Milk - To drink it or not to drink it...that is the question!

Milk has become a main source for humans to get many of the essential nutrients in their diets. It provides protein, calcium, carbohydrates, fats, and many vitamins and minerals (such as Biotin, Iodine, Potassium, Magnesium, Selenium, Thiamine, Vitamin A, Vitamin B, Riboflavin, Vitamin D, and Vitamin K). Recently, there has been a huge debate whether or not milk is a natural food source for humans. This is partially based on the fact that humans are the only mammals to consume breast milk from a different species other than their own. I learned this fact while I was taking the Microbiology course with Annie Prud'homme Genereux. I also learned, while reading Eating Well, Living Well, that only 50% of all humans are lactose-tolerant. That means that 1 in every 2 humans do not have the enzyme that allows the body to digest milk. I, being a vegetarian, have used milk products in the past as an easy way to fulfill my protein requirements but I have recently been trying to use other food sources because of this fact. I thought that maybe if animal milk wasn't a natural source of nutrients for humans than that must mean that we naturally don't need it and we must be able to get the same nutrients from other food sources. But before going dairy-free, I thought I might do a little research on the topic before I made the decision.

In the book, Eating Well, Living Well by Richard Beliveau and Denis Gingras, I came across a section that talked all about the milk debate. It said that humans naturally loose the ability to digest milk when they reach adulthood because the enzyme that breaks down lactose (the natural sugar is milk) disintegrates. The only reason that 50% of people can still consume lactose is because of the cattle farmers about 9,000 years ago. During the time when food was a challenge to find, the cattle farmers resorted to the milk of their goats, sheep, and cows. At first this was difficult because they did not have the enzyme that let them break down the lactose molecules. Instead, the lactose would be fermented by the bacteria in their intestines and cause bloating and irritation to their stomachs. Sometimes, it would even cause diarrhea and dehydration. These are the same symptoms people that are lactose-intolerant experience today. However, after consuming it many times, a gene mutated in their DNA that prevented the enzyme that breaks down lactose to not be lost when they got older. Therefore, everyone that can tolerate lactose today is a descendant of these cattle farmers.

What is really interesting is that these cattle farmers mostly lived in northern Europe. Because Europeans migrated West to the Americas, most people in Northern Europe and in North America have that gene mutation and are lactose-tolerant. Since very little migrated East, only about 1% of people in China and 5% of western Africa can tolerate lactose. This is the reason you'll find that Asian food and certain typed of African food contain little to no dairy.

One thing that it also mentions is that a different gene mutation happened in Eastern African countries such as Tansania, Kenya, and Sudan which allowed humans living there to digest lactose as well. This is somewhat of a phenomenon because this gene mutation happened around the same time as the other gene mutation in Northern Europe but differed in the specific gene that was altered. It is thought that the gene mutation in Eastern Africa first happened in pastoral populations in other parts of Europe but spread east to Eastern Africa.

But does this mean that it is unnatural for humans to drink milk from other mammals? Looking at it from the evolutionary stand point, it is natural for humans to drink it. With evolution, the species that can adapt to the changing environment will survive the longest. Therefore, some genes in species are altered to help the species live longer. Species that no gene mutations take place, simply go extinct. Therefore, the mutation in the gene that allows humans to digest lactose must have been an evolutionary change to help humans survive for a longer period of time.

However, it can also be looked at from a naturalist view. If humans were never intended to digest lactose after reaching adulthood, then it is unnatural for humans to consume it now. Another way of seeing it as unnatural is that humans forced it on themselves to have their bodies adjust to the lactose. And if no other mammal drinks milk from different species than their own, than humans should be no exception.

So I'll leave it up to you to decide whether consuming animal is natural or unnatural for humans. For me, I believe that it is natural for humans to consume lactose. Maybe it was not natural for the cattle farmers hundreds of years ago and the mutation didn't happen naturally because humans forced it on themselves, but today our bodies naturally produce the enzyme to tolerate it thus making it natural for humans today to consume it.

Despite my opinion on the topic, I am going to challenge myself to consume less dairy. This has nothing to do with the debate, but because it sounds like fun challenge to try and find the nutrients from other food sources. Since I love soy products so much, I don't think it will be that hard. Maybe I'll go vegan. hahaha just kidding. I could never give up chocolate! I'll let you know how it goes. hahaha.

Feel free to tell me your thoughts on the debate. Do you think it is natural for humans to consume milk?



:)

Childhood obesity: the factors that contributed to the new epidemic

Written by Jenny Clark

April 22, 2011

Childhood obesity is rapidly becoming a global issue. It has been estimated that over 42 million children under the age of 5 were overweight in 2010, with nearly 35 million of those children living in developing countries (WHO, 2010). In the US, the amount of children who are classified as obese has more than tripled in the past 30 years ( CDC, 2010). The percentage of obese children between the ages of 6-11 years increased from 6.5% in 1980 to 19.6% in 2008. Adolescents with obesity (ages 12-19) also increased from 5.0% in 1980 to 18.1% in 2008. The World Health Organization defines obesity as “abnormal or excessive fat that presents a risk to health” (WHO, 2011). They measure obesity using the Body Mass Index (BMI) which uses a person’s height and weight as variables to determine their risk of a disease. A BMI greater than 25 is considered overweight and a BMI greater than 30 is considered obese.

