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Wednesday, May 12, 2010

Vigorous exercise strengthens hip bones in young children

Researchers from Southhampton and Cambridge Universities in the UK have presented evidence that vigorous physical activity in young children results in stronger hip bones. The results were presented at the World Congress on Osteoporosis (IOF WCO-ECCEO10) in Florence, Italy.

More than 200 six-year olds participated in the study. Using advanced scanning technology, the researchers measured bone mass and analysed the structure of the femoral neck (hip) and thigh bone. Physical activity was assessed for seven continuous days.

The results showed that there was a relationship between time spent in vigorous activity and strength of the femoral neck, both in terms of shape and volumetric mineral density. This was independent of other factors such as diet, lifestyle and physical size.

This supports the argument that increasing physical activity in childhood is likely to improve childhood skeletal bone development, and is thus a potentially important public health strategy towards prevention of osteoporosis in later life.
Researchers from Southhampton and Cambridge Universities in the UK have presented evidence that vigorous physical activity in young children results in stronger hip bones. The results were presented at the World Congress on Osteoporosis (IOF WCO-ECCEO10) in Florence, Italy.

More than 200 six-year olds participated in the study. Using advanced scanning technology, the researchers measured bone mass and analysed the structure of the femoral neck (hip) and thigh bone. Physical activity was assessed for seven continuous days.

The results showed that there was a relationship between time spent in vigorous activity and strength of the femoral neck, both in terms of shape and volumetric mineral density. This was independent of other factors such as diet, lifestyle and physical size.

This supports the argument that increasing physical activity in childhood is likely to improve childhood skeletal bone development, and is thus a potentially important public health strategy towards prevention of osteoporosis in later life.
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Omega-3 linked to healthier, stronger bones: Rat study

Increased intakes of omega-3 fatty acids, and DHA in particular, may increase bone mineral content and produce healthier, stronger bones, suggest results from a study with rats.

Omega-3 is one of the stars of the nutrition industry, with the ingredients market valued at a whopping $1.6 billion by Frost & Sullivan. The fatty acids, most notably EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), have been linked to a wide-range of health benefits, including reduced risk of cardiovascular disease (CVD) and certain cancers, good development of a baby during pregnancy, joint health, and improved behaviour and mood.

According to findings of a new study with rats, DHA “appears to be a vital constituent of marrow” and enhances bone mineral content (BMC). The findings did not extend to EPA, however.

Scientists from Purdue University, Indiana University School of Medicine, Korea Maritime University, and the US National Institutes of Health (NIH), report their findings in the British Journal of Nutrition.

Study details

Led by Purdue’s Dr Bruce Watkins, the researchers used dual-energy X-ray absorptiometry to assess the impact of DHA on bone mineral content, compared with the omega-6 DPA (docosapentaenoic acid) or DHA plus DPA.

Rat pups bred to be omega-3 deficient were randomly assigned to receive linoleic acid (LA)- enriched rat milk, or the LA milk supplemented 1 per cent DHA, 1 per cent DPA, or 1 per cent DHA plus 0.4 per cent DPA. Once the animals reached adulthood, the fatty acid levels in their tissues were measured, and their bone mineral density (BMD) determined.
Increased intakes of omega-3 fatty acids, and DHA in particular, may increase bone mineral content and produce healthier, stronger bones, suggest results from a study with rats.

Omega-3 is one of the stars of the nutrition industry, with the ingredients market valued at a whopping $1.6 billion by Frost & Sullivan. The fatty acids, most notably EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), have been linked to a wide-range of health benefits, including reduced risk of cardiovascular disease (CVD) and certain cancers, good development of a baby during pregnancy, joint health, and improved behaviour and mood.

According to findings of a new study with rats, DHA “appears to be a vital constituent of marrow” and enhances bone mineral content (BMC). The findings did not extend to EPA, however.

Scientists from Purdue University, Indiana University School of Medicine, Korea Maritime University, and the US National Institutes of Health (NIH), report their findings in the British Journal of Nutrition.

Study details

Led by Purdue’s Dr Bruce Watkins, the researchers used dual-energy X-ray absorptiometry to assess the impact of DHA on bone mineral content, compared with the omega-6 DPA (docosapentaenoic acid) or DHA plus DPA.

Rat pups bred to be omega-3 deficient were randomly assigned to receive linoleic acid (LA)- enriched rat milk, or the LA milk supplemented 1 per cent DHA, 1 per cent DPA, or 1 per cent DHA plus 0.4 per cent DPA. Once the animals reached adulthood, the fatty acid levels in their tissues were measured, and their bone mineral density (BMD) determined.
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Eating nuts can lower cholesterol, say experts

Eating nuts may help lower cholesterol levels, US research suggests.

The review of 25 studies, involving nearly 600 people, showed eating on average 67g of nuts - a small bag - a day reduced cholesterol levels by 7.4%.

The US Loma Linda University team believes nuts may help prevent the absorption of cholesterol.

UK experts said the research showed nuts were an important part of a healthy diet, but warned against eating nuts covered in sugar or salt.

Previous work has indicated eating nuts regularly is beneficial, but the Archives of Internal Medicine study set out to put an accurate figure on the effect.

The people involved ate 67g of nuts a day on average, over a period of three to eight weeks.

As well as improving cholesterol levels, it also reduced the amount of triglyceride, a type of blood fat that has been linked to heart disease.

However, the impact was least pronounced among the overweight.

It is not yet clear why nuts have this effect, although one suggestion is that it is down to the plant sterols they contain, which are thought to interfere with cholesterol absorption.

Lead researcher Joan Sabate said increasing nut consumption as part of a healthy diet should be recommended.

He added: "The effects of nut consumption were dose related, and different types of nuts had similar effects."

