Inquiry Revisions

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Epidemiology of Obesity 1 Inquiry Revision - Epidemiology of Obesity Erin Shauna Human April 17, 2015 UWRT 1103-026

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Inquiry Revisions

Transcript of Inquiry Revisions

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Epidemiology of Obesity 1

Inquiry Revision - Epidemiology of Obesity

Erin Shauna Human

April 17, 2015

UWRT 1103-026

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Epidemiology of Obesity 2

Obesity, once perceived as a simple issue has exploded grown over the years(worldwide

obesity has increased 82% in the last two decades), capturing the attention of governments,

health policy makers and the general public and is today termed a global epidemic. The

consequences of its explosion have become oOf even greater concern, are the consequences of

its explosion which when extrapolated presents horrifying data that ifs not handled, will possibly

become a reality in the near future. Such is the case in that most of the world’s population live in

countries where overweight and obesity kill more people than underweight is more of a health

crisis than malnutrition (WHO, 2015). There is no doubt that Obesity causes certain

diseasescomes with ever-present co-morbidities, the most common being type II diabetes

(Kazaks, & Stern). In worst cases, this condition has been linked to increased mortality; a factor

that happen occurs with very little acknowledgement, hence the term “slow killer.” Over the past

years, professionals in the medical filed industry have attempted to raise some numerous theories

to help explain the underlying causes of obesity, and possible remediesthus possible methods of

treatment and prevention. These theories have come under sharp criticisms,; with later discovery

giving providing new information that often disqualifiesy the previous findings (Bray, &

DeLany, 1995). What is important is that we This work will begin by revisiting the history of

obesity. We can then relate the current ideas early theories on its causes, then it will relates the

current thinking about causes, co morbidities, and treatments with the aim of creating awareness

among the readersthose reading.

According to a multitude of clinical papers published on this topic, particularly those

authored by a popular group of international professionals asnd presented in the Lancet, several

factors and not just one contribute to cases of obesityobesity is a multifaceted condition with a

myriad of variables contributing to it. Led by Boyd Swinburn, the experts cite the global food

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system as one factor that encourages obesity this condition (Wilborn, et al, 2005). Here,

mechanization has been blamed for reducing people’s energy expenditure and leading them to

live sedentary lifestyles, a factor that according to these experts shifts the blame to the

government for overlooking such important facts. According to this argument, governments

should bear the blame for taking the issue of obesity as an individual’s responsibility

(Wickelgren, 1998). This argument goes further to suggestsuggests that during the Stone Age,

our ancestors were very much engaged in hunting and gathering, enjoying the diet of that period,

a factor that exposed them to much smaller risk of being obese. Boyd Eaton adds his weight on

the issue by insinuating that the majority of today’s non-communicable diseases, obesity

included, follow our desertion of the ancestral diets, which we are attuned to genetically.

Among the most renowned theories of obesity and its relation to diabetes mellitus

is the Thrifty Gene Hypothesis proposed by James V. Neel in 1962. Neel suggested that a

“thrifty genotype,” which modified the regulation of insulin release and glucose storage may

have provided a survival advantage for some of our hunter-gatherer ancestors predecessors

(Chakravarthy, MV & Booth, FW., 2004). This metabolic makeup would have allowed our

ancestors to match cycles of feast and famine with proportionately large fluctuations in blood

insulin levels, allowing them to store excess energy efficiently thus increasing chances of

survival through periods of food scarcity.

However, given today’s Western society with its modern, often dubbed “obesogenic”,

environment and plentiful food supply, this genetic disposition has come to be a huge

disadvantage detrimental to its current descendants. The hypothesis proposes that this thrifty

genotype may be responsible for the elevated insulin levels and excessive energy stores in some

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type-II diabetic individuals, and has contributed to the insulin resistance and obesity that has

come to characterize many of these patients.

When we think of the conventional view that the general public hold of obesity, we think

of the Energy Imbalance equation. It is the “commonsense” understanding that has been

reiterated over the years and is commonly referred to as the “Folk Theory of Obesity”. This

commonly-held theory suggests that the cause of obesity is simply “a long-term imbalance

between energy intake and energy expenditure” (Haslam, Sharma, & Le Roux, 2013). This

hypothesis finds its grounding on the first law of thermodynamics; effectively the law of

conservation of energy (as applied to a biological system over a period of time). A further theory

that is much popular purports that “weight gain/loss over some period is approximately

proportional to the energy stored” (Haslam, et al., 2013). Among the most renowned theories of

obesity from the past is the Folk theory which suggests the cause as being “a long-term

imbalance between energy intake and energy expenditure” (Haslam, Sharma, & Le Roux, 2013).

