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
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

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.

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

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."

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."

Read More

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
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

Read More

Obesity: The killer combination of salt, fat and sugar

For years I wondered why I was fat. I lost weight, gained it back, and lost it again – over and over and over. I owned suits in every size. As a former commissioner of the FDA (the US Food and Drug Administration), surely I should have the answer to my problems. Yet food held remarkable sway over my behaviour.

The latest science seemed to suggest being overweight was my destiny. I was fat because my body's "thermostat" was set high. If I lost weight, my body would try to get it back, slowing down my metabolism till I returned to my predetermined set point.

But this theory didn't explain why so many people, in the US and UK in particular, were getting significantly fatter. For thousands of years, human body weight had stayed remarkably stable. Millions of calories passed through our bodies, yet with rare exceptions our weight neither rose nor fell. A perfect biological system seemed to be at work. Then, in the 80s, something changed.

Three decades ago, fewer than one Briton in 10 was obese. One in four is today. It is projected that by 2050, Britain could be a "mainly obese society". Similar, and even more pronounced, changes were taking place in the US, where researchers found that not only were Americans entering their adult years at a significantly higher weight but, while on average everyone was getting heavier, the heaviest people were gaining disproportionately more weight than others. The spread between those at the upper end of the weight curve and those at the lower end was widening. Overweight people were becoming more overweight.

What had happened to add so many millions of pounds to so many millions of people? Certainly food had become more readily available, with larger portion sizes, more chain restaurants and a culture that promotes out-of-home eating. But having food available doesn't mean we have to eat it. What has been driving us to overeat?

It is certainly not a want born of fear of food shortages. Nor is it a want rooted in hunger or the love of exceptional food. We know, too, that overeating is not the sole province of those who are overweight. Even people who remain slim often feel embattled by their drive for food. It takes serious restraint to resist an almost overpowering urge to eat. Yet many, including doctors and healthcare professionals, still think that weight gainers merely lack willpower, or perhaps self-esteem. Few have recognised the distinctive pattern of overeating that has become widespread in the population. No one has seen loss of control as its most defining characteristic.

"Higher sugar, fat and salt make you want to eat more." I had read this in scientific literature, and heard it in conversations with neuroscientists and psychologists. But here was a leading food designer, a Henry Ford of mass-produced food, revealing how his industry operates. To protect his business, he did not want to be identified, but he was remarkably candid, explaining how the food industry creates dishes to hit what he called the "three points of the compass".

Sugar, fat and salt make a food compelling. They stimulate neurons, cells that trigger the brain's reward system and release dopamine, a chemical that motivates our behaviour and makes us want to eat more. Many of us have what's called a "bliss point", at which we get the greatest pleasure from sugar, fat or salt. Combined in the right way, they make a product indulgent, high in "hedonic value".

During the past two decades, there has been an explosion in our ability to access and afford what scientists call highly "palatable" foods. By palatability, they don't just mean it tastes good: they are referring primarily to its capacity to stimulate the appetite. Restaurants sit at the epicentre of this explosion, along with an ever-expanding range of dishes that hit these three compass points. Sugar, fat and salt are either loaded into a core ingredient (such as meat, vegetables, potato or bread), layered on top of it, or both. Deep-fried tortilla chips are an example of loading – the fat is contained in the chip itself. When it is smothered in cheese, sour cream and sauce, that's layering.

It is not just that fast food chains serve food with more fat, sugar and salt, or that intensive processing virtually eliminates our need to chew before swallowing, or that snacks are now available at any time. It is the combination of all that, and more.

Take Kentucky Fried Chicken. My source called it "a premier example" of putting more fat on our plate. KFC's approach to battering its food results in "an optimised fat pick-up system". With its flour, salt, MSG, maltodextrin, sugar, corn syrup and spice, the fried coating imparts flavour that touches on all three points of the compass while giving the consumer the perception of a bargain – a big plate of food at a good price.