Ellen Mason, senior cardiac nurse at the British Heart Foundation, agreed, but she urged people to go for unsalted nuts.

"Apart from salted peanuts at the pub, nuts in sugary cereals or the traditional Christmas selection, nuts have been largely lacking in our diets in the UK," she added.

The study was carried out by independent researchers, although it was partly funded by the International Tree Nut Council Nutrition Research and Education Foundation.
Eating nuts may help lower cholesterol levels, US research suggests.

The review of 25 studies, involving nearly 600 people, showed eating on average 67g of nuts - a small bag - a day reduced cholesterol levels by 7.4%.

The US Loma Linda University team believes nuts may help prevent the absorption of cholesterol.

UK experts said the research showed nuts were an important part of a healthy diet, but warned against eating nuts covered in sugar or salt.

Previous work has indicated eating nuts regularly is beneficial, but the Archives of Internal Medicine study set out to put an accurate figure on the effect.

The people involved ate 67g of nuts a day on average, over a period of three to eight weeks.

As well as improving cholesterol levels, it also reduced the amount of triglyceride, a type of blood fat that has been linked to heart disease.

However, the impact was least pronounced among the overweight.

It is not yet clear why nuts have this effect, although one suggestion is that it is down to the plant sterols they contain, which are thought to interfere with cholesterol absorption.

Lead researcher Joan Sabate said increasing nut consumption as part of a healthy diet should be recommended.

He added: "The effects of nut consumption were dose related, and different types of nuts had similar effects."

Ellen Mason, senior cardiac nurse at the British Heart Foundation, agreed, but she urged people to go for unsalted nuts.

"Apart from salted peanuts at the pub, nuts in sugary cereals or the traditional Christmas selection, nuts have been largely lacking in our diets in the UK," she added.

The study was carried out by independent researchers, although it was partly funded by the International Tree Nut Council Nutrition Research and Education Foundation.
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Preventing Fleas on Cats

Bradbury CA, Lappin MR: Evaluation of topical application of 10% imidacloprid–1% moxidectin to prevent Bartonella henselae transmission from cat fleas, J Am Vet Med Assoc 236:869, 2010.

Bartonella henselae is the gram-negative aerobic bacilli associated with the syndrome of cat scratch disease in immunocompetent humans. Ctenocephalides felis, the cat flea, is the vector for B. henselae. Infection is common in naturally exposed cats and their fleas, and >30% of cats with fleas are bacteremic. The objective of this study was to determine if monthly topical administration of a combination of 10% imidacloprid and 1 % moxidectin would lessen flea transmission of B. henselae among cats. Eighteen cats were housed in 3 groups of 6 cats. Each of the groups were placed in enclosures separated by mesh to allow fleas to pass among groups yet prevent cat-to-cat contact. The middle group of cats was inoculated with B. henselae and infection was confirmed. This group was flanked on one side by a group treated topically with 10% imidacloprid-1% moxidectin monthly for 3 months, and on the other side by an untreated group. Fleas were placed on the B. henselae infected group at periodic intervals. Blood samples were collected from all the cats weekly to detect Bartonella spp via PCR assay, bacterial culture, and serologic assay. B. henselae infection was confirmed in all untreated cats after flea exposure following the confirmed infection in the inoculated group. None of the cats treated with imidacloprid-moxidectin combination became infected. The results showed that a monthly topical administration of 10% imidacloprid-1% moxidectin reduces the flea load and thus prevented flea transmission of B. henselae to treated cats. Therefore, the likelihood of humans acquiring B. henselae infection may be lessened through monthly use of this flea control product in cats. [VT]

Related articles:
Kamrani A, Parreira VR, Greenwood J et al: The prevalence of Bartonella, hemoplasma, and Rickettsia felis infections in domestic cats and in cat fleas in Ontario, Can J Vet Res 72:411, 2008.

Breitschwerdt EB: Feline bartonellosis and cat scratch disease, Vet Immunol Immunopathol 123:167, 2008.

More on cat health: Winn Feline Foundation Library
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Bradbury CA, Lappin MR: Evaluation of topical application of 10% imidacloprid–1% moxidectin to prevent Bartonella henselae transmission from cat fleas, J Am Vet Med Assoc 236:869, 2010.

Bartonella henselae is the gram-negative aerobic bacilli associated with the syndrome of cat scratch disease in immunocompetent humans. Ctenocephalides felis, the cat flea, is the vector for B. henselae. Infection is common in naturally exposed cats and their fleas, and >30% of cats with fleas are bacteremic. The objective of this study was to determine if monthly topical administration of a combination of 10% imidacloprid and 1 % moxidectin would lessen flea transmission of B. henselae among cats. Eighteen cats were housed in 3 groups of 6 cats. Each of the groups were placed in enclosures separated by mesh to allow fleas to pass among groups yet prevent cat-to-cat contact. The middle group of cats was inoculated with B. henselae and infection was confirmed. This group was flanked on one side by a group treated topically with 10% imidacloprid-1% moxidectin monthly for 3 months, and on the other side by an untreated group. Fleas were placed on the B. henselae infected group at periodic intervals. Blood samples were collected from all the cats weekly to detect Bartonella spp via PCR assay, bacterial culture, and serologic assay. B. henselae infection was confirmed in all untreated cats after flea exposure following the confirmed infection in the inoculated group. None of the cats treated with imidacloprid-moxidectin combination became infected. The results showed that a monthly topical administration of 10% imidacloprid-1% moxidectin reduces the flea load and thus prevented flea transmission of B. henselae to treated cats. Therefore, the likelihood of humans acquiring B. henselae infection may be lessened through monthly use of this flea control product in cats. [VT]

Related articles:
Kamrani A, Parreira VR, Greenwood J et al: The prevalence of Bartonella, hemoplasma, and Rickettsia felis infections in domestic cats and in cat fleas in Ontario, Can J Vet Res 72:411, 2008.

