Mind Your Body Mar 2010
Mind Your Body Mar 2010
Thursday, March 25, 2010
Feline Permethrin Toxicity
Boland LA, Angles JM: Feline permethrin toxicity: retrospective study of 42 cases, J Feline Med Surg 12:61, 2010.
This study was a retrospective review of 42 cases of feline permethrin toxicity treated at a referral hospital in Australia. Most of the cases had a canine permethrin spot-on (PSO) flea product directly applied to the affected cats. Approximately half of the cases developed toxicity following a PSO product purchased from a supermarket. Most of the cases occurred in the summer. Cats are particularly sensitive to the effects of permethrin. Tremors and muscle fasciculations were the most common clinical sign exhibited in 86% of cats affected followed by twitches, hyperesthesia, seizures, pyrexia, ptyalism, ataxia, mydriasis, and temporary blindness. The clinical onset of signs was from a few hours up to 24-72 hours after application of the PSO. There was no correlation between the amount of permethrin applied and the severity of clinical signs induced. In this study, treatment involved decontamination, anticonvulsants, and supportive care. Methocarbamol was not used. Hypothermia was the most common complication found during treatment, followed by electrolyte abnormalities. One cat had to be euthanized during treatment. Results of this study suggest that the lack of availability of methocarbamol for treatment should not preclude treatment of permethrin toxicity. [VT]
Related articles:
Sutton NM, Bates N, Campbell A: Clinical effects and outcome of feline permethrin spot-on poisonings reported to the Veterinary Poisons Information Service (VPIS), London, J Feline Med Surg 9:335, 2007.
Dymond NL, Swift IM: Permethrin toxicity in cats: a retrospective study of 20 cases, Aust Vet J 86:219, 2008.
More on cat health: Winn Feline Foundation Library
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This study was a retrospective review of 42 cases of feline permethrin toxicity treated at a referral hospital in Australia. Most of the cases had a canine permethrin spot-on (PSO) flea product directly applied to the affected cats. Approximately half of the cases developed toxicity following a PSO product purchased from a supermarket. Most of the cases occurred in the summer. Cats are particularly sensitive to the effects of permethrin. Tremors and muscle fasciculations were the most common clinical sign exhibited in 86% of cats affected followed by twitches, hyperesthesia, seizures, pyrexia, ptyalism, ataxia, mydriasis, and temporary blindness. The clinical onset of signs was from a few hours up to 24-72 hours after application of the PSO. There was no correlation between the amount of permethrin applied and the severity of clinical signs induced. In this study, treatment involved decontamination, anticonvulsants, and supportive care. Methocarbamol was not used. Hypothermia was the most common complication found during treatment, followed by electrolyte abnormalities. One cat had to be euthanized during treatment. Results of this study suggest that the lack of availability of methocarbamol for treatment should not preclude treatment of permethrin toxicity. [VT]
Related articles:
Sutton NM, Bates N, Campbell A: Clinical effects and outcome of feline permethrin spot-on poisonings reported to the Veterinary Poisons Information Service (VPIS), London, J Feline Med Surg 9:335, 2007.
Dymond NL, Swift IM: Permethrin toxicity in cats: a retrospective study of 20 cases, Aust Vet J 86:219, 2008.
More on cat health: Winn Feline Foundation Library
Join us on Facebook
Follow us on Twitter
New for 2010: subscribe to our e-newsletter
Boland LA, Angles JM: Feline permethrin toxicity: retrospective study of 42 cases, J Feline Med Surg 12:61, 2010.
