Not getting enough vitamin D in your system may be linked to chronic pain.
Over the past 10 years, several researchers have found an association between extremely low vitamin D levels and chronic, general pain that doesn’t respond to treatment.
Many Americans are running low on vitamin D. A study published in the Archives of Internal Medicine in 2009 showed that vitamin D levels have plummeted among all U.S. ages, races, and ethnic groups over the past two decades.
But does not having enough vitamin D cause pain? That’s not yet clear. But here’s what you need to know about vitamin D and chronic pain.
Boosting Vitamin D, Easing Pain
Greg Plotnikoff, MD, senior consultant with the Allina Center for Health Care Innovations in Minnesota, still remembers the woman in her 40s who told him that he was the 30th doctor she’d seen.
“Twelve of them had told her she was crazy,” says Plotnikoff, formerly an associate professor of internal medicine and pediatrics at the University of Minnesota Medical School.
“She had weakness, achiness, fatigue – three pages worth of symptoms. Doctors had offered her antidepressants and seizure medications and all kinds of things that didn’t work. I checked her vitamin D levels – and they came back barely measurable.”
After six months on an aggressive, high-dose prescription vitamin D replacement, the woman could cross off every symptom on her three-page list. “I knew I wasn’t crazy!” Plotnikoff says she told him.
That’s just one woman. Her case doesn’t mean vitamin D will erase pain for everyone.
However, Plotnikoff published a study in 2003 on 150 people in Minneapolis who came to a community health clinic complaining of chronic pain. Virtually all of them – 93% – had extremely low vitamin D levels.
Vitamin D blood levels of 30-40 ng/mL are considered ideal. The average level in Plotnikoff’s study was about 12, and some people had vitamin D levels so low they were undetectable.
“The group with the lowest levels of vitamin D were white women of childbearing age,” Plotnikoff says. “Most of them were dismissed by their doctors as depressed or whiners. They attributed their pain to an inability to manage stress. But after we replenished their vitamin D, these people said, ‘Woo hoo! I’ve got my life back!'”
Plotnikoff notes that vitamin D is a hormone. “Every tissue in our bodies has [vitamin] D receptors, including all bones, muscles, immune cells, and brain cells,” he says.
And in March 2009, researchers at the Mayo Clinic published a study showing that patients with inadequate vitamin D levels who were taking narcotic pain drugs required nearly twice as much medication to control their pain as did patients with adequate D levels.
Jury Still Out
But other studies have shown no connection between vitamin D and chronic pain, and a research review published in January 2010 showed that the evidence on the subject is inconclusive.
“It would be nice if vitamin D worked for chronic pain. It would offer an inexpensive and simple treatment with known and probably limited adverse effects,” Sebastian Straube, MD, PhD, tells WebMD in an email. Straube is a physician-scientist at Germany’s University of Gottingen and led the research review, published in the Cochrane Library.
But it hasn’t been proven that boosting your vitamin D level will erase your pain.
“Looking at all the available evidence, the link is not convincing,” Straube says. “As far as treatment studies are concerned, we found a striking contrast in study outcome between randomized double blind trials that by virtue of their study design minimize bias, and other (non-double blind) studies that are more prone to bias. The latter largely do suggest a beneficial effect of vitamin D treatment; the former largely don’t.”
Plotnikoff says that there is no evidence from randomized, controlled trials that replenishing vitamin D levels will cure chronic pain. “But it doesn’t hurt to do it,” he notes.
So if you’ve got chronic pain, it can’t hurt to ask your doctor to check your vitamin D levels. “I believe this is absolutely medically indicated, and it should be the standard of care for everyone with chronic, nonspecific musculoskeletal pain,” Plotnikoff says.
“Considering that establishing the effectiveness (or lack thereof) of vitamin D in chronic painful conditions is a clinically important question, there is rather little high-quality evidence on this topic,” Straube says. “At present, we do not think the evidence in this area is of sufficient quality to guide clinical practice. There clearly is a need for more and better studies in the future.”
If you have severe vitamin D deficiency, any efforts to boost your D levels should be done by consulting with your doctor. Too much vitamin D can be dangerous and lead to an excess accumulation of calcium in your blood, which can lead to kidney stones.