Breitschwerdt EB: Feline bartonellosis and cat scratch disease, Vet Immunol Immunopathol 123:167, 2008.

More on cat health: Winn Feline Foundation Library
Join us on Facebook
Follow us on Twitter
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Sunday, May 9, 2010

Infants Need More Vitamin D

Why anyone listens to doctors when it comes to anything related to diet and environment is beyond me. They’re always getting it wrong. They were wrong on fiber and diverticular disease for decades. They were wrong on the impact of pesticides and xenoestrogens released into the environment for years, too. And of course they were wrong on trans fatty acids until just a couple of years ago. Now it looks like they’ve been wrong on exposure to sunlight and the use of vitamin supplements. Hardly surprising! Ever since we all began covering up, on their advice, to avoid getting skin cancer, vitamin D shortage has become a serious problem among both kids and adults. The problem is that there are only two ways to get vitamin D — exposure to ultraviolet light and supplementation. Without either enough sun exposure or adequate supplementation, we all face vitamin D shortage and the concomitant problems of weak bones and vulnerability to disease. And thanks to your doctor’s advice, you’re short on both.

Now, a new study has found that most infants, whether bottle or breast-fed, get far too little vitamin D. The study, conducted by the Centers for Disease Control (CDC), surveyed nine groups of mothers of children aged one to 10.5 months old. Each group contained between 1,633 and 1,952 mothers. The results showed that only five to 13% of breastfed infants (you read that correctly) and 20% to 37% of formula-fed babies get enough vitamin D daily. Back in 2008, the American Academy of Pediatrics recommended that the minimum daily requirement of vitamin D be doubled because children now get far less sun now than in the past. Well, the medical community missed on that one too. The new study reflects shortages even at those higher levels.

The news came as a surprise to many physicians and patients, who assumed that formula, at least, provided the requisite amount of vitamin D. But in order to get the required amount of vitamin D from formula, babies would need to drink a full liter (34 ounces) a day, and most don’t come close to drinking that much. Baby formula does provide a richer source of vitamin D than does breast milk (more on this later) — but, as it turns out, richer doesn’t necessarily mean rich enough, given that about 2/3 of all formula-fed babies are vitamin-D deficient (again, compared to 95 percent of breast-fed infants). And babies can’t make up the shortfall from food sources like eggs and fish. In fact, it’s virtually impossible for anyone to meet minimum requirements of vitamin D through food. Sun is the best source, but again experts recommend against exposing infants to sun without protection, given the risks.

The risks of vitamin D shortage are also considerable, particularly for infants. Historically, the possibility of rickets was the biggest concern, causing bowing of the legs bone deformities, slow growth, swelling of wrists and ankles, and possibly breathing problems. But as Dr. Carrie Drazba, M.D., a pediatrician at Rush University Medical Center, in Chicago, points out, “We’re finding out that there are other risks associated with vitamin D deficiency besides rickets. A lot of cells in our body have receptors for vitamin D.”

In fact, studies have found that vitamin D bolsters the immune system and may protect against heart disease, certain cancers, schizophrenia, autoimmune disorders, respiratory ailments, and type 1 diabetes in children. Several studies last year found that vitamin D shortages in childhood may lead to a host of heart-risk factors, including high blood pressure, high blood glucose, and low HDL (or good cholesterol), later in life.

Adding fuel to the fire of the CDC study, simultaneous research from Boston Medical Center, just published in Pediatrics, also found high levels of vitamin D deficiency, this time in newborns and their moms. In this Boston study, 433 women and 376 newborns provided blood samples obtained within 72 hours of birth. Shockingly, 58 percent of the newborns had vitamin D deficiencies, as did 36 percent of mothers, with severe deficiencies showing up in about two-thirds of those cases. (More on this later.)

The solution, the experts contend, is to supplement. “We found that most infants, not just those who are breast-fed, may require an oral vitamin D supplement daily, beginning within their first few days of life, to meet the 2008 AAP recommendation that infants consume at least 400 IU/day of vitamin D,” said study director Dr. Cria G. Perrine. (More on this later.)

Apparently, most doctors still don’t recommend supplementation to their patients. In fact, as few as one percent of formula-fed babies and five-percent of breast-fed babies actually take vitamin D supplements. Frank R. Greer, MD, who headed the committee that came up with the new guidelines for vitamin D intake, says, “I am frankly surprised that more pediatricians are not recommending supplementation, especially to new moms who are breastfeeding.” (More on this later.) The study authors believe that many doctors are unaware that the recommendations have increased. They note, “Because physicians’ knowledge of the AAP [vitamin D] recommendations has been positively associated with the likelihood of their recommending vitamin D supplements, both healthcare providers and parents need to be educated about the AAP guidelines and the importance of vitamin D nutrition, including that infants should not be exposed to sunlight and, thus, need an alternate source of vitamin D.”

In fact, the Institute of Medicine is actively considering again raising its guidelines for vitamin D intake for adults as well as for children and will announce its decision in the coming months. I’ve written before that even with the higher levels of recommended intake, the guidelines for vitamin D are conservative, at best. Currently, the guidelines call for 400 IU a day for kids, but even a few minutes of sun exposure can generate 2000-4000 or more IU. Vitamin D toxicity does not usually develop below 10,000 units per day (for adults), so there’s plenty of room to increase the recommended dose. The second study found that even among those mothers who took prenatal vitamin D supplements in the last trimester of pregnancy, 30 percent remained vitamin-D deficient at the time of birth, showing that at current recommended levels, supplementing isn’t sufficient. (More on this later.)