With children, obesity is also measured using BMI, but age and sex are also factored in since their bodies are still growing (Obesity Action Coalition, 2010). Therefore, instead of measuring obesity as a BMI higher than a specific number, it is calculated in BMI-for-age percentile which indicates where the child’s weight is in comparison to other children of the same age and sex. If a child’s BMI-for-age-percentile is greater than 85%, the child is considered overweight. If a child’s BMI-for-age percentile is greater than 95%, the child is considered obese.

Being overweight during childhood has brought up many concerns due to the many health risks associated with excess fat tissue. Childhood obesity has been associated with insulin resistance, high cholesterol, high blood pressure, asthma, sleep disorders, hardening of the arteries, and mental health problems during young adulthood (Steinberger & Daniels, 2003; Paxon, 2006). It is estimated that the health-costs associated with childhood obesity rose from $35 million in 1980 to $127 million in 1998. This cost is relatively small compared the estimated $51.5 to $78.5 billion spent on hospital costs in 1998 for adult obesity. However, prices are expected to rise as more children become obese.

What causes obesity is not entirely understood. Many scientists agree that the increase in caloric intake with the reduction in energy expenditure is the underlining reason for the childhood obesity epidemic. Yet, even babies who are not able to eat high-calorie foods and cannot participate in physical activity increased in obesity as much as 73% since 1980 (Begley,2009). Therefore, new studies have been conducted to determine all the factors of obesity. Many scientists are finding numerous possible factors including parental influences, social influences, media and advertising, and genetics (Federal Trade Commission, 2008).

The parenting techniques used by parents are also thought to influence the likelihood of their children becoming overweight or obese. One factor that has been considered is the length of time in which a child is breastfed. Harder, et al. (2005) conducted a meta-analysis of studies on duration of breastfeeding and the risk of being overweight later in life. From the studies, they found that for each extra month that a child is breastfed, their risk of being overweight decrease by 4%. This trend continued up until the baby reached 9 months old. Researchers hypothesize that this effect happens because extra sugars and fats are added into bottle formula, whereas breast milk is full of natural nutrients and fats (ASPE, 2011). Also, the foods that the parents provide in the household are thought to encourage unhealthy eating habits if the foods are low in nutritional quality. In a study conducted by Whitaker, et al. (1997), adolescents with at least one obese parent had a 79% chance of being obese during adulthood compared to the 8% chance for children without an obese parent. Researchers believe that this occurs because a child of the obese parent adopts the unhealthy habits that the obese parent demonstrates and the child is more likely to be offered food of low-nutritional quality (ASPE, 2011).

Many social influences have also been thought to contribute to the rise in childhood obesity in the past few decades. Some of these influences include the increase in the number of restaurants and fast-food restaurants around the world, the increase in processed foods, the price differences in fresh foods in comparison to processed foods, the increase in portion sizes, and the types of foods that have become socially acceptable to eat (French, et al., 2001; Maibach, 2007; ASPE, 2011). In addition, the easier access to cars and other forms of mechanical transportation has greatly reduced the amount of walking and physical exercise required for people to offset their current daily caloric intake, likely contributing to the obesity epidemic. Socio-economic status has also been shown to influence a child’s risk of becoming overweight or obese in many parts of the world (Drenowatz, et al., 2010; Sodjinou, et al., 2008). Lower socio-economic status has been linked to an increase likelihood of poor nutrition, sedimentary activity, and poor food habits (Groholt, et al.,2008). All the hypothesized social influences contribute to the increase in caloric intake and the reduction in physical activity, which are thought to be the underlining cause of the obesity epidemic.

As mentioned earlier, advertising to children has a significant effect in what children want to eat and how little they participate in physical activity. In 2006 alone, food, beverage, and fast-food restaurants spent nearly $1.6 billion on advertisements to generate almost 136 billion food ads, with children being their main targeted audience. With all these ads directed at children, it is estimated that each child in the US receives an average of 65 messages of advertisement each day from television alone (Batadam & Wootan, 2007). In addition, Hasting, et al. (2003) found that advertisements have a distinct effect on the food children choose to eat, thus affecting the amount of high-calorie and low-nutritional quality food intake of the children that frequently see the advertisements. At the same time, using media has been shown to increase sedimentary activities and reduce the amount of participation in physical activity by children (Boyce, 2006; Jago, et al., 2005). Together, the increase of caloric intake and the decrease in physical activity resulting from media has negatively influenced how children interpret healthy living, which has thus contributed to the increasing amount of overweight and obese children.