Gina Shaw, WebMD, Tue, 21 Sept 2010
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An increased intake of ‘good’ potassium salts could contribute significantly to improving blood pressure at the population level, according to new research. The favorable effect brought about by potassium is even estimated to be comparable with the blood pressure reduction achievable by halving the intake of ‘bad’ sodium salts (mostly from table salt).
Those are the conclusions drawn by Linda van Mierlo and her colleagues at Wageningen University, part of Wageningen UR, and Unilever in their investigation of the consumption of potassium in 21 countries. An article describing their findings appears in the journal Archives of Internal Medicine.
The risk of developing cardiovascular diseases rises as blood pressure increases. In Western countries only 20-30% of the population has ‘optimal’ blood pressure, with the systolic (maximum) pressure being lower than 120 mm Hg and the diastolic (minimum) pressure lower than 80 mm Hg. Blood pressure increases with age in most people. Men more often have a higher blood pressure than women.
Diet and lifestyle plays an important role in managing blood pressure. High intakes of sodium and low intakes of potassium have unfavorable effects on blood pressure. Therefore, reducing the consumption of sodium and increasing the consumption of potassium are both good ways to improve blood pressure.
The study carried out by food researchers from the Human Nutrition department at Wageningen University and from the Nutrition & Health department at Unilever demonstrates that the average potassium intake in 21 countries including the US, China, New Zealand, Germany and the Netherlands varies between 1.7 and 3.7 g a day. This is considerably lower than the 4.7 g a day, which has been recommended based on the positive health effects observed at this level of intake.
A hypothetical increase in the potassium intake to the recommended level would reduce the systolic blood pressure in the populations of these countries by between 1.7 and 3.2 mm Hg. This corresponds with the reduction that would occur if Western consumers were to take in 4 g of salt less per day. The intakes of both potassium and sodium are therefore of importance in preventing high blood pressure.
Earlier studies have shown that salt reduction of 3 g per day in food could reduce blood pressure and prevent 2500 deaths per year due to cardiovascular diseases in the Netherlands. In Western countries, salt consumption can be as high as 9-12 g a day whereas 5 g is the recommended amount according to WHO standards. Most household salt is to be found in processed foods such as bread, ready-made meals, soups, sauces and savory snacks and pizzas. An effective way of increasing potassium intake is to follow the guidelines for healthy nutrition more closely, including a higher consumption of vegetables and fruit. In addition, the use of mineral salts in processed foods — by which sodium is partly replaced by potassium — would contribute to an improved intake of both sodium and potassium.
ScienceDaily (Sep. 13, 2010)
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Is that cupcake an innocent indulgence? Or your next hit? We’re finding that a sweet tooth makes you just as much an addict as snorting cocaine
SETTLED on the sofa watching the usual rubbish on TV, I notice that predictable, uncontrollable, nightly craving. At first I sit there, fighting it. But the longer I fight, the worse it gets. After 20 minutes, I can’t concentrate on anything, I feel anxious, and start fidgeting like crazy. Finally, admitting my addiction, I break. I go to the freezer – to my stash of white stuff – and take a hit. Almost instantly, I relax, my brain in a state of bliss as the chemical courses through my veins. Isn’t it amazing what a few scoops of ice cream can do?
Before you dismiss my agitation as mere weakness, consider this: to my brain, sugar is akin to cocaine. There is now compelling evidence that foods high in sugar, fat and salt – as most junk foods are – can alter your brain chemistry in the same way as highly addictive drugs such as cocaine and heroin.
The idea, considered fringe just five years ago, is fast becoming a mainstream view among researchers as new studies in humans confirm initial animal findings, and the biological mechanisms that lead to “junk-food addiction” are being revealed. Some say there is now enough data to warrant government regulation of the fast food industry and public health warnings on products that have harmful levels of sugar and fat. One campaigning lawyer claims there could even be enough evidence to mount a legal fight against the fast food industry for knowingly peddling food that is harmful to our health, echoing the lawsuits against the tobacco industry in the 1980s and 90s.
