They are many benefits that come from adipose tissue (fat). It is an essential part of life, but it is often thought of as a human's worst enemy. With increasing trends in fad diets, and unsafe practices in weight loss being accepted by many, it is important to understand why we should love fat and why God designed our bodies to store it. Here is a description of four beneficial aspects of adipose tissue:
1. Adipose tissue secretes leptin. Leptin is a polypeptide hormone that has the potential to interact with several brain mechanisms and together, those may lower and maintain body fat. This may also play a key role in increasing metabolic fitness, reducing health risk factors, and improving overall health of obese people.
2. There are long-term adiposity signals - leptin and insulin - which act on brain mechanisms to inhibit food intake and increase energy expenditure.
3. Adipose tissue takes up glucose and uses it for the synthesis of glycerol 3-phosphate which feeds into the process of glycolysis. This is crucially important because glycolysis is a metabolic pathway in which ATP and NADH are produced.
4. Adipose tissue stores and releases fatty acids. When triacylglycerols are released into circulation, they are hydrolyzed by lipoprotein lipase in the adipose tissue capillary bed. After this occurs, and if a person enters into starvation (or just a hungry state), stored triacylglycerols are hydrolyzed by lipase, which is hormone-sensitive. This allows for free fatty acids and glycerol to be released into circulation. Free fatty acids yield a large amount of ATP, which provides energy to multiple tissues within the body. Glycerol is an important energizer to cellular metabolism.
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Sunday, September 27, 2009
Friday, September 11, 2009
The Origins of Obesity - A Comparison of Two Arguments
In a nation where the health care industry is currently in an upheaval and all eyes are being turned to preventative medicine to save on costs, it is important to try to understand where the origins lie for one of the biggest health threats in America. Obesity is the leading cause in several major health problems daunting the population today. From Coronary Heart Disease to several types of cancer, understanding obesity and how it can best be prevented will ultimately save many lives. There are varying opinions on the origins of obesity. Several studies have been conducted involving genetics, and also environmental factors. This research is aimed at leading toward the most efficient means of prevention. Whether that be through genetic alterations – as seen in rodent studies – or through environmental adjustments, obesity needs to be looked at through the progressive eye. Examples of this progress have been presented through the authors RJF Loos and Claude Bouchard in their article entitled, “Obesity-is it a genetic disorder,” as well as the authors Walter Poston II and John Foreyt in an article called, “Obesity is an environmental issue.” Both of which are discussed below.
It is well understood that a person’s familial circumstances play a role in their bodily development. However, how closely does this boil down to single genes, or a group of genes, causing the obesity epidemic? In an argument presented by RJF Loos and Claude Bouchard, it is proposed that obesity can be viewed as a genetic disorder. Through twin, adoption, and family studies, there have been links that show that obesity is an inheritable trait. Loos and Bouchard’s research looked at how historical biology and current day trends differ, and what the progression has looked like that has led to this health crisis. It was mentioned that the idea behind genetically caused obesity is not new. In 1962, James Neel proposed his “Thrifty genotype hypothesis,” posing that obesity in deed is caused by a series of genotype mutations. Loos and Bouchard addressed that obesity is a multifactorial disease that is stretching out over the population. They pointed out that environment does play a major role in the abundance of this condition, but they believe that a person’s reaction to a change in their lifestyle or environment depends on their “genetic predisposition.” Studies have been conducted that show that “…those with a high genetic predisposition for obesity will gain the most weight, whereas-those resistant will gain little if any” in an obesogenic environment. By calculating familial risk, it is easier to know how one might respond in such an environment. According to Loos and Bouchard, an individual is two to three times more likely to develop obesity if they have at least one first degree relative who also suffers from the disease. Loos and Bouchard also looked at the complexity behind whether or not obesity is caused by a single gene, or a group of genes. There are several Mendelian disorders that signify monogenic forms of obesity. Such disorders as Bardet-Biedle Syndrome, Prader-Willi Syndrome, and the experiments ran on mice all signal toward single genes. However, research is still being conducted to determine if, and to what degree, obesity is polygenic. Overall, Loos and Bouchard presented an understanding that one’s environment greatly impacts their ability to live a healthy lifestyle, but they also believe that a person’s genes dictate their regulation of energy balance in the long run.