The newest theory in obesity research involves looking at different genes that might be associated with a person’s ability to use dietary fats as fuel, the ability to store body fat, or the poor regulation of appetite that may cause a person to become obese even without the excess caloric intake and physical inactivity (CDC, 2011). These genes have been referred to as “energy-thrifty genes” because it is thought that they make people’s bodies unable to adapt to our society’s abundant food supply, which our ancestors did not have access to all year round. Currently, there have been three genes whose presence in the body have been found that correlate with obesity: FTO, MC4R, and PCSK1 (Hofker & Wijmenga, 2009). FTO and MC4R have been shown to correlate to BMI in obese individuals. PCSK1, along with MC4R, has been shown to be linked with severe or syndromic forms of obesity in mice and humans. However, the links between each of the genes are not fully understood and are still being researched. In addition, many more genes are being researched to determine whether there are more genes correlated to obesity. Nevertheless, future findings in obesity genetics will provide a better understanding of treatment and prevention methods for obese children and obese adults.

In conclusion, many factors have contributed to the childhood obesity epidemic that many developing countries are currently facing. In order to prevent childhood obesity from continuing to rise, more attention should be put towards changing these factors and educating children how to live healthily and develop healthy eating habits early in life.

References:

ASPE (2011). Childhood Obesity. U.S. Department of Health & Human Services: Assistant Secretary for Planning and Evaluation. [web] http://aspe.hhs.gov/health/reports/child_obesity/#_ftn93. Viewed on March 9, 2010.

Begley, S. Born to be big. Newsweek, 154, 12, p56-62.

Boyce, T. (2007). The media and obesity. The International Association of the Study of Obesity. Obesity Reviews 8, 1, 201-205.

CDC (2010). Childhood Obesity. National Center for Chronic Disease Prevention and Health Promotion, Division of Adolescent and School Health. [Web] http://www.cdc.gov/healthyyouth/obesity/. Viewed on March 9, 2011.

CDC (2011). Genomics and Health: Obesity and Genomics. Office of Surveillance, Epidemiology, and Laboratory Services, Public Health Genomics. [web] http://www.cdc.gov/genomics/resources/diseases/obesity/obesedit.htm. Viewed on March 9, 2010.

Drenwatz, C., Eisenmann, J.C., Pfeiffer, K. A., Welk, G., Heelan, K., Gentile, D. and Walsh, D. (2010). Influence of socio-economic status on habitual physical activity and sedentary behavior in 8- to 11-year old children. BMC Public Health, 10, 214.

Harder, T., Bermann, R., Kallischnigg, G., and Plagemann, A. (2005). Duration of breastfeeding and risk of overweight: a meta-analysis. American Journal of Epidemiology, 162, (5), 397-403

Hastings, G., Stead, M., McDermott, L., Forsyth, A., MacKintosh, A. M., Rayner, M., Godfrey, C., Caraher, M., and Angus, K. Review of research on the effects of food promotion to children: final report. Food Standards Agency. Downloaded at http://www.food.gov.uk/multimedia/pdfs/foodpromotiontochildren1.pdf

Groholt, E.K, Stigum, H., Nordhagen, R. Overweight and obesity among adolescents in Norway: cultural and socio-economic differences. Journal of Public Health, 30 (3): 258-265.

Hofker, M. and Wijmenga, C. A supersized list of obesity genes. Nature Genetics, 41 (2): 139-140.

Jago, R., Baranowski, T., Baranowski, J. C., Thompson, D. and Greaves, K.A. (2005). BMI from 3-6 of age is predicted by television viewing and physical activity, not diet. International Journal of Obesity, 29: 557-564.

Obesity Action Coalition (2010). All About Obesity. Obesity Action Coalition. [web] http://www.obesityaction.org/aboutobesity/childhoodobesity/childhood.php. Viewed on March 9, 2011.

Paxon, C. (2006). Childhood Obesity: The Future of Children. The Future of Children Journal, 16, 1, spring.

Sodjinou, R., Agueh, V., Fayomi, B, and Delisle, H. (2008). Obesity and cardio-metabolic risk factors in urban adults of Benin: Relationship with socio-economic status, urbanisation, and lifestyle patterns. BMC Public Health, 8,84.

Steinberger, J. and Daniels, S. R. Obesity, Insulin Resistance, Diabetes, and Cardiovascular Risk in Children: An American Heart Association Scientific Statement From the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). (2003). The American Heat Association Circulation, 107, 1448-1453.

Whitaker, R. C., Wright, J. A., Pepe, M.S., Seidel, K. D., and Dietz, W. H. Predicting obesity in young adulthood from childhood and parental obesity. The New England Journal of Medicine, 337 (13): 869-873.