“We have to educate people about how their brains get hijacked by fat, sugar and salt,” says David Kessler, former commissioner of the US Food and Drug Administration and now a director of the Center for Science in the Public Interest, based in Washington DC. With obesity levels rocketing across the world, it is clear that I am not alone in my love of sweet things, but can it really be as bad as drug addiction?
Arguably, it was the weight-loss industry that first introduced the idea to the public, long before there was any scientific evidence for it. For example, in her book Lick the Sugar Habit, published in 1988, the self-confessed “sugarholic” Nancy Appleton offered a checklist to determine whether you, too, are addicted to sugar. Since then, the notion has become commonplace.
In 2001, intrigued by this nascent cultural phenomenon, neuroscientists Nicole Avena, now at the University of Florida in Gainesville, and Bartley Hoebel at Princeton University, together began exploring whether the idea had a biological basis. They started by looking for signs of addiction in animals that had been eating junk food.
Hooked on sugar
Sugar is a key ingredient in most junk food, so they offered rats sugar syrup, similar to the sugar concentration in a typical soda beverage, for about 12 hours each day, alongside regular rat feed and water. After just a month on this diet, the rats developed behavior and brain changes that Avena and Hoebel claimed were chemically identical to morphine-addicted rats. They binged on the syrup and showed anxious behavior when it was removed – a sign of withdrawal. There were also changes in the neurotransmitters in the nucleus accumbens, a region associated with reward.
Crucially, the researchers noticed that the rats’ brains released the neurotransmitter dopamine each time they binged on the sugar solution, even after having eaten it for weeks (Neuroscience & Biobehavioral Reviews, vol 32, p 20). That’s not normal.
Dopamine drives the pursuit of pleasure – whether it is food, drugs or sex. It is a brain chemical vital for learning, memory, decision-making and sculpting the reward circuitry. You would expect it to be released when they eat a new food, says Avena, but not with one they are habituated to. “That’s one of the hallmarks of drug addiction,” she says. This was the first hard evidence of a biological basis for sugar addiction, and sparked a slew of animal studies.
Those results were among the most exciting news in obesity research in the last 20 years, says Mark Gold, an international authority on addiction research and chairman of the psychiatry department at the University of Florida College of Medicine.
Since Avena and Hoebel’s landmark study, scores of other animal studies have confirmed the findings. But it is recent human studies that have finally tipped the balance of evidence in favor of labeling a love of junk food as a proper addiction.
Addiction is commonly described as a dulling of the “reward circuits” triggered by the overuse of some drug. This is exactly what happens in the brains of obese individuals, says Gene-Jack Wang, chairman of the medical department at the US Department of Energy’s Brookhaven National Laboratory in Upton, New York. In another landmark study published in 2001, he discovered a dopamine deficiency in the striatum of the brains of obese individuals that was virtually identical to those of drug addicts (The Lancet, vol 357, p 354).
In subsequent studies, Wang showed that even when (not obese) individuals are shown their favorite foods, an area of their brain called the orbital frontal cortex – involved in decision-making – experiences a surge of dopamine. The same area is activated when cocaine addicts are shown a bag of white powder. It was a shocking discovery that showed you don’t have to be obese for your brain to exhibit addictive behavior. “I can tell they want it,” says Wang.
Another critical leap in identifying junk food as addictive was made by Eric Stice, a neuroscientist at the Oregon Research Institute in Eugene. Stice has been trying to predict a person’s propensity to junk food addiction. He has been watching how people’s brains respond when they are fed a brief burst of creamy chocolate milkshake. He then compares the brain activity of lean and obese individuals, to see if it differs.
In an as-yet-unpublished study he found that when fed milkshakes, lean adolescents with obese parents experienced a greater surge of dopamine – indicating a greater sense of satisfaction – than those who had lean parents. Stice suspects that this is where the problem begins. “There are people born for whom eating is just more orgasmic,” he says. It is this innate enjoyment of food that primes certain people to overeat.
Ironically, as they overeat, their reward circuitry dulls, which makes the food less satisfying and motivates them to eat more to compensate. They are essentially chasing the high of earlier heavenly eating experiences. This is precisely what we see with chronic alcohol or substance abuse, says Stice.
