| The study conductor(s)top |
| Bart Hoebel, Professor of Psychology, Princeton Neuroscience Institute |
| The participant(s)top |
| TKEM Lab Rats |
| Date study concludedtop |
| March 22, 2010 |
| Funded bytop |
| Princeton Neuroscience Institute |
| Purposetop |
|
To determine if a link exists between high-fructose corn syrup consumption and obesity when compared with sugar. |
| Summarytop |
|
The experiment found that rats consuming high-fructose corn syrup were much more likely to become obese and have various health problems, especially with cholesterol. |
| Methods usedtop |
|
In an initial experiment, Hoebel and colleagues from the Princeton Neuroscience Institute gave male rats water sweetened with either high-fructose corn syrup or sucrose (standard table sugar) in addition to their standard diet of rat feed. The concentration of sugar was roughly the same as that found in commercial sodas, while the concentration of high-fructose corn syrup was half that found in soda. |
| Resultstop |
|
The study, published online in the journal Pharmacology, Biochemistry and Behavior, found that, not only did rats consuming high-fructose corn syrup gain more weight than those eating sugar, but they also had abnormal increases in body fat, particularly in the abdomen and in the form of elevated triglyceride levels in the blood. In a second experiment, researchers tracked weight gain, body fat and triglycerides in rats eating only rat feed, compared with those regularly consuming high-fructose corn syrup. Researchers found that, compared with those on a standard rat diet, those eating the high-fructose corn syrup gained significantly more weight, and had higher concentrations of body fat and triglycerides, symptoms in keeping with what is known as metabolic syndrome in humans. Male rats in particular put on a significant amount of excess weight during the six-month study, gaining 48% more weight than those on the standard diet. |
| Notestop |
|
[+] This study has been peer reviewed and validated by various researchers from Princeton. |
| External Sourcestop |
| http://www.princeton.edu/main/news/archive/S26/91/22K07/ http://wellness.blogs.time.com/2010/03/23/study-high-fructose-corn-syrup-causes-more-weight-gain/ |
| APA Citation(s)top |
| High Fructose Corn Syrup and Obesity. (2010). Retrieved February 22, 2012, from Public Studies Web site: http://www.publicstudies.com/main/2010/03/high-fructose-corn-syrup-and-obesity/ |
| MLA Citation(s)top |
|
“High Fructose Corn Syrup and Obesity” Public Studies. 22 March 2010. February 22, 2012. <http://www.publicstudies.com/main/2010/03/high-fructose-corn-syrup-and-obesity/>. |
Archive for the ‘Health’ Category
High Fructose Corn Syrup and Obesity
Health Risks, Smoking and Obesity Comparison
| The study conductor(s)top |
| Dr. Martin Neovius (Karolinska Institute in Sweden) |
| The participant(s)top |
| 45,000 men who underwent mandatory military conscription tests in Sweden |
| Date study concludedtop |
| February 1, 2009 |
| Funded bytop |
| Unknown |
| Purposetop |
|
To determine the highest probable cause of death between cigarette smoking and obesity in males. |
| Summarytop |
|
45,000 men were tested for health factors and questioned about their smoking habits for the purpose of following up with them later. During the follow up period 2,897 subjects died, the incidence of death was lowest for people with normal weight and highest in obese subjects. The risk of premature death also correlated heavily with the increase of the number of cigarettes smoked per day. |
| Methods usedtop |
|
The participants all had their body mass index (BMI) measured and reported their smoking status at the age of 18 and were followed up for an average of 38 years. |
| Resultstop |
|
Being overweight at the age of 18 increased the risk of premature death by just over a third, while being obese more than doubled the risk. Being underweight carried no increased risk, irrespective of smoking status. However, being seriously underweight (a body mass index of less than 17) carried the same risk of premature death as being overweight. The combination of obesity and heavy smoking was associated with a large excess risk of early death (almost five times greater than normal weight non-smokers). However, there was no statistically significant interaction between these two factors. This means that being overweight or obese at the age of 18 increases the risk of premature death regardless of smoking status. Early death was also linked to the number of cigarettes participants smoked per day. This risk gradually increased the more participants smoked, with heavy smokers at more than double the risk of premature death compared to non-smokers. |
| Notestop |
|
| External Sourcestop |
| http://www.physorg.com/news154768226.html | http://www.webmd.com/news/20090225/teen-obesity-as-deadly-as-smoking |
| APA Citation(s)top |
| Health Risks, Smoking and Obesity Comparison. (2009). Retrieved February 22, 2012, from Public Studies Web site: http://www.publicstudies.com/main/2009/02/health-risks-smoking-and-obesity-comparison/ |
| MLA Citation(s)top |
|
“Health Risks, Smoking and Obesity Comparison” Public Studies. 1 February 2009. February 22, 2012. <http://www.publicstudies.com/main/2009/02/health-risks-smoking-and-obesity-comparison/>. |
Autism diagnosis and environment
| The study conductor(s)top |
| University of California researchers |
| The participant(s)top |
| Population sample of reported cases of Autism in CA from 1990 to 2001 |
| Date study concludedtop |
| January 1, 2009 |
| Funded bytop |
| State of California |
| Purposetop |
|
To isolate a statistically significant probably cause of Autism |
| Summarytop |
|
More than 3,000 new cases of autism were reported in California in 2006, compared with 205 in 1990. This increase does not correlate with increased willingness or ability to diagnose this condition. Changes in how and when doctors diagnose the disorder and when state officials report it can explain less than half of the increase. In 1990, 6.2 of every 10,000 children born in the state were diagnosed with autism by the age of five, compared with 42.5 in 10,000 born in 2001. |
| Methods usedtop |
|
Sample analysis. Hertz-Picciotto and Lora Delwiche of the UC Davis Department of Public Health Sciences analyzed 17 years of state data that tracks developmental disabilities, and used birth records and Census Bureau data to calculate the rate of autism and age of diagnosis. |
| Resultstop |
|
California’s sevenfold increase in autism cannot be explained by changes in doctors’ diagnoses and most likely is due to environmental exposures. The researchers have theorized that a pregnant woman’s exposure to chemical pollutants, particularly metals and pesticides, could be altering a developing baby’s brain structure, triggering autism. |
| Notestop |
|
[+] This study was peer reviewed at the source. |
| External Sourcestop |
| http://www.scientificamerican.com/article.cfm?id=autism-rise-driven-by-environment |
| APA Citation(s)top |
| Autism diagnosis and environment. (2009). Retrieved February 22, 2012, from Public Studies Web site: http://www.publicstudies.com/main/2009/01/autism-diagnosis-and-environment/ |
| MLA Citation(s)top |
|
“Autism diagnosis and environment” Public Studies. 1 January 2009. February 22, 2012. <http://www.publicstudies.com/main/2009/01/autism-diagnosis-and-environment/>. |