School Lunches and Nutritional Education

Written by Jennifer Clark

April, 13 2011

School lunch programs began in the US around 1890 after educators noticed that their students were too hungry to concentrate on learning half way through the day (Poppendieck, 2010). Food was donated to the schools by charity groups and women’s organizations. During the Great Depression in the 1930s, food became scarce and school lunches programs no longer had food to give to the students. Students began having troubles finding food in their homes as well as at school, leaving them to starve. In 1934, the Chicago Board of Education reintroduced school lunches in the city in an attempt to end the child hunger of the Depression (Levine, 2008). The programs were run by volunteers and food was donated by various farmers and companies. Many States saw the progress being made in Chicago and decided to ask legislators to authorize a portion of tax funds to go towards newly established school lunch programs (Poppendieck, 2010). However, when this happened, the schools were receiving surpluses of food, so much that there was no program to regulate which foods were to be distributed to certain schools. The government stepped in to help regulate the amount of food being put towards school lunches, and was eventually handed over to the USDA. By 1946, the National School Lunch Act was passed by congress which required States to grant aid to the school lunch program to ensure the health and well-being of the nation’s children, as well as donate the surplus of any agricultural commodities to continue the success of the school lunch programs ((Poppendieck, 2010). Ever since then, the school lunch system has been trying to establish a healthy food system for children regardless of their economic background, while balancing the amount of food contributed to each of the schools.

As of today, nearly 101,000 schools in the US have lunch programs ran by the National School Lunch Program (NSLP) (NSLP, 2011). On average, the NSLP serves approximately 60% of the entire student population (31.3 million students) per day. Also, approximately 87,000 schools participate in the School Breakfast Program, a partner federal-run program with the NSLP, which serves nearly 11 million children each day (NSBP, 2011). The federal programs began implementing nutritional standards in government-supported schools, whereby schools were contracted to supply a specific number of servings per food group for each student that receives free or reduced lunch prices (Poppendieck, 2010). The goal of these nutritional standards was to make sure that each child was getting at least a third of the recommended nutrients per day as well as a well-balanced meal. However, there have been many controversies regarding the effectiveness of theses programs and the nutritional benefits on the health of the children.

Firstly, if schools do not follow this policy with children that get free or reduced lunch prices, the schools will not get reimbursed from the government to pay for the meals (Poppendieck, 2010). To avoid not getting reimbursed, schools began modifying the menus to fit the preferences of the children, while continuing to satisfy each of the food groups required. For many of these changes, the new foods would be of less nutritional value than the original, but would follow the required food groups set by the government program. For example, instead of supplying cooked carrots as a vegetable serving, they began serving French fries because children showed more interest in them. Also, instead of serving whole milk for the children to drink, the schools began overstocking with chocolate milk. Since the government had no regulations on specific types of foods, French fries were considered as an appropriate vegetable choice and chocolate milk was considered an appropriate dairy choice. Furthermore, since the children were more likely to eat the French fries and chocolate than the alternatives, the schools were happier supplying them because they knew that they would be reimbursed.

Parents are also concerned with the prices of school lunches. Therefore, the school food programs alter the food choices in the menu to allow prices to reduce. However, school food programs struggle to make profit or even break even (Poppendieck, 2010). There are many reasons for this. One reason is because parents of the students demand that school lunch prices decrease. In order to do that, schools adjust their menu to serve cheaper food options to keep the prices of the meals at minimal charges. At the same time, the schools no longer have the flexibility to adjust the prices to make any profit, leaving them in a budget-tight situation. Another reason schools are struggling to balance their budget is because the demand for school lunches is unpredictable and unreliable. Since buying school lunch is not mandatory in all schools, the food staff have to estimate their budget. If they make too much food and not many students buy the food, then the kitchen looses money. Lastly, schools also have to budget for the amount of labour that goes into the food preparation and serving. Not only do the schools need to pay for the food, they also need to pay the staff that prepares and serves the food. With the already lowered prices, the strict regulations for reimbursement on meals, and not knowing the exact amount of students that will participate in the program each day, it makes it difficult for the school to prepare a budget for the lunch program. Therefore, schools buy mostly processed food because it costs less than fresh fruits, vegetables, and meats, it cuts down preparation costs because they no longer have to hire trained chefs to cook the food, and the foods have more appeal for the children.

In addition, schools want to sell as much food as possible to make some profit (Poppendieck, 2010). The best way, and the only way without making school lunch mandatory, is to sell foods that the students like and want. Since the schools only have policies to follow with the lunch program, many schools have added vending machines and a la carte stations in their schools, filled with all the foods not available in the lunch program. In fact, according to the School Nutrition Dietary Assessment Study-III, 80% of middle schools and 97% of high schools in the US had at least one vending machine on school property during the 2004-2005 school year (Gordon, et al., 2007). The a la carte stations included pieces of fruits and vegetables but the majority of the food included chips, crackers, ice cream, cookies, candy/candy bars, French fries, nachos, bagels, pizza, and pretzels (French, et al., 2003).

Also, processed food companies create contracts with the schools that give them benefits. For example, with soda machines, Coca-Cola made a 10-year contract with the Colorado Springs school district worth between $8-11 million, that included cash bonuses and incentives for exceeding the sale target (Jacobson, 2005; Nestle, 2007). These incentives included giving a brand new car to a superior senior who attended class everyday and had high grades, scholarships for college, and assisted with volunteer and fundraising programs at local schools. All in all, it appears to be a win-win situation for the schools, the parents, the government, and the children. However, the health and well-being of the children are being ignored.