Stice has also shown that people with certain variants of the DRD2 and DRD4 genes are endowed with less active dopamine circuits, and as a result have a dulled dopamine response when eating appetizing foods. Paradoxically, this places them at greater risk of obesity than a person without those gene variants because it means they have to eat more to get a sufficiently rewarding level of dopamine release (Science, vol 322, p 449; NeuroImage, vol 50, p 1618).
Together, these studies suggest there are two routes to food addiction corresponding to overactive or underactive dopamine systems, respectively: one if you find food more rewarding than the average person, and another if it isn’t rewarding enough.
Of course, fast food is more than just a sugar rush, it is often a rich cocktail of sugars, fats and salt. Neuroscientist Paul Kenny at The Scripps Research Institute in Jupiter, Florida, is probing the impact of a junk food diet on rat behavior and brain chemistry. One of his recent studies showed that these foods trigger the same changes in the brain as those caused by drug addiction in humans.
In animals, as in humans, repeated cocaine or heroin use dulls the brain’s reward system. This leads to heavier use because the memory of a more pleasurable effect spurs the user to take more to get the same feeling, essentially chasing the high.
Kenny wondered whether rats that eat junk food would have a similar response to the cocaine-addicted rats he had already studied. He used three groups of rats. The first was a control group that only had access to standard rat feed. The second group could eat junk food – bacon, sausage, icing and chocolate – for only 1 hour each day with regular rat feed and water available for the rest of the time. The third group had an all-you-can-eat, around-the-clock buffet that included junk food and rat feed. After 40 days, Kenny stopped access to the junk food in both experimental groups. The rats with unlimited access to junk food essentially went on a hunger strike. “It was as if they had become averse to the healthy food,” says Kenny. It took two weeks before the animals began eating as much as those in the control group.
Unlimited access to a powerfully addictive drug like cocaine has a big impact on the brain, says Kenny, so you might expect any addictive effect from food to be much less pronounced. But that is not the case. “Changes happened rapidly and we really saw very, very, striking effects. That’s what surprised me.”
The obese, unlimited junk food rats had dulled reward systems and were compulsive eaters. They would even tolerate electric shocks to their feet designed to deter them from eating junk food when the rat feed was still available shock-free. Cocaine-addicted rats behave the same way towards their drug.
When Kenny examined the brains of the obese rats with the unlimited junk food diet, they too had a dopamine deficiency in their striatum, similar to the obese individuals in Wang’s study in humans. In the rats’ brains, Kenny noticed there was a marked drop in a particular dopamine receptor, called D2. But it wasn’t clear whether this drop affected a rat’s propensity to become addicted to junk food.
To test the relevance of D2 receptors, he artificially reduced their number in the brains of a group of rats and then offered them only junk food for two weeks. The effect was dramatic. Compared to the control group offered the same diet, the reward circuitry in the brains of the modified rats showed a dulled response almost immediately. Unlike normal rats, they gorged on junk food even when eating it was penalized with an electric shock. Crucially, rats with reduced D2 receptors fed only regular rat food did not show the same change in their reward circuitry (Nature Neuroscience, vol 13, p 635). It seems there is an interaction between reduced D2 receptors and consumption of junk food that leads to addiction, says Kenny.
Taken together with Stice and Wang’s results, this suggests that people who from birth have a low number of D2 receptors could also be prone to junk-food addiction. Kenny cautions that more studies in humans are needed before the conclusion can be generalized beyond rats.
Gold says there is plenty of evidence that food and drug addiction are so similar that treatments proven safe and effective for other addictions – such as alcohol, nicotine, cocaine and heroin – should be tested for food addiction too. “The real test of the ‘hedonic eating’ or food addiction hypothesis is if it can yield new and effective treatments,” he says.
What some people claim is now beyond doubt is that junk foods rich in salt, sugar and fat switch on biological mechanisms that are just as powerful, and hard to fight, as drugs of abuse. Given that we regulate drugs because of the harms they can cause, is it time to begin tougher regulation of fast food too?
