Stress as a Cause of Sickness in Cats

Stella JL, Lord LK, Buffington CAT: Sickness behaviors in response to unusual external events in healthy cats and cats with feline interstitial cystitis, J Am Vet Med Assoc 238:67, 2011.

Millions of cats are relinquished or euthanized at shelters each year because of inappropriate elimination behaviors that are objectionable to owners. The most common behaviors are related to the lower urinary tract. Because this is a problem of major veterinary importance, the objective of this prospective, observational study was to compare sickness behaviors (SB) in healthy cats with those of cats with feline interstitial cystitis (FIC) in response to unusual external events (UEE). Twelve healthy cats and 20 cats with FIC were housed in an enriched colony environment and watched by a single observer for 77 weeks. SB referable to the gastrointestinal and urinary tracts, the skin, and behavior problems were recorded. Different instances of UEE (e.g., changes in caretakers, changes in vivarium routine, and lack of interaction with the investigator) were identified during 11 of the 77 weeks.  The remaining 66 weeks had no instances of identified UEE and were considered control weeks. The study had 4 noteworthy findings. First, there was no difference in mean number of SB identified between healthy cats and the cats with FIC under the enriched housing conditions in the colony. This suggests that husbandry and enrichment conditions present were related to a decrease in SB in the cats with FIC, compared to healthy cats. Second, exposure to UEE significantly increased the risk for an increase in the total number of SB in both groups of cats. SB may be more closely associated with UEE than with disease status.  Third, the most common SB associated to UEE includes decreases in food intake and elimination behaviors and increases in defecation and urination outside the litter box. This would suggest that when cats are evaluated for the presence of these clinical signs, the possibility the signs resulted from external as well as internal events should be considered. Fourth, an increase in age conferred a significant risk for upper gastrointestinal tract signs and avoidance behavior. The authors recommend that all clients with cats should be offered assistance with environmental enrichment to improve the health and welfare of their cats.  [VT]

Related articles:

Buffington CA: Comorbidity of interstitial cystitis with other unexplained clinical conditions, J Urol 172:1242, 2004.

More on cat health: Winn Feline Foundation Library

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Stella JL, Lord LK, Buffington CAT: Sickness behaviors in response to unusual external events in healthy cats and cats with feline interstitial cystitis, J Am Vet Med Assoc 238:67, 2011.

Millions of cats are relinquished or euthanized at shelters each year because of inappropriate elimination behaviors that are objectionable to owners. The most common behaviors are related to the lower urinary tract. Because this is a problem of major veterinary importance, the objective of this prospective, observational study was to compare sickness behaviors (SB) in healthy cats with those of cats with feline interstitial cystitis (FIC) in response to unusual external events (UEE). Twelve healthy cats and 20 cats with FIC were housed in an enriched colony environment and watched by a single observer for 77 weeks. SB referable to the gastrointestinal and urinary tracts, the skin, and behavior problems were recorded. Different instances of UEE (e.g., changes in caretakers, changes in vivarium routine, and lack of interaction with the investigator) were identified during 11 of the 77 weeks.  The remaining 66 weeks had no instances of identified UEE and were considered control weeks. The study had 4 noteworthy findings. First, there was no difference in mean number of SB identified between healthy cats and the cats with FIC under the enriched housing conditions in the colony. This suggests that husbandry and enrichment conditions present were related to a decrease in SB in the cats with FIC, compared to healthy cats. Second, exposure to UEE significantly increased the risk for an increase in the total number of SB in both groups of cats. SB may be more closely associated with UEE than with disease status.  Third, the most common SB associated to UEE includes decreases in food intake and elimination behaviors and increases in defecation and urination outside the litter box. This would suggest that when cats are evaluated for the presence of these clinical signs, the possibility the signs resulted from external as well as internal events should be considered. Fourth, an increase in age conferred a significant risk for upper gastrointestinal tract signs and avoidance behavior. The authors recommend that all clients with cats should be offered assistance with environmental enrichment to improve the health and welfare of their cats.  [VT]

Related articles:

Buffington CA: Comorbidity of interstitial cystitis with other unexplained clinical conditions, J Urol 172:1242, 2004.