Luckily, many changes are being made in schools to make it more nutritious for the students. In December 2010, President Barack Obama signed the Heathy, Hunger-Free Kids Act of 2010 which allocated $4.5 billion in new funding to make school lunches more affordable and more nutritious for students. The Act will take effect beginning in July 2011 (Child Nutrition Reauthorization: Healthy, Hunger-Free Kinds Act of 2010). This act gives the USDA the authority to enforce nutritional standards to all the foods sold in schools, including the vending machines and the á la carte stations. It will also allow the USDA to redesign the nutritional standards to improve the nutritional quality of the food. Also, the funding will help schools build a working relationship with local farms and helps design school gardens which will allow schools to offer local and organic produce. It will promote nutritional education policies in schools that will inform children on the importance of eating healthily and participating in regular exercise. Lastly, it will increase the access of drinking water to school. With the help of this bill, the US is on its way to reducing obesity and improving the health of children all around the country.

References:

Child Nutrition Reauthorization: Healthy, Hunger-free Kids Act of 2010. (2010). The White House: Office of the Press Secretary. http://www.whitehouse.gov/sites/default/files/Child_Nutrition_Fact_Sheet_12_10_10.pdf

French, S. A., Story, M., Fulkers, J. A., and Gerlach, A. F. (2003). Food environment in secondary schools: á la carte, vending machines, and food policies and practices. American Journal of Public Health, 93 (7), 1161-1168.

Gordon, A., Crepinsek, M. K., Nogales, Condon, E. (2007). School Nutrition Dietary Assessment Study-III: Volume I: School Foodservice, School Food Environment, and Meals Offered and Served: Executive Summary. USDA: Food and Nutrition Service Office Report. http://www.fns.usda.gov/ora/menu/published/cnp/files/sndaiii-vol1execsum.pdf

Jacobson, M. F. (2005). Liquid candy: how soft drinks are harming Americans’ health. Second Edition. Center for Science in the Public Interest.

Levine, S. (2008). School Lunch Politics: The surprising history of America’s Favorite Welfare Program. Princeton: Princeton University Press.

NSBP (2011). Fact Sheet: The School Lunch Plan. The USDA: Food and Nutrition Service. http://www.fns.usda.gov/cnd/breakfast/AboutBFast/SBPFactSheet.pdf

NSLP (2011). Fact Sheet: National School Lunch Program. The USDA: Food and Nutrition Service. http://www.fns.usda.gov/cnd/lunch/AboutLunch/NSLPFactSheet.pdf

Nestle, M. Food Politics: how the food industry influences nutrition and health. Berkley: University of California Press, 2007.

Poppendieck, J. (2010). Free for all: fixing school food in America. Los Angeles: University of California Press, Ltd.

The media and its influence on the physical and mental health of children

Written by Jennifer Clark

April 10, 2011

The media is all around us. With the drastic improvement in technology over the last few decades, media sources have skyrocketed (Maibach, 2007; French, et al., 2001). Today there are millions of websites available on the internet, hundreds of channels available on the television, and an increased accessibility to music and downloading sites, all of which expose us to thousands of advertisements each day. In fact, out of all US household in 2009, 75% owned a home computer, 71% had an internet connection, and 81% has at least one cell phone. Unfortunately, as much as it is one of our main sources of entertainment, it has also contributed to the increase in sedimentary lifestyles and our awareness of body perception, which has ultimately contributed to the increase health risks in our society.

However, the media is not only influencing the lifestyles and behaviours of adults. Children learn much about their social world through the images and characters they see in media, and has been shown to influence their food preferences (Bandura, 2001; Harris and Bargh, 2009). Children are one of the most targeted groups for advertisement agencies. A review study conducted by Robert, et al. (2005) found that children are exposed to 8.5 hours of media each day, 6.5 hours of which they are actually using the particular media themselves. In the study, use of television and music outweighed all the other media sources. In another study conducted by Batadam & Wootan (2007), the results suggested that each day, children received an average of 65 messages from advertisements on television alone.

The majority of the advertisements shown on children networks promote food products, 98% of which are foods low in nutritional value (Powell, et al., 2007). In 2006, the Federal Trade Commission (FTC) found that children would see approximately 5,538 different food ads from television, and teens would see approximately 5,512 in that year alone (Federal Trade Commission 2008). This comes as no surprise since in that same year, all children shows generated approximately 136 billion food ads with at least 50% had been targeted to children aged 2-11. Overall, It was estimated that food, beverage, and fast-food restaurants spent approximately $1.6 billion on advertisements with children as their main targeted audience.