This study was a retrospective review of 42 cases of feline permethrin toxicity treated at a referral hospital in Australia. Most of the cases had a canine permethrin spot-on (PSO) flea product directly applied to the affected cats. Approximately half of the cases developed toxicity following a PSO product purchased from a supermarket. Most of the cases occurred in the summer. Cats are particularly sensitive to the effects of permethrin. Tremors and muscle fasciculations were the most common clinical sign exhibited in 86% of cats affected followed by twitches, hyperesthesia, seizures, pyrexia, ptyalism, ataxia, mydriasis, and temporary blindness. The clinical onset of signs was from a few hours up to 24-72 hours after application of the PSO. There was no correlation between the amount of permethrin applied and the severity of clinical signs induced. In this study, treatment involved decontamination, anticonvulsants, and supportive care. Methocarbamol was not used. Hypothermia was the most common complication found during treatment, followed by electrolyte abnormalities. One cat had to be euthanized during treatment. Results of this study suggest that the lack of availability of methocarbamol for treatment should not preclude treatment of permethrin toxicity. [VT]
Related articles:
Sutton NM, Bates N, Campbell A: Clinical effects and outcome of feline permethrin spot-on poisonings reported to the Veterinary Poisons Information Service (VPIS), London, J Feline Med Surg 9:335, 2007.
Dymond NL, Swift IM: Permethrin toxicity in cats: a retrospective study of 20 cases, Aust Vet J 86:219, 2008.
More on cat health: Winn Feline Foundation Library
Join us on Facebook
Follow us on Twitter
New for 2010: subscribe to our e-newsletter
Read More
This study was a retrospective review of 42 cases of feline permethrin toxicity treated at a referral hospital in Australia. Most of the cases had a canine permethrin spot-on (PSO) flea product directly applied to the affected cats. Approximately half of the cases developed toxicity following a PSO product purchased from a supermarket. Most of the cases occurred in the summer. Cats are particularly sensitive to the effects of permethrin. Tremors and muscle fasciculations were the most common clinical sign exhibited in 86% of cats affected followed by twitches, hyperesthesia, seizures, pyrexia, ptyalism, ataxia, mydriasis, and temporary blindness. The clinical onset of signs was from a few hours up to 24-72 hours after application of the PSO. There was no correlation between the amount of permethrin applied and the severity of clinical signs induced. In this study, treatment involved decontamination, anticonvulsants, and supportive care. Methocarbamol was not used. Hypothermia was the most common complication found during treatment, followed by electrolyte abnormalities. One cat had to be euthanized during treatment. Results of this study suggest that the lack of availability of methocarbamol for treatment should not preclude treatment of permethrin toxicity. [VT]
Related articles:
Sutton NM, Bates N, Campbell A: Clinical effects and outcome of feline permethrin spot-on poisonings reported to the Veterinary Poisons Information Service (VPIS), London, J Feline Med Surg 9:335, 2007.
Dymond NL, Swift IM: Permethrin toxicity in cats: a retrospective study of 20 cases, Aust Vet J 86:219, 2008.
More on cat health: Winn Feline Foundation Library
Join us on Facebook
Follow us on Twitter
New for 2010: subscribe to our e-newsletter
Wednesday, March 24, 2010
High-Fructose Corn Syrup Prompts Considerably More Weight Gain, Researchers Find
ScienceDaily (Mar. 22, 2010) — A Princeton University research team has demonstrated that all sweeteners are not equal when it comes to weight gain: Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same.
In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. The researchers say the work sheds light on the factors contributing to obesity trends in the United States.
"Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn't true, at least under the conditions of our tests," said psychology professor Bart Hoebel, who specializes in the neuroscience of appetite, weight and sugar addiction. "When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they're becoming obese -- every single one, across the board. Even when rats are fed a high-fat diet, you don't see this; they don't all gain extra weight."
In results published online March 18 by the journal Pharmacology, Biochemistry and Behavior, the researchers from the Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup and obesity.
The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.
The second experiment -- the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals -- monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet.
"These rats aren't just getting fat; they're demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides," said Princeton graduate student Miriam Bocarsly. "In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes." In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.
High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars -- it is 50 percent fructose and 50 percent glucose -- but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.
This creates a fascinating puzzle. The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.
In the 40 years since the introduction of high-fructose corn syrup as a cost-effective sweetener in the American diet, rates of obesity in the U.S. have skyrocketed, according to the Centers for Disease Control and Prevention. In 1970, around 15 percent of the U.S. population met the definition for obesity; today, roughly one-third of the American adults are considered obese, the CDC reported. High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.