Initially, KFC meals were built around a whole chicken, with a pick-up surface that contained "an enormous amount of breading, crispiness and brownness on the surface. That makes the chicken look like more and gives it this wonderful oily flavour." Over time, the company began to realise there was less meat in a chicken nugget compared with a whole chicken, and a greater percentage of fried batter. But the real breakthrough was popcorn chicken. "The smaller the piece of meat, the greater the percentage of fat pick-up," said the food designer. "Now, we have lots of pieces of a cheaper part of the chicken." The product has been "optimised on every dimension", with the fat, sugar and salt combining with the perception of good value virtually to guarantee consumer appeal.

He walked me through some offerings at other popular food chains. Burger King's Whopper touched on the three points of the compass – then was altered for further effect. In its first, stripped-down form, the burger was explosively rich in fat, sugar and salt. Then the chain began adding more beef, extra cheese or a layer of bacon. McDonald's broke new ground in another way – by making food available on a whim. "The great growth has been the snacking occasion. You get hungry, you want something, your mind pushes off the reality of what you ought to eat, and you end up picking up a hamburger and a giant soda or french fries."

Next they introduced a high-fat, high-salt morning meal. "They took what they learned from the core lunch and dinner menu, and applied it to breakfast. The sausage McMuffin and the egg McMuffin are stand-ins for the hamburger. In effect, you are eating a morning hamburger."

This kind of food disappears down our throats so quickly after the first bite that it readily overrides the body's signals that should tell us, "I'm full." The food designer offered coleslaw as an example. When its ingredients are chopped roughly, it requires time and energy to chew. But when cabbage and carrots are softened in a high-fat dressing, coleslaw ceases to be "something with a lot of innate ability to satisfy".

This isn't to say that the food industry wants us to stop chewing altogether. It knows we want to eat a doughnut, not drink it. "The key is to create foods with just enough chew – but not too much. When you're eating these things, you've had 500, 600, 800, 900 calories before you know it." Foods that slip down don't leave us with a sense of being well fed. In making food disappear so swiftly, fat and sugar only leave us wanting more.

According to food consultant Gail Vance Civille, of management consultants Sensory Spectrum, fat is crucial to this process of lubrication, ensuring that a product melts in the mouth. In the past, she says, Americans typically chewed food up to 25 times before it was swallowed; now the average American chews 10 times. "If I have fat in there, I just chew it up and whoosh! Away it goes," she says. "You have a 'quick getaway', a quick melt."

The Snickers bar, Civille says, is "extraordinarily well engineered". Unlike many products whose nuts become annoyingly lodged between your teeth, the genius of Snickers is that as we chew, the sugar dissolves, the fat melts and the caramel picks up the peanut pieces, so the entire candy is carried out of the mouth at the same time. "You're not getting a build-up of stuff in your mouth."

Kettle chips are another success story. Made of sugar-rich russet potatoes, they have a slightly bitter background note and brown irregularly, which gives them a complex flavour. High levels of fat generate easy mouth-melt, and surface variations add a level of interest beyond that found in mass-produced chips. Heightened complexity is the key to modern food design.

Not so many decades ago, a single flavour of ice-cream was a special treat. Our options ran to vanilla, chocolate and strawberry – and when we could buy all three in a single carton, we saw that as a great innovation. Now ice-cream has countless flavours and varieties; it comes mixed with M&M's or topped with caramel sauce.

When layers of complexity are built into food, the effect becomes more powerful. Sweetness alone does not account for the full impact of a fizzy drink – its temperature and tingle, resulting from the stimulation of the trigeminal nerve by carbonation and acid, are essential contributors as well.

"The complexity of the stimulus increases its association to a reward," says Gaetano Di Chiara, an expert in neuroscience and pharmacology at the University of Cagliari in Italy. Elements of that complexity include tastes that are familiar and well liked, especially if not always readily available, and the learning associated with having had a pleasurable experience with the same food in the past.

Take a bowl of M&M's. If I've eaten them in the past, I'm stimulated by the sight of them, because I know they'll be rewarding. I eat one, and experience that reward. The visual cue gains power and stimulates the urge we call "wanting". The more potent and complex foods become, the greater the rewards they may offer. The excitement in the brain increases our desire for further stimulation.