More on cat health: Winn Feline Foundation Library

Join us on Facebook

Follow us on Twitter

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Vitamin D insufficiency could play a role in the development of Parkinson's disease

Researchers at Emory University report in the March, 2011 issue of Archives of Neurology the finding of a correlation between insufficient levels of vitamin D and the development of early Parkinson's disease (PD).

In the article's background information, Marian L. Evatt, MD, MS of Emory University School of Medicine and the Atlanta Veterans Affairs Medical Center and colleagues remark that "Vitamin D insufficiency has been reported to be more common in patients with Parkinson's disease than in healthy control subjects, but it is not clear whether having a chronic disease causing reduced mobility contributes to this relatively high prevalence."

The study included 157 placebo recipients who participated in The Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP) trial of men and women with early, untreated Parkinson's disease. Blood samples obtained upon enrollment and at the final visit after 13 months were analyzed for levels of 25-hydroxyvitamin D, the active form of the vitamin.

A high percentage of subjects had vitamin D insufficiency or deficiency at both points of the study. While 69.4 percent had vitamin D insufficiency defined as levels of less than 30 nanograms per milliliter (ng/mL) at the beginning of the study, 26.1 percent were classified as deficient with levels of less than 20 ng/mL. The prevalence of insufficiency at the final visit was 51.6 percent, and deficiency occurred in 7 percent.

"Previous studies in Asian populations reported a higher prevalence of hypovitaminosis D (deficiency or insufficiency) in patients with more advanced disease, suggesting that long-term effects of Parkinson's disease may contribute to the development of insufficient vitamin D concentrations," the authors write. "Contrary to our expectation that vitamin D levels might decrease over time because of disease-related inactivity and reduced sun exposure, vitamin D levels increased over the study period. These findings are consistent with the possibility that long-term insufficiency is present before the clinical manifestations of Parkinson's disease and may play a role in the pathogenesis of PD."

"To our knowledge, the study cohort is the largest and most well-characterized cohort of patients with PD in whom vitamin D status has been investigated," they observe. "We confirm a high prevalence of vitamin D insufficiency in patients with recent onset of PD, during the early clinical stages in which patients do not require symptomatic therapy."

Researchers at Emory University report in the March, 2011 issue of Archives of Neurology the finding of a correlation between insufficient levels of vitamin D and the development of early Parkinson's disease (PD).

In the article's background information, Marian L. Evatt, MD, MS of Emory University School of Medicine and the Atlanta Veterans Affairs Medical Center and colleagues remark that "Vitamin D insufficiency has been reported to be more common in patients with Parkinson's disease than in healthy control subjects, but it is not clear whether having a chronic disease causing reduced mobility contributes to this relatively high prevalence."

The study included 157 placebo recipients who participated in The Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP) trial of men and women with early, untreated Parkinson's disease. Blood samples obtained upon enrollment and at the final visit after 13 months were analyzed for levels of 25-hydroxyvitamin D, the active form of the vitamin.

A high percentage of subjects had vitamin D insufficiency or deficiency at both points of the study. While 69.4 percent had vitamin D insufficiency defined as levels of less than 30 nanograms per milliliter (ng/mL) at the beginning of the study, 26.1 percent were classified as deficient with levels of less than 20 ng/mL. The prevalence of insufficiency at the final visit was 51.6 percent, and deficiency occurred in 7 percent.

"Previous studies in Asian populations reported a higher prevalence of hypovitaminosis D (deficiency or insufficiency) in patients with more advanced disease, suggesting that long-term effects of Parkinson's disease may contribute to the development of insufficient vitamin D concentrations," the authors write. "Contrary to our expectation that vitamin D levels might decrease over time because of disease-related inactivity and reduced sun exposure, vitamin D levels increased over the study period. These findings are consistent with the possibility that long-term insufficiency is present before the clinical manifestations of Parkinson's disease and may play a role in the pathogenesis of PD."

