lead to synaptic dysfunction and neurodegeneration in Alzheimer’s disease” (Nature Reviews Neurology, 2013). Health and lifestyle factors induce the risk of Alzheimer’s. “Researcher suggests that a host of factors beyond genetics may play a role in the development of Alzheimer’s disease” (National Institute on Aging, 2016). Researchers mention that heart disease, stroke, high blood pressure and diabetes could play a role in increasing the risk of developing Alzheimer’s disease (National Institute on Aging, 2016). Beta-methyl-amino-L-alanine (BMAA) can also increase the risk of Alzheimer’s disease. BMAA is an amino acid produced by cyanobacteria (Ethno Medicine, n.d). The toxin is found in sea creatures such as sharks, fish and shellfish that ingest algae. “BMAA is inserted into human proteins, causing them to misfold replaces amino acid serine in the protein sequence” (Ethno Medicine, n.d). Beta-methyl-amino-L-alanine replaces the amino acid serine. Serine is an amino acid that is important in the functioning of the brain and central nervous system (Vitamins stuff, n.d). Replacing serine causes protein THE DEADLY BLOOM 6 aggregation and apoptosis (Ethno Medicine, n.d). BMAA is a trigger for Alzheimer’s in some people. An estimated 5.5 million Americans are diagnosed with Alzheimer’s in 2017 (Alzheimer’s Association, n.d). 200,000 are estimated to be under the age of 65 and 5.3 million are 65 and over (Alzheimer’s Association, n.d). Two thirds of Alzheimer’s patients are women (Alzheimer’s Association, n.d). African Americans are twice as likely to have Alzheimer’s as Caucasians (Alzheimer’s Association, n.d). Hispanics are one and one-half as likely to have Alzheimer’s as older Caucasians (Alzheimer’s Association, n.d). “Today, someone in the United States develops Alzheimer’s every 66 seconds” (Alzheimer’s Association, n.d). Alzheimer’s disease does not have a cure, however, individuals can take medications and participate in non-drug therapy (Alzheimer’s Association, n.d). Cholinesterase and memantine are used to stabilize the symptoms of Alzheimer’s temporarily (Alzheimer’s Association, n.d). Cholinesterase inhibitors are used to help delay mild to moderate Alzheimer’s (National Institute on Aging, 2016). These medications include donespezil and galantamine. These medicines help reduce the symptoms and prevent them from getting worst for an amount of time (National Institute on Aging, 2016). Although taking inhibitors is helpful, cholinesterase may lose effects as a result of the disease progressing (National Institute on Aging, 2016). To help moderate to severe Alzheimer’s doctors prescribe Namenda (memantine) (National Institute on Aging, 2016). These medications help maintain functions longer. While this can be helpful for most, medications and non-drug therapy do not reverse the THE DEADLY BLOOM 7 damage Alzheimer’s has caused in the brain. The prescriptions provide a temporary relief from the symptoms (Alzheimer’s Association, n.d). Doctors’ usually prescribed three different types of cholinesterase inhibitors; donespezil, is used to treat all stages of Alzheimer’s, Rivastigmine is used to treat mild to moderate Alzheimer’s and finally Galantamine is used to treat mild to moderate Alzheimer’s (Alzheimer’s Association, n.d). Caring for someone with Alzheimer’s is estimated to be $60,000 a year. Depending on the family of the patients, a nursing home or private care is used. The cost of living in a nursing home is around $82,000 per year. Coverage is not always covered by insurance. Family members cover some of the cost (Hanes, 2012). Alzheimer’s causes damage between the nerve cells in the brain and death of the nerve cells (National Institute on Aging, n.d). In the brain of a person with Alzheimer’s, the cortex and hippocampus shrink which injures the part of the brain that controls memory and thinking and the ventricles enlarge (Alzheimer’s Association, n.d). A magnetic resonance imaging (MRI) shows on average 0.44 percent of whole brain volume is lost in Alzheimer’s patients (ALZFORUM, n.d). In a brain of an Alzheimer’s patient, amyloid plaques are piled up between the nerve cells. “Amyloid is a general term for protein fragments that the body produces normally” (Bright Focus Foundation, n.d). Someone with a healthy brain can eliminate them, however, in a brain of an Alzheimer’s person, these fragments become insoluble plaques (Bright Focus Foundation, n.d). The brains also contain nerve cells containing tangles. “They primarily consist of a protein called tau, which forms part of a structure called microtubule” (Bright Focus THE DEADLY BLOOM Foundation, n.d). These proteins are not normal and the microtubule die out where tangles form (Bright Focus Foundation, n.d). Plaques do not stay in one place as Alzheimer’s progresses; they spread throughout the brain’s cortex. Depending on the stage at which a person is, the changes in the brain’s cortex very. (Alzheimer’s Association, n.d) 8 9 THE DEADLY BLOOM Methods and Materials BMAA is a neurotoxin that has been linked to Alzheimer’s and other neurological diseases. To investigate the presence of BMAA and its correlation to Alzheimer’s diagnosis a research study was conducted. With the permission of family members doctors at the National Institute of Neurological Disorders and Stroke gathered forty brain tissue samples to complete their experiment. Twenty of the samples came from people that had been diagnosed with Alzheimer’s, were deceased and were named the experimental group the other twenty who died of other causes, were named the control group. To find out if BMAA is an underlying cause of Alzheimer’s autopsy was performed to the forty patients who were diagnosed with Alzheimer’s as well as the controls. Standard procedures were used to remove the brains, which include “cutting the nerves to the blood vessels to the brain, the fibrous attachment to the skull and the nerves to the eyes,” (Encyclopedia, n.d). Twenty of the deceased had diagnoses of Alzheimer’s while living and the remaining twenty had not victims of Alzheimer’s disease. After obtaining the brains, pilling the lining of the surface of the brain from both the experimental and control group, data collection for both was obtained. To confirm a correlation between the presence of BMAA and Alzheimer diagnoses medical examiners performed an autopsy and removed the entire brain from forty deceased bodies. Examining the external features of the brain to identify atrophy. The brains were then placed in a cylinder filled with fluid to distinguish the average volume between the control and experimental group. Using a knife, the examiner cut each brain in half to evaluate the difference between a healthy brain and an Alzheimer THE DEADLY BLOOM 10 brain. Each brain was cut into smaller pieces to identify any similarities and