In theory there's a limit to how much stimulation rewarding foods can generate. We are supposed to habituate – to neuroadapt. When Di Chiara gave animals a cheesy snack called Fonzies, the levels of dopamine in their brains increased. Over time, habituation set in, dopamine levels fell and the food lost its capacity to activate their behaviour.

But if the stimulus is powerful enough, novel enough or administered intermittently enough, the brain may not curb its dopamine response. Desire remains high. We see this with cocaine use, which does not result in habituation. Hyperpalatable foods alter the landscape of the brain in much the same way.

I asked Di Chiara to study what happens after an animal is repeatedly exposed to a high-sugar, high-fat chocolate drink. When he'd completed his experiment, he sent me an email with "Important results!!!!" in the subject line. He had shown that dopamine response did not diminish over time with the chocolate drink. There was no habituation.

Novelty also impedes habituation, and intermittency is another driver. Give an animal enough sugar-laden food, withdraw it for the right amount of time, then provide it again in sufficient quantities, and dopamine levels may not diminish.

There's still a lot we don't know about the relationship between the dopamine-driven motivational system and our behaviour in the presence of rewarding foods. But we do know that foods high in sugar, fat and salt are altering the biological circuitry of our brains. We have scientific techniques that demonstrate how these foods – and the cues associated with them – change the connections between the neural circuits and their response patterns.

Rewarding foods are rewiring our brains. As they do, we become more sensitive to the cues that lead us to anticipate the reward. In that circularity lies a trap: we can no longer control our responses to highly palatable foods because our brains have been changed by the foods we eat.

I wanted to know how much the industry understood about how the food we eat affects us; about what I have termed "conditioned hypereating" – "conditioned" because it becomes an automatic response to widely available food, "hyper" because the eating is excessive and hard to control. I turned to Joseph Stiglitz, a Nobel laureate in economics.

"Does the industry know that what it feeds us gets us to eat more?" I asked.

"The industry has jacked up what works for it," Stiglitz said. "The learning is evolutionary." Practical experience has been its guide – it does not need lab rats when it can try out its ideas on humans. Its decision-makers do not have to analyse human brain circuitry to discover what sells.

A venture capitalist who knows the business intimately cited Starbucks as a company that has recognised and responded brilliantly to a cultural need. The caffeine and sugar in the coffee, with their energising effects, are certainly part of the equation, but the chain also offers something much more primal. "It's about warm milk and a bottle," he says. "One of my colleagues said, 'If I could put a nipple on it, I'd be a multimillionaire'."

But it was thinking creatively about how to attract more consumers that led Starbucks to the Frappuccino, the venture capitalist told me. Although its stores were crowded early in the day, by afternoon "they were so empty you could roll a bowling ball through them". The creation of a rich, sweet and comforting milkshake-like concoction utterly transformed the business. A Starbucks Strawberries & Crème Frappuccino comes with whipped cream and 18 teaspoons of sugar: all in all, this "drink" contains more calories than a personal-size pepperoni pizza, and more sweetness than six scoops of ice-cream. By encouraging us to consider any occasion for food an opportunity for pleasure and reward, the industry invites us to indulge a lot more often.

Starbucks learned a basic lesson: make enticing food easily and constantly available, keep it novel, and people will keep coming back for more. With food available in almost any setting, "the number of cues, the number of opportunities" to eat have increased, while the barriers to consumption have fallen, says David Mela, senior scientist of weight management at the Unilever Health Institute. "The environmental stimulus has changed."

Of course, when food is offered to us, we're not obliged to eat it. When it's on the menu, we don't have to order it. But this takes more than willpower. As an individual, you can practise eating the food you want in a controlled way. As a society, we can identify the forces that drive overeating and find ways to diminish their power. That's what happened with the tobacco industry: attitudes to smoking shifted. Similar changes could be brought about in our attitudes to food – by making it mandatory for restaurants to list calorie counts on their menus; by clear labelling on food products; by monitoring food marketing. But until then few of us are immune to the ubiquitous presence of food, the incessant marketing and the cultural assumption that it's acceptable to eat anywhere, at any time.

Call it the "taco chip challenge" – the challenge of controlled eating in the face of constant food availability. "Forty years ago, you might face the social equivalent of that taco chip challenge once a month. Now you face it every single day," Mela said. "Every single day and every single place you go, those foods are there, those foods are cheap, those foods are readily available for you to engage in. There is constant, constant opportunity."