"To our knowledge, the study cohort is the largest and most well-characterized cohort of patients with PD in whom vitamin D status has been investigated," they observe. "We confirm a high prevalence of vitamin D insufficiency in patients with recent onset of PD, during the early clinical stages in which patients do not require symptomatic therapy."

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How Sweet It Is: Why Your Taste Cells Love Sugar So Much

Newswise — PHILADELPHIA (March 7, 2011) – A new research study dramatically increases knowledge of how taste cells detect sugars, a key step in developing strategies to limit overconsumption. Scientists from the Monell Center and collaborators have discovered that taste cells have several additional sugar detectors other than the previously known sweet receptor.

“Detecting the sweetness of nutritive sugars is one of the most important tasks of our taste cells,” said senior author Robert F. Margolskee, M.D., Ph.D., a molecular neurobiologist at Monell. “Many of us eat too much sugar and to help limit overconsumption, we need to better understand how a sweet taste cell ‘knows’ something is sweet.”

Scientists have known for some time that the T1r2+T1r3 receptor is the primary mechanism that allows taste cells to detect many sweet compounds, including sugars such as glucose and sucrose and also artificial sweeteners, including saccharin and aspartame.

However, some aspects of sweet taste could not be explained by the T1r2+T1r3 receptor. For example, although the receptor contains two subunits that must join together for it to work properly, Margolskee’s team had previously found that mice engineered to be missing the T1r3 subunit were still able to taste glucose and other sugars normally.

Knowing that sugar sensors in the intestine are important to how dietary sugars are detected and absorbed, and that metabolic sensors in the pancreas are key to regulating blood levels of glucose, the Monell scientists used advanced molecular and cellular techniques to see if these same sensors are also found in taste cells.

The results, published in the Proceedings of the National Academy of Sciences USA, indicate that several sugar sensors from intestine and pancreas also are present in exactly those same sweet-sensing taste cells that have the T1r2+T1r3 sweet receptor.

“The taste system continues to amaze me at how smart it is and how it serves to integrate taste sensation with digestive processes,” said Margolskee.

The different sugar taste sensors may have varied roles. An intestinal glucose sensor also found to be located in the sweet-sensitive taste cells may provide an explanation for another mystery of sweet taste: why just a pinch of table salt tastes sweet or salt added to baked goods enhances sweet taste. Known as SGLT1, this sensor is a transporter that moves glucose into the sweet taste cell when sodium is present, thus triggering the cell to register sweetness.

In pancreas, the sugar sensor known as the KATP channel, monitors glucose levels and triggers insulin release when they rise. The authors speculate that KATP may function in sweet taste cells to modulate taste cell sensitivity to sugars according to metabolic needs. For example, this sensor may respond to hormonal signals from the gut or pancreas to make taste cells less responsive to sweets after we have just eaten a sugary piece of pecan pie and do not need additional energy.

“Sweet taste cells have turned out to be quite complex. The presence of the KATP channel suggests that taste cells may play a role in regulating our sensitivity to sweet taste under different nutritional conditions,” said first author Karen K. Yee, Ph.D., a cellular physiologist at Monell. “This knowledge may someday help us understand how to limit overconsumption of sweet foods.”

Future studies will focus on understanding the complex connections between taste cells and the digestive and endocrine systems.

Also contributing to the study were Sunil Sukumaran, Ph.D. and Ramana Kotha of Monell and Timothy Gilbertson, Ph.D. of Utah State University.

The Monell Chemical Senses Center is an independent nonprofit basic research institute based in Philadelphia, Pennsylvania. Monell advances scientific understanding of the mechanisms and functions of taste and smell to benefit human health and well-being. Using an interdisciplinary approach, scientists collaborate in the programmatic areas of sensation and perception; neuroscience and molecular biology; environmental and occupational health; nutrition and appetite; health and well-being; development, aging and regeneration; and chemical ecology and communication.