"Our findings lend support to the theory that the excessive consumption of high-fructose corn syrup found in many beverages may be an important factor in the obesity epidemic," Avena said.
The new research complements previous work led by Hoebel and Avena demonstrating that sucrose can be addictive, having effects on the brain similar to some drugs of abuse.
In the future, the team intends to explore how the animals respond to the consumption of high-fructose corn syrup in conjunction with a high-fat diet -- the equivalent of a typical fast-food meal containing a hamburger, fries and soda -- and whether excessive high-fructose corn syrup consumption contributes to the diseases associated with obesity. Another step will be to study how fructose affects brain function in the control of appetite.
In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. The researchers say the work sheds light on the factors contributing to obesity trends in the United States.
"Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn't true, at least under the conditions of our tests," said psychology professor Bart Hoebel, who specializes in the neuroscience of appetite, weight and sugar addiction. "When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they're becoming obese -- every single one, across the board. Even when rats are fed a high-fat diet, you don't see this; they don't all gain extra weight."
In results published online March 18 by the journal Pharmacology, Biochemistry and Behavior, the researchers from the Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup and obesity.
The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.
The second experiment -- the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals -- monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet.
"These rats aren't just getting fat; they're demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides," said Princeton graduate student Miriam Bocarsly. "In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes." In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.
High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars -- it is 50 percent fructose and 50 percent glucose -- but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.
This creates a fascinating puzzle. The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.
In the 40 years since the introduction of high-fructose corn syrup as a cost-effective sweetener in the American diet, rates of obesity in the U.S. have skyrocketed, according to the Centers for Disease Control and Prevention. In 1970, around 15 percent of the U.S. population met the definition for obesity; today, roughly one-third of the American adults are considered obese, the CDC reported. High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.
"Our findings lend support to the theory that the excessive consumption of high-fructose corn syrup found in many beverages may be an important factor in the obesity epidemic," Avena said.
The new research complements previous work led by Hoebel and Avena demonstrating that sucrose can be addictive, having effects on the brain similar to some drugs of abuse.
In the future, the team intends to explore how the animals respond to the consumption of high-fructose corn syrup in conjunction with a high-fat diet -- the equivalent of a typical fast-food meal containing a hamburger, fries and soda -- and whether excessive high-fructose corn syrup consumption contributes to the diseases associated with obesity. Another step will be to study how fructose affects brain function in the control of appetite.
ScienceDaily (Mar. 22, 2010) — A Princeton University research team has demonstrated that all sweeteners are not equal when it comes to weight gain: Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same.
In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. The researchers say the work sheds light on the factors contributing to obesity trends in the United States.
"Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn't true, at least under the conditions of our tests," said psychology professor Bart Hoebel, who specializes in the neuroscience of appetite, weight and sugar addiction. "When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they're becoming obese -- every single one, across the board. Even when rats are fed a high-fat diet, you don't see this; they don't all gain extra weight."
In results published online March 18 by the journal Pharmacology, Biochemistry and Behavior, the researchers from the Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup and obesity.
The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.
The second experiment -- the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals -- monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet.
"These rats aren't just getting fat; they're demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides," said Princeton graduate student Miriam Bocarsly. "In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes." In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.
High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars -- it is 50 percent fructose and 50 percent glucose -- but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.
This creates a fascinating puzzle. The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.
In the 40 years since the introduction of high-fructose corn syrup as a cost-effective sweetener in the American diet, rates of obesity in the U.S. have skyrocketed, according to the Centers for Disease Control and Prevention. In 1970, around 15 percent of the U.S. population met the definition for obesity; today, roughly one-third of the American adults are considered obese, the CDC reported. High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.
"Our findings lend support to the theory that the excessive consumption of high-fructose corn syrup found in many beverages may be an important factor in the obesity epidemic," Avena said.
The new research complements previous work led by Hoebel and Avena demonstrating that sucrose can be addictive, having effects on the brain similar to some drugs of abuse.