For years I wondered why I was fat. I lost weight, gained it back, and lost it again – over and over and over. I owned suits in every size. As a former commissioner of the FDA (the US Food and Drug Administration), surely I should have the answer to my problems. Yet food held remarkable sway over my behaviour.

The latest science seemed to suggest being overweight was my destiny. I was fat because my body's "thermostat" was set high. If I lost weight, my body would try to get it back, slowing down my metabolism till I returned to my predetermined set point.

But this theory didn't explain why so many people, in the US and UK in particular, were getting significantly fatter. For thousands of years, human body weight had stayed remarkably stable. Millions of calories passed through our bodies, yet with rare exceptions our weight neither rose nor fell. A perfect biological system seemed to be at work. Then, in the 80s, something changed.

Three decades ago, fewer than one Briton in 10 was obese. One in four is today. It is projected that by 2050, Britain could be a "mainly obese society". Similar, and even more pronounced, changes were taking place in the US, where researchers found that not only were Americans entering their adult years at a significantly higher weight but, while on average everyone was getting heavier, the heaviest people were gaining disproportionately more weight than others. The spread between those at the upper end of the weight curve and those at the lower end was widening. Overweight people were becoming more overweight.

What had happened to add so many millions of pounds to so many millions of people? Certainly food had become more readily available, with larger portion sizes, more chain restaurants and a culture that promotes out-of-home eating. But having food available doesn't mean we have to eat it. What has been driving us to overeat?

It is certainly not a want born of fear of food shortages. Nor is it a want rooted in hunger or the love of exceptional food. We know, too, that overeating is not the sole province of those who are overweight. Even people who remain slim often feel embattled by their drive for food. It takes serious restraint to resist an almost overpowering urge to eat. Yet many, including doctors and healthcare professionals, still think that weight gainers merely lack willpower, or perhaps self-esteem. Few have recognised the distinctive pattern of overeating that has become widespread in the population. No one has seen loss of control as its most defining characteristic.

"Higher sugar, fat and salt make you want to eat more." I had read this in scientific literature, and heard it in conversations with neuroscientists and psychologists. But here was a leading food designer, a Henry Ford of mass-produced food, revealing how his industry operates. To protect his business, he did not want to be identified, but he was remarkably candid, explaining how the food industry creates dishes to hit what he called the "three points of the compass".

Sugar, fat and salt make a food compelling. They stimulate neurons, cells that trigger the brain's reward system and release dopamine, a chemical that motivates our behaviour and makes us want to eat more. Many of us have what's called a "bliss point", at which we get the greatest pleasure from sugar, fat or salt. Combined in the right way, they make a product indulgent, high in "hedonic value".

During the past two decades, there has been an explosion in our ability to access and afford what scientists call highly "palatable" foods. By palatability, they don't just mean it tastes good: they are referring primarily to its capacity to stimulate the appetite. Restaurants sit at the epicentre of this explosion, along with an ever-expanding range of dishes that hit these three compass points. Sugar, fat and salt are either loaded into a core ingredient (such as meat, vegetables, potato or bread), layered on top of it, or both. Deep-fried tortilla chips are an example of loading – the fat is contained in the chip itself. When it is smothered in cheese, sour cream and sauce, that's layering.

It is not just that fast food chains serve food with more fat, sugar and salt, or that intensive processing virtually eliminates our need to chew before swallowing, or that snacks are now available at any time. It is the combination of all that, and more.

Take Kentucky Fried Chicken. My source called it "a premier example" of putting more fat on our plate. KFC's approach to battering its food results in "an optimised fat pick-up system". With its flour, salt, MSG, maltodextrin, sugar, corn syrup and spice, the fried coating imparts flavour that touches on all three points of the compass while giving the consumer the perception of a bargain – a big plate of food at a good price.