differences (Gentleman, 2012). The medical examiners used enzyme-linked immunosorbent assay (ELISA), which are used to detect the presence of antigen antibody in a sample (ELISA-antibody, n.d). The first step the examiners took in determining the presence of BMAA in the brain tissue was the use of standard solution. The medical providers added fifty microliters of solutions to the control and experimental group’s wells of the test strips. Secondly, the medical attendant added fifty microliters of enzyme conjugate to each wells using a pipette. Following, the addition of the enzyme conjugate, addition of fifty microliters of antibody solution was added to the individual wells. After the solution was added, tape was used to cover the wells then mixture of the contents was done, along with incubation for sixty minutes. The fourth step in determining the presence of BMAA was removing the tape and disposing the contents into a sink. 250 microliters of washing buffer was used to clean the wells. Next, 100 microliters of substrate color solution was added to each wells. During this step, the examiners covered the wells with tape and mixed the contents together, then incubated for thirty minutes. The sixth step for the examiners was adding 100 microliters of stop solutions using a multi-channel pipette. The final step in determining the presence was to calculate the results” (Abraxis, n.d). Health examiners were able to determine if BMAA was truly present in the brain of the experimental group. Also if its present in the brains of some of the control group. 11 THE DEADLY BLOOM Results Upon Medical examiners could see obvious brain atrophy in the experimental group and the brains of the control group remained with no atrophy. “Neurofibrillary tangles and B-amyloid plaques are the neurological hallmarks of Alzheimer’s” (Cox, 2016). The doctors concluded that BMAA replaced the amino acid serine in human proteins and it led to the death of motor neurons (Ethno Medicine, n.d). The control group brain maintained the average length and volume associated with normal size while the experimental group had a decrease in brain volume. Once the doctors placed the healthy brains in the cylinder, the liquid in rose approximately to 2800 centimeters cube on one of the tries. Using this number, examiners were able to subtract the brain volume, which is 1500 from 2800 (Shcupak, 2001). The lowest the water rose up to be 2600 cm3. The highest the fluid elevated to be 2900 cm3, which gave examiners the highest number. The medical examiners used the same method to determine the volume of the experimental group. Since the brains of the experimental group were smaller, than those of the control group, the fluid in the cylinder did not rise as high. The health providers simply took the volume of a healthy brain and subtracted the level at which the fluid reached. The water rose up to 800 cm3 on the first try and the doctor subtracted 1500 from 800 to determine the volume. On the second try the water rose up to 770 cm3, on another try the water raised to 599 and the highest the fluid and brain rose up to 2501. The medical provider subtracted the numbers from the healthy brain volume and obtained the results below. 12 THE DEADLY BLOOM Average brain volume between the control and experimental group Control/cm3 Experimental cm3 1100 700 1101 730 1120 750 1150 799 1170 800 1200 800 1201 800 1210 801 1220 810 1230 820 1250 830 1280 850 1300 870 1301 890 1310 900 1330 901 1350 930 1360 970 1380 1000 1400 1001 25062 cm3 16952 cm3 13 THE DEADLY BLOOM After taking the average of both the control and experimental group, the health examiners noticed obvious changes between a healthy brain and a brain of victims of Alzheimer’s. The average volume for the control group was calculated at 25,062 cm3 while the experimental group calculated at 16,952 cm3. Examiners were able to conclude their findings using this table. Average brain volume 9 8 7 6 5 4 3 2 Alzheimer's patients Healthy patients 1 0 Continuing the experiment, the specialists added 100 microliters to each well and incubated them for thirty-seven degree Celsius. The ELISA test revealed that there is presence of BMAA in the brain of Alzheimer’s patients. Only one sample from an Alzheimer’s brain did not have presence of BMAA. Alzheimer’s often results from hitting the head one too many times. Also, Alzheimer’s is genetic. Five to ten percent of Alzheimer cases are due to inherited genetic mutations. This means that that the one who did not have BMAA in their brain inherited the disease from a family member. Medical 14 THE DEADLY BLOOM examiner also determined the presence of BMAA in the control group. This is the result of absorption of seafood such as oyster and shrimp. (Stockholm University, 2015) ELISA results ELISA Results Experimental Group Control Group BMAA present 18 3 No BMAA 2 17 Total 20 20 As a result of these experiments, medical examiners concluded that at least six out of seven individuals who have died from Alzheimer’s have had BMAA in their system. BMAA may have increased the risk of Alzheimer’s in many. As determined in the experiment, some individuals may have been exposed to BMAA without their knowledge. 15 THE DEADLY BLOOM Conclusion BMAA has the potential to cause neurodegenerative diseases therefore awareness is needed to prevent exposure. Medical examiners at the National Institute of Neurological Disorders and Stroke (NINDS) have concluded that BMAA is found in the deceased Alzheimer’s brain tissues. With the help of ELISA, examiners concluded that eighteen deceased in the experimental group have presence of BMAA. “Individuals sometime recover from a head injury, however, when the inflammation that helps to heal the damaged brain tissue becomes chronic” the injury remains (Arnold, 2015). This is a cause for the two other patients who did not present BMAA in the brain. In contrast to the healthy brains, the presence of BMAA was seventeen. The healthy brains present a small amount of BMAA as a result of the individuals ingesting seafood. “The major route for human exposure is though consumption of seafood and shellfish as some species produce potent toxins that can be accumulated in fish and shellfish” (Barratt, 2010). This implies that a large population has a great risk of developing Alzheimer’s by digesting a large consumption of contaminated seafood. Medical examiners also have done an animal study to prove BMAA is present in the brain tissue of other living creatures. Researchers fed vervet monkeys’ fruits containing the toxin BMAA and another group of monkey a placebo type of fruit. After 140 days, the examiners “detected protein tangles and plaques, a hallmark of neurodeg ...
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Running head: AVOIDING OBESITY RELATED TO BPA IN PLASTIC MATERIALS