In the future, the team intends to explore how the animals respond to the consumption of high-fructose corn syrup in conjunction with a high-fat diet -- the equivalent of a typical fast-food meal containing a hamburger, fries and soda -- and whether excessive high-fructose corn syrup consumption contributes to the diseases associated with obesity. Another step will be to study how fructose affects brain function in the control of appetite.
Read More
In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. The researchers say the work sheds light on the factors contributing to obesity trends in the United States.
"Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn't true, at least under the conditions of our tests," said psychology professor Bart Hoebel, who specializes in the neuroscience of appetite, weight and sugar addiction. "When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they're becoming obese -- every single one, across the board. Even when rats are fed a high-fat diet, you don't see this; they don't all gain extra weight."
In results published online March 18 by the journal Pharmacology, Biochemistry and Behavior, the researchers from the Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup and obesity.
The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.
The second experiment -- the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals -- monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet.
"These rats aren't just getting fat; they're demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides," said Princeton graduate student Miriam Bocarsly. "In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes." In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.
High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars -- it is 50 percent fructose and 50 percent glucose -- but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.
This creates a fascinating puzzle. The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.
In the 40 years since the introduction of high-fructose corn syrup as a cost-effective sweetener in the American diet, rates of obesity in the U.S. have skyrocketed, according to the Centers for Disease Control and Prevention. In 1970, around 15 percent of the U.S. population met the definition for obesity; today, roughly one-third of the American adults are considered obese, the CDC reported. High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.
"Our findings lend support to the theory that the excessive consumption of high-fructose corn syrup found in many beverages may be an important factor in the obesity epidemic," Avena said.
The new research complements previous work led by Hoebel and Avena demonstrating that sucrose can be addictive, having effects on the brain similar to some drugs of abuse.
In the future, the team intends to explore how the animals respond to the consumption of high-fructose corn syrup in conjunction with a high-fat diet -- the equivalent of a typical fast-food meal containing a hamburger, fries and soda -- and whether excessive high-fructose corn syrup consumption contributes to the diseases associated with obesity. Another step will be to study how fructose affects brain function in the control of appetite.
Monday, March 22, 2010
Avoidance of four factors = four more years
An article published on March 23, 2010 in the journal PLoS Medicine reveals the conclusions of researchers from the Harvard School of Public Health and the University of Washington that smoking, high blood pressure, elevated blood glucose, and being overweight or obese decrease life expectancy by an average of 4.9 years for U.S. men and by 4.1 years for women.
Harvard School of Public Health associate professor of international health Majid Ezzati and associates evaluated 2005 data from the National Center for Health Statistics, the National Health and Nutrition Examination Survey and the Behavioral Risk Factor Surveillance System, along with a review of epidemiologic studies concerning the effects of these factors. They also estimated the risk factors' effects on 8 eight U.S. subgroups including Asians, Northland low-income rural whites, middle America, Appalachia and Mississippi Valley low-income whites, Western Native Americans, black middle America, high-risk urban blacks and Southern rural blacks.
Dr Ezzati and colleagues estimated the amount of deaths that would not have occurred in 2005 if exposure to the risk factors had been reduced to optimal levels or common guidelines. Elimination of obesity was calculated to increase life expectancy by an average of 1.3 years, normalization of hypertension was estimated to result in an added 1.5 years for men and 1.6 years for women, smoking cessation was correlated with an extra 2.5 years for men and 1.8 years for women, and optimization of blood glucose was estimated to confer an extra 0.5 years on male life expectancy and 0.3 years on that of females. Among those who had all four factors, Southern rural blacks experienced the greatest reduction in life expectancy and Asians had the least reduction. The four factors were determined to account for nearly 20 percent of U.S. life expectancy disparities, 75 percent of cardiovascular mortality disparities, and 50 percent of cancer disparities.