Initially, KFC meals were built around a whole chicken, with a pick-up surface that contained "an enormous amount of breading, crispiness and brownness on the surface. That makes the chicken look like more and gives it this wonderful oily flavour." Over time, the company began to realise there was less meat in a chicken nugget compared with a whole chicken, and a greater percentage of fried batter. But the real breakthrough was popcorn chicken. "The smaller the piece of meat, the greater the percentage of fat pick-up," said the food designer. "Now, we have lots of pieces of a cheaper part of the chicken." The product has been "optimised on every dimension", with the fat, sugar and salt combining with the perception of good value virtually to guarantee consumer appeal.

He walked me through some offerings at other popular food chains. Burger King's Whopper touched on the three points of the compass – then was altered for further effect. In its first, stripped-down form, the burger was explosively rich in fat, sugar and salt. Then the chain began adding more beef, extra cheese or a layer of bacon. McDonald's broke new ground in another way – by making food available on a whim. "The great growth has been the snacking occasion. You get hungry, you want something, your mind pushes off the reality of what you ought to eat, and you end up picking up a hamburger and a giant soda or french fries."

Next they introduced a high-fat, high-salt morning meal. "They took what they learned from the core lunch and dinner menu, and applied it to breakfast. The sausage McMuffin and the egg McMuffin are stand-ins for the hamburger. In effect, you are eating a morning hamburger."

This kind of food disappears down our throats so quickly after the first bite that it readily overrides the body's signals that should tell us, "I'm full." The food designer offered coleslaw as an example. When its ingredients are chopped roughly, it requires time and energy to chew. But when cabbage and carrots are softened in a high-fat dressing, coleslaw ceases to be "something with a lot of innate ability to satisfy".

This isn't to say that the food industry wants us to stop chewing altogether. It knows we want to eat a doughnut, not drink it. "The key is to create foods with just enough chew – but not too much. When you're eating these things, you've had 500, 600, 800, 900 calories before you know it." Foods that slip down don't leave us with a sense of being well fed. In making food disappear so swiftly, fat and sugar only leave us wanting more.

According to food consultant Gail Vance Civille, of management consultants Sensory Spectrum, fat is crucial to this process of lubrication, ensuring that a product melts in the mouth. In the past, she says, Americans typically chewed food up to 25 times before it was swallowed; now the average American chews 10 times. "If I have fat in there, I just chew it up and whoosh! Away it goes," she says. "You have a 'quick getaway', a quick melt."

The Snickers bar, Civille says, is "extraordinarily well engineered". Unlike many products whose nuts become annoyingly lodged between your teeth, the genius of Snickers is that as we chew, the sugar dissolves, the fat melts and the caramel picks up the peanut pieces, so the entire candy is carried out of the mouth at the same time. "You're not getting a build-up of stuff in your mouth."

Kettle chips are another success story. Made of sugar-rich russet potatoes, they have a slightly bitter background note and brown irregularly, which gives them a complex flavour. High levels of fat generate easy mouth-melt, and surface variations add a level of interest beyond that found in mass-produced chips. Heightened complexity is the key to modern food design.

Not so many decades ago, a single flavour of ice-cream was a special treat. Our options ran to vanilla, chocolate and strawberry – and when we could buy all three in a single carton, we saw that as a great innovation. Now ice-cream has countless flavours and varieties; it comes mixed with M&M's or topped with caramel sauce.

When layers of complexity are built into food, the effect becomes more powerful. Sweetness alone does not account for the full impact of a fizzy drink – its temperature and tingle, resulting from the stimulation of the trigeminal nerve by carbonation and acid, are essential contributors as well.

"The complexity of the stimulus increases its association to a reward," says Gaetano Di Chiara, an expert in neuroscience and pharmacology at the University of Cagliari in Italy. Elements of that complexity include tastes that are familiar and well liked, especially if not always readily available, and the learning associated with having had a pleasurable experience with the same food in the past.

Take a bowl of M&M's. If I've eaten them in the past, I'm stimulated by the sight of them, because I know they'll be rewarding. I eat one, and experience that reward. The visual cue gains power and stimulates the urge we call "wanting". The more potent and complex foods become, the greater the rewards they may offer. The excitement in the brain increases our desire for further stimulation.