On the adverse side of the gene-caused obesity argument, Walter Poston II, and John Foreyt, expressed their understanding that obesity is caused by the “toxic” environment. In their article, they took a straight-forward stance that obesity is an environmental issue. They stated that “…the primary environmental determinants of obesity are high caloric intake and low levels of activity.” Through logic and reason, these two authors explained how obesity trends have changed in progression with evolutionary advancements. As food supply becomes more readily available, and the need to exercise decreases, so does the rise in obesity continue. They quoted Bouchard himself in saying that “…genes account for only 5% of body mass index and subcutaneous fat.” If a person lives in a non-supporting environment, one that has created troublesome dietary and activity patterns, then they are much more likely to suffer from obesity. Poston II and Foreyt presented culture studies, in which two individuals from the same gene pool were raised in different environments. For example, a study was done on men of Japanese ancestry. The men that were raised in accordance to traditional Japanese culture were much healthier than those that lived closer in proximity to Westernized societies. The Japanese Americans who accepted Westernized culture, including diet, ended up being overweight, whereas the men raised in Japan were not. Poston II and Foreyt boiled it down to the idea that in the advanced culture today, there are strictly too many calories available for consumption. Food deprivation is very rarely an issue or concern, so the hunter-gatherer ideal of the earlier generations has been depleted, also leaving the trends in daily exercise diminished.
Although both of these articles presented clear evidence as to whether obesity is caused by genes or the environment, one of them stands out as the stronger argument. Poston II and Foreyt, in their article entitled, “Obesity is an environmental issue,” portrayed logical reasoning and a clear understanding as to why obesity is more affected by a person’s environment than it is by heredity. These authors used clear and practical studies that outlined why obesity is not solely caused within the genes. They noted that it was problematic that the single gene studies conducted by those attempting to prove that obesity was a genetic disorder had not yet been replicated in humans. The study brought forth, concerning the Pima Indian women, provided a clear understanding as to how one’s environment can affect the way in which adiposity develops. The two women that they looked at for this study were genetically related, but the one who had adopted an Americanized diet weighed much more than the woman who followed a traditional Pima Indian diet. This is a major downfall in the fight to see the cause of obesity get boiled down to genetics. Poston II and Foreyt also looked at evolution’s role in the rising obesity trend. They noted that over the last 100 years, the average male has gained 12 kilograms. As was pointed out, the human gene pool has not changed in that little amount of time. This much is clear however; Western society has changed drastically in terms of the availability of food, access to transportation, and excess intake in calories within the last century. Poston II and Foreyt presented the stronger argument as they created a realistic outline of how the human condition has been altered by an ever-changing environment.
It is unrealistic to say that obesity can be narrowed down to one single cause. It is a multi-faceted disease that affects each patient differently. It is very likely that there are genetic links to obesity. However, it is a lot easier and much more accessible to adjust a person’s interactions and reactions with and to their environment than it is to alter their genetic makeup. In the current Americanized culture, fast-food chains, faulty food labels, and a lack of need to exercise produce a rising obesity rate. Current public health initiatives need to be focused at prevention and intervention of this disease. This needs to start on the environmental playing field. By giving patients the tools they need to thrive in a “toxic” environment, the obesity trend should be lowered.
A vibrant pursuit against obesity could not come at a better time. Preventative measures need to be taken to reduce the more severe health care concerns that are related to obesity. By tackling the issues that initiate obesity, environmentally or genetically, great strides can be taken to alleviate the damage caused by the obesity epidemic. Loos and Bouchard presented why it is understandable to believe that genes have a powerful role in obesity, while Poston II and Foreyt expressed the impact a detrimental environment has on one’s ability to thrive nutritionally. Ultimately, obesity is a complex issue with many possible causes, but preventative and interventional measures should first be applied to the patient’s environment, giving them the resources they need to live a healthy, balanced lifestyle no matter where they are. This is the first step in the progression to end the rise in obesity.
Works Cited
Loos , Bouchard. (2003). Obeisty - is it a genetic disorder? Journal of Internal Medicine , 401-425.
Poston II, Foreyt. (1999). Obesity is an environmental issue. Atherosclerosis , 201-209.
It is well understood that a person’s familial circumstances play a role in their bodily development. However, how closely does this boil down to single genes, or a group of genes, causing the obesity epidemic? In an argument presented by RJF Loos and Claude Bouchard, it is proposed that obesity can be viewed as a genetic disorder. Through twin, adoption, and family studies, there have been links that show that obesity is an inheritable trait. Loos and Bouchard’s research looked at how historical biology and current day trends differ, and what the progression has looked like that has led to this health crisis. It was mentioned that the idea behind genetically caused obesity is not new. In 1962, James Neel proposed his “Thrifty genotype hypothesis,” posing that obesity in deed is caused by a series of genotype mutations. Loos and Bouchard addressed that obesity is a multifactorial disease that is stretching out over the population. They pointed out that environment does play a major role in the abundance of this condition, but they believe that a person’s reaction to a change in their lifestyle or environment depends on their “genetic predisposition.” Studies have been conducted that show that “…those with a high genetic predisposition for obesity will gain the most weight, whereas-those resistant will gain little if any” in an obesogenic environment. By calculating familial risk, it is easier to know how one might respond in such an environment. According to Loos and Bouchard, an individual is two to three times more likely to develop obesity if they have at least one first degree relative who also suffers from the disease. Loos and Bouchard also looked at the complexity behind whether or not obesity is caused by a single gene, or a group of genes. There are several Mendelian disorders that signify monogenic forms of obesity. Such disorders as Bardet-Biedle Syndrome, Prader-Willi Syndrome, and the experiments ran on mice all signal toward single genes. However, research is still being conducted to determine if, and to what degree, obesity is polygenic. Overall, Loos and Bouchard presented an understanding that one’s environment greatly impacts their ability to live a healthy lifestyle, but they also believe that a person’s genes dictate their regulation of energy balance in the long run.