The investigation is the first to examine the consequences of these preventable risk factors on life expectancy across the United States. "This study demonstrates the potential of disease prevention to not only improve health outcomes in the entire nation but also to reduce the enormous disparities in life expectancy that we see in the U.S.," Dr Ezzati commented.
"It's important that public health policy makers understand that these behavioral and metabolic risk factors are not just personal choices or the responsibility of doctors," added lead author and Harvard School of Public Health postdoctoral research fellow Goodarz Danaei. "To improve the nation's overall health and reduce health disparities, both population-based and personal interventions that reduce these preventable risk factors must be identified, implemented, and rigorously evaluated."
Harvard School of Public Health associate professor of international health Majid Ezzati and associates evaluated 2005 data from the National Center for Health Statistics, the National Health and Nutrition Examination Survey and the Behavioral Risk Factor Surveillance System, along with a review of epidemiologic studies concerning the effects of these factors. They also estimated the risk factors' effects on 8 eight U.S. subgroups including Asians, Northland low-income rural whites, middle America, Appalachia and Mississippi Valley low-income whites, Western Native Americans, black middle America, high-risk urban blacks and Southern rural blacks.
Dr Ezzati and colleagues estimated the amount of deaths that would not have occurred in 2005 if exposure to the risk factors had been reduced to optimal levels or common guidelines. Elimination of obesity was calculated to increase life expectancy by an average of 1.3 years, normalization of hypertension was estimated to result in an added 1.5 years for men and 1.6 years for women, smoking cessation was correlated with an extra 2.5 years for men and 1.8 years for women, and optimization of blood glucose was estimated to confer an extra 0.5 years on male life expectancy and 0.3 years on that of females. Among those who had all four factors, Southern rural blacks experienced the greatest reduction in life expectancy and Asians had the least reduction. The four factors were determined to account for nearly 20 percent of U.S. life expectancy disparities, 75 percent of cardiovascular mortality disparities, and 50 percent of cancer disparities.
The investigation is the first to examine the consequences of these preventable risk factors on life expectancy across the United States. "This study demonstrates the potential of disease prevention to not only improve health outcomes in the entire nation but also to reduce the enormous disparities in life expectancy that we see in the U.S.," Dr Ezzati commented.
"It's important that public health policy makers understand that these behavioral and metabolic risk factors are not just personal choices or the responsibility of doctors," added lead author and Harvard School of Public Health postdoctoral research fellow Goodarz Danaei. "To improve the nation's overall health and reduce health disparities, both population-based and personal interventions that reduce these preventable risk factors must be identified, implemented, and rigorously evaluated."
An article published on March 23, 2010 in the journal PLoS Medicine reveals the conclusions of researchers from the Harvard School of Public Health and the University of Washington that smoking, high blood pressure, elevated blood glucose, and being overweight or obese decrease life expectancy by an average of 4.9 years for U.S. men and by 4.1 years for women.
Harvard School of Public Health associate professor of international health Majid Ezzati and associates evaluated 2005 data from the National Center for Health Statistics, the National Health and Nutrition Examination Survey and the Behavioral Risk Factor Surveillance System, along with a review of epidemiologic studies concerning the effects of these factors. They also estimated the risk factors' effects on 8 eight U.S. subgroups including Asians, Northland low-income rural whites, middle America, Appalachia and Mississippi Valley low-income whites, Western Native Americans, black middle America, high-risk urban blacks and Southern rural blacks.
Dr Ezzati and colleagues estimated the amount of deaths that would not have occurred in 2005 if exposure to the risk factors had been reduced to optimal levels or common guidelines. Elimination of obesity was calculated to increase life expectancy by an average of 1.3 years, normalization of hypertension was estimated to result in an added 1.5 years for men and 1.6 years for women, smoking cessation was correlated with an extra 2.5 years for men and 1.8 years for women, and optimization of blood glucose was estimated to confer an extra 0.5 years on male life expectancy and 0.3 years on that of females. Among those who had all four factors, Southern rural blacks experienced the greatest reduction in life expectancy and Asians had the least reduction. The four factors were determined to account for nearly 20 percent of U.S. life expectancy disparities, 75 percent of cardiovascular mortality disparities, and 50 percent of cancer disparities.