In theory there's a limit to how much stimulation rewarding foods can generate. We are supposed to habituate – to neuroadapt. When Di Chiara gave animals a cheesy snack called Fonzies, the levels of dopamine in their brains increased. Over time, habituation set in, dopamine levels fell and the food lost its capacity to activate their behaviour.

But if the stimulus is powerful enough, novel enough or administered intermittently enough, the brain may not curb its dopamine response. Desire remains high. We see this with cocaine use, which does not result in habituation. Hyperpalatable foods alter the landscape of the brain in much the same way.

I asked Di Chiara to study what happens after an animal is repeatedly exposed to a high-sugar, high-fat chocolate drink. When he'd completed his experiment, he sent me an email with "Important results!!!!" in the subject line. He had shown that dopamine response did not diminish over time with the chocolate drink. There was no habituation.

Novelty also impedes habituation, and intermittency is another driver. Give an animal enough sugar-laden food, withdraw it for the right amount of time, then provide it again in sufficient quantities, and dopamine levels may not diminish.

There's still a lot we don't know about the relationship between the dopamine-driven motivational system and our behaviour in the presence of rewarding foods. But we do know that foods high in sugar, fat and salt are altering the biological circuitry of our brains. We have scientific techniques that demonstrate how these foods – and the cues associated with them – change the connections between the neural circuits and their response patterns.

Rewarding foods are rewiring our brains. As they do, we become more sensitive to the cues that lead us to anticipate the reward. In that circularity lies a trap: we can no longer control our responses to highly palatable foods because our brains have been changed by the foods we eat.

I wanted to know how much the industry understood about how the food we eat affects us; about what I have termed "conditioned hypereating" – "conditioned" because it becomes an automatic response to widely available food, "hyper" because the eating is excessive and hard to control. I turned to Joseph Stiglitz, a Nobel laureate in economics.

"Does the industry know that what it feeds us gets us to eat more?" I asked.

"The industry has jacked up what works for it," Stiglitz said. "The learning is evolutionary." Practical experience has been its guide – it does not need lab rats when it can try out its ideas on humans. Its decision-makers do not have to analyse human brain circuitry to discover what sells.

A venture capitalist who knows the business intimately cited Starbucks as a company that has recognised and responded brilliantly to a cultural need. The caffeine and sugar in the coffee, with their energising effects, are certainly part of the equation, but the chain also offers something much more primal. "It's about warm milk and a bottle," he says. "One of my colleagues said, 'If I could put a nipple on it, I'd be a multimillionaire'."

But it was thinking creatively about how to attract more consumers that led Starbucks to the Frappuccino, the venture capitalist told me. Although its stores were crowded early in the day, by afternoon "they were so empty you could roll a bowling ball through them". The creation of a rich, sweet and comforting milkshake-like concoction utterly transformed the business. A Starbucks Strawberries & Crème Frappuccino comes with whipped cream and 18 teaspoons of sugar: all in all, this "drink" contains more calories than a personal-size pepperoni pizza, and more sweetness than six scoops of ice-cream. By encouraging us to consider any occasion for food an opportunity for pleasure and reward, the industry invites us to indulge a lot more often.

Starbucks learned a basic lesson: make enticing food easily and constantly available, keep it novel, and people will keep coming back for more. With food available in almost any setting, "the number of cues, the number of opportunities" to eat have increased, while the barriers to consumption have fallen, says David Mela, senior scientist of weight management at the Unilever Health Institute. "The environmental stimulus has changed."

Of course, when food is offered to us, we're not obliged to eat it. When it's on the menu, we don't have to order it. But this takes more than willpower. As an individual, you can practise eating the food you want in a controlled way. As a society, we can identify the forces that drive overeating and find ways to diminish their power. That's what happened with the tobacco industry: attitudes to smoking shifted. Similar changes could be brought about in our attitudes to food – by making it mandatory for restaurants to list calorie counts on their menus; by clear labelling on food products; by monitoring food marketing. But until then few of us are immune to the ubiquitous presence of food, the incessant marketing and the cultural assumption that it's acceptable to eat anywhere, at any time.