Newswise — PHILADELPHIA (March 7, 2011) – A new research study dramatically increases knowledge of how taste cells detect sugars, a key step in developing strategies to limit overconsumption. Scientists from the Monell Center and collaborators have discovered that taste cells have several additional sugar detectors other than the previously known sweet receptor.

“Detecting the sweetness of nutritive sugars is one of the most important tasks of our taste cells,” said senior author Robert F. Margolskee, M.D., Ph.D., a molecular neurobiologist at Monell. “Many of us eat too much sugar and to help limit overconsumption, we need to better understand how a sweet taste cell ‘knows’ something is sweet.”

Scientists have known for some time that the T1r2+T1r3 receptor is the primary mechanism that allows taste cells to detect many sweet compounds, including sugars such as glucose and sucrose and also artificial sweeteners, including saccharin and aspartame.

However, some aspects of sweet taste could not be explained by the T1r2+T1r3 receptor. For example, although the receptor contains two subunits that must join together for it to work properly, Margolskee’s team had previously found that mice engineered to be missing the T1r3 subunit were still able to taste glucose and other sugars normally.

Knowing that sugar sensors in the intestine are important to how dietary sugars are detected and absorbed, and that metabolic sensors in the pancreas are key to regulating blood levels of glucose, the Monell scientists used advanced molecular and cellular techniques to see if these same sensors are also found in taste cells.

The results, published in the Proceedings of the National Academy of Sciences USA, indicate that several sugar sensors from intestine and pancreas also are present in exactly those same sweet-sensing taste cells that have the T1r2+T1r3 sweet receptor.

“The taste system continues to amaze me at how smart it is and how it serves to integrate taste sensation with digestive processes,” said Margolskee.

The different sugar taste sensors may have varied roles. An intestinal glucose sensor also found to be located in the sweet-sensitive taste cells may provide an explanation for another mystery of sweet taste: why just a pinch of table salt tastes sweet or salt added to baked goods enhances sweet taste. Known as SGLT1, this sensor is a transporter that moves glucose into the sweet taste cell when sodium is present, thus triggering the cell to register sweetness.

In pancreas, the sugar sensor known as the KATP channel, monitors glucose levels and triggers insulin release when they rise. The authors speculate that KATP may function in sweet taste cells to modulate taste cell sensitivity to sugars according to metabolic needs. For example, this sensor may respond to hormonal signals from the gut or pancreas to make taste cells less responsive to sweets after we have just eaten a sugary piece of pecan pie and do not need additional energy.

“Sweet taste cells have turned out to be quite complex. The presence of the KATP channel suggests that taste cells may play a role in regulating our sensitivity to sweet taste under different nutritional conditions,” said first author Karen K. Yee, Ph.D., a cellular physiologist at Monell. “This knowledge may someday help us understand how to limit overconsumption of sweet foods.”

Future studies will focus on understanding the complex connections between taste cells and the digestive and endocrine systems.

Also contributing to the study were Sunil Sukumaran, Ph.D. and Ramana Kotha of Monell and Timothy Gilbertson, Ph.D. of Utah State University.

The Monell Chemical Senses Center is an independent nonprofit basic research institute based in Philadelphia, Pennsylvania. Monell advances scientific understanding of the mechanisms and functions of taste and smell to benefit human health and well-being. Using an interdisciplinary approach, scientists collaborate in the programmatic areas of sensation and perception; neuroscience and molecular biology; environmental and occupational health; nutrition and appetite; health and well-being; development, aging and regeneration; and chemical ecology and communication.

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Mediterranean diet improves heart risk factors

The Mediterranean diet includes an abundance of fruits, vegetables, beans, nuts, olive oil, poultry and fish, with very little red meat. Scientists believe that eating this way has antioxidant and anti-inflammatory effects on the body.

"This study reinforces guidelines over the past 10 years, stressing the need to reduce consumption of refined carbohydrates and saturated fats" from meat and dairy products, Dr. Robert S. Rosenson of the Mount Sinai School of Medicine in New York told Reuters Health. He was not involved in the work.