In justifying this theory, the supporters have argued that weight gain is a completely endogenous

(dependent) variable while both energy intake and energy expenditure are exogenous

(independent) variables. Taking this stand is tantamount to the implication that the “right-hand

side of the energy imbalance equation (calories in–calories out) causes the left-hand side (weight

gain),” (Haslam, et al., 2013). This hypothesis finds its grounding on the first law of

thermodynamics; the law of conservation of energy as applied on biological system over some

period. A further theory that is much popular purports that “weight gain/loss over some period is

approximately proportional to the energy stored” (Haslam, Sharma, & Le Roux, 2013). In

justifying this theory, the supported have argued that weight gain is completely an endogenous

(dependent) variable while both energy intake and energy expenditure are exogenous

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(independent variables). Taking this stand is tantamount to the implication that the “right-hand

side of the energy imbalance equation (calories in–calories out) causes the left-hand side (weight

gain),” (Haslam, Sharma, & Le Roux, 2013). This factor does not resonate well with the 1st

law of thermodynamics. Additionally, this suggestion fails to give a reason as to why the same

this same process should not work in the reverse i.e., weight gain following the effects through

homeostatic mechanisms, may regulate and influence (thus determine) the energy intake and

expenditure.

For this theory to remain valid, we must assume be made to believe that people can

independently exogenously balance their energy intake and expenditure to be within 99 percent

of each other, a factor that does not come out reasonable.an unreasonable assumption. It is on

this ground that we are forced to assume the existence of particular homeostatic mechanisms,

which controls play a major role in determining the intake of calories and the expenditure of

energy by the body. This mechanism has been suggested as the reason for these variables being

partly independent and under the influence of weight gain. From this argument it is easy to

allude that when a person’s weight fluctuates, for example increases, this must be followed by

some negative feedback mechanisms that will effectively reduce intake of calorie and/or increase

the expenditure. This works in the reverse for the case of weight loss. These mechanisms give

reason to making these variables partly endogenous and influenced by weight gain. Such

mechanisms do exist, which means that a reverse relationship has been introduced to the energy

imbalance equation, therefore leaving it at a loss of theoretical justification.

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One recent argument has, Taubes, a co-founder of the Nutrition Science Initiative,

claiming that the "insulin hypothesis” although neglected, presents a long term history that once

offered a serious option to the traditional “calories in, calories out" theory. Taubes sees the

"energy balance" hypothesis as a mere tautology. In his argument he questions the idea that

people eat more, so they become fat. In his view, fat people take in more calories as a way of

maintaining their weight and as such obese people eat more for the reason that they are obese.

To explain his reasoning as to what he thinks isTo elaborate his theory on what the main cause of

obesity is, Taubes buys the proposal made by Wilhelm Falta and Gustav Von Bergmann,

Austrian and German scientists respectively. According to these two, “underlying biological

factors, not just what we eat, regulate how fat we get.” This supposition goes ahead to suggest

obesity as a "hormonal, regulatory disorder" and not merely a result of too much eating or lack of

exercise (Stevens, 2005). Such is the case that in human bodies, insulin goes up whenever

something is ingested that signals triggers the fat tissue to release sugar in the form of fat into the

blood stream. Based on this, Falta, argues that more insulin impliesy more sugar being changed

converted to fat, a factor that ultimately results in fatteningweight gain. Taubes brings up an

example from the past and states thatillustrates this by referring to a past experiment, stating that

"When insulin was injected into both diabetic dogs and humans in the laboratory as early as the

1920s, they would put on weight and fat." (Ferris, R. (2013).

For Gustav Von Bergmann, the concept of lipophilia, meaning "love of fat" is a better

explanation not just for why some individuals gain weight more than others, but also for why

some individuals gain weight in different places (Golay, Anderson, & Visser, 2010). This

concept holds the view those individuals that are "certainly predisposed to fatten" posses cells

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that depict lipophilic behavior. According to him, this explains furtherjustifies why people tend

to accumulated fat in particular places e.g. belly than others.