Call it the "taco chip challenge" – the challenge of controlled eating in the face of constant food availability. "Forty years ago, you might face the social equivalent of that taco chip challenge once a month. Now you face it every single day," Mela said. "Every single day and every single place you go, those foods are there, those foods are cheap, those foods are readily available for you to engage in. There is constant, constant opportunity."

Read More

Calcium may help you live longer: study

NEW YORK (Reuters Health) - Getting a bit more calcium in your diet could help you live longer, new research suggests.

Swedish researchers found that men who consumed the most calcium in food were 25 percent less likely to die over the next decade than their peers who took in the least calcium from food. None of the men took calcium supplements.

The findings are in line with previous research linking higher calcium intake with lower mortality in both men and women, the researchers point out in a report in the American Journal of Epidemiology.

While many researchers have looked at calcium and magnesium intake and the risk of chronic disease, less is known about the association between consumption of these nutrients in food and mortality.

To investigate, Dr. Joanna Kaluza of the Karolinska Institutet in Stockholm and her colleagues looked at more than 23,000 Swedish men who were 45 to 79 years old at the study's outset and were followed for 10 years. All had reported on their diet at the beginning of the study. During follow-up, about 2,358 died.

The top calcium consumers had a 25 percent lower risk of dying from any cause and a 23 percent lower risk of dying from heart disease during follow-up relative to men that had the least amount of calcium in their diet. Calcium intake didn't significantly influence the risk of dying from cancer.

Men in the top third based on their calcium intake were getting nearly 2,000 milligrams a day, on average, compared to about 1,000 milligrams for men in the bottom third. The US Recommended Dietary Allowance (RDA) for calcium intake is 1,000 milligrams for men 19 to 50 years old and 1,200 milligrams for men 50 and over.

"Intake of calcium above that recommended daily may reduce all-cause mortality," Kaluza and her colleagues conclude.

Calcium could influence mortality risk in many ways, they note, for example by reducing blood pressure, cholesterol, or blood sugar levels. For the men in the study, the main sources of calcium in the diet were milk and milk products and cereal products.

NEW YORK (Reuters Health) - Getting a bit more calcium in your diet could help you live longer, new research suggests.

Swedish researchers found that men who consumed the most calcium in food were 25 percent less likely to die over the next decade than their peers who took in the least calcium from food. None of the men took calcium supplements.

The findings are in line with previous research linking higher calcium intake with lower mortality in both men and women, the researchers point out in a report in the American Journal of Epidemiology.

While many researchers have looked at calcium and magnesium intake and the risk of chronic disease, less is known about the association between consumption of these nutrients in food and mortality.

To investigate, Dr. Joanna Kaluza of the Karolinska Institutet in Stockholm and her colleagues looked at more than 23,000 Swedish men who were 45 to 79 years old at the study's outset and were followed for 10 years. All had reported on their diet at the beginning of the study. During follow-up, about 2,358 died.

The top calcium consumers had a 25 percent lower risk of dying from any cause and a 23 percent lower risk of dying from heart disease during follow-up relative to men that had the least amount of calcium in their diet. Calcium intake didn't significantly influence the risk of dying from cancer.

Men in the top third based on their calcium intake were getting nearly 2,000 milligrams a day, on average, compared to about 1,000 milligrams for men in the bottom third. The US Recommended Dietary Allowance (RDA) for calcium intake is 1,000 milligrams for men 19 to 50 years old and 1,200 milligrams for men 50 and over.

"Intake of calcium above that recommended daily may reduce all-cause mortality," Kaluza and her colleagues conclude.

Calcium could influence mortality risk in many ways, they note, for example by reducing blood pressure, cholesterol, or blood sugar levels. For the men in the study, the main sources of calcium in the diet were milk and milk products and cereal products.

Read More

How to Prevent Low-Back Pain

Back pain is very common. It affects about 8 out of 10 people. But there are many steps you can take to avoid it. One of the best things you can do to prevent back pain is to exercise regularly and keep your back and abdominal muscles strong.

A program of regular low-impact exercises such as walking, swimming, or riding a bike—mobile or stationary—will be beneficial. Yoga can also help stretch and strengthen muscles and improve posture. Ask your doctor for a list of exercises appropriate for your age and physical condition.