On the adverse side of the gene-caused obesity argument, Walter Poston II, and John Foreyt, expressed their understanding that obesity is caused by the “toxic” environment. In their article, they took a straight-forward stance that obesity is an environmental issue. They stated that “…the primary environmental determinants of obesity are high caloric intake and low levels of activity.” Through logic and reason, these two authors explained how obesity trends have changed in progression with evolutionary advancements. As food supply becomes more readily available, and the need to exercise decreases, so does the rise in obesity continue. They quoted Bouchard himself in saying that “…genes account for only 5% of body mass index and subcutaneous fat.” If a person lives in a non-supporting environment, one that has created troublesome dietary and activity patterns, then they are much more likely to suffer from obesity. Poston II and Foreyt presented culture studies, in which two individuals from the same gene pool were raised in different environments. For example, a study was done on men of Japanese ancestry. The men that were raised in accordance to traditional Japanese culture were much healthier than those that lived closer in proximity to Westernized societies. The Japanese Americans who accepted Westernized culture, including diet, ended up being overweight, whereas the men raised in Japan were not. Poston II and Foreyt boiled it down to the idea that in the advanced culture today, there are strictly too many calories available for consumption. Food deprivation is very rarely an issue or concern, so the hunter-gatherer ideal of the earlier generations has been depleted, also leaving the trends in daily exercise diminished.
Although both of these articles presented clear evidence as to whether obesity is caused by genes or the environment, one of them stands out as the stronger argument. Poston II and Foreyt, in their article entitled, “Obesity is an environmental issue,” portrayed logical reasoning and a clear understanding as to why obesity is more affected by a person’s environment than it is by heredity. These authors used clear and practical studies that outlined why obesity is not solely caused within the genes. They noted that it was problematic that the single gene studies conducted by those attempting to prove that obesity was a genetic disorder had not yet been replicated in humans. The study brought forth, concerning the Pima Indian women, provided a clear understanding as to how one’s environment can affect the way in which adiposity develops. The two women that they looked at for this study were genetically related, but the one who had adopted an Americanized diet weighed much more than the woman who followed a traditional Pima Indian diet. This is a major downfall in the fight to see the cause of obesity get boiled down to genetics. Poston II and Foreyt also looked at evolution’s role in the rising obesity trend. They noted that over the last 100 years, the average male has gained 12 kilograms. As was pointed out, the human gene pool has not changed in that little amount of time. This much is clear however; Western society has changed drastically in terms of the availability of food, access to transportation, and excess intake in calories within the last century. Poston II and Foreyt presented the stronger argument as they created a realistic outline of how the human condition has been altered by an ever-changing environment.
It is unrealistic to say that obesity can be narrowed down to one single cause. It is a multi-faceted disease that affects each patient differently. It is very likely that there are genetic links to obesity. However, it is a lot easier and much more accessible to adjust a person’s interactions and reactions with and to their environment than it is to alter their genetic makeup. In the current Americanized culture, fast-food chains, faulty food labels, and a lack of need to exercise produce a rising obesity rate. Current public health initiatives need to be focused at prevention and intervention of this disease. This needs to start on the environmental playing field. By giving patients the tools they need to thrive in a “toxic” environment, the obesity trend should be lowered.
A vibrant pursuit against obesity could not come at a better time. Preventative measures need to be taken to reduce the more severe health care concerns that are related to obesity. By tackling the issues that initiate obesity, environmentally or genetically, great strides can be taken to alleviate the damage caused by the obesity epidemic. Loos and Bouchard presented why it is understandable to believe that genes have a powerful role in obesity, while Poston II and Foreyt expressed the impact a detrimental environment has on one’s ability to thrive nutritionally. Ultimately, obesity is a complex issue with many possible causes, but preventative and interventional measures should first be applied to the patient’s environment, giving them the resources they need to live a healthy, balanced lifestyle no matter where they are. This is the first step in the progression to end the rise in obesity.
Works Cited
Loos , Bouchard. (2003). Obeisty - is it a genetic disorder? Journal of Internal Medicine , 401-425.
Poston II, Foreyt. (1999). Obesity is an environmental issue. Atherosclerosis , 201-209.
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