John Banzhaf, a lawyer who teaches public interest law at George Washington University Law School in Washington DC, has been following the research for the last decade. In the 1960s, he won a court ruling that forced radio and TV stations across the US to provide free airtime for anti-smoking messages and played a major role in crafting lawsuits against the tobacco industry. Now he is turning his attention to the fast food industry and its role in fueling the obesity epidemic.
Banzhaf believes there is now enough research for the US Office of the Surgeon General to issue a report on food addiction, as it did for nicotine addiction in 1988. “The Health Consequences of Smoking: Nicotine Addiction”, a report weighing in at over 600 pages, concluded that cigarettes were addictive, nicotine was the cause, and that the chemical and behavioral processes that define heroine and cocaine addiction were the same for tobacco. “At that point people began to accept it,” Banzhaf says. But he acknowledges this is going to be a tricky fight. “Fast food isn’t a [single] chemical so you can’t meaningfully ask the question ‘Is a triple bacon cheeseburger addictive?’ ” he says. It would have to be something more specific about quantities of sugar, salt and fat.
Kelly Brownell, director of the Rudd Center for Food Policy and Obesity at Yale University, says that scientists would be likely to agree that low levels of addiction do occur. It is these low levels, Brownell argues, that are of real concern. It is easy to identify obese people who need help with their food addiction, what is more difficult to see is the slim people who are addicted and may eventually become obese because of their addiction. “Long term, that’s what’s effecting public health – it’s the healthy-looking kid who needs three Cokes a day, not the person who already weighs 400 pounds [180 kilograms].”
Signs of things to come can already be seen across the US. For example, trans fats were recently banned in restaurants in New York City and throughout California, and fizzy drinks are being voluntarily taken out of some school vending machines in anticipation of a law that will mandate it.
Unsurprisingly, the food and drink industry is putting up a fight. These foods are only addictive to a “certain subset of consumers who don’t exhibit the discipline required”, says Hank Cardello, a former executive at food companies including Coca Cola and General Mills, and now a visiting fellow at the Hudson Institute, a think tank based in Washington DC. “People aren’t going to change their behavior. To me it’s about getting calories off the streets.”
Discounting waste, spoilage and returns, the food available to us today is about 30 per cent higher in calories compared with 1970, says Cardello. He believes tax relief for companies producing low-calorie foods is one way to reduce calories consumed without destroying the companies that sell fast food.
Cardello says food companies don’t design food to be addictive, but admits many products are designed for “high hedonic value”, with carefully balanced combinations of salt, sugar and fat that, experience has shown, induce people to eat more.
Kessler points out that, of course, the ultimate power is in the consumers’ hands. Individuals have a responsibility to protect themselves, he says. I can vouch for the fact that it is possible to break the habit. After two weeks of going cold turkey, I can report I have successfully kicked my ice cream habit. Now, if only I could kick my junk TV addiction…
New Scientist, Bijal Trivedi is a writer based in Washington DC
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Twenty years ago, Archaeologists discovered a ship created In 130 BC from wood of walnut trees and bulging with a cargo hold of medicinal pills and Syrian glassware, that sank off the coast of Tuscany Italy.
For the first time archaeobotanists have been able to examine and analyze the pills that were prepared by the physicians of ancient Greece. DNA analysis show that each millennia old tablet is a mixture of more than ten different plant extracts; from hibiscus to celery. Most of the medicines are still completely dry according to Robert Fleischer of the Smithsonian’s National Zoological Park in Washington, D.C.
“For the first time, we have physical evidence of what we have in writing from the ancient Greek physicians Dioscorides and Galen,” stated Alain Touwaide of the Smithsonian Institution’s National Museum of Natural History in Washington, D.C.
Fleischer analysed DNA fragments in two of the pills and compared the sequences to the GenBank genetic database maintained by the U.S. National Institutes of Health. He was able to identify: carrot, radish, celery, wild onion, oak, cabbage, alfalfa and yarrow. He also found hibiscus extract that was probably imported from east Asia or the lands of present day India or Ethiopia.
“Most of these plants are known to have been used by the ancients to treat sick people,” says Fleischer. Yarrow staunched the flow of blood from wounds, and Pedanius Dioscorides, a physician and pharmacologist in Rome in the first century AD, described the carrot as a panacea for a number of problems. “They say that reptiles do not harm people who have taken it in advance; it also aids conception,” he wrote around 60 AD.