“The most obvious way to correct deficiency is sensible sun exposure,” said the director of the second study, Dr. Anne Merewood. “While a sunburn should be avoided, even a small amount of time spent outdoors was protective against deficiency.” Most pediatricians insist that babies should not get sun exposure — period — unless they have on sunscreen and clothing that protects them, so this advice won’t help with doctor-abiding infants though it might help their moms.

Throughout this blog, I’ve been repeatedly saying, “More on this later.” And now we come to it. There is one simple reason that ties all of these problems together, that accounts for babies being born vitamin D deficient, for breast milk being deficient, and for infants being vitamin D deficient. Thanks to the medical community’s recommendations to avoid the sun and to restrict vitamin D supplementation to dangerously low levels, mothers themselves are vitamin D deficient. If mom is deficient, any baby is going to be born deficient by definition. The fetus can’t manufacture vitamin D from thin air. Likewise, if mom is deficient, then her breast milk will be deficient. Again, vitamin D can’t appear in the milk out of thin air. And finally, if vitamin D levels are insufficient in breast milk, then where is the infant going to get their vitamin D from — particularly if their doctor has banned them from the sun and is prescribing insufficient levels of supplementation.

The solution is for parents to supplement at higher levels (up to 2000 IU daily), enjoy short stints of 10 to 15 minutes in the sun (early morning or late afternoon), and lose weight to enhance vitamin D absorption. Doing these things should minimize the likelihood of passing on a deficiency to offspring. (Note: studies show that the dose required to achieve a healthy blood level of vitamin D is somewhere in the neighborhood of 1,000–4,000 IU per day — which is still less than that obtained through several minutes of sun exposure. Vitamin D toxicity does not usually develop below 10,000 units per day.) As for the babies, a few minutes of unprotected exposure to sunlight (again, early morning or late afternoon) is still your best bet. And keep in mind that the body’s production of vitamin D is self regulating. You cannot OD on vitamin D based on sun exposure alone. But if you feel more comfortable following your pediatrician’s advice to keep your baby out of the sun, then you’ll want to give your child up to a 1,000 IU a day of a high-quality vitamin D supplement.
Why anyone listens to doctors when it comes to anything related to diet and environment is beyond me. They’re always getting it wrong. They were wrong on fiber and diverticular disease for decades. They were wrong on the impact of pesticides and xenoestrogens released into the environment for years, too. And of course they were wrong on trans fatty acids until just a couple of years ago. Now it looks like they’ve been wrong on exposure to sunlight and the use of vitamin supplements. Hardly surprising! Ever since we all began covering up, on their advice, to avoid getting skin cancer, vitamin D shortage has become a serious problem among both kids and adults. The problem is that there are only two ways to get vitamin D — exposure to ultraviolet light and supplementation. Without either enough sun exposure or adequate supplementation, we all face vitamin D shortage and the concomitant problems of weak bones and vulnerability to disease. And thanks to your doctor’s advice, you’re short on both.

Now, a new study has found that most infants, whether bottle or breast-fed, get far too little vitamin D. The study, conducted by the Centers for Disease Control (CDC), surveyed nine groups of mothers of children aged one to 10.5 months old. Each group contained between 1,633 and 1,952 mothers. The results showed that only five to 13% of breastfed infants (you read that correctly) and 20% to 37% of formula-fed babies get enough vitamin D daily. Back in 2008, the American Academy of Pediatrics recommended that the minimum daily requirement of vitamin D be doubled because children now get far less sun now than in the past. Well, the medical community missed on that one too. The new study reflects shortages even at those higher levels.

The news came as a surprise to many physicians and patients, who assumed that formula, at least, provided the requisite amount of vitamin D. But in order to get the required amount of vitamin D from formula, babies would need to drink a full liter (34 ounces) a day, and most don’t come close to drinking that much. Baby formula does provide a richer source of vitamin D than does breast milk (more on this later) — but, as it turns out, richer doesn’t necessarily mean rich enough, given that about 2/3 of all formula-fed babies are vitamin-D deficient (again, compared to 95 percent of breast-fed infants). And babies can’t make up the shortfall from food sources like eggs and fish. In fact, it’s virtually impossible for anyone to meet minimum requirements of vitamin D through food. Sun is the best source, but again experts recommend against exposing infants to sun without protection, given the risks.

The risks of vitamin D shortage are also considerable, particularly for infants. Historically, the possibility of rickets was the biggest concern, causing bowing of the legs bone deformities, slow growth, swelling of wrists and ankles, and possibly breathing problems. But as Dr. Carrie Drazba, M.D., a pediatrician at Rush University Medical Center, in Chicago, points out, “We’re finding out that there are other risks associated with vitamin D deficiency besides rickets. A lot of cells in our body have receptors for vitamin D.”

In fact, studies have found that vitamin D bolsters the immune system and may protect against heart disease, certain cancers, schizophrenia, autoimmune disorders, respiratory ailments, and type 1 diabetes in children. Several studies last year found that vitamin D shortages in childhood may lead to a host of heart-risk factors, including high blood pressure, high blood glucose, and low HDL (or good cholesterol), later in life.

Adding fuel to the fire of the CDC study, simultaneous research from Boston Medical Center, just published in Pediatrics, also found high levels of vitamin D deficiency, this time in newborns and their moms. In this Boston study, 433 women and 376 newborns provided blood samples obtained within 72 hours of birth. Shockingly, 58 percent of the newborns had vitamin D deficiencies, as did 36 percent of mothers, with severe deficiencies showing up in about two-thirds of those cases. (More on this later.)

The solution, the experts contend, is to supplement. “We found that most infants, not just those who are breast-fed, may require an oral vitamin D supplement daily, beginning within their first few days of life, to meet the 2008 AAP recommendation that infants consume at least 400 IU/day of vitamin D,” said study director Dr. Cria G. Perrine. (More on this later.)