Metabolic syndrome is a recent catchall for unhealthy traits that spell bad news for the heart, such as belly fat, high blood pressure, low levels of "good" HDL cholesterol, elevated fat levels in the blood (triglycerides), and high blood sugar. The condition is diagnosed when a person has at least three of those risk factors.

Reviewing 35 clinical trials, Dr. Demosthenes B. Panagiotakos at Harokopia University in Athens, Greece, and his team found that faithfully eating a Mediterranean diet can improve each of those traits.

For instance, those who stuck with the Mediterranean diet as compared to eating their regular foods or a low-fat diet trimmed their waistlines by about 0.43 cm (0.16 inches) on average.

They also showed slashed their blood pressure by 2.35 points on the top reading, and their fasting blood sugar by 3.89 milligrams per deciliter.

While these benefits may seem small, Dr. Elizabeth Mayer-Davis, who was not involved in the research, said they show a Mediterranean diet might be beneficial.

"So it's reasonable to recommend the Mediterranean diet to patients," she said. But she added that "we can't say that this diet reduces the risk of diabetes."

Nor does the study, published in Journal of the American College of Cardiology, show that the diet cuts the risk of death from heart disease, which has been linked to metabolic syndrome.

Mayer-Davis, professor of nutrition at the University of North Carolina at Chapel Hill, also said she was concerned that cost could be a barrier to adopting a diet that emphasizes fresh foods, olive oil and fish.

"This speaks to the need to improve availability of these kinds of foods to people who don't have a lot of extra money to spend," she told Reuters Health.

Olive oil is an important part of the Mediterranean diet because it is a so-called monounsaturated fat, which "protects" levels of HDL cholesterol.

However, it can cost a lot more than other cooking oils on supermarket shelves. Rosenson said that when he suggests this diet to his patients, he makes the point that the much cheaper canola oil is also high in monounsaturated fats.

Dr. Robert Eckel, a former president of the American Heart Association who reviewed the study for Reuters Health, noted that the Mediterranean diet "is part of a dietary pattern consistent with guidelines from the AHA, the USDA, and other bodies, that overall is consistent with reduced risk for cardiovascular disease, stroke and diabetes."

The Mediterranean diet includes an abundance of fruits, vegetables, beans, nuts, olive oil, poultry and fish, with very little red meat. Scientists believe that eating this way has antioxidant and anti-inflammatory effects on the body.

"This study reinforces guidelines over the past 10 years, stressing the need to reduce consumption of refined carbohydrates and saturated fats" from meat and dairy products, Dr. Robert S. Rosenson of the Mount Sinai School of Medicine in New York told Reuters Health. He was not involved in the work.

Metabolic syndrome is a recent catchall for unhealthy traits that spell bad news for the heart, such as belly fat, high blood pressure, low levels of "good" HDL cholesterol, elevated fat levels in the blood (triglycerides), and high blood sugar. The condition is diagnosed when a person has at least three of those risk factors.

Reviewing 35 clinical trials, Dr. Demosthenes B. Panagiotakos at Harokopia University in Athens, Greece, and his team found that faithfully eating a Mediterranean diet can improve each of those traits.

For instance, those who stuck with the Mediterranean diet as compared to eating their regular foods or a low-fat diet trimmed their waistlines by about 0.43 cm (0.16 inches) on average.

They also showed slashed their blood pressure by 2.35 points on the top reading, and their fasting blood sugar by 3.89 milligrams per deciliter.

While these benefits may seem small, Dr. Elizabeth Mayer-Davis, who was not involved in the research, said they show a Mediterranean diet might be beneficial.

"So it's reasonable to recommend the Mediterranean diet to patients," she said. But she added that "we can't say that this diet reduces the risk of diabetes."

Nor does the study, published in Journal of the American College of Cardiology, show that the diet cuts the risk of death from heart disease, which has been linked to metabolic syndrome.

Mayer-Davis, professor of nutrition at the University of North Carolina at Chapel Hill, also said she was concerned that cost could be a barrier to adopting a diet that emphasizes fresh foods, olive oil and fish.