The concoctions also provided the archaeobotanists a few surprises. Preliminary analysis suggest they contain sunflower, a plant that is not thought to have existed in the Old World before Europeans discovered the Americas in the 1400s. If the finding is confirmed, botanists may need to revise the traditional history of the plant and its diffusion, says Touwaide – but it’s impossible for now to be sure that the sunflower in the pills isn’t simply from recent contamination.
Drugs described by Dioscorides and another Greek physician known as Galen of Pergamon have often been dismissed as ineffectual quackery. “Scholars and scientists have often dismissed the literature on such medicines, and expressed doubt about their possible efficacy, which they attributed only to the presence of opium,” says Touwaide. He hopes to resolve this debate by exploring whether the plant extracts in the pills are now known to treat illnesses effectively.
He also hopes to discover therian, a medicine described by Galen in the second century AD that contains more than 80 different plant extracts and document the exact measurements ancient doctors used to manufacture the pills. “Who knows, these ancient medicines could open new paths for pharmacological research,” says Touwaide.
The team presented their findings at the Fourth International Symposium on Biomolecular Archaeology in Copenhagen, Denmark.
Casey Kazan via http://greece.greekreporter.com/2010/09/10/2000-year-old-pills-found-in-greek-shipwreck/
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Some 50 years ago, Australian physician John Cade observed the calming effect that lithium had on small animals. After testing the safety of lithium on himself, Cade ventured to try it on people suffering from the wild mood swings of manic depression.
Millions of prescriptions later, lithium remains the most popular choice for treating manic depression, although scientists do not understand how it quells mania or relieves depression. “It’s still a mystery,” says De-Maw Chuang of the National Institute of Mental Health in Bethesda, Md.
Now, there’s a new clue to this riddle. Chuang and his colleagues have found that lithium protects brain cells from being stimulated to death by glutamate, one of the many chemicals that transmit messages in the brain.
The new data suggest that lithium may calm overexcited areas of the brain or, more provocatively, preserve the life of brain cells whose presence guards against manic depression.
This finding “potentially contributes a lot to the field,” says Husseini K. Manji of Wayne State University in Detroit. “If we could figure out how lithium works, we could theoretically come up with better drugs and perhaps understand what’s going on in manic depression.”
Chuang and his colleagues tested the response of various types of rat brain cells to glutamate. Many normal cells and cells soaked in lithium for only a day died from a form of suicide that often results when this neurotransmitter over-stimulates a brain cell.
Yet rat brain cells soaked in lithium for about a week committed suicide much more rarely when exposed to glutamate, Chuang’s group reports in the Proceedings of the National Academy of Sciences. The effect was seen in cells from several brain regions.
The delay in protection is particularly striking, notes Manji, since a hallmark of lithium therapy is that it can take a week or longer to benefit people. Consequently, scientists have been looking for the long-term actions of lithium on brain cells.
Chuang’s team also examined the role of the NMDA receptor, the cell surface protein that glutamate binds to when it excites a cell. While cells soaked in lithium for a week had as many NMDA receptors as untreated cells, the treated cells responded differently.
Normally, activation of the NMDA receptor by glutamate triggers an influx of calcium ions, setting off a signaling cascade inside cells. However, cells soaked in lithium for a week let in far less calcium when exposed to glutamate.
In people with manic depression, lithium may correct a dysfunction of the NMDA receptor by limiting calcium influx, speculates Chuang.
Both Chuang and Manji also note that a small body of evidence suggests that people with mania or depression may lose brain cells. Lithium may thwart that cell death, they say. Indeed, Manji has some evidence that lithium-treated cells eventually begin to overproduce a protein that stymies the cell’s internal suicide program.
If lithium protects brain cells from death by glutamate over-stimulation, it may have uses beyond manic depression. This form of cell death occurs in strokes and in Alzheimer’s, Parkinson’s, and Huntington’s diseases. Chuang is investigating whether lithium protects mice from similar neurodegenerative illnesses.