In a study that investigated the types of advertisements shown on the Nickelodeon channel and the corresponding Nickelodeon’s magazine, the number-one entertainment company for children, it was found that 148 out of the 168 (88%) television food ads and 16 out of 21 (76%) of the magazine food ads promoted foods of poor nutritional quality (Batada & Wootan 2007). These advertisements included McDonald’s happy meals, Burger King’s kids meals, various carbonated drinks, sugary and salt snack foods, and sugary cereals (Powell, et al. 2007). This means that less that 20% of the food advertisements promoted healthy foods. Seeing as Nickelodeon is the top entertainment company for children, these advertisements are being exposed to the majority of the children in the North America. With these types of ads, they are ultimately encouraging unhealthy eating habits in all the children that use their media.

Furthermore, the advertisements incorporated the characters of the popular television shows that the children are watching. This brand recognition and positive association with the characters and the unhealthy food products is a popular method used in advertising to children in hopes of increasing interests in the processed foods market (Connor 2006). Unfortunately, marketers defend their choice to advertise to children because they have the right to free speech and that all foods, even the unhealthy foods, can be part of a balanced diet (Nestle, 2007). Since unhealthy food companies are willing to spend such large amounts of their budgets advertising to children, marketers are more than willing to make advertisements that make them the most money.

Ironically, Nickelodeon is a major sponsor for promoting childhood obesity awareness, and has partnered with Michelle Obama in her “Let’s Move” campaign to reduce childhood obesity. In doing so, Nickelodeon has incorporated small segments in between their shows that encourage children to go out and play. Yet, Nickelodeon continues to advertise unhealthy foods using brand recognition and positive association, sending mixed signals to children about what it means to live healthily.

Hastings, et al. (2003) conducted a review of more than 30,000 research articles regarding the effects of advertisements on children’s food choices and found that there was a distinct effect on the types of advertisements shown to children and the foods they chose to eat afterwards. Furthermore, many studies have shown that younger children are more likely to believe the health claims in advertisements and are more likely to ask their parents for the high-sugar foods they saw in the advertisements (ASPE 2011). Thus, advertising low-nutritional quality food towards children can influence their food choices early in life. With the increase in caloric intake from these low-nutritional foods, children are put at risk of developing nutritional deficiencies and other serious health issues like diabetes, obesity, and hypertension.

In addition, eating while watching television is linked to overeating. Conn, et al. (2001) conducted a study on the relationship between the amount of time spent watching television during meals and the amount of food consumed. The results showed that parent-child pairs that watched television during two or more meals a day consumed 6% more calories from meats, 5% more from pizza, 5% more salty snacks and soda, and almost 5% less in fruits, vegetables and juices, compared to parent-child pairs who watched television during one or no meals each day. The reasoning behind this extra caloric intake is believed to be because of the self-monitoring that is lost when watching media. Instead of concentrating on body signals that tell a person when they are full, people are concentrating on the entertainment from the media, therefore consuming more than they normal would if they were not distracted (French, et al. 2001). Scientist believe that this extra caloric intake contributes to the increase in body fat and puts children and adults at risk of developing serious health risks later in life.

Regardless to what type of media is being used, watching and reading media encourages a sedimentary lifestyle (Boyce, 2006; Marshall, et al. 2004). In a cohort study conducted on the association between BMI and the amount of participation in physical activity in 3-6 years of age, a strong correlation was found between the increased time spent on watching television and the decreased time spent on physical exercise (Jago, et al. 2005). At the same time, the National Center for Chronic Disease Prevention and Health Promotion (2011) suggests that participation in physical activity declines as a child gets older, with less than 20% of high school students regularly participating in at least 60 minute of physical activity per day. With the reduced amount of physical exercise and the increase in caloric intake, children have adapted unhealthy lifestyles that put them at risk of health problems in the future.

Also, media has been shown to influence the self-esteems of adolescents, contributing to body dissatisfaction and obsessions of body image (Groesz, et al., 2001; Taveras, et al., 2004). The media today has turned weight into a social issue and has created an idealistic perception of what beauty should look like. Being overweight or obese is seen as socially unacceptable. In a study conducted with adolescent girls and boys (ages 9-16), both sexes increased the amount of physical activity per week in hopes of constructing their bodies to look like those seen in the media (Taveras, et al., 2004). Although the increase of physical activity per week contributes to a healthy lifestyle, the body dissatisfaction that comes from disappointing results because of the unrealistic body images seen in the media contributes to an unhealthy mental well-being.

With the power that media has over children’s food choices, participation in physical activities, and their mental well-being, it comes as no surprise that children can develop unhealthy lifestyle choice when exposed to certain advertisements. To eliminate the increase in health risks associated with poor nutrition during childhood, advertisement should be restructured to encourage children to live healthily and understand that low-nutritional foods and sedimentary activities are not encouraged for their health and should be chosen on occasion rather than on a normal basis.

References:

ASPE (2011). Childhood Obesity. U.S. Department of Health & Human Services: Assistant Secretary for Planning and Evaluation. [web] http://aspe.hhs.gov/health/reports/ child_obesity/#_ftn93. Viewed March 9, 2010.

Bandura, A. (2001). Social cognitive theory of mass communication. Media Psychology, 3, 265-299.