Avoiding Obesity Related to BPA in Plastic Materials
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AVOIDING OBESITY RELATED TO BPA IN PLASTIC MATERIALS

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Avoiding Obesity related to BPA in plastic materials
Abstract
Since the early 1960s, the plastic manufacturers gave been using a chemical known as
Bisphenol A in the manufacturing of containers and other plastic items. Through the various
destructive practices such as the potential disruption of the endocrine, and result in the
interference with the metabolic processes, the chemical contributes substantially to the rising
cases of obesity individuals. The matter gets complex by the fact that in America and many other
countries, most people prefer to use plastics in the process of packaging their foods. To
demonstrate the manner in which this fact contributes to the cases of obesity, a study examined
students from three schools in Atlanta, Georgia. The learners have been drawn from a one
elementary level school, one middle-level school, and one high school. In this research, there
was an average of 98% of the students who responded (Barlow, 2009).
From these students, urine was collected, and the BPA concentration in the urine was
measured by qualified and properly trained research staff members. Additionally, the research
team received the anthropometric data that would be used in determining the possible causes of
the situation. Moreover, the team sought to know the lifestyles of the pupils so as to know or get
sufficient information that could be useful in determining the risk factors for obesity in this
group of people. Out of these people, it emerged that there is a perfect relationship between the
people who had a high concentration of BPA in their urine and obesity. Additionally, it emerged
that the rates at which BPA concentration in urine leads to obesity in boys are very different
from the manner in which it manifests itself among males. That fact is useful since it provides an
avenue to find means that would respond to the particular gender compositions and the needs of