The investigation is the first to examine the consequences of these preventable risk factors on life expectancy across the United States. "This study demonstrates the potential of disease prevention to not only improve health outcomes in the entire nation but also to reduce the enormous disparities in life expectancy that we see in the U.S.," Dr Ezzati commented.
"It's important that public health policy makers understand that these behavioral and metabolic risk factors are not just personal choices or the responsibility of doctors," added lead author and Harvard School of Public Health postdoctoral research fellow Goodarz Danaei. "To improve the nation's overall health and reduce health disparities, both population-based and personal interventions that reduce these preventable risk factors must be identified, implemented, and rigorously evaluated."
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Harvard School of Public Health associate professor of international health Majid Ezzati and associates evaluated 2005 data from the National Center for Health Statistics, the National Health and Nutrition Examination Survey and the Behavioral Risk Factor Surveillance System, along with a review of epidemiologic studies concerning the effects of these factors. They also estimated the risk factors' effects on 8 eight U.S. subgroups including Asians, Northland low-income rural whites, middle America, Appalachia and Mississippi Valley low-income whites, Western Native Americans, black middle America, high-risk urban blacks and Southern rural blacks.
Dr Ezzati and colleagues estimated the amount of deaths that would not have occurred in 2005 if exposure to the risk factors had been reduced to optimal levels or common guidelines. Elimination of obesity was calculated to increase life expectancy by an average of 1.3 years, normalization of hypertension was estimated to result in an added 1.5 years for men and 1.6 years for women, smoking cessation was correlated with an extra 2.5 years for men and 1.8 years for women, and optimization of blood glucose was estimated to confer an extra 0.5 years on male life expectancy and 0.3 years on that of females. Among those who had all four factors, Southern rural blacks experienced the greatest reduction in life expectancy and Asians had the least reduction. The four factors were determined to account for nearly 20 percent of U.S. life expectancy disparities, 75 percent of cardiovascular mortality disparities, and 50 percent of cancer disparities.
The investigation is the first to examine the consequences of these preventable risk factors on life expectancy across the United States. "This study demonstrates the potential of disease prevention to not only improve health outcomes in the entire nation but also to reduce the enormous disparities in life expectancy that we see in the U.S.," Dr Ezzati commented.
"It's important that public health policy makers understand that these behavioral and metabolic risk factors are not just personal choices or the responsibility of doctors," added lead author and Harvard School of Public Health postdoctoral research fellow Goodarz Danaei. "To improve the nation's overall health and reduce health disparities, both population-based and personal interventions that reduce these preventable risk factors must be identified, implemented, and rigorously evaluated."
Genetics of Feline Infectious Peritonitis Virus
Chang HW, de Groot RJ, Egberink HF et al.: Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene, J Gen Virol 91:415, 2010.
The virus of the lethal disease, feline infectious peritonitis (FIP), is closely related to the relatively innocuous form of feline coronavirus (FCoV). There is genetic and animal experimental evidence to indicate that the disease-causing form evolves time and time again from the harmless one by mutation in individual infected cats. What this specific mutation in the virus is remains unknown. One possible gene that may be involved, termed the “3c” gene, encodes a viral protein of unknown function. Previous studies have identified mutations in this gene that may be associated with FIP development. In this report, the investigators examined the 3c gene in the coronavirus infecting 27 healthy cats and 28 cats diagnosed with FIP in order to compare the viruses in this genetic region. Interestingly, the 3c gene in the virus of healthy cats was always intact, with no mutations. However, in cats with FIP, the majority (20/28) of viruses had mutations in this gene, varying from minor changes in a few amino acids to major changes leading to lack of function of the encoded protein. The researchers also tested the feces of cats with FIP for coronavirus. Virus was found in only 6 of 17 cats, indicating that in most cats with FIP, coronavirus has been cleared from the intestines and is only present in the tissues. In samples from 6 cats in which virus were detected, the 3c gene either had no mutations (5/6) or only one amino acid change (1/6). These investigators proposed the following scenario: Cats become infected by circulating virus that replicates in the gut. Replication in this compartment and efficient fecal shedding strictly require an intact viral 3c gene. A mutation in the virus occurs continually, one or more of which incidentally provides the virus with the ability to replicate in macrophages and monocytes, which then spread the – now FIPV – infection to organs throughout the body. Once in this new environment, virus propagation no longer requires the 3c gene; thus, mutations readily occur in the gene that may even improve the virus’ replication in tissue. The result is the disease feline infectious peritonitis. [MK]
Related articles:
Brown MA, Troyer JL, Pecon-Slattery J et al.: Genetics and pathogenesis of feline infectious peritonitis virus, Emerg Infect Dis 15:1445, 2009.