Batadam A. and Wootan, M. G. (2007). Nickelodeon markets nutrition-poor foods to children. American Journal of Preventive Medicine, 33, (1), 48-50.

Boyce, T. (2007). The media and obesity. The International Association of the Study of Obesity. obesity reviews 8, (1), 201-205.

Conn, K. A., Goldberg, J., Rogers, B. L., Tucker. K .L. (2001). Relationship between use of television during meals and children’s food consumption patterns. Pediatrics, 107, 1, 1-9.

Connor, S. M. (2006). Food-related advertising on preschool television: building brand recognition in young viewers. Pediatrics, 188, 1478-1485.

Federal Trade Commission (2008). Marketing food to children and adolescents: a review of industry expenditures, activities, and self-regulation. A Federal Trade Commission Report to Congress. Washington D.C: Federal Trade Commission.

French, S. A., Story, M., and Jeffery, R. (2001). Environmental Influences on Eating and Physical Activity. Annual Review of Public Health, 22, 309-335.

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Diabetes mellitus: theories to explain the malfunctions in the body’s insulin-regulation process in type 1, type 2, and gestational diabetes.

Written by Jennifer Clark

March 20, 2011

Diabetes Mellitus is a groups of chronic diseases characterized by high levels of blood-glucose levels caused by the body’s inability to produce insulin or the body’s cells unresponsiveness to insulin (Grosvenor & Smolin 2006). According to the World Health Organization (2011), there are approximately 220 million people worldwide that have at least one type of diabetes. However, many people with the disease do not get diagnosed. In the US, approximately 18.8 million people have been diagnosed with diabetes, yet it is estimated that 7.0 million people have diabetes but have not been diagnosed (CDC, 2011). This is much more significant than the approximated 1.7 million people in Canada that were diagnosed with diabetes in 2009 (Statistics Canada, 2010).

There are three types of diabetes mellitus: Type 1, Type 2, and gestational diabetes. All three types are caused by different malfunctions in the insulin-regulation process in the body. Therefore, diabetics experience episodes of extremely high and low blood-glucose levels. High blood-glucose levels can result in glucosuria, a condition that results excretion of large amounts of glucose through urine (Nelson & Cox 2005). This can lead to frequent urination, known as polyuria, as well as polydipsia when large amounts of water is consumed to compensate for the amount lost from urination. Low blood-glucose levels can be lethal or cause serious health problems such as damage to the heart, blood vessels, kidneys, eyes, and nerves. In fact, diabetes is the leading cause of both kidney failure and blindness in adults (Grosvenor & Smolin 2006; American Diabetes Association 2011).

Although the pathology of diabetes is fairly understood by scientists, the etiologies of what caused the malfunctions in the insulin-regulation process to occur are not entirely understood. For each types, different theories involving genetics and environmental factors have been suggested to explain why each type of diabetes develops.

Type 1 Diabetes Mellitus

Type 1 diabetes (T1DM), also known as insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes, accounts for nearly 5-10% of all diabetes cases and is usually diagnosed before the age of 30. It occurs when insulin is no longer produced in the body because the insulin-producing β-cells located in the islets of Langerhans of the pancreas have been destroyed. In result, glucose molecules can no longer be absorbed by the cells of the body. This causes blood-glucose levels to elevate when glucose is consumed as well as prevents cells from storing glucose to produce energy when blood-glucose levels are low. Therefore, the only way to ensure proper glucose metabolism is to inject insulin into the body before consuming glucose.

The etiology of T1DM is not entirely understood, but theories involving genetics, environmental factors, and diet propose explanations to what exactly is causing the destruction of the insulin-producing β-cells.

Genetic links to T1DM have been studied since the late 1970s. Many genes have been associated with the onset of T1DM, all of which are found in two chromosome regions: the human leukocyte antigen (HLA) region on chromosome 6p21 and the insulin gene region on chromosome 11p15 (Morran, et al. 2008). The HLA loci contributes approximately 42% to familial inheritance wheres the insulin gene loci only contributes about 10%. The HLA region is associated with proper immune system functioning and is thought to be responsible for the development and activation of the autoimmune response that causes the onset of T2DM. However, recent studies have shown that over forty more loci might be linked to the onset of T1DM, making the genetics of diabetes more complexed previously believed (Barrett, et al. 2009).

The theory that is most accepted by health professionals is that a viral infection triggers diabetes-susceptible genes to cause an autoimmune response, which attacks and destroy its own insulin-producing β-cells in the islets. This idea evolved from studies in the 1970s involving the encephalomyocarditis (EMC) virus in male mice that produced diabetes-like symptoms and the Kilham rat virus (KRV) in rats that produced rapidly-occurring autoimmune diabetes (Boucher, et al. 1975; Jun & Yoon 2001). Since then, research has focused on whether viruses can influence the diabetes-susceptible genes in humans. According to Jun & Yoon (2001), 13 different viruses have been associated with the onset of T1DM. The most common of these viruses are thought to be Coxsackie B, Rubella, and mumps which can directly infect and destroy the β-cells, and Coxsackie B4 which has been shown to cause severe T1DM in children (von Herrath 2009).