"This speaks to the need to improve availability of these kinds of foods to people who don't have a lot of extra money to spend," she told Reuters Health.

Olive oil is an important part of the Mediterranean diet because it is a so-called monounsaturated fat, which "protects" levels of HDL cholesterol.

However, it can cost a lot more than other cooking oils on supermarket shelves. Rosenson said that when he suggests this diet to his patients, he makes the point that the much cheaper canola oil is also high in monounsaturated fats.

Dr. Robert Eckel, a former president of the American Heart Association who reviewed the study for Reuters Health, noted that the Mediterranean diet "is part of a dietary pattern consistent with guidelines from the AHA, the USDA, and other bodies, that overall is consistent with reduced risk for cardiovascular disease, stroke and diabetes."

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Winn's goal is to help "Every Cat, Every Day" and we can only do this with your assistance. Stay in touch with our activities and learn how you can become involved in the future of feline health.

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Winn's goal is to help "Every Cat, Every Day" and we can only do this with your assistance. Stay in touch with our activities and learn how you can become involved in the future of feline health.

Join over 3,500 other cat lovers on our Facebook page.

Follow us on Twitter and help spread the word!

Subscribe to our email newsletter - we promise, no spam :-)

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Breakfast Is Not So Gr-r-reat When Your Only Option Is Frosted Flakes

One in four children goes without breakfast each morning, according to the U.S. Department of Agriculture. A tragedy to be sure -- but are Kellogg's breakfast products the solution?

Last week Kellogg announced its new project called Share Your Breakfast, part of a national advertising campaign. The project asks Americans to upload their breakfast photos to the Web site shareyourbreakfast.com, and for each breakfast photo shared, Kellogg Company will donate a school breakfast to a child in need -- up to $200,000 worth of (or one million) breakfasts.

Feeding hungry children sure sounds nice, but filling hungry bellies with highly-processed junk foods is hardly the answer. Let's take a look at some of the products Kellogg is promoting as part of this endeavor.

Frosted Flakes -- one of the products represented by Tony the Tiger at a National Breakfast Day event in New York last Tuesday -- contains 11 grams of sugar per three-fourths cup serving. After the first ingredient of milled corn, the next three read: Sugar, malt flavoring, and high-fructose-corn-syrup -- three forms of sugar by different names.

Nutri-Grain bars -- a product promoted as healthy -- contain more than 30 ingredients (minus the synthetic vitamins) and include high-fructose-corn syrup, artificial flavors, red #40, TBHQ, and host of other chemicals. Meanwhile, the front of the package reads: "More of the whole grains your body needs," "Good source of fiber," and "Made with real fruit." The only "real fruit" I could find is "strawberry puree concentrate" and it's listed after high-fructose-corn syrup and corn syrup. Each bar contains 11 grams of sugar and 3 grams of fiber.

Even Corn Flakes contain sugar, malt flavoring, and high-fructose-corn-syrup, listed as its second, third, and fourth ingredients. Kellogg is also offering promotions on Rice Krispies, Mini-Wheats, and Eggo Waffles -- the waffles contain partially-hydrogenated oils in addition to high-fructose-corn syrup.

But Kellogg Company knows that people are concerned about feeding their kids sugar and chemicals for breakfast every morning, so it has dedicated whole sections of its Web site to "correcting" false nutrition information. In one section, Kellogg refers to sugar as the "misunderstood nutrient." According to the Web site, "Sugar does not cause obesity, type 2 diabetes, heart disease or hyperactivity." This statement flies in the face of the most recent research and a host of mainstream studies that say the exact opposite.

One of the most recent studies, reported in TIME Magazine last year, found that consuming added sugars raises the risk for heart disease by raising cholesterol and triglycerides. The American Heart Association's (AHA) Web site states, "High intake of added sugars is implicated in numerous poor health conditions, including obesity, high blood pressure and other risk factors for heart disease and stroke." The AHA is so concerned about the amount of added sugars in the American diet that in 2009 it established upper limits for adults (none exist yet for children, oddly enough). The AHA says that women should get no more than six teaspoons a day and men no more than nine.