Apparently, most doctors still don’t recommend supplementation to their patients. In fact, as few as one percent of formula-fed babies and five-percent of breast-fed babies actually take vitamin D supplements. Frank R. Greer, MD, who headed the committee that came up with the new guidelines for vitamin D intake, says, “I am frankly surprised that more pediatricians are not recommending supplementation, especially to new moms who are breastfeeding.” (More on this later.) The study authors believe that many doctors are unaware that the recommendations have increased. They note, “Because physicians’ knowledge of the AAP [vitamin D] recommendations has been positively associated with the likelihood of their recommending vitamin D supplements, both healthcare providers and parents need to be educated about the AAP guidelines and the importance of vitamin D nutrition, including that infants should not be exposed to sunlight and, thus, need an alternate source of vitamin D.”

In fact, the Institute of Medicine is actively considering again raising its guidelines for vitamin D intake for adults as well as for children and will announce its decision in the coming months. I’ve written before that even with the higher levels of recommended intake, the guidelines for vitamin D are conservative, at best. Currently, the guidelines call for 400 IU a day for kids, but even a few minutes of sun exposure can generate 2000-4000 or more IU. Vitamin D toxicity does not usually develop below 10,000 units per day (for adults), so there’s plenty of room to increase the recommended dose. The second study found that even among those mothers who took prenatal vitamin D supplements in the last trimester of pregnancy, 30 percent remained vitamin-D deficient at the time of birth, showing that at current recommended levels, supplementing isn’t sufficient. (More on this later.)

“The most obvious way to correct deficiency is sensible sun exposure,” said the director of the second study, Dr. Anne Merewood. “While a sunburn should be avoided, even a small amount of time spent outdoors was protective against deficiency.” Most pediatricians insist that babies should not get sun exposure — period — unless they have on sunscreen and clothing that protects them, so this advice won’t help with doctor-abiding infants though it might help their moms.

Throughout this blog, I’ve been repeatedly saying, “More on this later.” And now we come to it. There is one simple reason that ties all of these problems together, that accounts for babies being born vitamin D deficient, for breast milk being deficient, and for infants being vitamin D deficient. Thanks to the medical community’s recommendations to avoid the sun and to restrict vitamin D supplementation to dangerously low levels, mothers themselves are vitamin D deficient. If mom is deficient, any baby is going to be born deficient by definition. The fetus can’t manufacture vitamin D from thin air. Likewise, if mom is deficient, then her breast milk will be deficient. Again, vitamin D can’t appear in the milk out of thin air. And finally, if vitamin D levels are insufficient in breast milk, then where is the infant going to get their vitamin D from — particularly if their doctor has banned them from the sun and is prescribing insufficient levels of supplementation.

The solution is for parents to supplement at higher levels (up to 2000 IU daily), enjoy short stints of 10 to 15 minutes in the sun (early morning or late afternoon), and lose weight to enhance vitamin D absorption. Doing these things should minimize the likelihood of passing on a deficiency to offspring. (Note: studies show that the dose required to achieve a healthy blood level of vitamin D is somewhere in the neighborhood of 1,000–4,000 IU per day — which is still less than that obtained through several minutes of sun exposure. Vitamin D toxicity does not usually develop below 10,000 units per day.) As for the babies, a few minutes of unprotected exposure to sunlight (again, early morning or late afternoon) is still your best bet. And keep in mind that the body’s production of vitamin D is self regulating. You cannot OD on vitamin D based on sun exposure alone. But if you feel more comfortable following your pediatrician’s advice to keep your baby out of the sun, then you’ll want to give your child up to a 1,000 IU a day of a high-quality vitamin D supplement.
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Junk-Food Addiction is REAL

http://www.jonbarron.org

When Homer Simpson first uttered the word “D’oh!‘ (which 300 linguists have agreed is The Simpson’s most important contribution to the English language), he might as well have had in mind the recent announcement by researchers that junk food actually is addictive. As anyone who ever finished a bag of Doritos three days into a diet knows, “D’oh!!! Of course the stuff is addictive.”

The researchers made their announcement in response to a new study led by the Scripps Research Institute in Jupiter, Florida. All joking aside, the study actually did contain some genuine surprises, particularly in revealing just how extraordinarily addictive junk food actually is. In essence, the researchers found that junk foods exert an addictive pull as powerful as that conferred by the most highly addictive narcotic drugs.

Dr. Kenny and his colleagues divided rats into three groups and then headed to the grocery store. “We basically bought all of the stuff that people really like — Ding-Dongs, cheesecake, bacon, sausage, [chocolate frosting, pound cake] — the stuff that you enjoy, but you really shouldn’t eat too often,” he said. They also bought healthy food. Each group of rats followed a different diet for 40 days. The rats in the first group ate healthy, regular rat food only. In the second group, the rats got healthy rat food plus an hour of access daily to junk food. The third group had unlimited access to both health food and junk — like most humans do.

The rats that had access to the treats only an hour a day managed to cram most of their eating into that blissful hour, eschewing the rat food the rest of the time. Meanwhile, the third group of rats — those who had round-the-clock access to treats — quickly turned obese and demonstrated a strong preference for Ding Dongs and cheesecake and the like. But their food preferences weren’t the only change the rats experienced. The researchers found that the brain circuitry in the junk-food-gorging rats actually changed. The more high-fat treats the rats ate, the more they craved treats in the future — the more treats it took on subsequent feedings for them to experience satisfaction. In other words, they developed “tolerance,” just the way junkies and alcoholics do, needing more and more of the “junk-food substance” in order to achieve a pleasure “rush.”

