Obesity Becoming the “Norm”? 1
Charlietheunicorn411
Obesity Becoming the “Norm”?
An epidemic is quickly spreading across the United States – obesity. It affects all
Americans regardless of their age-all Americans? My cousin is a stick. He is not affected.; fiftyfour percent of adults are considered overweight, of which twenty-two percent are obese.-What
is the difference? Twenty-five percent of children are experiencing obesity, as well (Hill &
Peters, 1998). The primary reason why obesity is a widespread problem in a developed nation,
such as the U.S., is inherited genes – what??? This doesn’t make sense to me. (Comuzzie &
Allison, 1998). This intro needs improvement. It is supposed to introduce the topic. What is
obesity? What causes it? The prevalence. Etc… Then it should transition into what the
manuscript will discuss.
In the early history of mankind, humans constantly searched for food in order to satiate
their pangs of hunger due to the lack of food. As a result, only humans with energy retaining
genes survived in this food-deprived environment. These survivors passed on their genes down
through generations to the people of today. However, in the twenty-first century, food has
become abundant, cheap, and fatty. Ultimately, the availability of energy-high foods coupled
with energy conserving genes lead to a one way path of obesity grammar (Hill & Peters, 1998). –
this is all introductory material and belongs in the introductory paragraph
Obesity-linked genes control the system of weight control through food consumption.-say
what? They regulate it by affecting the production of molecules that play important roles in the
system. Scientists have found and identified these important molecules. Molecules, Neuropeptide
Y (NPY), a protein that creates hunger, and Leptin, a protein that causes one to feel full by
Obesity Becoming the “Norm”? 2
disabling NPY, are two key factors. Evidently, cravings for food greatly impacts weight gain and
loss (Loftus, et al., 2000; Erickson, et al., 1996; Comuzzie & Allison, 1998). I am confused as to
where this is going. What is the point of this paper? You are not telling a story, you are blurting
out information sporadically.
The amount of fat stored in the body and food consumption both vary inversely to the
amount of NPY. NPY-repeating words side by side makes for poor ease of reading urges the
body to obtain more food when energy supply is low and also reduces energy utilization (Loftus,
et al., 2000; Erickson, et al., 1996). Experiments with two groups of obese mice show that
genetically engineering obese mice to produce less NPY alleviates the severity of obesity. The
first group of mice was Leptin-deficient and as a result was unable to block NPY.-do you think
the general reader is going to comprehend any of what you are saying. You need to be
considerate of the reader. Walk them step by step through the story you want to tell. Make sure
they know where you want to go at all times and where you are. This caused the group to overeat
because of a constant craving for food. Furthermore, the group rarely exercised and had slow
metabolism. The second group of Leptin-deficient mice was genetically engineered. This group
lacked both Leptin and NPY. Since there was less NPY, the mice experienced fewer symptoms.
However it did not completely compensate for the lack of Leptin. Hence, scientists became
confused by these results. They concluded that the answer to this confusion was that NPY is not
the sole target of Leptin. These other variables are still unknown and have yet to be found. NPY
removal is not being done to cure obesity in humans; however, the idea may resurface in the
future (Erickson, et al., 1996). I am lost. Still can’t figure out the point. These mice are
genetically engineered, but you implied that genetics is the cause of obesity in humans. You have
Obesity Becoming the “Norm”? 3
not discussed anything about this being the cause since you said it. The reader does not know the
point because I suspect that you do not know the direction you want to take the reader.
Energy consumption is primarily governed by molecules that break down brown adipose
tissue (BAT) and white adipose tissue (WAT), also simply known as brown and white fat,
respectively. The difference between these two fats is that brown fat is necessary for
thermogenesis, the creation of heat, and white fat is necessary for energy used in all processes –
like? except thermogenesis. In order for BATs to function and maintain its properties, BetaAdrenergic Receptors (βARs) are needed. It has been confirmed that βARs are needed for BATs
to be correctly broken down for heat. Without βARs, BATs would be nearly identical to WATs,
further proving the need for Beta-Adrenergic Receptors.-I have no idea what you are talking
about. Experiments show a rapid decrease in body temperature of mice that did not have BetaAdrenergic Receptors because it could cope with heat loss to the environment (Bachman, et al.,
2002). Furthermore, mice that lacked βARs did not have sufficient amounts of Uncoupling
Protein – 1 (UCP-1). UCP-1’s are necessary in the physical act of breaking down BATs.