Here are some quick pointers to prevent back problems:

Always stretch before any strenuous physical activity.

Don’t slouch when standing or sitting. When standing, keep your weight balanced on your feet. Curvature of the spine puts stress on back muscles.

Sit in chairs or car seats with good lumbar support. Switch sitting positions often and periodically walk around or gently stretch muscles to relieve tension.

Don’t bend over without supporting your back. For example, don’t lean over a low sink without bracing yourself with your hand. Also, don’t reach and lift an object out of a car trunk; first slide the object to the edge of the trunk.

Wear comfortable, low-heeled shoes.

Sleep on your side to reduce any curve in your spine. Always sleep on a firm surface.

Don’t try to lift objects too heavy for you. Lift with your legs keeping your back straight. Keep the object close to your body. Do not twist when lifting.

Try to control your weight, especially weight around the waistline that taxes lower back muscles.

If you smoke, quit. Smoking reduces blood flow to the lower spine and causes the spinal discs to degenerate.

To keep your spine strong, as with all bones, you need to get enough calcium and vitamin D every day. These nutrients help prevent osteoporosis, which is responsible for a lot of the bone fractures that lead to back pain.

Calcium is found in dairy products; green, leafy vegetables; and fortified products, like orange juice. Your skin makes vitamin D when you are in the sun. If you are not outside much, you can obtain vitamin D from your diet: almost all milk and some other foods are fortified with this nutrient. Most adults don’t get enough calcium and vitamin D, so talk to your doctor about how much you need per day.

In most cases, it is not necessary to see a doctor for back pain because pain usually goes away with or without treatment. However, a trip to the doctor is a good idea if your pain is severe and doesn’t improve, or if you have pain after a fall or an injury.

It is important to see your doctor if you have pain along with any of the following problems: trouble urinating; weakness, pain or numbness in your legs; fever; or unintentional weight

Back pain is very common. It affects about 8 out of 10 people. But there are many steps you can take to avoid it. One of the best things you can do to prevent back pain is to exercise regularly and keep your back and abdominal muscles strong.

A program of regular low-impact exercises such as walking, swimming, or riding a bike—mobile or stationary—will be beneficial. Yoga can also help stretch and strengthen muscles and improve posture. Ask your doctor for a list of exercises appropriate for your age and physical condition.

Here are some quick pointers to prevent back problems:

Always stretch before any strenuous physical activity.

Don’t slouch when standing or sitting. When standing, keep your weight balanced on your feet. Curvature of the spine puts stress on back muscles.

Sit in chairs or car seats with good lumbar support. Switch sitting positions often and periodically walk around or gently stretch muscles to relieve tension.

Don’t bend over without supporting your back. For example, don’t lean over a low sink without bracing yourself with your hand. Also, don’t reach and lift an object out of a car trunk; first slide the object to the edge of the trunk.

Wear comfortable, low-heeled shoes.

Sleep on your side to reduce any curve in your spine. Always sleep on a firm surface.

Don’t try to lift objects too heavy for you. Lift with your legs keeping your back straight. Keep the object close to your body. Do not twist when lifting.

Try to control your weight, especially weight around the waistline that taxes lower back muscles.

If you smoke, quit. Smoking reduces blood flow to the lower spine and causes the spinal discs to degenerate.

To keep your spine strong, as with all bones, you need to get enough calcium and vitamin D every day. These nutrients help prevent osteoporosis, which is responsible for a lot of the bone fractures that lead to back pain.

Calcium is found in dairy products; green, leafy vegetables; and fortified products, like orange juice. Your skin makes vitamin D when you are in the sun. If you are not outside much, you can obtain vitamin D from your diet: almost all milk and some other foods are fortified with this nutrient. Most adults don’t get enough calcium and vitamin D, so talk to your doctor about how much you need per day.

In most cases, it is not necessary to see a doctor for back pain because pain usually goes away with or without treatment. However, a trip to the doctor is a good idea if your pain is severe and doesn’t improve, or if you have pain after a fall or an injury.

It is important to see your doctor if you have pain along with any of the following problems: trouble urinating; weakness, pain or numbness in your legs; fever; or unintentional weight

Read More