“It was quite profound,” says study author Paul Kenny. “The reward-response effects in the junk-food rats were “very similar to what we see with animals that use cocaine and heroin.” The response became even more pronounced as the rats gained more weight. The fatty treats also seemed to lower levels of a dopamine receptor in the brain of the rats. In humans, lowered levels of dopamine receptors lead to increased pleasure-seeking behavior. Under normal conditions, dopamine deprivation excites normal desire or motivation, but in the case of the rats, eating junk foods made the deprivation severe enough to drive the mild desire to pathological levels.

The biggest surprise in the study was in the extreme behaviors that the compulsive cravings led to. The sadistic researchers launched a nasty plan. Every time the rodents–who by now were addicted to fatty treats — approached their pleasure buffet, they got a painful shock to their feet. Amazingly, this shock did not stop them from going to the junk food spread and continuing to eat, in spite of a bright light that warned them before each shock was issued, and even though they had the option of choosing a shock-free healthy meal instead. The other two groups of rats, including the group allowed only an hour of eating junk foods daily, opted for the healthy meal rather than the shock-laden foods. In other words, the more treats the rats enjoyed, the more hooked on treats they became, to the point where they would endure extreme punishment in order to get a fix, like junkies who behave in dangerous, self-destructive ways for a fix of drugs. And again, this behavior became more pronounced as the rats gained increasing amounts of weight.

Perhaps the most shocking tidbit of all, though, was the finding that the addicted rats absolutely refused regular food, even after their treats were taken away. They chose to starve rather than return to rat kibble. “They actually voluntarily starved themselves,” Kenny said.

What does all this information add up to, other than a good excuse for the zipper that no longer closes? While it’s understood that what’s true for rats isn’t necessarily true for humans, the behavioral response is close enough for at least some experts to suggest that obesity should be reclassified as a psychiatric disorder. “Once we start to consider obesity and pathological overeating as a psychiatric illness, we’re going to move a lot closer towards understanding how to come up with therapies or treatments,” says addiction biologist Jon Davis of the University of Ohio. He doesn’t mention the fact that addiction therapies certainly aren’t fail-proof. Even after completing drug-addiction recovery programs both in prison and in the community, male addicts have a recidivism rate of over 40 percent. Drug addiction is an extremely hard nut to crack.

On the other hand, 40 percent is a far lower failure rate than dieters experience, given that 95 percent of all diets ultimately fail (and that two-thirds of all adults in the US are now overweight). The Scripps Institute study certainly throws cold water on the cold turkey theory of dieting — the “just stop eating junk and go healthy” prescription. If people respond like the rats in the study — if they’d be willing to suffer extreme punishment for chocolate chip cheesecake — mere willpower probably will continue to fail while obesity statistics continue to rise. Here’s yet more evidence that food manufacturers need to be financially pressured to start migrating their product lines away from high-fat foods, high-fructose corn syrup, and processed junk and be prevented from having carte blanche to advertise their narcotic edibles on media frequented by children.

The bottom line is that merely offering healthy alternatives is not enough. As we just learned, addicted rats will starve themselves rather than eat healthy alternatives. Instead, manufacturers must be financially induced to steadily offer fewer and fewer addictive foods until people really have no choice but to eat healthier diets. In the meantime, keep in mind that if the addicted can manage to break their unhealthy routines long enough to lose substantial weight, they can rewire their brains back to normalcy enough to break the addictive cycle. As it is, five percent of people already manage to do that on their own.
http://www.jonbarron.org

When Homer Simpson first uttered the word “D’oh!‘ (which 300 linguists have agreed is The Simpson’s most important contribution to the English language), he might as well have had in mind the recent announcement by researchers that junk food actually is addictive. As anyone who ever finished a bag of Doritos three days into a diet knows, “D’oh!!! Of course the stuff is addictive.”

The researchers made their announcement in response to a new study led by the Scripps Research Institute in Jupiter, Florida. All joking aside, the study actually did contain some genuine surprises, particularly in revealing just how extraordinarily addictive junk food actually is. In essence, the researchers found that junk foods exert an addictive pull as powerful as that conferred by the most highly addictive narcotic drugs.

Dr. Kenny and his colleagues divided rats into three groups and then headed to the grocery store. “We basically bought all of the stuff that people really like — Ding-Dongs, cheesecake, bacon, sausage, [chocolate frosting, pound cake] — the stuff that you enjoy, but you really shouldn’t eat too often,” he said. They also bought healthy food. Each group of rats followed a different diet for 40 days. The rats in the first group ate healthy, regular rat food only. In the second group, the rats got healthy rat food plus an hour of access daily to junk food. The third group had unlimited access to both health food and junk — like most humans do.

The rats that had access to the treats only an hour a day managed to cram most of their eating into that blissful hour, eschewing the rat food the rest of the time. Meanwhile, the third group of rats — those who had round-the-clock access to treats — quickly turned obese and demonstrated a strong preference for Ding Dongs and cheesecake and the like. But their food preferences weren’t the only change the rats experienced. The researchers found that the brain circuitry in the junk-food-gorging rats actually changed. The more high-fat treats the rats ate, the more they craved treats in the future — the more treats it took on subsequent feedings for them to experience satisfaction. In other words, they developed “tolerance,” just the way junkies and alcoholics do, needing more and more of the “junk-food substance” in order to achieve a pleasure “rush.”

“It was quite profound,” says study author Paul Kenny. “The reward-response effects in the junk-food rats were “very similar to what we see with animals that use cocaine and heroin.” The response became even more pronounced as the rats gained more weight. The fatty treats also seemed to lower levels of a dopamine receptor in the brain of the rats. In humans, lowered levels of dopamine receptors lead to increased pleasure-seeking behavior. Under normal conditions, dopamine deprivation excites normal desire or motivation, but in the case of the rats, eating junk foods made the deprivation severe enough to drive the mild desire to pathological levels.