Most of the Kellogg's products I researched contained an average of 11 grams of sugar per serving, which is close to three teaspoons of sugar. If we assume that the average child weighs about half what the average woman weighs, then three teaspoons is the upper limit of how much a child should safely consume in one day, according to the AHA. That means the child couldn't eat any other added sugars for the rest of the day (not likely) and that he or she could only eat the single three-fourths cup serving (also, not likely). The AHA says the average American eats an alarming 22 teaspoons of added sugar a day.

One in four children goes without breakfast each morning, according to the U.S. Department of Agriculture. A tragedy to be sure -- but are Kellogg's breakfast products the solution?

Last week Kellogg announced its new project called Share Your Breakfast, part of a national advertising campaign. The project asks Americans to upload their breakfast photos to the Web site shareyourbreakfast.com, and for each breakfast photo shared, Kellogg Company will donate a school breakfast to a child in need -- up to $200,000 worth of (or one million) breakfasts.

Feeding hungry children sure sounds nice, but filling hungry bellies with highly-processed junk foods is hardly the answer. Let's take a look at some of the products Kellogg is promoting as part of this endeavor.

Frosted Flakes -- one of the products represented by Tony the Tiger at a National Breakfast Day event in New York last Tuesday -- contains 11 grams of sugar per three-fourths cup serving. After the first ingredient of milled corn, the next three read: Sugar, malt flavoring, and high-fructose-corn-syrup -- three forms of sugar by different names.

Nutri-Grain bars -- a product promoted as healthy -- contain more than 30 ingredients (minus the synthetic vitamins) and include high-fructose-corn syrup, artificial flavors, red #40, TBHQ, and host of other chemicals. Meanwhile, the front of the package reads: "More of the whole grains your body needs," "Good source of fiber," and "Made with real fruit." The only "real fruit" I could find is "strawberry puree concentrate" and it's listed after high-fructose-corn syrup and corn syrup. Each bar contains 11 grams of sugar and 3 grams of fiber.

Even Corn Flakes contain sugar, malt flavoring, and high-fructose-corn-syrup, listed as its second, third, and fourth ingredients. Kellogg is also offering promotions on Rice Krispies, Mini-Wheats, and Eggo Waffles -- the waffles contain partially-hydrogenated oils in addition to high-fructose-corn syrup.

But Kellogg Company knows that people are concerned about feeding their kids sugar and chemicals for breakfast every morning, so it has dedicated whole sections of its Web site to "correcting" false nutrition information. In one section, Kellogg refers to sugar as the "misunderstood nutrient." According to the Web site, "Sugar does not cause obesity, type 2 diabetes, heart disease or hyperactivity." This statement flies in the face of the most recent research and a host of mainstream studies that say the exact opposite.

One of the most recent studies, reported in TIME Magazine last year, found that consuming added sugars raises the risk for heart disease by raising cholesterol and triglycerides. The American Heart Association's (AHA) Web site states, "High intake of added sugars is implicated in numerous poor health conditions, including obesity, high blood pressure and other risk factors for heart disease and stroke." The AHA is so concerned about the amount of added sugars in the American diet that in 2009 it established upper limits for adults (none exist yet for children, oddly enough). The AHA says that women should get no more than six teaspoons a day and men no more than nine.

Most of the Kellogg's products I researched contained an average of 11 grams of sugar per serving, which is close to three teaspoons of sugar. If we assume that the average child weighs about half what the average woman weighs, then three teaspoons is the upper limit of how much a child should safely consume in one day, according to the AHA. That means the child couldn't eat any other added sugars for the rest of the day (not likely) and that he or she could only eat the single three-fourths cup serving (also, not likely). The AHA says the average American eats an alarming 22 teaspoons of added sugar a day.

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Opening sequence to Scoliosis Exercises for Correction and Prevention

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