Pedersen NC: A review of feline infectious peritonitis virus infection: 1963-2008, Journal of Feline Medicine & Surgery 11:225, 2009.
More on cat health: Winn Feline Foundation Library
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New for 2010: subscribe to our e-newsletter
The virus of the lethal disease, feline infectious peritonitis (FIP), is closely related to the relatively innocuous form of feline coronavirus (FCoV). There is genetic and animal experimental evidence to indicate that the disease-causing form evolves time and time again from the harmless one by mutation in individual infected cats. What this specific mutation in the virus is remains unknown. One possible gene that may be involved, termed the “3c” gene, encodes a viral protein of unknown function. Previous studies have identified mutations in this gene that may be associated with FIP development. In this report, the investigators examined the 3c gene in the coronavirus infecting 27 healthy cats and 28 cats diagnosed with FIP in order to compare the viruses in this genetic region. Interestingly, the 3c gene in the virus of healthy cats was always intact, with no mutations. However, in cats with FIP, the majority (20/28) of viruses had mutations in this gene, varying from minor changes in a few amino acids to major changes leading to lack of function of the encoded protein. The researchers also tested the feces of cats with FIP for coronavirus. Virus was found in only 6 of 17 cats, indicating that in most cats with FIP, coronavirus has been cleared from the intestines and is only present in the tissues. In samples from 6 cats in which virus were detected, the 3c gene either had no mutations (5/6) or only one amino acid change (1/6). These investigators proposed the following scenario: Cats become infected by circulating virus that replicates in the gut. Replication in this compartment and efficient fecal shedding strictly require an intact viral 3c gene. A mutation in the virus occurs continually, one or more of which incidentally provides the virus with the ability to replicate in macrophages and monocytes, which then spread the – now FIPV – infection to organs throughout the body. Once in this new environment, virus propagation no longer requires the 3c gene; thus, mutations readily occur in the gene that may even improve the virus’ replication in tissue. The result is the disease feline infectious peritonitis. [MK]
Related articles:
Brown MA, Troyer JL, Pecon-Slattery J et al.: Genetics and pathogenesis of feline infectious peritonitis virus, Emerg Infect Dis 15:1445, 2009.
Pedersen NC: A review of feline infectious peritonitis virus infection: 1963-2008, Journal of Feline Medicine & Surgery 11:225, 2009.
More on cat health: Winn Feline Foundation Library
Join us on Facebook
Follow us on Twitter
New for 2010: subscribe to our e-newsletter
Chang HW, de Groot RJ, Egberink HF et al.: Feline infectious peritonitis: insights into feline coronavirus pathobiogenesis and epidemiology based on genetic analysis of the viral 3c gene, J Gen Virol 91:415, 2010.