Also, recent research suggests that vitamin D deficiency can contribute to the onset of T1DM. The vitamin D system in the body interacts with the VDR and CYP27B1 genes located on chromosome 12, many of which are located in the β-cells of the islets (Mathieu & Badenhoop 2005). Mutations on the CYP37B1 gene causes rickets and other vitamin D deficiencies in children, whereas mutations on the VDR gene have been associated with the increase risk of many types of cancer, reduced bone mineral density, and immune disorders. With the immune disorders, researchers believe that vitamin D may act as an immunosuppressive agent that can protect against the autoimmune response seen in T1DM. Scientist hypothesize that this occurs due to vitamin D’s essential role in insulin secretion. Norman, et al. (1980) found that the pancreas contains vitamin D-dependent calcium-binding proteins and cytosol receptors that contribute to the proper secretion of insulin. Without proper vitamin D intake, inadequate secretion of insulin occurs, triggering an autoimmune response (Giulietti, et al. 2004). Although research supports this theory, the pathology of vitamin D in diabetes has still yet to be fully identified.

Type 2 Diabetes Mellitus

Type 2 diabetes (T2DM), also known as non-insulin dependent mellitus (NIDDM), is the most common type of diabetes, accounting for 90-95% of all diabetes cases. It occurs when there is a defect in the regulation of insulin activity in the body (Nelson & Cox 2005). Unlike in T1DM, int T2DM the body still has the ability to produce insulin, but the cells become unresponsive to the insulin molecules. By doing so, it reduces the amount of insulin uptake in the cells, forcing glucose to remain in the bloodstream. Studies also show that T2DM may also be caused by a decrease in β-cell mass and an increase in β-cell apoptosis, which reduces the amount of insulin released from the islets (Butler, et al. 2003). T2DM usually occurs with a combination of many diseases which is referred to as metabolic syndrome (Grosvenor & Smolin 2006). These diseases can include obesity, hypertension, high levels of blood lipids, and insulin insensitivity.

Both genetic and environmental factors contribute to the onset of T2DM. Like T1DM, specific genes have been associated with the increased risk of developing T2DM. The gene that has been found to have the strongest association with T2DM is the TCF7L2 gene (Saxena, et al. 2006). It is involved with impaired insulin secretion and increased hepatic glucose production. The other two genes that have strong correlations to T2DM are PPARγ, which has a strong correlation with insulin resistance, and KCNJ11, which is thought to be associated with decreased insulin secretion (Rios & Gutierrez Fuentes 2010).

The major environmental factor associated with T2DM is excess weight, particularly in the abdominal region. With the drastic increase in obesity rates in the last few decades, excess fat is believed to be associated with the increase in T2DM (Tamasan, et al. 2010). Research suggests that adipose tissue can communicate with the brain and peripheral tissues by secreting hormones responsible for the regulation of appetite and metabolism (Lazar, 2005). In particular, adipose tissue secretes many proteins including leptin that maintain glucose metabolism and insulin production. Thus, adipose tissue can cause an imbalance in glucose-insulin modulation, which fluctuates the blood-glucose levels in the body. Therefore, unlike T1DM, T2DM can be prevented and sometimes cured with the elimination of unhealthy living habits.

Gestational Diabetes Mellitus

Gestational diabetes mellitus (GDM) occurs in 5-10% of women during pregnancy. It happens when the pancreatic β-cells are unable to produce excess amounts of insulin to compensate for the insulin-blocking hormones released during pregnancy (Metzger, 2007). Fortunately, 90-95% of all women with GDM regain normal insulin production after giving birth (CDC, 2011). However, GDM is usually an early sign of diabetes with 35-60% of women developing diabetes 10-20 years after being diagnosed with the disease.

Although the etiology of GDM is not entirely understood, evidence suggests that a combination of the increase maternal adiposity and the increase hormonal effects of pregnancy on insulin-insensitivity are the main factors that contribute to the development of the disease (Buchanan & Xiang 2005). Since insulin resistance usually begins during mid-pregnancy and progresses till the end of the third trimester, the increase adipose tissue around the abdomen is thought to contribute to the cells’ insulin insensitivity, similar to excess body fat in T2DM. Also, since both insulin resistance and hormones re-stabilizes after delivery, it is thought the the hormones may contribute to the reduction in insulin production in the β-cells. In addition, certain factors can increase the risk of developing GDM during pregnancy such as being overweight, pre-diagnosed or undiagnosed with a type of diabetes, and genetic predisposition (Metzger 2007).

Conclusion

Although the etiology of diabetes is not fully understood, research has distinguished the specific malfunctions each type cause in the insulin-regulation process of the human body. With further research in the causes of the malfunctions, understanding of how insulin regulation is effected by genetic and environment factors can be established and can be used to reduce and prevent the development of diabetes in the future.

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