AVOIDING OBESITY RELATED TO BPA IN PLASTIC MATERIALS

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the individuals. The gender differences that emerge in this study is consistent with previous
papers that suggest that the susceptibility to obesity is different among the males and females in
the society.
On the fourteenth day of April 2008, the debate on BPA in plastics reached another level
of discussion when it appeared on the headlines of the Washington post. Concerning its safety
debate, there were a lot of commercial, political and the scientific interests involved. In America
alone, the country produces billion dollar worth of BPA products in the market each year. As a
result, due to the economic interests that are involved, there is likely to be political heat. The
political players would like to appease the electorate by encouraging job creation as opposed to
the killing off industries. Scientifically, however, research shows that there is a significant
relationship that exists between BPA in plastic materials and the rising cases of obesity among
American citizens (Ben-Jonathan & Brandebourg, 2009). In the same breath, the widespread
application of BPA in the entire globe has contributed significantly to the worldwide obesity
epidemic. In that regard, this research seeks to provide the possible mechanisms that can be
deployed to avoid or possibly drastically reduce the instances of obesity that are associated with
BPA in plastic materials.

AVOIDING OBESITY RELATED TO BPA IN PLASTIC MATERIALS

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Background
In the recent decades, the world has seen a soaring increase in the number of obesity
among populations. The most intriguing part of this realization is that most of the new cases are
children. In the United States, statistics indicate that an average of 20% of children is obese.
With this realization, it has become important that all the stakeholders including the government
seek the factors that contribute to this trend and make necessary improvements (Lang et al,
2008). Obesity is a condition that contributes to some health complications among those affected
especially children. Ordinarily, it predisposes the children to the type 2 diabetes, hypertension,
coronary heart disease and stroke. Besides, the children stand the risk of developing kidney and
liver diseases. Traditionally, people have linked obesity to ea...

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