The virus of the lethal disease, feline infectious peritonitis (FIP), is closely related to the relatively innocuous form of feline coronavirus (FCoV). There is genetic and animal experimental evidence to indicate that the disease-causing form evolves time and time again from the harmless one by mutation in individual infected cats. What this specific mutation in the virus is remains unknown. One possible gene that may be involved, termed the “3c” gene, encodes a viral protein of unknown function. Previous studies have identified mutations in this gene that may be associated with FIP development. In this report, the investigators examined the 3c gene in the coronavirus infecting 27 healthy cats and 28 cats diagnosed with FIP in order to compare the viruses in this genetic region. Interestingly, the 3c gene in the virus of healthy cats was always intact, with no mutations. However, in cats with FIP, the majority (20/28) of viruses had mutations in this gene, varying from minor changes in a few amino acids to major changes leading to lack of function of the encoded protein. The researchers also tested the feces of cats with FIP for coronavirus. Virus was found in only 6 of 17 cats, indicating that in most cats with FIP, coronavirus has been cleared from the intestines and is only present in the tissues. In samples from 6 cats in which virus were detected, the 3c gene either had no mutations (5/6) or only one amino acid change (1/6). These investigators proposed the following scenario: Cats become infected by circulating virus that replicates in the gut. Replication in this compartment and efficient fecal shedding strictly require an intact viral 3c gene. A mutation in the virus occurs continually, one or more of which incidentally provides the virus with the ability to replicate in macrophages and monocytes, which then spread the – now FIPV – infection to organs throughout the body. Once in this new environment, virus propagation no longer requires the 3c gene; thus, mutations readily occur in the gene that may even improve the virus’ replication in tissue. The result is the disease feline infectious peritonitis. [MK]
Related articles:
Brown MA, Troyer JL, Pecon-Slattery J et al.: Genetics and pathogenesis of feline infectious peritonitis virus, Emerg Infect Dis 15:1445, 2009.
Pedersen NC: A review of feline infectious peritonitis virus infection: 1963-2008, Journal of Feline Medicine & Surgery 11:225, 2009.
More on cat health: Winn Feline Foundation Library
Join us on Facebook
Follow us on Twitter
New for 2010: subscribe to our e-newsletter
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The virus of the lethal disease, feline infectious peritonitis (FIP), is closely related to the relatively innocuous form of feline coronavirus (FCoV). There is genetic and animal experimental evidence to indicate that the disease-causing form evolves time and time again from the harmless one by mutation in individual infected cats. What this specific mutation in the virus is remains unknown. One possible gene that may be involved, termed the “3c” gene, encodes a viral protein of unknown function. Previous studies have identified mutations in this gene that may be associated with FIP development. In this report, the investigators examined the 3c gene in the coronavirus infecting 27 healthy cats and 28 cats diagnosed with FIP in order to compare the viruses in this genetic region. Interestingly, the 3c gene in the virus of healthy cats was always intact, with no mutations. However, in cats with FIP, the majority (20/28) of viruses had mutations in this gene, varying from minor changes in a few amino acids to major changes leading to lack of function of the encoded protein. The researchers also tested the feces of cats with FIP for coronavirus. Virus was found in only 6 of 17 cats, indicating that in most cats with FIP, coronavirus has been cleared from the intestines and is only present in the tissues. In samples from 6 cats in which virus were detected, the 3c gene either had no mutations (5/6) or only one amino acid change (1/6). These investigators proposed the following scenario: Cats become infected by circulating virus that replicates in the gut. Replication in this compartment and efficient fecal shedding strictly require an intact viral 3c gene. A mutation in the virus occurs continually, one or more of which incidentally provides the virus with the ability to replicate in macrophages and monocytes, which then spread the – now FIPV – infection to organs throughout the body. Once in this new environment, virus propagation no longer requires the 3c gene; thus, mutations readily occur in the gene that may even improve the virus’ replication in tissue. The result is the disease feline infectious peritonitis. [MK]
Related articles:
Brown MA, Troyer JL, Pecon-Slattery J et al.: Genetics and pathogenesis of feline infectious peritonitis virus, Emerg Infect Dis 15:1445, 2009.
Pedersen NC: A review of feline infectious peritonitis virus infection: 1963-2008, Journal of Feline Medicine & Surgery 11:225, 2009.
More on cat health: Winn Feline Foundation Library
Join us on Facebook
Follow us on Twitter
New for 2010: subscribe to our e-newsletter
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