The biggest surprise in the study was in the extreme behaviors that the compulsive cravings led to. The sadistic researchers launched a nasty plan. Every time the rodents–who by now were addicted to fatty treats — approached their pleasure buffet, they got a painful shock to their feet. Amazingly, this shock did not stop them from going to the junk food spread and continuing to eat, in spite of a bright light that warned them before each shock was issued, and even though they had the option of choosing a shock-free healthy meal instead. The other two groups of rats, including the group allowed only an hour of eating junk foods daily, opted for the healthy meal rather than the shock-laden foods. In other words, the more treats the rats enjoyed, the more hooked on treats they became, to the point where they would endure extreme punishment in order to get a fix, like junkies who behave in dangerous, self-destructive ways for a fix of drugs. And again, this behavior became more pronounced as the rats gained increasing amounts of weight.

Perhaps the most shocking tidbit of all, though, was the finding that the addicted rats absolutely refused regular food, even after their treats were taken away. They chose to starve rather than return to rat kibble. “They actually voluntarily starved themselves,” Kenny said.

What does all this information add up to, other than a good excuse for the zipper that no longer closes? While it’s understood that what’s true for rats isn’t necessarily true for humans, the behavioral response is close enough for at least some experts to suggest that obesity should be reclassified as a psychiatric disorder. “Once we start to consider obesity and pathological overeating as a psychiatric illness, we’re going to move a lot closer towards understanding how to come up with therapies or treatments,” says addiction biologist Jon Davis of the University of Ohio. He doesn’t mention the fact that addiction therapies certainly aren’t fail-proof. Even after completing drug-addiction recovery programs both in prison and in the community, male addicts have a recidivism rate of over 40 percent. Drug addiction is an extremely hard nut to crack.

On the other hand, 40 percent is a far lower failure rate than dieters experience, given that 95 percent of all diets ultimately fail (and that two-thirds of all adults in the US are now overweight). The Scripps Institute study certainly throws cold water on the cold turkey theory of dieting — the “just stop eating junk and go healthy” prescription. If people respond like the rats in the study — if they’d be willing to suffer extreme punishment for chocolate chip cheesecake — mere willpower probably will continue to fail while obesity statistics continue to rise. Here’s yet more evidence that food manufacturers need to be financially pressured to start migrating their product lines away from high-fat foods, high-fructose corn syrup, and processed junk and be prevented from having carte blanche to advertise their narcotic edibles on media frequented by children.

The bottom line is that merely offering healthy alternatives is not enough. As we just learned, addicted rats will starve themselves rather than eat healthy alternatives. Instead, manufacturers must be financially induced to steadily offer fewer and fewer addictive foods until people really have no choice but to eat healthier diets. In the meantime, keep in mind that if the addicted can manage to break their unhealthy routines long enough to lose substantial weight, they can rewire their brains back to normalcy enough to break the addictive cycle. As it is, five percent of people already manage to do that on their own.
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Broccoli Component Limits Breast Cancer Stem Cells, Study Finds

ScienceDaily (May 5, 2010) — A compound derived from broccoli could help prevent or treat breast cancer by targeting cancer stem cells -- the small number of cells that fuel a tumor's growth -- according to a new study from researchers at the University of Michigan Comprehensive Cancer Center.

The study tested sulforaphane, a component of broccoli and broccoli sprouts, in both mice and cell cultures. Researchers found sulforaphane targeted and killed the cancer stem cells and prevented new tumors from growing.

"Sulforaphane has been studied previously for its effects on cancer, but this study shows that its benefit is in inhibiting the breast cancer stem cells. This new insight suggests the potential of sulforaphane or broccoli extract to prevent or treat cancer by targeting the critical cancer stem cells," says study author Duxin Sun, Ph.D., associate professor of pharmaceutical sciences at the U-M College of Pharmacy and a researcher with the U-M Comprehensive Cancer Center.

Results of the study appear in the May 1 issue of Clinical Cancer Research.

Current chemotherapies do not work against cancer stem cells, which is why cancer recurs and spreads. Researchers believe that eliminating the cancer stem cells is key to controlling cancer.

In the current study, researchers took mice with breast cancer and injected varying concentrations of sulforaphane from the broccoli extract. Researchers then used several established methods to assess the number of cancer stem cells in the tumors. These measures showed a marked decrease in the cancer stem cell population after treatment with sulforaphane, with little effect on the normal cells. Further, cancer cells from mice treated with sulforaphane were unable to generate new tumors. The researchers then tested sulforaphane on human breast cancer cell cultures in the lab, finding similar decreases in the cancer stem cells.

"This research suggests a potential new treatment that could be combined with other compounds to target breast cancer stem cells. Developing treatments that effectively target the cancer stem cell population is essential for improving outcomes," says study author Max S. Wicha, M.D., Distinguished Professor of Oncology and director of the U-M Comprehensive Cancer Center.

The concentrations of sulforaphane used in the study were higher than what can be achieved by eating broccoli or broccoli sprouts. Prior research suggests the concentrations needed to impact cancer can be absorbed by the body from the broccoli extract, but side effects are not known. While the extract is available in capsule form as a supplement, concentrations are unregulated and will vary.

This work has not been tested in patients, and patients are not encouraged to add sulforaphane supplements to their diet at this time.

Researchers are currently developing a method to extract and preserve sulforaphane and will be developing a clinical trial to test sulforaphane as a prevention and treatment for breast cancer. No clinical trial is currently available.
ScienceDaily (May 5, 2010) — A compound derived from broccoli could help prevent or treat breast cancer by targeting cancer stem cells -- the small number of cells that fuel a tumor's growth -- according to a new study from researchers at the University of Michigan Comprehensive Cancer Center.