Although humans have neither brown fat nor UCP-1’s, a protein similar to UCP-1’s is created in
ordinary fat and muscle cells. This observation shows promise to future treatments and therapy
(Gura, 1998). Evidently, the lack of βARs would cause thermogenesis resulting in failure due to
the BAT malfunctioning and ultimately decreasing the overall metabolism. This conclusion is
further reinforced by evidence of a 16 percent lower metabolism and higher weight of βARs
deficient mice compared to normal mice (Bachman, et al., 2002). – the general reader is lost.
How does this even relate to the previous paragraph?
C75 and Cerulenin created hope for scientists as a new therapeutic agent because of its
unique way of inhibiting eating.-now you are talking about therapeutic agents? Similar to the
Obesity Becoming the “Norm”? 4
function of Leptin, they block NPY. Under normal conditions, food-deprived mice have a
decrease in energy utilization (conservation of energy); however, C75 and Cerulenin go against
this evolutionary technique. In a controlled experiment, mice that have been injected with these
inhibitors lost large amounts of weight and surprisingly they did not seemed fatigued and
continued to have the same rate of metabolism and energy utilization as they had always been.
These ironic results are caused by the production of Leptin. Although these two molecules act as
a substitute for Leptin, it does not affect the production of Leptin in anyway. Both Leptin and
these molecules block NPY left and right. Therefore, mice did not feel the need to eat. The brain
begins to believe it has an adequate amount of energy because of the lack NPY expression when
actually the body is energy-deficient. Unfortunately, hopes for using these inhibitors for
therapeutic use were dashed. Mice needed continual injections of C75 and Cerulenin to stay lean
because effects of these molecules were dependent upon how long the drug was taken and thus,
they were temporary (Loftus, et al., 2000).
Despite the knowledge of these important molecules and hopes for new obesity
controlling agents,-how did you end up talking about obesity drugs? an effective drug with
minimal side effects has not been found (Loftus, et al., 2000; Erickson, et al., 1996; Bachman, et
al., 2002). Scientists are still striving to find the official “cure” for the large problem of obesity.
You need to gain some focus. What do you want to write about. You have basically
discussed a bunch of experiments out of any clear context. There is no story here, just
information. You need to decide what you want to focus on first. Do you want to focus on a
drug to alleviate obesity? I am not sure where you want to go with this.
Obesity Becoming the “Norm”? 5
The number below will change with each revision. These numbers are simply indicative of the amount of
improvement required at this point. When you receive a 9 or greater, the review is ready. DrT
4/10
References
Bachman, E.S., Dhillon, H., Zhang, C., Cinti, S., Bianco, A.C., Kobilka, B.K., & Lowell, B.B.
(2000) βAR Signaling Required for Diet-Induced Thermogenesis and Obesity
Resistance, Science, 297, 843-845.
Comuzzie, A.G., & Allison, D.B. (1998). The Search for Human Obesity Genes, Science, 280,
1374-1377.
Erickson, J.C., Hollopeter, G., & Palmiter, R.D. (1996). Attenuation of the Obesity Syndrome of
ob/ob Mice by the Loss of Neuropeptide Y, Science, 274, 1704-1707.
Gura, T. (1998). Uncoupling Proteins Provide New Clue to Obesity’s Causes, Science, 280,
1369-1370.
Hill, J.O., & Peters, J.C. (1998). Environmental Contributions to the Obesity Epidemic, Science,
280, 1371-1374.
Lazaar, M.A. (2005). How Obesity Causes Obesity: Not a Tal Tale, Science, 307, 373-375.
A tal tale? Is that correct? What is tal?
Obesity Becoming the “Norm”? 6
Loftus, T.M., Jaworsky, D.E., Frehywot, G.L., Townsend, C.A., Ronnett, G.V., Lane, M.D., &
Kuhajda, F.P. (2000). Reduced Food Intake and Body Weight In Mice Treated with
Fatty Acid Synthase Inhibitors, Science, 288, 2379-2381.