The issue of weight gain and loss as presented in the case of obesity still offer

much challenge In analyzing the few theories discussed, the issue of weight gain and loss as

presented in the case of obesity still offer much challenge, especially when looking at the many

theories propositions made. Scientific studies are ongoing in the missionquest to proving and

disproving existing hypotheses to gain more insight knowledge on this highly complex issue.

For many of us we can only keep our hopes alive that very soon somewhat of a conclusive

finding will be reached. For those of us who have been involved in the obesity story in modern

today’s times, it is frustrating that there is much confusion, debate, and misunderstanding

relating to the subject. In assessing analyzing the dietary aspect in addition to the other multitude

of factors responsible for weight gain and its consequences, we are constantly presented

bombarded with differing views in the medical world. This occurs before we even begin to think

about the methods and array of approaches to treating it. Ideas range from education to school

management, the value of workout facilities and support groups, urban planning and traffic

policies, clinical strategies and surgical intervention, and even fiscal and legislative measures.

It’s important that as a society we are not frightened intimidated by all these issues but

give acknowledgement to the fact that it is a topic which is now considered to be of such

importance significance that it involves everybody from basic scientists to physiologists,

endocrinologists, neuroscientists, and psychologists as well as an array of specialists in the

medical field. Initially it seemed that prevalence data about the explosion of this epidemic did

not give enough of an impression to figures of authority; however, it seems that the ensuing

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dramatic financial consequences have managed to send a stronger signal. As the predictions of

an unsustainable economic health burden emerge across the world, obesity is now a condition

that is taking central stage in places such as the United Nations General Assembly and the

Treasuries of the world.

Forming a truly objective opinion on obesity, the countless approaches to its treatment, and

what seemsseemingly impossible challenge of prevention is a difficult task, one which requires a

great deal of patience and discernment. What we can do for now, with all the information

gathered, is continue to educate ourselves (as well as others) and acknowledge the myriad of

variables involved in this condition, while actively trying to lead healthy lifestyles and encourage

others. As a population we have to reinforce the process of gaining an ever-increasing

understanding of obesity; this will lead to not only ascertaining the underlying mechanisms

involved but in also in determining the most appropriate forms of treatment, and more

importantly prevention. Given the urgency of the situation and the scale of this epidemic, we

don’t really have a choice.

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References

Bray, G., & DeLany, J. (1995). Opinions of Obesity Experts on the Causes and Treatment of

Obesity - A New Survey. Obesity Research, 3(S4), 419S-423S. doi:10.1002/j.1550-

8528.1995.tb00208.x

Chakravarthy, MV. & Booth, FW. (2004). Eating, exercise, and “thrifty” genotypes: connecting

the dots to-ward an evolutionary understanding of modern chronic diseases. J Appl

Physiol, 96: 3-10.

Ferris, R. (2013). Are We Ignoring The True Cause Of Obesity?. Business Insider. Retrieved 2

April 2015, from http://www.businessinsider.com/carbohydrates-insulin-and-obesity-

2013-4

Golay, A., Anderson, R., & Visser, A. (2010). Changing obesity: Theories, facts and

interventions. Patient Education And Counseling, 79(3), 275-276.

doi:10.1016/j.pec.2010.04.018

Haslam, D., Sharma, A., & Le Roux, C. (2013). Controversies in Obesity (pp. 63-65). London:

Springer Science & Business Media, 2013.

Kazaks, A., & Stern, J. (n.d.). Obesity Treatments and Controversies. Diabetes Spectrum, 231-

235.

Neel JV. (1962). Diabetes mellitus: a “thrifty” genotype rendered detrimental by “progress”.

Am J Hum Genet, 14: 353-62.

Stevens, J. (2005). Commentary: Obesity claims and controversies. International Journal of

Epidemiology, 77-78.

World Health Organization. (2015). Diabetes (Fact sheet No. 311). Retrieved 28 March 2015,

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from http://www.who.int/mediacentre/factsheets/fs311/en/

Wickelgren, I. (1998, May 29). Obesity: How big a problem? With obesity rates soaring,

experts debate whether everyone who is overweight needs to lose the excess pounds to

preserve his or her health.(includes related article on the risk of disease of abdominal fat

versus lower-body fat. Science.

Wilborn, C., Beckham, J., Campbell, B., Harvey, T., Galbreath, M., & La Bounty, P. et al.

(2005). Obesity: Prevalence, Theories, Medical Consequences, Management, and

Research Directions. J Int Soc Sports Nutr, 2(2), 4. doi:10.1186/1550-2783-2-2-4