The study tested sulforaphane, a component of broccoli and broccoli sprouts, in both mice and cell cultures. Researchers found sulforaphane targeted and killed the cancer stem cells and prevented new tumors from growing.

"Sulforaphane has been studied previously for its effects on cancer, but this study shows that its benefit is in inhibiting the breast cancer stem cells. This new insight suggests the potential of sulforaphane or broccoli extract to prevent or treat cancer by targeting the critical cancer stem cells," says study author Duxin Sun, Ph.D., associate professor of pharmaceutical sciences at the U-M College of Pharmacy and a researcher with the U-M Comprehensive Cancer Center.

Results of the study appear in the May 1 issue of Clinical Cancer Research.

Current chemotherapies do not work against cancer stem cells, which is why cancer recurs and spreads. Researchers believe that eliminating the cancer stem cells is key to controlling cancer.

In the current study, researchers took mice with breast cancer and injected varying concentrations of sulforaphane from the broccoli extract. Researchers then used several established methods to assess the number of cancer stem cells in the tumors. These measures showed a marked decrease in the cancer stem cell population after treatment with sulforaphane, with little effect on the normal cells. Further, cancer cells from mice treated with sulforaphane were unable to generate new tumors. The researchers then tested sulforaphane on human breast cancer cell cultures in the lab, finding similar decreases in the cancer stem cells.

"This research suggests a potential new treatment that could be combined with other compounds to target breast cancer stem cells. Developing treatments that effectively target the cancer stem cell population is essential for improving outcomes," says study author Max S. Wicha, M.D., Distinguished Professor of Oncology and director of the U-M Comprehensive Cancer Center.

The concentrations of sulforaphane used in the study were higher than what can be achieved by eating broccoli or broccoli sprouts. Prior research suggests the concentrations needed to impact cancer can be absorbed by the body from the broccoli extract, but side effects are not known. While the extract is available in capsule form as a supplement, concentrations are unregulated and will vary.

This work has not been tested in patients, and patients are not encouraged to add sulforaphane supplements to their diet at this time.

Researchers are currently developing a method to extract and preserve sulforaphane and will be developing a clinical trial to test sulforaphane as a prevention and treatment for breast cancer. No clinical trial is currently available.
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Sleeping for less than six hours may cause early death, study finds

Sleeping consistently for less than six hours a night may cause an early death, but too much sleep could also mean problems, according to a study that claims to have found unequivocal evidence of the potential harm from abnormal sleep patterns.

The research, by academics in the UK and Italy, analysed data from 16 separate studies across Europe, the US and Asia over 25 years, covering more than 1.3m people and more than 100,000 deaths.

It found that those who generally slept for less than six hours a night were 12% more likely to experience a premature death over a period of 25 years than those who consistently got six to eight hours' sleep. Evidence for the link was unequivocal, the researchers concluded.

The study, published in the scientific journal Sleep, was carried out by a team from the University of Warwick and the Federico II University medical school in Naples.

It also concluded that those who consistently sleep more than nine hours a night can be more likely to die early. Oversleeping itself is not seen as a risk but as a potential indicator of underlying ailments.

"Whilst short sleep may represent a cause of ill health, long sleep is believed to represent more an indicator of ill health," said Professor Francesco Cappuccio, who led the study and is head of the Sleep, Health and Society programme at the University of Warwick.

"Modern society has seen a gradual reduction in the average amount of sleep people take, and this pattern is more common amongst full-time workers, suggesting that it may be due to societal pressures for longer working hours and more shift-work. On the other hand, the deterioration of our health status is often accompanied by an extension of our sleeping time.

"Consistently sleeping six to eight hours per night may be optimal for health. The duration of sleep should be regarded as an additional behavioural risk factor, or risk marker, influenced by the environment and possibly amenable to change through both education and counselling as well as through measures of public health aimed at favourable modifications of the physical and working environments."

The study noted that previous research into lack of sleep had shown it was associated with ailments including heart disease, high blood pressure, obesity, and diabetes.
Sleeping consistently for less than six hours a night may cause an early death, but too much sleep could also mean problems, according to a study that claims to have found unequivocal evidence of the potential harm from abnormal sleep patterns.

The research, by academics in the UK and Italy, analysed data from 16 separate studies across Europe, the US and Asia over 25 years, covering more than 1.3m people and more than 100,000 deaths.

It found that those who generally slept for less than six hours a night were 12% more likely to experience a premature death over a period of 25 years than those who consistently got six to eight hours' sleep. Evidence for the link was unequivocal, the researchers concluded.

The study, published in the scientific journal Sleep, was carried out by a team from the University of Warwick and the Federico II University medical school in Naples.

It also concluded that those who consistently sleep more than nine hours a night can be more likely to die early. Oversleeping itself is not seen as a risk but as a potential indicator of underlying ailments.

"Whilst short sleep may represent a cause of ill health, long sleep is believed to represent more an indicator of ill health," said Professor Francesco Cappuccio, who led the study and is head of the Sleep, Health and Society programme at the University of Warwick.

"Modern society has seen a gradual reduction in the average amount of sleep people take, and this pattern is more common amongst full-time workers, suggesting that it may be due to societal pressures for longer working hours and more shift-work. On the other hand, the deterioration of our health status is often accompanied by an extension of our sleeping time.

"Consistently sleeping six to eight hours per night may be optimal for health. The duration of sleep should be regarded as an additional behavioural risk factor, or risk marker, influenced by the environment and possibly amenable to change through both education and counselling as well as through measures of public health aimed at favourable modifications of the physical and working environments."

The study noted that previous research into lack of sleep had shown it was associated with ailments including heart disease, high blood pressure, obesity, and diabetes.
Read More